tbuckley/cabot-search huggingface dataset:
Prediction of Probability of Pneumonectomy for Lung Cancer Using Tc-99m MAA Perfusion Lung Imaging
Authors: CHIH-YI CHEN, CHIA-HUNG KAO, NAN-YUNG HSU, CHUN-LIEH CHEN, CHUNG-PING HSU, PEI-YEN WANG
Journal: Clinical Nuclear Medicine (1994)

Pulmonary perfusion scintigraphy with Tc-99m MAA was performed on 182 patients, on whom either pneumonectomy or lobectomy was performed, because of primary nonsmall-cell lung carcinoma. Among them, 76 underwent pneumonectomy, and 106 underwent lobectomy. The mean value of the perfusion fraction (PF) of the affected lung of the patients undergoing pneumonectomy was 32.3 ± 13.6% (range, 4%-50%) and was less than that of the patients undergoing lobectomy, 43.5 ± 4.5% (range, 27%-50%). The difference was statistically significant (t-test,t= 6.82;P< 0.001). Among the 28 patients whose PF of the affected lung was equal to or less than 30%, 26 underwent pneumonectomy and only 2 had a lobectomy. Among the 154 patients whose PF of the affected lung was more than 30%, 50 underwent pneumonectomy and 104 had a lobectomy. These result suggest that “30%” can be a cutoff value (Yates correction X2 test, X2 = 33.09;P< 0.001).
Primary cutaneous T-cell lymphoma presenting as mycosis fungoides with a T-/null-cell phenotype: report of two cases
Authors: L. Bekel, G. Chaby, C. Lok, A. Dadban, D. Chatelain, S. Ingen-Housz-Oro, N. Ortonne
Journal: British Journal of Dermatology (2014)

Variations in the clinical and histological presentation of cutaneous T‐cell lymphoma (CTCL) can hamper diagnosis. We report two cases of a novel presentation of CTCL characterized by an aberrant immunophenotype with complete loss of pan T‐cell antigens including T‐cell receptor β chain and showing the clinical and histopathological appearance of erythrodermic and plaque‐stage mycosis fungoides.
Critical Role of Monocyte Chemoattractant Protein-1/CC Chemokine Ligand 2 in the Pathogenesis of Ischemic Cardiomyopathy
Authors: Nikolaos G. Frangogiannis, Oliver Dewald, Ying Xia, Guofeng Ren, Sandra Haudek, Thorsten Leucker, Daniela Kraemer, George Taffet, Barrett J. Rollins, Mark L. Entman
Journal: Circulation (2007)

Cardiac interstitial fibrosis plays an important role in the pathogenesis of ischemic cardiomyopathy, contributing to systolic and diastolic dysfunction. We have recently developed a mouse model of fibrotic noninfarctive cardiomyopathy due to brief repetitive myocardial ischemia and reperfusion. In this model, fibrotic changes are preceded by marked and selective induction of the CC chemokine monocyte chemoattractant protein-1 (MCP-1). We hypothesized that MCP-1 may mediate fibrotic remodeling through recruitment of mononuclear cells and direct effects on fibroblasts.Wild-type (WT) and MCP-1-null mice underwent daily 15-minute coronary occlusions followed by reperfusion. Additional WT animals received intraperitoneal injections of a neutralizing anti-MCP-1 antibody after the end of each ischemic episode. Hearts were examined echocardiographically and processed for histological and RNA studies. WT mice undergoing repetitive brief myocardial ischemia and reperfusion protocols exhibited macrophage infiltration after 3 to 5 days and marked interstitial fibrosis in the ischemic area after 7 days, accompanied by ventricular dysfunction. MCP-1-null mice had markedly diminished interstitial fibrosis, lower macrophage infiltration, and attenuated ventricular dysfunction compared with WT animals. MCP-1 neutralization also inhibited interstitial fibrosis, decreasing left ventricular dysfunction and regional hypocontractility. Cardiac myofibroblasts isolated from WT but not from MCP-1-null animals undergoing repetitive myocardial ischemia and reperfusion demonstrated enhanced proliferative capacity. However, MCP-1 stimulation did not induce cardiac myofibroblast proliferation and did not alter expression of fibrosis-associated genes.Defective MCP-1 signaling inhibits the development of ischemic fibrotic cardiomyopathy in mice. The profibrotic actions of MCP-1 are associated with decreased macrophage recruitment and may not involve direct effects on cardiac fibroblasts.
Soundings competition: the results
Authors: R Holland
Journal: BMJ (1994)

