tbuckley/cabot-search huggingface dataset:
Abstract 4382: Identification of Subclinical Right Ventricular Systolic and Diastolic Dysfunction in Stable Chronic Obstructive Pulmonary Disease - A Tissue Doppler Study
Authors: Qing Zhang, Fanny Ko, Jun-Min Xie, David Shu Cheong Hui, Gabriel Wai-Kwok Yip, Pui-Wai Lee, Chin-Pang Chan, Cheuk-Man Yu
Journal: Circulation (2008)

Introduction : Compared with conventional echocardiographic technologies, tissue Doppler imaging (TDI) is capable of detecting early impairment of myocardial function.   Hypothesis : Subclinical right ventricular (RV) dysfunction can be identified by using TDI in patients with chronic obstructive pulmonary disease (COPD).   Methods : 100 patients (73 ± 8 years, 80% males) with stable COPD (without acute exacerbation in the past 3 months) who had no history of right heart failure were compared with 50 healthy subjects. Color TDI was performed to assess tricuspid annular motion displacement, peak systolic (Sm) and peak early diastolic (Em) velocities in both basal and mid RV segments.   Results : Patients with COPD had a higher pulmonary artery systolic pressure (PASP) and increased RV wall thickness (RVWT), though RV areas and area change were comparable with controls. The tricuspid E velocity was decreased while A velocity was increased resulting in reduced E/A ratio. TDI showed significant reduction in tricuspid annular displacement as well as Sm and Em in both basal and mid segments. The extent of decline in Em (35%) was greater than that of Sm (13%). When the cutoff values were derived from the normal subjects (−2SD from mean) for basal Sm (7.1cm/s) and basal Em (4.8cm/s), the prevalence of systolic and diastolic dysfunction in COPD patients was 20% and 33%, respectively.   Conclusions : By using TDI, early asymptomatic impairment of RV systolic and diastolic function was evident in patients with stable COPD who had no clinical evidence of right heart failure.
Abstract 13988: Class II Major Histocompatibility Complex Transactivator (CIITA) Knockdown Prevents Immune Rejection of Allogeneic Bone Marrow Stem Cells in Cardiac Regeneration
Authors: Ana Ludke, Xi-Ping Huang, Sanjiv Dhingra, Jian Guo, Zhuo Sun, Shu-hong Li, Richard D Weisel, Ren-Ke Li
Journal: Circulation (2014)

Introduction:  Allogeneic young mesenchymal stem cells (MSCs) are excellent candidates for cardiac repair due to their great regenerative potential and immunoprivilege. However, their differentiation increases major histocompatibity complex II (MHC II) expression which induces transition from an immunoprivileged to an immunogenic state. The expression of MHC II is transcriptionally regulated by the class II MHC transactivator (CIITA). We assayed the effects of blocking MHC II upregulation using CIITA gene knockdown (CIITA − ) on survival of allogeneic MSCs  in vitro  and  in vivo .   Methods:  In vitro,  wild-type (WT) or CIITA knockout (CIITA − ) mouse MSCs were induced to differentiate using 5-azacytidine or cytokines. A co-culture system with allogeneic leukocytes was used to evaluate cytotoxicity (LDH release and leukocyte proliferation). Human MSCs (hMSCs) were treated with interferon-γ (INF-γ) to induce MHC II expression. siRNA was used to knockdown CIITA and evaluate immunoprivilege.  In vivo,  WT or CIITA −  MSCs were allogeneically implanted into infarcted myocardium. Allo-antibody formation in the recipients, cell survival, and cardiac function were assessed for the duration of the 5 week experiment.   Results:  Mouse data - MSC differentiation induced MHC II expression in WT cells whereas CIITA knockout completely prevented MHC II upregulation in differentiated MSCs. When these cells were co-cultured with allogeneic leukocytes, immune rejection was observed in differentiated WT-MSCs but immune tolerance was achieved with differentiated CIITA (-) -MSCs.  In vivo : knocking out CIITA in MSCs alleviated allogeneic immune response after cell therapy and prevented the rejection of transplanted cells, improving post-infarction cardiac function when compared to WT MSCs ( P   Human data  - MHC II upregulation by INF-γ exposure was associated with increased immunogenicity of hMSCs. Knocking down CIITA restored the immunoprivilege in the  in vitro  co-culture system.   Conclusions:  CIITA is a key factor which regulates the switch of allogeneic MSCs from an immunoprivileged to an immunogenic phenotype  in vitro  and  in vivo . CIITA knockdown rescued MSC immunoprivilege and prolonged the beneficial effect of allogeneic MSC therapy for cardiac repair.
CD4+VEGFR1HIGH T cell as a novel Treg subset regulates inflammatory bowel disease in lymphopenic mice
Authors: Jin-Young Shin, IL-Hee Yoon, Jong-Hyung Lim, Jun-Seop Shin, Hye-Young Nam, Yong-Hee Kim, Hyoung-Soo Cho, So-Hee Hong, Jung-Sik Kim, Won-Woo Lee, Chung-Gyu Park
Journal: Cellular and Molecular Immunology (2015)
Abstract 3546: Heart Failure-Derived Macrophages Induce Myocyte Oxidative Stress and Contractile Dysfunction in a Juxtacrine and iNOS-Dependent Manner
Authors: Justin R Kingery, Robert K Lewis, Charles R Partridge, Ameen Ismahil, Ernest Cardwell, Tariq Hamid, Steven P Jones, Sumanth D Prabhu
Journal: Circulation (2008)

