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T Tsujii

Publications and source records attributed to T Tsujii.

At least 73 records · Page 4Linked to original sources
PubMed1994

Parotin subunit as a potent polyclonal B cell activator binds to newly found glycosylphosphatidylinositol (GPI)-anchored proteins on human B cell surfaces.

Parotin subunit (PS) is a unique glycoprotein, isolated from bovine parotid glands, which possesses the ability to induce polyclonal antibody production and IL-1-like activity. The present studies investigated the existence of receptors for PS on B cell surfaces using PS-affinity chromatography. No PS-binding proteins (PSR) solubilized from human B cell surfaces with Triton X-100 were detected, whereas the PSR released from human B cell membranes with phosphatidylinositol-specific phospholipase C (PI-PLC) treatment were composed of 75- and 40-kDa proteins. PI-PLC treatment markedly reduced polyclonal antibody responses to PS but weakly inhibited the responses to PWM, xanthan gum, and LPS in human and mouse lymphocytes. Addition of PSR caused a dose-related reduction in polyclonal IgM and IgG antibody responses to PS. These results suggest that PSR can act as glycosylphosphatidylinositol-anchored receptors for PS.

Animals↗
PubMed1994

[Fatty liver].

Explore the source record for details and available documents.

Fatty Liver↗
PubMed1994

Cysteinyl leukotrienes in the urine of patients with liver diseases.

The significance of cysteinyl leukotrienes was investigated in patients with liver diseases by measurements of leukotriene E4 and N-acetyl-leukotriene E4 in urine. A marked increase of renal cysteinyl leukotriene excretion was observed in patients with cirrhosis without and with ascites, intrahepatic cholestasis, and obstructive jaundice as compared with healthy subjects (leukotriene E4: means 82, 264, 221 and 142 versus 40 nmol/mol creatinine, respectively; N-acetyl-leukotriene E4: means 25, 64, 61 and 47 versus 13 nmol/mol creatinine, respectively). The urinary concentration of leukotriene E4 was positively correlated with the one of N-acetyl-leukotriene E4 (r = 0.81, p < 0.001). In patients with cirrhosis, the excretion of cysteinyl leukotrienes was strongly increased in patients in Child-Turcotte stage C as compared with those in Child-Turcotte stages A and B. In patients with intrahepatic cholestasis and in those with obstructive jaundice, the excretion of leukotriene E4 plus N-acetyl-leukotriene E4 was positively correlated with total serum bilirubin. In patients with cirrhosis and in those with obstructive jaundice, the cysteinyl leukotrienes in urine were negatively correlated with creatinine clearance. The elevated renal excretion of cysteinyl leukotrienes decreased after biliary drainage in patients with obstructive jaundice. These data support the concept that increased urinary excretion of cysteinyl leukotrienes in patients with cirrhosis is due to a reduced functional liver mass and that in patients with cholestasis it is mainly due to an impaired elimination into the biliary tract that results in a diversion to renal excretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Antibody production system modulated by oral administration of human milk and TGF-beta.

Human milk contains large amounts of transforming growth factor-beta (TGF-beta), which exerts powerful suppressive effects on many immune functions. Oral administration of human milk and TGF-beta in mice strongly inhibited anti-sheep red blood cell (SRBC) responses obtained following oral immunization with SRBC, but enhanced the responses elicited by intraperitoneal, intrabronchial or intravenous immunization with SRBC. Anti-SRBC antibody responses stimulated by intraperitoneal or intravenous immunization with SRBC failed to augment when TGF-beta-depleted human milk was given orally. These findings suggest that TGF-beta in human milk functions as an adjuvant for protective antibody responses against parenteral infections.

Adjuvants, Immunologic↗
PubMed1994

Spontaneous passage of a colon cast in the absence of abdominal aneurysm.

The spontaneous passage of colon cast from a 76-year-old Japanese female patient is reported. Macroscopically, the colon case was shaped like the airbladder of a fish. Histopathologically, the cast consisted of degenerated colonal mucosa, including glands. No inflammatory reaction was apparent. The patient lacked any evidence of abdominal aneurysm. Since there have been only five reported cases of colon cast in the literature, and since in all of those association with abdominal aneurysms was always described, the present study represents the first report demonstrating the formation of a colon cast in the absence of associated abdominal aneurysm. However, the patient was found to exhibit several risk factors for ischemic colitis, such as arteriosclerosis on the wall of the abdominal aorta, chronic constipation, and colonic stenosis. Her colonal mucosal surface, indeed, suggested ischemic colitis. This case report, therefore, indicates that ischemic colitis, due to various causes, may be responsible for the formation of colon casts, and that the presence of an abdominal aneurysm is not necessarily a prerequisite for colon cast formation. This report may contribute to a better understanding of the pathogenesis of colon casts.

