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Nishiyama, A.

Publications and source records attributed to Nishiyama, A..

2 recordsLinked to original sources

Functional connectome linking child-parent relationships with psychological problems in adolescence

Paternal- and maternal-child relationships are associated with partly distinct psychobehavioral problems, which often manifest differently between boys and girls. In order to understand neural mechanisms underlying complicated mappings between child-parent relationship and adolescents problems, we used a dataset of early adolescents (N=93) and separately estimated the effects of paternal- and maternal-child relationships on resting-state functional connectivity and problems in boys and girls. General linear models identified the effects of paternal- and maternal-child relationships in different sets of functional connectivity, which we termed functional brain connectomes associated with paternal- and maternal-child relationship (FBCp and FBCm), respectively. Subsequent connectome-based models using these FBCs significantly predicted aggressive behaviors only for boys and internalizing problems selectively only girls. Lastly, a causal discovery method identified causal paths from daughter-mother relationship to FBCm, and then to daughters internalizing problems. These observations highlight sex-dependent mechanisms linking child-parent relationship, brain, and psychobehavioral problems in early adolescence.

neuroscience

The p21 dependent G2 arrest of the cell cycle in epithelial tubular cells links to the early stage of renal fibrosis

Renal fibrosis is accompanied with the progression of chronic kidney disease (CKD). Despite a number of past and ongoing studies, our understanding of the underlying mechanisms remains elusive. Here we explored the progression of renal fibrosis by using a mouse model, unilateral ureter obstruction (UUO). We found that in the initial stage of the progression where extracellular matrix did not deposit yet, the proximal tubular cells arrested at the G2 of the cell cycle. This G2 arrest was induced prior to activation of both DNA damage checkpoint and Wnt/{beta}-Catenin pathway. Further analyses in vivo and in vitro indicated the cyclin dependent kinase inhibitor p21 is involved in the G2 arrest after the damage. The newly produced monoclonal antibody against p21 revealed that the p21 levels were sharply upregulated in response to the damage during the initial stage, but dropped down toward the later stage. To examine the function of p21 in the progression of renal fibrosis, we constructed the novel p21 deficient mice by i-GONAD. Compared with wild-type mice, p21 deficient mice showed the exacerbation of the fibrosis. Thus we propose that during the initial stage of the fibrosis following the renal damage, tubular cells arrest in the G2 phase depending on p21, thereby safeguarding the kidney functions.

cell biology