The fundamental role of behavioral skills in crystalizing the budding managers

The mission and vision of Management education system had been exemplary in terms of evolving a true professional and efficient leader in every student and this pristine vision had been materialized and conceptualized in the vibrant ambience of a Gurukula. In continuation, the pupils were taught not only to earn their livelihood but also the humane principles for lifetime. Indeed, the Gurukulas adopted their own experiential learning pedagogy in order to train their pupils on various domains like interpersonal skills, intrapersonal skills, and professional skills, and so on… However, their pedagogical delivery was never constrained only for creating monetary machines but to evolve a human being.To interpret in the words of Swami Vivekananda, “Man making was the mission of education but not machine making”. In this contemporaneous world of monetary appetite, the lives of the people are completely saturated and engulfed by the monetary avarice. Accordingly, the precious dimensions of life have been monopolized by the dominating dimension called the economic status.Consequently, the same tendency is percolated into the younger generation wherein their success rate is measured by the yardstick of economic success and having no consideration for the true professional fiber.Interestingly, the academic role, which is responsible for evolving holistic personality in a student, has been redefined and drifted towards the metamorphosed role of building monetary generating humanoids.In continuation, the students who witness the transit of student-hood to professional-hood invariably witness a serious crisis in the role-adoption.Moreover, their theoretical or knowledge expertise may not encompass the vast corporate dimension that include interpersonal skills, intrapersonal skills, emotional intelligence, efficacy of communication skills, leadership skills and so on… Considering the subtle deficiencies and requirements of a professional, the paper suggests a few astute practices that are derived from the philosophies of Swami Vivekananda and other management gurus.Besides, the thoughts have been linked to the contemporaneous nomenclatures like emotional intelligence, transactional analysis, self-esteem etc… Moreover, the sagacious practices that are widely observed in the corporate corridors have been suggested in order to bridge the gap

EFFECTIVENESS OF SPIRULINA MOUTHWASH ON REDUCTION OF DENTAL PLAQUE AND GINGIVITIS: A CLINICAL STUDY

Objective: The present study evaluated the effectiveness of Spirulina mouthwash on the reduction of dental plaque and gingivitis.Methods: A single-blind clinical trial was conducted among thirty patient's aged 18-40 y visiting dental college and hospital in Bangalore city. Mouthwash was prepared using 0.5% Spirulina. Intervention protocol consisted of instructing the patients to rinse with 10 ml of mouthwash for 1 minute twice daily for 7 d. Plaque index and Gingival index were used to assess the variables at the baseline and after the intervention. The perception of the individual subjects with regard to the use of mouthwash was assessed using 10 cm long visual analog scale (VAS). Statistical analysis was carried out using Wilcoxon signed rank test for mean pre and post plaque and gingival scores respectively. Descriptive statistics was performed for VAS questionnaireResults: The results showed a highly significant difference (p<0.001) between the mean plaque scores at the baseline (2.16±0.34) and at the follow up (1.27±0.46). The mean gingival scores at the baseline (1.86±0.38) and at the follow-up (1.05±0.43) also showed a highly significant difference (p<0.001). Regarding the Visual Analog Scale, the mean values of 5 or greater than suggested the responses to be favourable as the values were reflectedConclusion: The study showed that Spirulina mouthwash resulted in significant reduction in dental plaque and gingivitis. Also, the mouthwash was convenient to use without any adverse effects. Hence, the use of herbal mouth rinses such as Spirulina should be supported

In Vitro and In Vivo Studies Identify Important Features of Dengue Virus pr-E Protein Interactions

Flaviviruses bud into the endoplasmic reticulum and are transported through the secretory pathway, where the mildly acidic environment triggers particle rearrangement and allows furin processing of the prM protein to pr and M. The peripheral pr peptide remains bound to virus at low pH and inhibits virus-membrane interaction. Upon exocytosis, the release of pr at neutral pH completes virus maturation to an infectious particle. Together this evidence suggests that pr may shield the flavivirus fusion protein E from the low pH environment of the exocytic pathway. Here we developed an in vitro system to reconstitute the interaction of dengue virus (DENV) pr with soluble truncated E proteins. At low pH recombinant pr bound to both monomeric and dimeric forms of E and blocked their membrane insertion. Exogenous pr interacted with mature infectious DENV and specifically inhibited virus fusion and infection. Alanine substitution of E H244, a highly conserved histidine residue in the pr-E interface, blocked pr-E interaction and reduced release of DENV virus-like particles. Folding, membrane insertion and trimerization of the H244A mutant E protein were preserved, and particle release could be partially rescued by neutralization of the low pH of the secretory pathway. Thus, pr acts to silence flavivirus fusion activity during virus secretion, and this function can be separated from the chaperone activity of prM. The sequence conservation of key residues involved in the flavivirus pr-E interaction suggests that this protein-protein interface may be a useful target for broad-spectrum inhibitors

