tbuckley/cabot-search huggingface dataset:
Dose-Dependent Dissociation of ACE-Inhibitor Effects on Blood Pressure, Cardiac Hypertrophy, and β-Adrenergic Signal Transduction
Authors: Michael Böhm, Maurizio Castellano, Enrico Agabiti-Rosei, Markus Flesch, Martin Paul, Erland Erdmann
Journal: Circulation (1995)

Background Dose-dependent effects of ACE inhibitors on blood pressure, cardiac hypertrophy, and β-adrenergic signal transduction were examined in an animal model with β-adrenergic desensitization, which has been identified in failing hearts and in hypertensive cardiac hypertrophy. It is unknown whether beneficial ACE-inhibitor effects are due to an unloading of the failing heart or a reduction of neuroendocrine activation with β-adrenergic resensitization. Methods and Results Low-dose (LD, 1 mg/kg) and high-dose (HD, 25 mg/kg) fosinopril treatment was performed in spontaneously hypertensive rats (SHR) and control (WKY) rats. Myocardial norepinephrine concentrations, adenylyl cyclase activity, β-adrenergic receptors (radioligand binding), G sα (functional reconstitution), and G iα (pertussis toxin labeling) were determined. Ventricular weights and blood pressures were measured. HD but not LD reduced blood pressure and left ventricular weights in SHR. Isoprenaline- and guanylylimidodiphosphate-stimulated adenylyl cyclase activities as well as β 1 -adrenergic receptors were reduced in SHR. The catalyst and G sα were unchanged, but G iα and norepinephrine concentrations were increased. Both LD and HD treatments restored β-adrenergic alteration. Conclusions LD treatment with ACE inhibitors restored β-adrenergic signal transduction defects independently of regression of cardiac hypertrophy. This could contribute to the effects of ACE inhibitors in patients, who are often treated with nonhypotensive doses.
Establishment and characteristics of a gastric cancer cell line (HuGC‐OOHIRA) producing high levels of G‐CSF, GM‐CSF, and IL‐6: The presence of autocrine growth control by G‐CSF
Authors: Masaru Baba, Hiroshi Hasegawa, Masahiro Nakayabu, Noriko Shimizu, Shiro Suzuki, Nanao Kamada, Kenzaburo Tani
Journal: American Journal of Hematology (1995)

Abstract We successfully established a human gastric cancer cell line, HuGC‐OOHIRA, from the ascites of a 60‐year‐old patient with advanced gastric cancer (poorly differentiated adenocarcinoma) complicated by peritonitis carcinomatosa and leukocytosis of unknown origin. Morphologically, the cells were polygonal and adhered weakly to the culture flask. They tended to pile up upon reaching confluence. Chromosome analysis revealed that the cell line has two modes of chromosome number, namely near diploidy and tetraploidy. Double minutes (DMs) were present in abundance in each cell. The doubling time was 25‐30 hr. The cell line was successfully transplanted into nude mice, and their peripheral leukocyte counts increased in proportion to the growth of the tumors. At 2 weeks after the transplantation, the serum rG‐CSF level was elevated to 2,893 üg/ml. The concentration of human G‐CSF in the culture supernatants was an extraordinary high level of 145,380 pg/ml/day. Secretion of GM‐CSF and IL‐6 was also detected. The intracellular localization of the G‐CSF was identified for the first time by immunofluorescence. Moreover, Northern blot analysis detected G‐CSF mRNA in this cell line. Anti‐recombinant human G‐CSF serum suppressed the propagation of HuGC‐OOHIRA cell line. Therefore, it is likely that the autocrine growth loop by G‐CSF is present in this cell line. This cell line would be very useful for understanding both the cellular and molecular basis for the production of various cytokines such as G‐CSF as well as cytokine‐dependent tumor proliferation.
LOSS OF VITREOUS HUMOR IN THE OPERATION FOR EXTRACTION OF CATARACT:ITS IMMEDIATE AND REMOTE EFFECT.
Authors: J. MORRISON RAY
Journal: JAMA (1907)

