10 results on '"Gupta, Vipin"'
Search Results
2. Comparative genomic analysis of novel Acinetobacter symbionts: A combined systems biology and genomics approach
- Author
-
Gupta, Vipin, Haider, Shazia, Sood, Utkarsh, Gilbert, Jack A, Ramjee, Meenakshi, Forbes, Ken, Singh, Yogendra, Lopes, Bruno S, and Lal, Rup
- Subjects
Biochemistry and Cell Biology ,Biomedical and Clinical Sciences ,Biological Sciences ,Microbiology ,Medical Microbiology ,Genetics ,Infectious Diseases ,Antimicrobial Resistance ,Biotechnology ,Emerging Infectious Diseases ,2.1 Biological and endogenous factors ,5.1 Pharmaceuticals ,Aetiology ,Development of treatments and therapeutic interventions ,Infection ,Acinetobacter ,Acinetobacter Infections ,Animals ,Bacterial Proteins ,Feces ,Genome ,Bacterial ,Moths ,Sheep ,Systems Biology - Abstract
The increasing trend of antibiotic resistance in Acinetobacter drastically limits the range of therapeutic agents required to treat multidrug resistant (MDR) infections. This study focused on analysis of novel Acinetobacter strains using a genomics and systems biology approach. Here we used a network theory method for pathogenic and non-pathogenic Acinetobacter spp. to identify the key regulatory proteins (hubs) in each strain. We identified nine key regulatory proteins, guaA, guaB, rpsB, rpsI, rpsL, rpsE, rpsC, rplM and trmD, which have functional roles as hubs in a hierarchical scale-free fractal protein-protein interaction network. Two key hubs (guaA and guaB) were important for insect-associated strains, and comparative analysis identified guaA as more important than guaB due to its role in effective module regulation. rpsI played a significant role in all the novel strains, while rplM was unique to sheep-associated strains. rpsM, rpsB and rpsI were involved in the regulation of overall network topology across all Acinetobacter strains analyzed in this study. Future analysis will investigate whether these hubs are useful as drug targets for treating Acinetobacter infections.
- Published
- 2016
3. Genomics of body fat distribution
- Author
-
SAINI, SIMMI, WALIA, GAGANDEEP KAUR, SACHDEVA, MOHINDER PAL, and GUPTA, VIPIN
- Published
- 2021
- Full Text
- View/download PDF
4. Prevalence of thyroid autoimmunity in first-degree relatives of patients with celiac disease
- Author
-
Soni, Snigdha, Agarwal, Ashish, Singh, Alka, Gupta, Vipin, Khadgawat, Rajesh, Chaturvedi, Pradeep K., Ahuja, Vineet, and Makharia, Govind K.
- Published
- 2019
- Full Text
- View/download PDF
5. Genetics of obesity and its measures in India.
- Author
-
Saini, Simmi, Walia, Gagandeep Kaur, Sachdeva, Mohinder Pal, and Gupta, Vipin
- Subjects
OBESITY genetics ,METABOLIC disorders ,PATHOLOGICAL physiology ,SEXUAL dimorphism ,GENETIC regulation - Abstract
Obesity is one of the largest global health problems associated with increased morbidity and mortality mediated by its association with several other metabolic disorders. The interaction between the genes and environment plays an important role in the manifestation of obesity. Despite a high heritability (40-70%) of obesity, the search for genetic variants associated with obesity susceptibility has been a challenging task. To date, limited studies have been conducted in India, restricted to the validation of few genetic variants identified by genomewide association studies. In this critical review, we sought to examine the current knowledge of genetic basis of obesity and its measures in the Indian population. A comprehensive literature search was performed using ‘PubMed’, ‘Medline’ and ‘IndMed’ databases to search for citations published until 31st May 2017, using the key terms as ‘Genetics’ AND ‘obesity’ AND ‘India’. We identified 48 potential studies which fulfilled the eligibility criteria. The findings indicated that FTO, MC4R, TNF-α
, PPAR-γ , UCP1, UCP2, LPL, LEPR, AMD1, IL6, APOE, ADIPOQ, DOK5, INSIG2, PBEF1, IL6R, Myostatin, CXCR4, HHEX, IRX3, POMC, NGN3, FOXA2, MTR, TCN and CHDH are some of the important genes studied among the Indian population. Importantly, the role of sexual dimorphism in the genetic regulation of obesity and body fat distribution was also reported in a few studies. Further, seven biological pathways have been identified that contribute to obesity pathogenesis in India. In conclusion, further exploration of pathway-based research on genetics of obesity can be useful for better understanding the pathophysiology of obesity in India. [ABSTRACT FROM AUTHOR] - Published
- 2018
- Full Text
- View/download PDF
6. Role of <italic>CYP1B1,</italic> p.E229K and p.R368H mutations among 120 families with sporadic juvenile onset open-angle glaucoma.
