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Biomedical subjects

A Tanimura

Publications and source records attributed to A Tanimura.

At least 19 recordsLinked to original sources
PubMed1996

Inositol 1,4,5-trisphosphate-dependent oscillations of luminal [Ca2+] in permeabilized HSY cells.

Oscillations in intracellular Ca2+ concentration ([Ca2+]i) are thought to play an important role in phosphoinositide-linked Ca2+ signaling events. We demonstrate corresponding inositol 1,4, 5-trisphosphate (IP3)-dependent oscillations of Ca2+ concentration within the lumen of the IP3-sensitive stores ([Ca2+]L) of saponin-permeabilized HSY cells by monitoring [Ca2+]L with the fluorescent Ca2+ indicator Mag-fura-2. The associated openings and closings of the IP3-sensitive Ca2+ release channel were detected via quenching of Mag-fura-2 fluorescence due to the entry of Mn2+, a Ca2+ surrogate, into the stores. Evidence for complimentary Ca2+ oscillations at the external surface of the stores was provided by the membrane-bound Ca2+ probe Calcium Green C18. The permeabilization of saponin-treated HSY cells to macromolecules was confirmed by demonstrating that permeabilized cells readily took up and lost (t1/2 approximately 46 s) a fluorescently tagged 70-kDa dextran. Our results impose a number of constraints on possible mechanisms for [Ca2+]i oscillations. In addition, they support recent proposals that [Ca2+]i oscillations arise directly from the (biphasic) effects of Ca2+ itself on IP3-sensitive Ca2+ channel activity.

Calcium↗
PubMed1996

Calcium release in HSY cells conforms to a steady-state mechanism involving regulation of the inositol 1,4,5-trisphosphate receptor Ca2+ channel by luminal [Ca2+].

In many cell types, low concentrations of inositol 1,4,5-trisphosphate (IP3) release only a portion of the intracellular IP3-sensitive Ca2+ store, a phenomenon known as "quantal" Ca2+ release. It has been suggested that this effect is a result of reduced activity of the IP3-dependent Ca2+ channel with decreasing calcium concentration within the IP3-sensitive store ([Ca2+]s). To test this hypothesis, the properties of IP3-dependent Ca2+ release in single saponin-permeabilized HSY cells were studied by monitoring [Ca2+]s using the Ca(2+)-sensitive fluorescent dye mag-fura-2. In permeabilized cells, blockade of the sarco/ER Ca(2+)-ATPase pump in stores partially depleted by IP3 induced further Ca2+ release via an IP3-dependent route, indicating that Ca2+ entry via the sarco/ER Ca(2+)-ATPase pump had been balanced by Ca2+ loss via the IP3-sensitive channel before pump inhibition. IP3-dependent Mn2+ entry, monitored via quenching of luminal mag-fura-2 fluorescence, was readily apparent in filled stores but undetectable in Ca(2+)-depleted stores, indicating markedly reduced IP3-sensitive channel activity in the latter. Also consistent with reduced responsiveness of Ca(2+)-depleted stores to IP3, the initial rate of refilling of these stores was unaffected by the presence of 0.3 microM IP3, a concentration that was clearly effective in eliciting Ca2+ release from filled stores. Analysis of the rate of Ca2+ release at various IP3 concentrations indicated a significant shift of the IP3 dose response toward higher [IP3] with decreasing [Ca2+]s. We conclude that IP3-dependent Ca2+ release in HSY cells is a steady-state process wherein Ca2+ efflux via the IP3 receptor Ca2+ channel is regulated by [Ca2+]s, apparently via changes in the sensitivity of the channel to IP3.

Calcium↗
PubMed1996

Expression of 135-kDa insecticidal protein gene from Bacillus thuringiensis in the yeast Saccharomyces cerevisiae.

Bacillus thuringiensis subsp. aizawai produces 130-kDa and 135-kDa (CryIA(a)) insecticidal proteins. When Saccharomyces cerevisiae was transformed by the vector carrying a cryIA(a) gene, the gene expression could not be observed. When the 5'-upstream region from the initiation codon was removed using a synthetic oligonucleotide, the CryIA(a) protein was successfully synthesized in yeast. The yeast extract containing CryIA(a) protein had insecticidal activity against Plutella xylostella larvae.

Bacillus thuringiensis↗
PubMed1996

[An allogeneic bone marrow transplantation for chronic myelocytic leukemia with a large extramedullary tumor in the pelvic cavity].

