Intravenous IgG: supertherapy for myocarditis and acute dilated cardiomyopathy.
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Acute Disease↗
Biomedical subjects
H Takada
Publications and source records attributed to H Takada.
Restricted diversification of T-cells in chronic active Epstein-Barr virus infection: potential inclination to T-lymphoproliferative disease.
To assess the abnormal T-cell expansion in chronic active Epstein-Barr virus infection (CAEBV), T-cell antigen receptor (TCR) repertoire was analyzed in four patients with the disease. All fulfilled the diagnostic criteria of CAEBV, presenting with fever, hepatosplenomegaly, cytopenia, abnormal high titers of anti EBV-antibodies, and positive EBV genome of unknown cause. Southern blotting probed with EBV-terminal repeats and TCR Cbeta gene indicated clonal expansion of the infected cells in 3 and 2 patients, respectively. The number of CD4+ HLA-DR+ cells appreciably increased in patients 1 (59%) and 2 (24%), who had a coronary aneurysm and central nervous system involvement, respectively. TCR gene expression examined by the inverse polymerase chain reaction methods revealed that Vbeta gene usages were preferential in all patients (Vbeta7 and Vbeta12: patient 1, Vbeta4: patient 2, Vbeta13: patients 3 and 4), compared with those in healthy controls. Valpha18 gene expression was remarkably high in patients 1 and 2. Moreover, Jbeta gene expression was skewing in the reigning Vbeta clones in all patients. Vbeta4-Jbeta1.5 and Vbeta13-Jbeta1.5 genes were clonally expressed in patients 2 and 4, respectively. These results suggest that CAEBV is associated with the restricted diversity of T-cells, which may stem from the sustained expansion of oligoclonal T-cells possibly driven by conventional viral antigens, but not, superantigens. Although the study is limited by the small number of patients, the unbalanced T-cell repertoire might contribute to the evolution of T-lymphoproliferative disease, otherwise, imply the innate defective immunity to EBV in CAEBV patients.
Adolescent↗
Escherichia coli infection induces only fetal thymus-derived gamma delta T cells at the infected site.
Intraperitoneal infection of mice with Escherichia coli induced activated TCR gamma delta T cells in the peritoneal cavity. We provide evidence that the E. coli-induced gamma delta T cells are derived only from the fetal thymus on the following grounds. The gamma delta T cells were not induced in athymic nude mice and irradiated bone marrow-transferred mice which lack fetal thymus-derived T cells. However, E. coli infection of fetal thymus-grafted nude mice did induce fetal thymus-derived gamma delta T cells. These results suggest that the fetal thymus-derived gamma delta T cells colonize the periphery during early ontogeny, and are maintained until adult age. The E. coli-induced gamma delta T cells express only the Vdelta1 gene. Vgamma6 was predominantly expressed whereas anti-Vgamma1 and anti-Vgamma4 monoclonal antibodies stained less than 3 % of the cells. Direct sequencing of PCR products revealed that Vgamma6 and Vdelta1 genes expressed by the E. coli-induced gamma delta T cells were invariant sequences identical to those expressed in the fetal thymus. The antigen (Ag) specificity of a T cell hybridoma expressing the fetal type Vgamma6 / Vdelta1(+) TCR could not be identified as the cells failed to respond to lipopolysaccharide, E. coli Ag, mycobacterial heat shock protein 65, or isopentenyl pyrophosphate. These results suggest that the Vgamma6 / Vdelta1(+) gamma delta T cells derived from fetal thymus can participate in immune responses against bacterial infection through recognition of a novel class of Ag which is not yet identified.
Animals↗
A solitary fibrous tumor in the perianal region with a 13-year follow-up: report of a case.
A case of a solitary fibrous tumor (SFT) of the perianal region in a 62-year-old man is reported herein. The patient had undergone an abdominoperineal excision of the rectum for an anorectal tumor 13 years previously, and had been referred to our hospital for a perineal mass. Computerized tomography and angiography revealed a markedly hypervascular tumor measuring 11 x 8 cm in size in the pelvic cavity. After preoperative radiotherapy (total 58 Gy) and the embolization of the feeding arteries, he underwent an en bloc excision of the tumor. Microscopically, the tumor was composed of spindle shaped cells with a "patternless" arrangement in a collagenous background. There was immunohistochemical evidence that these cells were strongly positive for CD34, thus suggesting the tumor to be SFT. The previously resected anorectal tumor showed similar histological and immunohistochemical findings. The patient's recovery was uneventful.
