Cell division without growth results in progressive cell size reductions during early embryonic development. How do the sizes of intracellular structures and organelles scale with cell size and what are the functional implications of such scaling relationships? Model organisms, in particular Caenorhabditis elegans worms, Drosophila melanogaster flies, Xenopus laevis frogs, and Mus musculus mice, have provided insights into developmental size scaling of the nucleus, mitotic spindle, and chromosomes. Nuclear size is regulated by nucleocytoplasmic transport, nuclear envelope proteins, and the cytoskeleton. Regulators of microtubule dynamics and chromatin compaction modulate spindle and mitotic chromosome size scaling, respectively. Developmental scaling relationships for membrane-bound organelles, like the endoplasmic reticulum, Golgi, mitochondria, and lysosomes, have been less studied, although new imaging approaches promise to rectify this deficiency. While models that invoke limiting components and dynamic regulation of assembly and disassembly can account for some size scaling relationships in early embryos, it will be exciting to investigate the contribution of newer concepts in cell biology such as phase separation and interorganellar contacts. With a growing understanding of the underlying mechanisms of organelle size scaling, future studies promise to uncover the significance of proper scaling for cell function and embryonic development, as well as how aberrant scaling contributes to disease. This article is categorized under Establishment of Spatial and Temporal Patterns > Regulation of Size, Proportion, and Timing Early Embryonic Development > Fertilization to Gastrulation Comparative Development and Evolution > Model Systems. © 2020 Wiley Periodicals, Inc.Drug-Target interaction (DTI) plays a crucial role in drug discovery, drug repositioning and understanding the drug side effects which helps to identify new therapeutic profiles for various diseases. However, the exponential growth in the genomic and drugs data makes it difficult to identify the new associations between drugs and targets. Therefore, we use computational methods as it helps in accelerating the DTI identification process. Usually, available data driven sources consisting of known DTI is used to train the classifier to predict the new DTIs. Such datasets often face the problem of class imbalance. Therefore, in this study we address two challenges faced by such datasets, i. e., class imbalance and high dimensionality to develop a predictive model for DTI prediction. The study is carried out on four protein classes namely Enzyme, Ion Channel, G Protein-Coupled Receptor (GPCR) and Nuclear Receptor. We encoded the target protein sequence using the dipeptide composition and drug with a molecular desc Weinheim.BACKGROUND Skeletal muscle is mainly responsible for insulin-stimulated glucose disposal. Dysfunction in skeletal muscle metabolism especially during obesity contributes to the insulin resistance. Astaxanthin (AX), a natural antioxidant, has been shown to ameliorate hepatic insulin resistance in obese mice. However, its effects in skeletal muscle are poorly understood. The current study aimed to investigate the molecular target of AX in ameliorating skeletal muscle insulin resistance. METHODS We fed 6-week-old male C57BL/6J mice with normal chow (NC) or NC supplemented with AX (NC+AX) and high-fat-diet (HFD) or HFD supplemented with AX for 24 weeks. We determined the effect of AX on various parameters including insulin sensitivity, glucose uptake, inflammation, kinase signaling, gene expression, and mitochondrial function in muscle. We also determined energy metabolism in intact C2C12 cells treated with AX using the Seahorse XFe96 Extracellular Flux Analyzer and assessed the effect of AX on mitochondrial oxidulin resistance and glucose intolerance through regulation of AMPK activation in the muscle, (ii) stimulated mitochondrial biogenesis in the muscle, (iii) enhanced exercise tolerance and exercise-induced fatty acid metabolism, and (iv) exerted antiinflammatory effects via its antioxidant activity in adipose tissue. CONCLUSIONS We concluded that AX treatment stimulated mitochondrial biogenesis and significantly ameliorated insulin resistance through activation of AMPK pathway in the skeletal muscle. check details © 2020 The Authors. Journal of Cachexia, Sarcopenia and Muscle published by John Wiley & Sons Ltd on behalf of Society on Sarcopenia, Cachexia and Wasting Disorders.OBJECTIVE To investigate the quality of life (QoL) and sexuality in women affected by pelvic organ prolapse (POP) and treated by bilateral sacrospinous ligament fixation (SSLF) with vaginal hysterectomy. METHODS This is a prospective observational study carried out at Isparta City Hospital from July 2017 to December 2018. A total of 26 sexually active women with symptomatic uterine prolapse POP-Q (Pelvic Organ Prolapse Quantification) stage II or higher requiring surgery were included in the study. Short Form Health Survey (SF-36) was used preoperatively and at 6 months to examine the impacts of vaginal reconstruction on QoL. To assess sexual functioning, the Pelvic Organ Prolapse/Urinary Incontinence Sexual Questionnaire (PISQ-12) was used preoperatively and at 6 months. RESULTS A significant improvement of POP-Q landmarks was found between pre- and posttreatment at 6 months of follow-up. The patients reported QoL improvement at the follow-up for all the categories of physical functioning, bodily pain, physical health, general health, vitality, social activity, emotional state, and mental health with respect to the baseline values (P  less then  .001). The results of PISQ-12 demonstrated a significant improvement for all the three fields behavioral emotive factor, physical factor, and partner-related factor, and the total score at 6 months after surgery (P  less then  .001). CONCLUSION This study clearly demonstrates that bilateral SSLF is able to significantly improve both QoL and sexual function in patients with POP. Improvement in sexuality and QoL after surgery may be explained by correction of avoidance of sexual intercourse due to prolapse and physical recovery. © 2020 John Wiley & Sons Australia, Ltd.