There seems to be great diversity of opinion among operators as to the exact consequences of loss of vitreous humor occurring as a complication in the operation for extraction of cataract. A general idea exists that it is an incident that they would rather not see occur, but that it has but little effect on the result of the operation. It has appeared to me that experience should give us more definite knowledge on this subject, and that we should know with exactness how much it militates against the final result. Being a more complicated structure than the aqueous, loss of vitreous makes more demands on the reparative powers of the eye than does loss of the aqueous fluid. When once it has escaped, the replaced humor never takes on the histologic make-up of the normal structure. A new fluid secreted from the same source as the aqueous and with
Decision Analysis: A Basic Clinical Skill?
Authors: Harold C. Sox
Journal: New England Journal of Medicine (1987)

The Medical Progress article by Pauker and Kassirer in this issue describes advances in applying the principles of decision analysis to patient care.1 Some problems remain and deserve comment.Decision analysis is a logically consistent approach to a common clinical problem: a decision whose consequences cannot be foretold with certainty. The uncertainties in medical practice stem from biologic variation and the inadequacies of clinical data. Uncertainty is intrinsic to the practice of medicine and cannot be eliminated by any analytical technique, however powerful. Decision analysis claims to identify the best decision, given the constraints imposed by uncertainty. This claim, valid . . .
Long-term Follow-up Study of HTLV-I Infection in Bottle-fed Children Born to Seropositive Mothers
Authors: Y. Ando, Y. Matsumoto, S. Nakano, K. Saito, K. Kakimoto, T. Tanigawa, Y. Ekuni, M. Kawa, T. Toyama
Journal: Journal of Infection (2003)
Abstract 5205: Galectin-3 and AP-1 mediate transcriptional effect of Arylsulfatase B (N-acetylgalactosamine-4-sulfatase) on versican in prostatic cells.
Authors: Sumit Bhattacharyya, Leonid Feferman, Joanne Kramer Tobacman
Journal: Cancer Research (2013)

Abstract N-acetylgalactosamine-4-sulfatase (Arylsulfatase B; ARSB) modifies the glycosaminoglycans (GAGs) chondroitin-4-sulfate (C4S) and dermatan sulfate by removing 4-sulfate groups from the non-reducing end and thereby regulating GAG degradation. Previous studies demonstrated that ARSB was reduced in malignant human colonic, mammary, and prostatic tissue and suggested that ARSB acts as a tumor suppressor. In this report, ARSB was silenced by siRNA in the WPMY-1 human prostate stromal myofibroblast cell line (ATCC), and effects on C4S, total sulfated glycosaminoglycans (GAGs), ErbB2, total EGFR, phospho-ERK, versican, and AP-1 were determined. Total sulfated GAGs were measured by Blyscan assay (Biocolor), and C4S was determined by Blyscan assay following immunoprecipitation by C4S antibody. Phospho(T202/Y204 for ERK1 or T185/Y187 for ERK2)-ERK, ErbB2, and total EGFR were measured by ELISA. Versican, an extracellular matrix chondroitin sulfate proteoglycan with EGF-like repeats at its C-terminus, was measured by ELISA and QPCR. ARSB and galectin-3 were silenced by siRNA (Qiagen). ARSB activity declined from 140.4 ± 8.4 to 21.4 ± 0.9 nmol/mg protein/hr following silencing. Total sulfated GAGs increased from 17.9 ± 0.7 μg/mg protein in control cells to 28.6 ± 1.4 μg/mg protein following ARSB silencing, and C4S increased from 7.4 ± 0.6 μg/mg protein to 15.5 ± 0.8 μg/mg protein following ARSB silencing. Total EGFR increased to 2.65 times baseline, and ErbB2 increased to over six-fold times baseline. Phospho-ERK increased to more than three times baseline, from 5.0 ± 0.5 ng/mg protein to 15.2 ± 0.8 ng/mg protein following silencing. Versican protein increased from 122.1 ± 5.3 ng/mg protein in control to 295.2 ± 11.2 ng/mg protein and mRNA increased more than two-fold. ARSB-silencing induced increases in versican mRNA and in activation of c-Jun and c-Fos, and these increases were inhibited when galectin-3 was also silenced. [All findings are highly significant (p&amp;lt;0.001, one-way ANOVA with Tukey-Kramer post-test)]. Previously, we have shown reduced binding of galectin-3 to C4S following ARSB silencing. Since there is an AP-1 binding site in the versican promoter, study data demonstrate that transcriptional effects of ARSB silencing on versican are mediated by galectin-3 and AP-1. The profound effects of ARSB silencing on versican and phospho-ERK in the prostatic myofibroblasts provide further evidence that ARSB acts as a tumor suppressor. Citation Format: Sumit Bhattacharyya, Leonid Feferman, Joanne Kramer Tobacman. Galectin-3 and AP-1 mediate transcriptional effect of Arylsulfatase B (N-acetylgalactosamine-4-sulfatase) on versican in prostatic cells. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 5205. doi:10.1158/1538-7445.AM2013-5205
Food Safety in China
Authors: Joan Stephenson
Journal: JAMA (2008)

