Vellore Institute of Technology (VIT) is a private university located in&nbsp;Tamil Nadu, India. Founded in 1984, as Vellore Engineering College, the institution offers 20 undergraduate, 34 postgraduate, four integrated and four research programs. It has campuses in Vellore, Amravati, Bhopal and Chennai.

VIT is one of the top ranked private universities in India according to NIRF, THE and QS Rankings.&nbsp;Govt. of India has recognized&nbsp;VIT, Vellore as an&nbsp;Institution of Eminence. This has allowed VIT to take independent quality initiatives and move up in world ranking.

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VIT University

Department of Biotechnology

Abstract: The main objective of this study (ABST and MIC) is used to recognize the possible drug resistance in microorganisms like Escherichia coli, Staphylococcus aureus and to assure susceptibility to drug of choice for particular infections. Here we use various medicinal plant extracts like Basil leaves (Ocimum tenuiflorum), Aloe vera (Aloe barbadensis miller), karpuravalli (Plectranthus amboinicus), kuppaimani (Acalypha indica) to determine an antimicrobial activity. By using different concentrations of these extracts, we evaluate whether the bacteria are susceptible to these compounds or not. We use Gram positive and Gram-negative microorganisms for the evaluation of pharmacological examinations and furthermore we have used immobilization technique for long term preservation. This technique will be useful to keep the medicinal plant extracts in an active form for a longer period of time.

School of Bio Sciences and Technology

Vellore Campus

INTERNATIONAL JOURNAL OF SCIENTIFIC & TECHNOLOGY RESEARCH

evaluation of culinary plants by using ABST and MIC for pharmacological studies

Cancer is a disease that is characterized by uncontrolled cell growth with the ability to penetrate or develop to the other parts of the body. Various studies have shown the significance of identifying drug targets for cancer, although this process continues challenging in the field of anti-cancer drug designing. The primary purpose of this study is to design a novel approach to identify target genes for cancer. The sub-network of colorectal, pancreatic, and prostate cancers were constructed from human protein–protein interaction network. The potential genes were analyzed using hubs and centrality measures. For the identification of target genes, we retrieve those genes that had the highest score in both mutation rates and graph centrality. Moreover, gene deletion analysis revealed that MYC, TP53, and EGFR genes remained potential targets in colorectal, pancreatic, and prostate cancer respectively. Results suggest that combining network measures with mutation frequencies in cancer genes might assist in recognizing several potential drug targets. Future enhancement of this current approach is to combine these network properties with the biological insights from gene expression data, and their functions will provide a reliable method for rational drug designing.

VIT Unitversity

Network Modeling Analysis in Health Informatics and Bioinformatics

Identification of target genes in cancer diseases using protein–protein interaction networks

Breast cancer (BC) is the most commonly diagnosed cancer among females worldwide, and among the BC-associated mutations in various proteins, mutations in the RAC-alpha serine/threonine-protein kinase (AKT1) remain the most dominant. We thus attempted to understand the potential molecular pathogenicity profile of the mutations in AKT1 using a comprehensive computational protocol involving analyses of biochemistry-disruption and destabilizing properties and conservation. Our predictions revealed that E17K, R67W, V164G, E319G, R391G, D32Y, L52H, L52R, and W80R were the most pathogenic mutations. In addition, the change of glutamate to lysine at position 17 of AKT1 (E17K) was found to be highly predominant. An extensive two-step molecular dynamics (simple and complex) simulation (MDS) using GROMACS (GROningen MAchine for Chemical Simulations) was then initiated to analyze and understand the structural impact of the E17K mutation on the function of AKT1. The simple MDS analysis revealed that the E17K mutation decreases the compactness and intramolecular hydrogen bonds of the protein. We also performed a virtual screening analysis with 19 AKT inhibitors obtained from the Selleck Chemicals website those satisfied the Lipinski rule of 5. Among these 19 compounds, Akti-1/2 exhibited the best binding affinity with both native AKT1 and the E17K mutant. The molecular interaction study also revealed that the co-crystallized AKT1 inhibitor N-(4-(5-(3-acetamidophenyl)-2-(2-aminopyridin-3-yl)-3H-imidazo [4,5-b]pyridin-3-yl)benzyl)-3-fluorobenzamide (12j) exhibited a better interaction with native AKT1 compared with the E17K mutant AKT1 protein, whereas, Akti-1/2 exhibited the opposite effects, i.e., a better interaction with the E17K mutant AKT1 than the native AKT1. These findings from the interaction analysis were further supported by the complex MDS, which measured the compactness and intermolecular hydrogen bonds of the proteins. The results obtained in this study suggest that Akti-1/2 might be a better inhibitor for the treatment of BC caused by the E17K mutation in AKT1. © 2019 Elsevier Ltd

Department of Integrative Biology

Computers in Biology and Medicine

A computational approach for investigating the mutational landscape of RAC-alpha serine/threonine-protein kinase (AKT1) and screening inhibitors against the oncogenic E17K mutation causing breast cancer

World University root node

Gene Reports

In silico studies on CNR1 receptor and effective cyanobacterial drugs: Homology modelling, molecular docking and molecular dynamic simulations

Regenerative Engineering and Translational Medicine

Neuropotency and Neurotherapeutic Potential of Human Umbilical Cord Stem Cell’s Secretome

Environmental Chemistry Letters

Enhanced bioleaching of copper from circuit boards of computer waste by Acidithiobacillus ferrooxidans

