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Biomedical subjects

K Wada

Publications and source records attributed to K Wada.

At least 559 records · Page 31Linked to original sources
PubMed1991

[Difference in effects of sodium fluoride and cholecystokinin on pepsinogen secretion from isolated guinea pig gastric chief cells].

In order to further investigate the precise mechanisms of cholecystokinin(CCK)-induced pepsinogen secretion from gastric chief cells, we compared the signal transducing mechanisms activated by CCK with those activated by sodium fluoride (NaF) in isolated guinea pig gastric chief cells. NaF stimulated a monophasic increase in diacylglycerol accumulation with a peak value observed at 15 sec, while CCK strongly stimulated its biphasic accumulation. NaF evoked an increase in initial Ca2+ influx rate with a slow and smooth increase in intracellular free Ca2+ concentration [( Ca2+]i) monitored by fura-2, while CCK stimulated a rapid increase in [Ca2+]i followed by a late sustained phase of [Ca2+]i increase. Lanthanum chloride (La3+) effectively (unlike either nifedipine or verapamil) blocked NaF-stimulated increase in [Ca2+], but it blocked only CCK-stimulated late sustained phase of [Ca2+]i increase. La3+ reduced NaF-or CCK-stimulated maximal pepsinogen secretion to 57.0 +/- 2.5% and 73.1 +/- 3.1% of control, respectively. These results suggest that NaF activates a signal transducing mechanism which seems to be distinct from that activated by CCK, thereby inducing an increase in diacylglycerol accumulation, Ca3+ influx and pepsinogen secretion in guinea pig gastric chief cells.

Animals↗
PubMed1991

Characterization of cholecystokinin receptors on guinea pig gastric chief cell membranes.

The binding of cholecystokinin (CCK) to its receptors on guinea pig gastric chief cell membranes were characterized by the use of 125I-CCK-octapeptide (CCK8). At 30 degrees C optimal binding was obtained at acidic pH in the presence of Mg2+, while Na+ reduced the binding. In contrast to reports on pancreatic and brain CCK receptors, scatchard analysis of CCK binding to chief cell membranes revealed two classes of binding sites. Whereas, in the presence of a non-hydrolyzable GTP analog, GTP gamma S, only a low affinity site of CCK binding was observed. Chief cell receptors recognized CCK analogs, with an order of potency of: CCK8 greater than gastrin-I greater than CCK4. Although all CCK receptor antagonists tested (dibutyryl cyclic GMP, L-364718 and CR1409) inhibited labeled CCK binding to chief cell membranes, the relative potencies of these antagonists in terms of inhibiting labeled CCK binding were different from those observed in either pancreatic membranes or brain membranes. The results indicate, therefore, that on gastric chief cell membranes there exist specific CCK receptors, which are coupled to G protein. Furthermore, chief cell CCK receptors may be distinct from pancreatic or brain type CCK receptors.

Animals↗
PubMed1991

Sequence and expression of genes encoding the large and small subunits of ribulose 1,5-bisphosphate carboxylase/oxygenase from Chromatium vinosum.

A DNA fragment bearing genes for the large (rbcL) and small (rbcS) subunits of ribulose 1,5-bisphosphate carboxylase/oxygenase (RuBisCO) was cloned from the photosynthetic purple sulfur bacterium Chromatium vinosum. Enzymatically fully active RuBisCO was synthesized in Escherichia coli cells when the cloned DNA was placed downstream of tac promoter. Nucleotide (nt) sequences of rbcL-rbcS were more homologous to cyanobacterial counterparts than to those from Alcaligenes eutrophus or higher plants. However, the amino acid (aa) sequence in a domain responsible for CO2 activation in the C. vinosum rbcL product resembled the corresponding aa sequence in higher plant RuBisCos, but not in the cyanobacterial enzymes. Chemically determined aa sequences at the N terminals of both subunits of RuBisCO purified from C. vinosum were not identical to those deduced from the nt sequences, although they were completely the same as aa sequences deduced from rbcA-rbcB, another locus encoding RuBisCO in C. vinosum. Therefore, the rbcL-rbcS locus seems to be barely expressed under a standard condition for photoautotrophic growth. The homology of the nt sequences between rbcL and rbcA was 82%, and that between rbcS and rbcB was 63%, whereas the codon usages of these genes were basically identical. The rbcL-rbcS and rbcA-rbcB loci therefore must have evolved from a common ancestral set of genes after duplication, instead of lateral gene transfer.

