tbuckley/cabot-search huggingface dataset:
Rehabilitation in Chronic Renal Failure
Authors: George Dunea
Journal: JAMA (1980)

This book is edited by the late Dr Samuel B. Chyatte, himself a sufferer from end-stage renal disease, who died in July 1978 after about three years of treatment with maintenance hemodialysis. The first three chapters deal with the cause, pathophysiology, and general treatment of chronic renal failure, including the principles of dialysis, transplantation, and dietary management. Then follows a chapter written by the editor himself, in which rehabilitation is described as the complex process of achieving psychological, vocational, and societal adjustment, ideally through the efforts of a team that includes the rehabilitation physician, the physical and occupational therapist, the social worker, the psychiatrist or psychologist, and the vocational rehabilitation counselor. There are detailed discussions of the overall physical and psychological evaluation and management of the dialysis patient, with special emphasis on counseling and vocational rehabilitation, on dietary management, and on problems peculiar to children and adolescents. The book should
South Korea's national health insurer sues tobacco industry for $51.9m in damages
Authors: J. Parry
Journal: BMJ (2014)

South Korea’s state health insurer has joined the ranks of countries suing the tobacco industry for the health related costs of disease caused by smoking. The country’s National Health Insurance Service (NHIS) announced on 14 April that it had filed a suit for damages of 53.7 billion won (£31m; €37.5m; $51.9m) from the local market leader KT&G Corporation and the local units of Philip Morris International and British American Tobacco.

“We believe the NHIS, as it takes responsibility for the health of the public and oversees the insurance budget, has a natural duty to bring this …
Hydroxylation Increases the Neurotoxic Potential of BDE-47 to Affect Exocytosis and Calcium Homeostasis in PC12 Cells
Authors: Milou M.L. Dingemans, Aart de Groot, Regina G.D.M. van Kleef, Åke Bergman, Martin van den Berg, Henk P.M. Vijverberg, Remco H.S. Westerink
Journal: Environmental Health Perspectives (2008)

Oxidative metabolism, resulting in the formation of hydroxylated polybrominated diphenyl ether (PBDE) metabolites, may enhance the neurotoxic potential of brominated flame retardants.Our objective was to investigate the effects of a hydroxylated metabolite of 2,2',4,4'-tetra-bromodiphenyl ether (BDE-47; 6-OH-BDE-47) on changes in the intracellular Ca2+ concentration ([Ca2+]i) and vesicular catecholamine release in PC12 cells.We measured vesicular catecholamine release and [Ca2+]i using amperometry and imaging of the fluorescent Ca2+-sensitive dye Fura-2, respectively.Acute exposure of PC12 cells to 6-OH-BDE-47 (5 microM) induced vesicular catecholamine release. Catecholamine release coincided with a transient increase in [Ca2+]i, which was observed shortly after the onset of exposure to 6-OH-BDE-47 (120 microM). An additional late increase in [Ca2+]i was often observed at > or =1 microM 6-OH-BDE-47. The initial transient increase was absent in cells exposed to the parent compound BDE-47, whereas the late increase was observed only at 20 microM. Using the mitochondrial uncoupler carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone (FCCP) and thapsigargin to empty intracellular Ca2+ stores, we found that the initial increase originates from emptying of the endoplasmic reticulum and consequent influx of extracellular Ca2+, whereas the late increase originates primarily from mitochondria.The hydroxylated metabolite 6-OH-BDE-47 is more potent in disturbing Ca2+ homeostasis and neurotransmitter release than the parent compound BDE-47. The present findings indicate that bioactivation by oxidative metabolism adds considerably to the neurotoxic potential of PBDEs. Additionally, based on the observed mechanism of action, a cumulative neurotoxic effect of PBDEs and ortho-substituted polychlorinated biphenyls on [Ca2+]i cannot be ruled out.
The CHARGE Study: An Epidemiologic Investigation of Genetic and EnvironmentalFactors Contributing to Autism
Authors: Irva Hertz-Picciotto, Lisa A. Croen, Robin Hansen, Carrie R. Jones, Judy van de Water, Isaac N. Pessah
Journal: Environmental Health Perspectives (2006)

