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Biomedical subjects

T Taniguchi

Publications and source records attributed to T Taniguchi.

At least 523 records · Page 29Linked to original sources
PubMed1993

[Treatment results of total cystectomy for patients with bladder cancer].

We assessed the treatment outcome of total cystectomy for 93 patients (71 men and 22 women) with bladder cancer treated in the Public Toyooka Hospital from 1970 to 1989. Patient age varied from 36 to 87 (mean 67). The overall actuarial survival rates at 5 and 10 years were 51% and 36%, respectively. The 5-year survival rates were 72% for grade 2 and 44% for grade 3 disease. The 5-year survival rates according to the pathological stage were 66% for pT0-1, 51% for pT2, 35% for pT3, 44% for pT4a disease. A statistical difference was noted between the 5-year survival rate of patients with pT0-2 disease and that with pT3. Patients with pT4aN0 disease showed a relatively high survival rate (67%). The 5-year survival rates were 54% for the patients with negative lymph node and 22% for those with positive lymph node. Although we could not demonstrate the efficacy of preoperative radiotherapy, the combination of radiation and chemotherapy was suggested to improve the survival after cystectomy. Patients who received simultaneous urethrectomy showed a higher 5-year survival rate as compared to those who did not.

Adult↗
PubMed1993

[Water-soluble eumelanin as a PCR-inhibitor and a simple method for its removal].

It has been confirmed that water-soluble eumelanins often extracted together with DNAs from natural black hairs act as an inhibitor of Taq DNA polymerase in the polymerase chain reaction (PCR). In the present investigation, an attempt to amplify the non-coding 333-bp region of mitochondrial DNA (mt333DNA) produced the following results: 1) Water-soluble preparations made from chemically synthesized melanin (Sigma products), as well as natural black eumelanins, inhibited the PCR amplification of mt333DNA at concentrations of more than 2 micrograms/ml. 2) Quantitative measurement of Taq DNA polymerase-catalyzed DNA synthesis in terms of the amount of [alpha-32P] dCMP incorporated into activated calf thymus DNA showed that both of the water-soluble melanins had the same inhibition activity as represented by the sigmoidal curve derived from a quadratic equation of melanin concentration. This observation suggested that Taq DNA polymerase combined with two molecules of melanin to form an inactivated complex. 3) Melanins did not appear to affect either the thermostability of Taq DNA polymerase at 94 degrees C, or the step of primer-annealing to template DNAs. On the other hand, we established a simple and useful method for removal of water-soluble eumelanins contaminating DNA preparations from hairs. The method was based on the adsorption of melanins to Bio-Gel. When a Bio-Gel P-60 minicolumn was equilibrated with 10 mM sodium acetate buffer, pH 4.2, water-soluble melanins were completely adsorpted to it whereas DNAs passed through, although the melanins showed incomplete adsorption to the gel when it was equilibrated with TE (10 mM Tris-HCl, pH 7.5, 0.1 mM EDTA).(ABSTRACT TRUNCATED AT 250 WORDS)

DNA, Mitochondrial↗
PubMed1993

Calmodulin activated adenylyl cyclase in ciliary processes: additivity of calcium and cyclic adenosine monophosphate signals on intraocular pressure response of the rabbit eye.

PURPOSE: The regulation of adenylyl cyclase by multiple signal systems was investigated by biochemical studies of the enzyme in ciliary processes and by in vivo intraocular pressure responses in the rabbit eye. METHODS: Adenylyl cyclase enzyme activity was determined by radiometric assay using alpha-32 P-ATP as substrate. Drugs were administered to the rabbit eye by intravitreal injection or topical application, and intraocular pressure was measured by pneumatonography. RESULTS: Adenylyl cyclase activity in the membrane/particulate fraction of the rabbit ciliary process was activated by calmodulin in the presence of Ca2+, Co2+, or Mn2+, and inhibited by the calmodulin antagonist calmidazolium. The activity was additive to stimulations of adenylyl cyclase by the activating G-protein (Gs) via isoproterenol or vasoactive intestinal peptide receptors, and by forskolin. The biochemical findings were supported by in vivo correlation experiments with intravitreal injection of MnCl2, and by topical treatment with the Ca(2+)-mobilizing alpha 1-adrenergic agonist phenylephrine and with agents affecting cyclic adenosine monophosphate levels (forskolin, isobutylmethylxanthine). The intraocular pressure response was augmented by combining threshold doses of phenylephrine with threshold doses of either forskolin or isobutylmethylxanthine. The maximal and most prolonged response (a decrease in intraocular pressure of 4 mm Hg for up to 8 hr) was obtained by combination treatment with all three agents at doses that produced no significant effect by themselves. CONCLUSIONS: These findings provide a biochemical mechanism for ocular hypotensive drugs having both a Ca(2+)-mobilizing activity as well as increasing cyclic adenosine monophosphate levels by receptor-coupled stimulation of adenylyl cyclase.