Chikungunya virus adaptation to Aedes albopictus mosquitoes does not correlate with acquisition of cholesterol dependence or decreased pH threshold for fusion reaction

<p>Abstract</p> <p>Background</p> <p>Chikungunya virus (CHIKV) is a mosquito transmitted alphavirus that recently caused several large scale outbreaks/epidemics of arthritic disease in tropics of Africa, Indian Ocean basin and South-East Asia. This re-emergence event was facilitated by genetic adaptation (E1-A226V substitution) of CHIKV to a newly significant mosquito vector for this virus; <it>Aedes albopictus</it>. However, the molecular mechanism explaining the positive effect of the E1-A226V mutation on CHIKV fitness in this vector remains largely unknown. Previously we demonstrated that the E1-A226V substitution is also associated with attenuated CHIKV growth in cells depleted by cholesterol.</p> <p>Methods</p> <p>In this study, using a panel of CHIKV clones that varies in sensitivity to cholesterol, we investigated the possible relationship between cholesterol dependence and <it>Ae. albopictus </it>infectivity.</p> <p>Results</p> <p>We demonstrated that there is no clear mechanistic correlation between these two phenotypes. We also showed that the E1-A226V mutation increases the pH dependence of the CHIKV fusion reaction; however, subsequent genetic analysis failed to support an association between CHIKV dependency on lower pH, and mosquito infectivity phenotypes.</p> <p>Conclusion</p> <p>the E1-A226V mutation probably acts at different steps of the CHIKV life cycle, affecting multiple functions of the virus.</p

A DNA Sequence Directed Mutual Transcription Regulation of HSF1 and NFIX Involves Novel Heat Sensitive Protein Interactions

BACKGROUND: Though the Nuclear factor 1 family member NFIX has been strongly implicated in PDGFB-induced glioblastoma, its molecular mechanisms of action remain unknown. HSF1, a heat shock-related transcription factor is also a powerful modifier of carcinogenesis by several factors, including PDGFB. How HSF1 transcription is controlled has remained largely elusive. METHODOLOGY/PRINCIPAL FINDINGS: By combining microarray expression profiling and a yeast-two-hybrid screen, we identified that NFIX and its interactions with CGGBP1 and HMGN1 regulate expression of HSF1. We found that CGGBP1 organizes a bifunctional transcriptional complex at small CGG repeats in the HSF1 promoter. Under chronic heat shock, NFIX uses CGGBP1 and HMGN1 to get recruited to this promoter and in turn affects their binding to DNA. Results show that the interactions of NFIX with CGGBP1 and HMGN1 in the soluble fraction are heat shock sensitive due to preferential localization of CGGBP1 to heterochromatin after heat shock. HSF1 in turn was found to bind to the NFIX promoter and repress its expression in a heat shock sensitive manner. CONCLUSIONS/SIGNIFICANCE: NFIX and HSF1 exert a mutual transcriptional repressive effect on each other which requires CGG repeat in HSF1 promoter and HSF1 binding site in NFIX promoter. We unravel a unique mechanism of heat shock sensitive DNA sequence-directed reciprocal transcriptional regulation between NFIX and HSF1. Our findings provide new insights into mechanisms of transcription regulation under stress

Epidemiology of Escherichia coli bacteraemia in England: results of an enhanced sentinel surveillance programme

Background: Escherichia coli causes over one third of the bacteraemia cases in England each year, and the incidence of these infections is increasing. Aim: To determine the underlying risk factors associated with E. coli bacteraemia. Methods: A three month enhanced sentinel surveillance study involving 35 National Health Service hospitals was undertaken in the winter of 2012/13 to collect risk factor information and further details on the underlying source of infection to augment data already collected by the English national surveillance programme. Antimicrobial susceptibility results for E. coli isolated from blood and urine were also collected. Findings: A total of 1,731 cases of E. coli bacteraemia were included. The urogenital tract was the most commonly reported source of infection (51.2% of cases) with prior treatment for a urinary tract infection being the largest independent effect associated with this infection source. Half of all patients had prior healthcare exposure in the month prior to the bacteraemia with antimicrobial therapy and urinary catheterisation being reported in one third and one fifth of these patients. Prior healthcare exposure was associated with a higher proportion of antibiotic non-susceptibility in the blood culture isolates (P=0.001). Conclusion: Analysis of risk factors suggests potential community and hospital-related interventions particularly better use of urinary catheters and improved antibiotic management of urinary tract infections. As part of the latter strategy, antibiotic resistance profiles need to be closely monitored to ensure treatment guidelines are up to date to limit inappropriate empiric therapy

Receptor Complementation and Mutagenesis Reveal SR-BI as an Essential HCV Entry Factor and Functionally Imply Its Intra- and Extra-Cellular Domains

