tbuckley/cabot-search huggingface dataset:
Gastrointestinal regulation of food intake
Authors: David E. Cummings, Joost Overduin
Journal: Journal of Clinical Investigation (2007)

Despite substantial fluctuations in daily food intake, animals maintain a remarkably stable body weight, because overall caloric ingestion and expenditure are exquisitely matched over long periods of time, through the process of energy homeostasis. The brain receives hormonal, neural, and metabolic signals pertaining to body-energy status and, in response to these inputs, coordinates adaptive alterations of energy intake and expenditure. To regulate food consumption, the brain must modulate appetite, and the core of appetite regulation lies in the gut-brain axis. This Review summarizes current knowledge regarding the neuroendocrine regulation of food intake by the gastrointestinal system, focusing on gastric distention, intestinal and pancreatic satiation peptides, and the orexigenic gastric hormone ghrelin. We highlight mechanisms governing nutrient sensing and peptide secretion by enteroendocrine cells, including novel taste-like pathways. The increasingly nuanced understanding of the mechanisms mediating gut-peptide regulation and action provides promising targets for new strategies to combat obesity and diabetes.
Intensive care in tetanus: management, complications, and mortality in 100 cases.
Authors: R S Edmondson, M W Flowers
Journal: BMJ (1979)

One hundred cases of tetanus were treated in the intensive care unit of Leeds General Infirmary during during 1961--1977. In 90 patients disease was severe enough to require paralysis and artificial ventilation; a further three needed tracheostomy but not paralysis; and in seven the condition was mild, requiring sedation only. Ten patients died, but all deaths were attributable to complications of treatment rather than to the disease itself and were theoretically avoidable. No evidence of permanent neurological damage from tetanus was found. In 65 patients a wound was the source of infection, most of which were minor, often receiving no medical attention. In five patients the source was probably varicose ulcers of the leg. Such patients, if lacking immunity, are at risk, particularly when farming or gardening. Only two patients had received a full course of tetanus toxoid, in one case eight years and in the other three years before injury; neither received a booster dose at the time of injury and in the second tetanus was mild. Of the 35 patients who did seek medical attention at the time of wounding, 21 received prophylactic antibiotics and 25 tetanus toxoid, but none received equine or human antitetanus serum. Early resort to tracheostomy and paralysis in severe tetanus resulted in a favourable mortality of 10% in the series. To implement such a policy full intensive-care facilities, with a trained nurse to care for each patient, must be available at all times.
A study of the secretion mechanism of the sebaceous gland using three-dimensional reconstruction to examine the morphological relationship between the sebaceous gland and the arrector pili muscle in the follicular unit
Authors: W-C. Song, K-S. Hu, H-J. Kim, K-S. Koh
Journal: British Journal of Dermatology (2007)

Journal Article A study of the secretion mechanism of the sebaceous gland using three‐dimensional reconstruction to examine the morphological relationship between the sebaceous gland and the arrector pili muscle in the follicular unit Get access W‐C. Song, W‐C. Song Department of Anatomy, College of Medicine, Konkuk University, 322 Danwol‐dong, Chungju, Chungbuk, 380‐701, Republic of Korea Search for other works by this author on: Oxford Academic Google Scholar K‐S. Hu, K‐S. Hu Division of Anatomy and Developmental Biology, Department of Oral Biology, Oral Science Research Center, Brain Korea 21 Project, College of Dentistry, Yonsei University, Seoul, Republic of Korea Search for other works by this author on: Oxford Academic Google Scholar H‐J. Kim, H‐J. Kim Division of Anatomy and Developmental Biology, Department of Oral Biology, Oral Science Research Center, Brain Korea 21 Project, College of Dentistry, Yonsei University, Seoul, Republic of Korea Search for other works by this author on: Oxford Academic Google Scholar K‐S. Koh K‐S. Koh Department of Anatomy, College of Medicine, Konkuk University, 322 Danwol‐dong, Chungju, Chungbuk, 380‐701, Republic of Korea Correspondence: Ki‐Seok Koh.E‐mail: kskoh@kku.ac.kr Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 157, Issue 2, 1 August 2007, Pages 325–330, https://doi.org/10.1111/j.1365-2133.2007.08036.x Published: 01 August 2007
Viruses and Lymphomas
Authors: Joseph S Pagano
Journal: New England Journal of Medicine (2002)

Do viruses cause lymphomas? Yes, at least some viruses can. The first evidence was found in the 1960s, when Epstein–Barr virus (EBV) was detected in an explanted Burkitt's lymphoma. Today's panoply is surprising, ranging from EBV in lymphomas in immunocompromised patients and EBV in Hodgkin's disease to leukemia and lymphoma produced by human T-cell leukemia virus type 1 (HTLV-1) (see Table). Now, in this issue of the Journal, Hermine et al. have provided evidence of an association between splenic lymphoma and hepatitis C virus (HCV) (see pages 89–94). What are we to make of these diverse associations, and how will . . .
Depression and CD4 Decline
Authors: Donald C. Barrett
Journal: JAMA (1994)

