E-cadherin expression in a particular subset of sensory neurons.

We found that the dorsal root ganglia (DRG) and trigeminal ganglia of mouse embryos express the E-cadherin cell-cell adhesion molecule and analyzed its expression profile. E-cadherin expression began around Embryonic Day 12 (E12) in these ganglia, thereafter increased, and persisted to the adult stage. This cadherin was expressed by 10 and 30% of DRG neurons in E17 and postnatal animals, respectively, as well as by satellite cells and some Schwann cells. E-cadherin-positive primary sensory fibers terminated only in a narrow region of the dorsal horn of the spinal cord, which was identified as part of lamina II by double-staining for E-cadherin and substance P or somatostatin. This E-cadherin expressing area of the spinal cord extended to part of the trigeminal nucleus in the medulla. These results showed that E-cadherin is expressed in a particular subset of primary sensory neurons which may have specific functional properties. We suggest that this adhesion molecule may play a role in the selective adhesion of sensory neuronal fibers.     

Efficacy of olmesartan and nifedipine on recurrent hypoxia-induced left ventricular remodeling in diabetic mice

AimsRecurrent hypoxia due to sleep apnea syndrome is implicated in cardiovascular events, especially in diabetic patients, but the underlying mechanisms remain controversial. We previously reported that angiotensin II receptor blockers can improve hypoxia-induced left ventricular remodeling. The aim of this study was to examine the effect on left ventricular remodeling of adding a calcium channel blocker to angiotensin II receptor blocker therapy in diabetic mice exposed to recurrent hypoxia.Main methodsMale db/db mice (8-week-old) and age-matched control db/+ mice were fed a Western diet and subjected to recurrent hypoxia (oxygen at 10 ± 0.5% for 8 h daily during the daytime) or normoxia for 3 weeks. Hypoxic db/db mice were treated with the vehicle, olmesartan (3 mg/kg/day), nifedipine (10 mg/kg/day), or both drugs.Key findingsRecurrent hypoxia caused hypertrophy of cardiomyocytes, interstitial fibrosis, and a significant increase in expression of the oxidative stress marker 4-hydroxy-2-nonenal (4-HNE) in the left ventricular myocardium. Treatment with olmesartan, nifedipine, or both drugs had no effect on systolic blood pressure, and each treatment achieved similar suppression of 4-HNE expression. Olmesartan and the combination with olmesartan and nifedipine significantly prevented cardiomyocyte hypertrophy more than treatment with nifedipine alone. On the other hand, olmesartan combined with nifedipine significantly reduced cytokine expression, superoxide production and matrix metalloproteinase (MMP)-9 activity, and significantly suppressed interstitial fibrosis in the left ventricular myocardium.SignificanceThe combination with olmesartan and nifedipine, as well as a monotherapy with olmesartan, exerts preferable cardioprotection in diabetic mice exposed to recurrent hypoxia.     

Augmentation and Suppression of TNF Release from Macrophages by Inflammatory Polymorphonuclear Leukocytes

It is known that polymorphonuclear leukocytes (PMNs) emerge first in local inflammatory sites, and then they are followed and scavenged by macrophages. We focused on the effect of PMN on tumor necrosis factor (TNF) release activity of macrophages, which is viewed as a possible indicator of the status of macrophage activation. One day after macrophages were cultured with fresh, intact murine PMNs which were induced with sodium casein, the release of TNF triggered by lipopolysaccharide (LPS) was augmented by low concentrations of PMNs, but suppressed by their high concentrations. When the PMN samples were fractionated into soluble and insoluble fractions, the augmenting and suppressing activity was partitioned; the relatively high concentrations of soluble fraction showed the suppressive effect whereas the insoluble fraction in lower concentrations showed augmentation. The suppressive activity was stable at 100 C, but the filtrates of the soluble fraction with membranes having cut-offs of 5,000 or 10,000 were not suppressive at all, suggesting the suppression is not due to low molecular compounds. It was also suggested that the suppressive effect for TNF release was not due to contaminating LPS or transforming growth factor-β. Inflammatory processes may thus be positively and negatively controlled by a quantitative factor of initial PMN populations by regulating the TNF release activity of the subsequent macrophages.     

