PubMed Health⌕ Search

Biomedical subjects

T Kasajima

Publications and source records attributed to T Kasajima.

At least 37 records · Page 2Linked to original sources
PubMed1997

Nitric oxide contributes to the progression of myocardial damage in experimental autoimmune myocarditis in rats.

BACKGROUND: Excess amounts of NO produced by an inducible NO synthase (iNOS) in response to cytokines may be cytotoxic and can be destructive to tissue. We investigated the role of NO in the development of myocardial damage and the effects of aminoguanidine (AG), an inhibitor of iNOS, on experimental autoimmune myocarditis in rats. METHODS AND RESULTS: Autoimmune myocarditis was induced in 20 Lewis rats by injection of porcine cardiac myosin. Ten of the 20 rats were administered AG. The severity of myocarditis was evaluated by measuring the size of myocarditic lesion and serum levels of CK-MB. Serum NO levels were determined using the Cd/Cu method. Tissue specimens were immunohistochemically examined for iNOS and nitrotyrosine. Histopathological study revealed extensive myocardial destruction and massive inflammatory cell infiltration in AG-untreated rats but only focal mononuclear cell infiltration in AG-treated rats. The mean percent areas of inflammatory lesions in the untreated and treated rats were 56 +/- 13% and 3 +/- 2%, respectively (P < .001). NO levels were 102 +/- 23 and 25 +/- 9 IU/L, respectively (P < .01). CK-MB levels were 68 +/- 13 and 16 +/- 13 nmol/L, respectively (P < .01). Superoxide production as measured with an ex vivo monitoring system was also significantly decreased in the treated rats. Nitrotyrosine relating to the generation of peroxynitrite was detected through immunostaining in the inflammatory lesions of untreated rats but not in those of treated rats. CONCLUSIONS: Excess amounts of NO produced by iNOS appear to contribute to the progression of myocardial damage in myocarditis. AG may prove to be useful in the treatment of myocarditis.

Animals↗
PubMed1997

Increased concentration of vascular endothelial growth factor/vascular permeability factor in cyst fluid of enlarging and recurrent thyroid nodules.

Human thyrocytes produce vascular endothelial growth factor (VEGF), a potent angiogenic factor, also known as vascular permeability factor (VPF), which increases vascular permeability. Based on the assumption that VEGF/VPF is involved in fluid accumulation in thyroid cysts, we determined the VEGF/VPF concentration in cyst fluids of thyroid nodules from 79 patients. VEGF/VPF was found to be abundantly present in the cyst fluids (0.02-183 ng/mL). There was no significant difference of VEGF/VPF concentration in the cyst fluid obtained from thyroid adenoma or from adenomotous goiter with cystic degeneration. Immunoreactive VEGF/VPF in cyst fluid was eluted mainly at 45 kDa, and stimulated endothelial cell proliferation, which was partially blocked by anti-VEGF/VPF antibody. The VEGF/ VPF concentration in the cyst fluid obtained from patients who required repeated aspiration or underwent surgical resection because of recurrent accumulation (84.8 +/- 58.3 ng/mL, mean +/- SD, n = 18) was significantly higher than that in the cysts that regressed or disappeared after a single aspiration (4.3 +/- 4.4 ng/mL, n = 12, P < 0.001). These in vitro and clinical findings suggest that VEGF/VPF is at least partly involved in the accumulation of cyst fluid in thyroid nodules, and that a high VEGF/VPF concentration predicts rapid accumulation of the cyst fluid, possibly necessitating interventional treatment.

Adenoma↗
PubMed1997

Distribution of inducible nitric oxide synthase in ulcerative colitis.

OBJECTIVE: To investigate reports that the biosynthesis of nitric oxide (NO) is increased in the colonic mucosa of patients with active ulcerative colitis (UC), which suggests that serum NOx levels may be an important indicator of UC activity. METHODS: To determine the role of NO within the colon, we purchased polyclonal antibodies against human-inducible NO synthase (iNOS). We then examined the distribution of iNOS-reactive cells in UC colon tissues. RESULTS: In specimens from 12 UC patients, iNOS-positive neutrophils and macrophages were observed at the base of the ulcer but not in distant areas in the active stage. iNOS expression in colon mucosa was virtually absent during the inactive stage of UC and within the colon of patients with non-UC colitis. CONCLUSIONS: We conclude that NO in colonic mucosa may play a potential role in the pathogenesis of UC.

Adult↗
PubMed1996

Contribution of Thy-1-CD4+ T cells to the disorganization of lymphoid follicles in retrovirus-induced immunodeficiency syndrome, MAIDS.

