The intervention significantly improve the health status of adults with metabolic diseases, in particular their exercise habits, HbA1c levels, body weight, empowerment and quality of life. The intervention provides more convenient and faster access to healthcare for busy individuals with time constraints. These results suggest that healthcare professionals could develop accessible and friendly interactive online interfaces for patients to expand the use of these interventions in the clinical setting.

Background During the second and third year after birth the gut microbiota (GM) is subjected to important development. The polycyclic aromatic hydrocarbon (PAH) exposure could influence the GM in animal and early postnatal exposure is associated with neurodevelopment disorder in children. This study was designed to explore the possible influence of the polycyclic aromatic hydrocarbons (PAHs) on the composition of the gut microbiota (GM) and neurodevelopment in a sample of 38 healthy children at the age of 3 years. Methods A brief development (Gesell Development Inventory, GDI) and behavior test (Child Behavior Checklist, CBCL) were completed on 3-yr-olds and stool samples were collected for 16S rRNA V4-V5 sequencing. The PAH-DNA adduct in the umbilical cord blood and the urinary hydroxyl PAHs (OH-PAHs) at the age of 12 months were measured as pre- and postnatal PAH exposure, respectively. Results The most abundant two phyla were Bacteroidetes (68.6%) and Firmicutes (24.2%). The phyla Firmicutes, Actinobacteria, Proteobacteria, Tenericutes, and Lentisphaerae were positively correlated with most domain behaviors of the GDI, whereas the Bacteroidetes, Cyanobacteria, and Fusobacteria were negatively correlated. Correspondingly, the phyla Bacteroidetes, Actinobacteria, and Fusobacteria showed positive correlations with most CBCL core and broadband syndromes, whereas the Firmicutes, Verrucomicrobia, Synergistetes, Proteobacteria and Tenericules were negatively correlated. The OH-PAH levels were not significantly associated with the Firmicutes phylum whereas the Bacteroidetes, Bacteroidia, and Bacteroidales all showed significant negative association with the OH-PAH levels. Conclusion The current findings suggest that composition of the GM is associated with neurodevelopment of the child. PAHs seem to change the relative abundance of some taxa (some deleted and some recruited) to counteract the negative effects of the PAHs.

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While therapeutic hypothermia improves the outcomes of individuals in cardiac arrest, the hemodynamic responses and mechanisms which underlie hypothermia-induced cardioprotection are not fully understood. Therefore, we investigated the mechanism by which induced hypothermia preserves cardiac function and protects against mitochondrial damage following cardiac arrest. Cardiac arrest was induced in adult male Wistar rats by asphyxiation for 8.5 min. Following resuscitation, the animals were randomly assigned to a hypothermia (32 °C) or normothermia (37 °C) group. Monitoring results showed that cardiac output at the fourth hour after resuscitation was significantly better in rats treated with hypothermia when compared to rats treated with normothermia (P < 0.01). Examinations by transmission electron microscopy showed that mitochondria in the left ventricle of rats in the hypothermia group were significantly less swollen compared to such mitochondria in the normothermia group (P < 0.001). Additionally, opening of mitochondrial permeability transition pores occurred less frequently in the hypothermic group. While complex I/III activity in the electron transport reaction was damaged after cardiac arrest and resuscitation, the degree of injury was ameliorated by hypothermia treatment (P < 0.05). The amount of STAT-3 phosphorylated at tyrosine 705 and its expression in mitochondria were significantly higher under hypothermia treatment compared to normothermia treatment. In vitro studies showed that inhibition STAT-3 activation abolished the ability of hypothermia to protect H9C2 cardiomyocytes against injury produced by simulated ischemia and reperfusion. Therapeutic hypothermia treatment can ameliorate cardiac dysfunction and help preserve both mitochondrial integrity and electron transport activity.