tbuckley/cabot-search huggingface dataset:
Cost-Effectiveness of Implantable Cardioverter–Defibrillators
Authors: Gillian D. Sanders, Mark A. Hlatky, Douglas K. Owens
Journal: New England Journal of Medicine (2005)

Eight randomized trials have evaluated whether the prophylactic use of an implantable cardioverter-defibrillator (ICD) improves survival among patients who are at risk for sudden death due to left ventricular systolic dysfunction but who have not had a life-threatening ventricular arrhythmia. We assessed the cost-effectiveness of the ICD in the populations represented in these primary-prevention trials.We developed a Markov model of the cost, quality of life, survival, and incremental cost-effectiveness of the prophylactic implantation of an ICD, as compared with control therapy, among patients with survival and mortality rates similar to those in each of the clinical trials. We modeled the efficacy of the ICD as a reduction in the relative risk of death on the basis of the hazard ratios reported in the individual clinical trials.Use of the ICD increased lifetime costs in every trial. Two trials--the Coronary Artery Bypass Graft (CABG) Patch Trial and the Defibrillator in Acute Myocardial Infarction Trial (DINAMIT)--found that the prophylactic implantation of an ICD did not reduce the risk of death and thus was both more expensive and less effective than control therapy. For the other six trials--the Multicenter Automatic Defibrillator Implantation Trial (MADIT) I, MADIT II, the Multicenter Unsustained Tachycardia Trial (MUSTT), the Defibrillators in Non-Ischemic Cardiomyopathy Treatment Evaluation (DEFINITE) trial, the Comparison of Medical Therapy, Pacing, and Defibrillation in Heart Failure (COMPANION) trial, and the Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT)--the use of an ICD was projected to add between 1.01 and 2.99 quality-adjusted life-years (QALY) and between 68,300 dollars and 101,500 dollars in cost. Using base-case assumptions, we found that the cost-effectiveness of the ICD as compared with control therapy in these six populations ranged from 34,000 dollars to 70,200 dollars per QALY gained. Sensitivity analyses showed that this cost-effectiveness ratio would remain below 100,000 dollars per QALY as long as the ICD reduced mortality for seven or more years.Prophylactic implantation of an ICD has a cost-effectiveness ratio below 100,000 dollars per QALY gained in populations in which a significant device-related reduction in mortality has been demonstrated.
Susceptibility to Disease.
Authors: W. H. Graves
Journal: JAMA (1904)

Goddard, Kans., Jan. 14, 1904. <h3>To the Editor:</h3> —I desire to call the attention of the profession to an important factor in the estimation of susceptibility to disease as influenced by age, namely, the decrease in the number of persons living as age increases. I have not been able to learn by a search of such literature as is available to me, and by a correspondence with several men of wide knowledge that this fact has ever been considered in the construction of tables intended to illustrate the varying susceptibility to a given disease at different ages. The tables or reports, as constructed, doubtless illustrate truly the prevalence of the disease at different ages, but fail signally in showing the varying susceptibility. Thus, a compilation before me shows that out of 434 cases of pneumonia, 42 occurred between the ages of 10 and 20, and 24 occurred in persons from
Antagonistic effect of nickel on the fermentative growth of Escherichia coli K-12 and comparison of nickel and cobalt toxicity on the aerobic and anaerobic growth.
Authors: L F Wu, C Navarro, K de Pina, M Quénard, M A Mandrand
Journal: Environmental Health Perspectives (1994)

The facultative anaerobic enterobacterium Escherichia coli requires the activity of nickel-containing hydrogenase for its anaerobic growth. Deficiency of the specific nickel transport system led to a hydrogenase-minus phenotype and slowed down the fermentative growth in the nik mutant. Addition of 300 microM nickel to the growth medium could restore the hydrogenase activity. This restoration resulted in the recovery of anaerobic growth. A further increase of nickel concentration inhibited growth. Thus nickel shows an antagonistic effect on the anaerobic growth of E. coli. To study the mechanism of nickel toxicity, two classes of nickel-resistant mutants were isolated. The nkr mutant was obtained by selecting colonies grown on nickel-containing minimal plate. It acquired simultaneously the resistance to cobalt. A nonspecific magnesium transport mutant corA was isolated on cobalt-containing plate. The corA mutant was also resistant to nickel. When analyzing the influence of nickel and cobalt on the bacterial growth, we obtained two interesting observations. First, anaerobic growth was less sensitive than aerobic growth to cobalt toxicity. In contrast, nickel toxicity did not vary from the growth conditions. Second, cobalt seems to abolish the growth, while nickel appears to slow down the growth rate under the condition used.
Association of Serum Fetuin-A With Insulin Resistance in Type 2 Diabetic and Nondiabetic Subjects
Authors: Katsuhito Mori, Masanori Emoto, Hisayo Yokoyama, Takahiro Araki, Megumi Teramura, Hidenori Koyama, Tetsuo Shoji, Masaaki Inaba, Yoshiki Nishizawa
Journal: Diabetes Care (2006)

