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M Shimokawa

Publications and source records attributed to M Shimokawa.

At least 37 records · Page 2Linked to original sources
PubMed1995

[Effects of selective radicular block for reflex sympathetic dystrophy].

We have analyzed therapeutic effects of selective radicular block for 30 patients of reflex sympathetic dystrophy with residual intractable pain after neurolytic sympathetic ganglion blockade. Ten patients showed complete pain relief after the therapy with a effective rate of 66.7%. Minor side effects were observed in 3 cases (10%). When examined 2 month after the therapy, the effect had persisted in 16 cases in successful 20 cases. The therapy could not relieve complaints induced by numbness and neuroma. By the therapy, patients with diffuse pain were more comfortable than patients with regional pain. In indicated cases, this therapy is useful for residual complain of reflex sympathetic dystrophy after neurolytic sympathetic ganglion block.

Adult↗
PubMed1995

[Myotonin protein kinase].

The mutation underlying myotonic dystrophy is the expansion of polymorphic CTG repeat in the 3'-noncoding region of the myotonin protein kinase (MtPK) gene mapping to chromosome 19q13.3. A full-length cDNA of human MtPK was cloned and expressed in COS-1 cells. MtPK is recovered from the COS cell extract as a 70 kDa protein, which coincides with the size deduced from the predicted amino acid sequence. Biochemical characteristics of MtPK expressed in COS cells and its expression are investigated.

Chromosomes, Human, Pair 19↗
PubMed1994

Different effect of 5,6-trans-prostaglandin E2 on plasminogen activation by urokinase and streptokinase.

We examined the effects of 5,6-trans-prostaglandin E2 (trans-PG E2) on fibrinolysis and plasminogen activation by either urokinase or streptokinase. trans-PG E2 was found to enhance fibrinolysis induced by urokinase and inhibit the one by streptokinase. These effects were also appeared in the method using synthetic chromogenic substrate S-2251, which suggested that the effects of trans-PG E2 were induced in the circumstances without coagulation factors such as fibrinogen, thrombin or fibrin. Moreover, the enhancement effect of trans-PG E2 on fibrinolysis by urokinase was investigated. The result of SDS-PAGE indicated that plasmin formation rate from plasminogen by urokinase was accelerated in the presence of trans-PG E2. As trans-PG E2 increased the hydrolyzing rate of S-2288 by urokinase, trans-PG E2 directly interacted with urokinase. Therefore, the enhancement effect of trans-PG E2 on plasminogen activation by urokinase could be explained, at least in part, as follows: at first trans-PG E2 directly exerts its effect on urokinase, then it causes the increase of generation rate of plasmin from plasminogen.

Amino Acid Sequence↗
PubMed1994

Effect of renal or hepatic dysfunction on neurotoxic convulsion induced by ranitidine in mice.

We investigated the effect of acute renal and hepatic dysfunction on the neurotoxicity of ranitidine, a histamine H2 receptor antagonist. Experimental acute hepatic and renal dysfunction in mice were produced by i.p. injection of uranyl nitrate (UN) and carbon tetrachloride (CT), respectively. Ranitidine was then constantly infused into the tail vein until the onset of clonic convulsion. When compared to control mice, UN treated mice had a significantly shorter onset time to clonic convulsion, lower total dose and higher plasma concentration at initiation of clonic convulsion. In contrast, the convulsive threshold concentration in the brain of UN treated mice was not significantly different from that of control mice. In CT treated mice, all pharmacokinetic and pharmacodynamic data described above were not significantly different from those of the control mice. No significant difference in the brain/plasma concentration ratio was observed between both disease models and the corresponding control mice. Finally, the effect of UN and CT treatment on the convulsive potency after intracerebral (i.c.) administration of ranitidine was investigated in mice. Potentiation of the intrinsic neurotoxic sensitivity to ranitidine could not be demonstrated for mice with renal or hepatic dysfunction. From these findings, we conclude that renal dysfunction is a risk factor for ranitidine neurotoxicity, and this increased risk results from increase in the drug concentration in plasma and brain as a result of impaired renal excretion. No apparent effect of acute hepatic dysfunction was observed on both the pharmacokinetic and pharmacodynamic behavior of the drug.

Acute Disease↗
PubMed1993

Identification of amyloid precursor protein in synaptic plasma membrane.

