NLO QCD Corrections to BcB_c-to-Charmonium Form Factors

The $B_c(^1S_0)$ meson to S-wave Charmonia transition form factors are calculated in next-to-leading order(NLO) accuracy of Quantum Chromodynamics(QCD). Our results indicate that the higher order corrections to these form factors are remarkable, and hence are important to the phenomenological study of the corresponding processes. For the convenience of comparison and use, the relevant expressions in asymptotic form at the limit of $m_c\rightarrow0$ for the radiative corrections are presented

A cluster randomised trial of educational messages to improve the primary care of diabetes

<p>Abstract</p> <p>Background</p> <p>Regular laboratory test monitoring of patient parameters offers a route for improving the quality of chronic disease care. We evaluated the effects of brief educational messages attached to laboratory test reports on diabetes care.</p> <p>Methods</p> <p>A programme of cluster randomised controlled trials was set in primary care practices in one primary care trust in England. Participants were the primary care practices' constituent healthcare professionals and patients with diabetes. Interventions comprised brief educational messages added to paper and electronic primary care practice laboratory test reports and introduced over two phases. Phase one messages, attached to Haemoglobin A1c (HbA1c) reports, targeted glycaemic and cholesterol control. Phase two messages, attached to albumin:creatinine ratio (ACR) reports, targeted blood pressure (BP) control, and foot inspection. Main outcome measures comprised practice mean HbA1c and cholesterol levels, diastolic and systolic BP, and proportions of patients having undergone foot inspections.</p> <p>Results</p> <p>Initially, 35 out of 37 eligible practices participated. Outcome data were available for a total of 8,690 patients with diabetes from 32 practices. The BP message produced a statistically significant reduction in diastolic BP (-0.62 mmHg; 95% confidence interval -0.82 to -0.42 mmHg) but not systolic BP (-0.06 mmHg, -0.42 to 0.30 mmHg) and increased the odds of achieving target BP control (odds ratio 1.05; 1.00, 1.10). The foot inspection message increased the likelihood of a recorded foot inspection (incidence rate ratio 1.26; 1.18 to 1.36). The glycaemic control message had no effect on mean HbA1c (increase 0.01%; -0.03 to 0.04) despite increasing the odds of a change in likelihood of HbA1c tests being ordered (OR 1.06; 1.01, 1.11). The cholesterol message had no effect (decrease 0.01 mmol/l, -0.04 to 0.05).</p> <p>Conclusions</p> <p>Three out of four interventions improved intermediate outcomes or process of diabetes care. The diastolic BP reduction approximates to relative reductions in mortality of 3% to 5% in stroke and 3% to 4% in ischaemic heart disease over 10 years. The lack of effect for other outcomes may, in part, be explained by difficulties in bringing about further improvements beyond certain thresholds of clinical performance.</p> <p>Trial Registration</p> <p>Current Controlled Trials, <a href="http://www.controlled-trials.com/ISRCTN2186314">ISRCTN2186314</a>.</p

Statin Therapy in Metabolic Syndrome and Hypertension Post-JUPITER: What is the Value of CRP?

Much evidence supports a pivotal role for inflammation in atherosclerosis. C-reactive protein (CRP), the prototypic marker of inflammation in humans, is a cardiovascular risk marker and may also promote atherogenesis. CRP levels are increased in metabolic syndrome and hypertension and confer increased risk of cardiovascular events in patients in these subgroups. Statins have been shown to lower low-density lipoproteins and CRP independently, and reduce cardiovascular events in subjects with and without metabolic syndrome and hypertension. In this review, we focus on the results from the primary prevention statin trial, Justification for the Use of statins in Primary prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER), which showed reductions in LDL, CRP, and cardiovascular events. Post-JUPITER, the new guidelines will now need to consider recommending high-sensitivity CRP testing to intermediate-risk metabolic syndrome patients and those with hypertension and intermediate risk so that we can better identify candidates at greater risk and reduce cardiovascular burden in these subjects with statin therapy

