A premature infant's discharge from the neonatal intensive care unit (NICU) is dependent on factors such as respiratory stability, adequate growth, and the ability to consume oral feeds. Once infants have achieved respiratory stability, a tool that can better predict age at discharge is desirable. Thus, we conducted a secondary data analysis to assess the association between ultrasound measurements of abdominal muscle thickness and postmenstrual age (PMA) at full oral feedings. Forty-nine (n = 49) healthy, premature infants (mean gestational age = 32 weeks) were recruited from the NICU. Anthropometric measurements and ultrasound measurements of the rectus abdominis were conducted when infants were medically stable. Fat-free mass (FFM) was obtained using air displacement plethysmography. The relationship between ultrasound measurements of muscle thickness and PMA at full oral feedings was assessed using linear regression analysis. The relationship between FFM z-scores and PMA at full oral feedings was alsoevelopment and validation of a prediction equation.Unbalanced copper (Cu2+ ) homeostasis is associated with the developmental defects of vertebrate myogenesis, but the underlying molecular mechanisms remain elusive. In this study, it was found that Cu2+ stressed zebrafish embryos and larvae showed reduced locomotor speed as well as loose and decreased myofibrils in skeletal muscle, coupled with the downregulated expression of muscle fiber markers mylpfa and smyhc1l and the irregular arrangement of myofibril and sarcomere. Meanwhile, the Cu2+ stressed zebrafish embryos and larvae also showed significant reduction in the expression of H3K4 methyltransferase smyd1b transcripts and H3K4me3 protein as well as in the binding enrichment of H3K4me3 on gene mylpfa promoter in skeletal muscle cells, suggesting that smyd1b-H3K4me3 axis mediates the Cu2+ -induced myofibrils specification defects. Additionally, whole genome DNA methylation sequencing unveiled that the gene smyd5 exhibited significant promoter hyper-methylation and increased expression in Cu2+ stressed embryos, and the ectopic expression of smyd5 in zebrafish embryos also induced the myofibrils specification defects as those observed in Cu2+ stressed embryos. Moreover, Cu2+ was shown to suppress myofibrils specification and smyd1b promoter transcriptional activity directly independent of the integral function of copper transporter cox17 and atp7b. All these data may shed light on the linkage of unbalanced copper homeostasis with specific gene promoter methylation and epigenetic histone protein modification as well as the resultant signaling transduction and the myofibrillogenesis defects.Retraction "Silence of lncRNA HEIH suppressed liver cancer cell growth and metastasis through miR-199a-3p/mTOR axis," by Yongbiao Ma, De Cao, Gaoxue Li, Jingxia Hu, Xin Liu, Jianling Liu, J Cell Biochem. 2019; 17757-17766 The above article, published online on 29 May 2019 in Wiley Online Library (https//onlinelibrary.wiley.com/doi/abs/10.1002/jcb.29041), has been retracted by agreement between the the journal's Editor in Chief, Prof. Dr. Christian Behl, and Wiley Periodicals LLC. The retraction has been agreed following an investigation based on allegations raised by a third party. Several flaws and inconsistencies between results presented and experimental methods described were found, the editors consider the conclusions of this article to be invalid. The authors collaborated in the investigation initially, but were not available for a final confirmation of the retraction.Retraction "Long noncoding RNA TALNEC2 plays an oncogenic role in breast cancer by binding to EZH2 to target p57KIP2 and involving in p-p38 MAPK and NF-κB pathways," by Enqi Qiao, Daobao Chen, Qinglin Li, Weiliang Feng, Xingfei Yu, Xiping Zhang, Liang Xia, Ju Jin, Hongjian Yang, J Cell Biochem. 2019; 3978-3988 The above article, published online on 30 October 2018 in Wiley Online Library (https//onlinelibrary.wiley.com/doi/abs/10.1002/jcb.27680), has been retracted by agreement between the the journal's Editor in Chief, Prof. Dr. Christian Behl, and Wiley Periodicals LLC. The retraction has been agreed following an investigation based on allegations raised by a third party. Several flaws and inconsistencies between results presented and experimental methods described were found, the editors consider the conclusions of this article to be invalid. The authors collaborated in the investigation initially, but were not available for a final confirmation of the retraction.Retraction "Emodin protects H9c2 cells against hypoxia-induced injury via regulation of miR-26a/survivin and the JAK1/STAT3 pathway," by Jiancheng Huang, Xiaobing Li, Pujuan Liu, Jun Wang, Hongying Li, J Cell Biochem. 2019; 11081-11090 The above article, published online on 30 January 2019 in Wiley Online Library (https//onlinelibrary.wiley.com/doi/abs/10.1002/jcb.28385), has been retracted by agreement between the journal's Editor in Chief, Prof. Dr. Christian Behl, and Wiley Periodicals LLC. The retraction has been agreed following an investigation based on allegations raised by a third party. Several flaws and inconsistencies between results presented and experimental methods described were found, the editors consider the conclusions of this article to be invalid. The authors collaborated in the investigation initially, but were not available for a final confirmation of the retraction. Giggle incontinence is a rare condition resulting in excessive urinary incontinence with laughter, where bladder function is otherwise "normal." Urodynamic descriptions of the condition to date are limited. We believe that giggle incontinence has characteristic urodynamic findings. We tested this hypothesis. We retrospectively reviewed the urodynamic investigations of patients with giggle incontinence managed in a tertiary regional bladder unit between February 2014 and November 2019. We identified the studies of seven patients, median age 13.5 years (10.4-15.7) of whom 6 were female. All had videourodynamics. Two went on to have further invasive investigation; one had urethral pressure profile and one had ambulatory urodynamics. Detrusor overactivity (DO) was observed in six. DO was asensate in all. HSP990 In five DO was triggered by laughter and was associated with laughter induced incontinence in four. Six had DO that was not provoked by laugher. In one amplitude of DO was proportional to vigour of laughter.