tbuckley/cabot-search huggingface dataset:
Acquiring computer literacy
Authors: D. Morris
Journal: BMJ (1998)

When the editor asked me to write this piece I responded that I was no expert on computers. That, he replied, was exactly what made me so suitable. So, how computer literate do you have to be to get by? Doctors, much like the rest of the population, straddle a whole range of positions from Luddite to nerd.

I have watched developments in computing since the 1970s with interest but without getting personally involved. By the mid-1990s the world had changed. The activity of general practice now needed so much counting that number crunchers were essential, the Family Health Services people were keen to get electronic links instead of paper, and commercial general practice systems were now impressive. We took the plunge, and in late 1995 we changed overnight from paper only to a paperless computerised practice.

Overnight? Well, yes and no. Yes, because from the day we went live with the computers we made no more paper notes or prescriptions. No, because going live wasn't overnight. We spent an entire year making the practice staff computer literate before our “Go live day,” and we continued up the learning curve for many months thereafter.

### Computer literacy: three basic stages

You have achieved basic competence when you can use your computer during a consultation as skilfully, and as unobtrusively to the patient, as you would use Lloyd George envelopes or A4 paper notes - both to record appropriate new history and findings and to refer back to older parts of the record as the consultation proceeds. If you don't have this level of competence with your computer, then both you and your patient will feel uneasy and distracted if you try to use it during a consultation.

There are three …
Successful treatment of Sweet's syndrome with doxycycline
Authors: R.K. JOSHI, D.N. ATUKORALA, A. ABANMI, O. KHAMIS, A. HALEEM
Journal: British Journal of Dermatology (1993)

Two patients with Sweet's syndrome are described, both of whom were treated with doxycycline 200 mg daily, and responded well to therapy. Doxycycline appears to be an effective alternative to corticosteroids for the treatment of Sweet's syndrome.
Convulsions associated with cyclosporin A in renal transplant recipients.
Authors: M Beaman, S Parvin, P S Veitch, J Walls
Journal: BMJ (1985)

Trois observations d'accidents neurotoxiques sous la forme de crises convulsives de type grand mal, attribues a la cyclosporine A. Dans les 3 cas les crises disparaissent sans sequelles apres interruption du traitement. Reprise possible de la cyclosporine sous surveillance etroite
Atherosclerotic aortic component quantification by noninvasive magnetic resonance imaging: an in vivo study in rabbits
Authors: Gérard Helft, Stephen G Worthley, Valentin Fuster, Azfar G Zaman, Clyde Schechter, Julio I Osende, Oswaldo J Rodriguez, Zahi A Fayad, John T Fallon, Juan J Badimon
Journal: Journal of the American College of Cardiology (2001)
Characterization of acidification in the cortical and medullary collecting tubule of the rabbit.
Authors: M E Laski, N A Kurtzman
Journal: Journal of Clinical Investigation (1983)

Ouabain and lithium decrease acidification in open-circuited bladders by eliminating the electrical gradient favoring acidification. The effect of ouabain and lithium on acidification in cortical and medullary collecting tubules derived from starved New Zealand white rabbits was studied by using the techniques of isolated nephron microperfusion and microcalorimetric determination of total CO2 flux. Bath and perfusion solutions were symmetric throughout all studies, and solutions contained 25 meq of bicarbonate and were bubbled with 93.3% O2/6.7% CO2 gas mixtures. In cortical collecting tubules, ouabain (10(-8) M) addition to bath resulted in a decrease in both potential difference (PD), from -16.4 to -2.2 mV (P less than 0.001), and total CO2 flux (JTCO2), from +6.0 to 1.5 pmol/mm per min (P less than 0.005). In medullary collecting tubules neither PD nor JTCO2 changed with the addition of ouabain in either 10(-8) or 10(-4) M concentration. Replacement of 40 mM NaCl with 40 mM LiCl in both perfusate and bath in cortical collecting tubules resulted in decreases in both PD, from -11.6 to 0.4 mV (P less than 0.005), and JTCO2, from +10.8 to +4.2 pmol/mm per min (P less than 0.025). This substitution had no effect on medullary collecting tubules. When control flux rates were plotted against animal bladder urine pH, both medullary and cortical tubules showed good inverse correlation between these variables, with higher values of flux rate for the medullary tubules. The data support a role for transepithelial PD in acidification in the cortical collecting tubule and also suggest that both cortical and medullary segments of the collecting tubule participate when urinary acidification is increased during starvation in the rabbit.
ADVANCED TREATMENT O PUERPERAL INFECTON
Authors: ROBERT T. GILLMORE
Journal: JAMA (1913)

