tbuckley/cabot-search huggingface dataset:
Abstract 13937: Human Microvascular Dysfunction Induced by Glucose and VLDL Lipolysis Products and Protective Effect of Exenatide in Hyperglycemia
Authors: Seth Truran, Raymond Q Migrino, Weiyang Zhang, Peter Reaven
Journal: Circulation (2011)

Type 2 diabetes mellitus and insulin resistance (T2DM/IR) are associated with microvascular complications in part due to direct toxic effects of hyperglycemia (HG) and free fatty acids on the vascu...
Impact of body position in premature newborn receiving nasal CPAP
Authors: Marisa Brunherotti, Francisco Martinez
Journal: European Respiratory Journal (2012)

Introduction:  The body position affects the cervical-thoracic-abdominal biomechanics and has impact on lung ventilation and perfusion. The impact of body position during CPAP is not well recognized.  Objective:  To evaluate the clinical impact of the prone and supine positions in newborn preterm infants breathing without support or on nasal CPAP.  Methods  :  Thirty two preterm infants with GA from 26 to 35 weeks, BW  Result s: The 16 infants of the nasal CPAP group presented GA of 30±2.0 weeks, BW of 1.353±281g, 56% were male and had 3±2.4 days of life at study. The 16 infants without breathing support presented respectively 33±1,5 weeks, 1.776±238 g, 37% were male and had 4±1,5 days of life at study. Clinical parameters of infants in nasal CPAP were not influenced by body position. Infants breathing without support presented at prone position better parameters, but with small clinical relevance, regarding oxygen saturation (95% ± 1.6 vs 94% ± 3.1, p Conclusion:  No difference in clinical parameters were found after changing the postural position in infants at nasal CPAP. When infants were breathing without support, prone position showed a small but statistically significant improvement in oxygen saturation and SA bulletin.
Abstract 18738: Use of Antithrombotic Therapies and Outcomes in Patients with Atrial Fibrillation and Heart Failure: Insights from the GARFIELD Registry
Authors: Ramon Corbalan, Antonio C Pereira Barretto, Giuseppe Ambrosio, Wael Al Mahmeed, Jean-Yves Le Heuzey, Gloria Kayani, Carlos Jerjes-Sanchez, Janina Stepinska, Alexander Parkhomenko, Jan Steffel, Elizaveta Panchenko, Ajay K Kakkar
Journal: Circulation (2014)

Background: Atrial fibrillation (AF) is commonly associated with heart failure (HF) and this combination is associated with a worse prognosis than either alone. However, it is unclear if these patients receive appropriate antithrombotic therapies and if they have a higher incidence of stroke or systemic embolism (SE). Methods: We compared clinical characteristics, antithrombotic therapies, and outcomes in patients with and without HF in the GARFIELD Registry, an ongoing, international, observational registry of consecutively recruited patients with newly diagnosed non-valvular AF and ≥1 additional stroke risk factor. A total of 12,458 prospective patients were enrolled in 30 countries between March 2010 and January 2013. Results are reported at 1-year follow-up. HF was defined at baseline as New York Heart Association (NYHA) I-II or III-IV. Antithrombotic therapy use and 1-year outcomes in patients with and without HF were analysed. Results: In total, 20% of patients had HF; they were older and had higher CHA2DS2-VASc and HAS-BLED scores compared with patients without HF. A higher proportion of patients with HF received antithrombotic therapies. The incidence of all-cause death was higher in HF patients than non-HF patients. Patients with NYHA class III-IV HF had a higher unadjusted incidence of all-cause death and stroke/SE compared with non-HF patients: 10.5 (95% confidence interval 8.8 to 12.7) vs 2.9 (2.7 to 3.2) per 100 person-years and 1.9 (1.2 to 3.0) vs 1.0 (0.8 to 1.2) per 100 person-years, respectively. Event rates slightly changed after adjustment for stroke risk factors. Conclusion: More AF patients with HF received antithrombotic therapies compared with those without HF. They also showed a higher incidence of all-cause death with increasing HF severity compared with AF patients without HF. After adjustment for stroke risk factors, this association was slightly attenuated.
Abstract 4399: Somatic HIF2A mutations identified in a new syndrome with multiple paragangliomas and somatostatinomas associated with polycythemia
Authors: Chunzhang Yang, Karel Pacak, Zhengping Zhuang
Journal: Cancer Research (2014)