Amino Acid Sequence↗
PubMed1991

Plasmin generation and fibrin(ogen)olysis following desmopressin infusion.

Desmopressin acetate (DDAVP) is known to stimulate the release of tissue-type plasminogen activator (t-PA) from endothelial cells, but it is unclear whether the increased t-PA actually elicits the plasmin generation and fibrin(ogen)olysis in the circulating blood. We measured plasma levels of plasmin-alpha 2-plasmin inhibitor complex, fibrinogen degradation products (FgDP) and fibrin degradation products (FbDP) following desmopressin infusion in 19 patients with bleeding disorders or thrombophilia. Administration of desmopressin (0.3-0.4 microgram/kg) produced a 4.0-fold increase in plasmin-alpha 2-plasmin inhibitor complex at 30 min, whereas neither FgDP nor FbDP was elevated significantly. These findings indicate that desmopressin infusion provokes the generation of plasmin in vivo, but most of the plasmin generated is complexed to alpha 2-plasmin inhibitor and does not degradate fibrin or fibrinogen.

Antifibrinolytic Agents↗
PubMed1991

Circulating thrombomodulin in thrombotic thrombocytopenic purpura.

Endothelial cell injury is thought to be one of the causative factors in thrombotic thrombocytopenic purpura (TTP). A novel index of endothelial injury, plasma thrombomodulin, was measured in 13 patients with acute TTP. The mean plasma concentration of thrombomodulin was elevated in patients with TTP (34.23 +/- 19.08 ng/ml) as compared with healthy subjects (16.99 +/- 2.63 ng/ml, P less than 0.001). Eight (61.5%) of 13 patients had high thrombomodulin values. Markedly elevated thrombomodulin levels were observed in TTP patients who had suffered from systemic lupus erythematosus, in whom plasma thrombomodulin was still elevated when they achieved remission. Five of these 13 patients with TTP had normal plasma levels of thrombomodulin. In addition, the plasma thrombomodulin concentrations were correlated well with von Willebrand factor antigen and tissue-type plasminogen activator antigen levels, both of which are released from stimulated or damaged endothelial cells. No difference was found in plasma thrombomodulin levels between patients who achieved remission and who did not. These findings suggest that the magnitude of the endothelial damage in TTP is variable among patients and that plasma thrombomodulin has limited clinical relevance to the severity of TTP.

Adult↗
PubMed1991

The inhibitory effect of anti-tumor drugs on phosphatidylcholine synthesis and its reversal by geranylgeranylacetone in the isolated guinea pig gastric glands.

To clarify the mechanism by which the administration of anti-tumor drugs, antibiotics or hypoglycemic agents causes gastric mucosal injury, the effects of these drugs on phosphatidylcholine synthesis in isolated guinea pig gastric glands were examined in vitro. Anti-tumor drugs such as tegafur, cyclophosphamide, and mitomycin C decreased [3H]choline incorporation into phosphatidylcholine. Furthermore, tegafur at 0.4 mg/ml decreased [3H]choline incorporation in the glands that had been pulsed with [3H]choline incorporation, suggesting that tegafur exerts its effect by inhibiting late step of phosphatidylcholine synthesis in the stomach. On the other hand, cefaclor and glibenclamide had no effect on [3H]choline incorporation. Geranylgeranylacetone, an anti-ulcer drug partially restored tegafur-induced reduction of [3H]choline incorporation into phosphatidylcholine. These results suggest that the anti-tumor drug-induced gastric mucosal injury may be due to drug-induced decrease in phosphatidylcholine synthesis, which the restoration of phosphatidylcholine synthesis by geranylgeranylacetone may explain its anti-ulcer action on drug-induced gastric mucosal lesions in vivo.

Animals↗
PubMed1991

Giant metastatic VIPoma in the liver.

A case of giant metastatic liver VIPoma manifesting WDHA syndrome is described. The patient was a 33-year-old Japanese male who was admitted because of persisting watery diarrhea and weight loss. Laboratory examinations revealed marked hypokalemia, mild hypercalcemia and highly elevated plasma vasoactive intestinal peptide (VIP) and glucagon levels. Intensive imaging examinations disclosed two large tumors in the liver but not in other organs, including the pancreas. Laparoscopy disclosed a slightly elevated purplish-colored large tumor on the surface of the apparently normal liver. At operation, however, a small hard nodule was observed in the tail of the pancreas. Histologically, it was revealed to be a VIPoma resembling a carcinoid or an islet cell tumor, and was identical to the liver tumors. Thus, this neoplasm was considered to be a VIPoma of pancreatic origin, with metastatic lesions in the liver.

