Moderating Effects of Mindfulness in the Relation between Bullying Victimization and Sleep Disturbance in Chinese Children: Sex Differences.

Bullying victimization is associated with sleep disturbance. The present study aimed to investigate the impact of bullying victimization on sleep disturbance, and the moderating effect of mindfulness on this association, also exploring differences across sex. A sample of 420 Chinese children (Mage = 9.60, SD age = 1.11, 48.10% girls) in grade 3 to grade 6 were recruited to complete the revised Bully/Victim Questionnaire, the Chinese version of Pittsburg Sleep Quality Index, the Child and Adolescent Mindfulness Measure, as well as the Family Affluence Scale. Results showed that bullying victimization was positively associated with sleep disturbance (ß = 0.20, p < 0.001). And the effect of bullying victimization on sleep disturbance was moderated by mindfulness (ß = -0.16, p < 0.001), and the effect was invalid for children with high mindfulness (ß = 0.04, p > 0.05). Subgroup analyses indicated the buffering effect of mindfulness only existed among boys (ß = -0.19, p < 0.01) but not girls (ß = -0.11, p > 0.05), suggesting that mindfulness may buffer this association, mainly for boys.

Development and characterization of mammary intraductal (MIND) spontaneous metastasis models for triple-negative breast cancer in syngeneic mice.

Triple-negative breast cancer (TNBC) has a more aggressive phenotype and higher metastasis and recurrence rates than other breast cancer subtypes. TNBC currently lacks a transplantation model that is suitable for clinical simulations of the tumor microenvironment. Intraductal injection of tumor cells into the mammary duct could mimic the occurrence and development of breast cancer. Herein, we injected 4T1 cells into the mammary ducts of BALB/C mice to build a preclinical model of TNBC and optimized the related construction method to observe the occurrence and spontaneous metastasis of tumors. We compared the effects of different cell numbers on tumorigenesis rates, times to tumorigenesis, and metastases to determine the optimal number of cells for modelling. We demonstrated that 4T1-MIND model mice injected with 20,000 cells revealed a suitable tumor formation rate and time, thus indicating a potential treatment time window after distant metastasis. We also injected 20,000 cells directly into the breast fat pad or breast duct for parallel comparison. The results still showed that the 4T1-MIND model provides sufficient treatment time for lung metastases in mice and that it is a more reliable model for early tumor development. The 4T1-MIND model requires continuous improvement and optimization. A suitable and optimized model for translational research and studies on the microenvironment in TNBC should be developed.

Maternal HCV infection is associated with intrauterine fetal growth disturbance: A meta-analysis of observational studies.

Since the evidence regarding the association between maternal hepatitis C virus (HCV) infection and impaired intrauterine fetal growth had not been conclusive, the aim of the present study was to evaluate the risk of maternal HCV infection in association with intrauterine fetal growth restriction (IUGR) and/or low birth weight infants (LBW). We performed an extensive literature search of PubMed, MEDLINE, and EMBASE through December 1, 2015. The odds ratios (ORs) of HCV infection and IUGR/LBW were calculated and reported with 95% confidence intervals (95% CIs). Statistical analysis was performed using RevMen 5.3 and Stata 10.0. Seven studies involving 4,185,414 participants and 5094 HCV infection cases were included. Significant associations between HCV infection and IUGR (OR = 1.53, 95% CI: 1.40-1.68, fixed effect model) as well as LBW were observed (OR = 1.97, 95% CI: 1.43-2.71, random effect model). The results still indicated consistencies after adjusting for multiple risk factors which could affect fetal growth, including maternal age, parity, maternal smoking, alcohol abuse, drugs abuse, coinfected with HBV/HIV and preeclampsia. Our findings suggested that maternal HCV infection was significantly associated with an increased risk of impaired intrauterine fetal growth. In clinical practice, a closer monitoring of intrauterine fetal growth by a series of ultrasound might be necessary for HCV-infected pregnant population.

