tbuckley/cabot-search huggingface dataset:
Harvey's Reluctance to Publish
Journal: JAMA (1987)

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 Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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 journal
Cross-linked cytokeratin polypeptides in liver and hepatoma cells: Possible association with the process of cell degeneration and death
Authors: K Fukuda
Journal: Hepatology (1993)

We investigated transglutaminase-induced crosslinking of cytokeratin polypeptides in liver and hepatoma cells. To overcome the difficulties in the biochemical analysis of highly cross-linked polymers and aggregates of cytokeratins, cross-linked cytokeratin dimers were analyzed by immunoblotting to evaluate the degree of cross-linking of cytokeratins. Covalently cross-linked cytokeratin dimers were not detectable in normal rat liver cells. However, cytokeratin dimers and high-molecular-weight cytokeratin polymers were detected in liver tissue with histological evidence of coagulative necrosis induced by ischemia or carbon tetrachloride. Treatment of cultured hepatoma cells with the Ca2+ ionophore A23187 showed a dosedependent, time-dependent decrease of cell viability. The appearance of cytokeratin dimers was shown to be correlated with cell death. These results suggest that the transglutaminase-induced cross-linking of cytokeratin polypeptides in liver and hepatoma cells is closely associated with the process of cell degeneration and death. (HEPATOLOGY 1993;17:118–124.)
ARGUMENT AGAINST SENATE BILL 34, FIFTY-SIXTH CONGRESS, FIRST SESSION, GENERALLY KNOWN AS THE "ANTIVIVISECTION BILL."
Authors: WILLIAM H. WELCH
Journal: JAMA (1900)

On February 21, 1900, the Senate Committee on the District of Columbia, with Senator Gallinger in the chair, gave to advocates and opponents of the "antivivisection bill" a public hearing, at which I presented in its main features the following argument. After this hearing, on March 9, 1900, an amended or substitute bill, still designated S. Bill 34, was printed for the committee. The principal changes from the original bill made by this substitute are as follows: 1. The title now reads: "A bill for the regulation of vivisection in the District of Columbia." 2. The restrictions apply for the most part only to experiments on warm-blooded animals instead of to those on all vertebrates. 3. Experiments to acquire "surgical experience" are now allowed. 4. The class of officers of the United States Government who may experiment without a license from the District Commissioners is defined. 5. The use of
Dietary and pharmacologic therapy for the lipid risk factors
Journal: JAMA (1983)

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
Who teaches physiological chemistry?
Authors: S. P. Bessman
Journal: JAMA (1966)

The development of the medical school department of biochemistry may soon transform it to an institute only remotely related to the activities of the school. This process has been caused by two factors. The first is the Flexner Report and the second is the extensive growth of the discipline itself. When the Flexner Report established the need for the incorporation of scientific principles into the teaching of medicine, departments of physiological chemistry began to appear in medical schools. The growing new departments became havens for increasing numbers of biochemists who had found little opportunity to develop independently in other areas of the universities. They soon expanded their studies beyond the immediate problems of animal and human biochemistry into the field of fermentation, then enzymology, then into bacterial metabolism and the chemistry of genetics. This was a natural result of the generality of biochemistry, but clinical departments began to question the
Abstract P296: Longitudinal Association of Changes in Abdominal Fat Quantity and Quality with Changes in Cardiovascular Disease Risk Factors
Authors: Jane J Lee, Alison Pedley, Udo Hoffmann, Joseph M Massaro, Caroline S Fox
Journal: Circulation (2016)