The failing heart exhibits low-level, but progressive, tissue macrophage infiltration. Although macrophages are sources of pro-oxidants, whether macrophage-myocyte interactions are of consequence in heart failure (HF) is unknown. We hypothesized that macrophage-myocyte juxtacrine interactions can induce myocyte dysfunction in HF. Wild-type (WT, C57BL/6) mice underwent coronary ligation (HF group) or sham operation. At 4 weeks in the HF group, echocardiography and hemodynamics confirmed LV dysfunction and remodeling. Flow cytometry showed a larger number of activated blood monocytes (F4/80+CD11b+: 11±2% vs. sham 7±2%, p &lt;0.05), and cardiac MOMA-2 immunostaining revealed a 2-fold increase in tissue activated macrophages. To assess macrophage-myocyte interactions, thioglycollate-elicited peritoneal macrophages were collected from WT naíve and HF mice, macrophages were co-cultured with isolated adult WT myocytes, and myocyte contraction was assessed in the presence or absence of myocyte-macrophage physical contact. Also, as macrophages lacking inducible nitric oxide synthase (iNOS) exhibit blunted activation, to deconstruct the role of macrophage activation, peritoneal macrophages were collected from ligated iNOS−/− HF mice. In the absence of macrophage association, myocyte contraction (1 Hz) was 9.5±1.3%. Contraction was significantly (p &lt; 0.05) depressed upon physical contact with either WT HF macrophages (4.6 ± 1.0%) or LPS-stimulated naíve WT macrophages, but not upon contact with unstimulated naíve WT macrophages. In contrast, physical contact with iNOS KO HF macrophages did not depress contraction (shortening 8.9±1%, p = NS), even with LPS pre-stimulation. Myocytes were loaded with the fluorescent indicators DCF-DA or HKGreen-2 to monitor reactive oxygen species (ROS) and peroxynitrite, respectively. Myocyte attachment to WT HF macrophages induced a 4-fold increase in myocyte ROS and peroxynitrite over baseline, events that did not occur with attachment to iNOS KO HF macrophages. We conclude that direct physical interaction with activated macrophages in HF is sufficient to induce myocyte oxidative and nitrative stress and contractile dysfunction, and this is dependent, at least in part, on macrophage-derived iNOS. This research has received full or partial funding support from the American Heart Association, AHA Great Rivers Affiliate (Delaware, Kentucky, Ohio, Pennsylvania &amp; West Virginia).
Pain in Childbirth: Report by Medical Women's Federation
Authors: K K CONRAD
Journal: BMJ (1949)

