tbuckley/cabot-search huggingface dataset:
Transpyloric fluid movement and antroduodenal motility in patients with gastro-oesophageal reflux.
Authors: P M King, A Pryde, R C Heading
Journal: Gut (1987)

The pattern of transpyloric fluid movement and associated antroduodenal motility was compared in patients with gastro-oesophageal reflux (GOR) and healthy controls using real time ultrasonic imaging. A similar number of cyclical periods of antroduodenal motor activity (GOR 94 and control 91) was studied in each group. Mean antral cycle times and the frequency of occurrence of related proximal duodenal contractions (antroduodenal coordination) were similar. Transpyloric fluid movement occurred as a number of discrete episodes in each cycle. Gastroduodenal flow was more frequent in the GOR group (mean 2.7 +/- 0.4 episodes per cycle) than in controls (mean 1.7 +/- 0.3). The mean duration of these episodes in both groups was similar at around 2.5 seconds. Duodenogastric flow (reflux) was observed in many cycles (GOR 63%; controls 54%), but there was no difference in the mean number of episodes per cycle (GOR 0.79; control 0.74) or their mean duration (two seconds for both). Transpyloric fluid flow only occurs when a pressure gradient is created across the open pylorus. These observations indicate that in GOR the gastroduodenal pressure gradient is positive more frequently than in normal controls. Gastroduodenal liquid flow but not duodenogastric reflux differs in GOR patients and controls.
Intrathymic clonal deletion of V beta 6+ T cells in cyclophosphamide-induced tolerance to H-2-compatible, Mls-disparate antigens.
Authors: M Eto, H Mayumi, Y Tomita, Y Yoshikai, K Nomoto
Journal: The Journal of Experimental Medicine (1990)

When C3H (H-2k, Mls-1b) mice were primed intravenously with 10(8) viable spleen cells from AKR (H-2k, Mls-1a) and treated intraperitoneally with 200 mg/kg of cyclophosphamide (CP) 2 d later, not only a long-lasting skin allograft tolerance but also a tolerance in mixed lymphocyte reaction to Mls-1a-encoded antigens was established. The cellular mechanisms of CP-induced tolerance were examined by assessing the V beta 6-bearing T cells that are strongly correlated with reactivity to Mls-1a-encoded antigens bound to MHC class II molecules. At the relatively early stage (2 or 5 wk) after the CP treatment, CD4+-V beta 6+ T cells of C3H origin were preferentially eliminated in the lymph nodes of the tolerant mice, whereas CD8+-V beta 6+ T cells remained. On the other hand, neither CD4+CD8- nor CD4-CD8+ thymocytes bearing a high density of V beta 6 was detected in the chimeric thymus. Namely, in the thymus of the tolerant C3H mice, neither mixed chimerism nor the clonal deletion of the V beta 6-bearing T cells was observed on day 14, whereas both of them were observed on day 35. The clonal deletion and mixed chimerism in the thymus were lasting for greater than 10 wk after the CP treatment. Expression of V beta 6 on the peripheral T cells in the tolerant C3H mice gradually reduced in the process of time. These results strongly suggested that the clonal deletion in the thymus was one of the essential mechanisms in the CP-induced tolerance system.
The Case of J. Hunter
Authors: ALLAN B. KIRSNER
Journal: Annals of Internal Medicine (1970)

Letters and Comments1 May 1970The Case of J. HunterALLAN B. KIRSNER, M.D.ALLAN B. KIRSNER, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-72-5-760_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: My chagrin at having missed review question No. 92 in Rheumatology was tempered by Dr. Rothermich's letter of dissent in the June issue (Ann Intern Med 70:1280, 1969).As he correctly pointed out, most rheumatologists would first think of gout rather than hemarthrosis in a patient with myocardial infarction who developed an acute joint even if the patient was anticoagulated.The following case is presented in support of Dr. Rothermich.Mr. John Hunter, surgeon, was in good health until the spring of 1769 when in his forty-first year he developed regular fits of gout. In early April...Reference1. HOME E: A short account of the author's life, in A Treatise on the Blood, Inflammation, and Gun-Shot Wounds, edited by HUNTER J, Philadelphia, Thomas Bradford, 1796, p. XXXIX Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: The Toledo Clinic 2001 Collingwood Blvd. Toledo, Ohio 43620 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 May 1970Volume 72, Issue 5Page: 760-761KeywordsGoutHemarthrosisMyocardial infarctionRheumatologySurgeons Issue Published: 1 May 1970 PDF DownloadLoading ...
Nitric Oxide Modulates Expression of Cell Cycle Regulatory Proteins
Authors: Felix C. Tanner, Peter Meier, Helen Greutert, Claudine Champion, Elizabeth G. Nabel, Thomas F. Lüscher
Journal: Circulation (2000)

