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[ { "answer_id": 23111, "body": "<p>1) Where are you measuring the temperature for the \"blood\" temperature versus \"core\" temperature?</p>\n\n<p>Blood is used, as you have mentioned, to transmit excess heat to superficial capillary beds, but in cases of hypothermia blood is preferentially directed towards the vital organs at the expense of the periphery. If you are measuring the core temperature (typically bladder temperature in someone critically ill, but could also be rectal or esophageal), then that is the temperature of that body area. All of the fluid within that area (inside and outside of the cells of the organs and tissues, including blood) is at approximately that temperature. If you are measuring temperature peripherally, you may get vastly different readings depending upon physical activity, environmental conditions, etc.</p>\n\n<p>2) Heat is generated through metabolism. In a very controlled manner, we do actually \"burn\" the food we eat into energy, carbon dioxide, water, and some other minor compounds during starvation when protein is broken down for energy. When at rest from a physical activity standpoint, the vast majority of this energy is generated in the \"core\" and typically this is the temperature our body attempts to regulate with relatively small variation. Water moving throughout the body conducts this heat from relatively warmer areas to relatively cooler areas, essentially equalizing this temperature within the \"core\" compartment.</p>\n\n<p>3) If friction in the blood was to be a significant source of heat then, given how delicate the solid components of blood are, people could not continue to exist. Increased physical force, due to microscopic fibrin thrombus formation, causes utter destruction of the red blood cells during disseminated intravascular coagulation (DIC), which leads to the typical microscopic appearance on a blood smear (shattered red blood cells or schistocytes).</p>\n", "score": 1 } ]

[ "blood", "body-temperature" ]

[ { "answer_id": 23102, "body": "<p>Short answer: it depends on the virus!</p>\n\n<p>For example, during the early stages of an acute HIV-infection in humans the virus will double every 0.65 days for a median of 14 days until it reaches a peak viral load. After this peak, the viral load will decrease at a half-life of 1.2 days until a steady-state is reached (Ribeiro et al., 2010)</p>\n\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2876646/pdf/0127-10.pdf\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2876646/pdf/0127-10.pdf</a></p>\n", "score": 1 }, { "answer_id": 23108, "body": "<p>As the saying goes &quot;it depends&quot;, but actually on quite a few factors: the virus strain, the host, and specific cells of the host, and the time frame considered <a href=\"https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0074863\" rel=\"nofollow noreferrer\">e.g.</a>:</p>\n<blockquote>\n<p>Influenza viruses exhibit large, strain-dependent differences in pathogenicity in mammalian hosts. Although the characteristics of severe disease, including uncontrolled viral replication, infection of the lower airway, and highly inflammatory cytokine responses have been extensively documented, the specific virulence mechanisms that distinguish highly pathogenic strains remain elusive. In this study, we focused on the early events in influenza infection, measuring the growth rate of three strains of varying pathogenicity in the mouse airway epithelium and simultaneously examining the global host transcriptional response over the first 24 hours. <strong>Although all strains replicated equally rapidly over the first viral life-cycle, their growth rates in both lung and tracheal tissue strongly diverged at later times, resulting in nearly 10-fold differences in viral load by 24 hours following infection.</strong> We identified separate networks of genes in both the lung and tracheal tissues whose rapid up-regulation at early time points by specific strains correlated with a reduced viral replication rate of those strains.</p>\n</blockquote>\n<p>So your question is not terribly easy to answer by a simple figure without establishing a time frame, cells of interest etc. But if you somehow care about that initial rate of replication, before any differences are observed across influenza strains...</p>\n<blockquote>\n<p>Remarkably, all three strains showed profiles of essentially identical, aggressive replication in the respiratory tract over the first 12 hours with the levels of viral M gene increasing by &gt;1000x (Figure 3 A and C). At 16 hours, however, the replication rates started to diverge with the low pathogenicity X31 lagging behind that of the high pathogenicity PR8 and VN strains. Over the next 32 hours, the quantity of X31 in the lung remained essentially constant while that of PR8 and VN continued to increase, reaching levels approximately 5x higher by 48 hours (Figure 3 C). In the trachea, as in the lung, all three strains replicated equally rapidly over the first 8 hours, with the M gene levels increasing approximately 100x (Figure 3B). From 8 hours onward however, the levels of VN remained constant while PR8 and X31 continued to grow rapidly with M gene levels increasing by more than 20x over the next 12 hours (Figure 3D). Importantly, the viral load measurements in the lungs and tracheas were performed in the same individuals, demonstrating the large, tissue-specific differences in replication rates between these three strains.</p>\n<p><a href=\"https://i.stack.imgur.com/MK6uz.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/MK6uz.png\" alt=\"enter image description here\" /></a></p>\n</blockquote>\n<p>So, more that 1000-fold replication within the first 12 hours for influenza in mice lungs (the most suitable cells), but only about 100-fold in the less suitable trachea cells (where replication differences between strains are also observed somewhat earlier, after 8 hours).</p>\n<p>Virus quantification was done by <a href=\"https://en.wikipedia.org/wiki/Virus_quantification#Quantitative_polymerase_chain_reaction_(qPCR)\" rel=\"nofollow noreferrer\">qPCR</a> in this study.</p>\n", "score": 1 } ]

[ "virus" ]

[ { "answer_id": 23198, "body": "<h3>PHE</h3>\n\n<p>12-4-2020 84279 - 78891 = 5388</p>\n\n<p>11-4-2020 78891 - 70272 = 8619</p>\n\n<p>10-4-2020 70272 - 65077 = 5195</p>\n\n<h3>ECDC</h3>\n\n<p>12-4-2020 8719</p>\n\n<p>11-4-2020 5195</p>\n\n<p>10-4-2020 4344</p>\n\n<p>It looks like the PHE data is a day ahead of the ECDC data</p>\n", "score": 2 } ]

[ "covid-19", "coronavirus", "healthcare-data", "database", "covid-19-datasets" ]

[ { "answer_id": 23201, "body": "<p>The care for a COVID-19 patient is totally different from that of a patient with other forms of pneumonia. A COVID-19 patient is highly contagious, and is able to aerosolize large amounts of potentially lethal virions into the environment infecting other hospital patients and staff. This happens particularly in intubation. These patients need to be treated in rooms quarantined from other patients, or, shared only with other COVID-19 patients.</p>\n\n<p>The care of a COVID-19 patient also involves the use of PPE. There is a huge shortage of PPE in a large numbers of countries especially in epicentres where people have been resorting to wearing trash bags to help protect them from infection. PPE has traditionally been disposable between patients but the shortage of PPE has meant that it has been reserved just for use when working with patients with known COVID-19, and been reused.</p>\n\n<p>These are three nurses from Northwick Park, London, a centre of clinical excellence.</p>\n\n<p><img src=\"https://video-images.vice.com/test-uploads/articles/5e8f02279a053c009d7a87b5/lede/1586434223278-ETpjugsXgAUl_og.jpeg\" alt=\"\"></p>\n\n<p>wearing trash bags as protection, and using surgical masks instead of N95 masks. All three nurses subsequently contracted COVID-19.</p>\n\n<p>Early in the disease in some countries medical staff had to be stood down for self isolation when they had unprotected contact with COVID-19 patients. And estimates range from 20-80% of COVID-19 patients are asymptomatic which means testing needs to be done.</p>\n\n<p><a href=\"https://www.vice.com/en_us/article/dygbdz/these-nurses-had-to-wear-trash-bags-as-ppe-now-they-have-coronavirus\" rel=\"nofollow noreferrer\">https://www.vice.com/en_us/article/dygbdz/these-nurses-had-to-wear-trash-bags-as-ppe-now-they-have-coronavirus</a></p>\n", "score": 3 }, { "answer_id": 23212, "body": "<p>This q is based on fairly incorrect premises e.g.</p>\n<blockquote>\n<p>why are governments primarily spending their testing capacity on those admitted to hospitals or otherwise in critical condition?</p>\n<p>[...]</p>\n<p>once a patient is in a hospital with breathing difficulties... what good does a test do?</p>\n</blockquote>\n<p>There seems to be a conflation here that &quot;admitted to hospitals&quot; is (nearly) always &quot;in critical condition&quot; and likewise that &quot;with breathing difficulties&quot; somehow also equates &quot;in critical condition&quot; <em>and</em> a Covid-19 diagnosis.</p>\n<p>Besides HCW safety, addressed in Dr. Chiu's answer, there's an obvious reason to test someone with &quot;breathing difficulties&quot; (for Covid-19) to establish a differential diagnosis. I think first a diagnosis of what the breathing difficulties actually are is done, e.g. is it pneumonia? Second, the guidelines for further diagnosing the serious cases of pneumonia generally recommend establishing the actual pathogen, <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5473649/\" rel=\"nofollow noreferrer\">e.g.</a>:</p>\n<blockquote>\n<p>Optimal treatment of lung infections relies on rapid and accurate detection of the offending pathogen. Delay in diagnosis can lead to increased morbidity and mortality.</p>\n</blockquote>\n<p>See also <a href=\"https://medicalsciences.stackexchange.com/questions/22913/use-of-antibiotics-with-chest-infections\">Use of antibiotics with chest infections</a> for a bit more detailed discussion on this.</p>\n<p>Additionally, early in the epidemic, <a href=\"https://journals.sagepub.com/doi/pdf/10.1177/0846537120913033\" rel=\"nofollow noreferrer\">evidence from China (Mar 4)</a> was that [their] virus tests were actually rather insensitive, i.e. they could only detect high viral loads:</p>\n<blockquote>\n<p>In the initial screening, computed tomography (CT) examination is needed for the auxiliary diagnosis. The diagnosis is\nthen confirmed by the positive results of the nucleic acid amplification test (NAAT) of the respiratory tract or blood specimens\nusing reverse transcription real-time fluorescence polymerase\nchain reaction (RT-PCR). However, this diagnosis method is\nhighly limited: (1) <strong>When the viral load is low, the detection rate\nis low, leading to false-negative results.</strong> (2) Only a positive\ndiagnosis can be made, but the severity of COVID-19 and its\nprogression cannot be judged (in contrast, CT imaging can\nreveal disease progression). (3) The supply of the reagents\ncannot keep up with the demand, and the quality of new products of major companies awaits to be studied and improved. (4)\nIt takes 1 day or longer to obtain the results after sampling. For\nthese reasons, <strong>Chinese researchers strongly recommend CT\nimaging as the main basis for the diagnosis of COVID-19 in\nthe current situation</strong>.</p>\n</blockquote>\n<p>So in such circumstances (low-sensitivity tests) the virus tests probably aren't even very useful for the mild cases, so &quot;saving&quot; [such insensitive] tests for these mild case is basically completely pointless.</p>\n<p>(See also related q here on that latter issue: <a href=\"https://medicalsciences.stackexchange.com/questions/23126/why-were-so-many-covid-19-negative-tests-among-close-contacts-of-the-early-chine\">Why were so many Covid-19 negative tests among close contacts of the early Chinese cases?</a> )</p>\n", "score": 1 } ]

[ "covid-19" ]

[ { "answer_id": 23341, "body": "<p>It has been previously observed that the SARS-CoV-2 virus was relatively stable at 1 mutation a month. However, recent studies, and the one you refer to suggest that this is incorrect.</p>\n\n<blockquote>\n <p>Based on current data, it seems as though SARS-CoV-2 mutates much more slowly than the seasonal flu. Specifically, SARS-CoV-2 seems to have a mutation rate of less than 25 mutations per year, whereas the seasonal flu has a mutation rate of almost 50 mutations per year.</p>\n</blockquote>\n\n<p>based on data stored at <a href=\"https://www.gisaid.org/\" rel=\"nofollow noreferrer\">Gisaid</a></p>\n\n<p>However, a paper just released on the 19th April 2020 lead by Li Lanjuan (it was on her advice that the city of Wuhan was quarantined ) based on 11 early samples taken from patients in Zhejiang at the beginning of the pandemic show otherwise. These patients had close travel links to Wuhan</p>\n\n<blockquote>\n <p>Professor Li Lanjuan and her colleagues from Zhejiang University found within a small pool of patients many mutations not previously reported. These mutations included changes so rare that scientists had never considered they might occur.</p>\n</blockquote>\n\n<p>and </p>\n\n<blockquote>\n <p>Li’s team detected more than 30 mutations. Among them 19 mutations – or about 60 per cent – were new.\n They found some of these mutations could lead to functional changes in the virus’ spike protein, a unique structure over the viral envelope enabling the coronavirus to bind with human cells. Computer simulation predicted that these mutations would increase its infectivity.</p>\n \n <p>To verify the theory, Li and colleagues infected cells with strains carrying different mutations. The most aggressive strains could generate 270 times as much viral load as the weakest type. These strains also killed the cells the fastest.</p>\n \n <p>It was an unexpected result from fewer than a dozen patients, “indicating that the true diversity of the viral strains is still largely underappreciated,” Li wrote in the paper.</p>\n</blockquote>\n\n<p>So, different mutations were found in the same patients, and different degrees of lethality when tested against cell cultures.</p>\n\n<p>They think this may explain why differing populations have been experiencing different degrees of disease severity across the world. These mutations had not been noticed before because the genomes published on worldwide databases were established using standard techniques</p>\n\n<blockquote>\n <p>Most of these samples, though, were sequenced by a standard approach that could generate a result quickly. The genes were read just once, for instance, and there was room for mistakes.</p>\n</blockquote>\n\n<p>But Li's team did deep sequencing to pick up these mutations</p>\n\n<blockquote>\n <p>Li’s team used a more sophisticated method known as ultra-deep sequencing. Each building block of the virus genome was read more than 100 times, allowing the researchers to see changes that could have been overlooked by the conventional approach.</p>\n</blockquote>\n\n<p><a href=\"https://www.livescience.com/coronavirus-mutation-rate.html\" rel=\"nofollow noreferrer\">https://www.livescience.com/coronavirus-mutation-rate.html</a></p>\n\n<p><a href=\"https://www.scmp.com/news/china/science/article/3080771/coronavirus-mutations-affect-deadliness-strains-chinese-study\" rel=\"nofollow noreferrer\">https://www.scmp.com/news/china/science/article/3080771/coronavirus-mutations-affect-deadliness-strains-chinese-study</a></p>\n\n<p>Patient-derived mutations impact pathogenicity of SARS-CoV-2\n<a href=\"https://www.medrxiv.org/content/10.1101/2020.04.14.20060160v1\" rel=\"nofollow noreferrer\">https://www.medrxiv.org/content/10.1101/2020.04.14.20060160v1</a></p>\n", "score": 1 } ]

[ "covid-19", "virus", "sars-cov-2", "non-pharmaceutical-interventions", "regulatory-agencies" ]

[ { "answer_id": 23288, "body": "<p>X-rays normally contain identification <a href=\"https://en.wikipedia.org/wiki/X-ray_marker\" rel=\"nofollow noreferrer\">markers</a> to indicate the side, the date, possibly name and other information. It looks like you've cut part of the x-rays off but it looks like there's a treating MD's name at the top. </p>\n\n<p>The date could be 9th August 1939, and the 1636 a clinic ID or something else. It's not a timestamp as it's the same in both x-rays. The L means left arm.</p>\n\n<p>It clearly is an x-ray of a <a href=\"https://bmcmusculoskeletdisord.biomedcentral.com/articles/10.1186/1471-2474-13-6\" rel=\"nofollow noreferrer\">greenstick fracture</a> of the distal radius in a child, because the epiphyses have not yet fused.</p>\n", "score": 4 } ]

[ "orthopedics", "x-rays" ]

[ { "answer_id": 23307, "body": "<p>Those are face shields to prevent primarily droplets reaching the eyes, and are worn as being more comfortable than goggles to protect the mucous membranes of the eyes, and they don't fog up like goggles can. However, they don't protect against droplet nuclei which float in the air, and there is no regulated design.</p>\n\n<blockquote>\n <p>Face shields are PPE that are commonly used as barrier protection for infection control purposes by numerous workers. There currently is no standard regarding face/eye protection from biological hazards and this deficit needs to be remedied as quickly as possible. Due to the lack of a good facial seal peripherally that can allow for aerosol penetration, face shields should not be used as solitary face/eye protection, but rather as adjunctive to other PPE (protective facemasks, goggles, etc.). Given the dearth of available data regarding the appropriate use of face shields for infection control, scientifically sound research needs to be conducted on the use of this form of PPE.</p>\n</blockquote>\n\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5015006/\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5015006/</a></p>\n", "score": 3 } ]

[ "covid-19", "air-quality", "face-mask-respirator", "personal-protective-equipment", "protection" ]

[ { "answer_id": 23358, "body": "<p>These viruses sit in animal populations and are transferred to humans by mosquitoes</p>\n\n<blockquote>\n <p>Flaviviruses are responsible for a growing disease burden in Argentina and other countries in the Americas. Non-human primates, such as monkeys, can be important hosts in the natural cycle of several flaviviruses. Yellow Fever virus outbreaks occurred in Argentina during 2007–2009 in areas of Misiones and Corrientes provinces inhabited by black howlers (Alouatta caraya), a monkey that is highly susceptible to the virus. During 2010 we tested 108 black howlers from Northeastern Argentina for flaviviruses. Most of these animals were negative for Yellow Fever virus but had antibodies to several other flaviviruses. Unexpectedly, the highest specific neutralizing antibody prevalence was to West Nile Virus; these results represent the first evidence of West Nile Virus circulation in a new host in Argentina. Detection of <strong>Dengue virus antibodies in black howlers</strong> highlights the potential for establishment of a dengue sylvatic cycle, not yet demonstrated in the Americas. We call for strengthening the monitoring of flaviviruses to evaluate risk for wildlife and human health in the region.</p>\n</blockquote>\n\n<p><a href=\"https://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.0005351\" rel=\"nofollow noreferrer\">https://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.0005351</a></p>\n", "score": 2 } ]

[ "virus" ]

[ { "answer_id": 23363, "body": "<p>This calculator suggests that the antibody tests aren't too bad in that they're suggesting that the official figures are way too low.</p>\n\n<p><a href=\"https://gabgoh.github.io/COVID/index.html\" rel=\"nofollow noreferrer\">https://gabgoh.github.io/COVID/index.html</a></p>\n\n<p>The first death in California was on the 6th Feb 2020 which means the disease was likely introduced in mid-January 2020.</p>\n\n<p>Assume a case fatality ratio of 0.014 (In NZ We have had 1116 cases, and 16 deaths)</p>\n\n<p>Infectious from day 3, R0 of 5.7 (worst case scenario reported so far)</p>\n\n<p>Population of 40M in California</p>\n\n<p>And lock down was 66 days later on 21st March 2020</p>\n\n<p>Then by day 40 (24th Feb 2020) you are seeing over 20M cases in California - so 50% of the population gets exposed at day 40. So, the true numbers lie somewhere between.</p>\n\n<p><a href=\"https://time.com/5825320/california-coronavirus-february-first-death/\" rel=\"nofollow noreferrer\">https://time.com/5825320/california-coronavirus-february-first-death/</a></p>\n", "score": 1 } ]

[ "covid-19", "test", "antibodies" ]

[ { "answer_id": 23404, "body": "<p>I think you're confused by what is meant as a genetic disease. A disease like <a href=\"https://en.wikipedia.org/wiki/Huntington%27s_disease\" rel=\"nofollow noreferrer\">Huntingdon's Chorea</a> is a genetic disease because we know the genetics, and we know that it occurs due to mutation in an autosomal dominant gene so the chance of inheritance is 50% with almost 100% penetrance.</p>\n\n<p>Diseases like T2DM have a genetic basis so that we know some groups are way more susceptible than others.</p>\n\n<blockquote>\n <p>The large variation in prevalence rates of type 2 diabetes among ethnic groups living in similar environments, the increased risk to siblings of affected individuals, and the high concordance rate for the disease in monozygotic twins compared with dizygotic twins indicate that this disease has a significant genetic component (rev. in 6). Studies in twins, and particularly in twins reared apart, have also produced high heritability estimates for BMI, ranging between 0.6 and 0.9 (7). However, the extent to which this familial aggregation reflects a small number of genes with major effects, a large number of genes each with small effect (polygenic inheritance), and environmental factors shared among family members remains unknown. For example, certain aspects of the intrauterine environment, such as the blood supply from the placenta, are shared more strongly between monozygotic compared with dizygotic twins, and intrauterine effects are known to have a significant impact on the future development of diabetes (8).</p>\n</blockquote>\n\n<p>but we don't consider it 100% genetic because for many if not most people it can be prevented by an appropriate life style, and it's the change in lifestyles that have caused the current epidemics of this disease.</p>\n\n<p><a href=\"https://diabetes.diabetesjournals.org/content/53/5/1181\" rel=\"nofollow noreferrer\">https://diabetes.diabetesjournals.org/content/53/5/1181</a></p>\n\n<p><a href=\"https://pubmed.ncbi.nlm.nih.gov/17098087/\" rel=\"nofollow noreferrer\">https://pubmed.ncbi.nlm.nih.gov/17098087/</a></p>\n", "score": 2 } ]

[ "diabetes", "genetics", "type-2-diabetes", "cause-and-effect", "insulin-resistance" ]

[ { "answer_id": 23386, "body": "<p>The paper is here <a href=\"https://www.scribd.com/document/456897616/DHSST#fullscreen&amp;from_embed\" rel=\"nofollow noreferrer\">https://www.scribd.com/document/456897616/DHSST#fullscreen&amp;from_embed</a></p>\n\n<p>It doesn't say but I presume that the Department of Homeland Security knows what sunlight is.</p>\n", "score": 1 } ]

[ "covid-19", "research", "sars-cov-2", "sunlight", "united-states" ]

[ { "answer_id": 23468, "body": "<p>The causes of <a href=\"https://www.mayoclinic.org/diseases-conditions/kawasaki-disease/symptoms-causes/syc-20354598\" rel=\"nofollow noreferrer\">Kawasaki disease/syndrome</a> are not well understood.</p>\n\n<p>Kawasaki involves inflammation of blood vessels, and is rare but almost exclusively found in young children.</p>\n\n<p>There are <a href=\"https://www.cnn.com/2020/04/27/health/children-covid-19-illness-intl-scli-gbr/index.html\" rel=\"nofollow noreferrer\">media reports</a> of associations of Kawasaki and COVID-19 but these are fairly early reports and it is unlikely (and I am unaware of any) that there are any sufficiently large samples of cases that have been organized to suggest a true causal role: these alerts are best directed towards physicians to be aware of the possibility when examining patients rather than to the general public.</p>\n", "score": 2 } ]

[ "covid-19" ]

[ { "answer_id": 23492, "body": "<p>These additives are required to get correct results.\nThey keep the blood from clotting. If blood is collected with a syringe, clotting factors will activate and this will give inaccurate results for clottingfactors and platelets, and possibly other tests as well.</p>\n", "score": 2 }, { "answer_id": 23509, "body": "<p>The article you linked calls those three additives <a href=\"https://en.m.wikipedia.org/wiki/Anticoagulant\" rel=\"nofollow noreferrer\">anticoagulants</a>, and provides a link to a page on that. It starts:</p>\n\n<blockquote>\n <p>Anticoagulants, commonly known as blood thinners, are chemical substances that prevent or reduce coagulation of blood, prolonging the clotting time.</p>\n</blockquote>\n\n<p>If you put blood in a glass tube, or most plastic tubes, it clots to a solid quite quickly. (<a href=\"https://en.m.wikipedia.org/wiki/Clotting_time\" rel=\"nofollow noreferrer\">A few minutes on glass</a> at body temperature.) This makes it impossible to test for anything related to clotting (since those factors may have been used up) and frankly difficult to test for anything else because you have a blob of jelly or even something the consistency of cheese, so you can't pour it, stir a reagent into it, and so on.</p>\n\n<p>To overcome this difficulty, someone went to a lot of trouble to invent a tube that would keep air out, and would have specific additives in it that wouldn't themselves interfere with the testing. I expect the exact details of how much of each additive, which tests are still accurate with heparin and which are not, which are ok with EDTA and which are not, and so on, would fill a book. For the purposes of your question, we can say yes, the additives are necessary for some tests, and that is why people use them.</p>\n", "score": 2 } ]

[ "blood-tests" ]

[ { "answer_id": 23591, "body": "<p>\"Its correlates\" refers to \"anything that correlates with depression/TRD\".</p>\n\n<p>They don't specify what those correlates are (though you could link the statement to the next one talking about bipolar disorder), but it could indeed include related disorders and conditions (such as anxiety disorders and substance abuse). It could also refer to surrogate measures or symptoms rather than particular diagnoses. It's a broadly worded call for further study.</p>\n", "score": 1 } ]

[ "terminology", "clinical-study" ]

[ { "answer_id": 23616, "body": "<p>The purpose of lock downs is to enforce social distancing and other measures to break the chain of disease transmission. There is no data to suggest that has occurred yet in the USA. </p>\n\n<p>Many countries that have employed mandatory lockdown have successfully contained the virus and stopped community transmission. China was the first successful example of this though there has now been a small outbreak of 6 cases in a residential compound in Wuhan, and the city of Shulan is in lockdown with 3 new cases reported. China has also just ordered the <a href=\"https://www.businessinsider.com.au/coronavirus-wuhan-orders-all-residents-tested-six-new-cases-2020-5?r=US&amp;IR=T\" rel=\"nofollow noreferrer\">testing of the 11 million residents</a> of Wuhan.</p>\n\n<p>Taiwan managed to contain the pandemic without lockdown but used early border controls, aggressive quarantine, and contact tracing as well as other social policies. They had 7 deaths in a population just larger than Sweden.</p>\n\n<p>New Zealand is emerging out of lockdown with people being allowed to return to work from tomorrow. 0 - 3 cases daily have been reported in the last week. NZ has had 20 deaths in a population of 5M. Sweden, which did not enforce lockdown, but relied on the public to adopt voluntary social distancing, has had 3,300 deaths with twice the population size. If you calculate the rate for the USA using Sweden as the basis, you would expect to see 33 * 3,300 = 108,900 deaths but so far the number of deaths has been 83,000 approx. So, as the USA eases its lockdown policies without evidence of controlling the chain of transmission, expect to see many more deaths.</p>\n\n<p><a href=\"https://www.dw.com/en/taiwan-coronavirus/a-52724523\" rel=\"nofollow noreferrer\">https://www.dw.com/en/taiwan-coronavirus/a-52724523</a><br>\n<a href=\"https://medicalxpress.com/news/2020-05-china-wuhan-virus-infection-month.html\" rel=\"nofollow noreferrer\">https://medicalxpress.com/news/2020-05-china-wuhan-virus-infection-month.html</a><br>\n<a href=\"https://en.wikipedia.org/wiki/COVID-19_pandemic_in_Sweden\" rel=\"nofollow noreferrer\">https://en.wikipedia.org/wiki/COVID-19_pandemic_in_Sweden</a></p>\n", "score": 3 } ]

[ "covid-19" ]

[ { "answer_id": 23629, "body": "<p>I can't find the CDC page you allude to, but I suppose you've read something <a href=\"https://waterandhealth.org/disinfect/cleaning-vs-disinfecting-whats-difference/\" rel=\"nofollow noreferrer\">like this</a>:</p>\n<blockquote>\n<p>Cleaning, accomplished with soap–or detergent–and water, refers to the physical removal of dirt and grime, and in the process, some portion of the germs on a given surface. Sometimes cleaning tools, including sponges and cloths, simply move germs from one surface to another. Disinfecting, on the other hand, refers to killing a high percentage of the germs on a surface or rendering them incapable of reproducing.</p>\n<p>Sanitizing is another relevant term in this discussion. [...] sanitizing lowers the number of germs on surfaces to a safe level, as judged by public health standards or requirements. The process works by either cleaning or disinfection to reduce the risk of spreading infection. Finally, sterilizing destroys all forms of microbial life and is used mainly in healthcare and laboratory settings. [...]</p>\n<p>If disinfecting a surface is the task at hand—for example, you might be tackling a food preparation counter that has just contacted raw meat or fish—the order of operations is important. Just remember “C” (cleaning) comes before “D” (disinfection).</p>\n</blockquote>\n<p>The point is largely that if you do it &quot;the other way around&quot; you risk actually [re-]contaminating the surfaces, e.g. with a sponge that isn't so clean. And as Bryan Krause says, a heavy buildup might not even be penetrated sufficiently in the decontamination step.</p>\n<p>Depending on the target virus, that page recommended various times for leaving the disinfectant (bleach) on the surface, e.g. flu for 10 minutes at the concentration they suggested, and for norovirus &quot;until dry&quot;. Also, after bleach disinfection</p>\n<blockquote>\n<p>If object is intended for food or mouth contact, rinse with plain water before using.</p>\n</blockquote>\n<p>This is because bleach leaves a solid residue that may still contain active substance(s).</p>\n<hr />\n<p>Having said that, it's not impossible to disinfect your hands, but you have to use a product that's suitable for skin use, <a href=\"https://www.ncbi.nlm.nih.gov/books/NBK507853/\" rel=\"nofollow noreferrer\">e.g.</a>:</p>\n<ul>\n<li>chlorhexidine</li>\n<li>&quot;iodine&quot; (iodopovidone)</li>\n<li>hydrogen peroxide</li>\n<li>alcohols (at high enough concentration), although this source says they only have &quot;minor activity against some viruses&quot;.</li>\n</ul>\n<p>And some more listed there... with a discussion of the most suitable pathogens; the ones I've picked above were mentioned as reasonably effective against viruses. (Some of these give burning sensation if you have any cuts or scrapes.)</p>\n<p>Regarding disinfection of hands, the CDC <a href=\"https://www.cdc.gov/handwashing/show-me-the-science-hand-sanitizer.html\" rel=\"nofollow noreferrer\">says</a> that in general</p>\n<blockquote>\n<p>Many studies show that hand sanitizers work well in clinical settings like hospitals, where hands come into contact with germs but generally are not heavily soiled or greasy. Some data also show that hand sanitizers may work well against certain types of germs on slightly soiled hands. However, hands may become very greasy or soiled in community settings, such as after people handle food, play sports, work in the garden, or go camping or fishing. When hands are heavily soiled or greasy, hand sanitizers may not work well. Handwashing with soap and water is recommended in such circumstances.</p>\n</blockquote>\n<p>Interestingly, that CDC page is heavily in favor of alcohol(s) as a general hand disinfectant, although it only talks about &quot;germs&quot; in general, without getting into sub-categories like viruses, bacteria etc.</p>\n", "score": 2 } ]

