Exacerbation by nicotine of the cyclosporine A-induced impairment of beta-adrenoceptor-mediated renal vasodilation in rats

Nicotine is implicated in smoking-related renovascular impairment and worsening of existing nephropathies. In the present study, we investigated whether nicotine aggravates the deleterious effect of the immunosuppressant drug cyclosporine A (CsA) on renal vasodilation induced by the beta-adrenoceptor agonist isoprenaline. Bolus isoprenaline (0.03-8.0 micromol) elicited dose-dependent vasodilation of phenylephrine-preconstricted perfused kidneys that was attenuated by infusion at 5 mL/min of nicotine (5 x 10(-4) mol/L) or CsA (2 micromol/L). Further, chronic administration of nicotine (0.4 mg/kg per day) or CsA (20 mg/kg per day) for 3 weeks reduced isoprenaline-induced vasodilation and elevated plasma urea and creatinine concentrations, effects that were magnified when both nicotine and CsA were administered concurrently. The role of endothelial and smooth muscle signalling in the acute nicotine/CsA renovascular interaction was investigated. Vasodilation caused by 0.25 micromol isoprenaline was attenuated by 6 micromol/L propranolol and 10 mmol/L tetraethylammonium (TEA), potentiated by 100 micromol/L hexamethonium and 7 micromol/L diclophenac, and virtually abolished in 80 mmol/L KCl-preconstricted tissues. N(G)-Nitro-L-arginine (L-NNA; 200 micromol/L), methylene blue (10 micromol/L), 3-[(3-cholamidopropyl)-dimethyl-ammonio]-1-propane-sulphonate (CHAPS; 0.2% for 30 s), nifedipine (750 nmol/L), atropine (1 micromol/L) and SQ22536 (an adenylyl cyclase inhibitor; 3 x 10(-5) mol/L) had no effect on isoprenaline responses. Nicotine (5 x 10(-4) mol/L) reduced isoprenaline-induced vasodilation and this effect was potentiated by concurrent CsA (2 micromol/L) infusion. Nicotine-induced impairment of the vasodilator response to isoprenaline was reduced by hexamethonium and potentiated by L-NNA, methylene blue, CHAPS and nifedipine. Alternatively, CsA exacerbation of the nicotine-isoprenaline interaction was abolished by propranolol, L-NNA, methylene blue, CHAPS, L-arginine, TEA and nifedipine. 5. In summary, nicotine and CsA produce additive impairment of kidney function and beta-adrenoceptor-mediated renovascular control, nitric oxide (NO)-cGMP signalling tonically restrains nicotine-induced impairment of isoprenaline vasodilation and the endothelial NO-K+ pathway modulates the aggravating effect of CsA on nicotine-isoprenaline interactions.     

Wear of human enamel and nano-filled composite resin denture teeth under different loading forces

Summary  To evaluate and correlate the two-body wear of human enamel and nano-filled composite resin teeth with the loading forces used in a dual-axis chewing simulator. Three groups of human enamel and three of nano-filled composite resin teeth were tested in a chewing simulator. Zirconia ceramic balls were used as antagonists. The teeth were tested with three different loading forces (20, 49 and 78 N). Wear was analysed by measuring the volume and vertical substance loss using a laser scanner after 300000 chewing cycles. Data were statistically analysed using two-way anova followed by the Scheffé test ( P  ≤ 0·05). Spearman correlation test was used to determine whether there was a relationship between the loading force and the degree to which the human enamel and composite resin had worn. An increase in the loading force significantly increased the wear of composite resin and of human enamel. The effect of the loading force on the wear was statistically significant at the 0·001 level. Human enamel showed a lower volume and vertical substance loss than composite resin under loading forces of 20 and 49 N and lower vertical loss under loading force of 78 N. The correlation between the volume loss and loading force was statistically significant ( r  = 0·616, P  < 0·001). Nano-filled composite resin and human enamel exhibited different amount of wear under different loading forces. In general, human enamel showed less vertical substance loss than nano-filled composite resin.     

Hand-assisted Laparoscopic Colorectal Surgery: Initial Experience of a Single Surgeon

Background/Aim:

As totally laparoscopic colorectal surgery is considered challenging and technically demanding with a long steep learning curve, we adopted hand-assisted laparoscopic colorectal surgery as a bridge to totally laparoscopic assisted colorectal surgery. This prospective study aims to highlight the initial experience of a single surgeon with this technique.

Materials and Methods:

A prospective analysis of the first 25 cases of hand-assisted laparoscopic colorectal resections which were performed by a single surgeon over a 15-month period. There were 15 males and 10 females with a mean age of 55.5 (range 20-82) years.

Results:

The indication in majority of cases was cancer (76%). The procedures consisted of 18 (72%) various colectomies and 7 (28%) anterior resections. The operative time ranged between 110-400 (mean 180) min. There was one conversion (4%) and the mean operative blood loss was 80 (range 60-165) ml. The number of lymph nodes retrieved in the cancer cases was 5-31 (mean 15) nodes. The mean length of hospital stay was five (range 3-10) days. The total number of short-term complications was six (24%) and there was one death due to anastomatic leak and multiorgan failure. Long-term complications after a maximum follow up of 30 months were two incisional hernias at the hand port site, but none of the patients developed adhesive small bowel obstruction or late anastomotic stricture. Currently all our colorectal procedures are conducted laparoscopically.

