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81.
Maria Pratheepa Sushil Kumar Jalali Robinson Silvester Arokiaraj Thiruvengadam Venkatesan Mandadi Nagesh Madhusmita Panda Sharath Pattar 《Bioinformation》2014,10(2):98-100
Insect Barcode Information System called as Insect Barcode Informática (IBIn) is an online database resource developed by the
National Bureau of Agriculturally Important Insects, Bangalore. This database provides acquisition, storage, analysis and
publication of DNA barcode records of agriculturally important insects, for researchers specifically in India and other countries. It
bridges a gap in bioinformatics by integrating molecular, morphological and distribution details of agriculturally important insects.
IBIn was developed using PHP/My SQL by using relational database management concept. This database is based on the client–
server architecture, where many clients can access data simultaneously. IBIn is freely available on-line and is user-friendly. IBIn
allows the registered users to input new information, search and view information related to DNA barcode of agriculturally
important insects.This paper provides a current status of insect barcode in India and brief introduction about the database IBIn.
Availability
http://www.nabg-nbaii.res.in/barcode 相似文献82.
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85.
Sivaram AG Suresh MV Indira M 《Comparative biochemistry and physiology. Toxicology & pharmacology : CBP》2003,134(3):397-401
Oxidative stress is a key step in the pathogenesis of ethanol associated liver injury. Ethanol administration induces an increase in lipid peroxidation either by enhancing the production of oxygen reactive species or by decreasing the level of endogenous antioxidants. In this present study, four groups of male guinea pigs (Cavia porcellus) were maintained for 45 days as follows: Control group (1 mg ascorbic acid (AA)/100 g body wt./day); Ethanol group (1 mg AA/100 g body wt./day+900 mg ethanol/100 g body wt./day); Selenium+AA group (25 mg AA+0.05 mg sodium selenite/100 g body wt./day); Ethanol+Se+AA group (25 mg AA+0.05 mg sodium selenite/100 g body wt.+900 mg ethanol/100 g body wt./day). Malondialehyde (MDA), hydroperoxides (HP) and conjugated dienes (CD) were significantly increased, while the activities of scavenging enzymes superoxide dismutase (SOD) and catalase were reduced in the alcohol administered groups. Co-administration of Se+AA along with alcohol increased the activities of scavenging enzymes and reduced the lipid peroxidation products level in hepatic tissues of guinea pigs. Activities of glutathione peroxidase (GPX) and glutathione reductase (GR) were enhanced in co-administered group. gamma-Glutamyl transpeptidase (GGT), a marker enzyme of alcohol induced toxicity, was also reduced, as was the glutathione content. This study suggests that the combined effect of Se+AA, provides protection against alcohol-induced oxidative stress as evidenced from the decreased levels of lipid peroxidation products and enhanced activities of scavenging enzymes. 相似文献
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Inflammatory cytokines and fatty acids regulate endothelial cell heparanase expression 总被引:10,自引:0,他引:10
Chen G Wang D Vikramadithyan R Yagyu H Saxena U Pillarisetti S Goldberg IJ 《Biochemistry》2004,43(17):4971-4977
Heparan sulfates, the carbohydrate chains of heparan sulfate proteoglycans, play an important role in basement membrane organization and endothelial barrier function. We explored whether endothelial cells secrete a heparan sulfate degrading heparanase under inflammatory conditions and what pathways were responsible for heparanase expression. Heparanase mRNA and protein by Western blot were induced when cultured endothelial cells were treated with cytokines, oxidized low-density lipoprotein (LDL) or fatty acids. Heparanase protein in the cell media was induced 2-10-fold when cells were treated with tumor necrosis factor alpha (TNFalpha) or interleukin 1beta (IL-1beta). Vascular endothelial growth factor (VEGF), in contrast, decreased heparanase secretion. Inhibitors to nuclear factor-kappaB (NFkappaB), PI3-kinase, MAP kinase, or c-jun kinase (JNK) did not affect TNFalpha-induced heparanase secretion. Interestingly, inhibition of caspase-8 completely abolished heparanase secretion induced by TNFalpha. Fatty acids also induced heparanase, and this required an Sp1 site in the heparanase promoter. Immunohistochemical analyses of cross sections of aorta showed intense staining for heparanase in the endothelium of apoE-null mice but not wild-type mice. Thus, heparanase is an inducible inflammatory gene product that may play an important role in vascular biology. 相似文献
88.
