tbuckley/cabot-search huggingface dataset:
Editorial: Prostaglandins--tour d'horizon
Authors: S. Vaisrub
Journal: JAMA (1974)

In February, Friday the 13th came on Tuesday, and the news was as expected. Dissident Nobel Laureate Alexander Solzhenitsyn was deprived of his Soviet citizenship and exiled from the country he loved and had striven in vain to improve. A news analyst commented that things hadn't changed much since the USSR was Russia ruled by tsars. The mid-East oil embargo prevailed. Thanks to the French—always a consistent people who had expected to fight World War II with tactics that had prevailed in World War I—a meeting of ministers of state in Washington failed to find a common ground for dealing with a worldwide energy crisis. In Britain, the striking coal miners kept the gloom on, and, ironically, on "The Price Is Right" a charming young woman won a trip for two for a week's stay in London. Israel and Syria were still pounding each other on the Golan Heights. On
Sustained azathioprine-induced remission in Wegener's granulomatosis.
Authors: A R Peermohamed, J Shafar
Journal: BMJ (1969)

It is conceivable, therefore, that the " enhancement " postulated by Floyd et al. (1966) is provided by the action of these two hormones.Turner (1968) has already shown in vitro that the insulinotropic effect of the amino-acid leucine is augmented by pancreozymin, while Ohneda et al. (1968) have recently reported that pancreozymin augments the insulinotropic effect of amino-acids in the dog.Further support for this hypothesis is provided by the present study, in which an increased insulinotropic effect of secretin and pancreozymin occurred in the presence of raised levels of circulating amino-acids.Circumstantial evidence for a significant role of seoretin and pancreozymin in the insulin response to protein, but not in response to glucose, may be adduced from the work of Estrich et al. (1967).These workers observed the effects of several oral test loads and could find no difference between the mean plasma insulin and glucose response to carbohydrate alone or to carbohydrate plus fat, yet fat is also known to stimulate secretin and pancreozymin release (Wang and Grossman, 1951).Carbo- hydrate plus protein, however, was associated with a significantly greater insulin but a lesser glucose response than a carbohydrate load alone, suggesting that the augmenting effect of intestinal hormones on insulin release occurs only in the presence of raised levels of plasma amino-acids.This inter- pretation of the role of these hormones is consistent with the failure to observe any effects of endogenous secretin and pancreozymin on glucose-induced insulin release, when intra- duodenal hydrochloric acid at physiological concentration was used as the secretory stimulus (Boyns et al., 1967; Mahler and Weisberg, 1968) and with the failure of intraduodenal infu- sions of glucose to affect external pancreatic secretion (Sum and Preshaw, 1967).
Life Imprints: Living in a Contaminated World
Authors: David Crews, Andrea C. Gore
Journal: Environmental Health Perspectives (2011)

Background: The links between nature and nurture need to be redefined to accommodate anthropogenic chemical contamination. Although some local remediation of contamination has occurred, at the global level this is simply not possible. Contaminants are spread by population migration, by introduction via the food chain, and through air and water currents, even to regions that were never exposed directly to these environmental insults. In recognizing and accepting this worldwide change, we must move on and consider the types of adaptations that could occur as a consequence.Objectives: We propose a paradigm shift in the field that integrates various disciplines involved in the study of environmental contamination to recognize that contamination is widespread and cannot be remedied at the global level.Discussion: Greater effort must be placed on integrative and interdisciplinary studies that explicitly illuminate how the causal mechanisms and functional outcomes of related processes operate at each level of biological organization while at the same time revealing the relations among the levels.Conclusions: To anticipate and understand the future, we must devote more study to what is likely to happen and less to what has happened. Only then will we begin to understand how ancestral environmental exposures act at both the level of the individual and the level of their descendants to influence all aspects of life history.
Rheumatic Fever and Rheumatic Heart Disease in Barbados: Detection and Prophylaxis
Authors: T. A. Hassell, S. Renwick, K. L. Stuart
Journal: BMJ (1972)

