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75) with the fewest features, indicating an excellent balance between avoiding redundant preprocessing task and higher accuracy in relation extraction on biomedical literature using our method. Many reports describe an association between preconceptional paternal exposure to environmental chemicals, including the persistent organic pollutant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) with an increased number of female offspring. We chronically treated wild-type C57BL/6 male mice with TCDD to investigate a role for the aryl hydrocarbon receptor (AHR) transcription factor. These mice had a 14% lower malefemale sex ratio than control mice, which was not observed in TCDD-treated Ahr knock out mice. AHR target genes Cyp1a1 and Ahrr were upregulated in the liver and testis of WT mice and Ahr expression was higher in the epididymis (2-fold) and liver (18-fold) than in whole testis tissue. The AHR protein was localized to round spermatids, elongating spermatids, and Leydig cells in the testis of WT mice. These studies demonstrate AHR involvement in the sex ratio distortion of TCDD-exposed males and the need for evaluating the molecular and genetic mechanism of this process. Accumulating evidences have pointed out that neuroinflammation is involved in Parkinson’s disease (PD) pathogenesis. Toll-like receptor 3 (TLR3), as a member of pattern-recognition receptors (PRRs), is known to play a pivotal role in inflammatory responses and immune responses. It was recently suggested that TLR3 was increased in the animal models of PD. The present study aimed to evaluate whether TLR3 gene (rs3775290) polymorphism was associated with PD susceptibility. We genotyped the single-nucleotide polymorphism (SNP) of TLR3 gene (rs3775290) using polymerase chain reaction and restriction fragment length polymorphism (PCR-RFLP) from 380 PD patients and 380 control subjects in Chinese Han population. Our data demonstrated that rs3775290 T allele carriers were associated with a reduced risk of PD between early-onset PD(EOPD)group and its healthy-matched control subgroup (OR = 0.571, 95 %CI = 0.366-0.891, P =  0.013 for TT + TC vs CC). Moreover, there were significant differences in genotype and allele distribution between EOPD group and the late-onset PD (LOPD) group (P = 0.024 and P  = 0.008, respectively). Therefore, our study suggested a possible association between TLR3 (rs3775290) gene polymorphism and PD susceptibility, indicating that T allele of rs3775290 might be a protective factor for sporadic PD in Han Chinese population. Hyperthyroidism may cause cognitive decline and increases the risk of Alzheimer’s disease (AD), the major form of dementia; however, the underlying mechanism of this relationship is unclear. AD is associated with increased serum levels of tau. In this study, we investigated the relationship between serum thyroid hormones (THs) and tau. Fifty participants diagnosed with hyperthyroidism and fifty euthyroid counterparts were included and received clinical examinations. Serum concentrations of thyroid-stimulating hormone (TSH), free thyroxine (FT4), free triiodothyronine (FT3) and tau protein were assessed. The total tau protein level was significantly higher in hyperthyroidism participants than in their euthyroid counterparts. The level of circulating total tau had a significant positive association with the serum concentrations of FT3 and FT4. Total tau level was increased in the low TSH group and the serum THs decreased with the increase of age. These findings reveal that peripheral THs are associated with the serum concentration of tau, which may be involved in the pathogenesis of Alzheimer’s disease (AD), suggesting a potential therapeutic target of AD via hyperthyroidism therapy. V.Post-translational modification of Tau, a microtubule-associated protein in the neuronal cell, plays a major role in Alzheimer’s disease. Tau is an axonal protein expressed in mature neurons that promote the self-assembly of tubulin into microtubules and its stabilization in neurons. Phosphorylation of Tau makes it prone to aggregation at the intra-neuronal region leading to impaired neurotransmission and dementia. Tau aggregates undergo trans-cellular propagation by the release of fibrillar species into the extra-cellular environment from damaged and infected neurons that can be internalized by neighbouring neuronal and glia cells and promotes aggregation in healthy cells. G-protein coupled receptors, the largest group of seven transmembrane receptors, are involved in neuronal signal transduction in response to various signals such as hormones and neurotransmitters. In Alzheimer’s disease, GPCRs are involved in phosphorylation of Tau through various downstream kinases such as GSK-3β, CDK-5 and ERKs signalling cascade. Several neuronal GPCRs that are involved in Tau phosphorylation are elaborated in this review. The astrocytic GPCR, Tau phosphorylation mediated by CaS receptors and its propagation by exosomes are also elaborated. In the microglia, the extra-cellular Tau binding to a chemokine GPCR, CX3CR1 triggers its internalization, whereas Tau phosphorylation at specific sites decreases its binding affinity to this receptor. NSC 119875 clinical trial Here we highlight the role of GPCRs in Tau phosphorylation and Tau interaction in different cells of the nervous system. Hence, the role of GPCRs are attaining more attention in the therapeutic field of Alzheimer’s disease. Specific agonists/antagonists and allosteric modulators could be the potential target for therapy against GPCR-mediated Tau phosphorylation in Alzheimer’s disease. We tested several predictions of the theory of motor control with spatial referent coordinates related to effects of muscle coactivation on force production and perception. In particular, we predicted that subjects would produce unintentional force increase by finger flexors and be unaware of this force increase. Healthy subjects performed steady force production task in isometric conditions with visual feedback on the force level. They coactivated muscles of the arm trying to keep the force constant in the absence of visual feedback. This led to a consistent force increase not perceived by the subjects as reflected by their verbal reports. In contrast, when asked to match the force with the contralateral hand, adequate force matching was observed. Using the “inverse piano” apparatus confirmed no change in the referent coordinate of the fingers and an increase in its apparent stiffness. The results confirm the earlier hypothesis on the reciprocal command being hierarchically higher than the coactivation command.