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 Publications 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
Isolation of mycobacterium-reactive CD1-restricted T cells from patients with human immunodeficiency virus infection.
Authors: J Gong, S Stenger, J A Zack, B E Jones, G C Bristol, R L Modlin, P J Morrissey, P F Barnes
Journal: Journal of Clinical Investigation (1998)

Because CD1-restricted T cells lack CD4 but produce IFN-gamma in response to nonpeptide mycobacterial antigens, they could play a unique role in immunity to tuberculosis. We studied CD1-restricted T cells in the context of HIV infection by expanding CD4(-) T cell lines from 10 HIV-infected patients. Upon stimulation with Mycobacterium tuberculosis antigen or upon exposure to macrophages infected with M. tuberculosis, these T cell lines proliferated, produced IFN-gamma, and showed cytolytic T cell (CTL) activity against macrophages pulsed with mycobacterial antigen, findings consistent with a protective role against M. tuberculosis. Anti-CD1b antibodies abrogated T cell proliferation, IFN-gamma production, and CTL activity, demonstrating that these T cells are CD1 restricted. IFN-gamma production in response to M. tuberculosis was enhanced by antitransforming growth factor-beta in 8/10 lines, and by IL-15 in 2/10 lines. IFN-gamma production was augmented in a nonantigen-specific manner by IL-12 in 4/8 lines. When live HIV was cocultured with CD1-restricted T cell lines, p24 antigen and proviral DNA were not detected, indicating that the T cells were not infectable with HIV. Vaccination strategies aimed at activation and expansion of M. tuberculosis-reactive CD1-restricted T cells in HIV-infected patients may constitute a novel means to provide protection against tuberculosis, while minimizing the risk of enhancing HIV replication through stimulation of CD4(+) cells.
Cardiomyocyte cell cycle activation improves cardiac function after myocardial infarction
Authors: R. J. Hassink, K. B. Pasumarthi, H. Nakajima, M. Rubart, M. H. Soonpaa, A. B. de la Riviere, P. A. Doevendans, L. J. Field
Journal: Cardiovascular Research (2007)

Cardiomyocyte loss is a major contributor to the decreased cardiac function observed in diseased hearts. Previous studies have shown that cardiomyocyte-restricted cyclin D2 expression resulted in sustained cell cycle activity following myocardial injury in transgenic (MHC-cycD2) mice. Here, we investigated the effects of this cell cycle activation on cardiac function following myocardial infarction (MI). MI was induced in transgenic and non-transgenic mice by left coronary artery occlusion. At 7, 60, and 180 days after MI, left ventricular pressure–volume measurements were recorded and histological analysis was performed. MI had a similar adverse effect on cardiac function in transgenic and non-transgenic mice at 7 days post-injury. No improvement in cardiac function was observed in non-transgenic mice at 60 and 180 days post-MI. In contrast, the transgenic animals exhibited a progressive and marked increase in cardiac function at subsequent time points. Improved cardiac function in the transgenic mice at 60 and 180 days post-MI correlated positively with the presence of newly formed myocardial tissue which was not apparent at 7 days post-MI. Intracellular calcium transient imaging indicated that cardiomyocytes present in the newly formed myocardium participated in a functional syncytium with the remote myocardium. These findings indicate that cardiomyocyte cell cycle activation leads to improvement of cardiac function and morphology following MI and may represent an important clinical strategy to promote myocardial regeneration.
Bone density at various sites for prediction of hip fractures
Authors: S.R. Cummings, W. Browner, S.R. Cummings, D.M. Black, M.C. Nevitt, W. Browner, H.K. Genant, J. Cauley, K. Ensrud, J. Scott, T.M. Vogt
Journal: The Lancet (1993)
What's Wrong with This Picture?
Authors: Michael Berkwits
Journal: Annals of Internal Medicine (1998)

