Department Of Human Genetics And Molecular Medicine

Permanent URI for this communityhttps://kr.cup.edu.in/handle/32116/103

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Author: search.filters.author.Singh, SandeepHas files: Yes

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    Dietary Patterns and Breast Cancer Risk: A Multi-Centre Case Control Study among North Indian Women
    (mdpi, 2018) Shridhar, Krithiga; Singh, Gurpreet; Dey, Subhojit; Dhatt, Sarvdeep Singh; Gill, Jatinder Paul Singh; Goodman, Michael; Magsumbol, Melina Samar; Pearce, Neil; Singh, Sandeep; Singh, Archna; Singh, Preeti; Thakur, Jarnail Singh; Dhillon, Preet Kaur
    Evidence from India, a country with unique and distinct food intake patterns often characterized by lifelong adherence, may offer important insight into the role of diet in breast cancer etiology. We evaluated the association between Indian dietary patterns and breast cancer risk in a multi-centre case-control study conducted in the North Indian states of Punjab and Haryana. Eligible cases were women 30–69 years of age, with newly diagnosed, biopsy-confirmed breast cancer recruited from hospitals or population-based cancer registries. Controls (hospital- or population-based) were frequency matched to the cases on age and region (Punjab or Haryana). Information about diet, lifestyle, reproductive and socio-demographic factors was collected using a structured interviewer-administered questionnaire. All participants were characterized as non-vegetarians, lacto-vegetarians (those who consumed no animal products except dairy) or lacto-ovo-vegetarians (persons whose diet also included eggs). The study population included 400 breast cancer cases and 354 controls. Most (62%) were lacto-ovo-vegetarians. Breast cancer risk was lower in lacto-ovo-vegetarians compared to both non-vegetarians and lacto-vegetarians with odds ratios (95% confidence intervals) of 0.6 (0.3–0.9) and 0.4 (0.3–0.7), respectively. The unexpected difference between lacto-ovo-vegetarian and lacto-vegetarian dietary patterns could be due to egg-consumption patterns which requires confirmation and further investigation.
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    Regulation of GAD65 expression by SMAR1 and p53 upon Streptozotocin treatment
    (2012) Singh, Sandeep; Raina, Varsheish; Chavali, Pavithra Lakshminarsimhan; Dubash, Taronish; Kadreppa, Sreenath; Parab, Pradeep; Chattopadhyay, Samit
    Background: GAD65 (Glutamic acid decarboxylase 65 KDa isoform) is one of the most important auto-antigens involved in Type 1 diabetes induction. Although it serves as one of the first injury markers of ?-islets, the mechanisms governing GAD65 expression remain poorly understood. Since the regulation of GAD65 is crucial for the proper functioning of insulin secreting cells, we investigated the stress induced regulation of GAD65 transcription.Results: The present study shows that SMAR1 regulates GAD65 expression at the transcription level. Using a novel protein-DNA pull-down assay, we show that SMAR1 binding is very specific to GAD65 promoter but not to the other isoform, GAD67. We show that Streptozotocin (STZ) mediated DNA damage leads to upregulation of SMAR1 and p53 expression, resulting in elevated levels of GAD65, in both cell lines as well as mouse ?-islets. SMAR1 and p53 act synergistically to up-regulate GAD65 expression upon STZ treatment.Conclusion: We propose a novel mechanism of GAD65 regulation by synergistic activities of SMAR1 and p53. ? 2012 Singh et al.; licensee BioMed Central Ltd.
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    miR-30c and miR-181a synergistically modulate p53?p21 pathway in diabetes induced cardiac hypertrophy
    (Springer New York LLC, 2016) Raut, Satish K.; Singh, Gurinder B.; Rastogi, Bhawna; Saikia, Uma Nahar; Mittal, Anupam; Dogra, Nilambra; Singh, Sandeep; Prasad, Rishikesh; Khullar, Madhu
    p53?p21 pathway mediates cardiomyocyte hypertrophy and apoptosis and is upregulated in diabetic cardiomyopathy (DbCM). We investigated role of microRNAs in regulating p53?p21 pathway in high glucose (HG)-induced cardiomyocyte hypertrophy and apoptosis. miR-30c and miR-181a were identified to target p53. Cardiac expression of microRNAs was measured in diabetic patients, diabetic rats, and in HG-treated cardiomyocytes. Effect of microRNAs over-expression and inhibition on HG-induced cardiomyocyte hypertrophy and apoptosis was examined. Myocardial expression of p53 and p21 genes was increased and expression of miR-30c and miR-181a was significantly decreased in diabetic patients, DbCM rats, and in HG-treated cardiomyocytes. Luciferase assay confirmed p53 as target of miR-30c and miR-181a. Over-expression of miR-30c or miR-181a decreased expression of p53, p21, ANP, cardiomyocyte cell size, and apoptosis in HG-treated cardiomyocytes. Concurrent over-expression of these microRNAs resulted in greater decrease in cardiomyocyte hypertrophy and apoptosis, suggesting a synergistic effect of these microRNAs. Our results suggest that dysregulation of miR-30c and miR-181a may be involved in upregulation of p53?p21 pathway in DbCM. ? 2016, Springer Science+Business Media New York.
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    Chitosan centered bionanocomposites for medical specialty and curative applications: A review
    (Elsevier B.V., 2017) Ahmad, Mudasir; Manzoor, Kaiser; Singh, Sandeep; Ikram, Saiqa
