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myo inositol/atrophy

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The neuropsychological effect of hyperammonemia is variable. This study tests the hypothesis that the effect of ammonia on the neuropsychological function in patients with cirrhosis is determined by the ability of the brain to buffer ammonia-induced increase in glutamine within the astrocyte by
Biochemical abnormalities in the retinal pigment epithelium of experimentally diabetic animals include increased sorbitol and decreased myo-inositol. Diabetes also causes a progressive reduction in the amplitude of the c-wave of the electroretinogram of the pigmented rat. The c-wave is generated by
We measured the alcohol sugars in sural nerves from 11 controls, 21 conventionally treated patients with diabetes and neuropathy, and 4 diabetics without neuropathy. The results were related to metabolic control and to clinical, neuropathological, and morphometric abnormalities in the nerves. The
OBJECTIVE To determine the effectiveness of the polyanionic, metal binding agent D-myo-inositol-1,2,6-triphosphate (alpha trinositol, AT), and its hexanoyl ester (HAT), in tissue wasting in cancer cachexia. METHODS The anti-cachexic effect was evaluated in the MAC16 tumour model. RESULTS Both AT and

Levels of myo-inositol in normal and degenerating peripheral nerve.

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This paper is addressed to investigate whether proton magnetic resonance spectroscopy ((1)H-MRS) may provide the means to investigate changes associated to alterations of neural activity and sensory experience in the blind. We examined the relationships between different brain metabolite levels in
BACKGROUND Mesial temporal lobe epilepsy (mTLE) is characterized by hippocampal atrophy, decreased N-acetyl-aspartate, and a low N-acetyl-aspartate/total creatine ratio, often attributed to neuron loss and gliosis. Qualitative studies reported that N-acetyl-aspartate content was significantly lower
BACKGROUND The aim of this study was to find biomarkers of disease severity in multiple system atrophy of cerebellar type by imaging disease specific regions using proton magnetic resonance spectroscopy on a 3.0 T system. METHODS We performed proton magnetic resonance spectroscopy separately in the
Frontotemporal lobar degeneration (FTLD) is a neurodegenerative disease of the frontal and temporal neocortex. The single most common pathology underlying FTLD is neuronal degeneration with ubiquitin-positive but tau-negative inclusions consisting of Tar DNA binding proteins (TDP-43). Inclusions
OBJECTIVE The establishment of biomarkers for amyotrophic lateral sclerosis (ALS) will be useful for early diagnosis and may provide evidence about pathogenesis. To elucidate whether high-field magnetic resonance (MR) findings and multimodal analysis of cerebrospinal fluid (CSF) levels of cystatin C

Intramural pericyte degeneration in early diabetic retinopathy study in vitro.

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An experimental model of diseased pericytes was established by using cultured bovine retinal capillary pericytes in high--glucose medium. The high glucose stimulated polyol pathway, reduced cellular myo-inositol content and disturbed inositol phospholipid metabolism which resulted in a decrease in
Neuropsychiatric manifestations can be a serious complication of systemic lupus erythematosus, affecting nearly 56% of these patients. Frequently, acceptable clinical outcome is observed in neurolupus with immunosuppressive therapy. Different metabolites identified with MR spectroscopy may be
To find imaging signs of active degenerative processes in vanishing white matter disease (VWM), six VWM patients and six matched controls underwent MR examinations. The data were analyzed with modified Scheltens scales for morphological findings and determined quantitatively for apparent diffusion

Retinal thinning and brain atrophy in early MS and CIS.

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Optical coherence tomography (OCT) could be complementary to magnetic resonance imaging (MRI) of the brain in monitoring course of multiple sclerosis (MS) and clinically isolated syndrome (CIS). Thinning of neurons in ganglion cell-inner plexiform layer (GCIPL) measured by OCT is
To determine the effect of diabetes on the development of axonal degeneration after acute nerve compression, the mobilized peroneal nerves of rats with streptozotocin-induced diabetes and of control rats were compressed at 150 mmHg (1 mmHg = 133 Pa) for 30 min by using specially devised cuffs. At
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