The Tai-Phake of Assam, India – A Morphometric Study and Population Comparison with Neighbouring Groups

Morphometric characters of the adult males of the Tai-Phake and the nature and extent of morphometric variation among five neighboring mongoloid groups of Assam have been examined in the present study. For the sake of investigation 12 anthropometric measurements have been taken and five indices have been calculated. In order to obtain the distance values size, shape and biological distance are calculated. It revels that the Tai-Phake maintains a far distance with other five neighboring groups (Ahom, Deuri, Chutia, Mishing and Moran). The Ahom also maintain far distance with other five groups. While, the Mishing and Moran, and Deuri and Chutia maintain close distance among themselves

Bisimidazole Selone Supported Zinc Compound: Synthesis and Characterizations

Metal-selenides have got vast applications in the field of metallurgy. In particular, the zinc selenide material is one of the most important materials that show excellent optical applications. In general, ZnSe is prepared by hydrothermal methods while the soft approach to prepare this material is limited, whereby Zn:Se ratio can be effectively controlled. Thus, a new 3,3’-methylenebis(1-isopropyl-1H-imidazole-2(3H)-selenone (3) ligand has been prepared by the reaction of 3,3’-methylenebis(1-isopropyl-1H-imidazole-3-ium) bromide and methyl bromide. The new zinc selenide complex has been prepared from the reaction of zinc tetrafluoroborate and (3), where one Zn is coordinated to four Se centres. The selenone ligand and the ZnSe complex have been characterized thoroughly by 1H NMR, 13C NMR, FT-IR, solution UV-vis and single crystal X-ray diffraction techniques. The thermal stability of the zinc selenide is also studied by TGA. In addition, novelbisimidazoselenone ligand with ethyl spacer and imidazoselenone ligand with biphenyl spacer have been prepared and characterized by 1H NMR, 13C NMR, FT-IR, solution UV-vis and single crystal X-ray diffraction technique

Comparison of hemodynamic and analgesic effects of interscalene block with bupivacaine versus bupivacaine-dexmedetomidine combination for shoulder arthroscopy under general anesthesia

Background: The interscalene block in shoulder arthroscopy is a well-established procedure. Many drugs have been used as adjuvants to local anesthetics to increase the quality of block in regional anesthesia, with variable results. Aims and Objectives: The present study was designed to evaluate the effect of dexmedetomidine as an adjuvant to bupivacaine during interscalene block in terms of intraoperative hemodynamic changes and postoperative analgesia. Materials and Methods: Thirty patients, aged 20–55 years of either sex, American Society of Anesthesiologists physical status I-II, scheduled for shoulder arthroscopic surgery for <2 h, were allocated into two equal groups to receive inj. bupivacaine (0.25%) with inj. dexmedetomidine 1 μg/kg (Group BD, n=15) or inj. bupivacaine (0.25%) with 1 mL normal saline (Group BS, n=15), total volume 20 mL in each case. After settlement of the interscalene block, both groups received general anesthesia as per standard protocol. Hemodynamic parameters (heart rate [HR] and systolic blood pressure [SBP]) were assessed in the intraoperative period, and postoperative pain was assessed using a visual analog scale score in the postoperative period at stipulated time points. Results: The mean values of HR and SBP were considerably low at all observed time points in the intraoperative period (i.e., at 10 min, 30 min, 60 min, 90 min, and120 min), in comparison with the saline group (P<0.0001). VAS scores between the two groups were considerably lower only at 8, 12, and 18 h in patients receiving dexmedetomidine (P<0.001). Conclusion: Dexmedetomidine as an adjuvant with bupivacaine can achieve a better hemodynamic profile (lower HR and SBP) in the intraoperative period. Also, the use of dexmedetomidine provides better postoperative analgesia profiles in the later part of the postoperative period (8–18 h), and the effect usually wanes by 24 h

Ab initio Study of the Effect of H2O Molecules Adsorption on the Semiconducting Graphene Nanoribbon

The H2O molecules adsorption effects over electronic transport properties of Armchair Graphene Nanoribbons (A-GNR) was theoretically studied using Non Equilibrium Green Function (NEGF) formalism along with Ab initio calculation. Three different orientations and adsorption sites are considered to calculate the adsorption energies. The calculated adsorption energies for those orientations also suggest that adsorption in metallic A-GNR has much smaller effect on its transport properties

Hdac6 Knock-Out Increases Tubulin Acetylation but Does Not Modify Disease Progression in the R6/2 Mouse Model of Huntington's Disease

Huntington's disease (HD) is a progressive neurodegenerative disorder for which there is no effective disease modifying treatment. Following-on from studies in HD animal models, histone deacetylase (HDAC) inhibition has emerged as an attractive therapeutic option. In parallel, several reports have demonstrated a role for histone deacetylase 6 (HDAC6) in the modulation of the toxicity caused by the accumulation of misfolded proteins, including that of expanded polyglutamine in an N-terminal huntingtin fragment. An important role for HDAC6 in kinesin-1 dependent transport of brain-derived neurotrophic factor (BDNF) from the cortex to the striatum has also been demonstrated. To elucidate the role that HDAC6 plays in HD progression, we evaluated the effects of the genetic depletion of HDAC6 in the R6/2 mouse model of HD. Loss of HDAC6 resulted in a marked increase in tubulin acetylation throughout the brain. Despite this, there was no effect on the onset and progression of a wide range of behavioural, physiological, molecular and pathological HD-related phenotypes. We observed no change in the aggregate load or in the levels of soluble mutant exon 1 transprotein. HDAC6 genetic depletion did not affect the efficiency of BDNF transport from the cortex to the striatum. Therefore, we conclude that HDAC6 inhibition does not modify disease progression in R6/2 mice and HDAC6 should not be prioritized as a therapeutic target for HD

