Publications by authors named "Gurinder B Singh"

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  • Recent research indicates that visfatin activates the NLRP3 inflammasome, which leads to podocyte injury, but the exact molecular mechanisms are still unclear.
  • The study found that visfatin triggers the clustering of NADPH oxidase subunits in membrane rafts of podocytes, forming a redox signaling platform that is crucial for NLRP3 activation.
  • Treatments that disrupt these membrane rafts or inhibit NADPH oxidase reduced the harmful effects of visfatin, suggesting that targeting these pathways could mitigate podocyte damage.
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  • India has a significant malaria burden, but Punjab is making progress towards elimination with low incidence rates; the study evaluated the effectiveness of its malaria surveillance system.
  • The evaluation included interviews and data reviews in two districts to assess various system attributes, revealing strengths in flexibility and weaknesses in representativeness and stability.
  • Recommendations for improvement include minimizing supplemental work for staff, ensuring private sector reporting, and providing ongoing training to enhance data quality and timeliness.
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  • AARS2 is a mitochondrial tRNA synthetase that plays a key role in charging tRNA-Ala with alanine and is linked to infantile cardiomyopathy when mutated.
  • The study discovered that the protein PCBP1 interacts with the Aars2 transcript, affecting its alternative splicing and crucial for Aars2's expression, influencing heart development.
  • Mice with cardiomyocyte-specific deletion of Pcbp1 exhibited heart defects similar to human congenital heart issues, and both Pcbp1 and Aars2 mutations disrupted the oxidative phosphorylation pathway, highlighting their roles in metabolic disruptions leading to congenital heart defects.
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  • - The study investigates how tRNA-derived fragments, specifically mt-Ty 5' tiRNAs, influence gene expression in skeletal muscle cell growth and development.
  • - Techniques like Northern blotting, RT-PCR, and RNA-Seq were used to analyze the impact of altering mt-Ty 5' tiRNA levels on muscle cell proliferation and differentiation.
  • - Findings revealed that lower levels of mt-Ty 5' tiRNAs hinder muscle cell growth and development, while increasing these fragments promotes healthier muscle cell function, suggesting their potential as new targets for treating muscle diseases.
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  • The India Hypertension Control Initiative (IHCI) is a collaborative program aimed at controlling hypertension in India, involving 21,895 adult patients from four different states.
  • A significant follow-up assessment revealed that blood pressure (BP) control improved from 26.3% to 59.8% among returning patients, indicating effective management, especially in primary care settings.
  • Despite promising results, the initiative faced challenges with patient retention, highlighting the need for strategies to ensure more patients return for ongoing hypertension care.
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  • - Skeletal muscles are crucial for various bodily functions, and understanding their development and regulation is key for maintaining muscle health and function.
  • - MicroRNAs (miRNAs) are small non-coding RNAs that play a significant role in regulating gene expression in skeletal muscle, affecting processes like myogenesis and overall muscle function.
  • - This review highlights recent findings on miRNAs in muscle development and disorders, such as sarcopenia and Duchenne muscular dystrophy, and briefly touches on their involvement in cancer cachexia.
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Background/aims: Recent studies have shown that nicotine induces podocyte damage. However, it remains unknown how nicotine induces podocyte injury. The present study tested whether nicotine induces NLRP3 inflammasomes activation and thereby contributes to podocyte injury.

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Efforts are being made to scale up human papillomavirus (HPV) vaccination for adolescent girls in India. Bivalent and quadrivalent HPV vaccines were licensed in the country in 2008, and a nonavalent vaccine was licensed in 2018. Demonstration projects initiated in Andhra Pradesh and Gujarat in 2009 introduced HPV vaccination in public health services in India.

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The intestinal microbe-derived metabolite trimethylamine N-oxide (TMAO) is implicated in the pathogenesis of cardiovascular diseases (CVDs). The molecular mechanisms of how TMAO induces atherosclerosis and CVDs' progression are still unclear. In this regard, high-mobility group box protein 1 (HMGB1), an inflammatory mediator, has been reported to disrupt cell-cell junctions, resulting in vascular endothelial hyper permeability leading to endothelial dysfunction.

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Background: The exact mechanism causing decreased expression of the dual specific phosphatase-1 ( DUSP-1) gene in diabetes-associated cardiac hypertrophy is not known. DNA promoter methylation is often associated with decreased gene expression in many diseases including cardiovascular diseases. So, we investigated whether epigenetic silencing via promoter methylation is involved in the decreased expression of DUSP-1 in diabetes-associated cardiac hypertrophy.

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Mitogen-activated protein kinases (MAPKs) (ERK1/2, JNK, and p38) are upregulated in diabetic cardiomyopathy (DCM). Dual-specific phosphatase-1 (DUSP-1) has been reported to regulate the activity of MAPKs in cardiac hypertrophy; however, the role of DUSP-1 in regulating MAPKs activity in DCM is not known. MicroRNAs have been reported to regulate the expression of several genes in hypertrophied failing hearts.

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  • The study explores how the p53-p21 pathway contributes to heart muscle cell (cardiomyocyte) growth and death, particularly in the context of diabetic heart disease (DbCM).
  • Researchers identified microRNAs (miR-30c and miR-181a) that regulate this pathway by targeting the p53 protein, showing they are less active in diabetic conditions.
  • Over-expressing these microRNAs in heart cells led to reduced levels of p53 and p21, decreasing cell growth and death, highlighting their potential role in preventing heart damage in diabetes.
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Aim: Cardiac hypertrophy and myocardial fibrosis significantly contribute to the pathogenesis of diabetic cardiomyopathy (DCM). Altered expression of several genes and their regulation by microRNAs has been reported in hypertrophied failing hearts. This study aims to examine the role of Cdc42, Pak1, and miR-30c in the pathogenesis of cardiac hypertrophy in DCM.

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Cardiovascular complications associated with diabetes significantly contribute to high mortality and morbidity worldwide. The pathophysiology of diabetic cardiomyopathy (DCM), although extensively researched upon, is partially understood. Impairment in various signaling pathways including nitric oxide (NO) signaling has been implicated in the pathogenesis of diabetes induced myocardial damage.

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Cardiovascular complications are a chief cause of mortality and morbidity in diabetic patients. Recent studies suggest that epigenetic changes which may arise as a consequence of environmental factors play an important role in predisposition to disease. Epigenetic mechanisms such as DNA methylation, chromatin remodeling and histone modifications regulate the gene expression in response to environmental signals.

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