This subcommittee was set up by the Council of the Medical Women's Federation at its meeting in Bournemouth in October, 1947.In the course of correspondence in The Tithes during August and September, 1947, one correspondent had suggested that only married women doctors with children of their own could speak with authority on the need or otherwise for anaesthetics in childbirth, and inquired whether any concerted and thorough study of the whole question had ever been undertaken.This sub- committee was set up with the object of obtaining information on that point. Method of InvestigationAt its first meeting the subcommittee concluded that it was important to collect the necessary information as quickly as possible.It was thought that this information could best be obtained by means of a questionary to married medical women.It was decided to question only those whose youngest child was not more than 10 years old.As a preliminary step, a " pilot" questionary was sent out to about 300 medical women.The subcommittee is satisfied that the questionaries were sent to a representative sample of medical women with children under 10 years.Names and addresses were supplied by members of the subcommittee and from information available at the head- quarters of the Medical Women's Federation.It was felt, by sending out questionaries rather than by inviting those interested to apply for them, that a more satisfactory cross-
Abstract 4008: PSGL-1-Expressing CD4 T Cells are Enriched in Culprit Coronary Artery Lesion of Acute Coronary Syndrome
Authors: Keiko Gomita, Kayoko Sato, Kazutaka Kitamura, Nobuhisa Hagiwara
Journal: Circulation (2008)

Background: Recently, several evidences on the crucial role of adhesion molecules in the development of atherosclerosis and plaque instability have been reported. While expression of VCAM-1, ICAM-1 and L-selectin has been consistently observed in atherosclerotic plaques it is still uncertain how adhesion molecules on T cells contribute to the incidence of acute coronary syndrome (ACS). In this study, we examined whether adhesion molecules on T cells in ACS have a significant role in the plaque stability and prone to cause ACS. Methods and Results: Fresh CD4 T cells were isolated from the peripheral blood of 76 ACS patients (AMI=35, UAP=41) and 74 age-matched controls (NC). CD69, an activation marker of T cells, was strongly expressed on CD4 T cells from ACS than from NC by FACS (P&lt;0.0001). CD4 T cells from ACS highly expressed p-selectin glycoprotein ligand-1 (PSGL-1) and integrin β (CD18), but not L-selectin by FACS (P &lt; 0.03, P &lt; 0.01, n.s., respectively). Soluble PSGL-1 (sPSGL-1) levels in plasma were lower in ACS patients than in NC (P=0.0001), which correlated negatively with the PSGL-1 expression on CD4 T cells (R=0.405, P&lt;0.02). We further investigated the thrombus-aspirating device samples (n=14) and fresh CD4 T cells derived from both the coronary artery and peripheral blood from the each same patient with ACS. CD4 T cells from the coronary artery strongly expressed PSGL-1 (P&lt;0.002), but not integrin β (CD18) and L-selectin by FACS. Finally, PSGL-1 was expressed on T cells, but not on CD68 positive macrophage, MPO positive neutrophil, or CD41 positive platelets in the thrombus-aspirating device samples. Conclusions: From these results, we demonstrated that PSGL-1-expressing CD4 T cells are enriched in the culprit coronary artery lesion of ACS, contributing to the acceleration of plaque instability and occurrence of ACS.
Abstract 16465: Once an Implantable Defibrillator, Always an Implantable Defibrillator?
Authors: Carmen Teodorescu, Audrey Uy-Evanado, Kyndaron Reinier, Harpriya Chugh, Jo Ayala, Ronald Mariani, Karen Gunson, Jonathan Jui, Sumeet S Chugh
Journal: Circulation (2011)

Introduction: A subset of patients with primary prevention implantable defibrillators (ICD) and severe LV systolic dysfunction are observed to undergo improvement/normalization of LV systolic funct...
Abstract 5286: Human AV Junctional Pacemaker Shift Due to Cholinergic and Adrenergic Stimulations: Optical Imaging with a Novel Long Wavelength Voltage-Sensitive Dye
Authors: Vadim V Fedorov, Christina M Ambrosi, William J Hucker, Alexey V Glukhov, Kelley V Foyil, Joe Wuskell, Leslie Loew, Nader Moazami, Igor R Efimov
Journal: Circulation (2008)

