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Background: In recent years, various phytomedicines have been used in the treatment of hepatic disorders. The aim of this study is to find out whether Peltophorum pterocarpum bark and leaves can help rats that have been exposed to isoniazid and rifampicin-induced hepatotoxicity. Materials and Methods: The rats were divided into 10 groups each with 6 rats. The liver damage is induced by isoniazid and rifampicin. The leaf and bark of P. pterocarpum extracted with ethanol are freshly mixed in sterile water (100, 200 and 400 mg/kg body weight), and given to rats orally in the early morning as a single dosage per day until the study period. The animals were sacrificed and the tissue and serum samples were collected for further investigations. Results: The liver damage induced by isoniazid and rifampicin altered the various biochemical parameters levels, but after the treatment of P. pterocarpum barks and leaves the levels were significantly altered when compared to the negative control rats. The drug silymarin was used as a standard. Conclusion: The extracts have the protective effect of liver markers and membrane-bound enzymes against the toxin-treated rats. This result highlights the hepatoprotective properties of the leaves and barks of the plant in a similar manner and the formulation (Group 10) have high beneficial effects than other groups.

Autism and autism spectrum disorders (ASD) affects the areas of social awareness and interaction, verbal and nonverbal communication, and behaviors and interests, which are grouped among neurobehavioral disorders. One in 68 children is affected with ASD according to the estimate from the Center for Disease Control and Prevention's autism and developmental disabilities monitoring network and an increasing prevalence observed worldwide. A characteristic heterogeneity in ASD determined genetic variability as a major contributor. Whole-exome sequencing of ASD individuals revealed that discrete de novo mutation (single-nucleotide variation or small indels) also contribute to the overall genetic risk of ASD apart from rare genetic variation affecting single nucleotides of protein-coding DNA or rare genomic copy number variants as assessed through other high-throughput genomic methods. These genes are involved in synaptic transmission and regulated during brain development by acting upstream or downstream of Wingless- related integration site (WNT), bone morphogenetic proteins/transforming growth factor-β, sonic hedgehog, fibroblast growth factor, and retinoic acid signaling pathways. The current review focuses on genes involved in synaptic function, undergoing de novo mutation leading to ASD condition.