A 16-year-old girl developed a pain and paresis in the right hip joint in April 1994. Abdominal CT scan revealed hepatosplenomegaly and large tumor mass (6 x 7 x 13 cm) invading the right psoas muscle in the pelvic cavity. Laboratory data disclosed marked granulocytosis, the presence of Ph1 translocation and bcr-abl rearrangement, thus a diagnosis of CML was made. The tumor was shown to be consisted of granulocytes at all stages of development by a fine needle aspiration cytology. According to the criteria of IBMTR, the disease was classified as accelerated phase solely because the sum of myeloblasts and promyelocytes exceeded over 20%. The patient was treated with hydroxycarbamide, 6MP and dexamethasone, and marked reduction of the tumor mass was observed. Then an allogeneic BMT was performed from her HLA- identical brother on August 1994. She did not develop clinically significant symptoms except for grade I skin GVHD. The tumor was completely disappeared after the BMT as assessed by the abdominal CT scan. No cytological and chromosomal relapse has been observed for 20 months after the BMT.

Adolescent↗
PubMed1996

[A case of so-called carcinosarcoma of the lung].

A 69-year-old male was followed at our institute for the purpose of hemo-dialization. During follow-up, a tumor shadow (phi 6.5 x 7.0 cm) was found in rt. S5 by chest X-ray. This tumor was diagnosed as squamous cell carcinoma by TBLB. Right middle lobectomy (R 2 a) was performed. Histological staging was pT 2 N 2 M 0, stage IIIa. This tumor was cystic, filled with keratin like substance. Histologically, the cyst wall was composed of well differentiated squamous cell carcinoma and sarcomatous stroma which didn't differentiate into bone, cartilage, muscle, and etc. Immunohistologically, sarcomatous stroma was positively stained by vimentin, negatively by keratin and EMA. This patient survived 7 months with recurrence.

Aged↗
PubMed1995

Involvement of direct phosphorylation in the regulation of the rat parotid Na(+)-K(+)-2Cl- cotransporter.

We identify a 175-kDa membrane phosphoprotein (pp175) in rat parotid acini whose properties correlate well with the Na(+)-K(+)-2Cl- cotransporter previously characterized functionally and biochemically in this tissue. pp175 was the only phosphoprotein immunoprecipitated by an anti-Na(+)-K(+)-2Cl- cotransporter antibody and the only membrane protein whose phosphorylation state was conspicuously altered after a brief (45-s) exposure of acini to the beta-adrenergic agonist isoproterenol. Phosphopeptide mapping provided evidence for three phosphorylation sites on pp175, only one of which was labeled in response to isoproterenol treatment. The half-maximal effect of isoproterenol on phosphorylation of pp175 (approximately 20 nM) was in excellent agreement with its previously demonstrated up-regulatory effect on cotransport activity. Increased phosphorylation of pp175 was also seen following acinar treatment with a permeant cAMP analogue and with forskolin, conditions that have likewise been shown to up-regulate the cotransporter. Combined with earlier results from our laboratory, these data provide strong evidence that the up-regulation of the cotransporter by these agents is due to direct phosphorylation mediated by protein kinase A. AlF(-)4 treatment, which results in an up-regulation of cotransport activity comparable with that observed with isoproterenol (approximately 6-fold), caused a similar increase in phosphorylation of pp175. However, hypertonic shrinkage and treatment with the protein phosphatase inhibitor calyculin A, which also up-regulate the cotransporter (approximately 3-fold and approximately 6-fold, respectively) caused no change in the phosphorylation level. Furthermore, although acinar treatment with the muscarinic agonist carbachol results in a dramatic up-regulation of cotransport activity and a concomitant phosphorylation of pp175, no phosphorylation of pp175 was seen with the Ca(2+)-mobilizing agent thapsigargin, which is able to fully mimic the up-regulatory effect of carbachol on transport activity. Taken together, these results indicate that direct phosphorylation is only one of the mechanisms involved in secretagogue-induced regulation of the rat parotid Na(+)-K(+)-2Cl- cotransporter.

Animals↗
PubMed1995

Surgically resected adrenal leiomyoma: report of a case.

This report describes the case of a 48-year-old woman found to have a leiomyoma of the left adrenal gland after presenting with anemia and hypertension. An upper gastrointestinal series revealed a mass in the posterior region of the body that distorted the stomach. A computed tomography (CT) scan showed a well-circumscribed mass with a high-density outline in the left adrenal gland, and magnetic resonance imaging (MRI) revealed a homogeneous mass. Multiple catheter samplings of vena cava blood revealed a slight elevation of epinephrine and norepinephrine in the left adrenal vein and the left renal vein. Thus, asymptomatic pheochromocytoma of the left adrenal gland was highly suspected as a preoperative diagnosis and a left adrenalectomy was performed. However, histologic examination subsequently revealed findings suggestive of leiomyoma of the adrenal gland, which was confirmed by electron microscopy. The patient's postoperative course was uneventful and she has remained free from any further symptoms.

