Biomedical subjects

K Wada

Publications and source records attributed to K Wada.

At least 577 records · Page 32Linked to original sources

PubMed1991

Control of growth and differentiation of the mammary gland by growth factors.

Mammary gland development is a complex process regulated by various steroid and polypeptide hormones. Although the systemic importance of hormones, such as estrogen, progesterone, prolactin, and growth hormone, in the growth of the mammary gland has been well documented, these hormones are virtually incapable of stimulating mammary cell growth in vitro. Thus, the growth stimuli for mammary cells requires clarification. In recent years, a number of growth factors have been discovered; this has prompted interest in examining possible involvement of these biologically active agents in the process of mammary gland development. Results presented herein indicate that several growth factors including epidermal growth factor, transforming growth factor alpha and beta, basic fibroblast growth factor, insulin-like growth factor-I, and mesenchyme-derived growth factor participate in the regulation of mammary cell growth and differentiation.

Animals↗

PubMed1991

[Protective effect of prostaglandin E2 on ethanol-induced injury of chief cells isolated from guinea pig].

The mechanism by which PGE2 directly protects individual gastric cells from ethanol-induced injury was studied by using isolated gastric chief cells from guinea pig. Ethanol dose-dependently caused chief cell injury which was estimated by the release of lactate dehydrogenase (LDH) from chief cells. Pretreatment of chief cells with PGE2 reduced the cell damage caused by ethanol in time- and dose-dependent manner. The pretreatment at 37 degrees C and pH 7.4 with PGE2 maximally reduced the cell damage. This protective effect was reduced when the pretreatment was performed at either acid or alkaline pH or at reduced temperature. PGE2 did not stimulate any increase in cytosolic free Ca2+ concentration and initial Ca2+ influx rate. On the other hand, PGE2 stimulated an increase of cAMP accumulation in chief cells. However, pretreatment of chief cells with secretion, VIP, dbcAMP or forskolin failed to reduce subsequent injury caused by ethanol. These results suggest that PGE2 may protect chief cells against ethanol-caused injury probably via PGE type receptors coupled to as yet unidentified signal in gastric chief cells.

Animals↗

PubMed1991

[A case of cerebral arteriovenous malformation revealed at repeated subcortical hematoma with initially normal angiogram].

An 18-year-old male admitted to our hospital suffered left temporal subcortical hemorrhage. No abnormality was demonstrated on carotid or vertebral angiography at that time. On the day following the onset, left frontotemporal craniotomy was performed and the subcortical hematoma was evacuated. No vascular malformation was found despite careful investigation. On 30th day after the onset, the repeat cerebral angiography was performed but failed to show any vascular abnormalities. After discharge he was in good health, and had had some follow up, CT were normal except for the hematoma cavity. Just two years after the first operation he suffered a second left temporal hemorrhage. Cerebral angiography was repeated and a temporal arteriovenous malformation (AVM) was found with feeding vessels from the M-1 and M-2 portion of the left middle cerebral artery and from the left anterior choroidal artery, and draining veins to vein of Rosenthal and the straight sinus. One month after the second hemorrhage, left frontotemporal craniotomy was performed and complete excision of the AVM was carried out. Only five cases of AVMs in patients with normal angiograms several years before have been reported previously in the literature. But there are no cases in which surgery has been performed. Differently to those cases, in this case it was investigated operatively whether there was a vascular abnormality at the first hemorrhage. We didn't think, however, that the AVM demonstrated at the second hemorrhage had developed spontaneously because there had been a hemorrhage of unknown origin previous to it. It was assumed that a small angiographically occult AVM connected to the hematoma cavity existed at the time of the first hemorrhage but it was too small to be found even during surgical procedure. Such an angiography occult AVM had been growing for two years, and its growth had probably been facilitated by the presence of the hematoma cavity left after the first operation.

Adult↗

PubMed1991

[Evaluation of clinical usefulness of a rapid quantitative measurement of D dimer (cross-linked fibrin degradation products)].

In order to evaluate precisely the fibrinolytic states in clinical disorders, plasma levels of D dimer (cross-linked fibrin degradation products) were measured by a newly developed, rapid quantitative method based on the latex photometric immunoassay in patients with hematological malignancies, diabetes mellitus, collagen disease, liver disease, thrombotic disease and disseminated intravascular coagulation (DIC). Plasma levels of D dimer were elevated in a variety of diseases, especially in DIC. Patients with hematological malignancies, liver disease and thrombotic disease also had relatively high levels of D dimer. On the whole, D dimer values were positively correlated with plasmin-alpha 2-plasmin inhibitor complex and thrombin-antithrombin III complex. In addition, plasma D dimer was measured during fibrinolytic therapy with urokinase or tissue-type plasminogen activator; its elevation was detected in some patients. These findings indicate that accelerated fibrinolysis is frequently observed in a variety of diseases, and that a rapid quantitative measurement of D dimer would be valuable for the precise assessment of fibrinolysis in these disease states.

