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T Matsubara

Publications and source records attributed to T Matsubara.

At least 55 records · Page 3Linked to original sources
PubMed2001

Pancreatic ductal adenocarcinoma associated with Potter type III cystic disease.

Although polycystic liver disease (PLD) is known to be associated with autosomal dominant polycystic kidney disease, a finding of PLD with pancreatic ductal adenocarcinoma is extremely rare. We have experienced one such case of a ductal adenocarcinoma of the pancreas in a patient with Potter type III cystic disease of the liver and kidney. A 63-year-old man was admitted to our hospital because of obstructive jaundice. Six months previously, on admission to a local hospital for treatment of diabetes mellitus, he had been found to have polycystic disease of the liver and kidney. Ultrasound examination revealed dilatation of the intrahepatic bile duct and the common bile duct. Blood tests showed an elevated total bilirubin level. Abdominal computed tomography scans and magnetic resonance imaging demonstrated polycystic lesions in the liver and the bilateral kidneys. Percutaneous transhepatic cholangio-drainage was performed, and fluorography of the biliary tree revealed obstruction of the lower common bile duct, causing jaundice. This appears to be a case of independent association of pancreatic ductal adenocarcinoma with polycystic disease of the liver and kidney. The patient's sister, who also had polycystic disease of the liver and kidney, had died of squamous cell carcinoma of the tongue. Although familial associations of carcinomas with polycystic liver disease may be extremely rare, they provide a perspective for the etiology of polycystic liver disease.

Abnormalities, Multiple↗
PubMed2001

Anatomical major resection versus nonanatomical limited resection for liver metastases from colorectal carcinoma.

BACKGROUND: Although systematic anatomical hepatic resection has been reported to improve patient survival in hepatocellular carcinoma, principles of hepatectomy procedure have not been clearly demonstrated in secondary hepatic malignancy. The purpose of the present study was to determine whether selection of surgical procedures for liver resection is associated with the pattern of tumor recurrence or patient survival. METHODS: During the period of 1980 through 1999, 174 cases underwent liver resection for hepatic metastasis from colorectal cancer. Of these, 96 underwent systematic anatomical major hepatic resection (anatomical group) and 78 cases underwent nonanatomical limited resection (nonanatomical group). Subset analysis of 115 patients with unilobar single or double tumors was also conducted. RESULTS: The overall 5-year survival rate of 174 patients was 43.2%. Univariate analysis did not show a significant difference in patient survival according to surgical procedure (anatomical group versus nonanatomical group). Operative morbidity and mortality rates were slightly higher in anatomical group. From the subset analysis in unilobar single or double tumors, anatomical major hepatectomy was unnecessary in 80.4% of the cases if the tumors were resectable by nonanatomical limited resection. Ninety percent of the ipsilateral recurrence, which could have been avoided if the first operation was anatomical hemihepatectomy, could undergo second hepatectomy with 5-year survival rate of 58.3%. CONCLUSIONS: There was not a significant difference in patient survival according to surgical procedure. To minimize surgical stress and operative risk, nonanatomical limited liver resection should be a basic surgical procedure for colorectal metastases.

Colorectal Neoplasms↗
PubMed2001

Coronary artery bypass grafting in octogenarians.

Preoperative profiles, postoperative complications, and the early and late results in 32 patients 80 yrs. of age and older (elderly group) who underwent coronary artery bypass grafting were compared with those in patients under 80 yrs. of age (control group). In the elderly group, the prevalence of patients with preoperative creatinine clearance (Ccr.) <50 l/day (34.4%), unstable angina pectoris (78.1%) and left main trunk disease (40.1%) was significantly higher than those in the control group. The incidences of arrhythmia and intensive care unit(ICU) syndrome were also significantly higher in the elderly group than in the control group, however, there was no death due to these complications. In the elderly group, one patient (3.1%) died in the hospital due to low cardiac output syndrome (LOS), while three patients (2.4%) of the control group died in the hospital. As for the long-term results, the 5-yr. survival rates for the elderly group and the control group were 82.6% and 85.2%, respectively, and the effectiveness of surgery was remarkable, with improved postoperative activity in 96.9% of the elderly group. These findings indicate that although the elderly patients have higher risks by undergoing surgery and have a disadvantage in the rate of postoperative complications, the postoperative improvement in activity and survival rate can be similar to those in the younger patients.

