tbuckley/cabot-search huggingface dataset:
Virus-induced decrease of insulin receptors in cultured human cells.
Authors: F Shimizu, J J Hooks, C R Kahn, A L Notkins
Journal: Journal of Clinical Investigation (1980)

Viral infections may produce abnormalities in carbohydrate metabolism in normal subjects and profound changes in glucose homeostasis in insulin-dependent diabetics. Using an in vitro radio-receptor assay with 125I-labeled insulin and human-amnion (WISH) cells, the effect of viral infections on insulin receptors was examined. Both herpes simplex virus and vesicular stomatitis virus produced a 50% decrease in insulin binding. There was no evidence that this decrease was due to degradation of insulin. On quantitative analysis, this decrease in binding was found to be the result of a decrease in receptor concentration with no change in receptor affinity. The decrease in receptors occurred between 4 and 12 h, at the time viral antigens were being inserted into the plasma membrane of infected cells. Because the t 1/2 of insulin receptors in uninfected cells was between 14 and 24 h, the decrease in insulin receptors cannot be explained solely by virus-induced shut-off of macromolecular synthesis. Moreover, viruses such as encephalomyocarditis that do not insert new antigens into the plasma membrane, did not cause changes in the number of insulin receptors. The most likely explanation is that virus-induced changes in the plasma membrane altered or displaced insulin receptors. It is concluded that the insulin receptor assay is a sensitive and quantitative method for studying the effect of viral infections on cell membranes. These data also suggest that abnormalities in glucose metabolism associated with some viral infections may be due, in part, to changes in the concentration of insulin receptors.
Cross sectional study of contribution of clinical assessment and simple cardiac investigations to diagnosis of left ventricular systolic dysfunction in patients admitted with acute dyspnoea
Authors: N. D Gillespie, G. McNeill, T. Pringle, S. Ogston, A. D Struthers, S. D Pringle
Journal: BMJ (1997)

<h3>Abstract</h3> <b>Objective:</b> To assess the comparative contribution of clinical assessment, electrocardiography, and chest radiography to the diagnosis of left ventricular systolic dysfunction in patients admitted to a general medical ward with acute dyspnoea. <b>Design:</b> Prospective cross sectional study. <b>Setting:</b> Acute medical admissions ward of a teaching hospital. <b>Subjects:</b> 71 randomly selected patients admitted with acute dyspnoea. <b>Main outcome measures:</b> Sensitivity and specificity of each investigation and logistic regression analysis of each variable in identifying left ventricular systolic dysfunction. <b>Results:</b> Clinical assessment in this cohort of patients with severe dyspnoea was generally sensitive (sensitivity 81%). Patients were divided into three groups on the basis of clinical assessment. In the first group (37 patients) the diagnosis of systolic dysfunction was clear, in the second (22) it was in doubt, and in the third (12) it was unlikely. The sensitivity of clinical assessment in identifying left ventricular systolic dysfunction was 81% and the specificity was 47%. The specificity of diagnosis was improved by electrocardiography (69%) and chest radiography (92%). Logistic regression analysis showed that isolated pulmonary crepitations were a comparatively poor predictor of left ventricular systolic dysfunction (<sup>2</sup>=10.215, P=0.0014) but that a full clinical examination had reasonable predictive value (<sup>2</sup>=24.82, P&lt;0.00001). The combination of clinical assessment and chest radiography improved the accuracy of diagnosis (<sup>2</sup>=28.08, P&lt;0.00001), as did the combination of clinical assessment and electrocardiography (<sup>2</sup>=32.41, P&lt;0.00001). <b>Conclusion:</b> Clinical assessment in patients admitted with acute dyspnoea is comparatively accurate. Patients with abnormal results on chest radiography, electrocardiography, and clinical examination have a high likelihood of having left ventricular systolic dysfunction. Echocardiography contributes little more to the diagnosis in these patients and may be more efficiently directed towards patients in whom the diagnosis is still in doubt after clinical assessment, chest radiography, and electrocardiography. <h3>Key messages</h3> The availability of echocardiography is limited for patients admitted to hospital with acute dyspnoea The presence of isolated lung crepitations is a poor predictor of left ventricular systolic dysfunction Full clinical assessment is sensitive in detecting left ventricular systolic dysfunction, with specificity being added by either chest radiography or electrocardiography Echocardiography should be reserved for cases with the most diagnostic doubt
Point mutations of the BCL-6 gene: clinical and prognostic correlation in B-diffuse large cell lymphoma
Authors: U Vitolo, B Botto, D Capello, D Vivenza, V Zagonel, A Gloghini, D Novero, G Parvis, R Calvi, C Ariatti, I Milan, M Bertini, C Boccomini, R Freilone, P Pregno, L Orsucci, G Palestro, G Saglio, A Carbone, E Gallo, G Gaidano
Journal: Leukemia (2002)
Bed Rest After Myocardial Infarction
Authors: RICHARD S. CRAMPTON
Journal: Annals of Internal Medicine (1973)