Disseminated Intravascular Coagulation↗

PubMed1991

[Detection of methicillin-resistant Staphylococcus aureus by polymerase chain reaction].

The low-affinity penicillin-binding protein (PBP 2') is associated with methicillin-resistance of Staphylococcus aureus and its structural gene (mecA) not present in methicillin-susceptible S. aureus could be detected by the polymerase chain reaction (PCR) method, in which a 533 bp region of mecA was amplified and detected by agarose gel electrophoresis. Survey for the mecA gene in 210 clinical isolates of S. aureus revealed that, while there was a gross correlation between the presence of the mecA gene and the resistance level to beta-lactams, three strains of mecA (+) tested showed beta-lactam susceptibility similar to those of mecA (-) strains. These three strains did not produce a detectable amount of PBP 2' constitutively nor inducibly, which was the cause of their high susceptibility to beta-lactams. One of them yielded a typical methicillin-resistant variant at a low frequency with a concomitant recovery of PBP 2' production when the bacterial cells of high density were spread onto an agar plate containing 10 micrograms/ml of oxacillin. These findings suggested that typical methicillin resistant S. aureus occurred during chemotherapy with beta-lactam antibiotics even when resistant strains could not be detected by the susceptibility test and thus all mecA (+) strains including those with high susceptibility should be precisely detected.

Bacterial Proteins↗

PubMed1991

Effects of 3-methylsulphonyl-4,5,3',4'-tetrachlorobiphenyl and 7,8-benzoflavone on aryl hydrocarbon hydroxylase activity in Ah responsive and Ah nonresponsive strains of mice.

In general, C57BL/6NQdj (C57) and DBA/2JCrj (DBA) strains of mice are considered to be the aryl hydrocarbon (Ah) responsive and Ah nonresponsive strains of mice, respectively, which are determined by whether the hepatic aryl hydrocarbon hydroxylase (AHH) activity is enhanced (Ah responsive) or not (Ah nonresponsive) after the treatment of 3-methylcholanthrene (MC). In this study, first, we examined that the Ah responsiveness was systemically regulated in the lungs and kidneys as well as in the liver and observed its systemic control in these three organs in the two strains of mice. Then, we prepared the hepatic microsomes of the two strains of mice after the treatment of MC (42 mg/kg, once), 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, 20 micrograms/kg, 6 times) and 2,3,4,7,8-pentachlorodibenzofuran (PenCDF 60 micrograms/kg, 6 times) in order to investigate the effects of 3-methylsulphonyl-4,5,3',4'-tetrachlorobiphenyl (3-MSF-TCB, 1.5-45 micrograms/ml) and 7,8-benzoflavone (ANF, 1.4-42 micrograms/ml) on the respective hepatic microsomal AHH activities and the following results were obtained. 1. As compared with the control enzyme activity, TCDD-induced AHH activity was the highest, PenCDF-induced one the second and MC-induced the lowest in both strains of mice. The inductions of the enzyme activity by these chemicals were much more remarkable in the Ah responsive C57 strain than those in the Ah nonresponsive DBA strain. 2. 3-MSF-TCB and ANF enhanced or reduced the enzyme activity depending on both their concentrations and kinds of microsomes, namely, those prepared from untreated control mice and mice treated with MC, TCDD or PenCDF.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

[The effect of organochlorine compounds on the induction of sister chromatid exchanges in cultured human lymphocytes].

