By using this method, we provide an efficient way to a wide variety of substituted thiolic compounds. Moreover, the catalyst is easily recovered using simple filtration and reused for 5 consecutive runs. CONCLUSION In this effort we developed a new Pd catalyst bonded on the surface of zeolite as substrate to prepare heterogeneous catalyst. We demonstrate that this novel catalyst offers reliable and convincing data that may offer valuable application in further developing the science and technology of Ullmann reaction protocols and allied industries. Additionally, the catalyst was reusable and kept its high activities over a number of cycles. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.Vitamin D is a neurosteroid hormone crucially involved in neurodevelopment. Neural cell proliferation, neurotransmission, oxydative stress and immune function, represent the main mechanisms mediated by vitamin D in the Central Nervous System. Therefore, its deficiency during pregnancy and early childhood may significantly impact on a developing brain, leading to possible adverse neuropsychological outcomes including Autism Spectrum Disorder (ASD). Significant vitamin D deficiency is described within children affected by ASD and in pregnant mothers whose offspring will later develop ASD, suggesting a possible role of the hormone as a contributing risk factor in the etiopathogenesis of ASD. We reviewed the actual literature on the potential contributing role of prenatal and early postnatal vitamin D deficiency in ASD etiopathogenesis, at both genetic and environmental level, and the possible effect of vitamin D supplementation in autistic children. Conflicting but promising results emerged on the topic. Further Randomized Controlled Trials studies carried out during pregnancy and early infancy are necessary for better understanding the possible contribution of vitamin D deficiency in the etiopathogenesis of autism and the potential efficacy of the hormone supplementation on the improvement of ASD core symptoms. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.BACKGROUND Despite the limited evidence about the effect of micronutrient supplementation on the semen quality, many micronutrient supplements have been used to improve male fertility. Approximately, 40%-50% of male infertility cases in general and up to 80% in men with idiopathic infertility cases are caused by oxidative stress and decreased level of seminal total antioxidant capacity. OBJECTIVE To investigate the beneficial effects of micronutrient supplementation on sperm concentration, motility and morphology. METHODS A Pub Med, Google Scholar, Embase data, web of Science and Cochrane Library database extensive research of the randomized controlled studies utilizing micronutrient vitamins and supplements was performed. RESULTS The existent international literature is rather heterogeneous and a definitive is difficult to be drawn. Several micronutrients have beneficial effects on sperm parameters. Rational use of micronutrients might be helpful for infertile patients. CONCLUSION Further randomized, controlled clinical trials are required to elucidate the efficacy and safety of micronutrients and propose proper protocols for their use.  https://www.selleckchem.com/products/liraglutide.html  A well-rounded, balanced diet is more preferable than the widespread use of micronutrient supplements beyond the recommended doses. Future studies should concern the pregnancy rate as a primary outcome in their designs. Further research should be done to determine the appropriate antioxidant compounds, the duration of the treatment, as well as a certain dose of antioxidants in clinical practices. The pre-treatment evaluation of the seminal oxidative status is also an important parameter to proceed with micronutrient supplementation without the risk of reductive stress. Under these conditions, supplements could support the quality of sperm and help to alleviate male infertility. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.BACKGROUND Cadmium is a worldwide spread toxicant that accumulates in tissues and affects many organs, mainly through oxidative damage. Oxidative stress is often associated with cardiovascular diseases and, when it affects vessels, it induces endothelial dysfunction, which, in turn, could precipitate atherosclerosis and hypertension. Therefore, it is reasonable to suggest antioxidant supplementation as a therapy against cadmium-induced endothelial dysfunction. OBJECTIVE This literature review aims to present the mechanisms involving oxidative stress by which cadmium induces endothelial dysfunction and the benefits of antioxidant supplementation as a therapeutic strategy against its harmful effects. METHODS On PubMed Central, articles that contemplated studies on cadmium intoxication and associated oxidative stress with endothelial dysfunction as well as articles that reported the use of antioxidant supplementation in an attempt to prevent or avoid endothelial dysfunction induced by cadmium exposure were selected. RESULTS Most of the studies that associated cadmium intoxication with endothelial dysfunction suggested oxidative stress as the major mechanism for this damage. Furthermore, experimental studies also revealed that the administration of substances with antioxidant properties, such as ascorbic acid and curcumin, has beneficial effects on the prevention of such dysfunction, reducing reactive oxygen species within the vessels, preventing a reduction in the amount of glutathione and the increase in blood pressure observed in animals exposed to cadmium. CONCLUSION Antioxidant therapy demonstrated to be a potential treatment to reduce cardiovascular injuries provoked by cadmium, but more studies are encouraged to determine the best antioxidant substance and dose to treat or avoid this complication. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.BACKGROUND We recently reported a role for the circadian rhythm protein Period 2 (PER2) in midazolam induced cognitive dysfunction. Based on previous studies showing a critical role for the adenosine A2B receptor (ADORA2B) in PER2 regulation, we hypothesized that hippocampal ADORA2B is crucial for cognitive function. METHODS Midazolam treated C57BL/6J mice were analyzed for Adora2b hippocampal mRNA expression levels, and spontaneous T-maze alternation was determined in Adora2b-/- mice. Using the specific ADORA2B agonist BAY-60-6583 in midazolam treated C57BL/6J mice, we analyzed hippocampal Per2 mRNA expression levels and spontaneous T-maze alternation. Finally, Adora2b-/- mice were assessed for mRNA expression of markers for inflammation or cognitive function in the hippocampus. RESULTS Midazolam treatment significantly downregulated Adora2b or Per2 mRNA in the hippocampus of C57BL/6J mice, and hippocampal PER2 protein expression or T-maze alternation was significantly reduced in Adora2b-/- mice. ADORA2B agonist BAY-60-6583 restored midazolam mediated reduction in spontaneous alternation in C57BL/6J mice.