tbuckley/cabot-search huggingface dataset:
Abortion
Authors: Stanley R. Levine
Journal: JAMA (1990)

<h3>To the Editor.—</h3> I first want to say how courageous I feel Dr Furth<sup>1</sup>is to have shared her experience, and also to emphasize what abortion was like prior to<i>Roe v Wade</i>. On page 1431 of the same issue,<sup>2</sup>the difference between abortions performed in 1973 and 1985, at least listed, is 100% +fold. I also want to compliment the American Medical Association on its amicus brief. At this time it is very important that physicians take the leadership in the pro-choice movement. It's obvious that a woman should have control over her body and should not, in any way, be limited in terms of an emotional issue. Simply stated, pro-choice is just that. It enables a woman to choose what she wants to do with her body, as opposed to pro-life, which may cause a woman to risk her life in not being able to
699 TGF-β ENHANCES ALCOHOL DEPENDENT HEPATOCYTE DAMAGE VIA DOWNREGULATION OF ALCOHOL DEHYDROGENASE I
Authors: L. Ciuclan, S. Ehnert, I. Ilkavets, H.-L. Weng, H. Gaitantzi, H. Tsukamoto, K. Breitkopf, S. Dooley, M.V. Singer
Journal: Journal of Hepatology (2009)
Corrections to the AASLD Practice Guideline
Authors: Doris B. Strader, Teresa L. Wright, David L. Thomas, Leonard B. Seeff
Journal: Hepatology (2004)

We fully acknowledge the issues raised by Dr. Hendrix and express our regret for omitting the Versant HCV RNA Qualitative Assay (Bayer Diagnostics, Tarrytown, NY) as one of the qualitative assays for HCV approved by the Food and Drug Administration, and especially for the error in Table 4 (Assays for Quantitation of HCV RNA in Serum) that incorrectly listed the upper dynamic range of the Versant HCV RNA Quantitative Assay as 700,000 instead of 7,700,000. Doris B. Strader, Teresa L. Wright, David L. Thomas, Leonard B. Seeff.
THE SPONTANEOUS HEALING OF CANCER.
Journal: JAMA (2007)

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
CLINIC.
Authors: E. FLETCHER INGALS
Journal: JAMA (1897)

<h3>Case 1.—Hypertrophy of the tonsils with frequently recurring tonsillitis.</h3> —Gentlemen: The first case I present to you is a girl 11 years of age who has been brought to me from a neighboring State on account of frequently recurring tonsillitis with which she has been troubled for several years. Her physician tells me that almost every time she takes cold she suffers from quinsy so that at least three or four times during the year she has this painful disease. He attempted to remove the tonsils, but was unable to do so. Upon examining the fauces I find that the tonsils are slightly enlarged. Neither of them is more than three-fourths of an inch long by half an inch broad and three-eighths of an inch in thickness. Both of them are covered by the anterior pillars of the fauces so that it would be impossible to engage the gland in
Gastritis and Gastrocytograms in Relation to Gastric Cancer: New Technique for Gastrocytogram
Journal: JAMA (1963)

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
Human hepatocyte growth factor in bile: An indicator of posthepatectomy liver function in patients with biliary tract carcinoma.
Authors: E Takeuchi
Journal: Hepatology (1997)

We measured the concentration of hepatocyte growth factor (HGF) in bile obtained from patients after hepatectomy. The HGF concentrations in the bile samples were quantified using an enzyme-linked immunosorbent assay (ELISA). By immunoblotting, using a monoclonal antibody raised against the HGF α-subunit, the bile HGF, which was purified on a Heparin-Sepharose column, showed a band of the same size as the recombinant HGF α-subunit (69 kd). Bile samples were obtained from 24 patients with biliary tract disease before and after hepatectomy by means of biliary drainage. Before surgery, the bile HGF concentrations were minimal (0.8 +/- 0.1 ng/mL); however, after hepatectomy on postoperative day 1 in patients without posthepatectomy liver failure (20 of 24), they increased severalfold (4.1 +/- 0.4 ng/mL, P < .05). The patients with posthepatectomy liver failure (4 of 24) showed no significant increase in bile HGF after hepatectomy (less than 2 ng/mL on postoperative day 1). The volume of the remnant liver correlated positively with the bile HGF concentration. The bile HGF concentration on postoperative day 1 exhibited a significant negative correlation with the maximum concentration of serum total bilirubin after hepatectomy. The concentration of bile HGF was generally higher than that in serum (2.1-fold). Thus, the bile HGF concentration after hepatectomy may be useful for the early assessment of posthepatectomy liver function. (Hepatology 1997 Nov;26(5):1092-9)
VIENNA
Journal: JAMA (1929)

