tbuckley/cabot-search huggingface dataset:
Follicular Lymphoma Cells Induce Changes in T-Cell Gene Expression and Function: Potential Impact on Survival and Risk of Transformation
Authors: Shahryar Kiaii, Andrew J. Clear, Alan G. Ramsay, Derek Davies, Ajanthah Sangaralingam, Abigail Lee, Maria Calaminici, Donna S. Neuberg, John G. Gribben
Journal: Journal of Clinical Oncology (2013)

Previous studies have demonstrated the prognostic importance of the immune microenvironment in follicular lymphoma (FL). To investigate the molecular mechanisms during which tumor-infiltrating T cells (TILs) are altered in the FL microenvironment, we studied highly purified CD4 and CD8 TILs from lymph node biopsies at diagnosis in treatment-naive patients with FL compared with reactive tonsils and the peripheral blood of healthy donors.Gene expression profiling of highly purified CD4 and CD8 TILs was performed on the Affymetrix platform. Diagnostic tissue microarrays from an independent patient set (n = 172) were used to verify protein expression and analyze any impact of TIL-expressed genes on outcome. Time-lapse imaging was used to assess T-cell motility.The most upregulated genes in both CD4 and CD8 TILs were PMCH, ETV1, and TNFRSF9. PMCH is not expressed in peripheral blood T cells, but expression is highly induced on culture with FL. Both CD4 and CD8 TILs from patients with FL have significantly impaired motility compared with those of healthy TILs from reactive tonsils and this can be induced on healthy T cells by FL cells. During multivariate analysis, a model incorporating the number and location of T cells expressing PMCH, NAMPT, and ETV1 showed prognostic significance for overall survival and for time to transformation.We showed altered gene expression in TILs in FL and demonstrated that altering the immune microenvironment in FL affects overall survival and time to transformation in this disease.
RAYNAUD'S SYNDROME: ACROSCLEROSIS; SCLERODERMA.
Authors: S. JABLONSKA, B. BUBNOW, B. LUKASIAK
Journal: British Journal of Dermatology (1958)

Journal Article RAYNAUD'S SYNDROME: ACROSCLEROSIS; SCLERODERMA. Get access S. JABLONSKA, S. JABLONSKA Department of Dermatology and Syphilology, Warsaw Medical School, Poland Search for other works by this author on: Oxford Academic Google Scholar B. BUBNOW, B. BUBNOW Department of Dermatology and Syphilology, Warsaw Medical School, Poland Search for other works by this author on: Oxford Academic Google Scholar B. LUKASIAK B. LUKASIAK Department of Dermatology and Syphilology, Warsaw Medical School, Poland Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 70, Issue 2, 1 February 1958, Pages 37–43, https://doi.org/10.1111/j.1365-2133.1958.tb13289.x Published: 01 February 1958
Adenosine Receptor Activation Induces Vascular Endothelial Growth Factor in Human Retinal Endothelial Cells
Authors: Maria B. Grant, Roy W. Tarnuzzer, Sergio Caballero, Mark J. Ozeck, Margaret I. Davis, Polyxenie E. Spoerri, Igor Feoktistov, Italo Biaggioni, John C. Shryock, Luiz Belardinelli
Journal: Circulation Research (1999)