Although the etiology of Alzheimer's disease has not been elucidated yet, dysfunction and loss of synapses are believed to cause dementia. Recent studies suggest that the primary cause of the disease is closely related to the aberrant processing of the amyloid precursor protein (APP). To investigate the localization of APP at synaptic sites, we obtained synaptic plasma membrane and synaptic vesicles from rat brain. Enhanced chemiluminescence (ECL) western blot analysis using two specific polyclonal antibodies against APP revealed strong APP immunoreactivity in the synaptic plasma membrane, but not in the synaptic vesicle fraction. These data indicate that APP is localized at the synaptic plasma membrane and may play a role in physiological synaptic activity. Alternative localization or aberrant processing of APP at the synaptic site may cause impairment of synaptic function in Alzheimer's disease.

Amyloid beta-Protein Precursor↗
PubMed1993

Simultaneous determination of amfenac sodium and its metabolite (7-benzoyl-2-oxindole) in human plasma by high-performance liquid chromatography.

A simple, selective, sensitive and rapid high-performance liquid chromatographic method for the simultaneous determination of amfenac sodium (AMF) and its metabolite (7-benzoyl-2-oxindole, S1) in plasma was established. To 100 microliters of plasma, purified water (100 microliters), ammonium sulphate (0.2 g) and ethanol (100 microliters) containing fenbufen (100 micrograms/ml, internal standard) were added. After centrifugation the ethanol layer was directly injected into a reversed-phase ODS column. AMF and S1 were eluted using a gradient buffer system of 20-80% acetonitrile-phosphate buffer (pH 7.0), and detected at 245 nm. The analytical recoveries of AMF at concentrations of 0.5, 2 and 10 micrograms/ml in plasma were ca. 92.1, 95.4 and 94.6%, respectively. The coefficients of variation of the AMF recoveries were below 4.6%. The S1 recoveries at the concentrations of 40, 200 and 400.ng/ml were ca. 93.4, 98.7 and 95.3%, and the coefficients of variation were below 6.0%. The coefficients of variation for intra- and inter-day variation of AMF (5 micrograms/ml) and S1 (100 ng/ml) were 4.5 and 3.6% and 4.2 and 4.2%, respectively. The detection limits of AMF and S1 in plasma were as low as 0.1 microgram/ml and 20 ng/ml, and the coefficients of variation were 4.0 and 4.4%, respectively. The method was applied to determine the plasma concentrations of AMF and S1 after oral administration of AMF capsules (100 mg of AMF) to human volunteers.

Administration, Oral↗
PubMed1993

Inhibitory spectra of purified protease nexin-II and related proteins towards cellular proteinases.

Amyloid beta protein (beta/A4) is deposited in senile plaques of patients with Alzheimer's disease. This protein is derived from a larger membrane-associated protein, termed amyloid precursor protein (APP). The constitutive processing of APP occurs at the central portion of beta/A4, resulting in the release of large N-terminal peptides. We have purified these peptides from the culture medium of cDNA-transfected COS-1 cells. Some of the isoforms contain the Kunitz-type protease inhibitor (KPI) domain and strongly inhibit trypsin, chymotrypsin and plasmin, but do not inhibit kallikrein, prolyl endopeptidase or granzyme A. The peptides also do not inhibit cysteine proteases such as cathepsin B or calpain. Soluble APPs lacking the KPI domain fail to inhibit any of these proteases. The results indicate that the KPI domain in soluble APPs has protease inhibitory activity against certain serine proteases.

Amino Acid Sequence↗
PubMed1993

Inhibition of GABAA receptor-mediated current responses by enoxacin (new quinolone) and felbinac (non-steroidal anti-inflammatory drug) in Xenopus oocytes injected with mouse-brain messenger RNA.

The convulsant interaction between enoxacin (ENX), a new quinolone antibacterial agent (NQ), and felbinac (FLB), a non-steroidal anti-inflammatory drug (NSAID), in vivo was reproduced as the change of GABA-induced current response in Xenopus oocytes injected with mouse brain mRNA. GABA (10 microM) response was inhibited by ENX in a dose-dependent manner, and IC50 of ENX was 96 microM. Moreover, the inhibitory effect of ENX was 80-fold potentiated in the presence of 10 microM FLB. The GABAA-antagonistic interaction between these two drugs in vitro was considered a possible mechanism of convulsant reaction after concomitant administration of NQs and NSAIDs in vivo.

