Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seven adult mares were used to determine the analgesic, CNS, and cardiopulmonary effects of detomidine hydrochloride solution after epidural or subarachnoid administration, using both regimens in random sequence. At least 1 week elapsed between experiments. A 17-gauge Huber point (Tuohy) directional needle was used to place a catheter with stylet into either the epidural space at the first coccygeal interspace or the subarachnoid space at the lumbosacral intervertebral junction. Catheters were advanced so that the tips lay at the caudal sacral (S5 to S4) epidural space or at the midsacral (S3 to S2) subarachnoid space. Position of the catheter was confirmed radiographically. A 1% solution of detomidine HCl was injected into the epidural catheter at a dosage of 60 micrograms/kg of body weight, and was expanded to a 10-ml volume with sterile water to induce selective caudal epidural analgesia (CEA). A dose of 30 micrograms of detomidine HCl/kg expanded to a 3-ml volume with spinal fluid was injected into the subarachnoid catheter to induce caudal subarachnoid analgesia (CSA). Analgesia was determined by lack of sensory perception to electrical stimulation (avoidance threshold > 40 V, 0.5-ms duration) at the perineal dermatomes and no response to superficial and deep muscular pinprick stimulation at the pelvic limb and lumbar and thoracic dermatomes. Maximal CEA and CSA extended from the coccyx to spinal cord segments T15 and T14 at 10 to 25 minutes after epidural and subarachnoid drug administrations in 2 mares. Analgesia at the perineal area lasted longer after epidural than after subarachnoid administration (142.8 +/- 28.8 minutes vs 127.1 +/- 27.7 minutes). All mares remained standing. Both CEA and CSA induced marked sedation, moderate ataxia, minimal cardiopulmonary depression, increased frequency of second-degree atrioventricular heart block, and renal diuresis. All treatments resulted in significantly (P < 0.05) decreased heart rate, respiratory rate, systemic arterial blood pressure, PCV, and plasma total solids concentration. To the contrary, arterial carbon dioxide tension, plasma bicarbonate, and standard base excess concentrations were significantly (P < 0.05) increased. Arterial oxygen tension, pH, and rectal temperature did not change significantly from baseline values. Results indicate that use of detomidine for CEA and CSA in mares probably induces local spinal and CNS effects, marked sedation, moderate ataxia, mild cardiopulmonary depression, and renal diuresis.
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PMID:Caudal analgesia induced by epidural or subarachnoid administration of detomidine hydrochloride solution in mares. 806 16

We studied cerebral blood flow, oxygen metabolism and their relation to clinical symptoms in 45 patients with spinocerebellar degeneration (SCD) and 12 normal control subjects using positron emission tomography (PET). Regions of interest were acquired for the cerebellar hemispheres, cerebellar vermis, brainstem, thalami, and cerebral cortices. PET studies in these patients revealed that regional cerebral blood flow (CBF), regional cerebral oxygen metabolic rate (CMRO2), CBF/mean CBF of each cerebral cortex (CBF/mCBF) and CMRO2/mean CMRO2 of each cerebral cortex (CMRO2/mCMRO2) in the cerebellar hemispheres, cerebellar vermis, and brainstem showed a significant decrease in comparison with the normal control subjects, while in the cerebral cortices and thalami, SCD patients showed normal values. CBF/mCBF and CMRO2/mCMRO2 were significantly decreased in patients with olivopontocerebellar atrophy (OPCA) and Menzel type of hereditary ataxia (Menzel type) in the cerebellar hemispheres, cerebellar vermis, and brainstem, whereas patients with late cortical cerebellar atrophy (LCCA) and Holmes type of hereditary ataxia (Holmes type) revealed a significant decrease of CBF/mCBF and CMRO2/mCMRO2 in the cerebellar hemispheres and cerebellar vermis, but not in the brainstem. Patients with OPCA showed a significant decrease of CBF in the cerebellar hemispheres, cerebellar vermis, brainstem and that of CMRO2 in the cerebellar hemispheres and cerebellar vermis. Patients with LCCA showed a significant decrease of CBF in the right cerebellar hemisphere and cerebellar vermis. However, a significant reduction of CBF and CMRO2 was not observed in patients with Menzel type or Holmes type in these regions. In patients with LCCA and Holmes type, the severity of upper limb ataxia and dysdiadochokinesis were significantly correlated with CBF/mCBF and CMRO2/mCMRO2 in the cerebellar hemispheres and brainstem.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Study of patients with spinocerebellar degeneration using positron emission tomography]. 829 3