with mercurial injection in the presence of a negative Wassermann.1 1 n favor of the syphilitic etiology is the fact that along with the cure due to the deep injection of mercury the complement fixation reaction became negative.This is of importance, because it is a substantiated fact, that in cases with non-specific positive reactions the non-spe¬ cific amboceptor in I be patient's serum docs not, as a rule, disappear after the institution of mercurial treat¬ ment.Whether this case is the result of inherited syphilis can only be suspected.In favor of Ibis, however, is the absence of any syphilitic manifestations in any of the third generation, who have been thoroughly examined, and the absence of history of miscarriage of any of the issue.I regret that photographs of the bladder lesion were not made at the first cystoscopy.They were seen at that time also by Dr. E. M. Sanders, who agreed with me that tuberculosis was the most probable diagnosis.A careful reading of the description will show that we were somewhat justified in this tentative diagnosis.
Abstract 3226: PKM2 metabolic activator slows lung cancer xenograft growth
Authors: Mark Parnell, Jason M. Foulks, Rebecca Nix, Bai Luo, Anna Senina, Yong Xu, Michael Saunders, Koc-Kan Ho, Michael V. McCullar, Steven B. Kanner
Journal: Cancer Research (2012)

Abstract Tumor cells primarily utilize aerobic glycolysis, rather than oxidative phosphorylation, to metabolize glucose (the Warburg effect). The M2 splice form of pyruvate kinase (PKM2), the enzyme catalyzing the rate-limiting final step of glycolysis, is highly upregulated in tumors. Unlike the M1 splice form (PKM1), a constitutively active tetramer found predominantly in non-cancerous tissues, PKM2 is an inactive dimer under normal physiological conditions. Tetramerization of PKM2 requires binding of the allosteric activator fructose-1,6-bisphosphate (FBP), an upstream glycolytic intermediate, resulting in a fully active enzyme. Inactivation of PKM2 by cancer cells may allow glycolytic intermediates to be diverted into other biosynthetic pathways necessary for biomass production. The finding that PKM2 rather than PKM1 expression enhances tumorigenicity suggests that activators of PKM2 may have anti-tumor properties. We have identified and developed a series of small molecule PKM2 activators that exhibit low nM activation activity in biochemical and cell-based assays that measure pyruvate and ATP production. The extent of activation of these compounds is equal to or greater than that of FBP in biochemical assays. In addition, preliminary studies show that PKM2 activators inhibit the growth of lung cancer cell lines in vitro. The current lead compound was tested in established subcutaneously implanted A549 lung adenocarcinoma xenografts, where we observed a statistically significant decrease in tumor growth, with no observable toxicity. These data suggest that this class of PKM2 activators is effective as tumor cell metabolic regulators with anti-tumor activity for lung cancer and potentially other malignancies. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 3226. doi:1538-7445.AM2012-3226
A hypoallergenic variant of Der p 1 as a candidate for mite allergy vaccines
Authors: David Walgraffe, Christel Mattéotti, Mohamed el Bakkoury, Lida Garcia, Céline Marchand, Dominique Bullens, Michel Vandenbranden, Alain Jacquet
Journal: Journal of Allergy and Clinical Immunology (2009)

