tbuckley/cabot-search huggingface dataset:
Bradykinin Production and Increased Pulmonary Endothelial Permeability during Acute Respiratory Failure in Unanesthetized Sheep
Authors: Hugh M. O'Brodovich, S. Alex Stalcup, Leila Mei Pang, Joel S. Lipset, Robert B. Mellins
Journal: Journal of Clinical Investigation (1981)

To investigate mechanisms of pulmonary edema in respiratory failure, we studied unanesthetized sheep with vascular catheters, pleural balloons, and chronic lung lymph fistulas. Animals breathed either a hypercapnic-enriched oxygen (n = 5) or a hypercapnic-hypoxic (n = 5) gas mixture for 2 h. Every 15 min blood gases, pressures, cardiac output, lymph flow (Qlym), plasma and lymph albumin (mol wt, 70,000), IgG (mol wt, 150,000), IgM (mol wt, 900,000), and blood bradykinin concentrations were determined. In both groups, cardiac output and pulmonary arterial pressures increased, whereas left atrial pressures were unchanged. Acidosis alone (arterial pH = 7.16, PaCO(2) = 81 mm Hg, PaO(2) = 250 mm Hg) resulted in a doubling of lymph flow, a small increase in protein flux, and a decrease in lymph to plasma protein concentration (L/P) ratio for all three proteins. Acidotic-hypoxic animals (arterial pH = 7.16, PaCO(2) = 84 mm Hg, PaO(2) = 48 mm Hg) tripled Qlym. In these animals the increase in lymphatic flux of albumin, IgG, and IgM was significantly (P < 0.05) greater than that seen in either the acidosis alone group or in animals where left atrial pressures were elevated (n = 5; P < 0.05). Also, their percent increase in flux of the large protein (IgM) was greater than for the small protein (albumin) (P < 0.05). With acidosis alone, only pulmonary arterial bradykinin concentration increased (1.27+/-0.25 ng/ml SE), whereas acidosis plus hypoxia elevated both pulmonary arterial bradykinin concentrations (4.83+/-1.14 ng/ml) and aortic bradykinin concentration (2.74+/-0.78 ng/ml). These studies demonstrate that hypercapnic acidosis stimulates in vivo production of bradykinin. With superimposed hypoxia, and therefore decreased bradykinin degradation, there is an associated sustained rise in Qlym with increased lung permeability to proteins.
Inflammatory bowel disease: study of cell mediated cytotoxicity for isolated human colonic epithelial cells.
Authors: B J Kemler, E Alpert
Journal: Gut (1980)

A better understanding of the mechanism(s) of cell mediated toxicity for colon cells in vitro may help clarify the pathogenesis of inflammatory bowel disease (IBD). We have examined both the cytotoxicity of IBD peripheral blood mononuclear cells and the kinetics of induction of such toxicity by soluble plasma factors. Peripheral blood mononuclear cells from IBD patients were found to be cytotoxic for the colon cells. With the use of Chang cells, this cytotoxicity was shown not to be due to an increase in spontaneous cell mediated cytotoxicity. Colon cell toxicity in vitro did not correlate with site of disease or severity, but decreased toxicity appeared to be associated with in vivo steroid administration. Plasma from some IBD patients was capable of inducing normal peripheral blood mononuclear cells to be toxic to colon cells. This ability was not affected by steroid therapy. The induction capacity of IBD plasma was not associated with the presence of circulating immune complexes, as measured by Raji RIA, suggesting that large complement fixing complexes are not the inducing and directing factors. Unlike findings in other systems, induction could be demonstrated after a one hour preincubation of mononuclear cells with IBD plasma. The kinetics of induction are consistent with the hypothesis that either cytophilic antibody or small circulating immune complexes arm K cells for specific colon cell lysis.
Oestrogen Receptor in Human Breast Cancer Tissue and Response to Endocrine Therapy
Authors: E. Engelsman, J. P. Persijn, C. B. Korsten, F. J. Cleton
Journal: BMJ (1973)

