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)

Water intoxication is considered to be one of the possible causes of haemoglobinuria in calves. As to predisposing factors, prognosis and particularly differential diagnosis, uncertainty is rather frequent. Therefore we tried to provoke this state in an experiment, in which the disiony-induced changes of the acid-base balance (pH, pCO2, HCO3, pO2, BE, SAT of venous blood) were determined in addition to clinical observations (general behaviour, respiratory and pulse rates, body temperatures) and blood analysis (red and white blood cells, PCV and haemoglobin). Experimental paroxysmal haemoglobinuria was induced in eight 2-months-old male calves of the Black Pied breed weighing 55-70 kg that were held on a green diet. After the animals had been given cold water (12-14 degrees C) at an amount of 12% of their body weight, increased volume of the abdominal cavity, muscle tremor, and a stooping posture could be seen, and in 45-60 min. following water administration the first spontaneous haemoglobinuria occurred. Except the first 20 minutes following water gavage, when pronounced tachycardia accompanied by arythmia (100-130 per min.) was recorded, a tendency towards hypothermy, mild bradycardia and bradypnoe was observed; correction of these values occurred within 24 hours. Haematological indices revealed a hydraemic trend that was most pronounced and long-lasting in haemoglobin. Twenty-four hours after water gavage haemoglobin, red blood cells and PCV values were still below their starting levels; the tendency toward leucopoenia changed into leucocytosis. The acid-base balance revealed a slight acidemic trend with decreasing pH, actual bicarbonate and BE levels in the first hour; later, equilibration and increase within the physiological range occurred.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Paroxysmal hemoglobinuria in calves and its effect on hematologic and acid-base profiles]. 823 28

459 microstimulations were done in 10 patients with tremor. The motor evoked response with reduction tremor drive was observed at 38 sites, of which 30 (79%) were noted in ventrointermedialis (vim) nuclei, and 5 (13.2%) in ventrocaudalis (vc) nuclei, 2 in ventroralis posterior (vop) nuclei, 1 in dorsal thalamus (dth). No increased tremor drive response was noted in all the sites. Paresthesia was the most common response (47.1%). Except pain at 1 site in vc nuclei, warm/cold and vertigo were noted in vop, vim, vc nuclei. No responses accounted for 43.8%.
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PMID:Effective response evoked by microstimulation of thalamus nuclei in patients with tremor. 840 81

We report a 75-year-old man with parkinsonism who died suddenly. The patient was well until 64 years of the age when he had an onset of tremor in his left hand. He was treated with a medicine in another hospital, and his tremor subsided. Five years after the onset, he started to note difficulty in fine finger movements and gait disturbance. He tended to lean backward with frequent falls. He was treated with bromocriptine, trihexyphenydil, and L-dops without apparent improvement. He visited our out patient clinic on November 11, 1993 when he was 75 years of the age. Neurologic examination at that time revealed an alert and well oriented man in no acute distress. Higher cerebral functions were intact. In the cranial nerves, he showed restriction in the upward as well as down ward gaze (40% of normal). He showed masking of the face and spoke in small voice. He walked in a stooped posture with small steps; retropulsion was present. Muscle rigidity was moderately positive in the neck, however, no rigidity was noted in the limbs. No abnormal involuntary movements were seen. He showed moderate bradykinesia and difficulty in finger tapping. Muscle stretch reflexes were normally elicited and the plantar response was flexor bilaterally. Sensation was intact. The autonomic nervous system appeared intact. He was treated with 300 mg/day of Sinemet with marginal improvement in his balance. In February 4, 1994, he had a common cold. On the next day, his parkinsonism worsened and he became unable to walk by himself. He was found unconscious in the bathroom on the same day. He was brought to our hospital by an ambulance. Upon arrival, he was unresponsive and was not breathing. Blood pressure could not be measured. Pupils were dilated without reaction to light. Cardiac resuscitation was attempted, however, ventricular fibrillation appeared on an EEG monitor, and he was pronounced dead at eleven o'clock in the morning. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that the patient had progressive supranuclear palsy because of vertical gaze palsy, axial rigidity, and poor response to levodopa. Regarding the cause of his sudden death, the chief discussant thought that he developed pulmonary embolism. Postmortem examination revealed non-bacterial thrombotic endocarditis in the heart, but this did not appeared to be related to his sudden death. Multiple disseminated small emboli were found occluding small arteries of the left lung; this was consistent with acute pulmonary embolism, and this was thought to be the cause of his sudden death. In the central nervous system, marked atrophy of the globus pallidus was noted; both internal as well as external segments showed marked atrophy; no myelinated fibers were seen in the globus pallidus. Neuronal cell loss was marked in the globus pallidus, the subthalamic nucleus, and the substantia nigra. No Lewy bodies or tangles were seen. The histologic diagnosis was consistent with pallido-nigro-luysian atrophy. Brownish pigments such as seen in Hallervorden-Spatz disease were seen in the globus pallidus. In addition, formy spheroids were seen in the substantia nigra. However, iron deposits were not so strong as to suggest Hallervorden-Spatz disease. Pallido-nigro-luysian atrophy is a rare neurodegenerative disorder. It is interesting to note that this condition may mimic progressive supranuclear palsy or pure akinesia clinically.
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PMID:[A 75-year-old man with parkinsonism and sudden death]. 853 59