In April a small notice appeared on this page, and also on Minerva's, inviting people to enter a competition to find a new author for Soundings. The winner would be required to write at least six pieces for the column, at £100 a go. The idea appealed to 276 writers and as a thank you to them, plus apology for taking so long to get a result, here is a brief explanation of what happened after the brown envelopes, and occasional desperate faxes, hit the in-trays in Tavistock Square.

Since the Soundings page was started in 1991 admission for contributors has been by invitation only. (The thinking behind this was that the page needs people who not only can write well but who are experienced, relatively sober, and won’t panic when the deadline has come and they haven’t got a single idea and anyway they’re about to board a plane for China.) The exception to this was Duncan Curr, who became one of the column's most admired writers after having sent in three articles on the off chance from Ingwavuma in South Africa. They were outstandingly good - gracefully written, full of …
Endogenous sex hormones and cardiovascular disease in men. A prospective population-based study.
Authors: E Barrett-Connor, K T Khaw
Journal: Circulation (1988)

Plasma obtained and frozen in 1972-1974 from 1,009 white men (40-79 years old) who have been followed for 12 years was examined for endogenous sex hormone levels according to prevalent or subsequent cardiovascular disease. In these older men, no sex hormone measured (testosterone, androstenedione, estrone, or estradiol) was significantly associated with known cardiovascular disease at baseline or with subsequent cardiovascular mortality or ischemic heart disease morbidity or mortality. Sex hormone-binding globulin levels were also similar by disease status. Analyses of hormone:sex hormone-binding globulin ratios or of estrogen:androgen ratios showed a similar lack of association with cardiovascular disease. Testosterone levels were significantly inversely associated with levels of blood pressure, fasting plasma glucose, and triglyceride and body mass index. In contrast, the only significant estrogen risk factor associations were positive correlations of estrone with total plasma cholesterol, triglyceride, and glucose. These data do not support a causal role for elevated endogenous estrogen levels and heart disease.
Hepatitis B virus infection and liver disease in ethiopian immigrants to Israel
Authors: Edna Ben-Porath, Lea Hornstein, Jerome Zeldis, Jacob Nahmias, Mignon Gruia, Batia Bilgoray, Yehudit Satinger
Journal: Hepatology (1986)

We assessed infection with hepatitis B virus in 357 Ethiopians who immigrated to Israel. Hepatitis B virus infection, as measured by the presence in the serum of HBsAg, anti-HBs, or anti-HBc, started at an early age (35% at the age of 1 to 4 years) and reached an overall rate of 98% in individuals over 40 years old. A high rate of HBsAg antigenemia in the young age group (19% at the age of 1 to 8 years) was associated with HBeAg and serum hepatitis B virus DNA. However, hepatitis B virus DNA was rarely detected in HBsAg-positive serum of older individuals who were anti-HBe-positive. No hepatitis B virus DNA sequences were detected in the serum of individuals who had anti-HBs. Despite the extremely high rate of hepatitis B virus infection that occurred at an early age, no clinical evidence of chronic liver disease in this population was detected.
PROGNOSTIC VALUE OF THE MAYO CLINIC RISK SCORE FOR CORONARY ARTERY REVASCULARIZATION USING THE AUSTRALASIAN SOCIETY OF CARDIAC AND THORACIC SURGEONS AND THE MELBOURNE INTERVENTIONAL GROUP REGISTRIES
Authors: Bryan P. Yan, Cheng-Hon Yap, Nick Andrianopoulos, Thomas J. Kiernan, Andrew E. Ajani, Julian A. Smith, David J. Clark, Stephen J. Duffy, Gilbert C. Shardey, Angela L. Brennan, Diem T. Dinh, Christopher M. Reid, Bernard J. Gersh
Journal: Journal of the American College of Cardiology (2010)
Intracranial Causes of Headache
Authors: H. Cohen
Journal: BMJ (1939)

