A CLINICAL EVALUATION OF PANCHAGAVYA GHRITA IN BAL APASMARA (EPILEPSY IN PAEDIATRIC AGE GROUP)

Background: Epilepsy is defined as the primary disorder of the brain due to an abnormal and excessive neuronal activity involving cerebral grey matter, resulting in a seizure.Objective: The objective was to do a clinical evaluation of Panchagavya ghrita in Bal apasmara (epilepsy in paediatric age group).Materials and Methods: It is a randomized open interventional parallel efficacy drug trial. A total number of 60 patients were selected from the age group of 4 years to 16 years of age. All the patients were recently diagnosed with Idiopathic type of epilepsy and were not on any kind of medication, before the start of the study. The selected patients were randomly divided into two groups – The patients in Group I (n = 30) were given Panchagavya ghrita and patients in Group II (n = 30) were kept on Tab. Tegretol for the study. Both the groups were studied for 12 months to see the efficacy of the drug.Results: Group I showed Statistically significant results in Frequency of convulsions, Duration of convulsion and Smritinasha (Amnesia). Where as in Group II highly significant results were observed in Frequency of convulsions and duration of convulsion; but not   significant results were observed in Smritinasha (Amnesia).Conclusion: Panchagavya ghrita has shown promising results in the management of Bal - apasmara (Epilepsy in paediatric age group) without any complications and side-effects

A COMPARATIVE STUDY OF BHUJANGASANA WITH KATIBASTI OVER ONLY KATIBASTI IN GRUDHRASI (SCIATICA)

Background: Grudhrasi (Sciatica) is one of the eighty Vatavyadhi mentioned in Ayurvedic Samhitas, which is caused by aggravated Vatadosha. This is characterized by Ruja (pain) in the waist, back, thigh, knee and calf regions along the course of Sciatic nerve. There are many treatment modalities available in Ayurveda and Modern medical science. They have some or the other shortcomings and drawbacks.Objectives: To evaluate the efficacy of Bhujangasana with Katibasti over only Katibasti.Materials and Methods: It is a randomized open interventional parallel efficacy drug trial. A total number of  40 patients were selected from OPD. All the patients were having classical presentation of Grudhrasi and SLR test positive between 300 and 700. The selected were randomly divided in to two groups, namely, Group A (study group n = 20) and Group B (control group n = 20). Group A was given Bhujangasana with Katibasti and Group B was given Katibasti only. The data were collected and observations were made before the treatment, on 8th day, 15th day and on 22nd day of the treatment. The data obtained from the result were subjected for statistical analysis and conclusions were drawn.Results: In Group A, 85% patients were totally relieved of pain and 15% patients were reported to have moderate pain. In Group B, 55% patients reported total relief from pain and 25% had mild pain. In 90% cases SLR became negative in Group A, whereas in Group B 75% patients reported negative result in SLR test.Conclusion: Analysis of overall effect of treatment in the present study reveals that Bhujangasana with Katibasti was statistically significant compared to that of Katibasti

Gut immune dysfunction through impaired innate pattern recognition receptor expression and gut microbiota dysbiosis in chronic SIV infection.

HIV targets the gut mucosa early in infection, causing immune and epithelial barrier dysfunction and disease progression. However, gut mucosal sensing and innate immune signaling through mucosal pattern recognition receptors (PRRs) during HIV infection and disease progression are not well defined. Using the simian immunodeficiency virus (SIV)-infected rhesus macaque model of AIDS, we found a robust increase in PRRs and inflammatory cytokine gene expression during the acute SIV infection in both peripheral blood and gut mucosa, coinciding with viral replication. PRR expression remained elevated in peripheral blood following the transition to chronic SIV infection. In contrast, massive dampening of PRR expression was detected in the gut mucosa, despite the presence of detectable viral loads. Exceptionally, expression of Toll-like receptor 4 (TLR4) and TLR8 was downmodulated and diverged from expression patterns for most other TLRs in the gut. Decreased mucosal PRR expression was associated with increased abundance of several pathogenic bacterial taxa, including Pasteurellaceae members, Aggregatibacter and Actinobacillus, and Mycoplasmataceae family. Early antiretroviral therapy led to viral suppression but only partial maintenance of gut PRRs and cytokine gene expression. In summary, SIV infection dampens mucosal innate immunity through PRR dysregulation and may promote immune activation, gut microbiota changes, and ineffective viral clearance

Molecular markers for grape characterization

Research NoteFive cultivars and 9 Pinot noir clones were used to test the usefulness of RFLP and RAPD markers and determine whether clonal selections could be differentiated

The dipeptidyl peptidase IV inhibitors vildagliptin and K-579 inhibit a phospholipase C: a case of promiscuous scaffolds in proteins.

