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Y Ikura

Publications and source records attributed to Y Ikura.

At least 19 recordsLinked to original sources
PubMed2006

Mast cells in diffuse large B-cell lymphoma; their role in fibrosis.

AIMS: Mast cells (MCs) are associated with fibrosis in various diseases. MCs comprise two phenotypes: the MC(TC) phenotype contains tryptase and chymase, whereas the MC(T) phenotype contains tryptase. Interleukin (IL)-4 promotes the development of MC(TC) from the MC(T) phenotype. The aim of this study was to determine the relationship between MC phenotypes and fibrosis in diffuse large B-cell lymphoma (DLBCL). METHODS AND RESULTS: We examined the distribution and density of MCs in 50 DLBCL and 20 reactive lymph nodes, and evaluated MC phenotypes and IL-4-expressing cells. To detect MCs, immunohistochemistry for tryptase and chymase was performed. The 50 DLBCLs were histologically divided into three groups: no fibrosis (32 cases), reticular type (eight cases) showing reticular fibrosis, and bundle type (10 cases) showing collagenous bundles. The density of tryptase-positive MCs was higher than that of chymase-positive MCs. The densities of tryptase-positive and chymase-positive MCs in fibrotic areas were significantly higher than those in the cellular areas in the reticular and bundle groups. Double immunostaining revealed that MCs in DLBCL comprised MC(T) and MC(TC) phenotypes. Chymase-positive MCs and T lymphocytes expressed IL-4. Although there were few chymase-positive MCs in reactive lymph nodes, the density of tryptase-positive MCs was not different from that in the 'no fibrosis' group. CONCLUSIONS: Tryptase-positive and chymase-positive MCs are associated with fibrosis in DLBCL.

Adult↗
PubMed2003

Mast cell chymase expression in Helicobacter pylori-associated gastritis.

AIMS: To study the role of mast cell chymase in the inflammatory processes of human chronic gastritis. Experimental studies have shown that mast cell chymase stimulates inflammatory cell accumulation, and contributes to angiotensin II formation. METHODS AND RESULTS: Tissue sections from human stomachs with Helicobacter pylori-associated gastritis (surgery/autopsy n = 20; biopsy n = 16) and normal stomachs (n = 10) were studied using immunohistochemical single and double labelling techniques. Monoclonal antibodies used were directed against mast cell chymase, tryptase, neutrophils (CD66b, elastase, and myeloperoxidase), macrophages, T-lymphocytes, and interleukin (IL)-4. The expression of angiotensin-converting enzyme and angiotensin II type 1 receptor was investigated using immunohistochemical analysis and the reverse transcription-polymerase chain reaction. The number of chymase-positive mast cells was significantly higher (P < 0.0001) in H. pylori-associated gastritis than in normal stomachs. Increased expression of chymase in inflamed mucosa was closely related to an increase in the accumulation of neutrophils, macrophages, T-lymphocytes, and IL-4-positive cells. The expression of angiotensin-converting enzyme and angiotensin II type 1 receptor was not altered in gastritis specimens. CONCLUSIONS: These observations suggest that mast cell chymase may be an important mediator in the inflammatory processes of human H. pylori-associated gastritis.

Chronic Disease↗
PubMed2003

Hepatitis C virus genotype testing in paraffin wax embedded liver biopsies for specimen identification.

Despite advances in medical technology, careful specimen identification is still a fundamental principle of laboratory testing. If pathological samples are mixed up, especially in the case of extremely small biopsy samples, large amounts of time and energy may be wasted in correctly identifying the specimens. Recently, two liver biopsy specimens were mixed up in this department, and a new pathological technology was used to resolve the issue. Liver biopsy was performed on two patients with hepatitis C virus (HCV) infection. During sample transfer or tissue processing, the biopsy specimens were mixed up. Because the ABO blood group of the two patients was identical (type AB), the specimens were subsequently identified by analysing the HCV genotypes. RNA extracted from the paraffin wax embedded liver specimens was examined by a polymerase chain reaction based HCV genotype assay. This enabled the correct identification of the specimens, and each patient received the appropriate treatment on the basis of the accurate diagnosis.