Aged↗
PubMed1994

Glial cell degeneration and hypomyelination caused by overexpression of myelin proteolipid protein gene.

Myelin proteolipid protein (PLP), the major myelin protein in the CNS, has been thought to function in myelin assembly. Thus, mutations within the gene coding for PLP (Plp) cause hypomyelination, such as the jimpy phenotype in mice and Pelizaeus-Merzbacher disease in humans. However, these mutants often exhibit premature death of oligodendrocytes, which form CNS myelin. To elucidate the functional roles of Plp gene products in the maturation and/or survival of oligodendrocytes, we produced transgenic mice overexpressing the Plp gene by introducing extra wild-type mouse Plp genes. Surprisingly, transgenic mice bearing 4 more Plp genes exhibited dysmyelination in the CNS, whereas those with 2 more Plp genes showed normal myelination at an early age (3 weeks after birth), but later developed demyelination. Overexpression of the Plp gene resulted in arrested maturation of oligodendrocytes, and the severity of arrest was dependent on the extent of overexpression. Overexpression also led to oligodendrocyte cell death, apparently caused by abnormal swelling of the Golgi apparatus. Thus, tight regulation of Plp gene expression is necessary for normal oligodendrocyte differentiation and survival, and its overexpression can be the cause of both dys- and demyelination.

Animals↗
PubMed1994

Parotin subunit and its synthetic peptide possess interleukin 1-like activity and exert stimulating effects on liver cells and brain cells.

We have investigated whether parotin subunit (PS) and its partial synthetic peptide (P-10.2: TDDTAIVLLK), possess interleukin 1 (IL-1)-like activities, and act on cell lines other than lymphocytes. When Chang liver cells were cultured with P-10.2, PS or IL-1, P-10.2 and PS augmented the growth of Chang liver cells. On the other hand, IL-1 enhanced the growth of Change liver cells at 1 day of the initial culture and subsequently failed to enhance during at least 4-day incubation. Next, effects of P-10.2 and PS on the growth of Alexander cells and MH134 were investigated. The proliferation of Alexander cells was inhibited with P-10.2 or PS but not with IL-1. P-10.2 inhibited the growth of MH134 at day 1 and 3, while the growth of MH134 was shown not to be inhibited with PS and IL-1 at day 1, but rather suppressed them at day 3. These results suggest that P-10.2 augments the growth of non-malignant liver cells (Chang liver cells) but inhibits that of hepatoma cells (Alexander cells and MH134). P-10.2 enhanced fibrinogen and hepatoglobin secretion from Chang liver cells. In addition to their liver cell activation, P-10.2 and PS stimulated ACTH and beta-endorphin secretion from AtT-20 cells.

Adrenocorticotropic Hormone↗
PubMed1994

Effect of prostaglandin E1 on experimental acute hepatic failure in rabbits: prostaglandin E1 prevents the development of multiple-organ failure.

Acute hepatic failure was induced in 50 male rabbits by D-galactosamine HCl (1 g per kg bw), and the effects of prostaglandin E1 on this model were investigated. Twelve hours after the administration of D-galactosamine HCl, a continuous infusion of prostaglandin E1 (2 micrograms.kg-1.h-1 or 20 micrograms.kg-1.h-1) was started. Ten animals in each group were observed until the time of death and mean survival times were compared between the groups. Five animals in each group were used for the determination of regional blood flows and brain water content. After the injections of D-galactosamine HCl, serum aspartate transaminase and alanine transaminase activity rose markedly and prothrombin time was prolonged. The administration of prostaglandin E1 did not affect these levels. However, the survival time in the prostaglandin E1 20 micrograms.kg-1.h-1 group (48.2 +/- 10.4 h) was significantly longer (p < 0.005, p < 0.01) than those in the untreated group (24.9 +/- 5.0 h) and the prostaglandin E1 2 micrograms.kg-1.h-1 group (28.1 +/- 5.8 h). Prostaglandin E1 20 micrograms.kg-1.h-1 inhibited elevations of blood urea nitrogen and creatinine and significantly inhibited the decrease of urine volume and urinary sodium excretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Alprostadil↗
PubMed1994

A modified fluid percussion device.

