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Biomedical subjects

I Nakano

Publications and source records attributed to I Nakano.

At least 145 records · Page 8Linked to original sources
PubMed1997

Naive and memory T cell infiltrates in chronic hepatitis C: phenotypic changes with interferon treatment.

The phenotypes of infiltrating lymphocytes in liver with chronic hepatitis C, including changes associated with interferon (IFN) treatment, were characterized. Specimens obtained from 22 patients treated with IFN were examined using avidin-biotin-peroxidase immunohistochemistry. In areas of lobular and periportal inflammation, most lymphocytes were CD8+ T cells of the CD45RO+ (memory) subset. The centres of lymphoid follicles were occupied by CD20+ B cells and a few CD4+ T cells which were CD45RA+ (naive subset). Follicular centres were surrounded mainly with CD4+ T cells. CD8+ T cells, mostly CD45RO+, were scattered through the mantle zones of follicles and extended around them. No significant changes in CD45RA+ lobular infiltrates accompanied IFN treatment. On the other hand, the number of CD45RO+ lobular infiltrates decreased after IFN treatment in complete responders (P < 0.01). Moreover, there were significant correlations between CD45RO+ cell counts and serum alanine aminotransferase concentrations, CD45RO+ cell counts and the liver histologic grade and CD45RO+ cell counts and CD8+ cell counts. These results suggest that CD8+ memory T cells participate in hepatocyte injury in chronic hepatitis C, and that a decrease of CD8+ memory T cells correlates with the decreased liver inflammation with IFN treatment.

Adult↗
PubMed1997

Japanese families with autosomal dominant pure cerebellar ataxia map to chromosome 19p13.1-p13.2 and are strongly associated with mild CAG expansions in the spinocerebellar ataxia type 6 gene in chromosome 19p13.1.

Autosomal dominant cerebellar ataxia is a group of clinically and genetically heterogeneous disorders. We carried out genomewide linkage analysis in 15 families with autosomal dominant pure cerebellar ataxia (ADPCA). Evidence for linkage to chromosome 19p markers was found in nine families, and combined multipoint analysis refined the candidate region to a 13.3-cM interval in 19p13.1-p13.2. The remaining six families were excluded for this region. Analysis of CAG-repeat expansion in the alpha1A-voltage-dependent calcium channel (CACNL1A4) gene lying in 19p13.1, recently identified among 8 small American kindreds with ADPCA (spinocerebellar ataxia type 6 [SCA6]), revealed that 8 of the 15 families studied had similar, very small expansion in this gene: all affected individuals had larger alleles (range of CAG repeats 21-25), compared with alleles observed in neurologically normal Japanese (range 5-20 repeats). Inverse correlation between the CAG-repeat number and the age at onset was found in affected individuals with expansion. The number of CAG repeats in expanded chromosomes was completely stable within each family, which was consistent with the fact that anticipation was not statistically proved in the SCA6 families that we studied. We conclude that more than half of Japanese cases of ADPCA map to 19p13.1-p13.2 and are strongly associated with the mild CAG expansion in the SCA6/CACNL1A4 gene.

Adult↗
PubMed1997

Single sperm analysis of the CAG repeats in the gene for Machado-Joseph disease (MJD1): evidence for non-Mendelian transmission of the MJD1 gene and for the effect of the intragenic CGG/GGG polymorphism on the intergenerational instability.

To investigate the mechanism of the meiotic instability of expanded CAG repeats in the gene for Machado-Joseph disease (MJD1), we analyzed the CAG repeat sizes of 1036 single sperm from six individuals with Machado-Joseph disease (MJD). The segregation ratio between single sperm with an expanded allele and those with a normal allele is significantly different (P <0.0001) from the expected 1:1 segregation ratio, which demonstrates segregation distortion of expanded alleles in male meiosis. In single sperm from individuals with the [expanded (CAG)n-CGG]/[normal (CAG)n-GGG] genotype, significantly greater instability of the CAG repeat was observed compared with single sperm from individuals with the [expanded (CAG)n-CGG]/[normal (CAG)n-CGG] genotype (F-test, P <0.001). These findings in single sperm confirm non-Mendelian transmission of the MJD1 gene and the effect of the intragenic CGG/GGG polymorphism on the intergenerational instability of the CAG repeats in the MJD1 gene, which have been observed in clinical and genetic studies. Our results indicate similarities and dissimilarities between MJD and Huntington's disease or myotonic dystrophy in terms of the inter-allelic interaction, segregation distortions and size distribution of trinucleotide repeats in mutant alleles. Further study is required to determine whether there is a common mechanism underlying the instability of the triplet repeats in 'triplet repeat diseases'.