Recombinant hypoallergens that display reduced allergenicity but retain T-cell reactivity represent promising candidates to improve the safety and efficacy of allergen-specific vaccines or immunotherapy.The current study reports the immunologic characterization of a hypoallergenic variant of the major mite allergen Der p 1.The recombinant proform of Der p 1 (ProDer p 1) was expressed in Escherichia coli (ProDer p 1 coli), purified and characterized at the level of its secondary structure, and IgE and T-cell reactivities. Moreover, the prophylactic potential of ProDer p 1 coli vaccinations was evaluated in a murine Der p 1 sensitization model.After purification and refolding, ProDer p 1 coli remained aggregated with a higher beta-sheet content and altered Der p 1 conformational epitopes compared with the correctly folded monomeric ProDer p 1 produced in Chinese hamster ovary cells. Both ProDer p 1 forms were able to retain the Der p 1-specific T-cell reactivity but direct ELISA, competitive inhibition, and rat basophil leukemia assays clearly showed that ProDer p 1 coli displays a very weak IgE reactivity. Mice vaccinations with aggregated ProDer p 1 adjuvanted with alum induced a T(H)1-biased immune response that prevented the subsequent allergic response after Der p 1 sensitization and airway challenge with aerosolized mite extracts. Furthermore, ProDer p 1 coli treatment inhibited the development of airway eosinophilia and airway hyperresponsiveness to inhaled methacholine.Aggregated forms of Der p 1 could represent hypoallergens suitable for the prevention of mite allergy.
GATA2 deficiency-associated bone marrow disorder differs from idiopathic aplastic anemia
Authors: Karthik A. Ganapathi, Danielle M. Townsley, Amy P. Hsu, Diane C. Arthur, Christa S. Zerbe, Jennifer Cuellar-Rodriguez, Dennis D. Hickstein, Sergio D. Rosenzweig, Raul C. Braylan, Neal S. Young, Steven M. Holland, Katherine R. Calvo
Journal: Blood (2014)
A Short Textbook of Orthopaedics and Traumatology
Authors: Reginald R. Cooper
Journal: JAMA (1977)

The author designed this relatively inexpensive, concise paperback primarily for the medical student desiring an overview of orthopedics and traumatology. This volume does indeed contain descriptions of a vast number of diseases and injuries. Perhaps this and the several diagrams rank as its most useful features. The initial section on trauma should suffice for most medical students. Discussions of many entities are somewhat dated, portray nearly a pure mechanical approach, and give little attention to musculoskeletal biology, physiology, and pathology. Some concepts rank as speculative. The section on osteomyelitis notes that infection arises in areas "where tissue vitality is lower than normal" as in a hematoma from injury. In fact, the metaphysis, the common location of acute hematogenous osteomyelitis, is an extremely dynamic portion of bone. Therapeutic concepts such as draining an infected joint in "severe cases" where "pus becomes too thick to be aspirated" should, in my opinion, no
Herpes Simplex Infections
Authors: Fred Levit
Journal: JAMA (1975)

<h3>To the Editor.—</h3> Some of the recent writings on herpes simplex infections of the genitalia give the impression that this disease has become common only recently. One author, speaking of herpes of the female genitalia, says that the disease "was almost never seen prior to 1956."<sup>1</sup>This impression is, of course, not correct. The disease is described in most textbooks of dermatology, and is frequently referred to as being "not uncommon." Crocker<sup>2</sup>does so in his text published in 1907. Duhring's textbook published in 1895 has two pages on genital herpes and includes the statement "Some women are much annoyed by its frequent recurrence."<sup>3</sup>But the disease is older than that. Nahmias and Roizman<sup>4</sup>in reviewing herpesvirus infections refer to a monograph on genital herpes published in 1886.<sup>5</sup>The oldest completely clear description of the disease in women that I can find is by Fuchs
HepaRG cells: A human model to study mechanisms of acetaminophen hepatotoxicity
Authors: Mitchell R. McGill, Hui-Min Yan, Anup Ramachandran, Gordon J. Murray, Douglas E. Rollins, Hartmut Jaeschke
Journal: Hepatology (2010)

Abstract Acetaminophen (APAP) overdose is the leading cause of acute liver failure in Western countries. In the last four decades much progress has been made in our understanding of APAP-induced liver injury through rodent studies. However, some differences exist in the time course of injury between rodents and humans. To study the mechanism of APAP hepatotoxicity in humans, a human-relevant in vitro system is needed. Here we present evidence that the cell line HepaRG is a useful human model for the study of APAP-induced liver injury. Exposure of HepaRG cells to APAP at several concentrations resulted in glutathione depletion, APAP-protein adduct formation, mitochondrial oxidant stress and peroxynitrite formation, mitochondrial dysfunction (assessed by JC-1 fluorescence), and lactate dehydrogenase (LDH) release. Importantly, the time course of LDH release resembled the increase in plasma aminotransferase activity seen in humans following APAP overdose. Based on propidium iodide uptake and cell morphology, the majority of the injury occurred within clusters of hepatocyte-like cells. The progression of injury in these cells involved mitochondrial reactive oxygen and reactive nitrogen formation. APAP did not increase caspase activity above untreated control values and a pancaspase inhibitor did not protect against APAP-induced cell injury. Conclusion: These data suggest that key mechanistic features of APAP-induced cell death are the same in human HepaRG cells, rodent in vivo models, and primary cultured mouse hepatocytes. Thus, HepaRG cells are a useful model to study mechanisms of APAP hepatotoxicity in humans. (Hepatology 2011)
'Realities of Medicine:' a week of the future
Authors: Beverly Merz
Journal: JAMA (1982)

