Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0040822 (
tremor
)
18,428
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The investigational use of prostaglandins to establish a safe, alternative method for the termination of pregnancy has shown significant development in the United States. The introduction of second generation compounds was initiated by chemically attaching a methyl group in the 15 carbon position of prostaglandins E2 and F2alpha. These compounds prevented enzymatic degradation by the enzyme prostaglandin 15 dehydrogenase. (15S)-15 methyl prostaglandin E2 methyl ester administered by intramuscular injection has been used successfully to therapeutically terminate pregnancy in 208 women of gestational age six through 20 weeks. Side effects, not major and considered acceptable by the investigator, were vomiting, diarrhea and temperature elevations associated with
shaking
and chills. (15S)-15 methyl prostaglandin F2alpha (THAM), administered by intramuscular injection, has been used to terminate pregnancy in 283 women. Efficacy rates under optimal dosage regimens have reached 100% with a complete abortion rate of 96%. Gastrointestinal side effects of vomiting and diarrhea occurred, but temperature elevations with associated
shaking
and chills were infrequent. The mean time from initial therapy to abortion with both compounds has remained under 16 hours. A route of drug therapy for therapeutic termination of human pregnancy has been explored and developed which avoids invasion of the uterus.
J Reprod Med 1975
Sep
PMID:The termination of human pregnancy with prostaglandin analogs. 121 55
A 43-year-old man who presented parkinsonism due to pontine and extrapontine myelinolysis was reported. Late in February, 1990, the patient presented suffered from a flu-like illness and was seen at a community hospital. Physical finding showed the pigmentation on the whole body and hypotension, and laboratory examination revealed severe electrolyte imbalance (serum sodium 100 mEq/l, serum potassium 6.9 mEq/l, serum chloride 68 mEq/l) and hypoglycemia (postprandial serum glucose 78 mg/dl). Given these results, adrenal failure was strongly suspected. Prompt correction of electrocyte imbalance was performed by the infusion of sodium chloride, and four days later the serum sodium level reached 131 mEq/l. On the other hand, the patient was noticed lethargic and showed parkinsonism i.e., rest
tremor
, cog-wheel rigidity, and hypokinesia. Fourteen days after the onset of neurological abnormalities, the patient was referred to our hospital for further evaluation of parkinsonism. Additionally, neurological examination revealed dysphagia, mutism and positive pyramidal tract sign. On admission brain computed tomography was unremarkable, but on the 14th hospital day it showed low density area in the pons. Brain magnetic resonance imaging also showed a striking increase in T2-weighted signal from the pons, the midbrain, and the bilateral thalamus. Based on these findings, a diagnosis of parkinsonism due to pontine and extrapontine myelinolysis was made, and levodopa therapy was started. After the initiation of levodopa therapy, improvement of
tremor
, rigidity, and hypokinesia ensued with marked functional benefit, and the patient was discharged on the 49th hospital day. Levodopa was stopped three weeks after discharge but, all neurological abnormalities were not recurrent.(ABSTRACT TRUNCATED AT 250 WORDS)
Rinsho Shinkeigaku 1992
Sep
PMID:[A case of parkinsonism due to pontine and extrapontine myelinolysis]. 130 Feb 56
We reported a 49-year-old mother and her 28-year-old son with autosomal dominantly inherited bulbar spinal muscular atrophy (AD-BSMA). They showed progressive bulbar paresis, muscle wasting and weakness dominant in the proximal groups of limb muscles, and finger
tremor
. Onset of illness was in adult life. In laboratory examinations, elevated creatine kinase in serum and neurogenic changes either in EMG or muscle biopsy were noted. The son had neither gynecomastia nor abnormal sexual hormone levels which were observed in the sex-linked recessive bulbar spinal muscular atrophy (SR-BSMA). Elongation due to the CAG repeats at the androgen receptor gene of the X chromosome in SR-BSMA was not detected. In conclusion, it is clear that AD-BSMA is different from SR-BSMA on the basis of clinical and genetical aspects.