The antimicrobial resistance (AMR) exhibited against broad spectrum and new generation antibiotics used for Pseudomonas infections is a major threat and renders the treatment ineffective. In our present study, we have used a computational approach to understand various drug resistance mechanisms which contribute to Multi-Drug Resistance (MDR) in P. aeruginosa. The interaction network of 60 AMR genes along with the 337 functional interactions was analyzed. Functional enrichment analysis of AMR genes has shown that the genes in the network are mainly associated with efflux pump mechanisms, alginate biosynthesis, biofilm formation, and ampC beta-lactamase biosynthesis. Interestingly, the genes phoP, phoQ, and cat genes are observed to have roles in more than one drug-resistant mechanism. The genes phoP and phoQ apart from their role in two-component regulatory systems also play major roles in multidrug efflux pumps and alteration in drug target. The gene cat involves in alteration of drug target and enzymatic inactivation. The interaction network analysis has shown that the AMR genes oprJ, oprM, oprN, ampC, gyrA, mexA, oprD, mexB and nfxB have higher number of direct interactors and they are considered as the hub nodes in the network and these genes can be used as potential drug targets for developing new drugs. The results from our study will be helpful in better understanding of the antibiotic resistance mechanisms in P. aeruginosa. The gene targets reported, can be used for new drug discovery against Pseudomonas infections. © 2019 Elsevier Ltd

Department of Bio-Sciences

Microbial Pathogenesis

Systems biology studies in Pseudomonas aeruginosa PA01 to understand their role in biofilm formation and multidrug efflux pumps

A pre-eminent subtype of lung carcinoma, Non-small cell lung cancer accounts for paramount causes of cancer-associated mortality worldwide. Undeterred by the endeavour in the treatment strategies, the overall cure and survival rates for NSCLC remain substandard, particularly in metastatic diseases. Moreover, the emergence of resistance to classic anticancer drugs further deteriorates the situation. These demanding circumstances culminate the need of extended and revamped research for the establishment of upcoming generation cancer therapeutics. Drug repositioning introduces an affordable and efficient strategy to discover novel drug action, especially when integrated with recent systems biology driven stratagem. This review illustrates the trendsetting approaches in repurposing along with their numerous success stories with an emphasize on the NSCLC therapeutics. Indeed, these novel hits, in combination with conventional anticancer agents, will ideally make their way the clinics and strengthen the therapeutic arsenal to combat drug resistance in the near future. © 2019 Elsevier Ltd

Fulltext

Seminars in Cancer Biology

Current progress and future perspectives of polypharmacology : From the view of non-small cell lung cancer

Main conclusion: Rice sheath blight research should prioritise optimising biological control approaches, identification of resistance gene mechanisms and application in genetic improvement and smart farming for early disease detection. Abstract: Rice sheath blight, caused by Rhizoctonia solani AG1-1A, is one of the most devasting diseases of the crop. To move forward with effective crop protection against sheath blight, it is important to review the published information related to pathogenicity and disease management and to determine areas of research that require deeper study. While progress has been made in the identification of pathogenesis-related genes both in rice and in the pathogen, the mechanisms remain unclear. Research related to disease management practices has addressed the use of agronomic practices, chemical control, biological control and genetic improvement: Optimising nitrogen fertiliser use in conjunction with plant spacing can reduce spread of infection while smart agriculture technologies such as crop monitoring with Unmanned Aerial Systems assist in early detection and management of sheath blight disease. Replacing older fungicides with natural fungicides and use of biological agents can provide effective sheath blight control, also minimising environmental impact. Genetic approaches that show promise for the control of sheath blight include treatment with exogenous dsRNA to silence pathogen gene expression, genome editing to develop rice lines with lower susceptibility to sheath blight and development of transgenic rice lines overexpressing or silencing pathogenesis related genes. The main challenges that were identified for effective crop protection against sheath blight are the adaptive flexibility of the pathogen, lack of resistant rice varieties, abscence of single resistance genes for use in breeding and low access of farmers to awareness programmes for optimal management practices. © 2019, Springer-Verlag GmbH Germany, part of Springer Nature.

Planta

Sheath blight of rice: a review and identification of priorities for future research

Genetic polymorphisms are mostly associated with inherited diseases, detecting and analyzing the biological significance of functional single-nucleotide polymorphisms (SNPs) using wet laboratory experiments is an arduous task hence the computational analysis of putative SNPs is essential before conducting a study on a large population. SNP in the leptin receptor (LEPR) could result in the retention of intracellular signalling due to the structural and functional instability of the receptor causing abnormal reproductive function in human. In this first comprehensive computational analysis of LEPR gene mutation, we have identified and analyzed the functional consequence and structural significance of the SNPs in LEPR using recently developed several computational algorithms. Thirteen deleterious mutations such as W13C, S93G, I232R, Q307H, Y354C, E497A, Q571H, R612H, K656N, T690A, T699M V741M, and L760R were identified in the LEPR gene coding region. Backpropagation algorithm has been developed to forestall the deleterious nature of SNP and to validate the outcome of the tested computational tools. From ConSurf prediction three SNPs (Q571H, R612H, and T699M) were highly conserved on LEPR protein and the most deleterious variant R612H had one hydrogen bond abolished and severely reduced protein stability. Molecular docking suggested that the mutant (R612H) LEPR had lowest binding energy than native LEPR with the ligand molecule. Thus the energetically destructive changeover of ARG to HIS in R612H could possibly affect the LEPR protein structural stability and functional constancy due to interruption in the amino acid interactions and could result in reproductive disorders in human and increases the complication in obstetric and pregnancy outcome. © 2019 Wiley Periodicals, Inc.