A linear stochastic formulation for distribution energy management systems considering lifetime extension of battery storage devices

Recently, the number of Battery Energy Systems (BESs) connected to the grid has grown significantly. These assets can alleviate some operational issues such as demand surges and occasional power fluctuations associated with the Renewable Energy Sources (RESs) connected to the grid. Nonetheless, both overcharging and frequent usage severely affect their health status and shorten their life expectancy. In this paper, an Energy Management System (EMS) framework with a linearised algorithm and in-depth analysis on BES life extension is presented, which optimises the techno-economic aspects of an Active Distribution Network (ADN) connected to RESs. By applying a mathematical linearisation formulation, a Mixed-Integer Linear Programming (MILP) model is proposed for linearising the Optimal Power Flow (OPF) problem. This technique, which has the merit of fair accuracy while having high speed, is used for scheduling BESs to increase their durability and decrease grid costs. To consider the inherent uncertainty associated with demand and RES generation, a two-stage Stochastic Programming (SP) method is implemented in the proposed model. In terms of battery Loss of Health (LoH) assessment, a linearised battery lifetime method is introduced. Ultimately, a modified 33-bus radial distribution test system with a day-ahead Real-Time Pricing (RTP) program was chosen to apply the proposed algorithm and assess its efficiency

MAPK and JAK/STAT pathways targeted by miR-23a and miR-23b in prostate cancer: computational and in vitro approaches

The long-lasting inadequacy of existing treatments for prostate cancer has led to increasing efforts for developing novel therapies for this disease. MicroRNAs (miRNAs) are believed to have considerable therapeutic potential due to their role in regulating gene expression and cellular pathways. Identifying miRNAs that efficiently target genes and pathways is a key step in using these molecules for therapeutic purposes. Moreover, computational methods have been devised to help identify candidate miRNAs for each gene/pathway. MAPK and JAK/STAT pathways are known to have essential roles in cell proliferation and neoplastic transformation in different cancers including prostate cancer. Herein, we tried to identify miRNAs that target these pathways in the context of prostate cancer as therapeutic molecules. Genes involved in these pathways were analyzed with various algorithms to identify potentially targeting miRNAs. miR-23a and miR-23b were then selected as the best potential candidates that target a higher number of genes in these pathways with greater predictive scores. We then analyzed the expression of candidate miRNAs in LNCAP and PC3 cell lines as well as prostate cancer clinical samples. miR-23a and miR-23b showed a significant downregulation in cell line and tissue samples, a finding which is consistent with overactivation of these pathways in prostate cancer. In addition, we overexpressed miR-23a and miR-23b in LNCAP and PC3 cell lines, and these two miRNAs decreased IL-6R expression which has a critical role in these pathways. These results suggest the probability of utilizing miR-23a and miR-23b as therapeutic targets for the treatment of prostate cancer. © 2015, International Society of Oncology and BioMarkers (ISOBM)

The Effects of Melatonin Supplementation on Parameters of Mental Health, Glycemic Control, Markers of Cardiometabolic Risk, and Oxidative Stress in Diabetic Hemodialysis Patients: A Randomized, Double-Blind, Placebo-Controlled Trial

Objective: This study evaluated the effects of melatonin supplementation on parameters of mental health, glycemic control, markers of cardiometabolic risk, and oxidative stress in diabetic hemodialysis (HD) patients. Design: A randomized, double-blind, placebo-controlled clinical trial was conducted in 60 diabetic HD patients, 18-80 years of age. Participants were randomly divided into 2 groups to take either melatonin (2 x 5mg/day) (n = 30) or placebo (n = 30) 1 hour before bedtime for 12 weeks. The effects of melatonin on mental health, metabolic status, and gene expression related to metabolic status were assessed using multiple linear regression adjusting for age and BMI. Results: Melatonin supplementation significantly decreased Pittsburgh Sleep Quality Index (P =.007), Beck Depression Inventory index (P =.001), and Beck Anxiety Inventory index (P =.01) compared with the placebo. Additionally, melatonin administration significantly reduced fasting plasma glucose (β = �21.77 mg/dL, 95 CI �33.22 to �10.33, P <.001), serum insulin levels (β = �1.89 μIU/mL, 95 CI �3.34 to �0.45, P =.01), and homeostasis model of assessment-insulin resistance (β = �1.45, 95 CI �2.10 to �0.80, P <.001), and significantly increased the quantitative insulin sensitivity check index (β = 0.01, 95 CI 0.007-0.02, P <.001) compared with placebo treated subjects. In addition, melatonin administration resulted in a significant reduction in serum high sensitivity C-reactive protein (β = �1.92 mg/L, 95 CI �3.02 to �0.83, P =.001) and plasma malondialdehyde (β = �0.21 μmol/L, 95 CI �0.36 to �0.06, P =.005); also, significant rises in plasma total antioxidant capacity (β = 253.87 mmol/L, 95 CI 189.18-318.56, P <.001) and nitric oxide levels (β = 2.99 μmol/L, 95 CI 0.71-5.28, P =.01) were observed compared with the placebo. Conclusion: Overall, melatonin supplementation for 12 weeks to diabetic HD patients had beneficial effects on mental health, glycemic control, inflammatory markers, and oxidative stress. © 2019 National Kidney Foundation, Inc