In this study, first, we investigated the effect of 7,8-benzoflavone (ANF), mitomycin C (MMC), a well-known genotoxic compound, and ANF plus MMC on the induction of sister chromatid exchanges (SCEs) in human whole-blood cultures. Second, we examined the effect of mixture of organochlorine compounds, which very resembled their contamination of healthy people in its composition, on the induction of SCEs in the same blood culture system in order to clarify their genotoxicity as a whole. The following results were obtained. 1. ANF and MMC significantly enhanced the number of SCEs/cell at the concentrations of 4 x 10(-5) M and 10(-8)M, respectively. When both of the compounds were simultaneously added in the blood cultures, their effects on the induction of SCEs seemed to be additive. 2. Without ANF in the blood culture system, namely, an usual system of the SCEs experiment, we could not find a dose-response relationship between the concentration of the mixture of organochlorine compounds and the induction of SCEs/cell. With ANF, however, we observed a fairly good dose-response relationship between them. 3. In the whole-blood culture system with ANF, we found significantly great number of SCEs/cell at the level of twenty times higher concentration of the organochlorine compounds than the ordinary level. According to the results described above and of our other studies, 50% effective concentration (EC50, about 2 SCEs/cell higher than control SCEs/cell) of the mixture was considered to be about 5 times greater level over the general one.(ABSTRACT TRUNCATED AT 250 WORDS)

Benzofurans↗

PubMed1991

[The inhibitory effect of cholecystokinin on phosphatidylcholine synthesis in isolated rat pancreatic acini].

The effects of cholecystokinin (CCK) and other pancreatic secretagogues on phosphatidylcholine (PC) synthesis were studied in isolated rat pancreatic acini. When acini were incubated with [3H] choline in the presence of 1 nM CCK-octapeptide (CCK8) for 60 min, the incorporations of [3H] choline to both water soluble choline metabolites and PC in acini were reduced by CCK8 to 74% and 41% of control, respectively. Pulse-chase study revealed that CCK reduced both the disappearance of phosphocholine and the synthesis of PC. Ca(2+)-mobilizing secretagogues such as carbamylcholine and Ca2+ ionophore A23187 also reduced PC synthesis to the same extent as CCK8. By contrast, neither cAMP-dependent secretagogues such as secretin and dibutyryl cAMP nor a phorbol ester had any effect on PC synthesis in acini. These results suggest that CCK inhibits PC synthesis by inducing both the reduction of choline uptake into acini and the inhibition of CTP: phosphocholine cytidylyltransferase activity. This hormonal regulation of PC synthesis via CDP-choline pathway appears to be mediated by Ca(2+)-dependent pathway but not by cAMP- or protein kinase C-dependent pathway.

Animals↗

PubMed1991

Changes in the prolactin response to thyrotropin-releasing hormone (TRH) throughout the proliferative phases in the ovulatory and anovulatory menstrual cycle.

This study was undertaken to determine the changes of prolactin (PRL) response to thyrotropin-releasing hormone (TRH) throughout the menstrual cycle. The infertile patients with normal ovulatory menstrual cycle and with normoprolactinemic anovulatory cycles were assigned to intravenous loading tests with TRH (0.5 mg) and gonadotropin-releasing hormone (Gn-RH)(0.1 mg) during the proliferative phase of the cycle. In normal ovulatory patients, the basal PRL and gonadotropin levels did not significantly vary, while the response to TRH was reduced to late proliferative phase, compared to early and mid-phases. The response of luteinizing hormone (LH), but not follicle-stimulating hormone (FSH) was approximately 2-fold higher in the late proliferative phase than in early or mid-phases. In patients with normal PRL and high LH (over 8 mIU/ml), both basal levels and responses to Gn-RH of the gonadotropins were higher than those in the normal ovulatory cycle, but PRL profiles was essentially equal to those in the late proliferative phase of normal cycle. No significant differences of basal and stimulated levels of gonadotropins and PRL were observed in patients with normal PRL and LH levels. Thus PRL response rather than basal level may be related to gonadotropin secretion and consequently menstrual cycle.

Adult↗

PubMed1991

[DNA analysis of resected pulmonary adenocarcinoma].

The nuclear DNA content was determined by flow cytometry (FCM) in 155 resected specimens (122 paraffin-embedded and 33 fresh frozen specimens) of primary adenocarcinoma of the lung obtained at our department during the 8 years from 1982 to July, 1990. Aneuploid patterns were observed in 106 specimens (68.4%), and the diploid patterns in 49 (31.6%). No difference was observed in the age, sex, or clinical stage between the two groups. As for the relationship of the presence or absence of vascular infiltration with the DNA index (DI) and the heterogeneity index score (HIS), the percent positivity of vascular infiltration was 38.1% in the group with 1 less than or equal to DI less than 1.5 but nearly twice higher at 63.6% in the group with 1.5 less than or equal to DI. The percent positivity of vascular infiltration was 29.4% in the group with HIS less than 100 but 62.5% in the group with 100 less than or equal to HIS. Concerning the relationship between the ploidy pattern and outcome, the 5-year survival rate was 28.0% in the aneuploidy group and 65.1% in the diploid group, the outcome being significantly poorer in the first group. Concerning the relationship between DI and outcome, the 5-year survival rate was 14.9% in the group with 1.5 less than or equal to DI as compared with 55.4% in the group with 1.0 less than or equal to DI less than 1.5. DNA analysis was made also in bronchoscopic brushing specimens to examine the possibility of preoperative evaluation of the prognosis of lung cancer.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenocarcinoma↗

PubMed1991

[Mitral prosthetic valve endocarditis diagnosed by transesophageal echocardiography--a surgical case report].

