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S Nakashima

Publications and source records attributed to S Nakashima.

At least 181 records · Page 10Linked to original sources
PubMed1995

Combined drug therapy with diltiazem, dextran, and hydrocortisone (DDH therapy) for late cerebral vasospasm after aneurysmal subarachnoid hemorrhage: assessment of efficacy and safety in an open clinical study.

Late cerebral vasospasm after subarachnoid hemorrhage (SAH) is a disastrous phenomenon for the patients and a definite treatment has not been established. We studied 48 consecutive patients receiving high-dose diltiazem (5 micrograms/kg/min) injection combined with dextran and hydrocortisone to late cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH). All but 2 patients underwent surgery within 72 hours after SAH. Diltiazem was continuously given via a central venous line for up to 2 weeks in conjunction with simple cisternal drainage. 5% of dextran solution (500 ml/day) was infused for 7-10 days. Hydrocortisone was given 1,600 mg on the first day, then the dose was gradually decreased over 14 days. Symptomatic vasospasm (SVS) occurred in 5 patients (10.4%), 4 patients recovered, but 1 had severe neurological deficit. A low density area on CT-scan was observed in 2 patients. Thirty patients (62.5%) had good recovery, 10 patients (20.8%) had moderate disability, 3 (6.3%) had severe disability and 3 (6.3%) had vegetative survival. Two patients died of the initial brain damage. There were no severely hypotensive side effects. However, 3 patients showed atrioventricular blockage on electrocardiogram. These side effects subsided after the dose of the drug was decreased or administration was stopped altogether. These findings show that high-dose calcium antagonist diltiazem therapy combined with dextran and hydrocortisone injection is safe and effective for prevention of late cerebral symptomatic vasospasm after SAH.

Adult↗
PubMed1995

[Inositol].

Explore the source record for details and available documents.

Diabetes Mellitus↗
PubMed1995

Design and synthesis of new cross-linking agents.

We have previously synthesized 6-vinylated guanosine derivatives by new Pd(0)-catalyzed cross-coupling reaction using guanosine 6-O-tosylate and vinyltributyl-stannane. Its potentials as a cross-linking agent have been demonstrated by adduct formation with guanosine and cytidine. But these 6-vinylated derivatives could not be incorporated to oligonucleotide because of chemical instability. In this paper, we report new deoxyguanosine derivatives with substituted olefin (2 and 3), which were designed to control the reactivity of vinyl functional group. Although either 2 or 3 did not formed the adducts with nucleobases, these compounds reacted with hydroxylamine hydrochloride in the presence of acid catalyst. The reactivity was in the order of 1 > 2 > 3. These results suggest that new guaosine derivatives (2 and 3) have moderate reactivity toward nucleophiles and are expected to be stable in incorporating into oligonucleotides as a cross-linking agent.

Cross-Linking Reagents↗
PubMed1995

[The involvement of protein kinase C isozymes in activation of phospholipase D and secretion of serotonin in rat basophilic leukemia cells].

Western blot analysis shows the presence of protein kinase C (PKC) alpha, beta1, beta2, delta, epsilon, zeta isozymes in rat basophilic leukemia (RBL-2H3) cells. Antigen stimulation caused preferential translocation of protein kinase C (PKC) delta and epsilon to membranes. On the other hand, when the cells were stimulated by phorbol 12-myristate 13-acetate (PMA) or ionophore (A23187), PKCalpha and beta were predominantly translocated. Phospholipase D (PLD) was activated by three stimulants in order: A23187 > PMA >> antigen. Therefore, PKCalpha and beta seem to be involved in the activation of PLD in RBL cells. The translocation of all PKC isozymes in A23187 stimulation was weak. Therefore, PLD activation in A23187 stimulation may require some other factors than PKC which are associated with the increase of Ca2+ in the cells. The cells stimulated by antigen secreted serotonin to the same level as the cells stimulated by A23187. In both stimulation, PKCalpha and epsilon were translocated to almost similar level, suggesting that PKCalpha and epsilon are involved in the secretion. All PKC isozymes except zeta were markedly translocated in PMA stimulation, but secretion did not occur. These results indicate that translocation of PKC alpha and beta may be associated with PLD activation and also that both translocation of PKCalpha and epsilon and intracellular calcium increase are required for serotonin secretion in RBL cells.

Animals↗
PubMed1994

Potent activation of phospholipase D by phenylarsine oxide in rat basophilic leukemia (RBL-2H3) cells.