Nephrin Regulates Lamellipodia Formation by Assembling a Protein Complex That Includes Ship2, Filamin and Lamellipodin

Actin dynamics has emerged at the forefront of podocyte biology. Slit diaphragm junctional adhesion protein Nephrin is necessary for development of the podocyte morphology and transduces phosphorylation-dependent signals that regulate cytoskeletal dynamics. The present study extends our understanding of Nephrin function by showing in cultured podocytes that Nephrin activation induced actin dynamics is necessary for lamellipodia formation. Upon activation Nephrin recruits and regulates a protein complex that includes Ship2 (SH2 domain containing 5′ inositol phosphatase), Filamin and Lamellipodin, proteins important in regulation of actin and focal adhesion dynamics, as well as lamellipodia formation. Using the previously described CD16-Nephrin clustering system, Nephrin ligation or activation resulted in phosphorylation of the actin crosslinking protein Filamin in a p21 activated kinase dependent manner. Nephrin activation in cell culture results in formation of lamellipodia, a process that requires specialized actin dynamics at the leading edge of the cell along with focal adhesion turnover. In the CD16-Nephrin clustering model, Nephrin ligation resulted in abnormal morphology of actin tails in human podocytes when Ship2, Filamin or Lamellipodin were individually knocked down. We also observed decreased lamellipodia formation and cell migration in these knock down cells. These data provide evidence that Nephrin not only initiates actin polymerization but also assembles a protein complex that is necessary to regulate the architecture of the generated actin filament network and focal adhesion dynamics

Pathogen Recognition Receptor Signaling Accelerates Phosphorylation-Dependent Degradation of IFNAR1

An ability to sense pathogens by a number of specialized cell types including the dendritic cells plays a central role in host's defenses. Activation of these cells through the stimulation of the pathogen-recognition receptors induces the production of a number of cytokines including Type I interferons (IFNs) that mediate the diverse mechanisms of innate immunity. Type I IFNs interact with the Type I IFN receptor, composed of IFNAR1 and IFNAR2 chains, to mount the host defense responses. However, at the same time, Type I IFNs elicit potent anti-proliferative and pro-apoptotic effects that could be detrimental for IFN-producing cells. Here, we report that the activation of p38 kinase in response to pathogen-recognition receptors stimulation results in a series of phosphorylation events within the IFNAR1 chain of the Type I IFN receptor. This phosphorylation promotes IFNAR1 ubiquitination and accelerates the proteolytic turnover of this receptor leading to an attenuation of Type I IFN signaling and the protection of activated dendritic cells from the cytotoxic effects of autocrine or paracrine Type I IFN. In this paper we discuss a potential role of this mechanism in regulating the processes of innate immunity

Analysis of the masses and decay constants of the heavy-light mesons with QCD sum rules

In this article, we calculate the contributions of the vacuum condensates up to dimension-6 including the $${\mathcal {O}}(\alpha _s)$$ corrections to the quark condensates in the operator product expansion, then we study the masses and decay constants of the pseudoscalar, scalar, vector, and axial-vector heavy-light mesons with the QCD sum rules in a systematic way. The masses of the observed mesons $$(D,D^*)$$, $$(D_s,D_s^*)$$, $$(D_0^*(2400),D_1(2430))$$, $$(D_{s0}^*(2317),D_{s1}(2460)),$$ $$(B,B^*)$$, $$(B_s,B_s^*)$$ can be well reproduced, while the predictions for the masses of $$(B^*_{0}, B_{1})$$ and $$(B^*_{s0}, B_{s1})$$ can be confronted with the experimental data in the future. We obtain the decay constants of the pseudoscalar, scalar, vector, and axial-vector heavy-light mesons, which have many phenomenological applications in studying the semi-leptonic and leptonic decays of the heavy-light mesons