Antigens, CD34↗
Malignant hemangioendothelioma of the small intestine: report of a case.
A case of malignant hemangioendothelioma (MH) of the small intestine in a 27-year-old woman is reported herein. The patient developed acute abdominal symptoms during investigations for anemia, weight loss, anorexia, and recurrent gastrointestinal bleeding. An emergency laparotomy revealed perforation of a jejunal tumor. The results of a histopathological study of the resected small bowel segment were interpreted as MH with lymph node involvement. Following this case report, a review of the relevant literature on small intestinal MH is presented.
Adult↗
Streptococcus intermedius-brain abscess in chronic granulomatous disease.
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Adult↗
Inflammatory cytokine production and specific antibody responses to lipopolysaccharide from endodontopathic black-pigmented bacteria in patients with multilesional periapical periodontitis.
We examined the induction of the cytokines interleukin (IL)-1 beta, IL-6, and IL-8 by lipopolysaccharides (LPSs) from several species of possible endodontopathic black-pigmented bacteria. Studies were conducted in human whole blood cultures from six patients (two from each group) with differing numbers of periapical periodontitis lesions (i.e. patients with radiographically clear periapical lesions in 10 or more teeth (high-lesion group, n = 4), in one or two teeth (low-lesion group, n = 6), and six healthy volunteers with no periapical lesions (no lesion group)). LPS from Prevotella intermedia ATCC 25611, Porphyromonas gingivalis 381, and Prophyromonas endodontalis ATCC 27067 induced a higher IL-8 response in the subjects of the high-lesion group, compared with the subjects of the other two groups. To ascertain the degree of sensitization by test bacteria, we examined the reactivities of antibodies in serum and saliva from the subjects to different bacterial species. LPS from P. gingivalis reacted strongly with sera from the high-lesion group. Thus, LPS from black-pigmented bacteria may be involved in multilesional periapical periodontitis by inducing particular cytokines and/or humoral immune responses.
Adult↗
Cerebrospinal fluid cytokine levels and dexamethasone therapy in bacterial meningitis.
OBJECTIVES: cerebrospinal fluid (CSF) levels of interleukin (IL)-1 beta and tumor necrosis factor (TNF) alpha were measured to assess the effect and application of dexamethasone (Dex) therapy for bacterial meningitis. METHODS: associations between clinical findings and CSF parameters were first investigated, and prognosis was compared between 25 patients with Dex and 12 without Dex therapy. RESULTS: patients with the presence of disturbed consciousness showed higher CSF levels of TNF alpha (mean: 3015 pg/ml) or protein (mean: 215 mg/dl) than those without it (both, P < 0.O5). Simultaneous increase of TNF alpha (> 1000 pg/ml) and protein (> 100 g/dl) was observed in 80%, of patients with profoundly disturbed consciousness. Patients with Dex therapy presented higher TNF alpha/protein levels at diagnosis than those without Dex therapy (P < 0.05). Despite worse conditions at diagnosis, only one of 14 Dex-treated patients whose initial CSF TNF alpha levels exceeded 1000 pg/ml developed deafness. On the other hand, two of four patients without Dex therapy who had the same TNF alpha level suffered from psychomotor retardation. The differences in the frequency of sequelae between those with and without Dex therapy were significant in patients showing high TNF alpha level (P < O.05), but not in those showing high CSF levels of IL-1 beta or protein. The logistic regression analysis indicated that high CSF protein level (P < O.0001), or no Dex therapy (P=0.0001) was the independent risk factor for sequelae. CONCLUSIONS: although the study number was small, our observations suggested that CSF TNF alpha/protein levels reflected the neurologic severity, and implied that early Dex therapy might be beneficial for patients with prominently high TNF alpha levels.
Adolescent↗
Outbreak of severe neurologic involvement associated with Enterovirus 71 infection.