Adenylyl Cyclases↗
PubMed1993

Regeneration of the rat carotid artery after clipping injury. Part I. A morphological study.

We investigated the natural course of the morphological regeneration of the endothelium and smooth muscle of the rat carotid artery after clipping injury. Vascular damage was produced by clipping the right carotid arteries of Wistar rats. Endothelial regeneration was confirmed by the injection of Evans blue dye and the detection of factor VIII-related antigen. The volume of the smooth muscle cell layer and the luminal size were measured by computer-assisted morphometric analysis. Immediately after arterial injury, Evans blue dye freely permeated the smooth muscle layer, suggesting that complete endothelial denudation had occurred. Endothelial regrowth started within 24 hours and was fastest on the third and fourth days after injury. The endothelial injury was repaired within 5 days. The area of the smooth muscle layer did not change immediately after clipping injury, but it gradually increased within a month. The luminal area of the injured artery increased during the 3-month recovery period. These findings suggest that endothelial regrowth is completed within a week after clipping injury, whereas smooth muscle cell regrowth is slower. In addition, arteriosclerotic luminal narrowing did not occur during recovery of the rat carotid artery from clipping injury.

Animals↗
PubMed1993

Regeneration of the rat carotid artery after clipping injury. Part II. A pharmacological study.

This study investigated the natural course of functional recovery of the vascular endothelium and smooth muscle after clipping injury of the rat carotid artery. Vascular injury was induced by clipping the right carotid arteries of Wistar rats. The contractile response to KCl, serotonin (5-hydroxytryptamine), and norepinephrine was decreased immediately after arterial injury. The response to KCl and serotonin recovered within 8 weeks, whereas the response to norepinephrine recovered after 12 weeks. Endothelium-dependent relaxation also disappeared immediately after clipping injury, but the recovery of relaxation in response to acetylcholine and adenosine triphosphate was observed within 1 week. Four weeks after clipping injury, higher doses of acetylcholine induced slight arterial contraction. These findings suggest that the recovery of smooth muscle contractility was slower than the process of endothelial regeneration in the rat carotid artery after clipping injury. Endothelium-dependent relaxation recovered within only a week, although the characteristics of the arterial cholinergic receptors may have changed in the chronic recovery stage.

Acetylcholine↗
PubMed1993

Effects of Al3+ and Be2+ ions combined with NaF on ciliary process adenylyl cyclase activity and aqueous humor dynamics in the rabbit eye.

PURPOSE: The activity of Al3+, Ga3+, and Be2+ ions in the presence of NaF to directly activate G-proteins was investigated by their potentiative effect on forskolin (FSK)-activated adenylyl cyclase in rabbit ciliary process membranes and their effects on aqueous humor dynamics in vivo. METHODS: Adenylyl cyclase (AC) was determined by radiometric conversion of ATP to cAMP by the particulate fraction of rabbit ciliary processes. Intravitreal injections of sterile solutions of analytical grade salts were made into the center of the vitreous in a volume of 20 microliters. Intraocular pressure, aqueous humor flow, and uveoscleral outflow measurements were made by pneumatonometry, fluorophotometry, and fluorescein-dextran method, respectively. Outflow facility was determined by tonography in the intact eyes and by two-level constant pressure perfusion in cannulated eyes. RESULTS: Both Al3+ (EC50, 40 mumol/l) and Be2+ (EC50, 11 mumol/l) in the presence of 0.5-2 mM NaF activated the stimulatory G-protein Gs. Ga3+ was ineffective and did not antagonize the activation by Al3+. Intravitreal injections of Al3+ (1 mumol/eye) or Be2+ (0.5 or 1 mumol/eye) had no significant intraocular pressure (IOP) effect, nor did 1.5 or 3 mumol/eye of NaF, but when either cation was injected together with NaF, IOP decreased by up to 40% for up to 140 hr. At the time of maximum IOP effect (72 hr) aqueous humor flow determined by fluorophotometry was decreased in BeCl2+ NaF-treated eyes by 40% relative to BeCl2-treated eyes; however, tonographic facility of outflow was unaffected. Uveoscleral flow was also decreased by 38% in BeCl2+ NaF treated eyes. CONCLUSIONS: These findings support the hypothesis that Gs activation of ciliary process adenylyl cyclase decreases aqueous humor formation rate in rabbit eyes, and that activation of G-proteins mediates contraction of ciliary muscles causing a decrease of aqueous humor outflow via the uveoscleral route. The results suggest that G-proteins putatively involved in trabecular facility changes are less sensitive to activation by BeF3- than are other parameters of aqueous humor dynamics.