Oestrogen receptor determinations were done in metastatic breast cancer tissue of patients with advanced breast cancer. In 37 patients with progressive disease evaluation of the response to endocrine treatment was possible, following the criteria of the E.O.R.T.C. Co-operative Breast Cancer Group. In 20 patients with receptor-negative tumours two objective remissions were noted; in 17 patients with receptor-positive tumours 14 objective remissions were seen. There seems to be a striking correlation between the presence or absence of oestrogen receptor in tumour tissue and the clinical response to hormonal therapy.
Recombinant Osteoprotegerin for Juvenile Paget's Disease
Authors: Tim Cundy, James Davidson, Michael D. Rutland, Carolyn Stewart, Alex M. DePaoli
Journal: New England Journal of Medicine (2005)

Juvenile Paget's disease, a genetic bone disease characterized by accelerated bone turnover, results from inactivating mutations in the gene encoding osteoprotegerin--a key regulator of osteoclastogenesis. The effects of recombinant osteoprotegerin were investigated in two adult siblings with juvenile Paget's disease. Bone resorption (assessed by N-telopeptide excretion) was suppressed by once-weekly subcutaneous doses of 0.3 to 0.4 mg per kilogram of body weight. After 15 months of treatment, radial bone mass increased in one patient by 9 percent and in the other by 30 percent, skeletal bisphosphonate retention decreased by 37 percent and 55 percent, respectively, and there was radiographic improvement. Apart from mild hypocalcemia and hypophosphatemia, no apparent adverse events occurred.
Change in Body Weight and Longevity
Authors: I-Min Lee
Journal: JAMA (1992)

<h3>Objective.</h3> —To investigate the effect of body weight change on longevity. <h3>Design.</h3> —Cohort analytic study, following men from 1977 through 1988. <h3>Setting.</h3> —The study was conducted among Harvard University alumni with mean age of 58 years. <h3>Patients.</h3> —Alumni, free of cardiovascular disease and cancer, completed questionnaires on weight, height, cigarette habit, and physical activities in 1962 or 1966 and in 1977 (n=11 703). We assessed weight change between questionnaires, based on self-reported weights. <h3>Main Outcome Measure.</h3> —Mortality from all causes (n=1441), coronary heart disease (n=345), and cancer (n=459), determined from death certificates. <h3>Results.</h3> —Lowest all-cause mortality was among alumni maintaining stable weight (±1 kg). With this category as referent (relative risk=1.00), relative risks of death associated with losing more than 5 kg, losing between 1 and 5 kg, (more than 1 kg and up to 5 kg) gaining between 1 and 5 kg (more than 1 kg and up to 5 kg), and gaining more than 5 kg were 1.57 (95% confidence interval, 1.34 to 1.84), 1.26 (1.10 to 1.46), 1.06 (0.90 to 1.24), and 1.36 (1.11 to 1.66), respectively. For coronary heart disease mortality, relative risks were 1.75 (1.26 to 2.43), 1.43 (1.05 to 1.93), 1.28 (0.91 to 1.80), and 2.01 (1.36 to 2.97), respectively. Weight change did not predict cancer mortality. Findings were not explained by cigarette habit, physical activity, or body mass index. We observed similar trends for follow-up between 1977 and 1982 and between 1983 and 1988. Those losing or gaining more weight also reported greater total lifetime weight loss, which may indicate weight cycling. <h3>Conclusions.</h3> —Both body weight loss and weight gain are associated with significantly increased mortality from all causes and from coronary heart disease but not from cancer. (<i>JAMA</i>. 1992;268:2045-2049)
Body Position and Activity, But Not Heart Rate, Affect Pump Flows in Patients With Continuous-Flow Left Ventricular Assist Devices
Authors: Kavitha Muthiah, Sunil Gupta, James Otton, Desiree Robson, Robyn Walker, Andre Tay, Peter Macdonald, Anne Keogh, Eugene Kotlyar, Emily Granger, Kumud Dhital, Phillip Spratt, Paul Jansz, Christopher S. Hayward
Journal: JACC Heart Failure (2014)