It is a Sunday morning late in August. A few casually but neatly dressed young men and women exchange greetings and anecdotes as they survey the brunch buffet: plump blueberries in a handcrafted ceramic bowl, coffee cakes stuffed with nuts and fruit, a chafing dish of spiced sausage, and pitchers of coffee and apple cider. They fill their plates and join the other guests in the sun-dappled living room. Throughout the summer, this group—mostly medical students—has enjoyed many such Sunday gettogethers at this home in Evanston, Ill. The brunches, which have become something of a tradition, are actually planning sessions for another tradition, "The Realities of Medicine," a week-long program designed to acquaint second-year medical students at the University of Illinois College of Medicine at Chicago with issues pertinent to the art and practice of medicine before they embark on their clinical rotations. The program is the brainchild of the
Hands-On Defibrillation
Authors: Michael S. Lloyd, Brian Heeke, Paul F. Walter, Jonathan J. Langberg
Journal: Circulation (2008)

Background— Brief interruptions in chest compressions reduce the efficacy of resuscitation from cardiac arrest. Interruptions of this type are inevitable during hands-off periods for shock delivery to treat ventricular tachyarrhythmias. The safety of a rescuer remaining in contact with a patient being shocked with modern defibrillation equipment has not been investigated. Methods and Results— This study measured the leakage voltage and current through mock rescuers while they were compressing the chests of 43 patients receiving external biphasic shocks. During the shock, the rescuer’s gloved hand was pressed onto the skin of the patient’s anterior chest. To simulate the worst case of an inadvertent return current pathway, a skin electrode on the rescuers thigh was connected to an electrode on the patient’s shoulder. In no cases were shocks perceptible to the rescuer. Peak potential differences between the rescuer’s wrist and thigh ranged from 0.28 to 14 V (mean 5.8±5.8 V). The average leakage current flowing through the rescuer’s body for each phase of the shock waveform was 283±140 μA (range 18.9 to 907 μA). This was below several recommended safety standards for leakage current. Conclusions— Rescuers performing chest compressions during biphasic external defibrillation are exposed to low levels of leakage current. The present findings support the feasibility of uninterrupted chest compressions during shock delivery, which may enhance the efficacy of defibrillation and cardiocerebral resuscitation.
(25) Port wine stain treated by infra-red coagulation
Authors: G.B. Colver, T.J. Ryan, R.P.R. Dawber
Journal: British Journal of Dermatology (1985)

Journal Article (25) Port wine stain treated by infra‐red coagulation Get access G.B. Colver, G.B. Colver The Slade Hospital, Oxford Search for other works by this author on: Oxford Academic Google Scholar T.J. Ryan, T.J. Ryan The Slade Hospital, Oxford Search for other works by this author on: Oxford Academic Google Scholar R.P.R. Dawber R.P.R. Dawber The Slade Hospital, Oxford Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 113, Issue s29, 1 July 1985, Pages 68–69, https://doi.org/10.1111/j.1365-2133.1985.tb13040.x Published: 01 July 1985
Smoking prevalence in England is below 20% for the first time in 80 years
Authors: J. Brown, R. West
Journal: BMJ (2014)

We would like to expand on the “who smokes” section of Zwar and Mendelsohn’s timely clinical review of smoking cessation by sharing the latest findings of a large national surveillance study, which has been tracking smoking prevalence in England since 2006.1 2 Each month a new sample of about 1800 people aged ≥16 years is selected by random location sampling to complete a computer assisted household survey with a trained interviewer. Prevalence data are weighted to …
To be good physicians, we must all fight against the battle against cancer
Authors: D. W. Berger
Journal: BMJ (2014)

I’m not a fighter, or at least I’m not a fighter when the fight is pointless. A fight “to beat” metastatic cancer is usually pointless.

