tbuckley/cabot-search huggingface dataset:
Abstract 9033: Cardiac Rehabilitation is Associated With Especially Improved Outcomes in Women and the Elderly: Results From a Large Cohort Study of Coronary Artery Disease Patients
Authors: Billie-Jean Martin, Trina Hauer, Adriane Lewin, William A Ghali, Merril Knudtson, Ross Arena, James A Stone, Sandeep G Aggarwal
Journal: Circulation (2010)

Background: Survival from acute coronary syndromes has improved in recent decades and attention is now focusing on reducing recurrent events in coronary artery disease (CAD) patients. Cardiac Rehab...
Hepatitis C in asymptomatic blood donors
Authors: C B Summerton
Journal: BMJ (1995)

The varied results in the literature make it possible to select studies that show an independent association between hypertriglyceridaemia and coronary heart disease, like the three that Peter H Winocour cites.2But many studies support the opposite conclusion.5"7Triglycerides may have a role in risk prediction when well standardised measurements of high density lipoprotein choles- terol are not available, as Winocour suggests.The negative correlation between the two measure- ments means that the triglyceride concentration can serve as a surrogate for the high density lipoprotein cholesterol concentration, albeit a rela- tively imprecise one.For any lipoprotein test, and especially for triglycerides, its accuracy in predicting risk depends on the quality of the measurement in the specific laboratory, so clinicians should learn about the accuracy of lipid tests available in the laboratory they use.Whether to measure triglycerides is a moot issue once hypercholesterolaemia is found and a decision made to measure low density lipoprotein choles- terol.Many laboratories use an indirect measure- ment of low density lipoprotein cholesterol which requires knowledge of the triglyceride concentra- tion.Consistent evidence that triglycerides have an important independent role in preventing coronary heart disease, however, remains elusive; calls for triglyceride testing must appeal to faith rather than established fact.
Abstract 17284: Selective Macrophage Ablation Attenuates Diet-Induced Obesity and Insulin Resistance and Reverses Diabetic Cardiomyopathy
Authors: Mehak Goel, Tariq Hamid, Mohamed Ameen Ismahil, Guihua Zhou, Kenneth Brittian, Heather Clair, Shangzhi Guo, Sumanth D Prabhu
Journal: Circulation (2011)

Although activated macrophages infiltrate the heart and adipose tissue in type 2 diabetes (T2D), the role of these cells in the genesis of cardiomyopathic phenotype is unknown. We tested the hypothesis that activated resident macrophages are fundamental mediators of diet-induced diabetic cardiomyopathy. Transgenic mice expressing an AP20187-inducible Fas-dependent suicide gene in macrophages and dendritic cells (MAFIA mice) were fed a high fat diet (HFD, 45% kcal fat) or control diet (CD, 10% kcal fat) for 28 weeks to induce T2D, and subsequently given either vehicle or AP20187 (0.5mg/kg IP every 10 d) for one month to induce macrophage apoptosis and depletion. HFD-fed mice exhibited a significant (p &lt; 0.05) 43% increase in body weight when compared to CD fed mice (43±5 vs 35±1 g) and developed hyperglycemia (199±44 vs 121±10 mg/dL), hyperinsulinemia (1.27±0.6 vs 0.43±0.14 µg/L) and decreased insulin sensitivity indicating T2D. Echocardiography revealed concentric LV hypertrophy in HFD-fed mice with increased wall thickness (anterior wall 1.2±0.1 vs 0.9±0.1 mm), decreased LV end-diastolic diameter (LVEDD 3.9±0.2 vs 4.2±0.4 mm), and unchanged LV ejection fraction. AP20187 treatment significantly reduced the caloric intake (0.3±0.08 vs 0.4±0.05 kcal/g/day) and body weight of HFD-fed mice (36±2 vs 47±5 g), attenuated hyperglycemia (108±8 vs 195±14 mg/dL) and hyperinsulinemia (0.6±0.2 vs 1.9±0.5 µg/L), and improved insulin sensitivity when compared to vehicle treated HFD-fed mice. Importantly, the improvements in metabolic parameters were accompanied by reversal of LV remodeling with decreased wall thickness (anterior wall 0.8±0.1 vs 1.3±0.1 mm) and increased LVEDD (4.6±0.5 vs 3.9±0.2 mm). White adipose tissue weights in AP20187-treated HFD-fed mice were also significantly decreased when compared to vehicle treated HFD-fed mice [epididymal (0.6±0.2 vs 1.4±0.3 g); inguinal (0.6±0.2 vs 1.1±0.3 g); retroperitoneal (0.8±0.5 vs 1.4±0.4 g). We conclude that resident activated macrophages play central and causative roles in the development of diet-induced T2D and diabetic cardiomyopathy. Targeting systemic macrophage activation may represent a therapeutic approach to reverse pathological cardiac remodeling associated with T2D and obesity.
Interleukin-6–Induced Inhibition of Multiple Myeloma Cell Apoptosis: Support for the Hypothesis That Protection Is Mediated Via Inhibition of the JNK/SAPK Pathway
Authors: Feng-hao Xu, Sanjesh Sharma, Agnes Gardner, Yiping Tu, Arthur Raitano, Charles Sawyers, Alan Lichtenstein
Journal: Blood (1998)
Abstract 15226: High Prevalence of Early Repolarization in Patients With Noncompaction Cardiomyopathy Presenting With Malignant Ventricular Arrhythmias.
Authors: Kadir Caliskan, Tamas Bauernfeind, Barbara Ujvari, Ron T van Domburg, Aggie H Balk, Luc Jordaens, Maarten L Simoons, Tamas Szili-Torok
Journal: Circulation (2010)