Romifidine, 100 micrograms/kg administered by intravenous injection, was evaluated as a premedicant to ketamine/halothane anaesthesia in 60 horses. Sedation developed within one to two minutes. In three cases mild staggering occurred within two minutes. Anaesthesia was induced after five minutes by the intravenous administration of ketamine (2 to 2.2 mg/kg). A mean time of 79 seconds elapsed before lateral recumbency was adopted. Fifty-four of the horses sank smoothly to the floor, with occasional steps sideways. Jaw tone, limb rigidity and mild muscle tremors often persisted for short periods after induction. Complete relaxation was achieved on average two minutes after the administration of ketamine. The transition to oxygen/halothane anaesthesia was excellent or good in 53 cases. The mean duration of anaesthesia was 79 minutes. Forty-seven of the horses were able to stand after one or two attempts with little or no ataxia. After halothane administration ceased, the mean time to sternal recumbency was 25 minutes and the mean time to standing was 33 minutes. Most horses appeared to be sedated upon standing, but they were able to walk soon after regaining their feet. The characteristics of the induction of anaesthesia were similar to those seen when detomidine/ketamine or xylazine/ketamine are used. The maintenance of anaesthesia with halothane was similar to that following other induction protocols, and the recovery from anaesthesia was smooth and free from excitement.
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PMID:Clinical evaluation of romifidine/ketamine/halothane anaesthesia in horses. 833 99

We studied cerebral oxygen and glucose metabolism as well as cerebral blood flow using positron emission tomography (PET) in a case with MELAS showing dementia, diabetes mellitus, ataxia and lactic acidosis without any signs of stroke. This case, confirmed to have a point mutation at position 3243 in the transfer RNA gene of mitochondrial DNA, developed a stroke-like episode 8 months after the PET study. Uncoupling was observed between cerebral oxygen metabolism and cerebral blood flow with reduced fractional oxygen extraction ratio, indicating "hyperemia", not ischemia. The "hyperemia" may be closely related to the malfunction of mitochondria in aerobic energy production. A drastic decrease in cerebral oxygen metabolism (CMRO2) was found globally in contrast to preserved cerebral glucose metabolism (CMRglu), resulting in a remarkable decrease in the metabolic ratio (CMRO2/CMRglu). The dissociation between cerebral glucose and oxygen metabolism may be characteristic of MELAS.
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PMID:Cerebral metabolism of oxygen and glucose in a patient with MELAS syndrome. 875 Jan 17

Two cases (case 1, a 45-year-old man; case 2, a 68-year-old man) of superficial siderosis of the central nervous system are presented. Main neurological symptoms were anosmia, sensorineural deafness, dysarthria, ataxia, and pyramidal tract signs. Lumbar puncture revealed bloody cerebrospinal fluid (CSF) in both cases. In case 1, the CSF became watery clear after administration of hemostatic medicines. T2-weighted magnetic resonance images showed cerebellar atrophy and marginal hypointensity of the brainstem, cerebellum, and the entire spinal cord. T2-weighted images of the cranial nerves showed hypointensity of the VIII nerves which were clinically impaired as compared with normointensity of the VII nerves which presented no clinical symptom. These findings may reflect difference in the degree of hemosiderin depostion between the VII and VIII nerves. While case 1 had a borderline score of WAIS-R (IQ79), case 2 showed overt dementia (performance IQ65). Positron emission tomography showed that cerebral blood flow and cerebral oxygen metabolism were reduced in the basal temporal lobes in both cases.
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PMID:[Two cases of superficial siderosis of the central nervous system. Findings of the cerebrospinal fluid, magnetic resonance imaging and positron emission tomography]. 882 97

Genetic programs and age-dependent changes in DNA and protein are involved in aging. The genetic program governs body weight, longevity, aging rate, sex-maturating period and metabolic rate in mammals, and such a number of life history variables are highly correlated with body size. Monogenic age-1 and daf-2 C. elegans mutants extend life span twice. However, human monogenic progeroids shorten lifespan. The Werner syndrome gene was mapped in 8p12. Mutations in the Cockayne syndrome genes (the CSA and CSB genes acting for preferential repair of active genes by interacting with transcription factor TFIIH) and in the ataxia telangictasia gene ATM (homologous with PI-3 kinase for signal transduction) have been disclosed. All such findings suggest a strong basis for the genetic program of aging. In addition, recent evidence indicates that genetic instability, such as telomere loss, somatic and mitochondrial DNA mutations, increases with age. In addition, amounts of carbonylated protein also increase during human aging, and greatly increase in an SOD-deficient C. elegans mutant, but to a less extent in long-living age-1. Therefore, the aging process involves gene action, genetic instability and protein oxidation. Dietary restriction and elimination of deleterious excessive reactive oxygen species may improve many abnormalities due to aging.
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PMID:[The mechanisms of aging and perspective for elimination of deleterious effects]. 889 Jun 1