Rinsho Shinkeigaku 1992
Sep
PMID:[A mother and her son with autosomal dominant bulbar spinal muscular atrophy]. 130 Feb 63
The neural mechanisms underlying the high pressure neurologic syndrome (HPNS), which limit man's safe advance to extreme diving depths, are still unclear. This work was aimed at a better understanding of HPNS through study of brainstem auditory-evoked potentials (BAEP). BAEP were repeatedly recorded within 2 experimental chamber dives, Titan VIII (2 divers, maximum depth of 560 msw, compression time to bottom 109 h) and Titan XI (3 divers, maximum depth of 615 msw, compression time to bottom 240 h). Prolongation of the IV/V-complex occurred in 2 divers upon reaching 525 msw during Titan VIII compression and was accompanied by vestibular disturbances and amplitude increases of finger
tremor
. Both categories of changes--clinical signs and IV/V delay--gradually diminished during a 4-day stay at 545 msw, suggesting that they depended on excessive compression rates and insufficient acclimation time. Longer holding times at intermittent depths during Titan XI clearly reduced both HPNS symptoms and magnitude of prolongation of IV/V latencies. Wave I and wave III latency did not significantly change, pointing to a suppression of pontomesencephalic transmission. We infer that pressure suppresses synaptic transmission or triggers an increase of cortical or subcortical efferent inhibitory modulation of upper pontine and midbrain auditory afferents. Postdive controls revealed no persistent changes of BAEP measures in either the Titan VIII or XI divers.
Undersea Biomed Res 1992
Sep
PMID:Human brainstem auditory-evoked potentials in deep experimental diving to pressures up to 62.5 bar. 135 11
Because of the number of different types of anti-Parkinsonian medications, a number of options in the treatment of PD are now available. Each patient's medication regimen should be individualized. Many of the medication choices are made based on the stage of the disease. For patients who have newly diagnosed PD, and who are on no medications, treatment with deprenyl should be strongly considered. While some controversy remains concerning its possible slowing of the rate of disease progression, there is no evidence to suggest that its use is detrimental. It is generally well tolerated in patients with early disease. These factors must be weighed against the cost of the medication, and the fact that little if any therapeutic effect is seen in most patients who are not being treated with LD. A useful analogy when considering this issue is the prophylactic use of aspirin for cerebrovascular or cardiovascular disease. Newly diagnosed patients requiring treatment, who have
tremor
as their only symptom or their most prominent symptom, may be given an anticholinergic medication. Patients who have significant bradykinesia, rigidity or gait disturbance can be given amantadine. A combination of these two medications may be useful, and a combination of deprenyl with an anticholinergic drug or amantadine may provide excellent relief of early symptoms. At some point, most patients' symptoms progress such that treatment with LD is considered. Given its possible, but unproven, acceleration of the rate of disease progression, this decision should be weighed carefully. In a relatively young patient who may be treated for many years, a dopamine receptor agonist can be initiated without LD therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
Compr Ther 1992
Sep
PMID:Recent progress in the treatment of Parkinson's disease. 135
The involvement of the excitatory neurotransmitter system in the lateral habenula and pedunculopontine nucleus in the initiation and propagation of limbic seizures induced by pilocarpine has been investigated in the rat. Limbic seizures occur in animals following bilateral microinjection into the lateral habenula of N-methyl-D-aspartate (NMDA) (5 and 12.5 nmol) or kainate (100 and 200 pmol), 15 min prior to a subconvulsant dose of pilocarpine (150 mg/kg, i.p.). In the absence of pilocarpine NMDA (5 and 12.5 nmol) or kainate (100 and 200 pmol), injected focally into the lateral habenula or pedunculopontine nucleus, produced sniffing, grooming and
tremor
but no electrographic or behavioural seizures. Limbic seizures also occur after a subconvulsant dose of pilocarpine when it is preceded by injection of NMDA (5 and 12.5 nmol) or kainate (50, 100 and 200 pmol) into the pedunculopontine nucleus. Behavioural and electrographic signs of limbic seizures following pilocarpine (380 mg/kg, i.p.) were attenuated or completely antagonized by focal injection into the lateral habenula of the NMDA antagonist, 2-amino-7-phosphonoheptanoate (AP7) (10 and 50 pmol) or kainate antagonist, gamma-D-glutamylaminomethylsulphonate (GAMS) (20 nmol). In addition, AP7 (0.05, 0.1 and 1.0 nmol) or GAMS (40 nmol) injected into the pedunculopontine nucleus suppressed limbic seizures induced by i.p. administration of pilocarpine (380 mg/kg). The relative efficacy of NMDA and non-NMDA receptor antagonists revealed that the selective NMDA antagonist, AP7, was more potent in its anticonvulsant activity in comparison to GAMS, a non-NMDA receptor antagonist.
