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Biomedical subjects

T Tsuji

Publications and source records attributed to T Tsuji.

At least 433 records · Page 24Linked to original sources
PubMed1997

Time dependent alterations of serum matrix metalloproteinase-1 and metalloproteinase-1 tissue inhibitor after successful reperfusion of acute myocardial infarction.

OBJECTIVE: To test the hypothesis that changes in serum matrix metalloproteinase-1 (MMP-1) and tissue inhibitors of metalloproteinase-1 (TIMP-1) after acute myocardial infarction reflect extracellular matrix remodelling and the infarct healing process. PATIENTS: 13 consecutive patients with their first acute myocardial infarction who underwent successful reperfusion. METHODS: Blood was sampled on the day of admission, and on days 2, 3, 4, 5, 7, 14, and 28. Serum MMP-1 and TIMP-1 were measured by one step sandwich enzyme immunoassay. Left ventricular volume indices were determined by left ventriculography performed four weeks after the infarct. RESULTS: Serum concentrations of both MMP-1 and TIMP-1 changed over time. The average serum MMP-1 was more than 1 SD below the mean control values during the initial four days, increased thereafter, reaching a peak concentration around day 14, and then returned to the middle control range. Negative correlations with left ventricular end systolic volume index and positive correlations with left ventricular ejection fraction were obtained for serum MMP-1 on day 5, when it began to rise, and for the magnitude of rise in MMP-1 on day 5 compared to admission. Serum TIMP-1 at admission was more than 1 SD below the mean control value, and increased gradually thereafter, reaching a peak on around day 14. Negative correlations with left ventricular end systolic volume index and positive correlations with left ventricular ejection fraction were obtained for serum TIMP-1 on days 5 and 7, and for the magnitude of rise in TIMP-1 on days 5 and 7 compared to admission. CONCLUSIONS: Both MMP-1 and TIMP-1 showed significant time dependent alteration after acute myocardial infarction. Thus MMP-1 and TIMP-1 may provide useful information in evaluating the healing process as it affects left ventricular remodelling after acute myocardial infarction.

Adult↗
PubMed1997

Assessment of UDP-galactosyl-transferase activity in gastric mucosa of patients with chronic liver disease using an enzyme-linked peanut agglutinin binding assay.

Gastric mucin plays an important role in protecting mucosa from irritants such as acids and pepsin, and UDP-galactosyltransferase is a key enzyme in mucin synthesis. In order to study the synthesis of gastric mucin in patients with chronic liver disease, we developed a new assay using a peanut agglutinin lectin to measure this enzyme in human gastric mucosa obtained by endoscopic biopsy. Enzyme activity correlated well with that determined with a previous method using radiolabeled galactose. The enzyme activity in gastric mucosa of cirrhotic patients was significantly lower than in patients with chronic hepatitis or in normal controls and correlated with the amount of mucin in surface epithelial cells. Our findings suggest that the synthesis of gastric mucin is impaired in patients with liver cirrhosis.

Adult↗
PubMed1997

Pathophysiological significance of the obese gene product, leptin, in ventromedial hypothalamus (VMH)-lesioned rats: evidence for loss of its satiety effect in VMH-lesioned rats.

To explore the pathophysiological significance of the obese (ob) gene product, leptin, in ventromedial hypothalamus (VMH)-lesioned rats, we examined the synthesis and secretion of leptin and its satiety effect in VMH-lesioned rats compared with those in sham-operated rats. Northern blot analysis revealed that ob gene expression is markedly augmented in the mesenteric and sc white adipose tissue, but remained unchanged in the epididymal white adipose tissue during the development of obesity in VMH-lesioned rats. Plasma leptin levels were relatively constant in sham-operated rats, but were elevated during the development of obesity in VMH-lesioned rats. In sham-operated rats, a single i.v. (1.0 mg/rat) or intracerebroventricular (2.0 micrograms/rat) injection of recombinant human leptin reduced food intake and body weight gain in sham-operated rats. By contrast, no significant effect on food intake or body weight gain was observed in VMH-lesioned rats. The present study provides evidence that VMH-lesioned rats overproduce leptin and increase its release but cannot respond to it and suggests that the loss of its satiety effect contributes to the development of obesity and the obesity-related phenotypes in VMH-lesioned rats.

