Biomedical subjects

N Murakami

Publications and source records attributed to N Murakami.

At least 127 records · Page 7Linked to original sources

PubMed1999

[A case of typical Melkersson-Rosenthal syndrome with possible autosomal dominant inheritance].

Here we presented a case of 40-year-old woman who suffered from bilateral facial palsy and headache. She had allegedly had an episode of facial palsy, and facial edema at her age of 14 years. Physical examination revealed swelling of the lips, upward disturbance of the left eye, hypogeusia, the fissured tongue, and bilateral facial palsy. Oral administration of prednisolone 20 mg/day yielded gradual but complete improvement of the facial palsy and hypogeusia within two weeks. Careful analysis of family history disclosed that four members had oro-facio-cervical edema and three had the fissured tongue. A diagnosis of Melkersson-Rosenthal syndrome with possible autosomal dominant inheritance was made based on the clinical findings and familial aggregation of the incomplete form of this syndrome.

Administration, Oral↗

PubMed1998

Sympatho-adrenal involvement in methamphetamine-induced hyperthermia through skeletal muscle hypermetabolism.

We investigated the involvement of the sympatho-adrenal axis in the hyperthermia induced by methamphetamine by using a biotelemetric system. The intraperitoneal injection of methamphetamine (1 mg/kg) induced hyperthermia preceded by an increase in oxygen consumption in freely moving rats. The hyperthermic effect of methamphetamine was completely blocked by chemical sympathectomy with 6-hydroxydopamine (50 mg/kg, i.p.). Adrenalectomy, but not adrenal demedullation, prevented the hyperthermia. In adrenalectomized rats, dexamethasone supplementation (0.5 mg/kg, s.c.) restored the methamphetamine-induced hyperthermia. Furthermore, dantrolene (1 or 2 mg/kg, i.v.), which blocks Ca2+ release from the sarcoplasmic reticulum in skeletal muscle, attenuated the hyperthermia. These results suggest that methamphetamine stimulates norepinephrine release from sympathetic nerve terminals, which then enhances thermogenesis in skeletal muscle under the permissive action of glucocorticoids.

Adrenal Glands↗

PubMed1998

Lysosomal glycogen storage disease with normal acid maltase with early fatal outcome.

In a male infant who had cardiomyopathy, generalized muscle weakness and increased serum creatine kinase levels, his muscle biopsy revealed myopathic changes with tiny intracytoplasmic vacuoles containing PAS-positive material and high acid phosphatase activity, but had normal acid maltase activity biochemically. These findings were consistent with those seen in lysosomal glycogen storage disease with normal acid maltase (Danon disease). Sarcolemmal indentations commonly seen in this disease were missing, but a complement membrane attack complex, C5b-9 was positive along the surface membrane of the muscle fibers as seen in X-linked vacuolar myopathy. The patient was on a respirator and died at 27 months of age from pneumonia and hypertrophic cardiomyopathy. Lysosomal glycogen storage disease with normal acid maltase may be manifested at birth with marked skeletal and cardiac involvement leading to death in early infancy.

Biomarkers↗

PubMed1998

Effects of a novel non-steroidal anti-inflammatory drug (M-5011) on bone metabolism in rats with collagen-induced arthritis.

The effects of a novel non-steroidal anti-inflammatory drug (NSAID), d-2-[4-(3-methyl-2-thienyl)phenyl]propionic acid: M-5011, and other NSAIDs (indomethacin, zaltoprofen and tiaprofenic acid) on bone metabolism in Dark Agouti (DA) strain rats with collagen-induced arthritis were evaluated. M-5011 (1.5 and 4.5 mg/kg) and other NSAIDs (1.5 mg/kg) were administered orally once a day from day 14 to day 35 after collagen immunization. In arthritic rats, paw volume and serum levels of anti-type II collagen antibody were increased on day 21 compared to those in non-immunized rats. M-5011 (4.5 mg/kg), indomethacin and zaltoprofen tended to prevent this increase in paw volume. Elevated urinary pyridinoline and deoxypyridinoline levels were found on days 28 and 35 in arthritic rats. M-5011 (4.5 mg/kg) also tended to prevent the increase in urinary pyridinoline level on day 28, but none of the other NSAIDs affected urinary deoxypyridinoline levels. Bone mineral densities in the hindpaw and vertebrae were also decreased in arthritic rats. M-5011 and tiaprofenic acid prevented this decrease in vertebral bone mineral density. These findings indicate that M-5011 partially inhibits the generalized bone loss accompanying the development of collagen-induced arthritis in rats.

Absorptiometry, Photon↗

PubMed1998

Anti-malarial activities of acylated bruceolide derivatives.