A putative protein tyrosine phosphatase inhibitor, phenylarsine oxide (PAO), potentiated phospholipase D (PLD) activity concentration-dependently in [3H] oleic acid-labeled rat basophilic leukemia (RBL-2H3) cells without significant increase in phosphatidylinositol-specific phospholipase C (PI-PLC) activity. Although PAO induced tyrosine phosphorylation of several proteins, both PAO-induced PLD activation and tyrosine phosphorylation were not affected by a protein tyrosine kinase inhibitor, genistein. Another tyrosine kinase inhibitor, herbimycin A, prevented the PAO-induced PLD stimulation but had no effect on protein tyrosine phosphorylation. However, depletion of protein kinase C (PKC) greatly reduced PAO-stimulated PLD activity. These results indicate that PKC but not tyrosine kinase may be involved in PAO-mediated PLD activation.

Animals↗
PubMed1994

Tyrosine phosphorylation and activation of mitogen-activated protein kinases by thrombin in human platelets: possible involvement in late arachidonic acid release.

Thrombin induced tyrosine phosphorylation of 41-kDa and 43-kDa mitogen-activated protein (MAP) kinases in human platelets which was detectable at 1 min and peaked at 2 min after thrombin stimulation as assessed by immunoprecipitation and immunoblotting. The kinase activity, measured by phosphorylation of myelin basic protein, increased concurrently with tyrosine phosphorylation. The present results indicate that thrombin activates MAP kinases which may not be involved in aggregation and secretory responses but may play a role in the late arachidonic acid release via activation of cytosolic phospholipase A2 in human platelets.

Arachidonic Acid↗
PubMed1994

Postnatal developmental changes in facial nerve morphology. Computer-aided 3-D reconstruction and measurement.

Accurate measurements of the lengths and angles of the facial nerve were obtained in eight normal human temporal bones of varying ages from 7 days to 76 years. Measurements were made on serial histological sections, using computer-aided three-dimensional (3-D) reconstruction. The most noteworthy of the findings demonstrated that both the mastoid portion of the facial nerve and the segment of the facial nerve between the second genu and the divergence of the chorda tympani nerve lengthened with age. The mastoid segment lengthened more significantly than the latter, indicating the facial canal grows more than the facial nerve in its mastoid portion. This difference in growth rates results in the site of the chorda tympani nerve divergence shifting with age relative to the stylomastoid foramen.

Adolescent↗
PubMed1994

Activation of phospholipase D in Chinese hamster ovary cells expressing platelet-activating factor receptor.

Platelet-activating factor (PAF) activated phospholipase D (PLD) in WT-H cells, CHO cells stably expressing cloned guinea-pig PAF receptor. The PLD activation was found to be dependent on extracellular Ca2+, protein kinase C (PKC), and a currently unidentified protein tyrosine kinase (PTK). PTK inhibitors ST-638 and genistein inhibited PLD activation induced by PAF as well as phorbol myristate acetate, indicating that PTK acts downstream of PKC. Furthermore, activation of MAP (mitogen-activated protein) kinases, as assessed by their phosphorylation, was also dependent on Ca2+, PKC, and PTK. The correlation between PLD activity and MAP kinase activation, together with the previously observed MAP kinase activation associated with arachidonic acid release by cPLA2 [Honda et al. (1994) J. Biol. Chem. 269, 2307-2315], led us to examine the involvement of MAP kinase in PLD activation. The results indicate that PLD and MAP kinases are activated through the common pathway consisting of Ca2+, PKC, and the unidentified PTK, which act in parallel, but not in a linear sequence.

Animals↗
PubMed1994

[A case of pineal teratoma with interesting radiological findings].

A rare case of mature pineal teratoma with interesting radiological findings in a 16-month-old infant is reported. The patient was referred to our clinic because of generalized convulsions. A CT scan showed marked hydrocephalus and a low density mass lesion without contrast enhancement in the pineal region. A CT cisternography demonstrated the lesion as a filling defect area on the image produced immediately after the emergent V-P shunt, and a filling area 24 hours later. The lesion was of signal intensity on T-1 weighted MR image and of high signal intensity on T-2 weighted MR image, equal to CSF intensity. These radiological findings were compatible with an arachnoid cyst in the quadrigeminal cistern, so we performed the excision of both anterior and posterior cyst walls using the occipital tentorial approach. However, the histology of the cyst wall was not compatible with that of an arachnoid cyst, showing neuroepithelial-like cell lining with positive staining for cytokeratine. The postoperative follow-up on MRI was continued for 31 months. An MRI performed 9 days after the first operation showed, compared with the gray matter, iso-signal intensity area and high signal intensity area on T-1 weighted image. At first, we thought this was because of bleeding of the pineal gland brought on by the operative maneuver. However, the mixed intensity lesion shown on T-1 weighted images gradually expanded and distorted, and finally showed the typical MR images for a teratoma. The operative findings using the occipital transtentorial approach were typical for a teratoma.(ABSTRACT TRUNCATED AT 250 WORDS)

Arachnoid Cysts↗
PubMed1994

An antiallergic drug, pemirolast potassium, inhibits inositol 1,4,5-trisphosphate production and Ca2+ mobilization in antigen-stimulated rat basophilic leukemia (RBL-2H3) cells.