Adolescent↗
PubMed2001

Maturation of macrophages from peripheral blood monocytes in Kawasaki disease: immunocytochemical and immunoelectron microscopic study.

Kawasaki disease (KD) is regarded as a cytokine-associated disorder. Despite intensive investigation into the etiology of KD, this remains unclear, although monocytes and macrophages are thought to play an important role. We examined peripheral blood monocytes using a monoclonal antibody, PM-2K, which recognizes mature macrophages but not monocytes. This study was conducted in 12 patients with KD, three patients with sepsis and 12 control subjects. Approximately 8% of whole peripheral blood monocytes from patients with acute KD were observed to be PM-2K positive. Approximately 15-20% of peripheral blood CD14+ monocytes from these patients were positive for PM-2K antibody (as determined by immunoelectron microscopy). PM-2K-positive monocytes had significantly fewer numbers of intracytoplasmic peroxidase-positive granules than monocytes from control subjects. In contrast, PM-2K-negative monocytes from patients with acute KD had a significantly greater number of peroxidase-positive granules in the cytoplasm than in those from controls. Monocytes from patients with sepsis displayed PM-2K immunocytochemical staining, similar to that in monocytes from patients with KD. These results suggest that during the acute stage of KD, monocytes partly differentiate into macrophages in the peripheral circulation.

Cellular Senescence↗
PubMed2001

Increase of cord blood cytokine-producing T cells in intrauterine infection.

BACKGROUND: Although infection is a frequent and important cause of morbidity and mortality in the neonatal period, evaluation of the immune system in cases of intrauterine infection is not easy. The subsets of T helper (Th) 1, which produce mainly interferon gamma (IFN-gamma), and Th2, which produce interleukin (IL) -4, have been implicated in the regulation of many immune responses. In this study, we investigated Th1 and Th2 subsets in the cord blood (CB) to evaluate the role of CB T cells in the intrauterine infections. METHODS: We used an intracellular cytokine-staining technique with determination by flow cytometry to study IFN-gamma-producing T cells and IL-4-producing T cells in the CB of six neonates with perinatal intrauterine infection and 17 uninfected neonates. RESULTS: The CB from neonates with intrauterine infections had more IFN-gamma-producing CD3+T cells than that from uninfected neonates. The percentage of CB IFN-gamma-producing CD3+T cells in the infected neonates correlated with the duration of membrane rupture before the onset of labor, but not with the level of C-reactive protein. The infected neonate born after the longest duration of membrane rupture showed an increased percentage of IL-4-producing CD3+T cells. CONCLUSIONS: Our results suggest that the increase of CB IFN-gamma and IL-4- producing T cells is part of the immune system directed against perinatal intrauterine infections.

Female↗
PubMed2001

Proliferative activity of intrahepatic colorectal metastases after preoperative hemihepatic portal vein embolization.

Although hemihepatic portal vein embolization (PVE) has been used preoperatively to extend indications for hepatectomy in patients with colorectal metastases, the effects of this procedure on tumor growth and outcome remain controversial. To address this issue, we assessed the proliferative activity of intrahepatic metastases after PVE and the long-term outcome of this procedure. Eighteen patients with colorectal metastases underwent preoperative PVE between 1996 and 2000 (PVE group). Twenty-nine patients who underwent major hepatic resection without PVE served as control (non-PVE group). The hepatic parenchymal fraction of the left lobe had significantly increased from 38.1 +/- 3.2% to 45.9 +/- 2.9% 3 weeks after PVE (+20.5%, P <.0001). Tumor volume and percent tumor volume had also significantly increased from 223 +/- 89 mL to 270 +/- 97 mL (+20.8%, P =.016) and from 13.7 + 4.3% to 16.2 + 4.9% (+18.5%, P =.014), respectively. There was no apparent correlation between the increase in parenchymal volume and that in tumor volume. The Ki-67 labeling index of metastatic lesions was 46.6 +/- 7.2% in the PVE group and 35.4 +/- 12.6% in the non-PVE group (P =.013). Long-term survival was similar in the PVE and non-PVE groups, however, disease-free survival was significantly poorer in the PVE group than in the non-PVE group (P =.004). We conclude that PVE increases tumor growth and probably is associated with enhanced recurrence of disease. Although PVE is effective in extending indications for surgery, patient selection for PVE should be cautious.