The objectives of this study were to improve our methods of secondary prophylaxis of rheumatic fever and rheumatic heart disease in Barbados, to estimate the overall prevalence of these diseases and the relative load imposed by them on available health services, and to measure the yield, feasibility, and effectiveness of mass programmes for the detection and prophylactic management of rheumatic heart disease in schoolchildren.Improved methods of surveillance and follow-up resulted in 97% adherence to therapy by patients on prophylactic penicillin. Thirty-four children, 27 with a first attack, were admitted with acute rheumatic fever, representing a 7% occupancy of children's medical beds during the 12-month period of the study. Out of a possible 3,942 schoolchildren aged 5-11 years, 3,882 (98%) were screened for rheumatic heart disease. Four cases (about 1 per 1,000) were discovered.
In Vitro Studies of Phospholipid Synthesis in Experimental Atherosclerosis
Authors: FRANK PARKER, JOHN W. ORMSBY, NORMAN F. PETERSON, GEORGE F. ODLAND, ROBERT H. WILLIAMS
Journal: Circulation Research (1966)

Using in vitro techniques and labeled linoleic acid and glucose, alterations in phospholipid synthesis in the aorta were correlated with electron microscopic studies at various intervals of time after feeding rabbits cholesterol. After 4 to 8 weeks of feeding, more phospholipid precursors were incorporated into the phospholipids of atherosclerotic blood vessels than of normal vessels. Concomitant with the metabolic alterations, the following ultrastructural changes occur. Smooth muscle cells of the plaque (myo-intimal cells) evolve into highly vacuolated cells containing a profusion of cytoplasmic organelles. The increase in membranous organelles suggests that the increase in phospholipid synthesis may be the result of a cellular requirement for increased intracytoplasmic structural phospholipid.
Women's Primary Health Care
Authors: Carolyn M. Clancy
Journal: JAMA (1996)

<i>Women's Primary Health Care</i>, edited by Vicki Seltzer and Warren Pearse, begins with a brief preface that carefully sidesteps the question of target audience. Instead, the editors have chosen to observe that clinicians of many disciplines provide and contribute to women's primary care: primary and preventive ambulatory health care needs of women are "as important for the subspecialist as for the generalist." This apparently diplomatic approach is ultimately both a strength and a weakness. It allows inclusion of a comprehensive array of topics relevant to women's primary care, but most chapters offer a superficial, although broad, overview of the subject at hand. This strategy begs the question of why a textbook on women's primary care at all? The main text has seven major parts. Part 1 includes tables of the leading causes of morbidity and mortality for women by age group, recommended preventive health interventions with a clear emphasis on
Cell calcium in the pathophysiology of ventricular fibrillation and in the pathogenesis of postarrhythmic contractile dysfunction.
Authors: Y Koretsune, E Marban
Journal: Circulation (1989)

The mechanism of ventricular fibrillation is poorly understood at the cellular level. We explored the role of intracellular free calcium in the pathophysiology and pathogenesis of ventricular fibrillation in perfused ferret hearts loaded with the Ca2+ indicator 5F-BAPTA. Nuclear magnetic resonance spectroscopy was used to measure [Ca2+]i, pH, and high-energy phosphates. During ventricular fibrillation induced by burst pacing, [Ca2+]i rose rapidly and dramatically, exceeding by four times the control within 5 minutes. [Ca2+]i remained markedly elevated throughout 20 minutes of fibrillation, but it returned to control values shortly after defibrillation. In a group of hearts kept isovolumic by a balloon in the left ventricle, acidosis and high-energy phosphate depletion developed despite the maintenance of normal coronary pressure. To distinguish the effects of superimposed ischemia from those of the arrhythmia itself, we lowered left ventricular volume during fibrillation in a second group of hearts. This maneuver decreased wall stress such that fibrillation had no significant adverse effect on intracellular pH, high-energy phosphates, or lactate efflux. [Ca2+]i still increased remarkably despite the absence of ischemic changes. Developed pressure did not recover to control levels after defibrillation in either group; the hearts appeared "stunned." We conclude that intracellular calcium increases as a direct consequence of ventricular fibrillation. The increase in [Ca2+]i may cause the contractile dysfunction observed in postarrhythmic hearts. Its possible role in initiating or maintaining the arrhythmia is less clear.
Evaluation of Surrogate Markers of Atherosclerosis in Patients with Venous Thromboembolism
Authors: Ahmet Kaya, Eftal Bakırcı, Zeki Yüksel Günaydın, Ali Bekir Kurt, Kamuran Kalkan, Selim Topçu, İbrahim Halil Tanboğa
Journal: Journal of the American College of Cardiology (2013)
Small molecule BDNF mimetics activate TrkB signaling and prevent neuronal degeneration in rodents
Authors: Stephen M. Massa, Tao Yang, Youmei Xie, Jian Shi, Mehmet Bilgen, Jeffrey N. Joyce, Dean Nehama, Jayakumar Rajadas, Frank M. Longo
Journal: Journal of Clinical Investigation (2010)

