Context:Dexmedetomidine as an adjuvant to local anesthetics in peripheral nerve blocks has been used in only a few studies.Aims:We aimed at assessing the effect of dexmedetomidine as an adjuvant to ropivacaine in supraclavicular brachial plexus block.Settings and Design:Random, controlled, and triple blind.Materials and Methods:Sixty American Society of Anesthesiologist grade I and II patients of either sex scheduled for elective upper limb surgery under supraclavicular brachial plexus block were divided into three equal groups in a prospective randomized double-blind controlled manner. For block patients in Group C received 0.5% ropivacaine (30cc), 0.5% ropivacaine with 50 μg dexmedetomidine (30cc) in Group D and 0.5% ropivacaine (30cc) in Group D-IV along with intravenous infusion of 50 μg dexmedetomidine in normal saline.Statistical Analysis Used:IBM-SPSS software version 17, Chi-square test, Mann-Whitney U-test.Results:Demographic profile and surgical characteristics were similar in all the three groups. Sensory block and motor block onset was earlier in group D than in group D-IV and group C. The sensory block and motor block duration was also prolonged in group D when compared with group D-IV and group C. The duration of analgesia was significantly longer in group D and D-IV when compared to group C.Conclusions:Dexmedetomidine as an adjuvant to 0.5%ropivacaine in ultrasound guided brachial plexus block shortens the sensory as well as motor block onset time, prolongs sensory and motor block duration and also increases the duration of analgesia. The action of dexmedetomidine most probably is local rather than centrally mediated.

Human papillomaviruses (HPVs) are epitheliotropic viruses with an affinity for keratinocytes and are principally found in the anogenital tract, urethra, skin, larynx, tracheobronchial and oral mucosa. On the basis of high, but variable frequency of HPV in oral squamous cell carcinoma (OSCC), malignant potential of HPV infection has been hypothesized but not definitely confirmed. The aim of this review was to highlight the genomic structure and possible mechanism of infection and carcinogenesis by HPV in the oral mucosa and to review the frequency of HPV prevalence in OSCC and oral potentially malignant disorders. A computer database search was performed through the use of PubMed from 1994 to 2014. Search keywords used were: HPV and oral cancer, HPV and oral leukoplakia, HPV and oral lichen planus, HPV and OSCC, HPV and verrucous carcinoma, HPV and proliferative verrucous leukoplakia, HPV and oral papilloma.

Although the newer therapies offer advantage over steroids for the management of OLP in recalcitrant cases, extensive lesions, and cases unresponsive to steroids, but sufficient clinical data on their use are still lacking. Hence, more RCTs with large sample size, adequate treatment duration, and long-term follow-up are required for clinical utility.

A haloalkalophilic Staphylococcus sp. SG-13 produced an alkalistable xylanase in wheat bran medium. A 12-fold purification was achieved by using standard purification techniques. The purified xylanase exhibited a dual pH optima of 7.5 and 9.2. The optimum temperature for enzyme activity was 50°C. The enzyme was stable at 50°C for more than 4 h. The xylanase exhibited K m and V max values of 4 mg ml −1 , 90 mmol min −1 per mg for birchwood xylan and 7 mg ml −1 , 55 mmol min −1 per mg for oatspelt xylan, respectively. The substrate binding affinity of xylanase was more for oatspelt xylan but birchwood xylan was hydrolysed more rapidly. The xylanase activity was stimulated by Fe 2¦ , Ni 2¦ , Cu 2¦ and dithiothreitol up to 60% and was strongly inhibited in the presence of Co 2¦ , Hg 2¦ , Pb 2¦ , phenyl methane sulphonyl fluoride, ethylenediaminetetraacetic acid, and acetic anhydride up to 100%. The xylanase dose of 1.8 U g −1 moisture free pulp, exhibited bleach boosting of kraft pulps optimally at pH 9.5-10.0 and 50°C after 4 h of reaction time. Pretreatment of pulp with xylanase and its subsequent treatment with 8% hypochlorite, reduced the kappa number by 30%, enhanced the brightness and viscosity by 11% and 1.8%, respectively, and improved the paper properties such as tensile strength and burst factor up to 10% and 17%, respectively.

Fibrosis can occur in any human tissue when the normal wound healing response is amplified. Such amplification results in fibroblast proliferation, myofibroblast differentiation, and excessive extracellular matrix deposition. Occurrence of these sequelae in organs such as the eye or lung can result in severe consequences to health. Unfortunately, medical treatment of fibrosis is limited by a lack of safe and effective therapies. These therapies may be developed by identifying agents that inhibit critical steps in fibrotic progression; one such step is myofibroblast differentiation triggered by transforming growth factor-␤1 (TGF␤1). In this study, we demonstrate that TGF␤1-induced myofibroblast differentiation is blocked in human fibroblasts by a candidate endogenous aryl hydrocarbon receptor (AhR) ligand 2-(1=H-indole-3=-carbonyl)-thiazole-4-carboxylic acid methyl ester (ITE). Our data show that ITE disrupts TGF␤1 signaling by inhibiting the nuclear translocation of Smad2/3/4. Although ITE functions as an AhR agonist, and biologically persistent AhR agonists, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin, cause severe toxic effects, ITE exhibits no toxicity. Interestingly, ITE effectively inhibits TGF␤1-driven myofibroblast differentiation in AhR ؊/؊ fibroblasts: Its ability to inhibit TGF␤1 signaling is AhR independent. As supported by the results of this study, the small molecule ITE inhibits myofibroblast differentiation and may be useful clinically as an antiscarring agent.