tbuckley/cabot-search huggingface dataset:
Hospital Liability for Physician Negligence
Authors: William B. Smith
Journal: JAMA (1984)

ONCE upon a time, the law recognized that hospitals were places in which physicians practiced medicine. The hospital merely furnished the facilities for the treatment that independent practitioners provided to their patients. If the physician's treatment was not up to the standard of care of the medical profession, he alone might be liable to the patient. This article will attempt to show how our society—and American law—has departed from that former state of affairs. Hospitals have always been liable for their own negligence and the negligence of their employees. The hospital has always had the legal obligation to maintain its equipment and facilities in good condition and efficient working order. Thus, when defective equipment or supplies used in the hospital injured the patient, the hospital could be held liable. Over the years hospital equipment has become more complex, more powerful, and more sophisticated, thus requiring more careful use and maintenance.
Distinct restitution properties in vagally mediated atrial fibrillation and six-hour rapid pacing-induced atrial fibrillation
Authors: Z. Lu, B. Cui, B. He, X. Hu, W. Wu, L. Wu, C. Huang, S. S. Po, H. Jiang
Journal: Cardiovascular Research (2010)

The atrial potential duration (APD) restitution has been suggested to play an important role in ventricular fibrillation; however, its role in atrial fibrillation (AF) has not been determined. This study sought to investigate the APD restitution properties in two different AF models: vagally mediated AF and 6-h rapid atrial pacing-induced AF. Twenty anaesthetized open-chest dogs were assigned to Group I, vagally mediated AF (n= 8) or Group II, 6-h rapid atrial pacing-induced AF (n= 12). In both groups, the monophasic APD was subsequently recorded at multiple pulmonary vein and atrial sites. The APD restitution curve was constructed using a dynamic pacing protocol and determined by plotting each APD90 against the preceding diastolic interval at incremental atrial pacing rates at eight sites. In Group I, vagal stimulation significantly shortened the APD90, flattened the APD restitution curve (slopes <1), and suppressed the APD alternans at each site, while increasing the AF inducibility and duration (P<0.05 for all). In Group II, 6-h rapid pacing-induced APD shortening steepened the restitution curves (slopes >1), facilitated the APD alternans, and also increased the incidence and duration of AF (P< 0.05 for all). The spatial dispersion of APD restitution was significantly increased in both groups. This study showed distinct atrial APD restitution properties in vagally mediated AF and 6-h rapid pacing-induced AF, indicating specific restitution kinetics in different mechanisms of AF.
An Iron-Binding Exochelin Prevents Restenosis Due to Coronary Artery Balloon Injury in a Porcine Model
Authors: Eli A. Rosenthal, Teri J. Bohlmeyer, Eric Monnet, Catriona MacPhail, Alastair D. Robertson, Marcus A. Horwitz, J.E.B. Burchenal, Lawrence D. Horwitz
Journal: Circulation (2001)

