Body Composition As A Frailty Marker For The Elderly Community.

Body composition (BC) in the elderly has been associated with diseases and mortality; however, there is a shortage of data on frailty in the elderly. To investigate the association between BC and frailty, and identify BC profiles in nonfrail, prefrail, and frail elderly people. A cross-sectional study comprising 235 elderly (142 females and 93 males) aged ≥65 years, from the city of Amparo, State of São Paulo, Brazil, was undertaken. Sociodemographic and cognitive features, comorbidities, medication, frailty, body mass index (BMI), muscle mass, fat mass, bone mass, and fat percent (%) data were evaluated. Aiming to examine the relationship between BC and frailty, the Mann-Whitney and Kruskal-Wallis nonparametric tests were applied. The statistical significance level was P<0.05. The nonfrail elderly showed greater muscle mass and greater bone mass compared with the prefrail and frail ones. The frail elderly had greater fat % than the nonfrail elderly. There was a positive association between grip strength and muscle mass with bone mass (P<0.001), and a negative association between grip strength and fat % (P<0.001). Gait speed was positively associated with fat mass (P=0.038) and fat % (P=0.002). The physical activity level was negatively associated with fat % (P=0.022). The weight loss criterion was positively related to muscle mass (P<0.001), bone mass (P=0.009), fat mass (P=0.018), and BMI (P=0.003). There was a negative association between fatigue and bone mass (P=0.008). Frailty in the elderly was characterized by a BC profile/phenotype with lower muscle mass and lower bone mass and with a higher fat %. The BMI was not effective in evaluating the relationship between BC and frailty. The importance of evaluating the fat % was verified when considering the tissue distribution in the elderly BC.101661-166

A high performance liquid chromatography method for determination of hydroxyzine hydrochloride in syrup

A simple isocratic method for quantification of hydroxyzine dihydrochloride by HPLC with UV detection at 232 nm in syrup has been developed and validated. Separation was achieved on a C18 column (250 x 4.6 mm, 5 μm) maintained at 90 ºC with 0.5 mol/L potassium dihydrogen phosphate buffer : acetonitrile (1:1, v/v) as mobile phase at a flow rate of 2.0 mL/min. The method was proven to be linear over the range of 80–120 μg/mL, accurate (recovery = 97.8 %), precise (coefficient of variation = 1.52 % for sample) and robust.Colegio de Farmacéuticos de la Provincia de Buenos Aire

A novel single amino acid deletion impairs fibronectin function and causes familial glomerulopathy with fibronectin deposits: case report of a family

Abstract Background Glomerulopathy with fibronectin deposits is an autosomal dominant disease associated with proteinuria, hematuria, hypertension and renal function decline. Forty percent of the cases are caused by mutations in FN1, the gene that encodes fibronectin. Case presentation This report describes two cases of Glomerulopathy with fibronectin deposits, involving a 47-year-old father and a 14-year-old son. The renal biopsies showed glomeruli with endocapillary hypercellularity and large amounts of mesangial and subendothelial eosinophilic deposits. Immunohistochemistry for fibronectin was markedly positive. Whole exome sequencing identified a novel FN1 mutation that leads to an amino-acid deletion in both patients (Ile1988del), a variant that required primary amino-acid sequence analysis for assessment of pathogenicity. Our primary sequence analyses revealed that Ile1988 is very highly conserved among relative sequences and is positioned in a C-terminal FN3 domain containing heparin- and fibulin-1-binding sites. This mutation was predicted as deleterious and molecular mechanics simulations support that it can change the tertiary structure and affect the complex folding and its molecular functionality. Conclusion The current report not only documents the occurrence of two GFND cases in an affected family and deeply characterizes its anatomopathological features but also identifies a novel pathogenic mutation in FN1, analyzes its structural and functional implications, and supports its pathogenicity.https://deepblue.lib.umich.edu/bitstream/2027.42/152212/1/12882_2019_Article_1507.pd