Hdac6 Knock-Out Increases Tubulin Acetylation but Does Not Modify Disease Progression in the R6/2 Mouse Model of Huntington's Disease

Huntington's disease (HD) is a progressive neurodegenerative disorder for which there is no effective disease modifying treatment. Following-on from studies in HD animal models, histone deacetylase (HDAC) inhibition has emerged as an attractive therapeutic option. In parallel, several reports have demonstrated a role for histone deacetylase 6 (HDAC6) in the modulation of the toxicity caused by the accumulation of misfolded proteins, including that of expanded polyglutamine in an N-terminal huntingtin fragment. An important role for HDAC6 in kinesin-1 dependent transport of brain-derived neurotrophic factor (BDNF) from the cortex to the striatum has also been demonstrated. To elucidate the role that HDAC6 plays in HD progression, we evaluated the effects of the genetic depletion of HDAC6 in the R6/2 mouse model of HD. Loss of HDAC6 resulted in a marked increase in tubulin acetylation throughout the brain. Despite this, there was no effect on the onset and progression of a wide range of behavioural, physiological, molecular and pathological HD-related phenotypes. We observed no change in the aggregate load or in the levels of soluble mutant exon 1 transprotein. HDAC6 genetic depletion did not affect the efficiency of BDNF transport from the cortex to the striatum. Therefore, we conclude that HDAC6 inhibition does not modify disease progression in R6/2 mice and HDAC6 should not be prioritized as a therapeutic target for HD

Short-Term Striatal Gene Expression Responses to Brain-Derived Neurotrophic Factor Are Dependent on MEK and ERK Activation

BACKGROUND: Brain-derived neurotrophic factor (BDNF) is believed to be an important regulator of striatal neuron survival, differentiation, and plasticity. Moreover, reduction of BDNF delivery to the striatum has been implicated in the pathophysiology of Huntington's disease. Nevertheless, many essential aspects of BDNF responses in striatal neurons remain to be elucidated. METHODOLOGY/PRINCIPAL FINDINGS: In this study, we assessed the relative contributions of multipartite intracellular signaling pathways to the short-term induction of striatal gene expression by BDNF. To identify genes regulated by BDNF in these GABAergic cells, we first used DNA microarrays to quantify their transcriptomic responses following 3 h of BDNF exposure. The signal transduction pathways underlying gene induction were subsequently dissected using pharmacological agents and quantitative real-time PCR. Gene expression responses to BDNF were abolished by inhibitors of TrkB (K252a) and calcium (chelator BAPTA-AM and transient receptor potential cation channel [TRPC] antagonist SKF-96365). Interestingly, inhibitors of mitogen-activated protein kinase kinases 1 and 2 (MEK1/2) and extracellular signal-regulated kinase ERK also blocked the BDNF-mediated induction of all tested BDNF-responsive genes. In contrast, inhibitors of nitric oxide synthase (NOS), phosphotidylinositol-3-kinase (PI3K), and CAMK exhibited less prevalent, gene-specific effects on BDNF-induced RNA expression. At the nuclear level, the activation of both Elk-1 and CREB showed MEK dependence. Importantly, MEK-dependent activation of transcription was shown to be required for BDNF-induced striatal neurite outgrowth, providing evidence for its contribution to striatal neuron plasticity. CONCLUSIONS: These results show that the MEK/ERK pathway is a major mediator of neuronal plasticity and other important BDNF-dependent striatal functions that are fulfilled through the positive regulation of gene expression

Cognitive Dysfunction in Huntington's Disease: Mechanisms and Therapeutic Strategies Beyond BDNF

One of the main focuses in Huntington's disease (HD) research, as well as in most of the neurodegenerative diseases, is the development of new therapeutic strategies, as currently there is no treatment to delay or prevent the progression of the disease. Neuronal dysfunction and neuronal death in HD are caused by a combination of interrelated pathogenic processes that lead to motor, cognitive and psychiatric symptoms. Understanding how mutant huntingtin impacts on a plethora of cellular functions could help to identify new molecular targets. Although HD has been classically classified as a neurodegenerative disease affecting voluntary movement, lately cognitive dysfunction is receiving increased attention as it is very invalidating for patients. Thus, an ambitious goal in HD research is to find altered molecular mechanisms that contribute to cognitive decline. In this review we have focused on those findings related to corticostriatal and hippocampal cognitive dysfunction in HD, as well as on the underlying molecular mechanisms, which constitute potential therapeutic targets. These include alterations in synaptic plasticity, transcriptional machinery, and neurotrophic and neurotransmitter signaling. This article is protected by copyright. All rights reserved