tbuckley/cabot-search huggingface dataset:
Environmental Connections: A Deeper Look into Mental Illness
Authors: Charles W. Schmidt
Journal: Environmental Health Perspectives (2007)

ental illnesses produce some of the most challenging health problems faced by society, accounting for vast numbers of hospitalizations, disabilities resulting in billions in lost productivity, and sharply elevated risks for suicide.Scientists have long known that these potentially devastating conditions arise from combinations of genes and environmental factors.Genetic research has produced intriguing biological insights into mental illness, showing that particular gene variations predispose some individuals to conditions such as depression and schizophrenia.Now, thanks to a growing union of epidemiology and molecular biology, the role of the environment in the etiology of mental illness has become more clear.Indeed, E. Fuller Torrey, president of the Treatment Advocacy Center, a nonprofit organization that promotes treatment advances in psychiatry, suggests that mental illnesses increasingly fall into the realm of environmental health.And from that platform, he says, new treatment advances could soon emerge."Some of the greatest advancements in twentieth-century medicine were achieved by identifying and preventing infectious diseases through vaccination, improved sanitary measures, improved nutrition, and diminished hazards of environmental contaminants," adds
A Nomogram to Predict Long-term Survival After Resection for Intrahepatic Cholangiocarcinoma
Authors: Omar Hyder, Hugo Marques, Carlo Pulitano, J. Wallis Marsh, Sorin Alexandrescu, Todd W. Bauer, T. Clark Gamblin, Georgios C. Sotiropoulos, Andreas Paul, Eduardo Barroso, Bryan M. Clary, Luca Aldrighetti, Cristina R. Ferrone, Andrew X. Zhu, Irinel Popescu, Jean-Francois Gigot, Gilles Mentha, Shen Feng, Timothy M. Pawlik
Journal: JAMA Surgery (2014)

Intrahepatic cholangiocarcinoma (ICC) is a primary cancer of the liver that is increasing in incidence, and the prognostic factors associated with outcome after surgery remain poorly defined.To combine clinicopathologic variables associated with overall survival after resection of ICC into a prediction nomogram.We performed an international multicenter study of 514 patients who underwent resection for ICC at 13 major hepatobiliary centers in the United States, Europe, and Asia from May 1, 1990, through December 31, 2011. Multivariate Cox proportional hazards regression modeling with backward selection using the Akaike information criteria was used to select variables for construction of the nomogram. Discrimination and calibration were performed using Kaplan-Meier curves and calibration plots.Surgical resection of ICC at a participating hospital.Long-term survival, effect of potential prognostic factors, and performance of proposed nomogram.Median patient age was 59.2 years, and 53.1% of the patients were male. Most patients (74.7%) had a solitary tumor, and median tumor size was 6.0 cm. Patients were treated with an extended hepatectomy (202 [39.3%]), a hemihepatectomy (180 [35.0%]), or a minor liver resection (<3 segments) (132 [25.7%]). Most patients underwent R0 resection (87.9%), and 35.7% of patients had N1 disease. Using the backward selection of clinically relevant variables, we found that age at diagnosis (hazard ratio [HR], 1.31; P < .001), tumor size (HR, 1.50; P < .001), multiple tumors (HR, 1.58; P < .001), cirrhosis (HR, 1.51; P = .08), lymph node metastasis (HR, 1.78; P = .01), and macrovascular invasion (HR, 2.10; P < .001) were selected as factors predictive of survival. On the basis of these factors, a nomogram was created to predict survival of ICC after resection. Discrimination using Kaplan-Meier curves, calibration curves, and bootstrap cross-validation revealed good predictive abilities (C index, 0.692).On the basis of an Eastern and Western experience, a nomogram was developed to predict overall survival after resection for ICC. Validation revealed good discrimination and calibration, suggesting clinical utility to improve individualized predictions of survival for patients undergoing resection of ICC.
STREPTOCOCCIC INFECTION AND MARMOREK'S SERUM.
Authors: GEO. W. COX
Journal: JAMA (1897)