Several O-acylated derivatives of bruceolide (2) were synthesized and their anti-malarial activities together with selective toxicities were examined. It was found that 3,15-di-O-acetyl-(3c), 3,15-di-O-propionyl-(3d) and 15-O-propionylbruceolide (3b), as well as bruceine B (3a), exhibited potent anti-malarial activities with high selective toxicities.

Acylation↗

PubMed1998

Two nonmuscle myosin II heavy chain isoforms expressed in rabbit brains: filament forming properties, the effects of phosphorylation by protein kinase C and casein kinase II, and location of the phosphorylation sites.

During the course of the expression of a 47-kDa COOH-terminal fragment of brain-type nonmuscle myosin heavy chain (MIIBF47), we found two closely related forms of MIIB, designated MIIB alpha and MIIB beta, in rabbit brains. The B alpha form corresponded to SMemb, described by Kuro-o et al. [(1991) J. Biol. Chem. 266, 3768] and was the more abundant form in rabbit brain, while the B beta form was novel. MIIB beta F47 differed from MIIB alpha F47 at six positions, three of which were within the carboxyl-terminal nonhelical domain; in MIIB beta F47, Ser, Pro, and Lys replaced Pro, Ser, and Glu, respectively. MIIB alpha F47 and MIIB beta F47 differed in filament assembly properties in the presence of various concentrations of salt, and a chimera containing the helical domain of MIIB beta F47 and the nonhelical domain of MIIB alpha F47 behaved very much like MIIB beta F47. Protein kinase C (PK C) incorporated 1 and 2 mol of phosphate/mol peptide of MIIB alpha F47 and MIIB beta F47, respectively, and caused similar levels of inhibition of assembly for both isoforms. Casein kinase II (CK II) incorporated 4 and 2 mol of phosphate/mol of MIIB alpha F47 and MIIB beta F47 peptides, respectively, and this caused strong inhibition of assembly for MIIB alpha F47 but only slight inhibition for MIIB beta F47. PK C sites in MIIB alpha F47 were localized within a region containing a cluster of Ser residues near the predicted junction of the helical and nonhelical domains: P-I-S(PO4)-F-S(PO4)-S(PO4)-S(PO4)-R-S(PO4)-. Out of the five potential PK C sites, only one site seemed to be phosphorylated per peptide. The PK C sites in MIIB beta F47 were localized as S(PO4)-I-S-F-S-S-(PO4)-R-S(PO4)-, with total incorporation of about 2 mol/mol of peptide. In addition, PK C phosphorylated a Ser within the predicted helical domain, E-V-S(PO4)-T-L, in both MIIB alpha F47 and MIIB beta F47. For CK II, five sites were identified within the COOH end of MIIB alpha F47: S(PO4)-L-E-L-S(PO4)-D-D-D-T(PO4)-E-S-K-T-S(PO4)-D-V-N-E-T-Q-P-P-Q-S(PO4) -E. The same sites were phosphorylated in MIIB beta F47 except for the first Ser, which was replaced by Pro in MIIB beta F47. An average of about two of the four potential sites were phosphorylated in MIIB beta F47, while in MIIB alpha F47 all five sites could be fully phosphorylated by CK II. Our results demonstrate that (1) the helical domains dictate the intrinsic salt dependence of assembly for nonmuscle myosin, (2) the isoforms are phosphorylatable by different kinases in an isoform specific manner mostly within the COOH-terminal nonhelical domain, and (3) the effects of the phosphorylation on assembly are isoform specific.

Amino Acid Sequence↗

PubMed1998

Asymmetrical changes in the fodrin alpha subunit in the superior temporal cortices in schizophrenia.

BACKGROUND: We examined possible abnormalities in neural structural proteins that may underlie morphometric changes reported in the left superior temporal cortices (Brodmann's area 22) of schizophrenics. METHODS: Particulate proteins of the superior temporal cortices taken at autopsy from 11 schizophrenic and 9 control brains were fractionated by gel electrophoresis. Target proteins, identified by reading their amino acid sequences, were immunoquantified using the specific antibody. RESULTS: Amino acid sequences of the 150-kDa proteins on sodium dodecyl sulfate/polyacrylamide gel electrophoresis, which were significantly increased on the left side of schizophrenic superior temporal cortices, revealed that they were proteolytic fragments of the alpha subunit of fodrin, a major cytoskeletal protein underlying the plasma membrane. Immunoquantification using the specific antibodies against alpha and beta subunits of fodrin indicated that there exist concomitant decreases in the full-length 240-kDa form and increases in the 150-kDa form of alpha-fodrin with no changes of the 235-kDa form of beta-fodrin in the left superior temporal cortices of the schizophrenic brains. CONCLUSIONS: The findings may be a possible molecular basis for linking morphometric changes to neurochemical pathophysiology in schizophrenia.

