tbuckley/cabot-search huggingface dataset:
Cimetidine and Granulopoiesis
Authors: S. ERIDANI
Journal: Annals of Internal Medicine (1982)

Letters and Corrections1 October 1982Cimetidine and GranulopoiesisS. ERIDANI, M.D., I.D.A. JOHNSTON, M.R.C.P., S. VILLA, B.SC.S. ERIDANI, M.D.Search for more papers by this author, I.D.A. JOHNSTON, M.R.C.P.Search for more papers by this author, S. VILLA, B.SC.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-97-4-620_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: Although there have been several reports of granulocytopenia associated with the use of cimetidine (1), inhibition of granulocyte-macrophage colony formation by in-vitro cimetidine has only recently been shown in two patients (2). We report a further case with bone marrow culture studies.A 72-year-old man was admitted from another hospital with acute renal failure after a laparotomy for a leaking aortic aneurysm. The patient was hemodialysed daily and needed ventilation on admission. On the third day of hospitalization he developed aspiration pneumonia. Intravenous gentamicin, erythromycin, and hydrocortisone were begun with cimetidine, 100 mg/dL, as a prophylactic measure....References1. FRESTON J. Cimetidine and granulocytopenia [Editorial]. Ann Intern Med. 1979;90:264-5. LinkGoogle Scholar2. FITCHENKOEFFLER JH. Cimetidine and granulopoiesis: bone marrow culture studies in normal man and patients with cimetidine associated neutropenia. Br J Haematol. 1980;46:361-6. CrossrefMedlineGoogle Scholar3. DE GALOCSYVAN YPERSELE DE STRIHOU CC. Pancytopenia with cimetidine. Ann Intern Med. 1979;90:274. LinkGoogle Scholar4. JOHNSONBLACKHUGHESCLARKE NAAS. Leucopenia with cimetidine [Letter]. Lancet. 1977;2:1226. CrossrefGoogle Scholar5. BYRON J. Pharmacodynamic basis for the interaction of cimetidine with the bone marrow stem cells (CFUs). Exp Hematol. 1980;8:256-63. MedlineGoogle Scholar6. LUKLUKHENDRIX GWT. Cimetidine and impaired renal function. Ann Intern Med. 1979;90:991-2. LinkGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: St Thomas' Hospital London SE1 England PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byCimetidine induced pancytopeniaHaematological Adverse Effects of Histamine H2-Receptor AntagonistsAdverse Reactions and Interactions with H2-Receptor AntagonistsEffect of cimetidine on granulocyte-macrophage colony formation by normal and chronic renal failure bone marrow cellsGastrointestinal drugs 1 October 1982Volume 97, Issue 4Page: 620-620KeywordsAcute renal failureAneurysmsBone marrowErythromycinHospitalizationsLaparotomyPneumonia Issue Published: 1 October 1982 PDF downloadLoading ...
Needle Biopsy-Reply
Authors: Harry J. Tamoney
Journal: JAMA (1976)

In Reply.—  In response to Dr Rush's comments on my article, I did not intend to condemn the use of needle biopsy as a valid diagnostic tool. I support Dr Crile's aspiration of thyroid nodules and, since my residency days at Memorial Hospital, have been an advocate of aspiration of breast masses. In these instances and others, I find it a very useful procedure.  I seriously question the value of needle biopsy in accurately diagnosing parotid swellings. It is not just the needle dissemination which Dr Rush mentions that alarms me. I am more concerned with the remote possibility of obtaining an accurate histologic identification. My second cause for concern is the inherent danger of injury to the facial nerve in such a blind maneuver as a needle biopsy. We do not encounter this hazard in needle biopsy of other areas, for example, liver, lung, or breast.  I am unfamiliar
Illuminating regeneration: noninvasive imaging of disease progression in muscular dystrophy
Authors: Jennifer R. Levy, Kevin P. Campbell
Journal: Journal of Clinical Investigation (2013)

Muscular dystrophies are characterized by progressive muscle weakness and wasting. Among the key obstacles to the development of therapies is the absence of an assay to monitor disease progression in live animals. In this issue of the JCI, Maguire and colleagues use noninvasive bioluminescence imaging to monitor luciferase activity in mice expressing an inducible luciferase reporter gene in satellite cells. These cells proliferate in response to degeneration, therefore increasing the level of luciferase expression in dystrophic muscle.
Patterns and Dynamics of SVZ Cell Migration in the Postnatal Forebrain
Authors: Akiyoshi Kakita, James E. Goldman
Journal: Neuron (1999)