Alleles↗
PubMed1997

Choroid plexus papilloma in the posterior third ventricle: case report.

OBJECTIVE AND IMPORTANCE: The case of a 42-year-old woman with a choroid plexus papilloma (CPP) arising from the posterior wall of the third ventricle is described. This case is very unusual because the tumor did not have any connection with the choroid plexus but was attached to the normal brain parenchyma. CLINICAL PRESENTATION: The patient presented with the symptoms of increasing intracranial pressure. Magnetic resonance imaging revealed hydrocephalus related to a small mass in the posterior third ventricle, occluding the aqueduct. INTERVENTION: Surgery confirmed that the tumor was located at the surface of the posterior commissure without having any connection to the normal choroid plexus. A histopathological examination revealed a CPP with no attachment to the choroidal tissue. CONCLUSION: A review of the literature demonstrates that CPPs without any connection to the choroid plexus are very unusual. To our knowledge, this is the first reported case of such a CPP that developed on the posterior wall of the third ventricle in which no choroid plexus was present. Furthermore, this tumor, to our knowledge, is also the smallest intraventricular CPP to be verified at surgery.

Adult↗
PubMed1997

Effect of Irsogladine on gap junctions in cerulein-induced acute pancreatitis in rats.

The capacity for intercellular communication (IC) via gap junctions is found in normal pancreatic acinar cells. The major role of IC is considered to be the maintenance of tissue homeostasis and the regulation of signal transmissions. Up to now, the participation of IC via gap junctions in acute pancreatitis has not been reported. We investigated the role of IC in cerulein (Cn)-induced acute pancreatitis in rats using irsogladine, an enhancer of IC via gap junction. Acute edematous pancreatitis was induced in rats by two intraperitoneal injections of 40 micrograms/kg Cn. Rats received various doses (25, 50, or 100 mg/kg body weight) of irsogladine orally, 15 and 2 h before the first Cn injection. The normal control group received only vehicle. The severity of pancreatitis was evaluated enzymatically and histologically 5 h after the first Cn injection. In Cn-induced acute pancreatitis, irsogladine significantly lowered the serum amylase level, the pancreatic wet weight, and the pancreatic amylase and DNA contents, in a dose-dependent manner. Particularly, the amylase content improved to the level of the normal controls. Histologically, the severity of pancreatitis was reduced significantly by treatment with irsogladine and no discernible vacuolization was seen in the group with 100 mg/kg irsogladine treatment. By immunofluorostaining pancreata with anti-connexin 32 (Cx32; a gap junction protein) antibody, we found that pancreatic acini were diffusely positive for Cx32 in the control group, but the number of Cx32-positive grains decreased markedly, to 19%, in the pancreatitis group. With 100 mg/kg irsogladine treatment, the number of Cx32 grains recovered to 70% of the normal control value. These findings indicate that IC via gap junction is disturbed in Cn-induced pancreatitis, which may result in the breakdown of tissue homeostasis and the progression of acute pancreatitis.

Acute Disease↗
PubMed1997

Serum levels of tissue inhibitor of metalloproteinases-2 and of precursor form of matrix metalloproteinase-2 in patients with liver disease.

Serum levels of tissue inhibitor of metalloproteinases-2 (TIMP2) and of precursor form of matrix metalloproteinase-2 (proMMP2) were determined in patients with chronic hepatitis and hepatocellular carcinoma by a one-step sandwich enzyme immunoassay. Serum levels of TIMP2 and proMMP2 were significantly higher in patients with chronic liver disease, than in normal controls. Serum levels of TIMP2 showed a weak negative correlation with the serum albumin level and prothrombin time (PT). Serum levels of proMMP2 in patients with chronic hepatitis were strongly correlated with those of type IV collagen and were negatively correlated with PT and serum albumin levels. Serum proMMP2 levels were also significantly correlated with histological stages. These data indicate that serum levels of proMMP2 might be useful in the follow-up of patients with chronic hepatitis.

