Results of aware breathing combined with sleep-inducing exercises within individuals together with insomnia.

We propose a novel nonlinearity measure called normalized differential correlation (NDC) to efficiently highlight nonlinearly expressed genes in transcriptome datasets. Validation using six real-world cancer datasets revealed that the NDC method could highlight nonlinearly expressed genes that could not be highlighted by t-test, MIC, edgeR, and DEseq2, although MIC could capture nonlinear correlations. The classification accuracy indicated that analysis of these genes could adequately distinguish cancer and paracarcinoma tissue samples. Furthermore, the results of biological interpretation of the identified genes suggested that some of them were involved in key functional pathways associated with cancer progression and metastasis. All of this evidence suggests that these nonlinearly expressed genes may play a central role in regulating cancer progression. Copyright © 2020 Wang, Zhang, Liang, Jiang, Tan, Luo, Yuan and Chen.Colorectal cancer (CRC) is the second most common cause of cancer-related death worldwide, and is well known for its strong invasiveness, rapid recurrence, and poor prognosis. Long non-coding RNAs (lncRNAs) have been shown to be involved in the development of various types of cancers, including colorectal cancer. Here, through transcriptomic analysis and functional screening, we reported that lncRNA LUCRC (LncRNA Upregulated in Colorectal Cancer) is highly expressed in colorectal tumor samples and is required for colorectal cancer cell proliferation, migration, and invasion in cultured cells and tumorigenesis in xenografts. LUCRC was found to regulate target gene expression of unfolded protein response (UPR) in endoplasmic reticulum (ER), such as BIP. The clinical significance of LUCRC is underscored by the specific presence of LUCRC in blood plasma of patients with colorectal cancers. These findings revealed a critical regulator of colorectal cancer development, which might serve as a therapeutic target in colorectal cancer. Copyright © 2020 Tang, Chen, Ding, Du, Lin, Xia, Lian, Ye, He and Liu.Meta-analysis, which combines the results of multiple studies, is an important analytical method in genome-wide association studies. In genome-wide association studies practice, studies employing meta-analysis may have overlapping data, which could yield false positive results. Recent studies have proposed models to handle the issue of overlapping data when testing the genetic main effect of single nucleotide polymorphism. However, there is still no meta-analysis method for testing gene-environment interaction when overlapping data exist. Inspired by the methods of testing the main effect of gene with overlapping data, we proposed an overlapping meta-regulation method to address the issue in testing the gene-environment interaction. We generalized the covariance matrices of the regular meta-regression model by employing Lin's and Han's correlation structures to incorporate the correlations introduced by the overlapping data. Based on our proposed models, we further provided statistical significance tests of the gene-environment interaction as well as joint effects of the gene main effect and the interaction. Through simulations, we examined type I errors and statistical powers of our proposed methods at different levels of data overlap among studies. We demonstrated that our method well controls the type I error and simultaneously achieves statistical power comparable with the method that removes overlapping samples a priori before the meta-analysis, i.e., the splitting method. On the other hand, ignoring overlapping data will inflate the type I error. Unlike the splitting method that requires individual-level genotype and phenotype data, our proposed method for testing gene-environment interaction handles the issue of overlapping data effectively and statistically efficiently at the meta-analysis level. Copyright © 2020 Jin and Shi.Rotor syndrome, a rare autosomal-recessive genetic disorder characterized by conjugated hyperbilirubinemia, is caused by biallelic pathogenic variants in both SLCO1B1 and SLCO1B3 genes. Long interspersed nuclear elements (LINEs) make up about 17% of the human genome and insertion of LINE-1 in genes can result in genetic diseases. In the current study, we examined SLCO1B1 and SLCO1B3 genes in two Chinese patients diagnosed with Rotor syndrome based on laboratory tests. In one patient, a novel exon 4 inversion variant was identified. This variant may have been induced by LINE-1 retrotransposon insertion into SLCO1B3 intron 3, and was identified using genome walking. Splicing assay results indicated that the exon inversion, resulting in SLCO1B3 exon 4 (122 bp) exclusion in the mature mRNA, might generate a premature termination codon. Here, we describe an exon inversion contributing to the molecular etiology of Rotor syndrome. Our results may inform future diagnoses and guide drug prescriptions and genetic counseling. Copyright © 2020 Zhou, Qi, Zhang, Wu, Xu, Li, Zhang, Li, Jia, Wang, Jia, Ou, Huang and You.Angiogenesis is a crucial event during cancer progression that regulates tumor growth and metastasis. EPZ011989 Activin receptor-like kinase 1 (ALK1), predominantly expressed in endothelial cells, plays a key role in the organization of neo-angiogenic vessels. Therapeutic targeting of ALK1 has been proposed as a promising strategy for cancer treatment, and microRNAs (miRNAs) are increasingly being explored as modulators of angiogenesis. However, the regulation of ALK1 by miRNAs is unclear. In this study, we identified that ALK1 is directly targeted by miR-199b-5p, which was able to inhibit angiogenesis in vitro and in vivo. Moreover, it was found that miR-199b-5p was repressed in breast cancer cells and its expression was decreased during the VEGF-induced angiogenesis process of human umbilical vein endothelial cells (HUVECs). Overexpression of miR-199b-5p inhibited the formation of capillary-like tubular structures and migration of HUVECs. Furthermore, overexpression of miR-199b-5p inhibited the mRNA and protein expression of ALK1 in HUVECs by directly binding to its 3'UTR. Additionally, overexpression of miR-199b-5p attenuated the induction of ALK1/Smad/Id1 pathway by BMP9 in HUVECs. Finally, overexpression of miR-199b-5p reduced tumor growth and angiogenesis in in vivo. Taken together, these findings demonstrate the anti-angiogenic role of miR-199b-5p, which directly targets ALK1, suggesting that miR-199b-5p might be a potential anti-angiogenic target for cancer therapy. Copyright © 2020 Lin, Qiu, Xiao, Ma, Xu, Zhang, Gao, Chen, Li, Li and Qian.EPZ011989