Various diseases often occur after delivery but the systemic examinations have not been studied before. Thyroid dysfunction frequently (4.4%) occurs after delivery through an immune rebound mechanism. If postpartum women complain of the symptoms caused by thyrotoxicosis (palpitation, weight loss, increased sweating, finger tremor, fatigue) or hypothyroidism (edema, cold intolerance, hoarseness, sleepiness, fatigue), it is essential to examine thyroid hormones, thyroid stimulating hormone, anti-thyroid microsomal antibody (MCHA) and anti-TSH receptor antibody. To predict who will develop postpartum thyroid dysfunction, the measurement of MCHA during pregnancy is useful because 62% of the subjects with positive MCHA show thyroid dysfunction after delivery. The individuals at high risk of postpartum onset of Graves' thyrotoxicosis can be found early in their pregnancy by the detection of thyroid stimulating antibody (TSAb). Other autoimmune diseases, such as rheumatoid arthritis, systemic lupus erythematosus, autoimmune hypophysitis and so on, also could develop after delivery. These findings indicate that laboratory tests in the postpartum period are essential to diagnose postpartum onset of autoimmune diseases and the measurement of autoantibodies in early pregnancy is useful for prediction of their onset in the postpartum period.
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PMID:[Postgravid health care and laboratory tests]. 855 72

Ninety children with acute asthma, equally divided into two study groups, were studied to compare the efficacy and safety of nebulized terbutaline with injected epinephrine in the treatment of acute exacerbation. The terbutaline group received 2 ml (5,0 mg) terbutaline solution diluted with 2 ml 0.9% saline for inhalation over 10 minutes; the epinephrine group received 0.01 ml/kg of 1:1000 epinephrine (maximum 0,3 ml) through subcutaneous injection at deltoid area. Spirometry, pulse oximetry, and clinical severity scoring system were evaluated at baseline and again 15 minutes after treatment. The baseline data of the two groups were not significantly different. The clinical severity score and spirometry of both groups were significantly improved after treatment. Compared with the terbutaline group, the epinephrine group had better mean oxygen saturation (SaO2; p < 0.001), frequency of oxygen desaturation (p = 0.0028) and forced expiratory flow 25-75% (FEF25-75%, p = 0.027). For those patients with initial forced expiratory volume in one second (FEV1) lower than 60% of predicted value, epinephrine treatment was more effective in the improvement of FEV1, FEF25-75%, and oxygen saturation (SaO2) (p = 0.011, 0.012, and 0.006, respectively). A Significantly higher rate of adverse effects occurred in patients given epinephrine (47% vs 11%, p = 0.0002); these included pallor, tremor, dizziness, headache, palpitation, soreness of legs, numbness of extremities, cold sweating, general weakness and nausea. Considering the general trend to noninvasive therapy in children and the more frequent adverse effects after epinephrine injection, such nebulized beta-2 agonists as terbutaline appear preferable for initial therapy of acute asthma if oxygen is supplemented to prevent possible hypoxemia. However, parenteral epinephrine still is worth trying, particularly in any severe, life-threatening attack.
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PMID:Terbutaline nebulization and epinephrine injection in treating acute asthmatic children. 890 60

Cold shivering in six chronic spinal dogs (T9-10), which became capable of weight-bearing standing and/or walking with their hindlimbs, was studied by electromyography (EMG). In the forequarters, EMG activities in the form of grouping discharges (GD) accompanied by visible tremor (VT) were induced at an ambient temperature of 15 degrees C in all the dogs. In the hindquarters, GD with VT were induced at 3 degrees C in one dog. Although GD with VT were not induced in in the remaining dogs, GD without VT were produced by additional cutaneous stimuli to the hindquarters at 3 degrees C. These stimuli never produced GD in the hindquarters at room temperature. Though the mean frequency of GD in the hindquarters was lower than that in the forequarters, the range of the frequency in the hindquarters was much the same as that in the forequarters. During the experiment, the drop in rectal temperature was less than 0.6 degrees C in all of the dogs. These findings suggest that the chronically isolated spinal cord is responsible for cold shivering, while its excitability to cold exposure is less than that of the spinal cord governed by the supraspinal center.
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PMID:Electromyographic (EMG) study of cold shivering in the chronic spinal dog. 915 46

