Humans are regularly and continuously exposed to ionizing radiation from both natural and artificial sources. Cumulating evidence shows adverse effects of ionizing radiation on both male and female reproductive systems, including reduction of testis weight and sperm count and reduction of female germ cells and premature ovarian failure. While most of the observed effects were caused by DNA damage and disturbance of DNA repairment, ionizing radiation may also alter DNA methylation, histone, and chromatin modification, leading to epigenetic changes and transgenerational effects. However, the molecular mechanisms underlying the epigenetic changes and transgenerational reproductive impairment induced by low-dose radiation remain largely unknown. In this study, two different types of human ovarian cells and two different types of testicular cells were exposed to low dose of ionizing radiation, followed by bioinformatics analysis (including gene ontology functional analysis and Ingenuity Pathway Analysis), to unravel and compare epigenetic effects and pathway changes in male and female reproductive cells induced by ionizing radiation. Our findings showed that the radiation could alter the expression of gene cluster related to DNA damage responses through the control of MYC. Furthermore, ionizing radiation could lead to gender-specific reproductive impairment through deregulation of different gene networks. More importantly, the observed epigenetic modifications induced by ionizing radiation are mediated through the alteration of chromatin remodeling and telomere function. This study, for the first time, demonstrated that ionizing radiation may alter the epigenome of germ cells, leading to transgenerational reproductive impairments, and correspondingly call for research in this new emerging area which remains almost unknown.
SUMMARYA separable variable method is introduced to find the exact homogeneous solutions of a two-dimensional transversely isotropic piezoelectric media to handle general boundary conditions. The usual method of separable variables for partial differentiation equations cannot be readily applicable due to the tangling of the unknowns and their derivatives. Introducing dual variables of stresses, we obtain a set of first-order Hamiltonian equations whose eigensolutions are symplectic spanning over the solution space to cover all possible boundary conditions. The solutions consist of two parts. The first part is the derogative zero-eigenvalue solutions of the Saint Venant type together with all their Jordan chains. The second part is the decaying non-zero-eigenvalue solutions describing the boundary layer effects. The classical solutions are actually the zero-eigenvalue solutions representing the simple extension, bending, equipotential field, and the uniform electric displacement. On the other hand, the non-zero-eigenvalue solutions represent the localized solutions, which are sensitive to the boundary conditions and are decaying rapidly with respect to the distance from the boundaries. Some rate-of-decay curves of the newly found non-zero-eigenvalue solutions are shown by numerical examples. Finally, the complete boundary layer effects are quantified for the first time.
Recent studies have shown hypoxia to be an endocrine disruptor that impairs sex differentiation and reproductive function, leading to male-biased F1 populations in fish. However, the molecular mechanisms through which hypoxia alters fish sex differentiation and therefore sex ratios remain poorly understood. In order to understand the potential role of miRNAs in mediating hypoxia-altered sex determination and differentiation in fish, we conducted small RNA sequencing and transcriptome sequencing on marine medaka (Oryzias melastigma) embryos that were exposed to hypoxia (2.0 ± 0.2 mg O2 L–1) for 40 h (encompassing a critical window of sex determination). We identified dysregulated miRNAs and mRNAs in the hypoxia-exposed embryo, and bioinformatic analysis of the integrative small RNA sequencing and transcriptome sequencing results revealed hypoxia to cause alterations of genes related to embryonic development through miRNA regulation. Importantly, we have identified miRNA-mRNA pairs that were reported to play roles in gonad development (novel miR-145-col9a3 and novel miRNA-94- arid5b), in sex hormone response (novel miRNA-210-ca2, novel miRNA-106-nr2f2, nbr-miR-29c-nr4a1, and ola-miR-92b-akr1d1), and in sex characteristic development (novel miRNA-145-mns1, nle-miR-20-sord, and ipu-miR-219b-abcc8). Our findings highlighted the possible roles of miRNA–mRNA in regulation of embryonic development and sex determination in response to hypoxic stress.
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