tbuckley/cabot-search huggingface dataset:
Molecular cloning of genes differentially regulated by TNF-α in bovine aortic endothelial cells, fibroblasts and smooth muscle cells
Authors: J Lin
Journal: Cardiovascular Research (1998)

Objective: Tumor necrosis factor-α (TNF-α) is a pleiotropic cytokine binding to and thereby stimulating vascular cells. TNF-α mediated intermediate stimulation of vascular cells is believed to play a pivotal role in the development of arteriosclerosis. While extensive information has recently become available on gene induction by TNF-α, less is known about gene suppression by TNF-α in vascular cells. Endothelial cells are the first cell layer within the vessel wall interacting with circulating, cytokine releasing cells. Therefore, they were selected as target for these study. Methods: A differential screening approach has been used to isolate cDNAs whose abundance was suppressed by incubating bovine aortic endothelial cells (BAEC) for 6 h with 1 nM TNF-α. The gene expression of 6 isolated cDNAs after TNF-α was investigated by dot blots and nuclear run-on analysis in BAEC. The investigated genes were partially or completely sequenced. Differential expression after TNF-α stimulation of BAEC, bovine fibroblasts and vascular smooth muscle cells (SMC) was studied by Northern blots. RNA transcripts of the clone C7 in aortic aneurysms were examined by in situ hybridization. Results: 49 independent cDNAs were isolated by the differential screening approach and 6 clones were further analyzed. These genes were downregulated in a time and dose dependent manner in BAEC. Sequence analysis revealed that 3 cDNAs encoded previously unidentified genes (C1, C5, C7), while 3 encoded known genes: connective tissue growth factor (CTGF; A1), fibronectin (A8) and the mitochondrial genome (B1). A1 and B1 were suppressed in BAEC, fibroblasts and SMC, whereas A8, C1, C5 and C7 were not uniformly downregulated in the investigated cells. C7 RNA transcripts were exclusively induced in the endothelium of an uninflamed aortic aneurysm. The transcripts were undetectable in an inflamed aortic aneurysm and control vessels. Conclusions: Gene suppression is a prominent feature of the intermediate effect of TNF-α on endothelial cells. Differences in the expression of the tested genes in endothelial cells, fibroblasts and vascular smooth muscle cells open possibilities for the study of cellular interactions in the vascular wall in disease situations with high local TNF-α concentrations.
SOME AETIOLOGICAL FACTOES IN OTITIS EXTERNA.
Authors: MYRA McKELVIE, P. McKELVIE
Journal: British Journal of Dermatology (1966)

Journal Article SOME AETIOLOGICAL FACTOES IN OTITIS EXTERNA. Get access MYRA McKELVIE, M.B., M.R.C.P., MYRA McKELVIE, M.B., M.R.C.P. Senior Registrar, Dermatology Department, University College Hospital, London, W.C.1 Search for other works by this author on: Oxford Academic Google Scholar P. McKELVIE, Ch.M., F.R.C.S., D.L.O. P. McKELVIE, Ch.M., F.R.C.S., D.L.O. Lecturer of Laryngology and Otology, Institute of Laryngology and Otology, London, W.C.1 Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 78, Issue 4, 1 April 1966, Pages 227–231, https://doi.org/10.1111/j.1365-2133.1966.tb12211.x Published: 01 April 1966
Antidepressants Normalize the Default Mode Network in Patients With Dysthymia
Authors: Jonathan Posner, David J. Hellerstein, Inbal Gat, Anna Mechling, Kristin Klahr, Zhishun Wang, Patrick J. McGrath, Jonathan W. Stewart, Bradley S. Peterson
Journal: JAMA Psychiatry (2013)