Animals↗
PubMed1992

trans-5-prostaglandin E2 stimulates plasminogen activation by tissue-type plasminogen activator.

The effect of trans-5-prostaglandin E2 (trans-PGE2) on fibrinolysis was examined in vitro using synthetic chromogenic substrate S-2251. trans-PGE2 was found to enhance plasminogen (PLG) activation mediated by tissue-type plasminogen activator (tPA). The enhancing effect was dependent on the concentration of trans-PGE2. cis-PGE2 and the other PGs (PGE1 and PGI2) did not show such an effect as trans-PGE2, despite to the fact that their structures are similar to that of trans-PGE2. trans-Configuration around the double bond at the 5-position seems to be important in the enhancement of the fibrinolytic activity.

Amino Acid Sequence↗
PubMed1992

Trans-prostaglandin E2 enhances fibrinolysis.

5,6-trans-Prostaglandin E2 (trans-PG E2) was found to accelerate the fibrinolysis in a cell-free system. trans-PG E2 decreased the lysis time by 15% in the fibrin clot lysis time method and increased the lysis area by 22% in the fibrin plate method. On the contrary, 5,6-cis-prostaglandin E2 did not have such effects. trans-PG E2 did not exert the effect in the absence of either tissue-plasminogen activator or plasminogen. These results suggest that trans-PG E2 enhances the generation of plasmin from plasminogen by tissue-plasminogen activator.

Cell-Free System↗
PubMed1992

[A case of angiotropic lymphoma diagnosed by adrenal biopsy].

We reported the first case of angiotropic lymphoma diagnosed by adrenal biopsy in Japan. Immunohistochemical study and southern blot hybridization analysis proved it to be B-lymphocyte origin. A 61-year-old man with history of mild hypertension and diabetes mellitus was admitted to our department because of recurrent minor stroke. On admission, general physical findings were normal. Laboratory investigations showed an elevated erythrocyte sedimentation rate and increased serum lactic dehydrogenase (LDH) level. The serial computed tomographic (CT) scan of the brain showed multifocal abnormal density lesions in bilateral hemispheres. Magnetic resonance imaging (MRI) of the brain demonstrated multiple lesions of increased signal intensity in the brainstem and bilateral hemispheres. A subsequent CT scan of the abdomen revealed swelling of bilateral adrenal glands. Adrenal biopsy was performed. Biopsy samples showed the intravascular proliferation of malignant lymphoma cells, non-Hodgkin, diffuse large cell type. These cells had the immunophenotype of a B cell lymphoma (reactive with the antileukocyte common antigen, anti-MB-1, anti-MB-2 and anti-MX-pan B, and unreactive with the anti-MT-1, anti-UCHL, anti-Ki, anti-kappa, anti-lambda and antifactor-VIII). Southern blot hybridization analysis showed monoclonal rearrangements of the immunoglobulin heavy-chain gene, which strongly suggested a B-lymphocyte origin. Thus, a diagnosis of angiotropic lymphoma was made. As soon as chemotherapy was begun, the patient fell into deep coma. A repeat CT scan of the brain was normal. His clinical status gradually deteriorated, and he died 18 months after his initial symptom. Autopsy, which was limited to the body, revealed characteristic systemic intravascular stagnation of lymphoma cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗
PubMed1991

Beneficial treatment with methyl 6-[3-(2-chloroethyl)-3-nitrosoureido]-6-deoxy-alpha-D-glucopyranoside in a patient with primary myelofibrosis.

We attempted treatment with methyl 6-[3-(2-chloroethyl)-3-nitrosoureido]-6-deoxy-alpha-D-glucopyranoside (MCNU), a novel nitrosourea derivative, in a 55-year-old man with advanced-stage primary myelofibrosis. MCNU was given intravenously at a dose of 50 mg once a month. Following MCNU treatment, his anemia and splenomegaly improved markedly. An increased dose of MCNU (100 mg, once a month) was even more effective for relieving the symptoms. Severe side effects resulting from this therapy, such as leukocytopenia or thrombocytopenia, were never observed. These observations indicate that MCNU treatment may be a beneficial management of advanced-stage primary myelofibrosis.