Background- Vascular smooth muscle cell (VSMC) proliferation is a critical factor in the neointima formation that causes restenosis after coronary angioplasty (PTCA). Desferri-exochelin 772SM (D-EXO), a highly diffusible, lipophilic iron chelator secreted by Mycobacterium tuberculosis, inhibits proliferation of VSMCs in culture. We hypothesized that treatment with D-EXO would inhibit neointima formation in balloon-injured vessels in vivo. Methods and Results- We subjected 24 pigs to overstretch coronary artery injury with standard PTCA balloons and then administered intramural injections of either D-EXO (n=14) or vehicle (n=10) through an Infiltrator catheter. Treatments were randomized, and the investigators were blinded with regard to treatment group until data analysis was completed. One month later, we euthanized the pigs, excised the injured coronary segments, made multiple sections of each segment, and identified the site of maximal neointima formation. An injury score based on the degree of disruption of the internal or external elastic lamina or media was assigned. D-EXO reduced stenosis index (neointima area divided by the area within the internal elastic lamina), adjusted for injury score, by 47%. Neointima thickness was also reduced. Conclusions- D-EXO, injected intramurally, substantially inhibited formation of neointima in a porcine vascular injury model.
ETC-1002, A MODULATOR OF ADENOSINE MONOPHOSPHATE-ACTIVATED PROTEIN KINASE AND ADENOSINE TRIPHOSPHATE-CITRATE LYASE, WAS SAFE AND REDUCED LOW-DENSITY LIPOPROTEIN-CHOLESTEROL IN HEALTHY VOLUNTEERS
Authors: Diane MacDougall, James Vanderlugt, Noah Rosenberg, Lorenzo DiCarlo, Mark Milad, Janice Margulies, Roger Newton
Journal: Journal of the American College of Cardiology (2013)
Drug-Eluting versus Bare-Metal Stents in Large Coronary Arteries
Authors: Christoph Kaiser, Soeren Galatius, Paul Erne, Franz Eberli, Hannes Alber, Hans Rickli, Giovanni Pedrazzini, Burkhard Hornig, Osmund Bertel, Piero Bonetti, Stefano De Servi, Hans-Peter Brunner-La Rocca, Ingrid Ricard, Matthias Pfisterer
Journal: New England Journal of Medicine (2010)

Recent data have suggested that patients with coronary disease in large arteries are at increased risk for late cardiac events after percutaneous intervention with first-generation drug-eluting stents, as compared with bare-metal stents. We sought to confirm this observation and to assess whether this increase in risk was also seen with second-generation drug-eluting stents.We randomly assigned 2314 patients needing stents that were 3.0 mm or more in diameter to receive sirolimus-eluting, everolimus-eluting, or bare-metal stents. The primary end point was the composite of death from cardiac causes or nonfatal myocardial infarction at 2 years. Late events (occurring during months 7 to 24) and target-vessel revascularization were the main secondary end points.The rates of the primary end point were 2.6% among patients receiving sirolimus-eluting stents, 3.2% among those receiving everolimus-eluting stents, and 4.8% among those receiving bare-metal stents, with no significant differences between patients receiving either drug-eluting stent and those receiving bare-metal stents. There were also no significant between-group differences in the rate of late events or in the rate of death, myocardial infarction, or stent thrombosis. Rates of target-vessel revascularization for reasons unrelated to myocardial infarction were 3.7% among patients receiving sirolimus-eluting stents, 3.1% among those receiving everolimus-eluting stents, and 8.9% among those receiving bare-metal stents. The rate of target-vessel revascularization was significantly reduced among patients receiving either drug-eluting stent, as compared with a bare-metal stent, with no significant difference between the two types of drug-eluting stents.In patients requiring stenting of large coronary arteries, no significant differences were found among sirolimus-eluting, everolimus-eluting, and bare-metal stents with respect to the rate of death or myocardial infarction. With the two drug-eluting stents, similar reductions in rates of target-vessel revascularization were seen. (Funded by the Basel Cardiovascular Research Foundation and the Swiss National Foundation for Research; Current Controlled Trials number, ISRCTN72444640.).
99 BASELINE PREDICTIVE FACTORS OF URSODEOXYCHOLIC ACID RESPONSE IN PRIMARY BILIARY CIRRHOSIS
Authors: M. Carbone, G. Mells, H.J. Cordell, M.A. Heneghan, J.M. Neuberger, P.T. Donaldson, A.J. Bathgate, A.K. Burroughs, M.H. Davies, D.B. Day, M.F. Dawwas, S. Thomson, G.J. Alexander, D.E. Jones, R.N. Sandford
Journal: Journal of Hepatology (2013)
Brief Communication: Physical Abuse of Boys and Possible Associations with Poor Adult Outcomes
Authors: William C. Holmes, Mary D. Sammel
Journal: Annals of Internal Medicine (2005)