[ "disinfection" ]

[ { "answer_id": 24434, "body": "<p>A good way to understand the 5 levels that are described in the paper might be to go to a website that presents information on the entire ICD-9 and permits the user to “click though” the levels of codes. Here is a good place to do this.</p>\n<p><a href=\"http://icd9.chrisendres.com/index.php\" rel=\"nofollow noreferrer\">http://icd9.chrisendres.com/index.php</a></p>\n<p>The hierarchy for the ICD-9 includes first the choice to classify based on Diseases and Injuries or on Procedures. Both are part of the ICD-9 Classification System. This &quot;choice&quot; is (unintuitively) the first level.</p>\n<p>Thus, using terminology in the paper, Level 1 is Diseases and Injuries (as opposed to Procedures). Level 2 is the Chapter where each chapter includes a large block of codes all of which mostly share the same first digit and pertain to an organ system (13 chapters) or another way to logically group diseases and conditions. Level 3 is a block of grouped three digit codes where the grouping reflects similar disease processes within the organ system. Level 4 is a specific three digit code for one disease or a set of related diseases or conditions within the Level 3 block. Level 5 is defined by the digits to the right of the decimal place of the Level 4 three digit code and comprises closely related but different diseases or conditions.</p>\n<p>In the example given in the cited paper,</p>\n<p>Level 1 is: Diseases and Injuries (not Procedures)</p>\n<p>Level 2 is: Chapter 17. INJURY AND POISONING (800-999)</p>\n<p>Level 3 is: OTHER AND UNSPECIFIED EFFECTS OF EXTERNAL CAUSES (990-995)</p>\n<p>Level 4 is: 992 Effects of heat and light</p>\n<p>Level 5 is: 992.0-992.8 (multiple codes. For 992, all have 1 digit to right of the decimal place but some three digit--level 4--codes have two digits to the right of the decimal place and some have no digits to the right of the decimal place)</p>\n", "score": 2 } ]

[ "icd-intrntl-classif-disea" ]

[ { "answer_id": 23735, "body": "<p>The CDC advice is pretty clear as to staying inside your own group</p>\n<blockquote>\n<p>Do: Stay 6 feet away from others (“social distancing”) and take other steps to prevent COVID-19</p>\n<p>If a park, beach, or recreational facility is open for public use, visiting is okay as long as you practice social distancing and everyday steps such as washing hands often and covering coughs and sneezes. Follow these actions when visiting a park, beach, or recreational facility:</p>\n<p>Stay at least six feet from others at all times. This might make some open areas, trails, and paths better to use. Do not go into a crowded area</p>\n<p><strong>Avoid gathering with others outside of your household</strong></p>\n<p>Wash hands often with soap and water for at least 20 seconds, especially after going to the bathroom, before eating, and after blowing your nose, coughing, or sneezing</p>\n<p>Bring hand sanitizer with at least 60% alcohol to use if soap and water are not available.</p>\n</blockquote>\n<p><a href=\"https://www.cdc.gov/coronavirus/2019-ncov/daily-life-coping/visitors.html\" rel=\"nofollow noreferrer\">https://www.cdc.gov/coronavirus/2019-ncov/daily-life-coping/visitors.html</a></p>\n", "score": 1 } ]

[ "covid-19", "disease-transmission", "prevention", "infectious-diseases" ]

[ { "answer_id": 23905, "body": "<p>In this pandemic it is important to take precautions at each and every step. Fruits and vegetables should be properly cleaned.\nWe don't know of fruit/vegetables vendors, who might be infected with COVID-19.\nEventhough there is no as such a scientific proof <a href=\"https://www.msn.com/en-us/health/nutrition/can-coronavirus-be-transmitted-via-fresh-fruits-and-vegetables/ar-BB10Kdu3\" rel=\"nofollow noreferrer\">that corona virus can spread through food</a></p>\n<p>But what's wrong in taking precautions and cleaning them properly?\nNow according to an <a href=\"https://www.researchgate.net/profile/John_Cluett/post/Are_there_studies_of_the_Effect_of_Social_Media_Memes_on_COVID_19_Information/attachment/5ed76d8739f1f30001614dd6/AS%3A898273850175490%401591176583828/download/Food+Safety+and+COVID-19++Precautionary+measures+to+limit+the+spread+of+COVID19+in+supply+chain+and+retail.pdf\" rel=\"nofollow noreferrer\">article</a> fruits and vegetables may be washed in chlorine, however chlorine changes their tastes.</p>\n<p>As you mentioned washing them in running water for 20 seconds extra, is a recommend method by the WHO. However there are news to wash them in baking soda, potassium permanganate, etc but none of the methods have been scientifically proven. <a href=\"https://www-thehindu-com.cdn.ampproject.org/v/s/www.thehindu.com/sci-tech/health/covid-19-how-to-handle-packaging-and-produce-when-you-are-back-from-your-grocery-run/article31501251.ece/amp/?amp_js_v=a3&amp;amp_gsa=1&amp;usqp=mq331AQFKAGwASA%3D#aoh=15921521223146&amp;referrer=https%3A%2F%2Fwww.google.com&amp;amp_tf=From%20%251%24s&amp;ampshare=https%3A%2F%2Fwww.thehindu.com%2Fsci-tech%2Fhealth%2Fcovid-19-how-to-handle-packaging-and-produce-when-you-are-back-from-your-grocery-run%2Farticle31501251.ece\" rel=\"nofollow noreferrer\">Newspaper</a></p>\n<p>Also there are ultrasonic cleaners and vegetable washer, however they can be used for your peace of mind but in actual there is no need. Washing them in running water is <a href=\"https://www.eatthis.com/how-to-wash-vegetables-fruit/\" rel=\"nofollow noreferrer\">enough</a></p>\n<p>Also rinsing them with soap is not a good idea, as there’s the danger of ingesting soap, which can cause gastrointestinal distress leading to vomiting and diarrhoea when consumed in large <a href=\"https://www-thehindu-com.cdn.ampproject.org/v/s/www.thehindu.com/sci-tech/health/covid-19-how-to-handle-packaging-and-produce-when-you-are-back-from-your-grocery-run/article31501251.ece/amp/?amp_js_v=a3&amp;amp_gsa=1&amp;usqp=mq331AQFKAGwASA%3D#aoh=15921521223146&amp;referrer=https%3A%2F%2Fwww.google.com&amp;amp_tf=From%20%251%24s&amp;ampshare=https%3A%2F%2Fwww.thehindu.com%2Fsci-tech%2Fhealth%2Fcovid-19-how-to-handle-packaging-and-produce-when-you-are-back-from-your-grocery-run%2Farticle31501251.ece\" rel=\"nofollow noreferrer\">quantities</a></p>\n<p>I hope I have answered your question :)</p>\n", "score": 3 } ]

[ "covid-19", "food-safety", "prevention", "disinfection" ]

[ { "answer_id": 23819, "body": "<p>I am not familiar with the particular media you have referenced, but there are many suture techniques that have been taught to generations of medical students from Ethicon (a manufacturer of sutures) with their <a href=\"http://surgsoc.org.au/wp-content/uploads/2014/03/Ethicon-Knot-Tying-Manual.pdf\" rel=\"nofollow noreferrer\">Knot Tying Manual</a>.</p>\n\n<p>As someone credentialed in many surgical procedures, but not actually a surgeon, I will admit that neither of the terms used are things I would consider uttering. However, what I believe would be referred to as a \"stick tie\" is actually a ligature suture where the bleeding vessel is clamped with a hemostat and a loop of suture is tied around the tip of the hemostat (see page 27 of the link above). In my practice of emergency medicine, the much more common method of ligation for bleeding vessels is a figure-of-eight suture. It is very infrequent for someone such as myself to be able to actually grab a large vessel with hemostats and to be the person to definitively manage the wound.</p>\n", "score": 2 } ]

[ "terminology", "sutures" ]

[ { "answer_id": 23885, "body": "<p>Copying from <a href=\"https://biology.stackexchange.com/questions/92770/why-do-some-viruses-cease-being-a-problem-even-though-no-vaccine-or-cure-is-foun/92776#92776\">another SE answer by me</a>:</p>\n\n<blockquote>\n <p>The elimination of SARS from the human population occurred via controlling the human-to-human spread through isolation and contact tracing. See <a href=\"https://apps.who.int/iris/handle/10665/70863\" rel=\"nofollow noreferrer\">https://apps.who.int/iris/handle/10665/70863</a> for a report on the epidemic and how cases and spread in different locations were handled.</p>\n</blockquote>\n\n<p>SARS was more severe overall, such that there was much less asymptomatic/presymptomatic spread like is observed with SARS-nCoV-2/COVID-19. It was therefore easier to identify and isolate the infected individuals, and to trace their contacts and isolate those people as well. The case fatality rate was much higher, unfortunately, but the lack of widespread transmission kept the number of affected individuals to a manageable scope. The WHO report in the link above goes into more detail on both the SARS epidemiology as well as the public health response.</p>\n", "score": 1 } ]

[ "coronavirus", "epidemiology" ]

[ { "answer_id": 23907, "body": "<p>ATP (adenosine triphosphate) is used by the cells as a source of energy. When you are awake, the brain cells use a lot of energy, and ATP is quickly consumed, and it becomes AMP (adenosine monophosphate).</p>\n\n<p>One decay product of AMP is adenosine. So, the more your \"fuel\" is running out, the more adenosine has accumulated. So high adenosine is a signal for the body to sleep.</p>\n\n<p>When you sleep, the activity in the body, and in particular the brain, is much lower, and is redirected from active functions (thinking, moving, eating, etc.) to passive function, and in particular regenerative functions. This is an opportunity for the body to concentrate on stockpiling ATP, and clean up adenosine.</p>\n\n<p>Source: <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3246291/\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3246291/</a></p>\n", "score": 2 }, { "answer_id": 23909, "body": "<p>To add additional information to the other answer, adenosine (<a href=\"https://doi.org/10.1007/s002469900129\" rel=\"nofollow noreferrer\">as a drug</a>) does not require anything for metabolism other than enzymes typically <a href=\"https://doi.org/10.1016/0014-2999(83)90026-2\" rel=\"nofollow noreferrer\">present in blood</a>. There are some genetic factors that interfere with this metabolism, and from personal practice it makes for a rather uncomfortable moment.</p>\n\n<p>Also, adenosine is not a neurotransmitter (directly signaling another neuron to cause depolarization), but <a href=\"https://doi.org/10.1073/pnas.89.18.8586\" rel=\"nofollow noreferrer\">it does inhibit neurotransmitter release</a> (and is therefore typically referred to as a neuromodulator in this capacity).</p>\n\n<p>Furthermore, adenosine triphosphate (ATP), as noted in the other answer, is quickly consumed. The body, without normal processes ongoing to replete the stores of ATP, will very rapidly run out of ATP (in the most vital tissues to life, such as brain and heart, within a matter of minutes). Without ATP, life is not possible. This is actually the process involved with what we call <a href=\"https://doi.org/10.1113/jphysiol.1947.sp004202\" rel=\"nofollow noreferrer\">rigor mortis</a>. When muscle cells run out of ATP (which, interestingly, is required to relax muscle tension) the body of the deceased person stiffens and remains so until the muscle proteins involved in contraction are degraded by enzymes.</p>\n", "score": 2 } ]

[ "sleep", "endocrinology", "metabolism" ]

[ { "answer_id": 24835, "body": "<p>This means that the diagnosis has been made and is present. As for whether it is a common phrase, this might depend on where you are looking: pubmed.gov does find the phrase, while scholar.google.com does (e. g.: <a href=\"https://scholar.google.com/scholar?hl=en&amp;as_sdt=0%2C5&amp;q=%22presence+of+a+diagnosis%22&amp;btnG=\" rel=\"nofollow noreferrer\">https://scholar.google.com/scholar?hl=en&amp;as_sdt=0%2C5&amp;q=%22presence+of+a+diagnosis%22&amp;btnG=</a>).</p>\n", "score": 2 } ]

[ "terminology" ]

[ { "answer_id": 23958, "body": "<p>The murmur from HOCM is from the mitral valve leaflet jamming into the septum, also called systolic anterior motion (SAM). This disappears when you increase the volume of LV because if you increase the volume, the ventricle becomes more distended and the leaflet is further away from the septum, so you have less murmur that can be heard.</p>\n<p>MVP murmur decreases during squatting because if you increase the volume in LV, there is more tension on the chordae tendinae so the leaflets can't prolapse as much.</p>\n", "score": 4 } ]

[ "heart", "cardiac-physiology" ]

[ { "answer_id": 23955, "body": "<p>The authors are fitting a regression model. It is common in regression with factors as predictors to consider one level of the factor as a &quot;reference&quot; level. Every other variable in the model expresses some difference relative to that reference level.</p>\n<p>Ultimately the choice of reference doesn't matter that much for the model, as long as appropriate comparisons are made, but it does help you understand how the numbers in the paper combine to get a result for a particular population.</p>\n", "score": 1 } ]

[ "cancer", "terminology", "clinical-study" ]

[ { "answer_id": 24041, "body": "<p>Yes it is most certainly possible.</p>\n<p>Glucose can be metabolised to glycogen, but it can also be metabolised to fatty acids and triglycerides.</p>\n<p>Glucose is converted into Acetyl-CoA through the anaerobic glycolysis, and Acetyl-CoA is used for the synthesis of fatty acids. An intermediate product of the anaerobic glycolysis is glycerinaldehyde-3-phosphate, which can be converted into glycerol and then be used as the backbone for triglycerides, which in turn can be stored in adipocytes and lead to increased weight. <a href=\"http://www2.csudh.edu/nsturm/CHE452/07_Fat%20Met-%20Overv.%20Synth.htm\" rel=\"nofollow noreferrer\">This graphic gives a good overview of the metabolism pathways.</a></p>\n<p>As a side note regarding &quot;<em>my understanding is that glucose can only be utilized immediately by body</em>&quot;, glucose can also be used to synthesise ribose through the pentose-phosphate pathway, and ribose can be used to synthesise DNA among other important molecules. Acetyl-CoA is also used for steroid and cholesterol synthesis.</p>\n", "score": 2 } ]

[ "nutrition", "diet", "weight", "sugar", "glucose" ]

[ { "answer_id": 24051, "body": "<blockquote>\n<p>This implies to me that there will be some sort of genetic signature attached to the virus by the person acting as a vector.</p>\n</blockquote>\n<p>The <em>people</em> don't attach anything to the virus, but the viral genome <em>does not stay constant</em>, it accumulates small changes. Those changes are only passed on to people from where the change originally occurs, other copies of the virus in different people don't change with it.</p>\n<p>Some of these changes could have effects on the properties of the virus (making it spread better or worse, cause more mild or severe illness), and changes that substantially damage the virus's ability to replicate and spread will tend to disappear by natural selection. However, many of the changes don't do much at all, for example they might be synonymous mutations via <a href=\"https://en.wikipedia.org/wiki/Codon_degeneracy\" rel=\"nofollow noreferrer\">codon degeneracy</a>, or they may change viral proteins or expression in ways that have modest effects.</p>\n<p>If you were to sample a population (say, in Victoria AU) and found everyone infected there had a pretty similar version of the virus, with the same differences relative to other circulating strains, that would be good evidence that they all got the virus from a similar origin: maybe one person spread it to others, who spread it to others, and so on.</p>\n<p>If, however, you sample a population and find three different strains: one that looks similar to viruses sequenced in the UK, one that looks similar to viruses sequenced in China, one that looks similar to viruses sequenced in Iran, it is more likely that each of those strains came (directly or indirectly) from a traveler from those places. If the security guard story is true, you'd also expect to find different guards with different strains, and then find strains in their communities that match each of the guards (this is assuming you did a whole lot of sequencing, which may or may not be feasible).</p>\n<p>The alternative would be that one person brought in a strain of the virus that then happened to randomly mutate to look similar to viruses from all those other places; the chances of that are very very slim.</p>\n<p>This is basically the same principle as paternity testing; though using a different type of genetic tool, it relies on genomes in the same lineage being more similar than one would expect by chance.</p>\n<p>There is a tool helpful for tracking/visualizing some of these changes throughout the pandemic: <a href=\"https://nextstrain.org/ncov/global\" rel=\"nofollow noreferrer\">https://nextstrain.org/ncov/global</a></p>\n", "score": 2 } ]

[ "covid-19", "epidemiology", "genetics" ]

[ { "answer_id": 24069, "body": "<p>The skin of a caucasian-skinned person with cyanosis <em>is</em> described as bluish, but <a href=\"https://osuwomeninphysics.wordpress.com/2015/03/11/everyday-physics-why-do-veins-look-blue/\" rel=\"nofollow noreferrer\">it is still more reddish than blue</a>. The bluish jumps out at us in comparison with healthy well-oxygenated blood.</p>\n<p>The colors we see are the product of the incoming light, and the proportion of the wavelengths that are absorbed, scattered, or reflected. Because skin and arteries/capillaries/veins are translucent, there's normally quite a bit of red light scattering and reflection going on. However when looking at veins or cyanotic skin, there's less reflection of the red wavelengths, and the skin looks darker and bluer than we're used to.</p>\n<p>If you look at a photograph of <a href=\"https://www.firstaidforfree.com/what-is-cyanosis/\" rel=\"nofollow noreferrer\">someone with Raynaud's or cyanotic hands,</a> you'll see that there's still quite a bit of red!</p>\n", "score": 1 } ]

[ "pathophysiology" ]

[ { "answer_id": 24202, "body": "<p>In mammalian cells the gene NKX2-5 is found on chromosome 5, more specifically on the long (q) arm of chromosome 5 at position 35.1. (Cytogenetic Location: 5q35.1)</p>\n<p>NKX2-5 is ~3,213 nucleotide bases long and is involved in biological processes that give an organism its shape. Disruption of NKX2-5 has proven to cause abnormal heart shape.</p>\n<p>More information can be found: <a href=\"https://geneticsperspective.blogspot.com/2020/04/nkx2-5-gene-overview.html\" rel=\"nofollow noreferrer\">here</a></p>\n", "score": 0 } ]

[ "cardiology", "genetics", "development-disorder" ]

[ { "answer_id": 24276, "body": "<blockquote>\n<p>The two major forms [of vitamin D] are vitamin D2 and vitamin D3. Vitamin D2 (ergocalciferol) is largely human-made and added to foods, whereas vitamin D3 (cholecalciferol) is synthesized in the skin of humans from 7-dehydrocholesterol and is also consumed in the diet via the intake of animal-based foods. [...] The differences do not affect metabolism (i.e., activation), and both forms function as prohormones. When activated, the D2 and D3 forms have been reported to exhibit identical responses in the body <a href=\"https://www.nap.edu/read/13050/chapter/5\" rel=\"nofollow noreferrer\">DRI - Institute of Medicine of the National Academies</a></p>\n</blockquote>\n<p>with that being said, in the same text we can find that</p>\n<blockquote>\n<p>There are a few naturally occurring food sources of vitamin D. These include fatty fish [such as salmon, tuna, and mackerel], fish liver oil, and egg yolk. Some foods are, however, fortified with vitamin D.</p>\n</blockquote>\n<p>for example in the United States, fluid milk is voluntarily fortified with 400 IU per quart</p>\n<p>The Food and Nutition Board has established the Recommended Dietary Allowances (RDA) to make nutrient recommendations <a href=\"https://www.ncbi.nlm.nih.gov/books/NBK56068/table/summarytables.t2/?report=objectonly\" rel=\"nofollow noreferrer\">Dietary Reference Intakes (DRIs)</a></p>\n", "score": 1 } ]

[ "vitamin-d" ]

[ { "answer_id": 24300, "body": "<p>For now the vaccines are in testing, and to some extent some validation of their efficacy will probably be necessary.</p>\n<p>Phase 1 trials check whether it is safe to check on efficacy of a drug, phase 2 trials check whether there is any efficacy. So by phase 2 trials some kind of testing needs to be on this (more details here: <a href=\"https://en.wikipedia.org/wiki/Phases_of_clinical_research\" rel=\"nofollow noreferrer\">https://en.wikipedia.org/wiki/Phases_of_clinical_research</a>).</p>\n<p>For some vaccines antibody levels (or surrogates) have been the measure of efficacy (see also here: <a href=\"https://www.immune.org.nz/vaccines/efficiency-effectiveness#:%7E:text=Vaccine%20immunogenicity%20is%20a%20measure,has%20been%20correlated%20with%20protection.\" rel=\"nofollow noreferrer\">https://www.immune.org.nz/vaccines/efficiency-effectiveness#:~:text=Vaccine%20immunogenicity%20is%20a%20measure,has%20been%20correlated%20with%20protection.</a>).</p>\n", "score": 1 } ]

[ "vaccination" ]

[ { "answer_id": 25012, "body": "<p>Since no one has responded, I offer the following information as far as I have been able to find out myself.</p>\n<p>There does not appear to be an official list of candidate drugs designated for RMAT at the moment. This means that until the drug is finally approved, we have to trust the news or the applicant's self-reporting.</p>\n<p>I've made a concerted effort to find that list on the FDA's website, but I cannot find any list of RMATs. Only the number of RMATs by status appears to be officially available to the public<a href=\"https://www.fda.gov/vaccines-blood-biologics/cellular-gene-therapy-products/cumulative-cber-regenerative-medicine-advanced-therapy-rmat-designation-requests-received-fiscal\" rel=\"nofollow noreferrer\">■</a>.</p>\n<p>One <a href=\"https://ipscell.com/rmat-list/\" rel=\"nofollow noreferrer\">unofficial list</a> says;</p>\n<blockquote>\n<p>Here is a list of firms/products that have self-reported that they have received FDA regenerative medicine advanced therapy designation or RMAT.<br>＜omit＞<br> Note that the FDA has recently updated it’s RMAT totals to indicate that it has approved 52 RMATs as of mid-2020 so about 8 are not in the public domain.</p>\n</blockquote>\n<p>They, also seem to have made the list by checking the press release by the applicant against the <a href=\"https://www.fda.gov/vaccines-blood-biologics/cellular-gene-therapy-products/cumulative-cber-regenerative-medicine-advanced-therapy-rmat-designation-requests-received-fiscal\" rel=\"nofollow noreferrer\">total number</a> released by the FDA.</p>\n<p>Note that <strong>being designated/approved as an RMAT</strong> and <strong>being approved as a regenerative medicine</strong> are different things. The former merely gives them the right to simplify the review process. The latter seems to mean that the product has received permission to be sold in the US. A list of products approved for use in regenerative medicine can be found <a href=\"https://www.fda.gov/vaccines-blood-biologics/cellular-gene-therapy-products/approved-cellular-and-gene-therapy-products\" rel=\"nofollow noreferrer\">here</a>.</p>\n<p><strong>So how many candidate drugs have been approved as regenerative medicine products via the RMAT way at this point?</strong> <br>\nThe following description was found in this <a href=\"https://www.rhoworld.com/rmat-designationwhat-is-it-and-is-it-right-for-your-therapeutic-product/\" rel=\"nofollow noreferrer\">article</a>.</p>\n<blockquote>\n<p>Although the Agency has granted 52 RMAT awards as noted in the table above, as of 30 June 2020, none of the products had received approval yet.</p>\n</blockquote>\n<p>However, I did not know how many of these were in clinical trials or under review and how many were jugged as Refusal to File (RTF).</p>\n", "score": 0 } ]

[ "clinical-study", "reference-request", "regulatory-agencies" ]

[ { "answer_id": 24369, "body": "<p>mirtazapine has a somewhat complex pharmacodynamic's: acts as an antagonist of the presynaptic alpha-2 autoreceptor and increases the release of both norepinephrine and seratonin; it is an antagonist of the 5-HT2 and 5-HT3 receptors; and it acts as a potent H1 antagonist, which is associated with the sedative effects of the drug.</p>\n<p>olanzapine, is a second-generation antispychotics antagonist of 5HT2a and D2 receptors.</p>\n<p>According to <a href=\"https://www.drugs.com/mtm/mesalamine.html\" rel=\"nofollow noreferrer\">drugs.com</a>:</p>\n<blockquote>\n<p>Mesalamine affects a substance in the body that causes inflammation, tissue damage, and diarrhea. Mesalamine is used to treat mild to moderate ulcerative colitis. Mesalamine is also used to prevent the symptoms of ulcerative colitis from recurring.</p>\n</blockquote>\n<p><strong>Interactions</strong></p>\n<p>Major drug to drug interactions: mirtazapine is metabolized by several CYP450 enzymes (2D6, 3A4, 1A2). Therefore, drugs that inhibit these isoenzymes may cause an increase of mirtazapine levels (the same logic is applied to olanzapine). Also, the sedative effects of mirtazapine can be cumulative with CNS depressants, such as alcohol and benzodiazepines.</p>\n<p>Minor interactions: according to <a href=\"https://www.drugs.com/drug-interactions/mirtazapine-with-olanzapine-1640-0-1744-0.html\" rel=\"nofollow noreferrer\">drugs.com</a> there is in fact an interaction between mirtazapine and olanzapine</p>\n<blockquote>\n<p>can increase the risk of an irregular heart rhythm that may be serious and potentially life-threatening, although it is a relatively rare side effect.</p>\n</blockquote>\n<p>(can't find any bibliographic reference to support this conclusion though)</p>\n<p>as much I was able to ascertain mesalamine does not interact with neither olanzapine nor mirtazapine.</p>\n<p><strong>References:</strong> basic and clinical pharmacology</p>\n", "score": 1 } ]

[ "medications" ]

[ { "answer_id": 24362, "body": "<p>Definitive manuals, or textbooks for drug interactions tend not to be published on their own any longer, due to their need to be constantly updated, and having been superseded by better ways to search for the information required, in a digital format. OR - they are tremendously expensive, like <a href=\"https://www.pharmpress.com/product/9780857113474/stockley\" rel=\"nofollow noreferrer\">this</a>. Otherwise, drug interactions and adverse reactions are integrated into clinical pharmacology textbooks such as Rang and Dale.</p>\n<p>Other study books, such as <a href=\"https://www.amazon.co.uk/Top-100-Drugs-Pharmacology-Prescribing/dp/070207442X/ref=sr_1_1?dchild=1&amp;keywords=prescribing&amp;qid=1596656972&amp;sr=8-1\" rel=\"nofollow noreferrer\">this</a>, do have commonly prescribed drugs with major interactions listed per each drugs.</p>\n<p>In the United Kingdom, we tend to use the British National Formulary (BNF) which is given to all doctors in a paper-copy, but is also online - <a href=\"https://bnf.nice.org.uk/\" rel=\"nofollow noreferrer\">here</a> which has a fully searchable interactions section. It can be bought in paper copy <a href=\"https://www.amazon.co.uk/British-National-Formulary-September-2020/dp/0857113690/ref=sr_1_1?dchild=1&amp;keywords=formulary&amp;qid=1596657102&amp;sr=8-1\" rel=\"nofollow noreferrer\">here</a> - but it's not a good study book, it's a reference for working prescribers.</p>\n<p><a href=\"https://www.drugs.com/\" rel=\"nofollow noreferrer\">https://www.drugs.com/</a> is reliable, an USA-based, with an interactions - but is again a website.</p>\n<p>If you want to let us know what specifically you are revising for, or what you need it for - perhaps we'll be able to point you to a more specific book. :)</p>\n", "score": 2 }, { "answer_id": 24366, "body": "<p>One of the most well-known books dedicated to drug interactions and serving as a comprehensive reference for this topic specifically is <a href=\"https://www.pharmpress.com/product/9780857113474/stockley\" rel=\"nofollow noreferrer\">Stockley's Drug Interactions</a>. You can find a sample chapter <a href=\"https://www.pharmpress.com/files/docs/Stockleys_Drug_Interactions_11_Sample.pdf\" rel=\"nofollow noreferrer\">here</a>.</p>\n<p>Highly recommended!</p>\n", "score": 1 } ]

[ "medications" ]

