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Inherited platelet disorders are rare but they can have considerable clinical impacts, and studies of their causes have advanced understanding of platelet formation and function. Effective hemostasis requires adequate circulating numbers of functional platelets. Quantitative, qualitative and combined platelet disorders with a bleeding phenotype have been linked to defects in platelet cytoskeletal elements, cell surface receptors, signal transduction pathways, secretory granules and other aspects. Inherited platelet disorders have variable clinical presentations, and diagnosis and management is often challenging. Evaluation begins with detailed patient and family histories, including a bleeding score. The physical exam identifies potential syndromic features of inherited platelet disorders and rules out other causes. Laboratory investigations include a complete blood count, blood film, coagulation testing and Von Willebrand factor assessment. A suspected platelet function disorder is further assessed by platelet aggregation, flow cytometry, platelet dense granule release and/or content, and genetic testing. The management of platelet function disorders aims to minimize the risk of bleeding and achieve adequate hemostasis when needed. Although not universal, platelet transfusion remains a crucial component in the management of many inherited platelet disorders.

To determine the crude and sex- and age-adjusted prevalence rates of atherogenic dyslipidemia (AD) and low HDL-cholesterol levels (low-HDLc), and to assess their associations with cardiovascular risk factors, chronic kidney disease, cardiovascular and cardiometabolic diseases.

Population-based cross-sectional study conducted in Primary Care, with randomly selected adult subjects. The AD was considered if the patients had hypertriglyceridemia (triglycerides≥150mg/dL) and low-HDLc (<40mg/dL [men];<50mg/dL [women]). Crude and sex- and age-adjusted prevalence rates were determined, and univariate and multivariate analysis were performed to assess related cardiometabolic factors.

Study population with 6,588 adults (55.9% women) with mean age 55.1 (±17.5) years. The mean HDLc levels were 49.2 (±12.6) mg/dL in men and 59.2 (±14.7) mg/dL in women. selleck chemical The crude prevalence rates of low-HDLc and AD were 30.8% (95%CI 29.7-31.9), and 14.3% (95%CI 13.5-15.2), respectively. The adjusted prevalence rates of low-HDLc were 28.0% in men and 31.0% in women, and AD were 16.4% in men and 10.6% in women. Seventy-three percent of the population with AD had high or very high cardiovascular risk. The independent factors associated with low HDLc or with AD were diabetes, smoking, abdominal obesity, and obesity. The major factors associated with low HDLc and AD were hypertriglyceridemia and diabetes, respectively.

Almost a third of the adult population had low HDL-C and half of them met AD criteria. Cardiometabolic factors were associated with low HDL-C and AD, highlighting hypertriglyceridemia with low HDLc, and DM with AD.

Almost a third of the adult population had low HDL-C and half of them met AD criteria. Cardiometabolic factors were associated with low HDL-C and AD, highlighting hypertriglyceridemia with low HDLc, and DM with AD.Dysfunction of perivascular adipose tissue of mesenteric bed participates in the pathophysiology of high blood pressure linked to metabolic syndrome. Thus, it might consider a new therapeutic objective to take account in cardiovascular and metabolic diseases. Besides its antihypertensive effect, there is a growing interest on the pleiotropic actions of losartan, an angiotensin II type 1 (AT1) receptor antagonist. The aim of the study was to analyze the actions of losartan treatment on adiposity index and prostanoids release from mesenteric vascular bed and its relationship with blood pressure as well as homeostasis model of assessment of insulin resistance (HOMA-IR) in Sprague-Dawley rats under a high-fat (HF) diet for 8 weeks. Four groups were used control (C), HF diet (HF, 50%, w/w bovine fat), losartan-treated (CL8, 30mg/kg/body weight/day in the drinking water) and losartan-treated HF diet (HFL, both treatments). A high-fat diet incremented systolic blood pressure, HOMA-IR, adiposity of mesenteric vascular bed and the release of vasoconstrictor prostanoids such as thromboxane (TX) B2 and prostaglandin (PG) F2α as well as PGE2, an inflammatory prostanoid in a context of insulin resistance and hypertension. We found a positive correlation between adiposity index and systolic blood pressure. Also, both parameters are positive correlated with the HOMA IR index. Moreover, we also found that these prostanoids release correlate with systolic blood pressure as well as with mesenteric vascular bed adiposity index. Losartan treatment prevented all these alterations and normalized the PGI2/TXA2 ratio in high-fat fed rats. We conclude that losartan may play beneficial actions on perivascular adipose tissue alterations and endothelial dysfunction through restoration of normal balance of vasoactive substances in this model.This study compared quantitative cartilage ultrasound metrics between people with (n = 12) and without (n = 12) arthroscopic cartilage damage after anterior cruciate ligament injury (age, 24.9 ± 3.7 y; sex, 33% female, 67% male; days since injury = 50 ± 52). A transverse suprapatellar ultrasound assessment imaged the femoral cartilage in participants' injured knees before a clinical arthroscopy. A custom program automatically separated a manual cartilage segmentation into standardized medial and lateral femoral regions and calculated mean thickness (i.e., cross-sectional area/length of cartilage-bone interface), mean echo intensity and echo-intensity heterogeneity. An orthopedic surgeon assessed arthroscopic cartilage damage in the medial and lateral femoral condyles using the Outerbridge grading system (cartilage damage = Outerbridge ≥ 1). Separate logistic regressions for medial and lateral femoral cartilage were used to determine the association between each ultrasound metric and arthroscopic cartilage damage. In medial femoral cartilage, for every 1 standard deviation decrease in echo-intensity mean and heterogeneity, there is, respectively, a 91% (adjusted odds ratio, 0.09; 95% confidence interval, 0.01-0.69) and 97% (adjusted odds ratio, 0.03; 95% confidence interval, 0.002-0.50) increase in the odds of having arthroscopic cartilage damage. Lateral cartilage ultrasound metrics are not associated with lateral arthroscopic cartilage damage. This study provides preliminary evidence that femoral cartilage ultrasound echo intensity is a non-invasive measure associated with medial femoral cartilage health after anterior cruciate ligament injury.