Aged↗

PubMed1998

Changing trends and prognoses for patients with papillary thyroid cancer.

OBJECTIVE: To analyze differences in the demographic backgrounds, and in treatments, prognosis, and risk factors of patients with papillary thyroid cancer operated on from 1965 to 1990, by dividing them into 3 chronological groups. DESIGN: Retrospective cohort study of 2423 patients with papillary thyroid cancer (tumor size, > or = 10 mm) who underwent curative surgery at the Noguchi Thyroid Clinic, Oita, Japan. SETTING: A center for the treatment of thyroid disease, at which about 1400 thyroid operations are performed per year. PATIENTS: There were 596 patients treated during from January 1, 1965, to December 31, 1973; 964 patients treated from January 1, 1974, to December 31, 1982; and 959 patients treated from January 1, 1983, to December 31, 1990. RESULTS: Of the 2519 patients treated, 96 were excluded from the study because they had undergone noncurative surgery. Therefore, the analyses are based on data for 2423 patients who underwent curative surgery. Three groups were defined as follows: group 1, underwent surgery during the period 1965-1973 (n = 577); group 2, underwent surgery during the period 1974-1982 (n = 924); and group 3, underwent surgery during the period 1983-1990 (n = 922). The mean age of the patients in group 1 was 42.4 years, in group 2, 45.0 years, and in group 3, 47.8 years. The mean tumor size was 30.4 mm, 26.5 mm, and 24.6 mm, respectively, for groups 1, 2, and 3. The 10- and 20-year disease-specific survival rates were significantly improved from group 1 (95.5% and 90.3%, respectively) to group 2 (97.8% and 93.9%, respectively), and the 10-year rate was significantly improved for group 3 (98.2%). In the multivariate analysis, age, sex, tumor size, and gross nodal metastasis were significant predictors of survival for group 1; however, only age and gross nodal metastasis were significant for group 3. CONCLUSIONS: Over time, papillary thyroid cancer has become diagnosed at an earlier stage, but the age of the patients at diagnosis is older. The disease-specific survival rate was significantly improved, mainly owing to earlier treatment, and the change in the risk factor profile for cancer mortality may be due to the changes in the demographic backgrounds and diagnostic and therapeutic modalities. These considerations derived from risk factor analysis should be considered for treating the patient and for the prediction of patient survival.

Adolescent↗

PubMed1998

Papillary thyroid carcinoma: modified radical neck dissection improves prognosis.

OBJECTIVE: To ascertain whether modified radical neck dissection offers a survival advantage for some subsets of patients with papillary cancer of the thyroid. DESIGN: A retrospective cohort study of 2966 patients curatively treated at the Noguchi Thyroid Clinic and Hospital Foundation, Oita, Japan, between 1946 and 1991. SETTING: A center for the treatment of thyroid disease, where about 1400 thyroid operations are performed per year. PATIENTS: Between 1946 and 1991, patients with papillary cancer whose primary tumor was 1 cm or larger and who were curatively treated were studied. Of the 2859 patients, 72.1% underwent modified radical neck dissection, 8.5% underwent partial node excision, and 19.4% underwent no node excision. RESULTS: A univariate analysis revealed a subset of patients who benefited from modified radical neck dissection. A multivariate analysis revealed that sex (P<.001), age at the time of the operation (P<.001), size of the primary tumor (P<.001), extrathyroidal invasion (P<.001), and the presence of nodal metastasis (P<.01) are significant risk factors. CONCLUSION: Patients with nodal metastasis, patients in whom the primary tumor invades beyond the thyroid capsule, and women older than 60 years can benefit from modified radical neck dissection.

Adult↗

PubMed1998

Mitochondrial abnormalities in selenium-deficient myopathy.

We report a man who developed selenium-deficient myopathy during long-term parenteral nutrition. Muscle biopsy showed marked mitochondrial depletion in the deep sarcoplasm and enlarged mitochondria at the periphery mainly in type 2 fibers. Muscle weakness improved gradually after the second course of selenium supplementation. The peculiar mitochondrial abnormalities in muscle fibers appear to play a key role in the pathogenesis of selenium-deficient myopathy.

Adult↗

PubMed1998

Antagonistic regulation of cell migration by epidermal growth factor and glucocorticoid in human gastric carcinoma cells.

