Presence of cytomegalovirus in the perilymphatic fluid of patients with profound sensorineural hearing loss caused by congenital cytomegalovirus infection

Conclusion: Not all patients diagnosed with congenital infection using umbilical cord assay were found to be positive for CMV-DNA by perilymphatic fluid assay. In addition, a CMV-DNA-positive result was observed in one patient who had not been diagnosed with congenital infection. Sampling of perilymphatic fluid from a large population of patients with congenital SNHL caused by congenital CMV infection or of unknown etiology is required to determine the prevalence of CMV-related profound HL. Objectives: Sensorineural hearing loss (SNHL) is one of the most frequent manifestations in patients with congenital cytomegalovirus (CMV) infection. Using dried umbilical cord, a PCR-based assay was recently developed for the retrospective detection of congenital CMV infection. This study analyzed the presence of CMV in the perilymphatic fluid and evaluated differences in the effect of cochlear implantation between CMV-positive and -negative groups. Method: Perilymphatic fluid was collected from each patient at the time of cochlear implantation and analyzed for the presence of CMV using a PCR method. Results: The perilymphatic fluid in two of the five patients suffering from congenital CMV infection and in one of the 17 patients without congenital CMV infection was found to be positive for CMV.     

Retro-transduction by virus pseudotyped with glycoprotein of vesicular stomatitis virus

A virus pseudotyped with glycoprotein of vesicular stomatitis virus (VSV-G) can enter various cell types at a relatively high titer. We observed that the amount of viral antigen from VSV-G pseudotyped human immunodeficiency virus type 1 (HIV-1) producing cells was much higher than that from their non-pseudotyped counterparts. This enhanced viral antigen production was not observed when we used HIV-1 pol mutant, viral enzyme inhibitors, HIV Env protein, or VSV-G fusion defective mutants. The transfection experiment using GFP-expressing virus showed time-dependent expansion of GFP-positive cells and viral DNA integration. These results suggested that the increase in viral antigen yield was caused by the release of a progeny virus following retro-transduction by the pseudotyped virus of the cells within the transfected cell culture. The infectivity as well as the amount of VSV-G on virus particles per unit of viral antigen was significantly different before and after the onset of the yield enhancement. This suggests that results of infection assays of the virus pseudotyped with VSV-G may be affected by the occurrence of such enhancement. This means that, while pseudotyping with VSV-G is a simple and effective method, this procedure should be carefully considered when the virus is produced for infectivity assays.     

Requirement of apelin-apelin receptor system for oxidative stress-linked atherosclerosis

The recently identified endogenous peptide apelin and its specific apelin receptor (APJ) are currently being considered as potential regulators in vascular tissue. Previously, we reported apelin mediates phosphorylation of myosin light chain and elicits vasoconstriction in vascular smooth muscle. In this study, physiological roles of the apelin-APJ system were investigated on atherosclerosis. In APJ and apolipoprotein E double-knockout (APJ(-/-)ApoE(-/-)) mice fed a high-cholesterol diet, atherosclerotic lesions were dramatically reduced when compared with APJ(+/+) ApoE(-/-) mice, in the absence of an effect of cholesterol levels. Immunohistochemical detection of smooth muscle cells, using a smooth muscle alpha-actin antibody, showed greatly reduced staining for these cells in lesions of APJ(-/-)ApoE(-/-) mice fed a high-cholesterol diet. Vascular production of superoxide radicals and the expression of nicotinamide-adenine dinucleotide phosphate oxidase subunits were decreased in APJ(-/-)ApoE(-/-) mice compared with APJ(+/+)ApoE(-/-) mice fed a standard normal diet. In vascular smooth muscle cells, apelin induced nicotinamide-adenine dinucleotide phosphate oxidase subunit expression. Apelin also induced vascular smooth muscle cell proliferation, which was inhibited by superoxide dismutase or diphenylene iodonium. The apelin-APJ system is a mediator of oxidative stress in vascular tissue, and thus we propose it to be a critical factor in atherogenesis under high-cholesterol dietary conditions. APJ deficiency is preventative against oxidative stress-linked atherosclerosis.     

Renal damage in obstructive nephropathy is decreased in Skp2-deficient mice

Ubiquitin-dependent degradation of the cyclin-dependent kinase inhibitor p27 mediated by SCF-Skp2 ubiquitin ligase is involved in cell cycle regulation. Proliferation of tubular cells is a characteristic feature in obstructed kidneys of unilateral ureteral obstruction. Comparing Skp2(+/+) mice with Skp2(-/-) mice, we investigated the involvement of Skp2, a component of SCF-Skp2 ubiquitin ligase for p27, in the progression of renal lesions in unilateral ureteral obstructed kidneys. mRNA expression of Skp2 was markedly increased in the obstructed kidneys from Skp2(+/+) mice and peaked 3 days after unilateral ureteral obstruction. Renal atrophy, tubular dilatation, tubulointerstitial fibrosis, and increases in alpha-smooth muscle actin expression, the number of tubular cells, and proliferating tubular cells positive for Ki67 were observed in the obstructed kidneys from Skp2(+/+) mice; however, these findings were significantly attenuated in Skp2(-/-) mice. The p27 protein level was increased in the obstructed kidneys but was significantly greater in Skp2(-/-) mice. The number of Ki67-positive p27-negative cells was lower in obstructed kidneys from Skp2(-/-) mice than Skp2(+/+) mice, whereas that of Ki67-negative p27-positive cells was greater in Skp2(-/-) mice. These findings suggest that p27 accumulation, which results from SCF-Skp2 ubiquitin ligase deficiency in Skp2(-/-) mice, is involved in the amelioration of renal damage induced by obstructive nephropathy.     

Anatomical names of skeletal surfaces: analysis and classification of Latin names, and comparison with corresponding Japanese names

For better understanding of the structures comprising the human body and in view of possible need for future revision, Latin anatomical names (Terminologia Anatomica) of the skeletal surfaces were analyzed and classified, and compared with the corresponding Japanese anatomical names. The words following Facies indicated: 1) morphological resemblance of the surface; 2) the structure that articulates with the surface; 3) the structure attached to the surface; 4) the structure in contact with the surface; 5) the way of connection between the surface and the structure that faces it; 6) the structure of which the surface is a component; 7) the structure that the surface faces; 8) the site that the surface faces; 9) the relative position of the surface; 10) the non-relative position of the surface; 11) an articulation of the surface; or 12) both the structure with which the surface articulates and the structure of which the surface is a component. Analysis of Latin names and comparison with Japanese names clarified some characteristics of both names and revealed some problems in them.