Adenylyl Cyclases↗
PubMed1993

Detection of interleukin-8 (IL-8) in seminal plasma and elevated IL-8 in seminal plasma of infertile patients with leukospermia.

OBJECTIVE: To determine if interleukin-8 (IL-8) is a normal constituent of seminal plasma and if leukospermia is a factor determining its elevation. DESIGN: Seminal plasma from 58 men obtained by masturbation was examined for the presence of IL-8 using an IL-8 specific sandwich ELISA. Semen samples were obtained from 34 infertile men without leukospermia, 10 infertile men with leukospermia, and 14 proven fertile men. The correlation of amount of IL-8 in seminal plasma with some spermiogram parameters and the amount of polymorphonuclear (PMN) elastase was statistically evaluated. RESULTS: Immunoreactive IL-8 was observed in the seminal plasma of all 58 subjects. The IL-8 titer in seminal plasma of patients with leukospermia (6.16 +/- 0.82 micrograms/L) was significantly higher than that in seminal plasma of patients without leukospermia (2.35 +/- 0.34 micrograms/L) and fertile men (1.64 +/- 0.29 micrograms/L). There was a high degree of correlation between PMN elastase and IL-8 levels in seminal plasma. CONCLUSIONS: These findings demonstrate IL-8 to be in seminal plasma and elevated IL-8 levels in infertile patients with leukospermia.

Humans↗
PubMed1993

[Clinical significance of multiple mucosal biopsies in new cases of superficial papillary bladder tumor].

We assessed the clinical significance of multiple mucosal biopsies in new cases of superficial papillary bladder tumor. Biopsy findings were abnormal (5 dysplasia, 5 transitional carcinoma) in 10 of the 71 cases examined. Abnormalities were observed exclusively at G2 or G3, and more frequently at pT1 than pTa. Cases with multiple tumors showed significantly more abnormalities than cases with a solitary tumor. Recurrence rates were not significantly different between the cases with abnormal biopsy findings and those with normal findings. However, the invasive tumor developed more frequently in the former. Mucosal biopsies seemed to be more useful in cases with multiple tumors than in those with a solitary tumor.

Adult↗
PubMed1992

Expression and regulation of the leukemia inhibitory factor/D factor gene in human T-cell leukemia virus type 1 infected T-cell lines.

The expression of the leukemia inhibitory factor/D factor (LIF) gene in human T-cell leukemia virus type 1 infected T-cell lines was examined. Human T-cell leukemia virus type 1 infected T-cell lines MT-1, MT-2, H89-59, H89-79, and H109 expressed LIF mRNA, but the T-cell lines MOLT-4 and TALL-1 did not. LIF mRNA expression was enhanced by interleukin 2 or 12-O-tetradecanoylphorbol-13-acetate in MT-2 cells. The biological activity of LIF was detected in culture medium enhanced by interleukin 2 in MT-2 cells. The expression of LIF mRNA was suppressed by 1 alpha,25-dihydroxyvitamin D3 and dexamethasone. These results imply that the expression of the LIF gene is involved in the development of hypercalcemia and abnormalities of the immune system observed in patients with adult T-cell leukemia.

Calcitriol↗
PubMed1992

Interleukin 2-induced activation of Ras requires two domains of interleukin 2 receptor beta subunit, the essential region for growth stimulation and Lck-binding domain.