Editorial Notes1 September 1973Bed Rest After Myocardial InfarctionRICHARD S. CRAMPTON, M.D.RICHARD S. CRAMPTON, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-79-3-449 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptDespite the apparent benefits of prehospital treatment and early mobilization, many physicians who are ignorant of the biological, psychological, and economic effects of acute myocardial infarction, leave prehospital treatment to chance, prolong bed rest unnecessarily, and unduly put off ambulation, discharge, and return to gainful work for their patients. The facts are that ending bed rest early does not increase complication or death rates (1-4), that 60% of patients who receive prehospital resuscitation return to active life (5), and that community mortality is reduced 15% by the community-wide coronary care system (6). In England, Ireland, The Netherlands, Russia, Scotland, and...References1. BECKWITHKERNODLELEHEW JDA: The management of myocardial infarction with particular reference to the chair treatment. Ann Intern Med 41:1189-1195, 1954 LinkGoogle Scholar2. Leading Article: Early mobilisation after myocardial infarction. Lancet 2:1359-1360, 1971 MedlineGoogle Scholar3. LAMERSDROSTKROON HWB: Early mobilization after myocardial infarction: a controlled study. Br Med J 1:257-259, 1973 CrossrefMedlineGoogle Scholar4. HUTTERSIDELSHINE AVK: Early hospital discharge after myocardial infarction. N Engl J Med 288:1141-1144, 1973 CrossrefMedlineGoogle Scholar5. CRAMPTONALDRICHSTILLERMAN RRR: Prehospital cardiopulmonary resuscitation in acute myocardial infarction. N Engl J Med 286:1320-1321, 1972 CrossrefMedlineGoogle Scholar6. CRAMPTONSTILLERMANGASCHO RRJ: Prehospital coronary care in Charottesville and Albemarle County. Va Med Mon 99:1191-1196, 1972 Google Scholar7. SHAH J: Early mobilisation after myocardial infarction. Lancet 1:534, 1972 CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: RICHARD S. CRAMPTON, M.D.Affiliations: Department of Internal Medicine University of Virginia School of Medicine Charlottesville, Virginia PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byThe experiences of myocardial infarction patients readmitted within six months of primary percutaneous coronary interventionReduction of prehospital, ambulance and community coronary death rates by the community-wide emergency cardiac care systemEarly Hospital Discharge in Myocardial InfarctionRICHARD S. CRAMPTON, M.D., F.A.C.P. 1 September 1973Volume 79, Issue 3Page: 449-449KeywordsAcute myocardial infarctionDeath ratesMortalityMyocardial infarctionResuscitationWalking ePublished: 1 December 2008 Issue Published: 1 September 1973 PDF downloadLoading ...
Pneumococcal Infection in Bone Marrow Transplant Recipients
Authors: JOHN L. BOICE
Journal: Annals of Internal Medicine (1980)

