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Alternative strategies geared towards general efficiency improvement and teamwork, rather than focusing on one patient group may be a higher yield approach for improving care in this paediatric emergency centre.

Acute exacerbations of idiopathic pulmonary fibrosis (AE-IPF) are the most frequent cause of death among patients with IPF. Here, we review the revised definition and diagnostic criteria for AE-IPF and discuss management strategies including mechanistically targeted investigational therapies for this complex syndrome.

Novel therapies targeting various pathways including inflammation, autoimmunity and coagulation cascade involved in AE-IPF have recently been reported. Although most of these reports are small and uncontrolled, they have provided evidence to design larger randomized, controlled, multicenter studies to improve outcomes among patients with AE-IPF.

AE-IPF has a dismal prognosis and current treatment consists mainly of supportive care and symptom palliation. There is a lack of consensus on current therapies for AE-IPF, including corticosteroids, but current randomized control studies for newer therapeutic strategies may hold promise.

AE-IPF has a dismal prognosis and current treatment consists mainly of supportive care and symptom palliation. There is a lack of consensus on current therapies for AE-IPF, including corticosteroids, but current randomized control studies for newer therapeutic strategies may hold promise.Host cytochrome P450s (P450s) play important roles in the bioactivation and detoxification of numerous therapeutic drugs, environmental toxicants, dietary factors, as well as endogenous compounds. Gut microbiome is increasingly recognized as our "second genome" that contributes to the xenobiotic biotransformation of the host, and the first pass metabolism of many orally exposed chemicals is a joint effort between host drug metabolizing enzymes including P450s and gut microbiome. Gut microbiome contributes to the drug metabolism via two distinct mechanisms direct mechanism refers to the metabolism of drugs by microbial enzymes, among which reduction and hydrolysis (or deconjugation) are among the most important reactions; whereas indirect mechanism refers to the influence of host receptors and signaling pathways by microbial metabolites. Many types of microbial metabolites, such as secondary bile acids (BAs), short chain fatty acids (SCFAs), and tryptophan metabolites, are known regulators of human diseases through modulating host xenobiotic-sensing receptors. To study the roles of gut microbiome in regulating host drug metabolism including P450s, several models including germ free mice, antibiotics or probiotics treatments, have been widely used. The present review summarized the current information regarding the interactions between microbiome and the host P450s in xenobiotic biotransformation organs such as liver, intestine, and kidney, highlighting the remote sensing mechanisms underlying gut microbiome mediated regulation of host xenobiotic biotransformation. In addition, the roles of bacterial, fungal, and other microbiome kingdom P450s, which is an understudied area of research in pharmacology and toxicology, are discussed.

The pathophysiology of idiopathic hypersomnia remains unclear, but some of its clinical features suggest the possibility of circadian dysfunction. This review will provide an overview of recent studies of circadian biology that have begun to elucidate the potential role of circadian rhythm dysfunction in idiopathic hypersomnia.

Clinically, people with idiopathic hypersomnia tend to have both a late chronotype and prominent sleep inertia or sleep drunkenness. Melatonin and cortisol profiles in people with IH confirm this tendency toward phase delay. More recently, it has been suggested that the night phase as defined by melatonin profile or period length as defined by BMA1 in dermal fibroblasts may also be prolonged in people with IH. Additionally, amplitude of melatonin rhythm and circadian gene expression, particularly BMAL1, PER1, and PER2, may be impaired in this disease.

Clinical features, melatonin profiles, and circadian gene expression all suggest abnormalities of the circadian system may be a contributor to the pathogenesis of IH.

Clinical features, melatonin profiles, and circadian gene expression all suggest abnormalities of the circadian system may be a contributor to the pathogenesis of IH.

Short gut syndrome is life-altering and life-threatening disease resulting most often from massive small bowel resection. Recent advances in understanding of the perturbed physiology in these patients have translated into improved care and outcomes. This paper seeks to review the advances of care in SBS patients.

Anatomic considerations still predominate the early care of SBS patients, including aggressive preservation of bowel and documentation of remnant bowel length and quality. Intestinal adaptation is the process by which remnant bowel changes to fit the physiologic needs of the patient. Grossly, the bowel dilates and elongates to increase intestinal weight and protein content. Architectural changes are noted, such as villus lengthening and deepening of crypts. In addition, gene expression changes occur that function to maximize nutrient uptake and fluid preservation. Management is aimed at understanding these physiologic changes and augmenting them whenever possible in an effort to gain enteral autonomy. Complication mitigation is key, including avoidance of catheter complications, bloodstream infections, cholestasis, and nutrient deficiencies.

Multidisciplinary teams working together towards intestinal rehabilitation have shown improved outcomes. JNJ-26481585 ic50 Today's practioner needs a current understanding of the ever-evolving care of these patients in order to promote enteral autonomy, recognize complications, and counsel patients and families appropriately.

Multidisciplinary teams working together towards intestinal rehabilitation have shown improved outcomes. Today's practioner needs a current understanding of the ever-evolving care of these patients in order to promote enteral autonomy, recognize complications, and counsel patients and families appropriately.

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