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

Groups of Alpk:AP (Wistar-derived) rats were fed diets containing 0, 500, 1000 or 2500 ppm permethrin for 2 years and Swiss-derived mice were maintained for their lifetime (80% mortality) on diets containing 0, 250, 1000, or 2500 ppm permethrin. Changes of toxicological significance were confined to the top dose level of 2500 ppm permethrin in both species. Tremors and hypersensitivity to noise were noted in rats at this dose during the first 2 weeks of study but such signs were not seen in mice. Pathological examination of the central and peripheral nervous systems did not reveal abnormalities attributable to permethrin administration. The effect on mice at 2500 ppm permethrin was shown by decreased body weight gain. Liver hypertrophy, associated with increase in liver weight, microsomal enzyme activity, and proliferation of smooth endoplasmic reticulum occurred in the rat with similar but less marked changes in the mouse. This was considered to be an adaptive response of no toxicological significance. No evidence of a carcinogenic effect was seen in the rat study. In the mouse study a slight elevation in benign lung tumor incidence in males only at 2500 ppm permethrin was observed but was not considered to represent a carcinogenic effect.
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PMID:Chronic toxicity and carcinogenic evaluation of permethrin in rats and mice. 322 Feb 9

The stereological technique was used to quantify glycogen areas and endoplasmic reticulum in fetal rat hepatocytes cultured for 24 hr in monolayer (monolayer cells) or following shaking by gyratory rotation (shaken cells). The volume density and volume per cell of glycogen areas decreased in order of freshly isolated hepatocytes, monolayer cells, and shaken cells. The surface density and area per cell of smooth endoplasmic reticulum increased in order of freshly isolated cells, monolayer cells, and shaken cells. The results show that the decrease of glycogen areas and proliferation of the smooth endoplasmic reticulum are more prominent in shaken cells than in monolayer cells. Prominent proliferation of the smooth endoplasmic reticulum in shaken cells may be due to the consumption of glycogen for energy release as a result of gyratory rotation.
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PMID:Morphometric analysis of fetal rat hepatocytes cultured in monolayer or following gyratory shaking. 377 80

Female heterozygotes of the shaking pup and myelin-deficient rat sex-linked recessive traits, show myelin mosaicism of the optic nerve and spinal cord. This is most marked in the optic nerve especially in the rat where mosaic patches persist with aging. In both the rat and dog, abnormal oligodendrocytes with distended rough endoplasmic reticulum are found in the abnormal patches and are a marker of the trait. Female heterozygote dogs can develop a marked tremor which disappears with age.
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PMID:Myelin mosaicism in female heterozygotes of the canine shaking pup and myelin-deficient rat mutants. 382 84

Intracerebral inoculation to guinea pigs of cerebrospinal fluid or brain suspensions from 6 patients with Creutzfeldt--Jakob disease was followed in 4 cases by the appearance, after a long incubation period, of a serially transmissible experimental disease. The disease was characterized by tremor, discrete ataxia and convulsions and led to a fatal outcome within several days. Microscopic lesions in the brain of guinea pigs with the experimental disease consisted in glial proliferation, spongiform change and vacuolation of neuron cytoplasm. Electron microscopy proved that the vacuoles were situated in the endoplasmic reticulum and in the cytoplasmic processes.
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PMID:Further data on experimental Creutzfeldt--Jakob disease (spongiform encephalopathy) in the guinea pig. 634 14

Quantification of glial cells, axonal size and myelin thickness and volume were carried out in selected areas of the three funiculi of the cervical spinal cord and the optic nerve of 'shaking pups' and normal littermates at 4 and 8 weeks of age. There was a marked reduction of oligodendrocytes in the affected pups with many of these cells having distended rough endoplasmic reticulum. Oligodendrocyte death was not noticeable. Astrocyte numbers were similar in both normal and affected pups. Axonal diameters were not reduced in the affected pups and there was no apparent correlation between myelination and axonal size in these animals. Total myelin volume and thickness were greatly reduced in the 'shaking pups.' Impaired stem cell division together with metabolic disturbance of oligodendrocytes are considered to be the main causes of the hypomyelination in this mutant.
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PMID:'Shaking pups': a disorder of central myelination in the spaniel dog. III. Quantitative aspects of glia and myelin in the spinal cord and optic nerve. 664 43

Young adult BALB/c mice were administered trimethyltin chloride (TMT) at a dosage of 3.0 mg TMT/kg body wt. Animals displayed severe toxic signs (tremor and aggression) within 24 hr and were sacrificed at 48 and 72 hr postinjection. The brain stems of these animals were examined with light and electron microscopy. Degenerative and vacuolar changes were observed in many large brain stem neurons, especially those in the mesencephalic trigeminal nuclei. These neurons acquired a chromatolytic character with eccentric nuclei, loss of Nissl substance, and hyalinoid cytoplasm. Extensive vacuolation was also found in these nerve cells. Electron microscopy examination revealed progressive loss of the Nissl substance (rough endoplasmic reticulum) and distention of the cytoplasmic membranes (endoplasmic reticulum and Golgi complex). Severe distention of these membranes resulted in large membrane-limited vacuoles within these nerve cells. This intraneuronal vacuolation reflects an intracellular edema condition of these nerve cells and is potentially reversible. Mitochondrial damage in these neurons was only moderate. Further investigation is needed to elucidate the full toxic impact and pathogenetic mechanisms of TMT in the nervous system.
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PMID:Neuropathology of trimethyltin intoxication. III. Changes in the brain stem neurons. 683 24