Abstract Hypoxia inducible factors (HIFs) control the cellular response to hypoxia and when dysregulated, contribute to tumorigenesis. We identified somatic HIF2A mutations in patients with a new disease syndrome of multiple paragangliomas and somatostatinomas associated with polycythemia. Five different somatic mutations in HIF2A were identified. All of them have a single amino acid substitution in the evolutionarily conserved oxygen-dependent degradation (ODD) domain resulting in disrupting the HIF-2α hydroxylation by prolyl hydroxylase domain-2 containing protein (PHD2). Changes of HIF-2α hydroxylation resulted in the stabilization of HIF-2α and cellular psuedohypoxia, that trigger activation of hypoxia-related genes expression and, dysregulate hematopoiesis leading to tumorigenesis. These results show for the first time that the intrinsic HIF mutations are present in tumors. Citation Format: Chunzhang Yang, Karel Pacak, Zhengping Zhuang. Somatic HIF2A mutations identified in a new syndrome with multiple paragangliomas and somatostatinomas associated with polycythemia. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 4399. doi:10.1158/1538-7445.AM2014-4399
Inactivation of Id1 increases taxol-induced apoptosis in androgen independent prostate cancer cells through activation of JNK signaling pathway
Authors: Y. C. Wong, Xiao Meng Zhang, M. T. Ling, X. H. Wang
Journal: Cancer Research (2006)

Proc Amer Assoc Cancer Res, Volume 47, 2006

1265 

Resistance to anticancer drugs is the major problem in the treatment of many advanced cancers including androgen-independent prostate cancer. Recently, increased expression of Id-1, a basic helix-loop-helix protein, is reported in several types of advanced cancer. It is suggested that high expression of Id-1 may provide an advantage for cancer cell survival and inactivation of Id-1 may be able to increase cancer cells’ susceptibility to apoptosis. To test this hypothesis, in this study, using RNA interfering technology, we inactivated the Id-1 gene in two androgen-independent prostate cancer cell lines, DU145 and PC3, and investigated if downregulation of Id-1 could lead to increased sensitivity to a commonly used anticancer drug, taxol. Using colony forming and MTT assays, we found that inactivation of Id-1 resulted in both decreased colony forming ability and cell viability in prostate cancer cells after taxol treatment. In addition, the si-Id-1 induced sensitization to taxol was associated with activation of apoptosis pathway demonstrated by increased apoptotic index, DNA laddering, sub-G1 phase of the cell cycle, as well as cleaved-PARP and Caspase 3. Furthermore, c-Jun N-terminal kinase (JNK), one of the common pathways responsible for taxol-induced apoptosis, was also activated in the si-Id-1 transfected cells. Inhibition of JNK activity by a specific inhibitor, SP600125, blocked the si-Id-1-induced sensitivity to taxol. These results indicate that increased Id-1 expression in prostate cancer cells may play a protective role against apoptosis, and downregulation of Id-1 may be a potential target to increase sensitivity of taxol-induced apoptosis in prostate cancer cells.(Supported by RGC grants:HKU7314/01M, hku7490/03M, HKU7470/04M, HKU7478/03M)
Abstract 21208: Subcompartments of the Nucleus are Differentially Modulated During the Development of Cardiac Hypertrophy and Failure in the Mouse
Authors: Sarah Franklin, Scherise Mitchell-Jordan, Haodong Chen, Vincent Ren, Peipei Ping, Yibin Wang, Michael Zhang, Thomas M Vondriska
Journal: Circulation (2010)