Epidermal growth factor (EGF) induced the disruption and scattering of colonies of TMK-1, a cell line derived from a human gastric carcinoma. A stimulatory action of EGF on cell migration was also observed as determined by a wound assay. However, these actions of EGF were inhibited if the cells were pretreated with dexamethasone, a synthetic glucocorticoid. Dexamethasone increased cell adhesion to collagen type IV and laminin, but not to poly-L-lysine and fibronectin. In contrast, EGF did not affect cell adhesion to these extracellular matrices whether dexamethasone was present or not. Dexamethasone enhanced the protein levels of both alpha1 and beta1 integrin subunits, and that of the alpha1 beta1 heterodimer. Further, flow cytometric analysis revealed that dexamethasone increased the expression of beta1 and alpha1 integrin subunits at the cell surface, whereas EGF increased expression of beta1 and alpha2 subunits at the cell surface. Antibodies against alpha1 and beta1 integrin subunits inhibited the increased cell adhesion seen in the presence of dexamethasone. An immunofluorescence study indicated that dexamethasone increased the formation of focal adhesions along the entire edges of cell colonies. In contrast, EGF led to the formation of focal adhesions preferentially at the cell front, and this EGF-induced preferential formation was not observed if the cells were pretreated with dexamethasone. These results suggest that glucocorticoid increased cell adhesion to the extracellular matrix via alpha1 beta1 integrin, and thereby antagonized EGF-induced cell migration.

Cadherins↗

PubMed1998

Chloroquine myopathy suggests that tau is degraded in lysosomes: implication for the formation of paired helical filaments in Alzheimer's disease.

We have found that amorphous tau deposits in chloroquine myopathy (CM), a vacuolar myopathy induced by the administration of chloroquine, a well-known lysosomotropic agent. The dynamics of tau in CM and immunocytochemistry strongly suggest that the accumulation of tau is due to defective tau degradation in the lysosomal compartment in the muscle. This observation may offer a new view on the formation of paired helical filaments in Alzheimer's disease: this selective protein degradation pathway may be defective and result in intracellular accumulation of tau, thereby forming the unusual filaments.

Alzheimer Disease↗

PubMed1998

The non-synaptic expression of transforming growth factor-beta 2 is neurally regulated and varies between skeletal muscle fibre types.

In adult skeletal muscles, transforming growth factor-beta 2 is restricted to the postsynaptic domain of the neuromuscular junction. The various putative functions of this transforming growth factor-beta 2 predict different patterns of transforming growth factor-beta 2 expression in denervated muscles. We therefore denervated rat tibialis anterior, extensor digitorum longus and soleus muscles and examined the expression of transforming growth factor-beta 2 using semi-quantitative reverse-transcription polymerase chain reaction and immunohistochemistry. Denervation up-regulated transforming growth factor-beta 2 expression extrasynaptically with little or no effect on synaptic expression. The up-regulation was detectable by one day, had become significant by three days and remained elevated for at least two weeks. This proves that the transforming growth factor-beta 2 associated with the neuromuscular junction is not under neural control and is consistent with transforming growth factor-beta 2 being a trophic factor for motoneurons. This pattern of transforming growth factor-beta 2 expression is similar to that described for other proteins associated with the neuromuscular junction, notably the acetylcholine receptor subunit genes. However, in contrast to the acetylcholine receptor subunit genes, the extent of up-regulation of transforming growth factor-beta 2 varied between fibre types, with the glycolytic IIB fibres being less affected than other fibre types.

Animals↗

PubMed1998

Severe infantile congenital myopathy with nemaline and cytoplasmic bodies: a case report.

A Japanese boy had marked generalized hypotonia and weakness and progressive respiratory failure since birth. Left biceps brachii muscle biopsy at 47 days of age showed marked variation in muscle fiber size, and nemaline and/or cytoplasmic bodies in approximately 10% of the muscle fibers. To our knowledge, the presence of nemaline and cytoplasmic bodies in the same muscle has not been previously reported. The severity of his respiratory failure and muscle weakness were thought to be related to muscle immaturity since there were many undifferentiated type 2C fibers.

Biopsy↗

PubMed1998

Distal myopathy with rimmed vacuoles.

Distal myopathy with rimmed vacuoles is an autosomal recessively inherited disorder with preferential involvement of the anterior tibial muscle. Recently the gene was discovered to be mapped to chromosome 9, the same region as in familial inclusion body myopathy (rimmed vacuole myopathy sparing the quadriceps). The onset of the disease was in young adults 20-40 years of age, averaging 26 years. The disease was progressive and most of the patients became non-ambulant within 12 years after the onset. The striking and common pathologic finding was the presence of rimmed vacuoles in muscle fibers with little evidence of necrotic or regenerative processes. Nuclear change with tubulofilamentous inclusions probably induces focal myofibrillar degeneration which activates the lysosomal system, resulting in active autophagocytosis and myelin body formation, i.e. rimmed vacuole formation.