Adrenal Gland Neoplasms↗
PubMed1995

Staurosporine enhances Ca2+ entry induced by depletion of intracellular Ca2+ stores in rat parotid acinar cells.

The effect of staurosporine on the Ca2+ signalling induced by the muscarinic receptor agonist carbachol (CCh) was studied in Fura-2-loaded rat parotid acinar cells. At concentrations > 1 nM, staurosporine dose-dependently enhanced the sustained increase in cytosolic free Ca2+ concentration ([Ca2+]i), but did not affect the peak [Ca2+]i seen just after stimulation. The enhancement of the sustained increase in [Ca2+]i was not attenuated by the protein kinase C activator, 4 beta-phorbol 12-myristate 13-acetate, and not mimicked by another inhibitor of protein kinase C, K-252a, suggesting that the effect of staurosporine on the CCh-induced Ca2+ signalling may be due to a mechanism independent of the inhibitory action on protein kinase C. Staurosporine also enhanced the increases in [Ca2+]i induced by the microsomal Ca(2+)-ATPase inhibitor thapsigargin (TG) and the Ca2+ ionophore ionomycin (Iono). When the cells were stimulated by CCh, TG, or Iono in the absence of extracellular Ca2+, a transient increase in [Ca2+]i due to Ca2+ release from intracellular stores was observed. This increase in [Ca2+]i was unaffected by preincubation with staurosporine. However, when Ca2+ was added to the extracellular medium after [Ca2+]i had returned to the resting level, the increase in [Ca2+]i was significantly enhanced by staurosporine. In addition, staurosporine accelerated the Mn2+ influx following the addition of CCh, TG, or Iono. These results suggest that staurosporine modulates the Ca2+ entry system activated by depletion of intracellular Ca2+ stores in rat parotid acinar cells.

Alkaloids↗
PubMed1995

Pentachlorophenol-induced oxidative DNA damage in mouse liver and protective effect of antioxidants.

8-Hydroxydeoxyguanosine (8-OH-dG) was determined as a marker of oxidative DNA damage in male B6C3F1 mice treated with the hepatocarcinogen pentachlorophenol (PCP). A single oral administration of PCP (0-80 mg/kg) significantly and dose-dependently increased the 8-OH-dG level specifically in the liver at 6 hr. Repeated doses (0-80 mg/kg) over 5 days caused a further increase. Elevation of the 8-OH-dG level caused by a single dose of PCP (60 mg/kg) was not affected by ip injection of buthionine sulfoximine (2 mmol/kg), an inhibitor of GSH synthesis, or aminotriazole (1 g/kg), an inhibitor of catalase, showing no clear evidence for enhancement by the oxidative stress due to reduction of antioxidative factors under these experimental conditions. However, examination of the effects of natural antioxidants on repeated PCP treatment (60 mg/kg/day, for 5 days) revealed that oral administration of vitamin E and diallyl sulfide 3 hr before each PCP challenge significantly protected against elevation of hepatic 8-OH-dG levels. beta-Carotene did not have any effect. Ellagic acid, epigallocatechin gallate and vitamin C demonstrated partial protection. These findings indicate that PCP causes oxidative DNA damage in the target organ liver which can be blocked by a number of antioxidant agents.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1995

Preventive effects of green tea against liver oxidative DNA damage and hepatotoxicity in rats treated with 2-nitropropane.

Male rats were given 2% green tea as their drinking water for 2 wk before a single ip injection of the carcinogen 2-nitropropane (2NP) (100 mg/kg body weight) and liver nuclear 8-hydroxydeoxyguanosine (8-OHdG) levels and hepatotoxicity parameters were determined 6 or 15 hr thereafter. The increase of 8-OHdG adducts in liver nuclear DNA caused by 2NP was depressed 50% at both time points with the green tea pretreatment. The time-dependent elevations of serum aminotransferases and lactate dehydrogenase values by 2NP were also effectively prevented. However, green tea had no obvious effects on the falls in serum lipid peroxide and triglyceride levels associated with carcinogen exposure. Increases of hepatic lipid peroxide levels with 2NP were depressed 100 and 30%, at 6 and 15 hr, respectively, by green tea and the decrease in hepatic glycogen content at 6 hr was clearly alleviated. Histopathological examination revealed effective protection against induction of hepatic degenerative changes by 2NP at 15 hr. Drinking crude catechin extract solution with the same concentration of (-)epigallocatechin gallate as green tea provided protection at 6 hr, but with only half the effectiveness. These findings demonstrate that green tea can effectively block oxidative DNA damage to the liver as well as hepatotoxicity in rats treated with 2NP.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1995

Chemical and chemotaxonomical studies on Dicranopteris species.