This use of military metaphors1 chimes with modern Western ideas about fighting injustice. It’s a compelling idea (how could anyone say fighting injustice was bad?), unites most of us with a common purpose, and helps …
National Vehicle Emissions Policies and Practices and Declining US Carbon Monoxide–Related Mortality
Authors: Joshua A. Mott
Journal: JAMA (2002)

Carbon monoxide (CO) has been reported to contribute to more than 2000 poisoning deaths per year in the United States.To evaluate the influence of national vehicle emissions policies and practices on CO-related mortality and to describe 31 years (1968-1998) of CO-related deaths in the United States.Longitudinal trend analysis using computerized death data from the Centers for Disease Control and Prevention, US Census Bureau population data, and annual CO emissions estimates for light-duty vehicles provided by the US Environmental Protection Agency.All deaths in the US for which non-fire-related CO poisoning was an underlying or contributing condition, classified by intent and mechanism of death. Negative binomial regression was used to incorporate every year of data into estimated percentage changes in CO emissions and mortality rates over time.During 1968-1998, CO-related mortality rates in the United States declined from 20.2 deaths to 8.8 deaths per 1 million person-years (an estimated decline of 57.8%; 95% confidence interval [CI], -62.4% to -52.6%). Following the introduction of the catalytic converter to automobiles in 1975, CO emissions from automobiles decreased by an estimated 76.3% of 1975 levels (95% CI, -82.0% to -70.4%) and unintentional motor vehicle-related CO death rates declined from 4.0 to 0.9 deaths per 1 million person-years (an estimated decline of 81.3%; 95% CI, -84.8% to -77.0%). Rates of motor vehicle-related CO suicides declined from 10.0 to 4.9 deaths per 1 million person-years (an estimated decline of 43.3%; 95% CI, -57.5% to -24.3%). During 1975-1996, an annual decrease of 10 g/mile of estimated CO emissions from automobiles was associated with a 21.3% decrease (95% CI, -24.2% to -18.4%) in the annual unintentional motor vehicle-related CO death rate and a 5.9% decrease (95%CI, -10.0% to -1.8%) in the annual rate of motor vehicle-related CO suicides.If rates of unintentional CO-related deaths had remained at pre-1975 levels, an estimated additional 11 700 motor vehicle-related CO poisoning deaths might have occurred by 1998. This decline in death rates appears to be a public health benefit associated with the enforcement of standards set by the 1970 Clean Air Act.
RNA Interference Improves Myopathic Phenotypes in Mice Over-expressing FSHD Region Gene 1 (FRG1)
Authors: Lindsay M Wallace, Sara E Garwick-Coppens, Rossella Tupler, Scott Q Harper
Journal: Molecular Therapy (2011)

Muscular dystrophies, and other diseases of muscle, arise from recessive and dominant gene mutations. Gene replacement strategies may be beneficial for the former, while gene silencing approaches may provide treatment for the latter. In the last two decades, muscle-directed gene therapies were primarily focused on treating recessive disorders. This disparity at least partly arose because feasible mechanisms to silence dominant disease genes lagged behind gene replacement strategies. With the discovery of RNA interference (RNAi) and its subsequent development as a promising new gene silencing tool, the landscape has changed. In this study, our objective was to demonstrate proof-of-principle for RNAi therapy of a dominant myopathy in vivo. We tested the potential of adeno-associated viral (AAV)-delivered therapeutic microRNAs, targeting the human Facioscapulohumeral muscular dystrophy (FSHD) region gene 1 (FRG1), to correct myopathic features in mice expressing toxic levels of human FRG1 (FRG1(-high) mice). We found that FRG1 gene silencing improved muscle mass, strength, and histopathological abnormalities associated with muscular dystrophy in FRG1(-high) mice, thereby demonstrating therapeutic promise for treatment of dominantly inherited myopathies using RNAi. This approach potentially applies to as many as 29 different gene mutations responsible for myopathies inherited as dominant disorders.