The protein constituents of biological subcompartments of the cardiac nucleus are unknown. Because of the importance of altered gene regulation during cardiac hypertrophy, failure and other disease...
Abstract 18611: Masked Hypertension in Prehypertensive African Americans After Dietary Stabilization
Authors: Praveen Veerabhadrappa, Keith M Diaz, Deborah L Feairheller, Kathleen M Sturgeon, Sheara T Williamson, Deborah L Crabbe, Jan Kretzschmar, Michael D Brown
Journal: Circulation (2010)

Objective: Office blood pressure (BP) measurements miss a significant number of individuals with masked hypertension (MHT). The aim of our study was to identify the prevalence of MHT and compare pl...
Abstract P160: Is Higher Educational Attainment or Higher Income Protective for Cardiovascular Risk in Deaf American Sign Language (ASL) Users?
Authors: Michael M McKee, Kimberly C McKee, Erika Sutter, Thomas Pearson
Journal: Circulation (2012)

Background: Deaf ASL users appear to be burdened with higher cardiovascular risk due to communication barriers in the health care setting and from lack of accessible health educational and outreach programs. It is well known among the general population that higher educational attainment and income are highly correlated and provide cardiovascular protection. It is unknown if the same effect is seen among Deaf ASL users. Objective We sought to examine whether educational attainment and/or annual household income are inversely associated with cardiovascular risk in a sample of Deaf ASL users. Methods: The Deaf Health Survey (DHS) is an adapted and translated Behavioral Risk Factor Surveillance System (BRFSS) into sign language. A sample of 339 Deaf adults from the Rochester, New York MSA participated in the 2008 DHS and is included in the analysis. We assessed education (≤high school [low education], some college, and 4 year college degree or higher [referent]) and annual household income (&lt;$25,000 versus ≥$25,000 [referent]). We constructed an aggregate (i.e. self-report of any of the four cardiovascular disease (CVD) equivalents: diabetes, myocardial infarction (MI), cerebral vascular attack (CVA), and angina) and conducted χ² tests of association for education and income. After excluding for any missing data on key variables, we conducted multi-logistic regression adjusting for : age, sex, race/ethnicity, and smoking. Results: In the study sample, 17.6% had ≤ high school education while 36.1% earned &lt;$25,000; income and education were poorly correlated (r= 0.355). Among this sample (mean age= 46.4, range= 18-88), the prevalence of outcomes was: diabetes (9.4%), MI (5.0%), CVA (0.9%), and angina (4.5%). Unadjusted, low education was significantly associated with reporting an aggregate outcome (χ² =15.6; p=0.0004) whereas income was not (χ² =0.79; p=0.37). Low education continued to be significantly associated with increased likelihood of reporting an aggregate outcome (OR 5.057; 95% CI 1.73-14.82) whereas income was not significantly associated with reporting an aggregate outcome (OR 0.91; 95% CI: 0.39-2.12) even after adjustment. Conclusion: This is the first known study documenting that low educational attainment is associated with higher likelihood of reported cardiovascular disease among Deaf individuals. Higher income did not appear to provide a cardiovascular protective effect, unlike in the general population. This may be partially explained by the poor correlation between educational attainment and income in the study sample. Effective and accessible health communication and education with Deaf individuals with lower educational attainment could be addressed by the use of language-concordant providers and interpreters and following principles of clear communication (e.g. teach-back) to address ongoing cardiovascular health disparities.
Incidence of Diabetes in Youth in the United States
Authors: Dana Dabelea, Ronny A Bell, Ralph B D'Agostino, Giuseppina Imperatore, Judith M Johansen, Barbara Linder, Lenna L Liu, Beth Loots, Santica Marcovina, Elizabeth J Mayer-Davis, David J Pettitt, Beth Waitzfelder
Journal: JAMA (2007)