[ { "answer_id": 24412, "body": "<p>While you seem to be asking several questions in this thread, I will try to answer them as well as I can.</p>\n<blockquote>\n<p>Is chronic fatigue syndrome a symptom of myocarditis?</p>\n</blockquote>\n<p>No, chronic fatigue syndrome can not be a symptom of myocarditis because CFS is a specific, separate medical condition that is pathophysiologically understood to be neurological, immunological, or endocrine in nature. Moreover, CFS is a chronic condition, while myocarditis is (mostly) an acute illness. A better question could be: &quot;Are CFS and myocarditis etiologically similar?&quot;</p>\n<blockquote>\n<p>because both these conditions can be induced by Epstein-Barr and enterovirus, and because both are debilitating conditions for which attempts to exercise can actually be harmful, I find myself wondering how much they have in common.</p>\n</blockquote>\n<p>While this is true, there are plenty of other causes for myocarditis (e.g., other viruses, bacteria, autoimmune disease, toxins like alcohol or heavy metals, etc.). The reason why exercise can be harmful in these patients is inherently different. While CFS patients usually just experience a subjective worsening of their symptoms, myocarditis patients suffer from heart failure due to their typically reduced ejection fraction, leading to a potentially fatal arrhythmia.</p>\n<blockquote>\n<p>Possibly TNF-alpha could be involved in the initial stimulus?</p>\n</blockquote>\n<p>It most certainly is. <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2883509/\" rel=\"nofollow noreferrer\">Research</a> has <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC548425/\" rel=\"nofollow noreferrer\">shown</a> that TNF-alpha promotes myocarditis, which comes at no surprise since TNF-alpha is a cytokine that is virtually ubiquitous in all inflammation involving macrophages, T-cells and NK cells.</p>\n<blockquote>\n<p>Could that signal that the heart is damaged and direct a &quot;lock-down&quot; of all activities requiring increased circulation?</p>\n</blockquote>\n<p>There is no real &quot;lock-down&quot; of activities requiring increased circulation in myocarditis; your heart just does not pump enough blood due to the muscle tissue being inflamed. Loss of function (&quot;functio laesa&quot;) was identified by Galen as a sign of <em>all</em> inflammation. It is understood to be either a neurological response to pain, or caused by swollen tissue inhibiting movement, or both. All this is not exclusive to myocarditis, but rather the final common path of all inflammation.</p>\n<p>I hope this helps to answer your questions!</p>\n", "score": 1 } ]

[ "covid-19", "heart" ]

[ { "answer_id": 24466, "body": "<p>The National Research Council has explained that:</p>\n<p>“Precision Medicine refers to the tailoring of medical treatment to the individual characteristics of each patient. It does not literally mean the creation of drugs or medical devices that are unique to a patient, but rather the ability to classify individuals into subpopulations that differ in their susceptibility to a particular disease, in the biology or prognosis of those diseases they may develop, or in their response to a specific treatment.”</p>\n<p>WIKIPEDIA accessed 8/17/2020</p>\n<p>National Research Council (US) Committee on A Framework for Developing a New Taxonomy of Disease. Toward Precision Medicine: Building a Knowledge Network for Biomedical Research and a New Taxonomy of Disease. Washington (DC): National Academies Press (US); 2011. PMID: 22536618. Appendix E. Glossary. Precision Medicine</p>\n<p>“Precision” treatments—ones that might work better in a particular subpopulation--still need to be studied to see if they do work better in a particular subpopulation. Some of these studies might involve use of a placebo.</p>\n<p>There are, however, some (a few) “precision” treatments that have been developed to treat a single patient. A good account of the development of a precision treatment for a single patient is given in a lay journal.</p>\n<p><a href=\"https://www.clinicalomics.com/topics/precision-medicine-topic/bch-n-of-1-trial-yields-approved-therapy-for-single-rare-disease-patient/\" rel=\"nofollow noreferrer\">https://www.clinicalomics.com/topics/precision-medicine-topic/bch-n-of-1-trial-yields-approved-therapy-for-single-rare-disease-patient/</a></p>\n<p>The case is also described in publication in the medical literature.\n<a href=\"https://www.nejm.org/doi/10.1056/NEJMoa1813279\" rel=\"nofollow noreferrer\">https://www.nejm.org/doi/10.1056/NEJMoa1813279</a></p>\n<p>In this instance, the drug to treat a rare condition was identified and tested in this patient in a study called an N-of-1 study. That is, the drug was tested in this and only this patient. The patient improved on the treatment. This N-of-1 study did <strong>not</strong> involve use of a placebo.</p>\n<p>So the answer to your question is “Yes, it is possible (sometimes) to eliminate the use of a placebo when evaluating a treatment that has been developed based on the principles of precision medicine.”</p>\n<p>Note that this patient improved but was not cured by this truly precision treatment. Precision medicine does not always cure a patient.</p>\n", "score": 1 } ]

[ "statistics", "clinical-study", "antibodies", "placebo", "antigen" ]

[ { "answer_id": 24407, "body": "<p>Topical products are applied directly to a part of the body, whereas other products are administered in other (more specific) ways. For example, oral products are used in or around the mouth.</p>\n<p>Snuff is a smokeless tobacco made from ground or pulverised tobacco leaves. Snuff is dry and usually consumed via the nasal route (via the nose) by sniffing it. In the case presented, the snuff is used topically (in hamster cheek pouches), probably in the form of <a href=\"https://en.wikipedia.org/wiki/Snus\" rel=\"nofollow noreferrer\">snus</a> or <a href=\"https://en.wikipedia.org/wiki/Dipping_tobacco\" rel=\"nofollow noreferrer\">dipping tobacco</a>, both of which are wet powdered smokeless tobacco products.</p>\n", "score": 3 }, { "answer_id": 24408, "body": "<p>I think it is a form of tobacco. Since the main etiology for squamous cell carcinoma is tobacco consumption.</p>\n<blockquote>\n<p>Tobacco and alcohol are the two most important known risk factors for the development of oral cancer.\n<a href=\"http://www.indianjcancer.com/article.asp?issn=0019-509X;year=2006;volume=43;issue=2;spage=60;epage=66;aulast=Mehrotra\" rel=\"nofollow noreferrer\">Reference</a></p>\n</blockquote>\n<p>Here is an <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5028589/\" rel=\"nofollow noreferrer\">article</a></p>\n<blockquote>\n<p>Herpes simplex virus (HSV) may enhance the development of oral carcinoma in individuals who are already at increased risk of the disease because of tobacco consumption and cigarette smoking and so must be considered as a possible etiologic agent in oral cancer and precancer.</p>\n</blockquote>\n<p>So yeah, the snuff should be a form of tobacco only.</p>\n<p>Also interestingly I found that study which the Burket's is referring to-\n<a href=\"https://www.sciencedirect.com/topics/medicine-and-dentistry/cheek-pouch\" rel=\"nofollow noreferrer\">Hamster study</a></p>\n", "score": 2 } ]

[ "dentistry", "herpes" ]

[ { "answer_id": 24464, "body": "<p>While visual changes from cataracts are probably more likely, it is possible that zoloft (generic name sertraline) could be causing your improved viion. It would be very unusual, as much more commonly it causes blurred vision rr double vision.</p>\n<p>Visual changes produced by serotonin reuptake inhibitors have become a subject of greater attention in the past few years.</p>\n<p>See\n<em>Antidepressants, Anti-anxiety Meds &amp; Your Eyes</em>\n<a href=\"https://www.bettervisionguide.com/antidepressants-anti-anxiety-meds-your-eyes/\" rel=\"nofollow noreferrer\">https://www.bettervisionguide.com/antidepressants-anti-anxiety-meds-your-eyes/</a></p>\n<p>Monitor the eyes for ocular effects from antidepressants, anti-anxiety medications\n<a href=\"https://www.eyeworld.org/monitor-eyes-ocular-effects-antidepressants-anti-anxiety-medications\" rel=\"nofollow noreferrer\">https://www.eyeworld.org/monitor-eyes-ocular-effects-antidepressants-anti-anxiety-medications</a></p>\n<p><em>Keep an eye on the SSRI: help avoid possible sight-threatening adverse events</em>\n<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4723200/\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4723200/</a></p>\n<p><em>Drugs for the Mind Affect the Eye</em>\n<a href=\"https://www.reviewofoptometry.com/article/drugs-for-the-mind-affect-the-eye\" rel=\"nofollow noreferrer\">https://www.reviewofoptometry.com/article/drugs-for-the-mind-affect-the-eye</a></p>\n<p><em>Ocular Effects of Serotonin Antidepressants</em>\n<a href=\"https://ww2.health.wa.gov.au/-/media/Files/Corporate/general-documents/WATAG/WAPDC/Serotonin-antidepressants-ocular-effects.ashx\" rel=\"nofollow noreferrer\">https://ww2.health.wa.gov.au/-/media/Files/Corporate/general-documents/WATAG/WAPDC/Serotonin-antidepressants-ocular-effects.ashx</a></p>\n<p>These effects are thought to be mediated through anticholinergic mechanisms for some antideressants (tricyclics and partoxetine especially) as well as via serotonergic mechanisms mediated by 5HT2B/C receptors and 5-HT7 autoreceptors in the iris-ciliary bodies.</p>\n<p>sample papers\n<em>Serotonin-2B/2C Receptors Mediate Bovine Ciliary Muscle Contraction: Role in Intraocular Pressure Regulation</em>\n<a href=\"https://www.researchgate.net/publication/322691582_Serotonin-2B2C_Receptors_Mediate_Bovine_Ciliary_Muscle_Contraction_Role_in_Intraocular_Pressure_Regulation\" rel=\"nofollow noreferrer\">https://www.researchgate.net/publication/322691582_Serotonin-2B2C_Receptors_Mediate_Bovine_Ciliary_Muscle_Contraction_Role_in_Intraocular_Pressure_Regulation</a></p>\n<p><em>[3H]-Serotonin Release from Bovine Iris-ciliary Body: Pharmacology of Prejunctional Serotonin (5-HT7) Autoreceptors</em></p>\n<p>Ciliary muscles are also be effected by catecholamines (norepinephrine or dopamine) , and some neuropeptides such as neuropeptide Y are also active which may be modulated indirectly by serotonin.</p>\n<p><em>Morphologic characteristics of the human ciliary muscle</em>\n<a href=\"https://www.sciencedirect.com/science/article/abs/pii/S0014483501910127\" rel=\"nofollow noreferrer\">https://www.sciencedirect.com/science/article/abs/pii/S0014483501910127</a></p>\n<p>Anything that can distort your vision could also correct it, if one's underlying ocular abnormality could be normalized through the action of the drug that usually produces burred vision. It would be highly unusual, but not impossible. If you discontinued sertraline or change to a different medication and your vision problems returned, it would provide further evidence of the link. I do not however, at all recommend going off the medication or switchung to a new medication if sertraline in working well for you just to check your vision. It might be work a trip to the ophthalmologist or optometrist to discuss it though, as well as consider other causes.</p>\n", "score": 1 } ]

[ "side-effects" ]

[ { "answer_id": 24468, "body": "<p>The brain is made up of oxygen-demanding gray matter and myelin-covered white matter.</p>\n<p>Hypoxic events initially damage the gray matter, but myelin is spared. However, new myelin secretion requires ATP-dependent enzymes which is impaired by hypoxic event. Since myelin takes about ~20 days to cycle, this coincides with the biphasic presentation of DPHL. Another theory is that oligodendrocytes (myelin-secreting cells) might have delayed apoptosis after hypoxic event, also leading to lack of new myelin formation once the old myelin degenerates.</p>\n<p>Source:</p>\n<p>Beeskow AB, Oberstadt M, Saur D, Hoffmann KT, Lobsien D. Delayed Post-hypoxic Leukoencephalopathy (DPHL)-An Uncommon Variant of Hypoxic Brain Damage in Adults. Front Neurol. 2018;9:708. Published 2018 Aug 27. doi:10.3389/fneur.2018.00708</p>\n", "score": 1 } ]

[ "brain", "neurology", "brain-damage" ]

[ { "answer_id": 24470, "body": "<p>I found the answer:</p>\n<ul>\n<li>&quot;CYL&quot; in Spherical section, means no correction needed</li>\n<li>&quot;SPH&quot; in Cylindrical section, means no correction needed</li>\n</ul>\n<p>If AXIS is zero, that is shorthand way some O.D.'s use to write 180.</p>\n", "score": 1 } ]

[ "optometry" ]

[ { "answer_id": 24649, "body": "<p>Preeclampsia has to be thought as imbalance in of vascular factors (a theory)\nCorrect way of thinking about Anti VEGF is thinking</p>\n<ul>\n<li>Anti VEGF are secreted by placenta (for unknown reasons),</li>\n<li>Decreased synthesis of PgI2 (vasodilator) and</li>\n<li>increased synthesis of TxA2 (vasoconstrictor) from vascular\nendothelium,</li>\n<li>increased sensitivity to Angiotensin II (pressor agent),</li>\n<li>NO decrease(vasodilator, decreases Plt aggregation, prevent intervillous thrombus)</li>\n<li>Endothelin -1 (vasoconstrictor)</li>\n<li>Inflammatory Cytokines (IL-6, TNF alpha)</li>\n<li>Imbalance of angiogenic and antiangiogenic proteins in placental vascular bed—there is\noverproduction of two antiangiogenic factors from the trophoblastic tissue. These two antiangiogenic\nfactors are: (a) soluble fms-like tyrosine kinase I (SFlt-1) and (b) soluble endoglin. SFlt-1 binds with\nVEGF and placental-like growth factor (PLGF) and causes endothelial cell dysfunction</li>\n</ul>\n<p>The balance of all these factors appears to be disturbed in preeclampsia, of which anti-VEGF is part off. Which means it might actually be responsible for preeclamsia (or rather we should say it is associated with) and <strong>not</strong> to be thought as single factor which is released in response to placental ischemia, it is one of multitude of factors responsible/associated with pathogenesis of preeclampsia.</p>\n<p>Source: DC Dutta textbook of Obstetrics, 8th ed. Pg 257</p>\n", "score": 0 } ]

[ "obstetrics", "pathogenesis" ]

[ { "answer_id": 24511, "body": "<p>On histamine: Histamine causes vasodilation, not vasoconstriction. The amount of histamine blocking agents ingested largely will not counteract the whole effect of histamine, however it may prevent more pronounced side effects that are not appreciated. One of these side effects, by vasodilation and vascular leak is edema. Edema can produce pressure on capillaries and further reduce perfusion of affected areas.\nSome more information on histamine: <a href=\"https://en.wikipedia.org/wiki/Histamine\" rel=\"nofollow noreferrer\">https://en.wikipedia.org/wiki/Histamine</a></p>\n<p>There are some data that hint at what you are suggesting, namely that some growth factors are accelerated by histamine (albeit the paper is on mice):\n<a href=\"https://www.sciencedirect.com/science/article/pii/S0022202X15329146\" rel=\"nofollow noreferrer\">https://www.sciencedirect.com/science/article/pii/S0022202X15329146</a></p>\n<p>A very old paper on the role of histamine in wound healing compared durability of keloid tissue: <a href=\"https://pubmed.ncbi.nlm.nih.gov/1791057/\" rel=\"nofollow noreferrer\">https://pubmed.ncbi.nlm.nih.gov/1791057/</a></p>\n<p>The study did not use OTC antihistamines however; they found though that exogenous histamine applied topically reversed the delayed healing induced by the experimental antihistamine. This may or may not be due to the increased proliferation of cells, growth factors or increased perfusion where previously it was inhibited.</p>\n<p>Finally, in <a href=\"https://en.wikipedia.org/wiki/Wound_healing\" rel=\"nofollow noreferrer\">https://en.wikipedia.org/wiki/Wound_healing</a> it is described how histamine allows inflammation communicating cells etc. to leave blood vessels, which are needed in wound healing e. g. for removal of dead tissue.</p>\n", "score": 3 } ]

[ "immune-system", "antihistamines", "histamine" ]

[ { "answer_id": 24586, "body": "<p>It's possible your news source confused deaths with hospitalizations, confused the cause of death, or that 2018 was particularly bad flu year in Argentina (but I rather doubt that).</p>\n<p>Peer-reviewed, albeit older <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5855154/\" rel=\"nofollow noreferrer\">publications</a> put the flu mortality figures much lower:</p>\n<blockquote>\n<p>During 2002–2009, we estimated that influenza contributed to an average of approximately 2000–9000 deaths and 8000–23,000 hospitalizations in Argentina</p>\n</blockquote>\n<p>And broken down by month</p>\n<p><a href=\"https://i.stack.imgur.com/lvIKp.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/lvIKp.jpg\" alt=\"enter image description here\" /></a></p>\n<p>Also they don't find the mortality substantially different from other American countries:</p>\n<blockquote>\n<p>our mortality rates are similar to those estimated in Argentina during 1992–1999, in neighboring Brazil, and in the United States</p>\n</blockquote>\n<hr />\n<p>I do see in a <a href=\"https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0221479\" rel=\"nofollow noreferrer\">more recent paper</a> some criticism that that older one may underestimate influenza...</p>\n<blockquote>\n<p>Several countries, including Argentina, Chile, and many Central American countries, have used virologic surveillance data to attribute hospitalizations to influenza, as we did in this analysis, but used a smaller subset of “pneumonia and influenza” ICD-10 hospital discharge codes, rather than all respiratory hospitalizations [7, 10, 36]. Using “pneumonia and influenza” hospitalizations likely under-estimated the true respiratory hospitalization burden from influenza, because patients with influenza can present with a wide spectrum of clinical respiratory symptoms, including exacerbations of chronic respiratory conditions [22, 37–40]. Our approach of using all respiratory codes, therefore, generated higher rates compared to the published rates using only “pneumonia and influenza” codes and are likely more inclusive and reflective of the full breadth of conditions seen in patients with influenza.</p>\n</blockquote>\n<p>Howerver, this more rencet paper doesn't estimate mortality, only incidence, and even for that they don't give per-country estimates, except as a (badly colord) <a href=\"https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0221479\" rel=\"nofollow noreferrer\">heat map</a>, on which (to my eye) Argentina seems to have between 10,000 and 50,000 hostpitalized cases (per year).</p>\n<p>So it's possible that the ministry (cited as sourcein that newspaper) changed their methodology, but even given this putative revised methodology, death exceeding hospitalizations seems fairly implausible.</p>\n", "score": 3 } ]

[ "covid-19", "influenza", "mortality-rate" ]

[ { "answer_id": 24548, "body": "<p>With all these vasectomy questions, you might be best off trying to interview a licensed urologist. You're correct that there appears to be very limited clinical research in humans regarding vasectomy in recent literature. From what I can find (<strong>emphasis</strong> mine):</p>\n<blockquote>\n<p><a href=\"https://www.sciencedirect.com/science/article/pii/S0015028200004829?casa_token=Qt0K11jA3Z0AAAAA:fZharNeCm0xQ2FyxEXNgHDrHpvku-paYf6sp2-agaXvT2_C-rlgLdjxrXCe44oDGCjxioWdAHg#BIB37\" rel=\"nofollow noreferrer\">Pamela J Schwingl, Harry A Guess,\nSafety and effectiveness of vasectomy,\n<em>Fertility and Sterility</em>,\nVolume 73, Issue 5,\nPages 923-936,\n2000.</a></p>\n<blockquote>\n<p>Peterson et al. suggest that there may be a trade-off between efficacy of an occlusion method and potential for reversibility. For example, <strong>open-ended vasectomies may be associated with a lower rate of congestive epididymitis and have a higher potential for reversal but may be associated with higher pregnancy rates</strong>. Removing a large portion of the vas may be associated with a low pregnancy rate, but re-anastomosis in this situation may be more difficult, with a low potential for reversibility. Cautery and coagulation methods tend to effectively seal off the ends of the vasa, but these require a more technically difficult vasoepididymostomy.</p>\n</blockquote>\n<blockquote>\n<p><strong>Open-ended vasectomy, or leaving the testicular end of the vas open, is performed to avoid the increased intraluminal pressure that leads to postvasectomy pain syndrome and to increase the chances of successful reversal</strong>. Some have shown that leaving the vas open eliminates potential for damage from increased pressure and is less likely than closed-ended vasectomy to be associated with congestive epididymitis, and in some cases, sperm granulomas. Others report that the method appears to result in increased rates of spontaneous recanalization. However, the method of occlusion of the closed-end and the use of fascial separation of the two ends seem to modify the rate of spontaneous recanalization.</p>\n</blockquote>\n</blockquote>\n<p>Of course, all of the citations this paper refers to are pre-2000, so these don't address your point that &quot;techniques for vasectomies and vasectomy reversal might have evolved since then.&quot; More recently:</p>\n<blockquote>\n<p>Peter TK Chan, Marc Goldstein, Vasectomy and Vasectomy Reversal, <em>Male Reproductive Dysfunction: Pathophysiology and Treatment</em>, Chapter 34, Pages 385-406, 2007.</p>\n<blockquote>\n<p>...men with postvasectomy congestive epididymitis may be relieved of their pain by open-ended vasectomy designed to purposefully produce a pressure-relieving sperm granuloma; however, <strong>it should be pointed out that some investigators have raised concern of potential vasectomy failure with the open-ended technique</strong>.</p>\n</blockquote>\n</blockquote>\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC529470/\" rel=\"nofollow noreferrer\">The associated reference</a> doesn't compare the closed- and open-ended techniques, but one might infer a more facile reversal is suggested by increased failure rates (compared to cauterization methods). Beyond this, even the 2019 textbook <em>Vasectomy Reversal</em> contains no direct mention of the open-ended technique, so I think your best resource will be a practicing clinician.</p>\n", "score": 3 } ]

[ "surgery", "sex" ]

[ { "answer_id": 24633, "body": "<p>No, according to <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4149942/\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4149942/</a> &quot;Single and double donor sperm intrauterine insemination cycles: Does double IUI increase clinical pregnancy rates?&quot;:</p>\n<blockquote>\n<p>Single and double donor IUI cycles had similar clinical pregnancy rates. This large data set did not demonstrate a benefit to routine double IUI in donor sperm cycles.</p>\n</blockquote>\n<p>Their introduction gives an interesting overview of the previous literature on that matter:</p>\n<blockquote>\n<p>Few studies have evaluated double IUI with donor sperm. These studies have been limited by small sample sizes and provide conflicting results. The first study to evaluate a double IUI regimen was performed by Khalifa et al. and demonstrated no benefit to double IUI (12). In contrast, Matilsky et al. demonstrated higher pregnancy rates using double IUI with frozen thawed donor sperm. The double IUI clinical pregnancy rate was 17.9% per cycle versus 5% per cycle with single IUI (13). More recently, Chavkin et al. conducted a retrospective study of 333 donor insemination cycles. Pregnancy rates over 3 cycles were 10.2% for single IUI compared to 13.7% for double IUI (p=0.47) (14). While the results were not statistically significant, the authors concluded that there may be a benefit to a second insemination.</p>\n</blockquote>\n", "score": 1 } ]

[ "obstetrics", "gynecology", "female", "artificial-insemination" ]

[ { "answer_id": 24665, "body": "<p><strong>TL;DR: Yes, but it's extremely rare and I could only find one example.</strong></p>\n<p>You asked:</p>\n<blockquote>\n<p>Has there ever been a medically verified case of someone having a big part of their body paralyzed for years, due to a car accident or similar event, who eventually recovered the normal functioning of their paralyzed body part?</p>\n</blockquote>\n<p>It's very rare but I did find <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3691521/\" rel=\"nofollow noreferrer\">one example</a>:</p>\n<blockquote>\n<p>The patient, a 58-year-old male, endured vertebral fractures at\ncervical levels C3–C6 in a motor vehicle accident at the age of 22.\nThe patient did not have any respiratory problem and his stay in the\nICU was limited to 5 days. Following the injury, the patient underwent\nmanual motor testing of lower and upper body muscles groups as well as\nsensory testing. The motor testing involved examination of flexion and\nextension of upper body (shoulder, elbow, and wrist), and lower body\njoints (hip, knee, and ankle), and sensory testing involved\nexamination of sensation to pinprick and light touch on both hands and\nfeet. Initially, the patient had no motor or sensory function below\nthe level of injury. Motor and sensory function at the sacral level\nwas also absent, which was tested during the bladder evacuation and\ncatheter placement procedure. This injury is equivalent to an ASIA A\n(ASIA: American Spinal Injury Association), or a “complete” injury,\naccording to today's ASIA impairment scale (AIS) (Maynard et al.,\n1997), which did not exist at the time of the patient's injury.</p>\n</blockquote>\n<p>The case history goes on to describe his recovery:</p>\n<blockquote>\n<p>He experienced slow and progressive neurological recovery that\ncontinued for 17 years after the injury. The first neurological\nrecovery, movement of the left big toe (a grade 1 motor function),\noccurred 6 weeks after the injury. The first recovery of sensation\noccurred 6 months after the injury in the form of a painful\ndysesthetic sensation in the pelvis. Eleven months after the injury,\nthe patient was able to perform complex upper body motor functions\nsuch as sitting up without assistance. Complex lower body motor\nfunctions such as ability to walk unassisted were recovered 15 months\nafter the injury. Concomitantly, the patient recovered autonomic\nnervous system functions (i.e., a high degree of bladder and bowel\nfunctions were recovered up to 64 months after the injury) although\nmany remain abnormal (Table ​(Table1).1). Currently, his injury is\ncategorized as ASIA D. His latest AIS evaluation (Figure ​(Figure1)1)\nshowed that he has regained 94% of motor function in the upper body\nand 100% in the lower body. The patient manifests incomplete and\nasymmetric motor recovery in his hands—i.e., his left hand is more\nfunctional then the right one. He has also regained 23% of sensory\nfunction in the upper body (above the level of T7), but only 10% in\nthe lower body.</p>\n</blockquote>\n<p>You then ask:</p>\n<blockquote>\n<p>If there are such records, what are the most plausible explanations?</p>\n</blockquote>\n<p>This is purely my opinion but I would say normal regrowth of neurons explains it. The fact that the first hint of recovery occurred after six weeks and then it took another 17 years for him to achieve the degree of partial recovery he ended up with is a strong argument for entirely natural processes. Neurons can reconnect, but it's known to be a very slow process.</p>\n", "score": 0 } ]

[ "medical-records", "recovery", "trauma", "medical-history", "vehicle-car-accident" ]

[ { "answer_id": 24657, "body": "<p>In simple infection-control terms, if you compare the US response to China's, the US measures pale in comparison. In China entire cities were <a href=\"https://www.theguardian.com/world/2020/mar/19/chinas-coronavirus-lockdown-strategy-brutal-but-effective\" rel=\"nofollow noreferrer\">locked down hard</a>, with people not being allowed to leave their residences (mostly apartments), with only select few delivering food etc. Transport in and out of such cities was almost entirely shut down. Even asymptomatic people were forced into ad-hoc treatment/containment <a href=\"https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)30744-3/fulltext\" rel=\"nofollow noreferrer\">facilities</a>.</p>\n<p>(A bit of an aside, or a &quot;natural experiment&quot;, Romania provides an <a href=\"https://www.euronews.com/2020/07/17/romanian-coronavirus-patients-can-t-be-made-to-go-to-hospital-court-rules\" rel=\"nofollow noreferrer\">example</a> of what happens when people intially forced into treatment/quarantine are allowed to leave en masse; Romania's Constitutional Court overturned an initial government decision in that regard, likely being the cause of a large increase in cases. Their 2nd/August wave being <a href=\"https://www.euronews.com/2020/09/09/is-europe-having-a-covid-19-second-wave-country-by-country-breakdown\" rel=\"nofollow noreferrer\">substantially larger</a> than their first/spring, although other Balkan countries have seen a similar pattern, so causality may not be that certain. Other sources <a href=\"https://www.euractiv.com/section/elections/news/covid-19-why-did-the-good-pupil-bulgaria-lag-behind/\" rel=\"nofollow noreferrer\">attribute</a> the rise (larger 2nd wave) in the Balkans to the [too] rapid relaxation of containment measures in general.)</p>\n<p>Lockdowns do work at reducing infection at least in the short run. A more &quot;apples to apples&quot; comparison being <a href=\"https://journals.sagepub.com/doi/10.1177/0141076820945282\" rel=\"nofollow noreferrer\">Sweden vs its neighbors</a>. By 23 June, Denmark, Norway or Finland had less than a third of Sweden's number of cases, per capita. (Now, in their defense, Swedish officials claim that in long run the total number of cases will &quot;equal out&quot;, an assertion yet to be proven.) Besides such cross-country comparisons, there is a <a href=\"https://www.thelancet.com/journals/eclinm/article/PIIS2589-5370(20)30201-7/fulltext\" rel=\"nofollow noreferrer\">micro-level study</a> from Italy on the effectiveness of lockdowns, using phone location data as a proxy measure for lockdown effectiveness at reducing travel/mobility.</p>\n<p>Other countries have developed alternative strategies to lockdown, South Korea is one, focusing on testing <em>and <a href=\"https://www.bloomberg.com/news/articles/2020-07-25/these-elite-contact-tracers-show-the-world-how-to-beat-covid-19\" rel=\"nofollow noreferrer\">rapid tracing</a></em>. The US pretty much failed to seriously implement any strategy that would have resulted in a substantial reduction in the spread of the infection, aside perhaps from banking on their pharma industry to rapidly produce a vaccine. (A &quot;check&quot; that has yet to be &quot;cashed&quot;.) Also, unlike most European countries, the US also &quot;reopened&quot; while its infection rate <a href=\"https://edition.cnn.com/2020/06/30/europe/european-union-travel-us-graphic-intl/index.html\" rel=\"nofollow noreferrer\">had not</a> gone down significantly, although in practice what this meant was that US states that were not hit hard in the initial wave failed to learn from the experience of those that were, reaching and <a href=\"https://www.cnbc.com/2020/07/25/florida-now-has-more-coronavirus-cases-than-new-york-and-california-leads-the-nation.html\" rel=\"nofollow noreferrer\">surpassing</a> their infection rates. (And speaking of history repeating itself, South Korea was not exactly immune to this either as a large August church rally was <a href=\"https://www.bbc.com/news/world-asia-53888219\" rel=\"nofollow noreferrer\">linked</a> to hundreds of new cases, reminiscent of the early days of the pandemic in that country.)</p>\n<p>One thing that you might have expected the current US administration to be good at was imposing travel restrictions, which would have bought the US more time. Alas, even in that department, a CDC study <a href=\"https://edition.cnn.com/2020/07/16/politics/us-travel-bans-late-new-york-city-coronavirus/index.html\" rel=\"nofollow noreferrer\">says</a> that travel bans from Europe came too late.</p>\n<p>Assigning political blame for these facts is beyond the scope of this post.</p>\n", "score": 4 } ]

