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Biomedical subjects

S Kojima

Publications and source records attributed to S Kojima.

At least 577 records · Page 32Linked to original sources
PubMed1993

[Hemolysis of isolated erythrocytes by UVA-sensitization of flavins].

Riboflavin (RF), flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD) caused hemolysis of isolated rabbit erythrocytes by UVA-sensitization. Hemolysis induced by UVA-sensitization with RF and FMN was inhibited by 1.0 mM histidine and EDTA, and was promoted by 0.15 mM histidine and 0.01 mM NaN3. Hemolysis induced by irradiation in anaerobic condition was smaller than those in aerobic condition. Hemolysis was proceeded in the dark for 5 hours after the UVA-irradiation with RF and FAD. Erythrocyte treated by UVA-sensitization with RF easily caused hypotonic hemolysis.

Animals↗
PubMed1993

[A case of Down syndrome complicated with Becker muscular dystrophy].

A 22-year-old man with Down syndrome had a history of progressive muscular wasting which began at the age of 12 years. Serum CK level was elevated to 545 U/l (normal < 150) and muscle CT scan revealed patchy low density areas in the proximal muscles. A muscle biopsy specimen revealed marked dystrophic changes with patchy immunostaining for dystrophin. Multiplex PCR analysis of the genomic DNA extracted from peripheral blood lymphocytes disclosed a deletion of exons 45-47 of the dystrophin gene, confirming a diagnosis of Becker muscular dystrophy (BMD). This is the first report of Down syndrome complicated with BMD. Careful observation is required in detecting a coexistence of myopathy in mentally retarded patients.

Adult↗
PubMed1993

Fatal spontaneous pneumocystosis in nude rats.

Spontaneously generated fatal pneumocystosis was found in a congenitally athymic nude (rnu/rnu) rat colony. Severe pulmonary pneumocystosis was seen in rnu/rnu rats, and 10(7) to 10(8) cysts per lung were detected. No histologic changes were seen nor were Pneumocystis carinii organisms detected in heterozygous rnu/+ rats. Indirect immunofluorescence revealed strong reactivity in the sera from rnu/+ rats with rat-P. carinii cysts (originated from Wistar strain), compared with mouse- or human P. carinii cysts. The cysts isolated from rnu/rnu rats reacted strongly with antirat-P. carinii rat serum in comparison with antimouse-P. carinii rabbit serum and serum from a human with pneumocystosis. Immunoblotting studies using rat-P. carinii antigen showed that 116-kDa antigen reacted with the antirat-P. carinii serum and sera from rnu/+ rats but not with the antimouse-P. carinii serum and the serum from a human with pneumocystosis, whereas 52-kDa antigens of rat-P. carinii were recognized by all the anti-P. carinii sera tested. On the basis of our findings, the outbreak was caused by the P. carinii indigenous to the rat.

Animals↗
PubMed1993

[Clinical types of spinocerebellar degeneration and evaluation with MR imaging].

Eighty one patients with the clinical diagnosis of non-hereditary or hereditary spinocerebellar degeneration were examined by magnetic resonance imaging (MRI). The MRI findings were subdivided into non-cerebellar atrophy, cerebellar atrophy without and with apparent enlargement of the fourth ventricle as a result of atrophy of the middle or superior cerebellar peduncles. The first pattern of non-cerebellar atrophy included ataxias such as Friedreich's ataxia and Machado-Joseph disease (MJD; type II). In the patients with MJD, atrophy of the brainstem was frequently recognized. The second pattern largely included late cortical cerebellar atrophy and hereditary ataxia of Holmes type. The third pattern was subdivided further into atrophies of the middle and superior cerebellar peduncles. The pattern of the former included olivo-ponto-cerebellar atrophy (OPCA) and hereditary ataxia of Menzel type, and the pattern of the latter included MJD and dentato-rubro-pallido-luysian atrophy (DRPLA). In the patients with OPCA and hereditary ataxia of Menzel type, increased signal intensity on T2-weighted image was always observed in the transverse pontine fibers, middle cerebellar peduncles. In several patients with MJD and DRPLA, atrophy of both cerebellar peduncles was demonstrated, but abnormal signal intensity was not observed in the pontocerebellar areas.

Cerebellum↗
PubMed1993

Clinical features of primary human herpesvirus-6 infection in an infant with acute lymphoblastic leukemia.

