tbuckley/cabot-search huggingface dataset:
Neuropathological Findings in Patients Dying after Open-heart Surgery
Authors: J. B. Brierley
Journal: Thorax (1963)

Although cerebral damage has been regarded as the cause of death in some patients dying after open operations on the heart, this conclusion rests almost entirely on clinical evidence such as an impaired level of consciousness after the opera- tion, abnormalities of muscle tone and reflexes, visual and extrapyramidal disorders or epilepsy.Accounts of cerebral pathology in fatal cases are limited to that of Bjork and Hultquist (1960) and a group of papers describing the cerebral emboli due to the anti-foam agent employed in the oxygenator (Yates, Cassie, Dark, Jack, and
Surgery versus intensive rehabilitation programmes for chronic low back pain
Authors: Bart W Koes
Journal: BMJ (2005)

Spinal fusion surgery has only modest, if any, effects 

The optimal management of patients with chronic low back pain remains a big challenge for today's healthcare services. In this week's BMJ Fairbank et al report how they assessed the effectiveness of surgical stabilisation of the spine compared to an intensive rehabilitation programme for patients who had had low back pain of at least a year and who were considered candidates for spinal fusion.1 The authors found no clear evidence that primary spinal fusion surgery was more beneficial than intensive rehabilitation, supporting the idea that spinal fusion plays, at best, only a small role in managing chronic low back pain.

The relevant and informative randomised trial by Fairbank et al was pragmatic by design.1 Patients with chronic low …
Alcoholic Myopathy
Authors: Reynold Spector, Aswini Choudhury, Pasquale Cancilla, Robert Lakin
Journal: JAMA (1979)

MANY agents, including drugs and alcohol, can cause rhabdomyopathy.<sup>1</sup>Alcoholic myopathy may have a varied presentation and is classified as acute, subacute, or chronic.<sup>2-6</sup>Acute or subacute alcoholic myopathy is related to the ingestion of excessive amounts of alcohol and generally characterized by diffuse or focal tenderness and muscle cramps.<sup>2-6</sup>The serum creatinine phosphokinase (CPK) activity is elevated, and muscle biopsy specimens frequently show a nonspecific pattern with degeneration and regeneration of muscle fibers.<sup>2-7</sup>Chronic alcoholic myopathy is characterized by proximal muscle weakness with minimal, nonspecific changes on muscle biopsy specimens.<sup>2,3,5</sup>Even in healthy volunteers receiving a nutritious diet supplemented with vitamins, 225 g of alcohol ingested daily for three weeks caused slight elevations in serum CPK activity and minimal but definite abnormalities on muscle biopsy specimens.<sup>8</sup> We present a case of a young man with a puzzling myopathy. After alengthy examination with nonspecific findings, a diagnostic alcohol challenge disclosed
Key part of US health reform is unconstitutional, Virginia court rules
Authors: J. H. Tanne
Journal: BMJ (2010)

A Virginia judge ruled yesterday that the “individual mandate” requiring US citizens to buy health insurance is unconstitutional.

Judge Henry Hudson, who was appointed by the former president George W Bush, ruled against the law in the US District Court in Richmond, Virginia. The case was originally brought by Virginia’s attorney general, Ken Cuccinelli II, also a Republican ( BMJ 2010;341:c4330, doi:10.1136/bmj.c4330).

Judge Hudson’s ruling does not halt the entire healthcare reform act, only the individual mandate. Some provisions of the act have already gone into effect, and more will do so in January. The requirement that US citizens have health insurance does not take effect until 2014, …
Diet, serum fatty acids, and atopic diseases in childhood
Authors: T. Dunder, L. Kuikka, J. Turtinen, L. Räsänen, M. Uhari
Journal: Allergy (2001)

