Preferential macrophage infiltration into OM fat is a general phenomenon exaggerated by central obesity, potentially linking central adiposity with increased risk of diabetes and coronary heart disease.
Efforts to develop metallic zinc for biodegradable implants have significantly advanced following an earlier focus on magnesium (Mg) and iron (Fe). Mg and Fe base alloys experience an accelerated corrosion rate and harmful corrosion products, respectively. The corrosion rate of pure Zn, however, may need to be modified from its reported~20 µm/year penetration rate, depending upon the intended application. The present study aimed at evaluating the possibility of using Fe as a relatively cathodic biocompatible alloying element in zinc that can tune the implant degradation rate via microgalvanic effects. The selected Zn-1.3wt %Fe alloy composition produced by gravity casting was examined in vitro and in vivo. The in vitro examination included immersion tests, potentiodynamic polarization and impedance spectroscopy, all in a simulated physiological environment (phosphate-buffered saline, PBS) at 37 • C. For the in vivo study, two cylindrical disks (seven millimeters diameter and two millimeters height) were implanted into the back midline of male Wister rats. The rats were examined post implantation in terms of weight gain and hematological characteristics, including red blood cell (RBC), hemoglobin (HGB) and white blood cell (WBC) levels. Following retrieval, specimens were examined for corrosion rate measurements and histological analysis of subcutaneous tissue in the implant vicinity. In vivo analysis demonstrated that the Zn-1.3%Fe implant avoided harmful systemic effects. The in vivo and in vitro results indicate that the Zn-1.3%Fe alloy corrosion rate is significantly increased compared to pure zinc. The relatively increased degradation of Zn-1.3%Fe was mainly related to microgalvanic effects produced by a secondary Zn 11 Fe phase.
MAPKs and inhibitory-kappaB kinase (IKK) were suggested to link various conditions thought to develop in adipose tissue in obesity (oxidative, endoplasmic reticulum stress, inflammation) with insulin resistance. Yet whether in obesity these kinases are affected in a fat-depot-differential manner is unknown. We assessed the expression and phosphorylation of these kinases in paired omental and abdominal-sc fat biopsies from 48 severely obese women (body mass index > 32 kg/m(2)). Protein and mRNAs of p38MAPK, ERK, c-Jun kinase-1, and IKKbeta were increased 1.5-2.5-fold in omental vs. sc fat. The phosphorylated (activated) forms of these kinases were also increased to similar magnitudes as the total expression. However, phosphorylation of insulin receptor substrate-1 on Ser312 (equivalent of murine Ser307) was not increased in omental, compared with sc, fat. Consistently, fat tissue fragments stimulated with insulin demonstrated that tyrosine phosphorylation and signal transduction to Akt/protein kinase B in omental fat was not inferior to that observable in sc fat. Comparison with lean women (body mass index 23.2 +/- 2.9 kg/m(2)) revealed similar ERK2 and IKKbeta expression and phosphorylation in both fat depots. However, as compared with lean controls, obese women exhibited 480 and 270% higher amount of the phosphorylated forms of p38MAPK and c-Jun kinase, respectively, in omental, but not sc, fat, and this expression level correlated with clinical parameters of glycemia and insulin sensitivity. Increased expression of stress-activated kinases and IKK and their phosphorylated forms in omental fat occurs in obesity, potentially contributing to differential roles of omental and sc fat in the pathophysiology of obesity.
The aim of the this study is to evaluate the in vivo behavior of Mg-1.5%Nd-0.5%Y-0.5%Zr implants with and without 0.4%Ca in comparison with inert Ti-6Al-4V reference implants. This was carried out by implanting cylindrical disks at the back midline of Wister male rats within the subcutaneous layer of the skin for up to 12 weeks. The degradation of magnesium-based implants in terms of hydrogen gas bubble formation was evaluated by radiography assessment; corrosion rate was analyzed by visual examination and weight loss measurements. The physiological response of the rats post-implantation was obtained by evaluating their wellbeing behavior and blood biochemical analysis including serum Mg, blood urea nitrogen, and serum creatinine. In addition, histological analyses of the soft tissue around the implants were carried out to assess local lesions relating to the implants such as inflammation, tissue necrosis, granulation, mineralization, and tumor development. The results obtained clearly indicate that apart from the normal degradation characteristics and subsequent formation of hydrogen gas bubbles, the in vivo behavior of Mg implants was adequate and comparable to that of Ti-6Al-4V reference alloy. In addition, it was evident that the corrosion degradation of the magnesium alloys was strongly related to the location of the implant within the animal's body. The addition of 0.4%Ca improves the biodegradation corrosion resistance of the tested magnesium implants.
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