Animals↗
PubMed1997

Use of serum creatine kinase MM isoforms for predicting the progression of left ventricular dilation in patients with hypertrophic cardiomyopathy.

Serum creatine kinase (CK) isoforms were examined to detect the progression of left ventricular (LV) enlargement with reduced motion, resembling dilated cardiomyopathy (DCM), in hypertrophic cardiomyopathy (HCM). Changes in LV indices were determined annually by echocardiography in 51 patients until serum measurements (first follow-up period, 6.5 +/- 2.2 years). Serum creatine isoforms (CKMM1, CKMM2 and CKMM3) were measured with high-voltage electrophoresis in 35 of these patients from 1991 to 1992, and the data for these latter patients are reported here. Serum total CK, CKMB, lactate dehydrogenase and its isoenzyme LDH1 were also measured. The changes in LV indices were further monitored until January, 1995 (second follow-up). During the 2 follow-up periods, the patients in the on-going group showed a reduction in the LV ejection fraction (LVEF) to < 55% with LV end-diastolic dimension (LVDd) < 55 mm, and those in the DCM-like group showed a reduction in LVEF to < 55% and an increase in LVDd to > 55 mm. During the first follow-up period, LVEF and LVDd remained at > or = 55% and < 55 mm, respectively, in 26 patients (nonprogressive-disease group), while 3 patients entered the on-going group and 6 entered the DCM-like group. The CKMM3/CKMM1 ratios in the on-going and DCM-like groups were significantly higher than those in the control and nonprogressive-disease groups. The CKMM3/CKMM1 ratio was significantly correlated with the annual rate of change for the LV end-systolic dimension (LVDs), LVDd, and LVEF, with the closest correlation observed for the annual change in LVDs. Moreover, 5 patients in the nonprogressive-disease group with elevation of the CKMM3/CKMM1 ratio to > + 2SD above the mean for the controls had an elevated annual change in LVDs within +/- 1SD of the mean in the DCM-like group. These results indicate that the ratio of CKMM3 to CKMM1 can be used to predict the progression of LV enlargement in HCM.

Aged↗
PubMed1997

Laminin alpha 1, alpha 2, alpha 4 and beta 1 chain mRNA expression in mouse embryonic, neonatal, and adult hearts.

We examined the relative expression of laminin alpha 1, alpha 2, alpha 4 and beta 1 chain genes in the heart of embryonic, neonatal and adult BALb/c mice. The reverse transcriptase-polymerase chain reaction was employed to determine the mRNA expression of these chains because of the relatively small amount of RNA extracted from rat embryonic hearts. Glyceraldehyde 3-phosphate dehydrogenase and beta-actin were used as internal controls. Among the hearts examined, a relatively high expression of laminin alpha 1 chain was observed in the embryonic hearts, while its expression was very weak in the neonatal and negligible in the adult hearts. Conversely, expression of laminin alpha 2 chain was virtually not observed in the embryonic hearts, but this chain was expressed weakly in the neonatal and substantially in the adult hearts. Similar to laminin alpha 1, laminin alpha 4 was expressed in the embryonic hearts, while its expression was relatively weak in the neonatal and adult hearts. Laminin beta 1 was expressed in the hearts of mice at all stages examined. These results demonstrate that the laminin chain gene expression changes in the different developmental stages of the hearts of BALb/c mice.

Animals↗
PubMed1997

A 15N GC/MS study of in vivo glutamine synthesis in liver failure rats.