Glial progenitors colonize the CNS widely in the perinatal period, but the pathways and mechanisms of migration are not well understood. We investigated the migration of progenitors from the neonatal rat forebrain subventricular zone (SVZ) by labeling them in vivo with a retrovirus encoding green fluorescent protein and visualizing movements by time lapse microscopy in slices. Cells within the dorsolateral SVZ moved in an undirected fashion but migrated radially and tangentially after emigration into white matter, cortex, and striatum. Cells in the striatal SVZ migrated parallel to the ventricular surface. During migration, elongation of the leading process and nuclear translocation were independent or linked. Orthogonal turning involved either cessation of cell body movement and formation of a new leading process or continuous cell body movement and bending of the leading process.
Low-Level Transcutaneous Electrical Vagus Nerve Stimulation Suppresses Atrial Fibrillation
Authors: Stavros Stavrakis, Mary Beth Humphrey, Benjamin J. Scherlag, Yanqing Hu, Warren M. Jackman, Hiroshi Nakagawa, Deborah Lockwood, Ralph Lazzara, Sunny S. Po
Journal: Journal of the American College of Cardiology (2015)
Stretch-mediated release of angiotensin II induces myocyte apoptosis by activating p53 that enhances the local renin-angiotensin system and decreases the Bcl-2-to-Bax protein ratio in the cell.
Authors: A Leri, P P Claudio, Q Li, X Wang, K Reiss, S Wang, A Malhotra, J Kajstura, P Anversa
Journal: Journal of Clinical Investigation (1998)

Physical forces activate apoptosis and gene expression, but the mechanism is unknown. For this purpose, adult myocytes were stretched in an equibiaxial stretch apparatus and the magnitude of cell death was examined 4 and 24 h later. The possibility of stretch-mediated activation of p53 and p53-dependent genes was evaluated at 30 min, 2, 4, 8, and 24 h. Myocyte apoptosis increased by 4.4- and 7.6-fold at 4 and 24 h after stretch. p53 binding to the promoter of angiotensinogen, AT1 receptor, and Bax also increased. Expression of angiotensinogen, AT1 receptor, p53, and Bax increased and Bcl-2 decreased in stretched myocytes. The changes in AT1 receptor, p53, Bax, and Bcl-2 became more apparent with the duration of stretch. Angiotensin II concentration in the medium increased at 10 min, reaching maximal levels at 1 and 20 h. The AT1 blocker, losartan, abolished apoptosis in stretched myocytes. Myocyte volume was not influenced by stretch. In conclusion, stretch-mediated release of angiotensin II is coupled with apoptosis and the activation of p53 which may be responsible for the prolonged upregulation of the local renin-angiotensin system and the increased susceptibility of myocytes to undergo apoptosis.
760. Overcoming Rhesus Macaque Endogenous Restriction Factors during HIV-1 Vector Transduction
Authors: Christina H. Swan, Udayan Chatterji, Philippe Gallay, Louis J. Picker, Bruce E. Torbett
Journal: Molecular Therapy (2006)

The ability to deliver genes into hematopoietic stem cells via HIV-1 derived vectors holds promise to investigate the pathobiology and therapeutic applications for infectious diseases. In vivo HIV-1 infection models are limited. The NOD/SCID-hu mouse has been an excellent model to study thymic function and HIV-1 thymic depletion. However, to better understand HIV-1 pathogenesis in humans, non-human primate models must be used. The rhesus macaque simian immunodeficiency virus (SIV) model recapitulates aspects of the pathology seen in human HIV-1 infection. Our laboratory has designed and previously described a CCR5 intrabody HIV-1 vector that efficiently prevents R5-tropic HIV-1 entry and provides transduced CD4+ T cells with a selective advantage during a dendritic cell-mediated infection. Unfortunately, transduction with a HIV-1 derived vector undergoes a post-entry restriction when introduced into rhesus macaque cells. The target for rhesus macaque endogenous restriction factors lies within the HIV-1 capsid protein, and may be due to rhesus macaque Cyclophilin A (CypA) incorporation and TRIM-5α capsid interactions. To increase transduction efficacy in both non-human primate and human hematopoietic cells we have assessed a naturally occurring HIV-1 capsid motif (V86P/H87Q/I91V/M96I), which evades both CypA- dependence in human cells and TRIM-5α-CypA restriction in owl monkey kidney cells during HIV-1 infection (Chatterji, et al. JBC, 2005). The V86P/H87Q/I91V/M96I capsid mutation within the CypA binding loop also rendered VSV-G pseudotyped HIV-1 vectors independent of CypA incorporation during human and non-human primate cell transduction. Interestingly, HIV-1 vectors with the V86P/H87Q/I91V/M96I capsid mutation were able to efficiently transduce non-human primate Vero and sMAGI cell lines and yielded a 1.4-fold increase in transduction efficiency in primary human CD4+ T cells. However, the V86P/H87Q/I91V/M96I HIV-1 vector did not efficiently transduce primary rhesus macaque CD4+ T cells. We are now in the process of evaluating novel HIV-1 capsid mutations that lie within and around the CypA binding loop in our HIV-1 vector system, such as H87Q and Q50Y/T54Q. Some of these capsid mutations in HIV-1 are required to efficiently infect primary rhesus macaque macrophages. We will present our findings on HIV-1 capsid mutations that allow HIV-1 vector entry into primary rhesus macaque CD4+ T cells.
Molecular cloning and characterization of a birch pollen minor allergen, Bet v 5, belonging to a family of isoflavone reductase–related proteins☆☆☆
Authors: Fariba Karamloo, Nicole Schmitz, Stephan Scheurer, Kay Foetisch, Andreas Hoffmann, Dieter Haustein, Stefan Vieths
Journal: Journal of Allergy and Clinical Immunology (1999)
Persistence of Organisms for Lyme Arthritis
Authors: Michael A. Patmas
Journal: Annals of Internal Medicine (1994)