Letters1 April 1980Pneumococcal Infection in Bone Marrow Transplant RecipientsJOHN L. BOICE, M.D.JOHN L. BOICE, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-92-4-571_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: In laboratory animals, two conditions are necessary to enhance the susceptibility to overwhelming pneumococcal infection after intraperitoneal inoculation: absence of the spleen; and absent or limited amounts of pre-existing antipneumococcal opsonizing antibody (1). Winston and colleagues (2) elegantly demonstrate in their paper in the December 1979 issue impaired serum opsonic activity secondary to low specific serum antibody or low complement activity in six of seven long-term bone marrow transplant survivors with episodes of severe pneumococcal infection. They speculate on several possible causes for these findings including immunologic immaturity secondary to therapy, absence of splenic production of specific...References1. HYSLOPMCCLUSKEY NR. Fever and circulatory collapse in an asplenic man. N Engl J Med. 1975;293:547-53. CrossrefMedlineGoogle Scholar2. WINSTONSCHIFFMANWANG DGD. Pneumococcal infections after bone-marrow transplantation. Ann Intern Med. 1979;91:835-41. LinkGoogle Scholar3. BISNO A. Hyposplenism and overwhelming pneumococcal infection: a reappraisal. Am J Med Sci. 1971;262:101-7. CrossrefMedlineGoogle Scholar4. HOOK E. Pneumococcal pneumonia. In: BEESON PB, MCDERMOTT W, WYNGAARDEN JB, eds. Cecil-Loeb Textbook of Medicine. 15th ed. Philadelphia: W. B. Saunders Co.; 1979:347-57. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: JOHN L. BOICE, M.D.Affiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byStreptococcus pneumoniae mycotic aortic aneurysm after allogeneic bone marrow transplantationChronic graft versus host disease is associated with long-term risk for pneumococcal infections in recipients of bone marrow transplantsChronic graft versus host disease is associated with long-term risk for pneumococcal infections in recipients of bone marrow transplants 1 April 1980Volume 92, Issue 4Page: 571-571KeywordsBone marrowInoculationResearch laboratoriesSpleen ePublished: 1 December 2008 Issue Published: 1 April 1980 PDF downloadLoading ...
Visible Drug Delivery by Supramolecular Nanocarriers Directing to Single-Platformed Diagnosis and Therapy of Pancreatic Tumor Model
Authors: Sachiko Kaida, Horacio Cabral, Michiaki Kumagai, Akihiro Kishimura, Yasuko Terada, Masaki Sekino, Ichio Aoki, Nobuhiro Nishiyama, Toru Tani, Kazunori Kataoka
Journal: Cancer Research (2010)

Nanoparticle therapeutics are promising platforms for cancer therapy. However, it remains a formidable challenge to assess their distribution and clinical efficacy for therapeutic applications. Here, by using multifunctional polymeric micellar nanocarriers incorporating clinically approved gadolinium (Gd)-based magnetic resonance imaging contrast agents and platinum (Pt) anticancer drugs through reversible metal chelation of Pt, simultaneous imaging and therapy of an orthotopic animal model of intractable human pancreatic tumor was successfully performed without any serious toxicity. The strong tumor contrast enhancement achieved by the micelles correlated with the 24 times increase of r(1) of the Gd chelates, the highest for the formulations using clinically approved Gd chelates reported to date. From the micro-synchrotron radiation X-ray fluorescence spectrometry scanning of the lesions, we confirmed that both the Gd chelates and Pt drugs delivered by the micelles selectively colocalized in the tumor interior. Our study provides new insights for the design of theranostic micelles with high contrast enhancement and site-specific clinical potential.
Potentiation of the antireactive, antiasthmatic effect of inhaled furosemide by inhaled lysine acetylsalicylate
Authors: S. Bianco, A. Vaghi, M. G. Pieroni, M. Robuschi, R. M. Refini, F. Berni, P. Sestini
Journal: Allergy (1993)

Nonsteroid antiinflammatory drugs interfere with the diuretic activity of furosemide, implying that this effect is at least partially dependent on renal prostaglandin synthesis. To investigate whether prostaglandin production could also modulate the bronchial antireactive activity of this diuretic drug, we investigated the effect of inhaled Iysine acetylsalicylate (162 mg) and of furosemide (18 mg), alone and in combination, on the bronchial obstructive response to ultrasonically nebulized water in asthmatic patients. The study was also prompted by the conflicting results obtained in previous studies of oral nonsteroid antiinflammatory drugs. Fifteen asthmatic patients underwent bronchial challenge with a mist of ultrasonically nebulized distilled water at the same time of day on four occasions, 2–4 days apart, 15 min after premedication according to a double‐blind, randomized protocol. After placebo, mean PD 15 to water mist did not differ from a preliminary test (2.1 ± 0.2 and 2.5 ± 0.4 ml, M ± SE, respectively). After lysine acetylsalicylate, mean PD., rose to 5.0 ± 0.7 ml (2.8 ± 0.6 times higher than placebo); after furosemide, to 9.0± 1.5 ml (4.4 ± 0.9 times over placebo); and after the two drugs in combination, to 32.2 ± 5.6 ml (16.3 ± 3.0 times higher than placebo). Similar results were obtained with inhaled indomethacin, whereas sodium salicylate had no effect. These data indicate that the bronchial antireactive activity of inhaled furosemide is greatly enhanced by inhaled lysine acetylsalicylate through a mechanism which probably involves inhibition of the local synthesis of prostaglandins, and could have therapeutic implications.
Intraischemic Preconditioning
Authors: Rainer Schulz, Heiner Post, Samir Sakka, David R. Wallbridge, Gerd Heusch
Journal: Circulation Research (1995)