Causes and contributing factors for autism are poorly understood. Evidence suggests that prevalence is rising, but the extent to which diagnostic changes and improvements in ascertainment contribute to this increase is unclear. Both genetic and environmental factors are likely to contribute etiologically. Evidence from twin, family, and genetic studies supports a role for an inherited predisposition to the development of autism. Nonetheless, clinical, neuroanatomic, neurophysiologic, and epidemiologic studies suggest that gene penetrance and expression may be influenced, in some cases strongly, by the prenatal and early postnatal environmental milieu. Sporadic studies link autism to xenobiotic chemicals and/or viruses, but few methodologically rigorous investigations have been undertaken. In light of major gaps in understanding of autism, a large case–control investigation of underlying environmental and genetic causes for autism and triggers of regression has been launched. The CHARGE (Childhood Autism Risks from Genetics and Environment) study will address a wide spectrum of chemical and biologic exposures, susceptibility factors, and their interactions. Phenotypic variation among children with autism will be explored, as will similarities and differences with developmental delay. The CHARGE study infrastructure includes detailed developmental assessments, medical information, questionnaire data, and biologic specimens. The CHARGE study is linked to University of California–Davis Center for Children's Environmental Health laboratories in immunology, xenobiotic measurement, cell signaling, genomics, and proteomics. The goals, study design, and data collection protocols are described, as well as preliminary demographic data on study participants and on diagnoses of those recruited through the California Department of Developmental Services Regional Center System.
Cognitive and psychiatric science beyond determinism
Authors: Dan J. Stein
Journal: Behavioral and Brain Sciences (1999)

Many of Rose's criticisms of determinism in biology have clear relevance to modern cognitive and psychiatric science; too narrow a focus on the brain as an information processing machine runs the risk of neglecting the context in which information processing takes place, and too narrow a focus on the neuroscience of psychopathology runs the risk of neglecting other levels of explanation for these phenomena. It should be emphasized, however, that animal and genetic studies of phenomena of interest to cognitive and psychiatric science (e.g., Alzheimer's disorder, schizophrenia, attention deficit/hyperactivity disorder, and violence), while perhaps only providing a partial perspective, may be useful in understanding these phenomena and in leading to appropriate psychiatric interventions.
The rational clinical examination
Authors: N. Devitt
Journal: JAMA (1992)

To the Editor.  —I was pleased to read your introduction to the new series on clinical examination. I thought the initial article 1 and Editorial 2 were both excellent. I would like to present the following case to pose a question: Four weeks ago, an 82-year-old woman came into my office with a 1-month history of right leg swelling. During this month, she had three separate episodes of pleuritic chest pain, the first two of which resolved spontaneously. She came to the office after the third episode of pain. On examination, she was found to have râles medial to her left scapula without audible rub. Her right leg was swollen and tender with a circumference of 40 cm compared with a left leg circumference of 35 cm. I felt absolutely certain that she had a deep-vein thrombosis with recurrent pulmonary emboli. I admitted her to the hospital where a venous
Decrease in the hepatic clearance of hepatocyte growth factor in carbon tetrachloride–intoxicated rats
Authors: Ke-Xin Liu, Yukio Kato, Masayo Yamazaki, Osamu Higuchi, Toshikazu Nakamura, Yuichi Sugiyama
Journal: Hepatology (1993)

