Gaming Disorder and Well-Being Among Emirati College Women

Background: The present study examined Internet Gaming Disorder (IGD) and depressive symptom levels among a predominantly female sample of college students from the United Arab Emirates (UAE). Methods: IGD was assessed among two successive cohorts of students at the beginning of the academic year in 2016 and 2019, respectively. All participants (n = 412) completed the Internet Gaming Disorder Scale – Short-Form (IGDS9-SF) and the WHO-5 Well-being Index (WHO-5), a tool widely used for the screening and assessment of depressive symptomatology. Results: Mean IGDS9-SF scores (15.85, SD = 6.40) were fairly similar to those observed in other nations. The prevalence of IGD was 1.45%, based on the stringent cut-off score (> = 40). Prevalence of IGD rose to 18.20% when using the less stringent cut-off (> = 21). There was an increase in the rate of IGD between 2016 and 2019, although not statistically significant. Higher IGDS9-SF scores were associated with greater depressive symptomatology; those scoring above the less stringent IGD cut-off had a greater likelihood of screening positive for depression OR = 2.28, 95% CI (1.176–4.428). Conclusions: This study provides insights about IGD among a predominantly female Arab population, finding a correlation with mood disorder symptomatology and suggesting an increase in problematic gaming over time. The results are discussed with reference to the mood repair hypothesis and the possibility of IGD being a dual disorder. The association with depressive symptoms is also discussed in light of the neurobiology of addictive behaviors and sexual dimorphism

Validation of less-invasive hemodynamic monitoring with Pulsioflex in critically ill patients

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Urbilaterian origin of paralogous GnRH and corazonin neuropeptide signalling pathways

This work was supported by funding from the China Scholarship Council (awarded to ST), Leverhulme Trust (grant RGP-2013-351, awarded to MRE), BBSRC (grant BB/M001644/1 awarded to MRE; grant BB/M001032/1 awarded to JHS) and a Company of Biologists (Journal of Experimental Biology) Travelling Fellowship awarded to MZ. IB is supported by a postdoctoral fellowship from the Research Foundation–Flanders (FWO)

Riding the techwave in an era of change: The healthcare guide to the future

FSW - Self-regulation models for health behavior and psychopathology - ou

Anthelmintic activity of trans-cinnamaldehyde and A- and B-type proanthocyanidins derived from cinnamon (Cinnamomum verum)

Cinnamon (Cinnamomum verum) has been shown to have anti-inflammatory and antimicrobial properties, but effects on parasitic worms of the intestine have not been investigated. Here, extracts of cinnamon bark were shown to have potent in vitro anthelmintic properties against the swine nematode Ascaris suum. Analysis of the extract revealed high concentrations of proanthocyanidins (PAC) and trans-cinnamaldehyde (CA). The PAC were subjected to thiolysis and HPLC-MS analysis which demonstrated that they were exclusively procyanidins, had a mean degree of polymerization of 5.2 and 21% of their inter-flavan-3-ol links were A-type linkages. Purification of the PAC revealed that whilst they had activity against A. suum, most of the potency of the extract derived from CA. Trichuris suis and Oesophagostomum dentatum larvae were similarly susceptible to CA. To test whether CA could reduce A. suum infection in pigs in vivo, CA was administered daily in the diet or as a targeted, encapsulated dose. However, infection was not significantly reduced. It is proposed that the rapid absorption or metabolism of CA in vivo may prevent it from being present in sufficient concentrations in situ to exert efficacy. Therefore, further work should focus on whether formulation of CA can enhance its activity against internal parasites

Retinoic acid induces HL-60 cell differentiation via the upregulation of miR-663

<p>Abstract</p> <p>Background</p> <p>Differentiation of the acute myeloid leukemia (AML) cell line HL-60 can be induced by all trans-retinoic acid (ATRA); however, the mechanism regulating this process has not been fully characterized.</p> <p>Methods</p> <p>Using bioinformatics and <it>in vitro </it>experiments, we identified the microRNA gene expression profile of HL-60 cells during ATRA induced granulocytic differentiation.</p> <p>Results</p> <p>Six microRNAs were upregulated by ATRA treatment, miR-663, miR-494, miR-145, miR-22, miR-363* and miR-223; and three microRNAs were downregulated, miR-10a, miR-181 and miR-612. Additionally, miR-663 expression was regulated by ATRA. We used a lentivirus (LV) backbone incorporating the spleen focus forming virus (SFFV-F) promoter to drive miR-663 expression, as the CMV (Cytomegalovirus) promoter is ineffective in some lymphocyte cells. Transfection of LV-miR-663 induced significant HL-60 cell differentiation <it>in vitro</it>.</p> <p>Conclusions</p> <p>Our results show miR-663 may play an important role in ATRA induced HL-60 cell differentiation. Lentivirus delivery of miR-663 could potentially be used directly as an anticancer treatment in hematological malignancies</p

NEDD9 Is a Positive Regulator of Epithelial-Mesenchymal Transition and Promotes Invasion in Aggressive Breast Cancer

Epithelial to mesenchymal transition (EMT) plays an important role in many biological processes. The latest studies revealed that aggressive breast cancer, especially the triple-negative breast cancer (TNBC) subtype was frequently associated with apparent EMT, but the mechanisms are still unclear. NEDD9/HEF1/Cas-L is a member of the Cas protein family and was identified as a metastasis marker in multiple cancer types. In this study, we wished to discern the role of NEDD9 in breast cancer progression and to investigate the molecular mechanism by which NEDD9 regulates EMT and promotes invasion in triple-negative breast cancer. We showed that expression of NEDD9 was frequently upregulated in TNBC cell lines, and in aggressive breast tumors, especially in TNBC subtype. Knockdown of endogenous NEDD9 reduced the migration, invasion and proliferation of TNBC cells. Moreover, ectopic overexpression of NEDD9 in mammary epithelial cells led to a string of events including the trigger of EMT, activation of ERK signaling, increase of several EMT-inducing transcription factors and promotion of their interactions with the E-cadherin promoter. Data presented in this report contribute to the understanding of the mechanisms by which NEDD9 promotes EMT, and provide useful clues to the evaluation of the potential of NEDD9 as a responsive molecular target for TNBC chemotherapy