Rabbit Anti-CANX monoclonal antibody, clone TO31-65

Background: Familial partial lipodystrophy of the Dunnigan type is one of the most common inherited lipodystrophies variables. These individuals have important metabolic disorders that cause predisposition to various diseases. In this study we aimed to demonstrate the relation between the metabolic abnormalities, inflammatory profile and the expression of genes involved in the activation of the endoplasmic reticulum stress (ERS) in subjects with FPLD. Methods: We evaluated 14 female FPLD patients and compared with 13 female healthy individuals. The subjects were paired with their respective BMI and age and categorized into two groups: Familial partial lipodystrophy of the Dunnigan type (FPLD) and control. Patients were fasted for 12 h before blood collection for measurement of HbA1c, glucose, insulin, lipids and inflammatory markers. Subcutaneous adipose tissue was collected by puncture aspiration of submental region during ambulatorial surgical aesthetic procedure. Results: We demonstrate that patients with FPLD show increased HbA1c (p < 0.01), fasting glucose (p < 0.002) and triglycerides (p < 0.005) while HDL/cholesterol (p < 0.001) was lower when compared to healthy individuals. We found that 64.2% FPLD patients had metabolic syndrome according to International Diabetes Federation definition. We also observe increased AUC of glucose (p < 0.001) and insulin during oGTT, featuring a frame of hyperglycemia and hyperinsulinemia, suggesting insulin resistance. Also we found hyperactivation of several genes responsible for ERS such as ATF-4 (p < 0.01), ATF-6 (p < 0.01), EIF2 alpha 3K (p < 0.005), CCT4 (p < 0.001), CHOP (p < 0.01), CALR (p < 0.001) and CANX (p < 0.005), that corroborate the idea that diabetes mellitus and metabolic syndrome are associated with direct damage to the endoplasmic reticulum homeostasis. Ultimately, we note that individuals with lipodystrophy have an increase in serum interleukins, keys of the inflammatory process, as IL-1 beta, TNF-alpha and IL-6 (p < 0.05 all), compared with healthy individuals, which can be the trigger to insulin resistance in this population. Conclusion: Individuals with FPLD besides having typical dysfunctions of metabolic syndrome, show a hyperactivation of ERS associated with increased systemic inflammatory profile, which together may explain the complex clinical aspect of this diseases.

The BRIght Target Explorer (BRITE)-Constellation is a group of Canadian/Austrian nanosatellites that will examine the apparently brightest stars in the sky for variability using precise differential photometry. The constellation consists of four low Earth-orbiting nanosatellites, divided into pairs, with each member of a pair having a different optical filter. Each BRITE satellite will observe a region of interest for up to 100 days or longer, allowing the measurement of stellar oscillations on the order of hours to months. Each BRITE satellite utilizes a number of new, innovative technologies including reaction wheels, star tracker and optical telescope, all sized and designed around space flight laboratory's 5-kg, 20 x 20 x 20 cm(3) CanX nanosatellite bus. The BRITE science instrument is a low power complementary metal oxide semiconductor (CMOS) detector coupled with a custom lens system designed to provide a telecentric, slightly defocused image optimized for observing stellar intensity with an accuracy of I mmag per data point per orbit down to a visual magnitude of +3.5. Photometric measurements will have an error amplitude spectrum no greater than 20 ppm over measurement periods longer than a month. The optics will have a small (30 mm) aperture and a maximum length of 100 mm in order to fit within the nanosatellite bus. (C) 2009 Published by Elsevier Ltd.