Adult↗
PubMed1997

Immunization with plasmid DNA encoding hepatitis C virus envelope E2 antigenic domains induces antibodies whose immune reactivity is linked to the injection mode.

Plasmids expressing different domains of the hepatis C virus (HCV) envelope E2 glycoprotein from a genotype 1a isolate were constructed to compare the immunogenic potential of E2 in nucleic acid-based immunizations. One plasmid, pCIE2t, expressed a C-terminally truncated form of E2, while others, pS2.SE2A to pS2.SE2E, encoded the adjacent 60-amino-acid (aa) sequences of E2 (inserts A to E) expressed as a fusion with the hepatitis B virus surface antigen. BALB/c mice were given injections of the plasmids intramuscularly (i.m.) or intraepidermally (i.e.) via a gene gun (biolistic introduction), and induced humoral immune responses were evaluated. The i.e. injections resulted in higher seroconversion rates and antibody titers, up to 100-fold, than did the i.m. injections (P = 0.01 to 0.04). Three restricted immunogenic domains, E2A (aa 384 to 443), E2C (aa 504 to 555), and E2E (aa 609 to 674), that yielded antibody titers ranging from 1:59 to > 1:43,700 could be identified. Subtype 1a- and 1b-derived E2 antigens and synthetic peptides were used in Western blot and enzyme-linked immunosorbent assay analyses, which revealed that the cross-reactivity of the plasmid-induced antibodies was linked both to the type of antigen expressed and to the injection mode. Induced anti-E2 antibodies could immunoprecipitate noncovalent E1E2 complexes believed to exist on the surface of HCV virions. This study allowed us to identify restricted immunogenic domains within E2 and demonstrated that different routes of injection of HCV E2 plasmids can result in quantitatively and qualitatively different humoral immune responses.

Animals↗
PubMed1997

Machado-Joseph disease: cerebellar ataxia and autonomic dysfunction in a patient with the shortest known expanded allele (56 CAG repeat units) of the MJD1 gene.

We describe an unusual case of a patient with Machado-Joseph disease (MJD) who showed autonomic dysfunctions in addition to cerebellar ataxia. The number of CAG repeat units in the expanded allele of the MJD1 gene of the patient is smaller (56 CAG repeat units) than all previously reported numbers of CAG repeat units in expanded alleles. Thus, the findings in this patient indicate that the clinical features of MJD cover a wider spectrum than previously thought.

Alleles↗
PubMed1997

Pathological characterization of astrocytic hyaline inclusions in familial amyotrophic lateral sclerosis.

To clarify the pathological characteristics of astrocytic hyaline inclusions (Ast-HIs) in patients with familial amyotrophic lateral sclerosis (FALS) with neuronal Lewy-body-like hyaline inclusions (LBHIs), eight autopsies on members of four different families, including two long-term surviving patients with clinical courses of over 10 years, were analyzed. Ast-HIs were found only in the two long-term surviving patients who belonged to different families and to different races. Ast-HIs were ultrastructurally composed of 15- to 25-nm granule-coated fibrils that had immunoreactivities to superoxide dismutase 1 (SOD1) and ubiquitin. Approximately 50% of the Ast-HIs expressed alpha B-crystallin, metallothionein, glutamine synthetase, and tubulin (alpha and beta) at various intensities. Some Ast-HIs reacted with antibodies to tau protein, S-100 protein, and heat shock protein 27. The Ast-HIs were not stained for glial fibrillary acidic protein. Our results suggest a cooperative role of superoxide dismutase 1, ubiquitin, and cytoskeletal proteins in the formation of granule-coated fibrils (namely, Ast-HIs) and provide evidence that Ast-HIs are formed in certain long-surviving familial amyotrophic lateral sclerosis patients with neuronal Lewy-body-like hyaline inclusions.

Adult↗
PubMed1997

A case of successfully treated giardiasis in pancreas.

