Bharathiar University

About: Bharathiar University is a education organization based out in Coimbatore, Tamil Nadu, India. It is known for research contribution in the topics: Thin film & Adsorption. The organization has 5812 authors who have published 8628 publications receiving 143934 citations. The organization is also known as: BU.

Metal-free branched alkyl tetrathienoacene (TTAR)-based sensitizers for high-performance dye-sensitized solar cells

Abstract: A new series of metal-free alkylated tetrathienoacene (TTAR)-based organic chromophores, TPA–TTAR–TA (R = branched-C8H17, 1, TTAR-b8; R = C15H31, 2, TTAR-15; R = C9H19, 3, TTAR-9), are synthesized for application in dye-sensitized solar cells (DSSCs). Due to the extensively conjugated TTAR π-bridge, all three dyes exhibit high extinction coefficients (1 × 105 M−1 cm−1). By systematically exploring the effects of the TTAR alkyl chain substituents, a significant influence of the dye coverage (orientation) on the TiO2 surfaces is observed. The branched-alkyl TTAR-b8 (1) promotes significant tilting and packing distortion on TiO2 in comparison to more ordered monolayers of linear long alkyls TTAR-15 (2) and TTAR-9 (3). Photophysical measurements on the dye-grafted TiO2 films reveal that the branched-alkylated TTA unit in 1 enhances the electron injection efficiency, in agreement with the high quantum efficiency. Notably, by utilizing a three-dimensional (3D) photonic crystal (PhC) layer to enhance the coherent scattering an increase the light absorption, TTAR-b8 exhibits higher short-circuit current densities and achieved a high PCE of 11.18%. TTAR-b8 is thus the best performing fused-thiophene-based organic DSSC dye reported to date.

Involvement of Mitogen-Activated Protein Kinase Pathway in T-2 Toxin-Induced Cell Cycle Alteration and Apoptosis in Human Neuroblastoma Cells

Abstract: T-2 toxin is the most toxic trichothecene and a frequent contaminant in many agriculture products Dietary ingestion represents the most common route of T-2 toxin exposure in humans T-2 toxin exposure leads to many pathological conditions like nervous disorders, cardiovascular alterations, immune depression and dermal inflammation However, the neuronal toxicity of T-2 toxin in vitro remains unclear In the present study, we investigated the mechanism of T-2 toxin-induced apoptosis in human neuroblastoma cells (IMR-32) T-2 toxin was cytotoxic at a low concentration of 10 ng/ml The 50 % inhibitory concentration (IC50) of T-2 toxin was found to be 40 ng/ml as assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, crystal violet dye exclusion test and lactate dehydrogenase (LDH) leakage T-2 toxin increased intracellular reactive oxygen species generation as early as 15 min and peaked at 60 min as analyzed by flow cytometry Annexin V + propidium iodide staining showed time-dependent increase in percent apoptotic cells DNA gel electrophoresis showed oligonucleosomal DNA fragmentation typical of apoptotic cells Additionally, casapse-3 activation and PARP cleavage indicated involvement of mitochondrial mediated caspase-dependent pathway of apoptosis Cell cycle analysis revealed time-dependent increase in sub-G1 population of cells and significant up-regulation of CDK2, CDK6, cyclin A and p21 messenger RNA (mRNA) levels Exposure to T-2 toxin induced the phosphorylation of extracellular signal-regulated kinase (ERK), p38-mitogen-activated protein kinase and c-jun N-terminal kinases (JNK) Analysis of human phospho-mitogen-activated protein kinase (MAPK) antibody array revealed time-dependent increase in phosphorylation Upstream of ERK pathway Grb2, Ras and Raf and downstream transcription factors c-fos and c-jun were significantly up-regulated Z-VAD-FMK and MAPK inhibitors (PD 98059, SB 203580 and ZM 336372) exposure prior to T-2 toxin treatment significantly decreased percent of apoptotic cells compared to only T-2 toxin-exposed cells Results of the present study show that T-2 toxin at nanogram concentrations can induce apoptosis in human neuronal cells through multiple signal transduction pathways The study provides possible leads for developing therapeutic approaches to prevent T-2 toxin-induced neurotoxicity