This report examines a modified fluid percussion device with specific improvements made to address deficiencies found in previously reported devices. These improvements include the use of a cylindrical saline reservoir made of stainless steel, placement of the reservoir in a 15-degree head-up position for the easy release of air bubbles, placement of the fluid flushing outlet and the pressure transducer close to the piston on the same plane, with both perpendicular to the direction of the piston, and adjustable reservoir volume to vary the waveform of the pressure pulse, and a metallic central injury screw secured to the animal's skull over the exposed dura. Using this device, midline fluid percussion (MFP) and lateral fluid percussion (LFP) injuries were performed in 70 rats. Histopathologic findings included diffuse axonal injury in the MFP model and cortical contusion in the LFP model. Survival rate was 41.4% in MFP animals and 100% in LFM animals when the device settings were 178 mm3 of the cylindrical reservoir and 50 degrees-60 degrees in height of the pendulum. Our results suggest that this modified fluid percussion device may offer significant improvements over previously reported fluid percussion models for use in experimental head injury.

Animals↗
PubMed1994

Effects of pituitary adenylate cyclase-activating polypeptide on gonadotropin secretion and subunit messenger ribonucleic acids in perifused rat pituitary cells.

Pituitary adenylate cyclase-activating polypeptide-38 (PACAP38) is a neuropeptide related to vasoactive intestinal peptide-secretin-glucagon which stimulates adenylate cyclase in cultured rat pituitary cells and stimulates LH and FSH release in vitro and in vivo. Because the cAMP-protein kinase-A pathway regulates the gonadotropin subunit messenger RNAs (mRNAs) and modulates GnRH-stimulated gonadotropin secretion in vitro, we examined the effects of PACAP38 on gonadotropin secretion and subunit mRNA levels. Anterior pituitary cells were prepared from 7-week-old male rats castrated at 5 weeks of age. In monolayer cultures stimulated with GnRH, 0.1-10 nM PACAP38 decreased (P < 0.05) the EC50 for GnRH dose-dependently without affecting the maximum LH secretory response. Cells were next stimulated with 1-min pulses of 2.5 nM GnRH every hour for 9 h in the absence or presence of 10 nM PACAP38, which was perifused continuously. The amplitude of GnRH-induced LH, FSH, and alpha-subunit secretory episodes from PACAP38-treated cells rose (P < 0.01) gradually to 233 +/- 54%, 197 +/- 44%, and 378 +/- 104%, respectively (mean +/- SEM; n = 5 experiments), of the value for control cells lacking PACAP38. This enhancement was sustained for at least 3 h after PACAP38 was removed from the perifusion medium. With PACAP treatment, interpulse secretion of LH and alpha-subunit increased gradually (P < 0.01) to 174 +/- 21% and 212 +/- 64% of the value for chambers stimulated with GnRH alone (control), respectively, whereas interpulse secretion of FSH declined (P < 0.001) to 75 +/- 7% of the control value. In contrast to the gradual effect of PACAP38 to enhance GnRH-induced hormone secretion, PACAP38 alone produced a transient burst of gonadotropin secretion. At the completion of the perifusions, total RNA was extracted and gonadotropin subunit mRNA levels were determined by Northern analysis. GnRH increased (P < 0.01) FSH beta mRNA to 438 +/- 52% of the level in cells stimulated with medium alone (control). Adding PACAP38 to the perifusion medium partially blocked (P < 0.01) the effect of GnRH (178 +/- 20% of the control value), and PACAP38 alone reduced (P < 0.01) FSH beta mRNA levels to 31 +/- 3% of the control value. By contrast, alpha-subunit mRNA levels were increased by both PACAP38 (143 +/- 4% of the control value; P < 0.01) and GnRH (121 +/- 2% of the control value; P < 0.05).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1994

[Interferon treatment for chronic hepatitis C].

