tbuckley/cabot-search huggingface dataset:
Diurnal Variation in Endothelium-Dependent Vasodilatation Is Not Apparent in Coronary Artery Disease
Authors: James A. Shaw, Jaye P. F. Chin-Dusting, Bronwyn A. Kingwell, Anthony M. Dart
Journal: Circulation (2001)

Background —Acute coronary syndromes present with an increased incidence from 6:00 am to 12:00 noon. Whether endothelial function follows a diurnal rhythm and whether this rhythm is impaired in coronary artery disease (CAD) has not previously been studied. Methods and Results —Diurnal variation in endothelium-dependent vasodilatation was examined in 10 CAD patients and 10 control subjects. Forearm blood flow responses to acetylcholine, sodium nitroprusside, and N G -monomethyl- l -arginine were determined by plethysmography at 8:00 am , 2:00 pm , and 8:00 pm . Heart rate, blood pressure, plasma cortisol, and inflammatory markers were also determined. Heart rate and the low-frequency component of heart rate variability were greatest in the morning in control subjects, suggesting a diurnal variation in sympathetic activity. Basal forearm blood flows were significantly reduced in control subjects at 8:00 pm compared with 8:00 am and 2:00 pm (1.2±0.2 versus 2.1±0.2 [8:00 am ] and 2.1±0.3 [2:00 pm ] mL · 100 mL −1 · min −1 ; P &lt;0.05) but unchanged in the CAD group. Acetylcholine (37 μg/min) responses were greater at 8:00 am than at 8:00 pm in control subjects (12.5±3.7 versus 19.6±2.9 mL · 100 mL −1 · min −1 , respectively; P &lt;0.05), but these responses were not time dependent in the CAD group. Responses to sodium nitroprusside were similar at all time points and between those with and without CAD. Conclusions —Thus, normal volunteers have a diurnal variation in their endothelium-dependent vasodilatation that may counteract other, potentially adverse, diurnal variations in hemodynamic and other parameters. In contrast, CAD patients who had presented with acute coronary syndromes showed a loss of this protective mechanism.
Sodium fusidate and increased remission rate of insulin-dependent diabetes mellitus
Authors: Ferdinando Nicoletti, PierLuigi Meroni, Michele Lunetta, Rosy Vigo, Tony Palermo, Domenico Papalia, Wilma Barcellini, MaurizioDi Mauro, Manuela Caruso-Nicoletti, Lanfranco Mughini, Carlo Zanussi
Journal: The Lancet (1991)
Alendronate and Estrogen–Progestin in the Long-Term Prevention of Bone Loss: Four-Year Results from the Early Postmenopausal Intervention Cohort Study: A Randomized, Controlled Trial
Authors: Pernille Ravn, Marianne Bidstrup, Richard D. Wasnich, James W. Davis, Michael R. McClung, Ana Balske, Carol Coupland, Opinder Sahota, Amarjot Kaur, Marianne Daley, Giovanni Cizza
Journal: Annals of Internal Medicine (1999)

Up to 3 years of treatment with alendronate, 5 mg/d, prevents postmenopausal bone loss.To determine whether the effect of alendronate is sustained at 4 years of treatment and persists after treatment is discontinued.Randomized, controlled trial.United States and Europe.1609 postmenopausal women 45 to 59 years of age.Participants were randomly assigned to receive oral alendronate, 5 mg/d or 2.5 mg/d; placebo; or open-label estrogen-progestin. Women in the alendronate groups received alendronate for the first 2 years of the study. Treatment was then continued without change or replaced with placebo for the last 2 years of the study.Annual measurement of bone mineral density.By year 4, the bone mineral density of participants in the placebo group had decreased by 1% to 6% (P < 0.001). Four years of treatment with 5 mg of alendronate per day increased bone mineral density at the spine (mean change [+/-SE], 3.8%+/-0.3%), hip (mean, 2.9%+/-0.2%), and total body (mean, 0.9%+/-0.2%) (P < 0.001 overall). By year 4, bone mineral density at most skeletal sites was greater in participants who switched from alendronate to placebo than in those who continuously received placebo. In years 3 and 4, bone loss in participants who switched from alendronate to placebo was similar to that seen during years 1 and 2 in those who continuously received placebo. Compared with 5 mg of alendronate per day, estrogen-medroxyprogesterone acetate produced similar increases in bone mineral density and estradiol-norethisterone acetate produced increases that were substantially greater.Four years of treatment with alendronate or estrogen-progestin prevented postmenopausal bone loss. A residual effect was seen 2 years after alendronate therapy was stopped; however, continuous alendronate treatment was more effective in preventing postmenopausal bone loss than 2 years of alendronate followed by 2 years of placebo.
Tumor Cell–Secreted Caveolin-1 Has Proangiogenic Activities in Prostate Cancer
Authors: Salahaldin A. Tahir, Guang Yang, Alexei A. Goltsov, Masami Watanabe, Ken-ichi Tabata, Josephine Addai, El Moataz Abdel Fattah, Dov Kadmon, Timothy C. Thompson
Journal: Cancer Research (2008)