Brain-derived neurotrophic factor (BDNF) activates the receptor tropomyosin-related kinase B (TrkB) with high potency and specificity, promoting neuronal survival, differentiation, and synaptic function. Correlations between altered BDNF expression and/or function and mechanism(s) underlying numerous neurodegenerative conditions, including Alzheimer disease and traumatic brain injury, suggest that TrkB agonists might have therapeutic potential. Using in silico screening with a BDNF loop–domain pharmacophore, followed by low-throughput in vitro screening in mouse fetal hippocampal neurons, we have efficiently identified small molecules with nanomolar neurotrophic activity specific to TrkB versus other Trk family members. Neurotrophic activity was dependent on TrkB and its downstream targets, although compound-induced signaling activation kinetics differed from those triggered by BDNF. A selected prototype compound demonstrated binding specificity to the extracellular domain of TrkB. In in vitro models of neurodegenerative disease, it prevented neuronal degeneration with efficacy equal to that of BDNF, and when administered in vivo, it caused hippocampal and striatal TrkB activation in mice and improved motor learning after traumatic brain injury in rats. These studies demonstrate the utility of loop modeling in drug discovery and reveal what we believe to be the first reported small molecules derived from a targeted BDNF domain that specifically activate TrkB.We propose that these compounds constitute a novel group of tools for the study of TrkB signaling and may provide leads for developing new therapeutic agents for neurodegenerative diseases.
Percutaneous Coronary Intervention and Drug-Eluting Stent Use Among Patients ≥85 Years of Age in the United States
Authors: Tracy Y. Wang, Frederick A. Masoudi, John C. Messenger, Kendrick A. Shunk, Andrew Boyle, J. Matthew Brennan, H. Vernon Anderson, Kevin J. Anstrom, David Dai, Eric D. Peterson, Pamela S. Douglas, John S. Rumsfeld
Journal: Journal of the American College of Cardiology (2012)
Properly designed trials
Authors: S. Jotkovitz
Journal: JAMA (1977)

<h3>In Reply.—</h3> Dr Wilkinson's comments raise an important factor in the treatment of status epilepticus: the potential danger of therapy due to the narrow margin of safety between therapeutic and lethal doses of anticonvulsants. All the drugs used to treat status epilepticus can be lethal if they are given in overdosage or too rapidly. Careful monitoring of respiration and cardiac function must be carried out during the administration of anticonvulsants. Any drug administered intravenously should be given slowly. The possibility of cardiac or respiratory arrest must be considered in every case and appropriate precautions taken. The physician must be prepared to resuscitate the patient. Drugs are not the only cause of cardiac system depression; the convulsive status per se often causes death by sudden cardiovascular collapse.<sup>1</sup> Dr Wilkinson's anecdotal description of his experience may lead to misinterpretation. Amobarbital sodium, as well as secobarbital sodium and hexobarbital, have been used
Silencing of miR-101 Prevents Cartilage Degradation by Regulating Extracellular Matrix–related Genes in a Rat Model of Osteoarthritis
Authors: Linghui Dai, Xin Zhang, Xiaoqing Hu, Qiang Liu, Zhentao Man, Hongjie Huang, Qingyang Meng, Chunyan Zhou, Yingfang Ao
Journal: Molecular Therapy (2015)