Causes of Head PainsThe causes of pains in the head are customarily, and for diagnostic purposes conveniently, grouped on an essentially anatomical basis:1. Intracranial-namely, diseases of the brain and meninges.2. Cranial-namely, diseases of the skull bones and the enclosed air sinuses.
Developmentally regulated expression of T cell receptor beta chain variable domains in immature thymocytes.
Authors: R C Budd, G C Miescher, R C Howe, R K Lees, C Bron, H R MacDonald
Journal: The Journal of Experimental Medicine (1987)

A minor subset of immature (CD4-,8-) thymocytes that lack expression of the B2A2 antigen was found to express low levels of surface TCR protein as detected by mAbs F23.1 and KJ16 (reacting with protein products of the V beta 8 gene family). Interestingly, F23.1/KJ16 determinants were expressed on a two- to three-fold higher proportion of B2A2- thymocytes than mature lymph node T cells in four independent haplotypes. When expanded in short-term culture with PMA and calcium ionophore, B2A2- thymocytes retained their overexpression of F23.1/KJ16 determinants and showed a fivefold elevated level (relative to lymph node) of V beta 8-specific mRNA. Taken together, these findings suggest that expression of TCR V beta genes, like Ig genes, is developmentally regulated.
An Alternative Inhibitor Overcomes Resistance Caused by a Mutation of the Epidermal Growth Factor Receptor
Authors: Susumu Kobayashi, Hongbin Ji, Yuki Yuza, Matthew Meyerson, Kwok-Kin Wong, Daniel G. Tenen, Balázs Halmos
Journal: Cancer Research (2005)

Abstract Mutations of the epidermal growth factor receptor (EGFR) gene have been identified in non–small cell lung cancer specimens from patients responding to anilinoquinazoline EGFR inhibitors. However, clinical resistance to EGFR inhibitor therapy is commonly observed. Previously, we showed that such resistance can be caused by a second mutation of the EGFR gene, leading to a T790M amino acid change in the EGFR tyrosine kinase domain and also found that CL-387,785, a specific and irreversible anilinoquinazoline EGFR inhibitor, was able to overcome this resistance on the biochemical level. Here, we present the successful establishment of a stable Ba/F3 cell line model system for the study of oncogenic EGFR signaling and the functional consequences of the EGFR T790M resistance mutation. We show the ability of gefitinib to induce growth arrest and apoptosis in cells transfected with wild-type or L858R EGFR, whereas the T790M mutation leads to high-level functional resistance against gefitinib and erlotinib. In addition, CL-387,785 is able to overcome resistance caused by the T790M mutation on a functional level, correlating with effective inhibition of downstream signaling pathways. Similar data was also obtained with the use of the gefitinib-resistant H1975 lung cancer cell line. The systems established by us should prove useful for the large-scale screening of alternative EGFR inhibitor compounds against the T790M or other EGFR mutations. These data also support the notion that clinical investigations of compounds similar to CL-387,785 may be useful as a treatment strategy for patients with resistance to EGFR inhibitor therapy caused by the T790M mutation.
The Automated Medical History: An Evaluation and Status Report.
Authors: P. I. Hershberg
Journal: Annals of Internal Medicine (1971)

Meeting Abstracts1 May 1971The Automated Medical History: An Evaluation and Status Report.P. I. Hershberg, M.D., E. R. McLean III, Ph.D., J. F. Rockart, Ph.D., R. HarrisonP. I. Hershberg, M.D.Search for more papers by this author, E. R. McLean III, Ph.D.Search for more papers by this author, J. F. Rockart, Ph.D.Search for more papers by this author, R. HarrisonSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-74-5-836_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptDuring the past 3 years over 30,000 patients have been examined with the assistance of an automated medical history questionnaire at the Lahey Clinic Foundation in Boston. This is believed to be the largest experience to date in which the automated medical history (AMH) has been an integral part of the physician's own examination of the patient rather than an addendum to it. To assess the role of the AMH in clinical practice of staff physicians, a detailed management study was performed to evaluate physician utilization. The results of this study are as follows. First, most physicians are willing and... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: P. I. Hershberg, M.D.; E. R. McLeanIII, Ph.D.; J. F. Rockart, Ph.D.; R. HarrisonAffiliations: Boston, Mass. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 May 1971Volume 74, Issue 5Page: 836-836KeywordsQuestionnaires ePublished: 1 December 2008 Issue Published: 1 May 1971 PDF downloadLoading ...
Limiting Confidentiality of Adolescent Health Services
Authors: Carol A. Ford, Abigail English
Journal: JAMA (2002)