Caveolin, a major structural component of specialized plasma membrane invaginations (caveolae) that participate in diverse cellular activities, has been implicated in the pathogenesis of several human diseases, including cancer. We showed in earlier studies that caveolin-1 (cav-1) is consistently and strongly overexpressed in metastatic prostate cancer and is secreted in a biologically active form by virulent prostate cancer cells. Using both in vitro and in vivo model systems, we now present evidence supporting a proangiogenic role for cav-1 in prostate cancer development and progression. Recombinant cav-1 (rcav-1) was taken up by cav-1(-/-) endothelial cells through either a lipid raft/caveolae- or clathrin-dependent mechanism, leading to specific angiogenic activities (tubule formation, cell migration, and nitric oxide production) that were mediated by rcav-1 stimulation of the PI3K-Akt-eNOS signaling module. Pathologic angiogenesis induced by cav-1 in prostate cancer-bearing mice correlated with an increased frequency, number, and size of lung metastases. We propose that in addition to its antiapoptotic role, cav-1 secreted by prostate cancer cells functions critically as a proangiogenic factor in metastatic progression of this tumor. These new insights into cav-1 function in prostate cancer may provide a base for the design of clinically applicable therapeutic strategies.
Prognosis of left ventricular geometric patterns in the Framingham heart study
Authors: Harlan M. Krumholz, Martin Larson, Daniel Levy
Journal: Journal of the American College of Cardiology (1995)

The goal of this study was to determine the incremental prognostic value of left ventricular geometric patterns beyond that provided by cardiovascular disease risk factors, including left ventricular mass. Left ventricular geometry may be classified into the following four mutually exclusive groups on the basis of left ventricular mass and relative wall thickness: concentric hypertrophy (increased mass and increased relative wall thickness), eccentric hypertrophy (increased mass and normal relative wall thickness), concentric remodeling (normal mass and increased relative wall thickness) and normal geometry (normal mass and normal relative wall thickness). The prognosis associated with these patterns in a population-based sample is not known. Proportional hazards regression models were used to evaluate the prognostic importance of left ventricular geometry in 3,216 subjects in the Framingham Heart Study who were ≥40 years old and free of clinically apparent cardiovascular disease, after adjustment for traditional cardiovascular risk factors and left ventricular mass. The follow-up period was 8 years. Subjects with concentric hypertrophy had the worst prognosis, followed by those with eccentric hypertrophy, concentric remodeling and normal geometry. Subjects with concentric hypertrophy also had the highest left ventricular mass. The association between type of geometry and prognosis was largely attenuated by adjustment for baseline differences in left ventricular mass. The odds ratio for incident cardiovascular disease in subjects with concentric hypertrophy compared with those who had normal geometry was 1.3 (95% confidence interval [CI] 0.8 to 2.1) in men and 1.2 (95% CI 0.6 to 2.3) in women after adjustment for other cardiovascular risk factors, including left ventricular mass. In a population-based sample of subjects without cardiovascular disease, knowledge of left ventricular geometry provided little prognostic information beyond that available from left ventricular mass and traditional cardiovascular risk factors.
Immune mediated mechanism for thrombosis: antiphospholipid antibody binding to platelet membranes.
Authors: M A Khamashta, E N Harris, A E Gharavi, G Derue, A Gil, J J Vazquez, G R Hughes
Journal: Annals of the Rheumatic Diseases (1988)