Adenosine, released in increased amounts by hypoxic tissues, is thought to be an angiogenic factor that links altered cellular metabolism caused by oxygen deprivation to compensatory angiogenesis. Adenosine interacts with 4 subtypes of G protein-coupled receptors, termed A(1), A(2A), A(2B), and A(3). We investigated whether adenosine causes proliferation of human retinal endothelial cells (HRECs) and synthesis of vascular endothelial growth factor (VEGF) and, if so, which adenosine receptor subtype mediates these effects. The nonselective adenosine receptor agonist 5'-N-ethylcarboxamidoadenosine (NECA), in a concentration-dependent manner, increased both VEGF mRNA and protein expression by HRECs, as well as proliferation. This proliferative effect of NECA was inhibited by the addition of anti-human VEGF antibody. NECA also increased insulin-like growth factor-I and basic fibroblast growth factor mRNA expression in a time-dependent manner and cAMP accumulation in these cells. In contrast, neither the A(1) agonist N(6)-cyclopentyladenosine nor the A(2A) agonist 2-p-(2-carboxyethyl) phenethylamino-NECA caused any of the above effects of NECA. The effects of NECA were not significantly attenuated by either the A(2A) antagonist SCH58261 or the A(1) antagonist 8-cyclopentyl-1, 3-dipropylxanthine. However, the nonselective adenosine receptor antagonist xanthine amine congener completely inhibited the effects of NECA. Addition of antisense oligonucleotide complementary to A(2B) adenosine receptor mRNA inhibited VEGF protein production by HRECs after NECA stimulation. Thus, the A(2B) adenosine receptor subtype appears to mediate the actions of adenosine to increase growth factor production, cAMP content, and cell proliferation of HRECs. Adenosine activates the A(2B) adenosine receptor in HRECs, which may lead to neovascularization by a mechanism involving increased angiogenic growth factor expression.
Impact of Raloxifene or Tamoxifen Use on Endometrial Cancer Risk: A Population-Based Case-Control Study
Authors: Angela DeMichele, Andrea B. Troxel, Jesse A. Berlin, Anita L. Weber, Greta R. Bunin, Elene Turzo, Rita Schinnar, Desiree Burgh, Michelle Berlin, Stephen C. Rubin, Timothy R. Rebbeck, Brian L. Strom
Journal: Journal of Clinical Oncology (2008)

Purpose Raloxifene reduces breast cancer risk in women with osteoporosis, and both tamoxifen and raloxifene prevent breast cancer in high-risk women. However, in vitro, raloxifene does not share the pro-estrogenic effects of tamoxifen on the endometrium. Randomized trials of these agents have provided limited information about endometrial cancer risk in the general population. We sought to compare endometrial cancer risks associated with raloxifene, tamoxifen, and nonusers of a selective estrogen receptor modulator (SERM) in the general population and characterize the endometrial tumors occurring in these groups. Methods We performed a case-control study of white and African American women age 50 to 79 years in the Philadelphia area. Patients were diagnosed with endometrial cancer between July 1999 and June 2002. Controls were identified through random-digit dialing. Results We analyzed 547 cases and 1,410 controls. Among cases, 3.3% had taken raloxifene; 6.2% had taken tamoxifen. Among controls, 6.6% had taken raloxifene; 2.4% had taken tamoxifen. After adjustment for other risk factors, the odds of endometrial cancer among raloxifene users was 50% that of nonusers (odds ratio [OR] = 0.50; 95% CI, 0.29 to 0.85), whereas tamoxifen users had three times the odds of developing endometrial cancer compared with raloxifene users (OR = 3.0; 95% CI, 1.3 to 6.9). Endometrial tumors in raloxifene users had a more favorable histologic profile and were predominantly International Federation of Gynecology and Obstetrics stage I and low grade. Conclusion Raloxifene users had significantly lower odds of endometrial cancer compared with both tamoxifen users and SERM nonusers, suggesting a role for raloxifene in endometrial cancer prevention and individualization of SERM therapy.
Prednisolone Inhibits Proliferation of Cultured Pulmonary Artery Smooth Muscle Cells of Patients With Idiopathic Pulmonary Arterial Hypertension
Authors: Aiko Ogawa, Kazufumi Nakamura, Hiromi Matsubara, Hideki Fujio, Tetsuya Ikeda, Kaoru Kobayashi, Ikuko Miyazaki, Masato Asanuma, Katsumasa Miyaji, Daiji Miura, Kengo Fukushima Kusano, Hiroshi Date, Tohru Ohe
Journal: Circulation (2005)