Coenzyme Q10 ameliorates trimethyltin chloride neurotoxicity in experimental model of injury in dentate gyrus of hippocampus: A histopathological and behavioral study

Background: Coenzyme Q10 has antioxidative and free radical scavenging effects. CoQ10 supplementation is known to have neuroprotective effects in some neurodegenerative diseases, such as Parkinson�s disease and Huntington�s disease. Objectives: The aim of this study was to evaluate both histopathologic and behavioral whether Coenzyme Q10 is protective against trimethyltin chloride (TMT) induced hippocampal damage. Materials and Methods: This was an experimental study. Thirty-six Balb/c mice were divided into four groups, as follows: 1) control group; 2) sham group of mice that received a 100 ±L intraperitoneal injection (IP) of sesame oil; 3) TMT group of mice that received a single 2.5 mg/kg/day IP injection of TMT; and 4) TMT + CoQ10 group of mice that received a 10 mg/kg IP injection of CoQ10. Body weight and Morris water maze (MWM) responses were investigated. In addition, the dentate gyrus neurons of the hippocampus were evaluated histopathologically by light and electron microscopes. Results: This study revealed that the body weight scale was found to be significantly higher in the CoQ10 group (21.39 ± 2.70), compared to the TMT group (19.39±2.74) (P < 0.05). In the TMT group, the animals showed body a weight loss that was significantly lower than that of the control group (22.33 ± 3.06) (P < 0.05). Our results showed that CoQ10 provided protection against MWM deficits. Furthermore, TMT impaired the ability of mice to locate the hidden platform, compared to the control group (P < 0.05). Microscopic studies showed that TMT caused histopathological changes in the dentate gyrus and increased the number of necrotic neurons (476±78.51), compared to the control group (208±40.84) (P < 0.001). But, CoQ10 significantly attenuated (31 9±60.08) the density of necrotic neurons compared to TMT (P < 0.05). Conclusions: The results of the present study indicate that Coenzyme Q10 diminished neuronal necrosis and improved learning memory. Part of its beneficial effect is due to its potential to discount oxidative stress. © 2016, Kowsar Medical Publishing Company. All rights reserved

Effect of vitamin d3 on mitochondrial biogenesis in granulosa cells derived from polycystic ovary syndrome

Background: Polycystic ovary syndrome (PCOS) is an endocrine disorder diagnosed by anovulation hyperandro-genism. Hyperandrogenism increases apoptosis, which will eventually disturb follicular growth in PCOS patients. Since mitochondria regulate apoptosis, they might be affected by high incidence of follicular atresia. This may cause infertility. Since vitamin D3 has been shown to improve the PCOS symptoms, the aim of study was to investigate the effects vitamin D3 on mtDNA copy number, mitochondrial biogenesis, and membrane integrity of granulosa cells in a PCOS-induced mouse model. Materials and Methods: In this experimental study, the PCOS mouse model was induced by dehydroepiandrosterone (DHEA). Granulosa cells after identification by follicle-stimulating hormone receptor (FSHR) were cultured in three groups: 1. granulosa cells treated with vitamin D3 (100 nM for 24 hours), 2. granulosa cells without any treatments, 3. Non-PCOS granulosa cells (control group). Mitochondrial biogenesis gene (TFAM) expression was compared between different groups using real-time PCR. mtDNA copy number was also investigated by qPCR. The mitochon-drial structure was evaluated by transmission electron microscopy (TEM). Hormonal levels were measured by an enzymelinked immunosorbent assay (ELISA) kit. Results: The numbers of pre-antral and antral follicles increased in PCOS group in comparison with the non-PCOS group. Mitochondrial biogenesis genes were downregulated in granulosa cells of PCOS mice when compared to the non-PCOS granulosa cells. However, treatment with vitamin D3 increased mtDNA expression levels of these genes compared to PCOS granulosa cells with no treatments. Most of the mitochondria in the PCOS group were spherical with almost no cristae. Our results showed that in the PCOS group treated with vitamin D3, the mtDNA copy number increased significantly in comparison to PCOS granulosa cells with no treatments. Conclusion: According to this study, we can conclude, vitamin D3 improves mitochondrial biogenesis and membrane integrity, mtDNA copy number in granulosa cells of PCOS mice which might improve follicular development and subsequently oocyte quality. © 2020, Royan Institute (ACECR). All rights reserved

