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)

Intraperitoneal administration of fenvalerate, a synthetic pyrethroid, in male rats for 45 days in doses of 100 and 200 mg/kg body weight/day induced hyperexcitability, tremors and paralysis. Tremors were observed after 7 days and gradually reached maxima on 45th day. The symptoms were more marked in rats treated with 200 mg/kg body weight/day. Fenvalerate provoked significant elevation of circulatory thyroid hormones, namely tri-iodothyronine (T3) and thyroxine (T4). A significant increase in total calcium as well as protein-bound calcium in whole brain and hypothalamus were recorded. The elevation of circulatory thyroid hormones as well as the active calcium pool could be together responsible for impairment of motor activity by altering various neuronal processes.
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PMID:Fenvalerate-induced alterations in circulatory thyroid hormones and calcium stores in rat brain. 895 8

The natural course of calcium-entry blocker-induced parkinsonism was evaluated in 13 elderly patients previously exposed to cinnarizine or flunarizine or both for a median period of 7 months. Clinical assessments were carried out before drug discontinuation and twice thereafter over a period lasting < or = 7 years. None of the patients showed a full recovery of extrapyramidal signs, indicating that the long-term prognosis of the parkinsonism is less benign than previously reported. Two main patterns of clinical outcome were recognized (i.e., "remittent" and "persistent and not progressive" parkinsonism), whereas the development of a progressive disorder was observed only in one patient. No significant correlation was found between the patterns of outcome and some clinical variables, such as total duration of exposure to cinnarizine and flunarizine, cumulative drug dosages, and age at onset of parkinsonism. There was no significant difference in terms of family history of essential tremor or parkinsonism or both among patients with the two main patterns of clinical course.
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PMID:A long-term follow-up study of cinnarizine- and flunarizine-induced parkinsonism. 1034 90

It is widely accepted that mechanical loading is necessary to construct the architecture of bone and to maintain bone mass. However, the mechanism of how bone cells respond to mechanical stimuli is not known. To clarify this, we stimulated osteoblast-like MC3T3E1 cells by mechanical shaking of the culture dishes and found that the level of the egr-1 gene, which is an early response gene induced by growth factors or serum and encodes a transcription factor, increased 15-45 min after the shaking, with a peak at 30 min. The egr-1 gene product increased 1 h after the shaking. The egr-1 gene elevation was not blocked by prior exposure to indomethacin, saralasin, Rp-cAMP, A23187, and colchicine, and it was blocked partially by cytochalasin D, H-7, and prolonged exposure to TPA. On the other hand, a prior incubation with cycloheximide, DRB, genistein, herbimycin A, and BAPTA/AM completely blocked the egr-1 gene level enhanced by shaking the culture dishes. Moreover, we found that in serum-deprived cells the egr-1 gene response to shaking was not induced. These results suggested that the egr-1 gene response is regulated at the transcriptional level and that it involves tyrosine kinase as well as labile or de novo protein and requires a particular level of intracellular calcium and serum.
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PMID:Fluid flow induces enhancement of the Egr-1 mRNA level in osteoblast-like cells: involvement of tyrosine kinase and serum. 901 82

Parkinsonism, tremor, chorea-ballismus, dystonia, tardive dyskinesia, myoclonus, tics and akathisia can be induced by many drugs. The drugs that are most frequently implicated in movement disorders are antipsychotics, calcium antagonists, orthopramides and substituted benzamides (e.g. metoclopramide, sulpiride, clebopride, domperidone), CNS stimulants, antidepressants, anticonvulsants, antiparkinsonian drugs and lithium. It is possible for a single drug to induce 2 or more types of movement disorders in the same patient. Movement disorders are not always reversible after drug withdrawal.
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PMID:Drug-induced movement disorders. 909 56