Adolescent↗

PubMed1998

Cognitive dysfunction and histological findings in rats with chronic-stage contusion and diffuse axonal injury.

The Morris water maze (MWM) technique is well known as a prominent method of evaluating learning acquisition and memory retention impairments in rats. We previously reported on a modified fluid percussion device that is able to consistently produce experimental cortical contusion (CC) and diffuse axonal injury (DAI) in separate groups of rats. The purpose of the present protocol is to evaluate the differences in learning acquisition and memory retention impairments between these two types of injured rats in the chronic stage using the MWM technique. CC and DAI rats are respectively induced by lateral and midline fluid percussion. We also compare the histological differences between these two different types of traumatic brain injury. The results show statistically significant differences in learning acquisition impairment between the sham and CC rats and between the sham and DAI rats. However, a difference in memory retention impairment was expected to be seen only between the sham and DAI rats. Histologically, the loss of CA3 pyramidal cells in the hippocampus was observed ipsilaterally in the CC and bilaterally in DAI. Neuronal cell loss was observed in bilaterally in layer II of the entorhinal cortex in DAI, but not in CC.

Animals↗

PubMed1998

Experimental brain injury induces expression of amyloid precursor protein, which may be related to neuronal loss in the hippocampus.

Previous reports have demonstrated that some focal brain injuries increase amyloid precursor protein (APP) immunoreactivity in the region surrounding the injury where it was localized, in damaged axons and in pre-alpha 2 cells of the entorhinal cortex. However, to date, APP expression in the hippocampus remote from the impact site has not been comprehensively studied. Therefore, we have evaluated APP expression not only in the locally injured cerebral cortex but also in the hippocampus remote from the impact site. In the present paper, diffuse axonal injury was induced in rats in midline fluid percussion injury. APP expression was examined post injury using Western blot analysis and immunohistochemistry. Western blot analysis demonstrated that the expression of 100-kd APP was increased in both the cerebral cortex and hippocampus 24 h after injury. It then decreased in the hippocampus, but did not change in the cerebral cortex, 7 days after injury. Immunohistochemical studies showed increased immunoreactivity of APP in the neuronal perikarya and reactive astrocytes near the region of injury in the cerebral cortex 24 h to 7 days after injury. In the hippocampus, APP accumulated in the CA3 neurons 24 h and 3 days after injury, although no hemorrhagic lesions were seen at that site. The APP positive neurons in CA3 showed shrunken cell bodies and pyknotic nuclei 3 days after injury, and some of the neurons in CA3 had disappeared by 7 days postinjury. The results of present study suggest that traumatic brain injury induces overexpression and accumulation of APP in neuronal perikarya and that these events are followed by degeneration of CA3 neurons. Further, the decline in APP expression in the hippocampus is thought to be due to neuronal loss in CA3 subsector.

Amyloid beta-Peptides↗

PubMed1998

Chronic thyroiditis as a favorable prognostic factor in papillary thyroid carcinoma.

A subgroup of patients with papillary thyroid carcinoma (PTC) also has chronic thyroiditis (CT) as an associated disease of the thyroid. To assess the prognostic value of CT in patients with PTC, we reviewed the histological slides of 2225 patients with PTC who had undergone surgery between 1971 and 1992. Of the 2225 patients, 692 were excluded from the analysis because regional lymph nodes and/or nonneoplastic thyroid tissues were unavailable for histological assessment. The series included 281 patients with CT in nonneoplastic thyroid tissue and 1252 without CT. We performed statistical analyzes by the log-rank test and Cox's proportional-hazard method. Sixty-two (5.0%) of the 1252 patients without CT died of metastatic disease during the follow-up period and the relapse-free 10-year survival rate was 85%. By contrast, only 2 (<1.0%) of the 281 patients with CT died, and their relapse-free 10-year survival rate was 95%. The difference between patients with CT and those without CT in terms of relapse-free and overall survival was statistically significant (p < 0.0001). Risk factors for unfavorable outcome were age 45 years or more, absence of psammoma bodies, and absence of CT (p < 0.0001), followed by vascular invasion (p = 0.0007), male sex (p = 0.0013), and metastasis to regional lymph nodes (p = 0.047). Multivariate analysis indicated that all of these factors with the exception of gender were independent factors in the final model for overall survival. Chronic thyroiditis in the nonneoplastic thyroid of patients with PTC is a powerful prognostic factor for both relapse-free and overall survival.

Adult↗