We examined the effect of NO on the proliferation and cell cycle regulation of human aortic vascular smooth muscle cells (VSMCs).The NO donor diethylenetriamineNONOate (10(-5) to 10(-3) mol/L) inhibited proliferation in response to 10% fetal calf serum (FCS) and 100 ng/mL platelet-derived growth factor-BB in a concentration-dependent manner. This effect was not observed with disintegrated diethylenetriamineNONOate or with the parent compound, diethylenetriamine. Adenoviral transfection of endothelial NO synthase (NOS) inhibited proliferation in response to FCS, which was prevented with N(G)-nitro-L-arginine methyl ester. NOS overexpression did not inhibit proliferation in response to platelet-derived growth factor, although the transfection efficiency and protein expression were similar to those of FCS-stimulated cells. Nitrate release was selectively enhanced from FCS-treated cells, indicating that NOS was activated by FCS only. NO caused G(1) cell cycle arrest. Cytotoxicity was determined with trypan blue exclusion, and apoptosis was assessed with DNA fragmentation. Cyclin-dependent kinase 2 expression level, threonine phosphorylation, and kinase activity were inhibited. Cyclin A expression was blunted, whereas cyclin E remained unchanged. p21 expression was induced, and p27 remained unaltered. The effect on cyclin A and p21 started within 6 hours and preceded the changes in cell cycle distribution. Proliferation in response to 10% FCS was barely inhibited with 8-bromo-cGMP (10(-3) mol/L) but was blunted with both forskolin and 8-bromo-cAMP. Proliferation in response to 2% FCS was inhibited with 8-bromo-cGMP, but it did not mimic the cell cycle effects of NO.NO inhibits VSMC proliferation by specifically changing the expression and activity of cell cycle regulatory proteins, which may occur independent of cGMP. Adenoviral overexpression of endothelial NOS represents a cytostatic strategy for gene therapy of vascular disease.
An environmental look at human health
Authors: Kimberly Glasbrenner
Journal: JAMA (1984)

Just 432 kilometers (270 miles) south of the Bethesda, Md, campus of the NIH lies yet another of the 11 NIH institutes—the National Institute of Environmental Health Sciences (NIEHS). Being apart from the main campus "takes a little extra effort on our part to ensure that the NIH and the Department of Health and Human Services remember that we're down here [in Research Triangle Park, NC]," says David P. Rall, MD, PhD, director of the institute. "But we make a deliberate effort to ensure a scientific cross-fertilization between the Bethesda campus and our folks." The institute is the principal federal agency for investigating the effects of chemical, physical, and biologic environmental agents on human health. It was created in 1966 as the Division of Environmental Health Sciences, as federal officials recognized the need for a focal center among government agencies to coordinate the study of environmental health issues. After three
What's in a name? From pathways to plans in end of life care
Authors: E. Borgstrom
Journal: BMJ (2013)

It is not surprising that the independent reviewers of the Liverpool care pathway suggested removing the term “pathway” from discussions about end of life care.1 2 Language influences the way people perceive the world and shapes the way we live.3 The term pathway metaphorically appeals to an irreversible journey of decline. Yet, as the Liverpool care pathway recognises, death is not …
Immune-mediated thrombocytopenia resulting from sensitivity to oxaliplatin
Authors: Brian R. Curtis, James Kaliszewski, Marisa B. Marques, M. Wasif Saif, Lisle Nabelle, Jules Blank, Janice G. McFarland, Richard H. Aster
Journal: American Journal of Hematology (2006)

Thrombocytopenia developing in the course of chemotherapy for malignant disease is usually attributed to drug-induced marrow suppression and/or marrow replacement by tumor. We describe two patients who developed severe thrombocytopenia and hemorrhagic symptoms while being treated with oxaliplatin, 5-fluorouracil, and leukovorin for metastatic colon cancer in whom platelet destruction appears to have been caused by oxaliplatin-dependent antibodies specific for the platelet glycoprotein IIb/IIIa complex (αIIb/β3 integrin). Drug-induced immune thrombocytopenia (DITP) should be considered in patients who experience a sudden, isolated drop in platelet levels while being treated with chemotherapeutic agents, especially when adequate numbers of megakaryocytes are present in the bone marrow. Am. J. Hematol. 81:193–198, 2006. © 2006 Wiley-Liss, Inc.
Most common cause of death in England and Wales in 2013 was heart disease in men and dementia in women
Authors: Z. Kmietowicz
Journal: BMJ (2015)