The study of bacteriology during the past few years has developed many interesting facts, not alone to the scientist, whose labors and interests are confined to the laboratory, but also to the clinician, whose work it is to practically apply the knowledge furnished him by the former. It would be difficult to name any one branch of the subject which could justly claim precedence if viewed merely in its scientific aspect, for all are of absorbing interest in this regard; but in the matter of practical application and tangible results it may be safely asserted that the study of the streptococcus microbe stands first in the list. It is the most widely distributed of any of the members of its class; it is more variable in its morphologic development than any of the others; it is unique in the matter of biologic characteristics, and it is decidedly the most far-reaching
CLINICAL OBSERVATIONS ON THE EMETIC ACTION OF DIGITALIS
Authors: CARY EGGLESTON
Journal: JAMA (1913)

Nausea and vomiting are probably the commonest of the side-actions encountered in the clinical use of the digitalis bodies. They have generally been attributed to a local irritant action of these substances on the mucous membrane of the alimentary canal. In two previous papers 1 Dr. Hatcher and I have shown that the digitalis bodies cause nausea and emesis in animals through their direct action on the vomiting center in the medulla. We have been unable to find in the literature, or to adduce from our own experiments, any evidence either to controvert this statement or to support the opposite view of local irritant action in the stomach or intestine. In view of our experimental findings we called attention to the need for a carefully controlled series of observations on the seat of the emetic action of therapeutic doses of this group of drugs when used clinically. It is the
DRUG SAMPLES FOR CHARITY HOSPITAL
Authors: A. M. Earle
Journal: JAMA (1960)

<h3>To the Editor:—</h3> I have read Sonneland's letter to the editor inThe Journal, May 21, page 295, and I would like to request Dr. Sonneland and any other physicians who throw their samples in the wastebasket to send these samples to me at the above address. I am collecting samples of drugs for the Albert Schweitzer Hospital in Haiti. This is a charity hospital in the Artebonite Valley. Any physicians wishing to send samples directly to the hospital may use this address: Albert Schweitzer Hospital % Allan &amp; Baussan P. O. Box 1304 Port-au-Prince, Haiti. If they would like further information regarding the Albert Schweitzer Hospital, they may obtain it from the Grant Foundation, 525 William Penn Pl., Pittsburgh 19.
p75 neurotrophin receptor signaling regulates hepatic myofibroblast proliferation and apoptosis in recovery from rodent liver fibrosis
Authors: Timothy J. Kendall, Selina Hennedige, Rebecca L. Aucott, Stephen N. Hartland, Madeleine A. Vernon, R. Christopher Benyon, John P. Iredale
Journal: Hepatology (2008)

Hepatic myofibroblast apoptosis is critical to resolution of liver fibrosis. We show that human hepatic myofibroblasts co-express p75NTR (p75 neurotrophin receptor) and sortilin, thus facilitating differential responses to mature and pro nerve growth factor (proNGF). Although mature NGF is proapoptotic, proNGF protects human hepatic myofibroblasts from apoptosis. Moreover, in recovery from experimental liver fibrosis, the decrease in proNGF parallels loss of hepatic myofibroblasts by apoptosis. Macrophage-derived matrix metalloproteinase 7 (MMP7) cleaves proNGF in a concentration-dependent manner, and its expression in the liver coincides with falling proNGF levels. To define the dominant effect of p75NTR-mediated events in experimental liver fibrosis, we have used a mouse lacking the p75NTR ligand-binding domain but expressing the intracellular domain. We show that absence of p75NTR ligand-mediated signals leads to significantly retarded architectural resolution and reduced hepatic myofibroblast loss by apoptosis. Lack of the ligand-competent p75NTR limits hepatocyte and oval cell proliferative capacity in vivo without preventing hepatic stellate cell transdifferentiation. Conclusion: NGF species have a differential effect on hepatic myofibroblast survival. Our data suggest that cleavage of proNGF by MMP7 during the early phase of recovery from liver fibrosis alters the pro/mature NGF balance to facilitate hepatic myofibroblast loss. Whereas fibrosis develops in the absence of p75NTR signaling, the dominant effects of loss of p75NTR ligand-mediated events are the retardation of liver fibrosis resolution via regulation of hepatic myofibroblast proliferation and apoptosis, and the reduction of hepatocyte and oval cell proliferation. (HEPATOLOGY 2009.)
Histoire du Curare: Les Poisons de Chasse en Amérique du Sud
Authors: Charles G. Roland
Journal: JAMA (1965)