[ "infection-control" ]

[ { "answer_id": 24666, "body": "<p>The basic structure of tooth consists of</p>\n<ol>\n<li>Outermost layer, enamel</li>\n<li>Next layer, dentin</li>\n<li>Innermost vital, vascularised tissue, pulp</li>\n<li>Hard tissue layer covering the root ( root doesn't have enamel), i. e. Cementum\n<img src=\"https://i.stack.imgur.com/7QyXy.jpg\" alt=\"enter image description here\" /></li>\n</ol>\n<p><a href=\"https://www.researchgate.net/figure/Tooth-structure-and-dental-tissues-with-the-respective-stem-cell-populations-A-The_fig1_341910373\" rel=\"nofollow noreferrer\">Reference</a></p>\n<p>Now enamel is a non vital tissue, having no cells, and vasculature. <a href=\"https://www.sciencedirect.com/science/article/abs/pii/S0033350632802635\" rel=\"nofollow noreferrer\">Reference</a></p>\n<p>Similarly dentin too doesn't have any cells, but has processes of cells in pulp(odontoblasts) , known as dentinal tubules.</p>\n<p>Hence even if tooth cancer is to happen, it will affect the pulpal cells, including the odontoblasts and their processes in dentin.</p>\n<p>Now talking about the odontoblasts,\nThere is an interesting <a href=\"https://www.researchgate.net/publication/240308348_Odontoblasts_in_odontogenic_tumors\" rel=\"nofollow noreferrer\">article</a>\nIt says that-</p>\n<blockquote>\n<p>The combination of cell contact and mechanical\nstressing can be related to models describing the significance of inter-cellular mechanical interactions in contact inhibition of proliferation (CIP).</p>\n</blockquote>\n<blockquote>\n<p>The model also could theoretically account for potential neoplastic behavior of odontoblasts if there was an initial disruption of tooth morphogenesis. Possibly, in those rare cases, in which an expansile odontogenic tumor contains dentin-producing odontoblasts, the cells are more than passive participants responding to inductive signals from neoplastic epithelial cells.</p>\n</blockquote>\n<p>Further for other cells of pulp, which include fibroblasts, defence cells, eg histiocytes,\nAgain quoting an interesting <a href=\"https://www.google.com/url?sa=t&amp;source=web&amp;rct=j&amp;url=https://pubmed.ncbi.nlm.nih.gov/17196513/&amp;ved=2ahUKEwjK-sSF6eLrAhWbXSsKHeqKD8oQFjADegQIAhAB&amp;usg=AOvVaw0nIzMCfqiUgdPkRgGrOfJs&amp;cshid=1599887213980\" rel=\"nofollow noreferrer\">article</a></p>\n<blockquote>\n<p>Malignant tumours affecting the dental pulp are\npredominantly found in fully emerged teeth of mature patients (in their fifth to sixth decade of life)</p>\n</blockquote>\n<p>According to this <a href=\"https://link.springer.com/referenceworkentry/10.1007%2F978-3-642-16483-5_1559#:%7E:text=Dental%20pulp%20neoplasms%20(DPNs)%20are,the%20tooth%20(secondary%20DPN)\" rel=\"nofollow noreferrer\">article</a></p>\n<blockquote>\n<p>Dental pulp neoplasms (DPNs) rare tumors of the dental pulp tissue which is not exposed to the oral cavity. Two types of DPNs can be distinguished: Type 1 originates from the dental pulp itself (primary DPN) and type 2 originates from tissue outside of the tooth (secondary DPN).</p>\n</blockquote>\n<p>Further the previous article says,</p>\n<blockquote>\n<p>There is no reason why cells of the dental pulp, such as fibroblasts, pericytes, stem cells and epithelial cell rests of Malassez, should not act in the same way, as all these cells have mitotic competence, which can be shown by the disease pattern of pulp polyps.\nBecause of the anatomically restricted space of the dental pulp, any clonal growth of the tumour would be limited and further associated with necrosis. And tumour expansion would increase the intrapulpal pressure, as would the resulting formation of hard tissue, which can even result in the strangulation of pulpal tissue.</p>\n</blockquote>\n<blockquote>\n<p>Additionally, the more apical the tumour growth, the higher the risk of a haemorrhagic infarct of the pulp, thus limiting its growth by itself. Because sarcoma has the capacity to exist in the dental pulp, predictions can be made about the tumours potential to metastasize. Chandler and colleagues’ states that the necessary cell mass for haematogenic metastasis of individual clonal cells is 106 cells, which equates to a spatial volume of about 1 cm3. Such a volume is not usually provided by the endodontic macroenvironment.</p>\n</blockquote>\n<p>However all these were for fully mature erupted teeth.\nThere is a class of tumors known as <strong>odontogentic</strong> tumors and these are common. Eg. Ameloblastoma</p>\n<blockquote>\n<p>odontogenic tumors arise from the tissues which make our teeth, they are unique to the jaws, and by extension almost unique to dentistry.\nThese develop from the epithelium and/or Ectomesenchyme tissue while the tooth is developing.\n<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5750825/\" rel=\"nofollow noreferrer\">Reference</a></p>\n</blockquote>\n<p>Hence 'cancer of tooth' the topic itself comprises of vast number of possibilities (thereby making this answer too long!!)\nHope I have satisfactorily answered your question :)</p>\n", "score": 3 } ]

[ "cancer", "dentistry" ]

[ { "answer_id": 27448, "body": "<p>For the results you are interested in you need the full text of the publications.</p>\n<p>For Pfizer/BioNTech vaccine (BNT162b2 mRNA):</p>\n<ul>\n<li><p>N Engl J Med 2020; 383:2603-2615</p>\n<p>DOI: <a href=\"https://doi.org/10.1056/NEJMoa2034577\" rel=\"nofollow noreferrer\">10.1056/NEJMoa2034577</a></p>\n<p>Clinical Trial: <a href=\"https://clinicaltrials.gov/ct2/show/NCT04368728\" rel=\"nofollow noreferrer\">NCT04368728</a></p>\n</li>\n</ul>\n<p>For Moderna vaccine (mRNA-1273):</p>\n<ul>\n<li><p>N Engl J Med 2020; 383:1920-1931</p>\n<p>DOI: <a href=\"https://doi.org/10.1056/NEJMoa2022483\" rel=\"nofollow noreferrer\">10.1056/NEJMoa2022483</a></p>\n<p>Clinical Trial: <a href=\"https://clinicaltrials.gov/ct2/show/NCT04283461\" rel=\"nofollow noreferrer\">NCT04283461</a></p>\n</li>\n</ul>\n<p>For Astra Zeneca vaccine (ChAdOx1 nCoV-19/AZD1222):</p>\n<ul>\n<li><p>Lancet. 2020 Aug 15;396(10249):467-478</p>\n<p>doi: <a href=\"https://doi.org/10.1016/S0140-6736(20)31604-4\" rel=\"nofollow noreferrer\">10.1016/S0140-6736(20)31604-4</a></p>\n<p>Clinical Trial: <a href=\"https://clinicaltrials.gov/ct2/show/NCT04324606\" rel=\"nofollow noreferrer\">NCT04324606</a></p>\n</li>\n</ul>\n<p>For Janssen vaccine (Ad26.COV2.S):</p>\n<ul>\n<li><p>N Engl J Med. 2021 Jun 10;384(23):2187-2201</p>\n<p>doi: <a href=\"https://doi.org/10.1056/NEJMoa2101544\" rel=\"nofollow noreferrer\">10.1056/NEJMoa2101544</a></p>\n<p>Clinical Trial: <a href=\"https://clinicaltrials.gov/ct2/show/NCT04505722\" rel=\"nofollow noreferrer\">NCT04505722</a></p>\n</li>\n</ul>\n", "score": 2 }, { "answer_id": 24701, "body": "<p>Finally found at least the Moderna Trial at <a href=\"https://clinicaltrials.gov/ct2/show/NCT04470427\" rel=\"nofollow noreferrer\">ClinicalTrials website</a>, still searching for others.</p>\n<p>This study description makes no mention of ethnicity targets, but Moderna's website (as of Sept 11 2020) has a graph of enrollees by ethnicity. Also states that as of Sept 11 2020 had not yet arrived at enrollment goal (24,000 of planned 30,000) <a href=\"https://www.modernatx.com/cove-study\" rel=\"nofollow noreferrer\">Moderna website</a></p>\n", "score": 0 } ]

[ "covid-19", "vaccination", "united-states" ]

[ { "answer_id": 24708, "body": "<p>I don't think he's referring to anything specific. &quot;May be&quot; is not a definitive statement, it just seems he is suggesting that it is plausible that a vaccine could be less protective than regular mask wearing. &quot;I might even go so far&quot; couches it even more.</p>\n<p>I think that's probably not a great statement to make, either, a better one might be to suggest that &quot;because a vaccine is not effective in everyone that gets it, mask-wearing may continue to be important even with a vaccine&quot;, but not every quote in front of the media is ever ideal. Really, the rest of his statement:</p>\n<blockquote>\n<p>if I don't get an immune response, the vaccine is not going to protect me. This face mask will</p>\n</blockquote>\n<p>seems like the part to focus on.</p>\n<p>For comparisons to influenza, this page talks about the annual flu vaccine efficiacy:</p>\n<p><a href=\"https://www.cdc.gov/flu/professionals/acip/immunogenicity.htm\" rel=\"nofollow noreferrer\">https://www.cdc.gov/flu/professionals/acip/immunogenicity.htm</a></p>\n<p>A quote, emphasis mine:</p>\n<blockquote>\n<p>IIV3 provided statistically significant protection against both the included B lineage (<strong>66%</strong>; 95%CI 58, 73) and the non-included B lineage (<strong>51%</strong>; 95%CI 36, 63) during the 2012– 13 season</p>\n</blockquote>\n<p>Another paper,</p>\n<p><em>Tricco, A. C., Chit, A., Soobiah, C., Hallett, D., Meier, G., Chen, M. H., ... &amp; Loeb, M. (2013). Comparing influenza vaccine efficacy against mismatched and matched strains: a systematic review and meta-analysis. BMC medicine, 11(1), 153.</em></p>\n<p>is a meta-analysis of flu vaccine efficacy in children. They write, quote, with emphasis mine:</p>\n<blockquote>\n<p>The live-attenuated influenza vaccine (LAIV) showed significant protection against mismatched (six RCTs, <strong>VE 54%</strong>, 95% confidence interval (CI) 28% to 71%) and matched (seven RCTs, <strong>VE 83%</strong>, 95% CI 75% to 88%) influenza strains among children aged 6 to 36 months</p>\n</blockquote>\n<blockquote>\n<p>VE was calculated using the following formula: (1 - relative risk × 100%)</p>\n</blockquote>\n<p>So it seems that 70% would be in the ballpark of the annual flu vaccine against the included strain. Obviously the 2019 coronavirus is not influenza, but we have no solid long-term efficacy data yet, and I think it's reasonable to expect that even a very useful vaccine (on par with the annual flu vaccine given to millions) would not approach 100% efficacy. Even with a vaccine, it will probably be important to continue basic public health protocols intended to limit virus spread, especially before many people are immunized.</p>\n<p>There's some mixing here between &quot;immune response&quot; and &quot;efficiacy&quot; but I think it would be fair to say that if someone gets sick, then whatever measured immune response they may have had was not effective, so we might as well consider it not an immune response for this purpose. Rewriting a paraphrased version of the quote, I would say:</p>\n<blockquote>\n<p>&quot;If the Covid vaccine provides similar protection to the annual influenza vaccine, the immunogenicity could be around 70%. If I don't get an immune response, the vaccine is not going to protect me but a face mask will still provide some protection.&quot;</p>\n</blockquote>\n", "score": 1 }, { "answer_id": 24709, "body": "<p>From a <a href=\"https://europepmc.org/article/med/32591466\" rel=\"nofollow noreferrer\">recent review</a> of &quot;Warp Speed&quot; vaccine candidates</p>\n<blockquote>\n<p>General experience, combined with emerging data, suggests that the most rapidly produced vaccines (i.e., nucleic acids and virus vectors) may also be the least capable of eliciting high titers of antibodies and NAbs to the S-protein.</p>\n</blockquote>\n<p>So, it's probably a safe bet to limit discussion to those for now... The review also says that</p>\n<blockquote>\n<p>it is unknown whether the results obtained in small animals will be matched in humans. The immunogenicity of mRNA and DNA vaccines is generally far stronger in small animals than in macaques, and more so in humans.</p>\n</blockquote>\n<p>And for the latter it cites <a href=\"https://europepmc.org/article/PMC/7185789\" rel=\"nofollow noreferrer\">a paper</a> on a MERS DNA vaccine, which interestingly happens to mention something like those ~70% numbers....</p>\n<blockquote>\n<p>T-cell responses were detected in 47 (71%) of 66 participants after two vaccinations and in 44 (76%) of 58 participants after three vaccinations. [...] At week 60, vaccine-induced humoral and cellular responses were detected in 51 (77%) of 66 participants and 42 (64%) of 66, respectively.</p>\n</blockquote>\n<p>There's also been a bit of a debate as to what measure(s) of immunity are most relevant. Most of the (short-term) Covid-19 vaccine data published so far, itself on the order of one-month, seems to have been mainly anti-bodies (e.g. a <a href=\"https://www.medrxiv.org/content/10.1101/2020.06.30.20142570v1.full.pdf\" rel=\"nofollow noreferrer\">recent study</a> on one of the mRNA vaccines found average levels exceeding convalescence), but some researchers <a href=\"https://news.berkeley.edu/2020/09/09/for-an-effective-covid-vaccine-look-beyond-antibodies-to-t-cells/\" rel=\"nofollow noreferrer\">disagree</a> this is the most relevant measure, pointing to T-cells response as more relevant. Actually the T-cells measure was reported for that vaccine candidate too, in a <a href=\"https://www.medrxiv.org/content/10.1101/2020.07.17.20140533v1\" rel=\"nofollow noreferrer\">separate</a> publication/preprint; it was on the order of 80% response [29/36 participants] for CD8+ T cells. And that <a href=\"https://www.evaluate.com/vantage/articles/news/trial-results/covid-19-vaccine-contest-turns-t-cell-responses\" rel=\"nofollow noreferrer\">seems</a> to be as good as it gets in terms of Covid-19 phase-1 published data.</p>\n<p>I guess there's some &quot;fudge factor&quot; to consider here given that phase I trials tend to select healthy volunteers in the 18-55 age range etc.</p>\n", "score": 1 }, { "answer_id": 24742, "body": "<p>Without questioning the CDC director specifically we are left to speculate why he said 70% as contrasted with 60% or 80%.\nHowever, the <a href=\"https://pfe-pfizercom-d8-prod.s3.amazonaws.com/2020-09/C4591001_Clinical_Protocol_0.pdf\" rel=\"nofollow noreferrer\">protocol</a> released by Pfizer may give some clue. The clinical trial for their candidate vaccine will last approximately two years, however they will be conducting Interim Analysis for Vaccine Efficacy at several points during that two year period.</p>\n<p>Pfizer will consider the vaccine an <strong>interim</strong> success, if after 32 persons contract Covid19, only 6 of those people were injected with the trial vaccine. That calculates to an efficacy of 77%.(see page 102 of protocol)</p>\n<p>Subsequent interim analysis the last being after 164 persons contract Covid-19. If, of the 164 persons only 53 were injected with the trial vaccine, that would also be deemed a success. That calculates to an efficacy of 52%. (same page)</p>\n<p>So from the Pfizer protocol we see efficacy targets for success of 52% or greater.</p>\n<p>However, Efficacy (the extent to which a vaccine provides a beneficial result) is not synonymous with Immunogenicity (the ability of a vaccine to provoke an immune response creating antibodies). Having antibodies (naturally or provoked) against COVID19 is clearly better than having no antibodies, but there is no assurance that any of the trial vaccines will produce antibodies in <strong>every single</strong> person (100% immunogenicity). As a practical matter the immunogenicity will likely be less than 100%, but 70% would be considered a great success, particularity if the antibodies are constantly being produced and renewed. For those who do not develop antibodies, or that their bodies do not continue to produce &quot;fresh&quot; antibodies they will have to rely on other protective means - such as masks.</p>\n<p>The Pfizer protocol is silent on the immunogenicity criteria for success.</p>\n", "score": 0 } ]

[ "covid-19", "immune-system", "vaccination" ]

[ { "answer_id": 24777, "body": "<p>Melatonin synthesis and secretion (pineal gland) is enhanced by darkness and inhibited by light (photons).</p>\n<p><a href=\"https://i.stack.imgur.com/jT9Mz.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/jT9Mz.jpg\" alt=\"Diagram of the major controlling mechanisms of melatonin release.\" /></a></p>\n<p><em>DOI: 10.1530/ror.0.0030013 PMID: 9509985</em></p>\n", "score": 3 } ]

[ "sleep", "sleep-cycles", "sleep-deprivation", "melatonin" ]

[ { "answer_id": 24965, "body": "<p>Your first reference points out the difference between a lateral ankle view versus an oblique view. The oblique view is taken from a lateral position but the joint is tilted so that the rays travel parallel to the joint surface. Otherwise, a lateral view results in superimposition of different parts of the joint being imaged rendering it unclear.</p>\n", "score": 1 } ]

[ "bone-fractures", "x-rays", "legs", "barefoot" ]

[ { "answer_id": 24851, "body": "<blockquote>\n<p>Why aren't lung machines / ECMO widely used for COVID-19?</p>\n</blockquote>\n<p>They are being used <a href=\"https://labblog.uofmhealth.org/health-tech/ecmo-last-resort-life-support-option-helped-majority-of-critically-ill-covid-19\" rel=\"nofollow noreferrer\">University of Michigan</a> and <a href=\"https://www.news-medical.net/news/20200926/ECMO-appears-to-be-saving-the-lives-of-many-critically-ill-COVID-19-patients.aspx\" rel=\"nofollow noreferrer\">News Medical</a></p>\n<p>Beyond that, you have already suggested the &quot;why&quot; not being used more widely, there are far fewer ECMO devices than ventilators.</p>\n<p>The remark about insurance companies is an inappropriate speculation.</p>\n", "score": 1 }, { "answer_id": 30622, "body": "<p>As others have mentioned <a href=\"https://www.bartshealth.nhs.uk/news/ecmo-explained-the-specialist-life-support-key-to-our-covid19-response-9345\" rel=\"nofollow noreferrer\">ECMO is used for covid-19 patients in some locations.</a> I think this information is readily available by searching.</p>\n<p>But I will try to provide some more information about why ECMO is not a first choice. Firstly ECMO is a step up from ventilation. Just as ventilation is a step up from providing non invasive positive airway pressure which is a step up from providing supplementary oxygen. As you progress up this pyramid the degree of resources decreases. There are less ventilators than there are e.g. NIV machines. Likewise there are less ECMO devices than there are ventilators. In fact depending on where you live most hospitals will not even have one.</p>\n<p>ECMO is not an alternative treatment to ventilation but a treatment to be relied on if ventilation fails. Why? <a href=\"https://pubmed.ncbi.nlm.nih.gov/29788836/\" rel=\"nofollow noreferrer\">Because it is associated with its own harms:</a></p>\n<blockquote>\n<p>it remains invasive and associated with significant complications, including tamponade, infection, thrombosis, gas embolism and bleeding. The most dreaded complication is intracranial hemorrhage (ICH)</p>\n</blockquote>\n<p>The risk of intracranial haemorrhage is significant:</p>\n<blockquote>\n<p><a href=\"https://www.frontiersin.org/articles/10.3389/fneur.2018.00548/full\" rel=\"nofollow noreferrer\">The incidence of ECMO-associated ICH varied between 1.8 and 21 %. Mortality rates in ICH-cohorts varied between 32 and 100 %, with a relative risk of mortality of 1.27–4.43 compared to non-ICH cohorts. </a></p>\n</blockquote>\n<p>These complications can be devastating in patients already severely ill from covid and deconditioned due to ICU stay.</p>\n<blockquote>\n<p>A ventilator does not do much to help when the lungs are full of fluid</p>\n</blockquote>\n<p>This is not necessarily true. Providing positive pressure to the lungs can improve gas exchange even when there is fluid in the alveoli. This is seen in the use of <a href=\"https://pmj.bmj.com/content/81/960/637\" rel=\"nofollow noreferrer\">CPAP for cardiogenic pulmonary oedema.</a> This not the same as covid but meant to illustrate that fluid in the lung doesn't render the lung useless for gas exchange. Covid pneumonia and ARDS are different situations but I wanted to point out this is not a correct assumption.</p>\n", "score": 1 } ]

[ "covid-19", "lungs", "mechanical-ventilation" ]

[ { "answer_id": 24880, "body": "<p>Measuring the concentration of amino acids &quot;in the body&quot; is a bit difficult. Your body is made up of lots of cells and organs, each one of which exists in a constant state of flux and contains many proteins and amino acids.</p>\n<p>Assuming perhaps that you meant &quot;in the blood&quot;, then yes, such kits do exist -- e.g. this enzyme-linked spectrophotomeric assay -- <a href=\"https://www.antibodies-online.com/kit/1503021/Cysteine+ELISA+Kit/\" rel=\"nofollow noreferrer\">https://www.antibodies-online.com/kit/1503021/Cysteine+ELISA+Kit/</a> -- but it costs €642,85 (+€40 shipping and 22% VAT) for 96 tests, and requires a molecular biology laboratory to use.</p>\n<p>The only commonly performed similar tests I am aware of are whole plasma amino acid counts, commonly performed on infants to look for inborn errors of metabolism -- i.e. specific birth defects of metabolism. You can find an example US Hospital page <a href=\"https://www.ucsfbenioffchildrens.org/tests/003361.html\" rel=\"nofollow noreferrer\">here</a> that contains the reference range for each amino acid.</p>\n", "score": 2 } ]

[ "nutrition", "supplement", "amino-acids" ]

[ { "answer_id": 24939, "body": "<p>The followings are English translations of quotations from one <a href=\"https://bsd.neuroinf.jp/wiki/%E3%83%8B%E3%83%A5%E3%83%BC%E3%83%AD%E3%83%B3%E6%96%B0%E7%94%9F#cite_note-ref10-10\" rel=\"nofollow noreferrer\">commentary</a>, written by a Japanese brain expert. (Unfortunately, the commentary itself is written in Japanese)</p>\n<blockquote>\n<p>By closely examining brain tissue samples from patients who died after taking anticancer drugs, researchers found that even in adult brains, neurons were nascent, at least in the dentate gyrus of the hippocampus.<br>\n<a href=\"https://pubmed.ncbi.nlm.nih.gov/9809557/\" rel=\"nofollow noreferrer\">https://pubmed.ncbi.nlm.nih.gov/9809557/</a></p>\n</blockquote>\n<blockquote>\n<p>On the other hand, a study using 14C as a tracer suggest that neurogenesis in the neocortex is very limited.<br>\n<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1567918/\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1567918/</a></p>\n</blockquote>\n<p>From the abstract of the first literature, you can achieve general understanding of how to prove neurogenesis. The following is a definitive statement of the <a href=\"https://pubmed.ncbi.nlm.nih.gov/9809557/\" rel=\"nofollow noreferrer\">first literature</a>.</p>\n<blockquote>\n<p>Human brain tissue was obtained postmortem from patients who had been treated with the thymidine analog, bromodeoxyuridine (BrdU), that labels DNA during the S phase.</p>\n</blockquote>\n<p>The nature of the anticancer drug of first literature was such that it was only taken up into the DNA when the cells were dividing. The fact that these anticancer drug-incorporated nerve cells were located near the hippocampus seems to prove neurogenesis.</p>\n<p>The second paper used 14C level in DNA as a date mark for when a cell was born based on following facts.</p>\n<ul>\n<li>Concentration of environmental 14C (these are produced in nuclear tests) has decreased exponentially since the 1963 Nuclear Test Ban Treaty.</li>\n<li>The DNA is stable after a cell has gone through its last cell division.</li>\n</ul>\n<p>The key is to use substances having both of following properties; if we can prove that the substance was taken up at least after adulthood, then we can prove that the cells divided after adulthood.</p>\n<ul>\n<li>only taken up into the cell when the cell divides, and</li>\n<li>stay stably inside the cell after the cell divides.</li>\n</ul>\n<p>For more information, read the references　(written in English) cited above.</p>\n", "score": 1 } ]

[ "brain", "neurology", "clinical-study" ]

[ { "answer_id": 24974, "body": "<p>Multiple tests can decrease the chance of a false negative.</p>\n<p>The probability of detection varies with the time since exposure. This <a href=\"https://www.nature.com/articles/d41586-020-02661-2\" rel=\"nofollow noreferrer\">Nature article</a> presents an informative (albeit rough) graph. Suppose, for example, your Saturday and Thursday tests occurred at the times I labeled on the graph below:</p>\n<p><a href=\"https://i.stack.imgur.com/Hnagd.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/Hnagd.png\" alt=\"enter image description here\" /></a></p>\n<p>Then it would be quite possible for the Saturday test to return a (false) negative result while the Thursday test returns a positive result, even though both were testing for the same infection.</p>\n<p>Notice (in the scenario above) that both tests occurred before the onset of symptoms, so it would be impossible to know if you were infected without testing.</p>\n<p>Both tests are valuable since detecting infections as early as possible reduces opportunities for the virus to spread (assuming the infected person quarantines themself).</p>\n<p>The second test may not always be the more accurate. With an antigen test, for example, it is conceivable that the Saturday test could occur near the peak of the orange curve (when probability of detection is most likely), and the Thursday test then occur when the probability of detection is much lower.</p>\n<p>Moreover, keep in mind that the graph is only depicting <em>probabilities</em>. If the Saturday test has, say, a 40% chance of detecting the virus, but the Thursday test has an 80% chance, then there is still an 8% chance (= 0.40 * (1 - 0.80)) that if the person is infected, the Saturday test returns a true positive while the Thursday test returns a false negative.</p>\n", "score": 3 } ]

[ "covid-19", "test", "intestine" ]