<h3>To the Editor.</h3> —Our recent findings on the relationship between depression and change in CD4 cell count<sup>1</sup>and Dr Lyketsos and colleagues'<sup>2</sup>failure to replicate our findings have added to the controversy concerning psychological distress and disease progression. Space limitations allow us to address only a few of the issues raised by the differences in articles and by the Editorial by Drs Perry and Fishman.<sup>3</sup> Perry and Fishman asserted that our significant findings may be a type I error attributable to our smaller sample size. The basis for this assertion is unclear. Smaller sample size diminishes power, thus making it more difficult to find a statistically significant effect (a type II error). Differences in results are therefore likely to be attributable to differences in procedures or in sample characteristics. The procedures of the two studies, though not identical, are similar. The study populations do differ on mean
Familial Aminoaciduria in Osteogenesis Imperfecta
Authors: Israel Chowers
Journal: JAMA (1962)

A metabolic disturbance in patients suffering from osteogenesis imperfecta is demonstrated. Abnormal aminoaciduria and low blood creatinine values were found in 6 such patients, belonging to 3 unrelated families. Low blood uric acid levels were found in 5 patients belonging to 2 of the 3 families. Among the clinically healthy relatives of the patients, abnormal aminoaciduria was found in 12 out of 17 persons examined. The blood creatinine levels, however, were normal. In 2 families blood uric acid values were low in 8 out of 13 persons.
The FDA's Classification System for New Drugs
Authors: Marion J. Finkel
Journal: New England Journal of Medicine (1980)

The October, 1978, issue of Consumer Reports contained an article on the Food and Drug Administration's (FDA's) classification of drugs at the time when they are approved for marketing.* This article focused primarily on the classification of a new molecular entity, with respect to whether and to what degree it represents a therapeutic advance, and it contained the FDA's ratings of new drugs or new formulations approved for marketing between October, 1975, and June, 1978. Undoubtedly, some physicians were asked by their patients about certain drugs that appeared in the list. Before explaining the genesis of such a classification system, . . .
Functional effects of a KCNQ1 mutation associated with the long QT syndrome
Authors: I BOULET, A RAES, N OTTSCHYTSCH, D SNYDERS
Journal: Cardiovascular Research (2006)

Long QT syndrome (LQTS) is an inherited disorder of ventricular repolarization caused by mutations in cardiac ion channel genes, including KCNQ1. In this study the electrophysiological properties of a LQTS-associated mutation in KCNQ1 (Q357R) were characterized. This mutation is located near the C-terminus of S6, a region that is important for the gate structure.Co-assembly of KCNE1 with the mutant Q357R elicited a current displaying slower activation compared to the wild-type KCNQ1/KCNE1 channels. The voltage dependence of activation of Q357R was shifted to more positive potentials. Moreover, a strong reduction in current density was observed that was partially attributed to the altered voltage dependence and kinetics of activation. The reduced current amplitude was also caused by intracellular retention of Q357R/KCNE1 channels as was shown by confocal microscopy. It indicated that the Q357R mutation disturbed protein expression by a trafficking or assembly problem of the Q357R/KCNE1 complex. To mimic the patient status KCNQ1, Q357R and KCNE1 were co-expressed, which revealed a dominant negative effect on current density and activation kinetics.The effects of the Q357R mutation on the activation of the channel together with a reduced expression at the membrane would lead to a reduction in I(Ks) and thus in "repolarization reserve" under physiological circumstances. As such it explains the long QT syndrome observed in these patients.
Conditional BDNF release under pathological conditions improves Huntington's disease pathology by delaying neuronal dysfunction
Authors: Albert Giralt, Olga Carretón, Cristina Lao-Peregrin, Eduardo D Martín, Jordi Alberch
Journal: Molecular Neurodegeneration (2011)

