Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hydrogen peroxide is used as a preserver in milk industry. Three cases of accidental ingestion of 60% hydrogen peroxide (oxygenated water 200 volumes). The patients were male stockbreeders aged 30, 45 and 62 years, respectively, who stored that powerful oxidizing agent in commercial drink containers without adequate labeling. One of them was admitted comatose and required assisted ventilation. After recovering consciousness migratory paresis of right limbs and of the VI cranial nerve were observed, which were reversed after ten days, and left hemiparesia that persisted for two months. Upper gastrointestinal tract lesions, particularly in stomach, were detected in all. The endoscopic and pathological findings are described in detail. The outcome was satisfactory in the three patients, with complete remission of the lesions. There appears to be a direct relationship between the severity of symptoms and the amount of ingested peroxide, dependent on the diameter of the opening of the container. Only five reports have been identified related to the oral poisoning by this substance.
 ...
PMID:[Ingestion of hydrogen peroxide. Apropos of 3 cases]. 204 3

This study used chemiluminescence, an "on-line" photon-counting technique, to detect and characterize activated O2 species in vitro and in isolated rat lungs. The sensitivity and specificity of enhanced chemiluminescence for superoxide anion (O2-.) and hydrogen peroxide (H2O2) was evaluated in vitro. The effect of media conditions (such as O2 tension, albumin concentration, and sulfhydryl group availability) on luminescence was assessed in vitro. Xanthine-xanthine oxidase (X-XO) primarily produced superoxide anion in vitro. Enhanced chemiluminescence varied directly with the dose of luminescent probe used and the quantity of activated O2 species administered. The strength of the luminescent signal was also dependent on the concentration of albumin and O2 in the media. Lucigenin was more sensitive than luminol to the presence of O2-. and, unlike luminol, lucigenin did not alter radical production by XO. However, neither luminescent probe was specific for O2-., as both detected H2O2 and O2 in vitro. H2O2-induced chemiluminescence was inhibited by catalase but not superoxide dismutase (SOD), while X-XO-induced luminescence was inhibited by SOD but not catalase. SOD-inhibitable chemiluminescence was a sensitive and specific marker for O2-. production in vitro. Once the sensitivity-specificity of enhanced chemiluminescence was defined in vitro, this technique was used to explore the mechanism by which exogenous X-XO reduced hypoxic vasoconstriction in isolated rat lungs. The vascular paresis, caused by administration of X-XO to the rat lung, resulted from a brief burst of O2-. production rather than a sustained alteration of lung radical levels.
 ...
PMID:Detection of activated O2 species in vitro and in rat lungs by chemiluminescence. 253 94

We report the case of a 3 year old boy who developed cardiac arrest during general anesthesia, immediately after the subcutaneous administration of hydrogen peroxide solution. Massive pulmonary embolization was hypothesized as the postoperative ECG showed an acute heart strain. However the occurrence of transient anisocoria, associated with a paresis affecting the left arm, remained unexplained. Since brain MR did not reveal any pathological data, a direct toxicity of hydrogen peroxide on a limited area of the CNS could be assumed.
 ...
PMID:[Severe pulmonary gas embolism caused by intraoperative administration of hydrogen peroxide]. 780 Jan 88

Cytosolic Cu/Zn superoxide dismutase (SOD1) is a ubiquitous small cytosolic metalloenzyme that catalyzes the conversion of superoxide anion to hydrogen peroxide (H(2)O(2)). Mutations in the SOD1 gene cause a familial form of amyotrophic lateral sclerosis (fALS). The mechanism by which mutant SOD1s causes ALS is not understood. Transgenic mice expressing multiple copies of fALS-mutant SOD1s develop an ALS-like motoneuron disease resembling ALS. Here we report that transgenic mice expressing a high concentration of wild-type human SOD1 (hSOD1(WT)) develop an array of neurodegenerative changes consisting of (1) swelling and vacuolization of mitochondria, predominantly in axons in the spinal cord, brain stem, and subiculum; (2) axonal degeneration in a number of long fiber tracts, predominantly the spinocerebellar tracts; and (3) at 2 years of age, a moderate loss of spinal motoneurons. Parallel to the development of neurodegenerative changes, hSOD1(WT) mice also develop mild motor abnormalities. Interestingly, mitochondrial vacuolization was associated with accumulation of hSOD1 immunoreactivity, suggesting that the development of mitochondrial pathology is associated with disturbed SOD1 turnover. In this study we also crossed hSOD1(WT) mice with a line of fALS-mutant SOD1 mice (hSOD1(G93A)) to generate "double" transgenic mice that express high levels of both wild-type and G93A mutant hSOD1. The "double" transgenic mice show accelerated motoneuron death, earlier onset of paresis, and earlier death as compared with hSOD1(G93A) littermates. Thus in vivo expression of high levels of wild-type hSOD1 is not only harmful to neurons in itself, but also increases or facilitates the deleterious action of a fALS-mutant SOD1. Our data indicate that it is important for motoneurons to control the SOD1 concentration throughout their processes, and that events that lead to improper synthesis, transport, or breakdown of SOD1 causing its accumulation are potentially dangerous.
 ...
PMID:Human Cu/Zn superoxide dismutase (SOD1) overexpression in mice causes mitochondrial vacuolization, axonal degeneration, and premature motoneuron death and accelerates motoneuron disease in mice expressing a familial amyotrophic lateral sclerosis mutant SOD1. 1111 61

A 23-year-old man presented with the right upper monoparesis. The right little finger paresis was apparent at first, and ring finger two weeks later, and middle, index, thumb were simultaneously four weeks later. Then the monoparesis gradually progressed to the proximal upper limb. Magnetic resonance imaging showed a small lesion at the knob of the left precentral gyrus. The lesion was low-intensity on T1-, and high-intensity on T2-weighted images, and clearly detected on high-intensity on FLAIR images, but showed no enhancement by gadolinium-diethylenetriamine pentaacetic acid (Gd-DTPA). Angiography and thallium scintigraphy showed no remarkable findings. Proton MR spectroscopy demonstrated lower N-acetylaspartate (NAA) and higher choline (Cho) level compared to the contralateral cortico-subcortical area. Diffusion weighted images demonstrated low apparent diffusion coefficient (ADC) value and high intensity on b = 1,000. To clarify the diagnosis of the lesion, we performed open biopsy by using the neuronavigation system to detect the lesion accurately and minimize the biopsy. Histological examination revealed an high grade astrocytoma with high MlIB-1 index over 30%. The progressive symptoms were due to highly infiltrative and proliferative nature of the tumor arising in the focal hand area of the primary motor cortex, according to the homunculus. We discuss herein the neuroimagings of the case that was considered to be in the initial stage of a malignant tumor.
 ...
PMID:[A case of high grade astrocytoma arising in the hand area of precentral gyrus]. 1602 48