Abstract Ischemic preconditioning (IP) and myocardial hibernation (MH) are both adaptive phenomena during acute myocardial ischemia, characterized by preserved myocardial viability and attenuated alterations of energy metabolism. Recent data from isolated buffer-perfused rabbit hearts pointed to a further link between IP and MH, in that an initial stimulus of no-flow ischemia was required to permit the development of MH during subsequent sustained low-flow ischemia. In the present study, we therefore investigated in the in situ pig heart whether a brief episode of no-flow ischemia enhances the myocardial tolerance to subsequent sustained low-flow ischemia. By blocking ATP-dependent potassium channels, we attempted to further determine whether such increased tolerance to ischemia is related to IP or MH, since blockade of ATP-dependent potassium channels abolishes the cardioprotection achieved by IP but not by MH. In 8 enflurane-anesthetized pigs serving as controls (group 1), the inflow into the cannulated left anterior descending coronary artery was reduced to achieve a 90% reduction in the anterior myocardial work index (sonomicrometry) for 90 minutes. In 15 pigs (group 2), a 10-minute no-flow ischemic episode preceded 80 minutes of sustained ischemia at a blood flow reduction identical to that in pigs of group 1. In 8 additional pigs (group 3), glibenclamide was administered before the 10-minute no-flow ischemic episode. In all pigs after 120 minutes of reperfusion, infarct size (IS, percentage of area at risk) was determined by triphenyltetrazolium chloride staining. In group 2, IS was reduced (6.8±6.0% [mean±SD], P &lt;.05) when compared with groups 1 (13.2±9.8%) and 3 (16.7±8.3%). In group 2, subendocardial blood flow of tissue that remained viable averaged 0.06±0.02 mL · min −1 · g −1 . This blood flow was lower than that in groups 1 (0.11±0.04 mL · min −1 · g −1 , P &lt;.05) and 3 (0.10±0.06 mL · min −1 · g −1 , P =NS), indicating an increased ischemic tolerance of the myocardium in pigs of group 2. Conclusions are as follows: (1) A brief episode of no-flow myocardial ischemia without intermittent reperfusion increases the tolerance to sustained low-flow ischemia. (2) The cardioprotective effect is mediated by activation of ATP-dependent potassium channels and therefore relates to IP rather than to MH.
Balloon-assisted enteroscopy using a single-balloon technique
Authors: D. Hartmann, A. Eickhoff, R. Tamm, J. Riemann
Journal: Endoscopy (2007)

The prototype of the single-balloon enteroscopy system (Olympus Medical Systems Europa GmbH, Hamburg, Germany; [Fig. 1]) consists of a high-resolution endoscope (XSIF-Q160Y) with a working length of 200 cm, and an outer diameter of 9.2 mm, and a flexible overtube (XST-BY3A; [Fig. 2]) with a working length of 132 cm and an outer diameter of 13.2 mm. A latex-free balloon is only attached at the tip of the single-use silicon overtube, and is inflated and deflated with air from a pressure-controlled pump system (Olympus balloon control unit MAJ-1440).
The Duffy antigen receptor for chemokines is up-regulated during acute renal transplant rejection and crescentic glomerulonephritis
Authors: Stephan Segerer, Heinz Regele, Matthias Mack, Renate Kain, Jean-Pierre Cartron, Yves Colin, Dontscho Kerjaschki, Detlef Schlöndorff
Journal: Kidney International (2000)
Some sexually transmitted infections rising, some falling
Authors: Michael Day
Journal: BMJ (2007)