[ { "answer_id": 25032, "body": "<p>The studies I found very significantly contradict each other.</p>\n<p>The 2020 systematic review {6} states that the risk of after the use of topical imiquimod 5% cream to treat a nodular basal cell carcinoma (BCC) is ~2%:</p>\n<p><a href=\"https://i.stack.imgur.com/G6OOU.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/G6OOU.png\" alt=\"enter image description here\" /></a></p>\n<p>The 2009 systematic review {5} summarized the likelihood of scarring and/or skin discoloration (e.g., hyper- or hypopigmentation) after the use of topical imiquimod 5% cream to treat a basal cell carcinoma (BCC):</p>\n<p><a href=\"https://i.stack.imgur.com/b641V.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/b641V.png\" alt=\"enter image description here\" /></a></p>\n<p><a href=\"https://i.stack.imgur.com/yAsMi.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/yAsMi.png\" alt=\"enter image description here\" /></a></p>\n<p><a href=\"https://i.stack.imgur.com/A8oYu.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/A8oYu.png\" alt=\"enter image description here\" /></a></p>\n<p>The 2018 study {4} states 0% of permanent hypopigmentation/depigmentation:</p>\n<blockquote>\n<p>Hypopigmentation depigmentation was present in 71% (17/24) of the lesions immediately after treatment and 6 months later. <strong>Hypopigmentation/depigmentation eventually healed, with normal skin pigmentation, in all patients</strong>.</p>\n</blockquote>\n<p>Whereas 67% of treated cases of BCC treated by imiquimod 5% cream had hypopigmentation in this 2007 study {1}.</p>\n<blockquote>\n<p>The cosmetic results were excellent in 33% of cases (n = 24), but a permanent hypopigmented macule was observed in 67% of cases (n = 12) (<a href=\"https://jamanetwork.com/journals/jamadermatology/fullarticle/410920#drs60017f2\" rel=\"nofollow noreferrer\">Figure 2</a>).</p>\n</blockquote>\n<p><strong>Important note</strong>: most patients in this study have a skin type 3 on the Fitzpatrick scale, which may strongly the impact the percentage of hypopigmentation cases, see below for more information.</p>\n<p>Example of hypopigmentation following a treatment of BCC treated by imiquimod 5% cream (see last picture <code>C</code>):</p>\n<p><a href=\"https://i.stack.imgur.com/rGrAR.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/rGrAR.jpg\" alt=\"enter image description here\" /></a></p>\n<p>Limitations:</p>\n<ol>\n<li><p>Small sample size.</p>\n</li>\n<li><p>Two authors of the study have disclosed a conflict of interest (paid by 3M Pharmaceuticals, which manufactures Imiquimod).</p>\n</li>\n<li><p>The study was published in 2007. Hopefully larger, more objective studies have been published since then.</p>\n</li>\n<li><p>Patients had different skin types, as assessed with the <a href=\"https://en.wikipedia.org/wiki/Fitzpatrick_scale\" rel=\"nofollow noreferrer\">Fitzpatrick scale</a>. I was told by a dermatologist the darker the skin, the more likely it is to get hypopigmentation from a imiquimod 5% cream. To be confirmed with a study. The following table shows the skin type distributions in the {1} study:</p>\n<p><a href=\"https://i.stack.imgur.com/Kp7Pb.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/Kp7Pb.png\" alt=\"enter image description here\" /></a></p>\n<p><a href=\"https://i.stack.imgur.com/rfwY4.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/rfwY4.png\" alt=\"enter image description here\" /></a></p>\n</li>\n</ol>\n<hr />\n<p>Regarding the location of the hypopigmentation, all studies I have found state the hypopigmentation, if any, is mostly limited to the site of application. Quote from {2}:</p>\n<blockquote>\n<p>Imiquimod-induced pigment loss has mainly been limited to the site of application.</p>\n</blockquote>\n<p>which collaborates {3}:</p>\n<blockquote>\n<p>Patient with multiple hypopigmented macules coalescing into large hypopigmented\npatches at the site of topical imiquimod therapy</p>\n</blockquote>\n<hr />\n<p>References:</p>\n<ul>\n<li>{1} Fifty-five Basal Cell Carcinomas Treated With Topical Imiquimod: Outcome at 5-Year Follow-up. <a href=\"https://jamanetwork.com/searchresults?author=David+Vidal&amp;q=David+Vidal\" rel=\"nofollow noreferrer\">David Vidal, MD, PhD</a>; <a href=\"https://jamanetwork.com/searchresults?author=Xavier+Mat%c3%adas-Guiu&amp;q=Xavier+Mat%c3%adas-Guiu\" rel=\"nofollow noreferrer\">Xavier Matías-Guiu, MD, PhD</a>; <a href=\"https://jamanetwork.com/searchresults?author=Agust%c3%adn+Alomar&amp;q=Agust%c3%adn+Alomar\" rel=\"nofollow noreferrer\">Agustín Alomar, MD, PhD</a>. <em>Arch Dermatol.</em> 2007;143(2):264-276. <a href=\"https://doi.org/doi:10.1001/archderm.143.2.266\" rel=\"nofollow noreferrer\">https://doi.org/doi:10.1001/archderm.143.2.266</a></li>\n<li>{2} Edgar, Natalie, Stacey Pilkington, and Daniel J. Hogan. &quot;Imiquimod-induced hypopigmentation following treatment of periungual verruca vulgaris.&quot; Cutis 101, no. 6 (2018): 466-468. <a href=\"https://www.mdedge.com/dermatology/article/167571/pigmentation-disorders/imiquimod-induced-hypopigmentation-following/page/0/1\" rel=\"nofollow noreferrer\">https://www.mdedge.com/dermatology/article/167571/pigmentation-disorders/imiquimod-induced-hypopigmentation-following/page/0/1</a> (<a href=\"https://web.archive.org/web/20201104074934/https://www.mdedge.com/dermatology/article/167571/pigmentation-disorders/imiquimod-induced-hypopigmentation-following/page/0/1\" rel=\"nofollow noreferrer\">mirror</a>); <a href=\"https://mdedge-files-live.s3.us-east-2.amazonaws.com/files/s3fs-public/Document/June-2018/CT101006466.PDF\" rel=\"nofollow noreferrer\">https://mdedge-files-live.s3.us-east-2.amazonaws.com/files/s3fs-public/Document/June-2018/CT101006466.PDF</a> (<a href=\"https://web.archive.org/web/20201104075123/https://mdedge-files-live.s3.us-east-2.amazonaws.com/files/s3fs-public/Document/June-2018/CT101006466.PDF\" rel=\"nofollow noreferrer\">mirror</a>)</li>\n<li>{3} Induction of Vitiligo-like Hypopigmentation with Use of Topical\nImiquimod for Superficial and Nodular Basal Cell Carcinomas\nRoxanne Rajaii, Elizabeth Young, DO, Sean Stephenson, DO, Michelle Legacy, DO, Lynn Sikorski, DO <a href=\"https://cdn.ymaws.com/www.aocd.org/resource/resmgr/jaocd/contents/volume41/41-03.pdf\" rel=\"nofollow noreferrer\">https://cdn.ymaws.com/www.aocd.org/resource/resmgr/jaocd/contents/volume41/41-03.pdf</a> (<a href=\"https://archive.vn/CssXF\" rel=\"nofollow noreferrer\">mirror</a>)</li>\n<li>{4} Bostanci, Seher, Pelin Kocyigit, Seçil Vural, Aylin Okcu Heper, and Aysenur Botsali. &quot;Long-term follow-up results of topical imiquimod treatment in basal cell carcinoma.&quot; Dermatologic Surgery 44, no. 1 (2018): 36-41. <a href=\"https://www.researchgate.net/profile/Secil_Vural/publication/320317367_Long-Term_Follow-Up_Results_of_Topical_Imiquimod_Treatment_in_Basal_Cell_Carcinoma/links/5b27ae41a6fdcc3cce9c2011/Long-Term-Follow-Up-Results-of-Topical-Imiquimod-Treatment-in-Basal-Cell-Carcinoma.pdf\" rel=\"nofollow noreferrer\">https://www.researchgate.net/profile/Secil_Vural/publication/320317367_Long-Term_Follow-Up_Results_of_Topical_Imiquimod_Treatment_in_Basal_Cell_Carcinoma/links/5b27ae41a6fdcc3cce9c2011/Long-Term-Follow-Up-Results-of-Topical-Imiquimod-Treatment-in-Basal-Cell-Carcinoma.pdf</a> (<a href=\"https://archive.vn/Nzt4K\" rel=\"nofollow noreferrer\">mirror</a>)</li>\n<li>{5} Love WE, Bernhard JD, Bordeaux JS. Topical imiquimod or\nfluorouracil therapy for basal and squamous cell carcinoma: a\nsystematic review. Arch Dermatol. 2009;145(12):1431–8. <a href=\"https://doi.org/10.1001/archdermatol.2009.291\" rel=\"nofollow noreferrer\">https://doi.org/10.1001/archdermatol.2009.291</a></li>\n<li>{6} Huang, Christina M., and Mark G. Kirchhof. &quot;Topical Imiquimod as a Treatment Option for Nodular Basal Cell Carcinoma: A Systematic Review.&quot; Journal of Cutaneous Medicine and Surgery (2020): 1203475420931770. <a href=\"https://doi.org/10.1177/1203475420931770\" rel=\"nofollow noreferrer\">https://doi.org/10.1177/1203475420931770</a></li>\n</ul>\n", "score": 1 } ]

[ "dermatology", "side-effects", "scar-tissue-scars", "basal-cell-carcinoma", "hyperpigmentation" ]

[ { "answer_id": 25062, "body": "<p>The 2009 systematic review {1} summarized the success rate of the use of topical <a href=\"https://en.wikipedia.org/w/index.php?title=Fluorouracil\" rel=\"nofollow noreferrer\">fluorouracil</a> cream to treat a superficial basal cell carcinoma (BCC). It found only 1 study, which reported a 90% success rate (at 3-week follow-up, so an important remaining question is what the success rate is after a few years). See the first row of this table (Gross et al.) from {1}:</p>\n<p><a href=\"https://i.stack.imgur.com/cUIxn.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/cUIxn.png\" alt=\"enter image description here\" /></a></p>\n<hr />\n<p>References:</p>\n<ul>\n<li>{1} Love WE, Bernhard JD, Bordeaux JS. Topical imiquimod or\nfluorouracil therapy for basal and squamous cell carcinoma: a\nsystematic review. Arch Dermatol. 2009;145(12):1431–8. <a href=\"https://doi.org/10.1001/archdermatol.2009.291\" rel=\"nofollow noreferrer\">https://doi.org/10.1001/archdermatol.2009.291</a></li>\n</ul>\n", "score": 1 } ]

[ "dermatology", "treatment", "basal-cell-carcinoma" ]

[ { "answer_id": 25013, "body": "<p><strong>In the final stage of FDA's approval process, what is the 'agency'? What is the role of them?</strong></p>\n<p>The agency is the Food and Drug Administration (FDA). <a href=\"https://www.fda.gov/about-fda/fda-organization\" rel=\"nofollow noreferrer\">They are an agency within the Department of Health and Human Services.</a> As the <a href=\"https://www.biospace.com/article/fda-rejects-mesoblast-s-remestemcel-l-for-graft-versus-host-disease/\" rel=\"nofollow noreferrer\">article</a> and quote in your question says,</p>\n<blockquote>\n<p>Although the agency isn't required to follow an advisory committee's recommendation, it usually does.</p>\n</blockquote>\n<p>Unfortunately in the instance you mentioned, they didn't, and there can be a number of reasons for that.</p>\n<blockquote>\n<p>In its CRL, the FDA recommended the company run at least one more randomized controlled trial in adults and/or children to generate more evidence of the drug’s effectiveness for SR-aGVHD.</p>\n</blockquote>\n<p>^{* <a href=\"https://medicalsciences.meta.stackexchange.com/q/972\">For those who may not know</a>, CRL stands for Complete Response Letter and SR-aGVHD stands for <a href=\"https://doi.org/10.1182/blood.2020007336\" rel=\"nofollow noreferrer\">steroid-refractory acute graft versus host disease</a>}</p>\n<p><strong>What kind of Committees or Groups involve the review at the final stage of approval? And, what is the relationship between the committees and the FDA?</strong></p>\n<p>The FDA advisory committees are <a href=\"https://www.fda.gov/drugs/drug-information-consumers/advisory-committees-critical-fdas-product-review-process\" rel=\"nofollow noreferrer\">critical to the FDA's Product Review Process</a> and the Oncologic Drugs Advisory Committee (ODAC) mentioned in the article you linked and quoted is one of many different committees.</p>\n<p>A calendar of FDA committee meetings can be found at <a href=\"https://www.fda.gov/advisory-committees\" rel=\"nofollow noreferrer\">https://www.fda.gov/advisory-committees</a> and the calendar mentions the names of the committees involved.</p>\n<p>The committees <a href=\"https://www.fda.gov/about-fda/fda-basics/what-fda-advisory-committee\" rel=\"nofollow noreferrer\">provide FDA with independent advice from outside experts</a>.</p>\n<blockquote>\n<p>In general, advisory committees include a chair, several members, plus a consumer, industry, and sometimes a patient representative. Additional experts with special knowledge may be added for individual committee meetings as needed. Although the committees provide advice to the agency, FDA makes the final decisions.</p>\n</blockquote>\n", "score": 2 } ]

[ "clinical-study", "reference-request", "regulatory-agencies" ]

[ { "answer_id": 25000, "body": "<p>During your rotations you will notice that not every disease will show itself with the classic &quot;Textbook&quot; presentation (this actually very rare). Moreover MG can be considered a cluster of different diseases: because of different groups of muscles affected by the disease (e.g. ocular or generalized) or because of pathogenesis (anti achR, anti MusK etc. etc.) - You can read more about it <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4156422/\" rel=\"nofollow noreferrer\">here</a>.\nSo, your pathophysiological reasoning is correct: without any Ach (to be precise, without a satisfactory interaction between Ach and its receptor), you have no DTR. Still, in MG it can be very variable depending on the type of MG that the patient had, on the clinical phase the patient was going through (MG can have a relapsing remitting disease course, as in <a href=\"https://pubmed.ncbi.nlm.nih.gov/26802912/\" rel=\"nofollow noreferrer\">this case</a> where patients were treated with azathioprine) and even on the medications the patient was on (such as Acetylcholinesterase inhibitors).</p>\n<p>So, long story short: in medicine there's no absolute truth and no thing such as 100%. Every piece must be carefully placed in the big frame.</p>\n<p>EDIT: I thought in the beginning that the question was going to be more general and less clinical. As of the clinical explanation to why in MG the DTR are spared (opposed to LEMS), here's a good neurophysiological basis for it:</p>\n<blockquote>\n<p>In MG as in LEMS the afferent limb of the reflex ark is unaffected as\nis the efferent up until the neuromuscular junction. The explanation\nof preserved reflexes in MG is that the initial barrage arrives at a\nrested neuromuscular junction. The initial release of acetylcholine is\nlarger than later in a train of impulses and this is sufficient to\novercome any deficit in the number of acetylcholine receptors. Only\nbrief transmission is needed to provide the mechanical response, and\nthis occurs before fatigability can set in.</p>\n</blockquote>\n<p>Source: <a href=\"https://onlinelibrary.wiley.com/doi/abs/10.1002/mus.880180821\" rel=\"nofollow noreferrer\">https://onlinelibrary.wiley.com/doi/abs/10.1002/mus.880180821</a></p>\n", "score": 2 } ]

[ "neurology", "reflex-impulse" ]

[ { "answer_id": 25010, "body": "<p>I'll write down what I've just found out as an answer. However, this is not a complete answer.</p>\n<p><strong>(F1)How do I find the review reports on FDA approved drug?</strong><br>\nThe FDA's database on medical devices appears to be compiled <a href=\"https://www.fda.gov/drugs/development-approval-process-drugs/drug-approvals-and-databases\" rel=\"nofollow noreferrer\">here</a>.</p>\n<p>For drug, following you can find the review reports from <a href=\"https://www.accessdata.fda.gov/scripts/cder/daf/\" rel=\"nofollow noreferrer\">here</a>.</p>\n<p>For example, if you search for the tamiflu, following two are hit.</p>\n<ul>\n<li>NDA <a href=\"https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&amp;ApplNo=021246\" rel=\"nofollow noreferrer\">021246</a></li>\n<li>NDA <a href=\"https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&amp;ApplNo=021087\" rel=\"nofollow noreferrer\">021087</a></li>\n</ul>\n<p>Note that, the FDA seems to make a distinction between drugs and OTCs.</p>\n<p><strong>(F2)How do I find the review reports on FDA approved medical devices?</strong><br>\nThe FDA's database on medical devices appears to be compiled <a href=\"https://www.fda.gov/medical-devices/device-advice-comprehensive-regulatory-assistance/medical-device-databases\" rel=\"nofollow noreferrer\">here</a>.</p>\n<p><strong>(F3)How do I find the review reports on FDA approved regenerative medicine?</strong><br>\n<a href=\"https://www.fda.gov/vaccines-blood-biologics/cellular-gene-therapy-products/approved-cellular-and-gene-therapy-products\" rel=\"nofollow noreferrer\">Here</a> is the official list of regenerative medicine products that have been finally approved by the FDA.</p>\n<p>Clicking on the name of each listed product will take you to a page where you can access the description and review information for each product. These pages has a link to a zip file containing all of the documents related to the review.\nFor example, following Fig is a capture of the page for <a href=\"https://www.fda.gov/vaccines-blood-biologics/cellular-gene-therapy-prod*ucts/gintuit-allogeneic-cultured-keratinocytes-and-fibroblasts-bovine-collagen\" rel=\"nofollow noreferrer\">GINTUIT</a>. On the following Fig, you can find the link for the Package Insert and &quot;Approval History, Letters, Reviews, and Related Documents&quot;\n<br>\n<a href=\"https://i.stack.imgur.com/f6Gxt.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/f6Gxt.png\" alt=\"enter image description here\" /></a></p>\n<p><strong>(F4)How do I find the meeting-minutes of FDA's committees?</strong><br>\nThanks to the @Chris Rogers 's <a href=\"https://medicalsciences.stackexchange.com/questions/24980/relationship-between-fda-agencies-and-the-advisory-committee/25013#25013\">answer</a> to previous my Q＆A, I found the following three articles on the FDA's website.</p>\n<ul>\n<li>(F4-1) <a href=\"https://www.fda.gov/drugs/drug-information-consumers/advisory-committees-critical-fdas-product-review-process\" rel=\"nofollow noreferrer\">https://www.fda.gov/drugs/drug-information-consumers/advisory-committees-critical-fdas-product-review-process</a></li>\n<li>(F4-2) <a href=\"https://www.fda.gov/advisory-committees\" rel=\"nofollow noreferrer\">https://www.fda.gov/advisory-committees</a></li>\n<li>(F4-3) <a href=\"https://www.fda.gov/advisory-committees/committees-and-meeting-materials\" rel=\"nofollow noreferrer\">https://www.fda.gov/advisory-committees/committees-and-meeting-materials</a></li>\n</ul>\n<blockquote>\n<p>If you want to jump to conclusions, the minutes of all FDA committees can be obtained from the (F4-3)'s website above.</p>\n</blockquote>\n<p>The (F4-1)'s web page has the following description, may indicating that the committee consults not all products.</p>\n<blockquote>\n<p>So, how does the agency determine which products will undergo advisory committee review in the first place?\n<br>\n<br>\n&quot;Surprisingly,&quot; Sherman says, &quot;many products do not make it to advisory committees.&quot; Those that do usually represent new technology or some element of controversy.</p>\n</blockquote>\n<p>The web page of (F4-1) has the following description, indicating that the committee will consult not all products. The FDA has five centers, and the director of each center seems to have the discretion to decide whether or not to use the committees / which committees to use.</p>\n<blockquote>\n<p>The decision to involve an advisory committee is usually at the discretion of the division director in one of the FDA's five product centers.</p>\n</blockquote>\n<p>However, for the pharmaceutical products, it is common sense that one of the subcommittees under the committee on pharmaceutical products. For the medical devices, it is common sense that one of the subcommittees under the committee on pharmaceutical products.</p>\n<p>The schedule of each committee can be found at the link of (F4-2).</p>\n<p>As one example, let's look for the minutes of a committee meeting on a regenerative medicine, Mesoblast's Ryoncil for Pediatric GVHD. (This regenerative medicine appears to have been rejected by the FDA in October 2020.) Presumably, the ODAC minutes mentioned in this <a href=\"https://www.biospace.com/article/fda-rejects-mesoblast-s-remestemcel-l-for-graft-versus-host-disease/\" rel=\"nofollow noreferrer\">article</a> can be accessed from <a href=\"https://www.fda.gov/advisory-committees/human-drug-advisory-committees/oncologic-drugs-advisory-committee\" rel=\"nofollow noreferrer\">here</a>.</p>\n<hr />\n<p><strong>(E1)How do I find the review reports on EMA approved drug and regenerative medicine?</strong><br></p>\n<p>You can find review reports on EMA approved drug and regenerative medicine from <a href=\"https://www.ema.europa.eu/en/medicines/field_ema_web_categories%253Aname_field/Human/ema_group_types/ema_medicine_en/ema_group_types/ema_medicine\" rel=\"nofollow noreferrer\">here</a></p>\n<p>Don't forget check On the &quot;European public assessment reports (EPAR)&quot;(See following Figure).</p>\n<p><a href=\"https://i.stack.imgur.com/1rvGm.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/1rvGm.png\" alt=\"enter image description here\" /></a></p>\n<p>For example, that of tamiflu(drug) and alofisel(regenerative medicine) are available from the following links.</p>\n<ul>\n<li><a href=\"https://www.ema.europa.eu/en/medicines/human/EPAR/tamiflu\" rel=\"nofollow noreferrer\">https://www.ema.europa.eu/en/medicines/human/EPAR/tamiflu</a></li>\n<li><a href=\"https://www.ema.europa.eu/en/medicines/human/EPAR/alofisel\" rel=\"nofollow noreferrer\">https://www.ema.europa.eu/en/medicines/human/EPAR/alofisel</a></li>\n</ul>\n<p>The database also seems to be able to search for &quot;animal medicine&quot; and &quot;Withdrawn applications&quot; depending on the settings.</p>\n", "score": 0 } ]

[ "clinical-study", "reference-request", "regulatory-agencies" ]

[ { "answer_id": 25063, "body": "<p>The 2018 systematic review {1} whether Imiquimod 5% cream (US brand: Aldara) is helpful as an adjunctive treatment of a facial basal cell carcinoma (BCC) prior to a Mohs surgery. Summary: Two studies show it is beneficial, and one shows it wasn't but that's unlikely because they looks at nasal BCC, which tends not to respond well to Imiquimod 5% cream. Quote from {1} with more details:</p>\n<blockquote>\n<p>Some of the literature explores the option of pretreatment\nwith imiquimod 5% cream before Mohs surgery. In one\nstudy, a total of 70 adults with primary nodular BCC were\nidentified, with one group given imiquimod 5% cream for\n4 weeks prior to Mohs and the other treated only with Mohs\nsurgery. It was found that there was less of an increase in\ntumor size and area from baseline, fewer Mohs stages, and\nshorter reconstruction times in the group given neoadjuvant\nimiquimod [22]. Another study used reflectance-mode\nconfocal microscopy as well as histological imaging to confirm\ndecreased tumor burden with the use of 5% imiquimod\ncream used before Mohs excision. When two, four, and six\nweek regimens were tested in comparison to vehicle cream,\nthe four and six week regimen groups showed significant\nreduction or clearance of tumors with confocal microscopic\nfindings that paralleled histologic diagnosis [23].</p>\n<p>Of note, one study was found to have different findings. In\nthis study, a total of 31 patients were followed. Some applied\nimiquimod cream each night for 6 weeks and underwent a\n4 week rest period prior to having Mohs surgery, while the\nothers underwent only Mohs surgery. No differences were\nfound in the number of Mohs stages, tumor sizes, or costs\nbetween the two groups. In the treatment group, 5 of 12\nremaining patients were confirmed on histology to be clear\nof tumor. In this study adjunctive imiquimod 5% cream\nbefore Mohs surgery was not found to be useful in treating\nnodular BCC, in fact the clearance of the nasal nodular BCC\npre-treated with imiquimod before Mohs was less than what\nhad been found in prior studies [24]. However, compared to\nother studies, this study had a smaller sample size. Furthermore,\nthis study specified nasal BCCs, which may respond\nless to imiquimod therapy.</p>\n<ul>\n<li>[22]. van der Geer S, Martens J, van Roij J, Brand E, Ostertag JU,\nVerhaegh ME, et al. Imiquimod 5% cream as pretreatment\nof Mohs micrographic surgery for nodular basal cell carcinoma\nin the face: a prospective randomized controlled study.\nBr J Dermatol. 2012;167(1):110–5. <a href=\"https://doi.org/10.1111/j.1365-2133.2012.10924.x\" rel=\"nofollow noreferrer\">https://doi.org/10.1111/j.1365-2133.2012.10924.x</a></li>\n<li>[23]. Torres A, Niemeyer A, Berkes B, Marra D, Schanbacher C, Gonzalez\nS, et al. 5% imiquimod cream and reflectance-mode confocal\nmicroscopy as adjunct modalities to Mohs micrographic surgery\nfor treatment of basal cell carcinoma. Dermatol Surg. 2004;30(12\nPt 1):1462–9. <a href=\"https://doi.org/10.1111/j.1524-4725.2004.30504.x\" rel=\"nofollow noreferrer\">https://doi.org/10.1111/j.1524-4725.2004.30504.x</a></li>\n<li>[24]. Butler DF, Parekh PK, Lenis A. Imiquimod 5% cream as adjunctive\ntherapy for primary, solitary, nodular nasal basal cell carcinomas\nbefore Mohs micrographic surgery: a randomized, double\nblind, vehicle-controlled study. Dermatol Surg. 2009;35(1):24–9. <a href=\"https://doi.org/10.1111/j.1524-4725.2008.34378.x\" rel=\"nofollow noreferrer\">https://doi.org/10.1111/j.1524-4725.2008.34378.x</a></li>\n</ul>\n</blockquote>\n<hr />\n<p>References:</p>\n<ul>\n<li>{1} Kamath, Preetha, Evan Darwin, Harleen Arora, and Keyvan Nouri. &quot;A review on imiquimod therapy and discussion on optimal management of basal cell carcinomas.&quot; Clinical drug investigation 38, no. 10 (2018): 883-899. <a href=\"https://doi.org/10.1007/s40261-018-0681-x\" rel=\"nofollow noreferrer\">https://doi.org/10.1007/s40261-018-0681-x</a></li>\n</ul>\n", "score": 0 } ]

[ "dermatology", "treatment", "basal-cell-carcinoma" ]

[ { "answer_id": 25004, "body": "<p>I have not found any whitening properties of tea tree oil but it can help prevent tooth discolouration and I have seen toothpaste with tea tree oil sold in shops.</p>\n<p><a href=\"http://saspublisher.com/wp-content/uploads/2014/03/SJAMS-21C253-257.pdf\" rel=\"nofollow noreferrer\">Jain et al. (2014)</a> states:</p>\n<blockquote>\n<p>Tea tree oil’s major active component is terpinen-4-ol (30%–40%). This compound is responsible for its antibacterial and antifungal\nproperties [(<a href=\"https://doi.org/10.1007/s007840050118\" rel=\"nofollow noreferrer\">Arweiler, et al. 2000</a>)].</p>\n</blockquote>\n<p><a href=\"https://doi.org/10.1016/j.jab.2017.08.001\" rel=\"nofollow noreferrer\">Chromogenic bacteria</a> can cause tooth discolouration, pore formation in teeth and also has the ability to form biofilm (<a href=\"https://doi.org/10.1016/j.jab.2017.08.001\" rel=\"nofollow noreferrer\">Ashe, et al. 2017</a>).</p>\n<p><a href=\"http://saspublisher.com/wp-content/uploads/2014/03/SJAMS-21C253-257.pdf\" rel=\"nofollow noreferrer\">Jain et al. (2014)</a> also states:</p>\n<blockquote>\n<p>Using tea tree oil orally is not recommended as it may cause possibly serious side effects such as confusion, loss of muscle control, or coma. In dentistry, tea tree oil has been used to destroy microorganisms in the mouth before dental surgery, removal of smear layer when used as a root canal irrigant and to relieve mouth soreness caused by dental procedures [9-12]. In studies\nof patients who suffered from oral candidiasis mouth rinses containing tea tree oil have shown some effectiveness in reducing symptoms when taken in a\ndose of one table spoonful of 5% tea tree oil solution as a mouth wash that is held in the mouth and then spit out\nfour times a day for up to 4 weeks [13, 14].</p>\n</blockquote>\n<h2>References</h2>\n<p>Arweiler, N. B., Donos, N., Netuschil, L., Reich, E., &amp; Sculean, A. (2000). Clinical and antibacterial effect of tea tree oil–a pilot study. <em>Clinical oral investigations, 4</em>(2), 70-73. <a href=\"https://doi.org/10.1007/s007840050118\" rel=\"nofollow noreferrer\">https://doi.org/10.1007/s007840050118</a></p>\n<p>Ashe, S., Agasti, S., Lakkoji, S., Rauta, P. R., Sahoo, H., Mishra, M., &amp; Nayak, B. (2017). Novel chromogenic bacteria characterized and their probable treatment options using herbal products and reagents to restrict biofilm formation. <em>Journal of Applied Biomedicine, 15</em>(4), 291-298. <a href=\"https://doi.org/10.1016/j.jab.2017.08.001\" rel=\"nofollow noreferrer\">https://doi.org/10.1016/j.jab.2017.08.001</a></p>\n<p>Jain, N., Rajwar, Y. C., Batra, M., Singh, H. P., Bhandari, R., &amp; Agarwal, P. (2014). Dentistry: Turning towards herbal alternatives: A review. <em>Scholars Journal of Applied Medical Sciences, 2</em>(1C), 253-7. <a href=\"http://saspublisher.com/sjams-21/\" rel=\"nofollow noreferrer\">http://saspublisher.com/sjams-21/</a></p>\n", "score": 1 } ]

[ "dentistry", "natural-remedy", "bleach-teeth-whitening" ]

[ { "answer_id": 25052, "body": "<p>There are many different ways of <a href=\"https://en.wikipedia.org/wiki/Fat#Classification\" rel=\"nofollow noreferrer\">classifying fats</a>, including:</p>\n<ul>\n<li>Chain length of the constituent fatty acids. This is mostly of interest in determining if the fat will be solid or liquid at room temperature, so it doesn't show up on nutrition labels.</li>\n<li>Presence of carbon-carbon double bonds in the constituent fatty acids. Saturated fats don't have any double bonds, while unsaturated fats do. (Monounsaturated fats have one double bond per fatty acid, while polyunsaturated fats have multiple double bonds.)</li>\n<li>The arrangement of atoms around any carbon-carbon double bonds. <em>Cis</em>-fatty acids have a &quot;C&quot; shape, while <em>trans</em>-fatty acids have a zig-zag shape.</li>\n</ul>\n<p>The nutrition label you show lists only some of the constituent fats of the product: the saturated fats, and those unsaturated fats with a <em>trans</em> arrangement. <em>Cis</em>-unsaturated fats aren't listed.</p>\n", "score": 2 }, { "answer_id": 25039, "body": "<p>The FDA's <a href=\"https://www.fda.gov/files/food/published/Food-Labeling-Guide-%28PDF%29.pdf\" rel=\"nofollow noreferrer\">food labeling guide</a> is a more complete reference.</p>\n<p>Importantly, these labels are not precise to any scientific standard. Fat quantities are rounded to the nearest gram or half gram, fat quantities &lt;0.5g are reported as zero, only saturated and trans fats must be labeled separate from total fat (if &gt;0.5g per serving) and others are up to the manufacturer. These are meant to provide general information to consumers, not to be an exact representation.</p>\n<p><a href=\"https://en.wikipedia.org/wiki/Omega-3_fatty_acid\" rel=\"nofollow noreferrer\">Omega-3</a> fats are a particular category of polyunsaturated fat. Manufacturers can add information about unsaturated fat as a whole or in categories, often separated into polyunsaturated and monounsaturated fats, but they don't have to. Often when they do it's because they are attempting to make some sort of health claim, so this is a form of allowed marketing rather than a government standard.</p>\n", "score": 1 } ]

