The article for the journal Current Computer-Aided Drug Design has been removed by the Publisher due to acute language inconsistencies and grammatical errors. see more Bentham Science apologizes to the readers of the journal for any inconvenience this may cause. The Bentham Editorial Policy on Article Withdrawal can be found at https//benthamscience.com/editorialpoliciesmain.php It is a condition of publication that manuscripts submitted to this journal have not been published and will not be simultaneously submitted or published elsewhere. Furthermore, any data, illustration, structure or table that has been published elsewhere must be reported, and copyright permission for reproduction must be obtained. Plagiarism is strictly forbidden, and by submitting the article for publication the authors agree that the publishers have the legal right to take appropriate action against the authors, if plagiarism or fabricated information is discovered. By submitting a manuscript, the authors agree that the copyright of their article is transferred to the publishers if and when the article is accepted for publication.It is a condition of publication that manuscripts submitted to this journal have not been published and will not be simultaneously submitted or published elsewhere. Furthermore, any data, illustration, structure or table that has been published elsewhere must be reported, and copyright permission for reproduction must be obtained. Plagiarism is strictly forbidden, and by submitting the article for publication the authors agree that the publishers have the legal right to take appropriate action against the authors, if plagiarism or fabricated information is discovered. By submitting a manuscript, the authors agree that the copyright of their article is transferred to the publishers if and when the article is accepted for publication. Design of sulfonamide-triazine derivatives as JAK1 inhibitors. JAK1 is a kinase involved in different autoimmune diseases. JAK1 inhibitors have shown promising results in treating autoimmune diseases. To design new JAK1 inhibitors based on sulfonamides-triazine conjugates capable of binding interactions comparable to observed interactions anchoring potent crystallographic JAK1 inhibitors. The crystallographic structures of 4 diverse nanomolar inhibitors complexed within JAK1 were used to guide the synthesis of new diaminotriazine-sulfonamide-based JAK1 inhibitors. Nineteen compounds have been prepared some of which exhibited low micromolar IC50 values against JAK1. Crystallographic complexes of diverse JAK1 inhibitors were successfully used to guide the synthesis of novel sulfonamide-triazine-based low micromolar JAK1 inhibitors.Crystallographic complexes of diverse JAK1 inhibitors were successfully used to guide the synthesis of novel sulfonamide-triazine-based low micromolar JAK1 inhibitors. C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) are routinely used to assess disease activity in spondyloarthritis. New biomarkers have been reported, such as neutrophil to lymphocyte ratio (NLR), platelet to lymphocyte ratio (PLR), CRP to albumin ratio (CAR), and albumin to fibrinogen ratio (AFR). Our study aimed to assess these ratios in spondyloarthritis and to determine the relationship between these ratios and the disease activity. We conducted a cross-sectional study, including patients with spondyloarthritis. The following ratios were calculated PLR, NLR, AFR, and CAR. Pearson correlation analysis was carried out to test the correlation of the data. Receiver operating characteristic curves were evaluated for each ratio using ASDASCRP as the gold standard for disease activity. Eighty-five patients were included. The sex ratio was 60 males to 25 females. The mean age was 42.58 ± 11.75 years. There was a positive correlation between the PLR and the following parameters CAR, CRP, and ESR. A negative correlation was found between AFR and the following ratios PLR, NLR, CRP, and ESR. The ASDAS correlated negatively with AFR and positively with both PLR and CAR. The cut-offs values of CAR and PLR to distinguish patients with very high disease activity (ASDASCRP>3.5) were 0.442 and 173.64, respectively. Given their good correlation with ESR and CRP, we suggest that PLR, CAR, and AFR can be used as potential indicators of inflammation in spondyloarthritis. The CAR and PLR are useful to identify patients with very high disease activity.Given their good correlation with ESR and CRP, we suggest that PLR, CAR, and AFR can be used as potential indicators of inflammation in spondyloarthritis. The CAR and PLR are useful to identify patients with very high disease activity. Neurogenesis, the key mechanism to generate new neurons from existing stem cell niches continues throughout the life in the adult mammalian brain, although decelerate with aging or the progression of neurodegenerative disorders like Alzheimer's disease (AD). In the past few years, impaired adult hippocampal neurogenesis emerged as a contributing hallmark of AD pathophysiology along with amyloid beta (Aβ) and tau hyper phosphorylation-induced neurotoxicity. However, no conclusive evidence exists that indicates the up/down-regulation of adult hippocampal neurogenesis during the course of AD progression. In this study, we examined alterations in adult hippocampal neurogenesis and cognitive deficits using Aβ(1-42)-induced mouse model of AD. Our results demonstrate that Aβ administration induces an anxiety like behavior and impairs spatial and non-spatial memory and learning in BALB/c mice. Extensive neuronal loss was also evident in the dentate gyrus (DG), CA1, CA2 and CA3 regions of hippocampus in Aβ-treated animals. Furthermore, Aβ-exposure markedly reduced the real-time expression of markers of cell proliferation and migration i.e. Ki67 and DCX, whereas immunohistochemistry analysis revealed a substantial reduction in the expression levels of Ki67 and NeuN. Our findings highlight the association of Aβ-induced neurotoxicity with altered neurogenesis and memory formation; however further insight is warranted to explore the underlying molecular pathway(s). Moreover, the treatment strategies aiming to repair the adult hippocampal neurogenesis hold potential as AD therapeutics.Our findings highlight the association of Aβ-induced neurotoxicity with altered neurogenesis and memory formation; however further insight is warranted to explore the underlying molecular pathway(s). Moreover, the treatment strategies aiming to repair the adult hippocampal neurogenesis hold potential as AD therapeutics.