To clarify the nature of nitrogen metabolism between branched chain amino acid (BCAA) and glutamine (Gln) in liver failure, we measured arterial plasma concentrations of Gln and 15N uptake to amino-N and amide-N of Gln in normal and D-galactosamine-induced fulminant hepatic failure (FHF) rats after 15N-leucine (Leu) injection. Fifteen, 30 and 60 min after Leu injection, the arterial plasma concentrations of Gln were significantly higher in FHF rats than in controls. The concentrations of amino-15N Gln were also significantly higher in FHF rats than in controls at 5, 15, 30 and 60 min after injection. The concentrations of amide-15N Gln did not significantly differ between FHF and controls at 5, 15 and 30 min. However, at 60 min, the concentration was significantly higher in the FHF rats. The higher uptake of 15N to amino-N of Gln in FHF rats suggests the presence of an enhanced ability to synthesize Gln from Leu in FHF rats. The higher uptake of 15N to amide-N of Gln in FHF rats at 60 min after injection suggests that excessive administration of BCAA to patients with severely impaired urea-cycle capacity suffering with hepatic failure may lead to greater levels of hyperammonemia.

Animals↗
PubMed1997

Comparison of cellular characteristics between human hepatoma cell lines with wild-type p53 and those with mutant-type p53 gene.

Characteristics of human hepatoma cell lines with the wild-type p53 were compared with those of human hepatoma cell lines with the mutant-type p53. The p21 protein located downstream of p53 was expressed in cell lines with the wild-type p53 but was not expressed in cell lines with the mutant-type p53. As to other tumor suppressor genes such as p16 and p27, there was no difference in their expression between both types of cell lines. In addition, no marked difference was observed in the activities of CDK2 and CDK4 between cell lines with the wild-type and the mutant-type p53. Phosphorylated Rb protein was detected in all cell lines except the HLE line, indicating that this cell line may have a deletion of and/or a mutation of the Rb gene. These results indicate that abnormalities of tumor suppressor genes other than p53, p16, p27, and Rb may be involved in hepatocarcinogenesis. The population doubling time of the wild-type p53 cells was significantly longer than that of the mutant p53 cells. Neither type of cell line showed a specific chromosome distribution which would indicate karyotype instability. The cell lines expressing the wild-type p53 produced tumors at lower frequency than those with the mutant p53 gene. Although there was no significant difference in effects of TGF-beta 1, EGF, cholera toxin, and db-cAMP on cell growth between the two types of cells, all three cell lines with the wild-type p53 were resistant to cytotoxicity of TNF-alpha, while two of the three with the mutant p53 were very sensitive to its cytotoxic effects.

Animals↗
PubMed1997

Increased serum levels of the carrier molecules of the carbohydrate antigen sialyl Lewis X in liver diseases.

The serum levels of the carbohydrate antigen sialyl Lewis X (SLEX) increase in liver diseases (Sunayama T, Okada Y, Tsuji T., J Hepatol 1994; 19: 451-458). However, it is not known whether the increased serum SLEX levels are associated with the increased levels of its carrier molecules and/or the increased density of SLEX per carrier molecule. By using of rabbit antibody against an SLEX-positive fraction from HepG2 culture supernatant, we developed an enzyme-linked immunosorbent assay to determine the serum levels of the carrier molecules of SLEX (CMSLEX). The CMSLEX-levels in patients with hepatocellular carcinoma were significantly higher than those of normal controls (P < 0.001) and benign chronic liver diseases, i.e., chronic active hepatitis, mild and severe form, and liver cirrhosis (P < 0.05). Patients with chronic persistent hepatitis and chronic active hepatitis, mild form, had higher CMSLEX-levels than normal controls (P < 0.05). The serum CMSLEX-levels did not differ significantly among benign liver diseases. We concluded that serum CMSLEX-levels increase nonspecifically in liver diseases. This is a possible molecular mechanism for the increased serum SLEX levels in liver diseases.

Adult↗
PubMed1997

Geranylgeranylacetone and cetraxate hydrochloride increase UDP-galactosyltransferase activity in rat gastric mucosa.