Background: Men's childhood physical abuse experiences are understudied. Objective: To obtain descriptions about men's personal childhood physical abuse histories and estimate their association with adult outcomes. Design: Population-based telephone survey. Setting: Urban areas with high frequency of domestic violence against girls and women. Participants: 298 men recruited through random-digit dialing. Measurements: 6 Conflict Tactics Scale items and psychiatric, sexual, and legal history questions. Results: One hundred of 197 (51%) participants had a history of childhood physical abuse. Most (73%) participants were abused by a parent. Childhood physical abuse history was associated with depression symptoms (P = 0.003), post-traumatic stress disorder symptoms (P < 0.001), number of lifetime sexual partners (P = 0.035), legal troubles (P = 0.002), and incarceration (P = 0.007) in unadjusted analyses and with depression symptoms (P = 0.015) and post-traumatic stress disorder symptoms (P = 0.003) in adjusted analyses. Limitations: There may have been inaccurate recall of past events. Lack of exposure time data disallowed direct comparison of abuse perpetration by mothers versus fathers. Other unmeasured variables related to childhood physical abuse might better explain poor adult outcomes. Conclusions: The high frequency of childhood physical abuse histories in this population-based male sample, coupled with the high proportion of parent perpetrators and the association between childhood physical abuse and adult outcomes that are often associated with perpetration of violence, argues for more study of and clinical attentiveness to potential adult outcomes of men's own childhood physical abuse histories.
Does the Functional Efficacy of Skeletal Myoblast Transplantation Extend to Nonischemic Cardiomyopathy?
Authors: Julia Pouly, Albert Hagège, Jean-Thomas Vilquin, Alvine Bissery, Andrée Rouche, Patrick Bruneval, Denis Duboc, Michel Desnos, Marc Fiszman, Yves Fromes, Philippe Menasché
Journal: Circulation (2004)

The benefits of skeletal myoblast (SM) transplantation on infarcted myocardium have been investigated extensively; however, little is known about its effects in nonischemic cardiomyopathy models. To address this issue, we tested SM transplantation in CHF147 Syrian hamsters, a strain characterized by a delta-sarcoglycan deficiency that phenotypically features the human setting of primary dilated cardiomyopathy.Cell culture techniques were used to prepare approximately 5x10(6) muscle cells from autologous tibialis anterior muscle, of which 50% were SMs (desmin staining). The cells were injected in 6 sites across the left ventricular wall (n=14). Control animals (n=12) received equivalent volumes of culture medium. Left ventricular systolic function was assessed in a blinded fashion from 2D echocardiographic left ventricular fractional area change, before transplantation, and 4 weeks later. Explanted hearts were processed for the detection of myotubes and quantification of fibrosis. Baseline functional data did not differ between the 2 groups. Four weeks after transplantation, 6 of the 10 surviving grafted hamsters were improved compared with 0 of the 8 survivors of the control group. This translated into a 6% decrease in fractional area change in controls compared with a 24% increase in cell-transplanted hamsters (P=0.001). Engrafted myotubes were consistently detected in all SM transplanted hearts by immunohistochemistry, whereas fibrosis was not worsened by cell injections.These data suggest that the functional benefits of SM transplantation might extend to nonischemic cardiomyopathy.
Ambulatory Monitoring Detects Sorafenib-Induced Blood Pressure Elevations on the First Day of Treatment
Authors: Michael L. Maitland, Kristen E. Kasza, Theodore Karrison, Kristin Moshier, Laura Sit, Henry R. Black, Samir D. Undevia, Walter M. Stadler, William J. Elliott, Mark J. Ratain
Journal: Clinical Cancer Research (2009)

