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Biomedical subjects

K Takeuchi

Publications and source records attributed to K Takeuchi.

At least 649 records · Page 36Linked to original sources
PubMed1995

[The clinical scoring system for predicting the risk of intraoperative and postoperative bronchospasm].

Patients with bronchial asthma (BA) are usually considered to have a high risk of developing bronchospasm (BS) during anesthesia. Our clinical scoring system for preoperative assessment in BA patients was used to predict the risk of intraoperative and postoperative BS. Thirty two patients with a history of BA were studied retrospectively, assessing preoperatively with our clinical scoring system; Bronchial Asthma Risk Index Score (BARIS). BARIS was composed of a total of ten items. Five of them were scored before inhalation of bronchodilators and remaining five items were scored after the inhalation. Each item was scored by 0, 1, or 2. Four of 32 patients developed BS peroperatively (BS group). Twenty eight patients developed no BS peroperatively (control group). The total scores of pre-inhalation five items were 4.8 +/- 1.9 in BS group and 2.0 +/- 1.3 in control group, and the total scores of post-inhalation five items were 4.0 +/- 1.4 in BS group and 1.3 +/- 1.0 in control group. There were significant differences between the two groups (P < 0.05, Mann-Whitney U-test). We conclude that BARIS is useful in evaluating the risk of peroperative bronchospasm in patients with a history of bronchial asthma.

Aged↗
PubMed1995

[Pulmonary malignant fibrous histiocytoma treated with cisplatin plus etoposide followed by surgery].

A 47-year-old woman was admitted to our hospital with a mass shadow in the upper lobe of the right lung. Undifferentiated carcinoma was diagnosed after transbronchial biopsy. Combination chemotherapy consisting of cisplatin and etoposide was given. After two cycles of chemotherapy, partial response was obtained, and surgery was done because there was no evidence of lymph node metastasis or distant metastasis. After successful surgery, malignant fibrous histiocytoma was diagnosed because histological examination revealed the typical storiform pattern and most tumor cells showed positive cytoplasmic staining for alpha 1-antitrypsin, alpha 1-antichymotrypsin, and CD68. No evidence of another primary lesion was found, so this tumor was thought to be a pulmonary malignant fibrous histiocytoma. Cisplatin and etoposide have synergistic effect in vivo, and this combination is widely used as a standard regimen for small cell lung cancer and other malignancies. It might also be effective against pulmonary malignant fibrous histiocytoma.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1995

[Prolonged preservation due to acceleration of anaerobic glycolysis with histidine buffered cardioplegia in canine heart].

Myocardial preservation has centered around the deep hypothermia with metabolic arrest to save energy loss. We evaluated the efficacy of histidine buffered cardioplegia containing 100 mM histidine formulated to promote anaeraboic energy production in a blood perfused canine heart subjected to 24 hours or 30 hours ischemia. The hearts were flushed with 100 mM histidine containing buffered solution (HBS) in one group and a second group and University Wisconsin solution (UWS) in a third group. The hearts were preserved at 4 degrees C for 24 hours in one and third group, and for 30 hours in a second group, then reperfused with autologous blood in an isolated heart perfusion apparatus. Standardized stroke volume, ejection fraction, developed pressure and end-systolic elastance were measured at 2 hours after reperfusion and compared with control non-preserved hearts. Better recovery of cardiac performance was attained in the hearts preserved with histidine containing cardioplegia for 24 hours or 30 hours than that in UW group. Although cardiac performances in the hearts preserved with histidine cardioplegia for 30 hours was worse than that in 24 hours preserved heart for 24 hour, those were comparable if low dose or high dose cathecolamine was given. We concluded that the histidine containing cardioplegia provides effective preservation of the canine heart with superior recovery of pump performance after 24 hours or 30 hours of preservation by buffering proton and lactate to promote anaerobic glycolysis.

Adenosine↗
PubMed1995

Effect of NG-nitro-L-arginine methyl ester, the nitric oxide synthase inhibitor, on duodenal alkaline secretion and mepirizole-induced duodenal lesions in rats.

