OBJECTIVEBetatrophin, a newly identified hormone, has been recently characterized as a potent stimulator that increases the production and expansion of insulin-secreting b-cells in mice, but the physiological role of betatrophin remains poorly understood. This study measured for the first time serum betatrophin levels in newly diagnosed patients with type 2 diabetes (T2DM) and explored the correlations between its serum levels and various metabolic parameters in T2DM. RESEARCH DESIGN AND METHODSWe analyzed the concentrations of betatrophin by ELISA in blood samples of 166 well-characterized individuals in whom anthropometric parameters, oral glucose tolerance test (OGTT), glycosylated hemoglobin, blood lipids, insulin sensitivity (1/homeostasis model assesment of insulin resistance [1/HOMA-IR] and Matsuda index [ISI M ]), and insulin secretion were measured. The participants were divided into newly diagnosed T2DM patients (n = 83) and age-, sex-and BMI-matched healthy control subjects (n = 83). RESULTSSerum betatrophin levels were significantly higher in T2DM patients than in healthy control subjects (613.08 [422.19-813.08] vs. 296.57 [196.53-509.46] pg/mL; P < 0.01). Serum betatrophin positively correlated with age, 2-h post-OGTT glucose (2hPG), and postprandial serum insulin (PSI), but negatively with 1/HOMA-IR and ISI M in T2DM patients. In the control group, betatrophin was only positively associated with age. In T2DM subjects, multivariate regression analyses showed that age, 2hPG, and PSI were independent factors influencing serum betatrophin levels. CONCLUSIONSCirculating concentrations of betatrophin are significantly increased in T2DM patients. Our results suggest that betatrophin may play a role in the pathogenesis of T2DM.Precise regulation of b-cell function is crucial for maintaining blood glucose homeostasis (1). In type 2 diabetes (T2DM), ambient insulin resistance forces b-cells to produce more insulin, which ultimately results in exhaustion of insulin production secondary to deterioration of b-cell functions. Unfortunately, neither pharmacotherapy nor insulin injections can reverse ongoing failure of b-cell function to prevent uncontrolled hyperglycemia and the devastating microvascular, neurologic, and macrovascular complications of diabetes. Treatments that replenish b-cell

Serum oxytocin levels were decreased in T2DM as well as OB subjects.

Spectroscopic refractive indices of monoclinic single crystal and ceramic lutetium oxyorthosilicate from 200 to 850nm J. Appl. Phys. 112, 063524 (2012) Full extraction methods to retrieve effective refractive index and parameters of a bianisotropic metamaterial based on material dispersion models J. Appl. Phys. 112, 064907 (2012) GaN-based light emitting diodes with micro-and nano-patterned structures by femtosecond laser nonlinear decomposition Appl. Phys. Lett. 101, 131103 (2012) On the method of photoluminescence spectral intensity ratio imaging of silicon bricks: Advances and limitations J. Appl. Phys. 112, 063116 (2012) Aluminium doped Zn1−xMgxO-A transparent conducting oxide with tunable optical and electrical properties A new technique for measuring the refractive index at high pressure in a diamond anvil cell is reported. This technique was applied to a 4:l methanohethanol mixture at room temperature and pressures up to 16.9 GPa. A parameterization is given for the refractive index that fits the data with a residual standard error of 4~ 10~~ at frequencies between 12 000 and 24 000 cm-l and pressures between 0.5 and 11.5 GPa. A sharp change in slope of the refractive index vs pressure was observed at the glass transition near 10 GPa. Modifications of the technique which should allow measurements of the refractive index to much higher pressures are discussed.