The long term side effects of any newly introduced drug is a subject of intense research, and often raging controversies. One such example is the dipeptidyl peptidase-IV (DPP4) inhibitor used for treating type 2 diabetes, which is inconclusively implicated in increased susceptibility to acute pancreatitis. Previously, based on a computational analysis of the spatial and electrostatic properties of active site residues, we have demonstrated that phosphoinositide-specific phospholipase C (PI-PLC) from Bacillus cereus is a prolyl peptidase using in vivo experiments. In the current work, we first report the inhibition of the native activity of PI-PLC by two DPP4 inhibitors - vildagliptin (LAF-237) and K-579. While vildagliptin inhibited PI-PLC at micromolar concentrations, K-579 was a potent inhibitor even at nanomolar concentrations. Subsequently, we queried a comprehensive, non-redundant set of 5000 human proteins (50% similarity cutoff) with known structures using serine protease (SPASE) motifs derived from trypsin and DPP4. A pancreatic lipase and a gastric lipase are among the proteins that are identified as proteins having promiscuous SPASE scaffolds that could interact with DPP4 inhibitors. The presence of such scaffolds in human lipases is expected since they share the same catalytic mechanism with PI-PLC. However our methodology also detects other proteins, often with a completely different enzymatic mechanism, that have significantly congruent domains with the SPASE motifs. The reported elevated levels of serum lipase, although contested, could be rationalized by inhibition of lipases reported here. In an effort to further our understanding of the spatial and electrostatic basis of DPP4 inhibitors, we have also done a comprehensive analysis of all 76 known DPP4 structures liganded to inhibitors till date. Also, the methodology presented here can be easily adopted for other drugs, and provide the first line of filtering in the identification of pathways that might be inadvertently affected due to promiscuous scaffolds in proteins

Progress toward the production of transgenic grapevines by Agrobacterium-mediated transformation

Grape possesses the basic prerequisites for Agrobacterium-mediated transformation it is a host for Agrobacterium and plant regeneration can be induced from cultured grape explants. Leaf explants were cocultivated with disarmed Agrobacterium vectors carrying kanamycin resistance and GUS genes and cultured on shoot-inducing medium containing kanamycin. After 21 d, intense and sharply-defined blue regions were observed, including some blue organized meristematic structures, consistent with plant-driven GUS gene expression. No GUS activity was detected in control explants. Among single leaf tips excised from over 200 regenerated shoots, one was GUS positive. The recovery of transgenic shoots might be improved by increasing the frequency or modifying the site of transformation and/or regeneration

Phosphatidylinositol (4,5) Bisphosphate Controls T Cell Activation by Regulating T Cell Rigidity and Organization

Here we investigate the role of Phosphatidylinositol (4,5) bisphosphate (PIP2) in the physiological activation of primary murine T cells by antigen presenting cells (APC) by addressing two principal challenges in PIP2 biology. First, PIP2 is a regulator of cytoskeletal dynamics and a substrate for second messenger generation. The relative importance of these two processes needs to be determined. Second, PIP2 is turned over by multiple biosynthetic and metabolizing enzymes. The joint effect of these enzymes on PIP2 distributions needs to be determined with resolution in time and space. We found that T cells express four isoforms of the principal PIP2-generating enzyme phosphatidylinositol 4-phosphate 5-kinase (PIP5K) with distinct spatial and temporal characteristics. In the context of a larger systems analysis of T cell signaling, these data identify the T cell/APC interface and the T cell distal pole as sites of differential PIP2 turnover. Overexpression of different PIP5K isoforms, as corroborated by knock down and PIP2 blockade, yielded an increase in PIP2 levels combined with isoform-specific changes in the spatiotemporal distributions of accessible PIP2. It rigidified the T cell, likely by impairing the inactivation of Ezrin Moesin Radixin, delayed and diminished the clustering of the T cell receptor at the cellular interface, reduced the efficiency of T cell proximal signaling and IL-2 secretion. These effects were consistently more severe for distal PIP5K isoforms. Thus spatially constrained cytoskeletal roles of PIP2 in the control of T cell rigidity and spatiotemporal organization dominate the effects of PIP2 on T cell activation

Intrathecal B-cell activation in LGI1 antibody encephalitis.

ObjectiveTo study intrathecal B-cell activity in leucine-rich, glioma-inactivated 1 (LGI1) antibody encephalitis. In patients with LGI1 antibodies, the lack of CSF lymphocytosis or oligoclonal bands and serum-predominant LGI1 antibodies suggests a peripherally initiated immune response. However, it is unknown whether B cells within the CNS contribute to the ongoing pathogenesis of LGI1 antibody encephalitis.MethodsPaired CSF and peripheral blood (PB) mononuclear cells were collected from 6 patients with LGI1 antibody encephalitis and 2 patients with other neurologic diseases. Deep B-cell immune repertoire sequencing was performed on immunoglobulin heavy chain transcripts from CSF B cells and sorted PB B-cell subsets. In addition, LGI1 antibody levels were determined in CSF and PB.ResultsSerum LGI1 antibody titers were on average 127-fold higher than CSF LGI1 antibody titers. Yet, deep B-cell repertoire analysis demonstrated a restricted CSF repertoire with frequent extensive clusters of clonally related B cells connected to mature PB B cells. These clusters showed intensive mutational activity of CSF B cells, providing strong evidence for an independent CNS-based antigen-driven response in patients with LGI1 antibody encephalitis but not in controls.ConclusionsOur results demonstrate that intrathecal immunoglobulin repertoire expansion is a feature of LGI1 antibody encephalitis and suggests a need for CNS-penetrant therapies