Adult↗
PubMed1991

Ethanol stimulates pepsinogen release by opening a Ca2+ channel of guinea pig gastric chief cells.

To better understand the mechanism by which ethanol causes gastric mucosal injury, the effects of ethanol on isolated guinea pig gastric chief cells were investigated in vitro. Ethanol at 300-900 mmol/L dose-dependently stimulated an increase in pepsinogen release without affecting chief cells' viability. Ethanol stimulated an increase in initial Ca2+ influx rate and intracellular Ca2+ concentration at the same concentrations as it stimulated pepsinogen release, whereas it did not stimulate cyclic adenosine monophosphate accumulation. Pepsinogen release stimulated by 900 mmol/L ethanol was almost equal to that stimulated by 10(-8) mol/L COOH terminal octapeptide of cholecystokinin. Ethanol did not stimulate an increase in the accumulation of inositol trisphosphates and tetrakisphosphates in [3H]inositol-labeled chief cells, whereas cholecystokinin octapeptide caused a significant increase in inositol trisphosphates and tetrakisphosphates. Ethanol-stimulated pepsinogen release and increases in the initial Ca2+ influx rate and intracellular Ca2+ concentration were inhibited by 0.5 mmol/L La3+ or 1 mmol/L ethylene glycol tetraacetic acid but were not inhibited by nifedipine or verapamil. These results suggest that the effect of ethanol on pepsinogen release from the gastric chief cells may be due to its opening of a Ca2+ channel that is sensitive to La3+ and that the pepsinogen releasing action of ethanol may be one of factors for ethanol-induced gastric mucosal injury.

Animals↗
PubMed1991

Intrahepatic metastasis of hepatocellular carcinoma: a histopathologic study.

Developmental processes of intrahepatic metastasis were examined in 75 selected cases of hepatocellular carcinoma (HCC) arising in cirrhotic livers. According to their prevalent sites of formation, metastatic nodules were divided into the portal type (59 of 75, 78.7%) and the acinar type (16 of 75, 21.3%). In general the tumor histology was similar to that of primary lesions. The acinar type usually developed via coalescence of scattered tumor cell clusters formed within pseudolobules. In seven cases classified as acinar type, the nodules were composed of well-differentiated tumor cells which were arranged in trabeculae of almost normal thickness (normotrabecular subtype). In four out of these seven cases, the lesions could be clearly defined as metastatic. The subtype could not be determined when only a few discrete nodules were present, as in the remaining three cases. The nodules of the normotrabecular subtype tended to contain a central core of less-differentiated HCC in association with tumor growth, giving rise to a feature of nodule-in-nodule lesions. It is concluded that there do occur metastatic nodules showing well-differentiated, normotrabecular pattern and that these nodules are available for studying developmental steps of early HCCs.

Carcinoma, Hepatocellular↗
PubMed1991

Rationale for frequency and dose of administration in gestrinone therapy for pelvic endometriosis in the experimental model of rabbit uterus.

1. Gestrinone has been used for treatment of pelvic endometriosis, in doses of 2.5 mg twice a week. This study is designed to clarify it from the dynamics of sex steroid receptors in rabbit uterus. 2. Four different regimens were scheduled, namely daily 1 microgram estradiol-17 beta (E2, consistent with endogenous level of women) for 3 days, and together with either 30, 60 (consistent with 2.5 microgram of clinical dose) or 120 microgram(s) gestrinone, in single dose or with 20 microgram(s) gestrinone daily (divided dose in single 60 microgram(s) gestrinone administration) for 3 days. Receptors for estrogen (ER, type I and II) or progestin (PR) were determined by charcoal adsorption in cytosol and KCl extract, or sedimentation in non-KCl extractable fraction, using [3H]E2 or [3H]promegestone respectively. 3. Gestrinone decreased total ER (type I and II) levels, dose-dependently, except the case of 20 micrograms gestrinone daily in ER type II. Total ER type I level did not return to the pre-level until 3 days only after 120 microgram(s) gestrinone administration. Total ER type II level was decreasing in 3 days after 30, 60 or 120 micrograms gestrinone therapy. Total PR level was decreased in the order of strength: 120 micrograms gestrinone greater than 60 micrograms gestrinone greater than 30 microgram gestrinone greater than 20 micrograms gestrinone in group, and the recovery was not obtained until 72 hr only after 120 micrograms gestrinone therapy. The uterine weight was decreasing with the same strength in 3 days of the therapy independently upon the regimen. 4. In conclusion, gestrinone dose of 60 micrograms (2.5 mg of clinical dose) every 3 days is considered to be effective for anti-steroid action in sex steroid receptor dynamics in the rabbit uterus, contributing to the rationale for gestrinone treatment of pelvic endometriosis.