Purpose: Early repolarizations are been associated with malignant ventricular arrhythmias, including idiopathic VF and sudden cardiac death (SCD). The possible mechanism include increased trabecula...
Signaling Proteins Boost Drug Activity
Authors: Tracy Hampton
Journal: JAMA (2006)

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 5248: Direct Cardiac Effect and Cellular Mechanism of Angiotensin-(1–7) in Heart Failure
Authors: Che-Ping Cheng, Peng Zhou, Heng-Jie Cheng, Michael Cross, William C Little
Journal: Circulation (2008)

Angiotensin-(1–7) {A-(1–7)} plays an important role in counteracting various actions of angiotensin II (AII) in the heart. However, its effect on cardiac contractility remains controversial. We previously demonstrated that in heart failure (HF), AII decreases left ventricle (LV) contractility. Whether A-(1–7) may antagonize AII-induced cardiac depression, thereby contributing to the beneficial actions of angiotensin-converting enzyme inhibitor (ACEI) therapy in HF, remains undefined. We assessed the hypothesis that A-(1–7) may produce positive modulation on Ca 2+ current (I Ca,L ) and increase LV and myocyte contractility via A-(1–7) receptors, acting through nitric oxide (NO)/bradykinin (BK)-mediated mechanism. We measured LV contractility changes after A-(1–7) (650 ng/kg, iv), which produced more than a 20-fold increase in plasma A-(1–7) levels, mimicking the elevations caused by ACEI in HF patients, and compared myocyte contractile and I Ca,L responses to A-(1–7) (10 −5 M) in 12 rats with isoproterenol (ISO)-induced HF (3 months after 170 mg/kg sq for 2 days). LV contractility was measured by pressure-volume analysis. I Ca,L was measured using whole-cell voltage clamp technique. In additional contractile studies, myocytes were pretreated to inhibit either NO synthase (L-NAME, 10 −5 M), BK (HOE 140, 10 −6 M) or A-1–7 receptor (D-Ala 7 ]-A-(1–7), 10 −5 M) followed with A-(1–7) exposure. Compared with baseline , after A-(1–7), E ES (44%, 1.1 vs 0.74 mmHg/μl) and M sw (37%, 91.2 vs 66.5 mmHg) were increased, indicating enhanced LV contractility. In HF myocytes, A-(1–7) increased myocyte percent shortening (28%, 7.3% vs 5.7%), the velocity of cell contraction (31%, 110.4 vs 84.2 μm/sec) and relengthening (41%, 71.8 vs 51.1 μm/sec) accompanied by significantly-increased peak I Ca,L (21%, 6.3±0.2 vs 5.2±0.2 pA/pF). L-NAME increased, HOE 140 decreased, and A-(1–7) receptor blockade prevented myocyte contractile responses to A-(1–7). In HF, clinically-relevant concentrations of A-(1–7) counteracted AII-induced cardiac depression, increased I Ca,L , and produced positive inotropic effects in both LV and myocytes. These effects are coupled with A-(1–7) receptors and involve activation of NO/BK pathways.
Abstract 1102: Cardiac-Specific Myosin Light Chain Kinase (MLCK), a Third Member of MLCK Family, Potentiates Sarcomere Formation and Cardiac Contraction
Authors: Jason Y Chan, Morihiko Takeda, Laura E Briggs, Jonathan T Lu, Nobuo Horikoshi, Ellen O Weinberg, Hiroki Aoki, Kenneth R Chien, Hideko Kasahara
Journal: Circulation (2007)

