, Hagen JA, Bremner CG, et al: Omeprazole does not reduce gastroesophageal reflux: new insights utilizing multichannel intraluminal impedance technologies. J Gastrointest Surg: Offic J Soc Surg Aliment Tract 2004, eight(7):89097. discussion 7-8. PubMed PMID: 15531244. Doumit M, Krishnan U, Jaffe A, Belessis Y: Acid and non-acid reflux during physiotherapy in young children with cystic fibrosis. Pediatr Pulmonol 2012, 47(2):11924. PubMed PMID: 22241570. Brodzicki J, Trawinska-Bartnicka M, Korzon M: Frequency, consequences and pharmacological remedy of gastroesophageal reflux in kids with cystic fibrosis. Med Sci Monit 2002, eight(7):CR529 R537. PubMed PMID: 12118204. Elkins MR, Robinson M, Rose BR, Harbour C, Moriarty CP, Marks GB, et al: A controlled trial of long-term inhaled hypertonic saline in sufferers with cystic fibrosis. New Engl J Med 2006, 354(3):22940. PubMed PMID: 16421364. McCoy KS, Quittner AL, Oermann CM, Gibson RL, Retsch-Bogart GZ, Montgomery AB: Inhaled aztreonam lysine for chronic airway Pseudomonas aeruginosa in cystic fibrosis. Am J Respir Crit Care Med 2008, 178(9):92128. PubMed PMID: 18658109.doi:10.1186/1471-2466-14-21 Cite this article as: DiMango et al.: Effect of esomeprazole versus placebo on pulmonary exacerbations in cystic fibrosis. BMC Pulmonary Medicine 2014 14:21.Submit your subsequent manuscript to BioMed Central and take complete advantage of:Hassle-free on-line submission Thorough peer review No space constraints or color figure charges Quick publication on acceptance Inclusion in PubMed, CAS, Scopus and Google Scholar Analysis which can be freely out there for redistributionSubmit your manuscript at www.biomedcentral/submit
Phosphatidylcholine transfer protein (PC-TP; also referred to as StARD2) is a liver-enriched cytosolic lipid binding protein that belongs towards the steroidogenic acute regulatory transferrelated (Commence) domain superfamily. PC-TP was initially characterized as a protein that catalyzes the intermembrane exchange of phosphatidylcholines in vitro (1). Its extremely selective lipid binding pocket accommodates a single phosphatidylcholine molecule and preferentially binds phosphatidylcholines with much more unsaturated sn-2 fatty acyl chains (1), which could in turn influence the conformation of PC-TP (4). By mechanisms that seem to be distinct from lipid transfer activity, PC-TP reduces hepatic insulin sensitivity. In chow fed Pctp-/-mice, decreased fasting plasma glucose concentrations are accompanied by decreased hepatic glucose production in hyperinsulinemic-euglycemic clamp research (6). Pctp-/-mice are also resistant to diet-induced diabetes, and therapy using a compact molecule inhibitor of PC-TP improves glucose tolerance and reduces hepatic glucose production in wild-type mice (7).Oligonucleotide Synthesis Coding area polymorphisms have also been reported in each mice (eight) and humans (9), which appear to confer protection against insulin resistance (four).β-Amanitin Improvements in glucose homeostasis are associated with enhanced hepatic insulin signaling through an unknown mechanism.PMID:25147652 In the absence of PC-TP or in response to its chemical inhibition, livers and major hepatocytes exhibit increased phosphorylation of Akt and its downstream targets (6, 7). PC-TP interacts with thioesterase superfamily member 2 (THEM2) (ten), a soluble homotetrameric fatty acyl-CoA thioesterase (also known as ACOT13) (11). Like PC-TP, THEM2 is enriched in liver, is a transcriptional target of peroxisome proliferation-activated receptor (PPAR) and reversibly associates with.