The leading cause of death among men in England and Wales in 2013 was ischaemic heart disease, accounting for 15.4% of deaths, while among women it was dementia and Alzheimer’s disease, which caused 12.2% of deaths, show the latest statistics.1 Dementia and Alzheimer’s disease overtook heart disease as the leading cause of death among women in 2012.

Altogether there were 506 790 deaths in England and Wales in 2013, up 1.5% from 2012. The second leading cause of death among …
ARTERIOVENOUS FISTULA OF THE LEFT INTERNAL CAROTID ARTERY AND JUGULAR VEIN
Authors: D. R. McIntyre
Journal: JAMA (1933)

R. H., a white man, aged 54, an American lawyer, consulted me, March 6, 1933, complaining of a blowing, pumping, steam-like noise in the left ear, together with extreme nervousness, anxiety, headache and easy fatigue. The noise in his left ear began in February, 1928, with a sudden onset while he was at ease reading in his library. Having just recovered from otitis media in the right ear, he first thought that possibly a like condition was making its appearance in the left ear. He consulted an ear specialist but a pathologic condition was not found. There had been no noticeable change in the noise heard, but he had progressively become more uneasy about his condition until he had reached the stage bordering on a nervous breakdown. The patient was well developed and fairly well nourished. On examination there was some swelling on the left side, and the external veins
Cardiovascular Benefit of Magnitude of Low-Density Lipoprotein Cholesterol Reduction
Authors: Catherine R. Rahilly-Tierney, Elizabeth V. Lawler, Richard E. Scranton, J. Michael Gaziano
Journal: Circulation (2009)

Background— We examined the effect of the magnitude of low-density lipoprotein cholesterol (LDL-C) reduction across subjects of various ages in a retrospective cohort study. Methods and Results— We selected 20 132 male veterans at high risk for an acute cardiovascular event and who had 2 or more LDL-C measurements before their first documented acute myocardial infarction, revascularization, death, or censoring date. LDL-C reduction was categorized as no reduction (&lt;10 mg/dL; reference), small reduction (between 10 and 40 mg/dL), moderate reduction (between 40 and 70 mg/dL), or large reduction (≥70 mg/dL). The primary outcome was combined acute myocardial infarction or revascularization. The first and last LDL-C levels in the databases were used to calculate the LDL-C reduction in patients who experienced no outcome or who died. Within each age quartile and in a subgroup of patients ≥80 years of age, a Cox proportional hazards model was used to determine hazard ratios for each category of LDL-C reduction compared with the reference category, with adjustment for age, body mass index, current smoking status, medications, and comorbidities. In all age groups, the magnitude of LDL-C reduction was proportional to the magnitude of cardiovascular risk reduction. Risk reduction for the combined outcome in patients who achieved a large LDL-C reduction was similar in all age quartiles, with multivariate-adjusted hazard ratios of approximately 0.30. Conclusions— In a cohort of veterans at high risk for cardiovascular events, patients of all ages, including those 80 years or older, benefitted the most from large reductions in LDL-C.
A Multifactorial Model for Pancreatic Cancer in Man
Authors: Ruey S. Lin
Journal: JAMA (1981)

In the past 30 years, the incidence of pancreatic cancer has increased substantially. The disease now causes more deaths than all other malignant neoplasms, except those of the colorectal region, lung, and breast. A study in over 115 hospitals in five metropolitan areas showed that males with pancreatic cancer were more often employed in the dry cleaning business or in occupations involving close exposure to gasoline, increasing the risk for pancreatic cancer up to five times. Females at risk for pancreatic cancer were more likely to smoke cigarettes, to have uterine myomas, and to have undergone oophorectomy or spontaneous abortions. Generally, these patients were of higher social class and drank more wine and decaffeinated coffee than demographically similar controls. Assessment of the effects of several factors showed that relative risks increased 34-fold among females and nearly sixfold among males. While no single factor accounts for the preponderance of pancreatic cancer, a combination of factors—each associated with a relatively small risk enhancement—may very well do so. (<i>JAMA</i>1981;245:147-152)
Ligand-Activated Peroxisome Proliferator–Activated Receptor-γ Protects Against Ischemic Cerebral Infarction and Neuronal Apoptosis by 14-3-3ε Upregulation
Authors: Jui-Sheng Wu, Wai-Mui Cheung, Yau-Sheng Tsai, Yi-Tong Chen, Wen-Hsuan Fong, Hsin-Da Tsai, Yu-Chang Chen, Jun-Yang Liou, Song-Kun Shyue, Jin-Jer Chen, Y. Eugene Chen, Nobuyo Maeda, Kenneth K. Wu, Teng-Nan Lin
Journal: Circulation (2009)