Fetuin-A (α2-Heremans Schmid glycoprotein) is a circulating glycoprotein that can inhibit insulin receptor autophosphorylation and subsequent downstream signaling in vitro (1, 2). Recently, it has been reported (3) that fetuin-A–deficient mice demonstrate enhanced insulin sensitivity. These data indicate that fetuin-A might be a negative regulator of insulin signaling. However, the physiological significance of fetuin-A in insulin resistance in humans remains unclear.

To address this, we investigated the relationship of serum fetuin-A levels and insulin resistance in nondiabetic ( n = 160) and type 2 diabetic ( n = 161) subjects. Serum fetuin-A was measured by an enzyme-linked immunosorbent assay kit (BioVender Laboratory Medicine, …
Induction of renal growth and injury in the intact rat kidney by dietary deficiency of antioxidants.
Authors: K A Nath, A K Salahudeen
Journal: Journal of Clinical Investigation (1990)

We report induction of renal growth and injury in the intact rat kidney using a diet deficient in vitamin E and selenium. This diet was imposed in 3-wk-old male weanling rats, and after 9 wk, enhancement of growth, characterized by increased wet weight, dry weight, protein content, and DNA content appeared. Morphometric analyses revealed increased kidney volume, tubular epithelial volume, and mean glomerular volume. There were no differences in nephron number. The animals on the deficient diet displayed increased urinary protein excretion at 9 wk. Renal injury was also characterized by an interstitial cellular infiltrate and diminutions in glomerular filtration rate. Enhanced growth and injury were antedated by increased renal ammoniagenesis. The deficient diet did not induce metabolic acidosis, potassium depletion, glucose intolerance, or elevated plasma amino acid concentration. Enhancement of renal growth and ammoniagenesis by the deficient diet was not suppressible by chronic alkali therapy. Stimulation of renal growth could not be ascribed to increased intrarenal iron, induction of ornithine decarboxylase, or alterations in glomerular hemodynamics. Stimulation of renal ammoniagenesis by dietary deficiency of antioxidants is a novel finding, as is induction of growth and injury. We suggest that increased renal ammoniagenesis contributes to induction of renal growth and injury.
Young male prostitutes. The physician's role in social rehabilitation
Authors: P. Gandy
Journal: JAMA (1970)

The physician can become a significant person in the recognition and job rehabilitation of the young male prostitute. The investigation of the lives of 50 individuals engaged in prostitution to homosexuals in an urban area revealed patterns of behavior unlike those of other groups alienated from society. The rejection of the authors' early attempts at interviewing these youths led to the development of the skills needed to reach these young men in order to provide vocational rehabilitation and to make other efforts to meet their real need, a worthwhile existence in every aspect of their lives.
Perinatal outcomes following maternal asthma and cigarette smoking during pregnancy
Authors: Nicolette A. Hodyl, Michael J. Stark, Wendy Scheil, Luke E. Grzeskowiak, Vicki L. Clifton
Journal: European Respiratory Journal (2013)

Does cigarette smoking in pregnancy explain the increased risk of adverse perinatal outcomes that occur with maternal asthma or does it compound the effect? Using population based birth records, a retrospective analysis was conducted of all singleton pregnancies in South Australia over 10 years (1999–2008; n=172 305), examining maternal asthma, cigarette smoking and quantity of smoking to estimate odds ratios. Compared with nonasthmatic females who did not smoke during pregnancy, both asthmatic females who smoked and those who did not smoke during pregnancy had a significantly increased risk of gestational diabetes, antepartum haemorrhage, polyhydramnios, premature rupture of membranes, emergency Caesarean section, and the child being small for gestational age and having congenital abnormalities. These associations suggest that asthma, independently of maternal smoking, increases the risk of these adverse perinatal outcomes. Maternal smoking was itself associated with an increased risk of a number of poor neonatal outcomes, with a dose–response relationship observed. Notably, maternal asthma combined with cigarette smoking significantly increased the risk of preterm birth and urinary tract infections to a greater degree than with either exposure alone. Maternal asthma and cigarette smoking during pregnancy are both independently associated with adverse perinatal outcomes and, combined, compound the risk of preterm birth and urinary tract infections.
Cholesterol distribution in the bulk tissues of man: variation with age
Authors: J. R. Crouse, S. M. Grundy, E. H. Ahrens
Journal: Journal of Clinical Investigation (1972)