Because thrombocytopenia occurs frequently in patients with anticardiolipin (aCL) antibodies and thrombosis, some investigators have proposed that aCL antibodies may play a direct part in thrombosis by binding and activating platelets. To test this proposal experiments were performed to determine whether aCL antibodies can bind platelets. Preincubation of aCL positive sera with freeze-thawed platelets caused significant inhibition of aCL activity in four serum samples tested. Antibodies with cardiolipin binding activity were subsequently eluted from these platelets. Total phospholipids extracted from platelets inhibited aCL activity, and the specific phospholipids bound were shown to be phosphatidylethanolamine, phosphatidylserine, and phosphatidylinositol. It is concluded that aCL antibodies can bind phospholipids in platelet membranes but pertubation of the membrane must first occur.
Morphoea and Systemic Sclerosis.
Authors: John T. Ingram.
Journal: British Journal of Dermatology (1964)

Journal Article Morphoea and Systemic Sclerosis. Get access John T. Ingram. John T. Ingram. Newcastle upon Tyne Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 76, Issue 5, 1 May 1964, Pages 238–239, https://doi.org/10.1111/j.1365-2133.1964.tb14523.x Published: 01 May 1964
Serodiagnosis of <i>Mycobacterium avium</i>–Complex Pulmonary Disease Using an Enzyme Immunoassay Kit
Authors: Seigo Kitada, Kazuo Kobayashi, Satoshi Ichiyama, Shunji Takakura, Mitsunori Sakatani, Katsuhiro Suzuki, Tetsuya Takashima, Takayuki Nagai, Ikunosuke Sakurabayashi, Masami Ito, Ryoji Maekura
Journal: American Journal of Respiratory and Critical Care Medicine (2007)

The diagnosis of Mycobacterium avium-complex pulmonary disease (MAC-PD) and/or its discrimination from pulmonary tuberculosis (TB) is sometimes complicated and time consuming.We investigated in a six-institution multicenter study whether a serologic test based on an enzyme immunoassay (EIA) kit was useful for diagnosing MAC-PD and for distinguishing it from other lung diseases.An EIA kit detecting serum IgA antibody to glycopeptidolipid core antigen specific for MAC was developed. Antibody levels were measured in sera from 70 patients with MAC-PD, 18 with MAC contamination, 37 with pulmonary TB, 45 with other lung diseases, and 76 healthy subjects.Significantly higher serum IgA antibody levels were detected in patients with MAC-PD than in the other groups (P < 0.0001). Setting the cutoff point at 0.7 U/ml resulted in a sensitivity and specificity of the kit for diagnosing MAC-PD of 84.3 and 100%, respectively. Significantly higher antibody levels were also found in patients with nodular-bronchiectatic disease compared with fibrocavitary disease in MAC-PD (P < 0.05). There was a positive correlation between the extent of disease on chest computed tomography scans and the levels of antibody (r = 0.43, P < 0.05) in patients with MAC-PD.The EIA kit is useful for the rapid diagnosis of MAC-PD and for differentiating MAC-PD from pulmonary TB and, if validated by studies in other populations, could find wide application in clinical practice.
<i>Aurora Borealis</i>
Authors: Thomas B. Cole
Journal: JAMA (2015)

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
Hyaluronic Acid Induces Osteopontin via the Phosphatidylinositol 3-Kinase/Akt Pathway to Enhance the Motility of Human Glioma Cells
Authors: Mi-Suk Kim, Myung-Jin Park, Eui-Jung Moon, So-Jeong Kim, Chang-Hun Lee, Heon Yoo, Sang-Hoon Shin, Eun-Sook Song, Seung-Hoon Lee
Journal: Cancer Research (2005)

Abstract Hyaluronic acid (HA) binds to cell-surface receptors such as CD44, and seems to be involved in cell adhesion, motility, and tumor progression in brain. To identify gene expression changes that are initiated by HA, we explored human cytokine arrays in U87MG glioma cells and identified osteopontin, a secreted matrix protein, as a transcriptional target of HA. Interestingly, expression of osteopontin was induced by HA in glioma cells lacking functional PTEN, a tumor suppressor gene (U87MG, U251MG, and U373MG), but not in wild-type (wt)-PTEN-harboring cells (LN18 and LN428). To confirm the role of PTEN, adenoviral (Ad)-wt-PTEN was used to induce ectopic expression of wt-PTEN in U87MG cells, leading to reduced HA-mediated osteopontin induction. Reciprocally, transfection with dominant-negative Akt repressed HA-induced osteopontin expression. Furthermore, HA promoted the motility of glioma cells, and down-regulation of induced osteopontin activity via a neutralizing anti-osteopontin antibody repressed HA-induced motility in vitro. Together, these results strongly suggest that induction of osteopontin expression by HA is dependent on activation of the phosphatidylinositol 3-kinase/Akt pathway. Furthermore, our data indicate that PTEN can effectively modulate the expression of osteopontin, and HA-induced osteopontin plays an important role in the motility response induced by HA in human glioma cells.
Dermatofibrosarcoma protuberans of the oral cavity
Authors: Shane A. Meehan, Joseph A. Napoli, Ann E. Perry
Journal: Journal of the American Academy of Dermatology (1999)