Identification of NR0B1 as a novel androgen receptor co-repressor in mouse Sertoli cells.

Nuclear receptor subfamily 0 group B member 1 (Nr0b1) is an atypical member of the nuclear receptor family that is predominantly expressed in mouse Sertoli cells (SCs). Mutations of NR0B1 in humans cause adrenal failure and hypogonadotropic hypogonadism. The targeted mutagenesis of Nr0b1 in mice has revealed a primary gonadal defect characterized by the overexpression of aromatase and cellular obstruction of the seminiferous tubules and efferent ductules, leading to germ cell death and infertility. The transgenic expression of Nr0b1 under the control of the Müllerian-inhibiting substance promoter (MIS-Nr0b1), which is selectively expressed in SCs, improves fertility. Testicular androgen receptor (AR) was also expressed in SCs. Many genes are directly regulated by androgen and its AR, which are involved in spermatogenesis and male infertility. As the association between NR0B1 and AR remains unclear in mouse SCs, we decided to further explore the relationship between them. In the present study, we have identified NR0B1 as a novel AR co-repressor in mouse SCs. Using RT­qPCR and immunofluorescence, we determined that NR0B1 was mainly expressed in mouse SCs in an age-dependent manner from 2-8 weeks of age postnatally. The inhibition of the effects of AR on AR target genes by NR0B1, in an androgen­dependent manner, was further demonstrated by western blot analysis and RT-qPCR in TM4 cells, a mouse Sertoli cell line. Finally, in vitro luciferase and co-immunoprecipitation assays validated that NR0B1, as an AR co-repressor, significantly inhibited the transcriptional activation of its target genes. These results suggest that novel inhibitory mechanisms underlie the effects of NR0B1 in modulating androgen-dependent gene transcription in mouse SCs.

Identification and characteristics of the testes-specific gene, Ccdc38, in mice.

Distinguishing the testes-specific genes in different species may disclose key genes associated with testes-specific functions and provide sufficient information for the study and treatment of male infertility. A testes­specific gene, coiled-coil domain containing 38 (Ccdc38), was identified by screening UniGene libraries. Systematic bioinformatics analysis demonstrated that the CCDC38 protein was conserved in various mammalian species. It was determined that CCDC38 was exclusively expressed in testes and its expression increased from 2­8 weeks of age. Additional immunohistochemical analysis indicated that CCDC38 was mainly expressed in spermatogonia and spermatocytes. It is of note that, immunofluorescence and co-immunoprecipitation assays demonstrated that CCDC38 interacted with ubiquitinated histone H2A in mouse testes. Therefore, these results suggest that Ccdc38 is a testes-specific gene, which may be important for mouse spermatogenesis.

[Expression of a testis-specific gene 1700001022RIK in mice and its bioinformatic analysis].

OBJECTIVE: To identify the expression characteristics of the 1700001022RIK (RIKEN cDNA 1700001022) gene in mice and explore its function by bioinformatic analysis. METHODS: Using the expression profile of gene microarray, we detected the expression of a new testis-specific gene, 1700001022RIK, in mice. We analyzed its expression characteristics in the testis tissue and their changes in different developmental stages of the testis by RT-PCR, real-time RT-PCR, Western blot, and immunohistochemistry. We performed bioinformatic analysis using a bioinformatic software. RESULTS: The 1700001022RIK gene was specifically expressed in the mouse testis in an age-dependent manner, most highly in the adult mice. The 1700001022RIK protein was mainly expressed in the spermatogonia, spermatocytes, and round spermatids of the adult mice. Bioinformatic analysis showed that the 1700001022RIK protein amino acid sequence had a high similarity in human and mice, which indicated that this gene was highly conserved in mammals. CONCLUSION: 1700001022RIK is a testis-specific gene mainly expressed in the spermatogonia, spermatocytes, and round spermatids of seminiferous tubules, which might be involved in the regulation of spermatogenesis.