Clerodane glycosides and flavonoids in Dicranopteris pedata and three varieties of D. linearis were investigated. All the ferns contained a new glycoside, (6S,13S)-6-[6-O-acetyl-beta-D-glucopyranosyl-(1-->4)-alpha-L-rhamnopy - ranosyloxy]-13-[alpha-L-rhamnopyranosyl-(1-->4)-beta-D-fucopyra nosyloxy]- cleroda-3,14-diene, as a chemical marker of this group. Flavonoids were limited to flavonol 3-O-glycosides. The ferns and isolated flavonoids are as follows; D. pedata: afzelin, quercitrin. D. linearis var. brevis: afzelin, quercitrin. D. linearis var. tenuis: quercitrin, isoquercitrin. D. linearis var. sebastiana: astragarin, isoquercitrin, rutin, kaempferol 3-O-(4-O-p-coumaroyl-3-O-alpha-L-rhamnopyranosyl)-alpha-L-rhamn opy ranosyl- (1-->6)-beta-D-glucopyranoside.

Carbohydrate Sequence↗
PubMed1995

Suppression of capacitative Ca2+ entry by serine/threonine phosphatase inhibitors in rat parotid acinar cells.

The effects of three serine/threonine protein phosphatase inhibitors, calyculin-A, tautomycin and okadaic acid, on the Ca2+ entry across the plasma membrane was studied in Fura-2-loaded rat parotid acinar cells. These protein phosphatase inhibitors did not affect the peak elevation of cytosolic free Ca2+ concentration ([Ca2+]i) just after stimulation with the muscarinic agonist carbachol (CCh), but they suppressed the sustained increase in [Ca2+]i. In the absence of extracellular Ca2+, CCh produced a transient increase in [Ca2+]i due to Ca2+ release from intracellular Ca2+ stores, and this increase in [Ca2+]i was unaffected by the phosphatase inhibitors. When Ca2+ was added to the external medium after the transient [Ca2+]i response, the increase in [Ca2+]i in the cells treated with the phosphatase inhibitors was significantly smaller than that in the control cells, indicating that the Ca2+ entry was reduced. Similar suppression of Ca2+ entry by the phosphatase inhibitors was observed when intracellular Ca2+ stores were previously depleted by the microsomal Ca(2+)-ATPase inhibitor thapsigargin (TG). In addition, the phosphatase inhibitors reduced the Mn2+ (Ca2+ surrogate) influx following the addition of CCh or TG. The enhancement of Ca2+ entry by the protein kinase inhibitor staurosporine was significantly attenuated by the phosphatase inhibitors. These results suggest that the phosphatase inhibitors suppressed the Ca2+ entry mechanism activated by depletion of intracellular Ca2+ stores in rat parotid acinar cells. The capacitative Ca2+ entry may be regulated by protein phosphorylation/dephosphorylation.

Alkaloids↗
PubMed1994

Modulatory effect of 4 beta-phorbol 12-myristate 13-acetate (PMA) on carbachol-induced Ca2+ mobilization in rat parotid acinar cells.

Treatment of rat parotid acinar cells with 4 beta-phorbol 12-myristate 13-acetate (PMA) significantly inhibited an increase in cytosolic free Ca2+ concentration ([Ca2+]i) induced by carbachol (CCh), a muscarinic agonist. The CCh-induced increase in [Ca2+]i was also inhibited by another active phorbol ester, 4 beta-phorbol 12,13-dibutyrate, but not by 4 alpha-phorbol 12,13-didecanoate, which does not activate protein kinase C. The treatment with PMA had no effect on increases in [Ca2+]i evoked by ionomycin and thapsigargin, which do not stimulate phosphoinositide hydrolysis. In contrast, an increase in [Ca2+]i induced by NaF, a direct activator of GTP-binding proteins, was delayed in the presence of PMA. The formation of inositol phosphates in response to CCh was suppressed significantly by PMA treatment. In radioligand binding assays, PMA did not directly interfere with the specific binding of [3H]quinuclidinyl benzilate ([3H]QNB), a muscarinic antagonist, to plasma membranes. Furthermore, the [3H]QNB binding to plasma membranes prepared from the PMA-pretreated cells was not different from that to the control membranes. These results indicate that PMA attenuated the CCh-induced increase in [Ca2+]i through inhibition of phosphoinositide hydrolysis. Activation of protein kinase C may play a role in negative-feedback control of the muscarinic pathway in rat parotid acinar cells.

