Hardness and Tensile Strength of Multifilamentary Metal-matrix Composite Superconductors for the Large Hadron Collider (LHC)

Conventional indentation hardness measurements to obtain load independent Vickers hardness values for the different phases in multifilamentary superconducting (SC) wires are described. The concept of composite hardness is validated for a binary metal-matrix metal-filament Nb-Ti/Cu composite wire. The tensile materials properties of the individual wire components are estimated from their indentation hardness. The potential and limitations of this approach are critically discussed, based on a comparison with tensile test results obtained for wires and extracted Nb-Ti filaments

Sex differences in age-related decline of urinary insulin-like growth factor-binding protein-3 levels in adult bonobos and chimpanzees

There is increasing interest in the characterization of normative senescence in humans. To assess to what extent aging patterns in humans are unique, comparative data from closely-related species, such as non-human primates, can be very useful. Here we use data from bonobos and chimpanzees, two closely-related species that share a common ancestor with humans, to explore physiological markers that are indicative of aging processes. Many studies on aging in humans focus on the somatotropic axis, consisting of growth hormone (GH), insulin-like growth factors (IGFs), and IGF binding proteins (IGFBPs). In humans, IGFBP-3 levels decline steadily with increasing age. We used urinary IGFBP-3 levels as an alternative endocrine marker for IGF-I, to identify the temporal pattern known to be related with age-related changes in cell proliferation, growth, and apoptosis. We measured urinary IGFBP-3 levels in samples from 71 bonobos and 102 chimpanzees. Focusing on samples from individuals aged ten years or older we found that urinary IGFBP-3 levels decline in both ape species with increasing age. However, in both species, females start with higher urinary IGFBP-3 levels than males, experience a steeper decline with increasing age, and converge with male levels around the age of 30 to 35 years. Our measurements of urinary IGFBP-3 levels indicate that bonobos and chimpanzees mirror human patterns of age-related decline in IGFBP-3 in older individuals (< 10 years) of both sexes. Moreover, like humans, both ape species show sex-specific differences in IGFBP-3 levels with females having higher levels than males, a result that correlates with sex-differences in life expectancy. Using changes in urinary IGFBP-3 levels as a proxy for changes in GH and IGF-I levels that mark age-related changes in cell proliferation, this approach provides an opportunity to investigate trade-offs in life history strategies in cross-sectional and in longitudinal studies, both in captivity and in the wild

Mineralocorticoid receptor antagonism attenuates vascular apoptosis and injury via rescuing protein kinase B activation

This article may also be found at the publisher's website at http://hyper.ahajournals.org/cgi/content/abstract/53/2/158?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=habibi&searchid=1&FIRSTINDEX=0&resourcetype=HWCITEmerging evidence indicates that mineralocorticoid receptor (MR) blockade reduces the risk of cardiovascular events beyond those predicted by its blood pressure-lowering actions; however, the underlying mechanisms remain unclear. To investigate whether protection elicited by MR blockade is through attenuation of vascular apoptosis and injury, independently of blood pressure lowering, we administered a low dose of the MR antagonist spironolactone or vehicle for 21 days to hypertensive transgenic Ren2 rats with elevated plasma aldosterone levels. Although Ren2 rats developed higher systolic blood pressures compared with Sprague-Dawley littermates, low-dose spironolactone treatment did not reduce systolic blood pressure compared with untreated Ren2 rats. Ren2 rats exhibited vascular injury as evidenced by increased apoptosis, hemidesmosome-like structure loss, mitochondrial abnormalities, and lipid accumulation compared with Sprague-Dawley rats, and these abnormalities were attenuated by MR antagonism. Protein kinase B activation is critical to vascular homeostasis via regulation of cell survival and expression of apoptotic genes. Protein kinase B serine473 phosphorylation was impaired in Ren2 aortas and restored with MR antagonism. In vivo MR antagonist treatment promoted antiapoptotic effects by increasing phosphorylation of BAD serine136 and expression of Bcl-2 and Bcl-xL, decreasing cytochrome c release and BAD expression, and suppressing caspase-3 activation. Furthermore, MR antagonism substantially reduced the elevated NADPH oxidase activity and lipid peroxidation, expression of angiotensin II, angiotensin type 1 receptor, and MR in Ren2 vasculature. These results demonstrate that MR antagonism protects the vasculature from aldosterone-induced vascular apoptosis and structural injury via rescuing protein kinase B activation, independent of blood pressure effects

The use of a proximal femoral nail as a hip prosthesis: A biomechanical analysis of a newly designed implant

Complication rates of hip fractures after proximal femoral nail are not rare. In such fractures, treatment invariably comprises the extraction of proximal femoral nail and the introduction of a different hip prosthesis. To solve this problem, we aimed to develop a new implant, the modular nail prosthesis, which combines an intramedullary nail with a hip prosthesis. The aim of this study was to determine the effect of stress load distribution on the stem using finite element analysis under laboratory conditions. For this, the shortest stem of 175 mm was chosen. In addition, six proximal femoral nail–hip prosthesis combinations were produced and tested with a biomechanical test device and passed 2300-N load bearing. According to the test results, our newly developed modular nail prosthesis can be converted to hip prosthesis securely.Afyon Kocatepe University Scientific Research Project Coordination Unit[15.TIP.07] ; Turkish Orthopaedic Research Council (subdivision of Turkish Society of Orthopaedics and Traumatology)[23

Direct Renin Inhibition Improves Systemic Insulin Resistance and Skeletal Muscle Glucose Transport in a Transgenic Rodent Model of Tissue Renin Overexpression

Renin is the rate-limiting enzyme in renin-angiotensin system (RAS) activation. We sought to determine the impact of renin inhibition on whole-body insulin sensitivity and skeletal muscle RAS, oxidative stress, insulin signaling, and glucose transport in the transgenic TG(mRen2)27 rat (Ren2), which manifests increased tissue RAS activity, elevated serum aldosterone, hypertension, and insulin resistance. Young (aged 6–9 wk) Ren2 and age-matched Sprague Dawley control rats were treated with aliskiren [50 mg/kg · d, ip] or placebo for 21 d and administered an ip glucose tolerance test. Insulin metabolic signaling and 2-deoxyglucose uptake in soleus muscle were examined in relation to tissue renin-angiotensin-aldosterone system [angiotensin (Ang) II, mineralocorticoid receptor (MR), and Ang type I receptor (AT1R)] and measures of oxidative stress as well as structural changes evaluated by light and transmission electron microscopy. Ren2 rats demonstrated systemic insulin resistance with decreased skeletal muscle insulin metabolic signaling and glucose uptake. This was associated with increased Ang II, MR, AT1R, oxidative stress, and reduced tyrosine insulin receptor substrate-1 phosphorylation, protein kinase B/(Akt) phosphorylation and glucose transporter-4 immunostaining. The Ren2 also demonstrated perivascular fibrosis and mitochondrial remodeling. Renin inhibition improved systemic insulin sensitivity, insulin metabolic signaling, and glucose transport along with normalization of Ang II, AT1R, and MR levels, oxidative stress markers, fibrosis, and mitochondrial structural abnormalities. Our data suggest that renin inhibition improves systemic insulin sensitivity, skeletal muscle insulin metabolic signaling, and glucose transport in Ren2 rats. This is associated with reductions in skeletal muscle tissue Ang II, AT1R, and MR expression; oxidative stress; fibrosis; and mitochondrial abnormalities