We investigated the HCO3- stimulatory mechanism of the nitric oxide (NO) synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) in the anesthetized rat duodenum and examined whether L-NAME protects against mepirizole-induced duodenal damage. The proximal duodenal loop was perfused with saline and HCO3- secretion was measured at pH 7.0 using a pH-stat with added HCl (10 mM). L-NAME (1-5 mg/kg, i.v.) increased HCO3- secretion in a dose-dependent manner, with concomitant elevation in arterial blood pressure and an apparent decrease in heart rate. These changes were mimicked by another NO synthase inhibitor, NG-monomethyl-L-arginine (L-NMMA; 50 mg/kg, i.v.) but not by NG-nitro-D-arginine methyl ester (D-NAME), and were all antagonized by co-administration of L-arginine but not by D-arginine (200 mg/kg, i.v.). The HCO3- stimulatory effect of L-NAME was also inhibited by vagotomy and pretreatment with atropine (1 mg/kg, s.c.) or indomethacin (5 mg/kg, s.c.). Vagotomy and atropine did not affect blood pressure response, but both inhibited the decrease of heart rate caused by L-NAME, whereas indomethacin did not affect either of these changes. In addition, L-NAME increased HCO3- secretion in the presence of mepirizole (200 mg/kg, s.c.) and prevented duodenal lesions caused by this agent. These results suggest that L-NAME stimulates duodenal HCO3- secretion in association with the inhibition of endogenous NO production, mediated by neural reflex through vagal efferent nerves, resulting from the pressor response to this agent, and may protect the duodenal mucosa against acid-related damage.

Animals↗
PubMed1995

Structure of translation initiation region of c-myc mRNA and thermostability of the c-myc mRNA/antisense ODN complex.

We enzymatically synthesized c-myc mRNA fragment containing the translation initiation (TI) region (36mer) and examined the structure by CD, 1H-NMR and RNaseV1 digestion. These study demonstrated that the c-myc mRNA fragment forms a hairpin structure at 37 degrees C. Six 15-mer antisense oligodeoxynucleotides(ODNs), which hybridize to the c-myc mRNA fragment were designed, and synhesized. Thermostabilities of the antisense ODNs-mRNA fragment complexes were examined. Antisense A (complementary to the c-myc mRNA from -9 to +6)-c-myc mRNA fragment complex had the highest melting temperature(Tm), and Antisense D (complementary to the c-myc mRNA from +1 to +15)-c-myc mRNA fragment complex had the most different Tm from a predicted Tm. Furthermore, Antisense D exhibited high inhibitory effect on HL60 cell proliferation, whereas Antisense A did not. The results suggest that the difference in the antisense effect is not simply due to the complex thermostability.

Cell Line↗
PubMed1994

Effect on fusion induction of point mutations introduced into the F protein of mumps virus.

We have tested the effect of substitution of an amino acid at position 195 of the F protein of mumps virus on cell-to-cell fusion caused by the virus. Introduction of amino acids with aromatic side chains into this position resulted in reduction of fusion induction. Furthermore the F protein was not cleaved when the amino acid at this position was substituted by several amino acids, suggesting that the amino acid at this position was essential to keep the tertiary structure of the protein that might be required not only for proper folding of the protein but also for induction of membrane fusion.

Mumps virus↗
PubMed1994

Complete obstruction of the inferior vena cava due to chronic relapsing pancreatitis: a case report.

A woman aged 62 with long history of chronic relapsing pancreatitis presented with swelling and ulcer in the lower limbs and occasional gastrointestinal bleeding. The radiological imaging showed complete obstruction of Inferior Vena Cava (IVC) at the level of the pancreas and well developed collateral vessels. Portal vein and splenic vein were also obstructed and superior mesenteric venous blood drained into the liver via coronary vein. She was originally found to have pancreas head tumor, which was not resectable. A palliative operation was performed, but histological examination of pancreatic specimen suggested only chronic inflammation and no evidence of malignancy. She was diagnosed as tumor-forming type chronic pancreatitis. Although SPV or SMV-PV obstruction has been recognized as a complication of chronic pancreatitis, IVC obstruction can occur by the same mechanism. This is the only case but one ever reported. Not only splenoportography but IVC-graphy will contribute to more precise understanding of patient's condition with chronic pancreatitis.

Chronic Disease↗
PubMed1994

Functional difference between two isoforms of rat kidney prostaglandin receptor EP3 subtype.