In order to quantify the tremorine and cold tremor activity in unanesthetized rats, a new ultrasonic motion transducer method was used. Both kinds of activity are reported as vibratory body motion that occurred between 18-32 Hz as determined by spectral analysis. The recorded signal was analyzed and its power spectrum was obtained through a fast Fourier transform operation. It was found that a negative linear relation occurs between shiver amplitude and ambient temperature (r = 0.999). A negative linear relation also occurs between metabolic rate and ambient temperature (r = 0.997). In addition, a positive linear relation between metabolic rate and cold shiver exists (r = 0.999). Both tremorine (30 mg/kg, i.p.) and cold tremor (Ta = 2-22 degrees C) activity monitored by the ultrasonic method were completely abolished by premedication with 1 mg/kg atropine. Thus, it appears that the advantages of this tremor detection method are that is non-invasive and non-contact. Therefore, the ultrasonic method provides a good choice for quantifying tremorine and cold tremor activity in unanesthetized animals during studies of thermoregulatory physiology or motor disorders.
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PMID:Ultrasonic analysis of tremorine and cold tremor activity in unanesthetized rats. 930 45

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

A 100-kDa protein was found to be a major cell wall protein in Saccharomyces cerevisiae cells cultured without shaking, but was not present in cells cultured with shaking. The amino acid sequence of this protein was identical to the sequence of Tir1p/Srp1p. TIR1/SRP1 has previously been identified as a gene induced by glucose, cold shock or anaerobiosis and was believed to be a cell membrane protein but not a cell wall protein. However, we found that beta-1,3-glucanase solubilized Tir1p/Srp1p from the cell wall and the purified Tir1p/Srp1p reacted with antiserum to beta-1,6-glucan and contained glucose. These results suggest that Tir1p/Srp1p is a major structural cell wall protein in the static-cultured yeast cells and is bound to the cell wall through beta-1,6-glucan. TIR1/SRP1 mRNA was transcribed only in the static culture and its transcription was regulated by the ROX1 repressor.
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PMID:Identification and analysis of a static culture-specific cell wall protein, Tir1p/Srp1p in Saccharomyces cerevisiae. 936 89

Simple cold storage of livers for transplantation activates glycolysis due to lack of oxygen. Energy derived from glycolysis may be critical for cell survival and liver cell death may occur once glycolysis is inhibited in the liver due to accumulation of end products or lack of substrates (glycogen). The relationship between cell death (lactate dehydrogenase, LDH release), anaerobic glycolysis (lactate production), and glycogen content of liver tissue was studied during cold incubation of liver slices in UW solution. Rat livers slices from male Sprague Dawley rats were incubated at 4 degrees C in UW solution, with continuous gentle shaking, under conditions of chemical hypoxia (KCN, 5 mM). The rate of lactate production, LDH release-ATP and glycogen content were measured spectrophotometrically and by HPLC. Lactate increased nearly linearly for the first 48 h of incubation; total lactate which had accumulated after 48 h was 33.9 +/- 0.81 mumol/g and at 96 h nearly the same, 31.3 +/- 1.2 mumol/g. Glycolysis stopped, apparently, because of the depletion of liver slice glycogen which was initially 228.8 +/- 1.7 mumol/g wet wt. It decreased to 34.7 +/- 2.7 mumol/g at 48 h and to 18.7 +/- 1.1 mumol/g at 72 h and remained at this level for the next 24 h. An increased leakage of LDH occurred once glycogen metabolism (and accumulation) ceased. LDH release could be stimulated after only a few hours of cold incubation of liver tissue slices by adding glycolysis inhibitor (iodoacetic acid) to the medium. After 24 h. LDH release was 24.4 +/- 1.8% and increased to 52.8 +/- 5.2% (P < 0.05, Student's t-text) with iodoacetic acid. Adding a glycolytic substrate (fructose, 10 mM) to the medium maintained lactate production for 96 h. The stimulation of glycolysis by fructose also reduced cell death: LDH release was significantly lower at 72- and 96-h incubation (P < 0.001, two-way ANOVA). The ATP content was significantly higher with fructose (P < 0.001). Adding glucose (20 mM) and fructose (10 mM) in combination resulted in prolonged cell survival, significantly delayed glycogen depletion and significantly higher ATP content at 48 and 72 h (two-way ANOVA). Livers from rats who had fasted for 24 h demonstrated the same LDH release at 48 h when incubated with glucose (20 mM) and fructose (10 mM). In conclusion, LDH leakage from hypoxic cold-stored liver slices is related to anaerobic glycolysis. Anaerobic glycolysis appears to continue slowly under hypothermia and provides sufficient energy for maintenance of cell viability. A stimulation of glycolysis in the cold is possible by fructose and results in prolonged cell survival under hypothermic conditions. Glycogen depletion can be slowed down by combining glucose and fructose.
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PMID:[Liver metabolism during cold ischemic incubation in UW solution in the rat model]. 949 7


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