The default mode network (DMN) is a collection of brain regions that reliably deactivate during goal-directed behaviors and is more active during a baseline, or so-called resting, condition. Coherence of neural activity, or functional connectivity, within the brain's DMN is increased in major depressive disorder relative to healthy control (HC) subjects; however, whether similar abnormalities are present in persons with dysthymic disorder (DD) is unknown. Moreover, the effect of antidepressant medications on DMN connectivity in patients with DD is also unknown.To use resting-state functional-connectivity magnetic resonance imaging (MRI) to study (1) the functional connectivity of the DMN in subjects with DD vs HC participants and (2) the effects of antidepressant therapy on DMN connectivity.After collecting baseline MRI scans from subjects with DD and HC participants, we enrolled the participants with DD into a 10-week prospective, double-blind, placebo-controlled trial of duloxetine and collected MRI scans again at the conclusion of the study. Enrollment occurred between 2007 and 2011.University research institute.Volunteer sample of 41 subjects with DD and 25 HC participants aged 18 to 53 years. Control subjects were group matched to patients with DD by age and sex.We used resting-state functional-connectivity MRI to measure the functional connectivity of the brain's DMN in persons with DD compared with HC subjects, and we examined the effects of treatment with duloxetine vs placebo on DMN connectivity.Of the 41 subjects with DD, 32 completed the clinical trial and MRI scans, along with the 25 HC participants. At baseline, we found that the coherence of neural activity within the brain's DMN was greater in persons with DD compared with HC subjects. Following a 10-week clinical trial, we found that treatment with duloxetine, but not placebo, normalized DMN connectivity.The baseline imaging findings are consistent with those found in patients with major depressive disorder and suggest that increased connectivity within the DMN may be important in the pathophysiology of both acute and chronic manifestations of depressive illness. The normalization of DMN connectivity following antidepressant treatment suggests an important causal pathway through which antidepressants may reduce depression.
The dos and don'ts of collaborating with industry
Authors: R. Moynihan
Journal: BMJ (2012)

Handy hints for getting the most out of relationships with drug companies



If you haven’t read the recent guidance on doctor-industry relationships, it’s certainly worth a look.1 Endorsed by leading professional groups, it argues that promising collaboration with industry “may be missed or even rejected” because of “misconceptions” arising from historical practices or rogue individuals. To set the record straight, the guidance emphasises the value of seeing sales representatives, the benefits of industry sponsored education, and the critical importance of health professionals serving on companies’ advisory boards.

To drive home its message, the guidance spells out some DOs and DON’T s for doctors, and this is where it starts to sound just a tad defensive, not least because of the use of BOLD CAPITALS . First among the DOs is the instruction to treat industry as a partner and to get involved with company funded trials and education. The DON’Ts feel like the desperate pleas of a lover fearing that a long term affair may be on the rocks: “ Don’t establish blanket policies denying interaction with industry,” and “ Don’t be tempted …
The Ten Commandments for Technical Exhibitors
Authors: Nathaniel E. Reich
Journal: JAMA (1966)

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
Abstract 3042: Glypican-1 (GPC1) promotes S-phase entry and DNA replication in human glioma cells
Authors: Dianhua Qiao, Kristy Meyer, Andreas Friedl
Journal: Cancer Research (2012)

Abstract Glypican-1 (GPC1), the most ubiquitously expressed member of the glypican family of heparan sulfate proteoglycans (HSPGs), is highly expressed in the developing brain and gliomas. In gliomas, GPC1 is overexpressed in both tumor blood vessel endothelial cells (ECs) and the neoplastic cells. Prior work by us in ECs indicates that GPC1 is overall mitogenic and essential for cell cycle progression and proliferation, implying a role in glioma angiogenesis. The present study focused on the role of GPC1 in glioma cells to explore potential roles in tumorigenesis and growth. The expression of GPC1 in U87 cells, a human glioma cell line with a relatively low basal level of GPC1, was titrated by adenoviral transduction. BrdU pulse-labeling showed a robust induction of S-phase entry and DNA replication by expression of GPC1 in a dose-dependent manner. GPC1 overexpression ultimately led to DNA re-replication and aneuploidy as well as enlarged nuclei and cell rounding. Consistent with these cell cycle effects, ectopic expression of GPC1 significantly induced downregulation of pRb, p21Cip1 and p27Kip1 and upregulation of cyclin E, CDK2 and E2F transactivation activity. These cellular and molecular activities of GPC1 were independent of serum concentrations in the growth medium, suggesting that they do not require exogenous growth factors. This activity required intact GPC1 as neither unglycanated GPC1 core protein nor isolated GPC1 HS chains induced the cell cycle and molecular alterations seen after intact GPC1 was added. The more general relevance of our observation to other cell types and the HS-dependency of the GPC1 activity were confirmed by GPC1 transduction of wild-type and HS synthesis-defective CHO cells. Overexpression of GPC1 induced dramatic S-phase entry in wild-type but not in HS-deficient mutant CHO cells. In summary, this work reveals a potent S-phase promoting activity of GPC1 in glioma cells, which may lead to accelerated cell growth and/or increased genomic instability and, therefore, implies a role for GPC1 in glioma tumorigenesis and growth. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 3042. doi:1538-7445.AM2012-3042
Antigen-specific soluble helper activity for murine major histocompatibility complex-encoded molecules. I. Kinetics of factor production after skin transplantation and genetic mapping of the H-2 region specificity.
Authors: J M Plate, C A McDaniel, L Flaherty, J H Stimpfling, R W Melvold, N Q Martin
Journal: The Journal of Experimental Medicine (1982)