Introduction: Subcutaneous (SAT) and visceral adipose tissue (VAT) are associated with adverse cardiometabolic risk profiles. We explored the degree to which changes in abdominal fat quantity and quality are associated with changes in cardiovascular disease (CVD) risk factors over time. Methods: Framingham Heart Study Third Generation cohort participants (n=1,106; 44.1% women; mean age 45.1 years) who underwent multi-detector computed tomography assessment for two consecutive examinations from 2002 to 2005 and from 2008 to 2011 were included in this analysis (mean interval 6.1 years). Abdominal adipose tissue volume in cm 3 and attenuation (indirect measure of fat quality) in Hounsfield units (HU) were determined by multi-detector computed tomography-acquired abdominal scans. Multivariable-adjusted linear and logistic regression models were constructed to examine the longitudinal associations between changes in abdominal fat volume and attenuation with changes in CVD risk factors. Multivariable-adjustment included baseline abdominal adipose tissue, baseline CVD risk factors, baseline age, smoking status, alcohol intake, physical activity, postmenopausal status, and hormone replacement therapy. Results: The mean fat volume change was 602 cm 3 for SAT and 703 cm 3 for VAT; and the mean fat attenuation change was -5.5 HU for SAT and 0.07 HU for VAT. An increase in fat volume and decrease in fat attenuation were associated with adverse changes in CVD risk factors. An additional 500 cm 3 increase in fat volume was associated with incident hypertension, hypertriglyceridemia, and metabolic syndrome (all p &lt;0.05). Similarly, each additional 5 HU decrease in fat attenuation was associated with adverse changes in CVD risk factor profiles. For example, a 5 HU decrease in SAT attenuation was associated with an increase of 2.89 mmHg of systolic blood pressure, 2.24 mmHg of diastolic blood pressure, 1.29 mg/dL of fasting plasma glucose, 5.01 mg/dL of total cholesterol, and 0.11 mg/dL of log triglycerides; and a decrease of 3.25 mg/dL of high density lipoprotein cholesterol (all p &lt;0.05). The majority of these associations remained significant even after further accounting for body mass index change, waist circumference change or respective abdominal adipose tissue volumes. Conclusions: Increasing accumulation of fat quantity and decreasing fat attenuation are associated with worsening of CVD risk factors beyond the associations with generalized adiposity, central adiposity, or respective adipose tissue volume. Our findings highlight the importance of quantitative and qualitative aspects of adipose tissue for a better understanding of CVD risk.
The centinormalized unit for reporting enzyme results. A note of caution
Authors: J. E. Buttery
Journal: JAMA (1981)

Centinormalized units (values expressed as a percentage of the upper limit of the reference range) have been proposed as a logical way of reporting enzyme results. We argue that this would not eliminate the need to refer to reference ranges, nor would it confer comparability of results between laboratories. The present confusing situation will be solved only by the adoption of standardized methods of estimation. (<i>JAMA</i>1981;245:2431-2432)
IARC Visiting Scientist Award, 1986–87
Journal: JNCI Journal of the National Cancer Institute (1985)

Journal Article IARC Visiting Scientist Award, 1986–87 Get access JNCI: Journal of the National Cancer Institute, Volume 75, Issue 3, September 1985, Pages 593–594, https://doi.org/10.1093/jnci/75.3.593-d Published: 01 September 1985
Professional Liability
Authors: James S. Todd
Journal: JAMA (1986)

For -A- or physicians it is not necessary to chronicle the ravages that the problem of professional liability has wreaked upon the medical profession and, more importantly, upon society. The statistics are there for all to see and, taken in the aggregate, by any reasonable interpretation, indicate a conundrum that so far has defied illumination or solution.<sup>1</sup>For all physicians, liability insurance premiums have increased by 236% over the last decade.<sup>2</sup>But the issue goes far beyond dollars and cents. It speaks to equity, to ethics, to medical progress, to availability of care, to confidence in medical professionals, and to what it is that society really expects of our profession. No one can deny that medical professionals are fallible, that they do make honest errors of judgment, that they do abhor incompetence. No physician sets out to be negligent. No patient is perfectly predictable in terms of response
Errors in Author Byline and Conflict of Interest Disclosures
Authors: Jussi Tikkanen, Chandima Divithotawela, Marcelo Cypel
Journal: JAMA Surgery (2020)

