tbuckley/cabot-search huggingface dataset:
Abstract 280: Reversal of Acute Coagulopathy Using Small-Volume 7.5% NaCl with Adenocaine and Mg2+ Resuscitation in a Rat Model of Severe Hemorrhagic Shock
Authors: Hayley L. Letson, Natalie M. Pecheniuk, Lebo P. Mhango, Geoffrey P. Dobson
Journal: Circulation (2011)

Acute traumatic coagulopathy occurs early in hemorrhagic trauma and is a major contributor to further bleeding, inflammation and mortality. Previously we showed that a small intravenous (IV) bolus of 7.5% NaCl with Adenocaine (adenosine and lidocaine) and Mg2+ could resuscitate mean arterial blood pressure (MAP) to within a permissive hypotensive range. Our aim was to examine the effect of the same fluid on activated partial thromboplastin times (aPTT) and prothrombin times (PT) following 60 min of resuscitation.

Methods: Male fed Sprague-Dawley rats (444 ± 10g, n=64) were anesthetized, non-heparinized and randomly assigned to one of eight groups: 1) Baseline blood, 2) 20 min bleed, 3) 60 min shock, 4) Untreated resuscitation, 5) 7.5% NaCl, 6) 7.5% NaCl Adenocaine, 7) 7.5% NaCl Mg2+ and 8) 7.5% NaCl, Adenocaine Mg2+. Hemorrhagic shock was induced by phlebotomy until MAP was 35-40 mmHg and continued for 20 min (~40% blood loss). Animals were left in shock for 60 min at 34°C. 0.3 ml IV bolus was injected over 2 sec. Arterial blood pressures, MAP, heart rate and rectal temperature were monitored. Arterial blood was collected in 3.2% Na-citrate tubes, centrifuged and the plasma was snap-frozen (-196°C) and stored at -80°C. aPTT and PT were measured on an Amelung KC4A microcoagulometer.

Results: Baseline aPTT and PT values were 17 ± 0.5 sec and 28 ± 0.8 sec, and increased significantly to 63 ± 21 and 107 ± 33 sec after blood withdrawal (20 min), and over 10 times baseline after 60 min shock. The large increases during shock were not due to hypothermia. Sixty minutes after 0.3 ml bolus resuscitation, the hypocoagulopathy worsened in all groups with the exception of 7.5% NaCl Adenocaine and Mg2+ with aPTT of 24 ± 1.7 sec and PT of 33 ± 1 sec. A partial restoration occurred with 7.5% NaCl Mg2+ (aPTT of 150 ± 43 and PT of 182 ± 47 sec) but was not significantly different from 7.5% NaCl alone.

Conclusion: aPTT and PT clotting times significantly increased during bleeding and shock prior to resuscitation. The hypocoagulopathy increased with 7.5% NaCl and was nearly completely reversed with 7.5% NaCl Adenocaine and Mg2+. We speculate that the mechanism(s) of reversal may shed light on understanding acute traumatic coagulopathy in out-of-hospital and far forward military settings.
Prediction of Age-related Macular Degeneration in the General Population
Authors: Gabriëlle H.S. Buitendijk, Elena Rochtchina, Chelsea Myers, Cornelia M. van Duijn, Kristine E. Lee, Barbara E.K. Klein, Stacy M. Meuer, Paulus T.V.M. de Jong, Elizabeth G. Holliday, Ava G. Tan, André G. Uitterlinden, Theru S. Sivakumaran, John Attia, Albert Hofman, Paul Mitchell, Johannes R. Vingerling, Sudha K. Iyengar, A. Cecile J.W. Janssens, Jie Jin Wang, Ronald Klein, Caroline C.W. Klaver
Journal: Ophthalmology (2013)
XIPHOSTERNAL CRUNCH: AN ANALYSIS OF 106 CASES AMONG 3,224 ARMY SEPARATEES
Authors: L SCHWAB, G L SMILEY, W P MEYN
Journal: Annals of Internal Medicine (1949)