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Endometritis is one of the main diseases that harms the dairy cow industry. Tanshinone IIA (TIIA), a fat-soluble alkaloid isolated from Salviae miltiorrhizae, has been reported to have potent anti-inflammatory properties. However, the anti-inflammatory effects of TIIA on a mouse model of lipopolysaccharide (LPS)-induced endometritis remain to be elucidated. The purpose of the present study was to investigate the effects of TIIA on LPS-induced mouse endometritis. TIIA was intraperitoneally injected 1 h before and 12 h after perfusion of LPS into the uterus. A histological examination was then performed, and the concentrations of myeloperoxidase (MPO) and nitric oxide (NO) in the uterine tissue were determined. The levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in a homogenate of the uterus were detected by enzyme-linked immunosorbent assay. The extent of phosphorylation of IκBα and p65 was detected by Western blotting. TIIA markedly reduced the infiltration of neutrophils, suppressed MPO activity and the concentration of NO, and attenuated the expression of TNF-α and IL-1β. Furthermore, TIIA inhibited the phosphorylation of the nuclear factor-kappa B (NF-κB) p65 subunit and the degradation of its inhibitor IκBα. All the results suggest that TIIA has strong anti-inflammatory effects on LPS-induced mouse endometritis.

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Pseudomonas aeruginosa (P. aeruginosa) is an opportunistic pathogen that can be found in individuals in which the immune system has been suppressed by HIV/AIDS or chronic alcoholism. We evaluated the role of inducible nitric oxide synthase (NOS II) as a modulator of lung concentrations of P. aeruginosa in normal rats and rats given a single dose of ethanol (ETOH). Rats were pretreated with either sterile saline (PBS, 0.1 ml/kg, i.v.) or the NOS II inhibitor L-N6-iminoethyl lysine (LNIL, 10 mg/kg, i.v.) 15 min before intraperitoneal administration of either PBS (4.5 ml/kg) or ETOH (4.5 g/kg). Thirty min after administration of PBS or ETOH the rats were placed in inhalation chambers and exposed to 45 min of an aerosol containing P. aeruginosa (5 x 10(4) colony forming units, CFU). A group of rats (n = 5-6/treatment/time period) were killed immediately (0 hr) or 4 hr after inhalation of P. aeruginosa. The lungs were homogenized and the P. aeruginosa were grown in nutrient broth to determine the number of viable CFU remaining in the lung. The NOS II and TNFalpha mRNA and protein content lung alveolar macrophages (AM) and neutrophils (PMN) were measured with RT-PCR and Western blot. The concentration of nitrate and nitrite anion in the bronchoalveolar lavage fluid (BALf) and ex vivo incubates of PMN were also measured. The CFU of P. aeruginosa present in the lungs of the four groups of rats at 0 hr did not differ. The CFU of P. aeruginosa in the lung increased (p < 0.05) in rats pretreated with ETOH when compared with that obtained from rats pretreated with PBS. However, pretreatment of rats with LNIL decreased (p < 0.05) the 4 hr lung content of P. aeruginosa. Coadministration of LNIL and ETOH to rats augmented the CFU of P. aeruginosa in lungs to amounts which did not differ from that of rats pretreated with ETOH. Inhalation of P. aeruginosa increased NOS II mRNA and protein in rat AM and PMN. Pretreatment of rats with ETOH alone, or in combination with LNIL, inhibited P. aeruginosa-induced NOS II transcription and translation and AM and PMN nitrate and nitrite generation whereas pretreatment with LNIL alone only inhibited nitrate and nitrite generation. Pretreatment of rats with ETOH suppressed P. aeruginosa stimulated PMN recruitment into the lung whereas LNIL enhanced (p < 0.05) P. aeruginosa-stimulated PMN recruitment into the lung. ETOH-induced increases of the lung content of P. aeruginosa were associated with increased PKC delta isozyme in the membrane of the PMN but could not be explained by altered plasma concentrations of hydrocortisone or ETOH. The data demonstrate that selective inhibition of NOS II-derived NO by LNIL decreases the lung content of P. aeruginosa whereas ETOH inhibits the lung clearance of P. aeruginosa. Speculatively, the difference between these effects of LNIL and ETOH may result from differences in drug-induced changes in lung recruitment of PMN.

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