A new technique allowing prolonged temporary cerebral artery occlusion.

Object: Clipping of complex cerebral aneurysms often requires temporary vessel occlusion. The risk of stroke, however, increases exponentially with occlusion time. The authors hypothesized that prolonged temporary occlusion might be tolerated if the occluded vessels were perfused with cold physiological saline solution (CPSS).

fMRI of supraspinal areas after morphine and one week pancreatic inflammation in rats.

Abdominal pain is a major reason patients seek medical attention yet relatively little is known about neuronal pathways relaying visceral pain. We have previously characterized pathways transmitting information to the brain about visceral pain. Visceral pain arises from second order neurons in lamina X surrounding the spinal cord central canal.

Reduction of brain injury by antithrombotic agent acutobin after middle cerebral artery ischemia/reperfusion in the hyperglycemic rat.

In vivo magnetic resonance imaging (MRI) was used to observe the effect of acutobin, a purified thrombin-like enzyme (TLE), isolated from the snake venom of Deinagkistrodon acutus, on MRI-detected brain lesion volume and tissue perfusion deficit in a hyperglycemic rat right middle cerebral artery occlusion/reperfusion (MCAO/R) model. Acutobin (0.75 U/ml) was intravenously injected with a dosage of 2.

Aspartoacylase deficiency does not affect N-acetylaspartylglutamate level or glutamate carboxypeptidase II activity in the knockout mouse brain.

Aspartoacylase (ASPA)-deficient patients [Canavan disease (CD)] reportedly have increased urinary excretion of N-acetylaspartylglutamate (NAAG), a neuropeptide abundant in the brain. Whether elevated excretion of urinary NAAG is due to ASPA deficiency, resulting in an abnormal level of brain NAAG, is examined using ASPA-deficient mouse brain. The level of NAAG in the knockout mouse brain was similar to that in the wild type.

Magnetic resonance histology: in situ single cell imaging of receptor cells in an invertebrate (Lolliguncula brevis, Cephalopoda) sense organ.

Utilizing contrast-enhanced MR histology, individual cell bodies were identified in situ and compared one-to-one with conventional histology. The squid Lolliguncula brevis served as a model where the receptor cells of the proprioceptive neck receptor organ were labeled with paramagnetic cobalt(II) ions by conventional cobalt iontophoresis. Stimulated echo images were obtained using a 9.

Canavan disease: a monogenic trait with complex genomic interaction.

Canavan disease (CD) is an inherited leukodystrophy, caused by aspartoacylase (ASPA) deficiency, and accumulation of N-acetylaspartic acid (NAA) in the brain. The gene for ASPA has been cloned and more than 40 mutations have been described, with two founder mutations among Ashkenazi Jewish patients. Screening of Ashkenazi Jews for these two common mutations revealed a high carrier frequency, approximately 1/40, so that programs for carrier testing are currently in practice.

Expression of glutamate transporter, GABRA6, serine proteinase inhibitor 2 and low levels of glutamate and GABA in the brain of knock-out mouse for Canavan disease.

Canavan disease (CD) is an autosomal recessive leukodystrophy characterized by spongy degeneration of the brain. The clinical features of CD are hypotonia, megalencephaly, and mental retardation leading to early death. While aspartoacylase (ASPA) activity increases with age in the wild type mouse brain, there is no ASPA activity in the CD mouse brain.

Effects of 2-deoxy-d-glucose on focal cerebral ischemia in hyperglycemic rats.

The authors examined the effects of pretreatment with 2-deoxy-d-glucose (2DG) on the middle cerebral artery occlusion-reperfusion (MCAO/R) model in hyperglycemic rats. Proton magnetic resonance imaging and spectroscopy were used to measure the lesion size, the level of cerebral perfusion deficit, and ratio of lactate to N-acetyl aspartate (NAA) in brain regions. By performing sequential diffusion weighted imaging, gradient echo bolus tracking, steady-state spin echo imaging, and water-suppressed proton magnetic resonance spectroscopy techniques, the time course of the early changes of the lactate/NAA peak ratio and perfusion deficit was examined in hyperglycemic rats undergoing 90-minute MCAO followed by 24-h reperfusion.

Adeno-associated virus-mediated aspartoacylase gene transfer to the brain of knockout mouse for canavan disease.

Canavan disease (CD) is an autosomal recessive leukodystrophy caused by deficiency of aspartoacylase (ASPA). Deficiency of ASPA leads to elevation of N-acetyl-L-aspartic acid (NAA) in the brain and urine. To explore the feasibility of gene transfer to replace ASPA in CD, we generated a knockout mouse and constructed an AAV vector that encodes human ASPA cDNA (hASPA) followed by green fluorescent protein (GFP) after an intraribosomal entry site.

A method for measuring cerebral glucose metabolism in vivo by 13C-NMR spectroscopy.

Current methods for estimating the rate of cerebral glucose utilization (CMR(glc)) typically measure metabolic activity for 40 min or longer subsequent to administration of [(13)C]glucose, 2-[(14)C]deoxyglucose, or 2-[(18)F]deoxyglucose. We report preliminary findings on estimating CMR(glc) for a period of 15 min by use of 2-[6-(13)C]deoxyglucose. After a 24-hr fast, rats were anesthetized, infused with [1-(13)C]glucose for 50 min, and injected with 2-[6-(13)C]deoxyglucose (500 mg/kg).