Background: The reasons behind the reported increase in the occurrence of childhood atopic sensitization rates are unclear. We wanted to evaluate the association between dietary fats, serum fatty acids, and the occurrence and development of atopic diseases. Methods: From a longitudinal database of a population‐based sample, 231 sex‐ and age‐matched pairs in 1980 and 154 pairs in 1986 were chosen, between whom we compared the dietary data, serum fatty acid composition, and occurrence of atopic diseases. The same variables were also compared between those who developed atopic disease later and those who did not during the 9‐year follow‐up. Results: Examination of the dietary data in 1980 for those who had developed atopic disease compared with those who had remained healthy showed that the atopic children had used less butter before the expression of atopy. According to the cross‐sectional data, the children with atopic disease consumed more margarine (mean 8.6 vs 7.3 [ P =0.04]), and less butter (mean 9.4 vs 11.6 g/1000 kcal [ P =0.002]), than the nonatopic children in 1980. Differences supporting these dietary findings were similarly found in the serum fatty acid data. Conclusions: The diet of the atopic children differed from that of the nonatopic children in the consumption of polyunsaturated fat.
Idiopathic Esophageal Ulceration Associated with Human Immunodeficiency Virus Infection: Efficacy of Thalidomide Treatment
Authors: D. Louvel, S. Musso, S. Métivier, O. Croizet, R.-M. Rouquet, P. Massip, J. Escourrou, J. Frexinos
Journal: Endoscopy (1996)
Od's Bodikins
Authors: Bernard Strauss
Journal: JAMA (1965)

<h3>To the Editor:—</h3> Your recent communications on Hodgkin's disease (<i>JAMA</i><b>190</b>:910 [Dec 7] 1964) have inspired the following immortal lines: Od's bodikins! Cried Hodgkin, Here is a canker Worse than a chancre. By the 23rd Psalm As I'm Hodgkin, Tom, We cannot endure it, Somebody must cure it!
Inhibitory Effect of Nicotine on Experimental Hypersensitivity Pneumonitis<i>In Vivo</i>and<i>In Vitro</i>
Authors: Marie-Renée Blanchet, Evelyne Israël-Assayag, Yvon Cormier
Journal: American Journal of Respiratory and Critical Care Medicine (2004)

The incidence of hypersensitivity pneumonitis (HP) is lower in smokers than in nonsmokers. Because nicotine is immunosuppressive, we hypothesized that it could have a protective effect on HP induction in vivo. HP was induced in mice that were treated with nicotine either intraperitoneally (IP) (0.5 to 2.0 mg/kg/day) or intranasally (IN) (0.025 to 2.0 mg/kg/day). Both IP- and IN-treated animals had fewer bronchoalveolar lavage total cells and lymphocytes and a decreased lung tissue inflammation. IFN-gamma but not interleukin-10 mRNA expression was reduced in lung tissue of 2.0-mg/kg IN-treated animals. To test the effect of nicotine on alveolar macrophages, AMJ2-C11 cells were treated with nicotine and stimulated with lipopolysaccharide or Saccharopolyspora rectivirgula, a causative agent of HP. Nicotine reduced tumor necrosis factor release and tumor necrosis factor, interleukin-10, and IFN-gamma mRNA expression after stimulation and decreased CD80 expression by 55% in lipopolysaccharide-stimulated cells and by 41% in S. rectivirgula-stimulated cells. We conclude that nicotine could be, at least in part, responsible for the protection observed in smokers against HP. The inhibitory effect of nicotine on alveolar macrophages could be one of the mechanisms involved.
Two Incidents of Tuberculous Infection by Milk from Attested Herds
Authors: J. M. Black, I. B. Sutherland
Journal: BMJ (1961)

<h3>Objective</h3> To describe the disease characteristics of patients with juvenile idiopathic arthritis (JIA) included in an inception cohort, to analyse how many patients from each JIA category reach an inactive disease state within the first year of specialised care and to determine predictors for attaining inactive disease. <h3>Methods</h3> Patients with JIA were enrolled in this study at 11 large German paediatric rheumatology units within the first 12 months after diagnosis. Laboratory and clinical parameters such as JIA core criteria and data on the medication used were collected every 3 months. Non-parametric statistical testing was performed for the comparison of the JIA core criteria at follow-up. Generalised linear models were used to analyse differences in the rates at which inactive disease was reached and to determine potential predictors. <h3>Results</h3> Of the 695 patients with JIA included in this analysis, approximately 75% experienced a period of inactive disease under treatment with disease-modifying antirheumatic drugs and systemic steroids in most cases with systemic-onset JIA or polyarthritis at least once during the first 12 months in ICON. Significant improvements were observed in all JIA core criteria, in disease activity and in functional status from baseline to the 12-month follow-up. Younger age at onset, a shorter duration between symptom onset and diagnosis and a positive antinuclear antibody status increased the probability of attaining an inactive disease state. <h3>Conclusions</h3> The 12-month outcome of JIA was good under real-life conditions, with half of the patients having attained inactive disease with contemporary treatments. Since a short duration between symptom onset and diagnosis was correlated to a period of inactive disease, children suspected of having JIA should be transferred to specialised care as soon as possible.
Stimulating hepatocyte renewal: a new paradigm for the treatment of severe alcoholic hepatitis unresponsive to corticosteroids?
Authors: Richard Moreau
Journal: Gut (2015)