- Author
-
Gupta, Viney, Somarajan, Bindu I., Walia, Gagandeep Kaur, Kaur, Jasbir, Kumar, Sunil, Gupta, Shikha, Chaurasia, Abadh K., Gupta, Dinesh, Kaushik, Abhinav, Mehta, Aditi, Gupta, Vipin, and Sharma, Arundhati
- Subjects
GLAUCOMA ,GLAUCOMA treatment ,GENETIC mutation ,DYSGENESIS ,NEUROPATHY ,GENETICS - Abstract
Background: To determine the frequency of
CYP1B1 p.E229K and p.R368H, gene mutations in a cohort of sporadic juvenile onset open-angle glaucoma (JOAG) patients and to evaluate their genotype/phenotype correlation.Methods: Unrelated JOAG patients whose first-degree relatives had been examined and found to be unaffected were included in the study. The patients and their parents were screened for p.E229K and p.R368H mutations. The phenotypic characteristics were compared between probands carrying the mutations and those who did not carry these mutations.Results: Out of 120 JOAG patients included in the study, the p.E229K mutation was seen in 9 probands (7.5%) and p.R368H in 7 (5.8%). The average age of onset of the disease (p = 0.3) and the highest untreated IOP (p = 0.4) among those carrying mutations was not significantly different from those who did not have these mutations. The proportion of probands with angle dysgenesis among those with p.E229K and p.R368H mutations was 70% (11 out of 16) in comparison to 65% (67 out of 104) of those who did not harbour these mutations (p = 0.56). Similarly, the probands with moderate to high myopia among those with p.E229K and p.R368H mutations was 20% (3 out of 16) in comparison to 18% (18 out of 104) of those who did not harbour these mutations (p = 0.59).Conclusion: The frequency of p.E229K and p.R368H mutations of theCYP1B1 gene is low even among sporadic JOAG patients. Moreover, there is no clinical correlation between the presence of these mutations and disease severity. [ABSTRACT FROM AUTHOR]- Published
