Publications by authors named "Seela Ramesh"

4 Publications

  • Page 1 of 1

Genetic polymorphisms in tumour necrosis factor receptors () illustrate differential treatment response to TNFα inhibitors in patients with Crohn's disease.

BMJ Open Gastroenterol 2019 1;6(1):e000246. Epub 2019 Feb 1.

Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, Florida, USA.

Background: Monoclonal antibodies inhibiting tumour necrosis factor-α (TNFα) signalling pathway (anti-TNFα) have been widely used in Crohn's disease (CD). However, treatment response varies among patients with CD and the clinical outcome is dependent on single nucleotide polymorphisms (SNP) in TNFα receptor superfamily 1A and 1B ().

Methods: We tested nine SNPs in and by TaqMan genotyping from peripheral blood samples of 104 subjects. Additionally, we quantified the effects of these SNPs on their corresponding gene expression by RT-PCR and susceptibility to subsp (MAP) infection by nested PCR.

Results: Four SNPs ( and ) were over-represented significantly (p<0.05) among patients with CD compared with healthy controls. The GG genotype was found in 15/54 patients with CD (28%), while it was only found in 2/50 healthy controls (4%) (OR 9.2, 95% CI 1.98 to 42.83). The TT genotype was found in 15/54 patients with CD (28%) compared with (4/50) healthy controls (8%) (OR 4.4, 95% CI 1.36 to 14.14). Furthermore, the SNPs and were associated with downregulating their corresponding genes significantly (p<0.05). MAP infection was predominantly found among patients with CD in comparison to healthy controls (57% vs 8%, respectively), which was also dependent on the SNPs and . Our SNP haplotype analysis of and indicates that the G-T haplotype is significantly distributed among patients with CD (46%) and MAP infection susceptibility is also associated with this specific haplotype (31%).

Conclusion: The SNPs and which are known to affect anti-TNFα clinical outcome in CD, were associated with lower corresponding gene expression and higher MAP infection susceptibility.
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http://dx.doi.org/10.1136/bmjgast-2018-000246DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6361334PMC
February 2019

Design, synthesis, molecular-docking and antimycobacterial evaluation of some novel 1,2,3-triazolyl xanthenones.

Medchemcomm 2017 Mar 3;8(3):559-570. Epub 2017 Jan 3.

Molecular Modeling and Medicinal Chemistry Group , Department of Chemistry , Osmania University , Hyderabad , Telangana-500 007 , India.

As part of an ongoing effort to develop new antitubercular and antimicrobial agents, a series of substituted xanthenone derivatives () were synthesized. Xanthenone derivatives () were prepared a one-pot three-component thermal cyclization reaction of β-naphthol (), substituted 1-aryl-1-[1,2,3]triazole-4-carbaldehydes (), and cyclic-1,3-diones (, ) in the presence of a catalytic amount of iodine. The newly synthesized compounds were characterized by IR, NMR, mass spectral data, and elemental analysis. These compounds ( and ) were screened for antitubercular activity against the HRv (ATCC 27294) strain, for antibacterial activity against Gram-positive and Gram-negative strains, and for antifungal activity against a pathogenic strain of fungi. Among the compounds tested, most of them showed good to excellent antimicrobial and antitubercular activity. The active compounds displaying good potency in the MTB were further examined for toxicity in a HEK cell line. In addition, the structure and antitubercular activity relationship were further supported by molecular-docking studies of the active compounds against the pantothenate synthetase (PS) enzyme of .
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http://dx.doi.org/10.1039/c6md00593dDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6072411PMC
March 2017

Evaluation and management of non-alcoholic steatohepatitis.

J Hepatol 2005 30;42 Suppl(1):S2-12. Epub 2004 Dec 30.

Division of Gastroenterology, Hepatology and Nutrition, Department of Internal Medicine, Virginia Commonwealth University, Richmond, VA, USA.

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http://dx.doi.org/10.1016/j.jhep.2004.11.022DOI Listing
July 2005

Hepatitis C and nonalcoholic fatty liver disease.

Semin Liver Dis 2004 Nov;24(4):399-413

Division of Gastroenterology, Hepatology and Nutrition, Department of Internal Medicine, Virginia Commonwealth University Medical Center, Richmond, VA 23298, USA.

Hepatitis C virus (HCV) and nonalcoholic fatty liver disease (NAFLD) are the two most common causes of chronic liver disease in North America. NAFLD represents a spectrum of liver lesions that occur in individuals who either do not consume any alcohol or only consume alcohol in quantities generally considered not to be harmful to the liver. This spectrum consists of isolated hepatic macrovesicular steatosis at one end and nonalcoholic steatohepatitis (NASH) at the other. Hepatic steatosis is present in approximately 50% of the subjects with HCV. Genotype 3 is independently associated with hepatic steatosis. In those with genotype 1 infection, steatosis is associated with features of the metabolic syndrome. The presence of hepatic steatosis correlates with the stage of hepatic fibrosis in patients with HCV. This has been related to the presence of insulin resistance. Hepatic steatosis also adversely affects the virologic response rates to anti-HCV therapy. In this article, we will review the epidemiology of HCV and NAFLD, their impact on each other, and the course of the liver disease in individuals afflicted with both conditions.
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http://dx.doi.org/10.1055/s-2004-860869DOI Listing
November 2004
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