The destruction of the lymphoid follicle (LF) and of the follicular dendritic cell network in the secondary lymphoid organs are major pathological features in murine acquired immunodeficiency syndrome (MAIDS). These pathological changes are associated with functional deficiency of lymphocytes. However, the mechanisms involved have not been established. In MAIDS-susceptible C57BL/6 (B6) mice, the destruction of the LF occurred as early as 2-3 weeks after the infection by LP-BM5 murine leukemia virus (MuLV) and was accompanied by the intrafollicular infiltration of T cells of an unusual phenotype, Thy-1-CD4+. B6 mice, which Thy-1+ T cells had been depleted by the repeated inoculation with monoclonal antibody to Thy-1 antigen, developed LF destruction after infection similar to the control B6 mice. The LP-BM5 MuLV-infected C57BL/6-nu/nu (B6-nu/nu) mice, otherwise resistant to MAIDS induction, also developed these abnormalities following the adoptive transfer of highly purified Thy-1-CD4+ T cells obtained from MAIDS mice. Thus, the production of Thy-1-CD4+ T cells and their infiltration into LF are thought to be involved in triggering the LF destruction. However, the cytolysis of follicular components by activated CD8+ T cells or by LP-BM5 MuLV itself was a less likely mechanism as MAIDS developed in B6 mice depleted of CD8+ T cell. A/J mice, which are resistant to viral infection in the presence of CD8+ T cells, also developed MAIDS and LF destruction after the depletion of CD8+ T cells. Furthermore, no follicular destruction was observed in infected B6-nu/nu mice even though they are highly sensitive to LP-BM5 MuLV.

Animals↗
PubMed1996

Apoptosis and DNA fragmentation in the bulbus cordis of the developing rat heart.

Histologic, ultrastructural and nick end labeling studies were made of the process of apoptosis in the bulbus cordis of rat embryos. Apoptosis was observed between the 14th and 16th days of gestational age, at which time the bulbus cordis undergoes extensive remodeling. Three types of mesenchymal cells were identified in this region: cells undergoing apoptosis, cells engaging in the phagocytic removal of apoptotic cells, and cells not involved in either of these two processes. Fragmentation of DNA, demonstrated by nick end labeling, was found only in the apoptotic cells. The combined use of morphologic and labeling techniques is extremely useful in the evaluation of the contribution of apoptosis to cardiac morphogenesis.

Animals↗
PubMed1996

Hypertrophic cardiomyopathy in Noonan syndrome.

Noonan syndrome, a well-known multiple congenital anomalies syndrome, is frequently accompanied by cardiovascular diseases including hypertrophic cardiomyopathy (HCM). The incidence of HCM in Noonan syndrome is approximately 20-30% and one-third of cases reveal ventricular outflow obstruction. HCM in Noonan syndrome is occasionally associated with a congenital heart defect, whereas classic HCM seldom accompanies cardiac malformations. Asymmetric septal hypertrophy and symmetric septal hypertrophy (concentric hypertrophy) can be observed both in HCM with Noonan syndrome and in classic HCM, but apical hypertrophy has not been reported in Noonan syndrome yet, although it appears in classic HCM. Congestive heart failure is the major cause of death in patients with HCM in Noonan syndrome, but cases of sudden death have also been reported. The histopathologic findings of ventricular myocardial tissue in HCM with Noonan syndrome are similar to those in classic HCM.

Adolescent↗
PubMed1996

Vasospastic angina in a patient with Fabry's disease who showed normal coronary angiographic findings.

It has been reported that coronary diseases in patients with Fabry's disease are induced by deposits in endothelial cells and coronary smooth muscle cells. Most of those are ischemia due to stenosis. This report describes a case of patient with Fabry's disease who showed severe vasospasms without coronary artery stenosis during acetylcholine loaded coronary angiography. In this case, a myocardial biopsy revealed that the deposits in the endothelial cells of the myocardial capillaries were lamellated appearance. Recently, it is reported that endothelial cell damage could be an important cause of coronary vasospasm. This case suggests that the some sort of functional disorder was induced by glyco-sphingolipid deposits in the coronary endothelial cells, and that this might have led to coronary artery spasms without the organic stenosis of coronary arteries.

Adult↗
PubMed1995

Restricted usage of T cell receptor V alpha-V beta genes in infiltrating cells in the hearts of patients with acute myocarditis and dilated cardiomyopathy.