To determine the factors influencing the response to interferon (IFN) therapy, we studied 156 patients with chronic hepatitis C who underwent IFN alpha treatment Either 9MU of recombinant IFN alpha 2a or 3MU of natural IFN alpha was administered daily for 2 weeks and then three times a week for 22 weeks. IFN responses were divided into three types on the basis of the results of the polymerase chain reaction (PCR) assay detecting the 5 noncoding regions of HCV in sera. A complete response (CR) was defined as sustained elimination of HCV for at least 6 months after treatment, partial response (PR) as HCV elimination for a limited period, no response (NR) as continuously HCV-RNA positive. HCV genotyping was done by PCR with genotype-specific primers, by analyzing the variations in nucleotide sequence within the core region of HCV, namely HCV-I, -II, -III and -IV. Quantitation of serum HCV-RNA was performed by competitive PCR assay using synthetic mutant RNA. CR was obtained in 43 patients, PR in 64, and NR in 49. The IFN responses, CR/PR/NR, were 7/10/3 in 20 patients with chronic persistent hepatitis histologically, 34/38/24 in 96 patients with chronic active hepatitis (CAH)2A, and 2/16/22 in 40 with CAH2B. Median values of pretreatment serum HCV-RNA amount (copies/ml) in CR, PR, and NR groups were 10(3.55), 10(4.56) and 10(5.97), respectively. On HCV genotyping of sera from 114 patients, HCV-I, -II, -III, -IV and mixed (II+of) were seen in 1, 94, 11, 6 and 2 patients, respectively. CR/PR/NR in patients infected with HCV-I, -II, -III, -IV and -II + IV were 0/0/1, 28/26/40, 3/5/3, 1/3/2 and 0/1/1, respectively. Patients who had low viremia levels were likely to show good IFN responses, and those who had progressed liver histologies were resistant to IFN therapy.

Chronic Disease↗
PubMed1994

[Study on decision support system for the interpretation of laboratory data by an artificial neural network--with a special reference to estimation for histological diagnosis of liver diseases with laboratory data on liver function].

An artificial neural network (ANN) was trained on laboratory data of liver function tests to estimate for histological diagnosis in patients with liver diseases such as chronic hepatitis, liver cirrhosis and fatty liver. ANN diagnosed accurately 95.3% of the cases for training and 50% of the test cases. Elimination of ZTT, GOT or A/G ratio from the data set for input reduced the ability of accurate diagnosis, whereas elimination of TBA raised this ability to 66.7%. On the other hand, accuracy of physician in diagnosing the test cases ranged from 20.8 to 62.5%. From our results it is expected that ANN may support a physician's decision on the interpretation of laboratory data.

Algorithms↗
PubMed1994

[A national surveillance study on alcoholic liver disease in Japan (1986-1991)].

National surveillance studies on alcoholic liver disease (ALD) in Japan were performed in 1978 and 1985, by a previous Japanese study group for ALD (Takeuchi group). In the present study, a subsequent nationwide surveillance study was performed from 1986 to 1991 and the results were compared with the previous two studies. In order to clarify the etiological relationships between hepatitis C virus (HCV) infection and ALD, an analysis was also done according to the new diagnostic criteria of ALD which was proposed by this group (Takada group). By the criteria of the Takeuchi group, the incidence of ALD was not significantly different during 1986 to 1991. However, the incidence of hepatocellular carcinoma (HCC) in alcoholic cirrhosis (AL-LC) clearly increased during this period. The analysis including the results of the previous study indicate that incidence of ALD reached a plateau in 1980 and then features of ALD in Japan entered a stable stage. However, HCC in AL-LC continued to show a linear increase from 1976 to 1991. Analysis with the new criteria of the Takada group was done in cases of 1990 and 1991. Approximately 2 out of 3 cases of ALD were caused by alcohol alone, and the remaining cases were caused by a combination of alcohol and HCV. Cases caused only by HCV were very rare. The main etiology in patients with alcoholic hepatitis and fibrosis was alcohol alone and that in chronic hepatitis of heavy drinkers was a combination of alcohol and HCV. In half of the patients with AL-LC, the etiology was alcohol alone and in the other half patients, it was a combination of both factors. In most patients with HCC, the etiology was a combination of alcohol and HCV, indicating that HCV infection may be important for the development of HCC in alcoholics.

Carcinoma, Hepatocellular↗
PubMed1993

Selective expression of foreign genes in glioma cells: use of the mouse myelin basic protein gene promoter to direct toxic gene expression.

