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Biomedical subjects

T Takano

Publications and source records attributed to T Takano.

At least 361 records · Page 20Linked to original sources
PubMed1994

Uncooked cornstarch treatment for hepatic phosphorylase kinase deficiency.

UNLABELLED: A 5-year-old boy with short stature, hepatomegaly and motor weakness due to hepatic phosphorylase kinase deficiency is described. Laboratory data showed mild hypoglycaemia and metabolic acidosis, hepatic dysfunction, and a low insulin-like growth factor-I level. Mild hypoglycaemia, marked ketosis and insufficient growth hormone secretion were revealed at night. Serum total and free carnitine levels were low and the acyl/total carnitine ratio was high. Urinary acylcarnitine profile using fast atom bombardment and tandem mass spectrometry showed increased excretion of acetylcarnitine and dicarboxylylcarnitines. These endocrinological and metabolic abnormalities and clinical symptoms were improved with uncooked cornstarch treatment. CONCLUSION: Uncooked cornstarch treatment may be helpful in hepatic phosphorylase deficiency.

Child↗
PubMed1994

Spermatocyte-specific transcription by calmodulin gene II promoter in transgenic mice.

Transgenic mice carrying a fused gene of the 294-base upstream and 68-base leader sequences of a rat calmodulin gene, CaMII, and beta-galactosidase gene were made. Only spermatocytes expressed the transgene mRNA in the testes of four independent transgenic lines. The localization of transgene mRNA was consistent with that of the mouse endogenous CaMII analyzed by in situ hybridization with the probe of 3'-noncoding region of mouse CaMII. Thus, this short promoter of CaMII evidently conferred the expression of transgene only on spermatocytes but not on spermatogonia nor on spermatids of the testis. The rat CaMII promoter up to -294 contained no sequences that corresponded to any of the reported sequence features of genes expressed in the testis. Therefore, this short promoter region of CaMII seemed to carry a certain novel machinery for the spermatocyte-specific gene expression.

Animals↗
PubMed1994

Staurosporine can inhibit the G1-S transition induced by a calcium channel agonist by blocking the pathway independent of phorbol ester-sensitive protein kinase C in rat thyroid cells (FRTL-5).

IGF-I, when added to TSH-primed FRTL-5 cells, can induce a long lasting Ca2+ influx followed by the DNA synthesis. BAY K8644, a Ca2+ channel agonist, can also induce the DNA synthesis in TSH-treated cells. Staurosporine, which is known to be a potent inhibitor of protein kinase C(PKC) strongly inhibited the DNA synthesis caused by these two reagents. However, in PKC-down regulated cells, IGF-I and BAY K8644 could also evoke the DNA synthesis and the inhibitory effect of staurosporine persisted. These inhibitory effects did not relay on inhibition of the Ca2+ influx induced by BAY K8644. Thus these results demonstrate that staurosporine acts at a point distal to Ca2+ influx to inhibit G1-S transition and this staurosporine-sensitive pathway possibly mediates the mitogenic signal in PKC-independent manner.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1994

Activation of phospholipase D in Chinese hamster ovary cells expressing platelet-activating factor receptor.

Platelet-activating factor (PAF) activated phospholipase D (PLD) in WT-H cells, CHO cells stably expressing cloned guinea-pig PAF receptor. The PLD activation was found to be dependent on extracellular Ca2+, protein kinase C (PKC), and a currently unidentified protein tyrosine kinase (PTK). PTK inhibitors ST-638 and genistein inhibited PLD activation induced by PAF as well as phorbol myristate acetate, indicating that PTK acts downstream of PKC. Furthermore, activation of MAP (mitogen-activated protein) kinases, as assessed by their phosphorylation, was also dependent on Ca2+, PKC, and PTK. The correlation between PLD activity and MAP kinase activation, together with the previously observed MAP kinase activation associated with arachidonic acid release by cPLA2 [Honda et al. (1994) J. Biol. Chem. 269, 2307-2315], led us to examine the involvement of MAP kinase in PLD activation. The results indicate that PLD and MAP kinases are activated through the common pathway consisting of Ca2+, PKC, and the unidentified PTK, which act in parallel, but not in a linear sequence.

Animals↗
PubMed1994

Immortalization-susceptible elements and their binding factors mediate rejuvenation of regulation of the type I collagenase gene in simian virus 40 large T antigen-transformed immortal human fibroblasts.

