Columnar GaN nanostructures (GaN nanocolumns) were grown on Al2O3(0001) by RF-radical source molecular beam epitaxy (RF-MBE) through a self-organization process. The nanocolumns were grown at high density, with the c-axis maintained perpendicular to the substrate surface. The dependence of column diameter and density on growth conditions was systematically investigated. The average diameter was minimized to 53 nm and the density of the GaN nanocolumns was 130×1012 columns per square meter.

Statins are known to lessen the severity of renal ischemia-reperfusion injury. The present study was undertaken to define the mechanism of renoprotective actions of statins using a mouse kidney injury model. Treatment of mice with pravastatin, a widely used statin, improved renal function after renal ischemia-reperfusion without lowering the plasma cholesterol level. Administration of pravastatin with mevalonate, a product of HMG-CoA reductase, eliminated renal protection suggesting an effect of pravastatin on mevalonate or its metabolism. In hypercholestrolemic apolipoprotein E knockout mice with reduced HMG-CoA reductase activity; the degree of injury was less severe than in control mice, however, there was no protective action of pravastatin on renal injury in the knockout mice. Treatment with a farnesyltransferase inhibitor (L-744832) mimicked pravastatin's protective effect but co-administration with the statin provided no additional protection. Both pravastatin and L-744832 inhibited the injury-induced increase in plasma IL-6 concentration to a similar extent. Our results suggest the protective effect of pravastatin on renal ischemia-reperfusion injury is mediated by inhibition of the mevalonate-isoprenoid pathway independent of its lipid lowering action.

The hypoglossal canals are an unusual location for dural arteriovenous fistulas (AVFs) to appear. One previous report of dural AVFs involving the hypoglossal canal has been published. In the present paper, the authors describe a dural AVF within the hypoglossal canal, which presented with ocular symptoms and was successfully treated by selective transvenous embolization. Magnetic resonance imaging and contralateral carotid arteriography were useful for determination of the exact location of the fistulous pouch, which was later packed with coils. Selective transvenous coil embolization with careful assessment of the location and pattern of the venous drainage of the dural AVF is a safe and effective treatment.

CD34(+) progenitors of human bone marrow are a rich source of mast cell progenitors capable of expressing granule and surface markers of mature mast cells in the presence of rhSCF and rhIL-6.

The high-density survival (HDS) assay was originally elaborated to assess cancer cell responses to therapeutic agents under the influence of intercellular communication. Here, we simplified the original HDS assay and studied its applicability for the detection of cellular radioresistance. We have recently defined clinically relevant radioresistant (CRR) cells, which continue to proliferate with daily exposure to 2 gray (Gy) of X-rays for more than 30 days in vitro. We established human CRR cell lines, HepG2-8960-R from HepG2, and SAS-R1 and -R2 from SAS, respectively. In an attempt to apply the HDS assay to detect radioresistance with clinical relevance, we simplified the original HDS assay by scoring the total number of surviving cells after exposure to X-rays. The modified HDS assay successfully detected radioresistance with clinical relevance. The modified HDS assay detected CRR phenotype, which is not always detectable by clonogenic assay. Therefore, we believe that the modified HDS assay presented in this study is a powerful tool to predict the effectiveness of fractionated radiotherapy against malignant tumors.