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Biomedical subjects

K Takase

Publications and source records attributed to K Takase.

At least 145 records · Page 8Linked to original sources
PubMed1996

Osteodystrophy in patients with chronic hepatitis and liver cirrhosis.

Bone mineral density (BMD) of the lumber vertebrae and factors related to bone metabolism were determined in patients with chronic viral hepatitis and patients with liver cirrhosis to clarify correlations between hepatic dysfunction, considered to be one of the causes of hepatic osteodystrophy, and decrease in bone mass. BMD of the second to fourth lumbar vertebrae was determined with a Lunar (Madison, WI, USA) DPX, a dual-energy X-ray absorptiometry diagnostic system. BMD was significantly lowest in patients with liver cirrhosis, followed by patients with chronic hepatitis, and healthy subjects, in this order. There was a significantly positive but weak correlation between albumin and BMD. Levels of 25(OH)D and 1,25(OH)2D were significantly lower in patients with liver cirrhosis than in those with chronic hepatitis. BMD and vitamin D were decreased in all patients whose cholinesterase (ChE) was below 0.3 delta pH. Urinary pyridinoline (Upyr) was significantly higher in the patients with liver cirrhosis, in whom bone mass was decreased, than in the patients with chronic hepatitis, whereas serum osteocalcin levels were distributed in the upper normal range in patients with chronic hepatitis and those with liver cirrhosis. There was a positive correlation between 25(OH)D and serum osteocalcin levels in patients with liver cirrhosis. These results indicate that osteogenesis is decreased and suggest that the decrease in BMD which occurs in viral liver cirrhosis, probably related to decreased, bone formation and slight promotion of bone resorption, reflects deranged hepatic function. This is the first report of Upyr and urinary deoxypyridinoline (UDpyr) determination in patients with liver cirrhosis and patients with chronic hepatitis. The negative correlation of Upyr and UDpyr with ChE is a novel finding.

Adult↗
PubMed1996

Pneumatosis intestinalis and necrotizing enterocolitis associated with liver cirrhosis.

We report a 58-year-old woman with pneumatosis intestinalis and necrotizing enterocolitis associated with liver cirrhosis. She was receiving treatment for liver cirrhosis and hepatic failure when sudden severe right upper abdominal pain and fever developed. Abdominal radiograph disclosed pneumatosis intestinalis, involving the ascending colon, and small collections of free air along the right hemidiaphragm. The pneumatosis intestinalis appeared in both cystic and linear form. Autopsy revealed necrosis and multiple gas-filled mural cysts in the ascending colon. To our knowledge, this is the first case to be reported of pneumatosis intestinalis and necrotizing enterocolitis associated with liver cirrhosis.

Colon↗
PubMed1996

Bacterial superantigens induce V beta-specific T cell receptor internalization.

Staphylococcal enterotoxins can cause toxic shock syndrome and autoimmune diseases. Circulating T cells from these diseases have a very wide range of expression in particular T cell receptor (TCR) beta chain variable regions (V beta). One possibility for this wide range of TCR V beta expression is that during acute infection with organisms secreting superantigens (SAg) these potent molecules might modulate TCR expression. To test this hypothesis, we investigated the potential effects of SAg on TCR V beta cell surface expression. Peripheral blood mononuclear cells (PBMC) from healthy donors were incubated with staphylococcal SAg. Toxic shock syndrome toxin-1 (TSST-1) induced downregulation of V beta 2 expression, whereas staphylococcal enterotoxin (SE) B induced V beta 3-and V beta 12-specific downregulation. TSST-1 did not interfere with anti-V beta 2 mAb binding. Therefore, this downregulation was not due to steric hindrance of Ab binding by TSST-1. TSST-1 induced V beta 2 downregulation was time-, dose- and temperature-dependent. CD3 expression decreased in parallel with reduction of V beta expression. CD4 and CD8 expression were only slightly decreased. CD2, CD25 and HLA-DR expression were upregulated following TSST-1 stimulation of T cell lines. To investigate the fate of TCR after toxin stimulation, V beta 8+ Jurkat T cells were incubated with SEE which is known to stimulate V beta 8+ T cells, and analysed with fluoresence microscopy, and immunoprecipitation and Western blotting. After SEE stimulation, there was an increase in V beta 8 molecules found in the cytoplasm which correlated with loss of cell surface V beta 8 molecules, suggesting internalization of cell surface V beta 8 molecules was induced by SEE stimulation. Shedding of V beta 8 molecules into the culture supernatant was not detected. These data demonstrate that SAg mediated downregulation of TCR expression occurs primarily as the result of TCR internalization. This downregulation phenomenon may have physiological and pathological consequences in patients infected with Staphylococcus aureus.