Lacking reliable data on cholesterol concentrations in muscle, adipose tissue, skin, and connective tissues (i.e., the "bulk tissues") in "normal" man, we have completed these analyses in 21 men and 8 women who died suddenly and unexpectedly; their ages ranged from 23 to 78 yr. In 11 of these subjects aged 20-40 yr, the mean cholesterol concentrations ranged from 180-440 mg/100 g dry tissue. In contrast, in 13 subjects aged 60-80 yr the values were 23-28% higher in muscle, adipose, and skin, while in dura mater, biceps, and psoas tendons the concentrations were 130, 260, and 460% higher (respectively). Esterified cholesterol in these connective tissues was found to be the major contributor, increasing 5- to 10-fold in the older group as opposed to a less than 5-fold rise in free cholesterol. In view of the large proportion of total body weight represented by these tissues, it is clear that large amounts of cholesterol can be accumulated there over a lifetime; indeed, the dense connective tissues appear to act uniquely as a trap for cholesterol, especially in the esterified form. Whether analyses of tendinous tissues in man, accessible during life, mirror the pattern of cholesterol deposition in arterial connective tissue remains to be determined.
W. PAISH "Diet in Sport"
Authors: Ivan M. Sharman
Journal: British Journal of Sports Medicine (1980)

This book, written by a National Athletics Coach, provides the reader with a succinct summary of the role of diet and its contribution, from a practical standpoint, to a sportsman's performance.The introductory chapter gives an account of the different food categories including the major nutrients: carbohydrates, fats and proteins.It also describes the other important items; vitamins, minerals, and dietary fibre.Subsequent chapters describe energy systems and expenditure and how such expenditure is met by dietary metabolism.Thus present physiological and biochemical theories, including the Cori and Kreb's cycles, are explained.The inclusion of such details is justified in the author's view because coaches nowadays pay considerable attention to these energy systems believing that each system responds differently to the various forms of training.
A role for pericytes as microenvironmental regulators of human skin tissue regeneration
Authors: Sophie Paquet-Fifield, Holger Schlüter, Amy Li, Tara Aitken, Pradnya Gangatirkar, Daniel Blashki, Rachel Koelmeyer, Normand Pouliot, Manuela Palatsides, Sarah Ellis, Nathalie Brouard, Andrew Zannettino, Nick Saunders, Natalie Thompson, Jason Li, Pritinder Kaur
Journal: Journal of Clinical Investigation (2009)

The cellular and molecular microenvironment of epithelial stem and progenitor cells is poorly characterized despite well-documented roles in homeostatic tissue renewal, wound healing, and cancer progression. Here, we demonstrate that, in organotypic cocultures, dermal pericytes substantially enhanced the intrinsically low tissue-regenerative capacity of human epidermal cells that have committed to differentiate and that this enhancement was independent of angiogenesis. We used microarray analysis to identify genes expressed by human dermal pericytes that could potentially promote epidermal regeneration. Using this approach, we identified as a candidate the gene LAMA5, which encodes laminin alpha5, a subunit of the ECM component laminin-511/521 (LM-511/521). LAMA5 was of particular interest as we had previously shown that it promotes skin regeneration both in vitro and in vivo. Analysis using immunogold localization revealed that pericytes synthesized and secreted LAMA5 in human skin. Consistent with this observation, coculture with pericytes enhanced LM-511/521 deposition in the dermal-epidermal junction of organotypic cultures. We further showed that skin pericytes could also act as mesenchymal stem cells, exhibiting the capacity to differentiate into bone, fat, and cartilage lineages in vitro. This study suggests that pericytes represent a potent stem cell population in the skin that is capable of modifying the ECM microenvironment and promoting epidermal tissue renewal from non-stem cells, a previously unsuspected role for pericytes.
Risk-Related Health Insurance
Authors: William K. Natale
Journal: JAMA (1993)