Background: Two myosin light chain kinase (MLCK) proteins, skeletal (encoded by mylk2 gene) and smooth muscle MLCK (encoded by mylk1 gene) have been shown to be expressed in mammals. Human mylk2 has been mapped as a disease locus for familial cardiac hypertrophy (OMIM 606566 ), suggesting that abnormal function of skeletal MLCK stimulates cardiac hypertrophy. While phosphorylation of the putative substrate of skeletal MLCK, myosin light chain 2 (MLC2), is recognized as a key regulator of cardiac contraction, the abundance of skeletal MLCK in the heart is controversial, suggesting the existence of an additional MLCK that is preferentially expressed in cardiac muscle. Methods and Results: We characterized a new kinase named cardiac MLCK that is encoded by a gene homologous to mylk1 and 2 and is specifically expressed in the heart in both atrium and ventricle. Expression of cardiac MLCK was highly regulated by the cardiac homeobox transcription factor, Nkx2.5, in neonatal cardiomyocytes. The overall structure of cardiac MLCK protein is conserved with skeletal and smooth muscle MLCK including putative catalytic and adjacent Ca2+/calmodulin binding domains at the carboxyl-terminus. The amino-terminus is unique without significant homology to other known proteins. Cardiac MLCK phosphorylated MLC2v with a catalytic value of Km=4.3 micro M (Lineweaver-Burk analysis) indicating high affinity of cardiac MLCK to MLC2v, similar to the affinity of skeletal muscle MLCK to skeletal muscle MLC2 and smooth muscle MLCK to smooth muscle MLC2. Adenoviral-mediated overexpression of cardiac MLCK and knockdown of cardiac MLCK using RNAi in cultured cardiomyocytes revealed that cardiac MLCK regulates MLC2v phosphorylation, sarcomere organization and cardiac myocyte contraction. Expression of cardiac MLCK protein was significantly decreased in severe heart failure in vivo (post-myocardial infarction heart failure mouse model). Conclusion: Cardiac MLCK is a new key regulator of cardiac contraction and sarcomere organization. Reduction of cardiac MLCK function leading to decreased phosphorylation of MLC2v may contribute to compromised contractile function in the failing heart.
Abstract 3454: Fine Mapping Of A Chromosome 16 Locus Associated With Low High-density Lipoprotein Cholesterol Level (HDL-C) In French Canadian Subjects
Authors: Zari Dastani, Michel Marcil, Jenny C Lee, Paivi Pajukanta, Daniel Gaudet, Jacques Genest, James C Engert
Journal: Circulation (2007)

Low HDL-C is a known independent risk factor for coronary heart disease. Levels of HDL-C are influenced by both genetic and environmental factors. We previously performed a quantitative linkage analysis in two independent studies of the French Canadian founder population: a Quebec-wide study (QUE) consisted of 362 individuals from multigenerational families, and 410 individuals from families of the Saguanay-Lac St-Jean region (SLSJ). The results demonstrated a linkage to the locus 16q23–24 in both studies. This locus has been implicated in previous linkage scans for HDL-C in multiple studies from different populations. All of them resulted in linkage peaks that are less than 12 cM far from our peak, suggesting the existence of one or more genes in this specific locus. We examined the region by SNP fine mapping and used family based association and case-control association analysis. Using families from the QUE study, defining HDL-C &lt;5th percentile (age/gender-matched) as cases, the region was narrowed from 25 cM to 18.1 cM. Affected members from four families share a 2 microsatellite haplotype. SNPs genotyped in this locus allowed us to narrow down the shared haplotype to 4Mb. A case-control association study in the SLSJ study sample (cases &lt;5 percentile HDL-C, controls &gt;40 percentile HDL-C) identified several significant SNPs, one of which was located in the same region as the shared haplotype from the QUE families. Constructing a haplotype of this SNP and a nearby SNP, increased the evidence for association (p =0.016 to 0.0097). The CHST6 gene, located within this region, has been previously identified in macular corneal dystrophy. Because of the presence of occular manifestations with other genes associated with low HDL-C (e.g. LCAT, ApoA1), we sequenced the CHST6 gene and also its homologue CHST5, which is located in the same region. We found three non-synonymous variants in these two genes. One of the variants in the CHST6 gene showed a strong segregation in the four families sharing the microsatellite haplotype. This same variant also demonstrated an odds ratio &gt;2 in the case/control sample, but this was not significant due to the small sample size. Our data present strong evidence for a HDL-C gene on chromosome 16q23–24 that may be related to the CHST6 or CHST5 loci.
Effect of Long-Term Exposure to Lower Low-Density Lipoprotein Cholesterol Beginning Early in Life on the Risk of Coronary Heart Disease
Authors: Brian A. Ference, Wonsuk Yoo, Issa Alesh, Nitin Mahajan, Karolina K. Mirowska, Abhishek Mewada, Joel Kahn, Luis Afonso, Kim Allan Williams, John M. Flack
Journal: Journal of the American College of Cardiology (2012)
Combined Hepatic Arterial Occlusion and Chemotherapy for Primary or Secondary Tumors of the Liver
Authors: Constantine P. Karakousis
Journal: Liver Cancer (1985)

