Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two forms of cellulase, buffer soluble (BS) and buffer insoluble (BI), are induced as a result of auxin treatment of dark-grown pea epicotyls. These two cellulases have been purified to homogeneity. Antibodies raised against the purified cellulases were conjugated with ferritin and were used to localize the two cellulases. Tissue sections were fixed in cold paraformaldehyde-glutaraldehyde and incubated for 1 h in the ferritin conjugates. The sections were washed with continuous shaking for 18 h and subsequently postfixed in osmium tetroxide. Tissue incubated in unconjugated ferritin was used as a control. A major part of BI cellulase is localized at the inner surface of the cell wall in close association with microfibrils. BS cellulase is localized mainly within the distended endoplasmic reticulum. Gogli complex and plasma membrane appear to be completely devoid of any cellulase activity. These observations are consistent with cytochemical localization and biochemical data on the distribution of these two cellulases among various cell and membrane fractions.
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PMID:Subcellular localization of cellulases in auxin-treated pea. 76 48

The cause of the degeneration of dopamine-containing cells in the zona compacta of the substantia nigra in Parkinson's disease remains unknown. The ability of the selective nigral toxin 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine (MPTP) (via its metabolite MPP+) to destroy nigral dopamine cells selectively by inhibiting complex I of the mitochondrial energy chain may provide a clue. Indeed, recent studies of post-mortem brain tissue have suggested the presence of an on-going toxic process in the substantia nigra in Parkinson's disease leading to excess lipid peroxidation. This appears also to involve a disruption of mitochondrial function since mitochondrial superoxide dismutase activity is increased and there is impairment of complex I. These changes may in turn relate to a selective increase in the total iron content of substantia nigra coupled to a generalised decrease in brain ferritin content. Piribedil is used in the symptomatic treatment of Parkinson's disease and is particularly effective against tremor. Piribedil (and its metabolites) acts as a dopamine D-2 receptor agonist. However, in our studies in contrast to other dopamine agonists, in vivo piribedil interacts with dopamine receptors in the substantia nigra and nucleus accumbens but not those in the striatum. In patients with Parkinson's disease the beneficial effects of piribedil may be limited by nausea and drowsiness. Indeed, in MPTP-treated primates piribedil reverses motor deficits but marked side-effects occur. However, pre-treatment with the peripheral dopamine receptor antagonist domperidone prevents the unwanted effects and piribedil produces a profound and longer-lasting reversal of all components of the motor syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Parkinson's disease: pathological mechanisms and actions of piribedil. 163 7

A cross-sectional epidemiological study was carried out among 141 male subjects exposed to inorganic manganese (Mn) in a Mn oxide and salt producing plant (mean age 34.3 years; duration of exposure, mean 7.1 years, range 1-19 years). The results were compared with those of a matched control group of 104 subjects. The intensity of Mn exposure was moderate as reflected by the airborne Mn levels and the concentrations of Mn in blood (Mn-B) and in urine (Mn-U). A significantly higher prevalence of cough in cold season, dyspnea during exercise, and recent episodes of acute bronchitis was found in the Mn group. Lung ventilatory parameters (forced vital capacity, FVC; forced expiratory volume in one second, FEV1; peak expiratory flow rate, PEFR) were only mildly altered in the Mn group (smokers) and the intensity and the prevalence of these changes were not related to Mn-B, Mn-U, or duration of exposure. There was no synergistic effect between Mn exposure and smoking on the spirometric parameters. Except for a few nonspecific symptoms (fatigue, tinnitus, trembling of fingers, increased irritability), the prevalence of the other subjective complaints did not differ significantly between the control and Mn groups. Psychomotor tests were more sensitive than the standardized neurological examination for the early detection of adverse effects of Mn on the central nervous system (CNS). Significant alterations were found in simple reaction time (visual), audioverbal short-term memory capacity, and hand tremor (eye-hand coordination, hand steadiness). A slight increase in the number of circulating neutrophils and in the values of several serum parameters (ie, calcium, ceruloplasmin, copper, and ferritin) was also found in the Mn group. There were no clear-cut dose-response relationships between Mn-U or duration of Mn exposure and the prevalence of abnormal CNS or biological findings. The prevalences of disturbances in hand tremor and that of increased levels of serum calcium were related to Mn-B. The response to the eye-hand coordination test suggests the existence of a Mn-B threshold at about 1 microgram Mn/100 ml of whole blood. This study demonstrates that a time-weighted average exposure to airborne Mn dust (total dust) of about 1 mg/m3 for less than 20 years may present preclinical signs of intoxication.
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PMID:Epidemiological survey among workers exposed to manganese: effects on lung, central nervous system, and some biological indices. 357 89