Travelers' romantic tales about curare have had a relaxing effect on the critical faculties of many writers. Publications discussing curare continue to appear containing quotations from Spanish authors of the 16th century, which conjure up desperate battles, the clash of arms, and hordes of armored Spaniards quailing before flights of poisoned arrows. The agonized death of the wounded is portrayed in chilling details; and the poison, these romanticists contend, was curare. Vellard denies this, pointing out that, at least among the Nambikwara Indians of the Matto Grosso, who have manufactured and used the arrow poison for centuries, there is a powerful taboo forbidding the use of curare against man. Certainly these early "clinical" descriptions have little in common with the known effects of curare; the wounded Spaniards often lingered on, in agony, for a day or longer. Vellard has traveled and lived among the South American Indian tribes for many
IMPACT OF LIPID RICH PLAQUE AT THE STENT EDGE ASSESSED BY OPTICAL COHERENCE TOMOGRAPHY ON EDGE RESTENOSIS AFTER EES IMPLANTATION
Authors: Yasushi Ino, Daisuke Higashioka, Takashi Kubo, Yosuke Katayama, Yasutsugu Shiono, Makoto Orii, Keisuke Satogami, Yoshiki Matsuo, Takashi Yamano, Tomoyuki Yamaguchi, Tsuyoshi Nishiguchi, Ikuko Teraguchi, Tomoko Nakamura, Kumiko Hirata, Akira Taruya, Haruhi Nishio, Atsushi Tanaka, Takashi Akasaka
Journal: Journal of the American College of Cardiology (2015)
Abstract P5-20-11: Bevacizumab in metastatic breast cancer: a retrospective matched-pair analysis.
Authors: SP Gampenrieder, F Romeder, C Muß, M Pircher, S Ressler, G Rinnerthaler, R Bartsch, C Sattlberger, B Mlineritsch, R Greil
Journal: Cancer Research (2012)

Abstract Background: In November 2011 the FDA withdrew accelerated approval of the breast cancer indication for bevacizumab, because “the drug has not been shown to be safe and effective for this use” (FDA Commissioner M. A. Hamburg, MD). The objective of this analysis was to evaluate efficacy and safety of bevacizumab in non-selected patients with stage IV breast cancer. Patients and methods: All patients with metastatic breast cancer treated with bevacizumab in combination with chemotherapy in our institution between 2005 and 2011 were retrospectively analysed. At least 1 cycle of bevacizumab was required for safety analysis, 3 applications for efficacy evaluation. A control group was matched according to the following criteria: receptor status, line of treatment, chemotherapy backbone, visceral or non-visceral disease and age. Results: A total of 213 patients fulfilled the inclusion criteria. All of them were evaluable for toxicity, 199 for response. 503 potential controls allowed a complete matching for 103 patients. Fifty-eight percent of patients received first-line, 15% second-line and 27% of patients beyond second-line treatment. Visceral metastases were present in 69% of patients in both groups. The most common chemotherapy backbones were paclitaxel, capecitabine and docetaxel with 44%, 32% and 19%, respectively. Most common grade 3/4 toxicities related to bevacizumab were hypertension (27%), proteinuria (1%), thromboembolism (9%) and bleeding events (1%). Interestingly, patients developing hypertension during bevacizumab treatment had a more favourable outcome (PSF 11.7 vs. 5.7 months, p &amp;lt; .001; OS 27.4 vs. 14.5 months, p &amp;lt; .001). Since the median time until apparent blood pressure elevation was only 1.4 months, this provides a simple biologic biomarker for bevacizumab efficacy. Conclusion: Bevacizumab in combination with chemotherapy appears to be an effective, well-tolerated regimen in the treatment of advanced breast cancer even in a non-selected, partly intensively pre-treated population. Bevacizumab induced hypertension predicted a better PFS and OS. Citation Information: Cancer Res 2012;72(24 Suppl):Abstract nr P5-20-11.
Endoplasmic reticulum stress induces hepatic steatosis via increased expression of the hepatic very low‐density lipoprotein receptor
Authors: Hyunsun Jo, Sung Sik Choe, Kyung Cheul Shin, Hagoon Jang, Jae Ho Lee, Je Kyung Seong, Sung Hoon Back, Jae Bum Kim
Journal: Hepatology (2012)