Mechanisms underlying the selective vulnerability of the lateral striatal area to the toxic effects of 3-nitropropionic acid (3-NPA) were investigated in rats. A single exposure to 3-NPA (20 mg/kg, s.c.) induced no deficits in behavior and histology, but subsequent injection produced motor symptoms, catalepsy, lip smacking, abnormal gait, paddling, rolling, opisthotonos, tremor, recombence, somnolence and so on, in 30% of the animals within a few hours. Diffusion-weighted magnetic resonance imaging of the brains revealed an area of high signal intensity in the bilateral striata. By this stage (within a few hours), striatal astrocytes had become swollen and disintegrated. Extravasation of immunoglobulin G was detected, indicating blood-brain barrier (BBB) dysfunction. Electron microscopy revealed edema and disorganization of structures inside the astrocytic end-feet around the branches of the lateral striatal artery. Neurons were less vulnerable than astrocytes to the 3-NPA injury. Treatment of the rats with D2 receptor agonist prior to exposure to 3-NPA attenuated the behavioral abnormalities and histological damage whereas pretreatment with D2 antagonist exacerbated these changes. The concentrations of extracellular dopamine (DA) and dihydroxyphenyl acetic acid (DOPAC) were both increased in rats exposed to 3-NPA. In vitro imaging of astrocytes revealed a progressive increase in [Ca2+]i after superfusion with 3-NPA, and the 'ceiling' level was maintained even after extensive washing. DA superfusion also increased the astrocytic [Ca2+]i and this increase was reversible. Data indicate that 3-NPA-induced striatal damage was associated with astrocytic cell death and dysfunction of the BBB. Intracellular edema and extreme Ca2+ overload induced by the toxin were further aggravated by an increase in the level of DA activity. These factors acting either singly or in combination may trigger astrocyte destruction.
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PMID:Acute 3-nitropropionic acid intoxication induces striatal astrocytic cell death and dysfunction of the blood-brain barrier: involvement of dopamine toxicity. 915 47

We modified the isolation procedure of muscle and heart mitochondria. In human muscle, this resulted in a 3.4 fold higher yield of better coupled mitochondria in half the isolation time. In a preparation from rat muscle we studied factors that affected the stability of oxidative phosphorylation (oxphos) and found that it decreased by shaking the preparation on a Vortex machine, by exposure to light and by an increase in storage temperature. The decay was found to be different for each substrate tested. The oxidation of ascorbate was most stable and less sensitive to the treatments. When mitochondria were stored in the dark and the cold, the decrease in oxidative phosphorylation followed first order kinetics. In individual preparations of muscle and heart mitochondria, protection of oxidative phosphorylation was found by adding candidate stabilizers, such as desferrioxamine, lazaroids, taurine, carnitine, phosphocreatine, N-acetylcysteine. Trolox-C and ruthenium red, implying a role for reactive oxygen species and calcium-ions in the in vitro damage at low temperature to oxidative phosphorylation. In heart mitochondria oxphos with pyruvate and palmitoylcarnitine was most labile followed by glutamate, succinate and ascorbate. We studied the effect of taurine, hypotaurine, carnitine, and desferrioxamine on the decay of oxphos with these substrates. 1 mM taurine (n = 6) caused a significant protection of oxphos with pyruvate, glutamate and palmitoylcarnitine, but not with the other substrates. 5 mM L-carnitine (n = 6), 1 mM hypotaurine (n = 3) and 0.1 mM desferrioxamine (n = 3) did not protect oxphos with any of the substrates at a significant level. These experiments were undertaken in the hope that the in vitro stabilizers can be used in future treatment of patients with defects in oxidative phosphorylation.
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PMID:Rapid isolation of muscle and heart mitochondria, the lability of oxidative phosphorylation and attempts to stabilize the process in vitro by taurine, carnitine and other compounds. 930 66

It has been proposed that parkinsonian tremor is produced either by the activity of an intrinsic thalamic pacemaker or by the oscillation of an unstable long loop reflex arc. The former (central) hypothesis proposes that overactivity of neurons in the internal segment of the globus pallidus inhibits or hyperpolarizes thalamic neurons. When hyperpolarized, thalamic cells oscillate with bursting of the type associated with low threshold calcium spikes (low threshold spike-bursts). Low threshold spike-bursts can be identified by particular patterns of interspike intervals within the burst. The alternative (peripheral) hypothesis proposes that tremor results from oscillation of a reflex arc transmitting activity from muscle stretch receptors to thalamus, motor cortex, and back to the stretched muscle. When the gain of this reflex is increased, the arc may become unstable and oscillate. Oscillations produced by peripheral inputs may produce an acceleration-deceleration pattern within the burst which results in sinusoidal modulation of a spike train if bursting is periodic. We have assessed these two hypotheses by studying the pattern of interspike intervals occurring within bursts recorded in patients with parkinsonian tremor. The spike trains were analysed for 118 cells located in the ventral nuclear group including ventralis intermedius (thalamic cerebellar relay nucleus, n=48) and ventralis oralis posterior (thalamic pallidal relay nucleus, n=39) of patients with parkinsonian tremor. Two cells recorded in ventralis intermedius of a sleeping patient with chronic pain showed bursting activity similar to the low threshold spike-bursts recorded in sleeping animals, suggesting a common mechanism for low threshold spike-bursts across species. Forty-two cells recorded in patients with parkinsonian tremor (ventralis intermedius, n=19; ventralis oralis posterior, n=12) were classified as tremor-related cells because their activity was characterized by both a concentration of power at tremor frequency and significant correlation with tremor. Eleven tremor-related cells, 10 located in ventralis intermedius or ventralis oralis posterior and most responding to sensory inputs, had an acceleration-deceleration pattern of intraburst firing. Only one cell, a tremor-related cell in ventralis intermedius, showed the pattern expected of presumed low threshold spike-bursts. Therefore, intraburst interspike interval patterns consistent with either the central or the peripheral hypothesis were recorded in the thalamus of patients with parkinsonian tremor. Twenty-one tremor-related cells (15 cells in ventralis intermedius or ventralis oralis posterior) had bursts with intraburst interspike intervals which were independent of position of the interspike interval within the burst. Therefore, the activity of the majority of cells was not consistent with either hypothesis, suggesting that another oscillatory process may contribute to parkinsonian tremor.
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PMID:Patterns of bursting occurring in thalamic cells during parkinsonian tremor. 946 2

