Cerebral Glutamate Alterations Using Chemical Exchange Saturation Transfer Imaging in a Rat Model of Lipopolysaccharide-Induced Sepsis.

Glutamate-weighted chemical exchange saturation transfer (GluCEST) is a useful imaging tool to detect glutamate signal alterations caused by neuroinflammation. This study aimed to visualize and quantitatively evaluate hippocampal glutamate alterations in a rat model of sepsis-induced brain injury using GluCEST and proton magnetic resonance spectroscopy (H-MRS). Twenty-one Sprague Dawley rats were divided into three groups (sepsis-induced groups (SEP05, = 7 and SEP10, = 7) and controls ( = 7)).

Is aryl hydrocarbon receptor antagonism after ischemia effective in alleviating acute hepatic ischemia-reperfusion injury in rats?

Aryl hydrocarbon receptors (AhRs) have been reported to be important mediators of ischemic injury in the brain. Furthermore, the pharmacological inhibition of AhR activation after ischemia has been shown to attenuate cerebral ischemia-reperfusion (IR) injury. Here, we investigated whether AhR antagonist administration after ischemia was also effective in ameliorating hepatic IR injury.

Preclinical Long-term Magnetic Resonance Imaging Study of Silymarin Liver-protective Effects.

Background And Aims: Efficacy evaluations with preclinical magnetic resonance imaging (MRI) are uncommon, but MRI in the preclinical phase of drug development provides information that is useful for longitudinal monitoring. The study aim was to monitor the protective effectiveness of silymarin with multiparameter MRI and biomarkers in a thioacetamide (TAA)-induced model of liver injury in rats. Correlation analysis was conducted to assess compare the monitoring of liver function by MRI and biomarkers.

In Vivo Measurement of Neurochemical Abnormalities in the Hippocampus in a Rat Model of Cuprizone-Induced Demyelination.

This study quantitatively measured the changes in metabolites in the hippocampal lesions of a rat model of cuprizone-induced demyelination as detected using in vivo 7 T proton magnetic resonance spectroscopy. Nineteen Sprague Dawley rats were randomly divided into two groups and fed a normal chow diet or cuprizone (0.2%, w/w) for 7 weeks.

Optimization of Keyhole Imaging Parameters for Glutamate Chemical Exchange Saturation Transfer MRI at 7.0 T.

Purpose: To evaluate the effects of a reference image and keyhole factor (K) selections for high-frequency substitution on keyhole imaging technique for applications in glutamate chemical exchange saturation transfer (GluCEST) imaging.

Procedures: The CEST data were obtained using a 7.0 T MRI scanner.

Cerebral mapping of glutamate using chemical exchange saturation transfer imaging in a rat model of stress-induced sleep disturbance at 7.0T.

Background: Glutamate chemical exchange saturation transfer (GluCEST) imaging has been widely used in brain psychiatric disorders. Glutamate signal changes may help to evaluate the sleep-related disorders, and could be useful in diagnosis.

Purpose: To evaluate signal changes in the hippocampus and cortex of a rat model of stress-induced sleep disturbance using GluCEST.

Changes to gamma-aminobutyric acid levels during short-term epileptiform activity in a kainic acid-induced rat model of status epilepticus: A chemical exchange saturation transfer imaging study.

Purpose: To evaluate temporal changes in gamma-aminobutyric acid (GABA) signals in the hippocampus during epileptiform activity induced by kainic acid (KA) in a rat model of status epilepticus using chemical exchange saturation transfer (CEST) imaging technique.

Methods: CEST imaging and H magnetic resonance spectroscopy (H MRS) were applied to a systemic KA-induced rat model to compare GABA signals. All data acquisition and analytical procedures were performed at three different time points (before KA injection, and 1 and 3 h after injection).

Retrospective Brain Motion Correction in Glutamate Chemical Exchange Saturation Transfer (GluCEST) MRI.

Purpose: To evaluate the feasibility of motion correction in glutamate chemical exchange saturation transfer (GluCEST) imaging, using a rat model of epileptic seizure.

