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101.
Aditya Kumar Sharma Neha Dhasmana Neha Dubey Nishant Kumar Aakriti Gangwal Meetu Gupta Yogendra Singh 《Indian journal of microbiology》2017,57(1):1-10
Virulence is described as an ability of an organism to infect the host and cause a disease. Virulence factors are the molecules that assist the bacterium colonize the host at the cellular level. These factors are either secretory, membrane associated or cytosolic in nature. The cytosolic factors facilitate the bacterium to undergo quick adaptive—metabolic, physiological and morphological shifts. The membrane associated virulence factors aid the bacterium in adhesion and evasion of the host cell. The secretory factors are important components of bacterial armoury which help the bacterium wade through the innate and adaptive immune response mounted within the host. In extracellular pathogens, the secretory virulence factors act synergistically to kill the host cells. In this review, we revisit the role of some of the secreted virulence factors of two human pathogens: Mycobacterium tuberculosis—an intracellular pathogen and Bacillus anthracis—an extracellular pathogen. The advances in research on the role of secretory factors of these pathogens during infection are discussed. 相似文献
102.
Raju K. Mandal Naseem Akhter Shafiul Haque Aditya K. Panda Rama D. Mittal Mohammed A. A. Alqumber 《PloS one》2014,9(8)
Aim
Tissue inhibitor of metalloproteinase (TIMP2) is involved in the regulation of matrix metalloproteinase 2 (MMP2) and shown to implicate in cancer development and progression. The results from the published studies based on the association between TIMP2 -418 G>C polymorphism and cancer risk are inconsistent. In this meta-analysis, we aimed to evaluate the potential association between TIMP2 -418 G>C polymorphism and cancer risk.Methodology
We searched PubMed (Medline) and EMBASE web databases to cover all studies based on relationship of TIMP2 -418 G>C polymorphism and risk of cancer until October 2013. The meta-analysis was performed for selected case-control studies and pooled odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated for all genetic models.Results
A total of 2225 cancer cases and 2532 controls were included from ten eligible case-control studies. Results from overall pooled analysis suggested no evidence of significant risk between TIMP2 -418 G>C polymorphism and cancer risk in any of the genetic models, such as, allele (C vs. G: OR = 1.293, 95% CI = 0.882 to 1.894, p = 0.188), homozygous (CC vs. GG: OR = 0.940, 95% CI = 0.434 to 2.039, p = 0.876), heterozygous (GC vs. GG: OR = 1.397, 95% CI = 0.888 to 2.198, p = 0.148), dominant (CC+GC vs. GG: OR = 1.387, 95% CI = 0.880 to 2.187, p = 0.159) and recessive (CC vs. GG+GC: OR = 0.901, 95% CI = 0.442 to 1.838, p = 0.774) models. No evidence of publication bias was detected during the analysis.Conclusions
The present meta-analysis suggests that the TIMP2 -418 G>C polymorphism may not be involved in predisposing risk factor for cancer in overall population. However, future larger studies with group of populations are needed to analyze the possible correlation. 相似文献103.
Abhishek Sharma Satyawati Sharma Aditya Mittal Satya Narayan Naik 《Annals of microbiology》2014,64(2):515-520
The development of biofriendly and economical alternatives to chemical pesticides is a globally important scientific challenge. In this work, Karanja-based media conditions were optimized for obtaining high production of biomass and spores of a biocontrol agent, the entomopathogenic fungus Paecilomyces lilacinus 6029, using a two-step statistical approach coupled with rigorous experimentation. In the first step, non-edible Karanja cake was screened out as a major substrate from other oil cakes. In the second step, biomass production was maximized by applying response surface methodology to experimental variations in key physico-chemical factors: carbon/nitrogen (C/N) ratio and pH. This approach eventually predicted a maximum biomass production of 10.559 g/l with a medium having a C/N ratio of 35.88 and pH 5.9. An experimental production of 10.529 g/l biomass was obtained. The remarkable agreement between the predicted and the experimentally obtained biomass confirm the validity of the approach utilized to maximize production of P. lilacinus. 相似文献
104.
