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5 years) age groups. In new born kid the glands were small, white cord like. It became "?" shaped at 6 months and "S" shaped at 12 months of age. A significant growth in size and weight of gland occurred at 6 month, then up to 12 month and beyond it grew slowly. The secretory acini of the lobules were lined by pseudostratified ciliated columnar epithelium which contained A-tall columnar, B-basal and C-narrow columnar type of cells. The number per unit area and size of the gland increased with age significantly from birth in the prepubertal animals and up to puberty. In post-pubertal animals it did not grow significantly, rather the connective tissue elements were increased in the capsule (adventitia). The intralobular connective tissue however, decreased at the expense of growth of acini at all ages.]]>

Nanostructured thin films of Cu2O modified by overlayering SrTiO3 with varying thickness have been studied for the first time as photoelectrode in photoelectrochemical (PEC) water splitting. Effective mass calculations for electrons and holes in bulk SrTiO3 and Cu2O using DFT first-principles have also been attempted to explain the enhanced charge separation at Cu2O/SrTiO3 interface. All samples were characterized using XRD, SEM, and UV–vis spectrometry. The influence of surface modification of Cu2O with varying thickness of SrTiO3 on PEC performance has been investigated. Photocurrent density for Cu2O/SrTiO3 heterojunction with overall thickness of 343 nm at 0.8 V/SCE was found to be 2.52 mA cm–2 which is 25 times higher than that of pristine Cu2O (0.10 mA cm–2 at 0.8 V/SCE). Theoretical studies showed that the electrons in SrTiO3 had large effective masses as compared to electrons in Cu2O at conduction band minima indicating weak mobility of photogenerated electrons in SrTiO3 and strong mobility in Cu2O leading to improved separation of charge carriers resulting in the enhancement of photocurrent densities at the Cu2O/SrTiO3 heterojunction.

Focal cortical dysplasia (FCD) is one of the most common pathologies associated with drug-resistant epilepsy (DRE). The pharmacological targets remain obscured, as the molecular mechanisms underlying FCD are unclear. Implications of epigenetically modulated aberrant gene expression in disease progression are reported in various DRE pathologies except FCD. Here we performed genome-wide CpG-DNA methylation profiling by methylated DNA immunoprecipitation (MeDIP) microarray and RNA sequencing (RNAseq) on cortical tissues resected from FCD type II patients. A total of 19088 sites showed altered DNA methylation in all the CpG islands. Of these, 5725 sites were present in the promoter regions, of which 176 genes showed an inverse correlation between methylation and gene expression. Many of these 176 genes were found to belong to a cohesive network of physically interacting proteins linked to several cellular functions. Pathway analysis revealed significant enrichment of receptor tyrosine kinases (RTK), EGFR, PDGFRA, NTRK3, and mTOR signalling pathways. This is the first study that investigates the epigenetic signature associated with FCD type II pathology. The candidate genes and pathways identified in this study may play a crucial role in the regulation of the pathogenic mechanisms of epileptogenesis associated with FCD type II pathologies.