We have cloned two isoforms of rat kidney prostaglandin E2 receptor EP3 subtype (rEP3A and rEP3B), which differ only in their cytosolic carboxyl-terminal tails (30 and 29 amino acids, respectively). The aim is to clarify the functional difference between two rEP3 receptor isoforms by examining formation of adenosine 3',5'-monophosphate (cAMP) and change in cytosolic free calcium ([Ca2+]i) in cultured cells transiently transfected with cloned rEP3A or rEP3B receptor cDNA. In immortalized renal distal tubule cells (TKC2), vasopressin (VP) stimulated cAMP formation, and the cAMP formation was significantly attenuated by a non-peptide VP receptor antagonist, OPC-31260. The VP-induced increase in cAMP formation was also attenuated by over-expression of rEP3A receptor but not that of rEP3B receptor. On the other hand, in COS-7 cells transfected with rEP3B receptor cDNA, PGE2 induced an increase in [Ca2+]i, but no increase in [Ca2+]i was observed in the cells transfected with rEP3A cDNA. In conclusion, rEP3A receptor is suggested to antagonize VP (V2) receptor by inhibiting cAMP formation, whereas rEP3B receptor is linked with Ca2+ messenger system.

Animals↗
PubMed1994

Influenza virus M2 protein ion channel activity is not required to maintain the equine-1 hemagglutinin in its native form in infected cells.

The equine-1 influenza virus A/Cornell/74 (H7N7) hemagglutinin (HA) is cleaved to HA1 and HA2 in the trans Golgi network (TGN) of infected cells. The avian influenza virus A/chicken/Germany/34 (fowl plague virus Rostock) H7 HA is also cleaved to HA1 and HA2 intracellularly in the TGN. To maintain the fowl plague virus Rostock HA in its native form during transport through the TGN, a functioning M2 ion channel activity is required, otherwise the HA undergoes its transition to the low-pH form (Sugrue et al., 1990, EMBO J. 9, 3469-3476). Studies were initiated to investigate if the equine H7 HA has intracellular requirements different from those of the fowl plague virus Rostock HA. We report here that the pH of transition to the low-pH form of the equine-1 HA is approximately pH 5.3 and that the M2 protein ion channel blocker, amantadine, does not have a discernable effect on the native conformation of equine-1 HA during transport through the TGN. Moreover, the equine-1 HA expressed from cDNA does not require coexpression of a functional M2 protein to maintain HA in its native conformation.

Amantadine↗
PubMed1994

Different cellular mechanisms of vasopressin receptor V1 and V2 subtype in vasopressin-induced adenosine 3', 5'-monophosphate formation in an immortalized renal tubule cell line, TKC2.

Vasopressin (VP) stimulates adenosine 3',5'-monophosphate (cAMP) formation in an immortalized renal tubule cell line, TKC2, which is derived from transgenic mouse harboring temperature-sensitive SV40 T-antigen gene. VP (10(-8) M)-induced cAMP formation was significantly attenuated by either non-peptide vasopressin receptor V1 or V2 subtype antagonist, OPC-21268 (10(-8) and 10(-6) M) or OPC-31260 (10(-8) and 10(-6) M), respectively, and it was completely abolished by combination of both agents (10(-6) M). VP (10(-8) M) also induced an increase in cytosolic free Ca2+ and prostaglandin (PG) E2 synthesis, both of which were significantly inhibited by OPC-21268 (10(-8) M), but not by OPC-31260 (10(-6) M). Either OPC-21268 (10(-8) M), depletion of extracellular Ca2+ or inhibition of cyclooxygenase attenuated both VP-induced PGE2 synthesis and cAMP formation. In conclusion, both V1 and V2 receptors can stimulate cAMP formation. V1 receptor, however, stimulates cAMP formation via Ca(2+)-dependent PGE2 synthesis, whereas V2 receptor may stimulate it directly.

Animals↗
PubMed1994

Expression of human nm23-H1 and nm23-H2 proteins in hepatocellular carcinoma.