Idiopathic pulmonary arterial hypertension (IPAH) is associated with proliferation of smooth muscle cells (SMCs) in small pulmonary arteries. There is no therapy that specifically inhibits SMC proliferation. Recent studies reported that prednisolone (PSL) inhibits the postangioplasty proliferation of SMCs in atherosclerotic arteries. In this study, we tested the hypothesis that PSL has antiproliferative effects on pulmonary artery SMCs of patients with IPAH.Pulmonary artery SMCs were harvested from the pulmonary arteries of 6 patients with IPAH who underwent lung transplantation. Control SMCs were obtained from 5 patients with bronchogenic carcinoma who underwent lung lobectomy. After incubation in the presence of platelet-derived growth factor (PDGF), PSL was added at different concentrations and cell proliferation was assessed by 3H-thymidine incorporation. PSL (2x10(-4) and 2x10(-3) mol/L) significantly inhibited PDGF-stimulated proliferation (P<0.05) of SMCs from patients with IPAH but did not affect cell viability of SMCs, as confirmed by trypan blue staining. In cell cycle analysis using a microscope-based multiparameter laser scanning cytometer, PSL inhibited the progression of SMCs from G(0)/G1 to the S phase. This inhibition was associated with increased p27 expression level. PSL (2x10(-4) mol/L) also inhibited PDGF-induced SMC migration.Our results indicate that PSL has an antiproliferative effect on cultured SMCs of pulmonary arteries from patients with IPAH and suggest that PSL may be potentially useful therapeutically in patients with IPAH.
Neck and Total Body Fat Deposition in Nonobese and Obese Patients with Sleep Apnea Compared with That in Control Subjects
Authors: I. L. MORTIMORE, I. MARSHALL, P. K. WRAITH, R. J. SELLAR, N. J. DOUGLAS
Journal: American Journal of Respiratory and Critical Care Medicine (1998)

Around 50% of patients with the sleep apnea/hypopnea syndrome (SAHS) are not obese: body mass index (BMI) < 30 kg/m2. We hypothesized that local fat deposition around the upper airway may be different in nonobese patients with SAHS from that in normal subjects with the same body mass. We therefore examined the relationship between indices of general obesity; BMI, neck circumference (NC), and percentage total body fat with neck fat deposition measured by magnetic resonance imaging in three matched subject groups. Nine nonobese, nonsnoring control subjects (BMI, 25 SE 0.7 kg/m2; NC, 38.1 SE 0.5 cm; age, 37.5 SE 2.5 yr), nine nonobese patients with SAHS (BMI, 25.7 SE 0.4 kg/m2; NC, 39.8 SE 0.8 cm; age, 40 SE 4.2 yr), and nine obese patients with SAHS matched to the other groups for age (BMI, 34 SE 1.1 kg/m2; NC, 43.9 SE 0.6 cm; age, 40 SE 2.7 yr). Neck volume and fat content were assessed from the hard palate to the vocal cords using T1-weighted images. Percentage total body fat was 30 and 44% greater in nonobese and obese patients with SAHS, respectively, than in control subjects. Neck tissue volume was 10% greater in nonobese and 28% greater in obese patients with SAHS than in control subjects. The percentage of neck tissue volume attributed to fat was 27% greater in nonobese and 67% greater in obese patients with SAHS than in control subjects. The excess fat in both the nonobese and obese patients with SAHS compared with that in control subjects was localized to areas anterolateral to the upper airway, the differences were 52 and 88%, respectively. There were no significant differences between nonobese patients with SAHS and control subjects with respect to fat located in other areas of the neck; obese patients with SAHS had 42% more fat than control subjects (p < 0.05). We conclude that even relatively nonobese patients with SAHS have excess fat deposition, especially anterolateral to the upper airway when compared with control subjects with the same level of obesity assessed using BMI and NC. This may contribute to their predisposition to SAHS.
Cortisone et Corticostimuline (ACTH) en Rhumatologie
Authors: O. Savage
Journal: Annals of the Rheumatic Diseases (1953)