Procedures: Epileptic seizure was induced in six male Wistar rats by intraperitoneal injection of kainic acid (KA). CEST data were obtained using a 7.

Does the Apparent Diffusion Coefficient Value Predict Permanent Cerebral Ischemia/Reperfusion Injury in Rats?

Rationale And Objectives: Variation in tissue damage after cerebral ischemia/reperfusion (I/R) can cause uncertainty in stroke-related studies, which can be reduced if the damage can be predicted early after ischemia by measuring the apparent diffusion coefficient (ADC). We investigated whether ADC measurement in the acute phase can predict permanent cerebral I/R injury.

Materials And Methods: The middle cerebral artery occlusion model was established using the intraluminal suture method to induce 60 minutes of ischemia followed by reperfusion in rats.

In Vivo Mapping and Quantification of Creatine Using Chemical Exchange Saturation Transfer Imaging in Rat Models of Epileptic Seizure.

Purpose: To evaluate signal changes in the hippocampus of epileptic seizure rat models, based on quantified creatine chemical exchange saturation transfer (CrCEST) signals.

Procedures: CEST data and H magnetic resonance spectroscopy (H MRS) data were obtained for the two imaging groups: control (CTRL) and epileptic seizure-induced (ES; via kainic acid [KA] injection) groups. CrCEST signals in the hippocampal regions were quantitatively evaluated; correlations between CrCEST signals and phosphocreatine (PCr) and total creatine (tCr; PCr + Cr) concentrations, derived from the analysis of H MRS data, were investigated as a function of time changes (before KA injection, 3 and 5 h after KA injection).

The administration of hydrogen sulphide prior to ischemic reperfusion has neuroprotective effects in an acute stroke model.

Emerging evidence has suggested that hydrogen sulfide (H2S) may alleviate the cellular damage associated with cerebral ischemia/reperfusion (I/R) injury. In this study, we assessed using 1H-magnetic resonance imaging/magnetic resonance spectroscopy (1H-MRI/MRS) and histologic analysis whether H2S administration prior to reperfusion has neuroprotective effects. We also evaluated for differences in the effects of H2S treatment at 2 time points.

Induction of G2/M arrest and apoptosis by water extract of Strychni Semen in human gastric carcinoma AGS cells.

The seed of Strychnos nux-vomica (Loganiaceae) has been used in traditional Oriental medicine as a folk remedy for the treatment of cancer. However, the mechanism responsible for the anticancer effects of Strychni Semen is not clearly understood. The study tested whether and how the water extract of Strychni Semen (ESS) treatment would affect the growth of AGS human gastric carcinoma cells.

Induction of apoptosis by linoleic acid is associated with the modulation of Bcl-2 family and Fas/FasL system and activation of caspases in AGS human gastric adenocarcinoma cells.

In this study, we investigated the effects of linoleic acid (LA), a polyunsaturated fatty acid found in most vegetable oils and certain food products, on the growth of AGS human gastric adenocarcinoma cells. LA treatment resulted in a concentration-dependent growth inhibition of AGS cells by inducing apoptosis, as evidenced by the formation of apoptotic bodies, chromatin condensation, and the accumulation cells in the sub-G1 phase. LA treatment induced cyclin-dependent kinase inhibitor p21 in a p53-independent manner; however, this compound did not affect the cell cycle distribution.

Induction of Egr-1 is associated with anti-metastatic and anti-invasive ability of beta-lapachone in human hepatocarcinoma cells.

beta-lapachone, a quinone compound obtained from the bark of the lapacho tree (Tabebuia avellanedae), was reported to have anti-inflammatory and anti-cancer activities. In this study, we investigated novel functions of beta-lapachone in terms of anti-metastasis and anti-invasion abilities using human hepatocarcinoma cell lines, HepG2 and Hep3B. beta-lapachone dose-dependently inhibited cell viability and migration of both HepG2 and Hep3B cells, as determined by methylthiazoletetrazolium (MTT) assay and wound healing assay.