PURPOSE: The primary infection with human herpesvirus-6 developed concurrently with diagnosis of acute lymphoblastic leukemia and initiation of intensive chemotherapy for the disease in a 4-month-old girl. RESULTS: Prolonged viremia persisted for 7 days in the presence of neutralizing antibodies, and clinical features such as prolonged febrile and diarrheal period, no appearance of skin rash, and marked bulging fontanelle for 7 days in the absence of the virus DNA in spinal fluid may suggest an atypical clinical course of exanthem subitum and an unusual viral replication in immunocompromised condition.

DNA, Viral↗
PubMed1993

[Bilateral internal carotid artery stenoses in a patient with meningovascular neurosyphilis].

We report a 37-year-old man with cerebral infarction due to meningovascular neurosyphilis. He developed right hemiplegia and motor aphasia preceded by left retroorbital pain lasting a month. Bilateral tonic pupils were also observed. Magnetic resonance imaging (MRI) disclosed cerebral infarction in the distribution of perforating branches of the left middle cerebral artery. Abnormal enhancement was absent in the meninges on T1-weighted MRI examination. SPECT study with I-123 iodoamphetamine showed decreased perfusion in the area of the left middle cerebral artery on early phase. A delayed SPECT 4 hour later demonstrated redistribution of the cerebral blood flow in the area of its cortical branches. On cerebral angiograms, marked stenoses were disclosed at the supraclinoid segments of the bilateral internal carotid arteries as well as the M1 segment of the left middle cerebral artery. These stenoses were associated with increased collateral circulations on the left side. Atherosclerosis was not apparent, on angiography. The cerebrospinal fluid (CSF) showed pleocytosis and positive TPHA. The CSF/serum ratio of TPHA was 1/16. Oligoclonal IgG band was present in the CSF. CSF IgG index was elevated. These findings were consistent with meningovascular neurosyphilis. Causes of angiitis other than syphilis were excluded. A test for antibodies against human immunodeficiency virus was negative. The clinical course of his recovery was similar to that in patients with atherosclerotic thrombosis. The stenosis of the right internal carotid artery demonstrated by angiography could not be expected from the clinical manifestations and SPECT study.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Wernicke's encephalopathy in a child with acute lymphoblastic leukemia.

PURPOSE: We describe the case of a 9-year-old boy who developed Wernicke's encephalopathy while receiving chemotherapy for acute lymphoblastic leukemia (ALL). PATIENTS AND METHODS: After suffering anorexia for 4 weeks following chemotherapy, he exhibited nystagmus and ataxia. Symptoms rapidly worsened following an increased glucose load, and included a depressed consciousness, irregular respiration, and ophthalmoplegia. The serum thiamine level was 9 ng/ml (normal: 20-50). Cranial computed tomography (CT) revealed a low density area bilaterally at the neostriatum. Thiamine 100 mg/day was administered intravenously. RESULTS: The patient's neurological signs improved dramatically. However, he subsequently developed pancytopenia and died of pneumonia. CONCLUSION: The possibility of Wernicke's encephalopathy should be considered in children who are receiving chemotherapy for malignant disease when a persistent loss of appetite is followed by such neurological symptoms as nystagmus and ataxia.

Anorexia↗
PubMed1993

[Late onset seizures in cerebral infarction--clinical study of late onset seizures in cortical branch infarction].

We retrospectively analyzed the clinical features, prognosis, CT scans and electroencephalograms in 527 patients with cerebral infarction in the Toranomon hospital between 1983 and 1990. CT scans revealed cortical involvement in 130 cases and subcortical infarcts in the territory of the perforating branch arteries in 397 cases. The mean duration of the follow up was 38.5 +/- 27 months (M +/- SD). Of these, late onset seizures developed in 5.69% (30/527). The incidence of seizures after cortical branch infarcts was 20% (26/130), which was significantly higher than that after subcortical infarcts (1%; 4/397) (p < 0.05). These late seizures could be either generalized or partial seizures. The interval between stroke and the onset of seizures was 2.4 years (mean), and 78% of late onset seizures developed within 3 years after the stroke. CT scans of the patients with late seizures showed that infarcted area was located mainly in the territory of the left middle cerebral artery. The incidence of late seizures was significantly higher in patients with left cortical infarction (12/41, 29.3%) than those with right one (6/29, 15.4%, p < 0.05). These results suggest that left-sided cortical involvement may have some liability to late onset seizures in patients with cerebral infarction. Further study on indication of prophylactic use of anticonvulsants might be requested in patients with right hemiparesis and aphasia.