Interleukin 2 (IL-2) can stimulate the proliferation of various kinds of T-cell lines. The receptor for IL-2 is composed of at least two subunits (alpha and beta), of which beta subunit plays the major role in transducing growth signals into the cells. A nonreceptor-type tyrosine kinase, Lck, is associated with IL-2 receptor beta subunit, and the binding of IL-2 to its receptor induces the activation of Lck. On the other hand, it has been shown that stimulation of T-cells with IL-2 causes rapid activation of Ras protein. In this paper, we describe that both of the two regions in IL-2 receptor beta subunit, the indispensable region for the induction of cell growth (serine-rich region) and the binding region of Lck protein (acidic region), are required for the activation of Ras. These two regions are also required for tyrosine phosphorylation of an 85-kDa cellular protein (p85) and the accumulation of fos and jun mRNAs. This observation suggests also that the activation of a receptor-associated tyrosine kinase in response to IL-2-stimulation is primarily responsible for subsequent activation of the pathway through Ras to Fos and Jun.

Animals↗
PubMed1992

Effects of the subcutaneous administration of enkephalins on tail-flick response and righting reflex of developing rats.

The s.c. administration of [Met5]-enkephalin to 10-day-old rats pretreated with the mixture of 3 peptidase inhibitors, amastatin, captopril and phosphoramidon, produced the inhibition of tail-flick response and loss of righting reflex. When infant rats were pretreated with the mixture of any combination of two peptidase inhibitors, however, the change in both the response and the reflex were not produced at all by enkephalin injection, indicating that 3 kinds of enzymes, amastatin-sensitive aminopeptidase(s), captopril-sensitive peptidyl dipeptidase A and phosphoramidon-sensitive endopeptidase 24.11, played an important role in the inactivation of enkephalin after its systemic administration. Additionally, the fact that the two enkephalin-induced effects were more effectively antagonized by naloxone, a relatively selective mu-opioid antagonist, than by naltrindole, a specific delta-antagonist, or by nor-binaltorphimine, a specific kappa-antagonist, showed that these two effects were produced by the interaction of enkephalin with mu receptors. Moreover the involvement of mu receptors in the production of these two effects was shown by the fact that the s.c. administration of [D-Ala2,N-Me-Phe4,Gly5-ol]-enkephalin, a selective mu agonist, also produced these two effects which were more effectively antagonized by naloxone than by naltrindole or nor-binaltorphimine. Since the magnitude of the two effects induced by enkephalins in 15-day-old rats was significantly lower than that in 10-day-old rats, and the two enkephalin-induced effects were not produced at all in 20-day-old rats, a maturation-induced decrease in the permeability of the blood-brain barrier against opioid peptides was indicated.

Aging↗
PubMed1992

Cloning and characterization of gastrin receptor from ECL carcinoid tumor of Mastomys natalensis.

We report here the cDNA cloning of a putative gastrin receptor from enterochromaffin-like (ECL) carcinoid tumor of Mastomys natalensis. For this study, we used the polymerase chain reaction technique to amplify transmembrane domain sequences related to rat pancreatic cholecystokinin (CCK)-A receptor from the ECL tumor cDNA library. The amino acid sequence deduced from the cloned cDNA showed 85.7% and 49.0% identity to canine parietal cell gastrin receptor and rat pancreatic CCK-A receptor, respectively. Ligand binding studies using COS-7 cells transfected with the cDNA showed the same binding specificity for gastrin and CCK-8 as the gastrin receptor on the Mastomys carcinoid tumor membrane. Both gastrin and CCK-8 elevated free cytosolic calcium concentration in COS-7 cells expressing the cloned receptor. RNA blot analysis revealed the expression of the gastrin receptor in both Mastomys stomach and brain.

Amino Acid Sequence↗
PubMed1992

Thrombin-induced human platelet aggregation is inhibited by protein-tyrosine kinase inhibitors, ST638 and genistein.

We have investigated the involvement of protein-tyrosine kinases in thrombin-induced aggregation of human platelets, using ST638 and genistein which are known inhibitors of protein-tyrosine kinase. Preincubation of platelets with 50 microM of ST638 or 25 micrograms/ml of genistein completely blocked the platelet aggregation induced with 0.05 unit/ml of thrombin. The increase of protein-tyrosine phosphorylation bands (135-, 124-, 76-, 64-, and 60-kDa) induced with thrombin was also inhibited by these inhibitors in a dose-dependent manner. These inhibitors also blocked the platelet aggregation and protein-tyrosine phosphorylation induced with thrombin in aspirin-treated platelets. Increase of the intracellular Ca2+ concentration induced by thrombin was also inhibited by higher concentrations of genistein. These results suggest that the protein-tyrosine phosphorylation plays a certain role in platelet activation having some relation to the intracellular Ca2+ concentration.