Latex immunoassay is a nonisotopic method based on agglutination, by protein, of calibrated latex particles coated with a specific antibody. The assay has been automated in a simple continuous-flow system by incubating the reaction mixture in a heated mixing coil for 25 min and measuring the agglutination with a cell counter. No external shaking of the latex suspension and no additional reagent is required for the agglutination. The method can accurately and precisely quantify a wide variety of proteins in plasma and urine, including human ferritin, beta 2-microglobulin, retinol-binding protein, and albumin. Depending on the antigen-antibody system, the detection limit ranges from 10(-10) to about 10(-12) mol/L. Within- and between-assay CVs are less than 10%. In the assay of ferritin, sera are pretreated to eliminate interferences from chylomicrons, complement, and rheumatoid factor.
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PMID:Continuous-flow system for automation of latex immunoassay by particle counting. 634 48

Sensory hairs from antennae of male saturniid moths (Antheraea polyphemus) were separated while deep-frozen by shaking antennal branches with glass beads. The hairs were collected through their differential adhesion to the surface of a petri dish. The yield, determined by the length of the isolated hair fragments, was about 38% of the estimated total hair length per antenna. The dendritic membrane was separated from the hair fragments by centrifugation through Sephadex and further purified by ultracentrifugation in sucrose buffers. Transmission electron microscopy was used to monitor the steps of the hair and membrane isolation and to investigate the membrane pellet. Some membrane vesicles bound cationized ferritin, thus indicating a negatively charged cell surface coat. Negatively stained membrane vesicles exhibited a pattern of repetitive substructures irregularly distributed over the vesicle surface. The units had a diameter of about 3 nm and a maximal density of 30,000/micron2.
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PMID:Dendritic membrane from insect olfactory hairs: isolation method and electron microscopic observations. 653 23

A sensitive immunoassay based on latex particle agglutination (latex immunoassay) has been developed for the determination of serum ferritin. Polystyrene particles (0.8 micron) to which anti-ferritin antibody is adsorbed are incubated with serum for 30 min with shaking or 60 min without shaking. The resulting agglutination is quantified by measuring the decrease of absorbance of the latex suspension at 360 nm. Pretreatment of the serum is required to prevent interference from complement, rheumatoid factor and chylomicrons. The lowest detectable concentration of ferritin in serum is about 5 micrograms/l. Within-runs and between-runs coefficients of variation, based on analysis of samples containing 14-820 micrograms/l ferritin, ranged from 3.6 to 13.8%. A correlation coefficient of 0.95 between latex immunoassay and radioimmunoassay was obtained for the determination of ferritin in 46 sera.
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PMID:Turbidimetric latex immunoassay for serum ferritin. 673 56

Ninety preselected children, aged between 8 and 14 years, living in two rural West African (Gambian) villages, were randomly divided into three groups, matched for age and sex. One group received a placebo (lactose) tablet, one received riboflavin (5 mg) on 5 d every week, which was sufficient to correct an endemic riboflavin deficiency, and one received a multivitamin supplement (Protovit; Hoffmann La Roche), on 5 d every week, together with FeSO4 (200 mg) once weekly, and the supplements were given for 1 year. Neuromuscular tests, including arm tremor and manipulative skills, were performed on three occasions: once just before the introduction of the supplements; again 6 weeks after commencing the supplements; and again 1 year later. Venous blood samples were collected at the same time as the first two sets of neuromuscular tests. These samples were used for haematology and nutrient status indices: plasma ferritin, ascorbic acid, cyanocobalamin and pyridoxal phosphate, and erythrocyte tests for folate status, for riboflavin status (erythrocyte glutathione reductase activation coefficient) and thiamine status (erythrocyte transketolase activation coefficient). The riboflavin in both supplements achieved a clear-cut response in biochemical status, which was dose-dependent. The pyridoxine, ascorbic acid and Fe components of the multivitamin also affected the associated biochemical indices. Although overall the arm tremor and related neuromuscular function tests did not respond significantly to the supplements, significant improvement was seen in the boys for the arm-tremor test in both the supplemented groups.
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PMID:Biochemical indices and neuromuscular function tests in rural Gambian schoolchildren given a riboflavin, or multivitamin plus iron, supplement. 798 90