BACKGROUND: The expression of nm23-H1 and nm23-H2 proteins in 25 hepatocellular carcinomas was studied immunohistochemically. METHODS: Tissue specimens were reacted with anti-human nm23-H1 and nm23-H2 monoclonal antibodies (MoAb) (H1-229 and H2-206, respectively) and then stained by the biotin-streptoavidin complex method. RESULTS: Adjacent nontumorous tissues were intensely stained with nm23-H1 and nm23-H2. Of the 25 hepatocellular carcinomas, 60% were positive for MoAb H1-229, and 68% were positive for MoAb H2-206. These immunoreactivities were most common in the cytoplasm of tumor cells. There was no significant correlation between the expression of nm23-H1 protein and tumor size, Edmondson's histopathologic classification, or invasion of the capsule. However, the authors observed an inverse relationship between nm23-H1 expression and intrahepatic metastases of hepatocellular carcinomas. There was no significant correlation between the expression of nm23-H2 protein and clinicopathologic findings. Only a short survival period was observed in patients with hepatocellular carcinoma with reduced nm23-H1 or nm23-H2 proteins. CONCLUSIONS: The results suggest that nm23-H1 protein plays a role in the suppression of intrahepatic metastasis of hepatocellular carcinoma and that the combined expression of nm23-H1 is associated with favorable prognosis.

Carcinoma, Hepatocellular↗
PubMed1994

Methoxamine-induced release of endogenous ATP from rabbit pulmonary artery.

Methoxamine, an alpha 1-adrenoceptor agonist, significantly increased the overflow of ATP, ADP and AMP, but not adenosine, by a prazosin-sensitive mechanism in the rabbit pulmonary artery. Among the adenine nucleotides released, the amount of ATP was larger than those of the other two. Such release of adenine nucleotides was not induced by clonidine, an alpha 2-adrenoceptor agonist, and isoproterenol, a beta-adrenoceptor agonist. Methoxamine-induced release was observed in the absence of extracellular calcium, but was not observed at a low temperature, 27 degrees C. This suggests an extracellular calcium-independent and temperature-dependent ATP-releasing mechanism coupled with alpha 1-adrenoceptors in rabbit pulmonary artery.

Adenosine Triphosphate↗
PubMed1994

Two isoforms of the rat kidney EP3 receptor derived by alternative RNA splicing: intrarenal expression co-localization.

Two different clones, named rEP3A (approximately 2.2 kb) and rEP3B (approximately 5.2 kb), were isolated from a rat kidney cDNA library by a homology screening approach. rEP3A was shown to encode the rat kidney prostaglandin E receptor EP3 subtype (rEP3A receptor) (Takeuchi, K. et al. B.B.R.C. (1993) 194: 885). rEP3B receptor differs only in its carboxyl-terminal tail (Ile-336 to Pro-364) from rEP3A receptor. Southern blot analysis of genomic DNA has suggested that the EP3 receptor gene is a single copy gene. RT-PCR using microdissected nephron segments showed co-expression of both receptor mRNAs specifically in distal nephron segments such as mTAL, cTAL, CCD and IMCD, whereas no significant expression of both receptor mRNAs was detected from GL, PCT, and PST. In conclusion, we have cloned an isoform of the rat kidney EP3 receptor, rEP3B receptor. rEP3A and rEP3B receptors are suggested to be derived by alternative RNA splicing, and both receptors are co-localized to distal tubules exerting an effect on water and electrolyte metabolism.

Alternative Splicing↗
PubMed1994

Inhibition of the soluble and the tumor cell receptor-bound plasmin by urinary trypsin inhibitor and subsequent effects on tumor cell invasion and metastasis.

The present study was undertaken to determine whether highly purified human urinary trypsin inhibitor (UTI) efficiently inhibits the soluble and the tumor cell receptor-bound plasmin. The ability of plasmin inhibitors to regulate invasion by tumor cells which express membrane-associated plasmin was also examined. UTI and two other plasmin inhibitors [alpha 2-anti-plasmin (alpha 2AP) and alpha 2-macroglobulin (alpha 2M)] were used. alpha 2AP and alpha 2M, as well as UTI, rapidly inactivate the soluble plasmin that is not bound to cells. Experiments were performed in vitro using cultures of ovarian cancer HOC-I cells and gestational choriocarcinoma SMT-ccl cells. HOC-I and SMT-ccl cells had plasmin(ogen) on their cell surface, and the plasmin activity was detected on their cell surface enzymologically and immunologically. Receptor-bound plasmin reacted effectively with UTI and was directly inactivated by UTI. In contrast, receptor-bound plasmin was not inhibited by alpha 2AP and alpha 2M. Using a modified Boyden chamber and an artificial basement membrane, Matrigel, it was found that UTI, but not alpha 2AP or alpha 2M, can inhibit HOC-I and SMT-ccl cells invasion in vitro. Furthermore, in the experimental lung metastasis model, UTI inhibited the formation of lung metastasis by Lewis lung carcinoma cells. The inhibition of tumor cell invasion was not due to direct antitumor effects of UTI. These results suggest that inhibition of receptor-bound plasmin by UTI is associated with significantly reduced tumor cell invasiveness in vitro and with a decreased number of metastasis in vivo.