Article1 August 1949XIPHOSTERNAL CRUNCH: AN ANALYSIS OF 106 CASES AMONG 3,224 ARMY SEPARATEESLOUIS SCHWAB, M.D., GORDON L. SMILEY, M.D., WERNER P. MEYN, M.D.LOUIS SCHWAB, M.D.Search for more papers by this author, GORDON L. SMILEY, M.D.Search for more papers by this author, WERNER P. MEYN, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-31-2-228 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptINTRODUCTIONSolis-Cohen1 has recently called attention to a peculiar heart sound heard in the tricuspid area among normal individuals, which is designated as the xiphosternal crunch. His report emphasized that:1. It occurred in 17.8 per cent of 4,982 normal Army inductees and in 21.1 per cent of the last 3,115 of this same group who were studied more carefully. It is apparently a normal functional sound.2. It is commonly misinterpreted as indicating mitral or tricuspid regurgitation, pericarditis or congenital heart disease.3. It is described in only one of the standard texts on physical diagnosis.Solis-Cohen's exhaustive review...Bibliography1. SOLIS-COHEN M: The xiphosternal crunch and its incidence in healthy inductees, Am. Jr. Med. Sci., 1945, ccx, 333. CrossrefGoogle Scholar2. Ibid., p. 340. Google Scholar3. OCHSNERDEBAKEY AM: Chonechondrosternon; report of case and review of literature, Jr. Thorac. Surg., 1939, viii, 469. CrossrefGoogle Scholar4. MONEY A: On great frequency of cardiac murmurs in puerperal state, Med. Chir. Trans., London, 1882, lxv, 87. CrossrefGoogle Scholar5. RUSSELL W: The murmurs of debility in the pulmonary and tricuspid areas, Edinburgh Med. Jr., 1882, xxviii, 130. Google Scholar6. BENEDICT AL: Adventitious murmurs accompanying the first heart sound, Arch. Diag., 1910, iii, 340. Google Scholar7. FISHBERG AM: Heart failure, 1st Ed., 1937, Lea and Febiger, Philadelphia, p. 391. Google Scholar8. HILL B: Principles of medical statistics, Post Graduate Series, Vol. III, 3rd Ed., 1946, The Lancet Limited, London, p. 93. Google Scholar9. SOLIS-COHEN M: An analysis of 63 cases exhibiting the xiphosternal crunching sound, Penn. Med. Jr., 1909, xiii, 216. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: *Received for publication March 4, 1948. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byBibliographyThe late systolic murmurCardiovascular SystemSystolic clicks and the late systolic murmurSystolic triple rhythmsSystolic clicks: A clinical, phonocardiographic, and hemodynamic evaluation 1 August 1949Volume 31, Issue 2Page: 228-234KeywordsCongenital heart diseaseHeart Issue Published: 1 August 1949 PDF downloadLoading ...
The Lost Art of Healing
Authors: D J Weatherall
Journal: BMJ (1997)

Bernard Lown: Houghton Mifflin, £15.99 ISBN 0 395 82525 3

Many, especially older, clinicians believe that medical practice has lost its way. Gone are the caring physicians who could take a thorough history and carry out a competent physical examination, or so the argument goes, and they have been replaced by super-specialised technicians who process their patients by means of laboratory tests and complex, high technology diagnostic machinery. Through a combination of the need for haste, engendered by the increasing commercialisation of medical care, and fear of litigation, patients are exposed to innumerable unnecessary investigations; clinical wisdom, kindness, and pastoral care are at a premium. In short, healing is a lost art.

This pessimistic view may have influenced the General Medical Council's recent pronouncements on the future of medical education in Britain. Similar thinking in the United States is reflected in this book by Bernard Lown, the distinguished Boston cardiologist and acceptor of the 1985 Nobel Peace …
An inconvenient truth
Authors: Des Spence
Journal: BMJ (2007)

As a child I was good with a knife. Preparing 4 kg of potatoes in 10 minutes—anything was preferable to milking the goat. No ready meals for us. At school the air was thick with the smell of burnt toast and the sound of bubbling cauldrons of custard, for home economics classes were compulsory. At university I worked in a restaurant washing dishes, graduated to vegetable preparation, and eventually specialised in making the starters. Later, armed with a Delia Smith idiot's guide cookbook, I discovered a passion for food and cooking. Cooking, however, has become mere “entertainment,” ever more voyeurism, and about the celebrities rather than the food. We are losing our food culture.