Adult↗
PubMed2001

Mast cell chymase expression and mast cell phenotypes in human rejected kidneys.

BACKGROUND: Mast cells (MCs) are known to participate in various types of chronic disease, but their role in chronic renal rejection is poorly understood. Recently, distinct phenotypes of MCs have been described in humans by the demonstration of one protease, chymase. Hence, we questioned whether chymase in MCs could play a role in the pathogenesis of renal rejection in humans. METHODS: We investigated MC chymase expression and MC phenotypes, using immunohistochemical single- and double-staining techniques, in nephrectomy (N = 13) and biopsy (N = 8) specimens of human rejected kidneys. Tissue chymase levels were determined by enzymatic assay for chymase activity. We also examined the association between MC chymase expression and the degree of interstitial fibrosis in these renal allografts. RESULTS: Based on chymase positivity, rejected kidneys were divided into two groups, a chymase-negative [Chy(-)] group and a chymase-positive [Chy(+)] group. Quantitative analysis showed that the number of chymase-positive MCs and tissue chymase levels were significantly higher in the Chy(+) group than in the Chy(-) group. Furthermore, the interstitial fibrotic area in the Chy(+) group was significantly larger than that in the Chy(-) group. Immunodouble staining analysis also demonstrated that a new MC phenotype, positive for chymase but negative for tryptase, was present in the human rejected kidney. CONCLUSIONS: These results show that increased expression of chymase in MCs is related to the severity of interstitial fibrosis in human rejected kidneys.

Adolescent↗
PubMed2001

An experimental study on hepatotoxicity of sclerosant ethanolamine oleate flowed into portal vein.

Although endoscopic injection sclerotherapy has been a main treatment option for gastroesophageal varices, intraportal inflow of the sclerosant, ethanolamine oleate, induce liver damage. The aim of this study was to clarify the liver damage due to intraportal inflow of ethanolamine oleate. Ethanolamine oleate suspension was injected into livers of male Wistar rats via the portal (ileocolic) vein. Degrees of liver damage were evaluated by serum levels of transaminases and by histological examination. Intraportal injection of ethanolamine oleate led to extensive liver necrosis, which was marked 1 day after the injection and recovered by 7 days after injection. Liver necrosis became severe as the dose of the injected sclerosant increased. Histologically, neither portal thrombosis nor embolism was evident. Carbon powder particles of India ink, which were injected together with ethanolamine oleate, reached and deposited in sinusoids of the necrotic portions of the liver. These findings suggested that the liver damage had not developed simply as a result of impairment of portal blood flow. Ethanolamine oleate may itself have direct hepatotoxic effects.

Animals↗
PubMed2000

Primary choriocarcinoma and human chorionic gonadotrophin-producing giant cell carcinoma of the lung: are they independent entities?

AIMS: Human chorionic gonadotrophin (hCG) is a useful marker for chorionic proliferative disorders, such as choriocarcinoma. Although hCG synthesis in lung cancers is frequent, primary pulmonary choriocarcinoma (PCC) is rare. To clarify the differences between primary choriocarcinoma and hCG-producing giant cell carcinoma (GCC) of the lung, we compared the clinicopathological and immunohistochemical findings of these tumours. METHODS AND RESULTS: Three patients, one with PCC and two with hCG-producing GCC, were included in this study. They were all middle-aged men and habitual smokers. The growth of these tumours and the progression of the clinical courses were extremely rapid, and the patients all died within 8 months after the pulmonary tumours were found. Haemorrhagic appearance was a common macroscopic feature of the specimens obtained. Microscopically, both types of tumours mainly consisted of atypical polygonal cells. While PCC contained many syncytial trophoblast-like multinucleated cells that had strong immunoreactivity for anti-hCG, such cells were relatively few in hCG-producing GCC. These histological and immunohistochemical findings reflected the serum test result for hCG, which was higher in the case of PCC. CONCLUSIONS: There are a few differences between PCC and hCG-producing GCC, as described above. Reliable distinction between them seems to be difficult for pathologists and worthless for clinicians.