Regulation of the cd38 promoter in human airway smooth muscle cells by TNF-α and dexamethasone

<p>Abstract</p> <p>Background</p> <p>CD38 is expressed in human airway smooth muscle (HASM) cells, regulates intracellular calcium, and its expression is augmented by tumor necrosis factor alpha (TNF-α). CD38 has a role in airway hyperresponsiveness, a hallmark of asthma, since deficient mice develop attenuated airway hyperresponsiveness compared to wild-type mice following intranasal challenges with cytokines such as IL-13 and TNF-α. Regulation of CD38 expression in HASM cells involves the transcription factor NF-κB, and glucocorticoids inhibit this expression through NF-κB-dependent and -independent mechanisms. In this study, we determined whether the transcriptional regulation of CD38 expression in HASM cells involves response elements within the promoter region of this gene.</p> <p>Methods</p> <p>We cloned a putative 3 kb promoter fragment of the human <it>cd38 </it>gene into pGL3 basic vector in front of a luciferase reporter gene. Sequence analysis of the putative <it>cd38 </it>promoter region revealed one NF-κB and several AP-1 and glucocorticoid response element (GRE) motifs. HASM cells were transfected with the 3 kb promoter, a 1.8 kb truncated promoter that lacks the NF-κB and some of the AP-1 sites, or the promoter with mutations of the NF-κB and/or AP-1 sites. Using the electrophoretic mobility shift assays, we determined the binding of nuclear proteins to oligonucleotides encoding the putative <it>cd38 </it>NF-κB, AP-1, and GRE sites, and the specificity of this binding was confirmed by gel supershift analysis with appropriate antibodies.</p> <p>Results</p> <p>TNF-α induced a two-fold activation of the 3 kb promoter following its transfection into HASM cells. In cells transfected with the 1.8 kb promoter or promoter constructs lacking NF-κB and/or AP-1 sites or in the presence of dexamethasone, there was no induction in the presence of TNF-α. The binding of nuclear proteins to oligonucleotides encoding the putative <it>cd38 </it>NF-κB site and some of the six AP-1 sites was increased by TNF-α, and to some of the putative <it>cd38 </it>GREs by dexamethasone.</p> <p>Conclusion</p> <p>The EMSA results and the cd38 promoter-reporter assays confirm the functional role of NF-κB, AP-1 and GREs in the cd38 promoter in the transcriptional regulation of CD38.</p

Transcultural Diabetes Nutrition Therapy Algorithm: The Asian Indian Application

India and other countries in Asia are experiencing rapidly escalating epidemics of type 2 diabetes (T2D) and cardiovascular disease. The dramatic rise in the prevalence of these illnesses has been attributed to rapid changes in demographic, socioeconomic, and nutritional factors. The rapid transition in dietary patterns in India—coupled with a sedentary lifestyle and specific socioeconomic pressures—has led to an increase in obesity and other diet-related noncommunicable diseases. Studies have shown that nutritional interventions significantly enhance metabolic control and weight loss. Current clinical practice guidelines (CPGs) are not portable to diverse cultures, constraining the applicability of this type of practical educational instrument. Therefore, a transcultural Diabetes Nutrition Algorithm (tDNA) was developed and then customized per regional variations in India. The resultant India-specific tDNA reflects differences in epidemiologic, physiologic, and nutritional aspects of disease, anthropometric cutoff points, and lifestyle interventions unique to this region of the world. Specific features of this transculturalization process for India include characteristics of a transitional economy with a persistently high poverty rate in a majority of people; higher percentage of body fat and lower muscle mass for a given body mass index; higher rate of sedentary lifestyle; elements of the thrifty phenotype; impact of festivals and holidays on adherence with clinic appointments; and the role of a systems or holistic approach to the problem that must involve politics, policy, and government. This Asian Indian tDNA promises to help guide physicians in the management of prediabetes and T2D in India in a more structured, systematic, and effective way compared with previous methods and currently available CPGs