Adult↗
PubMed2001

Clarithromycin inhibits NF-kappaB activation in human peripheral blood mononuclear cells and pulmonary epithelial cells.

Macrolide antibiotics modulate the production of proinflammatory cytokines in vivo and in vitro. Transcription of the genes for these proinflammatory cytokines is regulated by nuclear factor kappaB (NF-kappaB). We examined whether or not clarithromycin inhibits the activation of NF-kappaB induced by tumor necrosis factor alpha (TNF-alpha) or staphylococcal enterotoxin A (SEA) in human monocytic U-937 cells, a T-cell line (Jurkat), a pulmonary epithelial cell line (A549), and peripheral blood mononuclear cells (PBMC). Flow cytometry revealed that clarithromycin suppresses NF-kappaB activation induced by TNF-alpha in U-937 and Jurkat cells in a concentration-related manner. Western blot analysis also demonstrated that clarithromycin inhibits NF-kappaB activation induced by TNF-alpha in U-937, Jurkat, and A549 cells and PBMC and by SEA in PBMC. Western blot analysis of cytoplasmic extracts of A549 cells revealed that this inhibition is not linked to preservation of expression of the IkappaBalpha protein. The chloramphenicol acetyltransferase assay indicated that NF-kappaB-dependent reporter gene expression is suppressed in U-937 cells pretreated with clarithromycin. These findings are consistent with the idea that clarithromycin suppresses the production of proinflammatory cytokines via inhibition of NF-kappaB activation.

Anti-Bacterial Agents↗
PubMed2001

Purification, characterization, and overexpression of flavin reductase involved in dibenzothiophene desulfurization by Rhodococcus erythropolis D-1.

The dibenzothiophene (DBT)-desulfurizing bacterium, Rhodococcus erythropolis D-1, removes sulfur from DBT to form 2-hydroxybiphenyl using four enzymes, DszC, DszA, DszB, and flavin reductase. In this study, we purified and characterized the flavin reductase from R. erythropolis D-1 grown in a medium containing DBT as the sole source of sulfur. It is conceivable that the enzyme is essential for two monooxygenase (DszC and DszA) reactions in vivo. The purified flavin reductase contains no chromogenic cofactors and was found to have a molecular mass of 86 kDa and four identical 22-kDa subunits. The enzyme catalyzed NADH-dependent reduction of flavin mononucleotide (FMN), and the K(m) values for NADH and FMN were 208 and 10.8 microM, respectively. Flavin adenine dinucleotide was a poor substrate, and NADPH was inert. The enzyme did not catalyze reduction of any nitroaromatic compound. The optimal temperature and optimal pH for enzyme activity were 35 degrees C and 6.0, respectively, and the enzyme retained 30% of its activity after heat treatment at 80 degrees C for 30 min. The N-terminal amino acid sequence of the purified flavin reductase was identical to that of DszD of R. erythropolis IGTS8 (K. A. Gray, O. S. Pogrebinsky, G. T. Mrachko, L. Xi, D. J. Monticello, and C. H. Squires, Nat. Biotechnol. 14:1705-1709, 1996). The flavin reductase gene was amplified with primers designed by using dszD of R. erythropolis IGTS8, and the enzyme was overexpressed in Escherichia coli. The specific activity in crude extracts of the overexpressed strain was about 275-fold that of the wild-type strain.