To examine whether a decrease in hepatic uptake, clearance or both of hepatocyte growth factor contributes to increased plasma hepatocyte growth factor levels, we kinetically analyzed hepatic hepatocyte growth factor handling using rats with carbon tetrachloride-induced liver injury in both in vivo and perfused liver systems. After the intravenous administration of tracer 125I-hepatocyte growth factor, the time profile of trichloroacetic acid-precipitable 125I-hepatocyte growth factor was analyzed, and tissue clearance and total body plasma clearance were determined. For the tissues examined (liver, kidney, lung, spleen and adrenal), liver and adrenal clearance of 125I-hepatocyte growth factor decreased significantly. It was found that the hepatic clearance explains the bulk of the total body plasma clearance. The hepatic clearance and the total body clearance decreased to minimums (approximately 40% of control) 24 hr after carbon tetrachloride administration and recovered to near-control values over a 6-day period. At 24 hr after carbon tetrachloride administration, a single-pass liver perfusion of 125I-hepatocyte growth factor was performed, and its results were compared with the control results. After a 15-min perfusion of 125I-hepatocyte growth factor, we washed the liver sequentially with heparin and then with acid buffer to separately determine the cell-surface-bound and internalized 125I-hepatocyte growth factor. In carbon tetrachloride-intoxicated rats, both the acid-washable binding and the internalized 125I-hepatocyte growth factor dropped to almost half of the control values, but the decrease in heparin-washable binding was minimal. In contrast, when 125I-hepatocyte growth factor was perfused with excess unlabeled hepatocyte growth factor (135 pmol/L), mostly saturating the cell-surface receptors, the change in cell-surface-bound 125I-hepatocyte growth factor and internalized 125I-hepatocyte growth factor in carbon tetrachloride-intoxicated rats was minimal. This finding, along with our previous finding that the cell-surface hepatocyte growth factor receptors are greatly down-regulated in carbon tetrachloride-intoxicated rats, suggests that the hepatic clearance of hepatocyte growth factor through receptor-mediated endocytosis decreases in carbon tetrachloride-intoxicated rats. The decrease in the hepatic clearance of hepatocyte growth factor could be one of the causes of the elevated hepatocyte growth factor level in the circulating blood in liver diseases.
Causes of lower gastrointestinal haemorrhage.
Authors: W. G. Everett
Journal: BMJ (1992)

clinic, and an abnormally placed testis should be detected.3As some undescended testes descend spontaneously we suggest that all boys with an undescended testis at 8 months should be reviewed at 1 year and, if the testis has still not descended, referred to a surgeon so that orchidopexy can be arranged during the second year of life.To reduce the toll of testicular cancer better health education is required as this would also benefit all potential victims, 90% of whom have normally descended testes.Self examination should be taught at an early age and may lead to earlier presentation of testicular tumours.
miRNA-128 Suppresses Prostate Cancer by Inhibiting BMI-1 to Inhibit Tumor-Initiating Cells
Authors: Min Jin, Tao Zhang, Can Liu, Mark A. Badeaux, Bigang Liu, Ruifang Liu, Collene Jeter, Xin Chen, Alexander V. Vlassov, Dean G. Tang
Journal: Cancer Research (2014)

microRNA-128 (miR128) is reduced in prostate cancer relative to normal/benign prostate tissues, but causal roles are obscure. Here we show that exogenously introduced miR128 suppresses tumor regeneration in multiple prostate cancer xenograft models. Cancer stem-like cell (CSC)-associated properties were blocked, including holoclone and sphere formation as well as clonogenic survival. Using a miR128 sensor to distinguish cells on the basis of miR128 expression, we found that miR128-lo cells possessed higher clonal, clonogenic, and tumorigenic activities than miR128-hi cells. miR128 targets the stem cell regulatory factors BMI-1, NANOG, and TGFBR1, the expression of which we found to vary inversely with miR128 expression in prostate cancer stem/progenitor cell populations. In particular, we defined BMI-1 as a direct and functionally relevant target of miR128 in prostate cancer cells, where these genes were reciprocally expressed and exhibited opposing biological functions. Our results define a tumor suppressor function for miR128 in prostate cancer by limiting CSC properties mediated by BMI-1 and other central stem cell regulators, with potential implications for prostate cancer gene therapy.
Abstract 4661: Levels of C22:0- and C24:0-dihydroceramide correlate with cytotoxicity in T-cell acute lymphoblastic leukemia cell lines
Authors: Michael W. Holliday, Steven B. Cox, Min H. Kang, Barry J. Maurer
Journal: Cancer Research (2012)