Prolonged myocardial cell damage initiated by acute myocarditis is thought to be one of the most important etiology of dilated cardiomyopathy. To investigate the immunological mechanisms involved in the pathogenesis of dilated cardiomyopathy, we analyzed the phenotypes of infiltrating cells and examined the expression of perforin in infiltrating cells in the hearts of patients with dilated cardiomyopathy as well as acute myocarditis. We also examined the expression of HLA and intercellular adhesion molecule-1 (ICAM-1) in myocardial tissue of these patients. Furthermore, to evaluate the antigen specificity of infiltrating T cells and persistence of viral genomes in the myocardial tissue, we analyzed the expression of T cell receptor (TCR) V alpha and V beta genes as well as enterovirus genomes by PCR. We found infiltration of perforin-expressing killer cells and enhanced expression of HLA class I and ICAM-1 in the myocardial tissue. We also found that the repertoires of TCR V alpha as well as V beta gene transcripts were restricted, indicating that a specific antigen in the hearts was targeted. Because no enterovirus genomes were detected in all patients, it is strongly suggested that a cell-mediated autoimmune mechanism triggered by virus infection may play a critical role in the pathogenesis of dilated cardiomyopathy. However, we could not exclude the possibility that viruses other than enteroviruses could be pathogenic in these patients.

Acute Disease↗
PubMed1995

An unclassified cerebral small cell tumor in a patient with human T-cell lymphotropic virus type 1-induced primary extranodal lymphoma.

We describe an autopsy case of a thalamic tumor in a patient with human T-cell lymphotropic virus type 1 (HTLV-1)-induced extranodal lymphoma of the skull. Neither brain tumors associated with adult T-cell leukemia nor HTLV-1-induced extranodal lymphoma of bone have previously been reported. The tumor, which resembled an oligodendroglioma or dysembryoplastic neuroepithelial tumor, was composed of medium-sized cells with dark, round-to-polygonal nuclei and a mucinous matrix that formed pericellular lakes. Tumor cells were immunoreactive with S-100 protein and neuron-specific enolase but not with glial fibrillary acid protein, synaptophysin, or vimentin. Tumor cells had prominent rough endoplasmic reticulum and free ribosomes with short processes, compatible with an oligodendroglial or small neuronal nature. Many atypical lymphocytes had infiltrated the leptomeningeal space, subependymal zone along the ventricular walls, fornices, corpus callosum, and right frontal lobe. Multinucleated or bizarre astrocytes and macrophages were found exclusively in the right frontal white matter. The coexistence of this unclassified peculiar brain tumor with bizarre astrocytosis suggests a cytopathic effect of HTLV-1 on human glioneuronal cells.

Adult↗
PubMed1994

Morphometrical analysis of cystadenolymphoma (Warthin's tumor). Subclassification and characterization of the lymphoid stroma in comparison with gastric lymphoid follicles.

Morphometrical analysis was applied to cystadenolymphoma (Warthin's tumor, adenolymphoma: CAL). By quantitative analysis of tissue sections, the examined cases were divided into three subtypes according to the ratio of the lymphoid stroma (LS) to the whole tissue: type I "stroma-rich type", the LS of this type was more than 57% of the whole tissue; type II "typical type", the LS of this type was 37% to 56% of the whole tissue; and type III "stroma-poor type", the LS of this type was less than 36% of the whole tissue. The average age of the patients in subtypes I, II and III was 57.7, 68.0, and 62.4 years, respectively. The age of the patients with type I CAL was significantly lower than that of those with type II CAL. In many type II cases, a reticular distribution of IgE in the germinal centers was frequently observed. From an analysis of the sections immunohistochemically stained with monoclonal antibodies to B and T cells, there appeared to be a trend that the greater the percentage of the LS to the whole tissue, the lower the ratio of B cell region to the LS. In contrast to CAL, an analysis of the change of the ratio of B cell region to the lymphoid follicles (LF) seen in the gastric mucosa of patients with chronic gastritis showed that the larger the volume of LF, the higher the ratio of the B cell region to the entire LF.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenolymphoma↗
PubMed1994

Hypoxia induces apoptosis with enhanced expression of Fas antigen messenger RNA in cultured neonatal rat cardiomyocytes.

