Buck Wade (taxtrout0)

To investigate the association between dose and frequency of prenatal alcohol exposure (PAE) and sleep problems in children, after controlling for established risk factors for sleep problems. Data from the birth cohort of the Longitudinal Study of Australian Children (LSAC) was used. Mothers of 3447 children provided information on alcohol consumption during pregnancy, children's sleep problems from 2- to 9-years, and potential confounders associated with sleep problems. Children were classified into PAE groups based on distinct patterns of maternal drinking during pregnancy abstinent, occasional, low, moderate, and heavy. The effect of PAE on the number and persistence of sleep problems across childhood (2-9 years) was examined. After controlling for multiple covariates that impact sleep, children with heavy PAE had 1.13 more sleep problems across childhood (2-9 years) relative to children whose mothers were abstainers, in particular 0.37 more at 2- to 3-years (0.504, 95 % CI 0.053, 0.956), and 0.34 more at 6- to 7-years (0.847, 95 % CI 0.299, 1.396). Compared to children of abstainers, heavy PAE increases the probability of having persistent sleep problems from 2- to 9-years by 22.57 %. No negative associations between moderate or low PAE and sleep were observed. Autophagy inhibitor Parenting, family, economic, and child health factors also significantly affected child sleep. Heavy PAE was associated with significantly more sleep problems across childhood and a higher probability of reporting persistent sleep problems, relative to children with no PAE. Implications for the understanding and management of sleep in young children with PAE and FASD are discussed. Heavy PAE was associated with significantly more sleep problems across childhood and a higher probability of reporting persistent sleep problems, relative to children with no PAE. Implications for the understanding and management of sleep in young children with PAE and FASD are discussed.The highly bidirectional dialogue between the gut and the brain is markedly stimulated and influenced by the microbiome through integrated neuroendocrine, neurological and immunological processes. Gut microbiota itself communicate with the host producing hormonal intermediates, metabolites, proteins, and toxins responsible for a variety of biochemical and functional inputs, thereby shaping host homeostasis. Indeed, a dysregulated microbiota-gut-brain axis might be the origin of many neuroimmune-mediated disorders, e.g. autism, multiple sclerosis, depression, Alzheimer's and Parkinson's disease, which appear months or even years prior to a diagnosis, corroborating the theory that the pathological process is spread from the gut to the brain. A much deeper comprehension of how commensal microbe can be manipulated to interfere with disease progression is crucial for developing new strategies to diagnose and treat diseases. In recent years, the potential of positron-emission-tomography (PET) in the field of bacteria detection has gained attention. The uptake of several PET tracers has been evaluated to investigate infection pathophysiology, e.g. sterile or pathogen-mediated infection, monitoring of progression, or as a surrogate endpoint in clinical trials. In this minireview, we briefly describe the role of microbiome-gut-brain axis in health and disease and we discuss the imaging modalities and agents that could be applied to study the dynamic interactions between microbiome, gut and brain. These are key aspects in understanding the biochemical lexicon underpinning the microbiome-host crosstalk that would enable the development of diagnostics and therapeutics by targeting the human microbiota.Chronic cough is multifactorial in origin, may affect quality of life adversely, and often poses a diagnostic challenge for physicians. Laryngopharyngeal reflux (LPR) is one common contributing factor for chronic cough, but the mechanism by which reflux ca