This is the era of the convenience meal in all its guises. Our main streets are full of takeaways: fish and chips, Chinese, kebabs, pizza, and Indian. But at least there is a degree of honesty in these colourful shop fronts. We pull into the supermarkets and stuff our trolleys with ready meals of couscous, duck, Jambalaya, deluding ourselves that this is proper food, but these are just takeaways too, processed imitations of real food, stuffed full of hidden calories, salt, and preservatives.

But our children fare the worst; in a society that venerates the needs of children they have become culinary Napoleons. They eat only what they like, and so what they like becomes all that is offered. Junk explanations are offered: food “allergies” or “intolerance.” Behind the closed doors of many of our most affluent households, no one cooks, and kids get processed foods, with fat chance of escaping obesity or eating disorders. Our society is “allergic” to accepting responsibly, so it is all the fault of advertising and the food industry. Our children's diet is parental passivity at its worst. All the excuses about time or cost are just that: excuses. We got what we wanted—wealth, comfort, and, above all else, convenience—but on the way we have lost much.

The Lancet has just published evidence that food additives adversely affect conduct (doi: 10.1016/S0140-6736(07)61306-3). This is not much of a surprise. But the real issue is our consumption of processed convenience foods. We need to value our traditional food culture, reconnect with food production, and see cooking as importantly as we do the “three Rs.” Schools should relinquish their blinkered obsession with academic performance and instead be filled with the smell of burnt custard. Likewise, families should give up the pointless merry go round of tutors and extracurricular lessons and use this time to prepare food together. Children can learn to do something positive with knives rather than just seeing them as something that teenage gang members wield. Let them cut their fingers and burn their hands. Believe me, this is considerably safer than milking a goat.
Plaque Prolapse After Stent Implantation in Patients With Acute Myocardial Infarction
Authors: Young Joon Hong, Myung Ho Jeong, Youngkeun Ahn, Doo Sun Sim, Jong Won Chung, Jung Sun Cho, Nam Sik Yoon, Hyun Ju Yoon, Jae Youn Moon, Kye Hun Kim, Hyung Wook Park, Ju Han Kim, Jeong Gwan Cho, Jong Chun Park, Jung Chaee Kang
Journal: JACC. Cardiovascular imaging (2008)
Quality of Care
Authors: Janet M. Torpy, Alison E. Burke, Richard M. Glass
Journal: JAMA (2008)

Quality of Care Health care quality means that patients receive appropriate care for medical problems in order to achieve the best possible outcomes.Quality of care is a cooperative effort that involves patients, doctors, nurses, and other health care professionals, as well as institutions (such as hospitals, nursing homes, mental health centers, and home health care agencies).Part of providing quality health care involves following standards, guidelines, and evidence-based practices.Evidence-based medicine involves using results from research studies such as clinical trials (scientific tests of treatments) and findings from other investigations to guide medical decisions.When results from such research indicate that a particular way of treating a disease is best, guidelines are developed to help clinicians and patients make good decisions about medical care.The October 22/29, 2008, issue of JAMA is a theme issue on the health of the nation and includes articles about the US health care system.
Non-MALT marginal zone B-cell lymphomas: a description of clinical presentation and outcome in 124 patients
Authors: Françoise Berger, Pascale Felman, Catherine Thieblemont, Thierry Pradier, Lucille Baseggio, Paul-Andre Bryon, Gilles Salles, Evelyne Callet-Bauchu, Bertrand Coiffier
Journal: Blood (2000)
Antidepressant prescribing and suicide
Authors: Wayne D Hall, Andrea Mant, Phillip B Mitchell
Journal: BMJ (2003)

EDITOR—Our critical finding was the relation between decline in suicide rate and exposure to antidepressants across age groups in both sexes. We agree that time series data must be interpreted cautiously; that is why we considered alternative explanations.