We report a case of giardiasis in the pancreas in a patient with diabetes mellitus. The patient is interesting in the following: 1) Giardia lamblia was found only in the pancreas and not in the gall bladder by cytology on endoscopic retrograde cholangiopancreaticography (ERCP) and by cerulein-secretin test (CST). 2) ERCP revealed multiple small cysts scattered throughout the pancreas. 3) Decreased pancreatic exocrine function was recovered by treatment with metronidazole.

Aged↗
PubMed1996

Nucleotide sequence diversity of hypervariable region 1 of hepatitis C virus in Japanese hemophiliacs with chronic hepatitis C and patients with chronic posttransfusion hepatitis C.

Hemophiliac patients with chronic hepatitis C might be exposed to and become infected with multiple hepatitis C virus (HCV) strains by means of frequent use of blood products, even if they are infected with a single subtype of HCV. To test this hypothesis, we analyzed the genetic diversity of hypervariable region 1 (HVR1) of HCV in chronically infected hemophiliacs and in patients with chronic posttransfusion hepatitis with a single HCV inoculation. The diversity of nucleotide sequences in HVR1 of serum HCV RNA was compared between 21 hemophiliacs infected with a single HCV subtype and 16 patients with posttransfusion HCV infection. The number of HCV quasispecies was determined by fluorescence single-strand conformation polymorphism (SSCP) analysis. Direct sequencing was performed to determine the diversity in HVR1. The number of HCV quasispecies in the blood was 5.2 +/- 2.0 clones in hemophiliacs and 4.0 +/- 2.3 clones in posttransfusion patients, a nonsignificant difference (P = .0943). The number of sites at which the nucleotide was not homogenous in all quasispecies was significantly higher in hemophiliacs (13.0% +/- 7.4%) than in posttransfusion hepatitis patients (2.7% +/- 2.8%; P < .0001). In conclusion, there was a high degree of genetic variation in HVR1 of HCV specimens isolated from hemophiliacs compared with posttransfusion patients. These findings indicate the possibility that multiple infections of a single HCV subtype may occur among patients frequently exposed to blood products; single HCV subtypes may therefore derive from multiple origins.

Adult↗
PubMed1996

The induction of cardioangitis by Lactobacillus casei cell wall in mice. I. The cytokine production from murine macrophages by Lactobacillus casei cell wall extract.

A single intraperitoneal injection of the water-soluble cell wall extract from Lactobacillus casei (LCWE) in mice can induce acute inflammatory heart involvement such as cardiac arteritis, similar to the heart lesions in Kawasaki disease. To clarify whether inflammatory cytokines participate in pathogenic mechanisms of LCWE-induced cardioangitis in mice, we studied in vitro cytokine production (IL-1, TNF alpha, and IL-6) from peritoneal macrophages (M phi) stimulated with LCWE in comparison with that of lipopolysaccharide (LPS). LCWE significantly activated M phi of BALB/c in production of IL-1 and TNF alpha compared with LPS. However, the magnitude of IL-6 synthesis by LCWE was approximately similar to that of LPS. These results demonstrate that the pathogenesis of LCWE- induced cardiac lesions may be associated with increased production of inflammatory cytokines.

Animals↗
PubMed1996

Collagen-encapsulated coagulation necrosis in cerebral infarcts: a pathological study.

Coagulation necrosis (CN)--a type of necrosis characterized by firm, eosinophilic parenchyma with recognizable cell outlines--is thought to be a result of rapid degeneration of tissue protein to a gel state and loss of water which prevents the necrotic tissue from undergoing autolysis and cellular digestion. In this study, we observed CN in cerebral infarcts of 11 of 150 consecutive autopsy cases of large cerebral infarction. Cerebral CN in patients who had survived for about 1 month had already started to be surrounded by newly formed vessels and type I collagen-positive tissue. In patients who had survived for more than 1 year, CN was deposited with calcium and cholesterin crystals and encapsulated by thick, dense collagenous tissue. Encapsulation, however, was not always complete, a finding that suggests that other factors, such as gel transformation at an early stage of CN and calcification at a later stage, are important for the persistence of CN in the infarct. The results of our study suggest that cerebral CN occurs more frequently than is generally believed.