Letters1 September 1994Persistence of Organisms for Lyme ArthritisMichael A. Patmas, MS, MDMichael A. Patmas, MS, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-121-5-199409010-00017 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:The provocative report by Bradley and colleagues [1] supports the emerging view that persistence of spirochetes is important in the pathogenesis of chronic, relapsing Lyme disease [2, 3]. It is disturbing that the patients described have not responded to courses of antibiotic therapy exceeding those previously thought to be curative in studies with only short-term follow-up [4]. The long periods of clinical latency (sample, 25 patients) spanning 5 years also raise doubt about the presumption that routinely prescribed, short-duration antibiotic treatment is curative and that persistent or relapsing symptoms are necessarily caused by the development of fibromyalgia ...References1. Bradley JF, Russell LJ, Goodman JL. The persistence of spirochetal nucleic acids in active Lyme arthritis. Ann Intern Med. 1994; 120:487-9. Google Scholar2. Preac-Mursic V, Weber K, Pfister HW, Wilske B, Gross B, Bauman, A, et al. Survival of Borrelia burgdorferi in antibiotically treated patients with Lyme borreliosis. Infection. 1989; 17:355-9. Google Scholar3. Leigner KB, Rosenklide CE, Campbell GL, Quan TJ, Dennis DT. Culture-confirmed treatment failure of cefotaxime and minocycline in a case of Lyme meningoencephalitis in the United States. In: Program and Abstracts of the Fifth International Conference on Lyme Borreliosis, Arlington, Virginia, May 30-June 2, 1992. Bethesda, Maryland: Federation of American Societies for Experimental Biology; 1992. Google Scholar4. Steere AC, Taylor E, McHugh GL, Logigan EL. The overdiagnosis of Lyme disease. JAMA. 1993; 269:1812-6. Google Scholar5. Hsu VM, Patella SJ, Sigal LH. “Chronic Lyme disease” as the incorrect diagnosis in patients with fibromyalgia. Arthritis Rheum. 1993; 36:1493-500. Google Scholar Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 September 1994Volume 121, Issue 5Page: 383-384KeywordsAntibioticsBorrelia burgdorferiFibromyalgiaLyme diseasePathogenesisSpirochetes Issue Published: 1 September 1994 CopyrightCopyright © 1994 by American College of Physicians. All Rights Reserved.PDF DownloadLoading ...
A single FIT (≥ 50 ng Hb/mL) detected 38% of screen-detected advanced colorectal neoplasia
Authors: Richard F. Logan
Journal: Annals of Internal Medicine (2012)

Source Citation de Wijkerslooth TR, Stoop EM, Bossuyt PM, et al. Immunochemical fecal occult blood testing is equally sensitive for proximal and distal advanced neoplasia. Am J Gastroenterol. 2012;107:1570-8. 22850431
Focus: Washington: Enthoven criticises Clinton's health care reforms
Authors: J Roberts
Journal: BMJ (1994)

An eighteenth century measure intended to prevent the British from seizing American colonists' property has returned to haunt President Clinton's attempts to reform the US health care system. The measure is the clause in the fifth amendment saying “Nor shall private property be taken for public use without just compensation.” And it is being wielded by an unlikely opponent.

Alain Enthoven, architect of British and American health reforms, is claiming that Clinton's proposals for global budgeting are unconstitutional. The argument is a complicated one - but Enthoven's main complaint is that Clinton has moved from the idea of a managed market place to government regulation.