We disagree with Moncrieff that we should have used ratios of daily dependent doses. This would have been an alternative measure of change in exposure but not of overall antidepressant exposure. We agree that the daily dependent doses will underestimate prescribing levels of tricyclic …
Murine Autoantibodies to a Cryptic Membrane Antigen: Possible Explanation for Neuraminidase-Induced Increase in Cell Immunogenicity2
Authors: Steven A. Rosenberg, Susan Schwarz
Journal: JNCI Journal of the National Cancer Institute (1974)

The normal sera of several mouse strains contained cytotoxic activity toward lymphocytes treated with neuraminidase (Nase) but not to untreated cells. The greatest cytotoxic activity was in C3H/HeJ mice. CBA/J and AKR/J mice also had high levels. In C57BL/6J mice, there was no cytotoxic activity toward Nase-treated lymphocytes. This cytotoxic activity (probably antibody) was complement dependent and stable at 56° C for 30 minutes, but was inactivated by heating to 80° C for 30 minutes. Nase-treated C3H/HeJ and C57BL/6J cells contained equal amounts of this “hidden” antigen, as determined by absorption studies. Untreated cells contained no detectable antigen. These natural antibodies to a “cryptic” antigen exposed by Nase treatment were the basis of a theory to explain the increased immunogenicity of Nase-treated cells.
Ultrasound of the Whole Arm to Manage Suspected Upper-Extremity Deep Venous Thrombosis
Authors: Scott M. Stevens, Scott C. Woller
Journal: JAMA Internal Medicine (2015)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Internal Medicine HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Internal Medicine journal
The Mad Yard
Authors: Mark Evan Chimsky
Journal: JAMA (2003)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Abstract 694: Different pancreatic cancer cells have their own core signaling pathway
Authors: Eunkyung Kim, Sujin Kang, So Y. Kim, Dongxu Kang, Seungha Lee, Hye J. Choi, Joo-Hang Kim, Jae Jin Song
Journal: Cancer Research (2014)

Abstract Gemcitabine as the standard chemotherapy agent to pancreatic cancer has proved effective; however, the response rate remains at 5.4% and the 5-year survival rate is extremely poor. Due to the shortcomings of gemcitabine and the presence of gemcitabine-resistant pancreatic cancer, the development of targeted agents into an anti-neoplastic agent remains a viable option. We have investigated the transforming growth factor-beta (TGF-β), which is known to play a central role in pancreas cell function. We have already observed that the suppression of TGF-β2 induced an unexpected down-regulation of both TGF-β1 and TGF-β3 with concomitant decreases of survival-related signals, such as N-caderin, β-catenin, pp65 in melanoma cell line. Here, two different pancreatic cancer cell lines (HPAC, BxPC3), which have opposite genetic backgrounds (K-ras, p53, Smad4, EGFR), have shown differing sensitivities to the down-regulation of TGF-β2. Through transcriptome analysis, HPAC showed a high expression of TGF-β2, MUC4, HSP27, BMP4 which are deeply related to tumor progression and metastasis and are composed to core signaling complex initiating from TGF-β2. This was confirmed by TGF-β2 down-regulation with gemcitabine to show a greater decrease in survival potential compared to BxPC3. On the contrary, BxPC3, which has more of the mutant type p53, exhibited greater down-regulation of MUC4 by downregulation of p53 compared to that of TGF-β2. Such observations suggest that BxPC3 is composed of a different core signaling pathway, p53-MUC4 rather than TGF-β2-related signalings.In conclusion, it is necessary that the core signaling pathways which are implicated in individual pancreatic carcinogenesis are more specifically considered so that the various gemcitabine-resistant pancreatic cancer cells on the basis of customized treatment can be controlled. Citation Format: Eunkyung Kim, Sujin Kang, So Y. Kim, Dongxu Kang, Seungha Lee, Hye J. Choi, Joo-Hang Kim, Jae Jin Song. Different pancreatic cancer cells have their own core signaling pathway. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 694. doi:10.1158/1538-7445.AM2014-694
Cannabis use and the risk of developing a psychotic disorder
Authors: WAYNE HALL, LOUISA DEGENHARDT
Journal: World Psychiatry (2008)