Escherichia coli↗
PubMed2001

Respiratory alkalosis does not alter NOx concentrations in human plasma and erythrocytes.

To test the hypothesis that NOx (NO and NO, metabolites of NO) accumulates in red blood cells (RBC) in response to changes in PCO(2) and bicarbonate (HCO) concentration in blood, we examined the effect of changes in PCO(2) and HCO induced by hyperventilation in healthy adults on partitioning of NOx in whole blood. NOx in hemolysate was measured by a high-performance liquid chromatography-Griess system equipped with a C(18) reverse phase column to trap hemoglobin, which enables determination of whole blood NOx concentration and calculation of NOx concentration in RBC with high accuracy and reproducibility. NOx concentration in RBC was lower than that in plasma, and equilibrium between plasma and RBC was achieved rapidly after addition of NO. Changes in PCO(2) and HCO by hyperventilation failed to influence NOx concentrations in both plasma and RBC. Plasma NOx concentrations correlated with whole blood NOx and RBC NOx concentrations. Our results indicate that changes in PCO(2) or HCO induced by hyperventilation do not influence NOx compartmentalization in plasma and RBC.

Adult↗
PubMed2001

A comparison of FcepsilonRI-mediated RANTES release from human platelets between allergic patients and healthy individuals.

BACKGROUND: Recently some studies have suggested that human platelets may play an important role in allergic inflammation through the high affinity IgE receptor (FcepsilonRI), the low affinity IgE receptor (FcepsilonRII/CD23) and the low affinity IgG receptor (FcgammaRIIA/CD32) expressed on the cell surface. We reported that human platelets via the FcepsilonRI induced the release of the chemical mediator serotonin and the chemokine RANTES (regulated upon activation, normal T expressed and presumably secreted), but the biological implication of human platelets in type I allergy has not yet been understood clearly. METHODS: We compared the levels of RANTES release from platelets obtained from allergic patients and healthy individuals, stimulated with monoclonal antibody (Ab) to human FcepsilonRI alpha-chain, or human myeloma IgE and anti-human IgE Ab. RESULTS: We confirmed that the level of RANTES release from platelets of allergic patients stimulated with human IgE and anti-human IgE was significantly higher than that of healthy individuals. CONCLUSIONS: We demonstrated that the surface expression levels of FcepsilonRI on the platelets from allergic patients and healthy individuals were not significantly different, but that the platelets of allergic patients were more activated by the IgE-FcepsilonRI pathway than those of healthy individuals. Taken together, these results suggest a novel and important role for human platelets in perpetuating allergic inflammation through the IgE and FcepsilonRI.

Adult↗
PubMed2001

Increased frequency of alleles associated with elevated tumor necrosis factor-alpha levels in children with Kawasaki disease.

Genetic polymorphisms influence the magnitude of the cytokine response after an inflammatory stimulus. To determine whether such polymorphisms might play a role in Kawasaki disease (KD), we analyzed white and Japanese children with KD and control populations for two polymorphic loci in which the A allele is associated with high tumor necrosis factor-alpha secretion. The lymphotoxin-alpha+250 A/A genotype was overrepresented among white children with KD compared with controls (0.59 versus 0.36; p = 0.013). The tumor necrosis factor-alpha-308 A/G genotype was overrepresented among whites with KD who had coronary artery abnormalities compared with those with normal echocardiograms (0.36 versus 0.09; p = 0.044). No significant difference was seen at either locus between Japanese children with KD and Japanese controls. The increased frequency of the high secretor alleles in white children with KD suggests that these loci may be related to susceptibility to KD and to outcome after disease.

Alleles↗
PubMed2001

Screening of natural compounds for inhibitory activity on colon cancer cell migration.