UDP-galactosyltransferase (UDP-Gal-T) is a key enzyme in the synthesis of mucus glycoprotein which plays an important role in gastric mucosal defensive mechanisms. Analysis of gastric UDP-Gal-T activity should clarify the mechanisms of the action of antiulcer drugs regarding gastric defensive factors. Here, we examined UDP-Gal-T activity in rat gastric mucosa treated with the antiulcer drugs geranylgeranylacetone (GGA) and cetraxate hydrochloride (CET). The effects of coadministration of indomethacin and exogenous administration of prostaglandins (PGs) were also studied. GGA and CET significantly increased UDP-Gal-T activity, and coadministration of indomethacin inhibited the increase of enzyme activity. UDP-Gal-T activity level with GGA was significantly higher than the control level, even in the presence of indomethacin. With CET, however, this was not the case. Among PGs, PGE1 significantly increased enzyme activity. Concomitant administration of PGE1 and GGA or CET increased UDP-Gal-T activity even with indomethacin to the levels achieved when these antiulcer drugs were administered without indomethacin. Our findings suggest that GGA and CET exert antiulcer effects by increasing mucus glycoprotein synthesis and that endogenous PG synthesis may be involved in this process. However, mechanisms not mediated by endogenous PGs may also exist in the stimulatory action of GGA on UDP-Gal-T activity.

Animals↗
PubMed1997

Yeast functional assay of the p53 gene status in human cell lines maintained in our laboratory.

We used a yeast functional assay (functional analysis of separated alleles in yeast: FASAY) to determine the p53 gene status of human cell lines maintained in our laboratory. This assay enables the researcher to score wild-type p53 expression on the basis of the ability of expressed p53 to transactivate the reporter gene HIS 3 via the p53-responsive GAL 1 promoter in Saccharomyces cerevisiae. The cell lines examined were ten hepatoma, two hepatoblastoma, three in vitro immortalized fibroblast, two osteosarcoma, a chondrosarcoma, an ovarian teratocarcinoma and a colon cancer cell line. Out of 20 cell lines, 11 cell lines had mutations in both alleles of the p53 gene, and another 8 cell lines had no mutation in the p53 gene. Thus, 55% of the cell lines examined had mutations in the p53. Interestingly, PA-1 cells had both the normal and the mutant p53 alleles, showing that FASAY is a useful method for detecting the wild-type and mutated p53 genes simultaneously. As for the three liver cell lines harboring HBsAg, there was no relationship between their p53 gene status and the presence of HBsAg. Two cell lines were normal for p53 status, while the other had a mutation of the p53 gene.

Alleles↗
PubMed1997

Two cases of renal hypouricemia with nephrolithiasis.

We treated two cases of renal hypouricemia with nephrolithiasis. The serum uric acid level of the first patient was 1.5 mg/dl, and the ratio of uric acid clearance to creatinine clearance (CUA/Ccr) was 75.7%. In the benzbromarone (BZB) suppression test, CUA/Ccr was increased from 60.4% to 130.0%, but was not decreased in response to the pyrazinamide (PZA) suppression test. This patient was considered to have a presecretory reabsorptive urate transportation defect. His condition was also associated with IgA nephropathy. The serum uric acid level in the second patient was 1.0 mg/dl and CUA/Ccr was 56.0%. Neither PZA nor BZB had a significant effect on CUA/Ccr. He was considered to have a subtotal uric acid transportation defect. Both patients were incidentally found to have nephrolithiasis. The second patient had abnormal maximum tubular secretory capacity for para-aminohippurate (PAH) (TmPAH), and was found to have two kinds of proximal tubular abnormalities related to uric acid and PAH.

Adult↗
PubMed1997

Decremental oscillation curve fitting of heart rate response following face immersion into cold water.

Using 18 healthy volunteers, we attempted to fit the heart rate response to a decremental oscillation curve by the least-squares method following facial immersion into cold water. The decremental oscillation equation was as follows: HR = alpha.e(-betat) sin omegat + gamma, where HR is the instantaneous heart rate at t s, alpha the maximum amplitude of the decremental oscillation, beta the decremental rate, omega the angular velocity and gamma the basal heart rate. Each subject immersed his/her face fully in a basin filled with ice-cold water (4 degrees C) for 30 s. The heart rate response to facial immersion was significantly fitted to the decremental oscillation curve with a correlation coefficient > 0.75 in all the trials. Double trials with a 15-min intertrial interval did not show any significant change in the coefficients. Atropine sulfate decreased the value of coefficient omega and increased that of gamma but did not change alpha or beta, indicating that omega is determined mainly by parasympathetic tone. There were no differences for any coefficient between men and women. The coefficients beta and gamma increased in association with age. Given the significant fitting to the decremental oscillation curve of the heart rate response, we propose that the corresponding electrical circuit consists of a resistance and an inductor connected in series, with a condenser in a parallel circuit with a direct current impulse. This method of fitting with the corresponding electric circuit may be useful for analysis of the heart rate response to physiological stimulus.