Antibodies, Monoclonal↗
PubMed1996

Ventricular arrhythmogenic dose of adrenaline during sevoflurane, isoflurane, and halothane anaesthesia either with or without ketamine or thiopentone in cats.

The doses of adrenaline required to induce ventricular arrhythmia during sevoflurane, isoflurane and halothane anaesthesia, either with or without infusions of ketamine (76 micrograms kg-1 min-1) or thiopentone (0.5 mg kg-1 min-1), were determined in cats. Groups of six to eight cats were maintained at end-tidal concentrations equivalent to 1.25 times the minimal alveolar concentration of each anaesthetic. The mean dose of adrenaline required to induce arrhythmia during sevoflurane anaesthesia (19.0 micrograms kg-1) was approximately 11 times higher than that required during halothane anaesthesia (1.66 micrograms kg-1) and the same as that required during isoflurane anaesthesia (19.0 micrograms kg-1). Ketamine tended to decrease the requirement of adrenaline during halothane anaesthesia, but not significantly, and did not change the requirement during isoflurane or sevoflurane anaesthesia. Thiopentone did not change the requirement for adrenaline during halothane, isoflurane or sevoflurane anaesthesia. It was concluded that either with or without ketamine or thiopentone, the effect of sevoflurane on the sensitisation of the feline myocardium to the arrhythmogenic effects of adrenaline was significantly less than that of halothane and not different from that of isoflurane.

Anesthesia, General↗
PubMed1996

Infection with GB virus C (GBV-C) in patients with fulminant hepatitis.

BACKGROUND/METHODS: There appear to be hepatitis viruses other than hepatitis A, B, C, D and E. One of these has been proposed with a designation of GB virus C. Sera from 44 patients with fulminant hepatitis were tested for RNA of GB virus C by reverse-transcription polymerase chain reaction with nested primers deduced from the putative non-structural 3 (helicase) region. RESULTS: RNA of GB virus C was detected in three (20%) of 15 patients with hepatitis B virus infection and three (12%) of 25 patients without markers of hepatitis A-E virus infection. Overall, GB virus C RNA was detected in six (14%) of the 44 patients with fulminant hepatitis, at a frequency significantly higher (p < 0.001) than that in three (0.9%) of 326 blood donors matched for age with the patients. CONCLUSIONS: These results indicate a role of GB virus C in inducing fulminant hepatitis either by itself or in concert with the other hepatitis viruses.

Acute Disease↗
PubMed1996

Fulminant hepatic failure caused by ecarazine hydrochloride (a hydralazine derivative).

The cause of fulminant hepatic failure is reported to be unknown in more than half the cases in Japan. We recently reviewed 23 cases of fulminant hepatic failure that had been treated at our hospital. The cause of disease had been regarded as unknown before this study. It was found that seven of these patients had been under ecarazine hydrochloride therapy when they developed fulminant hepatic failure. We examined the reasons why fulminant hepatic failure in these seven patients had not been previously attributed to ecarazine, and found that it could be explained by the following factors: (1) the time from the start of ecarazine therapy to the onset of hepatic failure was long; (2) in all cases, hepatic failure developed more than 10 days after the clinical recognition of hepatitis; and (3) characteristic signs of drug-induced hepatic failure such as a skin rash and positive lymphocytes stimulation test with the drug were absent in all cases. Fulminant hepatic failure in these cases could be characterized by: (1) rapid decrease in serum alanine transaminase (ALT) level after discontinuation of ecarazine, (2) prolonged jaundice despite discontinuation of ecarazine, (3) high incidence of anti-nuclear antibody (ANA) (57%), and (4) histological findings of extensive hepatocellular necrosis ranging from bridging necrosis to massive necrosis. Of the seven patients, four died of fulminant hepatic failure. These four patients had received high doses of ecarazine hydrochloride for prolonged periods. Our data suggest that there may be many cases in which the cause of fulminant hepatic failure or acute hepatitis was not previously determined that can be attributed to long-term drug therapy for chronic diseases.