Carcinoembryonic Antigen↗
PubMed2000

Cytomegalovirus associated pancreatitis in a patient with systemic lupus erythematosus.

Pancreatitis can develop as a complication of systemic lupus erythematosus (SLE). Steroids are considered one of the possible causes of this complication, but the pathological mechanism is unclear. We describe an autopsy case of a 29-year-old woman with cytomegalovirus (CMV) associated pancreatitis that developed during steroid therapy for her SLE. Many parenchymal cells with cytomegalic inclusions were seen in the patient's pancreas, especially in lesions showing active inflammation, and transcripts of CMV major immediate-early and late genes, markers of active viral replication, were detected. These findings suggest that CMV played an etiological role in the pancreatic disorder.

Adult↗
PubMed1999

Quantitative analysis and in situ localization of human telomerase RNA in chronic liver disease and hepatocellular carcinoma.

Telomerase is a specialized type of reverse transcriptase that catalyzes the synthesis and extension of telomeric DNA. High levels of telomerase activity have been detected in most hepatocellular carcinoma (HCC) tissues; very weak telomerase activity is, however, detected in approximately half of nontumorous chronic liver disease tissues. The purpose of this study was to investigate the possible source of this weak telomerase activity in these tissues using quantitative competitive reverse transcription (RT)-polymerase chain reaction (PCR) and in situ RT-PCR. Competitive RT-PCR indicated that the relative amount of human telomerase RNA (hTR) was significantly higher in chronic hepatitis or liver cirrhosis compared with the normal liver (p < 0.005), and in HCC compared with the normal liver (p < 0.001) and with chronic hepatitis or liver cirrhosis (p < 0.0001). In the normal liver tissue, hTR was detected by in situ RT-PCR in occasional sinusoidal cells and nuclei of occasional hepatocytes. In tumor-free liver or tumor-bearing liver, hTR was detected in sinusoidal cells, infiltrating lymphocytes, occasional proliferative bile ductal epithelial cells, and the nuclei of occasional hepatocytes. In HCC, hTR was detected in nuclei of all HCC cells as an intense signal and in sinusoidal cells. These results indicate that the amount of hTR increases in the nuclei of hepatocytes during hepatocarcinogenesis, and that the cells associated with the weak telomerase activity in approximately half of the nontumorous chronic liver lesions are mainly migrating lymphocytes and sinusoidal cells.

Adult↗
PubMed1998

Levels of tau phosphorylation at different sites in Alzheimer disease brain.

The microtubule-associated protein tau is abnormally hyperphosphorylated in Alzheimer's disease (AD) brain. To date, 21 phosphorylated sites of tau have been identified. In the present study the levels of phosphorylation at Ser199/Ser202, Thr231/Ser235, Ser262/Ser356 and Ser396/Ser404 of tau in AD brain homogenate and its 100,000 x g supernatant were determined using radioimmuno-dot-blot assay. In homogenate, Ser199/Ser202 and Ser262/Ser356 were phosphorylated to similar level and were more phosphorylated than Thr231 or Ser396/Ser404. In supernatant, there was no significant difference in phosphorylated tau level among the investigated sites except for Thr231/Ser235 which was least phosphorylated. These results suggest that Ser199/Ser202 and Ser262/Ser356 are major sites of phosphorylation of tau in AD brain.

Aged↗
PubMed1998

Increased tau protein level in postmortem cerebrospinal fluid.