miR-497 and miR-302b regulate ethanol-induced neuronal cell death through BCL2 protein and cyclin D2 总被引:1,自引:0,他引:1
Yadav S Pandey A Shukla A Talwelkar SS Kumar A Pant AB Parmar D 《The Journal of biological chemistry》2011,286(43):37347-37357
In chronic alcoholism, brain shrinkage and cognitive defects because of neuronal death are well established, although the sequence of molecular events has not been fully explored yet. We explored the role of microRNAs (miRNAs) in ethanol-induced apoptosis of neuronal cells. Ethanol-sensitive miRNAs in SH-SY5Y, a human neuroblastoma cell line, were identified using real-time PCR-based TaqMan low-density arrays. Long-term exposure to ethanol (0.5% v/v for 72 h) produced a maximum increase in expression of miR-497 (474-fold) and miR-302b (322-fold). Similar to SH-SY5Y, long-term exposure to ethanol induced miR-497 and miR-302b in IMR-32, another human neuroblastoma cell line. Using in silico approaches, BCL2 and cyclin D2 (CCND2) were identified as probable target genes of these miRNAs. Cotransfection studies with 3'-UTR of these genes and miRNA mimics have demonstrated that BCL2 is a direct target of miR-497 and that CCND2 is regulated negatively by either miR-302b or miR-497. Overexpression of either miR-497 or miR-302b reduced expression of their identified target genes and increased caspase 3-mediated apoptosis of SH-SY5Y cells. However, overexpression of only miR-497 increased reactive oxygen species formation, disrupted mitochondrial membrane potential, and induced cytochrome c release (mitochondria-related events of apoptosis). Moreover, ethanol induced changes in miRNAs, and their target genes were substantially prevented by pre-exposure to GSK-3B inhibitors. In conclusion, our studies have shown that ethanol-induced neuronal apoptosis follows both the mitochondria-mediated (miR-497- and BCL2-mediated) and non-mitochondria-mediated (miR-302b- and CCND2-mediated) pathway. 相似文献
105.
Aditya Abha Singh Meenakshi Chaurasia Vaishali Gupta Madhoolika Agrawal S. B. Agrawal 《Acta Physiologiae Plantarum》2018,40(5):92
Increase in surface level of ozone (O3) in last 30 years is one of the major problems for global agriculture. Field experiment was conducted using open top chambers on two Indian maize cultivars (Buland and Prakash) grown under ambient (AO) and elevated (EO) O3 concentrations to evaluate the effect of an antiozonant ethylene diurea (EDU) given as soil drench. EDU application reduced the ROS production with concomitant decrease in lipid peroxidation. Inductions in activities of enzymatic antioxidants along with increased content of non-enzymatic antioxidants were observed in EDU-treated plants, though the response varied between the cultivars. Photosynthetic proteins (PEP carboxylase and RuBisCO large and small subunits) detected through SDS–PAGE analysis increased with EDU treatment. EDU also led to an increase in jasmonic acid and a decline in salicylic acid contents. The protective effect of EDU was further accompanied by increased pigments (chlorophyll and carotenoids), foliar carbohydrates (starch and total soluble sugars), enhanced biomass, and economic yield. Effectiveness of EDU was more evident at higher O3 concentration and cultivar Prakash exhibited a more positive response with EDU as compared to Buland. 相似文献
106.
Shomu Bohora Amit Vora Aditya Kapoor Vanita Arora Nitish Naik Raja Selvaraj Narayan Namboodiri Anil Saxena Ajay Naik Balbir Singh C. Narsimhan Mohan Nair T.S. Kler 《Indian pacing and electrophysiology journal》2018,18(6):188-192
Cardiac implantable electronic device (CIED) procedures are being done by many operators/centers and it is projected that this therapy will remarkably increase in India in the coming years. This document by IHRS, aims at guiding the Indian medical community in the appropriate use and method of implantation with emphasis on implanter training and center preparedness to deliver a safe and effective therapy to patients with cardiac rhythm disorders and heart failure. 相似文献
107.
