Publications by authors named "Balasubramaniyan N"

Whether early life acetaminophen (APAP) exposures injure the developing lung is controversial. We sought to correlate murine pulmonary developmental expression profiles of to susceptibility to APAP exposure. P14 C57BL/6 mice were exposed to APAP (140 mg/kg x 1, IP) and assessed for evidence of a histologic, metabolic, functional, and/or transcriptional pulmonary response.

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Researchers have been motivated to develop photovoltaic systems that can efficiently convert artificial light into power with the growing use of indoor electrical devices for the Internet of Things. Understanding the impact of molecular design strategies involving morphological optimization through the terminal group of the non-fullerene acceptors (NFAs) is crucial. This is critically important to enhancing the photovoltaic efficiency of organic photovoltaic devices under diverse irradiation conditions.

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A 20-year-old female presents with a painless, progressive, normal color smooth surface sublingual swelling extending to chin that had gradually increased in size over the preceding 2 months, which severely impaired her speech and swallowing. Fine-needle aspiration biopsy was suggestive of benign cystic lesion. Following surgical excision, the mass was found to contain a large amount of sebaceous keratin material removed along with the entire capsule of the cyst.

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Background: The developmental immaturity of the innate immune system helps explains the increased risk of infection in the neonatal period. Importantly, innate immune signaling pathways such as p65/NFκB and c-Jun/AP1 are responsible for the prevention of hepatocyte apoptosis in adult animals, yet whether developmental immaturity of these pathways increases the risk of hepatic injury in the neonatal period is unknown.

Methods: Using a murine model of endotoxemia (LPS 5 mg/kg IP x 1) in neonatal (P3) and adult mice, we evaluated histologic evidence of hepatic injury and apoptosis, presence of p65/NFκB and c-Jun/AP1 activation and associated transcriptional regulation of apoptotic genes.

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The ability to detect hydrogen peroxide is important due to the presence in biological systems. Researchers are highly interested in developing efficient electrochemical hydrogen peroxide sensors. Metal-organic frameworks (MOFs) with their composites, an emerging class of porous materials, are ideal candidates for heterogeneous catalysts because of their versatile functionalities.

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Maintenance of hepatocyte homeostasis plays an important role in mediating the pathogenesis of many diseases. A growing body of literature has established a critical role played by tumor necrosis factor-α (TNFα) in maintaining hepatocyte homeostasis; however, the transcriptional mechanisms underlying constitutive expression are unknown. Whole liver fractions and primary hepatocytes from adult control C57BL/6 mice and the murine hepatocyte cell line AML12 were assessed for constitutive expression.

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Establishing an S-scheme heterojunction is a promising method for increasing the photocatalytic activity of synthetic materials. In this study, nitrogen-doped g-CN/TiO S-scheme photocatalysts have been synthesized and examined for photocatalytic hydrogen production using thermal decomposition methods. Nitrogen-doped g-CN/TiO composites performed better than pure nitrogen-doped g-CN and TiO alone.

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Rationale: In Indian subcontinent, every adult may have suffered from chicken pox during their early childhood and harbour the virus, which eventually becomes inactive over years. These latent organisms can undergo sudden activation when triggered by injection of local anaesthesia in the oral cavity. Probably, some symptoms develop along the distribution of the nerve.

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Herein, simple acceptor-donor-acceptor (A-D-A)-type small molecules denoted as DICTF and DRCTF with modification in terminal units were synthesized and used as electron acceptors. With the tuning of the electron-withdrawing units in electron acceptors, their photovoltaic properties were investigated when combined with low-band-gap BODIPY-thiophene-backboned donor material, named P(BdP-HT). The P(BdP-HT):DICTF-based organic solar cells (OSCs) displayed excellent efficiency of around 11.

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Management of condylar fractures includes the closed and open methods. The closed method, although is conservative, has disadvantages such as inadequate reduction, disturbances in occlusion, and a decrease in ramal height. To overcome these disadvantages, surgeons prefer open reduction and internal fixation.

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Background And Aims: Cholestatic liver diseases, including primary sclerosing cholangitis, are characterized by periportal inflammation with progression to hepatic fibrosis and ultimately cirrhosis. We recently reported that the thioredoxin antioxidant response is dysregulated during primary sclerosing cholangitis. The objective of this study was to examine the impact of genetic and pharmacological targeting of thioredoxin reductase 1 (TrxR1) on hepatic inflammation and liver injury during acute cholestatic injury.

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Article Synopsis
  • - The study investigates the role of miR-199a-5p in reducing the expression of the ABCB11 efflux transporter in mice with cholestasis, which is a condition affecting bile acid transport in the liver.
  • - After common bile duct ligation (CBDL), miR-199a-5p was found to be significantly upregulated, leading to the inhibition of ABCB11 by targeting its mRNA.
  • - Treatment with obeticholic acid (OCA), a nuclear receptor FXR agonist, increased ABCB11 levels and decreased miR-199a-5p expression, suggesting a mechanism for regulating ABCB11 during cholestasis.
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Article Synopsis
  • Researchers developed a mouse model to study parenteral nutrition-associated cholestasis (PNAC), demonstrating that intestinal inflammation combined with parenteral nutrition (PN) leads to liver issues and transporter gene suppression.
  • The study examined the role of TNFα, finding that it suppresses important liver transporters and is elevated in cases of PNAC.
  • Treatment with infliximab (a drug targeting TNFα) prevented the progression of PNAC, suggesting that targeting TNFα could be a potential therapy for this condition.
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Background And Aims: Parenteral nutrition (PN)-associated cholestasis (PNAC) complicates the care of patients with intestinal failure. In PNAC, phytosterol containing PN synergizes with intestinal injury and IL-1β derived from activated hepatic macrophages to suppress hepatocyte farnesoid X receptor (FXR) signaling and promote PNAC. We hypothesized that pharmacological activation of FXR would prevent PNAC in a mouse model.

