THE COMPARATIVE DEPOSITIONAL HETEROGENEITY OF MANCHHAR FORMATION (SIWALIK GROUP), SOUTHERN INDUS BASIN, PAKISTAN

Present study is carried out for detailed description, distribution and interpretation of lithofacies and textural analysis of Manchhar Formation from Gaj River, Manchhar Lake and Lal Bagh Sections of Southern Indus Basin Pakistan. Four different clastic lithofacies are identified during present study, which are conglomeratic sandstone (Gt), shale (Fm), fine to coarse grain flat bedded sandstone (Sh) and fine to coarse grain trough cross-bedded sandstone (St). These Facies suggest that Manchhar Formation is deposited in the Beach to shallow agitated water and fluvial system. Twenty-nine (29) unconsolidated loose and friable sandstone samples were selected for textural analysis. Grain-size parameters such as mean, median, standard deviation, Skewness and Kurtosis were used for transport history, mode and hydrodynamic energy condition to recognize the depositional environment. Stewart Diagram shows deltaic/wave water process takes active role under the influence of wave process. Linear discriminant functions analysis show that the fluvial environment of deposition dominates and influences shallows water and beach environment. Passega diagram reveals that transport mode was rolling and suspension by the tractive current that shows the fluvio-deltaic to deltaic wave with the influence of wave depositional environment of Miocene-Pliocene (Neogene) Manchhar Formation

From the genetic architecture to synaptic plasticity in autism spectrum disorder.

International audienceGenetics studies of autism spectrum disorder (ASD) have identified several risk genes that are key regulators of synaptic plasticity. Indeed, many of the risk genes that have been linked to these disorders encode synaptic scaffolding proteins, receptors, cell adhesion molecules or proteins that are involved in chromatin remodelling, transcription, protein synthesis or degradation, or actin cytoskeleton dynamics. Changes in any of these proteins can increase or decrease synaptic strength or number and, ultimately, neuronal connectivity in the brain. In addition, when deleterious mutations occur, inefficient genetic buffering and impaired synaptic homeostasis may increase an individual's risk for ASD