An antiallergic drug, pemirolast potassium (TBX) at concentrations between 0.01 and 10 micrograms/ml inhibited antigen (Ag)-stimulated degranulation in RBL-2H3 cells, which have the properties of mucosal mast cells. At the same concentrations, the drug suppressed both the formation of inositol 1,4,5-trisphosphate and the mobilization of Ca2+, indicating the prevention of phospholipase C activation. The production of 1,2-diacylglycerol and phosphatidic acid, which was mainly due to phosphatidylcholine hydrolysis, was also suppressed. Moreover, TBX reduced Ag-induced liberation of arachidonic acid, a precursor of eicosanoids, implying the inhibition of phospholipase A2. These data suggest that TBX inhibits the activation of phospholipase C, leading to decreased formation of the signal transducing molecules necessary for cell activation.

Animals↗
PubMed1994

[Clinico-epidemiologic study of infantile hydrocephalus in Japan].

A nation-wide survey on congenital hydrocephalus, including secondary hydrocephalus occurring within one year after birth, was carried out in 1988. The number of patients with congenital hydrocephalus treated during the previous one year was estimated to be 3,200-3,500 throughout Japan. The number of new cases of this disease which occurred during the year was calculated to be 800. This indicates a rate of 0.58 per 1,000 live births. Clinico-epidemiologic features were compared with regard to three subjects listed below. (1) The difference between the epidemiologic profile of term and preterm infants with hydrocephalus was investigated. As for etiology, the incidences of primary hydrocephalus and hydrocephalus complicated by Arnold-Chiari malformation type II and meningocele were significantly higher in term infants than in preterm infants. It was estimated that about 30% of the hydrocephalus in preterm infants and only 7.7% in term infants occurred as a consequence of intracranial hemorrhage. The degree of neurological impairment and the mortality rate were higher in preterm infants than term infants. (2) The changing panorama of infantile hydrocephalus in Japan was investigated comparing the epidemiologic data of four groups according to the birth year. As for pregnancy period, preterm infants with hydrocephalus were gradually increasing recently. Hydrocephalus secondary to intracranial hemorrhage was increasing and that secondary to intracranial infection was decreasing. The rate of shunt malfunction was decreasing significantly. (3) Clinico-epidemiologic features of intractable hydrocephalus based on the diagnostic criteria of the research committee was investigated comparing intractable with non-intractable groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Humans↗
PubMed1993

Heavy-chain isoforms of non-muscle myosin in human tissues.

The heavy-chain isoforms of myosin in human non-muscle and smooth muscle tissues were analyzed by means of SDS/PAGE and using three distinct newly developed monoclonal anti-(human cerebrum myosin) Ig (HBM-1, HBM-3 and HBM-4). Purified cerebrum myosin contained three electrophoretic variants of non-muscle myosin heavy chain (NM1, NM2 and NM3, with apparent molecular masses of about 200, 198 and 196 kDa, respectively). Both NM1 and NM2 were recognizable by the brain-specific antibody HBM-1, while NM3 was recognizable by HBM-3. Each of the variants reacted with HBM-4 to a similar extent. Purified cerebellum myosin gave three electrophoretic variants of the heavy chain which were indistinguishable electrophoretically or immunologically from those of cerebrum myosin. Aortic myosin contained four electrophoretic variants, including the two smooth muscle myosin heavy chain isoforms and NM2-like and NM3-like heavy chains. Liver, platelet and kidney myosins contained a heavy chain very similar to NM3. Kidney myosin also contained a small fraction of an NM2-like electrophoretic variant. In addition, cerebrum, kidney, liver and platelet myosins appeared to contain minor, 194-kDa myosin heavy-chain-like polypeptide(s) (NM4). NM1, as well as NM2 and NM3, thus appear to be the brain-type and non-brain-type non-muscle myosin heavy-chain isoforms, respectively, and additional minor heavy-chain isoforms are also likely to be present in human tissues.

Animals↗