Enterovirus 71 has been associated with several outbreaks, as well as sporadic cases, of central nervous system infection and has a worldwide distribution. Seven children with encephalitis and five with aseptic meningitis caused by Enterovirus 71 were seen at Otsu Municipal Hospital during the summer of 1997. The infections were confirmed serologically, although detection of the viral genome in cerebrospinal fluid was unsuccessful. Seven children were diagnosed as having hand-foot-and-mouth syndrome, two were diagnosed as having herpangina, and three patients younger than 12 months old developed no eruptions. The skin or mucosal manifestations of this outbreak demonstrated considerable variation. The Enterovirus 71 strain that caused the outbreak had a strong neurovirulent tendency. Among the patients with encephalitis, symptoms originating from the impairment of diencephalon were seen in four patients, and those originating from cerebellar impairment were seen in two patients. Brain magnetic resonance imaging in one patient revealed an abnormality in the pons. The neurologic manifestations associated with Enterovirus 71 infection may be characterized by involvement of the cerebellum, brainstem, and diencephalon. Enterovirus 71 is one of the pathogenic viruses that cause hand-foot-and-mouth syndrome, as well as a variety of other clinical manifestations. The most important of these is neurologic disease, especially in infants and young children.
Antibodies, Viral↗
Differential roles of TLR2 and TLR4 in recognition of gram-negative and gram-positive bacterial cell wall components.
Toll-like receptor (TLR) 2 and TLR4 are implicated in the recognition of various bacterial cell wall components, such as lipopolysaccharide (LPS). To investigate in vivo roles of TLR2, we generated TLR2-deficient mice. In contrast to LPS unresponsiveness in TLR4-deficient mice, TLR2-deficient mice responded to LPS to the same extent as wild-type mice. TLR2-deficient macrophages were hyporesponsive to several Gram-positive bacterial cell walls as well as Staphylococcus aureus peptidoglycan. TLR4-deficient macrophages lacked the response to Gram-positive lipoteichoic acids. These results demonstrate that TLR2 and TLR4 recognize different bacterial cell wall components in vivo and TLR2 plays a major role in Gram-positive bacterial recognition.
Animals↗
Synergistic action of apoptosis induced by eicosapentaenoic acid and TNP-470 on human breast cancer cells.
The effects of eicosapentaenoic acid (EPA) and an angiogenesis inhibitor (TNP-470) on the suppression of breast cancer cell growth were examined in five human breast cancer cell lines (MDA-MB-231, T-47D, MCF-7, KPL-1, and MKL-F). In all five cell lines, EPA and TNP-470 alone both showed tumor growth inhibition in a time- and dose-dependent manner, and in combination, a synergistic effect was seen at high concentrations. EPA plus TNP-470 treatment evoked apoptosis as confirmed by the appearance of sub G1 populations, by DNA fragmentation, and by cell morphology. With the combination, the expression of Bax and Bcl-xS, the apoptosis-enhancing proteins, was more up-regulated and that of Bcl-2 and Bcl-xL, the apoptosis-suppressing proteins, was more down-regulated compared to the use of EPA or TNP-470 alone, suggesting that their synergistic effect was due to an acceleration of apoptosis.
Apoptosis↗
Down-regulation of TGF-beta receptors in human colorectal cancer: implications for cancer development.
Many colorectal cancer cells are resistant to the anti-proliferative effects of transforming growth factor-beta (TGF-beta). TGF-beta also acts as paracrine factor from cancer cells on their mesenchymal cells. The aim of this study was to examine the expression of TGF-beta and its receptors in human colorectal cancer tissue and determine any relationship with cancer growth. In situ hybridization and Northern blot hybridization detection of TGF-beta1, type I and type II receptor mRNA and immunohistochemical staining of TGF-beta1 were performed using 11 human colorectal adenomas, 22 colorectal cancers and ten normal colorectal mucosas as control. TGF-beta receptor mRNAs were expressed mainly by normal colorectal epithelial cells and adenoma. However, mRNAs for TGF-beta receptors were only faintly, if at all, expressed in eight of 22 human colorectal cancers. In addition, intense signals of TGF-beta1 mRNA and the protein were detected in all colorectal cancers. TGF-beta receptor mRNAs and TGF-beta1 protein were also distributed in fibroblasts and endothelial cells in the interstitium. Moreover, Smad 4 protein was translocated to nucleus in primarily cultured adenoma cells, but not in cancer cells after TGF-beta stimulation. The escape of human colon cancer from TGF-beta-mediated growth inhibition by down-regulation of TGF-beta receptors as well as the effects of TGF-beta on stroma formation and angiogenesis indicate a possible role for TGF-beta in the progression of colon cancer in an intact host.
Adenoma↗
Enhancement by galactosamine of lipopolysaccharide(LPS)-induced tumour necrosis factor production and lethality: its suppression by LPS pretreatment.