Enthoven, professor of public and private management at Stanford University, California, can claim the credit for providing the blueprints for two major reforms of health care. His ideas provided the rough sketches that …
Tumor Necrosis Factor-α Is Associated With Increased Protein C Activation in Nonobese Type 2 Diabetic Patients
Authors: Yutaka Yano, Esteban C. Gabazza, Nagako Kitagawa, Nelson E. Bruno, Kazutaka Matsumoto, Kaname Nakatani, Rika Araki, Akira Katsuki, Yukihiko Adachi, Yasuhiro Sumida
Journal: Diabetes Care (2004)

Tumor necrosis factor-α (TNF-α) plays a critical role in the pathogenesis of vascular injury in diabetic patients (1). Increased circulating levels of TNF-α have been reported in diabetic patients (2,3). Hyperglycemia stimulates TNF-α secreted from monocytes and endothelial cells (4,5). Moreover, TNF-α may cause vascular injury by affecting the balance between coagulation and fibrinolysis. For example, TNF-α stimulates the expression of tissue factor that is the initiator of blood coagulation activation and the secretion of plasminogen activator inhibitor-1 that inhibits fibrinolysis (1).

Activated protein C (APC) is a serine protease that inhibits activation of the blood coagulation system by proteolytically inactivating factors Va and VIIIa and by stimulating fibrinolysis (6,7). APC may indirectly promote fibrinolysis by inhibiting thrombin generation and by inhibiting the action of plasminogen activator inhibitor-1 (8). Recently, it was reported that APC has an anti-inflammatory effect and that it inhibits vascular injury induced by TNF-α …
Prevalence of Participation in Methadone Programs
Authors: MARVIN E. PERKINS, ALEX RICHMAN
Journal: American Journal of Psychiatry (1972)

The authors' study of the two-year prevalence of participation during five successive years in a particular methadone maintenance system disclosed no evidence of worsening of results for first admissions as time went on. Although the admission criteria differed somewhat, the rate of retention after ambulatory induction was higher than that for inpatient induction. The authors point out the need for a statistical index that considers retention of patients in any treatment facility rather than only in one particular program or modality of treatment.
Antiproliferative effects of interferon alpha on hepatic progenitor cells<i>in vitro</i>and<i>in vivo</i>
Authors: Rebecca Lim, Belinda Knight, Keyur Patel, John G. McHutchison, George C. Yeoh, John K. Olynyk
Journal: Hepatology (2006)

Hepatic progenitor cells (called oval cells in rodents) proliferate during chronic liver injury. They have been suggested as targets of malignant transformation in chronic liver diseases, including chronic hepatitis C. Interferon alpha therapy reduces the risk of hepatocellular carcinoma (HCC) in chronic hepatitis C regardless of viral clearance. The aim of this study was to determine whether interferon alpha could reduce the risk of HCC by modifying preneoplastic events in the hepatic progenitor cell population. Pre- and post-treatment liver biopsies were evaluated for changes in t he hepaticprogenitor cell population in 16 patients with non-responding chronic hepatitis C Interferon alpha-based treatment significantly reduced the numbers of c-kit-positive hepatic progenitor cells by 50%. To determine the mechanism of cell number reduction, the effects of interferon alpha on murinehepatic progenitor cells were studied in vitro. MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) proliferation assay and proliferating cell nuclear antigen staining showed that interferon alpha had a dose-dependent, anti-proliferative effect Interferon alpha stimulated hepatocytic and biliary differentiation of the oval cell lines reflected by increased expression of albumin and cytokeratin19 accompanied by decreased expression of alphafetoprotein and Thy-1. To validatethese results in vivo, mice were placed on the choline-deficient, ethionine-supplemented diet to induce liver injury and oval cell proliferation and treated with pegylated interferon alpha 2b for 2 weeks. This resulted in a significant four-fold reduction in the number of oval cells (P < .05). In conclusion, interferon alpha-based treatment reduced the number of hepatic progenitor cells in chronic liver injury by modulating apoptosis, proliferation, and differentiation. Supplementay material for this article can
An open clinical pilot study of the efficacy and safety of oral terbinafine in dry non-inflammatory tinea capitis
Authors: T.S. HAROON, I. HUSSAIN, A. MAHMOOD, A.H. NAGI, I. AHMAD, M. ZAHID
Journal: British Journal of Dermatology (1992)