HCV entry into cells is a multi-step and slow process. It is believed that the initial capture of HCV particles by glycosaminoglycans and/or lipoprotein receptors is followed by coordinated interactions with the scavenger receptor class B type I (SR-BI), a major receptor of high-density lipoprotein (HDL), the CD81 tetraspanin, and the tight junction protein Claudin-1, ultimately leading to uptake and cellular penetration of HCV via low-pH endosomes. Several reports have indicated that HDL promotes HCV entry through interaction with SR-BI. This pathway remains largely elusive, although it was shown that HDL neither associates with HCV particles nor modulates HCV binding to SR-BI. In contrast to CD81 and Claudin-1, the importance of SR-BI has only been addressed indirectly because of lack of cells in which functional complementation assays with mutant receptors could be performed. Here we identified for the first time two cell types that supported HCVpp and HCVcc entry upon ectopic SR-BI expression. Remarkably, the undetectable expression of SR-BI in rat hepatoma cells allowed unambiguous investigation of human SR-BI functions during HCV entry. By expressing different SR-BI mutants in either cell line, our results revealed features of SR-BI intracellular domains that influence HCV infectivity without affecting receptor binding and stimulation of HCV entry induced by HDL/SR-BI interaction. Conversely, we identified positions of SR-BI ectodomain that, by altering HCV binding, inhibit entry. Finally, we characterized alternative ectodomain determinants that, by reducing SR-BI cholesterol uptake and efflux functions, abolish HDL-mediated infection-enhancement. Altogether, we demonstrate that SR-BI is an essential HCV entry factor. Moreover, our results highlight specific SR-BI determinants required during HCV entry and physiological lipid transfer functions hijacked by HCV to favor infection

Human cytomegalovirus immediate-early 1 protein rewires upstream STAT3 to downstream STAT1 signaling switching an IL6-type to an IFNγ-like response

MN and CP were supported by the Wellcome Trust (www.wellcome.ac.uk) Institutional Strategic Support Fund and CP was supported by the Deutsche Forschungsgemeinschaft (PA 815/2-1; www.dfg.de).The human cytomegalovirus (hCMV) major immediate-early 1 protein (IE1) is best known for activating transcription to facilitate viral replication. Here we present transcriptome data indicating that IE1 is as significant a repressor as it is an activator of host gene expression. Human cells induced to express IE1 exhibit global repression of IL6- and oncostatin M-responsive STAT3 target genes. This repression is followed by STAT1 phosphorylation and activation of STAT1 target genes normally induced by IFNγ. The observed repression and subsequent activation are both mediated through the same region (amino acids 410 to 445) in the C-terminal domain of IE1, and this region serves as a binding site for STAT3. Depletion of STAT3 phenocopies the STAT1-dependent IFNγ-like response to IE1. In contrast, depletion of the IL6 receptor (IL6ST) or the STAT kinase JAK1 prevents this response. Accordingly, treatment with IL6 leads to prolonged STAT1 instead of STAT3 activation in wild-type IE1 expressing cells, but not in cells expressing a mutant protein (IE1dl410-420) deficient for STAT3 binding. A very similar STAT1-directed response to IL6 is also present in cells infected with a wild-type or revertant hCMV, but not an IE1dl410-420 mutant virus, and this response results in restricted viral replication. We conclude that IE1 is sufficient and necessary to rewire upstream IL6-type to downstream IFNγ-like signaling, two pathways linked to opposing actions, resulting in repressed STAT3- and activated STAT1-responsive genes. These findings relate transcriptional repressor and activator functions of IE1 and suggest unexpected outcomes relevant to viral pathogenesis in response to cytokines or growth factors that signal through the IL6ST-JAK1-STAT3 axis in hCMV-infected cells. Our results also reveal that IE1, a protein considered to be a key activator of the hCMV productive cycle, has an unanticipated role in tempering viral replication.Publisher PDFPeer reviewe

Shape coexistence in the neutron-deficient lead region: A systematic study of lifetimes in the even-even 188−200^{188-200}Hg with GRIFFIN

Lifetimes of $2^+_1$ and $4^+_1$ states, as well as some negative-parity and non-yrast states, in $^{188-200}$Hg were measured using $\gamma-\gamma$ electronic fast timing techniques with the LaBr$_3$(Ce) detector array of the GRIFFIN spectrometer. The excited states were populated in the $\epsilon/\beta^+$-decay of $J^\pi =7^+/2^-$ $^{188-200}$Tl produced at the TRIUMF-ISAC facility. The deduced B(E2) values are compared to different interacting boson model predictions. The precision achieved in this work over previous ones allows for a meaningful comparison with the different theoretical models of these transitional Hg isotopes, which confirms the onset of state mixing in $^{190}$Hg