Parkinson's disease, known also as striatal dopamine deficiency syndrome, is a degenerative disorder of the central nervous system characterized by akinesia, muscular rigidity, tremor at rest, and postural abnormalities. In early stages of parkinsonism, there appears to be a compensatory increase in the number of dopamine receptors to accommodate the initial loss of dopamine neurons. As the disease progresses, the number of dopamine receptors decreases, apparently due to the concomitant degeneration of dopamine target sites on striatal neurons. The loss of dopaminergic neurons in Parkinson's disease results in enhanced metabolism of dopamine, augmenting the formation of H2O2, thus leading to generation of highly neurotoxic hydroxyl radicals (OH.). The generation of free radicals can also be produced by 6-hydroxydopamine or MPTP which destroys striatal dopaminergic neurons causing parkinsonism in experimental animals as well as human beings. Studies of the substantia nigra after death in Parkinson's disease have suggested the presence of oxidative stress and depletion of reduced glutathione; a high level of total iron with reduced level of ferritin; and deficiency of mitochondrial complex I. New approaches designed to attenuate the effects of oxidative stress and to provide neuroprotection of striatal dopaminergic neurons in Parkinson's disease include blocking dopamine transporter by mazindol, blocking NMDA receptors by dizocilpine maleate, enhancing the survival of neurons by giving brain-derived neurotrophic factors, providing antioxidants such as vitamin E, or inhibiting monoamine oxidase B (MAO-B) by selegiline. Among all of these experimental therapeutic refinements, the use of selegiline has been most successful in that it has been shown that selegiline may have a neurotrophic factor-like action rescuing striatal neurons and prolonging the survival of patients with Parkinson's disease.
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PMID:Oxidative stress and antioxidant therapy in Parkinson's disease. 883 Mar 46

Degeneration of dopaminergic neurons that project from substantia nigra to striatum is the primary mechanism that causes Parkinson disease (PD). This death of dopaminergic cells disturbs control over impulses sent from the motor cortex and hence results in the presence of three cardinal motor signs: tremor, rigidity, bradykinesia. The cause of Parkinson disease is unknown. Current treatments relieve symptoms but do not halt the progression of the disease. It is not yet known what causes neurons to degenerate. Influences of aging, environmental toxins, genetic susceptibility have been pointed out by researchers, but the theory of oxidative stress seems to be the most convincing. It is supposed that SN neurons are exposed to oxidative reactions from dopamine metabolism (production) during which hydrogen peroxide and toxic semiquinones are formed. Additionally, in brains of PD patients there are decreased concentrations of defence mechanisms such as glutathion and compensatory ferritin that binds iron, maintaining it in its safe state (Fe2+ iron takes part in Fenton reaction that leads to free radicals production). However, we have to admit that Parkinson disease is probably multifactorial, and the combination of the above stated factors may cause the disease.
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PMID:[Factors which can play important role in pathogenesis of Parkinson disease]. 1061 5

In mammalian cells, regulation of the expression of proteins involved in iron metabolism is achieved through interactions of iron-sensing proteins known as iron regulatory proteins (IRPs), with transcripts that contain RNA stem-loop structures referred to as iron responsive elements (IREs). Two distinct but highly homologous proteins, IRP1 and IRP2, bind IREs with high affinity when cells are depleted of iron, inhibiting translation of some transcripts, such as ferritin, or turnover of others, such as the transferrin receptor (TFRC). IRPs sense cytosolic iron levels and modify expression of proteins involved in iron uptake, export and sequestration according to the needs of individual cells. Here we generate mice with a targeted disruption of the gene encoding Irp2 (Ireb2). These mutant mice misregulate iron metabolism in the intestinal mucosa and the central nervous system. In adulthood, Ireb2(-/-) mice develop a movement disorder characterized by ataxia, bradykinesia and tremor. Significant accumulations of iron in white matter tracts and nuclei throughout the brain precede the onset of neurodegeneration and movement disorder symptoms by many months. Ferric iron accumulates in the cytosol of neurons and oligodendrocytes in distinctive regions of the brain. Abnormal accumulations of ferritin colocalize with iron accumulations in populations of neurons that degenerate, and iron-laden oligodendrocytes accumulate ubiquitin-positive inclusions. Thus, misregulation of iron metabolism leads to neurodegenerative disease in Ireb2(-/-) mice and may contribute to the pathogenesis of comparable human neurodegenerative diseases.
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PMID:Targeted deletion of the gene encoding iron regulatory protein-2 causes misregulation of iron metabolism and neurodegenerative disease in mice. 1117 92


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