We examined whether apoptosis occurs in cardiomyocytes by hypoxia in vitro. Neonatal rat cardiomyocytes and nonmyocytes were cultured in 95% N2-5% CO2 atmosphere to produce hypoxic conditions. DNA fragmentation into integer multiples of the internucleosomal DNA length was observed in cardiomyocytes as early as 12 hours, whereas nonmyocytes did not show fragmentation of DNA up to 72 hours. DNA fragmentation of cardiomyocytes induced by hypoxia was also confirmed by nick-end labeling in situ. Messenger RNA for Fas antigen, a mediator of apoptotic cell death, was expressed in both cardiomyocytes and nonmyocytes as revealed by Northern blotting and in situ hybridization. In hypoxic condition, Fas messenger RNA levels in cardiomyocytes were upregulated by twofold over controls, whereas those of nonmyocytes were downregulated. These results indicate that cardiomyocyte death by hypoxia can occur via apoptosis and that Fas antigen may be associated with the mechanism of this apoptotic process.

Animals↗
PubMed1993

An autopsied case of Williams syndrome complicated by moyamoya disease.

An 18 year old girl with typical clinical features of Williams syndrome suddenly died of intracerebral hemorrhage due to moyamoya disease. Autopsy revealed vascular abnormalities, such as supravalvular aortic stenosis (SAS) and an abnormal complicated cerebrovascular network in the cerebral arteries. The arterial wall of the SAS lesion consisted of thickened medial tissue showing elastic disorganization with prominence of the smooth muscle cells. The narrowed vessels of the circle of Willis showed intimal thickening with an extremely wavy internal elastic lamina and marked thinning of the media. To our knowledge, this is the first report of moyamoya disease associated with Williams syndrome.

Abnormalities, Multiple↗
PubMed1993

Increased 1,25-(OH)2D2 concentration in a patient with malignancy-associated hypercalcemia receiving intravenous hyperalimentation inadvertently supplemented with vitamin D2.

A 55-year-old patient with hypercalcemic crisis due to gastric carcinoma with bone marrow metastasis was treated with bisphosphonate (pamidronate) and calcitonin. Urinary excretion of parathyroid hormone-related protein (PTHrP) was increased. When normocalcemia had been attained, intravenous hyperalimentation was started, in which 1,000 U vitamin D2 was inadvertently supplemented on days 5-18, On days 15-18, hypercalcemia rapidly recurred, accompanied by markedly increased serum levels of 25-OHD2 (9.1 ng/dl) and 1,25-(OH)2D2 (161 pg/ml). This clinical course suggests that PTHrP, like PTH, stimulated 1 alpha-hydroxylase activity and produced excessive 1,25-(OH)2D2. Vitamin D should not be administered to patients with malignancy-associated hypercalcemia, particularly that due to PTHrP-producing tumors.

Calcitriol↗
PubMed1992

A case of pediatric cardiomyopathy with severely restrictive physiology.

A rare case of a 6-year-old male with idiopathic familial cardiomyopathy manifesting severely restrictive physiology is reported. The patient showed congestive heart failure with dilatation of both atria with a normal ventricular cavity. A square-root configuration was revealed in the ventricular pressure tracings. His elder brother had died of hypertrophic cardiomyopathy at the age of 3 years. Endomyocardial biopsy disclosed marked disorganization of muscle bundles with hypertrophy of the myocytes and interstitial fibrosis. The patient died suddenly during hospitalization. Autopsy revealed diffuse hypertrophy of both the ventricular walls and the ventricular septum with extensive myocardial disorganization and interstitial fibrosis. These advanced myopathic changes in the myocardium may have been related to the restrictive physiology in this case.

Bundle-Branch Block↗
PubMed1992

A case of transfusion-associated graft-versus-host disease not prevented by white cell-reduction filters.

A case of transfusion-associated graft-versus-host disease (TA-GVHD) in a patient with non-Hodgkin's lymphoma is reported. The patient, a 67-year-old woman, was diagnosed as having diffuse, mixed type non-Hodgkin's lymphoma, at clinical stage IIIA. She was treated with combination chemotherapy and received multiple blood transfusions for anemia and thrombocytopenia. Although white cells (WBCs) were reduced in the transfused components by WBC-reduction filters, the patient developed TA-GVHD that was confirmed by skin biopsy. It is suggested that the WBC reduction attained with these filters does not prevent TA-GVHD in immunocompromised patients. It is recommended that all blood components should be irradiated before transfusion to such patients.

Aged↗
PubMed1992

A case of lymphadenosis benigna cutis of the earlobe: an immunohistochemical study.

We report a 38-year-old woman who developed an erythematous nodule on her earlobe after wearing pierced-type 18-carat gold earrings. Biopsy specimens revealed dense cellular infiltration predominantly composed of lymphocytes and plasma cells in the dermis and subcutaneous tissue with formation of lymph follicles. Morphological and immunohistochemical analyses were compatible with lymphadenosis benigna cutis.

Adult↗