Thiazolidinediones have been reported to protect against ischemia-reperfusion injury. Their protective actions are considered to be peroxisome proliferator-activated receptor-gamma (PPAR-gamma)-dependent; however, it is unclear how PPAR-gamma activation confers resistance to ischemia-reperfusion injury.We evaluated the effects of rosiglitazone or PPAR-gamma overexpression on cerebral infarction in a rat model and investigated the antiapoptotic actions in the N2-A neuroblastoma cell model. Rosiglitazone or PPAR-gamma overexpression significantly reduced infarct volume. The protective effect was abrogated by PPAR-gamma small interfering RNA. In mice with knock-in of a PPAR-gamma dominant-negative mutant, infarct volume was enhanced. Proteomic analysis revealed that brain 14-3-3epsilon was highly upregulated in rats treated with rosiglitazone. Upregulation of 14-3-3epsilon was abrogated by PPAR-gamma small interfering RNA or antagonist. Promoter analysis and chromatin immunoprecipitation revealed that rosiglitazone induced PPAR-gamma binding to specific regulatory elements on the 14-3-3epsilon promoter and thereby increased 14-3-3epsilon transcription. 14-3-3epsilon Small interfering RNA abrogated the antiapoptotic actions of rosiglitazone or PPAR-gamma overexpression, whereas 14-3-3epsilon recombinant proteins rescued brain tissues and N2-A cells from ischemia-induced damage and apoptosis. Elevated 14-3-3epsilon enhanced binding of phosphorylated Bad and protected mitochondrial membrane potential.Ligand-activated PPAR-gamma confers resistance to neuronal apoptosis and cerebral infarction by driving 14-3-3epsilon transcription. 14-3-3epsilon Upregulation enhances sequestration of phosphorylated Bad and thereby suppresses apoptosis.
Abstract 5029: Comparative combination cancer immunotherapy with vaccination, checkpoint inhibition and TNFRSF stimulation
Authors: Taylor H. Schreiber, Neal Schilling, Vadim Deyev, Eckhard R. Podack
Journal: Cancer Research (2014)

Abstract Therapeutic tumor immunity requires the presence and appropriate activation of tumor antigen specific CD8+ T cells and migration of activated tumor-antigen specific CD8+ T cells into a tumor microenvironment where immunosuppressive barriers have been eliminated. Antibody mediated blockade of CTLA-4 and PD-1 is a clinically effective strategy to dampen tumor mediated immunosuppression in a minority of patients with advanced cancer, and this approach may be potentiated through vaccination to prime additional CTL clones and through direct stimulation of T cell costimulatory molecules of the TNF superfamily. Here we provide a systematic comparison of anti-tumor vaccination with either heat shock protein gp96-Ig or traditional peptide/adjuvant vaccines given alone or in combination with CTLA-4 or PD-1 blockade and direct T cell costimulation via OX40, 4-1BB and TNFRSF25. Through the tracking of tumor-antigen specific CD4+ and CD8+ T cell responses, these studies demonstrate that both TNFRSF4 and TNFRSF25 independently and additively costimulate vaccine induced CD8+ T cell proliferation following both primary and secondary antigen challenge. In contrast, the activity of TNFRSF4 and TNFRSF25 were observed to be divergent in the costimulation of CD4+ T cell immunity. Interestingly, antigen-specific cellular and humoral responses were uncoupled upon secondary immunization, which was dramatically effected by the presence of OX40, 4-1BB or TNFRSF25 costimulation. When combined with checkpoint inhibition in therapeutic murine orthotopic tumor models, synergistic anti-tumor activity was observed with various triple combinations with vaccine, checkpoint inhibition and T cell costimulation. These studies highlight the complementary activity of vaccination, checkpoint inhibition and direct T cell costimulation, which may guide the application of combination immunotherapy for effective anti-tumor immunity. Citation Format: Taylor H. Schreiber, Neal Schilling, Vadim Deyev, Eckhard R. Podack. Comparative combination cancer immunotherapy with vaccination, checkpoint inhibition and TNFRSF stimulation. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 5029. doi:10.1158/1538-7445.AM2014-5029
Renal Cell Carcinoma Presenting as a "Hot" Lesion in Kidney, with "Cold" Metastasis in the Skeleton
Authors: CARLOS A. BORZUTZKY, ELLIOTT H. TURBINER
Journal: Clinical Nuclear Medicine (1985)