The Effects of Synbiotic Supplementation on Metabolic Status in Diabetic Patients Undergoing Hemodialysis: a Randomized, Double-Blinded, Placebo-Controlled Trial

This study was conducted to evaluate the effects of synbiotic supplementation on metabolic profiles in diabetic patients undergoing hemodialysis (HD). This randomized, double-blinded, placebo-controlled clinical trial was performed in 60 diabetic HD patients. Participants were randomly assigned into two groups to receive either synbiotic capsule, containing Lactobacillus acidophilus, Lactobacillus casei, and Bifidobacterium bifidum (2 � 109 CFU/g each), plus 0.8 g/day of inulin (n = 30) or placebo (n = 30) for 12 weeks. Synbiotic supplementation significantly decreased fasting plasma glucose (β � 13.56 mg/dL; 95 CI, � 23.82, � 3.30; P = 0.01), insulin levels (β � 5.49 μIU/mL; 95 CI, � 6.92, � 4.05; P &lt; 0.001), and insulin resistance (β � 2.25; 95 CI, � 3.02, � 1.48; P &lt; 0.001), while increased the quantitative insulin sensitivity check index (β 0.02; 95 CI, 0.01, 0.02; P &lt; 0.001) compared with the placebo. Additionally, synbiotic intake resulted in a significant reduction in high-sensitivity C-reactive protein (β � 2930.48 ng/mL; 95 CI, � 3741.15, � 2119.80; P &lt; 0.001) and malondialdehyde levels (β � 0.60 μmol/L; 95 CI, � 0.99, � 0.20; P = 0.003). Moreover, we found a significant increase in total antioxidant capacity (β 142.99 mmol/L; 95 CI, 61.72, 224.25; P = 0.001) and total glutathione levels (β 131.11 μmol/L; 95 CI, 89.35, 172.87; P &lt; 0.001) in the synbiotic group compared with the placebo group. Overall, synbiotic supplementation for 12 weeks had beneficial effects on glycemic control, biomarkers of inflammation, and oxidative stress in diabetic patients under HD. This study was registered in the Iranian website (www.irct.ir) for registration of clinical trials (http://www.irct.ir: IRCT2017090133941N17). http://www.irct.ir: IRCT2017090133941N17. © 2018, Springer Science+Business Media, LLC, part of Springer Nature

Human unrestricted somatic stem cells ameliorate sepsis-related acute lung injury in mice

Background Aims: Sepsis and related disorders, especially acute lung injury (ALI), are the most challenging life-threatening diseases in the hospital intensive care unit. Complex pathophysiology, unbalanced immune condition, and high rate of mortality complicate the treatment of sepsis. Recently, cell therapy has been introduced as a promising option to recover the sepsis symptoms. The aim of this study was to investigate the therapeutic potential of human unrestricted somatic stem cells (USSCs) isolated from human umbilical cord blood in the mouse model of ALI. USSCs significantly enhanced the survival rate of mice suffering from ALI and suppressed concentrations of proinflammatory mediators TNF-α, and interleukin (IL)-6, and the level of anti-inflammatory cytokine IL-10. ALI mice injected by USSCs showed notable reduction in lung and liver injury, pulmonary edema, and hepatic enzymes, compared with the control group. These results determined the in vivo immunomodulatory effect of USSCs for recovery of immune balance and reduction of tissue injury in the mouse model of ALI. Therefore, USSCs can be a suitable therapeutic approach to manage sepsis disease through the anti-inflammatory potentia

Homozygous loss-of-function mutations in SLC26A7 cause goitrous congenital hypothyroidism.

Defects in genes mediating thyroid hormone biosynthesis result in dyshormonogenic congenital hypothyroidism (CH). Here, we report homozygous truncating mutations in SLC26A7 in 6 unrelated families with goitrous CH and show that goitrous hypothyroidism also occurs in Slc26a7-null mice. In both species, the gene is expressed predominantly in the thyroid gland, and loss of function is associated with impaired availability of iodine for thyroid hormone synthesis, partially corrected in mice by iodine supplementation. SLC26A7 is a member of the same transporter family as SLC26A4 (pendrin), an anion exchanger with affinity for iodide and chloride (among others), whose gene mutations cause congenital deafness and dyshormonogenic goiter. However, in contrast to pendrin, SLC26A7 does not mediate cellular iodide efflux and hearing in affected individuals is normal. We delineate a hitherto unrecognized role for SLC26A7 in thyroid hormone biosynthesis, for which the mechanism remains unclear