<h3>To the Editor.</h3> —Physicians are well aware that poor health behavior is a major cause of illness in our society, and many benefits would accrue if patients would assume greater responsibility for their own health.<sup>1</sup>It is therefore disappointing that in his otherwise comprehensive examination,<sup>2</sup>Dr Light breezily dismisses the potential connection of risk-rated life insurance with self-induced illness in a single sentence claiming that "little evidence exists that such [risk-rated] rates are effective and that such risk rating leads to a tangle of problems about where to draw lines and how to monitor them." But the relationship of self-destructive conduct to insurance is central, not collateral, as he unfortunately implies by this summary treatment of the topic. He suggests that this is material for another article, but given the broad ramifications of his sweeping statement, he could at least have given us a few explanatory paragraphs. While
Pathogenic Cycle Between the Endogenous Nitric Oxide Synthase Inhibitor Asymmetrical Dimethylarginine and the Leukocyte-Derived Hemoprotein Myeloperoxidase
Authors: Eike-Christin von Leitner, Anna Klinke, Dorothee Atzler, Jessica L. Slocum, Natalie Lund, Jan T. Kielstein, Renke Maas, Robin Schmidt-Haupt, Michaela Pekarova, Olaf Hellwinkel, Dimitrios Tsikas, Louis G. D'Alecy, Denise Lau, Stephan Willems, Lukas Kubala, Heimo Ehmke, Thomas Meinertz, Stefan Blankenberg, Edzard Schwedhelm, Crystal A. Gadegbeku, Rainer H. Böger, Stephan Baldus, Karsten Sydow
Journal: Circulation (2011)

The nitric oxide synthase inhibitor asymmetrical dimethylarginine (ADMA) and the leukocyte-derived hemoprotein myeloperoxidase (MPO) are associated with cardiovascular diseases. Activation of monocytes and polymorphonuclear neutrophils (PMNs) with concomitant release of MPO is regulated in a nitric oxide-dependent fashion. The aim of the study was to investigate a potential 2-way interaction between ADMA and MPO.Ex vivo, ADMA uptake by isolated human PMNs, the principal source of MPO in humans, significantly impaired nitric oxide synthase activity determined by gas chromatography-mass spectrometry. In humans, short-term ADMA infusion (0.0125 mg · kg(-1) · min(-1)) significantly increased MPO plasma concentrations. Functionally, PMN exposure to ADMA enhanced leukocyte adhesion to endothelial cells, augmented NADPH oxidase activity, and stimulated PMN degranulation, resulting in release of MPO. In vivo, a 28-day ADMA infusion (250 μmol · kg(-1) · d(-1)) in C57Bl/6 mice significantly increased plasma MPO concentrations, whereas this ADMA effect on MPO was attenuated by human dimethylarginine dimethylaminohydrolase1 (hDDAH1) overexpression. Moreover, the MPO-derived reactive molecule hypochlorous acid impaired recombinant hDDAH1 activity in vitro. In MPO(-/-) mice, the lipopolysaccharide-induced increase in systemic ADMA concentrations was abrogated.ADMA profoundly impairs nitric oxide synthesis of PMNs, resulting in increased PMN adhesion to endothelial cells, superoxide generation, and release of MPO. In addition, MPO impairs DDAH1 activity. Our data reveal an ADMA-induced cycle of PMN activation, enhanced MPO release, and subsequent impairment of DDAH1 activity. These findings not only highlight so far unrecognized cytokine-like properties of ADMA but also identify MPO as a regulatory switch for ADMA bioavailability under inflammatory conditions.
TUBERCULIN HYPERSENSITIVENESS IN NON-TUBERCULOUS GUINEA PIGS INDUCED BY INJECTIONS OF BACILLUS-FREE FILTRATES
Authors: Frank A. McJunkin
Journal: The Journal of Experimental Medicine (1921)

1. When a guinea pig with well developed peritoneal tuberculosis is injected intraperitoneally with about 20 cc. of a heavy suspension of a virulent tubercle bacillus (Culture H37) death occurs within 24 hours or the animal becomes extremely toxic. Such a peritoneal tuberculosis develops in about 1 month after 1 cc. of. a very heavy suspension of Culture H37 has been introduced into the abdominal cavity. If the viscid fluid which is contained within the peritoneal cavity is mixed with saline solution and passed through a Berkefeld filter a bacillus-free filtrate is obtained which induces in normal guinea pigs a certain degree of cutaneous hypersensitiveness to tuberculin. 2. The abdominal organs and the parietal peritoneum, to which masses of leucocytes and tubercle bacilli are adherent, when crushed and extracted with saline solution yield a filtrate which likewise induces a cutaneous hypersensitiveness. 3. The cutaneous hypersensitiveness does not appear before the 7th or 8th day after the filtrate injection and is therefore considered to be the result of an active sensitization of the animal.
TCT-13 Renal resistive indices, urinary albumin excretion and renal function in patients with resistant hypertension after catheter-based renal sympathetic denervation
Authors: Felix Mahfoud, Bodo Cremers, Christian Ukena, Henry Krum, Paul Sobotka, Markus Schlaich, Bruno Scheller, Ulrich Laufs, Michael Böhm
Journal: Journal of the American College of Cardiology (2012)
Overexpression of Indoleamine 2,3-Dioxygenase in Human Endometrial Carcinoma Cells Induces Rapid Tumor Growth in a Mouse Xenograft Model
Authors: Norio Yoshida, Kazuhiko Ino, Yoshiyuki Ishida, Hiroaki Kajiyama, Eiko Yamamoto, Kiyosumi Shibata, Mikio Terauchi, Akihiro Nawa, Hidetoshi Akimoto, Osamu Takikawa, Ken-ichi Isobe, Fumitaka Kikkawa
Journal: Clinical Cancer Research (2008)