Antineoplastic Agents↗
PubMed1991

[Comparison of methylprednisolone and droperidol in the prevention of nausea and vomiting following major gynaecological surgery].

The efficacy of methylprednisolone (MP) (500 or 250 mg) or droperidol 2.5 mg administered i.v., was studied in 200 women undergoing major gynaecological surgery. Following a standardised general anaesthesia technique with intrathecal morphine, the incidence of nausea and vomiting was assessed. The frequency of postoperative nausea and vomiting in the non-treated group was 59% and 35%; the group of MP 500 mg has a significant reduction of nausea and vomiting to 21% and 13%. Droperidol 2.5 mg decreased the incidence of postoperative nausea alone (nausea: 36%, vomiting: 19%). MP 250 mg was not effective in reducing either nausea or vomiting (nausea: 44%, vomiting: 38%). It was concluded that, of the drugs studied, MP 500 mg was most effective in preventing nausea and vomiting after major gynaecological surgery.

Adult↗
PubMed1989

[Impaired B lymphocyte function during open heart surgery].

Sequential in vitro lymphocyte function tests in 13 patients undergoing cardiac operation were performed to study B lymphocyte function following operation. Lymphocytes were stimulated with phytohemagglutinin (PHA), pokeweed mitogen (PWM) and Staphylococcus aureus Cowan 1 (SAC). Mitogen responses were measured by 3H-labeled thymidine incorporation. The SAC responses were significantly depressed following operation. Immunoglobulin secreting cells were measured by protein A plaque forming cell assay. The numbers of immunoglobulin secreting cells induced by PWM or SAC decreased remarkably at least as long as 3 day after the operation. The percentage of circulating B lymphocytes increased significantly postoperatively. This indicates that the B lymphocytes remaining after the operation were functionally impaired.

Antibody-Producing Cells↗
PubMed1981

[Separation of free and bound radiolabeled antigen using protein A-sepharose CL-4B in hCG radioimmunoassay (author's transl)].

Protein A isolated from Staphylococcus aureus can bind the Fc portion of IgG of several species. We used Protein A coupled to Sepharose CL-4B (Protein A-S) for the separation of antibody-bound and free radiolabeled hCG in the radioimmunoassay, and the results were compared to the double antibody method. One gram of Protein A-S containing 7 mg of Protein A was dissolved in 17.5 ml of 1/15M phosphate buffer saline pH 7.4. Two hundred fifty microliters of this suspension were added to the assay tubes 24 hours after mixing 125I-hCG, anti-hCG and hCG standards or serum samples. After further incubation for 10 minutes at room temperature, the tubes were centrifuged and the radioactivity in the precipitates was measured by a gamma spectrometer. The standard curve obtained by the Protein A-S method was virtually identical to that obtained using the double antibody method. The intra- and interassay coefficients of variation in the hCG radioimmunoassay using the Protein A-S method ranged from 6.6 to 8.2% and from 7.2 to 11.9% respectively, which were close to those obtained by the double antibody method. IgG in serum inhibited the binding of Protein A-S to anti-hCG, and thus it was necessary to dilute the samples more than one-hundred fold. Under these conditions a good correlation exists in the serum hCG levels determined by either the Protein A-S method or the double antibody method. Thus, Protein A-S permitted the rapid separation of antibody-bound and free radiolabeled hCG in the radioimmunoassay and could be substituted for the second antibody.

Antigens↗
PubMedDate not supplied

Measurement of thyroid iodine by CT.

For evaluation of thyroidal iodine kinetics and thyroid nodules, we carried out quantitative in vivo measurement of thyroid iodine concentration by CT. Neuron activation analysis of iodine content was conducted on 48 thyroid fragments without calcification operatively obtained from 18 patients who had undergone CT of the thyroid without contrast enhancement. The CT attenuation values were obtained from the regions of interest in the CT image that corresponded to the analyzed fragment. When iodine concentration in the thyroid tissue was greater than 0.02 mg/g, the CT values correlated linearly with the iodine concentrations in thyroid nodules, thyroids with diffuse thyroid disease, and normal thyroids. The relationship is represented by the following formula: iodine concentration (mg/g) = (CT value-65)/104. The relationship between iodine concentration and CT value in diffuse thyroid disease, thyroid nodules, and normal thyroids was not significantly different.

Humans↗