Aim: The present study was undertaken to establish a suitable drying process for Garcinia cowa and Garcinia pedunculata fruits for maximum retention of their nutritional qualities. Methodology: Slices of three different thickness with 0.3, 0.6, 0.9 cm of G. cowa and G. pedunculata fruits were dried by sun drying, solar drying and by cabinet drying at three different temperatures (50°C, 70°C and 90°C). Results: The mean crude fat and ash content were higher in G. cowa than G. pedunculata while later was found rich in crude protein and Fe contents. Total phenol content ranged between 881.31-888.65 and 719.00-736.74 mg gallic acid equivalent 100 g-1, total flavonoid content between 89.21-90.06 and 51.00-52.54 mg quercetin equivalent 100 g-1 and mean HCA contents ranged between 3.13-3.92% and 1.84-1.99% for G. cowa and G. pedunculata, respectively. The methanolic extracts exhibited significant antioxidant activity. With lower IC50 values, G. cowa had higher antioxidant activity than G. pedunculata. Interpretation: Oven drying at 50°C and 0.9 cm slice thickness for drying resulted in better retention of total phenolic and flavonoid contents with better antioxidant activities.
Background
Atherosclerosis is one of the major causes of cardiovascular disease. It is characterized by the accumulation of atherosclerotic plaque in arteries under the influence of inflammatory responses, proliferation of smooth muscle cell, accumulation of modified low density lipoprotein. The pathophysiology of atherosclerosis involves the interplay of a number of genes and metabolic pathways. In traditional translation method, only a limited number of genes and pathways can be studied at once. However, the new paradigm of network medicine can be explored to study the interaction of a large array of genes and their functional partners and their connections with the concerned disease pathogenesis. Thus, in our study we employed a branch of network medicine, gene network analysis as a tool to identify the most crucial genes and the miRNAs that regulate these genes at the post transcriptional level responsible for pathogenesis of atherosclerosis.
Result
From NCBI database 988 atherosclerotic genes were retrieved. The protein–protein interaction using STRING database resulted in 22,693 PPI interactions among 872 nodes (genes) at different confidence score. The cluster analysis of the 872 genes using MCODE, a plug-in of Cytoscape software revealed a total of 18 clusters, the topological parameter and gene ontology analysis facilitated in the selection of four influential genes viz., AGT, LPL, ITGB2, IRS1 from cluster 3. Further, the miRNAs (miR-26, miR-27, and miR-29 families) targeting these genes were obtained by employing MIENTURNET webtool.
Conclusion
Gene network analysis assisted in filtering out the 4 probable influential genes and 3 miRNA families in the pathogenesis of atherosclerosis. These genes, miRNAs can be targeted to restrict the occurrence of atherosclerosis. Given the importance of atherosclerosis, any approach in the understanding the genes involved in its pathogenesis can substantially enhance the health care system.
Colistin resistance has increased due to the increasing and inappropriate use of this antibiotic. The mechanism involves modification of lipid A with phosphoethanolamine (PEtN) and/or 4-amino-4deoxy-l-arabinose (L-Ara4N). EptA and eptB catalyze the transfer of phosphoethanolamine to lipid A. In this study, gene network was constructed to find the associated genes related to colistin resistance, and further in vitro validation by transcriptional analysis was performed. In silico studies showed that eptB gene is a highly interconnected node in colistin resistance gene network. To ascertain these findings twelve colistin-resistant clinical isolates of Escherichia coli were selected in which five were harboring the plasmid-mediated mcr-1. Screening for colistin resistance was performed by broth microdilution (BMD) method and Rapid polymyxin NP test. PCR confirmed the presence of the eptA and eptB genes in all isolates and five isolates were harboring mcr-1. Transcriptional expression in five isolates harboring mcr-1, showed an enhanced expression of eptB when exposed under sub-inhibitory colistin stress. The present study for the first time highlighted genetic interplay between mcr-1 and eptA and eptB under colistin exposure.
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