Aged↗
PubMed1996

Are breaches in the glia limitans the primary cause of the micropolygyria in Fukuyama-type congenital muscular dystrophy (FCMD)? Pathological study of the cerebral cortex of an FCMD fetus.

A light and electron microscopic study of the brain of an 18-week fetus with a prenatal genetic diagnosis of Fukuyama-type congenital muscular dystrophy revealed a widespread mantle of abnormal neurogliomesenchymal tissue that covered a dysplastic cerebral cortex. In this area alone, the glia limitans that adjoined the abnormal mantle via one or two layers of basal lamina had frequent breaches, through which neuroglial elements extruded. In the most severely affected cortical region, which had only a rudimentary and fragmentary glia limitans, the majority of cortical neurons had migrated into the neurogliomesenchymal tissue. The massive overmigrated neurons still maintained a somewhat columnar arrangement, and the marked dysplasia abruptly shifted to a neurogliomesenchymal tissue-free normal cortical structure with an intact glia limitans, thus indicating essentially vertical overmigration of neurons without significant tangential migration of them. Together the above findings imply that breaches in the glia limitans may be the primary cause of the micropolygyria seen in this genetic disorder.

Cerebral Cortex↗
PubMed1996

Progressive supranuclear palsy with asymmetric lesions in the thalamus and cerebellum, with special reference to the unilateral predominance of many torpedoes.

This report concerns a notable case of progressive supranuclear palsy exhibiting asymmetric dentate nucleus and thalamic degeneration with numerous torpedoes. The neuronal loss in the ventral lateral nucleus of the thalamus was predominant on the right side, while in the cerebellum, a quantitative study revealed the contralateral predominance of the neuronal loss in the dentate nuclei and torpedo formation, with preserved Purkinje cells. The abnormal tau-protein-related profiles in the two nuclei did not show any laterality in their distribution, indicating that the dentatothalamic tract may have been affected in a non-specific way in this case. In addition, the fact that the prominent sites of torpedo formation and loss of dentate nucleus neurons are identical supports the hypothesis that the torpedoes may be formed in association with neuronal loss in the dentate nucleus because of a plausible metabolic change in Purkinje cells through synaptic detachment of their axon terminals.

Aged↗
PubMed1996

Some unusual responses of astrocytes to ghost tangles in a long duration case of juvenile Alzheimer's disease: an electron microscopic study.

The ghost tangles (GTs) in usual Alzheimer's disease are separated into small bundles of abnormal straight filaments by many invading astrocytic processes lacking a basal lamina (BL). An electron microscopic study of GTs in the Ammon's horn of a case of juvenile Alzheimer's disease of 25 years' duration, however, revealed that only a small number of astrocytic processes had infiltrated the GTs, resulting in the GTs being composed of large bundles. Moreover, the majority of glial processes that had invaded or apposed GTs possessed an interrupted but still fairly well-developed BL with hemidesmosome-like profiles. Although pia-arachnoid cells are required for astrocytes to form a continuous BL, astrocytes can have a segmental BL on their surface facing even empty intercellular spaces within the brain parenchyma. The much greater frequency and better development of the GT-associated BL in our case indicate that the GT filaments somehow increased the ability of astrocytes to form a BL. On the other hand, the scarcity of GT-invading astrocytic processes implies that many of the glial processes that had once penetrated GTs had been withdrawn, with the result that GTs escaped expectable endocyto-phagocytosis by astrocytes.

Alzheimer Disease↗
PubMed1996

An autopsy case of Marchiafava-Bignami disease with peculiar chronological CT changes in the corpus callosum: neuroradiopathological correlations.

We conducted a comparative analysis of the autopsy findings in a case of Marchiafava-Bignami disease with the X-ray computed tomography (CT) and magnetic resonance imaging (MRI) findings obtained while the patient was alive. Histologically, massive deposits of hemosiderin were demonstrated in the astrocytes and macrophages located in the walls of the callosal cystic lesion, suggesting that the transient increase in density during the subacute stage observed on X-ray CT is secondary to significant hemorrhage.

Adult↗