Abstract Fenretinide (4-HPR) is a synthetic retinoid that is cytotoxic to several T-cell acute lymphoblastic leukemia (ALL) cell lines, and has demonstrated activity in a variety of cancer cell lines in vitro. Reported mechanisms of action for fenretinide include both increased reactive oxygen species (ROS) generation in some cell lines and increased dihydroceramide levels. Dihydroceramides are the product of N-acylation of sphinganine with fatty acid chains varying in carbon length and degree of saturation. Although synthetic, short-acyl chain dihydroceramides have been reported to be non-cytotoxic in cell culture in vitro, the cytotoxic potencies of native-acyl chain dihydroceramides are unknown. In the current study, increased synthesis of specific native-acyl chain dihydroceramides was targeted through a novel cell culture method employing concurrent exogenous administration of sphinganine, GT-11, a dihydroceramide desaturase inhibitor, and specific individual fatty acids. Sphingolipids were analyzed using LC/MS/MS. Cytotoxicity was measured using the fluorescence-based cytotoxicity assay DIMSCAN. Non-parametric correlation analysis of cytotoxicity and absolute sphingolipid levels revealed a strong positive correlation between cytotoxicity and C22:0-dihydroceramide (α = 0.75, P &amp;lt; 0.001) and C24:0-dihydroceramide (α = 0.84, P &amp;lt; 0.001) in the CCRF-CEM ALL cell line, with similar results observed independently in MOLT-4, COG-LL-317 and COG-LL-332 ALL cell lines. Additionally, fenretinide cytotoxicity was significantly increased by co-treatment with C22:0-fatty acid in association with an increase of C22:0- and C24:0-dihydroceramides. These findings suggest that the addition of specific fatty acids, perhaps in a tumor-type specific manner, through simple dietary or intravenous supplementation, or via concurrent incorporation into drug delivery vehicles, may improve the clinical efficacy of dihydroceramide-increasing anticancer agents, such as fenretinide. 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 4661. doi:1538-7445.AM2012-4661
After correcting for worse baseline characteristics, women treated with thrombolytic therapy for acute myocardial infarction have the same mortality and morbidity as men except for a higher incidence of hemorrhagic stroke. The Investigators of the International Tissue Plasminogen Activator/Streptokinase Mortality Study.
Authors: H D White, G I Barbash, M Modan, J Simes, R Diaz, J R Hampton, J Heikkilä, A Kristinsson, S Moulopoulos, E A Paolasso
Journal: Circulation (1993)

In the prethrombolytic era, women with myocardial infarction were reported to have a worse outcome than men. This analysis evaluates the association of sex with morbidity and mortality after thrombolytic therapy.Data were analyzed from 8261 of the 8387 randomized patients with acute myocardial infarction who received thrombolytic therapy in the International Tissue Plasminogen Activator/Streptokinase Mortality Study (baseline data were missing for 126 patients) and were followed for 6 months. Women made up 23% (n = 1944) of the study population. Baseline characteristics were worse in women: they were 6 years older, were more likely to have a history of previous infarction (P < .01), antecedent angina (P < .01), hypertension (P < .0001), or diabetes (P < .0001); were in a higher Killip class on admission (P < .0002); and received thrombolytic therapy 18 minutes later than men (P < .0001). Fewer women were smokers (P < .0001). Women had a higher hospital (12.1% versus 7.2%, P < .0001) and 6-month mortality (16.6% versus 10.4%, P < .0001) and were more likely to develop cardiogenic shock (9.1% versus 6.3%, P < .0001), bleeding (7.2% versus 5.3%, P < .01), and hemorrhagic (1% versus 0.3%, P < .001) or total stroke (2.2% versus 1.1%, P < .0001) during hospitalization. Reinfarction rates and requirement for angioplasty or surgery did not differ. After correction for worse baseline characteristics, women had similar morbidity and mortality apart from a significantly higher incidence of hemorrhagic stroke, which remained significant even after accounting for weight and treatment allocation (odds ratio, 2.90; P < .01).After thrombolytic therapy for acute myocardial infarction, women have similar morbidity and mortality to men but suffer from a higher incidence of hemorrhagic stroke.
Psychosis and Convulsions Following Withdrawal From Ethchlorvynol
Authors: Monica D. Blumenthal, Melvin J. Reinhart
Journal: JAMA (1964)

AFTER extensive publicity given the addicting properties of barbiturates over the last decade, many physicians have turned to nonbarbiturate sedatives in hopes of avoiding physical and psychological dependence. Unfortunately, more extensive experience in the use of these drugs as long-term daily sedatives, has demonstrated that many which were originally thought to be "safe" are capable of producing drug dependence. We would like to report that ethchlorvynol (Placidyl), or ethyl β-chlorovinyl ethynyl carbinol, may be another example of such a drug. Ethchlorvynol was introduced in 1955 and it was initially thought that it would not produce dependence.<sup>1</sup>The drug was sold for four years without a prescription in Canada, and this policy was not changed until 1959, when Cahn<sup>2</sup>reported four cases of excessive ethchlorvynol intake. Two of his patients showed marked ataxia, accompanied by confusion and disorientation in one patient, and two further patients suffered from withdrawal phenomena
Lineage Infidelity of MDA-MB-435 Cells
Authors: Shankar Sellappan, Rebecca Grijalva, Xiaoyan Zhou, Wentao Yang, Menashe Bar Eli, Gordon B. Mills, Dihua Yu
Journal: Cancer Research (2004)