Free fatty acids associated with the high molecular weight aminoacyl-tRNA synthetase complex influence its structure and function 总被引:1,自引:0,他引:1
Aminoacyl-tRNA synthetases from higher eukaryotes often are isolated as high molecular weight complexes associated with other components such as lipids. Since hydrophobic interactions are involved in the organization of the complex, it has been suggested that interaction of synthetases with these lipids might be important for their structure and function. Delipidation is known to affect certain properties of synthetases within the complex including sensitivity to detergents plus salts, temperature inactivation, hydrophobicity, sensitivity to proteases, and, as shown here, sensitivity to p-mercuribenzoate and sites of papain cleavage. Of the lipids known to co-purify with the complex, cholesterol esters, phospholipids and free fatty acids, we show that the particular lipids responsible for many of these changes are the free fatty acids. Specific removal of fatty acids results in a complex with properties similar to one totally delipidated by detergent treatment, and readdition of the fatty acid fraction reverses the effects. The fatty acid fraction contains both saturated and unsaturated fatty acids, but unsaturated fatty acids are much more effective in reversing the properties of the delipidated complex that are saturated fatty acids. These results indicate that the free fatty acids co-purifying with the synthetase complex bind to the synthetases and affect their structure and function. 相似文献
89.
Surya P. Bhatt Hrudaya P. Nath Young-il Kim Rekha Ramachandran Jubal R. Watts Nina L. J. Terry Sushil Sonavane Swati P. Deshmane Prescott G. Woodruff Elizabeth C. Oelsner Sandeep Bodduluri MeiLan K. Han Wassim W. Labaki J. Michael Wells Fernando J. Martinez R. Graham Barr Mark T. Dransfield for the SPIROMICS investigators 《Respiratory research》2018,19(1):257
Background
Chronic obstructive pulmonary disease (COPD) is associated with a two-to-five fold increase in the risk of coronary artery disease independent of shared risk factors. This association is hypothesized to be mediated by systemic inflammation but this link has not been established.Methods
We included 300 participants enrolled in the SPIROMICS cohort, 75 each of lifetime non-smokers, smokers without airflow obstruction, mild-moderate COPD, and severe-very severe COPD. We quantified emphysema and airway disease on computed tomography, characterized visual emphysema subtypes (centrilobular and paraseptal) and airway disease, and used the Weston visual score to quantify coronary artery calcification (CAC). We used the Sobel test to determine whether markers of systemic inflammation mediated a link between spirometric and radiographic features of COPD and CAC.Results
FEV1/FVC but not quantitative emphysema or airway wall thickening was associated with CAC (p?=?0.036), after adjustment for demographics, diabetes mellitus, hypertension, statin use, and CT scanner type. To explain this discordance, we examined visual subtypes of emphysema and airway disease, and found that centrilobular emphysema but not paraseptal emphysema or bronchial thickening was independently associated with CAC (p?=?0.019). MMP3, VCAM1, CXCL5 and CXCL9 mediated 8, 8, 7 and 16% of the association between FEV1/FVC and CAC, respectively. Similar biomarkers partially mediated the association between centrilobular emphysema and CAC.Conclusions
The association between airflow obstruction and coronary calcification is driven primarily by the centrilobular subtype of emphysema, and is linked through bioactive molecules implicated in the pathogenesis of atherosclerosis.Trial Registration
ClinicalTrials.gov: Identifier: NCT01969344.90.