Age Factors↗
PubMed1997

[Coronary artery bypass grafting in patients over 70 years old].

We examined the outcome of CABG in 157 patients aged over 70 years. The average age was 72.7 +/- 2.4 years: the number of the diseased vessels, 2.5 +/- 0.7/pt; the mean preoperative LVEF, 0.55 +/- 0.17 and the number of patients with left main trunk disease, 40 (26%). The mean number of bypass grafts was 2.8 +/- 0.8/pt. In 131 patients (83.4), left internal thoracic artery (LITA) was used to bypass the left anterior descending artery (LAD). The postoperative hospital mortality rate was 6.4%. After 10 years of follow-up, the actuarial survival rate and cardiac event-free rate were 73.6% and 88.9%, respectively calculated by the Kaplan-Meier method. A comparison of the long-term results of CABG with and without ITA grafting, showed no statistical difference with respect to actuarial survival rate. However, the cardiac event-free rate was improved by using an ITA graft (92.4% with an ITA vs 77.3% without an ITA, p = 0.047). This result suggested that the use of ITA in patients over 70 years old reduced the incidence of postoperative cardiac events without increasing the operative risk.

Age Factors↗
PubMed1997

[p53 alterations and chromosome 17 aberrations in non-small cell lung cancer].

We studied the relationship between DNA index, numerical abberation of chromosome 17 and alterations of the p53 gene in 23 non-small cell lung cancers. Diploid and aneuploid cells from 23 non-small cell lung cancer with DNA aneuploidy were flow sorted into each cell population using FACStar(plus). They were examined by PCR-SSCP analysis for p53 mutation and by microsatellite analysis for loss of heterozygosity at TP53 locus (17p13.1). They were also analyzed by FISH for copy number of chromosome 17. p53 mutations were found in aneuploid cells from the 11 cases (48%). Among them, 8 cases were informative at TP53 locus, and all showed loss of heterozygosity. Aneuploid cells from 16 cases exhibited gain of chromosome 17 copy number in FISH analysis. DNA index was significantly associated with th mean copy number of chromosome 17, suggesting that the number of chromosome 17 changed with DNA index. There were no associations between p53 mutation and DNA index or mean copy number of chromosome 17. In some cases, we also analyzed structural abberation of short arm of chromosome 17 by FISH using p53-cosmid (17p13.1) and Distal 17p (17p13.3-ptel) probes. The p53 gene located on the increased chromosome 17 was lost due to point mutation or deletion of 17p.

Aneuploidy↗
PubMed1997

[True "PICA communicating artery" aneurysm: a case report].

We present an unusual case of an aneurysm of the distal posterior inferior cerebellar artery (PICA). A 51-year-old female presented a subarachnoid hemorrhage with mild consciousness disturbance on August 6, 1992. Computed tomography (CT) on admission showed subarachnoid hemorrhage with thick hematoma in the cisterna magna and intraventricular hematoma in the 4th, 3rd and both lateral ventricles. The angiogram on admission revealed no definite vascular anomalies. Repeated angiograms on the 11th day after onset showed an aneurysm on anastomotic branch between the bilateral distal PICAs. The aneurysm was clipped successfully through a suboccipital craniectomy 14 days after the onset. In the literature reviewed, only one such aneurysm, located at an anastomotic vessel of the bilateral PICAs, has been reported by Hlavin et al in 1991. They reported that the aneurysm was associated with a unilateral PICA that supplied both cerebellar hemispheres and arose from an anastomotic vessel in the contralateral circulation. They called the aneurysm as "a PICA communicating artery" aneurysm. We assume that this "PICA communicating artery" is a remnant of a primitive lateral vertebrobasilar anastomosis, which appears in the embryo at the 9 mm stage. It is suggested that the pathogenesis may be not only the hemodynamic factor but also a congenital anomaly.

Arterio-Arterial Fistula↗