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MiR-483-5p overexpression significantly increased hypoxia-induced cardiomyocyte apoptosis and oxidative stress, while knockdown attenuated these effects. Mechanistically, miR-483-5p directly targets MAPK3 in AC16 cells. Furthermore, the protective effects of miR-483-5p knockdown against hypoxia-induced cardiomyocyte injury are partially dependent on MAPK3. Conclusions MiR-483-5p, which targets MAPK3, might be a potential therapeutic target for the diagnosis and prevention of hypoxia-induced myocardial injury. © The Author(s) 2020.Background It has been shown that miR-144-3p regulates cell proliferation, apoptosis, migration and invasion in various cancers. However, the function and expression of miR-144-3p in colorectal cancer (CRC) remained obscure. Methods Immunohistochemical (IHC) staining was performed to investigate the protein expression of BCL6 in CRC tissues. The effect of BCL6 and miR-144-3p on CRC cells was explored through methylthiazolyl tetrazolium (MTT) assay, colony formation and cell cycle assays. Luciferase reporter assays, reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blot assay were carried out to determine that BCL6 is directly regulated by miR-144-3p. Results Our results showed that miR-144-3p is down-regulated in CRC and correlates with the tumor progression of CRC patients. miR-144-3p inhibits cell proliferation and delays G1/S phase transition of CRC cells. Moreover, we found that BCL6 is a new target of miR-144-3p. Furthermore, BCL6 is a mediator of miR-144-3p repression of cell proliferation and cell cycle arrest in CRC cells. miR-144-3p repression of Wnt/β-catenin signaling is mediated by BCL6 in CRC cells. Conclusions Overall, the effect of the miR-144-3p/BCL6 axis on regulating CRC carcinogenesis was demonstrated, and miR-144-3p was identified as a potential prognostic and therapeutic target in colorectal cancer. © The Author(s) 2020.Background Apgar score is currently an accepted method for newborn infant assessment immediately after delivery. Low fifth minute Apgar score was strongly associated with the risk of neonatal and infant death. Even though much has been done, still, the levels of neonatal mortality in sub-Saharan African countries including Ethiopia were significant. Therefore, this study is aimed at identifying the risk factors so as providing strategies for decreasing the morbidity and mortality of newborns and identifying determinants of low fifth minute Apgar score among newborns delivered in Jimma University Medical Center, Southwest Ethiopia, 2018. Method Institution-based cross-sectional study was conducted involving 366 neonates delivered at Jimma University Medical Center. Data was collected by using interview questionnaire. Apgar score was assessed by standard tool at the 1st, 5th, and 10th minutes after birth and only 5th minute Apgar score was used as outcome variable. Consecutive sampling technique was used to select the participants. The collected data were analyzed using SPSS version 20.0. Chi-square test was done at bivariate level and P value was used to select candidate variables for multivariate analysis. Finally, a 95% confidence interval was used to assess significance. ZCL278 Results A response rate of this study was 95%. The proportion of low 5th minute Apgar score in this study was 11.5%. Prolonged duration of labor (AOR = 15.18, 95% CI 5.51-40.27), maternal history of khat use (AOR = 3.21, 95% CI 1.26-8.85), and low birth weight (AOR = 1.65, 95% CI 1.02-3.11) were predictors of low fifth minute Apgar score. Conclusion About one tenth of newborns were having low 5th minute Apgar score. The likelihood of low 5th minute Apgar score was found to increase with prolonged duration of labor, history of mother's khat use, and low birth weight. Copyright © 2020 Bekalu Getachew et al.Adenosine receptors A1 (A1AR) and A2a (A2aAR) play an important role in regulating glutamate uptake to avoid glutamate accumulation that causes excitotoxicity in the brain; however, the precise mechanism of the effects of A1AR and A2aAR is unclear. Herein, we report that expression of the A1AR protein in the astrocyte membrane and the level of intracellular glutamate were decreased, while expression of the A2aR protein was elevated in cells exposed to oxygen-glucose deprivation (OGD) conditions. Coimmunoprecipitation (Co-IP) experiments showed that A1AR interacts with A2aAR under OGD conditions. The activation of A1AR and inactivation of A2aAR by 2-chloro-N6-cyclopentyladenosine (CCPA) and SCH58251, respectively, partly reversed OGD-mediated glutamate uptake dysfunction, elevated EAAT2, and PPARγ protein levels, and suppressed the expression of Ying Yang 1 (YY1). Both the silencing of YY1 and the activation of PPARγ upregulated EAAT2 expression. Moreover, YY1 silencing elevated the PPARγ level under both normal and OGD conditions. Histone deacetylase (HDAC)1 was found to interact with YY1, and HDAC1 silencing improved PPARγ promoter activity. Taken together, our findings suggest that A1AR-A2aAR heteromers regulate EAAT2 expression and glutamate uptake through the YY1-mediated recruitment of HDAC1 to the PPARγ promoter region. Copyright © 2020 Xianhua Hou et al.Primary neuroendocrine carcinomas of the urinary bladder are rare. A 60-year-old male presented with gross hematuria for the past 3 months. Diagnostic flexible cystoscopy revealed a papillary lesion above the right ureteric orifice. Transurethral resection of bladder tumor was performed and resected tissue was sent for histopathology that revealed high-grade urothelial carcinoma with small-cell neuroendocrine differentiation. Lamina propria, muscularis propria, and perineural invasion was seen which was later also confirmed by immunohistochemistry. The patient received neoadjuvant four cycles of chemotherapy and then underwent radical cystoprostatectomy with ileal conduit. The patient's recovery was uneventful and he is on regular follow-up from the past 12 months without any disease recurrence. Early detection and aggressive management can improve the survival and prognosis of these patients. Copyright © International Journal of Health Sciences.