Brain-Derived Neurotrophic Factor (BDNF) is the main candidate for neuroprotective therapy for Huntington's disease (HD), but its conditional administration is one of its most challenging problems.Here we used transgenic mice that over-express BDNF under the control of the Glial Fibrillary Acidic Protein (GFAP) promoter (pGFAP-BDNF mice) to test whether up-regulation and release of BDNF, dependent on astrogliosis, could be protective in HD. Thus, we cross-mated pGFAP-BDNF mice with R6/2 mice to generate a double-mutant mouse with mutant huntingtin protein and with a conditional over-expression of BDNF, only under pathological conditions. In these R6/2:pGFAP-BDNF animals, the decrease in striatal BDNF levels induced by mutant huntingtin was prevented in comparison to R6/2 animals at 12 weeks of age. The recovery of the neurotrophin levels in R6/2:pGFAP-BDNF mice correlated with an improvement in several motor coordination tasks and with a significant delay in anxiety and clasping alterations. Therefore, we next examined a possible improvement in cortico-striatal connectivity in R62:pGFAP-BDNF mice. Interestingly, we found that the over-expression of BDNF prevented the decrease of cortico-striatal presynaptic (VGLUT1) and postsynaptic (PSD-95) markers in the R6/2:pGFAP-BDNF striatum. Electrophysiological studies also showed that basal synaptic transmission and synaptic fatigue both improved in R6/2:pGAP-BDNF mice.These results indicate that the conditional administration of BDNF under the GFAP promoter could become a therapeutic strategy for HD due to its positive effects on synaptic plasticity.
Physique of Female Swimmers and Divers From the 1976 Montreal Olympics
Authors: T. Khosla
Journal: JAMA (1984)

Appreciable differences in heights and adjusted weights were observed between women finalists and nonfinalists in four swimming and two diving events at Montreal in 1976. The finalists in swimming events were both taller (3.5 cm) and heavier (2.8 kg) than nonfinalists. Substantial differences were observed between the physical characteristics of finalists in swimming and diving events. The divers were older (2.9 years), shorter (6.7 cm), and lighter for their height (5 kg) than swimmers. Of the 60 medalists from ten swimming events at Munich and Montreal, only two (3%) had heights below the mean height for women (162 cm) in the United States, compared with three (25%) of 12 medalists in diving.
26. Microsphere Delivery of Adenoviral-Liposome Complexes Reduces Adenoviral Immunogenicity and Allows Successful Re-Administration of the Virus without Loss of Gene Expression Efficiency
Authors: Jason C. Steel, John C. Morris, Mark A. Burton, Heather M.A. Cavanagh, Wouter H.J. Kalle
Journal: Molecular Therapy (2005)

The successful use and repeat administration of adenoviral vectors for gene therapy is hampered by the virus's immunogenicity and poor tissue localization. Following initial exposure to the virus, antibody production occurs often limiting the therapeutic benefit of secondary administration. Further, the small size and the ubiquitous expression of the adenoviral receptor limits the ability of the virus to remain localized within a treatment site. In order to overcome these problems we examined a combination of liposomes and microspheres for the delivery of adenovirus. We found that conjugation of liposomes to adenovirus can provide shielding from neutralizing antibodies, and that binding the adenovirus-liposome complexes to microspheres increased the level of protection. We examined microsphere-adenovirus-liposome (MAL) complexes in vivo and compared the antibody production, transgene expression and localization of gene expression to that of naked adenovirus (NA) and adenovirus complexed to liposomes (AL complexes). Our results showed that the MAL complexes induced significantly lower antibody titers than either the AL complexes or NA. In animals pre-exposed to adenovirus, NA induced 14-fold greater antibody levels than the MAL complexes (P < 0.05). Similarly, AL complexes induced significantly higher levels of antibodies when compared to the MAL complexes with 10-fold more antibodies induced (P < 0.05). With respect to transgene expression, animals pre-exposed to adenovirus and treated with MAL complexes exhibited 99% greater transgene expression than those treated with NA and 35% more expression than those treated with AL complexes (P < 0.05). When comparing the level of gene expression in animals not exposed to adenovirus to those pre-exposed, we showed that expression with both the AL complexes and NA decreased significantly while expression in animals treated with MAL complexes remained constant indicating that re-administration of the adenovirus without loss of expression was achievable using the MAL complexes. In addition to the benefits of reduced immunogenicity and an enhanced ability to re-dose the animals, we also show the MAL complexes provided greater localization of gene expression than either the AL complexes or NA. After an intratumoral injection of MAL complexes up to 90% of gene expression was retained in the tumor. This was significantly greater than the levels observed in the tumor following treatment with NA (65%) or AL complexes (75%). Conclusion: The use of MAL complexes to deliver adenovirus provides a simple method to enhance vector localization and inhibit neutralization by the immune system while maintaining high transfection efficiency.
Binding of high molecular weight kininogen to human endothelial cells is mediated via a site within domains 2 and 3 of the urokinase receptor.
Authors: R W Colman, R A Pixley, S Najamunnisa, W Yan, J Wang, A Mazar, K R McCrae
Journal: Journal of Clinical Investigation (1997)