Letters15 February 1998What's Wrong with This Picture?Michael Berkwits, MDMichael Berkwits, MDVeterans Affairs Medical Center; University of Pennsylvania Medical Center; Philadelphia, PA 19104Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-128-4-199802150-00029 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:In his description of a syncopal patient with aortic stenosis and gastrointestinal bleeding caused by cancer, Brody [1] nicely portrayed some of the perils of fee-for-service care. He did not acknowledge, however, the lingering question about whether a significant association between these clinical conditions exists. Heyde [2] first suggested a link between aortic stenosis and idiopathic gastrointestinal bleeding in 1958. Since then, the Heyde syndrome (as it has sometimes been called) has been different things to different people. Subsequent authors both confirmed and challenged Heyde's impressions. Some found a risk for idiopathic bleeding, others a link with ...References1. Brody SA. What's wrong with this picture? Ann Intern Med. 1997; 126:997-8. Google Scholar2. Heyde EC. Gastrointestinal bleeding in aortic stenosis. N Engl J Med. 1958; 259:196. Google Scholar3. Imperiale TF, Ransohoff DF. Aortic stenosis, idiopathic gastrointestinal bleeding, and angiodysplasia: is there an association? Gastroenterology. 1988; 95:1670-6. Google Scholar4. Bhutani MS, Gupta SC, Markert RJ, Barde CJ, Donese R, Gopalswamy N. A prospective controlled evaluation of endoscopic detection of angiodysplasia and its association with aortic valve disease. Gastrointest Endos. 1995; 42:398-402. Google Scholar5. Ransohoff DF, Lang CA. Suggested techniques for fecal occult blood testing and interpretation in colorectal cancer screening. Ann Intern Med. 1997; 26:808-10. Google Scholar Author, Article, and Disclosure InformationAffiliations: Veterans Affairs Medical Center; University of Pennsylvania Medical Center; Philadelphia, PA 19104 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 15 February 1998Volume 128, Issue 4Page: 323-324KeywordsBloodCancer preventionCancer screeningColorectal cancerHematologic testsHemorrhageInformation storage and retrievalStenosisUlcersValvular diseases Issue Published: 15 February 1998 CopyrightCopyright © 1998 by American College of Physicians. All Rights Reserved.PDF DownloadLoading ...
Walsh and Hoyt's Clinical Neuro-Ophthalmology
Authors: Thomas R. Hedges
Journal: JAMA (1988)

This is the third volume of a planned five-volume text on neuro-ophthalmology, a monumental task that is enviably done. Dr William Hoyt, who coauthored the third edition in three volumes in 1969 with Dr Frank B. Walsh, is given due credit for his help along with many others. One who knows the history of this work from Dr Walsh's singular first edition in 1947 and the second 1952 edition to its state-of-the-art content at present can only admire the very capable effort performed by Dr Miller in rendering for the present and for posterity a work of great value. The format and organization of the third volume follow volume 1, which covers the visual sensory system and the optic nerve, and volume 2, which deals with the autonomic nerves, the ocular motor system, and sensory innervation of the eye and orbit and has a wonderfully readable chapter on headache. The
Outbreak of Group A Streptococcus Septicemia in Children
Authors: Mary C. Wheeler
Journal: JAMA (1991)

To determine the epidemiologic, clinical, and microbiological features of group A streptococcus septicemia in children.A descriptive series of 34 cases over an 11-year period from 1980 through 1990.An academically affiliated tertiary-care pediatric hospital, the principal referral center for the state of Colorado and surrounding states.Thirty-four patients with positive blood cultures for group A streptococcus (33 medical records were available).Yearly incidence and clinical features of cases; microbiological features of isolated organisms.There was a significant increase (P = .01) in the incidence of group A streptococcus bacteremia over an 11-year period, with 14 (41%) of these cases occurring in 1989 and 1990. Patients had a rapidly progressing illness, usually without preceding pharyngitis. The prominent M and T types were 1 (4) and 12 (4). Eleven (73%) of the 15 strains produced pyrogenic exotoxin B that significantly correlated with production of proteinase.There appears to be an increase in group A streptococcus bacteremia in children that is associated with a strain phenotype that suggests a change in organism virulence.
Application of ACTH Stimulation to Adrenal Imaging with Radioiodocholesterol
Authors: M NAKAJO, H SAKATA, K SHIRONO, K SHIMABUKURO, S ONOHARA, S SHINOHARA
Journal: Clinical Nuclear Medicine (1983)