Brain Res 1992
Sep
25
PMID:Excitatory neurotransmitters in the lateral habenula and pedunculopontine nucleus of rat modulate limbic seizures induced by pilocarpine. 135 21
An incubator/shaker device proved to be a convenient alternative to a waterbath for the incubation of enzyme immunoassays (EIA). The device achieved effective and even heat transfer. In two of five EIAs it increased reactivity and in three of five EIAs it slightly increased the discrimination between seronegative and seropositive specimens though, for the samples investigated, extra sensitivity was not thereby achieved. At a high
shaking
frequency (1400 rpm) there was cross-contamination between wells, but this did not occur at 900 rpm. The relative contributions of heating and of
shaking
to the incubation of EIAs deserve further investigation.
J Virol Methods 1992
Sep
PMID:Is the IEMA combined incubator/shaker device preferable to a waterbath for incubating enzyme immunoassays? 143 64
In this report, we described a case of acute lymphoblastic leukemia with leukoencephalopathy that responded to oxygenation under hyperbaric pressure (OHP) therapy. The patient was 6 year-old female who was diagnosed as acute lymphoblastic leukemia (ALL) one year and 9 months earlier. After the first relapse of the central nervous system (CNS) leukemia, intrathecal administration of methotrexate (MTX) and skull irradiation induced CNS remission. The patient was readmitted because of second CNS relapse. After the third administration of weekly intrathecal MTX injection, apathy and finger
tremor
were observed. Her conscious disturbance continued for two weeks and magnetic resonance imaging (MRI) revealed abnormal findings in the white matter of her brain. Subsequently OHP therapy was commenced, and the conscious disturbance was improved gradually. One month later, neuro-disturbance resolved completely and the findings of MRI were improved. We could not find any case of leukoencephalopathy which was treated with OHP in the literature. But our case suggested that OHP therapy is valuable in patient with leukoencephalopathy in the early stage.
Rinsho Ketsueki 1992
Sep
PMID:[A case report of childhood acute lymphoblastic leukemia with leukoencephalopathy that responded to oxygenation under hyperbaric pressure therapy]. 143 44
We report a 72-year-old woman who showed marked orolingual dyskinesia and choreoathetoid movements of the neck, with rolling and nodding of the head. She had been treated for postural
tremor
and other complaints with multiple drugs, including trihexyphenidyl HCl (THP) 6 mg/day for about two years. Moreover, two months before admission to our hospital, a doctor added tricyclic antidepressant, dosulepin HCl (DL) because of her state of anxiety. Two weeks following DL administration, the persistent dyskinesia described above appeared. Suspecting the dyskinesia to be induced by anticholinergics, we withdrew THP, which decreased the intensity of the dyskinesia. Then, when DL was ceased the dyskinesia almost completely disappeared, slightly recurring only during calculating, when excited or writing. In order to confirm that anticholinergics were the cause of the dyskinesia, we administered THP 6 mg/day again. In a few days the same dyskinesia reappeared, disappearing following THP withdrawal. In this case the overlap of anticholinergics might have resulted in the dyskinesia, because both THP and DL have anticholinergic effects. It should be stressed that inappropriate administration of anticholinergics could cause severe dyskinesia in the elderly.
Nihon Ronen Igakkai Zasshi 1992
Sep
PMID:[A case of choreoathetoid movements induced by anticholinergic drugs, trihexyphenidyl HCl and dosulepin HCl]. 143 66
Tetrahydroaminoacridine (THA) and metrifonate are cholinesterase inhibitors used in the treatment of Alzheimer's disease. In experimental animals they inhibit acetylcholinesterase activity and have been reported to increase levels of brain acetylcholine. This paper presents results from studies of their effect at two dose levels on the dynamics of acetylcholine in mouse brain. Metrifonate at two doses (10 and 30 mg/kg intraperitoneally), known to cause cholinesterase inhibition, had no effect on levels of acetylcholine or choline or on the rate of synthesis of acetylcholine. THA (3 mg/kg intraperitoneally) had no effect on levels of acetylcholine and choline but had a shortlasting decreasing effect on the synthesis rate of acetylcholine. THA (10 mg/kg intraperitoneally) increased levels of acetylcholine and choline and markedly decreased the synthesis rate of acetylcholine. At this dose, the animals showed severe cholinergic effects, e.g.
tremor
and salivation. It is suggested that a moderate cholinesterase inhibition in brain facilitates cholinergic nerve transmission which is obtained at a broader dose range for metrifonate than for THA.
Pharmacol Toxicol 1992
Sep
PMID:Metrifonate and tacrine: a comparative study on their effect on acetylcholine dynamics in mouse brain. 143 50
<< Previous
1
2
3
4
5
6
7
8
9
10
Next >>