Examining the health and drug exposures among Canadian children residing in drug-producing homes

Objective: To examine the health and well-being of children residing in residences where drug production is occurring. Study design: Starting in January 2006, children identified by police and the Children's Aids Society in the York region of Ontario, Canada, were referred to the Motherisk Program at the Hospital for Sick Children for pediatric assessment of their general health and well-being, with specific focus on illicit-drug exposure. We used a standard protocol to collect all available medical and environmental history, conducted physical and neurologic examinations, and collected hair for analysis of illicit drugs. Results: In total, 75 children, at the mean age of 6.5 years, were referred to us after being removed from homes where marijuana was grown (80%) or other operations linked to drug production were occurring (20%). Overall, rates of health issues in this cohort fell below reference values for Canadian children. Of the hair tests, 32% were positive for illicit substances. In the majority there were no clinical symptoms related to these drugs. Conclusion: The majority of children removed from drug-producing homes were healthy and drug free. Comprehensive evaluations should be performed on a case-by-case basis in order to determine what is ultimately in the best interest of the child.Fil: Moller, Monique. University Of Toronto. Hospital For Sick Children; Canadá. University of Toronto; CanadáFil: Koren, Gideon. University of Toronto; Canadá. University Of Toronto. Hospital For Sick Children; CanadáFil: Karaskov, Tatyana. University Of Toronto. Hospital For Sick Children; CanadáFil: García Bournissen, Facundo. University Of Toronto. Hospital For Sick Children; Canadá. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentin

Liberal transfusion strategy improves survival in perioperative but not in critically ill patients. A meta-analysis of randomised trials

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Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes Afford New Opportunities in Inherited Cardiovascular Disease Modeling

Fundamental studies of molecular and cellular mechanisms of cardiovascular disease pathogenesis are required to create more effective and safer methods of their therapy. The studies can be carried out only when model systems that fully recapitulate pathological phenotype seen in patients are used. Application of laboratory animals for cardiovascular disease modeling is limited because of physiological differences with humans. Since discovery of induced pluripotency generating induced pluripotent stem cells has become a breakthrough technology in human disease modeling. In this review, we discuss a progress that has been made in modeling inherited arrhythmias and cardiomyopathies, studying molecular mechanisms of the diseases, and searching for and testing drug compounds using patient-specific induced pluripotent stem cell-derived cardiomyocytes

Sulforaphane Improves Abnormal Lipid Metabolism via Both ERS-Dependent XBP1/ACC &SCD1 and ERS-Independent SREBP/FAS Pathways

Scope: To investigate the effect of sulforaphane (SFN) on the abnormal lipid metabolism and underlying mechanisms.  Methods and results: Models with abnormal lipid metabolism were established both in rats and human hepatocytes. Hepatic steatosis was detected by H&E and oil red O staining. The structure of endoplasmic reticulum was visualized by transmission electron microscopy. The expressions of X-box binding protein 1 (XBP1), protein kinase-like ER kinase (PERK), sterol regulatory element binding protein-1c (SREBP1c) and lipogenic enzymes were determined by real-time PCR and western blot analysis. SFN lowered the content of triglyceride and cholesterol. SFN alleviated the swelling of endoplasmic reticulum (ER) and decreased the perimeter of ER. SFN significantly decreased the expressions of acetyl CoA carboxylase 1 (ACC1), stearoyl-CoA desaturase 1 (SCD1) and fatty acid synthase. SFN inhibited SREBP1c by blocking the PERK. Meanwhile, SFN suppressed ACC1 and SCD1 via blocking the formation of splicing-type XBP1. The key roles of XBP1 and SREBP1c in SFN-reduced lipid droplets were confirmed by a timed sequence of measurement according to time points.  Conclusion: SFN improved abnormal lipid metabolism via both ER stress -dependent and -independent pathways