Egholmjohansson9195

g., hooking up is fun, hooking up provides sexual freedom) helped differentiate reported involvement in various types of hookup behaviors. The most prominent and consistent correlate was number of different hookup partners in the last 12 months (increased likelihood of all behaviors, except deep kissing). Recommendations for understanding hooking up as a developmental and/or cultural experience are discussed.Although the evolution of differentiated thyroid cancer (DTC) is usually indolent, some tumors grow fast, metastasize, and may be fatal. Viruses have been associated with many human tumors, especially the Epstein-Barr virus (EBV), which shows a high viral load in DTC. In order to evaluate the ability of the virus to cause morphological and molecular changes in neoplastic thyroid cell lines TPC-1, BCPAP, and 8505C, a viral adaptation was performed for the analysis of EBV cytopathic effect (CPE), viral kinetics and gene expression analysis of oncogenes KRAS, NRAS, HRAS, and TP53. Comparison of inoculated cells with non-inoculated control cells showed that all tumor cell lines were permissive to the virus. The virus caused CPE in the TPC-1 and 8505C, but not in BCPAP cells. Viral kinetic was similar in both BCPAP and 8505C with a point of eclipse at 24 h post infection. TPC-1 cell line displayed a decreasing growth curve, with highest viral load right after inoculation, which decreased over time. There was hyperexpression of TP53 and NRAS in BCPAP cell (p = 0.012 and p = 0.0344, respectively). The 8505C cell line presented NRAS hyperexpression (p = 0.0255), but lower TP53 expression (p = 0.0274). We concluded that neoplastic thyroid cell lines are permissive to EBV that the virus presents different viral kinetic patterns in different cell lines and produces a CPE on both well-differentiated and undifferentiated thyroid cell lines. We also demonstrated that EBV interferes in oncogene expression in thyroid neoplastic cell lines, suggesting that these effects could be related to different tumor progression patterns.PURPOSE This meta-analysis was conducted given the inconsistent findings of studies regarding the sex discrepancy in the relationship between type 1 diabetes (T1D) and the risk of end-stage renal disease (ESRD). METHODS Articles published on PubMed between January 1, 1966 and March 31, 2019 were systematically retrieved without language restrictions. The included articles all presented sex-specific data of the incidence rate ratio, standardized incidence or mortality ratio, hazard ratio, relative risk, or odds ratio, or provided data to estimate the association between T1D and ESRD or kidney disease-related mortality. The gender-specific effect estimates and pooled ratio (female-to-male) for ESRD and for deaths from T1D-related renal disease were acquired via a random-effects meta-analysis with inverse variance weighting, regardless of heterogeneity evaluated based on the I2 statistic. RESULTS Nineteen studies, including 122,842 individuals, were finally selected for this meta-analysis. Sex differences in effect estimates were found in ESRD (pooled ratio = 0.81 (95% confidence interval 0.69-0.94)) with considerable heterogeneity (I2 = 66.9%), but not in mortality with T1D-associated renal disease. CONCLUSION Women with T1D have a lower risk of ESRD compared with that in men, but this finding may be biased by potential confounding factors and must be verified by other well-planned prospective studies.PURPOSE Triple negative breast cancers (TNBCs) are enriched in cells bearing stem-like features, i.e., cancer stem cells (CSCs), which underlie cancer progression. Thus, targeting stemness may be an interesting treatment approach. The epigenetic machinery is crucial for maintaining the stemness phenotype. Bromodomain and extra-terminal domain (BET) epigenetic reader family members are emerging as novel targets for cancer therapy, and have already shown preclinical effects in breast cancer. HexadimethrineBromide Here, we aimed to evaluate the effect of the BET inhibitor JQ1 on stemness in TNBC. METHODS Transcriptomic, functional annotation and qRT-PCR studies were performed on JQ1-exposed TNBC cells in culture. The results obtained were confirmed in spheroids and spheroid-derived tumours. In addition, limiting dilution, secondary and tertiary tumour sphere formation, matrigel invasion, immunofluorescence and flow cytometry assays were performed to evaluate the effect of JQ1 on CSC features. For clinical outcome analyses, the onlinefamily G Member 2 (ABCG2) and RUNX2, and predicted a low response to chemotherapy in TNBC patients, which supports a role for RUNX2 as a potential predictive marker for chemotherapy response in TNBC. CONCLUSIONS We identified a stemness-related gene panel associated with JQ1 and describe how this inhibitor modifies the stemness landscape in TNBC. Therefore, we propose a novel role for JQ1 as a stemness-targeting drug. Loss of the stem cell phenotype via JQ1 treatment could lead to less aggressive and more chemo-sensitive tumours, reflecting a better patient prognosis. Thus, the identified gene panel may be of interest for the clinical management of patients with aggressive TNBC.PURPOSE DCBLD2 expression dysregulation has been reported in several types of human cancer. As yet, however, the role of DCBLD2 in colorectal cancer (CRC) is not known. METHODS CRC tissues were obtained from patients undergoing surgery from February 2009 to May 2014 (n = 90). Tissue microarray construction and immunohistochemistry were carried out to determine DCBLD2 expression. In vivo studies were performed in 4-week-old BALB/c nude mice. In vitro studies were conducted using CRC-derived HT29 and HCT116 cell lines. RESULTS DCBLD2 expression was found to be significantly increased in CRC tissues compared to adjacent normal tissues (p  less then  0.001). In addition, we found that DCBLD2 expression was positively correlated with the stage of the disease, the degree of differentiation and vascular invasion. High DCBLD2 expression was significantly associated with a poor overall survival. In vitro, DCBLD2 expression downregulation significantly reduced CRC cell proliferation and invasion. In a mouse xenograft model, DCBLD2 expression downregulation reduced lung metastasis and increased overall survival.