Dramatic changes occur in expression of the type I collagenase gene during the process of immortalization in simian virus 40 large T antigen-transformed human fibroblasts (S. Imai and T. Takano, Biochem. Biophys. Res. Commun. 189:148-153, 1992). From transient transfection assays, it was determined that these changes involved the functions of two immortalization-susceptible cis-acting elements, ISE1 and ISE2, located in a 100-bp region about 1.7 kb upstream. The profiles of binding of an activator, Proserpine, to the enhancer ISE1 were similar in the extracts of young, senescent preimmortalized and immortalized cells. ISE2 contained both negative and positive regulatory elements located adjacent to each other. The positive regulatory element consisted of a tandem array of putative Ets family- and AP-1-binding sites. An activator, Pluto, interacted with this positive regulatory element and had an AP-1-related component as a complex. The binding activity of Pluto was predominantly detected only in the extract from senescent preimmortalized cells. In contrast, a repressor, Orpheus, which bound to the ATG-rich negative regulatory element of ISE2, was prominently detected in extracts from both young preimmortalized and immortalized cells and appeared to suppress transcription in an orientation-dependent manner. Thus, the interplay of Pluto and Orpheus was suggested to be crucial for regulation of the collagenase gene accompanying in vitro aging and immortalization. Proserpine seemed to interact with Pluto to mediate strong expression of the collagenase gene in cellular senescence. On the basis of these results, we propose a model for regulation of the collagenase gene during in vitro aging and immortalization.

Antigens, Viral, Tumor↗
PubMed1994

[The prevalence and significance of abnormal thyroid hormone metabolism in acute myocardial infarction].

In order to clarify the relationship between thyroid function and left ventricular function in acute myocardial infarction (AMI), 52 patients (63.3 +/- 11.0 years old) admitted to the coronary care unit within 24 hours after the onset were studied. Both FT3 and FT4 levels measured at 48-72 h after the onset (1.66 +/- 0.59 pg/ml, 1.02 +/- 0.37 ng/dl) were significantly lower than those on admission (2.99 +/- 0.76 pg/ml; p < 0.01, 1.14 +/- 0.25 ng/dl; p < 0.05) and controls (3.27 +/- 0.66 pg/ml; p < 0.01, 1.22 +/- 0.23 ng/dl; p < 0.05). The decline of these thyroid hormone levels correlated well with the severity of AMI (Killip's classification), hemodynamic deterioration and liver function (low levels of albumin and cholinesterase). Low thyroid hormone levels were also associated with the elevation of catecholamine and alpha-hANP levels on admission. Low cortisol and impaired renal function were recognized as factors which might prolong the condition of low thyroid hormones. Non-survivors showed significantly lower levels of FT3 and FT4 48 hours after onset, and a lower level of FT4 in aged patients was consistent with a poor prognosis. In conclusion, the measurement of thyroid hormones in AMI is important in evaluating the severity of the condition and waking a prognosis.

Aged↗
PubMed1994

Pamidronate treatment in patients with tumor-associated hypercalcemia: pharmacological effects and pharmacokinetics.

The purpose of this study was to investigate the effects of pamidronate, a second generation bisphosphonate, on the change in calcium homeostasis in patients with tumor-associated hypercalcemia. Eight patients with tumor-associated hypercalcemia received intravenous infusion of pamidronate (45 mg) and their high mean serum calcium concentration significantly decreased from 3.56 mmol/L to 2.62 mmol/L7 days after treatment. Serum intact PTH before treatment had been suppressed to below normal in all patients but returned to normal range in six patients within 7 days after treatment. Urinary PTH related peptide (PTHrP) excretion before treatment had been elevated in seven patients and then significantly increased further after pamidronate therapy. The serum bone Gla protein concentration was not apparently changed by the treatment. Pamidronate in serum was rapidly eliminated after the treatment and urinary excretion reached a plateau on the second day (13.8% of the administered dose), suggesting that the major portion of the infused dose had been distributed to the bone and other tissues. These findings suggest that pamidronate has a potent hypocalcemic effect and that PTHrP production in malignant tumors could be affected by pamidronate therapy.

Aged↗
PubMed1994

Genistein but not staurosporine can inhibit the mitogenic signal evoked by lithium in rat thyroid cells (FRTL-5).

Long-term administration of lithium is one of the well-known causes of goiter. It can stimulate DNA synthesis in rat thyroid cells (FRTL-5) treated with thyroid-stimulating hormone (TSH). To investigate the mitogenic signal transduction system activated by lithium, lithium-induced DNA synthesis and Ca2+ influx were studied using two protein kinase inhibitors, genistein as a specific tyrosine kinase inhibitor and staurosporine as a potent inhibitor of protein kinase C. Genistein but not staurosporine blocked the DNA synthesis induced by lithium in TSH-primed cells but neither compound had any effect on the Ca2+ entry stimulated by lithium. Genistein clearly attenuated the phosphotyrosine content of the 175 kDa substrate in the presence of lithium but staurosporine failed to do so. Moreover, lithium could also stimulate DNA synthesis in protein kinase C down-regulated cells. These data demonstrate that lithium may require the activation of a particular genistein-sensitive kinase, possibly a tyrosine kinase, to induce cell proliferation. It is suggested that the phorbol ester-sensitive protein kinase C family might not participate in the mitogenic signal transduction pathway activated by lithium.