Dörthe Seidel; Stephan Diedrich, Dr med; Florian Herrle, PD, Dr med, MSc; Henryk Thielemann, Dr med; Frank Marusch, Prof Dr med; Rebekka Schirren, Dr med; Recca Talaulicar; Tobias Gehrig, Dr med; Nadja Lehwald-Tywuschik, PD; Matthias Glanemann, Prof Dr med; Jörg Bunse, Dr med; Martin Hüttemann, Dr med; Chris Braumann, Prof Dr med; Oleg Heizmann, PD Dr med; Marc Miserez, Prof; Thomas Krönert, Dr med; Stephan Gretschel, Prof Dr med; Rolf Lefering, Prof Dr rer medic
Psychological Responses to Continuous Terror: A Study of Two Communities in Israel
Authors: Arieh Y Shalev, Rivka Tuval, Sarah Frenkiel-Fishman, Hilit Hadar, Spencer Eth
Journal: American Journal of Psychiatry (2006)

Objective: The authors evaluated psychological responses to continuous terror. Method: Data were collected after 10 months of escalating hostilities against civilians in Israel. The study's participants were randomly selected adults living in two suburbs of Jerusalem, one frequently and directly exposed to acts of terrorism (N=167) and the other indirectly exposed (N=89). Participants provided information about exposure to terror-related incidents, disruption of daily living, symptoms of posttraumatic stress disorder (PTSD), and general distress (assessed with the Brief Symptom Inventory). Results: Residents of the directly exposed community reported more frequent exposure to terror and deeper disruption of daily living. Notwithstanding, the directly and indirectly exposed groups reported comparable rates of PTSD and similar levels of symptoms: 26.95% of the directly exposed group and 21.35% of the indirectly exposed group met DSM-IV PTSD symptom criteria (criteria B through D), and about one-third of those with PTSD symptoms (35.7% in the directly exposed group and 31.5% in the indirectly exposed group) reported significant distress and dysfunction. Subjects who did not meet PTSD symptom criteria had very low levels of PTSD symptoms, and their Brief Symptom Inventory scores were within population norms. Exposure and disruption of daily living contributed to PTSD symptoms in the directly exposed group. Disruption of daily routines contributed to Brief Symptom Inventory scores in both groups. Conclusions: Continuous terror created similar distress in proximal and remote communities. Exposure to discrete events was not a necessary mediator of terror threat. A subgroup of those exposed developed serious symptoms, whereas others were surprisingly resilient. Disruption of daily routines was a major secondary stressor.
Practical Anatomy
Journal: JAMA (1934)

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
Leads from the MMWR. Tuberculosis among Asians/Pacific Islanders--United States, 1985
Journal: JAMA (1987)

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
Incomplete Conflict of Interest Disclosure
Journal: JAMA Oncology (2016)

Joanne Armstrong, MD, MPH; Michele Toscano, MS; Nancy Kotchko, MA; Sue Friedman, DVM; Marc D. Schwartz, PhD; Katherine S. Virgo, MBA, PhD; Kristian Lynch, PhD; James E. Andrews, PhD; Claudia X. Aguado Loi, MPH, PhD; Joseph E. Bauer, PhD; Carolina Casares, MD, MPH; Elizabeth Bourquardez Clark, BA; Matthew R. Kondoff, BS; Ashley D. Molina, BS; Mehrnaz Abdollahian, MS; Gregg Walker, MBA; Rebecca Sutphen, MD
A reduction in the rate of PSA rise following chemotherapy in patients with metastatic hormone refractory prostate cancer (HRPC) predicts survival: Results of a pooled analysis of CALGB HRPC trials
Authors: A. V. D'Amico, S. Halabi, N. J. Vogelzang, E. J. Small
Journal: Journal of Clinical Oncology (2004)

