HIV-Associated Cardiovascular Disease

Currently, 17 million people worldwide are receiving antiretroviral therapy (ART) for human immunodeficiency viral (HIV) infection. There has been a dramatic decline in mortality from HIV infection in the last decade due to increased availability of ART. HIV-associated cardiac failure is on the increase, with more cases of diastolic dysfunction reported in the ART era. HIV increases the risk of CVD, because of longer survival on ART, ongoing subclinical inflammation, traditional cardiovascular risk factors and the complications of chronic ART use. HIV-associated CVD encompasses a wide spectrum of heterogeneous clinical entities, which include diastolic dysfunction, asymptomatic left ventricular dysfunction, cardiomyopathy, myocarditis, heart failure, myocardial fibrosis, myocardial steatosis, pulmonary hypertension, peripheral arterial disease, cerebrovascular disease, infective endocarditis, coronary artery disease and cardiac neoplasms (e.g. Kaposi sarcoma and B-cell immunoblastic lymphoma). In this chapter, we review the complex association of HIV infection and CVD. We describe important recent developments and perspectives based on a systematic analysis of the important advances in this field published in the last decade

Design and Fabrication of Radio Frequency Amplifier with 3 dB π-Network Attenuator Isolation

This paper presents the design and fabrication of radio frequency amplifier (RFA), which operates at 5.8 GHz unlicensed frequency for WiMAX application. The RFA designed used T-matching network consisting of lump reactive elements, 3 dB attenuator and microstrip line at the input and output impedance. The RFA developed in this project contribute a gain of 15.6 dB with overall noise figure of 2.4 dB. The overall measured bandwidth is 1.240 GHz with S parameters S11, S12 and S22 measured are -12.4 dB, -25.5 dB and -12.3 dB respectively. The isolation result shows that there is a significant contribution using 3 dB π-network. The RFA used FET transistor EPA018A from Excelics Semiconductor Inc

Adénocarcinome pulmonaire primitif: expérience d’un centre hospitalier tunisien

La fréquence de l'adénocarcinome pulmonaire primitif est en nette augmentation au dépend des autres types histologiques de cancer bronchique primitif. En effet, il représente environ 40% des cas des carcinomes bronchiques non à petites cellules (CNPC). Il se distingue par certaines particularités. Décrire les aspects épidémiologiques, cliniques, thérapeutiques et évolutifs de l'adénocarcinome pulmonaire primitif. Etuderétrospective incluant 322 patients porteurs d'adénocarcinome pulmonaire primitif, hospitalisés au service de pneumologie du centre hospitalouniversitaire de Monastir (Tunisie) entre janvier 1990 et septembre 2013. L'âge moyen de nos patients était de 59,4 ans. 25,8% sont âgés de moins de 50 ans. Une prédominance masculine (86,3%) a été notée. 81,7% des patients étaient tabagiques. La symptomatologie respiratoire était dominée par la douleur thoracique (57,1%) et la toux (46%). Au moment du diagnostic, 73,3 % des patients étaient au stade métastatique. Les localisations secondaires les plus fréquentes étaient le poumon controlatéral (25,5%), la plèvre (21,1%) et l'os (19,25%). La prise en charge thérapeutique s'est basée essentiellement sur la chimiothérapie (48,5% des cas). Seulement 10,3% des patients ont bénéficié d'un traitement chirurgical. La médiane de survie de nos patients était de 6 mois avec une survie à 1 an, 3 ans et 5 ans respectivement de 25,9%, 3,2% et 2%. L'adénocarcinome bronchique primitif est un sous type histologique particulier parmi les cancers broncho-pulmonaires primitifs. Son incidence est en augmentation depuis une vingtaine d'année. Malgré les progrès thérapeutiques, il reste de mauvais pronostic

Histological changes of liver tissue and serobiochemical relation in does with pregnancy ketosis

Histological changes of liver in does with pregnancy ketosis were characterized. Twenty pregnant does at day 80 of pregnancy were used for this experiment. A total of 10 does were fed by grass (Napier) and goat concentrate with water ad libitum. Those 10 goats considered as healthy pregnant goat, and another 10 goats showing clinical and subclinical signs of ketosis considered as unhealthy pregnant does. Liver biopsies were performed when clinical signs appeared. Beta-Hydroxybutyrate (BHBA), free fatty acid (FFA), and glucose were dosed. Histological preparation revealed similar incidence and intensity of mild liver steatosis with lower cellular vacuolation in hepatocyte presence in healthy late pregnant does. Almost all of the pregnant does with ketosis state (n=8/10) had large amount of small lipid droplets in almost every hepatocyte over the whole liver acinus with higher number of cellular vacuolation, and related with higher BHBA and FFA levels while low in glucose level

Microscopic Evaluation Of The Natural Coral (Porties spp.) Post-implantation In Sheep Femur.