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
The Patents-Based Pharmaceutical Development Process
Authors: John H. Barton, Ezekiel J. Emanuel
Journal: JAMA (2005)

The pharmaceutical industry is facing substantial criticism from many directions, including financial barriers to access to drugs in both developed and developing countries, high profits, spending on advertising and marketing, and other issues. Underlying these criticisms are fundamental questions about the value of the current patent-based drug development system. Six major problems with the patent system are (1) recovery of research costs by patent monopoly reduces access to drugs; (2) market demand rather than health needs determines research priorities; (3) resources between research and marketing are misallocated; (4) the market for drugs has inherent market failures; (5) overall investment in drug research and development is too low, compared with profits; and (6) the existing system discriminates against US patients. Potential solutions fall into 3 categories: change in drug pricing through either price controls or tiered pricing; change in drug industry structure through a "buy-out" pricing system or with the public sector acting as exclusive research funder; and change in development incentives through a disease burden incentive system, orphan drug approaches, or requiring new drugs to demonstrate improvement over existing products prior to US Food and Drug Administration approval. We recommend 4 complementary reforms: (1) having no requirement to test new drug products against existing products prior to approval but requiring rigorous comparative postapproval testing; (2) international tiered pricing and systematic safeguards to prevent flow-back; (3) increased government-funded research and buy-out for select conditions; and (4) targeted experiments using other approaches for health conditions in which there has been little progress and innovation over the last few decades.
Shall The Journal be Removed to Washington?
Authors: JNo. W. Trader
Journal: JAMA (1891)

<h3>To the Editor.</h3> —As a member of the Association I oppose the removal ofThe Journalto Washington City. I cannot see any advantage to be gained from the more central point—Chicago. If a removal is demanded, and the convenience of the members is to be considered, why not seek a central point, and establish headquarters at St. Louis, Mo.? Sedalia, Mo., Jan. 26, 1891.
Autoreactive T-cells in Goodpasture's syndrome recognize the N-terminal NC1 domain on α3 type IV collagen
Authors: Frank Merkel, Raghuram Kalluri, Martin Marx, Uwe Enders, Stefan Stevanovic, Gerhard Giegerich, Eric G. Neilson, Hans-G Rammensee, Billy G. Hudson, Manfred Weber
Journal: Kidney International (1996)
Microsomal enzymes in malnutrition as determined by plasma half life of antipyrine.
Authors: K Krishnaswamy, A N Naidu
Journal: BMJ (1977)

Nutritional-pharmacological interactions were studied in a group of malnourished subjects. Antipyrine was used to evaluate mixed-function oxidase in man. The results indicated that the rate of disappearance of antipyrine from plasma was strongly influenced by the nutritional status of the individual. The half life of antipyrine was modified in undernourished subjects and those with nutritional oedema. This finding indicates that drug regimens may have to be adjusted in patients who have antipyrine half lives that are shorter or longer than normal. Otherwise drug treatment may be inadequate or, in patients with impaired microsomal enzyme activity, potentially dangerous.
Early Discharge and Evidence-based Practice
Authors: Paula Braveman
Journal: JAMA (1997)

