GABA Measurement in a Neonatal Fragile X Syndrome Mouse Model Using H-Magnetic Resonance Spectroscopy and Mass Spectrometry.

Fragile X syndrome (FXS) is the leading monogenetic cause of autism spectrum disorder and inherited cause of intellectual disability that affects approximately one in 7,000 males and one in 11,000 females. In FXS, the gene is silenced and prevents the expression of the fragile X mental retardation protein (FMRP) that directly targets mRNA transcripts of multiple GABA subunits. Therefore, FMRP loss adversely impacts the neuronal firing of the GABAergic system which creates an imbalance in the excitatory/inhibitory ratio within the brain.

In vivo H MRS of human gallbladder bile in understanding the pathophysiology of primary sclerosing cholangitis (PSC): Immune-mediated disease versus bile acid-induced injury.

Primary sclerosing cholangitis (PSC) has been considered to be either an "autoimmune disease" or a "bile acid-induced injury." In vitro MRS studies on PSC patients have limitations due to the contamination of bile with contrast agent (commonly administered during endoscopic retrograde cholangiopancreatography) and/or the use of patient cohorts with other diseases as controls. The objective of this study was to quantify biliary metabolites using in vivo H MRS and gain insight into the pathogenesis of PSC.

In vivo 1H MRS of human gallbladder bile at 3 T in one and two dimensions: detection and quantification of major biliary lipids.

In vitro (1)H MRS of human bile has shown potential in the diagnosis of various hepatopancreatobiliary (HPB) diseases. Previously, in vivo (1)H MRS of human bile in gallbladder using a 1.5 T scanner demonstrated the possibility of quantification of choline-containing phospholipids (chol-PLs).

Influence of ATP-dependent K+ channels on nicotine-induced inhibition of withdrawal in morphine-dependent mice.

In the present study, we have investigated the effect of nicotine and diazoxide, a potassium channel opener and glibenclamide, a potassium channel (K(ATP)) blocker on naloxone-precipitated physical withdrawal signs, including jumping and diarrhea. Then, the interactions of nicotine with diazoxide and glibenclamide were tested. Mice were rendered dependent on morphine by subcutaneous (s.