Animals↗
PubMed1993

Evidence that substance-P receptors do not exist in mouse parotid and submandibular acinar cells.

Substance P (SP) had no effect on cytosolic Ca2+ concentration ([Ca2+]i) and inositol phosphate formation in mouse parotid and submandibular acinar cells, but induced a rapid increase in [Ca2+]i and production of inositol phosphates in rat acinar cells. In addition, SP did not stimulate amylase release from mouse parotid acini, but SP-induced amylase release was seen in rats. These results indicate that the mouse lacks SP receptors on parotid and submandibular acinar cells.

Amylases↗
PubMed1993

A new regulatory element that augments the Tax-dependent enhancer of human T-cell leukemia virus type 1 and cloning of cDNAs encoding its binding proteins.

The Tax protein of human T-cell leukemia virus type 1 (HTLV-1) trans activates the 21-bp enhancer of HTLV-1. A sequence of more than two copies of the 21-bp enhancer is efficiently activated by Tax, but one copy is not activated extensively. Another sequence (TRE-2, positions -163 to -117) adjacent to the 21-bp enhancer in the long terminal repeat of HTLV-1 can enhance a single copy of the 21-bp enhancer activity in trans activation by Tax. This sequence contains motifs related to the Ets- and NF-kappa B-binding sequences, but mutations at these sites indicated that neither is responsive to cooperation with the 21-bp enhancer. A deletion mutation of TRE-2 identified 25 bases at positions -158 to -134 (TRE-2S) as an essential sequence, and TRE-2S was sufficient to give maximum cooperation with one copy of the 21-bp enhancer in trans activation by Tax protein. Using TRE-2S as a probe, we screened a cDNA library of HUT102 cells by the Southwestern (DNA-protein) procedure and isolated two cDNA clones, THP-1 and -2. These two clones encode TRE-2S-binding proteins, and they differ by only an extra 17 amino acids in THP-2. Both THP proteins contain five zinc finger motifs which are strikingly similar to those of the GLI family, an amplified gene product in glyoma cells. The binding site of THP-1 and -2 was GAACCACCCA in TRE-2S, which is highly homologous to the GLI-binding site. These results suggest that binding of THP to TRE-2S may be involved in cooperation with one copy of the 21-bp enhancer in responding to Tax trans activation.

Base Sequence↗
PubMed1993

The cytosolic acidification in rat parotid cells is associated with an increase in cytosolic Ca2+ concentration.

A transient decrease in cytosolic pH ([pH]i) in rat parotid cells was evoked by the addition of carbachol (CCh), phenylephrine, or substance P, whereas isoproterenol and dibutyryl cyclic AMP had little or no effect on [pH]i. The decrease in [pH]i induced by the Ca(2+)-mobilizing agonists was also observed in Ca(2+)-free medium, but not when the intracellular Ca2+ stores were previously depleted. Ionomycin and thapsigargin elicited a decrease in [pH]i with an increase in cytosolic Ca2+ concentration ([Ca2+]i). The protein kinase C activator and inhibitor had no effect on the agonist-induced decrease in [pH]i. These results suggest that the cytosolic acidification is associated with an increase in [Ca2+]i.

Animals↗
PubMed1993

Carbachol-induced potassium release in rat parotid acini: comparison of the roles of cytosolic Ca2+ and protein kinase C.

Carbachol (CCh) stimulated K+ release from rat parotid acini. Treatment with the intracellular Ca2+ antagonist 8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate (TMB-8) or the intracellular Ca2+ chelator 1,2-bis(O-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA) strongly suppressed the CCh-induced K+ release. Combined addition of the Ca2+ ionophore ionomycin and the microsomal Ca(2+)-ATPase inhibitor thapsigargin caused a rapid increase in cytosolic Ca2+ concentration ([Ca2+]i) and resulted in a marked release of K+. In the absence of extracellular Ca2+, CCh or a combination of ionomycin and thapsigargin caused a transient release of K+ which correlated well with the transient change in [Ca2+]i. On the other hand, phorbol 12-myristate 13-acetate (PMA) did not potentiate the CCh-induced K+ release, although the CCh-induced amylase release was significantly enhanced in the presence of PMA. Staurosporine, a protein kinase C-inhibitor, did not inhibit the CCh-induced K+ release, which was in contrast with its inhibitory effect on amylase release. These results suggest that the K+ release from rat parotid acini induced by CCh stimulation is mediated by a rapid increase in [Ca2+]i but is not associated with activation of protein kinase C. This signal pathway is different from that for amylase release where activation of protein kinase C plays an important role.

Alkaloids↗