Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q16637 (SMA)
 8,107 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This report describes a new specific colorimetric procedure for uric acid assay with AutoAnalyzer II and SMA (Technicon) systems, made specific by the application of uricase. Hydrogen preroxide, formed in this reaction, effects the oxidative coupling of 4-aminophenazone and 2,4-dichlorophenol under the catalytic influence of peroxidase. The red dye formed is measured at 505 or 520 nm. A sample blank measurement is not necessary, and the reagents show very good stability. The test shows linearity up to 714 mumol of uric acid per liter. Results of thie method correlate very well with those by the uricase-ultraviolet and uricase--catalase methods. There is no interference by hemoglobin, bilirubin, lipemia, and various drugs, except a minor interference by alpha-methyldopa. Interference from ascorbate is eliminated by ascorbate oxidase. This method can be regarded as a considerably improved routine test for uric acid on continuous-flow systems in clinical laboratories as compared with the commonly used phosphotungstate method.
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PMID:Determination of uric acid on continuous-flow (AutoAnalyzer II and SMA) systems with a uricase/phenol/4-aminophenazone color test. 62 57

We describe the enzymatic determination of uric acid (uricase/peroxidase) with the SMAC system. The method correlates well with known SMA 12 and Autoanalyzer methods. The change from the original uric acid method to the enzymatic one is simple and does not require any change of the software.
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PMID:[Adaptation of the SMAC for the determination of uric acid with an uricase/perioxidase procedure (author's transl)]. 64 55

The simultaneous assays of glucose and uric acid in blood plasma use first a specific oxidase, then a peroxidase and the same chromogenic system. The coupling of the two methods on Autoanalyser SMA 12/60 use five reagents, three of which are identical in the two methods.
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PMID:[Continuous flow determination of plasma uric acid by an enzyme method using a sequential autoanalyzer. Combination with glucose determination in the presence of glucose oxidase]. 100 27

An automatic micromethod is described for the estimation of plasma uric acid. The hydrogen peroxide formed when uric acid is oxidised by uricase, condenses by oxidation two molecules of p-hydroxyphenil-acetic acid in the presence of peroxidase. The product formed (dicarboxymethyl-5,5' dihydroxy-2,2' biphenyl) is fluorescent. This method permits one to estimate quantitites of uric acid of the order of 1 microng and permits measurement of uric acid in 50 microll of plasma. The values obtained for human plasma are compared to those supplied by a reductrimetric technique (SMA 12-60).
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PMID:[Automatic ultramicrotechnic for the determination of plasma uric acid]. 102 25

A continuous flow method is described for the determination of uric acid in serum using uricase and peroxidase, with omicron-dianisidine as the chromogen. The method can be used with single channel systems and with the multichannel system SMA 12/60 (Technicon). The new method was compared with six other manual and mechanized methods for the dosage of uric acid, and the results were analyzed statistically. The results from all the enzymic methods showed a good correlation, whereas the "chemical oxidation" methods showed systematic deviations.
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PMID:[A mechanized enzymic method for the determination of uric acid (author's transl)]. 118 25

Trinder's method for glucose has nearly all the attributes of an ideal automated colorimetric glucose oxidase procedure. The chemicals used in the color reaction with peroxidase are readily available, the solutions are stable and can be prepared by the user, the method is highly specific and largely free of interferences, the sensitivity can be adjusted by the user to cover a wide range of glucose concentrations, and the reagents are not hazardous. We found very good agreement between results by this method and by the hexokinase and Beckman Glucose Analyzer methods. The method has been modified and adapted to the AutoAnalyzer I and SMA 6/60 (Technicon) with manifolds that give very little interaction between specimens. A study of the method by the simplex technique revealed that the glucose oxidase activity in the reagent is the most critical variable.
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PMID:Evaluation of Trinder's glucose oxidase method for measuring glucose in serum and urine. 123 63

We localized alpha-smooth muscle actin (alpha-SMA) in the quail ovary, using the peroxidase-anti-peroxidase technique. Special attention was paid to the influence of fixation on the immunoreactivity of the antigen. The immunostaining of alpha-SMA largely depended on the nature of the fixative. The antigen could most successfully be localized in ovaries fixed in Carnoy's fluid. We also localized alpha-SMA and desmin in semi-thin glycol methacrylate sections of the pre-ovulatory follicle, using the immunogold-silver staining method. The sections were pretreated with Lugol's iodine or sodium metaperiodate to enhance the immunoreactivity. alpha-SMA was demonstrated in the cells of the chordae, the tunica albuginea, and the theca externa of each follicle. These structures were inter-connected, forming an ovarian suspensory apparatus. The thecal cells of prelampbrush follicles also expressed alpha-SMA. In the wall of the pre-ovulatory follicle, desmin was found in the cells of the chordae and the tunica albuginea, and in a few cells of the theca externa. In the theca interna, desmin, and sometimes alpha-SMA, was observed in cells adjacent to the endothelium of sinusoids, which are probably pericytes. Our results support the hypothesis that in birds the ovarian follicles possess a thecal contractile system, that is presumably involved in the ovulatory process.
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PMID:Immunolocalization of smooth muscle-like cells in the quail ovary. 128 32