Skeletal scintigraphy is useful for detecting primary renal carcinomas and associated osseous metastatic deposits. Usually, renal masses present as photondeficient foci, and osseous metastases, as foci of increased response. A case is presented with the unusual combination of focal increased Tc-99m MDP localization to the primary renal cell carcinoma and photopenic osseous metastatic foci. Proposed mechanisms are discussed.
Expression of pro-opiomelanocortin gene and quantification of adrenocorticotropic hormone-like immunoreactivity in human normal peripheral mononuclear cells and lymphoid and myeloid malignancies.
Authors: R Buzzetti, L McLoughlin, P M Lavender, A J Clark, L H Rees
Journal: Journal of Clinical Investigation (1989)

Using Northern blotting with a human genomic DNA probe for the pro-opiomelanocortin (POMC) gene, we have shown specific mRNA in normal human peripheral mononuclear cells (PBMC); the presence of specific mRNA was also observed in a T lymphocyte cell line derived from a patient with lymphoma. We then demonstrated that PBMC translate the message into protein. Thus, using a radioimmunoassay with an antibody for ACTH, a median of 29 pg of ACTH-like immunoreactivity (ACTH-LIR) was found in 10(7) PBMC. ACTH-LIR was also detected in seven different cell lines derived from patients with lymphoid and myeloid malignancies, two of them JM and U937 showing the highest values 135 and 108 pg/10(7) cells, respectively. The chromatographic characterization of this ACTH-LIR showed, at least, three molecular forms of immunoreactive ACTH with molecular weights of the order of 31,000 POMC, 22,000 ACTH, and 4,500 ACTH, in addition to high-molecular-weight material (greater than 43,000). We conclude that PBMC produce ACTH-LIR which may act as a paracrine immunomodulator in a similar way to lymphokines and/or may signal the adrenal gland to secrete glucocorticoids.
Very Late Stent Thrombosis After Drug-Eluting Stent in Segment With Neointimal Tissue Coverage
Authors: Tsuyoshi Nishiguchi, Hironori Kitabata, Atsushi Tanaka, Hideaki Kataiwa, Kohei Ishibashi, Kenichi Komukai, Takashi Tanimoto, Yasushi Ino, Shigeho Takarada, Takashi Kubo, Nobuo Nakamura, Masato Mizukoshi, Toshio Imanishi, Takashi Akasaka
Journal: JACC. Cardiovascular imaging (2010)
Drug-Induced Lipemia.
Authors: Daniel Porte
Journal: Annals of Internal Medicine (1968)

s1 May 1968Drug-Induced Lipemia.Daniel Porte Jr., M.D. (Associate), Benjamin Belknap, M.D., John D. Bagdade, M.D., Edwin L. Bierman, M.D., F.A.C.P.Daniel Porte Jr., M.D. (Associate), Benjamin Belknap, M.D., John D. Bagdade, M.D., Edwin L. Bierman, M.D., F.A.C.P.Author, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-68-5-1189_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTwo patients treated with adrenal steroids and two patients treated with thiazides have been found to be lipemic only during drug therapy. Steroid treatment in these patients produced marked hypertriglyceridemia (triglycerides (TG) > 5,000 mg/ 100 ml) and severe deterioration of carbohydrate (CHO) tolerance with decreased insulin responses to glucose. Postheparin lipolytic activity (PHLA, an index of TG removal via tissue lipoprotein lipase) was low (0.17 µEq/ml per minute), and dietary fat particles circulated in plasma. These findings suggested an exogenous lipemia due to a reduced ability to metabolize dietary fat and resembled "diabetic lipemia," a recently described syndrome in... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Seattle, Washington PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 May 1968Volume 68, Issue 5Page: 1189-1189KeywordsDrug therapyDrugsFatsGlucoseHyperlipidemiaInsulinLipasesLipoproteinsPatientsSteroids Issue Published: 1 May 1968 PDF downloadLoading ...