We examined the effects of 75 kinds of natural compounds, such as alkaloids, phenylpropanoids, flavonoids, steroids and terpenoids on the in vitro migration and proliferation of colon 26-L5 cells, in comparison with anti-cancer drugs used for chemotherapy. Twenty-three of the 75 compounds inhibited markedly tumor cell migration. Among the 23 compounds, evodiamine showed the most potent and selective inhibitory activity on tumor cell migration with an IC50 value of 1.25 microg/ml, which was about 20 times lower than that for tumor cell proliferation. The migratory inhibition reached about 70% at 10 microg/ml of evodiamine. On the other hand, most of anti-cancer drugs tested, except for paclitaxel, had little effect on tumor cell migration at the concentrations strongly inhibiting tumor cell proliferation. Paclitaxel suppressed tumor cell migration in a concentration-dependent manner and achieved about 70% inhibition at 10 microg/ml with a marginal effect on cell proliferation. These results suggest that evodiamine and paclitaxel may be regarded as leading compounds for anti-metastatic agents acting through the inhibition of tumor cell migration without cytotoxicity.

Animals↗
PubMed2001

Inhibitory effects of evodiamine on in vitro invasion and experimental lung metastasis of murine colon cancer cells.

We have previously reported that evodiamine had a marked inhibitory activity on tumor cell migration in vitro. To extend our study, the effects of evodiamine on invasion, growth, and metastatic development of colon 26-L5 cells were examined here. Evodiamine inhibited the invasion of tumor cells into Matrigel in a concentration-dependent manner, and achieved 70% inhibition at 10 microg/ml. Treatment of tumor cells with evodiamine for 24 h showed little effect on tumor growth at concentrations of less than 10 microg/ml, whereas an over 48-h treatment resulted in a concentration- and time-dependent inhibition. Pretreatment of tumor cells with 10 microg/ml evodiamine before inoculation into mice caused 70% reduction in their lung metastasis formation. When evodiamine at 10 mg/kg was administered into mice from the 6th day after tumor inoculation, the number of tumor nodules in lungs was decreased by 48% as compared to control. The inhibition rate was equivalent to that produced by cisplatin, a potent anti-cancer drug. Evodiamine did not affect the body weight of mice in the experimental period, whereas cisplatin caused serious weight loss. These results suggest that evodiamine may be regarded as a promising agent in tumor metastasis therapy.

Adenocarcinoma↗
PubMed2001

Lipid peroxidation may predict restenosis after coronary balloon angioplasty.

The present study assessed whether lipid peroxidation in plasma might predict restenosis after coronary balloon angioplasty. A total of 87 patients, who had undergone successful coronary balloon angioplasty using standard techniques, were enrolled. Fasting blood samples before the intervention were measured for plasma levels of thiobarbituric acid reactive substances (TBARS, an indicator of lipid peroxidation). Angiography was carried out before and 15 min after angioplasty, and at follow-up (4 months after angioplasty), and evaluated using a quantitative approach. There were 23 patients with restenosis (group R) and 64 patients without restenosis (group N) after coronary balloon angioplasty. The plasma TBARS level (mean+/-SEM) of 4.3+/-0.1 micromol/L in group R was significantly higher than that of 3.2+/-0.1 micromol/L in group N (p<0.01). There were no significant differences in other parameters, including plasma lipid levels, between the 2 groups. The plasma level of TBARS positively correlated with lumen loss of the coronary artery at the time of follow-up angiography (r=0.57, p<0.01). Our results suggest that oxidative stress contributes to restenosis and indicate that an elevated plasma level of TBARS may be a reliable predictor of restenosis.

Aged↗
PubMed2001

Regulation of endothelial nitric oxide synthase and endothelin-1 expression by fluvastatin in human vascular endothelial cells.