Patients with severe alcoholic hepatitis who are admitted to the hospital usually have evidence of decompensated cirrhosis with high serum bilirubin levels, low prothrombin time associated with dysfunction or failure of other organs/systems (kidney, brain, circulation).1 Spontaneous 1-month mortality is 35%.2

Pathophysiology of severe alcoholic hepatitis is incompletely understood.2–4 Alcohol consumption results in alterations of gut microbiome, increased intestinal permeability and subsequent translocation of Gram-negative bacteria. These bacteria may release pathogen-associated molecular patterns (PAMPs) such as lipopolysaccharide (LPS). In the liver, PAMPs stimulate Kupffer cells to produce high levels of proinflammatory chemokines (eg, interleukin-8 (IL-8)) or cytokines such as tumour necrosis factor α (TNF-α). TNF-α may activate cell death pathways and induce the production of reactive oxygen species (ROS) by hepatocyte mitochondria, leading to cell death. Acetaldehyde metabolism also contributes to hepatocyte ROS production. These findings led to the traditional view that excessive inflammation and oxidative stress are involved in the development of liver damage in patients with alcoholic hepatitis.

Corticosteroid therapy (40 mg of oral prednisolone per day) is now considered as the first-line treatment for severe alcoholic hepatitis.2 However, according to the Lille model ∼40% of patients with severe alcoholic hepatitis do not respond to corticosteroids,2 and this group has high 6-month mortality (close to 80%).5 This is why novel, pathophysiology-based, medical therapies should be developed for patients who do not respond to corticosteroids.

Dubuquoy et al 6 provide new insights into the pathophysiology of severe alcoholic hepatitis. They investigated liver explants from patients with severe alcoholic hepatitis who underwent salvage transplantation, from patients with alcoholic cirrhosis and no alcoholic hepatitis and fragments of normal livers. …
Woman With Three Girls
Authors: Janet M. Torpy
Journal: JAMA (2011)

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
Meningitis complicating acute otitis media
Authors: G J E M Bates, A B Drake-Lee
Journal: BMJ (1988)

general purpose gloves his peak flow fell from 580 1/min to 350 I/min within 15 minutes, necessitating inhalation of a bronchodilator.This challenge test with suspected and control gloves was repeated, and again a pronounced fall in peak flow occurred only with the general purpose gloves.A dozen each of the microtouch and general purpose gloves were enclosed in conical flasks.Pure filtered air was drawn over them at 0-5 1/min and passed through a tube of activated charcoal; this was desorbed with carbon disulphide and analysed by gas chromatography and mass spectrometry.The vapours from the two types of gloves were compared and included many chemicals in common.Nevertheless, one peak was observed in the vapour from the general purpose gloves which was not present in the microtouch glove vapour; this was identified as a bicyclic terpene, probably carene.Semiquantitative analysis by selected monitoring showed that it was given off from the gloves in concentration ofabout 10 parts per billion per glove.
Endoscopic Injection of Fibrin Glue versus Polidocanol in Peptic Ulcer Hemorrhage: A Pilot Study
Authors: P. L. Berg, W. Barina, P. Born
Journal: Endoscopy (1994)

See also: Endoscopic Injection of Fibrin GlueEndoscopy 1996; 28(03): 327-327DOI: 10.1055/s-2007-1005469
Abstract 975: Employing functional genomics to reveal emergent dependencies
Authors: Kathryn Cappell, Amy When, Patrick Taus, Kimberly Maxfield, Angelique Whitehurst
Journal: Cancer Research (2012)