Osteoarthritis (OA) is a common, degenerative joint disease characterized by articular cartilage degradation. Currently, clinical trials based on microRNA therapy have been performed to treat various diseases. However, no treatment has been found for arthritis. This study investigated the functions of miR-101 in cartilage degradation in vivo and evaluated the feasibility of using miR-101 as a therapeutic agent for OA. Mono-iodoacetate-induced arthritis (MIA) rats were used as an animal model of OA. miR-101 mimic or miR-101 inhibitor was injected into the rats' knees to evaluate its effects on cartilage degradation. Cartilage degradation aggravated at 14 days after the injection of miR-101 mimic. By contrast, miR-101 silencing reduced cartilage degradation. Moreover, the administration of miR-101 mimic is sufficient to cause cartilage degradation in the normal cartilage of rats. By contrast, miR-101 inhibitor could prevent this change. Microarray and qPCR were used to investigate the different expressed genes after injecting miR-101 mimic and miR-101 inhibitor in the rats' articular cartilage. Several cartilage degradation-related genes were selected and validated to function in cartilage degradation with miR-101. Our results demonstrated the therapeutic effect of miR-101 inhibition on cartilage degradation in MIA rats by regulating several cartilage degradation–related genes. Osteoarthritis (OA) is a common, degenerative joint disease characterized by articular cartilage degradation. Currently, clinical trials based on microRNA therapy have been performed to treat various diseases. However, no treatment has been found for arthritis. This study investigated the functions of miR-101 in cartilage degradation in vivo and evaluated the feasibility of using miR-101 as a therapeutic agent for OA. Mono-iodoacetate-induced arthritis (MIA) rats were used as an animal model of OA. miR-101 mimic or miR-101 inhibitor was injected into the rats' knees to evaluate its effects on cartilage degradation. Cartilage degradation aggravated at 14 days after the injection of miR-101 mimic. By contrast, miR-101 silencing reduced cartilage degradation. Moreover, the administration of miR-101 mimic is sufficient to cause cartilage degradation in the normal cartilage of rats. By contrast, miR-101 inhibitor could prevent this change. Microarray and qPCR were used to investigate the different expressed genes after injecting miR-101 mimic and miR-101 inhibitor in the rats' articular cartilage. Several cartilage degradation-related genes were selected and validated to function in cartilage degradation with miR-101. Our results demonstrated the therapeutic effect of miR-101 inhibition on cartilage degradation in MIA rats by regulating several cartilage degradation–related genes.
Abstract 167: Myricetin suppresses UVB-induced photoaging, skin cancer, and angiogenesis by targeting multiple kinases
Authors: Sung Keun Jung, Ki Won Lee, Ann M. Bode, Hyong Joo Lee, Zigang Dong
Journal: Cancer Research (2012)

Abstract Chronic exposure to solar ultraviolet is a major cause of photoaging and skin carcinogenesis. In the present study, we investigated the effect of myricetin on UVB-induced photoaging, skin cancer, and angiogenesis in JB6 P+ cells and a mouse skin tumorigenesis model. Myricetin inhibited wrinkle formation induced by UVB irradiation (0.18 J/cm2, 3 days/week for 15 weeks) in mouse skin. Myricetin treatment reduced UVB-induced epidermal thickening of mouse skin and also suppressed UVB-induced matrix metalloproteinase-9 (MMP-9) protein expression and enzyme activity. In vitro and in vivo pull-down and kinase assays revealed that myricetin suppressed Raf activity by binding with Raf. Secondly, myricetin suppressed UVB-induced COX-2 expression and mitogen-activated protein kinases in JB6 P+ cells and mouse skin. Pull-down and kinase assay results showed that myricetin directly inhibited UVB-induced Fyn kinase activity by binding with Fyn in an ATP-competitive manner. Mouse skin tumorigenesis data clearly showed that pretreatment with myricetin significantly suppressed UVB-induced skin tumor incidence in a dose-dependent manner. Topical treatment with myricetin suppressed repetitive UVB-induced neovascularization in the SKH-1 hairless mouse skin. The induction of vascular endothelial growth factor, matrix metalloproteinase (MMP)-9 and MMP-13 expression by chronic UVB irradiation was substantially suppressed by myricetin treatment. Immunohistochemical and Western blot analyses revealed that myricetin attenuated UVB-induced hypoxia inducible factor-1alpha expression in mouse skin. In vivo kinase and pull down assay data revealed that myricetin suppressed UVB-induced phosphatidylinositol 3 (PI3)-kinase activity by direct binding with PI3-kinase. Overall, together these results suggest that the anti-photoaging, anti-skin carcinogenesis, and anti-angiogenesis effects of myricetin are due to mainly targeting Raf, Fyn, and PI3-K, respectively. 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 167. doi:1538-7445.AM2012-167
Annual incidence of MRSA falls in England, but <i>C difficile</i> continues to rise
Authors: Helen Mooney
Journal: BMJ (2007)