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
AUTHOR'S REPLY
Authors: P. George, M. Pearson, R. Rudd, M. Hetzel
Journal: Thorax (1991)

Bronchography in the assessment of patients with lung collapse for endo- scopic laser therapy We would like to make the following comments on the bronchographic technique described in the study by Dr PJM George and colleagues (July 1990;45:503-8).Firstly, the iodine content and the osmolarity of the contrast medium Omnipaque used in the study were not mentioned, nor was it clear
Impaired stress and interleukin-1beta-induced hypothalamic expression of the neuronal activation marker FOS in cholestatic rats
Authors: M Swain
Journal: Hepatology (1996)

Both interleukin (IL)-1beta and psychological stress activate the hypothalamic-pituitary-adrenal (HPA) axis by stimulating neuronal activity within the paraventricular nucleus of the hypothalamus via different pathways. Because it has been shown previously that cholestatic rats show defective cytokine-and stress-induced HPA axis activation, neuronal activation in the paraventricular nucleus of rats with cholestasis caused by bile duct resection and in noncholestatic sham-resected (sham) controls was examined. To do this, the expression of the neuronal activation marker FOS in the hypothalamic paraventricular nucleus of bile duct-resected (BDR) and sham rats exposed to restraint stress and intracerebroventricularly infused IL-1beta, two stimuli known to activate the HPA axis by stimulating neurons in the paraventricular nucleus, was quantitated. BDR rats showed decreased FOS expression in the paraventricular nucleus after both stimuli compared with similarly treated sham controls. These data show that BDR rats show an impaired ability to activate hypothalamic neurons within the paraventricular nucleus and suggest that hypofunctioning of the HPA axis in response to immune (i.e., IL-1beta) and psychological stressors, which have been documented previously for BDR rats, may be caused by a specific defect in the intracellular machinery involved in the activation of neurons within the hypothalamic paraventricular nucleus. (Hepatology 1996 Oct;24(4):914-8)
Editorial Board
Authors: Joanna Schaffhausen, Milka Kostic, Basil Nyaku, Peggy Kristanto, S Amara, N Birdsall, N Bowery, J Crawley, A Cuello, B Fredholm, L Hunyady, T Kenakin, M Mishina, W Moolenaar, C Page, R Ruffolo, R Summers, Australia Tanaka, Japan Watson
Journal: Trends in Pharmacological Sciences (2011)
Signal Transduction and Cell Function
Authors: Rachel Mcmahan, Silvia Giugliano, Cara Porsche, Lucy Golden- Mason, Hugo Rosen, Lucy Golden-Mason, Samjhana Thapaliya, Ciaran Fealy, Anny Mulya, Chris Flask, John Kirwan, Srinivasan Dasarathy
Journal: Hepatology (2013)