Hypertension is a mechanism-based toxicity of sorafenib and other cancer therapeutics that inhibit the vascular endothelial growth factor (VEGF) signaling pathway. This prospective, single-center, cohort study characterized ambulatory blood pressure monitoring as an early pharmacodynamic biomarker of VEGF signaling pathway inhibition by sorafenib.Fifty-four normotensive advanced cancer patients underwent 24-hour ambulatory blood pressure monitoring before and between days 6 and 10 of sorafenib therapy. After blood pressure changes were detected among the first cohort within 10 days, ambulatory blood pressure monitoring was done during the first 24 hours of treatment for the second cohort.For the entire patient population, the blood pressure increase [mean systolic, +10.8 mm Hg; 95% confidence interval (95% CI), 8.6-13.0; range, -5.2 to +28.7 mm Hg; mean diastolic, +8.0 mm Hg; 95% CI, 6.3-9.7; range, -4.4 to +27.1 mm Hg] was detected between days 6 and 10 (P < 0.0001 for both) and plateaued thereafter. Variability in blood pressure change did not associate with: age, body size, sex, self-reported race, baseline blood pressure, or steady-state sorafenib plasma concentrations. In the second cohort, the blood pressure elevation was detected during the first 24 hours (mean systolic, +8.2 mm Hg; 95% CI, 5.0-11.3; mean diastolic, +6.5 mm Hg; 95% CI, 4.7-8.3; P < 0.0001 for both).Ambulatory blood pressure monitoring detects the blood pressure response to VEGF signaling pathway inhibition by sorafenib during the first 24 hours of treatment. The magnitude of blood pressure elevation is highly variable and unpredictable but could be important in optimizing the therapeutic index of VEGF signaling pathway inhibitor therapy.
Induction of endoplasmic reticulum stress and apoptosis by a marine prostanoid in human hepatocellular carcinoma
Authors: Po-Cheng Chiang, Chung-Liang Chien, Shiow-Lin Pan, Wen-Pin Chen, Che-Ming Teng, Ya-Ching Shen, Jih-Hwa Guh
Journal: Journal of Hepatology (2005)
First-line assessment of patients with chronic liver disease with non-invasive techniques and without recourse to liver biopsy
Authors: Thierry Poynard
Journal: Journal of Hepatology (2010)

It was initially an error that led me to develop non-invasive biomarkers of liver diseases [1]. After perforating the gallbladder of a friend in 1990, I wished that one day the assessment of patients with chronic liver disease could be carried out rapidly with noninvasive techniques and without the use of a liver biopsy. My first biomarker had no industrial development [2] but the others thereafter had professional developments, such as FibroTest with 500,000 tests prescribed worldwide in the last 7 years [3]. Twenty years later, it seems that there is little controversy concerning the utility of the most validated biomarkers versus biopsy [4–6]. Over the last 7 years, the opinions of more than 50 leaders from Nid Afdhal [7] to Vlad Ratziu [8] have been published on these biomarkers. From the evidence-based data, I will summarize my understanding of the main points of agreement and disagreement in 2010 and the main priorities for the years ahead.
Uptake and mitochondrial dysfunction of alpha-synuclein in human astrocytes, cortical neurons and fibroblasts
Authors: Nady Braidy, Wei-Ping Gai, Ying Hua Xu, Perminder Sachdev, Gilles J Guillemin, Xing-Mai Jiang, J William O Ballard, Martin P Horan, Zhi Ming Fang, Beng H Chong, DanielKam Yin Chan
Journal: Translational Neurodegeneration (2013)

