The aim of this study was to investigate the intra-familial distribution of mutans streptococci in some Chinese families. Eighteen families consisting of mother, father and a 3-yr-old child without any older siblings participated. Clinical examination and interview were performed to obtain information about level of mutans streptococci in saliva, caries prevalence scored by DMFT or deft, general health, diet regimens, breast-feeding time, principal caretaker of the child and the parents' profession. At the same appointment, two pooled plaque samples from each subject were collected with the tips of sterile tooth picks. From these plaque samples, mutans streptococci were isolated on MSB-agar plates and identified by serotyping. Pure isolates were obtained from all subjects of 11 families. These isolates were genotyped using restriction endonuclease HaeIII. The results showed that in 4 families the mothers shared genotype with the child, and in 3 families it was the father and the child who harboured a similar genotype. In 2 families, all subjects harboured an identical genotype. Further, the spouses in one parental pair showed an identical genotype, and, finally, in one family all subjects harboured their unique genotypes. None of the investigated factors could explain the differences in the intra-familial distribution of mutans streptococci. The pattern of similar genotypes in these Chinese families differs from that reported for western families.
Mammalian male germ cell development is a stepwise cell-fate transition process; however, the full-term developmental profile of male germ cells remains undefined. Here, by interrogating the high-precision transcriptome atlas of 11,598 cells covering 28 critical time-points, we demonstrate that cell-fate transition from mitotic to post-mitotic primordial germ cells is accompanied by transcriptome-scale reconfiguration and a transitional cell state. Notch signaling pathway is essential for initiating mitotic arrest and the maintenance of male germ cells’ identities. Ablation of HELQ induces developmental arrest and abnormal transcriptome reprogramming of male germ cells, indicating the importance of cell cycle regulation for proper cell-fate transition. Finally, systematic human-mouse comparison reveals potential regulators whose deficiency contributed to human male infertility via mitotic arrest regulation. Collectively, our study provides an accurate and comprehensive transcriptome atlas of the male germline cycle and allows for an in-depth understanding of the cell-fate transition and determination underlying male germ cell development.
The significant increase in liver SWE values in neonates and infants with biliary atresia supports their application for differentiating biliary atresia from infantile hepatitis syndrome.
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