The liver develops primary tumors, usually of epithelial origin, i.e., either hepatocellular or cholangiocarcinomas, but also tumors arising from tissues derived from the primitive mesenchyme, i.e., the various sarcomas. When a primary tumor is resectable, this is the treatment of choice in the absence of other metastatic disease.
Symptom responses of female Vietnam veterans to Operation Desert Storm [published erratum appears in Am J Psychiatry 1992 Aug;149(8):1129]
Authors: J Wolfe, P J Brown, M L Bucsela
Journal: American Journal of Psychiatry (1992)

This study examined the status of symptoms of posttraumatic stress disorder (PTSD) in a cohort of women after the onset of Operation Desert Storm.Seventy-six non-treatment-seeking Vietnam veterans were obtained from lists of those who recently had participated in other research projects conducted at the National Center for Post-Traumatic Stress Disorder. Before the onset of Operation Desert Storm, subjects had completed a set of psychometrically valid instruments measuring general psychological symptoms and PTSD symptoms (e.g., SCL-90-R, Mississippi Scale for Combat-Related Posttraumatic Stress Disorder). On the basis of the latter scale, subjects were divided into groups with and without PTSD symptoms. At the height of the military conflict, subjects were recontacted and asked to complete the SCL-90-R and the Veterans Update Form, a measure assessing changes in PTSD symptoms.Multivariate analyses indicated that while most female Vietnam veterans experienced some intensification of stress-related symptoms during Operation Desert Storm, those who had previously reported high levels of PTSD were significantly more susceptible to greater distress.Results of this survey indicate that female Vietnam veterans with prior wartime exposure are an at-risk population for the intensification of stress symptoms after the recurrence of a military conflict.
Antibiotic Resistance from Food
Authors: Denis E. Corpet, . C.R.a Toulouse
Journal: New England Journal of Medicine (1988)

Antimicrobial resistant Escherichia coli are found in most fecal samples from the normal population. The present study tested the hypothesis that antibiotic-resistant bacteria come from contaminated food. Six healthy volunteers ate a sterile diet for 3 weeks after a control period. The fecal incidence of resistance to ampicillin, tetracycline, and streptomycin in lactose-fermenting enteric bacilli was determined daily. During the control period, the populations of fecal resistant lac+ enteric bacilli varied with time, periodically reaching a high level of 108 per gram. After the start of the sterile diet, the fecal concentration of resistant bacteria dropped. Three days later, no resistant strain could be detected in the feces of three volunteers, whereas in those of the other three, some could be detected sporadically. The sterile diet reduced the number of resistant bacilli in all volunteers (p<0.001). Thus, most fecal resistant lac+ enteric bacilli come from contaminated food: transient strains enter the intestines with food and are excreted in feces.
Abstract 268: From Advanced Cardiac Life Support (ACLS) to Airway-Circulation-Leadership-Support (A-C-L-S): A Novel Team Training Model for Resuscitation Teams
Authors: Kah-Meng Chong, Chih-Wei Yang, Eric H Chou, Huang-Fu Yeh, Edward P Huang, Cheng-Yi Wu, Hui-Chih Wang, Yueh-Ping Liu, Wen-Chu Chiang, Patrick C Ko, Matthew H Ma
Journal: Circulation (2011)