Bone defects resulting from congenital defects, tumor or trauma are conventionally repaired using bone graft. Allogenic and xenogenic bone grafts are used as alternatives but several problems are generally associated with them such as virus transfer, considerable care, high cost and regular immuna-defensive reaction

Kinin b(1) receptor in adipocytes regulates glucose tolerance and predisposition to obesity

BACKGROUND: Kinins participate in the pathophysiology of obesity and type 2 diabetes by mechanisms which are not fully understood. Kinin B(1) receptor knockout mice (B(1) (-/-)) are leaner and exhibit improved insulin sensitivity. METHODOLOGY/PRINCIPAL FINDINGS: Here we show that kinin B(1) receptors in adipocytes play a role in controlling whole body insulin action and glucose homeostasis. Adipocytes isolated from mouse white adipose tissue (WAT) constitutively express kinin B(1) receptors. In these cells, treatment with the B(1) receptor agonist des-Arg(9)-bradykinin improved insulin signaling, GLUT4 translocation, and glucose uptake. Adipocytes from B(1) (-/-) mice showed reduced GLUT4 expression and impaired glucose uptake at both basal and insulin-stimulated states. To investigate the consequences of these phenomena to whole body metabolism, we generated mice where the expression of the kinin B(1) receptor was limited to cells of the adipose tissue (aP2-B(1)/B(1) (-/-)). Similarly to B(1) (-/-) mice, aP2-B(1)/B(1) (-/-) mice were leaner than wild type controls. However, exclusive expression of the kinin B(1) receptor in adipose tissue completely rescued the improved systemic insulin sensitivity phenotype of B(1) (-/-) mice. Adipose tissue gene expression analysis also revealed that genes involved in insulin signaling were significantly affected by the presence of the kinin B(1) receptor in adipose tissue. In agreement, GLUT4 expression and glucose uptake were increased in fat tissue of aP2-B(1)/B(1) (-/-) when compared to B(1) (-/-) mice. When subjected to high fat diet, aP2-B(1)/B(1) (-/-) mice gained more weight than B(1) (-/-) littermates, becoming as obese as the wild types. CONCLUSIONS/SIGNIFICANCE: Thus, kinin B(1) receptor participates in the modulation of insulin action in adipocytes, contributing to systemic insulin sensitivity and predisposition to obesity

The global response to the COVID-19 pandemic: how have immunology societies contributed?

The COVID-19 pandemic is shining a spotlight on the field of immunology like never before. To appreciate the diverse ways in which immunologists have contributed, Nature Reviews Immunology invited the president of the International Union of Immunological Societies and the presidents of 15 other national immunology societies to discuss how they and their members responded following the emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)

Meta-analysis of type 2 Diabetes in African Americans Consortium

Type 2 diabetes (T2D) is more prevalent in African Americans than in Europeans. However, little is known about the genetic risk in African Americans despite the recent identification of more than 70 T2D loci primarily by genome-wide association studies (GWAS) in individuals of European ancestry. In order to investigate the genetic architecture of T2D in African Americans, the MEta-analysis of type 2 DIabetes in African Americans (MEDIA) Consortium examined 17 GWAS on T2D comprising 8,284 cases and 15,543 controls in African Americans in stage 1 analysis. Single nucleotide polymorphisms (SNPs) association analysis was conducted in each study under the additive model after adjustment for age, sex, study site, and principal components. Meta-analysis of approximately 2.6 million genotyped and imputed SNPs in all studies was conducted using an inverse variance-weighted fixed effect model. Replications were performed to follow up 21 loci in up to 6,061 cases and 5,483 controls in African Americans, and 8,130 cases and 38,987 controls of European ancestry. We identified three known loci (TCF7L2, HMGA2 and KCNQ1) and two novel loci (HLA-B and INS-IGF2) at genome-wide significance (4.15 × 10(-94)<P<5 × 10(-8), odds ratio (OR)  = 1.09 to 1.36). Fine-mapping revealed that 88 of 158 previously identified T2D or glucose homeostasis loci demonstrated nominal to highly significant association (2.2 × 10(-23) < locus-wide P<0.05). These novel and previously identified loci yielded a sibling relative risk of 1.19, explaining 17.5% of the phenotypic variance of T2D on the liability scale in African Americans. Overall, this study identified two novel susceptibility loci for T2D in African Americans. A substantial number of previously reported loci are transferable to African Americans after accounting for linkage disequilibrium, enabling fine mapping of causal variants in trans-ethnic meta-analysis studies.Peer reviewe