Within 10 minutes of intraperitoneal injection of penitrem A (3 mg/kg), rats develop severe generalized tremors and ataxia that persist for up to 48 hours. These are accompanied by a three- to fourfold increase in cerebellar cortical blood flow. Mitochondrial swelling occurs in cerebellar stellate and basket cells within 30 minutes of dosing and persists for more than 12 hours without leading to cell death. From 2 hours, Purkinje cell dendrites show early cytoplasmic condensation accompanied by fine vacuolation of smooth endoplasmic reticulum and enlargement of perikaryal mitochondria. From 6 hours, many Purkinje cells develop intense cytoplasmic condensation with eosinophilia that resembles "ischemic cell change," and from 12 hours, many other Purkinje cells show marked watery swelling. Astrocytes begin to swell from 0.5 hours after injection and show hypertrophy of organelles from 6 hours. Also from 6 hours onward, discrete foci of necrosis appear in the granule cell layer, while permeability of overlying meningeal vessels to horseradish peroxidase becomes evident at 8 hours. All changes are more severe in vermis and paravermis. Despite widespread loss of Purkinje cells, the animals' behavior becomes almost normal within a week. While tremor occurs with doses of 1.5 and 0.5 mg/kg, cellular damage is minimal. The tremor mechanism differs from that of harmaline since destruction of inferior olivary nuclei abolishes neither the tremor response to penitrem A nor the cellular damage. No morphological changes are found in other brain regions. The affinities of penitrem A for high-conductance calcium-dependent potassium channels and for gamma-aminobutyric acid receptors with the probability of resultant excitotoxity are considered to be important underlying factors for these changes.
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PMID:The effects of the tremorgenic mycotoxin penitrem A on the rat cerebellum. 954 35

Haematological and serum biochemical measurements in male spontaneously epileptic rats (SER; double mutants homozygous for zitter and tremor genes) were compared with the values for related rat strains. Some haematological values were low in TRM rats and total leukocyte counts were high in ZI and TRM rats. TRM rats showed higher total cholesterol, phospholipid, high-density lipoprotein cholesterol and calcium values, and lower albumin value than Kyo: Wistar rats. Zitter homozygous rats including SER exhibited low total cholesterol, phospholipid and high-density lipoprotein cholesterol values. The SER showed an increase in urea nitrogen, aspartate aminotransferase and alanine aminotransferase values, and a decrease in glucose value, suggesting deterioration of the whole body with age.
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PMID:Haematological and serum biochemical values in spontaneously epileptic male rats and related rat strains. 958 5

Cow's, ewe's, and goat's milk samples were treated with carbon dioxide gas until a pH of 6.1 was reached and stored at 4 degrees C to determine the resulting modifications in the mineral balance. The amounts of calcium and phosphorus dissolved during the acidification were similar in the three species. The acidification with CO2 produced the dissolution of phosphorus and magnesium in concentrations similar to those attained by acidification with lactic acid or hydrochloric acid. Still, the contents of soluble calcium and ionic calcium were higher with the CO2 treatment. The increase of ionic calcium due to the addition of CO2 could explain why milk subjected to such treatment is better suited for coagulation. Removal of added CO2 by shaking the milk for several hours at atmospheric pressure resulted in a higher concentration of ionic-calcium than was found in control milks to which no CO2 had been added. Thus the addition of CO2 improved milk's technological suitability for cheesemaking.
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PMID:Salt balance and rennet clotting properties of cow's, ewe's, and goat's milks preserved with carbon dioxide. 970 55


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