Scanning Electron Microscopic Studies on Microvascular Architecture of Human Coronary Vessels by Corrosion Casts: Normal and Focal Necrosis

Microvascular architecture of the normal human heart and myocardial focal necrosis were studied by scanning electron microscopy of corrosion casts. Casts macroscopically identical in form to the left ventricular posterior wall were prepared. The following results were obtained in the normal human heart. (I) Most of the arterioles communicated with capillary plexuses smoothly and straight forwardly in the left ventricular posterior free wall. (2) Arterioles which branched from the arteries ran in various directions and continued into capillaries either at right angles or obliquely in the trabeculae carneae. (3) capillaries running parallel with the cardiac muscle fibers ran in different directions to cross over with each other in different layers of myocardium. Capillaries in the myocardium formed a continuous and coarse net-like architecture with many bifurcations and anastomoses. Capillaries were about 5-7 μm in diameter. (4) Some veins gathering capillaries in the epicardium ran into the myocardium and the others ran in the epicardium. Veins connecting with capillaries in the myocardium ran in the myocardial layer and communicated with larger veins. (5) An arteriovenous anastomosis and two different types of venous-venous anastomoses were observed in the left ventricular posterior wall. At the site of focal necrosis, cross sections of dilated vessels were observed in large numbers by light microscopy and scanning electron microscopy. (I) At the site of focal necrosis, dilated capillaries running with tortuosity were seen in large numbers by scanning electron microscopy of corrosion casts. (2) When compared with vessels in the normal myocardium, small arterial branches were dilated and run tortuously. (3) These dilated capillary plexuses were observed in the area which communicated with twigs branching off at the right angle from the arterial branch

Mild Electrical Stimulation with Heat Shock Ameliorates Insulin Resistance via Enhanced Insulin Signaling

Low-intensity electrical current (or mild electrical stimulation; MES) influences signal transduction and activates phosphatidylinositol-3 kinase (PI3K)/Akt pathway. Because insulin resistance is characterized by a marked reduction in insulin-stimulated PI3K-mediated activation of Akt, we asked whether MES could increase Akt phosphorylation and ameliorate insulin resistance. In addition, it was also previously reported that heat shock protein 72 (Hsp72) alleviates hyperglycemia. Thus, we applied MES in combination with heat shock (HS) to in vitro and in vivo models of insulin resistance. Here we show that 10-min treatment with MES at 5 V (0.1 ms pulse duration) together with HS at 42°C increased the phosphorylation of insulin signaling molecules such as insulin receptor substrate (IRS) and Akt in HepG2 cells maintained in high-glucose medium. MES (12 V)+mild HS treatment of high fat-fed mice also increased the phosphorylation of insulin receptor β subunit (IRβ) and Akt in mice liver. In high fat-fed mice and db/db mice, MES+HS treatment for 10 min applied twice a week for 12–15 weeks significantly decreased fasting blood glucose and insulin levels and improved insulin sensitivity. The treated mice showed significantly lower weight of visceral and subcutaneous fat, a markedly improved fatty liver and decreased size of adipocytes. Our findings indicated that the combination of MES and HS alleviated insulin resistance and improved fat metabolism in diabetes mouse models, in part, by enhancing the insulin signaling pathway

Coexistence of charge order and antiferromagnetism in (TMTTF)(2)SbF6: NMR study

The electronic state of (TMTTF)(2)SbF6 was investigated by the H-1 and C-13 NMR measurements. The temperature dependence of T-1(-1) in H-1 NMR shows a sharp peak associated with the antiferromagnetic transition at T-AF = 6 K. The temperature dependence of T-1(-1) is described by the power law T-2.4 below T-A. This suggests the nodal gapless spin wave excitation in antiferromagnetic phase. In 13C NMR, two sharp peaks at high temperature region, associated with the inner and the outer carbon sites in TMTTF dimer, split into four peaks below 150 K. It indicates that the charge disproportionation occurs. The degree of charge disproportionation Delta rho is estimated as (025 +/- 0.09)e from the chemical shift difference. This value Delta rho is consistent with that obtained from the infrared spectroscopy. In the antiferromagnetic state (AFI), the observed line shape is well fitted by eight Lorentzian peaks. This suggests that the charge order with the same degree still remains in the AF state. From the line assignment, the AF staggered spin amplitude is obtained as 0.70 mu(B) and 0.24 mu(B) at the charge rich and the poor sites, respectively. These values corresponding to almost 1 mu(B) per (timer are quite different from 0.11 mu(B) of another AF (AFII) state in (TMITF)(2)Br with effective higher pressure. As a result, it is understood that the antiferromagnetic staggered spin order is stabilized on the CO state in the AFI phase of (TMTTF)2(S)bF(6)