Abstract Using a pangenomic loss of function strategy, our group has recently discovered that a cohort of gametogenic genes modulates chemoresponsiveness in tumor cells. Numerous studies focused on identifying aberrant gene expression patterns in tumors have previously correlated the presence of gametogenic genes with the tumorigenic state. Our functional genomics approach has now revealed that these tumor-activated aberrant gene products may play essential roles in supporting tumor cell fitness in the presence of insults, such as genotoxic stress. Specifically, depletion of each of the 8 gametogenic genes identified in our screen results in an increase in mitotic transit time and a reduction in mitotic fidelity in the presence of paclitaxel, demonstrating a requirement for their function at the level of chromosome segregation. At the cell biological level, these components contribute to mitotic spindle architecture by supporting centrosomal coalescence, centrosome duplication and/or microtubule stability. Given that the expression of these genes is otherwise biased towards the germline, they could present pharmacological entry points with an extraordinary therapeutic window. For example, we find that the CT-antigen, ACRBP, specifies poor outcome in ovarian patients and depletion of ACRBP can enhance sensitivity to paclitaxel in ovarian tumor explants in vitro and an ovarian orthtopic xenografts in vivo. In addition, we find that a small molecule that targets the gametogenic protein, TACC3, synergizes with paclitaxel to reduce tumor cell growth. We propose that the dependency on these gametogenic components may arise as a consequence of passage through a selection bottleneck, during tumor evolution, which requires acquisition of traits that normalize the mitotic perturbations originally driving the plasticity of preneoplastic genomes. We show that such traits, when defined by otherwise anomalous gene products, may represent conceptually ideal intervention targets with wide therapeutic windows. 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 975. doi:1538-7445.AM2012-975
Abstract 1412: Two-photon imaging of cancer cell extravasation in live mice
Authors: Michelle A. Digman, Jose S. Aguilar, Enrico Gratton, Atsushi Suetsugu, Robert M. Hoffman
Journal: Cancer Research (2011)

Abstract MDA-MB-231 breast cancer cells were engineered to express cytoplasmic paxillin-GFP and nuclear H2B-mCherry. In order to image extravasation, the cancer cells were injected in the blood stream of nude mice. Using 2-photon excitation microscopy we can simultaneously excite the two probes and also visualize the autofluorescence of tissues. A skin flap was opened to visualize blood vessels and recognize the position of the cancer cells. Two-photon imaging showed that after an initial phase in which the cells are non-adherent, some cells spread on the internal surface of the capillaries. Days later some cells started to appear on the external side of the capillary. The extravasated cells extend very long protrusions into the tissue. The goal was to determine if at the end of the long protrusion, if it is possible to observe the formation of focal adhesions by imaging paxillin-GFP. Preliminary results show that when cells start to adhere to the blood vessel wall they form focal adhesions as determined by the characteristic elongated features observed in the paxillin-GFP channel. New approaches will allow the tracking of the tip of the protrusion to determine if focal adhesions are forming there as the cells extravasate. This is important in establishing the mechanism of cell extravasation and migration in tissues. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1412. doi:10.1158/1538-7445.AM2011-1412
Identification of Pathways for Bipolar Disorder
Authors: John I. Nurnberger, Daniel L. Koller, Jeesun Jung, Howard J. Edenberg, Tatiana Foroud, Ilaria Guella, Marquis P. Vawter, John R. Kelsoe
Journal: JAMA Psychiatry (2014)

IMPORTANCE-Genome-wide investigations provide systematic information regarding the neurobiology of psychiatric disorders.OBJECTIVE-To identify biological pathways that contribute to risk for bipolar disorder (BP) using genes with consistent evidence for association in multiple genome-wide association studies (GWAS).DATA SOURCES-Four independent data sets with individual genome-wide data available in July 2011 along with all data sets contributed to the Psychiatric Genomics Consortium Bipolar Group by May 2012.A prior meta-analysis was used as a source for brain gene expression data.STUDY SELECTION-The 4 published GWAS were included in the initial sample.All independent BP data sets providing genome-wide data in the Psychiatric Genomics Consortium were included as a replication sample.
Myocardial ischemia in patients with hypertrophic cardiomyopathy: contribution of inadequate vasodilator reserve and elevated left ventricular filling pressures.
Authors: R O Cannon, D R Rosing, B J Maron, M B Leon, R O Bonow, R M Watson, S E Epstein
Journal: Circulation (1985)