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Background: Biliary atresia (BA) is an inflammatory pediatric cholangiopathy with only surgical means for treatment. Many contributors to bile acid synthesis and transport have previously been reported to be downregulated in patients with BA; yet, the driving factors of the abnormal bile acid synthesis and transport in regard to BA have not been previously studied.

Materials And Methods: Wild type or Ig-α mice were injected with salt solution (control) or rotavirus on day of life 0, and analyses were performed on day of life 14.

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Adenosine triphosphate-binding cassette subfamily C member 2 (ABCC2/Abcc2) is critically important to biliary excretion of many endobiotic and xenobiotic compounds, and is a major driving force for bile acid-independent bile flow. Abcc2 expression is reduced at the messenger RNA (mRNA) and protein levels in various forms of experimental cholestasis. In a microRNA (miRNA) screen of mouse liver after biliary obstruction, we found that miRNA let7a-5p was significantly up-regulated approximately 4-fold.

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In infants intolerant of enteral feeding because of intestinal disease, parenteral nutrition may be associated with cholestasis, which can progress to end-stage liver disease. Here we show the function of hepatic macrophages and phytosterols in parenteral nutrition-associated cholestasis (PNAC) pathogenesis using a mouse model that recapitulates the human pathophysiology and combines intestinal injury with parenteral nutrition. We combine genetic, molecular, and pharmacological approaches to identify an essential function of hepatic macrophages and IL-1β in PNAC.

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Introduction: Anxiety towards exodontic procedures is a common occurrence in dental practice. In hypertensive patients this anxiety induced stress may have an effect on cardiovascular system which may be clinically significant.

Aim: To evaluate the cardiovascular changes in hypertensive patients that may manifest following anxiety induced stress in patients undergoing exodontic procedures under local anaesthesia.

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Background: Recently eye effects of Diabetes Mellitus (DM) are an important concern due to increase in its trend especially in developing countries.

Objectives: To assess the awareness related to eye effects of DM and its prevention practices among people with diabetes.

Methods: This cross sectional study was conducted from January 2013 to April 2013 in Villupuram district of Tamil Nadu, India.

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In this study we identified the mechanisms underlying the inhibitory effects of NF-κB on the expression of genes encoding multiple liver transport proteins. Well-conserved NF-κB binding sites were found in the promoters of farnesoid X receptor (FXR)-target genes. An electromobility shift assay (EMSA) demonstrated the specific interaction between the NF-κB p65 protein and a (32)P-labeled BSEP NF-κB response element (NF-κBE).

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The Peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (PGC-1α) is a transcriptional co-activator that plays a central role in adapted metabolic responses. PGC-1α is dynamically methylated and unmethylated at the residue K779 by the methyltransferase SET7/9 and the Lysine Specific Demethylase 1A (LSD1), respectively. Interactions of methylated PGC-1α[K779me] with the Spt-Ada-Gcn5-acetyltransferase (SAGA) complex, the Mediator members MED1 and MED17, and the NOP2/Sun RNA methytransferase 7 (NSUN7) reinforce transcription, and are concomitant with the m(5)C mark on enhancer RNAs (eRNAs).

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Elevated serum concentrations of the vasoactive protein endothelin-1 (ET-1) occur in the setting of systemic inflammatory response syndrome and contribute to distal organ hypoperfusion and pulmonary hypertension. Thus, understanding the cellular source and transcriptional regulation of systemic inflammatory stress-induced ET-1 expression may reveal therapeutic targets. Using a murine model of LPS-induced septic shock, we demonstrate that the hepatic macrophage is the primary source of elevated circulating ET-1, rather than the endothelium as previously proposed.

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The control of transcription is regulated through the well-coordinated spatial and temporal interactions between distal genomic regulatory elements required for specialized cell-type and developmental gene expression programs. With recent findings CFTR has served as a model to understand the principles that govern genome-wide and topological organization of distal intra-chromosomal contacts as it relates to transcriptional control. This is due to the extensive characterization of the DNase hypersensitivity sites, modification of chromatin, transcription factor binding sites and the arrangement of these sites in CFTR consistent with the restrictive expression in epithelial cell types.

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Background: Small ubiquitin-like modifiers (SUMO) are covalently conjugated to other proteins including nuclear receptors leading to modification of various cellular processes.

Results: Ligand-dependent SUMOylation of farnesoid X receptor (FXR) negatively regulates the expression of its target genes.

Conclusion: SUMO modification attenuates the capacity of FXR to function as a transcriptional activator.

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Base amino acid lysine residues play an important role in regulation of nuclear receptors [e.g., farnesyl X receptor (FXR)], leading to enhanced or suppressed biologic activity.

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