INTRODUCTION The 2010 AHA Guidelines for Cardiopulmonary Resuscitation (CPR) and Emergency Cardiovascular Care emphasize providers should coordinate and perform chest compressions and ventilations in a team-based approach. We developed a team training model called Airway-Circulation-Leadership-Support (A-C-L-S) to improve resuscitation performance, and presented our preliminary experience of A-C-L-S model in resuscitation team training for emergency department (ED) staff. METHODS CPR technical and non-technical tasks were prioritized and bundled into a mnemonic - ‘A-C-L-S’ which comprises 4 domains: Airway (A), Circulation (C), Leadership (L), and Support (S). A-team is assigned to manage airway, avoid hyperventilation, and monitor EtCO2. C-team focuses on rapid defibrillation and high-quality chest compression with feedback from an accelerometer. L-team assumes coordination and situation monitoring. S-team is responsible for intravenous access, drugs administration, time keeping, and recording. Each team training course consists of: (1) a video-assisted lecture on A-C-L-S model; (2) two high-fidelity simulation-based cardiac arrest scenarios before and after the lecture, each followed by (3) video-facilitated debriefing emphasizing the A-C-L-S model. A 10-item questionnaire using 5-point Likert scale was administered to evaluate perception of CPR teamwork before (i.e. prior clinical experiences) and after the course. RESULTS Seven A-C-L-S team training courses were delivered to 52 ED staff (17 residents and 35 nurses, all qualified ACLS providers) at a university teaching hospital from April to May 2011. Perception of CPR teamwork improved significantly in leadership (48.9% to 78.7%, p = 0.017), task assignment (34.1% to 74.5%, p = 0.002), role commitment (42.6% to 85.1%, p = 0.000), workload distribution (34.1% to 67.4%, p = 0.024), and shared goal (44.7% to 76.1%, p = 0.002) after the A-C-L-S team training. CONCLUSIONS Our novel A-C-L-S team training model can facilitate and reinforce the perception of CPR teamwork among ED staff. Application of this model in different scenarios and disciplines, and its impact on actual resuscitation performance and patient outcomes deserve further study.
Abstract 4730: Restoring Forces and Lengthening Load are Independent and Important Determinants of Peak Early-Diastolic Mitral Annulus Velocity
Authors: Anders Opdahl, Espen W Remme, Thomas Helle-Valle, Erik Lyseggen, Trond Vartdal, Eirik Pettersen, Thor Edvardsen, Otto A Smiseth
Journal: Circulation (2008)

Background: Mechanisms of early-diastolic mitral annulus velocity (E′) are poorly understood. We investigated if restoring forces, generated by contraction below unstressed length, and lengthening load , the expanding effect of LV pressure during early filling, may be determinants of E′ in addition to LV relaxation ( tau ). Methods: In 15 anesthetized dogs we evaluated LV transmural pressure-diameter loops to define unstressed LV long-axis diameter (L 0 ). As a reflection of restoring forces we used the difference between minimum LV long-axis diameter and L 0 (L min −L 0 ). As a measure of LV lengthening load we used LV pressure at the time of mitral valve opening (LVP MVO ). E′ was measured by sonomicrometry and tissue Doppler imaging (TDI) at baseline, during volume loading, dobutamine infusion (n=9), and after 15 minutes and 3 hours (n=8) of LAD-occlusion. Results: Changes in E′ during dobutamine and ischemia correlated inversely with changes in tau (R=−0.58), confirming a relationship between E′ and relaxation. Furthermore, E′ showed an even stronger correlation with L min −L 0 (R=−0.79, Fig 1 ), suggesting a close relationship between E′ and restoring forces. During increased LVP MVO , however, there was a marked increase in E′ which could not be attributed to changes in tau or in L min −L 0 , but E′ correlated well with LVPMVO (R =0.78, Fig 2 ). Conclusion: The present study indicates that in the non-failing ventricle restoring forces and lengthening load are important determinants of E′. Furthermore, the apparent preload-dependency of E′ is explained by the effect of lengthening load. Fig 1 Fig 2
Comparison of efficacy of social skills training for deficit and nondeficit negative symptoms in schizophrenia
Authors: A Kopelowicz, R P Liberman, J Mintz, R Zarate
Journal: American Journal of Psychiatry (1997)

The purpose of this pilot study was to compare the efficacy of social skills training for individuals with schizophrenia who did or did not have the deficit syndrome.Three subjects with the deficit syndrome and three with nondeficit negative symptoms received 12 weeks of social skills training. Social skills and negative symptoms were evaluated before and after training and at 6-month follow-up.Patients with schizophrenia who did not have the deficit syndrome demonstrated significantly better social skills and lower negative symptoms both after training and at follow-up than did those who had the deficit syndrome.Schizophrenic patients with nondeficit negative symptoms appear amenable to intensive social skills training, but schizophrenic patients with the deficit syndrome may have significant deficits in skill acquisition.
International spondyloarthritis inter-observer reliability exercise - The inspire study
Authors: D D Gladman, R D Inman, R R Cook, W Maksymowych, D Van der Heijde, R Landewe, J Braun, J Davis, P Mease, J Brandt, R B Vargas, Chandran, R Helliwell, A Kavanaugh, F D O'Shea, M A Khan, N Pipitone, P Rahman, J D Reveille, M Stone, W Taylor, D J Veale
Journal: Annals of the Rheumatic Diseases (2006)