tbuckley/cabot-search huggingface dataset:
Increased segmental activity and intraluminal pressures in the sigmoid colon of patients with the irritable bowel syndrome.
Authors: J Rogers, M M Henry, J J Misiewicz
Journal: Gut (1989)

Intraluminal pressure activity has been recorded in the unprepared true sigmoid colon of seven normal controls (mean age 37 years, range 22-55, three men) and seven patients with irritable bowel syndrome (IBS) (45 years, 24-75, four men) for 30 minutes before and 100 minutes after a standard 1000 kcal meal. Results differ from previously published data by showing much higher indices of pressure activity with amplitudes up to 490 mmHg in IBS, and 450 mmHg in controls. Study segment activity index and mean pressure wave amplitudes were significantly (p less than 0.015 and p less than 0.01) higher in IBS than controls, but per cent duration of activity was similar for the whole period of study. During the basal period in controls mean amplitudes recorded from the proximal sigmoid (40 cm from anus) were significantly (p less than 0.01) higher than those in the descending colon (50 cm), distal sigmoid (30 cm) and rectum (15 cm). This study shows that the increased colonic activity in IBS is characterised by increased amplitude, but not duration of pressure waves. In the basal state there is a high pressure zone in the proximal sigmoid colon of controls. Pressures in the unprepared colon of controls and IBS were higher than those measured under other experimental conditions.
Unfelicitous Medical Writing
Authors: William Hines
Journal: JAMA (1975)

To the Editor.—  In the very same issue (233:897, 1975) in which an editorial on Unfelicitous Medical Writing appeared, this little gem was printed (p 851) in a MEDICAL NEWS item on Dr George H. Whipple and the Strong Memorial Hospital in Rochester, New York.  If `a great institution is the lengthening shadow of one man,' then that shadow, or more precisely, that guiding light, was—and in many ways still is—George Hoyt Whipple, now 96 years of age.  Now, go back and read that over once more, slowly, carefully, and with feeling. It clearly says that Dr Whipple is the Strong Memorial Hospital.
Lipoprotein-Associated Phospholipase A2 Activity Is Associated With Risk of Coronary Heart Disease and Ischemic Stroke
Authors: Hok-Hay S. Oei, Irene M. van der Meer, Albert Hofman, Peter J. Koudstaal, Theo Stijnen, Monique M.B. Breteler, Jacqueline C.M. Witteman
Journal: Circulation (2005)

Lipoprotein-associated phospholipase A2 (Lp-PLA2) has been proposed as an inflammatory marker of cardiovascular disease. In the present study, we investigated whether Lp-PLA2 is an independent predictor of coronary heart disease and ischemic stroke.The Rotterdam Study is a population-based follow-up study in 7983 subjects > or =55 years of age. We performed a case-cohort study, including 308 coronary heart disease cases, 110 ischemic stroke cases, and a random sample of 1820 subjects. We used Cox proportional-hazard models with modification of the standard errors based on robust variance estimates to compute hazard ratios adjusted for age, sex, body mass index, systolic blood pressure, non-HDL cholesterol, HDL cholesterol, diabetes, smoking, alcohol consumption, cholesterol-lowering medication, white blood cell count, and C-reactive protein. Compared with the first quartile of Lp-PLA2 activity, multivariate-adjusted hazard ratios for coronary heart disease for the second, third, and fourth quartiles were 1.39 (95% CI, 0.92 to 2.10), 1.99 (95% CI, 1.32 to 3.00), and 1.97 (95% CI, 1.28 to 3.02), respectively (P for trend=0.01). Corresponding multivariate-adjusted hazard ratios for ischemic stroke were 1.08 (95% CI, 0.55 to 2.11), 1.58 (95% CI, 0.82 to 3.04), and 1.97 (95% CI, 1.03 to 3.79) (P for trend=0.03). The relation between Lp-PLA2 and coronary heart disease was present in both subjects with non-HDL cholesterol levels below the median and those with non-HDL cholesterol levels above the median.This study shows that Lp-PLA2 activity is an independent predictor of coronary heart disease and ischemic stroke in the general population.
Conclusions of review of dietary sugars and body weight are unwarranted
Authors: R. C. Cottrell, A. Wittekind
Journal: BMJ (2013)