Journal Article An open clinical pilot study of the efficacy and safety of oral terbinafine in dry non‐inflammatory tinea capitis Get access T.S. HAROON, T.S. HAROON Departments of Dermatology, King Edward Medical College/Mayo Hospital, Lahore, Pakistan Professor T.S. Haroon, Department of Dermatology, King Edward Medical College/Mayo Hospital, Nila Gumbad, Lahore, Pakistan. Search for other works by this author on: Oxford Academic Google Scholar I. HUSSAIN, I. HUSSAIN Departments of Dermatology, King Edward Medical College/Mayo Hospital, Lahore, Pakistan Search for other works by this author on: Oxford Academic Google Scholar A. MAHMOOD, A. MAHMOOD Departments of Dermatology, King Edward Medical College/Mayo Hospital, Lahore, Pakistan Search for other works by this author on: Oxford Academic Google Scholar A.H. NAGI, A.H. NAGI Department of Pathology, King Edward Medical College/Mayo Hospital, Lahore, Pakistan Search for other works by this author on: Oxford Academic Google Scholar I. AHMAD, I. AHMAD Department of Pathology, King Edward Medical College/Mayo Hospital, Lahore, Pakistan Search for other works by this author on: Oxford Academic Google Scholar M. ZAHID M. ZAHID Department of Pathology, King Edward Medical College/Mayo Hospital, Lahore, Pakistan Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 126, Issue s39, 1 February 1992, Pages 47–50, https://doi.org/10.1111/j.1365-2133.1992.tb00010.x Published: 01 February 1992
Chemical form of cadmium (and other heavy metals) in rice and wheat plants.
Authors: M Kaneta, H Hikichi, S Endo, N Sugiyama
Journal: Environmental Health Perspectives (1986)

Chemical forms of heavy metals such as Cd, Cu, Ni, and Pb in rice and wheat plants grown in nutrient solution containing a heavy metal were investigated. Fractionation of an extract of Cd-treated rice plants on Sephadex G-75 showed cadmium to be associated with organic compounds of high (fraction A), intermediary (fraction B), and low molecular weight (fraction C). Material A, whose molecular weight was greater than 440,000, is probably nonspecific binding of Cd to normal cell components. Materials B and C can be classified as types of metallothionein. The molecular weight of B was 33,100. This material contains 12 mg Cd/g protein. The UV-absorption spectrum of B showed absorptions at 280 and 250 nm. Material B was not eluted even at a very high ionic strength from the DEAE-cellulose column, but it was eluted at a very low ionic strength from a CM-cellulose column, indicating a highly anionic molecule which differs from metallothionein in animals. Fraction C contains two materials: one a Cd-containing material whose molecular weight was estimated to be approximately 7000 and the other an inorganic Cd salt. In addition to cadmium, copper, lead, and nickel in rice and wheat have been studied. As a result, heavy metal-containing materials whose molecular weights were estimated to be approximately 16,000 and 8900 (Ni-treated rice plants), 7000 (Pb-treated rice plants), 5000 (Cd-treated wheat plants), and 21,000 (Cu-treated wheat plants) were isolated.
Adults hospitalised with acute respiratory illness rarely have detectable bacteria in the absence of COPD or pneumonia; viral infection predominates in a large prospective UK sample
Authors: Tristan W. Clark, Marie-jo Medina, Sally Batham, Martin D. Curran, Surendra Parmar, Karl G. Nicholson
Journal: Journal of Infection (2014)

Many adult patients hospitalised with acute respiratory illness have viruses detected but the overall importance of viral infection compared to bacterial infection is unclear.Patients were recruited from two acute hospital sites in Leicester (UK) over 3 successive winters. Samples were taken for viral and bacterial testing.Of the 780 patients hospitalised with acute respiratory illness 345 (44%) had a respiratory virus detected. Picornaviruses were the most commonly isolated viruses (detected in 23% of all patients). Virus detection rates exceeded 50% in patients with exacerbation of asthma (58%), acute bronchitis and Influenza-like-illness (64%), and ranged from 30 to 50% in patients with an exacerbation of COPD (38%), community acquired pneumonia (36%) and congestive cardiac failure (31%). Bacterial detection was relatively frequent in patients with exacerbation of COPD and pneumonia (25% and 33% respectively) but was uncommon in all other groups. Antibiotic use was high across all clinical groups (76% overall) and only 21% of all antibiotic use occurred in patients with detectable bacteria.Respiratory viruses are the predominant detectable aetiological agents in most hospitalised adults with acute respiratory illness. Antibiotic usage in hospital remains excessive including in clinical conditions associated with low rates of bacterial detection. Efforts at reducing excess antibiotic use should focus on these groups as a priority. Registered International Standard Controlled Trial Number: 21521552.