Antigen-specific soluble helper molecules are produced during major histocompatibility complex-disparate allograft priming. Genetic mapping studies with appropriate recombinant and mutant lines of mice have defined the antigen specificities of the soluble helper molecules described here as being directed against the H-2Dd molecules. The production of antigen-specific helper molecules is a relatively early event after H-2Dd-region allograft priming. A later phase of factor production near the time of graft rejection also contains nonspecific helper factors and IL-2.
On Lateral Curvature of the Spine: Its Prevention and Treatment
Authors: R. Barwell
Journal: BMJ (1899)

Excellent Health very good. 2 1888 Returned with ventral hernia in 1895. 3I893 , "I have not had good health; never free from pain, ,,especially in the lower part of my back." 4 1894 " I have had very good health since my oper-ation." 5 I894 Very good health: earns her living by mangling. 62894 ,, "I lhave no pain, but much general weakness, which makes one think of all kinds of imaginary diseases."I I894 "Since my operation I have had very good health." 82894 Much better since operation.92894 "My health has been fairly good." 10 2895 *, "I have enjoyed the best of health 'since my opera- tion."2I1895 Has had excellent health since operation. 122895 Thrombo-"I am fairly well in health, but my leg still troubles'me sis of veins very much." of left leg 23 2895 Excellent "I have had excellent health since the operation."
Neurotensin increases mortality and mast cells reduce neurotensin levels in a mouse model of sepsis
Authors: Adrian M. Piliponsky, Ching Cheng Chen, Toshihiko Nishimura, Martin Metz, Eon J. Rios, Paul R. Dobner, Etsuko Wada, Keiji Wada, Sherma Zacharias, Uma M. Mohanasundaram, James D. Faix, Magnus Abrink, Gunnar Pejler, Ronald G. Pearl, Mindy Tsai, Stephen J. Galli
Journal: Nature Medicine (2008)
High pro-inflammatory cytokine secretion and selective depletion of high avidity cross-reactive cytotoxic T-cells in the pathogenesis of acute secondary dengue virus infection
Authors: Tao Dong, Edward Moran, Nguyen Vinh Chau, Cameron Simmons, Yanchun Peng, Tran Tinh Hien, Andrew McMichael, Jeremy Farrar, Sarah Rowland-Jones
Journal: Journal of Infection (2007)
Pericatheter Leak in a Peritoneal Dialysis Patient
Authors: Kyaw N. Tun, Mark Tulchinsky
Journal: Clinical Nuclear Medicine (2012)

A 62-year-old patient with end-stage renal disease who is managed with continuous ambulatory peritoneal dialysis developed anterior abdominal wall swelling and pain that extended from just above peritoneal catheter site caudally. CT of the abdomen suggested pericatheter abscess with panniculitis. Tc-99m sulfur colloid peritoneal distribution planar scintigraphy suggested the diagnoses of pericatheter leak. The addition of SPECT/CT confirmed the latter diagnosis and pinpointed the exact location of the peritoneal leakage that was around insertion site. SPECT/CT was useful in establishing unequivocal diagnosis of peritoneal leak.
Endovascular Stents in the Pulmonary Circulation
Authors: Rami Fogelman, David Nykanen, Jeffrey F. Smallhorn, Brian W. McCrindle, Robert M. Freedom, Lee N. Benson
Journal: Circulation (1995)