Previous morphometric or biochemical investigations have yielded different data on the distribution of free and membrane-bound ribosomes in midgut cells of Aedes aegypti. In the present paper ribosomal distribution has been morphometrically analysed to determine whether different mosquito strains, different food and different narcosis used in these previous studies, and/or methodological errors, could account for the different results. Most of the cellular parameters in the stomach epithelium of female A. aegypti, strain Rockefeller, and their changes during blood digestion, are comparable to those measured for another Aedes strain (Segemaganga, Hecker and Rudin, 1979), and ae generally similar to those of Anopheles stephensi (Hecker 1978). Proteolytic activity against casein is similar for both Aedes strains with a maximum activity being registered around 30 h after a blood meal. During digestion of human serum there is no increase in the ratio of membrane-bound to free ribosomes, and no significant increase in the surface area of the rough endoplasmic reticulum or of the number of bound or free ribosomes. Proteolytic activity is distinctly lower than during blood digestion. Immobilization of mosquitoes prior to dissection by either narcosis or by shaking in a test tube has no significant influence on cellular parameters in females fed on sugar solution and investigated 3 days after emergence. It is concluded that the differences in ribosomal parameters previously obtained by morphometrical (Hecker and Rudin 1979) and biochemical (Gander et al. 1980) methods, can only partly be explained by the selection of different food for the mosquitoes, and must also have been caused by methodological inadequacies.
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PMID:Morphometric parameters of the midgut cells of Aedes aegypti L. (Insecta, Diptera) under various conditions. 702 89

BALB/c mice were injected IP with a single dose of trimethyltin chloride (3.0 mg TMT/kg body weight). Severe body tremor was observed within 12 hours post-injection. All animals were sacrificed 48 hours post-injection by means of intracardial perfusion with 2.5% buffered glutaraldehyde. Light microscopic examination revealed extensive neuronal necrosis in the granule cells of the fascia dentata of the hippocampus. Scattered neuronal loss was also observed in the pyriform cortex, the neocortex, amygdaloid nucleus, and the brainstem. Electron microscopic examination of the hippocampus revealed lysosomal accumulation in both the granule cells and pyramidal neurons. While extensive cellular necrosis was observed in the granule cells, the pyramidal neurons only displayed some dilatation and vacuolation of their endoplasmic reticulum. This report represents the first in depth pathological study in the mouse hippocampus following an acute exposure to TMT.
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PMID:Neuropathology of mouse hippocampus in acute trimethyltin intoxication. 708 42

Myelin deficiency (md) is a new mutant in the Wistar rat caused by an X-linked recessive lethal gene. One-half of the male offspring develop tremor and ataxia at 10-12 days of age and seizures at 16-21 days. Usually, the animals die 24-28 days postnatally unless survival is prolonged by anticonvulsants. Light microscopic examination of the C.N.S. shows a complete lack of myelin. The P.N.S. is normally myelinated, however. Frontal cortex, corpus callosum, optic nerves, cerebellum and spinal cord were studied routinely in affected animals aged 3-46 days. Abnormal males were identified three days after birth by the absence of myelinated axons from the ventral funiculus of the cervical cord. In mutants aged 3-16 days, axons had the usual ultrastructural features but were either entirely non-myelinated or, rarely, were invested by poorly organized, non-compacted, myelin-like loops of membranes, 2 to 4 in number. In mutants aged 17-20 days, axonal swellings appeared. These increased in number with longer survival times and contained large numbers of microtubules, neurofilaments, mitochondria and dense bodies. Normal C.N.S. myelin was not observed at any age. Two types of abnormal glial cell occur in md. The first, present in white matter at three days of age, is an abnormal oligodendrocyte. The cytoplasm contains dilatation of the rough-surfaced endoplasmic reticulum and the nuclear envelope is widened. A second cell-type, conspicuous by 10 days, has an electron-dense nucleus with prominently clumped chromatin and large cytoplasmic lipid droplets. This second cell type is believed to be a microgliacyte. The number of cytologically-normal oligodendrocytes decreases as mutants age while hypertrophied, filament-rich astrocytes occur in increasing numbers. The myelin defect in md C.N.S. is probably due to an abnormality of oligodendrocytes. Axonal alterations are probably secondary. Myelin deficiency resembles the murine mutant, Jimpy (jp), although ultrastructural changes in oligodendrocytes appear to be dis-similar and md, in contrast to jp, contains no normal-appearing C.N.S. myelin.
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PMID:Ultrastructure of the central nervous system in a myelin deficient rat. 713 Oct 49


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