Recent publications on commercial porcine bioprosthetic cardiac valves have stated that the endothelium disappears during the glutaraldehyde processing and that in many cases histological evidence of early tissue deterioration was found. Our experiences have shown that porcine aortic valves can be processed in glutaraldehyde without loss of the integrity of the endothelium and with the development of optimum collagen fibre structure. The valve mounted in a Dacron tube is not restricted in diameter and performs well under biological conditions up to a period of six months.
581 QUANTITATIVE LONGITUDINAL EVALUATION OF HEPATITIS DELTA VIRUS RNA AND HEPATITIS B VIRUS DNA SHOWS A DYNAMIC COMPLEX REPLICATIVE PROFILE IN CHRONIC B/D COINFECTION
Authors: D. Tabernero, M. Schaper, F. Rodríguez-Frías, R. Jardi, M. Homs, G. Ruiz, M. Buti-Ferret, R. Esteban
Journal: Journal of Hepatology (2009)
Use of Prophylactic Antibiotics for Prevention of Intravascular Catheter-Related Infections in Interleukin-2-Treated Patients
Authors: L. C. HARTMANN, W. J. URBA, R. G. STEIS, J. W. SMITH, L. A. VANDERMOLEN, S. P. CREEKMORE, M. SZNOL, M. A. CASCIANO, N. ENGLER, D. L. LONGO
Journal: JNCI Journal of the National Cancer Institute (1989)

Journal Article Use of Prophylactic Antibiotics for Prevention of Intravascular Catheter-Related Infections in Interleukin-2-Treated Patients Get access LYNN C. HARTMANN, LYNN C. HARTMANN Program Resources, Inc. NCI-Frederick Cancer, Research FacilityFrederick, MD Search for other works by this author on: Oxford Academic PubMed Google Scholar WALTER J. URBA, WALTER J. URBA Program Resources, Inc. NCI-Frederick Cancer, Research FacilityFrederick, MD Search for other works by this author on: Oxford Academic PubMed Google Scholar RONALD G. STEIS, RONALD G. STEIS Biological Response Modifiers Program Division of Cancer Treatment National Cancer Institute NCI-Frederick Cancer Research Facility Search for other works by this author on: Oxford Academic PubMed Google Scholar JOHN W. SMITH, II, JOHN W. SMITH, II Biological Response Modifiers Program Division of Cancer Treatment National Cancer Institute NCI-Frederick Cancer Research Facility Search for other works by this author on: Oxford Academic PubMed Google Scholar LOUIS A. VANDERMOLEN, LOUIS A. VANDERMOLEN Biological Response Modifiers Program Division of Cancer Treatment National Cancer Institute NCI-Frederick Cancer Research Facility Search for other works by this author on: Oxford Academic PubMed Google Scholar STEPHEN P. CREEKMORE, STEPHEN P. CREEKMORE Biological Response Modifiers Program Division of Cancer Treatment National Cancer Institute NCI-Frederick Cancer Research Facility Search for other works by this author on: Oxford Academic PubMed Google Scholar MARIO SZNOL, MARIO SZNOL Cancer Therapy Evaluation Program Division of Cancer Treatment National Cancer InstituteBethesda, MD Search for other works by this author on: Oxford Academic PubMed Google Scholar MANUEL A. CASCIANO, MANUEL A. CASCIANO Frederick Memorial HospitalFrederick, MD Search for other works by this author on: Oxford Academic PubMed Google Scholar NANCY ENGLER, NANCY ENGLER Frederick Memorial HospitalFrederick, MD Search for other works by this author on: Oxford Academic PubMed Google Scholar DAN L. LONGO DAN L. LONGO * *Correspondence to: Dr. Dan L. Longo, Biological Response Modifiers Program, Division of Cancer Treatment, National Cancer Institute, NCI-Frederick Cancer Research Facility, Bldg, 567, Rm 135, Frederick, MD 21701. Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 81, Issue 15, 2 August 1989, Pages 1190–1193, https://doi.org/10.1093/jnci/81.15.1190 Published: 02 August 1989