Dermatofibrosarcoma protuberans (DFSP) is a low grade, malignant spindle cell tumor with an infiltrative growth pattern and a high rate of local recurrence. This tumor's cell of origin is controversial. DFSP usually presents in adult life and is most frequently located on the trunk and proximal extremities. Although 10% to 15% of cases involve the head and neck, this tumor has not been previously described in the oral cavity.
Dendritic Cell Vaccination in Combination with Anti-CD25 Monoclonal Antibody Treatment: A Phase I/II Study in Metastatic Melanoma Patients
Authors: Joannes F.M. Jacobs, Cornelis J.A. Punt, W. Joost Lesterhuis, Roger P.M. Sutmuller, H. Mary-lène H. Brouwer, Nicole M. Scharenborg, Ina S. Klasen, Luuk B. Hilbrands, Carl G. Figdor, I. Jolanda M. de Vries, Gosse J. Adema
Journal: Clinical Cancer Research (2010)

Abstract Purpose: The success of cancer immunotherapy depends on the balance between effector T cells and suppressive immune regulatory mechanisms within the tumor microenvironment. In this study we investigated whether transient monoclonal antibody–mediated depletion of CD25high regulatory T cells (Treg) is capable of enhancing the immunostimulatory efficacy of dendritic cell vaccines. Experimental Design: Thirty HLA-A2.1+ metastatic melanoma patients were vaccinated with mature dendritic cells pulsed with tumor peptide and keyhole limpet hemocyanin (KLH). Half of the patients were pretreated with daclizumab, a humanized antibody against the interleukin-2 (IL-2) receptor α-chain (CD25), either four or eight days before dendritic cell vaccinations. Clinical and immunologic parameters were determined. Results: Daclizumab efficiently depleted all CD25high immune cells, including CD4+FoxP3+CD25high cells, from the peripheral blood within four days of administration. Thirty days after administration, daclizumab was cleared from the circulation and all CD25+ cells reappeared. The presence of daclizumab during dendritic cell vaccinations prevented the induction of specific antibodies in vivo but not the presence of antigen-specific T cells. Daclizumab, however, did prevent these CD25+ T cells from acquiring effector functions. Consequently, significantly less patients pretreated with daclizumab developed functional, vaccine-specific effector T cells and antibodies compared with controls. Daclizumab pretreatment had no significant effect on progression-free survival compared with the control group. Conclusions: Although daclizumab depleted the CD4+FoxP3+CD25high Tregs from the peripheral circulation, it did not enhance the efficacy of the dendritic cell vaccine. Residual daclizumab functionally suppressed de novo induced CD25+ effector cells during dendritic cell vaccinations. Our results indicate that for immunotherapeutic benefit of transient Treg depletion, timing and dosing as well as Treg specificity are extremely important. Clin Cancer Res; 16(20); 5067–78. ©2010 AACR.
Pulmonary hypertension therapy and COPD: still many questions to be answered
Authors: C. Jardim, R. Souza
Journal: European Respiratory Journal (2009)

To the Editors: 

After great development in the knowledge of pulmonary arterial hypertension (PAH) during the last decades, there is now an increasing interest in the pathophysiology of other forms of pulmonary hypertension, such as chronic obstructive pulmonary disease (COPD). The results obtained in the study by Stolz et al. 1 have shown that for an average COPD Global Initiative for Chronic Obstructive Lung Disease stage III-IV population, …
Randomised trial of effect of alendronate on risk of fracture in women with existing vertebral fractures
Authors: Dennis M Black, Steven R Cummings, David B Karpf, Jane A Cauley, Desmond E Thompson, Michael C Nevitt, Douglas C Bauer, Harry K Genant, William L Haskell, Robert Marcus, Susan M Ott, James C Torner, Sara A Quandt, Theodore F Reiss, Kristine E Ensrud
Journal: The Lancet (1996)
A Three-Kilobase Fragment of the Human Robo4 Promoter Directs Cell Type–Specific Expression in Endothelium
Authors: Yoshiaki Okada, Kiichiro Yano, Enjing Jin, Nobuaki Funahashi, Mie Kitayama, Takefumi Doi, Katherine Spokes, David L. Beeler, Shu-Ching Shih, Hitomi Okada, Tatyana A. Danilov, Elizabeth Maynard, Takashi Minami, Peter Oettgen, William C. Aird
Journal: Circulation Research (2007)