Adult↗
PubMed1996

Immunohistochemical study of CA 19-9 and SPan-1 in cases of hydronephrosis.

Although the serum level of carbohydrate antigen (CA) 19-9 is reportedly increased in patients with hydronephrosis, virtually no immunohistochemical studies of this condition have been performed. Therefore, we examined immunohistochemically 11 hydronephrotic kidneys and 3 normal control kidneys using antibodies against CA 19-9 and SPan-1, another sialylated carbohydrate antigen. Immunoreactivity for CA 19-9 was seen in the transitional and tubular epithelia in most of the hydronephrotic kidneys (9 of the 11 cases), and also detected in 2 of the 3 control specimens, although there the distribution appeared to be limited. SPan-1 immunoreactivity showed the same trend. CA 19-9 and SPan-1 immunoreactivity in hydronephrosis appeared to be more widely distributed than in controls, although its mechanism remains unclear.

Adult↗
PubMed1996

Susceptibility of chicken embryos to highly virulent infectious bursal disease virus.

The susceptibility of chicken embryos to highly virulent infectious bursal disease virus (hvIBDV), strains F539 and DV86, was examined with respect to three inoculation routes and compared with the classical type of IBDV, strain G691. Death patterns of embryos infected with strains F539 and DV86 of hvIBDV were observed constantly and most of the infected embryos died; however, the death pattern associated with the strain G691 of classical IBDV was erratic and not related to the virus titer inoculated. The chorioallantoic membrane (CAM) route was the most sensitive route of infection, while the allantoic sac (AS) route was the least, regardless of the strain. The difference in titer of hvIBDV between the CAM and yolk sac (YS) route was less than that of classical IBDV. Constant lethality to embryos seems to be distinctive characteristic of hvIBDV.

Allantois↗
PubMed1996

[Treatment of scrotal hydrocele using fibrin adhesive].

For the purpose of adhesion of the tunica vaginalis in scrotal hydrocele, we used fibrin adhesive, Bolheal. Between September 1993 and December 1994, 13 patients with scrotal hydrocele received occlusion therapies using Bolhead. The therapy was effective in 1 of the 6 patients (17%) administered 2.4 mg of fibrinogen and 750 units of thrombin into the vaginal cavity after aspiration of fluids, and in 5 of the 7 patients (71%) administered 240 mg of fibrinogen and 7.5 units of thrombin. Therefore, fibrin adhesive may be useful in the treatment of scrotal hydrocele.

Aged↗
PubMed1996

[Consideration of therapeutic choice for grade 3 superficial bladder cancer].

Between January, 1977 and December, 1994, 90 patients with grade 3 (G3) superficial bladder cancer were treated at Yokohama City University Hospital, Yokohama Municipal Hospital and Kanagawa Cancer Center. These patients were clinically observed. The prognostic factors of the patients with G3 superficial bladder tumors were age and growth pattern of tumors. Patients older than 67 showed significantly poor survival compared with younger patients (p < 0.01). Patients with non-papillary sessile tumors showed significantly poor survival compared with the other groups (p < 0.05). The five-year survival rate of the patients with G3 superficial tumors who were treated by total cystectomy was 75%, whereas all the patients who were treated by bladder preservation therapy died within 4 years, the difference being significant (p < 0.05). Eleven patients with G3 superficial bladder tumors died of cancer, and most of these patients had multiple and non-papillary sessile tumors. These findings suggest that the patients with G3 superficial tumors, which are non-papillary sessile tumors, should be treated by radical cystectomy.

Adult↗
PubMed1995

Rapamycin inhibits ribosomal protein synthesis and induces G1 prolongation in mitogen-activated T lymphocytes.