The patient was a 39-year-old female who had undergone mitral valve replacement 2 years previously. Staphylococcus epidermidis was detected on blood culture. Transesophageal echocardiography revealed vegetation attached to the left atrial site of the mitral prosthesis, whereas precordial echocardiography did not reveal any abnormal echo structure. The patient was performed an emergency operation, during which the echocardiographic finding was confirmed. We conclude that performance of transesophageal echocardiography is useful when clinical features suggest prosthetic valve endocarditis.

Adolescent↗

PubMed1991

[Acute unclassified leukemia with bone marrow necrosis].

Massive bone marrow necrosis was seen in a 42-year-old male with acute leukemia. In December, 1988, on admission, laboratory data revealed pancytopenia and a high level of serum LDH and ALKP. Bone marrow aspiration resulted in dry-tap and showed bone marrow necrosis in the bone marrow biopsy specimen. A bone marrow scintigraphy with 111In faintly visualized the bone marrow but visualized area was expanded in the extremities compared with normal subjects. The second bone marrow biopsy showed proliferation of blasts. In the middle of March, blasts began to appear in peripheral blood. The blasts were cytochemically negative for POX, Es, PAS, AcP, TdT and had surface markers CD3-, CD19-, CD33-, CD13-, LCA-, HLA-DR-. Even by investigation on rearrangement of the immunoglobulin heavy chain region, an origin of the blasts could not be determined. In April, the number of blasts in peripheral blood increased and hepatosplenomegaly developed rapidly. Therefore, he was put on the chemotherapy with vincristine and prednisolone, but he died of cerebral hemorrhage. The autopsy revealed widespread bone marrow necrosis. It has rarely been reported that massive bone marrow necrosis is found prior to the occurrence of acute unclassified leukemia.

Acute Disease↗

PubMed1991

[Characterization of muscarinic acetylcholine receptors in the isolated gastric chief cells from guinea pig].

The muscarinic receptor system involved in pepsinogen secretion from isolated guinea pig gastric chief cells was investigated by assessing the effect of muscarinic receptor antagonists on carbamylcholine (CCh)-induced pepsinogen secretion. CCh stimulated pepsinogen secretion in a dose dependent manner with the maximal and the half-maximal stimulatory concentrations at 10(-4) and 3 x 10(-6) M, respectively. Each of five different muscarinic receptor antagonists such as atropine, pirenzepine, 4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP), AF-DX116 and scopolamine reduced pepsinogen secretion stimulated by graded concentration of CCh, but did not alter the maximum secretion. The increase in concentration of each antagonist caused parallel rightward shift of the dose response curve to CCh. Schild analysis of the inhibition of CCh-induced pepsinogen secretion by the antagonists showed that pA2 values of atropine, scopolamine and 4-DAMP are 8.8, 9.2 and 9.0, respectively. On the other hand, pA2 values of pirenzepine and AF-DX116 are 6.5 and 5.9, respectively, suggesting that the muscarinic receptor mediating pepsinogen secretion from chief cells has a intermediate affinity for pirenzepine and a low affinity for AF-DX116. These results suggest that the muscarinic acetylcholine receptor mediating pepsinogen secretion from gastric chief cells is the M3 subtype.

Animals↗

PubMed1990

Antibodies to a C-terminal peptide of the rat brain glutamate receptor subunit, GluR-A, recognize a subpopulation of AMPA binding sites but not kainate sites.

Antibodies were made to a thirteen amino acid synthetic peptide corresponding to the C-terminal portion of the glutamate (glu) receptor, GluR-A. The immunoprecipitation of kainic acid (KA) and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) binding sites by the anti-peptide antibodies was studied using a detergent-solubilized preparation of rat brain membranes. Under these conditions a subpopulation of AMPA binding sites was recognized by the antibodies, but no KA binding sites were recognized. Scatchard analysis of this subpopulation of AMPA binding sites yields a curvilinear plot which fits a two-site model with dissociation constants of 4.6 and 323 nM. These studies show that the glu receptor complex, GluR-A, binds AMPA but not KA and suggest that (i) the binding sites for these two ligands reside on different proteins, and (ii) the KA receptor identified physiologically is not equivalent to the KA binding sites identified with 3H-labelled KA.