Animals↗
PubMed1991

Ferredoxin and ferredoxin-NADP reductase from photosynthetic and nonphotosynthetic tissues of tomato.

Ferredoxin and ferredoxin-NADP+ oxidoreductase (FNR) were purified from leaves, roots, and red and green pericarp of tomato (Lycopersicon esculentum, cv VFNT and cv Momotaro). Four different ferredoxins were identified on the basis of N-terminal amino acid sequence and charge. Ferredoxins I and II were the most prevalent forms in leaves and green pericarp, and ferredoxin III was the most prevalent in roots. Red pericarp of the VFNT cv yielded variable amounts of ferredoxins II and III plus a unique form, ferredoxin IV. Red pericarp of the Momotaro cv contained ferredoxins I, II, and IV. This represents the first demonstration of ferredoxin in a chromoplast-containing tissue. There were no major differences among the tomato ferredoxins in absorption spectrum or cytochrome c reduction activity. Two forms of FNR were present in tomato as judged by anion exchange chromatography and by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. FNR II had a lower apparent relative molecular weight, a slightly altered absorption spectrum, and a lower specific activity for cytochrome c reduction than FNR I. FNR II could be a partially degraded form of FNR I. The FNRs from the different tissues of tomato plants all showed diaphorase activity, with FNR II being more active than FNR I. The presence of ferredoxin and FNR in heterotrophic tissues of tomato is consistent with the existence of a nonphotosynthetic ferredoxin/FNR redox pathway to support the function of ferredoxin-dependent enzymes.

Amino Acid Sequence↗
PubMed1991

Shift in the megakaryocyte ploidy in MDS patients: microcytofluorometry with DAPI staining after destaining of Wright-Giemsa stain.

We applied DAPI (4',6-diamidino-2-phenylindole) staining to the determination of nuclear DNA content in single megakaryocytes in 12 normal subjects and 12 patients with myelodysplastic syndrome (MDS). After the megakaryocytes had been identified on Wright-Giemsa stained smear and classified according to modified Feinendegen's classification, they were photographed. Then Wright-Giemsa stain was removed by immersion in 50% ethanol at 37 degrees C for 1 h and 100% methanol at 37 degrees C for 1 h. The specimens were then stained with DAPI solution (DAPI 0.01 mg/ml, pH 7.4 Tris-EDTA-2Na buffer solution and 0.01 M 2-mercaptoethylamine hydrochloride mixed at the ratio of 0.5:98.5:1.0) for more than 30 min. The amount of nuclear DNA in the previously identified megakaryocytes was measured by microcytofluorometry. The maximum population of megakaryocytes ploidy was in 16N in normal subjects, 8N in 10/12 MDS patients, and 4N in the remaining two patients. These findings suggest impairment of the development of the megakaryocytes nucleus in the MDS patients.

Adolescent↗
PubMed1991

A study on driving status in 98 epileptic patients with driving licences.

As to the driving status in the period between January 1984 and December 1988, 98 epileptic patients with driving licences were examined, paying regard to their clinical conditions. Sixty-one (62%) of the patients were seizure-free for the last five years or more in December 1988. Eighty-one (83%) were actually driving motor vehicles at the time of this study, and 27 (33%) of the 81 drivers still had fits during the past five years. Nine patients (9%) had caused traffic accidents, but no accident had occurred due to seizures. The type of the nine accidents was as follows: One case of a slight physical injury to the other person, four cases of the driver's own car damage without other material damage, and four of the accidents involving other cars.