Conclusion:

Hand-assisted laparoscopic colorectal procedures are easy to learn as a good bridge to master totally laparoscopic colorectal surgery.     

The role of CXCR4 signaling in the migration of transplanted oligodendrocyte progenitors into the cerebral white matter

Enhancing the ability of either endogenous or transplanted oligodendrocyte progenitors (OPs) to engage in myelination may constitute a novel therapeutic approach to demyelinating diseases of the brain. It is known that in adults neural progenitors situated in the subventricular zone of the lateral ventricle (SVZ) are capable of generating OPs which can migrate into white matter tracts such as the corpus callosum (CC). We observed that progenitor cells in the SVZ of adult mice expressed CXCR4 chemokine receptors and that the chemokine SDF-1/CXCL12 was expressed in the CC. We therefore investigated the role of chemokine signaling in regulating the migration of OPs into the CC following their transplantation into the lateral ventricle. We established OP cell cultures from Olig2-EGFP mouse brains. These cells expressed a variety of chemokine receptors, including CXCR4 receptors. Olig2-EGFP OPs differentiated into CNPase-expressing oligodendrocytes in culture. To study the migratory capacity of Olig2-EGFP OPs in vivo, we transplanted them into the lateral ventricles of mice. Donor cells migrated into the CC and differentiated into mature oligodendrocytes. This migration was enhanced in animals with Experimental Autoimmune Encephalomyelitis (EAE). Inhibition of CXCR4 receptor expression in OPs using shRNA inhibited the migration of transplanted OPs into the white matter suggesting that their directed migration is regulated by CXCR4 signaling. These findings indicate that CXCR4 mediated signaling is important in guiding the migration of transplanted OPs in the context of inflammatory demyelinating brain disease.     

Performance of Five Commercially Available Tooth Color-Measuring Devices

PURPOSE: Visual tooth color assessment is neither accurate nor precise due to various subjective and objective factors. As newly developed tooth color-measuring devices for dental application provide the possibility of a more objective means of color determination, their performances in vitro and in vivo must be evaluated. The objective of this study was to evaluate the accuracy and precision of five commercially available tooth color-measuring devices in standardized and in clinical environments. MATERIALS AND METHODS: In an in vitro study, standards (A1, A2, A3, A3.5, and A4 shade tabs of Vita Lumin) were measured five times with five electronic devices (ShadeScan, Easyshade, Ikam, IdentaColor II, and ShadeEye) by two operators. In an in vivo study, the right upper central incisors of 25 dental students were measured with the same electronic devices by a single operator. Vita shade tab codes were expressed as CIE (International Commission on Illumination) L*a*b* values and in terms of the precision and accuracy of DeltaE color differences. The Mann-Whitney statistical test was used to analyze the differences between the two operators in the in vitro study, and the Kruskal-Wallis one-way analysis of variance on ranks with the post-hoc Tukey test was used to analyze the accuracy and precision of electronic devices. RESULTS: No statistically significant difference was found between the different operators in the in vitro study. The obtained precision was Easyshade > ShadeScan approximately equal Ikam > IdentaColor II > ShadeEye. The obtained accuracy was Easyshade > ShadeScan approximately equal Ikam > ShadeEye > IdentaColor II. In the in vivo study, the Easyshade and the Ikam were the most precise, and the ShadeEye and the IdentaColor II were more precise than the ShadeScan. With respect to accuracy, there was no statistical difference between the ShadeScan, Ikam, and the Easyshade. The IdentaColor II was considered inaccurate (DeltaE(a)= 3.4). CONCLUSIONS: In the clinical setting, the Easyshade and Ikam systems were the most reliable. The other devices tested were more reliable in vitro than in vivo.     

Lymphotoxins and cytomegalovirus cooperatively induce interferon-beta, establishing host-virus détente.

Tumor necrosis factor (TNF)-related cytokines regulate cell death and survival and provide strong selective pressures for viruses, such as cytomegalovirus (CMV), to evolve counterstrategies in order to persist in immune-competent hosts. Signaling by the lymphotoxin (LT)-beta receptor or TNF receptor-1, but not Fas or TRAIL receptors, inhibits the cytopathicity and replication of human CMV by a nonapoptotic, reversible process that requires nuclear factor kappa B (NF-kappa B)-dependent induction of interferon-beta (IFN-beta). Efficient induction of IFN-beta requires virus infection and LT signaling, demonstrating the need for both host and viral factors in the curtailment of viral replication without cellular elimination. LT alpha-deficient mice and LT beta R-Fc transgenic mice were profoundly susceptible to murine CMV infection. Together, these results reveal an essential and conserved role for LTs in establishing host defense to CMV.