Abstract Recent evidence suggests that obese animals exhibit increased endoplasmic reticulum (ER) stress in the liver and adipose tissue. Although ER stress is closely associated with lipid homeostasis, it is largely unknown how ER stress contributes to hepatic steatosis. In this study, we demonstrate that the induction of ER stress stimulates hepatic steatosis through increased expression of the hepatic very low-density lipoprotein receptor (VLDLR). Among the unfolded protein response sensors, the protein kinase RNA-like ER kinase–activating transcription factor 4 signaling pathway was required for hepatic VLDLR up-regulation. In primary hepatocytes, ER stress–dependent VLDLR expression induced intracellular triglyceride accumulation in the presence of very low-density lipoprotein. Moreover, ER stress–dependent hepatic steatosis was diminished in the livers of VLDLR-deficient and apolipoprotein E–deficient mice compared with wild-type mice. In addition, the VLDLR-deficient mice exhibited decreased hepatic steatosis upon high-fat diet feeding. Conclusion : These data suggest that ER stress–dependent expression of hepatic VLDLR leads to hepatic steatosis by increasing lipoprotein delivery to the liver, which might be a novel mechanism explaining ER stress–induced hepatic steatosis.
CROSS CORRELATION OF TISSUE DOPPLER MYOCARDIAL ACCELERATION AT BASELINE BEFORE CARDIAC RESYNCHRONIZATION THERAPY IS A MARKER FOR SUBSEQUENT VENTRICULAR ARRHYTHMIAS
Authors: Bhupendar Tayal, Antonia Delgado-Montero, Keiko Ryo, Akiko Goda, Kristina Haugaa, Niels Risum, Peter Sogaard, John Gorcsan
Journal: Journal of the American College of Cardiology (2014)
Regional ischemic 'preconditioning' protects remote virgin myocardium from subsequent sustained coronary occlusion.
Authors: K Przyklenk, B Bauer, M Ovize, R A Kloner, P Whittaker
Journal: Circulation (1993)

BACKGROUND One or more brief episodes of coronary artery occlusion protect or "precondition" the myocardium perfused by that artery from a subsequent episode of sustained ischemia. We sought to determine whether ischemic preconditioning protects only those myocytes subjected to brief coronary occlusion or whether brief occlusions in one vascular bed also limit infarct size and/or attenuate contractile dysfunction in remote virgin myocardium subjected to subsequent sustained coronary occlusion. METHODS AND RESULTS In the preliminary limb of the study, six anesthetized dogs underwent four episodes of 5-minute circumflex branch occlusion plus 5-minute reperfusion, followed by 1 hour of sustained left anterior descending coronary artery occlusion and 4.5 hours of reflow. Subendocardial blood flow during left anterior descending coronary artery occlusion (measured by injection of radiolabeled microspheres) was 0.07 +/- 0.03 mL.min-1 x g tissue-1, similar to the value of 0.07 +/- 0.02 mL.min-1 x g-1 observed in a group of eight concurrent control dogs. However, infarct size (assessed by triphenyltetrazolium staining) in the circumflex preconditioned group averaged 4 +/- 1% of the myocardium at risk, significantly less (p &lt; 0.05) than the value of 13 +/- 4% observed in the concurrent controls. An additional 18 dogs were then randomized to undergo either four episodes of circumflex branch occlusion (n = 8) or no intervention (n = 10) before 1 hour of left anterior descending coronary artery occlusion and 4.5 hours of reflow. Subendocardial blood flow averaged 0.08 +/- 0.02 versus 0.08 +/- 0.03 mL.min-1 x g-1 in the control versus circumflex preconditioned groups, yet infarct size was significantly smaller in circumflex preconditioned dogs than in the controls (6 +/- 2% versus 16 +/- 5% of the risk region; p &lt; 0.05). At 4.5 hours following reperfusion, segment shortening in the left anterior descending coronary artery bed (assessed by sonomicrometry) averaged -21 +/- 19% of baseline in control animals versus 13 +/- 12% of baseline in the preconditioned group (p = NS). Circumflex preconditioning did not, however, have an independent beneficial effect on contractile function: Regression analysis revealed that the trend toward improved function in circumflex preconditioned dogs reflected the smaller infarct sizes in this group. CONCLUSIONS Brief episodes of ischemia in one vascular bed protect remote, virgin myocardium from subsequent sustained coronary artery occlusion in this canine model. These data imply that preconditioning may be mediated by factor(s) activated, produced, or transported throughout the heart during brief ischemia/reperfusion.
Mitochondrial remodeling in adipose tissue associated with obesity and treatment with rosiglitazone
Authors: Leanne Wilson-Fritch, Sarah Nicoloro, My Chouinard, Mitchell A. Lazar, Patricia C. Chui, John Leszyk, Juerg Straubhaar, Michael P. Czech, Silvia Corvera
Journal: Journal of Clinical Investigation (2004)