Background The use of endovascular stents to relieve obstructions in the setting of non–balloon dilatable pulmonary artery stenosis has been encouraging. The benefits in management and the potential for restenosis, however, have not been defined. This study attempts to assess the impact of such implants on clinical outcomes and the pattern of stent incorporation within the vessel wall. Methods and Results Fifty-five balloon-expandable stents were implanted in 42 patients 6.1±4.7 years of age. Patients were followed prospectively (median, 15 months) and recatheterized 1 year after implantation. Thirty-eight patients had the implants positioned percutaneously (49 implants), while 4 patients (6 implants) had intraoperative implantations. There was a diameter increase in the stenotic area of 109±79% ( P &lt;.0001) and a gradient reduction of 74±26% ( P &lt;.0001). Twelve stents straddled the orifice of side-branch pulmonary arteries and reduced flow to the branch vessel acutely in 7 patients. Twenty-nine patients underwent recatheterization, and various degrees and locations of acquired intraluminal narrowing were observed in all cases, particularly in areas of diameter mismatch between the stented and nonstented vessels. Eleven patients had further dilation with diameter improvement. Of the 38 patients who underwent percutaneous implantation, planned surgery for pulmonary artery stenosis was avoided in 33 and deferred in 4 patients. One patient who was considered inoperable had stent implantation as a palliative procedure. Symptomatic improvement was reported in 27 patients, and 15 patients remained asymptomatic. Conclusions Endovascular stents have a role in the treatment of pulmonary artery stenoses and positively affect clinical care. The stenosis relief, however, may be tempered by the development of intraluminal stent obstruction, which may require redilation (15 of 55 stents) and mandates long-term follow-up.
Changes in BMI Before and During Economic Development and Subsequent Risk of Cardiovascular Disease and Total Mortality: A 35-Year Follow-up Study in China
Authors: Yao He, Tai Hing Lam, Bin Jiang, Lan Sun Li, Dong Ling Sun, Lei Wu, Miao Liu, Shan Shan Yang, Yi Yan Wang, Deirdre K. Tobias, Qi Sun, Frank B. Hu
Journal: Diabetes Care (2014)

OBJECTIVE It is unclear whether changes in BMI during rapid economic development influence subsequent mortality. RESEARCH DESIGN AND METHODS We analyzed whether BMI in 1976 and 1994 and changes in BMI during 1976–1994 predict cardiovascular disease (CVD) and all-cause mortality in a 35-year follow-up cohort of 1,696 Chinese (1,124 men and 572 women, aged 35–65 years) in Xi'an, China. Participants were categorized as underweight (&amp;lt;18.5 kg/m2), normal weight (18.5–24.9 kg/m2), and overweight (≥25.0 kg/m2). RESULTS During 51,611 person-years of follow-up, we identified 655 deaths from all causes and 234 from CVD. From 1976 to 1994, the prevalence of overweight rose from 9.2 to 27.8%. With each unit increment in 1976 BMI, multivariate hazard ratios (HRs) (95% CI) were 0.78 (0.72–0.84) for CVD and 0.91 (0.87–0.95) for all-cause mortality. In contrast, corresponding HRs were 1.14 (1.08–1.19) and 1.05 (1.01–1.08) in 1994 BMI. The HRs for each unit increment in BMI change from 1976 to 1994 were 1.35 (1.25–1.41) for CVD and 1.09 (1.05–1.13) for all-cause mortality. Compared with participants with stable normal weight in 1976 and 1994, HRs of all-cause mortality for those who had normal weight in 1976 but became overweight in 1994 and for those who were persistently overweight during 1976–1994 were 1.42 (1.12–1.80) and 1.80 (1.04–3.14), respectively. CONCLUSIONS Gaining weight with increased BMI at middle age in Chinese during economic development was associated with elevated risks of all-cause and CVD mortality. Higher BMI measured before economic development was associated with lower mortality risk, whereas BMI measured afterward was associated with increased mortality.
FDA panel recommends banning "aversive" shock devices
Authors: M. McCarthy
Journal: BMJ (2014)