The monkey mesial area 6 comprises two distinct cytoarchitectonic areas: F3 [supplementary motor area properly defined (SMA-proper)], located caudally, and F6 (pre-SMA), located rostrally. The aim of the present study was to describe the corticocortical connections of these two areas. To this purpose restricted injections of neuronal tracers (wheat germ-agglutinin conjugated to horseradish peroxidase, fluorescent tracers) were made in different somatotopic fields of F3, F6, and F1 (area 4) and their transport plotted. The results showed that F3 and F6 differ markedly in their cortical connections. F3 is richly linked with F1 and the posterior premotor and cingulate areas (F2, F4, 24d). Connections with the anterior premotor and cingulate areas (F6, F7, F5, 24c) although present, are relatively modest. There is no input from the prefrontal lobe. F3 is also connected with several postrolandic cortical areas. These connections are with areas PC, PE, and PEa in the superior parietal lobule, cingulate areas 23 and PEci, the opercular parietal areas (PFop, PGop, SII) and the granular insula. F6 receives a rich input from the anterior premotor areas (especially F5) and cingulate area 24c, whereas its input from the posterior premotor and cingulate areas is very weak. A strong input originates from area 46. There are no connections with F1. The connections with the postrolandic areas are extremely meagre. They are with areas PG and PFG in the inferior parietal lobule, the disgranular insula, and the superior temporal sulcus. A further result was the demonstration of a differential connectivity pattern of the cingulate areas 24d and 24c. Area 24d is strongly linked with F1 and F3, whereas area 24c is connected mostly with F6. The present data support the notion that the classical SMA comprises two functionally distinct areas. They suggest that F6 (the rostral area) is responsible for the "SMA" so-called high level motor functions, whereas F3 (the caudal area) is more closely related to movement execution.
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PMID:Corticocortical connections of area F3 (SMA-proper) and area F6 (pre-SMA) in the macaque monkey. 750 40

The limited knowledge of the cellular mediators of renal scarring hampers progress in the management of progressive chronic renal failure (CRF). We have studied 38 patients with biopsy-proven mesangial IgA nephropathy with emphasis on attempting to define the role of myofibroblasts (alpha-smooth muscle actin/SMA-positive cells) in renal scarring. In 18 untreated patients, correlations were undertaken between known histological parameters of progression as well as the presence of myofibroblasts in tissues and the clinical outcome. alpha-SMA staining by an avidin-biotin-peroxidase method was confined to a large extent to the vascular smooth muscle cells of normal kidneys but extended to the tubulointerstitium and periglomerular space in scarred kidneys. Mild glomerular staining was also noted. The interstitial immunostain followed a similar distribution to that of interstitial type III collagen. Morphometric analysis showed the interstitial alpha-SMA staining to be a reliable histological predictor of outcome as it discriminated between progressors and non-progressors (chi 2 = 4.923, P = 0.026). The intensity of the interstitial alpha-SMA staining correlated with renal functional outcome; inversely with the reciprocal of serum creatinine slopes (r = -0.466, P < 0.025) and positively with the serum creatinine value at the end of the observation period (r = 0.704, P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Myofibroblasts, predictors of progression of mesangial IgA nephropathy? 781 54

This paper presents a summary of results which concern the neuronal mechanisms underlying the control of gaze. The development of techniques of recording from alert animals and combining functional analysis of neuronal activity with intracellular marking by horse-radish peroxidase has allowed a study of the neuronal mechanisms underlying the vestibulo-ocular reflex and the generation of saccades. The results of these analysis show that there is a close interaction at the level of the brainstem between this two elements of the oculomotor repertoire. This interaction involves both the action of premotor burst neurons involved in the generation of the saccade but also ponto-bulbar reticulo-spinal neurons belonging to the tecto-reticulo-spinal system and involved in the coordination between eye and head movements. This interactions has a very important consequence in the field of recuperation from vestibular lesions. It has been suggested that after vestibular lesions, in addition to local plasticity at the level of the vestibular nuclei it has been suggested that recuperation of function can be due to a functional creation of pseudo-vestibular reflexes by a sequence of blended saccades induced by the saccadic generator mechanisms and with the contribution of the reticulo-spinal system. These interactions have been studied in humans. We have also shown that after prism adaptation the non functional vestibulo-ocular reflex could be replaced by saccades confirming our previous studies in animals. In order to try to approach the neuronal mechanisms underlying these cortical influences we have been able to delineate by position emission tomography techniques the areas of the brain contributing to the generation of voluntary or remembered saccades (parietal cortex, frontal eye fields, supplementary motor eye field, cingulate gyrus, etc.). We have also shown that in patients with lesions of these areas the major deficit in the execution of saccades derived from vestibular information about body motion was the prefrontal cortex and SMA.
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PMID:[Recent data on the physiopathology of gaze]. 795 93


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