Data on the incidence of diabetes mellitus (DM) among US youth according to racial/ethnic background and DM type are limited.To estimate DM incidence in youth aged younger than 20 years according to race/ethnicity and DM type.A multiethnic, population-based study (The SEARCH for Diabetes in Youth Study) of 2435 youth with newly diagnosed, nonsecondary DM in 2002 and 2003, ascertained at 10 study locations in the United States, covering a population of more than 10 million person-years.Incidence rates by age group, sex, race/ethnicity, and DM type were calculated per 100,000 person-years at risk. Diabetes mellitus type (type 1/type 2) was based on health care professional assignment and, in a subset, further characterized with glutamic acid decarboxylase (GAD65) autoantibody and fasting C peptide measures.The incidence of DM (per 100,000 person-years) was 24.3 (95% confidence interval [CI], 23.3-25.3). Among children younger than 10 years, most had type 1 DM, regardless of race/ethnicity. The highest rates of type 1 DM were observed in non-Hispanic white youth (18.6, 28.1, and 32.9 for age groups 0-4, 5-9, and 10-14 years, respectively). Even among older youth (> or =10 years), type 1 DM was frequent among non-Hispanic white, Hispanic, and African American adolescents. Overall, type 2 DM was still relatively infrequent, but the highest rates (17.0 to 49.4 per 100,000 person-years) were documented among 15- to 19-year-old minority groups.Our data document the incidence rates of type 1 DM among youth of all racial/ethnic groups, with the highest rates in non-Hispanic white youth. Overall, type 2 DM is still relatively infrequent; however, the highest rates were observed among adolescent minority populations.
Effects of nebivolol and ivabradine on the left ventricular diastolic function in patients (pts) with COPD and stable angina
Authors: Olexandr Fesenko, Tetyana Pertseva
Journal: European Respiratory Journal (2014)

Aim:  To study influence of nebivolol and ivabradine on diastolic left ventricular (LV) dysfunction in pts with COPD and concomitant stable angina.   Materials and Methods:  We studied 44 pts in stable stage of COPD divided into 2 groups: 1st – 22 (50,0%) males (age – 59,3±6,2 yrs) with stable angina and arrhythmias taking nebivolol (Nebilet®), 2nd – 22 (50,0%) males (age – 57,5±5,9 yrs) with angina alone taking ivabradine (Coraxane®), before and after 6-months course of complex treatment. Measurements included clinical status and echocardiography with pulsed-wave Doppler.   Results:  Results are presented in the Table.   Conclusion:  6-month course of treatment of COPD and stable angina pts with either nebivolol or ivabradine leads to the improvement of LV diastolic function, LV relaxation, and decrease of LV filling pressure.
Primate Torpor: Regulation of Stress-Activated Protein Kinases during Daily Torpor in the Gray Mouse Lemur, <i>Microcebus Murinus</i>
Authors: Kyle K. Biggar, Cheng-Wei Wu, Shannon N. Tessier, Jing Zhang, Fabien Pifferi, Martine Perret, Kenneth B. Storey
Journal: Genomics Proteomics & Bioinformatics (2015)