The tyrosine kinase inhibitor sunitinib was recently approved for use against gastrointestinal stromal tumors and advanced renal cell carcinoma. Yet, the protective effect of sunitinib against breast cancer has been poorly investigated. In this study, we investigated the antiproliferative and apoptogenic effects of sunitinib and the possible mechanism involved against the MCF7 human breast cancer cell line. Treatment of MCF7 cells with sunitinib caused concentration-dependent cell growth suppression due to apoptosis. Apoptotic death induced by sunitinib in MCF7 cells was mediated by activation of caspase-3 and p53 mRNA and protein expression and an increase in the percentage of apoptotic cells (40%) as determined by flow cytometry. Apoptosis was associated with a significant inhibition of nuclear factor-kappa B mRNA and protein expression. Mechanistically, blocking of de novo RNA synthesis by actinomycin D significantly inhibited sunitinib-induced expression of p53 mRNA, but not that of caspase-3, indicating involvement of a transcriptional mechanism. This apoptosis-mediated inhibition of MCF7 cell growth was attributed to inhibition of cell cycle-related genes (cyclin D1 and cyclin E2) and arrest of MCF7 cells in the G<sub>2</sub>/M phase in the cell cycle, allowing up-regulation of expression of DNA repair genes such as x-ray repair cross-complementing protein 1. In addition, sunitinib exhibited concentration-dependent induction of oxidative stress genes (heme oxygenase 1 and glutathione transferase A1) through the nuclear factor erythroid 2–related factor 2 pathway. These findings lead us to propose that sunitinib suppressed the proliferation of MCF7 cells via cell-cycle arrest and apoptotic- and oxidative stress-mediated pathways.
STUDIES ON THE CHEMOTHERAPY OF THE HUMAN MALARIAS. III. THE PHYSIOLOGICAL DISPOSITION AND ANTIMALARIAL ACTIVITY OF THE CINCHONA ALKALOIDS 123
Authors: John V. Taggart, David P. Earle, Robert W. Berliner, Charles G. Zubrod, William J. Welch, Nancy Bowman Wise, Edmond F. Schroeder, Irving M. London, James A. Shannon
Journal: Journal of Clinical Investigation (1948)
Judge allows force feeding of mentally competent patient
Authors: C Dyer
Journal: BMJ (1994)

The Mental Health Act 1983 allows detained patients to be treated against their will even if they are mentally competent to refuse treatment and the treatment is against their best interests, a High Court judge ruled last week. Mr Justice Thorpe granted Croydon Health Authority a declaration that it could force feed a 24 year old detained patient suffering from borderline personality disorder.

The judge made the declaration despite deciding that the patient was competent to refuse treatment and that force feeding would not be in her best interests “unless and until her physical state was so debilitated as to threaten her survival.” He said that it was “disquieting” that the act legalised what the common law would not.

Lawyers for the patient, named only as …
Augmented forearm vasoconstriction during dynamic exercise in healthy older men.
Authors: J A Taylor, G A Hand, D G Johnson, D R Seals
Journal: Circulation (1992)

BACKGROUND We tested the hypothesis that the nonactive limb vasoconstriction evoked during large-muscle dynamic exercise becomes augmented with aging in humans. METHODS AND RESULTS Sixteen young control subjects (age, 26 +/- 1 year) and twelve older (65 +/- 1 year) healthy men with similar chronic physical activity levels were studied during supine leg cycling exercise. Both peak work load (1,100 +/- 60 versus 1,400 +/- 40 kpm/min) and peak O2 uptake (1.85 +/- 0.10 versus 2.38 +/- 0.07 l/min) were lower in the older men (p &lt; 0.05). There were no differences in the two groups under conditions of quiet supine (basal) rest. During cycling for 5 minutes each at mild, moderate, and heavy submaximal intensities (approximately 45%, 65%, and 85% of peak O2 uptake), the increases in arterial blood pressure generally were similar in the young and older subjects; however, heart rate rose less in the older men (p &lt; 0.05). Whole forearm blood flow (venous occlusion plethysmography) was lower and vascular resistance was higher (approximately 55-90%) in the older men at all loads (p &lt; 0.05), but the steady-state forearm skin blood flow responses (laser Doppler velocimetry) were not different in the two groups. The increases in antecubital venous norepinephrine concentrations were greater in the older men at each work load (p &lt; 0.05), although the plasma epinephrine responses were similar in the two groups. In other studies, 1) peak whole forearm reactive hyperemia and vascular conductance after sustained circulatory arrest (ischemia) were slightly (approximately 20%) but not significantly lower in the older men and 2) the forearm vasoconstrictor and plasma norepinephrine responses to a nonexercise sympathoexcitatory stimulus (limb immersion in ice water) tended to be blunted in the older men. CONCLUSIONS During brief, submaximal, large-muscle dynamic exercise, healthy older men demonstrate augmented forearm vasoconstriction that is probably caused by greater constriction of skeletal muscle resistance vessels; this appears to be mediated, at least in part, by increased sympathetic outflow. These altered sympathetic vasoconstrictor adjustments do not represent a nonspecific hyperresponsiveness to acute stress with human aging. Finally, the regulation of arterial blood pressure appears to be normal in these healthy older men.