[ "nutrition" ]

[ { "answer_id": 25104, "body": "<p><a href=\"https://emedicine.medscape.com/article/276624-workup#c8\" rel=\"nofollow noreferrer\">https://emedicine.medscape.com/article/276624-workup#c8</a> (<a href=\"https://web.archive.org/web/20201113033425/https://emedicine.medscape.com/article/276624-workup\" rel=\"nofollow noreferrer\">mirror</a>) explains that using a shave biopsy is the typical biopsy to use but a punch biopsy is preferable in some situations:</p>\n<blockquote>\n<p>A skin biopsy is often required to confirm the diagnosis and determine the histologic subtype of basal cell carcinoma (BCC). Most often, a <strong>shave biopsy</strong> is all that is required. Nevertheless, in the case of a pigmented lesion where there may be difficulty distinguishing between pigmented BCC and melanoma, an excisional or <strong>punch biopsy</strong> may be indicated; this is to ensure that the depth of the lesion can be determined if it proves to be a malignant melanoma.</p>\n<p>In most cases, a superficial biopsy specimen that contains dermis is all that is required to confirm the diagnosis of BCC, although it is possible to miss the tumor. For example, an ulcerated BCC may reepithelialize with normal epidermis while tumor is still present at a deeper level. Part or all of the BCC may be sampled, but avoid going beyond the clinical margins if the biopsy is only for diagnostic purposes.</p>\n<p>Punch biopsy is an easy method to obtain a thick specimen, but is rarely required. The most suspicious area of a lesion may be sampled, or multiple biopsy samples may be taken if the tumor is large or has a varied appearance in different areas. Avoid punch biopsy if curettage is planned for final treatment.</p>\n</blockquote>\n", "score": 1 } ]

[ "dermatology", "biopsy", "basal-cell-carcinoma" ]

[ { "answer_id": 25180, "body": "<p>I think this question is too vague for a definite answer, but areas to consider would include:</p>\n<ul>\n<li>confounding vs effect modifier: where do smoking and condition A lie in relation to the outcome of mortality?</li>\n<li>matched pairs study: if it is ethical, you could get a simple random sample consisting of people with condition A that do not smoke and pair each individual in that sample with another individual in a simple random sample consisting of people with condition A that do smoke.</li>\n<li>case-control study: this study design is useful for if condition A is a rare disease (note: not rare exposure; in that case you would use a cohort study). You would then adjust for confounding variables based on your study population.</li>\n</ul>\n", "score": 1 } ]

[ "research", "smoking", "cause-and-effect" ]

[ { "answer_id": 25162, "body": "<p>The 2010 study {1} reviewed a few existing studies and seems to lean toward age as not having an impact on the recurrence rate (however, note that 1 of the reviewed studies does indicate youth+female as a risk factor of recurrence after Mohs surgery):</p>\n<p>(NMSC = non-melanoma skin cancer, e.g. basal cell carcinoma (BCC))</p>\n<blockquote>\n<p>Young Age Is Not a Clinical Risk Factor\nAlthough young age (typically &lt; 40 years) is generally\nviewed as a clinical risk factor for aggressive NMSC behavior, after much deliberation the panel\ndecided it is not. The published biomedical literature\ndoes not strongly support “young age,” per se, as a\nrisk factor. Leffell et al.{46} documented an increased\npercentage of basal cell cancer with aggressive histologic\ngrowth patterns in young persons, but this\nhistologic feature is already a separate risk factor in\nthe algorithm</p>\n<p>When the features of 54 basal cell cancers in\nyoung patients referred for Mohs surgery were compared\nwith similar tumors in older patients,{47} tumor\nlocation, histology, and clinical morphology did not\ndiffer appreciably between the groups. In fact, initial\nlesion and final defect sizes were statistically smaller\nin the younger group. In a study from the United\nKingdom in which 39 young patients with basal cell\ncancer were followed up for a minimum of 5 years,{48}\n4 tumors were incompletely excised, 2 recurred, and\n1 metastasized. Another study observed a higher\nnumber of recurrent tumors in younger women referred\nfor Mohs surgery than in other demographic\ngroups.{49} Finally, 2 more recent studies found no difference\nin either recurrence rates or presence of aggressive\nhistologic subtypes in younger versus older\npatients with basal cell skin cancer.{50,51}</p>\n<p>The panel decided that, taken together, these\nstudies do not support the suggestion that young age\nalone is a high-risk factor for NMSC behavior. Any\ntumor showing an aggressive histologic growth pattern,\nregardless of patient age, becomes a high-risk\ntumor.</p>\n</blockquote>\n<hr />\n<p>References:</p>\n<ul>\n<li>{1} Miller SJ, Alam M, Andersen J, et al. Basal cell and squamous cell skin cancers. J Natl Compr Canc Netw 2010; 8:836. <a href=\"https://jnccn.org/view/journals/jnccn/8/8/article-p836.xml;\" rel=\"nofollow noreferrer\">https://jnccn.org/view/journals/jnccn/8/8/article-p836.xml;</a> DOI: <a href=\"https://doi.org/10.6004/jnccn.2010.0062\" rel=\"nofollow noreferrer\">https://doi.org/10.6004/jnccn.2010.0062</a></li>\n<li>{46} Leffell DJ, Headington JT, Wong DS, Swanson NA. Aggressivegrowth\nbasal cell carcinoma in young adults. Arch Dermatol\n1991;127:1663–1667.</li>\n<li>{47} Dinehart SM, Dodge R, Stanley WE, et al. Basal cell carcinoma\ntreated with Mohs surgery. A comparison of 54 younger patients\nwith 1050 older patients. J Dermatol Surg Oncol 1992;18:560–566.</li>\n<li>{48} Cox NH. Basal cell carcinoma in young adults. Br J Dermatol\n1992;127:26–29.</li>\n<li>{49} Robins P, Albom MJ. Recurrent basal cell carcinomas in young\nwomen. J Dermatol Surg 1975;1:49–51.</li>\n<li>{50} Milroy CJ, Horlock N, Wilson GD, Sanders R. Aggressive basal\ncell carcinoma in young patients: fact or fiction? Br J Plast Surg\n2000;53:393–396.</li>\n<li>{51} Roudier-Pujol C, Auperin A, Nguyen T, et al. Basal cell carcinoma\nin young adults: not more aggressive than in older patients.\nDermatology 1999;199:119–123.</li>\n</ul>\n", "score": 1 } ]

[ "dermatology", "basal-cell-carcinoma" ]

[ { "answer_id": 25226, "body": "<p>I second Thomas' suggestion of pubmed.gov! Below are some details of my favorite sources for this kind of thing.</p>\n<p>NOTE - It can definitely be tricky to find reliable sources that aren't behind a paywall using databases, but once you know a specific article you can often chuck the citation into regular google to find a free version. If you can't find a specific article that you really want to read, you can always reach out to one or more of the authors; (in most cases) they can legally send you a copy for free and many will.</p>\n<p><strong><a href=\"https://pubmed.gov\" rel=\"nofollow noreferrer\">Pubmed</a></strong></p>\n<ul>\n<li>Run by National Library of Medicine (VERY reliable)</li>\n<li>Citations for 30 million+ journal articles and textbooks</li>\n<li>User-friendly searching</li>\n<li>Usually free abstract</li>\n<li>Usually links to full article (though many links lead behind a paywall)</li>\n</ul>\n<p><strong><a href=\"https://cochranelibrary.com\" rel=\"nofollow noreferrer\">Cochrane Library</a></strong></p>\n<ul>\n<li>Run by the same company as Cochrane Reviews, pretty much the gold standard in review articles</li>\n<li>Search journal articles and/or Cochrane Reviews\n<ul>\n<li>In reviews, experts look all the literature available on the subject and write a summary about what the literature says as a whole. I like this because you're less likely to be led astray by a single study, which might contradict dozens of other, better-designed studies.</li>\n</ul>\n</li>\n<li>For reviews, usually have the citation, a free abstract, and a free plain-language summary of the findings</li>\n<li>Full articles are (usually) behind a paywall</li>\n</ul>\n<p><strong><a href=\"https://medlineplus.com\" rel=\"nofollow noreferrer\">MedlinePlus</a></strong></p>\n<ul>\n<li>Run by National Library of Medicine</li>\n<li>Search a broad range of sources:\n<ul>\n<li>FDA medication summaries (here's the one for <a href=\"https://medlineplus.gov/statins.html\" rel=\"nofollow noreferrer\">statins</a>, for example)</li>\n<li>Online articles from reliable, but not peer-reviewed, sources (e.g., an article from the Mayo Clinic on <a href=\"https://www.mayoclinic.org/diseases-conditions/high-blood-cholesterol/expert-answers/rhabdomyolysis/FAQ-20057817?p=1\" rel=\"nofollow noreferrer\">Rhabdomyolosis and Statins</a>)</li>\n<li>Information on ongoing clinical trials (obligatory <a href=\"https://clinicaltrials.gov/search/open/condition=%22Hydroxymethylglutaryl-CoA+Reductase+Inhibitors%22\" rel=\"nofollow noreferrer\">statin example</a>)</li>\n<li>etc.</li>\n</ul>\n</li>\n<li>All free!</li>\n</ul>\n<p><strong>Merck Manual, <a href=\"https://www.merckmanuals.com/professional\" rel=\"nofollow noreferrer\">Professional</a> and <a href=\"https://www.merckmanuals.com/home\" rel=\"nofollow noreferrer\">Consumer</a> Editions</strong></p>\n<ul>\n<li>This is the online version of the print dictionaries Merck has produced for decades. My grandfather, a research-enthusiast primary care doctor, was a HUGE fan\n<ul>\n<li>Extremely reliable</li>\n<li>Reflects actual current recommendations; recent journal publications don't always reflect how things are done &quot;in the real world&quot;</li>\n</ul>\n</li>\n<li>Thousands of pages explaining diseases and medications, plus clinical calculators, reference values (e.g. for bloodwork)</li>\n<li>The Professional Edition is more science-y, but you don't need to be an MD to understand most of it. The Consumer Edition is very easy to understand.</li>\n<li>I write fiction as a hobby, and I use this all the time as a quick reference for pretty much anything related to health and medicine</li>\n<li>I also find this to be the most user-friendly, and they have a pretty nice iOS app</li>\n<li>All free!</li>\n</ul>\n<p>If you're really looking for original research, Pubmed and Cochrane Library are your best bets.</p>\n<p>If you're looking for free, reliable info that isn't necessarily from original research articles, MedlinePlus and Merck Manual will serve you well.</p>\n", "score": 4 } ]

[ "research" ]

[ { "answer_id": 25259, "body": "<p>Both of these studies involve a rodent inflammation model where complete freund's adjuvant is injected to incite inflammation, and then rats are given an alcohol-based coriander seed extract or other injections.</p>\n<p>These are pretty low-quality papers in low-quality journals. I'll start with the one you link second:</p>\n<hr />\n<p>Deepa, B., Acharya, S., &amp; Holla, R. (2020). Evaluation of antiarthritic activity of Coriander seed essential oil in Wistar albino rats. Research Journal of Pharmacy and Technology, 13(2), 761-766.</p>\n<p>This study, which declares &quot;The TNF α levels were statistically reduced by CSEO group compared to Indomethacin group.&quot; makes this declaration based on &quot;p&lt;0.05&quot; where the p-value they actually report is 0.055. 0.055 is not less than 0.05, and based on their statistical threshold they should not have rejected the null hypothesis of no effect.</p>\n<p>Importantly, they also completely failed their Stats 101 class and instead of comparing the interaction between Time (i.e., baseline vs 21 days) and Treatment, they just compare Baseline to Day 21 in individual groups. This is wrong, and not meaningful. At worst, they should have compared Day 21 among treatment groups, but they did not do this. Their statistical tests do not measure what they say they do.</p>\n<p>You can throw this study in the bin, it's worthless as presented, and it's embarrassing to the journal, the researchers, and their institution that it was published.</p>\n<hr />\n<p>Nair, V., Singh, S., &amp; Gupta, Y. K. (2012). Evaluation of disease modifying activity of Coriandrum sativum in experimental models. The Indian journal of medical research, 135(2), 240.</p>\n<p>The other paper is not quite as bad, but still lacking in statistical methodology. They don't really provide enough information to critique their analysis, which to me is sufficient to consider it junk. You don't make your case better by leaving out details that can be used to critique, we have to assume that those details are hiding something when they are missing. They present standard errors that are miniscule compared to what one would expect in these sorts of experiments, so I have to assume that they may have included pseudoreplication by testing multiple samples from the same animals and not accounting for these multiple comparisons in the statistical analysis.</p>\n<p>They've also used a vehicle (control) that is sufficiently different from their treatment that it is just as likely that the non-active ingredients cause the effects they see.</p>\n<p>Their IL-6 results are purely qualitative, and even the qualitative approach they use is seriously lacking. Basically &quot;look at these example pictures and trust us&quot;.</p>\n<hr />\n<p>In summary, these studies do not actually conflict because they do not actually show anything robust - on this they are actually quite in agreement.</p>\n", "score": 3 } ]

[ "immune-system", "autoimmune-disease", "inflammation", "cytokines" ]

[ { "answer_id": 25284, "body": "<p>No one coordinates global vaccine production. Vaccines, like other pharmaceuticals, are produced by individual companies. Individual companies have been entering into agreements with individual governments to deliver vaccine for the residents of their countries.</p>\n<p>The Bill and Melinda Gates foundation has made <a href=\"https://www.gavi.org/\" rel=\"nofollow noreferrer\">GAVI</a> (along with partners in the WHO and UNICEF) as a <a href=\"https://en.wikipedia.org/wiki/GAVI\" rel=\"nofollow noreferrer\">public-private partnership</a> to do something like maybe what you are thinking of as coordination to try to ensure poorer countries have vaccine access, and they now have a Covid-19 vaccination program, but this is really just an effort to combine resources among those that have the fewest resources. They don't have any say over what other countries do.</p>\n", "score": 4 } ]

[ "covid-19" ]

[ { "answer_id": 25309, "body": "<p>I am unaware of any mechanism by which exercise can cause &quot;blood alkalization&quot; (usually called &quot;alkalosis&quot;).</p>\n<p>Blood pH is VERY tightly regulated at 7.35-7.45 (slightly alkaline), so it rarely changes much except in severe illness.</p>\n<p>That said, slight acidosis can occur in exercise due to an increase in carbon dioxide released from muscles (<a href=\"https://medlineplus.gov/ency/article/000092.htm\" rel=\"nofollow noreferrer\">Medline Plus - Respiratory Acidosis</a>). Onset would depend heavily on a person's conditioning and the intensity of exercise, with poor conditioning and high intensity being associated with faster onset. In most cases, any acidosis would dissipate quickly after stopping exercise - i.e. within minutes. After heavy exercise it may take a bit longer. (<a href=\"https://pubmed.ncbi.nlm.nih.gov/1568991/\" rel=\"nofollow noreferrer\">PubMed - Acid-base regulation during exercise and recovery in humans</a>)</p>\n<p>Over production of lactic acid may also cause acidosis during exercise, but this is up for debate (<a href=\"https://bjsm.bmj.com/content/38/5/622?__cf_chl_jschl_tk__=9586c059d64990bbc2715aa49eaf0497ff122170-1608160071-0-AZWfSoKW2FiITIHgj5NYCTVy6-77XXYNB-A_5heDcfHPWLv_prTI4-3iLjTG3YK4D8cB2sb2HoGIdVz5XYbhek6wfqaoa1mzUpOYWglaQe1O9qDMMbTw5wp9xsrvwgLJ6NU2NBMrWS-NPTAQzU1L1VbQSqyuyH2M5tACG96t3kpr-iXDLEUq9RpdoKvc6ddGpjfvCbC0NJq9QrlOIcjTjiYiIB9DlwtYwmluQcNfC-_0_sFHWLBGHUm9xqpXNGxRCyk_B4sBdZTVDA21W1b6OgnPFD0PXpPwTewNqNP4IRUsepUoq6ZHOAR93TDOqnV-Kb-viyfFADNyBoA2Xo7_af0\" rel=\"nofollow noreferrer\">this BMJ article</a> says yes, whereas <a href=\"https://journals.physiology.org/doi/full/10.1152/ajpregu.00114.2004#:%7E:text=The%20development%20of%20acidosis%20during,the%20acid%20salt%20sodium%20lactate\" rel=\"nofollow noreferrer\">this review from the American Journal of Physiology</a> says no, for example).\nIn any case, severe lactic acidosis occurs much more commonly due to serious diseases like AIDs, sepsis, or kidney failure (<a href=\"https://medlineplus.gov/ency/article/000391.htm\" rel=\"nofollow noreferrer\">Medline Plus - Lactic Acidosis</a>).</p>\n<p>Further, heavy breathing in exercise doesn't &quot;build up acidity&quot;, it counter-acts acidosis by getting rid of the excess carbon dioxide. Severe hyperventilation not during exercise (e.g. during a panic attack) can cause slight alkalosis because it causes a person to exhale more carbon dioxide than their body is producing (<a href=\"https://medlineplus.gov/ency/article/000111.htm\" rel=\"nofollow noreferrer\">Medline Plus - Respiratory Alkalosis</a>).</p>\n<p>In addition to the links above, I suggest you look at these Medline Plus pages; they do a good job explaining blood acidosis and alkalosis:</p>\n<p><a href=\"https://medlineplus.gov/ency/article/000335.htm\" rel=\"nofollow noreferrer\">Metabolic Acidosis</a></p>\n<p><a href=\"https://medlineplus.gov/ency/article/001183.htm\" rel=\"nofollow noreferrer\">Alkalosis - General</a></p>\n", "score": 3 } ]

[ "exercise", "blood-tests", "acidic", "hyperventilation", "alkaline" ]

[ { "answer_id": 25389, "body": "<p>Two things that come to mind:</p>\n<ul>\n<li>Unlike COVID-19, the herpes virus does not completely shut down society. So there's much more incentive and hence funding to finding a vaccine for COVID-19.</li>\n<li>We already have researched (but not completed) vaccines for other corona-type diseases like SARS and MERS, and luckily this knowledge helped in accelerating the process of finding a vaccine for COVID-19. See e.g. <a href=\"https://jbiomedsci.biomedcentral.com/articles/10.1186/s12929-020-00695-2\" rel=\"nofollow noreferrer\">the recently published article 'Coronavirus vaccine development: from SARS and MERS to COVID-19'</a>.</li>\n</ul>\n", "score": 5 } ]

[ "covid-19", "vaccination", "herpes" ]

[ { "answer_id": 25438, "body": "<p>The long-term side effects are typically studied within the framework of the <a href=\"https://en.m.wikipedia.org/wiki/Survival_analysis#:%7E:text=Survival%20analysis%20is%20a%20branch,and%20failure%20in%20mechanical%20systems.\" rel=\"nofollow noreferrer\">survival analysis</a>. E.g., a cohort if individuals is followed throughout many years, recording the number of cases of adverse side effects and deaths, or none happening (<em>censored data</em>). Previous medicalninterventions, short-term side effects, and other risk factors are included as statistical covariates. One can then use the methods of the survival analysis, such as Cox regression, to establish whether any of these risk factors is related to the incidence of the adverse conditions.</p>\n<p>In the context of new types of medication/intervention, such a study essentially constitutes the Phase IV clinical study, which often lasts throughout all the time while the medication/intervention is in use.</p>\n", "score": 1 } ]

[ "medications" ]

[ { "answer_id": 25683, "body": "<p>It's not clear to me if any of this has been confirmed to a good degree (meaning in terms of actual mechanisms), but in the realm of hypotheses, a fairly cited <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7167588/\" rel=\"nofollow noreferrer\">paper</a> indeed links ACE2 deficiency (caused by a combination of genetic and viral factors) with thrombotic processes:</p>\n<blockquote>\n<p>Clinical reports of patients infected with SARS-CoV-2 show that several features associated with infection and severity of the disease (i.e., older age, hypertension, diabetes, cardiovascular disease) share a variable degree of ACE2 deficiency. We suggest that ACE2 down-regulation induced by viral invasion may be especially detrimental in people with baseline ACE2 deficiency associated with the above conditions. The additional ACE2 deficiency after viral invasion might amplify the dysregulation between the ‘adverse’ ACE→Angiotensin II→AT1 receptor axis and the ‘protective’ ACE2→Angiotensin1-7→Mas receptor axis. In the lungs, such dysregulation would favor the progression of inflammatory and thrombotic processes triggered by local angiotensin II hyperactivity unopposed by angiotensin1-7.</p>\n</blockquote>\n<p>But even this paper notes that there are obviously competing or concurrent mechanisms, at least in the lungs, responsible for lung symptoms:</p>\n<blockquote>\n<p>the damage of pneumocytes type II due to the binding of coronavirus to ACE2 receptors is devastating for at least three reasons: 1) local unopposed ACE→Angiotensin II→AT1 receptor axis over-activity; 2) reduced production of alveolar surfactant by injured pneumocytes type II leading to reduced lung elasticity; 3) reduced repair of pneumocytes type I leading to impaired gas exchanges and fibrosis.</p>\n</blockquote>\n<p>There's <a href=\"https://www.ahajournals.org/doi/full/10.1161/CIRCRESAHA.120.317447\" rel=\"nofollow noreferrer\">another paper</a> (citing the above) on &quot;(micro)thrombosis&quot; in Covid-19 patients, but again it does little more than\nrepeat that hypothesis, although it does mention a couple of experiments:</p>\n<blockquote>\n<p>human blood vessel organoids, which closely resemble human capillaries, contain viral RNA after exposure to COVID-19 in vitro. Strikingly, the application of human recombinant soluble ACE-2 markedly inhibited viral infection in human capillary organoids, pointing to a direct role for endothelial ACE-2 in viral uptake in blood vessels. Intriguingly, the uptake of SARS-CoV-2 into cells is associated with the downregulation of ACE-2 expression. This appears to play an important role in promoting a proinflammatory and prothrombotic milieu since ACE-2 plays a pivotal role in regulating the RAS (renin-angiotensin system), by degrading angiotensin II to angiotensin 1–7. While angiotensin II induces vasoconstriction and promotes a proinflammatory/prothrombotic phenotype, angiotensin 1–7 opposes these effects via binding to the MAS receptor, which is widely expressed including on endothelial cells and platelets.</p>\n</blockquote>\n", "score": 1 } ]

[ "coronavirus", "blood-pressure" ]

[ { "answer_id": 25507, "body": "<p>No, there is no infection &quot;found or originating primarily or solely in the nape&quot;. Any skin infection (eg. Staphyloccus, Streptococcus) can affect the nape of the neck. Hope this helps.</p>\n", "score": 1 } ]

[ "virus", "bacteria", "infectious-diseases", "neck", "fungal-infection" ]

[ { "answer_id": 25609, "body": "<p>Yes of course; it would not be possible to create epidemiological models without some measure of time.</p>\n<p>The equivalent of what you ask for is usually expressed as the number of infection-causing contacts per unit time, or as a total rate of contacts times a probability of transmission. Typically R is derived from this number rather than the other way around, since R is given by (rate of infected)*(time infectious).</p>\n<p>See <a href=\"https://en.m.wikipedia.org/wiki/Basic_reproduction_number\" rel=\"nofollow noreferrer\">https://en.m.wikipedia.org/wiki/Basic_reproduction_number</a> and <a href=\"https://en.m.wikipedia.org/wiki/Compartmental_models_in_epidemiology\" rel=\"nofollow noreferrer\">https://en.m.wikipedia.org/wiki/Compartmental_models_in_epidemiology</a></p>\n", "score": 1 }, { "answer_id": 25610, "body": "<h2>Clinical</h2>\n<p>The term &quot;<a href=\"https://en.wikipedia.org/wiki/Serial_interval\" rel=\"nofollow noreferrer\">serial interval</a>&quot; refers to the time between successive cases; there are a number of similar serial interval statistics.</p>\n<p>The clinical onset serial interval is defined in terms of symptoms: the mean time between symptoms appearing in an infected person, and the symptoms appearing in the infectees. This can also be used to estimate the serial interval empirically.</p>\n<p>The diagnostic serial interval is the mean time between diagnoses for the infector and infectees.</p>\n<p>The interval between successive infections is usually called <em>the</em> serial interval. The theoretical value of the serial interval is estimated to be the sum of the mean latent period (time from infection to infectiousness) and half the infectious period; whether this value has its own name, I haven't been able to determine. The &quot;average transmission interval&quot; is the sum of the mean latent period and the full infectious period.</p>\n<p>See &quot;<a href=\"https://academic.oup.com/aje/article/158/11/1039/162725\" rel=\"nofollow noreferrer\">The Interval between Successive Cases of an Infectious Disease</a>&quot; for a more extensive description.</p>\n<h2>Modeling</h2>\n<p>For a prevalent class of epidemiological models, compartmental models, the population is partitioned into groups, such as susceptible, infectious and immune (called &quot;removed&quot;). The transition rate between susceptible and infectious compartments (∂(S/N)/∂t) corresponds to the concept in the question. With:</p>\n<ul>\n<li><code>β</code> being the average number of contacts per person over a unit of time,</li>\n<li><code>S</code> being the number of susceptible individuals,</li>\n<li><code>I</code> being the number of infected individuals, and</li>\n<li><code>N</code> being the total population,</li>\n</ul>\n<p><img src=\"https://chart.googleapis.com/chart?cht=tx&amp;chl=%5Cfrac%7B%5Cpartial+%5Cfrac%7BS%7D%7BN%7D%7D%7B%5Cpartial+t%7D%3D%5Cfrac%7B-%5Cbeta+S+I%7D%7BN%5E%7B2%7D%7D\" alt=\"d(S/N)/dt = -βSI/N²\" /></p>\n", "score": 1 } ]

[ "epidemiology", "statistics" ]

[ { "answer_id": 25714, "body": "<p>The <strong>official</strong> source for information on death records is the Office of National Statistics (ONS) and there are stats available with <a href=\"https://www.ons.gov.uk/peoplepopulationandcommunity/birthsdeathsandmarriages/deaths/datasets/monthlyfiguresondeathsregisteredbyareaofusualresidence\" rel=\"nofollow noreferrer\">monthly figures</a> and <a href=\"https://www.ons.gov.uk/peoplepopulationandcommunity/birthsdeathsandmarriages/deaths/datasets/weeklyprovisionalfiguresondeathsregisteredinenglandandwales\" rel=\"nofollow noreferrer\">weekly figures</a>.</p>\n<p>When you look at the weekly total deaths figures for 2019 for example, you notice a drop in numbers during the last week of May, the last 2 weeks of August, and Christmas week.</p>\n<p>When you look at the monthly figures, the figures are pretty consistent except there is a much higher figure in January and there are lower figures in June, August and September. Strangely, July's figures are fairly consistent with the rest of the year.</p>\n<p>Averages are:</p>\n<blockquote>\n<p>based on the actual number of death registrations recorded for each corresponding week over the previous five years. Moveable public holidays, when register offices are closed, affect the number of registrations made in the published weeks and in the corresponding weeks in previous years.</p>\n</blockquote>\n<p>This could also explain the high figure for January as Christmas will shift some of the December figures into January.</p>\n<p>The weekly stats spreadsheets downloadable from the ONS give figures for</p>\n<blockquote>\n<p>All respiratory diseases (ICD-10 J00-J99) ICD-10 v 2013 (IRIS)</p>\n</blockquote>\n<p>The trouble is that without access to ONS data held within their IRIS software, deaths by cause is difficult to ascertain for causes other than respiratory diseases, and you cannot make any meaningful data comparisons with the ONS sheets on suicides as they are <a href=\"https://www.ons.gov.uk/peoplepopulationandcommunity/birthsdeathsandmarriages/deaths/bulletins/suicidesintheunitedkingdom/previousReleases\" rel=\"nofollow noreferrer\">recorded in annual figures</a> rather than weekly or monthly.</p>\n<p>As far as I am able to find, there is no meaningful information that can be sought regarding causes for the dips in the figures you mention</p>\n", "score": 1 } ]

[ "statistics", "death", "mortality-rate", "united-kingdom" ]

[ { "answer_id": 25800, "body": "<p><a href=\"https://en.wikipedia.org/wiki/CT_scan#Adverse_effects\" rel=\"nofollow noreferrer\">CT scans use ionizing radiation</a>. It's safe to get a CT scan for a medical purpose: the marginal risks of the scan are outweighed by the diagnostic benefits. However, repeated CT scans can potentially raise the risk of cancer. Monitoring ones progress in a fitness program can easily be done with other methods that do not cause cancer. I would consider it medical malpractice to offer CT scans for the purposes you describe.</p>\n<p>MRI does not use radiation, but the machines are quite expensive to purchase and operate and potentially dangerous due to the strong magnets interacting with metal. In the US, the <a href=\"https://www.gehealthcare.com/feature-article/how-much-does-an-mri-cost\" rel=\"nofollow noreferrer\">average cost of an MRI scan is ~$2600</a>. I'm not sure what a reputable source would be for estimating the cost of an MRI in Singapore, but I see estimates in the $100s. For research or diagnosis these costs are reasonable, but I doubt there is a market of patients willing to pay that cost regularly, and are likely subsidized figures that would not be available for non-medically necessary scans.</p>\n", "score": 3 } ]