We investigated the effects of rapamycin (RAP) on cell cycle progression and protein synthesis in mitogen-activated primary T lymphocytes. Stimulation of resting human T lymphocytes with phorbol ester and calcium ionophore rendered cells capable of initiating DNA synthesis within 30 h; roughly 60% of the cells entered the first G2/M phase of the cell cycle within 96 h. Addition of RAP delayed the entry into S phase by 9 h, although a similar percentage (approximately 50%) of cells entered the first G2/M phase and proliferated. On this basis, we concluded that RAP primarily induced a G1 prolongation without blocking cell cycle progression. Addition of the co-mitogens to resting T lymphocytes up-regulated the translation of ribosomal protein mRNA concurrent with activation of p70s6k. RAP inhibited this translational up-regulation of ribosomal protein mRNA as well as the activation of p70s6k without affecting translation of nonribosomal protein mRNA. RAP also prevented the synthesis and accumulation of ribosomal proteins. Further, this failure to increase ribosomal proteins, which probably reflects the failure to increase numbers of ribosomes, resulted in suppression of the synthesis of total cellular protein and a delay in the escalation of cell size. RAP-treated cells eventually initiated DNA synthesis when cell size became equivalent to that of the control cells entering S phase of the cell cycle. Thus, inhibition of protein synthesis caused by the primary inhibition of ribosomal protein mRNA translation probably explains the effect of RAP on cell cycle progression of mitogen-activated resting T lymphocytes.

Amino Acid Sequence↗
PubMed1995

Effects of iron-depletion on cell cycle progression in normal human T lymphocytes: selective inhibition of the appearance of the cyclin A-associated component of the p33cdk2 kinase.

Iron removal by the chelating-agent deferoxamine (DFO) arrests cell cycle progression of activated human T cells in late G1 phase, before the G1/S border. The effects of the drug on molecules that regulate progression through the cell cycle were defined. DFO (10 mumol/L) inhibited induction of transcription of the cdc2 gene, but had no effect on accumulation of cdk2, cdk4, or interleukin (IL)-2-transcripts. No detectable p34cdc2 protein accumulated, but synthesis of the p33cdk2 protein was begun. It accumulated to normal levels during the first 20 to 30 hours of incubation in the presence of DFO. Furthermore, p33cdk2 was activated as an H1 histone kinase. As active p33cdk2 primarily represents complexes of the p33 protein with cyclin E or cyclin A, the effects of DFO on these cyclins were examined. Although the induction of synthesis and early accumulation of cyclin E and cyclin E-associated kinase activity appeared normal, the appearance of cyclin A and cyclin A-associated kinase activity were inhibited by DFO. However, the production of cyclin A mRNA appeared to be normal in the presence of DFO. A major effect of DFO in blocking cell cycle progression may be mediated through inhibition of the appearance of cyclin A protein and, therefore, a major component of p33cdk2 activity. The results also indicate that the p33cdk2/cyclin E activity produced in the presence of DFO was not sufficient for completion of the G1 phase of the cell cycle.

CDC2 Protein Kinase↗
PubMed1995

Induction of G1 arrest by down-regulation of cyclin D3 in T cell hybridomas.

The relationship between activation-induced growth inhibition and regulation of the cell cycle progression was investigated in T cell hybridomas by studying the function of the cell cycle-regulating genes such as G1 cyclins and their associated kinases. Activation of T cell hybridomas by anti-T cell receptor antibody induces growth arrest at G1 phase of the cell cycle and subsequently results in activation-driven cell death. Rapid reduction of both messenger RNA and protein level of the cyclin D3 is accompanied by growth arrest upon activation. Although the residual cyclin D3 protein forms a complex with cdk4 protein, cyclin D3-dependent kinase activity is severely impaired. Stable transfectants engineered to express cyclin D3 override the growth arrest upon activation. These results imply that the activation signal through T cell receptor induces the down-regulation of cyclin D3 expression and cyclin D3-dependent kinase activity, leading to growth arrest in G1 phase of the cell cycle in T cells.

Animals↗
PubMed1995

Epstein-Barr virus replicative gene transcription during de novo infection of human thymocytes: simultaneous early expression of BZLF-1 and its repressor RAZ.

