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)

An assay has been developed and evaluated that quantifies the surface tension lowering ability of amniotic fluid surfactant. The formation of stable foam following vigorous shaking of amniotic fluid was evaluated by the addition of various amounts of dipalmitoyl lecithin in a solution of ethanol and saline and by fine adjustments of the ethanol volume fraction in the final assay mixture. The foam stability index (FSI) for a particular sample of amniotic fluid was defined as the highest ethanol volume fraction that would permit the formation of stable foam after vigorously shaking a mixture of ethanol and amniotic fluid. The assay is referred to as the FSI test. We report the FSI values in amniotic fluid specimens from 59 patients obtained within 72 hours of delivery. The L/S ratio was measured in 50 of the same 59 specimens. We observed 6 cases of neonatal hyaline membrane disease (HMD) and 2 cases of transient tachypnea of the newborn (TTNB) in this study. No cases of HMD or TTNB occurred with FSI values of greater than 0.47, while 2 cases of HMD were recorded in association with L/S ratios of 2.5 and 2.8, respectively. The potential clinical value of the FSI test is discussed.
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PMID:Assessing fetal lung maturation by the foam stability index test. 58 10

A boy aged 1.5 year with deficient weight and height, retardation of motor development, decreased muscle tonus, finger tremor and periodic tachypnoea without detectable respiratory system changes is presented. Gasometry demonstrated metabolic acidosis with respiratory alkalosis, high concentration of lactic acid in serum and cerebrospinal fluid, increasing metabolic acidosis after glucose load, and lack of hyperglycaemic response after alanine load, and cortical atrophy in CT. On the basis of these changes Leigh's disease was diagnosed.
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PMID:[Leigh disease in a 17-year-old boy]. 227 48

Clinical observations and results of investigations of pyruvic acid metabolism are reported in 4 children in whom subacute necrotizing encephalomyelopathy of Leigh was diagnosed intravitally. Attention is called to the similarity of the clinical manifestations with its onset in the first year of life, deficient body weight and growth, progressing neurological disturbances (weakening of muscle power, tremor, ataxia, nystagmus), course with periods of exacerbations, tachypnoea, skin changes (hirsutism, telangiectasia, perspiration), death at the age of 2-3 years. The biochemical changes in all children included raised serum levels of lactic acid, pyruvic acid and alanine, and acid-base equilibrium disturbances with metabolic acidosis (relatively balanced respiratory alkalosis). The results of the test of intravenous loading with glucose and alanine carried out in all children indicated indirectly reduced activity of pyruvate carboxylase. In one child histological examination of the brain carried out postmortem confirmed the diagnosis of Leigh's disease.
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PMID:[Suspected pyruvate carboxylase deficiency in 4 children with Leigh disease]. 309 72

The effect on behavior of eight anticholinergic agents: atropine, scopolamine, trihexyphenidyl, biperiden, homatropine, eucatropine, hexocyclium and propantheline, injected into the cerebral ventricle (ICV) of the cat was investigated and compared. The anticholinergic agents evoked: (1) psychomotor stimulation such as miaowing, loud calling, restlessness, impelling locomotion, jumping, vacant staring, apprehension and loss of interest of the surroundings; (2) aggression, hissing, threat, attack, defense, fighting with paws and flight; (3) autonomic responses including mydriasis, tachypnea, dyspnea, licking, vomiting, salivation, micturition and defection; and (4) motor phenomena comprising scratching, ataxia, rigidity, tremor, weakness with adynamia or myoclonic jerks. Convulsions appeared only after ICV injections of atropine and homatropine. The most characteristic behavioral effect of anticholinergic agents was psychomotor stimulation accompanied by mild aggressive responses. The only exception was propantheline which caused a muscular weakness and adynamia. Atropine and scopolamine alone induced a dose-dependent impelling locomotion as well as fighting behavior. Carbachol and eserine injected intracerebroventricularly reversed the locomotion autonomic and motor phenomena produced by anticholinergic agents administered similarly. It is suggested that anticholinergic agents acting as partial agonists, can produce their behavioral effects through central cholinoceptive sites.
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PMID:Comparative behavioral effects of anticholinergic agents in cats: psychomotor stimulation and aggression. 370 93