Accidents, Traffic↗
PubMed1991

Hemostatic alterations caused by ventricular assist devices for postcardiotomy heart failure.

The hemostatic alterations in two adult patients who were supported by left ventricular assist devices (LVADs) because of postcardiotomy heart failure were evaluated. In both patients, fibrinopeptide A and thrombin-antithrombin III complex increased markedly during the first several days, and thereafter decreased moderately but remained above normal over the entire procedure. Furthermore, fibrinopeptide B beta 15-42 and alpha 2 plasmin inhibitor-plasmin complex were also markedly increased over the entire course of LVAD treatment. These data show that the LVAD system strongly activates both the coagulation and the fibrinolytic system, even when thromboembolic or bleeding complications are not clinically evident. Furthermore, the decrease in physiological coagulation inhibitors, especially protein C, indicates that these factors are activated and consumed during LVAD treatment. Because protein C is important in regulating the coagulation cascade during LVAD treatment, exhaustion of this system might result in thromboembolic complications during LVAD treatment.

Aged↗
PubMed1991

Peritoneal fluid interleukin-1 beta and tumor necrosis factor in patients with benign gynecologic disease.

The levels of interleukin 1 beta (IL-1 beta) and tumor necrosis factor (TNF) in peritoneal fluid (PF-IL-1 beta and PF-TNF) and production of IL-1 beta and TNF by peritoneal macrophages were determined in patients with benign gynecologic disease. The level of PF-IL-1 beta was elevated in the acute pelvic inflammatory disease (PID) and stages I and II endometriosis (E I/II) groups compared with the normal pelvis group, but not in the myoma of the uterus, ovarian cyst, and postinflammatory pelvic adhesion groups. The level of PF-TNF was elevated in the PID, EI/II and stages III and IV endometriosis (EIII/IV) groups. There was no correlation between the levels of PF-IL-1 beta and PF-TNF. Neither the level of PF-IL-1 beta nor that of PF-TNF was correlated with the concentration of peritoneal macrophages. Peritoneal macrophages produced IL-1 beta and TNF in vitro in the absence of stimulants. The levels of PF-IL-1 beta and PF-TNF are presumably linked to the activation of peritoneal macrophages.

Adult↗
PubMed1991

Identification of methicillin-resistant strains of staphylococci by polymerase chain reaction.

A simple and reliable method using a polymerase chain reaction (PCR) was devised to identify methicillin-resistant staphylococci. By using lysates of the strain to be tested as templates and 22-mer oligonucleotides as primers, a 533-bp region of mecA, the structural gene of a low-affinity penicillin-binding protein (PBP 2'), was amplified by PCR and detected by agarose gel electrophoresis. Results obtained by this method were compared with those obtained by broth microdilution MIC determination for 210 and 100 clinical isolates of Staphylococcus aureus and coagulase-negative staphylococci, respectively. Of 99 mecA-negative S. aureus isolates, 100% of the strains were methicillin susceptible and 98% of the strains were oxacillin susceptible. Three strains (3%) of 111 mecA-positive S. aureus isolates exhibited almost the same susceptibility to beta-lactams as the mecA-negative ones and did not produce detectable amounts of PBP 2' despite the presence of the mecA gene. One of them yielded typically methicillin-resistant variants at a low frequency with concomitant recovery of PBP 2' production. The mecA gene was also found in coagulase-negative Staphylococcus epidermidis, Staphylococcus haemolyticus, Staphylococcus sciuri, Staphylococcus saprophyticus, and Staphylococcus caprae and conferred resistance on most of the bacteria.

Bacterial Proteins↗
PubMed1991

Different effects on oestrogen binding sites and anti-oestrogenic action of danazol and progesterone.

Rabbit uterus contains type I and II oestrogen binding sites in the cytosol, and nuclear fractions. Oestrogen-stimulated increase in uterine weight was inhibited by concurrent treatment with progesterone or danazol. Oestrogen-induced type I binding sites were decreased by progesterone and to a lesser extent by danazol, while oestrogen-induced type II sites were decreased almost equally in the two groups. Neither progesterone nor danazol alone caused any detectable changes in uterine weight. These findings may suggest that the anti-oestrogenic effect on uterine weight is more correlated with the change in type II binding sites of oestrogen than that in type I sites. Thus, danazol may exert anti-oestrogenic actions through a pathway independent from that of progesterone.

Animals↗