Epstein-Barr virus (EBV) is known to infect B cells and epithelial cells. We and others have shown that EBV can also infect a subset of thymocytes. Infection of thymocytes was accompanied by the appearance of linear EBV genome within 8 hr of infection. Circularization of the EBV genome was not detected. This is in contrast to the infection in B cells where the genome can circularize within 24 hr of infection. The appearance of the BamHI ZLF-1 gene product, ZEBRA, by RT-PCR, was observed within 8 hr of infection. The appearance of a novel fusion transcript (RAZ), which comprised regions of the BZLF-1 locus and the adjacent BRLF-1 locus, was detected by RT-PCR. ZEBRA protein was also identified in infected thymocytes by immunoprecipitation. In addition, we demonstrated that the EBNA-1 gene in infected thymocytes was transcribed from the Fp promoter, rather than from the Cp/Wp promoter which is used in latently infected B cells. Transcripts encoding gp350/220, the major coat protein of EBV, were identified, but we did not find any evidence of transcription from the LMP-2A or EBER-1 loci in infected thymocytes. These observations suggest that de novo EBV infection of thymocytes differs from infection of B cells. The main difference is that with thymocytes, no evidence could be found that the virus ever circularizes. Rather, EBV remains in a linear configuration from which replicative genes are transcribed.

Antigens, Viral↗
PubMed1995

Control of cell cycle entry and progression in mitogen-stimulated human B lymphocytes.

Tonsillar B lymphocytes were stimulated to proliferate by the mitogenic combination of phorbol dibutyrate and ionomycin. Progression through the cell cycle was monitored by measurements of cellular DNA and RNA content using flow cytometry. Changes in surface expression of class II MHC antigens and CD20 antigen were also monitored as early parameters of B lymphocyte activation and cell cycle progression. The results showed that about 60% of the population synchronously entered and progressed through the cell cycle. The transition from the resting state, signaled by increased RNA content, occurred about 12 to 24 hr after stimulation; S phase entry occurred at about 36 hr. Small, variable populations of cells appeared to be unresponsive to the stimuli, either because they were "preactivated" before in vitro stimulation or were already dying. The kinetics of appearance and accumulation of several cell cycle regulated/regulatory proteins were followed by immunoblotting. The proliferating cell nuclear antigen (PCNA) cyclin A and p33cdk2 proteins were either absent or present in very low amounts in resting cells and first became detectable in increased amount beginning at about 24 hr after stimulation; increased p34cdc2 protein was not detected until about 36 hr. Increased cellular content and phosphorylation of the p110Rb protein was already obvious by 24 hr after stimulation. The effects of several immunosuppressive agents were examined using purified B cells. Both cyclosporin A and an FK506 analogue were shown to inhibit proliferation of B lymphocytes, at the low doses also inhibitory to T cells.

Antigens, CD↗
PubMed1995

Hepatocyte regeneration in chronic hepatitis C and interferon treatment: analysis of immunohistological identification of proliferating cell nuclear antigen (PCNA).

To evaluate the usefulness of proliferating cell nuclear antigen (PCNA) immunostaining in the assessment of the efficacy of interferon (IFN) therapy in chronic hepatitis C, we investigated the proliferative activity of hepatocytes in 67 patients with chronic hepatitis C, using this immunostaining method. The percentage of PCNA-positive hepatocytes was 2.4% in patients with chronic persistent hepatitis, 2.5% in those with chronic aggressive hepatitis 2A, and 3.9% in those with chronic aggressive hepatitis 2B. The PCNA count increased with the progression of the liver disease. Patients were classified as complete, partial, and non-responders to IFN; the percentage of PCNA-positive hepatocytes before IFN therapy was 1.6% in the complete responders, 3.9% in the partial responders, and 4.9% in the non-responders. There was a significant negative correlation between the percentage of PCNA-positive hepatocytes and the response to IFN treatment. Thirty-two of 53 cases (60.4%) in which the PCNA labeling index (LI) was less than 5.0 were complete responders compared with 13 of 14 cases (92.9%) in which the PCNA LI was higher than 5.0, representing partial responders or non-responders (P < 0.001). Most complete responders had a low PCNA LI, irrespective of HCV genotype. Our findings indicate that PCNA immunostaining is a simple and reliable index of cell proliferation in liver regeneration, and may be a useful predictor of the response to IFN treatment in chronic hepatitis C.

Adult↗