The aim of this study was to determine the contribution of pre-load and heart rate to pump flow in patients implanted with continuous-flow left ventricular assist devices (cfLVADs).Although it is known that cfLVAD pump flow increases with exercise, it is unclear if this increment is driven by increased heart rate, augmented intrinsic ventricular contraction, or enhanced venous return.Two studies were performed in patients implanted with the HeartWare HVAD. In 11 patients, paced heart rate was increased to approximately 40 beats/min above baseline and then down to approximately 30 beats/min below baseline pacing rate (in pacemaker-dependent patients). Ten patients underwent tilt-table testing at 30°, 60°, and 80° passive head-up tilt for 3 min and then for a further 3 min after ankle flexion exercise. This regimen was repeated at 20° passive head-down tilt. Pump parameters, noninvasive hemodynamics, and 2-dimensional echocardiographic measures were recorded.Heart rate alteration by pacing did not affect LVAD flows or LV dimensions. LVAD pump flow decreased from baseline 4.9 ± 0.6 l/min to approximately 4.5 ± 0.5 l/min at each level of head-up tilt (p < 0.0001 analysis of variance). With active ankle flexion, LVAD flow returned to baseline. There was no significant change in flow with a 20° head-down tilt with or without ankle flexion exercise. There were no suction events.Centrifugal cfLVAD flows are not significantly affected by changes in heart rate, but they change significantly with body position and passive filling. Previously demonstrated exercise-induced changes in pump flows may be related to altered loading conditions, rather than changes in heart rate.
Novel strategy to monitor apparent tumor-specific T cells in patients with cancer
Authors: Rieneke van de Ven, Traci L Hilton, Christopher J Dubay, Sachin Puri, Hong-Ming Hu, Rom S Leidner, R Bryan Bell, Walter J Urba, Brendan D Curti, Sandra Aung, Bernard A Fox
Journal: Journal for ImmunoTherapy of Cancer (2013)

Meeting abstracts We hypothesize that immune responses that develop following immunotherapy, particularly in patients with objective responses, are directed against a wide range of antigenic determinants. However, in the absence of autologous tumor cells, monitoring is frequently limited to a small
Familienstruktur und Psychose
Authors: Gisela Pankow
Journal: Psychotherapy and Psychosomatics (1968)

Research Articles| February 12 2010 Familienstruktur und Psychose Subject Area: Psychiatry and Psychology Gisela Pankow Gisela Pankow Paris Search for other works by this author on: This Site PubMed Google Scholar Psychother Psychosom (1968) 16 (6): 366–374. https://doi.org/10.1159/000285968 Article history Published Online: February 12 2010 Content Tools Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn MailTo Tools Icon Tools Get Permissions Cite Icon Cite Search Site Citation Gisela Pankow; Familienstruktur und Psychose. Psychother Psychosom 1 June 1968; 16 (6): 366–374. https://doi.org/10.1159/000285968 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsPsychotherapy and Psychosomatics Search Advanced Search This content is only available via PDF. 1968Copyright / Drug Dosage / DisclaimerCopyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements. Article PDF first page preview Close Modal You do not currently have access to this content.
Fluoroquinolone resistance in <i>Salmonella</i> Typhi
Authors: Fiona J Cooke, John Wain, E John Threlfall
Journal: BMJ (2006)

Replication studies play an essential role in corroborating research findings and ensuring that subsequent experimental works are interpreted correctly. A previously published paper indicated that the neurotransmitter glutamate, along with the compounds <i>N</i>-methyl-d-aspartate (NMDA) and d-(−)-2-amino-5-phosphonopentanoic acid (AP5), acts as positive allosteric modulators of inhibitory glycine receptors. The paper further suggested that this form of modulation would play a role in setting the spinal inhibitory tone and influencing sensory signaling, as spillover of glutamate onto nearby glycinergic synapses would permit rapid crosstalk between excitatory and inhibitory synapses. Here, we attempted to replicate this finding in primary cultured spinal cord neurons, spinal cord slice, and <i>Xenopus laevis</i> oocytes expressing recombinant human glycine receptors. Despite extensive efforts, we were unable to reproduce the finding that glutamate, AP5, and NMDA positively modulate glycine receptor currents. We paid careful attention to critical aspects of the original study design and took into account receptor saturation and protocol deviations such as animal species. Finally, we explored possible explanations for the experimental discrepancy. We found that solution contamination with a high-affinity modulator such as zinc is most likely to account for the error, and we suggest methods for preventing this kind of misinterpretation in future studies aimed at characterizing high-affinity modulators of the glycine receptor. <h3>SIGNIFICANCE STATEMENT</h3> A previous study indicates that glutamate spillover onto inhibitory synapses can directly interact with glycine receptors to enhance inhibitory signalling. This finding has important implications for baseline spinal transmission and may play a role when chronic pain develops. However, we failed to replicate the results and did not observe glutamate, d-(−)-2-amino-5-phosphonopentanoic acid, or <i>N</i>-methyl-d-aspartate modulation of native or recombinant glycine receptors. We ruled out various sources for the discrepancy and found that the most likely cause is solution contamination.
Abstract 1989: The effect of resveratrol combined with DFMO or DenSpm on MCF-7 breast cancer cells and MCF-10a non-cancerous cells
Authors: Isabella Benassi, Riley M. Smith, KateLyn White, Shanna Dennis, Niki Nelson, Russ Feirer
Journal: Cancer Research (2012)