Very few selected species of primates are known to be capable of entering torpor. This exciting discovery means that the ability to enter a natural state of dormancy is an ancestral trait among primates and, in phylogenetic terms, is very close to the human lineage. To explore the regulatory mechanisms that underlie primate torpor, we analyzed signal transduction cascades to discover those involved in coordinating tissue responses during torpor. The responses of mitogen-activated protein kinase (MAPK) family members to primate torpor were compared in six organs of control (aroused) versus torpid gray mouse lemurs, Microcebus murinus. The proteins examined include extracellular signal-regulated kinases (ERKs), c-jun NH2-terminal kinases (JNKs), MAPK kinase (MEK), and p38, in addition to stress-related proteins p53 and heat shock protein 27 (HSP27). The activation of specific MAPK signal transduction pathways may provide a mechanism to regulate the expression of torpor-responsive genes or the regulation of selected downstream cellular processes. In response to torpor, each MAPK subfamily responded differently during torpor and each showed organ-specific patterns of response. For example, skeletal muscle displayed elevated relative phosphorylation of ERK1/2 during torpor. Interestingly, adipose tissues showed the highest degree of MAPK activation. Brown adipose tissue displayed an activation of ERK1/2 and p38, whereas white adipose tissue showed activation of ERK1/2, p38, MEK, and JNK during torpor. Importantly, both adipose tissues possess specialized functions that are critical for torpor, with brown adipose required for non-shivering thermogenesis and white adipose utilized as the primary source of lipid fuel for torpor. Overall, these data indicate crucial roles of MAPKs in the regulation of primate organs during torpor.
Alemtuzumab vs. Interferon Beta-1a in Early Multiple Sclerosis
Authors: The CAMMS223 Trial Investigators
Journal: New England Journal of Medicine (2008)

Alemtuzumab, a humanized monoclonal antibody that targets CD52 on lymphocytes and monocytes, may be an effective treatment for early multiple sclerosis.In this phase 2, randomized, blinded trial involving previously untreated, early, relapsing-remitting multiple sclerosis, we assigned 334 patients with scores of 3.0 or less on the Expanded Disability Status Scale and a disease duration of 3 years or less to receive either subcutaneous interferon beta-1a (at a dose of 44 microg) three times per week or annual intravenous cycles of alemtuzumab (at a dose of either 12 mg or 24 mg per day) for 36 months. In September 2005, alemtuzumab therapy was suspended after immune thrombocytopenic purpura developed in three patients, one of whom died. Treatment with interferon beta-1a continued throughout the study.Alemtuzumab significantly reduced the rate of sustained accumulation of disability, as compared with interferon beta-1a (9.0% vs. 26.2%; hazard ratio, 0.29; 95% confidence interval [CI], 0.16 to 0.54; P<0.001) and the annualized rate of relapse (0.10 vs. 0.36; hazard ratio, 0.26; 95% CI, 0.16 to 0.41; P<0.001). The mean disability score on a 10-point scale improved by 0.39 point in the alemtuzumab group and worsened by 0.38 point in the interferon beta-1a group (P<0.001). In the alemtuzumab group, the lesion burden (as seen on T(2)-weighted magnetic resonance imaging) was reduced, as compared with that in the interferon beta-1a group (P=0.005). From month 12 to month 36, brain volume (as seen on T(1)-weighted magnetic resonance imaging) increased in the alemtuzumab group but decreased in the interferon beta-1a group (P=0.02). Adverse events in the alemtuzumab group, as compared with the interferon beta-1a group, included autoimmunity (thyroid disorders [23% vs. 3%] and immune thrombocytopenic purpura [3% vs. 1%]) and infections (66% vs. 47%). There were no significant differences in outcomes between the 12-mg dose and the 24-mg dose of alemtuzumab.In patients with early, relapsing-remitting multiple sclerosis, alemtuzumab was more effective than interferon beta-1a but was associated with autoimmunity, most seriously manifesting as immune thrombocytopenic purpura. The study was not powered to identify uncommon adverse events. (ClinicalTrials.gov number, NCT00050778.)
Importance of the MKK6/p38 pathway for interleukin-12–induced STAT4 serine phosphorylation and transcriptional activity
Authors: Roberta Visconti, Massimo Gadina, Mario Chiariello, Elbert H. Chen, Louis F. Stancato, J. Silvio Gutkind, John J. O'Shea
Journal: Blood (2000)
Abstract 12994: Sarpogrelate Use and Clinical Outcomes After Drug-Eluting Stent in Patients With Diabetes Mellitus(s-code), a Single Center Trial
Authors: Kohei Fukuchi, Tsukasa Inada, Fujio Hayashi, Kazuya Nagao, Naoki Takahashi, Motoko Tokunaga, Haruyasu Ito, Masaru Tanaka
Journal: Circulation (2014)

