BackgroundA link between uric acid (UA) levels and cardiovascular diseases has been previously reported. However, its importance as a risk factor is still controversial. This study sought to determine whether elevated serum uric acid levels are associated with cardiovascular disease (CVD) in middle-aged and elderly Chinese individuals.MethodsWe conducted a population-based cross-sectional study in Shanghai, with a total of 8510 participants aged ≥40 years. The CVD included diagnosed coronary heart disease (CHD) and stroke. MetS was defined according to the updated National Cholesterol Education Program Adult Treatment Panel III criteria for Asian Americans.ResultsUric acid levels were positively associated with BMI, waist circumference, triglycerides, systolic blood pressure, diastolic blood pressure, glycohemoglobin, fasting plasma glucose, postprandial 2-hour plasma glucose (all P < 0.05), and negatively associated with HDL-cholesterol (P < 0.001). The prevalence of CVD significantly increased with increasing quartiles of UA in those without MetS group (p trend < 0.001), but not necessarily increased in those with MetS. After adjustment for metabolic syndrome and other cardiovascular risk factors, multivariate logistic regression analysis showed that odds ratios (OR) for CHD, stroke, and CVD in those in the fourth quartiles were 2.34 (95% confidence interval [CI] 1.73 to 3.45), 2.18 (95% CI 1.86 to 3.28), and 2.16 (95% CI 1.80 to 3.29), respectively, compared with those in the first quartile of UA.ConclusionsElevated serum uric acid level was associated with CVD, independent of conventional cardiovascular disease risk factors and metabolic syndrome.
BackgroundExtracellular matrix (ECM) disarray is found in calcific aortic valvular disease (CAVD), yet much remains to be learned about the role of individual ECM components in valvular interstitial cell (VIC) function and dysfunction. Previous clinical analyses have shown that calcification is associated with decreased collagen content, while previous in vitro work has suggested that the presence of collagen attenuates the responsiveness of VICs to pro-calcific stimuli. The current study uses whole leaflet cultures to examine the contributions of endogenous collagen in regulating the phenotype and calcification of VICs.MethodsA “top-down” approach was used to characterize changes in VIC phenotype in response to collagen alterations in the native 3D environment. Collagen-deficient leaflets were created via enzymatic treatment and cultured statically for six days in vitro. After culture, leaflets were harvested for analysis of DNA, proliferation, apoptosis, ECM composition, calcification, and gene/protein expression.ResultsIn general, disruption of collagen was associated with increased expression of disease markers by VICs in whole organ leaflet culture. Compared to intact control leaflets, collagen-deficient leaflets demonstrated increased VIC proliferation and apoptosis, increased expression of disease-related markers such as alpha-smooth muscle actin, alkaline phosphatase, and osteocalcin, and an increase in calcification as evidenced by positive von Kossa staining.ConclusionsThese results indicate that disruption of the endogenous collagen structure in aortic valves is sufficient to stimulate pathological consequences in valve leaflet cultures, thereby highlighting the importance of collagen and the valve extracellular matrix in general in maintaining homeostasis of the valve phenotype.
Screening auf spezifische Hepatopathien Welcher Wert ist wann erhöht?Wichtig für die diagnostische Weichenstellung ist die Di erenzierung in ein "hepatitisches" (Erhöhung der Transaminasen) oder "cholestatisches" (Erhöhung der cholestatischen Enzyme, AP, Bilirubin und Gamma-GT) Schädigungsmus-ter. Typisch für eine akute oder chronische Hepatitis ist die Transaminasenerhöhung. Bei einer alkoholischen oder nicht-alkoholischen Fettleber sind typischerweise GPT und die Gamma-GT erhöht, bei einer Fettleberhepatitis steigen die Trans aminasen und meist auch das Bilirubin dann stärker an.Eine isolierte Erhöhung der alkalischen Phosphatase (AP) spricht gegen eine Lebererkrankung, da dieses Enzym nicht nur von der Leber, sondern auch von Knochen, Niere und Plazenta gebildet wird. Sind jedoch auch andere Leberwerte erhöht, insbesondere Gamma-GT bzw. Bilirubin, so handelt es sich um eine Cholestase. Extrahepatische Cholestase-Ursachen sind Ab ussbehinderungen der Galle im Bereich der großen Gallenwege durch einen Gallengangstein oder einen Tumor. Sonogra sch sieht man erweiterte Gallengänge.
BackgroundStatins are commonly used to lower total cholesterol levels in the general population to prevent cardiovascular events. However, the effects of statins in patients with chronic kidney disease remain unclear. We therefore performed a meta-analysis to assess the effects of statin therapy on cardiovascular outcomes in patients with mild to moderate chronic kidney disease.MethodsWe systematically searched PubMed, EmBase, the Cochrane Central Register of Controlled Trials, proceedings of major meetings, and reference lists of articles for relevant literature. Only randomized clinical trials were included. Outcomes analysed included cardiovascular disease, total mortality, myocardial infarction, stroke, cardiovascular death, and possible drug-related adverse events. Subgroup analyses were also performed based on the population characteristics and clinical indexes.ResultsTwelve trials met our inclusion criteria. Overall, statin therapy resulted in a 24% reduction in the risk of cardiovascular disease (RR = 0.76,95% confidence interval [CI], 0.72– 0.80), a 21% reduction in the risk of total mortality (RR = 0.79,95% CI, 0.72–0.86), a 34% reduction in the risk of myocardial infarction (RR = 0.66,95% CI, 0.52–0.83), a 30% reduction in the risk of stroke (RR = 0.70,95% CI, 0.57–0.85), and a 17% reduction in the risk of cardiovascular mortality (RR = 0.83,95% CI, 0.73– 0.93). No statistically significant drug-related adverse events were noted. Subgroup analysis indicated that some important factors such as baseline creatinine level ≥1.5 mg/dL, baseline glomerular filtration rate (GFR), and cardiovascular disease history could affect cardiovascular outcomes.ConclusionStatin therapy had a clear effect on cardiovascular disease, total mortality, stroke, and myocardial infarction in patients with mild to moderate renal disease. Subgroup analysis indicated that baseline GFR, baseline creatinine level, and a history of cardiovascular disease might play an important role in the cardiovascular outcomes.
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