To study the mechanism and hemodynamic significance of myocardial ischemia in hypertrophic cardiomyopathy, 20 patients (nine with resting left ventricular outflow tract obstruction greater than or equal to 30 mm Hg) with a history of angina pectoris and angiographically normal coronary arteries underwent a pacing study with measurement of great cardiac vein flow, lactate and oxygen content, and left ventricular filling pressure. Compared with 28 control subjects without hypertrophic cardiomyopathy, their resting coronary blood flow was higher (91 +/- 27 vs 66 +/- 17 ml/min; p less than .001) and their coronary resistance was lower (1.13 +/- 0.38 vs 1.55 +/- 0.45 mm Hg/ml/min; p less than .001). Left ventricular end-diastolic pressure (16 +/- 6 vs 11 +/- 3 mm Hg; p less than .001) and pulmonary arterial wedge pressure (13 +/- 5 vs 7 +/- 3 mm Hg; p less than .001) were significantly higher in patients with hypertrophic cardiomyopathy. During pacing, coronary flow rose in both groups, although coronary and myocardial hemodynamics differed greatly. In contrast to the linear increase in flow in control subjects up to heart rate of 150 beats/min (66 +/- 17 to 125 +/- 28 ml/min), patients with hypertrophic cardiomyopathy demonstrated an initial rise in flow to 133 +/- 31 ml/min at an intermediate heart rate of 130 beats/min. At this point, 12 of 20 patients developed their typical chest pain. With continued pacing to a heart rate of 150 beats/min, mean coronary flow fell to 114 +/- 29 ml/min (p less than .002), with 18 of 20 patients experiencing their typical chest pain and metabolic evidence of myocardial ischemia. This fall in coronary flow was associated with a substantial rise in left ventricular end-diastolic pressure (30 +/- 9 mm Hg immediately after peak pacing). In the 14 patients whose coronary flow actually fell from intermediate to peak pacing, the rise in left ventricular end-diastolic pressure in the same interval was greater than that of the six patients whose flow remained unchanged or increased (11 +/- 8 vs 2 +/- 2 mm Hg; p less than .01). In addition, despite metabolic and hemodynamic evidence of myocardial ischemia, the arteriovenous O2 difference actually narrowed at peak pacing. Thus most patients with hypertrophic cardiomyopathy achieved maximum coronary vasodilation and flow at modest increases in heart rate. Elevation in left ventricular filling pressure, probably related to ischemia-induced changes in ventricular compliance, was associated with a decline in coronary flow.(ABSTRACT TRUNCATED AT 400 WORDS)
Abstract 5404: Metabolic stress played a role in dasatinib-induced EGFR degradation and apoptosis in head and neck cancer.
Authors: Yu-Chin Lin, Meng-Hsuan Wu, Tzu-Tang Wei, Kuen-Feng Chen, Ann-Lii Cheng, Ching-Chow Chen
Journal: Cancer Research (2013)

Abstract Head and neck squamous cell carcinoma (HNSCC) is a worldwide disease with aggressive course and dismal outcome. Dasatinib, a Bcr-abl and Src in hibitor, has been approved clinically for CML and shown activities against solid tumors in vitro. In our recent work, degradation of epidermal growth factor receptor (EGFR) plays a role in dasatinib-induced apoptosis in HNSCC cells. We further revealed the role of metabolic stress in dasatinib-induced EGFR degradation and apoptosis. Dasatinib decreased cellular ATP, and activated AMPK activation and induced endoplasmic reticulum stress (ER stress) as well. Inhibition or knockdown of AMPK reversed dasatinib-induced EGFR degradation, and pharmacological activation of AMPK led to ER stress and EGFR degradation. Addition of ER stress inhibitor to dasatinib reversed EGFR degradation and apoptosis, and pharmacologic activation of ER stress resulted in EGFR degradation. In conclusion, metabolic stress may play a role in dasatinib-induced EGFR degradation and apoptosis in HNSCC cells. Citation Format: Yu-Chin Lin, Meng-Hsuan Wu, Tzu-Tang Wei, Kuen-Feng Chen, Ann-Lii Cheng, Ching-Chow Chen. Metabolic stress played a role in dasatinib-induced EGFR degradation and apoptosis in head and neck cancer. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 5404. doi:10.1158/1538-7445.AM2013-5404
Chemical Genomics Identifies Small-Molecule MCL1 Repressors and BCL-xL as a Predictor of MCL1 Dependency
Authors: Guo Wei, Adam A. Margolin, Leila Haery, Emily Brown, Lisa Cucolo, Bina Julian, Shyemaa Shehata, Andrew L. Kung, Rameen Beroukhim, Todd R. Golub
Journal: Cancer Cell (2012)