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)

We have recently experienced a case of Vibrio vulnificus septicemia which occurred in a patient with hepatic cirrhosis, and as we were able to give early antibiotic treatment, the patient survived. We would like to report this case here together with another case experienced 2 years ago. Case 1 was a 58-year-old male who was attending our hospital as an outpatient for hepatic cirrhosis. At 5:30 pm on August 8, 1987, he consumed abalone and giant clam and at 9 pm complained of high fever with shaking chills. He was admitted to our department as an emergency case. Cefoperazone was administered resulting in a decline of fever on the following day. During the course of treatment he fell transiently into pre-DIC, but due mainly to the administration of antibiotics his condition was subsided. Case 2 was a 53-year-old male who was under medical care in our hospital for grave hepatic cirrhosis. On October 11, 1985, he consumed sushi and two days later suffered chills and pyrexia. A blood culture revealed Vibrio vulnificus. His condition improved transiently with administration of Cefazolin, but oliguria, hypotension and ascites occurred subsequently, and finally the patient died on the 22nd day.
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PMID:[Two case reports of septic shock due to Vibrio vulnificus with liver cirrhosis]. 250 32

A 63-year-old man was admitted to our hospital with tremor and somnolence, followed soon by coma. Anemia and retinal bleeding were observed. The blood smear exhibited rouleaux formation and leukoerythroblastosis. A bone marrow aspiration resulted in dry tap. The biopsy specimens revealed remarkable infiltration of myeloma cells with fibrosis. The M-component of IgG-lambda type and hyper-ammonemia were detected in the serum. Liver and renal functions, however, were within normal range. His consciousness recovered after plasmapheresis. Two courses of VMCP (vincristine, melphalan, carboquone and prednisolone) did not affect the paraproteinemia. Five courses of VAD (vincristine, adriamycin and dexamethasone) could lower the level of IgG. He died of pneumonia. The plasma of some patients with multiple myeloma may contain unidentified factors which increase the plasma ammonia.
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PMID:[Coma, hyperviscosity syndrome, hyperammonemia and myelofibrosis in a patient with IgG, lambda type multiple myeloma]. 250 73

An effective HPLC method for detecting deoxyribonucleoside triphosphates in hyphae from the fungus Neurospora crassa has been developed. In rapidly growing cells the nucleotide levels vary from 11.8 pmoles/micrograms DNA for dGTP to 24.2 pmoles/micrograms DNA for dTTP. These levels fall by approximately one half in stationary-phase cultures but the ratio of each pool to dGTP remains the same. The dNTP pools in conidia are at least 5-fold lower than in rapidly growing cells. The pool sizes are the same in static and shaking cultures. When the ribonucleotide reductase inhibitor, hydroxyurea (30 mM), is added to rapidly growing cultures, DNA synthesis is stopped and the dGTP pool is reduced by 39%, while the size of the other pools remains the same. In the presence of 11 mM histidine, DNA synthesis is also stopped and the size of the dGTP pool reduced by 46% while the deoxypyrimidine pools are somewhat increased. This suggests that the toxicity of excess histidine in Neurospora may be due to its ability to interact with the ribonucleotide reductase, inactivating the enzyme. Histidine may react with the free radical at the active site, as does hydroxyurea.
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PMID:Deoxyribonucleoside triphosphate pools in Neurospora crassa: effects of histidine and hydroxyurea. 296 78

A 9-year-old boy manifested acute cerebellar ataxia associated with mumps infection. He developed opsoclonus, myoclonus, tremor, and truncal ataxia 7 days after mumps infection. Lumbar puncture revealed pleocytosis without elevation of protein; ELISA demonstrated an increased IgM titer of cerebrospinal fluid against mumps virus. From these results it was determined that acute cerebellar ataxia was induced by a direct invasion of mumps virus. Electroencephalography demonstrated normal background activity, although alpha-like activity appeared bilaterally in the frontal regions which was induced by eye closure and decreased by eye opening. Polygraphic electroencephalography revealed that the alpha-like activity corresponded to the ocular movement recorded above or lateral to the eyelids by electro-oculography; therefore, the alpha-like activity was considered to be derived from the opsoclonus which was secondary to cerebellar involvement. His neurologic symptoms improved gradually and resolved completely within 3 months after the onset of acute cerebellar ataxia.
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PMID:Mumps-induced opsoclonus-myoclonus and ataxia. 324 24

Lipid chemical analysis of a case of membranous lipodystrophy (Nasu-Hakola disease) was reported. The case is a 43 yr-old man (at death). Onset of the disease was at his age of 10 when he had complained of leg pain. Since his age of 14, he had bone fractures of the lower extremities many times. At the age of 35, he was admitted to a hospital for the neurological examination. At that time, he showed exaggerated tendon reflexes and intension tremor of the upper extremities. He was euphoric and demented. His IQ was 31. Histological examination of biopsy specimen from the bone marrow revealed the typical membrano-cystic lesion. He had status epilepticus which was followed by comatous state for a week. The disease progressed gradually and he fell into decorticated state. He died at the age of 43. The total clinical course was 33 years. The brain weighed 680 g. Remarkable atrophy was observed in the whole brain. Loss of nerve cells in the upper layers of the cortex was marked. There were loss of myelin sheath and severe gliosis in the white matter. A part of the brain, liver and subcutaneous fat was frozen at the time of autopsy for the chemical examination. Quantitative determination of cholesterol, glycolipid, phospholipid, free fatty acid in the brain and liver, cholesterol, free fatty acid, triglyceride in the subcutaneous fat were carried out. Cholesterol was decreased about 33% in the cortex and 42% in the white matter in comparing with those of controls and the content of cerbroside in the white matter was about 1/3 of that of controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Lipid chemical study of an autopsy case of Nasu-Hakola disease]. 337 Jan 66