Te Morenga and colleagues’ review sheds some light on the confused literature regarding dietary sugars and body weight.1 The authors acknowledge that the small change in body weight (~0.8 kg) attributed to alterations in sugar intake in the intervention trials cited probably results from changes in energy intake, rather than some characteristic unique …
Transfer of Research Technology to Clinical Practice — What Are the Criteria?
Authors: Rex B. Conn, Russell K. Brynes
Journal: New England Journal of Medicine (1980)

This issue of the Journal contains an article by Levitt, Ellis, and Meier that will be of interest to physicians who must make decisions about the presence of pancreatic disease; another, by Nakahara, Hirano, and their co-workers, describes a surface marker on the blast cells of patients with acute lymphoblastic leukemia. These articles present new information about serum amylase isoenzymes and membrane glycolipids on lymphoblasts. Such information is valuable for the light it sheds on biologic mechanisms in health and disease, but a question raised by all such reports is whether the new observations should be transmuted into diagnostic tests . . .
Syncope: Current Diagnostic Evaluation and Management
Authors: Antonis S. Manolis
Journal: Annals of Internal Medicine (1990)

Objective: To provide a comprehensive review of the causes, current diagnostic evaluation, and treatment of syncope. Data Identification: New data and knowledge in this evolving field were critically analyzed by doing a MEDLINE search on syncope supplemented by selective review of English language literature citations in the Index Medicus before 1980. Study Selection: We reviewed approximately 200 published articles on syncope and closely related topics as well as using our own clinical experience. We selected articles if they addressed the pathophysiology of syncope, classification and causes, differential diagnosis, noninvasive and invasive evaluation, and current therapy. Results of Data Synthesis: Syncope is a common clinical problem, occurring in 30% to 50% of the adult population. The prognosis for syncope depends on its cause. Cardiac syncope has the worst prognosis and therefore mandates thorough evaluation and prompt treatment. Diagnostic evaluation is made difficult by the transient nature of the episodes and the many causes. Noninvasive testing reveals the cause of syncope in approximately 50% of cases. More extensive evaluation, including invasive electrophysiologic studies, has assumed a larger role in defining the cause of syncope in selected patients with structural heart disease in whom a noninvasive evaluation has been nondiagnostic. Recently tilt-table studies have been proposed as a clinically useful noninvasive test for vagally mediated syncope. Conclusions: A rational stepwise diagnostic and therapeutic approach to patients with syncope can be developed by initially doing a careful history and physical examination followed by a noninvasive evaluation and selective use of additional, more specialized or invasive tests. Future research should focus on defining the validity and utility of current diagnostic testing in syncope and on exploring further the pathophysiology of patients with recurrent, unexplained syncope.
Squamous cell carcinoma arising in chronic lymphoedema
Authors: R.K. LISTER, M.M. BLACK, E. CALONJE, K.G. BURNAND
Journal: British Journal of Dermatology (1997)

Two patients are reported in whom a squamous cell carcinoma arose in chronic lymphoedematous skin on the lower legs. Although lymphangiosarcoma is a well recognized complication of chronic lymphoedema, squamous cell carcinoma has only been reported on seven previous occasions. The pathogenesis of malignant tumours in chronic lymphoedema is discussed.
Next-Generation Drug-Eluting Stents
Authors: Manesh R. Patel, David R. Holmes
Journal: JAMA (2008)

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 Angiogenic Factor PlGF Mediates a Neuroimmune Interaction in the Spleen to Allow the Onset of Hypertension
Authors: Daniela Carnevale, Fabio Pallante, Valentina Fardella, Stefania Fardella, Roberta Iacobucci, Massimo Federici, Giuseppe Cifelli, Massimiliano De Lucia, Giuseppe Lembo
Journal: Immunity (2014)
Abstract 1210: Tetraspanin CD63 interacts with extranuclear estrogen receptor alpha and regulates non-genomic signaling pathways in breast cancer
Authors: Jian Huang, Alexander Craig Mackinnon, Liying Jiang
Journal: Cancer Research (2012)