Amino Acid Sequence↗

PubMed1990

Novel forms of ferredoxin and ferredoxin-NADP reductase from spinach roots.

Ferredoxin and the enzyme catalyzing its reduction by NADPH, ferredoxin-NADP reductase (ferredoxin-NADP+ oxidoreductase or FNR), were found to be present in roots of spinach (Spinacia oleracea). Localization experiments with endosperm of germinating castor beans (Ricinus communis), a classical nonphotosynthetic tissue for cell fractionation studies, confirmed that ferredoxin and FNR are localized in the plastid fraction. Both proteins were purified from spinach roots and found to resemble their leaf counterparts in activity, spectral properties, and complex formation, but to differ in amino acid composition and amino terminal sequence. The results indicate that the primary structures of the FNR and ferredoxin of spinach roots differ from that of the corresponding leaf proteins. Together with earlier findings, the present results provide evidence that nonphotosynthetic plastids, including those of roots, are capable of reducing ferredoxin with heterotrophically generated NADPH.

Amino Acid Sequence↗

PubMed1990

Nerve growth factor rapidly induces expression of the 68-kDa neurofilament gene by posttranscriptional modification in PC12h-R cells.

We have isolated a subclonal cell line of PC12, PC12h-R, which is characterized by its rapid response to nerve growth factor (NGF) in extending its neurites. The mRNA levels of the 68-kDa neurofilament (NF-L) increased severalfold as early as 3 h after the addition of NGF, but this was not accompanied by an increase in the transcription rate. Analysis of the stabilities of 3.5- and 2.3-kilobase (kb) NF-L mRNAs using actinomycin D revealed that 2.3-kb mRNA was degraded much faster than the 3.5-kb species and that NGF apparently stabilized NF-L mRNAs. These results show that the NF-L gene can be regulated posttranscriptionally, a finding that may be important in responding to the acute demand for neurofilament syntheses.

Adrenal Gland Neoplasms↗

PubMed1990

Structure of the 68-kDa neurofilament gene and regulation of its expression.

The complete structure of the mouse 68-kDa neurofilament (NF-L) gene was elucidated. We cloned cDNAs corresponding to 3.5- and 2.3-kb NF-L mRNA, including their polyadenylation sites. Sequence analysis revealed that these NF-L mRNAs arose from the alternative use of two polyadenylation sites in exon 4. Promoter analysis using NF-L promoter-beta-galactosidase fusion plasmids determined regions responsible for its basic promoter activity, which were located between -328 and -36 base pairs from the transcription initiation site. These promoter fusion plasmids induced a significant level of beta-galactosidase in NF-nonproducing C6 cells as well as in NF-producing PC12h cells. The in vitro transcription assay using HeLa cell extract also showed that this promoter exhibited strong transcriptional activity. Little difference in NF-L mRNA stability was observed between the two cells. However, nuclear run-off assay revealed that the NF-L gene was not transcribed in NF-nonproducing C6 cells. These data suggest that the strong promoter activity of the NF-L gene is repressed in vivo at the transcription initiation level in a tissue-specific manner.

Animals↗

PubMed1990

Fibrinolysis and fibrinogenolysis in disseminated intravascular coagulation.

In order to assess precisely the fibrinolytic state in disseminated intravascular coagulation (DIC), plasma levels of fibrinogenolysis products (FgDP), fibrinolysis products (FbDP) and fibrinogenolysis plus fibrinolysis products (TDP) were measured with newly developed enzyme-linked immunosorbent assays based on monoclonal antibodies in 72 patients with DIC at presentation. Not only FbDP and TDP but also FgDP were markedly elevated in patients with DIC. When analyzed according to the underlying disease categories, the relative proportion of FgDP to TDP was high in patients with acute promyelocytic leukemia and vascular diseases, and it was the lowest in patients with sepsis. Correlation analysis revealed that plasma levels of FgDP correlated negatively with alpha 2-antiplasmin and positively with plasmin-alpha 2-antiplasmin complex (PAP) and a ratio of PAP to thrombin-antithrombin III complex (TAT). These findings indicate that besides fibrinolysis, fibrinogenolysis is markedly accelerated in the majority of the patients with DIC.

Disseminated Intravascular Coagulation↗