Introduction: Diabetes mellitus (DM) still remains a strong risk factor for the early restenosis and target lesion revascularization (TLR) after implanting drug-eluting stent (DES). 5-Hydroxytryptamine (5-HT) is known to induce platelet aggregation, proliferation of vascular smooth muscle cells and vasoconstriction. Sarpogrelate is the selective 5-HT2A receptor antagonist, which has been used clinically to prevent atherosclerosis. Hypothesis: We assessed the hypothesis that adding sarpogrelate with standard dual antiplatelet therapy (DAPT) would lower restenosis after DES implantation in the CAD patients with DM or impaired glucose tolerance (IGT). Methods: We undertook a prospective, open-label randomized trial in 148 patients with DM or IGT, who were planned for elective percutaneous coronary intervention (PCI) using DES for de-novo native coronary artery lesions. Patients were assigned to receive standard DAPT (aspirin 100mg daily and clopidogrel 75mg daily or ticlopidine 200mg daily) or sarpogrelate 3...
Alveolar type II cells transplantation in pulmonary fibrosis: effect on the lung macrophage activation
Authors: Raquel Guillamat-Prats, Sabrina Gea-Sorli, Gemma Gay-Jordi, Daniel Closa, Luis-Ignacio Sanchez-Lopez, Valeria Sirenko, Fernanda Hernandez-Gonzalez, Oriol Bulbena, Antoni Xaubet, Anna Serrano-Mollar
Journal: European Respiratory Journal (2013)

The phenotype adopted by alveolar macrophages (AM) and interstitial macrophages (IM) could determine the progression of fibrosis. Macrophages activation is classified into M1 or M2. M1 is a proinflammatory phenotype and M2 is involved in tissue remodeling. Our group has shown that alveolar type II cells (ATII) transplantation is able to reverse pulmonary fibrosis. Therefore, the objective of the study was to evaluate the effect of ATII transplantation in macrophages activation in an experimental model of pulmonary fibrosis.  The induction of fibrosis was performed in rats by the intratracheal instillation of bleomycin (3.5U/kg). The animals were transplanted with ATII (2.5x10 6  cells/animal) 15 days after bleomycin instillation and were sacrificed 21 days after the induction of fibrosis. AM were obtained by bronchoalveolar lavage and IM by digestion of the lung tissue. Macrophages activation was determined by RT-PCR of TNFα and IL1β specific M1 markers and arginase-I, mannose receptor (MR), IL10 and TGFβ specific M2 markers.  In AM, the expression of M2 markers as arginase-I, IL10 and TGFβ significantly increased in the fibrotic group. ATII transplantation was able to decrease the expression of all these markers. In contrast, M1 markers were unchanged. In IM, expression of all M1 and M2 markers increased significantly in the fibrotic group. ATII transplantation was able to decreased the expression of IL1β, arginase-I, IL10 and TGFβ.  During pulmonary fibrosis, all the macrophages adopted a M2 phenotype characteristic of tissue remodeling. ATII transplantation decreases M2 phenotype of both macrophage populations, which could be related to the reduction of fibrotic lesions.
Abstract 2704: Effect Of Statin Treatment On Long-Term Clinical outcome In Patients With End-Stage Heart Failure
Authors: Dimitris Tousoulis, Apostolis Drolias, Charalambos Antoniades, Nikos Papageorgiou, Penny Gounari, John Andreou, Elli Stefanadi, Christos Pitsavos, Christodoulos Stefanadis
Journal: Circulation (2007)

Introduction: Statin treatment has a major impact on clinical outcome in patients with atherosclerosis, but its role in patients with end-stage heart failure is controversial, since low LDL is asso...