Abstract Purpose: Indoleamine 2,3-dioxygenase (IDO) is a tryptophan-catabolizing enzyme that induces immune tolerance in mice. Our prior study showed that high tumoral IDO expression in endometrial cancer tissues correlates with disease progression and impaired patient survival. The purpose of the present study was to clarify the functional role of IDO in human endometrial cancer cells and to investigate the therapeutic potential of IDO inhibitors. Experimental Design: IDO cDNA was transfected into the human endometrial carcinoma cell line AMEC, resulting in the establishment of stable clones of IDO-overexpressing AMEC cells (AMEC-IDO). AMEC-IDO cells were characterized in vitro as well as in vivo using a mouse xenograft model. Results: There was no significant difference in in vitro cell proliferation, migration, or chemosensitivity to paclitaxel between AMEC-IDO and control vector–transfected cells (AMEC-pcDNA). However, in vivo tumor growth was markedly enhanced in AMEC-IDO–xenografted nude mice when compared with AMEC-pcDNA–xenografted mice. Splenic natural killer (NK) cell counts in AMEC-IDO–xenografted mice were significantly decreased when compared with control mice. Furthermore, conditioned medium obtained from AMEC-IDO cell cultures markedly reduced the NK lysis activity of nude mice. Finally, oral administration of the IDO inhibitor 1-methyl-d-tryptophan in combination with paclitaxel in AMEC-IDO–xenografted mice strongly potentiated the antitumor effect of paclitaxel, resulting in significantly prolonged survival. Conclusions: This is the first evidence showing that IDO overexpression in human cancer cells contributes to tumor progression in vivo with suppression of NK cells. Our data suggest that targeting IDO may be a novel therapeutic strategy for endometrial cancer.
Erythroderma associated with mixed lymphocyte endothelial cell interaction and Staphylococcus aureus infection
Authors: MADALENE C.Y. HENG, S. G. KLOSS, D. G. CHASE
Journal: British Journal of Dermatology (1986)

Journal Article Erythroderma associated with mixed lymphocyte endothelial cell interaction and Staphylococcus aureus infection Get access MADALENE C.Y. HENG, MADALENE C.Y. HENG Division of Dermatology, Department of Medicine, U.C.L.A. San Fernando Valley Internal Medicine Program, Veterans Administration Medical Center, Sepulveda, California, U.S.A. Madalene C.Y.Heng. Search for other works by this author on: Oxford Academic Google Scholar S. G. KLOSS, S. G. KLOSS Division of Dermatology, Department of Medicine, U.C.L.A. San Fernando Valley Internal Medicine Program, Veterans Administration Medical Center, Sepulveda, California, U.S.A. Search for other works by this author on: Oxford Academic Google Scholar D. G. CHASE D. G. CHASE Division of Dermatology, Department of Medicine, U.C.L.A. San Fernando Valley Internal Medicine Program, Veterans Administration Medical Center, Sepulveda, California, U.S.A. Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 115, Issue 6, 1 December 1986, Pages 693–705, https://doi.org/10.1111/j.1365-2133.1986.tb06650.x Published: 01 December 1986 Article history Accepted: 04 June 1986 Published: 01 December 1986
Increased expression of CD44v6 and CD44v3 in ulcerative colitis but not colonic Crohn's disease
Authors: W.M.C. Rosenberg, D.G. Jackson, J.M. Trowell, J.I. Bell, W.M.C. Rosenberg, C. Prince, R.W. Chapman, J.M. Trowell, D.P. Jewel, L. Kaklamanis, S.B. Fox, D.L. Simmons
Journal: The Lancet (1995)