    The polyfunctional nature of chitosan enables its application not only in polymer technology but also shows their importance in the field of nanotechnology for the fabrication of the wide spectrum of functional nanomaterials in biomedical field. Chitosan is a poly aminosaccharide with appealing structure composed of ?-(1???4)-linked D-glucosamine (deacetylated unit) and N-acetyl-D-glucosamine (acetylated unit). It has various functional groups that enriches for various properties such as antibacterial, mucoadhasive, nontoxic, biodegradable, biocompatible. With the advancement of material technologies, chitosan is being chemically modified into self-assembled nanocomposites for advanced biomedical applications. This review article demonstrate the various schemes for the preparation of chitosan nanocomposites from different functional material, focusing on their application specifically in tissue engineering, drug and gene delivery, wound healing and bioimaging. ? 2017 Elsevier B.V.
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    Oxidative stress and inflammation in diabetic complications
    (Hindawi Publishing Corporation, 2014) Vikram, Ajit; Tripathi, Durga Nand; Kumar, Ashutosh; Singh, Sandeep
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    CYP/PON genetic variations as determinant of organophosphate pesticides toxicity
    (Springer India, 2017) Kaur, GURPREET; Jain, A.K.; Singh, Sandeep
    In the present scenario of increased accumulation of pesticides in the environment, it is important to understand its impact on human health. The focus is on gene?environment interaction, highlighting the consequences and factors that may halt the biotransformation of some pesticides and change their actual dose response curve due to mixed exposure to pesticides. The paraoxonase and cytochrome P450 gene families are involved in the metabolism of oxon derivate (toxic than its parent compound) of organophosphate pesticides, thus, mutations in these genes may impact the metabolic outcome of pesticides and subsequent health hazards. The complex multi gene?environment interaction and one gene ? one risk factor are two different aspects to understand the potential health effect related to environmental exposure studies. The genetic polymorphisms are associated with varying levels of risk within the population, as gene products of varied genotype alter the biotransformation of exogenous/endogenous substrates. This paper is aimed to review the impact of endogenous and exogenous factors on a mechanistic pathway of organophosphate pesticide biotransformation and various risk associated with it among the human population. Understanding the genetic polymorphism of genes involved in pesticide metabolism and highlighting the gene isoform dependent interindividual differences to metabolize particular pesticides may help us to unravel the reasons behind differential toxicity for pesticides exposure than expected. ? 2017, Indian Academy of Sciences.
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    Editorial: Signal Transduction Inhibitors as Promising Anticancer Agents
    (Hindawi, 2015) Kumar, Raj; Santos, Cedric Dos; Ahluwalia, Tarunveer Singh; Singh, Sandeep
    Cancer is a group of diseases sharing common features like unrestrictive growth, metastasis, and angiogenesis; however the basic signal transduction pathways are deregulated to such an extent that every cancer case itself poses new challenges for the therapeutics. Worldwide approximately 7.6 million people died of cancer in year 2008 and it has been projected that 13.1 million deaths will be due to cancer by year 2030. Understanding the disease etiology and dysregulation of tissue microenvironment, signal transduction pathways are the potential directions, which may help us find the possible cure for the disease. However, recent advances in cancer therapeutics are proving to be beneficial for the patients but there is still a lot to be desired. Continuous research worldwide is focusing on developing better therapeutics as well as finding novel druggable targets for better efficacy. Another recent development is novel multitarget drugs, which may increase the efficacy manyfold.
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    Pesticide Induced Cytotoxicity Analysis in Human Cells
    (Krishi Sanskriti Publications, 2017) Kaur, Gurpreet; Singh, Sandeep; Jain, A.K.
    The aim of our work was to evaluate the effect of pesticides on cell survival, oxidative stress mechanism in hPBMC (human Peripheral Blood Mononucleated Cells) and lung cancer cells (A549 cell line). Cells were exposed to each atrazine, butachlor, chlorpyriphos and Dichlorvos pesticides of varying concentration individually and in combination of pesticides to evaluate pesticide- pesticide interaction. The hPBMNc and A549 cancer cells have been exposed to 1, 10, 50, 100 μg/ml concentration of each atrazine, butachlor, chlorpyriphos and Dichlorvos for 24 h exposure period. The cytotoxicity study revealed that the atrazine, butachlor, chlorpyriphos and Dichlorvos resulted in statistically significant decrease in cell survival rate in dose dependent manner in hPBMC and A549 cells. The cell cycle arrest has also been observed following 10 μg/ml concentration in cancer cells. The oxidative stress analysis has been done to evaluate the toxicity mechanism behind the cytotoxicity of pesticides under investigation. Our results suggest the increased oxidative stress, and cell cytotoxicity in both hPBMC and A549 Cells. The combined treatments of various pesticides suggest their combinatorial and/or synergistic impact on human cells.