HYDROGEL FORMULATION FROM CALOTROPIS GIGANTEA PLANT EXTRACT AGAINST FOOT ULCER CAUSING BACTERIA IN DIABETES

Objective: The objective of present study was to develop hydrogel formulations loaded with Calotropis gigantea leaves extract. Methods: The prepared hydrogel formulations were compliance with their color, odor, homogeneity, pH, and spreadability. Results: As all the formulations were complies with the all parameters and it can be suggest as a Good antibacterial gel. It is evident that, ethanolic extract of Calotropis gigantea showed a maximum inhibitory zone against bacteria associated with foot ulcer. Conclusions: The In vitro studies showed a quantity dependent increase in antibacterial activity against foot ulcer causing bacteria, a contraction which is higher than that produced by the control groups. These contractions were statistically significant (p<0.05), during the study with leave extract against foot ulcer causing bacteria in diabetes

A study on the antimicrobial property of the cotton fabric imparted with Michaelia champaca leaf extract loaded nanoparticles

In the present work ethanol, methanol, ethyl acetate, chloroform and benzene extract of the Michaelia champaca leaves were screened for their antimicrobial activity. The ethanolic extracts of M. champaca leaves were proved to have the maximum antimicrobial activity; thus the ethanolic leaf extract was selected and the nanoparticles were synthesized using ionic gelification method. The nanoparticles were characterized physically and chemically using TEM and FTIR respectively. The herbal extract loaded nanopartricles were coated on to the non woven cotton fabric using the pad dry cure method. The antimicrobial activity of the untreated and treated (M. champaca leaf extracts coated fabric and leaf extract loaded nanoparticles coated fabric) fabric were assessed by the standard AATCC 147, AATCC 30 and laundering durability. The herbal leaf extract loaded nanoparticles coated fabric showed the better antimicrobial activity and particularly highest wash durability when compared with other treated fabric. The controlled and sustained releasing property of the herb extract loaded nanoparticles could be attributed to its very effective antimicrobial activity. These particles could further have numerous applications in the field of medical textiles. The study revealed that the fabric coated with herbal extract loaded nanoparticles could act against microorganism in the fabric

Molecular docking studies on potent adsorbed receptor of Thrh protein: A new target for biodegradation of indigo dye

Vat dyes are aromatic compounds widely used for denim textile industries, this result in a great wastewater problem from this industry due to recalcitrant nature of these dyes. The active protein (ThrH) was purified from Pseudomonas aeruginosa by DEAE-Sepharose A-50 column chromatography and this 3D crystal structure was reported recently. The present study aimed to demonstrate the binding energy between 3D crystal structures of indigo dye and ThrH. We have calculated the gliding score as well as gliding energy based on the hydrophobic interactions between targeted sites (amino acid and dye residue) and the main think is binding energy which was observed maximum level because of the presence of magnesium ions along with catalytic molecules located at the binding sites. The dye degraded mineralized compound was predicted by mass spectrum and infrared spectroscopy

A DNA Vaccine against Chikungunya Virus Is Protective in Mice and Induces Neutralizing Antibodies in Mice and Nonhuman Primates

Chikungunya virus (CHIKV) is an emerging mosquito-borne alphavirus indigenous to tropical Africa and Asia. Acute illness is characterized by fever, arthralgias, conjunctivitis, rash, and sometimes arthritis. Relatively little is known about the antigenic targets for immunity, and no licensed vaccines or therapeutics are currently available for the pathogen. While the Aedes aegypti mosquito is its primary vector, recent evidence suggests that other carriers can transmit CHIKV thus raising concerns about its spread outside of natural endemic areas to new countries including the U.S. and Europe. Considering the potential for pandemic spread, understanding the development of immunity is paramount to the development of effective counter measures against CHIKV. In this study, we isolated a new CHIKV virus from an acutely infected human patient and developed a defined viral challenge stock in mice that allowed us to study viral pathogenesis and develop a viral neutralization assay. We then constructed a synthetic DNA vaccine delivered by in vivo electroporation (EP) that expresses a component of the CHIKV envelope glycoprotein and used this model to evaluate its efficacy. Vaccination induced robust antigen-specific cellular and humoral immune responses, which individually were capable of providing protection against CHIKV challenge in mice. Furthermore, vaccine studies in rhesus macaques demonstrated induction of nAb responses, which mimicked those induced in convalescent human patient sera. These data suggest a protective role for nAb against CHIKV disease and support further study of envelope-based CHIKV DNA vaccines

Genetic mechanisms of critical illness in COVID-19.

Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 ×  10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

GSTN - The New Network

A robust IT infrastructure holds the key to the successful implementation of GST in India. Much like the GST scheme, the GST Network has also been the subject of much critique. The author in this article discusses two major concerns that have been voiced with the structure of the GSTN. First, the structure and functioning of the GSTN as a NIU has been discussed along with the possibility of interference by non-governmental bodies. Second, the author has dealt with the privacy concerns emerging from such a large scale collection of data by GSTN. This has been analysed in the backdrop of the debate surrounding whether the right to privacy is a fundamental right at all. The article concludes with suggestions on how these two concerns could be best addressed without compromising on the effectiveness of the GSTN

GSTN - The New Network

A robust IT infrastructure holds the key to the successful implementation of GST in India. Much like the GST scheme, the GST Network has also been the subject of much critique. The author in this article discusses two major concerns that have been voiced with the structure of the GSTN. First, the structure and functioning of the GSTN as a NIU has been discussed along with the possibility of interference by non-governmental bodies. Second, the author has dealt with the privacy concerns emerging from such a large scale collection of data by GSTN. This has been analysed in the backdrop of the debate surrounding whether the right to privacy is a fundamental right at all. The article concludes with suggestions on how these two concerns could be best addressed without compromising on the effectiveness of the GSTN

Data Leakage Identification and Blocking Fake Agents Using Pattern Discovery Algorithm

ABSTRACT: A data distributor has given sensitive data to a set of supposedly trusted agents (third parties). If the data distributed to third parties is found in a public/private domain then finding the guilty party is a nontrivial task to distributor. Traditionally, this leakage of data is handled by water marking technique which requires modification of data. If the watermarked copy is found at some unauthorized site then distributor can claim his ownership. To overcome the disadvantages of using watermark, data allocation strategies are used to improve the probability of identifying guilty third parties. In this project, we implement and analyse a guilt model that detects the agents using a protocol. The guilty agent is one who leaks a portion of distributed data. The idea is to distribute the data intelligently to agents based on data request and explicit data request in order to improve the chance of detecting the guilty agents. The algorithms implemented using fake objects will improve the distributor chance of detecting guilty agents. It is observed that by minimizing the sum objective the chance of detecting guilty agents will increase. We also developed a framework for generating fake objects. Our goal is to detect when the distributor's sensitive data have been leaked by agents, and if possible to identify the agent that leaked the data