Cyclopiazonic acid (CPA) was found to have many pharmacological properties in common with the antipsychotic drugs chlorpromazine and reserpine. Thus, in mice CPA at ip doses of 5-14 mg/kg body weight produced hypokinesia, hypothermia, catalepsy, ptosis, sedation without loss of righting reflex, tremor, gait disturbance, dyspnoea, opisthotonus, atypical convulsion and prolonged barbiturate-induced sleep. The ip LD50 of CPA was found to be 13 +/- 0.05 mg/kg. The tremors induced by near-lethal doses of CPA were associated with voluntary or forced movements (action tremors); they worsened during the days following treatment, but they were weak compared with the exhausting and continuous tremors of the whole body caused by 20 mg tremorine/kg (used for comparison). When death occurred only 24-259 min after administration of CPA (11-14 mg/kg), it was preceded by dypsnoea, cyanosis, opisthotonus and clonic leg movements and tonic extension of hind legs (convulsions). When death was delayed (2-6 days after CPA administration), it was preceded by prostration, ptosis, hypothermia, tremor and cessation of food and water intake resulting in cachexia; convulsions were not seen in this group of mice. CPA did not affect the rate of convulsion or death caused by either maximal electroshock or metrazol administration but it did delay the onset of metrazol-induced seizures. In rabbits, 10 mg CPA/kg body weight initially produced tachycardia, tachypnoea and sedation with an activated electroencephalogram. Of three rabbits given 10 mg CPA/kg one died, and in this rabbit slow delta waves were seen just before and during a brief period with clonic leg movements. In this animal death was accompanied by tonic extension of the hind legs, respiratory arrest and cardiac fibrillation; and epileptiform EEG was not seen at any time. The unexpected EEG activation with sedation in rabbits treated with CPA was similar to the effect of reserpine on EEG.
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PMID:Toxicity and neuropharmacology of cyclopiazonic acid. 404 83

1. In unanaesthetized rabbits 5-hydroxytryptophan (5-HTP) and 5-hydroxytryptamine (5-HT) were injected into the cisterna magna or into the cannulated left lateral cerebral ventricle while rectal temperature was recorded.2. 5-HTP injected intracisternally in a dose of 1.5-3 mg produced a fall in temperature often followed by a rise beyond the pre-injection level. With 6 mg the main effect was a rise in temperature. The intraventricular injection of 1-2 mg 5-HTP usually produced a fall followed by a rise.3. 5-HT injected intracisternally in a dose of 0.2 mg produced a fall in temperature similar to that produced with this dose injected intraventricularly. Following an intracisternal injection of 1-4 mg 5-HT there was either a fall, or a fall followed by a rise, but in a few experiments the effect consisted mainly of a rise in temperature.4. Additional effects regularly observed with these injections were tachypnoea, ear twitching, rapid movements of the vibrissae, shaking of the head, wiping and scratching movements, ataxia, nodding and sideways movements of the head and long-lasting catalepsy.5. The sites where 5-HTP and 5-HT act when producing the temperature responses and the various behavioural effects are discussed.
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PMID:Temperature responses and other effects of 5-hydroxytryptophan and 5-hydroxytryptamine when acting from the liquor space in unanaesthetized rabbits. 530 31

The effects of ranitidine hydrochloride, a histamine H2-receptor antagonist, on the reproductivity of male and female rats of Crj:CD (SD) strain and the development of their fetuses were examined. Ranitidine hydrochloride was intravenously administered once daily at dose levels of 5, 15 and 40 mg/kg in base weight respectively, to males from 60 days before mating until the completion of mating, and to females from 14 days before mating up to day 7 of gestation. All pregnant females were killed on day 20 of gestation and their fetuses were examined morphologically. Tachypnea, prone position and transient tremor were observed for a short period of time directly after an intravenous administration of ranitidine in the dose of 40 mg/kg, which were probably induced by a rapid fall in blood pressure. There was a significant decrease in the weight of spleen in males of 15 and 40 mg/kg groups. Treatment with ranitidine hydrochloride did not have any influence on mating performances and pregnancy at all dose levels. In observation of the fetuses, there was no influence of ranitidine hydrochloride administration on fetal growth and development. A few external, skeletal and visceral malformations were seen sporadically in each group, and 19 cases of dwarf fetuses were observed in 2 dams of 40 mg/kg group, but these changes were not attributable to administration of the drug. These results indicated that ranitidine hydrochloride intravenously administered to males and females before mating and to pregnant females in early stages of gestation had no toxic effects on reproductivity in either sex at the dose of 40 mg/kg/day or less.
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PMID:[Effects of intravenous administration of ranitidine hydrochloride on the fertility of the male and female rats]. 609 56