1. D-Galactosamine (GalN) depletes UTP primarily in the liver, resulting in decreased RNA synthesis in hepatocytes. Co-injection of GalN and lipopolysaccharide (LPS) into mice produces fulminant hepatitis with severe hepatic congestion, resulting in rapid death. Although the underlying mechanism is uncertain, GalN enhances the sensitivity to tumour necrosis factor (TNF). Administration of uridine (a precursor of UTP) prior injection of either LPS itself or interleukin-1 (IL-1) reduces the lethality of GalN+LPS. The present study focused on the effects of these agents on TNF production. 2. Intraperitoneal injection of GalN+LPS into mice greatly elevated serum TNF. Although large doses of LPS alone also greatly elevated serum TNF, LPS itself induced neither hepatic congestion nor rapid death. Administration of a macrophage depletor, liposomes encapsulated with dichloromethylene bisphosphonate, reduced both the TNF production and mortality induced by GalN+LPS. 3. Uridine, when injected 0.5 h after the injection of GalN+LPS, reduced the production of TNF. Prior injection of LPS, but not of IL-1, also reduced this TNF production. 4. Serum from LPS-injected mice reduced the TNF production induced by GalN+LPS, but it was less effective at reducing the lethality. Its ability to reduce TNF production was abolished by heat-treatment. 5. We hypothesize that a factor inhibiting TNF production by macrophages is produced by hepatocytes in response to LPS. Possibly, production of this hepatocyte-derived TNF-down-regulator (TNF-DRh) may be: (i) inhibited by GalN, causing over-production of TNF by macrophages and (ii) stimulated by LPS-pretreatment (and restored by uridine), causing reduced TNF production.
Animals↗
Oversecretion of IL-18 in haemophagocytic lymphohistiocytosis: a novel marker of disease activity.
We investigated the significance of interleukin (IL)-18 levels in the pathophysiology of haemophagocytic lymphohistiocytosis (HLH). IL-18 levels were significantly elevated in all nine patients with active HLH compared with those of healthy controls. Serial determination of IL-18 levels in three cases, showed a gradual decrease compared with those of IL-12, interferon (IFN)-gamma or soluble Fas ligand (sFasL) in the course of clinical improvement, and seemed to be elevated until complete disappearance of disease activity. IL-18 and IFN-gamma (CC 0.711, P = 0.018), and IFN-gamma and sFasL (CC 0.849, P = 0.0049) levels were significantly correlated. On the other hand, correlation between IL-12 and IFN-gamma, IL-18 and sFasL, or IL-18 and IL-12 was not observed. IL-18, IFN-gamma and sFasL levels significantly correlated with disease activity such as fever and alanine transaminase (ALT) levels. IL-18 mRNA expression was enhanced in spleen, but not in peripheral blood mononuclear cells (MNC), bone marrow MNC, liver from patients of active HLH, or the tumour from a patient with lymphoma-associated haemophagocytic syndrome (LAHS). These results suggest that IL-18 may play important roles in the pathogenesis of HLH, particularly through induction of Th1 cells. IL-18 measurement may be useful for the diagnosis and for the detection of smouldering disease activity.
Cell Communication↗
Lipopolysaccharide-dependent down-regulation of CD27 expression on T cells activated with superantigen.
To investigate the mechanisms underlying T-cell responses during superantigen (SAg) stimulation, we analysed the effects of SAg on CD27 expression with or without lipopolysaccharide (LPS) as a novel regulator of T-cell function. CD27 is expressed on the majority of resting peripheral blood T cells (CD27low). Activation of T cells by SAg induces high levels of CD27 surface expression (CD27high) accompanied with simultaneous CD30 receptor expression. After prolonged activation in vitro, the level of CD27 expression became intermediate. The effects of LPS on down-regulation of CD27high expression on CD30+ T cells were dose-dependent. Separating LPS-stimulated monocytes from T cells by mechanical dispersion abolished its inhibitory effect, indicating the requirement for direct interactions between monocytes and T cells. We also found that SAg up-regulated CD80 expression on CD14+ monocytes and LPS inhibited SAg-induced CD80 expression after 24 hr of stimulation. Up-regulation of CD152 (CTLA-4) was selective, since it was found to be preferentially expressed on the CD30+ population. Competitive experiments using soluble blocking peptides showed that addition of CD28 or CD80 peptide recovered LPS-induced down-regulation of CD27high expression on CD30+ T cells. These observations suggested that the presence of low levels of CD80 on monocytes may partially inhibit CD27 expression due to inefficient delivery of positive signals via CD28/CD80 interaction, and that the increased levels of CD80 enhance the inhibition through interactions with CD152 which is expressed at the highest levels after 48 hr of activation.