Adipose tissue plays a central role in the control of energy homeostasis through the storage and turnover of triglycerides and through the secretion of factors that affect satiety and fuel utilization. Agents that enhance insulin sensitivity, such as rosiglitazone, appear to exert their therapeutic effect through adipose tissue, but the precise mechanisms of their actions are unclear. Rosiglitazone changes the morphological features and protein profiles of mitochondria in 3T3-L1 adipocytes. To examine the relevance of these effects in vivo, we studied white adipocytes from ob/ob mice during the development of obesity and after treatment with rosiglitazone. The levels of approximately 50% of gene transcripts encoding mitochondrial proteins were decreased with the onset of obesity. About half of those genes were upregulated after treatment with rosiglitazone, and this was accompanied by an increase in mitochondrial mass and changes in mitochondrial structure. Functionally, adipocytes from rosiglitazone-treated mice displayed markedly enhanced oxygen consumption and significantly increased palmitate oxidation. These data reveal mitochondrial remodeling and increased energy expenditure in white fat in response to rosiglitazone treatment in vivo and suggest that enhanced lipid utilization in this tissue may affect whole-body energy homeostasis and insulin sensitivity.
ERK2 but not ERK1 plays a key role in hepatocyte replication: An RNAi-mediated ERK2 knockdown approach in wild-type and ERK1 null hepatocytes
Authors: Christophe Frémin, Frédéric Ezan, Pierre Boisselier, Anne Bessard, Gilles Pagès, Jacques Pouysségur, Georges Baffet
Journal: Hepatology (2007)

The mitogen-activated protein kinases (MAPKs) ERK1 and ERK2 have been implicated in various physiological events, and specific targeting of these MAPKs could affect cell proliferation in many cell types. First, to evaluate the potential specific roles of these two MAPKs, we analyzed the mitogenic response in regenerating liver after partial hepatectomy (PH) and in primary culture of hepatocytes isolated from ERK1-deficient mice. We show that ERK1 knockout and wild-type (wt) cells replicate with the same kinetics after PH in liver, in vivo, and in primary cultures of hepatocytes, in vitro. Indeed, Cyclin D1 and Cdk1 appear to be expressed concomitantly in knockout and wt cells, highlighting that hepatocytes progress in the cell cycle independently of the presence of ERK1. Second, we specifically abolished ERK2 expression by RNA interference in mouse and rat hepatocytes. We investigated whether small interfering RNA (siRNA) targeting ERK2 could specifically inhibit its expression and interfere with the process of replication. In ERK1-deficient hepatocytes, silencing ERK2 expression by RNA interference and ERK2 activation by U0126 clearly demonstrate that DNA replication is regulated by an ERK2-dependent mechanism. Furthermore, in rat wt hepatocytes, whereas ERK2 targeting inhibits late G(1) and S phase progression, ERK1 silencing is devoid of any effect on cell proliferation, indicating that ERK1 cannot rescue ERK2 deficiency.Our results emphasize the importance of the MAPK cascade in hepatocyte replication and allow us to conclude that ERK2 is the key form involved in this regulation, in vivo and in vitro.
Physicians as Double Agents
Authors: Stephen M. Shortell, Teresa M. Waters, Kenneth W. B. Clarke, Peter P. Budetti
Journal: JAMA (1998)

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
1420 THE EFFICACY AND SAFETY OF THE INTERFERON-FREE COMBINATION OF BI201335 AND BI207127 IN GENOTYPE 1 HCV PATIENTS WITH CIRRHOSIS - INTERIM ANALYSIS FROM SOUND-C2
Authors: V. Soriano, E. Gane, P. Angus, F. Stickel, J.-P. Bronowicki, S. Roberts, M. Manns, S. Zeuzem, L. Dai, W. Boecher, J. Stern, F. Mensa
Journal: Journal of Hepatology (2012)