Aphasia↗
PubMed1993

[Treatment of aplastic anemia with antithymocyte globulin, Lymphoser Berna].

Twenty-four patients with aplastic anemia (19 severe: 5 moderate) were treated with combined immunosuppression consisting of antithymocyte globulin (ATG: Lymphoser Berna, Swiss Serum and Vaccine Institute Berne) and high-dose methylprednisolone. Danazol or meptiostane was administered concurrently for at least 3 months. Three batches of ATG were used, two were not absorbed with thrombocytes and one was absorbed with thrombocytes for the prevention of thrombocytopenia. Nine of 20 evaluable patient (45%) had sustained improvement in hematopoiesis within 3 months of treatment. Nine of 14 patients (64%) showed a response to ATG without thrombocyte absorption, on the other hand, none of 6 patients responded to ATG with thrombocyte absorption. By life table analysis, the 3 year probability of survival was 81 +/- 27% after the combined immunosuppressive therapy. These results indicated that ATG therapy was very effective in Japanese patients with aplastic anemia.

Adolescent↗
PubMed1993

[Magnetic resonance imaging in chronic toluene abuse, and volitional hyperkinesia].

We described the central nervous system impairments and findings of magnetic resonance imaging (MRI) of the brain in three chronic toluene abusers. Patient 1 and 2 had a history of chronic toluene inhalation for 1 or 2 years and patient 3 has a history of it for 16 years. The patients were evaluated after an abstinence period of at least 4 weeks, to avoid neurologic effects of acute intoxication. Neurologic signs included cerebellar, cognitive and pyramidal dysfunctions in all 3 patients and hyperkinésie volitionnelle (HV; volitional hyperkinesia) in patient 3 who had a long history of toluene inhalation. This HV was found to be tremulous by surface electromyography. Appearance of HV in chronic toluene abuse seems to be related to a period or quantity of inhalation of toluene. T2-weighted MRI in the 3 patients revealed the following abnormalities: (1) increased signal intensity of middle cerebellar peduncle and cerebellar white matter, deep cerebral white matter, and posterior limb of internal capsule; and (2) decreased signal intensity of thalamus and basal ganglia. Proton-weighted MRI in patient 3 with HV showed decreased signal intensity of lateral portion of the thalamus and tegmentum of the brainstem. These MRI findings correlate remarkably well with the neurologic signs seen in the 3 patients. Cerebellar, cognitive, and pyramidal dysfunctions appear to be related to involvement of middle cerebellar peduncle (cerebellar white matter), deep cerebral white matter, and internal capsule, respectively, and HV seems to correlate with involvement of the thalamus or tegmentum of the brainstem, especially the latter.

Adult↗
PubMed1993

Inhibitory effect of 5,6,7,8-tetrahydroneopterin on adriamycin-induced cardiotoxicity.

The protective effect of the reduced form of neopterin, 5,6,7,8-tetrahydroneopterin (NPH4), against the cardiotoxicity of adriamycin (ADR) was evaluated in mice by assay of serum creatine phosphokinase (CPK) and heart lipid peroxide (i.e., thiobarbituric acid reactive substances, TBARS). The activity of CPK was drastically elevated at around 3 days after a single s.c. injection of ADR and had returned to normal at 6 days. There were no marked changes in the TBARS content of the heart by 6 days, but a significant increase was apparent at about 8 days after ADR treatment. The effect of NPH4 was evaluated in terms of the serum CPK activity at the 4th day and in terms of TBARS content at the 8th day after ADR treatment. The elevation of CPK activity induced by ADR was significantly suppressed by two treatments with NPH4 every day for 4 days, i.e., from day 0 to day 3 after injection of ADR, at doses of 3 mg/kg and 0.3 mg/kg. The increase of TBARS content in the heart at 8 days after ADR treatment was also suppressed at both doses of NPH4. The effect of the timing of NPH4 treatment on the suppression of elevated CPK was examined. The suppressive potency of NPH4 could not be elicited by any treatment schedule that terminated at or before 2 days after injection of ADR. Consecutive treatments from day 0 to day 3 after injection of ADR were effective, as was a simple schedule of only two treatments with NPH4 on day 3.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Two distinct portions of LTG19/ENL at 19p13 are involved in t(11;19) leukemia.