Microtubule-associated protein tau has been reported to be significantly increased in cerebrospinal fluid (CSF) of the patients with Alzheimer's disease (AD), which suggests that it is possibly a biological marker for the diagnosis of AD. The underlying mechanism of the increased tau level in CSF, however, is not known. In this study, the tau levels were compared between antemortem and postmortem CSF. The postmortem tau levels in CSF were significantly increased in all groups including AD, neurological control, and nondemented control. A striking elevation of CSF tau was observed during the postmortem change with the nondemented subjects. These findings may offer some insight into the understanding of the mechanism of the increased tau level in CSF with AD and other related disorders.

Aged↗
PubMed1998

Patient background of the Pokemon phenomenon: questionnaire studies in multiple pediatric clinics.

Many children in Japan developed various neuropsychological problems, including seizures, while watching the program Pocket Monster, televised on 16 December 1997. To examine the basis for this incident, we have performed a survey of volunteering children and their parents who visited our pediatric clinics for other reasons from 8 January to 28 February 1998. Children and their parents filled out questionnaires. Among the total of 662 children surveyed, the great majority (603, 91.1%) was found to have watched the Pocket Monster program and 30 individuals (5.0% of viewers) complained of variable degrees of neuropsychological abnormalities. These included seizures (two cases), headache (nine cases), nausea (eight cases), blurred vision (four cases), vertigo (two cases), dysthymia (two cases) and vomiting (one case). Nearly half (14) of these children developed symptoms during or immediately after watching the program, while the remainder did so later. Representative cases are reported and other statistical aspects are discussed.

Adolescent↗
PubMed1998

White matter changes in the gerbil brain under chronic cerebral hypoperfusion.

BACKGROUND AND PURPOSE: An animal model of chronic cerebral hypoperfusion was developed with coiled clips applied to both carotid arteries of adult Mongolian gerbils for between 1 week and 2 months. In the brain of this animal model, rarefaction of white matter with dilatation of the ventricles was frequently observed. To better understand the mechanism of white matter alteration under cerebral hypoperfusion, the chronological sequence of molecular changes in the cerebral white matter of the animal model was determined. METHODS: Specially designed coiled clips were placed around both carotid arteries of Mongolian gerbils to create stenosis without occlusion. Changes in levels of myelin basic protein (MBP) as a marker of myelin, neurofilament H (NFH) as a marker of axonal proteins, and glial fibrillary acidic protein (GFAP) in astroglia after 2 months of cerebral hypoperfusion were analyzed with Western blotting and enzyme-linked immunosorbent assay. RESULTS: Western blotting of the white matter after 2 months of hypoperfusion showed that the levels of MBP and NFH decreased, whereas that of GFAP increased. The time course of MBP and NFH changes determined with enzyme-linked immunosorbent assay revealed that the change of MBP preceded that of NFH. CONCLUSIONS: In the present study it was shown that the damage to myelin precedes that to the axon in the white matter in a chronic cerebral hypoperfusion animal model, suggesting that the change in myelin is the primary pathological event in the cerebral white matter under chronic hypoperfusion. The present study may help in understanding the mechanisms of white matter pathology in leukoaraiosis.

Animals↗
PubMed1997

Expression of platelet-derived growth factor and its receptor in livers of patients with chronic liver disease.

To find if platelet-derived growth factor contributes to liver fibrosis in chronic liver disease, we studied the expression of the B-chain of this cytokine and its beta-receptor in livers of patients with chronic hepatitis or cirrhosis. Seventeen patients were included in this study. Five specimens of liver tissue obtained during autopsy from subjects without liver disease were used as controls. The location of the peptides was identified by an immunohistochemical technique with monoclonal antibodies. Expression of mRNA for the B-chain was assessed by in situ hybridization. Cells stained for the B-chain and expressing its mRNA were identified as macrophages. In control tissues, only a few cells were stained. In the patients' specimens, most stained cells were in portal areas and their number increased with histologic liver damage. In intralobular areas, the stained cells were seen in regions of focal necrosis. Portal mesenchymal and perisinusoidal cells expressed beta-receptor. These cells were dense in periportal areas, where many myofibroblast-like cells were seen. These findings suggest that the B-chain of platelet-derived growth factor is released mainly by macrophages involved in inflammatory reactions. This cytokine probably acts on myofibroblast-like mesenchymal cells, and may be implicated in liver fibrosis in chronic liver disease.