Abstract The origin of cell lines is critical in defining cell type-specific biological functions. Several reports (D. T. Ross et al., Nat Genet 2000;24:227–35; G. Ellison et al., J Clin Pathol Mol Pathol 2002;55:294–9) suggested that the MDA-MB-435 cell line, a cell line extensively used for studying breast cancer biology, has a gene expression pattern most compatible with melanocyte origin. However, we demonstrate that MDA-MB-435 cells express breast-specific or epithelial-specific markers. Also, MDA-MB-435 cells were induced to express breast differentiation-specific proteins and secrete milk lipids as observed in other well-established breast cancer cell lines. Notably, MDA-MB-435 cells also expressed melanocyte-specific proteins as did another highly aggressive breast cancer cell line. MDA-MB-435 xenograft tissue sections stained entirely positive for epithelium-specific markers but only partially positive for melanocyte-specific markers. Thus, MDA-MB-435 is most likely a breast epithelial cell line that has undergone lineage infidelity.
F-18 FDG PET/CT in Rectal Carcinoma
Authors: Gaia Grassetto, Maria Cristina Marzola, Annamaria Minicozzi, Adil Al-Nahhas, Domenico Rubello
Journal: Clinical Nuclear Medicine (2011)

This short review aims at summarizing the available data pertaining to the usefulness of F-18 FDG PET/CT in rectal cancer. It is specifically focused on the emerging role of F-18 FDG PET/CT in assessing the response to neoadjuvant combined radiochemotherapy in locally advanced rectal cancer. It also probes the possibility of finding standardized PET/CT parameters that are capable of differentiating responders from nonresponders in whom therapeutic approach could be modified.
Invasive Fibrous (Riedel's) Thyroiditis With Bilateral Fibrous Parotitis
Authors: Ralph C. Hines
Journal: JAMA (1970)

Invasive fibrous (Riedel's) thyroiditis is usually insidious in onset with a protracted clinical course. Its etiology is obscure but its occasional acute onset and rapid progression suggest more than one possible cause. It is sometimes associated with similar fibrosclerotic processes in other areas (mediastinum, lungs, orbits, retroperitoneal tissues, common bile duct) in the syndrome of so-called multifocal fibrosclerosis. A patient presented with previously unreported association of Riedel's thyroiditis and bilateral fibrous parotitis.
Exercise Training in Coronary Artery Disease and Coronary Vasomotion
Authors: S. Gielen, G. Schuler, R. Hambrecht
Journal: Circulation (2001)

Exercise training has assumed a major role in cardiac rehabilitation, mostly because of its positive effects on myocardial perfusion in patients with coronary artery disease. The mechanisms involved in mediating this key effect have long been debated: both regression of coronary artery stenosis and improvement of collateralization have been suggested as potential adaptations. However, the comparatively minute changes in luminal diameter and myocardial contrast staining do not fully explain the significant changes in myocardial perfusion. During the last decade, endothelial dysfunction was identified as a trigger of myocardial ischemia. The impaired production of endothelium-derived nitric oxide (NO) in response to acetylcholine and flow leads to paradoxic vasoconstriction and exercise-induced ischemia. Recently, it was confirmed in humans that training attenuates paradoxic vasoconstriction in coronary artery disease and increases coronary blood flow in response to acetylcholine. Data from cell-culture and animal experiments suggest that shear stress acts as a stimulus for the endothelium to increase the transport capacity for L-arginine (the precursor molecule for NO), to enhance NO synthase activity and expression, and to increase the production of extracellular superoxide dismutase, which prevents premature breakdown of NO. Exercise also affects the microcirculation, where it sensitizes resistance arteries for the vasodilatory effects of adenosine. These novel findings provide a pathophysiological framework to explain the improvement of myocardial perfusion in the absence of changes in baseline coronary artery diameter. Because endothelial dysfunction has been identified as a predictor of coronary events, exercise may contribute to the long-term reduction of cardiovascular morbidity and mortality.