In the foreword the authors point out that, although Hench, Kendall, and their collaborators still refer to work with cortisone and ACTH as a "therapeutic experiment", this attitude is no longer tenable.These drugs are being used so widely in the field of rheumatic and other diseases that discussion on their value can no longer remain in the field of pure science.The present work deals only with the rheumatic and para-rheumatic diseases, and is concerned with decisions as to its suitability in certain cases and the best mnethods of administration.The experience has been gained in the study of over 460 cases of rheumatic disease, mainly at the H6pital Cochin in Paris, and the findings are com-
Intracoronary radiation therapy for patients with in-stent restenosis. Interim report from a randomized clinical study
Authors: R. Waksman, R.L. White, R.C. Chan, L.M. Gierlach, B.G. Bass, L.F. Satler, R. Mehran, M. Porrazzo, K.M. Kent, A.D. Fichard, J.J. Popma, G.S. Mintz, M.B. Leon
Journal: Journal of the American College of Cardiology (1998)
I-REGION GENES ARE EXPRESSED ON T AND B LYMPHOCYTES
Authors: Peter Lonai, Hugh O. McDevitt
Journal: The Journal of Experimental Medicine (1974)

Unidirectional mixed lymphocyte reactions (MLR) were performed between mouse strains differing for various segments within the H-2 complex. Thymocytes and purified lymph node T cells and B cells were used as stimulator cells. In three of five combinations studied, differing only within the I region, both T and B cells stimulated in the MLR. This suggests that the region codes for both T- and B-cell surface structures. However, if the difference was restricted to one I subregion (I-C), only T cells stimulated. This finding suggests that some of the I-region genes may be expressed either in T or in B cells.
Every workplace should have a mental health first aider, says government
Authors: A. O'Dowd
Journal: BMJ (2012)

All workplaces should ensure an employee is trained in “first aid” mental health for any members of staff who need help, according to the government.

In its new No health without mental health: implementation framework , published on 24 July, the Department of Health called for mental health to be treated as seriously as physical health.1

The framework for England sets out practical steps and action that organisations can take to make the six high-level objectives of last year’s mental health strategy No health without mental health a reality.2

Mental ill health is estimated to cost British businesses almost £30bn (€39bn; $47bn) across the UK economy a year—mostly because of lost production from staff being …
Distinct roles of matrix metalloproteases in the early- and late-phase development of neuropathic pain
Authors: Yasuhiko Kawasaki, Zhen-Zhong Xu, Xiaoying Wang, Jong Yeon Park, Zhi-Ye Zhuang, Ping-Heng Tan, Yong-Jing Gao, Kristine Roy, Gabriel Corfas, Eng H Lo, Ru-Rong Ji
Journal: Nature Medicine (2008)
Molecular definition of distinct cytoskeletal structures involved in complement- and Fc receptor-mediated phagocytosis in macrophages.
Authors: L A Allen, A Aderem
Journal: The Journal of Experimental Medicine (1996)

It has long been known from the results of ultrastructural studies that complement- and immunoglobulin G (IgG)-opsonized particles are phagocytosed differently by macrophages (Kaplan. G. 1977. Scand. J. Immunol. 6:797-807). Complement-opsonized particles sink into the cell, whereas IgG-coated particles are engulfed by lamellipodia, which project from the cell surface. The molecular basis for these differences is unknown. We used indirect immunofluorescence and confocal microscopy to examine how cytoskeletal proteins associate with phagosomes containing complement-opsonized zymosan (COZ) particles or IgG beads in phorbol-myristateacetate-treated peritoneal macrophages. During ingestion of COZ, punctate structures rich in F-actin, vinculin, alpha-actinin, paxillin, and phosphotyrosine-containing proteins are distributed over the phagosome surface. These foci are detected beneath bound COZ within 30 s of warming the cells to 37 degrees C, and their formation requires active protein kinase C. By contrast, during Fc receptor-mediated phagocytosis, all proteins examined were uniformly distributed on or near the phagosome surface. Moreover, ingestion of IgG beads was blocked by tyrosine kinase inhibitors, whereas phagocytosis of COZ was not. Thus, the signals required for particle ingestion, and the arrangement of cytoskeletal proteins on the phagosome surface, vary depending upon which phagocytic receptor is engaged. Moreover, complement receptor (CR)-mediated internalization required intact microtubules and was accompanied by the accumulation of vesicles beneath the forming phagosome, suggesting that membrane trafficking plays a key role in CR-mediated phagocytosis.
Removal of One-Third of the Stomach with Three and A-Half Inches of Duodenum for Cancer
Authors: J. L. Thomas
Journal: BMJ (1902)