WE BRIEFLY REVIEW THE EVIDENCE THAT CANNABIS USE IN ADOLESCENCE AND YOUNG ADULTHOOD IS A CONTRIBUTORY CAUSE OF SCHIZOPHRENIFORM PSYCHOSES, BY SUMMARISING LONGITUDINAL STUDIES THAT: a) have examined relationships between cannabis use and the risk of psychosis or psychotic symptoms; and b) have controlled for potential confounders, such as other forms of drug use and personal characteristics that predict an increased risk of psychosis. There is now reasonable evidence from longitudinal studies that regular cannabis use predicts an increased risk of schizophrenia and of reporting psychotic symptoms. These relationships have persisted after controlling for confounding variables such as personal characteristics and other drug use. The relationships did not seem to be explained by cannabis being used to self-medicate symptoms of psychosis. A contributory causal relationship is biologically plausible because psychotic disorders involve disturbances in the dopamine neurotransmitter system with which the cannabinoid system interacts, as has been shown by animal studies and a human provocation study. We briefly explore the clinical and public health implications of the most plausible hypothesis, that cannabis use precipitates schizophrenia in persons who are vulnerable because of a personal or family history of schizophrenia.
Abstract 611: Co-targeting the PI3K and androgen receptor signal pathways in castration resistant prostate cancer
Authors: Marco A. De Velasco, Yurie Kura, Naomi Ando, Emiko Fukushima, Yuji Hatanaka, Yutaka Yamamoto, Nobutaka Shimizu, Kazuhiro Yoshimura, Masahiro Nozawa, Kazuhiro Yoshikawa, Kazuto Nishio, Hirotsugu Uemura
Journal: Cancer Research (2014)

Abstract PTEN-deficient castration-naïve prostate tumors respond well to PI3K pathway inhibition, however, treatment response is largely ineffective in castration-resistant prostate cancer (CRPC). Reciprocal feedback regulation between the PI3K and androgen receptor (AR) signaling pathways helps maintain survival. We hypothesized that combined PI3K and AR pathway inhibition would improve the therapeutic outcome. Using an in vivo model of prostate cancer, we assessed the rational therapeutic combination of the mTOR inhibitor, everolimus, and the anti-androgen, chlormadinone acetate (CA), in PTEN deficient tumors. Treatment efficacy was examined in conditional PTEN-mutant mice that developed CRPC after surgical castration. Drug efficacy was evaluated by comparing differences in tumor burden, inhibition of tumor cell proliferation and induction of apoptosis. Treatment-specific responses were measured by downstream PI3K signal molecules, nuclear translocation of AR and activation of compensatory signaling pathways. Mice treated with everolimus or CA alone did not show a significant reduction in tumor burden compared to controls, however, the combination of everolimus and CA significantly inhibited tumor burden. Combination therapy also significantly inhibited cellular proliferation and increased apoptosis. PI3K pathway activation was effectively suppressed by everolimus as measured the levels of phosphorylated S6. No significant differences were noted in the nuclear translocation of the AR between control and treatment groups. Mice treated with the combination therapy demonstrated suppression of MAPK pathway activation. Interestingly, all treatments resulted in an increase of STAT3 activation. In summary, our findings show that AR re-challenge can sensitize CRPC to PI3K inhibition. This study provides a rationale for the developing combination therapies for CRPC by co-targeting the AR and PI3K signal transduction pathways. Citation Format: Marco A. De Velasco, Yurie Kura, Naomi Ando, Emiko Fukushima, Yuji Hatanaka, Yutaka Yamamoto, Nobutaka Shimizu, Kazuhiro Yoshimura, Masahiro Nozawa, Kazuhiro Yoshikawa, Kazuto Nishio, Hirotsugu Uemura. Co-targeting the PI3K and androgen receptor signal pathways in castration resistant prostate cancer. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 611. doi:10.1158/1538-7445.AM2014-611