Two articles in this issue ofThe Journalreach apparently conflicting conclusions regarding the safety of the short postpartum hospital stays that are now—and are likely to remain—standard for apparently well mothers and newborns. Both studies, 1 from Washington State<sup>1</sup>and 1 from Wisconsin,2used case-control designs and large secondary databases to examine the association between early discharge and neonatal readmissions. Although this question has been explored before, few studies have been so large or have addressed limitations so skillfully. Interpreting the implications of these studies and their seemingly contradictory conclusions raises difficult issues about science and society; the issues are not unique to these studies. Using linked birth certificate and hospital discharge abstracts from eligible vaginal singleton live births in Washington State from 1991 through 1994, Liu and colleagues<sup>2</sup>investigated whether "early" (&lt;30 hours after delivery) compared with "later" (30-78 hours after delivery) discharge increased the risk
An Inv(16)(p13.3q24.3)-Encoded CBFA2T3-GLIS2 Fusion Protein Defines an Aggressive Subtype of Pediatric Acute Megakaryoblastic Leukemia
Authors: Tanja A. Gruber, Amanda Larson Gedman, Jinghui Zhang, Cary S. Koss, Suresh Marada, Huy Q. Ta, Shann-Ching Chen, Xiaoping Su, Stacey K. Ogden, Jinjun Dang, Gang Wu, Vedant Gupta, Anna K. Andersson, Stanley Pounds, Lei Shi, John Easton, Michael I. Barbato, Heather L. Mulder, Jayanthi Manne, Jianmin Wang, Michael Rusch, Swati Ranade, Ramapriya Ganti, Matthew Parker, Jing Ma, Ina Radtke, Li Ding, Giovanni Cazzaniga, Andrea Biondi, Steven M. Kornblau, Farhad Ravandi, Hagop Kantarjian, Stephen D. Nimer, Konstanze Döhner, Hartmut Döhner, Timothy J. Ley, Paola Ballerini, Sheila Shurtleff, Daisuke Tomizawa, Souichi Adachi, Yasuhide Hayashi, Akio Tawa, Lee-Yung Shih, Der-Cherng Liang, Jeffrey E. Rubnitz, Ching-Hon Pui, Elaine R. Mardis, Richard K. Wilson, James R. Downing
Journal: Cancer Cell (2012)
The Psychology of Preventive Health
Authors: S. Enright
Journal: BMJ (1996)

Marian Pitts Routledge, £11.99, pp160 ISBN 0 415 10683 4

A psyhchologist's skill lies in understanding and influencing aspects of human thought and behaviour. It therefore naturally falls to health psychologists to explain why it is so difficult to encourage people to engage in behaviour which is in the best interests of their own health. Despite the explosion of theories in this area over the past two decades the reader may not be surprised to find that for most of us our health related behaviour defies …
1065-176 Role of endothelin-1 and coronary flow reserve in hypertensive patients without coronary artery disease
Authors: Hideki Fujii, Shin Takiuchi, Shinichirou Niizuma, Kei Kamide, Takeshi Horio, Satoshi Nakatani, Yuhei Kawano
Journal: Journal of the American College of Cardiology (2004)
Monitoring Resuscitation of the Injured Patient
Authors: Allan M. Parham
Journal: JAMA (1977)

<h3>To the Editor.—</h3> The authors of "Monitoring Resuscitation of the Injured Patient" (237:242, 1977) have attempted to simplify a complex task, but in so doing have entirely neglected a basic principle of vascular physiology. As a result, they have made recommendations that are frankly dangerous. They state that mean pulmonary artery pressure (PAP) "is the best single means for assessing adequacy of restoration of fluid volume," and that "continued fluid administration in the presence of an elevated PAP is hazardous and could lead to development or aggravation of posttraumatic pulmonary insufficiency." The authors would have encountered little disagreement if these statements had been made about the pulmonary artery wedge pressure rather than the mean pulmonary artery pressure. It is the pulmonary artery wedge pressure that most accurately reflects (1) the adequacy of volume restoration to maintain left ventricular filling pressure, and (2) the pulmonary venous pressure— hence the tendency for
Phospholipase C-gamma 1 association with CD3 structure in T cells.
Authors: J D Dasgupta, C Granja, B Druker, L L Lin, E J Yunis, V Relias
Journal: The Journal of Experimental Medicine (1992)

Recently, we and others have reported tyrosine phosphorylation of phospholipase C-gamma 1 (PLC gamma 1) enzyme after CD3 activation of T cells, and have proposed that PLC gamma 1 mediates signal transduction through the T cell receptor (TCR/CD3). Here, using immunoblotting and immune complex PLC assays, we show that CD3 stimulation of Jurkat cells induces the association of PLC gamma 1 enzyme with CD3 complex. PLC activity is also found to co-precipitate with the CD3 zeta chain from activated cells. In addition, in vitro PLC assays show that CD3 activation leads to about 10-fold stimulation of PLC gamma 1 activity. These results, along with the observation that Jurkat cells preferentially express PLC gamma 1, indicate that PLC gamma 1 participates in CD3 signaling.