The effects of ranitidine hydrochloride, a histamine H2-receptor antagonist, on development and general behavior of F1 generation of Crj: CD (SD) rats were examined. Ranitidine hydrochloride was intravenously administered once daily from day 7 to 17 of gestation at dose levels of 5, 15 and 40 mg/kg in base weight respectively. Two-thirds of females were killed on day 20 of gestation to examine the development of fetuses, the remaining females were allowed to litter naturally and the postnatal development of the offsprings was observed. Tachypnea, prone position and transient tremor were observed for approximately 15 from 30 seconds directly after an intravenous administration of ranitidine hydrochloride in the dose of 40 mg/kg, which were probably induced by a rapid fall in blood pressure. During the gestation period, there occurred a slight depression of the maternal body weight gain in the ranitidine-treated groups. At the stage of lactation, the body weights of dams showed slightly lower levels than control and their liver weights of dams were also inclined to decrease in 15 and 40 mg/kg groups. In the observation of the fetuses, there were no significant differences between the control and ranitidine-treated groups concerning fetal growth and development, external, skeletal and internal anomalies in fetuses. In delivery and postpartum observation, no influence of ranitidine administration was observed on the litter size, mortality rate of F1 pups. There was a tendency towards decrease in body weight in males of the ranitidine-treated groups. But no significant changes were observed in general behavior, postnatal development, various functions such as reflex response, learning and reproductive performances of F1 generation. Therefore, it was concluded that ranitidine hydrochloride had no effects on fetal and postnatal development, general behavior and various functions of F1 generation at the dose of 40 mg/kg/day or less.
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PMID:[Effects of intravenous administration of ranitidine hydrochloride to the pregnant rat in organogenesis period]. 609 57

The effects of ranitidine hydrochloride, a histamine H2-receptor antagonist, on delivery, lactation, postnatal development of F1 generation of Crj:CD (SD) rats were examined. Ranitidine hydrochloride was intravenously administered once daily from day 17 of gestation to day 21 after delivery at dose levels of 5, 15 and 40 mg/kg in base weight respectively. All females were allowed to litter naturally, and postnatal development of offsprings was observed. Tachypnea, prone position and transient tremor were observed for approximately one minute directly after an intravenous administration of ranitidine in the dose of 40 mg/kg, which were probably induced by a rapid fall in blood pressure. In delivery and postpartum observation, there occurred no influence of the ranitidine administration on maternal body weight, delivery and lactation. In studies on general behavior of F1 rats, no abnormal changes were observed on postnatal development and various functions such as reflex response and learning. Ranitidine treatment did not affect reproductive performances of F1 generation. A slight inhibition in body weight gain and a slight decrease in average weight of liver were observed in F1 females of 40 mg/kg group, but no other influence attributable to the ranitidine administration was observed on the general state and development of offsprings. In necropsy of offsprings, hydronephrosis, transitional epithelial carcinoma, kinky tail, unilateral absence of testis and epididymis were observed in one case of ranitidine-treated groups. But they were not attributable to administration of ranitidine. In summary, it was concluded that ranitidine hydrochloride had no effects on delivery and lactation of dams, and also on viability, development and various functions of F1 generation at the dose of 40 mg/kg/day or less.
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PMID:[Effects of intravenous administration of ranitidine hydrochloride to the female rat in perinatal and postnatal periods]. 609 58

Nifedipine and verapamil injected into the cerebral ventricles of unanaesthetized cats produced a longlasting rise in the body temperature. The hyperthermic effect of nifedipine and verapamil were not dose-dependent. The hyperthermic effect of verapamil was preceded by a shortlasting fall in the body temperature, which was not dose-dependent. Calcium antagonists, nifedipine and verapamil also produced mydriasis, tachypnoea, dyspnoea, ataxia, tremor and muscular weakness. These symptoms were inconsistent and of slight intensity. In agreement with the theory of ionic set point controlling the body temperature, the most probable explanation is that calcium antagonists, nifedipine and verapamil produced changes in the body temperature by acting on sodium and calcium fluxes in the posterior hypothalamus.
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PMID:[Effects of nifedipine and verapamil on body temperature in cats]. 624 Oct 13


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