We have previously demonstrated that retrovirus-mediated genes were transferred to mouse glioma cells in a meningeal gliomatosis model (Yamada et al.: Japanese Journal of Cancer Research 83:1244-1247, 1992). This retrovirus vector contains the Escherichia coli. beta-galactosidase (beta-gal) gene as a marker for integration of the lacZ gene, which is controlled by the SV40 early promoter. We investigated whether lacZ genes could be specifically controlled in mouse glioma cells by glial-specific promoters, including the 2.5 kb 5' flanking region of the mouse glial fibrillary acidic protein (GFAP) gene, the 1.3 kb 5' flanking region of the myelin basic protein (MBP) gene, and the 1.5 kb 5' flanking region of the myelin proteolipid protein (PLP) gene. Psi-2 packaging cells were transfected with each retrovirus vector (GFAP promoter-, MBP promoter-, and PLP promoter-lacZ) and the infectious virus particles were recovered from the supernatants. Blue staining for beta-gal was detected in various fibroblast, myeloma, and glioma cell lines transduced with the retrovirus BAG vector. On the other hand, blue staining was only detected in glioma cells after transduction with the lacZ gene-bearing retrovirus controlled by glial-specific promoters. The strongest promoter activity was detected after transduction with the retrovirus in which the MBP promoter controlled the lacZ gene. Mouse glioma cells transduced with retrovirus containing the MBP promoter directing the herpes simplex virus type 1 thymidine kinase (HTK) gene were extremely sensitive to ganciclovir, while the parental cells and cells transduced with retrovirus containing the lacZ gene were not sensitive to ganciclovir.(ABSTRACT TRUNCATED AT 250 WORDS)

3T3 Cells↗
PubMed1993

Metabolic fate of endotoxin and blood tumour necrosis factor levels in rats with acute and chronic alcohol loading.

To investigate the metabolic fate of endotoxin in alcoholics and its possible relationship to cytokines and liver injury, we administered a low-dose radiolabelled endotoxin to rats given alcohol in various conditions and studied the organ distribution of endotoxin and measured plasma levels of tumour necrosis factor (TNF). In the chronic alcohol-fed rats (Lieber-DeCarli liquid diets for 6 weeks) 3H-endotoxin was rapidly cleared by the liver and excreted into faeces. However, the endotoxin clearance was decreased after an acute ethanol load to rats (5 mg/g body wt ethanol i.p.) or in the chronic ethanol-fed rats with an additional 5 mg/g body wt ethanol load. Plasma TNF was not elevated in the control or in the acute ethanol load rats, slightly elevated in the chronic ethanol-fed rats and markedly elevated in the chronic ethanol-fed rats with an additional high-dose ethanol load. Serum GPT was elevated only in the chronic ethanol-fed rats with an additional high-dose ethanol. In conclusion, an additional administration of a high dose ethanol to chronic alcohol-fed rats led to decrease of endotoxin clearance and elevation of plasma TNF, which may play an important role in the pathogenesis of alcoholic hepatitis.

Alcoholic Intoxication↗
PubMed1993

Effect of alcohol on the functions of Kupffer cells and splenic macrophages in rats.

Uptake of endotoxin and production of tumor necrosis factor (TNF) by Kupffer cells and splenic macrophages were measured in chronically alcohol-fed rats. Twenty male Sprague-Dawley rats, weighing 200-250 g, were pair-fed by isocaloric control and ethanol-containing Lieber-DeCarli liquid diets for 6 weeks. Endotoxin uptake and TNF production of Kupffer cells and splenic macrophages in the chronic ethanol load-group were significantly (P < 0.001) greater than those in the control group. The increase in endotoxin uptake was more prominent in Kupffer cells and the increase in TNF production was more marked in splenic macrophages in the chronic ethanol group. When these cells were precultured in the medium containing 10-100 mM ethanol, the endotoxin uptake and TNF production of Kupffer cells isolated from control and chronic ethanol-fed rats were decreased in proportion to the concentration of ethanol in the culture medium. However, the addition of ethanol to the culture medium did not affect the endotoxin uptake and TNF production of splenic macrophages. These results support the hypothesis that the splenic macrophages are important for endotoxin uptake, and excessive production of TNF in rats given large amounts of alcohol.

Alcoholism↗