In 10 patients (five females) suffering from multiple sclerosis with mild degree of disability, (EDSS ranging from 0 to 2) and in 10 age and sex matched control subjects we investigated lung function, respiratory muscles strength and cardiorespiratory response to incremental exercise in order to assess the metabolic cost of exercise. In the absence of any impairment of lung volumes and flows and in- and expiratory maximal mouth pressures, at peak of exercise oxygen consumption (VO2max = 1886 +/- 145 ml/min) and workload (Wmax = 137 +/- 9.8 watts) were slightly diminished in patients, as compared with controls (VO2max = 2246 +/- 196 ml/min and Wmax = 164 +/- 14.7 watts). These findings were associated with an increased heart rate (HR) and reduced oxygen pulse (VO2/HR) at the same workloads. During the whole exercise, however, the slope of the linear relationship between VO2 and work exhibited by the patients, amounting to 9.9 +/- 0.6 ml/min/watt, was similar to that of the controls (10.9 +/- 0.42 ml/min/watt). Incidentally, both at rest and during exercise, the patients showed a significantly greater minute ventilation (VE) due to a faster respiratory rate, associated with an augmented dead space (P < 0.05). We conclude that an increase of metabolic cost of exercise does not occur in multiple sclerosis patients with mild disability, suggesting a lack or a low degree of spasticity and/or ataxia elicited by the effort. Thus, their exertional capacity appears to be limited mainly by a poor training. The tachypnea observed in these patients at rest and during exercise was unexpected and the reason for adopting such a pattern of breathing is unclear.
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PMID:Energy cost of exercise in multiple sclerosis patients with low degree of disability. 934 81

We report a 65-year-old woman with paraneoplastic cerebellar degeneration (PCD) who showed reduced cerebellar metabolism with preserved blood flow. She was admitted to Gunma University Hospital because of progressive gait and speech disturbances. Neurologic examination revealed nystagmus, dysphagia, explosive speech, reduced muscle tone in limbs, and marked truncal and limb ataxia, and mild hypesthesia in hands and feet. Cranial MRI demonstrated slight cerebellar atrophy. Laboratory findings disclosed high levels of serum CA19-9 and other tumor markers, and positive anti-Yo antibody, indicating that she had PCD. A specimen obtained from an axillary lymph node revealed metastasis of poorly differentiated adenocarcinoma, although systemic and vigorous checkup failed to find its origin. Cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) were measured using positron emission tomography (PET) 15 months after the onset. CMRO2 was clearly decreased in the cerebellum, while CBF was almost normal. Moreover, PET with 2 18F-fluoro-2-deoxy-D-glucose (FDG) revealed that glucose metabolism was also reduced in the cerebellum. Single photon emission tomography using 99mTc-ethyl cysteinate dimer (ECD) showed a normal blood flow pattern in the whole brain. These results indicated that uncoupling of circulation and metabolism in the cerebellum of this patient. There are several reports showing uncoupling of cerebral perfusion and metabolism in ischemic disorders, encephalitis, mitochondrial diseases, brain tumors, epilepsy and Gaucher disease, although its pathophysiology is not elucidated. Because anti-Yo antibody evidently gives a suppressive influence on the cerebellar neurons, understanding the way the autoantibody acts may give a clue to the mechanism of reduced cerebellar metabolism with preserved perfusion in PCD.
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PMID:[Uncoupling of cerebellar blood flow and metabolism in paraneoplastic cerebellar degeneration: report of a case]. 936 81

Ataxia due to prolonged vitamin E (RRR-alpha-tocopherol) deficiency still remains the only human neurodegenerative disorder that can be positively attributed to insufficient levels of an essential antioxidant. In affected nerve cells during vitamin E deficiency there is an increase in peroxidation of mitochondrial membranes and a progressive reduction in respiration-dependent axonal transport processes, ultimately resulting in cell death. The possibility of inhibition of electron transport and the increased generation of oxygen radicals that may arise due to prolonged exposure to the toxic nitric oxide radical within mitochondria of vitamin E-deficient neurones is discussed as a pathway to nerve cell death that is characteristically seen in the syndrome.
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PMID:The possible role of nitric oxide and impaired mitochondrial function in ataxia due to severe vitamin E deficiency. 969 Jul 73

Ionizing radiation activates not only signalling pathways in the nucleus as a result of DNA damage, but also signalling pathways initiated at the level of the plasma membrane. Proteins involved in DNA damage recognition include poly(ADP ribose) polymerase (PARP), DNA-dependent protein kinase, p53 and ataxia- telangiectasia mutated (ATM). Many of these proteins are inactivated by caspases during the execution phase of apoptosis. Signalling pathways outside the nucleus involve tyrosine kinases such as stress-activated protein kinase (SAPK)/c-Jun N-terminal kinase (JNK), protein kinase C, ceramide and reactive oxygen species. Recent evidence shows that tumour cells resistant to ionizing radiation-induced apoptosis have defective ceramide signalling. How these signalling pathways converge to activate the caspases is presently unknown, although in some cell types a role for calpain has been suggested.
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PMID:Molecular mechanisms of ionizing radiation-induced apoptosis. 1036 Dec 59


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