The effect of moderate alcohol consumption on adiponectin oligomers and muscle oxidative capacity: a human intervention study

Aims/hypothesis The aim of this study was to investigate whether moderate alcohol consumption increases plasma high molecular weight (HMW) adiponectin and/or muscle oxidative capacity. Materials and methods Eleven lean (BMI 18 - 25 kg/m(2)) and eight overweight ( BMI >= 27 kg/m(2)) men consumed 100 ml whisky (similar to 32 g alcohol) or water daily for 4 weeks in a randomised, controlled, crossover trial. After each treatment period, muscle biopsies and fasting blood samples were collected. Results Adiponectin concentrations increased ( p <0.001) by 12.5% after 4 weeks of moderate alcohol consumption. Moderate alcohol consumption tended to increase HMW adiponectin by 57% ( p= 0.07) and medium molecular weight adiponectin by 12.5% ( p= 0.07), but not low molecular weight (LMW) adiponectin. Skeletal muscle citrate synthase, cytochrome c oxidase and beta-3-hydroxyacyl coenzyme A dehydrogenase (beta-HAD) activity were not changed after moderate alcohol consumption, but an interaction between alcohol consumption and BMI was observed for cytochrome c oxidase ( p= 0.072) and citrate synthase ( p= 0.102) activity. Among lean men, moderate alcohol consumption tended to increase cytochrome c oxidase ( p= 0.08) and citrate synthase activity ( p= 0.12) by 23 and 26%, respectively, but not among overweight men. In particular, plasma HMW adiponectin correlated positively with activities of skeletal muscle citrate synthase ( r= 0.64, p= 0.009), cytochrome c oxidase ( p= 0.59, p= 0.009) and beta-HAD ( r= 0.46, p= 0.056), while such correlation was not present for LMW adiponectin. Whole-body insulin sensitivity and intramyocellular triacylglycerol content were not affected by moderate alcohol consumption. Conclusions/interpretation Moderate alcohol consumption increases adiponectin concentrations, and in particular HMW adiponectin. Concentrations of HMW adiponectin in particular were positively associated with skeletal muscle oxidative capacity

Fatigue strength of nodular cast iron with different surface conditions under bending loading

The aim of this study is to evaluate the effects of surface conditions on the fatigue life of nodular cast iron under cyclic plane bending where the maximum stress is reached at the surface of interest. In order to evaluate the effect of surface conditions, fatigue tests were carried out on five sets of specimens with different surfaces. The surface conditions were as-cast, sand blasted, fine grinded, nitrided and carbonitrided. The results show differences in fatigue strength, which are associated with the surface conditions. The characteristics of the surface layers in the different test specimens were examined by metallography. The fracture surfaces were fractographically analyzed to find places of fatigue crack initiation and to explain different fatigue life

Biochemical analysis of the living human vitreous

Background: To date, our understanding of the biochemical composition of the living human vitreous relies on extrapolations from animal or human post-mortem studies. Methods: This was a cross-sectional study of vitreous samples from 27 individuals scheduled for retinal surgery within a tertiary hospital. From each vitreous sample, the concentrations of sodium, potassium, chloride, calcium, magnesium, glucose, lactate, β- hydroxybutyrate, copper, zinc, selenium, iron, ferritin and transferrin and osmolality were measured. Perioperative serum samples were also obtained for comparison. Results: The following vitreous mean ± standard deviation (95% confidence interval of the mean) was observed for each analyte: sodium, 146.7 ± 3.3 (145.4–148.0) mmol/L; potassium, 5.73 ± 0.86 (5.39–6.08) mmol/L; chloride, 121.6 ± 2.6 (120.6–122.7) mmol/L; calcium, 1.128 ± 0.518 (0.923–1.333) mmol/L; magnesium, 0.900 ± 0.158 (0.838–0.962) mmol/L; glucose, 2.97 ± 0.98 (2.58–3.36) mmol/L; lactate, 3.97 ± 1.09 (3.54–4.40) mmol/L; osmolality, 289.5 ± 6.9 (286.6–292.5) mOsm/kg; BOHB, 0.0937 ± 0.0472 (0.0750–0.1124) mmol/L; copper, 0.519 ± 0.269 (0.412–0.625) µmol/L; zinc, 1.95 ± 1.09 (1.52–2.38) µmol/L; selenium, 0.1035 ± 0.0276 (0.0923–0.1146) µmol/L; iron, 3.11 ± 1.40 (2.56–3.66) µmol/L; ferritin, 19.5 ± 10.3 (15.5–23.6) µg/L; transferrin, 0.0878 ± 0.0526 (0.0670–0.1086) g/L. Vitreous biochemistry was not significantly different between male and female participants. Vitreous biochemistry was significantly different between non-diabetic and diabetic participants. Vitreous biochemistry was significantly different from the vitreous substitute BSS Plus (Alcon, USA). The vitreous extracted from living humans was markedly different from the commonly reported reference values obtained from animal studies. Conclusions: The current data provide hitherto unavailable information about the biochemical composition of the living human vitreous.Jan Kokavec, San H Min, Mei H Tan, Jagjit S Gilhotra, Henry S Newland Shane R Durkin John Grigg, Robert J Casso

Goldenhar syndrome: a cause of secondary immunodeficiency?

<p>Abstract</p> <p>Goldenhar syndrome (GS) results from an aberrant development of the 1^st and 2^nd branchial arches. There is a wide range of clinical manifestations, the most common being microtia, hemifacial microsomia, epibulbar dermoids and vertebral malformations. We present two cases of GS and secondary immunodeficiency due to anatomical defects characteristic of this disorder. Case 1 (3-year-old female) averaged 6 episodes of sinusitis and otitis media per year. Case 2 (7-year-old female) also had recurrent otitis media, an episode of bacterial pneumonia, and 2 episodes of bacterial meningitis. Their immune evaluation included a complete blood count with differential, serum immunoglobulin levels and specific antibody concentrations, lymphocyte phenotyping, and mitogen and antigen responses, the results of which were all within normal ranges. Both children demonstrated major structural abnormalities of the inner and middle ear structures, retention of fluid in mastoid air cells, and chronic sinusitis by computed tomography. These two cases illustrate how a genetically-associated deviation of the middle ear cleft can cause recurrent infections and chronic inflammation of the middle ear and adjacent sinuses, even meninges, leading to a greatly reduced quality of life for the child and parents.</p