The urokinase receptor (uPAR) binds urokinase-type plasminogen activator (u-PA) through specific interactions with uPAR domain 1, and vitronectin through interactions with a site within uPAR domains 2 and 3. These interactions promote the expression of cell surface plasminogen activator activity and cellular adhesion to vitronectin, respectively. High molecular weight kininogen (HK) also stimulates the expression of cell surface plasminogen activator activity through its ability to serve as an acquired receptor for prekallikrein, which, after its activation, may directly activate prourokinase. Here, we report that binding of the cleaved form of HK (HKa) to human umbilical vein endothelial cells (HUVEC) is mediated through zinc-dependent interactions with uPAR. These occur through a site within uPAR domains 2 and 3, since the binding of 125I-HKa to HUVEC is inhibited by vitronectin, anti-uPAR domain 2 and 3 antibodies and soluble, recombinant uPAR (suPAR), but not by antibody 7E3, which recognizes the beta chain of the endothelial cell vitronectin receptor (integrin alphavbeta3), or fibrinogen, another alphavbeta3 ligand. We also demonstrate the formation of a zinc-dependent complex between suPAR and HKa. Interactions of HKa with endothelial cell uPAR may underlie its ability to promote kallikrein-dependent cell surface plasmin generation, and also explain, in part, its antiadhesive properties.
Bacteriologic and Serologic Evidence for Neisseria meningitidis in Acute Pneumonia.
Authors: William H. Wood
Journal: Annals of Internal Medicine (1971)

Meeting Abstracts1 May 1971Bacteriologic and Serologic Evidence for Neisseria meningitidis in Acute Pneumonia.William H. Wood Jr., M.D., Emanuel Wolinsky, M.D.William H. Wood Jr., M.D.Search for more papers by this author, Emanuel Wolinsky, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-74-5-829_4 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptA group of 20 patients was selected from a large number of patients with acute pneumonia seen over a period of 18 months. Four had positive blood cultures forNeisseria meningitidis. The rest had admission sputum cultures containing large numbers of meningococci. The cases were grouped into three categories on the basis of clinical data. Four cases in bacteremic patients without evidence of meningitis were classified as definite meningococcal pneumonia; presumptive meningococcal pneumonia—five cases in which the only bacterial pathogen found in the sputum wasN. meningitidis;and questionable meningococcal pneumonia —11 cases in which there were large numbers of... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Cleveland, Ohio PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 May 1971Volume 74, Issue 5Page: 829-829KeywordsBacterial pathogensBacterial pneumoniaBloodMeningitisNeisseria meningitidisPneumoniaSputum Issue Published: 1 May 1971 PDF DownloadLoading ...
Authors respond to editorial
Authors: L. V. d. Block, R. Deschepper, J. Bilsen, N. Bossuyt, V. V. Casteren, L. Deliens
Journal: BMJ (2009)

In the editorial accompanying our study, Byock says that we focus on practices that rarely occur at the end of life, such as euthanasia and physician assisted suicide, and pay little attention to more common decisions.1 2 However, detailed empirical reporting is necessary because …
Opportunistic Infections and Kaposi's Sarcoma in Homosexual Men
Authors: David T. Durack
Journal: New England Journal of Medicine (1981)

In the summer of 1981, the Centers for Disease Control (CDC) alerted the medical world to an unexpected outbreak of Pneumocystis carinii pneumonia and Kaposi's sarcoma in young homosexual men who had no known reason to contract these uncommon diseases.1 , 2 New and surprising though this association may be, enough cases have already been collected to establish its reality. More than 160 examples are now being analyzed at the CDC, and five or six new cases are being reported each week. Recently, eight cases of Kaposi's sarcoma in young homosexual men in New York City were reported in Lancet.3 In . . .
The Biography of the Factitious-Disorder Patient
Authors: Reinhard Plassmann
Journal: Psychotherapy and Psychosomatics (1994)

Review Articles| February 18 2010 The Biography of the Factitious-Disorder Patient Subject Area: Psychiatry and Psychology Reinhard Plassmann Reinhard Plassmann Burg-Klinik, Stadtlengsfeld, Deutschland Search for other works by this author on: This Site PubMed Google Scholar Psychother Psychosom (1994) 62 (1-2): 123–128. https://doi.org/10.1159/000288912 Article history Published Online: February 18 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 Reinhard Plassmann; The Biography of the Factitious-Disorder Patient. Psychother Psychosom 31 December 1994; 62 (1-2): 123–128. https://doi.org/10.1159/000288912 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. 1994Copyright / 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.
Pregnancy and liver disease.
Authors: M M Steven
Journal: Gut (1981)

Progress reportIn considering liver disease in pregnancy, it is useful to use Sherlock's classification6 and consider (1) liver disease peculiar to pregnancy;(2) intercurrent liver disease occurring during pregnancy;(3) pregnancy complicating liver disease.Previous authors have considered jaundice during pregnancy,46 but, as jaundice may be absent or subclinical, we have elected not to use this classifi- cation.There have been several studies of the incidence of jaundice, clinical and biochemical, occurring in pregnancy, and figures quoted for the incidence 592 on July 17,