We previously isolated cDNA clones, MLL-a and MLL-b, derived from the 11q23 breakpoint region and detected gene rearrangements with MLL-b cDNA in infantile leukemia cell lines with 11q23 abnormalities. We also showed chimeric mRNAs between MLL and genes on partner chromosomes such as 4q21 and 19p13. In the present study, we isolated overlapping MLL cDNA clones of 11 kb and demonstrated that MLL-a and MLL-b were derived from the same gene, MLL/ALL-1/HRX. Northern analysis with an MLL cDNA probe detected different signals in t(11;19) cell lines, one being sized 10 kb in two cell lines, KOCL-33 and KOCL-44, and the other being 9.2 kb in the cell line, KOPN-1. To elucidate the molecular basis for the heterogeneity, we isolated cDNA clones of a translocation-associated gene on chromosome 19, LTG19, as well as chimeric cDNAs from KOPN-1. Northern analysis with LTG19 cDNA demonstrated the identical gene, encoding serine/proline rich 559 amino acid polypeptide, to be involved in all three cell lines. Sequence comparison revealed that the LTG19 portion of the predicted chimeric protein of KOPN-1 was fused in frame and contained the C-terminal 189 amino acids. This was shorter by 366 amino acids than those of KOCL-33 and KOCL-44, also fused in frame. Reverse transcriptase-PCR analysis demonstrated complex chimeric mRNAs in cell lines and leukemia samples. Although a chimeric mRNA of KOPN-1 type was rare, its presence suggested that the shared C-terminal portion of 189 amino acids of LTG19 contains important signal(s) for malignant transformation.

Amino Acid Sequence↗
PubMed1993

[Aberrant expression of major histocompatibility complex class II antigen in inflammatory myopathies].

Although major histocompatibility complex (MHC) class I molecules have been consistently demonstrated on muscle fibers of patients with inflammatory myopathies (IM), results concerning the expression of MHC class II molecules have been conflicting and mechanism of the expression remains to be elucidated. Expression of MHC and neural cell adhesion molecules (N-CAM) was analyzed in 38 cases of IM and in 13 cases of normal and disease controls by the immunocytochemical method. The sarcolemmaL HLA-ABC molecules were seen in all IM cases, and were visualized on the every muscle fiber in 68% of the cases. In contrast, the HLA-DR, -DP, or -DQ expression was seen on scattered fibers in 37%, 11%, 5% of IM cases, respectively. The HLA-DR reactivity was often seen on muscle fibers in the vicinity of infiltrating cells or on the perifascicular fibers. The HLA-DR positive fibers did not express N-CAM, suggesting a degenerating/regenerating process of muscle fibers was not contributory to the aberrant expression of MHC class II molecules. The perifascicular HLA-DR expression was related to the perifascicular atrophy and was more frequent in polymyositis complicated with interstitial pneumonitis. Those results suggest that increased expression of MHC class I molecules precede the aberrant expression of MHC class II molecules, and the perifascicular atrophy might reflect immunopathological processes.

Adult↗
PubMed1993

[IgA nephropathy with acute exacerbation of idiopathic interstitial pneumonia: an autopsy case].

A 73-year old man was admitted to the hospital because of dyspnea. His proteinuria was pointed out in 1981. He felt dyspnea after exertion and abnormal chest X-ray shadow was pointed out in 1984. He was admitted to our hospital for further examination for the first time in 1988. He was diagnosed as IgA nephropathy by renal biopsy, and idiopathic interstitial pneumonia (IIP) by transbronchial lung biopsy. Then steroid therapy was begun because of progression of renal dysfunction in November 1990. But thereafter dyspnea, hypoxia and fine diffuse reticulonodular shadow on chest X-ray film was exacerbated. And he died because of respiratory failure. In this case, progression of IgA nephropathy seemed associated with exacerbation of IIP.

Aged↗
PubMed1993

[A case of multiple broncholithiasis caused by mucus retention].

The patient was a 57-year-old male with long-standing bronchiectasis who developed severe respiratory failure and died in 1991. Autopsy revealed multiple broncholithiasis in both lungs, but no calcified lymph nodes in the hilar region. Since histological examination of the broncholiths showed only stratified structures but no tissue structure, most likely cause was considered to be calcification of mucus in the bronchi. Analysis of the stone components revealed 78% calcium and 22% protein. This patient represents a case of multiple broncholithiasis caused by mucus retention, which is thought to be very rare.

Adult↗