Animals↗
PubMed1994

Intercellular adhesion induced by anti-alpha 3 integrin (VLA-3) antibodies.

We generated four monoclonal antibodies (mAbs) specific for human alpha 3 integrin (VLA-3 alpha subunit). All of them were found to induce homotypic cell aggregation of HT1080 fibrosarcoma and SN12C renal carcinoma cells, both of which express high levels of alpha 3 integrin. The antibodies also induced the cell aggregation of K562 erythroleukemic cells transfected with alpha 3 integrin cDNA, but not the parental K562 cells. The aggregation was observed in a temperature-dependent manner and was not inhibited by the addition of EDTA. Immunofluorescence microscopic observation showed that alpha 3 integrin on HT1080 cells was translocated into the contact regions after the mAb treatment. The intercellular adhesion between cells expressing alpha 3 integrin and cells without alpha 3 integrin was also induced by the anti-alpha 3 antibody treatment.

Antibodies, Monoclonal↗
PubMed1994

Cloning, heterologous expression, and localization of a novel crystal protein gene from Bacillus thuringiensis serovar japonensis strain buibui toxic to scarabaeid insects.

Recombinant Escherichia coli strains harboring pAG1, pAG2, pKBB100, and pKBB101 were cloned by using antiserum constructed against 130-kDa crystal protein antigen of Bacillus thuringiensis serovar japonensis strain Buibui. DNAs in the recombinant strains hybridized to the 26-base oligonucleotide probe corresponding to N-terminal amino acids of the 130-kDa crystal protein of strain Buibui. Cultures of the recombinant strains were toxic to larvae of the cupreous chafer, Anomala cuprea. Furthermore, the production of the 130-kDa polypeptide was demonstrated in the cells harboring pAG1 and pAG2 by immunoblot analysis with antiserum against the 130-kDa crystal protein. Southern hybridization analysis showed that the 130-kDa crystal protein gene is located on the chromosomal DNA of strain Buibui. On the other hand, DNA probes derived from cryIA(a) and cryIIIA genes did not hybridize to the DNA of strain Buibui.

Animals↗
PubMed1994

Influences of urethane anesthesia on indomethacin-induced gastric mucosal lesions in rats. Relation to blood glucose levels.

Effects of urethane on gastric motility and mucosal ulcerogenic responses induced by indomethacin were investigated in the rat in relation to blood glucose levels (BGL) and compared with those of pentobarbital Na. Urethane (1.25 g/kg) given intraperitoneally, caused a progressive and significant rise in BGL, while pentobarbital (30 mg/kg) given intraperitoneally did not affect BGL. Subcutaneous administration of indomethacin (25 mg/kg) caused high-amplitude gastric contractions and induced hemorrhagic lesions in the stomachs of conscious rats. These lesions were significantly inhibited by urethane but not pentobarbital. Administration of urethane abolished basal gastric motility and almost completely suppressed the motility responses induced by indomethacin, while pentobarbital did not have much effect on gastric motility under basal and indomethacin-stimulated conditions. Acid secretion was significantly decreased by urethane and increased by pentobarbital. Pretreatment of the animals with yohimbine (5 mg/kg, subcutaneously) but not prazosin (0.5 mg/kg) inhibited the elevation in BGL seen after administration of urethane and allowed resumption both gastric motility and ulcerogenic responses induced by indomethacin, with less change in acid secretion. These results suggest that intraperitoneal administration of urethane prevented indomethacin-induced gastric lesions, probably by inhibiting the enhanced gastric motility response, and this effect may relate to its hyperglycemic action mediated by alpha 2-adrenoceptors. These findings also provide further evidence to support the importance of gastric motility in the pathogenesis of these lesions.

Anesthesia, General↗