2-Amino-isonicotinic acid/4-Pyridinecarboxylic acid, 2-amino-/2-amino-4-carboxypyridine/acide 2-aminoisonicotinique/2-Amino-4-pyridinecarboxylic acid/2-Amino-4-pyridine carboxylic acid/2-Aminopyridine-4-carboxylic acid
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provides coniferyl ferulate(CAS#:13362-28-2) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Antithrombin III (AT) is the main inhibitor of blood coagulation proteases like thrombin and factor Xa. In this study we report the identification and characterization of several variants of AT for the first time in Indian population. We screened 1950 deep vein thrombosis (DVT) patients for AT activity and antigen levels. DNA sequencing was further carried out in patients with low AT activity and/or antigen levels to identify variations in the AT gene. Two families, one with type I and the other with type II AT deficiency were identified. Three members of family I showed an increase in the coagulation rates and recurrent thrombosis in this family was solely attributed to the rs2227589 polymorphism. Four members of family II spanning two generations had normal antigen levels and decreased AT activity. A novel single nucleotide insertion, g.13362_13363insA in this family in addition to g.2603T>C (p.R47C) mutation were identified. AT purified from patient’s plasma on hi-trap heparin column showed a marked decrease in heparin affinity and thrombin inhibition rates. Western blot analysis showed the presence of aggregated AT. We also report a novel point mutation at position g.7549 A>G (p.T280A), that is highly conserved in serpin family. Variant protein isolated from patient plasma indicated loss of regulatory function due to in-vivo polymerization. In conclusion this is the first report of AT mutations in SERPINC1 gene in Indo-Aryan population where a novel point mutation p.T280A and a novel single nucleotide insertion g.13362_13363insA are reported in addition to known variants like p.R47C, p.C4-X and polymorphisms of rs2227598, PstI and DdeI.
Antithrombin III Deficiency in Indian Patients with Deep Vein Thrombosis: Identification of First India Based AT Variants Including a Novel Point Mutation (T280A) that Leads to Aggregation
Teena Bhakuni, 1 Amit Sharma, 2 Qudsia Rashid, 1 Charu Kapil, 1 Renu Saxena, 2 Manoranjan Mahapatra, 2 and Mohamad Aman Jairajpuri 1 ,*
HIV patients develop hepatic steatosis. We investigated hepatic steatosis in transgenic mice expressing the HIV-1 accessory protein Vpr (Vpr-Tg) in liver and adipose tissues, and WT mice infused with synthetic Vpr. Vpr-Tg mice developed increased liver triglyceride content and elevated ALT, bilirubin and alkaline phosphatase due to three hepatic defects: 1.6-fold accelerated de novo lipogenesis (DNL), 45% slower fatty acid ß-oxidation, and 40% decreased VLDL-triglyceride export. Accelerated hepatic DNL was due to coactivation by Vpr of liver X receptor-α (LXRα) with increased expression of its lipogenic targets Srebp1c, Chrebp, Lpk, Dgat, Fasn and Scd1, and intranuclear SREBP1c and ChREBP. Vpr enhanced association of LXRα with Lxrα and Srebp1c promoters, increased LXRE-LXRα binding, and broadly altered hepatic expression of LXRα-regulated lipid metabolic genes. Diminished hepatic fatty acid ß-oxidation was associated with decreased mRNA expression of Pparα and its targets Cpt1, Aox, Lcad, Ehhadh, Hsd10 and Acaa2, and blunted VLDL export with decreased expression of Mttp and its product microsomal triglyceride transfer protein. With our previous findings that Vpr circulates in HIV patients (including those with undetectable plasma HIV-1 RNA), co-regulates the glucocorticoid receptor and PPARγ and transduces hepatocytes, these data indicate a potential role for Vpr in HIV-associated fatty liver disease.
HIV-1 viral protein R (Vpr) induces fatty liver in mice via LXRα and PPARα dysregulation: implications for HIV-specific pathogenesis of NAFLD
Neeti Agarwal,1 Dinakar Iyer,1,9 Chiara Gabbi,2 Pradip Saha,1 Sanjeet G. Patel,3 Qianxing Mo,4 Benny Chang,1 Biman Goswami,1 Ulrich Schubert,5 Jeffrey B. Kopp,6 Dorothy E. Lewis,7 and Ashok Balasubramanyamcorresponding author1,8
To examine the association between 18F-fluorodeoxyglucose (18F-FDG) uptake in positron emission tomography/computed tomography (PET/CT) and the response to anti-programmed cell death-1 (PD-1) monoclonal antibody therapy in non-small cell lung cancer (NSCLC) patients, 89 patients with advanced or recurrent NSCLC were retrospectively analysed. Maximum standardized uptake value (SUVmax) in 18F-FDG PET/CT and the response to anti-PD-1 antibodies were recorded. A cut-off value of SUVmax was determined by receiver operating characteristic curve analysis for patient stratification. Among the 89 patients evaluated, 24 were classified as responders (all partial response), and 65 as non-responders. The average SUVmax of the responders was 15.60 (range, 6.44-51.10), which was significantly higher than that of the non-responders (11.61; range, 2.13-32.75; P = 0.0168, Student’s t-test). The cut-off SUVmax value selected for stratification was 11.16 (sensitivity and specificity, 0.792 and 0.585, respectively). The response rate of patients with SUVmax value ≥ 11.16 (41.3% [19/46]) was significantly higher than that of patients with SUVmax < 11.16 (11.6% [5/43], P = 0.0012, Chi-squared test). The SUVmax in 18F-FDG PET/CT is a potential predictive marker of response to anti-PD-1 antibody therapy in NSCLC patients. Further prospective studies of large populations are necessary to validate these results. Subject terms: Predictive markers, Non-small-cell lung cancer, Tumour biomarkers
18F-FDG uptake in PET/CT is a potential predictive biomarker of response to anti-PD-1 antibody therapy in non-small cell lung cancer
Kazuki Takada,corresponding author1 Gouji Toyokawa,2 Yasuto Yoneshima,3 Kentaro Tanaka,3 Isamu Okamoto,3 Mototsugu Shimokawa,4 Sho Wakasu,1 Akira Haro,1 Atsushi Osoegawa,1 Tetsuzo Tagawa,1 Yoshinao Oda,5 Yoichi Nakanishi,3 and Masaki Mori1