Alkaloids↗
PubMed1994

Popliteal venous aneurysm with pulmonary embolism.

A 29-year-old female was admitted to the hospital because of increasing exertional dyspnea, chest oppressive feeling and palpitation. Lung perfusion scan, pulmonary angiography, and venography of the lower extremities revealed multiple pulmonary embolism and a right popliteal venous aneurysm as the probable source of emboli. B-mode/Doppler echography and magnetic resonance imaging were useful for the preoperative evaluation. Following anticoagulant therapy and thrombolytic therapy using intravenous heparin and urokinase, respectively, the popliteal venous aneurysm was surgically excised; the walls contained organized thrombus. She delivered a baby without any complication 2 years after the surgery.

Adult↗
PubMed1994

Abundant existence of 40kD-cdc2-related protein in rat thyroid cells.

The cdc2 kinase family is known to be one of the important factors for cell proliferation in both yeast and mammalian cells. By using polyclonal antibodies against PSTAIRE region of cdc2HS, we studied the amount of cdc2-related kinases in the rat thyroid cell line, FRTL-5, during the cell cycle. The immunoreactive protein with molecular weight 34kD was hardly detectable, instead, 40kD protein exists constantly in amount through G0 phase to S phase. Further, it did not decrease when the cells were cultured in serum- and hormone-free medium. Moreover, we observed an increase of this protein in the nuclear fraction as the cells enter S phase. On the contrary, we could not detect any immunoreactive 40kD protein in primary cultures of rat thyroid cells. These results may indicate abundant existence of this protein might concern cell cycle regulation of FRTL-5 or its immortal feature.

Animals↗
PubMed1994

Phorbol ester inhibits DNA synthesis induced by interleukin-6 in TSH-pretreated FRTL-5 cells.

Combination of TSH and Interleukin-6 (IL-6) can stimulate DNA synthesis in FRTL-5 cells. Phorbol 12-myristate 13-acetate (PMA) stimulates G0 to G1 transition but inhibits G1 to S transition in these cells. We studied the effect of IL-6 on DNA synthesis in TSH-pretreated FRTL-5 cells in the presence or absence of PMA. IL-6 induced DNA synthesis when it was added to TSH-pretreated cells. Further, PMA inhibited the DNA synthesis induced by IL-6. These data might suggest that in FRTL-5 cells IL-6 can show its mitogenic effect in G1 phase of their cell cycle progression.

Animals↗
PubMed1994

Antihypertensive effect of the peptides derived from casein by an extracellular proteinase from Lactobacillus helveticus CP790.

Peptides derived from alpha s1- and beta-caseins by the Lactobacillus helveticus CP790 proteinase were investigated for their inhibitory activities against angiotensin I-converting enzyme. The antihypertensive effect of casein hydrolysates in strain SHR spontaneously hypertensive rats was also investigated. Both alpha s1- and beta-casein hydrolysates inhibited this enzyme. Some of these peptides showed enzyme inhibitory activity, and one of them from beta-casein inhibited the enzyme greatly; the concentration of an angiotensin I-converting enzyme inhibitor needed to inhibit 50% of the enzyme activity was 4 microM. The hydrolysate of casein demonstrated antihypertensive activity in spontaneously hypertensive rats at an orally administered dosage of 15 mg/kg of body weight. MILK fermented with L. helveticus CP790, containing about .3% peptides, also showed antihypertensive activity in SHR rats with 5 ml/kg of body weight (15 mg of peptide/kg); however, the milk fermented with L. helveticus CP791, a variant defective for proteinase activity, did not show this activity. Results suggested that the peptides liberated from casein by the proteinase in the culture medium showed antihypertensive effect in SHR rats.

Amino Acid Sequence↗
PubMed1994

Characterization of glutathione efflux from Hep G2 cells.

Previous studies have suggested that both cAMP-dependent signal transduction pathway and Ca2+/protein kinase C-dependent pathway are involved in GSH efflux from hepatocytes. In the present study, GSH efflux from Hep G2 cells, a human-derived hepatoma cell line, was further characterized. Both epidermal growth factor (0.1-10 ng/ml) and insulin (1 microgram/ml) significantly increased GSH efflux from Hep G2 cells. A fall in the membrane potential produced by the replacement of Na+ with equivalent K+ did not affect GSH efflux significantly. Neither ouabain, a Na+/K+ ATPase inhibitor, vanadate, a Ca2+ ATPase inhibitor, nor BaCl2, a K+ channel blocker, significantly affected the GSH efflux. Methionine (1mM) decreased GSH efflux from the cells, although total GSH content in the cells was not affected during the incubation time of 60 min. Signal transductions through tyrosine kinase-coupled receptors may also be involved in GSH efflux from hepatocytes.

Adenosine Triphosphatases↗