Abstract Tetraspanin is a four transmembrane protein family whose members are regarded as molecular linkers. They also serve as scaffold proteins for many signaling processes. CD63 is a member of the tetraspanin family that serves as a lysosomal protein. Estrogen receptor alpha (ERα) plays critical roles in breast carcinogenesis. Extranuclear ERα could initiate rapid estrogen responses by forming protein complexes with many signaling molecules. Here, we report a novel protein complex formed between tetraspanin CD63 and extranuclear ERα. Immunoprecepitation (IP) experiments in MCF-7 and BT474 cells showed that CD63 interacts with ERα at endogenous levels. IP experiments using extracts from different cellular compartments (nucleus, cytoplasm and plasma membrane) showed that the interaction between CD63 and ERα is mainly located on the plasma membrane. Moreover, using co-immunofluorescence (IF) staining, we found CD63 co-localized with ERα on plasma membrane and/or in the cytoplasm. To further explore the effects of CD63 on ERα signaling pathways, we stably knocked down CD63 by shRNA in MCF-7 and BT474 cells. Interestingly, the expression of ERα was increased with lower expression of CD63. We further examined ERα from extracts of nucleus, cytoplasm, and membrane by western blots, and found that ERα in cytoplasm and/or membrane was increased by knocking down CD63 whereas the ERα level in the nucleus was not changed. IF staining showed similar results. Furthermore, P-MAPK level was up-regulated in both MCF-7 and BT474 cell lines with suppressed expression of CD63. These data suggest that the tetraspanin CD63 may facilitate the transport of ERα between plasma membrane and/or cytoplasm and nucleus, an important new function. CD63 may play a key role on organizing and regulating non-genomic ERα signaling pathways in breast cancer. 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 1210. doi:1538-7445.AM2012-1210
CHRONIC OR PERSISTING IDENTITY DIFFUSION
Authors: WERNER KOENIG
Journal: American Journal of Psychiatry (1964)

This paper discusses the psychiatric examination of over 200 former concentration camp survivors in connection with their restitution claims. By extending Erikson's concept of acute identity diffusion at the end of adolescence to the concept of a chronic or persisting identity diffusion, satisfactory theoretical framework for the understanding of the characterological changes in former adolescent camp survivors was developed. The paper seeks to illustrate the theoretical issues by use of general background and direct quotations of the individuals and closes with a short comment on the therapeutic goal.
Meprobamate Sedative or Tranquilizer
Authors: Mortimer Ostow
Journal: JAMA (1965)

ABSTRACT To the Editor:— A news item in this morning's New York Times reported that meprobamate has been dropped from the US Pharmacopoeia. The decision was based upon a ruling that the drug is a sedative, not a true tranquilizer, and could cause addiction  dosage levels not much above recommended.These actions and statements unfortunately tend to discredit a drug which I consider to be one of the finest sedatives introduced to medical practice within several decades. When first introduced it was called a tranquilizer as were several other drugs introduced at the same time. The term tranquilizer should be reserved for those drugs which exert a therapeutic effect in certain types of schizophrenia and mania. Such a definition applies to the antipsychotic phenothiazines and to reserpine as well as to a few other compounds. It does not apply to meprobamate, to chlordiazepoxide hydrochloride, or to diazepam.Meprobamate has in
PROGRESSIVE STRAIN IMAGING CHANGE AND ROLE OF THE NATRIURETIC PEPTIDES AS PREDICTORS OF LEFT VENTRICULAR DYSFUNCTION AND FIBROSIS IN AGING MYOCARDIUM
Authors: Diego Bellavia, Jeson S. Sangaralingham, Elise Oehler, Alessandro Cataliotti, Paul McKie, Gerald E. Harders, Margaret M. Redfield, Fletcher A. Miller, John C. Burnett
Journal: Journal of the American College of Cardiology (2010)
Effects of <i>n</i>‐3 polyunsaturated fatty acids and of rosuvastatin on left ventricular function in chronic heart failure: a substudy of GISSI‐HF trial
Authors: Stefano Ghio, Laura Scelsi, Roberto Latini, Serge Masson, Ermanno Eleuteri, Michela Palvarini, Olga Vriz, Michele Pasotti, Marco Gorini, Roberto Marchioli, Aldo Maggioni, Luigi Tavazzi
Journal: European Journal of Heart Failure (2010)
Abstract 741: CpG methylation abrogates KLF2-mediated transcriptional repression of telomerase in human T cells.
Authors: Toshifumi Hara, Manami Yoshita, Masataka Nakamura
Journal: Cancer Research (2013)