Abstract The accumulation and aggregation of alpha-synuclein (α-syn) in several tissue including the brain is a major pathological hallmark in Parkinson’s disease (PD). In this study, we show that α-syn can be taken up by primary human cortical neurons, astrocytes and skin-derived fibroblasts in vitro . Our findings that brain and peripheral cells exposed to α-syn can lead to impaired mitochondrial function, leading to cellular degeneration and cell death, provides additional evidence for the involvement of mitochondrial dysfunction as a mechanism of toxicity of α-syn in human cells.
Thymus transplantation in complete DiGeorge syndrome: immunologic and safety evaluations in 12 patients
Authors: M. Louise Markert, Marcella Sarzotti, Daniel A. Ozaki, Gregory D. Sempowski, Maria E. Rhein, Laura P. Hale, Francoise Le Deist, Marilyn J. Alexieff, Jie Li, Elizabeth R. Hauser, Barton F. Haynes, Henry E. Rice, Michael A. Skinner, Samuel M. Mahaffey, James Jaggers, Leonard D. Stein, Michael R. Mill
Journal: Blood (2003)
Hepatic stimulator substance protects against acute liver failure induced by carbon tetrachloride poisoning in mice
Authors: Mei Mao-Hua, An Wei, Zhang Bao-Hong, Shao Qing, Gong De-Zheng
Journal: Hepatology (1993)

Hepatic stimulator substance was extracted from the liver of weanling Sprague-Dawley rats according to the method of LaBrecque. Quang-Ming mice were injected with carbon tetrachloride to induce acute liver failure. Hepatic stimulator substance suppressed the elevation of ALT and AST induced by carbon tetrachloride in a dose-dependent manner. Hepatic histological changes indicated that hepatic stimulator substance reduced the severity of hepatic lesion induced by carbon tetrachloride and reversed carbon tetrachloride-induced reduction of hepatic mitochondrial succinic dehydrogenase activity. In attempting to elucidate the mechanism or mechanisms of this protective effect, we found that hepatic stimulator substance significantly restored the carbon tetrachloride-induced decrease of hepatocyte plasmalemma and mitochondrial and microsomal membrane fluidity. Hepatic stimulator substance also decreased the malondialdehyde content of carbon tetrachloride-intoxicated mice; restored the liver-reduced glutathione content, which was lowered by carbon tetrachloride intoxication; stimulated liver regeneration, as shown by enhanced DNA synthesis; and increased the H-thymidine incorporation into DNA of hepatocytes. We propose that hepatic stimulator substance protects the liver against acute liver failure induced by carbon tetrachloride poisoning, probably by an antioxidative effect on hepatocyte membrane lipid peroxidation, which was increased by free radicals produced from carbon tetrachloride. In addition, hepatic stimulator substance stimulates hepatocyte proliferation. These protective mechanisms may act in concert to protect against carbon tetrachloride injury. (Hepatology 1993;17:638-644.)
Neurodegenerative changes initiated by presynaptic dysfunction
Authors: Toru Yasuda, Yasuto Nakata, Chi-Jing Choong, Hideki Mochizuki
Journal: Translational Neurodegeneration (2013)

α-Synucleinopathies are a subgroup of neurodegenerative diseases including dementia with Lewy bodies (DLB) and Parkinson's disease (PD). Pathologically, these disorders can be characterized by the presence of intraneuronal aggregates composed mainly of α-synuclein (αSyn), which are called Lewy bodies and Lewy neurites. Recent report showed that more than 90% of αSyn aggregates are present in the form of very small deposits in presynaptic terminals of the affected neurons in DLB. However, the mechanisms responsible for presynaptic accumulation of abnormal αSyn remain unclear. In this article, we review recent findings on the involvement of presynaptic dysfunction in the initiation of neuronal dysfunctional changes. This review highlights that the presynaptic failure can be a potential trigger of the dying-back neuronal death in neurodegenerative diseases.
Suppression of Lymphoma and Epithelial Malignancies Effected by Interferon γ
Authors: Shayna E.A. Street, Joseph A. Trapani, Duncan MacGregor, Mark J. Smyth
Journal: The Journal of Experimental Medicine (2002)

