Abstract：
OBJECTIVE: To study whether male factor infertility and insomnia share genetic risk variants and identify any molecular, cellular, and biologic interactions between these traits.
METHODS: The in silico study was performed. Two lists of genetic variants were manually curated through a literature review, one of those associated with male factor infertility and the other with insomnia. Genes were assigned to these variants to compose male factor infertility-associated (454 genes) and insomnia-associated (921 genes) gene lists.
METHODS: Not applicable.
METHODS: Not applicable.
METHODS: Not applicable.
METHODS: Enrichment of biologic pathways and protein-protein interaction analysis.
RESULTS: Twenty-eight genes were common to both lists, representing a greater overlap than would be expected by chance. In the 28 genes contained in the intersection list, there was a significant enrichment of pathways related to kinesin binding. A protein-protein interaction analysis using the intersection list as input retrieved 25 nodes and indicated that two of them were kinesin-related proteins (PLEKHM2 and KCL1).
CONCLUSIONS: The shared male factor infertility and insomnia genes, and the biologic pathways highlighted in this study, suggest that further functional investigations into the interplay between fertility and sleep are warranted.
METHODS: The in silico study was performed. Two lists of genetic variants were manually curated through a literature review, one of those associated with male factor infertility and the other with insomnia. Genes were assigned to these variants to compose male factor infertility-associated (454 genes) and insomnia-associated (921 genes) gene lists.
METHODS: Not applicable.
METHODS: Not applicable.
METHODS: Not applicable.
METHODS: Enrichment of biologic pathways and protein-protein interaction analysis.
RESULTS: Twenty-eight genes were common to both lists, representing a greater overlap than would be expected by chance. In the 28 genes contained in the intersection list, there was a significant enrichment of pathways related to kinesin binding. A protein-protein interaction analysis using the intersection list as input retrieved 25 nodes and indicated that two of them were kinesin-related proteins (PLEKHM2 and KCL1).
CONCLUSIONS: The shared male factor infertility and insomnia genes, and the biologic pathways highlighted in this study, suggest that further functional investigations into the interplay between fertility and sleep are warranted.
摘要：
目的：研究男性不育和失眠是否具有遗传风险变异，并识别任何分子，这些性状之间的细胞和生物相互作用。
方法：进行了计算机模拟研究。通过文献综述手动策划了两个遗传变异列表，其中一个与男性不育有关，另一个与失眠有关。将基因分配给这些变体以组成男性不育（454个基因）和失眠（921个基因）相关的基因列表。
方法：不适用。
方法：不适用。
方法：生物途径的富集和蛋白质-蛋白质相互作用（PPI）分析。
结果：28个基因在两个列表中是共同的，代表比偶然预期的更大的重叠。在交叉列表中包含的28个基因中，与驱动蛋白结合相关的通路显著富集。使用交叉列表作为输入的PPI分析检索到25个节点，并表明其中2个是驱动蛋白相关蛋白（PLEKHM2和KCL1）。
结论：男性不育和失眠的共同基因，以及这项研究中强调的生物学途径，这表明有必要对生育能力和睡眠之间的相互作用进行进一步的功能性研究.
方法：进行了计算机模拟研究。通过文献综述手动策划了两个遗传变异列表，其中一个与男性不育有关，另一个与失眠有关。将基因分配给这些变体以组成男性不育（454个基因）和失眠（921个基因）相关的基因列表。
方法：不适用。
方法：不适用。
方法：生物途径的富集和蛋白质-蛋白质相互作用（PPI）分析。
结果：28个基因在两个列表中是共同的，代表比偶然预期的更大的重叠。在交叉列表中包含的28个基因中，与驱动蛋白结合相关的通路显著富集。使用交叉列表作为输入的PPI分析检索到25个节点，并表明其中2个是驱动蛋白相关蛋白（PLEKHM2和KCL1）。
结论：男性不育和失眠的共同基因，以及这项研究中强调的生物学途径，这表明有必要对生育能力和睡眠之间的相互作用进行进一步的功能性研究.