MEDIALH 99 minority-retching and vomiting are continually repeated, and these are particularly bad cases owing to the consequent escape of stomach contents into the abdomen.(According to Fenwick, vomiting occurs in about 29 per cent.)The actual interval of time which elapses between perfora- tion and operation also influences the prognosis.The longer the irritating material is allowed to lie in the abdominal cavity the greater the danger of a fatal septic peritonitis.The evil of delay in these cases is well brought out in the table given by Robson and Moynihan in their Diseases of the Stomach, p. i6i. Interval between Perforation and Operation.Death-rate.Under I2 hours ... .
Primary intrapulmonary benign schwannoma. A case with ultrastructural and immunohistochemical confirmation
Authors: X Bosch, J Ramirez, J Font, JA Bombi, J Ferrer, J Vendrell, M Ingelmo
Journal: European Respiratory Journal (1990)

Neurogenic pulmonary tumours are rare. Neurofibromas are the most common variety and tend to occur in patients with generalized neurofibromatosis, whereas schwannomas arise sporadically in patients who have no evidence of this disorder. A case of solitary benign schwannoma arising in a segmental bronchus is presented, and the published cases reviewed. Microscopically, the tumour had a spindle-shaped cell proliferation with palisade formation in several fields and low cellularity in other areas. The diagnosis was supported by positive immunostaining for S-100 protein and by ultrastructural examination which showed elongated cells surrounded by well-preserved basal lamina and numerous cytoplasmic processes also possessing a basal lamina.
Endoglin Has a Crucial Role in Blood Cell–Mediated Vascular Repair
Authors: Linda W. van Laake, Sander van den Driesche, Simone Post, Alie Feijen, Maurits A. Jansen, Mariette H. Driessens, Johannes J. Mager, Repke J. Snijder, Cornelius J. J. Westermann, Pieter A. Doevendans, Cees J. A. van Echteld, Peter ten Dijke, Helen M. Arthur, Marie-José Goumans, Franck Lebrin, Christine L. Mummery
Journal: Circulation (2006)

Endoglin, an accessory receptor for transforming growth factor-beta in vascular endothelial cells, is essential for angiogenesis during mouse development. Mutations in the human gene cause hereditary hemorrhagic telangiectasia type 1 (HHT1), a disease characterized by vascular malformations that increase with age. Although haploinsufficiency is the underlying cause of the disease, HHT1 individuals show great heterogeneity in age of onset, clinical manifestations, and severity.In situ hybridization and immunohistochemical analysis of mouse and human hearts revealed that endoglin is upregulated in neoangiogenic vessels formed after myocardial infarction. Microvascularity within the infarct zone was strikingly lower in mice with reduced levels of endoglin (Eng+/-) compared with wild-type mice, which resulted in a greater deterioration in cardiac function as measured by magnetic resonance imaging. This did not appear to be because of defects in host inflammatory cell numbers in the infarct zone, which accumulated to a similar extent in wild-type and heterozygous mice. However, defects in vessel formation and heart function in Eng+/- mice were rescued by injection of mononuclear cells from healthy human donors but not by mononuclear cells from HHT1 patients.These results establish defective vascular repair as a significant component of the origin of HHT1. Because vascular damage or inflammation occurs randomly, it may also explain disease heterogeneity. More generally, the efficiency of vascular repair may vary between individuals because of intrinsic differences in their mononuclear cells.
Papaverine stimulation of prostaglandin E2 production by cultured rabbit gastric mucosa
Authors: M. Ligumsky, D. Rachmilewitz, U. Zor
Journal: Gut (1979)