Abstract Resveratrol, (3,5,49-trihydroxy-trans-stilbene), was first reported to act as a chemo-preventative anticancer compound in mice by Jang et al. in 1997. Resveratrol has been shown to induce apoptosis and reduce both cell viability and mitotic index in many cancer cell lines, including MCF-7. The current work extends these studies to determine its effects on glucose utilization and enzymes involved in polyamine metabolism. Glucose uptake was found to be reduced in MCF-7 cells treated with resveratrol. Work in other labs has shown resveratrol to sensitize cancer cells to other chemotherapeutic compounds. In the present study, the effects of combinations of resveratrol with compounds that affect polyamine metabolism, DFMO (difluoromethylornithine) and DenSpm (N1, N11-diethylnorspermine), were tested. Both DFMO and DenSpm were found to reduce cell proliferation and mitotic index in MCF-7 cell lines and more importantly, a synergistic effect was observed when these compounds were used in combination with resveratrol. In this investigation resveratrol was also found to induce apoptosis and reduce cell viability, mitotic index, and glucose uptake in non-cancerous, transformed mammary epithelial cells (MCF-10a). Similar findings have been reported with other non-cancerous cells including intestinal smooth muscle cells (Garcia et al., 2011). The combination of resveratrol and DFMO also reduced glucose uptake, proliferation, and mitotic index in this non-cancerous cell line (MCF-10a). These compounds were found to affect the expression of ODC (ornithine decarboxylase) and SSAT (spermidine/spermine acetyl transferase), enzymes involved in polyamine metabolism, and other proteins involved in cell cycle regulation. 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 1989. doi:1538-7445.AM2012-1989
The high-affinity IgE receptor (FcεRI) blocks apoptosis in normal human monocytes
Authors: Norito Katoh, Stefan Kraft, Jörg H.M. Weßendorf, Thomas Bieber
Journal: Journal of Clinical Investigation (2000)

Monocytes have a limited life span, and their homeostasis is regulated by apoptosis in vivo. When cultured in the absence of appropriate exogenous stimuli, they undergo apoptosis, but under the influence of survival signals, these cells differentiate into macrophages or dendritic cells. Here we show that ligation of the high-affinity IgE receptor (FcεRI) on human monocytes from nonatopic individuals markedly reduces apoptosis induced by serum deprivation or by CD95/Fas ligation. Aggregation of FcεRI reduces its own expression but fails to modulate CD95/Fas expression. In contrast, FcεRI ligation enhances the expression of the antiapoptotic molecules Bcl-2 and Bcl-xL, but not Mcl-1, in monocytes. Incubation of unstimulated cells with culture supernatants of FcεRI-activated monocytes prolongs their life span, whereas CD95/Fas expression remains unaffected. The incidence of apoptosis is restored considerably when the supernatant is depleted of TNF-α, whereas elimination of IL-1β, GM-CSF, or IL-12 has no effect. These results indicate that FcεRI mediates signals preventing monocyte apoptosis directly by increasing the levels of Bcl-2 and Bcl-xL, and indirectly by means of TNF-α in an autocrine and paracrine fashion. This process may contribute to the establishment of chronic allergic disorders such as atopic dermatitis.
Low Cerebrospinal-Fluid Sugar Content in Meningeal and Intracranial Neoplasia
Authors: Maurice H. Laszlo
Journal: JAMA (1965)