We investigated the effects of fluvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, on endothelial vasoactive substances using human umbilical vein endothelial cells (HUVECs). Incubation of HUVECs with fluvastatin for 12 h increased endothelial nitric oxide synthase (eNOS) mRNA expression in a concentration-dependent manner (peak, 276 +/- 38%, mean +/- S.D., of the control, at 1.0 microM fluvastatin, P<0.01). In addition, fluvastatin increased eNOS protein production (245 +/- 51% of the control level, P<0.05) as well as nitrite production (165 +/- 35% of the control level, P<0.01). In contrast, incubation of HUVECs with 1.0 microM fluvastatin for 12 h significantly reduced the production of endothelin-1 (ET-1) and preproET-1 mRNA expression in HUVECs (28 +/- 1% and 39 +/- 1% of the control level, respectively, P<0.01). Our results suggest that fluvastatin might be involved in improvement of endothelial function and prevention of the progression of atherosclerosis.

Base Sequence↗
PubMed2001

Inverse correlation between the changes of lumbar bone mineral density and serum undercarboxylated osteocalcin after vitamin K2 (menatetrenone) treatment in children treated with glucocorticoid and alfacalcidol.

We have reported that alfacalcidol plus menatetrenone, a vitamin K2 with four isoprene units (menaquinone-4), treatment is useful for improving bone problems in children with skeletal unloading. The aim of this study was to evaluate the effect of menatetrenone on bone metabolism in long-term glucocorticoid-treated children with alfacalcidol treatment. Twenty children who had been treated with fixed dosages of prednisolone and alfacalcidol (0.03 microg/kg/day) for 24 weeks were enrolled in a prospective pilot study, and assigned to receive alfacalcidol (0.03 microg/kg/day) or alfacalcidol (0.03 microg/kg/day) plus menatetrenone (approximately 2 mg/kg/day). Bone biochemical markers and bone mineral density (BMD) were measured at baseline and after the 12-week treatment. In the group receiving alfacalcidol plus menatetrenone, serum carboxylated osteocalcin (OC) (p =0.0022) and lumbar BMD (p=0.0029) increased and serum undercarboxylated OC (p=0.0004) decreased significantly in comparison to the group receiving alfacalcidol; further, the change of lumbar BMD showed an inverse correlation to the change of serum undercarboxylated OC (r=-0.744, p=0.0134) and positive correlations to the baseline values of bone turnover markers such as serum levels of intact OC, bone-specific alkaline phosphatase and type I procollagen carboxyl extension peptide and urinary levels of deoxypyridinoline and N-telopeptide of type I collagen. No adverse effect was observed. This is a small short-term study, but its results suggest that menatetrenone effectively and safely increases lumbar BMD probably through carboxylation of OC in long-term prednisolone-treated children with alfacalcidol treatment who have a high bone turnover. Randomized double-blind controlled trials are needed to confirm our findings.

Adolescent↗
PubMed2001

Comparison of ticlopidine and cilostazol for the prevention of restenosis after percutaneous transluminal coronary angioplasty.

Prevention of restenosis after percutaneous transluminal coronary angioplasty (PTCA) continues to be a significant problem. Recent controlled studies have demonstrated that cilostazol suppresses restenosis after PTCA. The effects of ticlopidine, another antiplatelet agent, were compared in terms of outcomes of patients randomized for treatment with the two drugs after PTCA. A total of 35 patients (47 lesions) were assigned prospectively and randomly to ticlopidine (17 patients, 24 lesions) and cilostazol (18 patients, 23 lesions) groups. Minimal luminal diameter (MLD) and percentage of stenosis to reference diameter were estimated before PTCA, just after the procedure and after 4 months follow-up. All patients underwent 4 months angiographic follow-up, at the end of which MLD was 2.03+/-0.71 mm in the ticlopidine group and 2.05+/-0.68 mm in the cilostazol group (p = 0.95), and the percentage of stenosis to reference diameter was 31.4+/-16.7% and 30.0+/-17.0%, respectively (p = 0.78). The restenosis rate was 12.5% in the ticlopidine group and 17.4% in the cilostazol group (p = 0.69), relatively low as compared to the 20% to 30% reported in previous studies. Adverse drug reactions during the follow-up period were observed in two of the ticlopidine group and none of the cilostazol group. We conclude that both ticlopidine and cilostazol are effective for the prevention of restenosis after PTCA, however the former may be associated with slight side effects.

Aged↗