It is well known that under different physiological and pathologic conditions, the atrioventricular junction (AVJ) may become the pacemaker of the heart. However, unlike the well-characterized AVJ pacemaker in animal models, autonomic control of the human AVJ pacemaker has not been studied. Explanted human hearts with different types of cardiomyopathy (n=7) were obtained at the time of cardiac transplantation and perfused with cardioplegic solution. The AVJ was cannulated, isolated from the rest of the heart, immobilized with the excitation-contraction uncoupler blebbistatin (10 μmol/L) and optically mapped using the infrared voltage sensitive dye di-ANBDQBS. Imaging was conducted with 100x100 CMOS camera from endocardial field of view ranging 24x24 to 36x36mm 2 , which allowed to simultaneously map right side of intratrial and intraventricular septa, coronary sinus (CS) and His bundle regions. In control, we found AVJ rhythm of 31+/−15 bpm (2409+/−1264 ms) in all human preparations which originated in compact AV node (N-region, n=4) and/or region between AV node and His bundle (NH-region, n=3). Isoproternol (Iso, 1 μM) induced AVJ rhythm acceleration up to 68+/−12 bpm (913+/−192 ms), temporary pacemaker shift to CS region (n=2) and improved conduction in both slow and fast pathways, which induced reentrant arrhythmias in 3/5 preparations. Acetylcholine (ACh, 1–3 μM) slowed rhythm to 21+/−6 bpm (3130+/−1146 ms) and conduction in both pathways up to complete block, and induced temporary pacemaker shift to CS region in 3/4 preparations. Moreover, we found bifocal activation in 3/4 preparation when two main pacemakers (CS and compact AV node) worked asynchronously with different frequencies, accompanied by the exit block from AV node. We showed by high-resolution optical mapping for the first time that unlike in animal models (rabbit and rat) in isolated coronary perfused human AVJ leading pacemaker localized mostly in the N- or NH-regions. Beta-adrenergic (Iso) and cholinergic (ACh) stimulations of AVJ can significantly accelerate or slow rhythm and conduction, as well as induced pacemaker shift to CS, and result in reentrant arrhythmias. This research has received full or partial funding support from the American Heart Association, AHA Midwest Affiliate (Illinois, Indiana, Iowa, Kansas, Michigan, Minnesota, Missouri, Nebraska, North Dakota, South Dakota &amp; Wisconsin).
A phase II trial of doxorubicin (DXR) and gemcitabine (GMZ) administered in patients with metastatic breast cancer (MBC)
Authors: A. Bensalem, K. Bouzid
Journal: Journal of Clinical Oncology (2005)

777 Background: The aim of this phase II study was to assess safety and efficacy of the combination of DXR-GMZ in patients with MBC Methods: Chemonaive patients with histologically or cytologically confirmed MBC, ECOG PS ≤2, aged 18–75 years, and adequate hepatic, renal, and cardiac functions were eligible. Patients received DXR 25 mg/m2 and GMZ 1250 mg/m2 on days 1 and 8 every 21 days for 6 cycles. Results: From November 2001 to January 2004, 51 patients with a median age of 47.1 years (range, 28–73) were enrolled. All patients had stage IV disease. A total of 306 cycles were administered. All patients were evaluable for safety. Grade 3/4 toxicities were neutropenia (9.8% of cycles), anemia (3.6%), and thrombocytopenia (3.6%). Nonhematologic grade 2/3 toxicities included nausea and vomiting (18.0%), there were no other grade 3 nonhematologic toxicities and no grade 4 hematologic toxicities. Of the 49 patients evaluable for efficacy, 30 patients (61.2%) had a complete response, and 13 patients (26.5%) had a partial response for an overall response rate of 87.7%. Five pts had stable disease and one patient (2.0%) had progressive disease. The median time to progression was 13.3 months (range, 2–36+ months). Survival data will be presented in next year’s publication. Conclusions: The combination of DXR-GMZ in patients with MBC appears to be an active regimen with a favorable toxicity profile. No significant financial relationships to disclose.
Effects of Ramipril on Endothelial Function and the Expression of Proinflammatory Cytokines and Adhesion Molecules in Young Normotensive Subjects With Successfully Repaired Coarctation of Aorta
Authors: Stella Brili, Dimitris Tousoulis, Charalambos Antoniades, Carmen Vasiliadou, Maria Karali, Nikos Papageorgiou, Nikos Ioakeimidis, Kyriakoula Marinou, Elli Stefanadi, Christodoulos Stefanadis
Journal: Journal of the American College of Cardiology (2008)
Abstract 2318: Selective Mitochondrial Translocation of Phosphorylated PKC{varepsilon} in Viable Myocytes Overexpressing Urocortin after Cardioplegic Arrest and Reperfusion: Physical Interaction of Phosphorylated PKC{varepsilon} with the Kir6.1 Cardiac Potassium Channel Subunit as a Potential Mechanism of Cardioprotection
Authors: Carol Chen-Scarabelli, Giuseppe Faggian, Maddalena Tessari, Zhaokan Yuan, Justin Di Rezze, Louis Saravolatz, Alessandro Mazzucco, Tiziano M Scarabelli
Journal: Circulation (2008)
Abstract 20882: Predictors of Suboptimal TIMI Flow after Primary Angioplasty for Acute Myocardial Infarction: Results from the HORIZONS-AMI Trial
Authors: Adriano Caixeta, Alexandra J Lansky, Roxana Mehran, Bernhard Witzenbichler, Giulio Guagliumi, Jan Z Peruga, Bruce Brodie, Dariusz Dudek, Ran Kornowski, Franz Hartmann, Bimmer Claessen, Martin Fahy, George Dangas, Gregg W Stone
Journal: Circulation (2010)