Wilson's disease is a multisystem disorder. Heart involvement in Wilson's disease, however, has rarely been recognized. A prospective study was undertaken of 53 consecutive patients (28 men and 25 women, mean age of 21.4 years) with Wilson's disease. Electrocardiographic abnormalities occurred in 18 of 53 patients (34 percent), including left ventricular hypertrophy, biventricular hypertrophy, early repolarization, ST depression and T inversion, premature atrial or ventricular contractions, atrial fibrillation, sino-atrial block, Mobitz type 1 atrioventricular block, and tremor artifact. In contrast, 26 medical students and 14 carriers of Wilson's disease as control subjects (mean age of 22.6 years) all showed normal ECG. Eight out of 43 patients (19 percent) demonstrated asymptomatic orthostatic hypotension. An abnormal response to the Valsalva maneuver occurred in six of 18 patients (33 percent). There were two cardiac deaths; one died of repeated ventricular fibrillation (the copper content in the myocardium was 2.28 micrograms/g, and in the bundle of His 1.21 micrograms/g wet weight in the autopsy specimen); and the other, of dilated cardiomyopathy. It is concluded that four modes of cardiac manifestations in Wilson's disease include arrhythmias, cardiomyopathy, cardiac death, and autonomic dysfunction. Such possible cardiac involvement should be added to the clinical picture of Wilson's disease involving the hepatic and central nervous system.
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PMID:Cardiac Wilson's disease. 382 52

To develop an efficient method for the production of urocanic acid, optimal conditions for the production of microbial L-histidine ammonia lyase and for the conversion of L-histidine to urocanic acid by this enzyme were studied. A number of microorganisms were screened to test their ability to form and accumulate urocanic acid from L-histidine. Achromobacter liquidum was selected as the best organism. With this organism, enzyme activity as high as 2.0 units/ml could be produced by a shaking culture at 30 C in a medium containing glucose, urea, potassium phosphate, L-histidine, yeast extract, peptone, and inorganic salts. Appropriate addition of a surface-active agent to the reaction mixture shortened the time required for the conversion. A large amount of L-histidine was converted stoichiometrically to urocanic acid in 48 h at 40 C. Accumulated urocanic acid was readily isolated in pure form by ordinary procedures with isoelectric precipitation. Yields of isolated urocanic acid of over 92% from L-histidine were easily attainable. When the culture of Achromobacter liquidum was added to DL-histidine, D-histidine and urocanic acid were simultaneously obtained in high yields.
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PMID:Enzymatic production of urocanic acid by Achromobacter liquidum. 415 Nov 17

The patient was a 59-year-old man who had been in hospital suffering from aplastic anemia with transfusion hemosiderosis. Sudden onset of weakness, shaking chills and headache was observed after his staying out overnight on July 25, 1981. His temperature was 39.3 degrees C and he complained of abdominal pain and abdominal distension. His blood pressure dropped to a dangerous level and tonic convulsions that had begun in the upper body gradually extended to the whole body and he died 23 hours after his return. V. vulnificus was isolated by the blood culture performed before death. During his stay away from the hospital, he had eaten raw cuttlefish, which was considered to be the source of infection. V. vulnificus is one of the halophilic marine vibrios and is isolated frequently in summertime from the sea foods and sea water near Japan. It has been disclosed that the presence of underlying diseases such as liver cirrhosis, hemochromatosis can predispose a person to fatal sepsis by V. vulnificus. In this case, besides leukocytopenia, the presence of hemosiderosis induced by many transfusions was considered to be a major cause leading to the fulminating course of the disease.
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PMID:[Fatal Vibrio vulnificus infection in a patient with aplastic anemia]. 667 24

The ability of thyrotrophin-releasing hormone (TRH), its metabolites and several analogues to induce wet-dog shaking (WDS) was tested by their injection into the periaqueductal grey region of male rats. TRH and its metabolite deamido-TRH (TRH-OH) both stimulated WDS, though TRH-OH gave a longer duration of response; other TRH metabolites were inactive. Of the TRH analogues studied, RX77368 (pGlu-His-3,3'-dimethyl-ProNH2) was the most potent in this behavioural test system. Both CG3509 and CG3703 were also very active in inducing WDS, as were their deamidated metabolites. The relative stability of the TRH analogues to enzymic degradation in the brain may be related to their enhanced behavioural activity over TRH. The production from these analogues of biologically-active metabolites may also explain the increased activity in stimulating WDS of the parent peptides.
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PMID:Induction of wet-dog shaking in rats by analogues and metabolites of thyrotrophin-releasing hormone (TRH). 682 Jan 71

A second case of Hb York (beta 146 His leads to Pro), was discovered in a patient with polycythemia. The oxygen equilibrium curves (OEC) of red cell suspensions in a buffer (pH 7.4) at 37 degrees C revealed a biphasic curve with a P50 of only 12.5 mm Hg (normal value: 26.5 +/- 1.0 mm Hg). The purified Hb York had an extremely high affinity for oxygen with diminished cooperativity and decreased Bohr effect. The oxygen affinity was significantly reduced by inositol hexaphosphate. Molecular stability studies by mechanical shaking of various liganded forms of Hb York revealed stabilities between those of Hb A and Hb S. Isolated beta Y-subunits were more unstable than beta A-subunits at every pH examined. Hb York was 1.4 times more unstable than Hb A in 18.9% isopropanol.
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PMID:Characterization and properties of Hb York (beta 146 His leads to Pro). 687 72


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