Abstract Many genes in tumor cells are DNA-methylated and transcriptionally repressed. Constitutive expression of the limiting catalytic subunit of telomerase, hTERT, is one of the common signatures of tumor cells, even though its promoter is DNA-methylated. On the other hand, in normal somatic cells the promoter is unmethylated and transcription of hTERT is strictly regulated. In this study, we examined transcriptional regulation of the hTERT gene in normal and tumor cells. We identified a novel promoter element, which bound the zinc-finger transcription factor Krüpple-like factor 2 (KLF2) in normal human T Lymphocytes. The binding of KLF2 to the hTERT promoter element paralleled repression of hTERT transcription in resting normal T cells. T cell growth induced KLF2 release from the element and hTERT transcription. Forced reduction of KLF2 expression by siRNA in normal resting T cells increased the level of endogenous hTERT mRNA. The hTERT promoter is methylated in the KLF2-positive human T leukemic cell line, Kit 225, and KLF2-negative human T leukemic cell line, Jurkat. Treatment with the DNA methyltransferase inhibitor, Zebularine, reduced levels of CpG methylation in the hTERT promoter, resulting in downregulation of hTERT mRNA expression in KLF2-positive Kit 225 cells, while the Zebularine treatment did not cause any appreciable effects on hTERT expression in KLF2-negative Jurkat cells. Methylation of CpG sequences in endogenous and exogenous hTERT promoter elements inhibited the KLF2 binding to the element. Furthermore, KLF2 binding to the promoter is associated with histone H3 repressive marks, indicating KLF2-mediated epigenetic silencing of the hTERT promoter. Our results suggest that KLF2 partly controls strict transcriptional regulation of the hTERT gene through association and dissociation with the promoter in normal T cells, but in tumor cells these important interactions are prevented by DNA methylation. Citation Format: Toshifumi Hara, Manami Yoshita, Masataka Nakamura. CpG methylation abrogates KLF2-mediated transcriptional repression of telomerase in human T cells. [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 741. doi:10.1158/1538-7445.AM2013-741
Controlling methicillin resistant Staphylococcus aureus
Authors: G. Duckworth
Journal: BMJ (2003)

Time to return to more stringent methods of control in the United Kingdom? 

Methicillin resistant Staphylococcus aureus (MRSA) is a major cause of hospital acquired infection worldwide, posing a growing threat to public health. It belongs to a species of ubiquitous and versatile organisms that are continually adapting to new antimicrobial and environmental challenges, often through gene transfers even from distantly related organisms such as vertebrates. Why is MRSA important? Some strains are eminently transmissible, resulting in large numbers of infections in hospitals. Bacteraemia data for England and Wales show that MRSA as a proportion of total Staphylococcus aureus bacteraemias rose from under 2% in 1990 to 42% in 20001 2—one of the highest reported rates in Europe.

Methicillin resistance was first reported in 1961 shortly after the introduction of methicillin (similar to flucloxacillin), the first penicillin resistant to destruction by staphylococcal β -lactamase. The discovery of methicillin was an important development as many hospital strains of S aureus had become penicillin resistant in the 1950s through the production of β -lactamase.w1 Some European countries experienced problems with MRSA in the 1960s, but this was followed by …
Enhanced Sensitivity to the HER1/Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor Erlotinib Hydrochloride in Chemotherapy-Resistant Tumor Cell Lines
Authors: Qun Dai, Yi-He Ling, Marie Lia, Yi-Yu Zou, Glenn Kroog, Kenneth K. Iwata, Roman Perez-Soler
Journal: Clinical Cancer Research (2005)