Background: NAFLD is a prevalent problem throughout the Western world.LSECs have been shown to play important roles in liver injury and repair but their role in the underlying pathogenetic mechanisms of NAFLD remains undefined.Here we evaluated the effects of steatosis on LSEC expression of genes involved in inflammation, apoptosis, angiogenesis and cell adhesion in a murine model of NAFLD and an immortalized human LSEC line.Methods: To evaluate gene expression changes in LSEC during NAFLD C56BL/6 mice were fed a western diet (21% anhydrous milkfat (butterfat), 34% sucrose, and a total of 0.2% cholesterol) or regular chow for 3 months.LSECs (CD45negCD31+) were purified on a FACSAria cell sorter followed by RNA isolation.The Mouse Endothelial Cell Biology RT2 Profiler PCR Array (SA Biosciences) was used to evaluate gene expression changes in LSEC from lean or obese mice.The immortalized human-liver endothelial cell line TMNK-1 was incubated with oliec acid (0.66mM) and palmitic acid (0.33mM) for 24 hours followed by RNA isolation and quantitative PCR.Results: Using PCR array technology we identified distinct gene expression profiles in LSECs from mice with NAFLD.Gene pathway analysis in LSECs from mice fed a high fat or low fat diet showed a number of differentially expressed genes including those involved in apoptosis (12), angiogenesis (20), cell adhesion (13) and inflammation (16).Interestingly, feeding a high fat diet led to an increase in the expression of anti-inflammatory molecules, including the chemokine CX3CL1 (Fraktaline), in LSECs.The high fat diet also led to a decrease in proinflammatory chemokines including CXCL2 (Mip-2) and CCL2 (MCP-1).In vitro incubation of the human LSEC line, TMNK-1, with palmitic acid and oliec acid also led to a significant increase in the expression of CXC3CL1 and a corresponding decrease in CCL2.Conclusions: LSECs isolated from steatotic livers demonstrated a shift towards a pro-apoptotic, anti-inflammatory phenotype.These pathways may represent a compensatory mechanism to reverse the liver damage associated with NAFLD.
International Abstracts
Journal: JAMA (1989)

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
Nonvolatile Organic Compounds in Treated Waters
Authors: C. D. Watts, B. Crathorne, M. Fielding, S. D. Killops
Journal: Environmental Health Perspectives (1982)

Over the past decade much information has been published on the analysis of organics extracted from treated water. Certain of these organics have been shown to be by-products of the chlorination disinfection process and to possess harmful effects at high concentrations. This has resulted in increased interest in alternative disinfection processes, particularly ozonation. The data on organics had been largely obtained by using gas chromatography-mass spectrometry, which is only capable of analyzing, at best, 20% of the organics present in treated water. Research in key areas such as mutagenicity testing of water and characterization of chlorination and ozonation by-products has emphasized the need for techniques suitable for analysis of the remaining nonvolatile organics. Several methods for the isolation of nonvolatile organics have been evaluated and, of these, freeze-drying followed by methanol extraction appears the most suitable. Reverse-phase HPLC was used for separation of the methanol extract, but increased resolution for separation of the complex mixtures present is desirable. In this context, high resolution size exclusion chromatography shows promise. Characterization of separated nonvolatiles is possible by the application of state-of-the-art mass spectrometric techniques. Results obtained by these techniques have shown that the nonvolatile organic fraction of chlorinated drinking water consists of many discrete compounds. Among these, some of the chlorinated compounds are almost certainly by-products of disinfection. Studies of the by-products of ozonation of fulvic and humic acids isolated from river waters have indicated a similar proportion of nonvolatile organics. Further, ozonation can result in the release of compounds that are trapped in the macromolecules.
Acute myocardial infarction
Authors: J. L. Villanua, M. Morell, M. V. de la Torre, A. García Aicantara, J. L. Carpintero, A. García, P. Pascual, J. A. Rivero, M. Martinez del Campo, M. Roth, R. v. Essen, K. -L. Neuhaus, J. Carlsson, A. Vogt, W. Feuerer, U. Tebbe, W. Niederer, J. M. Serrano, E. Torrado, J. C. Escudero, J. M. Hernandez, M. Herrera, J. A. Arboleda, J. Caturla, M. Delgado, J. Canovas, C. Muñoz, F. Criado, B. Alvarez, R. Reig, F. Del Rio, V. Estrada, C. Cardenal, J. Ferrero, Santos F. Martin, A. Fernández-Cruz, A. Silla, J. Caturia, A. Perez, M. Mauri, D. Barja, J. Acosta
Journal: Intensive Care Medicine (1992)
Single-dose treatment of gonorrhea with selected antibiotic agents
Authors: T. F. Keys
Journal: JAMA (1969)