Prostaglandins (PGs) are synthesised by gastric mucosa, and have been shown to inhibit gastric acid secretion and ulcer formation in man and experimental animals. Recently exogenous PGs, mainly of the E group, have been used for the treatment of peptic ulcer disease. We therefore searched for a drug that would stimulate endogenous gastric prostaglandin E(2) (PGE(2)) synthesis. Rabbit gastric mucosa slices were cultured for 22 hours at 77 degrees C. PGE(2), measured by radioimmunoassay, was found to be linearly secreted into the culture medium. PGE(2) accumulation in the medium during 22 hours of culture was 7.9+/-0.5 (SE) ng/mg tissue (N=20). Addition of papaverine (100 mu/ml), a cyclic nucleotide phosphodiesterase inhibitor, resulted in a significant increase (250% of control) in PGE(2) accumulation in the medium: 24.3+/-1.8 ng/mg tissue (N=25). Isobutylmethylxanthine (IBMX 100 mug/ml), another phosphodiesterase inhibitor, only slightly increased PGE(2) accumulation, while 8 bromo-cyclic AMP (1 mM) had no effect. Under these conditions IBMX increased by 20-fold mucosal cyclic AMP levels: 3.9+/-0.3 pmol/mg tissue (N=8) as compared with control levels: 0.2+/-0.03 pmol/mg tissue (N=8). Papaverine, however, did not alter mucosal cyclic AMP accumulation. These results indicate that papaverine stimulates PGE(2) production by cultured rabbit gastric mucosa and that this stimulation is not related to the inhibition of phosphodiesterase activity and accumulation of mucosal cyclic AMP. Papaverine induced stimulation of PGE(2) production should be further evaluated regarding its possible beneficial effects in protecting gastric mucosa and in reducing acid secretion in peptic ulcer patients.
The premature beat
Authors: R. Coronel, J. W T Fiolet, M. J Janse, J. T Vermeulen
Journal: Cardiovascular Research (1992)

Journal Article The premature beat Get access Ruben Coronel, Ruben Coronel Laboratory of Experimental Cardiology, University of Amsterdam, The Netherlands. Search for other works by this author on: Oxford Academic PubMed Google Scholar Jan W T Fiolet, Jan W T Fiolet Laboratory of Experimental Cardiology, University of Amsterdam, The Netherlands. Search for other works by this author on: Oxford Academic PubMed Google Scholar Michiel J Janse, Michiel J Janse Laboratory of Experimental Cardiology, University of Amsterdam, The Netherlands. Search for other works by this author on: Oxford Academic PubMed Google Scholar Jessica T Vermeulen Jessica T Vermeulen Laboratory of Experimental Cardiology, University of Amsterdam, The Netherlands. Search for other works by this author on: Oxford Academic PubMed Google Scholar Cardiovascular Research, Volume 26, Issue 7, July 1992, Page 720a, https://doi.org/10.1093/cvr/26.7.720a Published: 01 July 1992
(+)-Cyanidanol-3 in the Treatment of Acute Viral Hepatitis: A Randomized Controlled Trial
Authors: Hans Schomerus, Karl H. Wiedmann, Wolfgang Dölle, Herrmann Peerenboom, Georg Strohmeyer, Klaus Balzer, Harald Goebell, Hans K. Dürr, Christian Bode, André L. Blum, Gert Frösner, Wolfram Gerlich, Peter A. Berg, Klaus Dietz
Journal: Hepatology (1984)

One-hundred sixty patients (81 cyanidanol, 79 placebo) were included in a double-blind placebo-controlled clinical trial to evaluate the effect of 3 gm (+)-cyanidanol-3 per day for 8 weeks on the clinical course of acute viral hepatitis and HBsAg elimination. Quantitative determination of HBsAg was performed at frequent intervals. The mean time for serum bilirubin to decrease to 1.3 mg per dl was 30.8 ± 3.5 days in the treated group and 52.2 ± 9.8 days in the control group, (p &lt; 0.025). The time for SGOT to decrease to 100 IU per liter was 17.98 ± 1.82 in the treated group and 26.53 ± 3.7 in the control group (p &lt; 0.025). No significant difference in the evolution of other laboratory values or symptoms was found. The elimination rate of HBsAg was identical in both groups. Treatment did not alter the incidence of chronicity.