ACTH-stimulation adrenal imaging (ACTH-I) was performed in 14 patients after baseline imaging (B-I) was performed. In six patients with no adrenal diseases in whom the findings of B-I were equivocal, morphologic normality of the adrenals was confirmed by ACTH-I because of increased adrenal uptake of radioiodocholesterol. In three patients with cortisol-producing tumors, visualization of contralateral glands by ACTH-I provided indirect evidence for autonomous cortisol secretion of the tumors. In three patients with pheochromocytoma or cyst, ACTH-I increased adjacent cortical radioactivity to more clearly delineate the lesions. In two patients with primary adrenocortical insufficiency, exogenous ACTH had no effect on adrenal uptake of the tracer. Correlation was observed between response of the adrenal net counts and urinary excretion of 17-OHCS and 17-KS. ACTH-I is useful when B-I does not provide sufficient diagnostic information or further information is needed due to low or absent radioiodocholesterol uptake by the adrenal gland(s).
Transcription of the activating receptor NKG2D in natural killer cells is regulated by STAT3 tyrosine phosphorylation
Authors: Shiguo Zhu, Prasad V. Phatarpekar, Cecele J. Denman, Vladimir V. Senyukov, Srinivas S. Somanchi, Hoainam T. Nguyen-Jackson, Emily M. Mace, Alexandra F. Freeman, Stephanie S. Watowich, Jordan S. Orange, Steven M. Holland, Dean A. Lee
Journal: Blood (2014)
Alkalosis and Urate Clearance
Authors: LAWRENCE RAMSAY
Journal: Annals of Internal Medicine (1975)

Comments1 December 1975Alkalosis and Urate ClearanceLAWRENCE RAMSAY, M.R.C.P. (UK), DAVID LEVINE, M.R.C.P. (UK), JOHN SHELTON, B.SC., ROBERT BRANCH, M.R.C.P. (UK), RICHARD AUTY, M.R.C.P. (UK)LAWRENCE RAMSAY, M.R.C.P. (UK)Search for more papers by this author, DAVID LEVINE, M.R.C.P. (UK)Search for more papers by this author, JOHN SHELTON, B.SC.Search for more papers by this author, ROBERT BRANCH, M.R.C.P. (UK)Search for more papers by this author, RICHARD AUTY, M.R.C.P. (UK)Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-83-6-903 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: We read with interest about the increased prevalence of hyperuricaemia and gouty arthritis in patients with Bartter's syndrome (Ann Intern Med83:56-59, 1975), but the authors' conclusions that systemic alkalosis can decrease the clearance of uric acid, and that physicians should be aware of this inhibitory effect of alkalosis on urate clearance, do not seem justified by the evidence presented. This evidence was obtained in a careful study of five patients with normal renal function, and the results were given in Table 2 of the paper. Systemic alkalosis was induced by substituting 100 meq sodium bicarbonate for...References1. STEELERIESELBACH TR: The renal mechanism for urate homeostasis in normal man. Am J Med 43:868-875, 1967 CrossrefMedlineGoogle Scholar2. ZWEIFLERTHOMPSON AG: Correction of thiazide hyperuricaemia by potassium chloride and ammonium chloride. Arthritis Rheum 8:1134-1144, 1965 CrossrefMedlineGoogle Scholar3. GRIEBLEJOHNSTONFULLER HLJ: Treatment of arterial hypertensive disease with diuretics. Arch Intern Med 110:33-44, 1962 Google Scholar4. RAMSAYAUTYHORTH LRC: Plasma uric acid level related to the urinary excretion of aldosterone and of electrolytes in normal subjects. Clin Sci Mol Med, in press Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Department of Medicine University of Glasgow Glasgow, Scotland G11 6NT PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByImplications of Disorders of Purine Metabolism for the Kidney and the Urinary TractDEffects of smoking and physical activity on serum uric acid in a Jerusalem population sampleFactors influencing the serum uric acid level. A study based on a population survey in Hisayama town, Kyushu, JapanAbnormal Urate Excretion Associated with Renal and Systemic Disorders, Drugs, and ToxinsThe Effect of Urine Flow Rate on Urate Clearance 1 December 1975Volume 83, Issue 6Page: 903-904KeywordsArthritisBicarbonatesSodiumUric acid Issue Published: 1 December 1975 PDF DownloadLoading ...