Single-dose, injectable antigonorrheal agents were evaluated at Navy facilities in the Pacific region. One hundred and one of 103 patients receiving 2.4 million units of procaine penicillin G with orally administered probenecid, and 105 of 106 patients receiving 2 gm of ampicillin sodium with orally administered probenecid were cured of infection. Ninety-seven cures resulted from 105 patients treated with 2 gm of kanamycin sulfate, and 81 cures from 97 patients treated with 2 gm of cephaloridine. Eighty percent of the gonococcal strains from the Philippines and Japan were insensitive to procaine penicillin G (0.1μg/ml). Serum levels of the drugs one hour following injection ranged from 1.5μg to 24μg per milliliter for penicillin and 10.8μg to 70.0μg per milliliter for ampicillin. With the increasing numbers of penicillin-insensitive gonococci, ampicillin may become the drug of choice for gonorrhea.
Reply:
Authors: Muhammad Y. Sheikh
Journal: Hepatology (2008)

We acknowledge the appreciation and comments by Drs. Amedeo Lonardo and Paola Loria. In our review, the metabolic syndrome (MS) represents hepatitis C virus (HCV)-related insulin resistance (IR) and its clinical consequences, with IR being a common denominator.1 The intensity of IR and its consequences vary based on underlying cause(s) and the body's ability to compensate for IR.2 Although all HCV patients may not manifest the typical phenotype of MS, they have significant potential of developing these features due to similar underlying pathophysiology.1 MS has also been recently described in 26% of patients with HCV.3 It is also known that there is considerable interplay of both viral and host factors in accelerating the natural course of disease in HCV.4 It is therefore difficult to isolate pathogenic mechanisms induced by the virus from any coexisting additional insult(s). It seems premature to limit the spectrum of HCV-induced MS by labeling it as "dysmetabolic syndrome". The causes of mortality in patients with HCV are variable. It ranges from liver-related mortality to those attributable to drug, alcohol, trauma, suicide, and cardiovascular mortality.5 Moreover, onset of portal hypertension and decompensated cirrhosis can alter several clinical features of MS syndrome. On the other hand, there is presently a lot of controversy about the utility of MS to predict cardiovascular risk in an individual.6, 7 The role of IR in HCV is a relatively new subject, and more studies are needed in order to clearly delineate the effect it has on the natural history of the disease process. The difficulty lies in the complex natural history of chronic liver disease and unraveling the effects of specific factors that may alter its course over the lifespan of an individual. Muhammad Y. Sheikh M.D., FACP, FACG*, * Division of Gastroenterology and Hepatology, University of California San Francisco, Fresno Medical Education Program, Community Regional Medical Center, Fresno, CA.
POSTGRADUATE COURSE OF THE AMERICAN ACADEMY OF OPHTHALMOLOGY AND OTO-LARYNGOLOGY
Journal: JAMA (1921)

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
ANNUAL REPORT ON GRADUATE MEDICAL EDUCATION IN THE UNITED STATES
Journal: JAMA (1962)

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
Hyperphagia and obesity. Relationship to medial hypothalamic lesions
Authors: G. G. Celesia
Journal: JAMA (1981)

Progressive left hemiparesis followed by face and trunk cutaneous vasodilation and hyperphagia developed in a 28-year-old man. He began eating five to six meals a day and gained 16 kg in 60 days. Computed tomography disclosed a neoplastic lesion involving the midline via the hypothalamus and reaching the contralateral lenticular nucleus. Findings from endocrine studies, including thyroid-stimulating hormone, growth hormone, prolactin, and cortisol serum levels, were normal. Hyperphagia and consequent obesity were associated with bilateral destruction of the ventromedial hypothalamic area; cutaneous vasodilation was related to involvement of the preoptic area. (<i>JAMA</i>1981;246:151-153)
In Reply
Authors: Howard I. Scher, Susan Halabi, Ian F. Tannock, Michael Morris, Cora N. Sternberg, Michael A. Carducci, Mario A. Eisenberger, Celestia Higano, Glenn J. Bubley, Robert Dreicer, Daniel P. Petrylak, Philip Kantoff, Ethan Basch, Wm Kevin Kelly, William D. Figg, Eric J. Small, Tomasz M. Beer, George Wilding, Alison Martin, Maha Hussain
Journal: Journal of Clinical Oncology (2008)