Abstract Purpose: Erlotinib (Tarceva, OSI-774) is a potent and specific inhibitor of the HER1/epidermal growth factor receptor (EGFR) tyrosine kinase. In phase II clinical studies, oral erlotinib monotherapy has shown antitumor activity in patients with advanced non–small cell lung cancer, head and neck cancer, and ovarian cancer after the failure of standard chemotherapy. We hypothesized that some tumors treated with multiple cytotoxic therapies may become more dependent on the HER1/EGFR signaling pathways for survival. Experimental Design: The growth-inhibitory effect of erlotinib was tested on 10 pairs of chemosensitive, parental, and chemoresistant tumor cell lines. Results: Enhanced sensitivity to erlotinib was observed in the doxorubicin-resistant human breast cancer cell line MCF-7, paclitaxel-resistant human ovarian carcinoma cell line A2780, and cisplatin-resistant human cervical carcinoma cell line ME180. The IC50 values of erlotinib in the resistant cell lines were 2- to 20-fold lower than those in the corresponding parental cell lines. This enhanced sensitivity to erlotinib correlated with higher HER1/EGFR and phospho-HER1/EGFR expression when compared with the corresponding parental cell lines. Acquired resistance to cytotoxic agents was not associated with cross-resistance to erlotinib. AE-ME180/CDDP-resistant xenografts showed greater sensitivity to erlotinib than parental ME180 xenografts did. Conclusions: Our findings suggest that acquired resistance to cytotoxic therapy in some tumors is associated with enhanced sensitivity to HER1/EGFR inhibitors, which correlates with increased HER1/EGFR expression. These data may explain some of the observed clinical activity of HER1/EGFR inhibitors in patients previously treated with multiple therapies. HER1/EGFR tyrosine kinase inhibitors may be more effective as second- or third-line treatment for certain patients with tumors that were previously treated with multiple chemotherapy regimens.
PM(10) exposure, gaseous pollutants, and daily mortality in Inchon, South Korea.
Authors: Y C Hong, J H Leem, E H Ha, D C Christiani
Journal: Environmental Health Perspectives (1999)

To evaluate the relative importance of various measures of particulate and gaseous air pollution as predictors of daily mortality in Inchon, South Korea, the association between total daily mortality and air pollution was investigated for a 20-month period (January 1995 through August 1996). Poisson regression was used to regress daily death counts on each air pollutant, controlling for time trends, season, and meteorologic influences such as temperature and relative humidity. Regression coefficients of a 5-day moving average of particulate matter less than or = to 10 microm in aerodynamic diameter (PM(10)) on total mortality were positively significant when considered separately and simultaneously with other pollutants in the model. PM(10) remained significant when the models were confined to cardiovascular or respiratory mortality. Sulfur dioxide (SO(2)) and carbon monoxide (CO) were significantly related to respiratory mortality in the single-pollutant model. Ozone exposure was not statistically significant with regard to mortality in the above models, and graphic analysis showed that the relationship was nonlinear. A combined index of PM(10), nitrogen dioxide, SO(2), and CO seemed to better explain the exposure-response relationship with total mortality than an individual air pollutant. Pollutants should be considered together in the risk assessment of air pollution, as opposed to measuring the risk of individual pollutants.
Deactivation of cultured human liver myofibroblasts by Trans -resveratrol, a grapevine-derived polyphenol
Authors: Sandrine Godichaud, Stéphanie Krisa, Baptiste Couronné, Liliane Dubuisson, Jean-Michel Mérillon, Alexis Desmoulière, Jean Rosenbaum
Journal: Hepatology (2000)

Liver myofibroblasts are major actors in the development of liver fibrosis and cancer progression. There is a large interest in drugs that might deactivate these cells. Many studies have shown that the grapevine-derived polyphenol, trans -resveratrol, and other stilbenes have therapeutic potential in some diseases. In this work, we have studied the effect of grapevine polyphenols on cultured human liver myofibroblasts. We have shown that trans -resveratrol profoundly affects myofibroblast phenotype. Trans -resveratrol induced morphological modifications. It markedly reduced proliferation of myofibroblasts in a dose-dependent manner. Trans -resveratrol also decreased the expression of α smooth muscle actin (α-SMA) without affecting vimentin or β-cytoplasmic actin expression. It decreased myofibroblast migration in a monolayer wounding assay. We also showed that trans -resveratrol inhibited the messenger RNA (mRNA) expression of type I collagen. Finally, it decreased the secretion of matrix metalloproteinase 2 (MMP-2). We conclude that trans -resveratrol can deactivate human liver myofibroblasts. In the second part of this study, we have shown that neither trans -piceid (a glycosylated analog) nor trans -piceatannol (a hydroxylated analog) reproduces trans -resveratrol effects on liver myofibroblasts. We finally show that, although trans -resveratrol decreases the proliferation of skin fibroblast and vascular smooth muscle cells, it does not affect their expression of α-SMA, which indicates some cell specificity.