[ "mri" ]

[ { "answer_id": 25815, "body": "<p>As you found, HbA1c is glycated Haemoglobin (<a href=\"https://www.diabetes.co.uk/what-is-hba1c.html\" rel=\"nofollow noreferrer\">Hb</a>) the <a href=\"https://www.webmd.com/diabetes/guide/glycated-hemoglobin-test-hba1c\" rel=\"nofollow noreferrer\">A1c</a> bit refers to the type of Haemoglobin.</p>\n<p>POCT is Point of Care Testing. (See <a href=\"https://dx.doi.org/10.1177/1932296814538940\" rel=\"nofollow noreferrer\">https://dx.doi.org/10.1177/1932296814538940</a></p>\n<p>IFCC is International Federation of Clinical Chemistry and Laboratory Medicine (<a href=\"https://www.ifcc.org/\" rel=\"nofollow noreferrer\">https://www.ifcc.org/</a>) a standardisation program for HbA1c testing</p>\n<p>DCCT is the Diabetes Control and Complications Trial. (See <a href=\"https://www.niddk.nih.gov/about-niddk/research-areas/diabetes/blood-glucose-control-studies-type-1-diabetes-dcct-edic\" rel=\"nofollow noreferrer\">https://www.niddk.nih.gov/about-niddk/research-areas/diabetes/blood-glucose-control-studies-type-1-diabetes-dcct-edic</a>)</p>\n<p>NGSP is an organisation looking to standardise HbA1c testing (<a href=\"http://www.ngsp.org/\" rel=\"nofollow noreferrer\">http://www.ngsp.org/</a>).</p>\n<blockquote>\n<p>When the NGSP began in 1996 it was originally called the “National Glycohemoglobin Standardization Program”.  As the program grew and became international in scope the official name was shortened to the acronym.</p>\n</blockquote>\n", "score": 1 } ]

[ "diabetes", "endocrinology", "type-2-diabetes", "glycated-hemoglobin-hba1c" ]

[ { "answer_id": 25822, "body": "<p>The eGFR is calculated differently based on several factors, including sex and race. So there are different calculation formulas based on male vs female, and African American vs Caucasian. There are not currently differences for other ethnicities, but there are some studies working on validating those.</p>\n<p><a href=\"https://www.kidney.org/sites/default/files/docs/12-10-4004_abe_faqs_aboutgfrrev1b_singleb.pdf\" rel=\"nofollow noreferrer\">Source</a></p>\n", "score": 1 } ]

[ "diabetes", "kidney", "coloration-discoloration", "urine", "glomerular-filtration-grf" ]

[ { "answer_id": 25818, "body": "<p>I have found on the internet (see sources below) that the answer is in general no, for two reasons:</p>\n<ul>\n<li>the serological test must detect the antibodies related to the Spike protein, and this condition is not respected by most of rapid tests. In particular, some look for the nucleocapside protein which is contained inside the virus (not on its <em>corona</em> like the Spike protein) and it is not induced by the vaccine;</li>\n<li>the tests are actually very low in reliability.</li>\n</ul>\n<p>This result is meaningful especially for a study in a large number of people: other kind of tests have to be performed. Indeed, specific tests which look for the vaccine induced Spike protein are used.</p>\n<p>Sources:</p>\n<p><a href=\"https://www.focus.it/scienza/salute/dopo-il-vaccino-come-capire-se-si-e-immuni-alla-covid\" rel=\"nofollow noreferrer\">https://www.focus.it/scienza/salute/dopo-il-vaccino-come-capire-se-si-e-immuni-alla-covid</a>\n<a href=\"https://iris.paho.org/bitstream/handle/10665.2/53057/v44e1492020.pdf?sequence=1&amp;isAllowed=y\" rel=\"nofollow noreferrer\">https://iris.paho.org/bitstream/handle/10665.2/53057/v44e1492020.pdf?sequence=1&amp;isAllowed=y</a></p>\n<p>Hope this could help. Bye</p>\n", "score": 3 } ]

[ "covid-19", "vaccination", "test" ]

[ { "answer_id": 25827, "body": "<p><a href=\"https://en.wikipedia.org/wiki/Dry_heat_sterilization\" rel=\"nofollow noreferrer\">Dry heat sterilization</a> is fairly inefficient, time-wise, in general. According to Wikipedia, which cites the CDC for this:</p>\n<blockquote>\n<p>The proper time and temperature for dry heat sterilization is 160 °C (320 °F) for 2 hours or 170 °C (340 °F) for 1 hour or in the case of High Velocity Hot Air sterilisers 190°C (375°F) for 6 to 12 minutes.</p>\n</blockquote>\n<p>But this is for all mirco-organisms, which some of which are more hardy than coronaviruses. I'm not sure if there's a study just on the latter in re dry heat.</p>\n<p>Also this is not exactly what you're asking here, as you want to sterilize the air, but it is somewhat relevant if you're trying to do that by heat transfer from a surface, e.g. a hot plate, coil etc. Because of inefficiency relative to other methods, this way of sterilizing air it might not have been studied too much, <a href=\"https://www.sciencedirect.com/science/article/pii/S0065216408701321\" rel=\"nofollow noreferrer\">e.g.</a>:</p>\n<blockquote>\n<p>Many ways have been suggested for sterilizing air. These include destruction of microorganisms by: dry heat-gas fired or electrical; adiabatic compression; and irradiation or removal of microorganism. The removal of microorganisms involve: scrubbing, electrostatic precipitation, sieving, and filtration fibrous or granular beds. Of these, only adiabatic compression, filtration through beds of fibrous materials, and filtration through beds of granular materials have found widespread usage on an industrial scale.</p>\n</blockquote>\n<p>(Albeit that's a 1960's article, but physics didn't change much since...)</p>\n<p>The (1st) <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7340062\" rel=\"nofollow noreferrer\">(2020) paper</a> you've linked to uses a <em>heated filter</em>, so it's really a combination method. (The filter had non-zero effect even without it being heated, if you look at their graphs--fig 3.) That paper also mentions the air flow rate at which they've tested their system. Which of course is a factor in heat transfer too; e.g. they quantified the observed temperature drop with increased air flow, albeit only at couple of points.</p>\n<p>See also <a href=\"https://en.wikipedia.org/wiki/Sterility_assurance_level\" rel=\"nofollow noreferrer\">sterility assurance level</a> for what professionals mean when they say something is sterilized. Basically, it's a statistical measure/guarantee, not an absolute one. In the 2020 paper you've linked to, they set/measured that at 99.8%.</p>\n", "score": 3 } ]

[ "covid-19", "sars-cov-2", "heat", "air-temperature" ]

[ { "answer_id": 25857, "body": "<p>Stabilization means taking action so that a patient's state does not degrade. While this is often performed by paramedics, in order to be able to transport a patient to a medical facility for further treatment, it is also performed in hospitals, e.g. to stop bleeding during surgery.</p>\n<p>Surgical stabilization is stabilization through surgical means. For instance, plating a fracture to ensure primary bone healing may be considered a form of surgical stabilization. In this case, it is a stabilization in the mechanical sense of the word as well, as the two bone fragments are stably held together.</p>\n", "score": 1 } ]

[ "surgery" ]

[ { "answer_id": 25886, "body": "<p>I am unable to give medical advice here. However, the issue that they correct with a CABG is not inflammation of the arteries, it’s a buildup of plaque within the arteries in your heart.</p>\n<p>A CABG usually occurs when the plaque is too extensive to simply open up the arteries with a stent, or a combination of stenting and CABG may be used.</p>\n<p>Magnesium is an electrolyte. It is particularly important for the heart muscle, and, if too low (or too high), it can cause arrhythmias.</p>\n<p>I don’t know anything about magnesium and inflammation, but I wouldn’t start any supplements or vitamins without consulting your cardiologist or surgeon.</p>\n", "score": 1 } ]

[ "inflammation", "cabg-coronary-art-bypass" ]

[ { "answer_id": 25932, "body": "<p>Based on provisional data, yes, the death rate among vaccine recipients is much lower than that of non-recipients. But this kind of raw comparison leaves out important details, as I'll mention at the end of this post.</p>\n<p>It's not too hard to run the numbers here. Your quote says that from 2020/12/14 through 2021/03/15, there were 1913 deaths. I went to <a href=\"https://www.cdc.gov/nchs/nvss/vsrr/COVID19/index.htm\" rel=\"nofollow noreferrer\">this CDC page</a> which gives (provisional!) weekly death counts from all causes. I selected the weeks ending 2020/12/19 through 2020/12/13 as this is the closest to matching the date range you gave. Adding up the weekly totals gives a total of 843,804 deaths from all causes over that time period. Subtracting the 1913 vaccine-recipient deaths leaves 841,891 deaths that we assume were among those who did not receive the vaccine.</p>\n<p><a href=\"https://covid.cdc.gov/covid-data-tracker/#vaccinations\" rel=\"nofollow noreferrer\">This other CDC page</a> tracks the number of people who received a COVID-19 vaccine. According to that, 79,367,225 people have received at least one dose of vaccine. (Note this is less than the 109 million you quoted, as some people received two doses.) If we estimate US population at 330 million, that means the other 250,632,775 have not received a vaccine.</p>\n<p>Thus the death rate among vaccine recipients is <code>1913 / 79367225</code> or (scaling for easier-to-interpret numbers) about 2.4 deaths per 100,000 people. The death rate among non-recipients is <code>841891 / 250632775</code> or about 335.9 deaths per 100,000.</p>\n<p>Of course, there's a lot of sloppiness in these calculations. The date ranges do not correspond exactly, and even if they did, it's difficult to find reliable data on deaths up to such a recent date. There were almost surely deaths before March 13 which are not yet represented in the CDC data for various reasons. (That's why the CDC page lists <em>provisional</em> death counts.) The same is true of vaccine totals. And of course the value used for the total US population is just a very rough estimate.</p>\n<p>Also, although I don't have data on this, I would be especially suspicious of the vaccinated death count given by the CDC. As noted on that page, that death count is based on reports submitted to VAERS, which tracks adverse events. Healthcare providers are required to report deaths of vaccinated individuals. However, due to the rapid, varying, and often chaotic rollout of the vaccine, record-keeping may lag, I could easily imagine that there are people who were vaccinated and then died without their death being flagged as a death of a vaccinated person, let alone reported as such to VAERS. This would mean that the death would be included in the total of all deaths but not in the total of vaccinated deaths. (For instance, I received my first dose of the vaccine three days ago; no one has a record of this except the pharmacy where I got it. At some point they may transmit that to my insurance company or somewhere else, but if I happen to get hit by a bus next week I have serious doubt that my vaccination record would be linked up with that, at least not for some time.)</p>\n<p>As I mentioned at the beginning, though, this whole calculation is an extremely coarse way of looking at the vaccine. We are dividing the entire US population into only four groups, based on whether they are dead or alive and whether or not they received a COVID vaccine. The populations that were vaccinated first included disparate groups with wildly different mortality patterns. The benefit in reduced death rate may be even larger among the elderly, who are at high risk of death from COVID if infected; on the other hand, the figures for total deaths and total population include children under 16, who cannot yet even receive the vaccine.</p>\n<p>Over the time period in question about a quarter of all deaths in the US &quot;involved COVID-19&quot; according to the CDC. The death rates above are broadly consistent with the idea that the vaccine is reducing the death rate due to COVID, but I wouldn't want to read too much into them.</p>\n", "score": 2 } ]

[ "covid-19", "death" ]

[ { "answer_id": 25994, "body": "<p>According to <a href=\"https://www.researchgate.net/publication/260432019_Neural_Mechanisms_Underlying_Lower_Urinary_Tract_Dysfunction\" rel=\"nofollow noreferrer\">this paper</a> (full text freely available), &quot;the somatic pudendal nerve stimulates striated muscle of the external urethral sphincter, mediated by ACh activating nicotinic (N) receptors&quot; (from Figure 2 caption).</p>\n<p>And here is Figure 2 from that paper:\n<a href=\"https://i.stack.imgur.com/vXxR8.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/vXxR8.png\" alt=\"enter image description here\" /></a></p>\n<p>On page 83 of the paper the Guarding Reflex - which is the bladder-to-external urethral sphincter (EUS) reflex - is explained, and in the top-right it says:</p>\n<blockquote>\n<p>In order for the guarding reflex to be reversed and the EUS relaxed, a final inhibitory signal is generated from the pontine micturition center (PMC). Bladder afferent fibers\nin the pelvic nerve form synapses in the spinal cord, and axons from the second-order neurons travel rostrally to the micturition center. The center integrates this sensory information with signals from more rostral brain regions and ultimately generates inhibitory input to the sympathetic and somatic centers in the spinal cord and stimulatory input to the parasympathetic center (Fig. 5). This spino-bulbo-spinal reflex results in relaxation of the EUS and internal urethral sphincter, followed by contraction of detrusor muscles, increase in bladder pressure, and flow of urine [4].</p>\n</blockquote>\n", "score": 1 } ]

[ "side-effects", "physiology", "drug-metabolism", "drug-administration", "urinary-system" ]

[ { "answer_id": 26000, "body": "<p>As suggested by @CareyGregory you need to speak to PubMed about that. I have noticed that recently too with quite a few articles.</p>\n<p>The one linked can actually be read at <a href=\"https://www.ajmc.com/view/a09_12aug_rls_sethi\" rel=\"nofollow noreferrer\">https://www.ajmc.com/view/a09_12aug_rls_sethi</a> as it is open access.</p>\n<p>Going off tangent a little, interestingly the author information is weird to me too as there are only 2 authors, and 2 authors don't make an <em>et al.</em> citation as far as I am aware. The citation for this article is</p>\n<p>Sethi, K. D., &amp; Mehta, S. H. (2012). A clinical primer on restless legs syndrome: what we know, and what we don't know. <em>The American journal of managed care, 18</em>(5 Suppl), S83-88.</p>\n", "score": 1 } ]

[ "research" ]

[ { "answer_id": 32325, "body": "<p>I asked a real doctor, and the answer is thirty minutes.</p>\n", "score": 0 } ]

[ "medications" ]

[ { "answer_id": 26035, "body": "<p>The US' National Institute of Health maintains the <a href=\"https://dailymed.nlm.nih.gov/dailymed/index.cfm\" rel=\"nofollow noreferrer\">Daily Med database</a>, which is searchable by active and inactive ingredients.</p>\n<hr />\n", "score": 2 } ]

[ "medications", "vaccination", "research" ]

[ { "answer_id": 26332, "body": "<p>The most common technical term would probably be &quot;spinal manipulation&quot; in general, and &quot;manipulation of the cervical spine&quot; / &quot;cervical spinal manipulation&quot; to denote the treatment of the neck portion of the spine specifically.</p>\n<p>&quot;Cavitation&quot; is the term for the sound that can be produced during the quick separation of joint surfaces.</p>\n<p>Unfortunately, @Desai seems to be not quite correct to include the term &quot;crepitation&quot; or &quot;crepitus&quot; here, however, it is related to the sounds that joints can produce. My understanding is that crepitus is frequently caused by pathologic conditions (for example hypermobility, damage of the joint cartilage, muscle weakness) and rather not as a common side effect during spinal manipulation.</p>\n<p>The technique that brought you to ask your question here is a general technique. There are <em>general</em> techniques for &quot;hitting several joints at once&quot; (I observed that a certain therapist would rather be <em>hoping</em> that the pain-causing segment would be affected by the general technique) - and <em>specifically</em> targeted techniques which require more skill and experience for adequate localization and angular position of the joint (portion) to be treated, as well as for the execution of the technique itself. But these specific techniques also require more time, as well in practicing as also in execution... chiropractors, orthopedic manual therapists or doctors of osteopathic medicine may have the greatest expertise with &quot;High-Velocity-Low-Amplitude&quot;-techniques, as &quot;spinal manipulation&quot; is sometimes also called (&quot;HVLA&quot;-techniques).</p>\n<p>&quot;Low amplitude&quot; suggests that &quot;if you use high velocity&quot; (apply more force than with the softer, slower &quot;<em><strong>mobilisation</strong></em>&quot;, which is probably <em>the</em> central term in manual therapy), then &quot;you better head for a very small movement that you try to guide the joint to&quot;. If you think of what these words mean, it could be easy to &quot;go a little bit too far&quot;. It is much easier for a therapist - and safer for the patient - to use (slower) <em>mobilisation</em> instead of (faster) <em>manipulation</em> techniques. With them, you have a lot more time, during the application, to change direction, position, intensity, duration ... so, your own brain has more time to actually learn &quot;how joints feel&quot;. As a learning professional, I do find value in such a viewpoint.</p>\n<p>While the evidence base supports the use of these techniques in modern musculoskeletal practice (1), the effect of manipulation techniques is correlating with the kind of subjective hope (expectation) patients may direct towards it. For example, the source I use here states that the technique of spinal manipulation may cause &quot;a reduction of [<em>perception</em>] of pain&quot; (1).</p>\n<p>The original goal of reflexively applied manipulation and mobilisation techniques is, of course, to improve range of movement exactly where it is needed (nowhere else, hopefully). There is a somewhat clarifying story worth to tell, written by one of the more famous manual therapists, Geoffrey Maitland. In the 3rd edition of his book about spinal manipulation (2) he reflects that [&quot;a decade ago, of the patients that would improve on application of passive moment, 85% would need mobilisation, while 15% would require manipulation&quot;]. One sentence later, he displays his personal professional development in stating that he came to the conclusion that a rate of 99% (mobilisation) to 1% (manipulation) seemed to be the more adequate estimate for him.</p>\n<p>While that would have been a good point to end this little trip through the universe of spinal <em>manipulation</em>, it is still worth to at least mention the bias or blindness that generalized perception seems to have towards specific <em>mobilisation</em>, which is less effect-presenting, but not less effective. Also, while both methods are known to not permanently relieve pain, I feel the serious obligation to argue that adequate <em><strong>mild heel lifts</strong></em> - even <em><strong>as a back pain prevention tool</strong></em> for the general population - will push overall symmetric movement in all our spines facet joints on the long run (and thus lower back pain efficiently). For the biomechanical genesis of spinal pain, manual therapy and its relatives provide diagnostic skill that, if taken seriously, by far transcends its &quot;special fx unit&quot; :) ... for example, <em>functional</em> radiology is not up to this level of restricted movement detection yet, it is, by today, very much still a <em>static</em> radiology facing very specific and localizable problems from its own and evolved angle. When we speak to it about <em>movement</em> ... the current focus of therapies is upon exercise and load transfer (to my mind, <em>mild leg length differences</em> are gravely overlooked in modern clinical practice, according to the high influence of their causal link to spinal pain, even enough to with some urgency refer towards this phenomenon in an article about spinal manipulation).</p>\n<p>References:<br />\n(1) Grieve's Modern Musculoskeletal Therapy, 4th ed., 2015, p. 277 ff.<br />\n(2) Maitland, Manipulation der Wirbelsäule, 3rd ed., 2006, p. 182</p>\n", "score": 1 } ]

[ "physiotherapy", "neck" ]

[ { "answer_id": 26155, "body": "<p>TL;DR — The transmission of HIV through blood products is very rare, but examples have occurred in some low-income countries which lack the equipment to test all blood.</p>\n<p>You said:</p>\n<blockquote>\n<p>Around the world organizations that seek blood donations usually have a policy to discourage men who have sex with men (MSM) from donating blood. This is due to the risk of Human Immunodeficiency Virus (HIV) in the blood.</p>\n</blockquote>\n<p>This is not entirely accurate. There have been blanket bans in the past with regard to MSM blood donations in the US and the UK. I am unsure on the US, but in the UK the ban included women who have had sex recently with a man who has sex with men. However, there have been changes in the rules to remove restrictions <strong>in certain circumstances</strong>.</p>\n<p>Other countries have followed suit.</p>\n<blockquote>\n<p>Other countries have similarly amended MSM-specific restrictions on blood donation in the past decade, including Argentina, Bolivia, Chile, Israel, Mexico, Peru, and South Africa. In 2016, France began allowing MSM to donate apheresis plasma under the same policy as other donors (ie, plasma from people with more than one recent sexual partner is quarantined for at least 2 months until the donor can return for HIV retesting). Then, in 2019, the country announced whole blood donation regulations would be aligned for gay and straight donors by 2022. In 2020, both Hungary and Brazil repealed bans on blood donation by MSM, with Brazil's Supreme Court ruling that such restrictions were unconstitutional (<a href=\"https://doi.org/10.1016/S2352-3026(20)30326-4\" rel=\"nofollow noreferrer\">Skelly, et al. 2020</a>).</p>\n</blockquote>\n<p>Bans such as this rely on self-reporting donors, and the FAIR report on BBIs from MSM blood donation (which I talk about later - in the UK section) even covers the fact that there is non-compliance in positive donors reporting sex between men.</p>\n<h2>HIV vs other blood borne infections (BBIs)</h2>\n<p>The thing is, there are many other BBIs other than HIV which are a cause for concern for the Blood Transfusion teams around the world. Among others, there is syphilis and hepatitis. And, just like with these BBIs, <a href=\"https://medicalsciences.stackexchange.com/questions/5261/how-do-you-get-infected-with-hiv\">there is more than one way to get HIV</a> other than a man having sex with another man.</p>\n<h2>What are the chances of receiving blood infected with BBIs</h2>\n<p>Avert — a UK-based charity that has been providing accurate and trusted information about HIV and sexual health worldwide for over 30 years — points out that in order to prevent transmission of BBIs, international health regulations require all blood products, such as organs or tissues, to be screened for a number of viral or bacterial contaminants before they are used.</p>\n<p>And:</p>\n<blockquote>\n<p>During the screening process any blood products which contain HIV, hepatitis B, hepatitis C, or syphilis will be disposed of.</p>\n<p>This means that the transmission of HIV through blood products is very rare, but examples have occurred in some low-income countries which lack the equipment to test all blood (<a href=\"https://www.avert.org/hiv-transmission-prevention/blood-transfusions-transplants\" rel=\"nofollow noreferrer\">Avert, n.d.</a>).</p>\n</blockquote>\n<h2>In the US</h2>\n<blockquote>\n<p>In 2015, US policy changed from a lifetime ban on donations (‘indefinite referral’) from any man who reported having sex with another man after 1977, to a 12-month deferral period. This means that men who last had sex with another man more than a year ago are eligible to donate blood, while men who have had sex more recently are not (<a href=\"https://www.aidsmap.com/news/mar-2020/no-increase-hiv-blood-donations-rules-gay-men-were-relaxed\" rel=\"nofollow noreferrer\">AIDS Map, 2020</a>).</p>\n</blockquote>\n<p>Referring to the Conference on Retroviruses and Opportunistic Infections (<a href=\"https://www.croiconference.org/croi-2020/\" rel=\"nofollow noreferrer\">CROI 2020</a>), there was a study (<a href=\"https://doi.org/10.1182/blood.2020007003\" rel=\"nofollow noreferrer\">Grebe, et al. 2020</a>) which found that</p>\n<blockquote>\n<ul>\n<li>HIV incidence in first-time donors was similar before and after implementation of the 12-month MSM deferral, both overall and in males.</li>\n<li>The residual risk of HIV transfusion transmission for components sourced from first-time donors was low and did not change significantly.</li>\n</ul>\n</blockquote>\n<div class=\"s-table-container\">\n<table class=\"s-table\">\n<thead>\n<tr>\n<th><a href=\"https://i.stack.imgur.com/nhZPC.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/nhZPC.png\" alt=\"chart of incidence differences\" /></a><br></th>\n</tr>\n</thead>\n<tbody>\n<tr>\n<td>image from page 50 of <a href=\"https://www.croiconference.org/wp-content/uploads/sites/2/resources/2020/ebook/croi2020-boston-abstract-ebook.pdf\" rel=\"nofollow noreferrer\">CROI 2020 Oral Abstracts PDF Book</a></td>\n</tr>\n<tr>\n<td>Bivariable and multivariable Poisson regression models using data from the entire TTIMS period showed that MSM deferral policy was not a significant correlate of incidence, although male sex (risk ratio 5.0, 95% CI: 2.8–9.5), age 18-24 (RR: 4.3, 1.5–18.3), black race (RR: 10.1, 5.8–17.9), Hispanic ethnicity (RR: 2.6, 1.3–5.0) and Southern region (RR: 2.0, 1.4–7.9) were significant (<a href=\"https://www.croiconference.org/wp-content/uploads/sites/2/resources/2020/ebook/croi2020-boston-abstract-ebook.pdf\" rel=\"nofollow noreferrer\">CROI 2020 Oral Abstract</a>).</td>\n</tr>\n</tbody>\n</table>\n</div>\n<p>It was concluded that:</p>\n<blockquote>\n<p>There is no evidence that the implementation of a 12-month MSM deferral policy resulted in increased HIV incidence in, and therefore transfusion transmission risk from, first-time blood donors in the United States</p>\n</blockquote>\n<h2>In the UK</h2>\n<blockquote>\n<p>The criteria that are used by the UK blood services to select blood donors on the basis of behaviours that may increase the risk of acquiring and transmitting blood borne infections (BBI) last underwent major review by SaBTO [Advisory Committee on the Safety of Blood, Tissues and Organs] in 2011. That review led to a change in selection criteria for potential blood donors who are men who have sex with men (MSM). The selection criteria were changed from a permanent deferral to a twelve month deferral from last sexual contact in England, Scotland and Wales Blood Services in 2011, and by The Northern Irish Blood Transfusion Service in 2016 (<a href=\"https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/809909/sabto-donor-selection-criteria-report-2017-v2.pdf\" rel=\"nofollow noreferrer\">UK Government, 2017</a>).</p>\n</blockquote>\n<p>In December last year, the UK Government announced <a href=\"https://www.gov.uk/government/news/landmark-change-to-blood-donation-criteria\" rel=\"nofollow noreferrer\">a further change in the rules to allow more gay and bisexual men to donate blood in the UK</a> (<a href=\"https://www.nat.org.uk/blog/changes-blood-donation-rules-explained\" rel=\"nofollow noreferrer\">National AIDS Trust, 2020</a>) and the UK Government state that changes will take place by Summer 2021 and will have no impact on the safety of blood donated in the UK (<a href=\"https://www.gov.uk/government/news/landmark-change-to-blood-donation-criteria\" rel=\"nofollow noreferrer\">UK Government 2020</a>).</p>\n<p>NHS Blood and Transplant (NHSBT) led a steering group called FAIR (For the Assessment of Individualised Risk).</p>\n<blockquote>\n<p>FAIR membership includes representatives from the four UK blood services (NHS Blood and Transplant, Scotblood, the Welsh Blood Service and the Northern Ireland Blood Transfusion Service), Public Health England, Nottingham University, the National Aids Trust (NAT), Stonewall, Freedom to Donate, Terrence Higgins Trust (THT), and includes experts in epidemiology, virology and psychology and other key stakeholders (<a href=\"https://www.blood.co.uk/news-and-campaigns/news-and-statements/fair-steering-group/\" rel=\"nofollow noreferrer\">NHSBT, 2020</a>).</p>\n</blockquote>\n<p>It was set up to consider how risk could be assessed on a more individual basis when people go to donate blood.</p>\n<p>New criteria, based on findings from the FAIR report (<a href=\"https://nhsbtdbe.blob.core.windows.net/umbraco-assets-corp/21001/fair_sabto_20201211.pdf\" rel=\"nofollow noreferrer\">FAIR, 2020</a>), focuses on individual behaviours, and lifts a blanket deferral for men who have had sex with men in the last 3 months.</p>\n<blockquote>\n<p>The FAIR (For the Assessment of Individualised Risk) steering group has recently concluded that donors who have had the same sexual partner in the last three months and who don’t have an STI should be eligible to donate (<a href=\"https://www.blood.co.uk/news-and-campaigns/news-and-statements/fair-steering-group/\" rel=\"nofollow noreferrer\">NHSBT, 2020</a>).</p>\n</blockquote>\n<h2>References</h2>\n<p>AIDS Map (2020). <em>No increase in HIV in blood donations since rules for gay men were relaxed</em> <a href=\"https://www.aidsmap.com/news/mar-2020/no-increase-hiv-blood-donations-rules-gay-men-were-relaxed\" rel=\"nofollow noreferrer\">https://www.aidsmap.com/news/mar-2020/no-increase-hiv-blood-donations-rules-gay-men-were-relaxed</a></p>\n<p>Avert (n.d.). <em>Blood transfusions &amp; transplants and HIV</em> <a href=\"https://www.avert.org/hiv-transmission-prevention/blood-transfusions-transplants\" rel=\"nofollow noreferrer\">https://www.avert.org/hiv-transmission-prevention/blood-transfusions-transplants</a></p>\n<p>CROI (2020). <em>Conference on Retroviruses and Opportunistic Infections 2020</em> <a href=\"https://www.croiconference.org/croi-2020/\" rel=\"nofollow noreferrer\">https://www.croiconference.org/croi-2020/</a></p>\n<p>FAIR (2020). <em>Can donor selection policy move from a population-baseddonor selection policy to one based on a more individualised risk assessment? Conclusions from the For the Assessment of Individualised Risk (FAIR) group</em> <a href=\"https://nhsbtdbe.blob.core.windows.net/umbraco-assets-corp/21001/fair_sabto_20201211.pdf\" rel=\"nofollow noreferrer\">https://nhsbtdbe.blob.core.windows.net/umbraco-assets-corp/21001/fair_sabto_20201211.pdf</a></p>\n<p>Grebe, E., Busch, M. P., Notari, E. P., Bruhn, R., Quiner, C., Hindes, D., ... &amp; Custer, B. (2020). HIV incidence in US first-time blood donors and transfusion risk with a 12-month deferral for men who have sex with men. <em>Blood, The Journal of the American Society of Hematology, 136</em>(11), 1359-1367. <a href=\"https://doi.org/10.1182/blood.2020007003\" rel=\"nofollow noreferrer\">https://doi.org/10.1182/blood.2020007003</a></p>\n<p>National AIDS Trust (2020). <em>Changes to blood donation rules explained</em> <a href=\"https://www.nat.org.uk/blog/changes-blood-donation-rules-explained\" rel=\"nofollow noreferrer\">https://www.nat.org.uk/blog/changes-blood-donation-rules-explained</a></p>\n<p>NHSBT (2020). <em>Blood donor selection policy: the work of the FAIR steering group</em> <a href=\"https://www.blood.co.uk/news-and-campaigns/news-and-statements/fair-steering-group/\" rel=\"nofollow noreferrer\">https://www.blood.co.uk/news-and-campaigns/news-and-statements/fair-steering-group/</a></p>\n<p>Skelly, A. N., Kolla, L., Tamburro, M. K., &amp; Bar, K. J. (2020). Science over stigma: the need for evidence-based blood donation policies for men who have sex with men in the USA. <em>The Lancet Haematology, 7</em>(11), e779-e782. <a href=\"https://doi.org/10.1016/S2352-3026(20)30326-4\" rel=\"nofollow noreferrer\">https://doi.org/10.1016/S2352-3026(20)30326-4</a></p>\n<p>UK Government (2017). <em>Donor Selection Criteria Report (2017) Version 2</em> <a href=\"https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/809909/sabto-donor-selection-criteria-report-2017-v2.pdf\" rel=\"nofollow noreferrer\">https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/809909/sabto-donor-selection-criteria-report-2017-v2.pdf</a></p>\n<p>UK Government (2020). <em>Landmark change to blood donation criteria</em> [Press Release] <a href=\"https://www.gov.uk/government/news/landmark-change-to-blood-donation-criteria\" rel=\"nofollow noreferrer\">https://www.gov.uk/government/news/landmark-change-to-blood-donation-criteria</a></p>\n", "score": 1 } ]

