Hollissylvest6617

However, the closest associations to ∆PWV/year were found for the ratio of these two factors (skin AGEs/sRAGE) [β coeff = 0.0747 (SE 0.0189), p  less then  0.0001]. In a categorized manner, subjects with skin AGEs/sRAGE ratio ≥ 3.3 showed about twofold higher risk having ΔPWV/year ≥ 0.2 m/s [adjusted odds ratio was 2.09 (95% CI 1.35-3.22), p = 0.001]. In contrast, neither circulating AGEs nor circulating AGEs/sRAGE showed any significant relation to ΔPWV/year. In conclusion, skin AGEs/sRAGE ratio seems to be a more sensitive biomarker of vascular aging than these single factors themselves or circulation status of AGEs.Whether dynamic change in waist circumference is associated with progression from prehypertension to hypertension is not well understood. We explored this issue. A total of 4221 prehypertensive adults ≥18 years were enrolled during 2007-2008 and followed up during 2013-2014. Participants were classified by percentage waist-circumference change at follow-up ≤-2.5, -2.5 to ≤2.5, 2.5 to ≤5.0, and >5.0%. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated with logistic regression models, with stable waist-circumference change (-2.5 to 2.5%) as the reference. During the 6 years of follow-up, 1464 prehypertensive patients (851 women) showed progression to hypertension, with an incidence rate of 32.7% for men and 36.3% for women. As compared with stable waist circumference, a waist-circumference gain > 5.0% was associated with increased hypertension risk adjusted ORs (95% CI) were 1.08 (1.01-1.14) for men and 1.09 (1.04-1.15) for women. The risk also decreased significantly for men with ≥2.5% waist-circumference loss (OR = 0.94, 95% CI 0.88-1.00). We found a linear association between percentage waist-circumference gain and risk of progression from prehypertension to hypertension for both sexes by restricted cubic splines (pnonlinearity = 0.772 for men and 0.779 for women). For each 10% gain in waist circumference, the risk increased by 8% for men and 5% for women. The association remained significant for both sexes in a subgroup analysis by abdominal obesity at baseline. The long-term gain in waist circumference significantly increased the risk of progression from prehypertension to hypertension for both sexes in a rural Chinese population, regardless of abdominal obesity status at baseline.BACKGROUND To investigate the effect of frailty on short-term postoperative outcomes in patients with prostate cancer treated with radical prostatectomy (RP). METHODS Within the National Inpatient Sample database, we identified 91,618 RP patients treated between 2008 and 2015. The Johns Hopkins Adjusted Clinical Groups frailty-defining indicator was applied, and we examined the rates of frailty over time, as well as its effect on overall complications, major complications, nonhome-based discharge, length of stay (LOS), and total hospital charges (THCs). Time trends and multivariable logistic, Poisson and linear regression models were applied. RESULTS Overall, 12,185 (13.3%) patients were frail. Rates of frail patients increased over time (from 10.3 to 18.2%; p  less then  0.001). Frail patients had higher rates of overall complications (16.6 vs. 8.6%), major complications (4.9 vs. 2.6%), nonhome-based discharge (5.9 vs. 5%), longer LOS (2 vs. 1), and higher THCs ($37,186 vs. $35,241) (all p  less then  0.001). selleck kinase inhibitor Moreover, frailty was an independent predictor of overall complications (OR 1.95), major complications (OR 1.76), nonhome-based discharge (OR 1.20), longer LOS (RR 1.19), and higher THCs (RR $3160) (all p  less then  0.001). Of frail patients, 10,418 (85.5%) neither exhibited body mass index ≥ 30 nor Charlson comorbidity index ≥ 2. CONCLUSIONS On average, every seventh RP patient is frail and that proportion is on the rise. Frail individuals are at higher risk of adverse short-term postoperative outcomes, that cannot be predicted by other risk factors, such as obesity or comorbidities.BACKGROUND The combination of abiraterone acetate and prednisone (AA/P) is used to treat metastatic prostate cancer, but molecular predictors of treatment response are not well elucidated. We evaluated plasma circulating tumor DNA- (ctDNA-) based copy number alterations (CNAs) to determine treatment-related predictive and prognostic biomarkers for metastatic castration-resistant prostate cancer (mCRPC). METHODS Serial plasma specimens were prospectively collected from 88 chemotherapy-naive mCRPC patients before and after 12 weeks of AA/P treatment. Sequencing-based CNA analyses were performed on 174 specimens. We evaluated CNA-associated 12-week responses for primary resistance, time to treatment change (TTTC) for secondary resistance, and overall survival for prognosis (P  less then  0.05). Associations with primary resistance were analyzed using the Fisher exact test. Kaplan-Meier survival curves and Cox regression analyses were used to determine the associations of CNAs with acquired resistance and overalloutcomes.BACKGROUND Statins inhibit HMG-CoA reductase, the rate-limiting enzyme of the mevalonate pathway. Epidemiological and pre-clinical evidence support an association between statin use and delayed prostate cancer (PCa) progression. Here, we evaluated the effects of neoadjuvant fluvastatin treatment on markers of cell proliferation and apoptosis in men with localized PCa. METHODS Thirty-three men were treated daily with 80 mg fluvastatin for 4-12 weeks in a single-arm window-of-opportunity study between diagnosis of localized PCa and radical prostatectomy (RP) (ClinicalTrials.gov NCT01992042). Percent Ki67 and cleaved Caspase-3 (CC3)-positive cells in tumor tissues were evaluated in 23 patients by immunohistochemistry before and after treatment. Serum and intraprostatic fluvastatin concentrations were quantified by liquid chromatography-mass spectrometry. RESULTS Baseline characteristics included a median prostate-specific antigen (PSA) level of 6.48 ng/mL (IQR 4.21-10.33). The median duration of fluvastatin treae data warrant further investigation into the anti-neoplastic effects of statins in prostate tissue.