Proliferation of meniscal fibrochondrocytes cultured on a new polyurethane scaffold is stimulated by TGF-β.

The aim of this study was to investigate if newly developed polyurethane (PU) scaffolds are suitable as scaffold for cell-seeded meniscus tissue engineered constructs. Scaffolds were seeded with goat meniscal fibrochondrocytes and cultured to assess changes in biological and mechanical properties. Furthermore, the effect of TGF-β on these properties was investigated.

DNA double-strand break repair in parental chromatin of mouse zygotes, the first cell cycle as an origin of de novo mutation.

In the human, the contribution of the sexes to the genetic load is dissimilar. Especially for point mutations, expanded simple tandem repeats and structural chromosome mutations, the contribution of the male germline is dominant. Far less is known about the male germ cell stage(s) that are most vulnerable to mutation contraction.

Motile human normozoospermic and oligozoospermic semen samples show a difference in double-strand DNA break incidence.

Background: Among ICSI children de novo structural chromosome aberrations of male descent are increased. Misrepair of double-strand DNA breaks (DSBs) is a prerequisite for such aberrations to occur. To date, no absolute assessment of the number of DSBs in human sperm nuclei after gamete fusion has been described.

Chromosome-wide nucleosome replacement and H3.3 incorporation during mammalian meiotic sex chromosome inactivation.

In mammalian males, the first meiotic prophase is characterized by formation of a separate chromatin domain called the sex body. In this domain, the X and Y chromosomes are partially synapsed and transcriptionally silenced, a process termed meiotic sex-chromosome inactivation (MSCI). Likewise, unsynapsed autosomal chromatin present during pachytene is also silenced (meiotic silencing of unsynapsed chromatin, MSUC).

gammaH2AX signalling during sperm chromatin remodelling in the mouse zygote.

In the mouse, the paternal post-meiotic chromatin is assumed to be devoid of DNA repair after nuclear elongation and protamine-induced compaction. Hence, DNA lesions induced thereafter will have to be restored upon gamete fusion in the zygote. Misrepair of such lesions often results in chromosome type aberrations at the first cleavage division, suggesting that the repair event takes place prior to S-phase.