Dmitry Shishmarev Emily Rowland Shouvik Aditya Srinivasan Sundararaj Aaron J. Oakley Angela F. Dulhunty Marco G. Casarotto 《Protein science : a publication of the Protein Society》2022,31(5)
Excitation‐contraction coupling (ECC) is the physiological process in which an electrical signal originating from the central nervous system is converted into muscle contraction. In skeletal muscle tissue, the key step in the molecular mechanism of ECC initiated by the muscle action potential is the cooperation between two Ca2+ channels, dihydropyridine receptor (DHPR; voltage‐dependent L‐type calcium channel) and ryanodine receptor 1 (RyR1). These two channels were originally postulated to communicate with each other via direct mechanical interactions; however, the molecular details of this cooperation have remained ambiguous. Recently, it has been proposed that one or more supporting proteins are in fact required for communication of DHPR with RyR1 during the ECC process. One such protein that is increasingly believed to play a role in this interaction is the SH3 and cysteine‐rich domain‐containing protein 3 (STAC3), which has been proposed to bind a cytosolic portion of the DHPR α1S subunit known as the II–III loop. In this work, we present direct evidence for an interaction between a small peptide sequence of the II–III loop and several residues within the SH3 domains of STAC3 as well as the neuronal isoform STAC2. Differences in this interaction between STAC3 and STAC2 suggest that STAC3 possesses distinct biophysical features that are potentially important for its physiological interactions with the II–III loop. Therefore, this work demonstrates an isoform‐specific interaction between STAC3 and the II–III loop of DHPR and provides novel insights into a putative molecular mechanism behind this association in the skeletal muscle ECC process. 相似文献
108.
109.
Satish Srinivas Kitambi Enrique M. Toledo Dmitry Usoskin Shimei Wee Aditya Harisankar Richard Svensson Kristmundur Sigmundsson Christina Kalderén Mia Niklasson Soumi Kundu Sergi Aranda Bengt Westermark Lene Uhrbom Michael Andäng Peter Damberg Sven Nelander Ernest Arenas Per Artursson Julian Walfridsson Karin Forsberg Nilsson Lars G.J. Hammarström Patrik Ernfors 《Cell》2014
110.
Patrick Marcinek Aditya Nath Jha Vidyagouri Shinde Arun Sundaramoorthy Raja Rajkumar Naveen Chandra Suryadevara Sanjeev Kumar Neela Hoang van Tong Vellingiri Balachander Vijaya Lakshmi Valluri Kumarasamy Thangaraj Thirumalaisamy P Velavan 《PloS one》2013,8(8)
In recent years, genome wide association studies have discovered a large number of gene loci that play a functional role in innate and adaptive immune pathways associated with leprosy susceptibility. The immunological control of intracellular bacteria M. leprae is modulated by NOD2-mediated signaling of Th1 responses. In this study, we investigated 211 clinically classified leprosy patients and 230 ethnically matched controls in Indian population by genotyping four variants in NOD2 (rs9302752A/G), LRRK2 (rs1873613A/G), RIPK2 (rs40457A/G and rs42490G/A). The LRRK2 locus is associated with leprosy outcome. The LRRK2 rs1873613A minor allele and respective rs1873613AA genotypes were significantly associated with an increased risk whereas the LRRK2 rs1873613G major allele and rs1873613GG genotypes confer protection in paucibacillary and leprosy patients. The reconstructed GA haplotypes from RIPK2 rs40457A/G and rs42490G/A variants was observed to contribute towards increased risk whereas haplotypes AA was observed to confer protective role. Our results indicate that a possible shared mechanisms underlying the development of these two clinical forms of the disease as hypothesized. Our findings confirm and validates the role of gene variants involved in NOD2-mediated signalling pathways that play a role in immunological control of intracellular bacteria M. leprae. 相似文献