Introduction: Not achieving TIMI 3 flow after primary PCI in ST-segment elevation myocardial infarction (STEMI) is strongly related to mortality. The predictors of TIMI flow <3 after PCI in patient...
Abstract 9169: Down-Regulation of miR-15 Family is Responsible for Overexpression of GATA-4 Mediated Cytoprotection
Authors: Bin Yu, Zeeshan Pasha, Zhisong He, Yigang Wang, Muhammad Ashraf, Meifeng Xu
Journal: Circulation (2011)

We have previously reported that mesenchymal stem cells (MSC) preprogrammed to express GATA-4 (MSC GATA-4 ) significantly increased their survival in ischemic myocardium. However, it is unclear how upregulation of GATA-4 in MSC mediates cytoprotection. MicroRNAs (miR) post-transcriptionally regulate the expression of thousands of distinct mRNAs. While some regulatory interactions help to maintain basal cellular functions, others are likely relevant in more specific settings, such as response to stress. In this study, we transduced GATA-4 into MSC. The expression of miR in MSC was assessed using miR microarray and quantitative real-time PCR. Bcl-2-like 2 (Bcl-w), one protein of miR-15 family targeted genes, was analyzed using qRT-PCR and western blot. Anoxia was used to mimic ischemic injury. FACS for annexin-V labeling cells was used to evaluate cell apoptosis and MTT intake was employed to study MSC survival. Our study indicated that overexpression of GATA-4 modulates the expression of several miR in MSC, including significantly decreased miR-15 family (e.g. miR-15b, miR-16, and miR-195) ( Fig. 1 ). Bcl-2-like-2 (Bcl-w), which is one of target genes of miR-15 family and has an anti-apoptotic effect, was increased in MSC GATA-4 . However, overexpression of miR-195 in MSC GATA-4 (MSC GATA-4-miR-195 ) using a lentiviral vector transfection system significantly reduced Bcl-w compared to that in the negative control miR transfected MSC (MSC GATA-4-miR-NC ) ( Fig. 2 ). The apoptosis of MSC GATA-4 following exposed to anoxia for 8 hours was lower than MSC Null , and it was abolished by transfecting miR-195 and siRNA-Bcl-w into MSC GATA-4 ( Fig. 3 ). These results indicate that overexpression of GATA-4 downregulates miR-15 family resulting in upregulation of Bcl-w, responsible for GATA-4 mediated cytoprotection.
Abstract 9699: Short Sleep Duration and Glycemic Control Have Synergic Effect on Cardiovascular Events in Hypertensive Patients
Authors: Kazuo Eguchi, Satoshi Hoshide, Shizukiyo Ishikawa, Kazuyuki Shimada, Kazuomi Kario
Journal: Circulation (2011)