Aged↗
PubMed1996

Development of an animal model for neuroleptic malignant syndrome: heat-exposed rabbits with haloperidol and atropine administration exhibit increased muscle activity, hyperthermia, and high serum creatine phosphokinase level.

The neuroleptic malignant syndrome (NMS) is a life-threatening complication of neuroleptic treatment. To elucidate the pathogenesis of NMS, an animal model has been developed. Experimental rabbits treated with haloperidol (1 mg/kg) by intramuscular injection, were studied for the diagnostic symptoms of increased muscle rigidity, elevated body temperature, and high serum creatine phosphokinase (CPK) level. Administration of haloperiodol (1 mg/kg) and atropine (0.4 mg/kg), and exposure to high ambient temperature (35 degrees C) induced a significant increase in electromyographic activity with muscle rigidity similar to that observed in patients with NMS. Such rabbits also showed elevated body temperature and serum CPK value. In addition to the similarity of the signs and symptoms, all parameters measured (muscle rigidity, body temperature, and serum CPK level) were normalized by dantrolene treatment. The effectiveness of dantrolene in the experimental animal partially confirms the validity of this animal model for NMS. This experimental animal model for NMS may be useful to elucidate the pathogenesis of NMS.

Animals↗
PubMed1996

Mixed germ-cell tumor of the brain. Pathologic study of six autopsy cases.

Intracranial mixed germ-cell tumors are rare. We describe the findings from six autopsies of patients with these tumors. The patients were all young at presentation (mean age, 16 years), and five of the six were male. Headache, vomiting, polyuria and diplopia were common symptoms. Radiographic evaluation demonstrated a mass on the midline of the brain. The patients were treated mainly with radiation, but survival (mean, 3.7 years) was not as long as predicted. At autopsy, the tumors occupied most of the ventricular spaces, and ranged from being well-circumscribed to invasive. All tumors contained both germinoma components and nongerminomatous germ-cell tumor components. Because the distribution of these components was not homogenous, at least two sections were necessary for the diagnosis. Immunoreactivity for placental alkaline phosphatase was found in all tumors. Immunostaining for human chorional gonadotropin, alpha-fetoprotein and carcinoembryonic antigen was usually associated with abnormally high serum levels of these tumors markers in life. A number of the cells in both kinds of tumor components expressed proliferating cell nuclear antigen, probably reflecting the intense malignant potential.

Adolescent↗
PubMed1996

Relationship between hepatic iron deposits and response to interferon in chronic hepatitis C.

OBJECTIVES: The response to interferon in chronic hepatitis C is believed to be affected by hepatic iron content. We histopathologically examined liver biopsy specimens from patients with chronic hepatitis C to determine whether the presence or absence of hepatic iron deposits correlated with the response to interferon. METHODS: Sixty-three patients with hepatitis C treated with interferon-alpha were examined. Liver biopsy specimens obtained just before treatment were sliced and stained with Perls' Prussian blue. Twenty patients had complete responses, 24 patients had transient responses, and 19 patients had no response. RESULTS: Iron deposits stained by Prussian blue were seen in hepatocytes, sinusoidal cells, and portal mesenchymal cells. The degree of hepatocytic and sinusoidal iron deposits did not correlate with the response to interferon. However, the degree of portal iron deposits did correlate with hepatic inflammation activity (tau = 0.55, p < 0.001) and the severity of liver fibrosis (tau = 0.60, p < 0.001), and it correlated negatively to the response to interferon (tau = -0.49, p < 0.001). CONCLUSIONS: The results suggest that portal iron deposits are a factor in the response to interferon. The presence of portal iron deposits seems to be related to a poor response.

Adult↗