- 2018
- Full Text
- View/download PDF
7. Association of Common Genetic Variants with Lipid Traits in the Indian Population.
- Author
-
Walia, Gagandeep Kaur, Gupta, Vipin, Aggarwal, Aastha, Asghar, Mohammad, Dudbridge, Frank, Timpson, Nicholas, Singh, Nongmaithem Suraj, Kumar, M. Ravi, Kinra, Sanjay, Prabhakaran, Dorairaj, Reddy, K. Srinath, Chandak, Giriraj Ratan, Smith, George Davey, and Ebrahim, Shah
- Subjects
- *
HUMAN genetic variation , *BLOOD lipids , *LOW density lipoproteins , *LOCUS (Genetics) , *HIGH density lipoproteins - Abstract
Genome-wide association studies (GWAS) have been instrumental in identifying novel genetic variants associated with altered plasma lipid levels. However, these quantitative trait loci have not been tested in the Indian population, where there is a poorly understood and growing burden of cardiometabolic disorders. We present the association of six single nucleotide polymorphisms in 1671 sib pairs (3342 subjects) with four lipid traits: total cholesterol, triglycerides, high density lipoprotein cholesterol (HDL-C) and low density lipoprotein cholesterol (LDL-C). We also investigated the interaction effects of gender, location, fat intake and physical activity. Each copy of the risk allele of rs964184 at APOA1 was associated with 1.06 mmol/l increase in triglycerides (SE = 0.049; p = 0.006), rs3764261 at CETP with 1.02 mmol/l increase in both total cholesterol (SE = 0.042; p = 0.017) and HDL-C (SE = 0.041; p = 0.008), rs646776 at CELSR2-PSRC1-SORT1 with 0.96 mmol/l decrease in cholesterol (SE = 0.043; p = 0.0003) and 0.15 mmol/l decrease in LDL-C levels (SE = 0.043; p = 0.0003) and rs2954029 at TRIB1 with 1.02 mmol/l increase in HDL-C (SE = 0.039; p = 0.047). A combined risk score of APOA1 and CETP loci predicted an increase of 1.25 mmol/l in HDL-C level (SE = 0.312; p = 0.0007). Urban location and sex had strong interaction effects on the genetic association of most of the studied loci with lipid traits. To conclude, we validated four genetic variants (identified by GWAS in western populations) associated with lipid traits in the Indian population. The interaction effects found here may explain the sex-specific differences in lipid levels and their heritability. Urbanization appears to influence the nature of the association with GWAS lipid loci in this population. However, these findings will require replication in other Indian populations. [ABSTRACT FROM AUTHOR]
- Published
- 2014
- Full Text
- View/download PDF
8. Genetic underpinnings of lung function and COPD.
- Author
-
Ranjan, Astha, Singh, Amanjot, Walia, Gagandeep Kaur, Sachdeva, Mohinder Pal, and Gupta, Vipin
- Published
- 2019
- Full Text
- View/download PDF
9. Genetics of nonalcoholic fatty liver disease in Asian populations.
- Author
-
Kumar, Arun, Shalimar, Walia, Gagandeep Kaur, Gupta, Vipin, and Sachdeva, M. P.
- Abstract
Nonalcoholic fatty liver disease (NAFLD) is characterized by the accumulation of fat in the liver without any historyof chronic alcohol consumption. It encompasses a wide spectrum of diseases that range from simple steatosis to nonalcoholicsteatohepatitis. NAFLD is strongly associated with obesity, insulin resistance / type-2 diabetes mellitus and the metabolic syndrome.NAFLD is a complex disorder; environmental and genetic factors interact with NAFLD manifestation and determine its progression.In this review, an attempt was made to provide current information on the genetic variants of NAFLD in Asian populations. Literaturesearch was performed by using PubMed, Medline and Google Scholar database. Candidate gene, validation and genomewideassociation studies (GWASs) were included in this review. A total of 41 studies fulfilled inclusion criteria of which 12 candidategene studies exclusively focussed on thePNPLA3gene and 17 other studies on other important candidate genes such asNCAN-CILP2,PPARG,AGTR1,FABP1,APOC3etc. reported significant association with NAFLD. Eight validation studies identifiedassociations of variants onPNPLA3,LYPLAL1,TM6SF2,ADIPOR2,STAT3,GCKR,SAMM50etc. with NAFLD. Thus, so far,four GWASs have been conducted in Asian population that reportedPNPLA3,SAMM50,PARVBandGATAD2Agenes which weresignificantly associated withNAFLD. Findings indicate thatPNPLA3,APOC3,PPARG,NCANandGCKRgenes emerge out to bethe important biological markers associated with NAFLD. [ABSTRACT FROM AUTHOR]
- Published
- 2019
- Full Text
- View/download PDF
10. Explanation of genetic component of human height by recent genome-wide association studies.
- Author
-
Gupta, Vipin and Sachdeva, M. P.
- Subjects
- *
STATURE , *BODY size , *HUMAN genetics , *GENOMES , *GENETICS , *HUMAN biology , *DEVELOPMENTAL biology - Abstract
In the article the author examines the genetic component of human height through genome-wide association studies (GWAS) in India. It highlights the sources being considered by GWAS to define a part of genetic spectrum of anthropometric traits in human height, considering the help of physical anthropology literature on human growth and developmental research. It also presents data on the association of genetic variants among the general population, that were seen to possibly affect human height.
- Published
- 2010
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.