Robo4, a member of the roundabout family, is expressed exclusively in endothelial cells and has been implicated in endothelial cell migration and angiogenesis. Here we report the cloning and characterization of the human Robo4 promoter. The 3-kb 5'-flanking region directs endothelial cell-specific expression in vitro. Deletion and mutation analyses revealed the functional importance of two 12-bp palindromic DNA sequences at -2528 and -2941, 2 SP1 consensus motifs at -42 and -153, and an ETS consensus motif at -119. In electrophoretic mobility shift assays using supershifting antibodies, the SP1 motifs bound SP1 protein, whereas the ETS site bound a heterodimeric member of the ETS family, GA binding protein (GABP). These DNA-protein interactions were confirmed by chromatin immunoprecipitation assays. Transfection of primary human endothelial cells with small interfering RNA against GABP and SP1 resulted in a significant (approximately 50%) reduction in endogenous Robo4 mRNA expression. The 3-kb Robo4 promoter was coupled to LacZ, and the resulting cassette was introduced into the Hprt locus of mice by homologous recombination. Reporter gene activity was observed in the vasculature of adult organs (particularly in microvessels), tumor xenografts, and embryos, where it colocalized with the endothelial cell-specific marker CD31. LacZ mRNA levels in adult tissues and tumors correlated with mRNA levels for endogenous Robo4, CD31, and vascular endothelial cadherin. Moreover, the pattern of reporter gene expression was similar to that observed in mice in which LacZ was knocked into the endogenous Robo4 locus. Together, these data suggest that 3-kb upstream promoter of human Robo4 contains information for cell type-specific expression in the intact endothelium.
Anaphylactic Shock, Acute Renal Failure, and Disseminated Intravascular Coagulation
Authors: V. Taylor Smith
Journal: JAMA (1982)

ZOMEPIRAC sodium is a nonsteroidal, anti-inflammatory agent available since November 1980. It was developed as an analgesic and has been described by the manufacturer as safe and well tolerated. There is a previous report of an anaphylactic reaction, secondary to zomepirac, in the literature.<sup>1</sup>This report presents the occurrence of anaphylactic shock, disseminated intravascular coagulation, and acute renal failure following the ingestion of zomepirac. <h3>Report of a Case</h3> A 66-year-old man came to the emergency room with a six-hour history of nausea, vomiting, and diarrhea. He also noted chills, but his temperature was not taken at home. Some occasional mild abdominal cramping was noted with the diarrhea. One week before admission the patient noted a similar type of illness with chills, nausea, vomiting, and diarrhea, but it lasted only two hours and subsided spontaneously. He felt well prior to and in between these episodes. Additional history indicated that he
The Treatment of Laryngeal Phthisis
Authors: G. H. Mackenzie
Journal: BMJ (1887)

<h3>Abstract</h3> The gastrointestinal (GI) tract is inhabited by a complex microbial community, which contributes to its homeostasis. Disrupted microbiome can cause GI-related diseases, including inflammatory bowel disease, therefore identifying host-microbe interactions is crucial for better understanding gut health. Bacterial extracellular vesicles (BEVs), released into the gut lumen, can cross the mucus layer and access underlying immune cells. To study cross-kingdom communication between BEVs and host, we focused on the influence of BEVs, generated by <i>Bacteroides thetaiotaomicron</i> (VPI-5482), on host immune cells. Using single-cell RNA sequencing data and host-microbe protein-protein interaction networks, we examined the potential effect of BEVs on dendritic cells, macrophages and monocytes with particular focus on the Toll-like receptor (TLR) pathway. We identified biological processes affected in each immune cell type, and also cell-type specific processes (e.g myeloid cell differentiation). The TLR pathway analysis highlighted that BEV targets differ among cells and even between the same cells in healthy versus disease (ulcerative colitis) conditions. Our <i>in silico</i> findings were validated in BEV-monocyte co-cultures demonstrating the requirement for TLR4 in BEV-elicited NF-κ B activation. This study demonstrates that both cell-type and health condition influence BEV-host communication. The results and the pipeline can facilitate BEV-based therapy development for the treatment of IBD.