4506 Background: A prostate-specific antigen (PSA) decline of > 50% is associated with a prolongation in survival for patients with metastatic hormone refractory prostate cancer (HRPC). However, whether any reduction in the rate of PSA rise following chemotherapy prolongs survival remains unanswered. Methods: Four pooled multi-institutional Cancer and Leukemia Group B randomized phase III trials containing a minimum of 3 pre-treatment and 3 post-treatment PSA values, and follow up information on 153 men with metastatic HRPC who received chemotherapy for progressive metastatic HRPC formed the study cohort. The ability of the ratio (R) of the post to pre-chemotherapy PSA slope and its constituents to predict time to death following chemotherapy was assessed using the proportional hazards regression model. Results: At the time of this analysis, 139 men had died. When evaluated by tertiles, R was associated (pCox ≤ 0.09) with time to death following chemotherapy controlling for the value of the pre-chemotherapy PSA slope (pCox = 0.02). The median survival following chemotherapy for patients whose R-value was in the best (< - 0.8), middle (- 0.8 or more and up to - 0.3) or worse response tertile (> - 0.3) was 25 months [95% Confidence Interval (CI): 19–30], 23 months [95% CI: 18–29], and 18 months [95% CI: 14–23] respectively. The adjusted Hazard Ratio for death was 0.7 [95% CI: 0.45–1.05; pCox = 0.09] and 0.7 [95% CI: 0.45–1.04; pCox = 0.08] for patients with an R-value in the best and middle response tertile respectively as compared to the worse response tertile. Conclusion: A reduction in the rate of PSA rise following chemotherapy is associated with a prolongation in survival. Therefore, R may be an intermediate end point for mortality in patients with metastatic HRPC. Prospective validation is warranted. No significant financial relationships to disclose.
Patient behavior for blood pressure control. Guidelines for professionals
Journal: JAMA (1979)

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 Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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 journal
Abstract 515: Progesterone receptor inhibition of efficient type I interferon signaling in breast cancer
Authors: Katherine Rose Walter, Merit Goodman, Christy Hagan
Journal: Cancer Research (2019)

Abstract A vast majority (65-70%) of breast cancers express the progesterone receptor (PR), a nuclear receptor that is activated in response to its ligand progesterone. Compelling clinical trial data have suggested that progestins have a role in breast cancer development, independent of the widely studied estrogen receptor. The mechanism by which this occurs, however, is vastly understudied. Traditionally, PR exerts its effects following ligand activation by translocating to the nucleus and binding to DNA where it affects the transcription of a variety of genes involved in growth, survival, and proliferation. Our lab has identified a novel subset of genes that have altered expression following PR activation. Interferon Stimulated Genes (ISGs)–primarily activated in response to interferon signaling (viral response pathway) –are repressed when PR is activated by its ligand. In attempting to elucidate a mechanism by which PR exerts this effect, we have investigated crosstalk of PR with canonical interferon signaling proteins and have found that PR interacts with these proteins and significantly reduces their ability to become activated. STAT1, a crucial protein involved in the interferon signaling cascade, is unable to efficiently be phosphorylated when PR is activated with ligand. ChIP experiments have also shown that PR inhibits the machinery necessary for ISG transcription from efficiently binding ISG promoters, possibly explaining the reduction in ISG expression observed following PR activation. Because of the importance of this particular signaling cascade in normal cell biology, multiple mechanisms most likely exist to fully inhibit interferon signaling and experiments are currently underway to identify other possibilities to better define PR’s functionality in this context. Evasion of the immune system is considered a Hallmark of Cancer and our preliminary data suggest a potential mechanism by which breast cancer is able to accomplish this. Activation of type I interferon signaling is an early step in marking tumors for immune clearance. By repressing ISG protein expression, it is possible that these tumors are able to avoid detection by host immune cells leading to tumor establishment and subsequent progression. This novel role of PR and progestins offers insight that could aid in improving upon established estrogen only-based therapies for prevention and treatment of hormone dependent breast cancers. Citation Format: Katherine Rose Walter, Merit Goodman, Christy Hagan. Progesterone receptor inhibition of efficient type I interferon signaling in breast cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 515.