Occurrence of autoimmune antibodies to liver microsomal proteins in association with fulminant hepatitis in the LEC strain of rats

The Long Evans Cinnamon (LEC) rat, which has been established as a strain showing hereditary hepatitis and hepatic carcinoma, was found to possess autoimmune antibodies to liver microsomal proteins, particularly to a protein with the molecular weight of 56kD. The antibodies also recognized a protein(s) in liver microsomes from Long Evans Agouti and Sprague-Dawley rats. About 42 and 15 percent of respective female and male LEC rats died within a week after acute hepatitis; sera from all of the animals contained the antibodies. About 43 and 0 percent of the surviving female and male LEC rats possessed the antibodies, respectively. These results suggest that the autoantibodies occur in association with acute lethal hepatitis in the LEC rats.     

Cell-Cell adhesion molecule: Identification of a glycoprotein relevant to the Ca2+-independent aggregation of chinese hamster fibroblasts

Molecules making up the Ca²⁺-independent cell-cell adhesion sites (CIDS) of Chinese hamster V79 cells have been investigated. Previous studies showed that Fab fragments (Fab) of the antibody raised against the surface of V79 cells inhibit the Ca²⁺-independent aggregation of V79 cells, and that this inhibitory effect is neutralized by the addition of some proteinous substance released from the surface of V79 cells treated with 0.01% trypsin. In the present study, we found that the antibody raised against this substance (anti-TRF) displays the complement-dependent cytotoxicity more strongly to the cells with active CIDS than to those without it. The Fab of this antibody inhibited the Ca²⁺-independent aggregation of V79 cells strongly, particularly in the presence of a hyaluronidase. Electrophoresis of the materials immunoprecipitated with anti-TRF from lysates of cells labeled with radioactive iodine, monosaccharides or methionine showed that a glycoprotein with a molecular weight of 125,000 is the only component to react with this antibody in cells with the active CIDS. Indirect immunofluorescence of anti-TRF showed that the antigens are distributed over the entire surface of V79 cells, and are present only in fibroblastic cells in the primary culture of Chinese hamster hepatic cells. These results suggest that the glycoprotein with a molecular weight of 125,000 has a specific role in the Ca²⁺-independent adhesion of Chinese hamster fibroblastic cells.     

Spontaneous rosette formation of rat thymus cells with guinea pig erythrocytes.

C57 black mice were immunised intraperitoneally with a DBA2 lymphoma (SL2). Fourteen days later spleen cells were prepared. These cells lysed the specific target (SL2) in vitro. Spleen cells were cultured for 24 hr at 37 ° C. Cell-free culture supernatants contained IgG and lysed SL2 cells either in the presence of a source of complement or in the presence of a monolayer of macrophages (a good source of antibody-dependent effectors). The cells producing cell-dependent antibody adhered to nylon wool and were unaffected by anti-theta serum. It was found that the production of antibody in vitro did not make a significant contribution to the observed cytolysis of SL2 by sensitised spleen cells. This effect was mediated by thymus-derived lymphocytes.     

Chitosan staple fibers and their chemical modification with some aldehydes

Nine wet-spinning conditions were examined for the preparation of chitosan staple fibers, and novel five N-alkylidene and N-arylidene-chitosan staple fibers were obtained by the post-treatment of the chitosan fibers with aldehydes including vanillin. The tenacity and elongation values of the chitosan filaments were almost unchanged by their post-treatment with monoaldehydes except that with formaldehyde and glyoxal. However, these values decreased significantly in the partially N-modified filaments, which were obtained by the pre-treatment with vanillin. The chitosan filaments (31–79 μm in diameter) had a scaly structure on the filament surface as examined by SEM observation.