[ "blood-tests", "hiv", "blood-donation" ]

[ { "answer_id": 26136, "body": "<p><a href=\"https://www.cdc.gov/vaccines/hcp/vis/vis-statements/tdap.html\" rel=\"nofollow noreferrer\">Tdap</a> is the tetanus+diptheria+pertussis vaccine, usually given to adolescents but some people miss it and get as an adult (may also vary by country, but see <a href=\"https://www.cdc.gov/vaccines/schedules/hcp/imz/child-adolescent.html\" rel=\"nofollow noreferrer\">this CDC page for recommended vaccine ages in the US</a>), and also to pregnant women.</p>\n<p><a href=\"https://www.cdc.gov/vaccines/hcp/vis/vis-statements/td.html\" rel=\"nofollow noreferrer\">Td</a> is a tetanus+diptheria vaccine given as a booster, typically every 10 years or more frequently if there has been a recent wound/other higher risk exposure. It's not really that Td is for &quot;adults only&quot; but rather that if you are following the recommended schedule adults have had Tdap by the time they are adults, so they'll only be getting the booster, whereas adolescents have either not gotten Tdap so they'd be preferred for Tdap over Td, or they already got Tdap and won't typically need a booster as an adolescent because the inexorable passage of time means they will be adults by the time 10 years have passed. CDC guidance has no problem with Tdap being given instead of Td as a booster, though, if it's more available/convenient (the important bit is that people <em>get the Td booster part</em>; it's not important that they avoid the pertussis part).</p>\n<p>It's common for employers to require employees to be up-to-date on these vaccinations because employers don't want to be liable for workers getting infected with tetanus due to an injury on the job.</p>\n<p>The first phrasing is pretty nonsensical English. The simplest interpretation is that they require being current on Td/Tdap, which would suggest having a Tdap sometime in the past and either Td or Tdap within the last 10 years. If someone has never had Tdap, then the recommendation would be to get Tdap (&quot;substitute for&quot;) one time only, and then to get Td every ten years after that.</p>\n", "score": 2 } ]

[ "vaccination" ]

[ { "answer_id": 26238, "body": "<h2>TL;DR;\n3 - IgG for S protein</h2>\n<p>From <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7561304/\" rel=\"nofollow noreferrer\">Safety and immunogenicity of an inactivated SARS-CoV-2 vaccine, BBIBP-CorV: a randomised, double-blind, placebo-controlled, phase 1/2 trial</a>:</p>\n<blockquote>\n<p>The secondary outcome was immunogenicity, assessed as the neutralising\nantibody responses against infectious SARS-CoV-2.</p>\n</blockquote>\n<p>From <a href=\"https://www.abingdonhealth.com/what-are-covid-19-neutralising-antibody-rapid-tests/\" rel=\"nofollow noreferrer\">What are COVID-19 neutralising antibody rapid tests and why use them?</a></p>\n<blockquote>\n<p>Neutralising antibodies bind to the SARS-CoV-2 Spike protein and\ninterfere with the virus’ ability to enter human cells. IgG antibodies\nare the most common antibody in blood and have the largest part to\nplay in conferring immunity to bacteria or viruses.</p>\n</blockquote>\n", "score": 0 } ]

[ "covid-19", "vaccination", "antibodies" ]

[ { "answer_id": 26232, "body": "<p><a href=\"https://en.wikipedia.org/wiki/Alopecia_areata#Treatment\" rel=\"nofollow noreferrer\">Wikipedia</a> suggests that there are no known reliable and safe treatments. Corticosteroids have been used but evidence for efficacy is weak. The US FDA <a href=\"https://investor.lilly.com/news-releases/news-release-details/lilly-receives-fda-breakthrough-therapy-designation-baricitinib\" rel=\"nofollow noreferrer\">has allowed breakthrough use of at least one drug</a> that is ordinarily prescribed for rheumatoid arthritis following early trial successes, with a <a href=\"https://clinicaltrials.gov/ct2/show/NCT03899259\" rel=\"nofollow noreferrer\">phase 3 trial ongoing</a>, but there is no FDA-approved treatment.</p>\n<p>In general as a rule there is a lot more financial (and other) incentive to say there is a magic cure for something, and almost no incentive to say there is not. Even if someone provides before and after &quot;evidence&quot;, this is not reliable unless it is coming from a reputable source (such as a scientific article in a reputable journal, a trusted government regulatory agency or public health institute, etc). For a simple example, you could take an &quot;after&quot; photo, remove some hair and take a &quot;before&quot; photo, and claim whatever treatment you want worked.</p>\n", "score": 2 } ]

[ "alopecia" ]

[ { "answer_id": 26242, "body": "<p>mRNA (messenger RNA) is the &quot;working copy&quot; of gene that the machinery in the cell's cytoplasm uses to direct synthesis of a protein (translation). Thus, if you can get a suitable-looking mRNA into the cytoplasm (e.g. by coating it with NLP), the cell will start translating it.</p>\n<p>DNA, on the other hand, first needs additional machinery to make an mRNA working copy from it (transcription), which process takes place in the cell's nucleus. It's much harder to get things into the nucleus from outside the cell. Adenoviruses are not only robust (hence their long shelf life under refrigeration), but as double-stranded DNA viruses they are already specialized to get their DNA contents into the nucleus and get it transcribed.</p>\n<p>It's all a matter of the right tool for the job.</p>\n<p>Edit: Regarding transport of the viral DNA into the nucleus, here's part of an abstract from a relevant paper: (&quot;Viral entry into the nucleus&quot; PMID: 11031249 DOI: 10.1146/annurev.cellbio.16.1.627)</p>\n<p>&quot;Because many viruses replicate in the nucleus of their host cells, they must have ways of transporting their genome and other components into and out of this compartment. For the incoming virus particle, nuclear entry is often one of the final steps in a complex transport and uncoating program. Typically, it involves recognition by importins (karyopherins), transport to the nucleus, and binding to nuclear pore complexes. Although all viruses take advantage of cellular signals and factors, viruses and viral capsids vary considerably in size, structure, and in how they interact with the nuclear import machinery. Influenza and adenoviruses undergo extensive disassembly prior to genome import&quot;</p>\n<p>Just injecting DNA into the cytoplasm won't do much of anything - a lot of machinery is needed to get it to and into the nucleus, some supplied by the virus and some supplied by the cell. NLPs have none of that.</p>\n", "score": 4 }, { "answer_id": 29262, "body": "<p><a href=\"https://www.nature.com/articles/s41598-020-65059-0\" rel=\"nofollow noreferrer\">There are</a> experimental vaccines that deliver DNA of interest (e.g. that would express spike protein) merely tied to a plasmid encapsulated in a LNP (liquid nano-particle). Some animal trials indicate that LNP-encapsulated plasmid-DNA vaccines would achieve approximately 10-20 times better delivery efficiency than &quot;naked&quot; plasmid-DNA injection, i.e. LNP encapsulation would lead to that 10-20 times less active substance (and possibly fewer booster doses as well).</p>\n<p>The recently approved (in India) ZyCoV-D, which is a plasmid-DNA vaccine (exact plasmid <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8166516/\" rel=\"nofollow noreferrer\">used</a> is pVAX-1, which has been commercially available for at least a decade), doesn't seem use a LNP encapsulation though. ZyCoV-D requires <em>three</em> doses as the initial schedule, so delivery efficiency (via a jet injector) is probably not as good as what could achieve with additional LNP encapsulation.</p>\n<p>Basically, a plasmid is circular piece of DNA (typically found in bacteria) that if it makes it into the nucleus, results in mRNA being produced from a certain part of it--part which follows the promoter region/gene. pVAX-1 [for instance] uses the promoter from the cytomegalovirus (CMV). CREB binding sites in this promoter region <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5705778/\" rel=\"nofollow noreferrer\">facilitate</a> movement to the nucleus, although that might not be whole story of how it achieves nuclear import. The current plasmid-based vaccines seem to rely on rather inefficient means of nuclear import. Something like 1-3% of plasmids injected into cytoplasm make it into the nucleus.(The full CMV appears substantially more complicated in this regard, with additional nuclear localization sites in other large proteins, only more recently <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3648141/\" rel=\"nofollow noreferrer\">identified</a>.)</p>\n<p>LNP encapsulation is a fairly expensive procedure, which requires investing in highly specialized microfluidics equipment, so there's probably a commercial tradeoff between &quot;brute forcing&quot; the solution with more DNA vs. encapsulating in LNP.</p>\n<p>For mRNA the benefits of LNP encapsulation are perhaps even higher; <a href=\"https://link.springer.com/article/10.1007/s12195-020-00619-y\" rel=\"nofollow noreferrer\">one paper</a> reported 40-fold increase in expression with LNP encapsulation than without.</p>\n<p>I'm not totally sure about this, but currently it seems that plasmid-DNA vaccines cannot be made by the mostly synthetic route that mRNA vaccines use, i.e. plasmids still need to be grown in bacteria inside bioreactors, which makes them less attractive than mRNA-LNP vaccines in that regard.</p>\n<hr />\n<p>Adenovirus vectored vaccines (like Astra Zeneca's) are grown with the virus infecting actual cells, so you cannot easily replace the DNA inside this DNA-based virus (family) with RNA. The &quot;trick&quot; with an adenovirus-vectored vaccine is that it doesn't replicate in <em>most</em> cells, but it does replicate in the ones in which it is actually grown; these cells are themselves <a href=\"https://genomemedicine.biomedcentral.com/articles/10.1186/s13073-021-00859-1\" rel=\"nofollow noreferrer\">modified</a> to actually supply the missing replication gene for the virus.</p>\n<blockquote>\n<p>Adenovirus-based vectors typically have two regions of the virus genome removed, known as E1 and E3. The E1 region contains early genes required to trigger a transcription cascade enabling viral replication; E1-deleted vectors therefore need to be grown in E1 trans-complementing cell lines such as HEK293 cells. HEK293 cells have a 4-kbp region of human adenovirus type 5 (HuAd5) integrated into the cellular genome that provides the E1 genes in trans enabling efficient virus vector replication and recombinant virus production. [...] Usually, the transgene to be expressed [e.g. spike] is inserted into the virus genome in place of the E1 region under the control of a highly active promoter.</p>\n</blockquote>\n<p>There is <a href=\"https://www.criver.com/eureka/viral-vector-quandary\" rel=\"nofollow noreferrer\">actually</a> a small risk that some of the viruses produced this way are replication\ncompetent, by including (via recombination events) the original E1 gene from the cell in which they are grown. One of the reasons for selecting a virus that is not adapted to humans <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5842362/\" rel=\"nofollow noreferrer\">is to minimize</a> the chance of bad outcomes stemming from this risk. (The other/major reason is to limit the likelihood the immune response will react to the vector before it can deliver is transgene payload.)</p>\n<p>There are also some further similarities between the ZyCoV-D vaccine and the AZ vaccine: both use the CMV promoter to mark the start of the transgene, which is also terminated by the same BGH poly-A sequence. So, on this level, they rely on the same cookbook once in the nucleus.</p>\n<p>Finally, RNA viruses have also been <a href=\"https://doi.org/10.3390/genes10030189\" rel=\"nofollow noreferrer\">tried</a> as viral vectors. There were even some head-to-head comparisons with DNA vectored-vaccines; like between ChAd3 and rVSV viral vectors <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5705229/\" rel=\"nofollow noreferrer\">for Ebola (2017)</a>; as far as I can tell, there wasn't much difference in either safety or effectiveness in that trial. The RNA-virus-vectored vaccine for Ebola was <a href=\"https://www.fda.gov/news-events/press-announcements/first-fda-approved-vaccine-prevention-ebola-virus-disease-marking-critical-milestone-public-health\" rel=\"nofollow noreferrer\">approved</a> by the FDA in 2020. There's also an <a href=\"https://www.nature.com/articles/s41467-020-20228-7\" rel=\"nofollow noreferrer\">experimental</a> Covid-19 vaccine based on the same rVSV platform. I'm not entirely sure why this was not pursued, but I suspect that it's because RNA-viral-vectored vaccines <a href=\"https://academic.oup.com/jid/article/217/suppl_1/S48/4999139\" rel=\"nofollow noreferrer\">need</a> -60 degrees C storage, so the DNA-based vaccines definitely have an advantage here.</p>\n", "score": 0 } ]

[ "vaccination", "virus", "genetic-engineering", "immunology" ]

[ { "answer_id": 26270, "body": "<p>This is normal, anatomy is a complex subject to grasp at first. I can suggest the following to help you study more efficiently:</p>\n<p><strong>Learning Strategies</strong></p>\n<ul>\n<li>Begin by knowing all <a href=\"https://en.wikipedia.org/wiki/List_of_systems_of_the_human_body\" rel=\"nofollow noreferrer\">systems</a> of the human body\n(learn the skeletal system first and then the muscular system etc.)</li>\n<li>Focus on a particular system and <a href=\"https://human.biodigital.com\" rel=\"nofollow noreferrer\">visualize</a> its parts\n(learn the head and go down or start with fingers then limbs etc.)</li>\n</ul>\n<p><strong>Learning Approaches</strong></p>\n<ul>\n<li>Exercise your knowledge and ability to recollect using anatomy <a href=\"https://www.google.ca/books/edition/Anatomy_Flashcards/qbZNMQEACAAJ\" rel=\"nofollow noreferrer\">flashcards</a></li>\n<li>Actively engage in your learning (don't only read), <a href=\"https://www.google.ca/books/edition/The_Anatomy_Coloring_Book/x3eArHrj6x4C\" rel=\"nofollow noreferrer\">color</a> and explain relations</li>\n</ul>\n", "score": 1 }, { "answer_id": 26320, "body": "<p>Aitía gave you good answers to start with in structuring your learning: If you sort into digestable chunks what is up for learning, you can feed your long term potentiation with the necessary repetition.</p>\n<p>A friend once told me that he started to learn the (peripheral) nervous system first, so he found it easier, later, to attach muscles, and then muscles to bones - this approach is a functional one, not a structural one, though.</p>\n<p>I happen to memorize things better - and research has shown that to be effective for the brain - when I imagine a patient case (a pathology) related to an anatomical structure. If that is what you like, books of functional anatomy (you can lay them out side to side with those of structural anatomy) tend to explain more clinical cases or &quot;why's&quot;. Find something that connects the content to your life, so that your brain thinks, &quot;aah, that is why that matters&quot;, for example, if you do fitness, think of how muscles stretch or contract when you make a movement or how ligaments limit a certain movement etcetera. Many books come with clinical cases (take, for example, golfer's elbow - you may palpate your own Epicondylus medialis when making a fist - this lets you remember where the flexor muscles have their origin). The sensory experience of palpating what you just &quot;learned&quot; turns theoretical knowledge into practical knowledge. &quot;Learning&quot; often meant to the brain that the two were apart, and this performative approach often meant fatigue, thus, the disappearance of joy, which is a central motivating factor in the physiological learning of children.</p>\n<p>You can also be rigorous and make a learning plan. That is suggested in an exam preparation book series (The GK Series by Thieme, referring to a forum for German medial students, medi-learn.de), here a summary in my free and brief simplification:</p>\n<ul>\n<li><p>reserve 6-8 hours / day for learning, 5 days a week</p>\n</li>\n<li><p>keep track of until when you want to (or &quot;have to&quot;) learn &quot;what&quot;</p>\n</li>\n<li><p>don't learn too much &quot;all new&quot; stuff on one day/session, repetition is okay</p>\n</li>\n<li><p>if it is too complicated, learn it in chunks</p>\n</li>\n<li><p>read/learn before noon on one day, what you check/ask yourself in the afternoon of the next day (you can connect the dots with Aitía's flashcard example here)</p>\n</li>\n<li><p>truly seek in yourself what you know already, before you look at the back of a flashcard too fast</p>\n</li>\n<li><p>Let me add: There are also flashcard learning systems that put aside those cards you either labeled &quot;I don't need to repeat THAT&quot;, &quot;I could repeat that&quot; and &quot;I should repeat that&quot;.</p>\n</li>\n</ul>\n<p>It may also be worth to note that learning benefit from healthy sleep, even only naps, if the brain becomes tired after learning (studies show that after sleep, long term potentiation is improved). Most probably, if you ask it, your brain tells you about the way it likes to digest certain types of information. The more neurons blink, the more connections you make because things and their interdependence become important to your growing understanding, the better the connection between them gets and long term potentiation is reinforced. Podcasts, for example, can be a medium to listen to in supermarkets or subways, still keeping your mind &quot;at it&quot; ... I also imagined me being very small and the structures of the body like roads I'd travel (the french series &quot;Il était une fois… la Vie&quot; may have stimulated that). There is also good 3D visualisation software out there, if you look for it.</p>\n<p>There are types of questions explicity linking the &quot;chunks&quot; of structural anatomy, like &quot;What nerve innervates this muscle/organ&quot;, &quot;what muscle sits on that part of this bone&quot;, &quot;which ligament restricts that joint movement&quot; - you see that my anatomy is more or less based on musculoskeletal needs, but you might want to take that as a metaphor. In school we had a guy whom I talked to about his learning, and he said: &quot;I don't <em>learn</em> muscle functions at all, I simply remember where they are and then imagine what happens when they contract&quot;. He was somehow already thinking like the body when I was still learning some thinking. (However, the full scope of some muscle function also can't be explained by just looking at a drawing of them, but he made an important point to my slightly overfocused and a little bit narrow minded brain at the time. I was so busy in attempting &quot;to get it all right&quot; that I lost the big picture, &quot;that I can, basically, grasp things&quot;, just not all at once).</p>\n<p>If you speak with a buddy (like with us, here), but maybe off-Internet, you get a taste of the personal depth their learning had. One of my other buddies was the son of a doctor. He had a serious love for the stuff. Man, that still inspires me today! It helps me to understand that whatever I understand, &quot;why do I have the feeling he'd understand it better&quot;? But through always knowing-or-feeling that, I always learn, and it never gets <em>really</em> boring ... :)</p>\n<p>In the end, I wish to you that you can make learning fun and sometimes think of the smiles of the people that are grateful, when you help them .. it is really the most rewarding thing. My greatest joy is in balancing mild leg length differences with marginal heel lifts and check the results of possibly symmetrically aligned zygapophysial joint movement (with palpation, while radiology hardly is there so far). Here, I desperately <em>need</em> functional anatomy :)! Hardly anyone does mild leg length difference compensation in such relative precision, it is very successful and people are so thankful. Really strange that there's not much more science about &quot;the hard problem of practical relevance&quot; for LLD/LLI, which is of course my favorite example for why learning matters and is fun. I wish you all the success you can have, and that you find your own &quot;favourite problem&quot; to work with! Go for it :) !</p>\n", "score": 0 } ]

[ "anatomy" ]

[ { "answer_id": 26275, "body": "<p>OK, it seems this is more what you were asking for:</p>\n<p>Food Data Chart\n<a href=\"http://apjcn.nhri.org.tw/server/info/books-phds/books/foodfacts/html/data/data2e.html\" rel=\"nofollow noreferrer\">http://apjcn.nhri.org.tw/server/info/books-phds/books/foodfacts/html/data/data2e.html</a></p>\n<p>Table of Phenylalanine Content of Foods: Comparative Analysis of Data Compiled in Food Composition Tables\n<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5509543/\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5509543/</a></p>\n", "score": 1 } ]

[ "nutrition", "labeling", "amino-acids" ]

[ { "answer_id": 26282, "body": "<p>No it's not zero, even in the US. The March 20 Vox report is talking about the clinical trials, which were conducted on tens of thousands of people, who were generally healthy.</p>\n<p>In the subsequent rollout in the US, some vaccinated people have died as CNN <a href=\"https://edition.cnn.com/2021/04/14/health/breakthrough-infections-covid-vaccines-cdc/index.html\" rel=\"noreferrer\">reported</a> in mid-April:</p>\n<blockquote>\n<p>About 5,800 people who have been vaccinated against coronavirus have become infected anyway, the US Centers for Disease Control and Prevention tells CNN.</p>\n<p>Some became seriously ill and 74 people died, the CDC said. It said 396 -- 7% -- of those who got infected after they were vaccinated required hospitalization.</p>\n<p>This is the CDC's first public accounting of breakthrough cases, and the agency is searching for patterns based on patient age and gender, location, type of vaccine, variants and other factors. [...]</p>\n<p>About 77 million people in the US are fully vaccinated against coronavirus, according to a CNN analysis of CDC data.</p>\n</blockquote>\n<p>So that's almost 1 in a million deaths among the vaccinated, in the US. Clearly not something that would have been likely caught in the clinical trials.</p>\n<p>By April 26, <a href=\"https://www.cdc.gov/vaccines/covid-19/health-departments/past-breakthrough-data.html\" rel=\"noreferrer\">CDC's website</a> reported 132 deaths in the US among the vaccinated, which had reached 95 million by then. However, this report also says that &quot;20 (15%) of the 132 fatal cases were reported as asymptomatic or not related to COVID-19.&quot; These [20 or so] might have been excluded from CNN's earlier report.</p>\n<p>There most recent data, as I'm writing this, <a href=\"https://www.cdc.gov/vaccines/covid-19/health-departments/breakthrough-cases.html\" rel=\"noreferrer\">seems</a> to be from May 10: 223 deaths among the vaccinated (42 of which &quot; asymptomatic or not related to COVID-19&quot;) out of 115 million fully vaccinated.</p>\n", "score": 5 } ]

[ "covid-19", "vaccination", "epidemiology", "covid", "immunology" ]

[ { "answer_id": 26303, "body": "<p>If you are just starting with a whole bunch of patients that are on mechanical ventilation, then you have identified a <em>cohort</em> and you aren't doing case-control.</p>\n<p>However, this sounds like it could be <a href=\"https://en.wikipedia.org/wiki/Case%E2%80%93control_study\" rel=\"nofollow noreferrer\">case-control</a> approach <em>if you approach and analyze it as such</em>. In a case-control approach, you identify cases by some outcome measure, and take controls from a similar population without the outcome. So, if you started with a group of patients who died after mechanical ventilation, and then take some controls who did not die but were also on mechanical ventilation, you could call that case-control. The figure on Wikipedia shows how a case-control and retrospective cohort study are nearly the same, except for what the investigator takes as &quot;known&quot; going in.</p>\n<p>In a non-experimental paradigm, there is little distinction between &quot;independent&quot; and &quot;dependent&quot; variables, since neither is manipulated by the investigator; everything is just an observation, and the estimated relationships are all correlative. In a cohort study, you fit a model of the form:</p>\n<p>Outcome ~ Exposures + error</p>\n<p>whereas in a case-control study you fit a model:</p>\n<p>Exposures ~ Outcome + error</p>\n<p>In the classic &quot;lung cancer vs cigarettes&quot; example, this is the difference between asking &quot;Are people who smoke (exposure) more likely to get lung cancer (outcome)?&quot; and asking &quot;Are people who get lung cancer (outcome) more likely to be smokers (exposure) than people who are cancer-free?&quot;</p>\n<p>Note that while case-control studies often involve some sort of <a href=\"https://en.wikipedia.org/wiki/Matching_(statistics)\" rel=\"nofollow noreferrer\">matching</a>, the matching approach has been under more scrutiny lately and the popular <a href=\"https://en.wikipedia.org/wiki/Propensity_score_matching\" rel=\"nofollow noreferrer\">propensity score matching</a> is disfavored.</p>\n<p>Often you use a case-control approach because cases are rare. It's more efficient in that circumstance to instead start with a bunch of cases and then identify controls that go with them to have a (at least roughly) balanced sample; otherwise, you might need 1000s of subjects in a study to find just a couple cases, and yet not have enough statistical power to say anything about them.</p>\n<p>As with other correlative studies, whichever approach you take you need to be wary of drawing <a href=\"https://xkcd.com/552/\" rel=\"nofollow noreferrer\">causative conclusions from correlation</a>. If different ventilator settings are used for sicker patients, then you're likely to find correlations between settings and mortality that are not causative.</p>\n", "score": 3 } ]

[ "mechanical-ventilation" ]

[ { "answer_id": 26322, "body": "<p>The pathophysiology of NAFLD is not fully understood, so it makes sense that there isn't much literature exploring differences in pathophysiology between people with PCOS and people without. There is an excellent explanation of the current understanding of NAFLD pathophysiology in <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5127277/\" rel=\"nofollow noreferrer\">this review article - see &quot;Pathogenesis&quot;</a>. You'll notice a lot of &quot;this suggests&quot; languages as opposed to &quot;we know this is what happens.&quot;</p>\n<p>I found a few review articles that suggest PCOS is a risk factor for NAFLD because people with PCOS are more likely to be obese, and more likely to have metabolic syndrome - insulin resistance, high cholesterol and triglycerides, etc. I've included a list below. There may also be other hormonal influences. Several of the review articles suggest that hyperandrogenism in PCOS can contribute to fast progression of NAFLD, for example, but the evidence is inconsistent (i.e. not every study has found an association).</p>\n<p>I'm not sure what you mean by &quot;different comorbidities.&quot; Most common comorbidities with NAFLD are also common with PCOS, such as type 2 diabetes. If you mean complications of NAFLD, there is some evidence that PCOS is associated with faster progression of NAFLD (see review articles below), so all complications could be more common.</p>\n<p>Review Articles:</p>\n<ul>\n<li><a href=\"https://academic.oup.com/edrv/article/41/1/66/5601173\" rel=\"nofollow noreferrer\">Endocrine Reviews Review Article on NAFLD from Endocrine Reviews</a> - nice section on potential endocrine influences under &quot;Epidemiology of NAFLD&quot;</li></li>\n<li><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4093689/\" rel=\"nofollow noreferrer\">World Journal of Gastroenterology Review Article on NAFLD &amp; PCOS (1)</a> - mostly focuses on screening &amp; treatment</li>\n<li><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4202347/\" rel=\"nofollow noreferrer\">World Journal of Gastroenterology Review Article on NAFLD &amp; PCOS (2)</a> - large section on possible pathogenesis mechanisms for NAFLD in PCOS</li>\n<li><a href=\"https://eje.bioscientifica.com/view/journals/eje/177/3/EJE-16-1063.xml\" rel=\"nofollow noreferrer\">Clinical &amp; Translational Endocrinology Review Article on NAFLD &amp; PCOS</a> - focuses on hormonal influences on NAFLD</li>\n<li><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5946415/#:%7E:text=According%20to%20the%20results%20of,risk%20of%20NAFLD%20than%20controls.\" rel=\"nofollow noreferrer\">Reproductive Health Meta-analysis on NAFLD &amp; PCOS</a> - suggests relationship between NAFLD &amp; PCOS may be independent of features like obesity and insulin resistance</li>\n</ul>\n", "score": 2 } ]

[ "pcos", "fatty-liver-disease" ]