IN EVALUATING a patient with central-nervoussystem (CNS) disease and meningeal irritation of unknown etiology, low spinal-fluid sugar content calls attention to the possibility of diffuse CNS tumor acting as the cause. Meningeal or cerebral carcinomatosis or both must be considered in the differential diagnosis. It is the purpose of this paper to call attention to the association of CNS tumor and decreased cerebrospinal-fluid (CSF) sugar content.  Report of a Case  A 54-year-old Cuban woman was admitted to the Psychiatric Institute of Jackson Memorial Hospital, Miami, Fla, on Jan 23, 1963, with a tentative diagnosis of involutional depressive reaction. Six months previously she had fled her homeland and sought refuge in Jamaica, where she lived under crowded and unsanitary conditions. One month prior to admission she arrived in Miami and visited the emergency room of Jackson Memorial Hospital on several occasions with complaints of head, neck, and back ache. On each
Insulin-Like Growth Factors I and II. Peptide, Messenger Ribonucleic Acid and Gene Structures, Serum, and Tissue Concentrations*
Authors: WILLIAM H. DAUGHADAY, PETER ROTWEIN
Journal: Endocrine Reviews (1989)

HYPOPHYSECTOMIZED rats have a defect in the synthesis of matrix protein which is rapidly repaired by the administration of GH in vivo. In 1957, it was first reported that this defect, as determined by measuring the incorporation of [35S]sulfate into chondroitin sulfate, could not be corrected by addition of GH to media containing cartilage segments (1). The defect, however, was rapidly corrected by the addition of diluted normal rat serum to such media, but serum from hypophysectomized rats was virtually inactive. It was proposed that GH acted on skeletal tissues by inducing the formation of a direct acting intermediary growth factor. This hypothesis, commonly referred to as the somatomedin hypothesis, has been extensively confirmed and recently extended to include autocrine and paracrine roles of somatomedins in many tissues as well as the originally recognized endocrine role of this growth factor. Research in the somatomedins has increased so much in recent years that a comprehensive review of the subject is no longer possible within the length constraints of this Journal. In this review, we will focus on the insulin-like growth factors (IGFs) that are present in body fluids and tissues. We will review the rapidly developing information about the molecular biology of the biosynthesis of IGFs and their regulation in fetal and postnatal life and the possible role of IGF biosynthesis in tissue repair and hypertrophy. Last, we will consider the relative contribution of endocrine as opposed to autocrine/paracrine actions of IGF-I in skeletal growth. Not included in this review will be a consideration of IGF binding proteins, IGF receptors, and postbinding effector mechanisms. Readers are referred to recent reviews for consideration of these topics (2–4).
Homocysteine and coagulation factors as a risk factor of myocardial infarction at a young age
Authors: Masahiko Saigo, Satoshi Abe, Masakazu Ogawa, Sadatoshi Biro, Shinichi Minagoe, Tsuminori Yamashita, Tatsuru Matsuoka, Hiroyuki Torii, Hitoshi Toda, Yoshihiko Atsuchi, Koushi Mawatari, Ikuro Maruyama, Chuwa Tei
Journal: Journal of the American College of Cardiology (2002)
The divorce of REM sleep and dreaming
Authors: Anton Coenen
Journal: Behavioral and Brain Sciences (2000)

The validity of dream recall is discussed. What is the relation between the actual dream and its later reflection? Nielsen proposes differential sleep mentation, which is probably determined by dream accessibility. Solms argues that REM sleep and dreaming are double dissociable states. Dreaming occurs outside REM sleep when cerebral activation is high enough. That various active sleep states correlate with vivid dream reports implies that REM sleep and dreaming are single dissociable states. Vertes &amp; Eastman reject that REM sleep is involved in memory consolidation. Considerable evidence for this was obtained by REM deprivation studies with the dubious water tank technique. [Nielsen; Solms; Vertes &amp; Eastman]