Amino Acid Sequence↗
PubMed1992

IL-2 and EGF receptors stimulate the hematopoietic cell cycle via different signaling pathways: demonstration of a novel role for c-myc.

Stimulation via cytokine receptors such as IL-2 and IL-3 receptors, but not by the EGF receptor (EGFR), induces cells of the BAF-B03 hematopoietic cell line to transit the cell cycle. We demonstrate that the IL-2 receptor beta chain (IL-2R beta) is linked to at least two intracellular signaling pathways. One pathway may involve a protein tyrosine kinase of the src family, which leads to the induction of the c-jun and c-fos genes, among others. A second pathway, involving an as yet unknown mechanism, leads to c-myc gene induction. Stimulation of the EGFR, expressed following transfection of an appropriate recombinant construct, can activate the former, but not the latter, pathway in this cell line and cause the cells to enter S phase but not progress further. This deficiency can be rescued by ectopic expression of the c-myc gene, indicating a novel role for this proto-oncogene in the S to G2/M transition of the cell cycle.

Animals↗
PubMed1992

Protein-tyrosine kinase p72syk is activated by wheat germ agglutinin in platelets.

We previously reported a molecular cloning of porcine gene syk encoding a non-receptor type 72-kDa protein-tyrosine kinase (Taniguchi et al. (1991) J. Biol. Chem. 266, 15790-15796). In this study, we have demonstrated that p72syk is expressed in porcine platelets at 0.1-0.2% of total protein and that the lectin wheat germ agglutinin induces an activation of p72syk against both auto- and exogenous-substrate-phosphorylation in porcine platelets. The activation of p72syk was abrogated by the coexistence of N-acetyl-D-glucosamine with wheat germ agglutinin. These data suggest that p72syk is a candidate of responsible protein-tyrosine kinase for platelet activation and that cell surface glycoprotein is involved in the activation of p72syk in platelets.

Acetylglucosamine↗
PubMed1992

New human gene encoding a positive modulator of HIV Tat-mediated transactivation.

The human immunodeficiency virus-1 (HIV-1) protein Tat is a potent activator of virus gene expression. Tat functions through a sequence known as TAR, located immediately downstream of the transcription start site in the long terminal repeat. Several observations suggest that cellular factors cooperate with Tat in the overall transactivating process. We have isolated a human complementary DNA from the new gene MSS1, which may encode such a cellular factor, by transcomplementation of a yeast sgv1- mutant. The MSS1 protein shares 42% sequence identity with the human TBP-1 protein, which binds Tat in vitro and suppresses Tat-mediated transactivation in vivo (ref. 6). We report here that the levels of HIV activation by Tat correlate with endogenous levels of MSS1 messenger RNA. Furthermore, we provide evidence that expression of MSS1 enhances the Tat-mediated transactivation. Our results suggest that MSS1 has a key role in activation of HIV genes regulated by Tat.

ATPases Associated with Diverse Cellular Activitie↗
PubMed1992

Protein-tyrosine phosphorylations induced by concanavalin A and N-formyl-methionyl-leucyl-phenylalanine in human neutrophils.

The ability of the lectin concanavalin A (ConA) and N-formyl-methionyl-leucyl-phenylalanine (fMLF) to induce protein-tyrosine phosphorylation in human neutrophils was examined by immunoblot analysis. ConA caused an increase in tyrosine phosphorylation of protein bands with apparent molecular masses of 120, 80, 76, 66 and 40 kDa; on the other hand, fMLF caused an increase in those of only 80-kDa and 40-kDa proteins. These protein-tyrosine phosphorylations were time- and dose-dependent. The tyrosine phosphorylation of 40-kDa protein induced by fMLF was suppressed but that by ConA was not suppressed by pertussis toxin pretreatment. At the same time, pertussis toxin pretreatment also inhibited lysozyme release and aggregation of neutrophils induced by fMLF but did not inhibit those responses induced by ConA. These results suggest that the tyrosine phosphorylation of 40-kDa protein may be involved in a part of neutrophil activation and be regulated via pleiotropic signal transduction pathways. In addition, immunoblot analysis employing antibodies against microtubule-associated protein 2 (MAP2) kinase suggested that this tyrosine-phosphorylated 40-kDa protein might be the MAP2 kinase.

Blood Proteins↗