Abatacept↗
Effects of exercise for 1 month on serum lipids in adolescent females.
BACKGROUND: The present study was done to clarify the effects of 1 month of exercise on levels of total cholesterol (TC) and high-density lipoprotein cholesterol (HDLC) and on the ratio TC/HDLC and also to evaluate the relationship of body fat to amount of exercise and TC/HDLC ratio. METHODS: Twenty-seven female athletes (aged 15-18 years) were divided into two groups: the participant's group, in which players trained and attended a tournament, and the non-participant's group, in which players did not attend the tournament. We assessed the amount of exercise, body composition, serum TC and HDLC and TC/HDLC on four occasions: before (T0), during (T1), 1 day after (T2) and a week after (T3) the experimental period. Levels of TC and HDLC adjusted for changes in plasma volume were compared for each occasion. Two multiple regression models for change in TC/HDLC from T0 to T2 and from T0 to T3 were employed. RESULTS: (i) The changing patterns in TC and HDLC throughout the program were different between the two groups; (ii) the decreased level of TC/HDLC after 1 month of exercise may easily revert to its original level; and (iii) the relevant factor for the decline in TC/HDLC was the amount of exercise, not body fat reduction. CONCLUSIONS: Exercise may be a more important factor for the improvement of TC/HDLC than concomitant body fat reduction and non-strenuous exercise may maintain a more stable and higher HDLC level than strenuous exercise.
Adolescent↗
Significance of the atherosclerogenic index and body fat in children as markers for future, potential coronary heart disease.
BACKGROUND: The purpose of this study is to establish a simple marker in children for future, potential risks of coronary heart disease. METHODS: We measured serum total cholesterol (TC) and triglyceride (TG) by enzymatic methods, high-density lipoprotein cholesterol (HDLC) by the dextran sulfate-magnesium method and estimated body fat by the new impedance method in 1289 children (651 boys and 638 girls) in the fourth grade (9 or 10 years old) to obtain the atherosclerogenic index (AI). We also investigated the children's lifestyle. RESULTS: The probability of an AI score of 3 or more was significantly higher in children with an estimated 23-25% body fat than in those with body fat less than 17%. Moreover, the odds ratio increased along with an increase in the percentage of body fat. When body fat was estimated as being greater than 29%, the odds ratio was 11-fold higher than those with body fat less than 17%. When body fat was greater than 23%, the children's physical activity, as assessed by the questionnaire, was found to be poorer than those with lower body fat. Levels of TC and TG were significantly higher and that of HDLC was lower in those with less body fat. CONCLUSIONS: The AI is a useful indicator of obesity in children. The combination of AI and percentage body fat is a good indicator for evaluating children who would be at a greater risk of obesity, hyperlipidemia, unhealthy eating habits and inadequate physical activity. The hypothetical risk levels for future coronary heart disease are an AI score of > or = 3 and percentage body fat > or = 23% in Japanese children.
Arteriosclerosis↗
Sudden death in school children: role of physical activities and meteorological conditions.
BACKGROUND: This current study is aimed at investigating the effect of physical activities and meteorological conditions on the sudden deaths of children without obvious causes at school. METHODS: The subjects are 76 victims of sudden death at school in the 12 years from 1983 to 1994 in Aichi Prefecture, Japan. The incidence of these sudden deaths is shown by month of the year, day of the week and hour of the day in relation to physical activities and meteorological factors. The analysis of Hayashi's quantitation type II was used for evaluation of the relationship between sudden deaths under the different physical conditions, such as sedentary (at rest or slow walking) or active (running, competitive sports or swimming) conditions, and meteorological or weather factors such as, season of the year, wind-chill factor, atmospheric pressure and relative humidity. RESULTS: Of 76 cases, 21 died suddenly under sedentary physical conditions and 55 under active conditions. The incidence of sudden death was highest from 10.00 to 11.00 h and on Thursday. Sudden death under sedentary conditions was associated with autumn and winter or with winter with high humidity and low atmospheric pressure. Sudden deaths during running were associated with spring with low humidity and high pressure and sudden deaths during competitive sports were associated with dry and cloudy weather. CONCLUSION: Sudden deaths in children at school may be associated with physical activities and meteorological conditions.
Cause of Death↗