The immunosurveillance of transformed cells by the immune system remains one of the most controversial and poorly understood areas of immunity. Gene-targeted mice have greatly aided our understanding of the key effector molecules in tumor immunity. Herein, we describe spontaneous tumor development in gene-targeted mice lacking interferon (IFN)-γ and/or perforin (pfp), or the immunoregulatory cytokines, interleukin (IL)-12, IL-18, and tumor necrosis factor (TNF). Both IFN-γ and pfp were critical for suppression of lymphomagenesis, however the level of protection afforded by IFN-γ was strain specific. Lymphomas arising in IFN-γ-deficient mice were very nonimmunogenic compared with those derived from pfp-deficient mice, suggesting a comparatively weaker immunoselection pressure by IFN-γ. Single loss of IL-12, IL-18, or TNF was not sufficient for spontaneous tumor development. A significant incidence of late onset adenocarcinoma observed in both IFN-γ– and pfp-deficient mice indicated that some epithelial tissues were also subject to immunosurveillance.
Report of the Medical Schools Section Primary Care Task Force
Authors: George T. Bryan
Journal: JAMA (1992)

THE percentage of physicians practicing a primary care specialty has declined, from about one half of total physicians in 1963 to about one third in 1986. One reason for this change is the retirement of general practitioners from medical practice. 1 These physicians are not being replaced at the same level, due to the decreased interest in primary care displayed by more recent US medical school graduates. 2 For example, results from the 1992 National Residency Matching Program showed that about 62% of the available positions in family practice, 64% of the positions in pediatrics, and 60% of the positions in internal medicine were filled with US seniors (memorandum from Norman Kahn, Jr, MD, American Academy of Family Physicians, to Commission on Education, March 17, 1992). In addition, 60% of the individuals initially entering residencies in internal medicine and 40% of those in pediatrics later pursue subspecialty training (Lyttle et
Association of Metabolic Syndrome in Nondiabetic Patients with Increased Risk for Chronic Kidney Disease
Authors: John R. Sedor, Jeffrey R. Schelling
Journal: Journal of the American Society of Nephrology (2005)

In a recent editorial, we suggested that more data are required to determine if metabolic syndrome is associated with progressive chronic kidney disease (CKD) in the absence of overt diabetes ([1][1]). This is clearly an important issue; metabolic syndrome, characterized by abdominal obesity,
Systemic amyloidosis AL with temporal artery involvement revealing lymphoplasmacytic malignancy in a man presenting as polymyalgia rheumatica.
Authors: P Lafforgue, E Senbel, D Figarella-Branger, J Boucraut, N Horschowsky, J F Pellissier, P C Acquaviva
Journal: Annals of the Rheumatic Diseases (1993)

A 68 year old man presented with a clinical and biological picture that suggested polymyalgia rheumatica. Temporal artery biopsy disclosed no inflammatory change but massive light chain amyloid deposits in the media. Further exploration showed a malignant lymphoplasmacytic haemopathy with a triclonal gammopathy and a muscular, rectal, and probable cardiac amyloidosis. Cryoglobulinaemia and high concentrations of soluble interleukin 2 receptor (sIL-2R) were also found. This is the fifth case with confirmed involvement of the temporal artery. The especially high sIL-2R concentration was thought to reflect the tumour mass rather than lymphocyte activation.
FLUORESCENCE MOLECULAR IMAGING
Authors: Vasilis Ntziachristos
Journal: Annual Review of Biomedical Engineering (2006)

There is a wealth of new fluorescent reporter technologies for tagging of many cellular and subcellular processes in vivo. This imposed contrast is now captured with an increasing number of available imaging methods that offer new ways to visualize and quantify fluorescent markers distributed in tissues. This is an evolving field of imaging sciences that has already achieved major advances but is also facing important challenges. It is nevertheless well poised to significantly impact the ways of biological research, drug discovery, and clinical practice in the years to come. Herein, the most pertinent technologies associated with in vivo noninvasive or minimally invasive fluorescence imaging of tissues are summarized. Focus is given to small-animal imaging. However, while a broad spectrum of fluorescence reporter technologies and imaging methods are outlined, as necessary for biomedical research, and clinical translation as well.