Backgrounds: Short duration of sleep is associated with increased prevalence of diabetes. We tested the hypothesis that short sleep duration is not only a risk of diabetes, but the combination of these is associated with increased risk of incident cardiovascular disease (CVD). Methods: We analyzed 1255 hypertensives who performed ambulatory BP monitoring (ABPM). The mean age was 70.4 ± 9.9 years, and they were followed for 50 ± 23 months. Sleep duration was evaluated by self-report. Diabetes was defined by a history or taking diabetic medications. Short sleep duration was defined as the 20th percentile of the whole population (&lt;7.5hrs). Hard CVD event was defined as either myocardial infarction, stroke, or sudden cardiac death; and All CVD event was defined as Hard CVD events plus angina, heart failure and end stage renal disease. Cox proportional hazard models were used to calculate hazard ratios (HR) and 95% confidence intervals (CI) controlling for significant covariates. Results: There were 299 diabetic and 956 non-diabetic subjects. The sleep duration was significantly shorter in diabetics than in non-diabetics (8.3±1.4 vs. 8.5±1.4, P=0.005). There were a total of 99 Hard CVD events and 123 All CVD events. When the subjects were divided by 4 categories: Diabetes+Short sleep (n=94); Diabetes+ Long sleep (n=205); Non-diabetes+Short sleep (n=257); Non-diabetes+Long sleep (n=699), the group with Diabetes+Short sleep had significantly higher incidence of Hard CVD events (HR=2.27, 95%CI=1.17-4.42, P=0.015) and All CVD events (HR=2.47, 1.37-4.43, P=0.003) compared with the group with Non-diabetes+Long sleep independent of age, sex, BMI, creatinine, and 24-h SBP. Although there was no interactions between diabetes and short duration of sleep on the impact of CVD events, a subanalysis of diabetic subjects (N=203) have shown that there were significant interactions between the sleep duration and average hemoglobin A1c levels on the impact of Hard and All CVD events. Conclusion: The combination of diabetes and short duration of sleep was associated with higher risk of incident cardiovascular disease (CVD) than those without. Worse glycemic control along with short sleep duration had a tendency to act synergistically as risks of future cardiovascular events.
基层卫生工作者的良师益友：对《中华全科医师杂志》的感悟
Authors: 李净潜, 高青山, 姜文忠
Journal: BMJ (2008)

光阴易逝，转眼《中华全科医师杂志》创刊已经6周年了，在此我以读者的身份向贵刊反馈一下自己的感受。该杂志于2002年9月份创刊，当时，我国全科医学刚起步，基层全科医学工作者都渴望有自己专业的刊物，她的创刊，使从事这方面的工作者欣喜若狂，给全科医学搭建了发展的平台。6年来为满足广大读者的需求，已经发展到月刊，
Abstract 12281: Two Years of LDL Lowering Does Not Improve Calf Muscle Physiology or Functional Capacity in Peripheral Arterial Disease
Authors: Amy West, Justin D Anderson, Craig H Meyer, Frederick H Epstein, Klaus D Hagspiel, Stuart S Berr, Arthur L Weltman, Nancy L Harthun, Hongkun Wang, Joseph M DiMaria, Jennifer R Hunter, John M Christopher, Christopher M Kramer
Journal: Circulation (2010)
Nova et Vetera
Authors: D G JAMES
Journal: BMJ (1962)

On June 3 the Bishop of Colchester will conduct a service of rededication at Hempstead Church (near Saffron Walden, Essex), where the remains of William Harvey lie.This small country church has been worthily restored as an international shrine housing the mortal remains of an immortal figure.Twenty-three days after his death on June 3, 1657, in Roehampton, Harvey's body was laid in a vault, built two years earlier by his merchant brother, Eliab Harvey, and over it was erected a chapel.Although unburied, his body had been encased in lead, as was the custom of the day, such that the moulded metal envelope bore a general outline of the body it contained, with a rude semblance of head, face, and neck.The vault was later to be filled with the bodies of many other members of the Harvey family; some were laid in coffins, others "lapt in lead" like their illustrious forebear.Although the Harveys were originally Kentish Yeomen of Folkestone, later members had prospered 'Echo.October 19, 1883.