A "cock-up" by the UK government has impeded the ability of the Healthcare Commission to assess independent sector treatment centres (ISTCs), says the watchdog's chief executive, Anna Walker.She says that a government oversight has impeded the commission's ability to assess the safety and quality of the centres.The commission declared this week that the Department of Health had failed to ensure that the data collected on the controversial clinics were compatible with the data used to monitor the rest of the NHS.The commission had aimed to review the first 23 centres, which were set up to carry out high volumes of straightforward elective surgery to cut NHS waiting lists.The commission interviewed 2000 patients, made inspections, and checked health records.Ms Walker said that there were gaps, however, because "comparative data has not been systematically collected."Where independent providers serve NHS patients we must ensure we have the proper systems to provide reassurance about what is being provided," she said."That is why we are calling for one sys-tem that allows comparable information to be published on all major healthcare providers, whether public or private, whether they are treating NHS patients or otherwise."Beginning in October, the Royal College of Surgeons will carry out its own study, funded by the Department of Health, to assess the success of operations carried out in the centres.Bernard Ribeiro, president of the Royal College of Surgeons, said, "It is imperative that patients receive a sustained, safe, and [high] quality service, which is consistent across surgical providers."See www.healthcarecommission.org.uk. Failure to monitor independent centres prevents comparison, say�s watchdog
55 Genetic polymorphisms in promoter region of osteopontin gene as a marker to determine hepatitis activity in patients with chronic hepatitis C
Authors: A MATSUI, S MOCHIDA, M NAITO, M INAO, S NAGOSHI, M HASHIMOTO, S MISHIRO, K FUJIWARA
Journal: Hepatology (2003)

Autosomal dominant polycystic kidney disease (ADPKD) leads to renal failure. The hallmark of ADPKD is increased epithelial proliferation, which has been proposed to be due to atypical signaling including abnormal JAK-STAT activity. However, the relative contribution of JAK-STAT family members in promoting proliferation in ADPKD is unknown. Here, we present siRNA JAK-STAT–focused screens discovering a previously unknown proliferative role for multiple JAK-STAT components (including STAT1, STAT2, STAT4, STAT5a, and STAT5b). Amongst these, we selected to study the growth hormone/growth hormone receptor/STAT5-axis because of its known role as a regulator of growth in nonrenal tissues. Loss of STAT5 function, facilitated by pharmacological inhibition or siRNAs, significantly reduced proliferation with an associated reduction in cyst growth in vitro. To study whether STAT5 is abnormally activated in vivo, we analyzed its expression using two independent mouse models of ADPKD. STAT5 was nuclear, thus activated, in renal epithelial cyst lining cells in both models. To test whether forced activation of STAT5 can modulate proliferation of renal cells in vivo, irrespective of the Pkd1 status, we overexpressed growth hormone. These mice showed increased STAT5 activity in renal epithelial cells, which correlated with de novo expression of cyclin D1, a STAT5 target gene. Chromatin immunoprecipitation experiments revealed that STAT5 transcriptionally activated cyclin D1 in a growth hormone–dependent fashion, thus providing a mechanism into how STAT5 enhances proliferation. Finally, we provide evidence of elevated serum growth hormone in Pkd1 mutant mice. Thus, the growth hormone/STAT5 signaling axis is a novel therapeutic target in ADPKD.
Is tibiofemoral osteoarthritis in the knee joint a new disease?
Authors: J Rogers, P Dieppe
Journal: Annals of the Rheumatic Diseases (1994)

OBJECTIVES--To compare the prevalence of osteoarthritis (OA) of the hip, tibiofemoral and patellofemoral joints in a skeletal population. METHODS--A total of 785 adult English skeletons (695 Saxon or Mediaeval origin) were examined for OA using established criteria. RESULTS--Twenty nine skeletons had hip OA, compared with 14 with patellofemoral joint OA, and only four tibiofemoral joint OA. CONCLUSION--Tibiofemoral OA was far less prevalent in ancient skeletons than hip or patellofemoral disease. Tibiofemoral OA may be a 9new9 disease.
Improving Quality and Reducing Disparities
Authors: Kaytura Felix Aaron, Carolyn M. Clancy
Journal: JAMA (2003)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Journals JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal