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Biomedical subjects

M Noda

Publications and source records attributed to M Noda.

At least 361 records · Page 20Linked to original sources
PubMed1995

Big insulin-like growth factor II-producing hepatocellular carcinoma associated with hypoglycemia.

A 76-year-old female with a hepatitis C virus (HCV)-related hepatocellular carcinoma (HCC) was hospitalized because of fasting hypoglycemia. Her sera contained a low concentration of immunoreactive insulin and insulin-like growth factor (IGF)-I, while the IGF-II level was normal. However, most of the IGF-II consisted of the high molecular weight form (big IGF-II). The tumor tissue contained fetal type of IGF-II mRNA (6.0 kb). Furthermore, we found that one of the four patients examined with HCV-related HCC had big IGF-II in serum. This indicates that non-islet cell tumor hypoglycemia (NICTH) in HCV-related HCC might be accompanied by production of big IGF-II by the tumor.

Aged↗
PubMed1995

[Effects of prostaglandin E1 (PGE1) on pulmonary hypertension and lung vascular remodeling in a rat monocrotaline model of human pulmonary hypertension].

Prostaglandin E1 (PGE1) has been shown to be a potent pulmonary vasodilator in humans and in many animals. The effects of PGE1 on the development of pulmonary hypertension and on pulmonary vascular remodeling were studied in a rat monocrotaline (MCT) model of human pulmonary hypertension. By 3 weeks after injection, MCT (80 mg/kg S.C.) had resulted in high values of mean pulmonary arterial pressure and of the ratio of right ventricular weight to left ventricle+septum weight (RV/LV+S). PGE1 inhibited the development of pulmonary hypertension (300 micrograms/kg) and right ventricular hypertrophy (300 and 100 micrograms/kg) induced by MCT. Three weeks after the injection, the media walls of pulmonary arteries in lungs from rats given MCT were significantly thicker than those from lungs of control rats. PGE1 (300, 100, and 30 micrograms/kg) resulted in significantly less of this morphologic change, in a dose-dependent manner. These results indicate that PGE1 inhibits the development of pulmonary hypertension associated with lung vascular thickening induced by MCT. PGE1 may be useful for the treatment of pulmonary hypertension in humans.

Alprostadil↗
PubMed1995

[Effect of adhesiveness of white blood cells on pulmonary vascular permeability and resistance].

We studied pulmonary vascular injury evoked by mechanically activated white blood cells (WBCs). In isolated perfused rat lungs, changes in pulmonary vascular resistance were measured, and a gravimetric method was used to measure the pulmonary vascular filtration coefficient, which was taken as an index of pulmonary vascular injury. WBCs were activated by gentle agitation in a glass container for 10 sec. The filtration coefficient was measured under baseline conditions, and then inactive or activated WBCs were added to the perfusate. The perfusion was stopped for 90 minutes and then the lungs were reperfused. The expression of CD18 on the surface of WBCs was measured by flow cytometry. The filtration coefficient and the pulmonary vascular resistance in lungs exposed to activated WBCs were about 2.5 times and 3.3 times higher, respectively, than those in the lungs exposed to inactive WBCs. These results indicate increases in resistance and in pulmonary vascular permeability. The results of flow cytometry indicated that the mechanical agitation increased the expression of CD18 on the surface of WBCs. In conclusion, WBCs in which adhesiveness has been increased can induce pulmonary vascular injury and can increase pulmonary vascular resistance.

Animals↗
PubMed1995

[Characteristics of early gastric cancer accompanied by lymph node metastasis].

We studied the phenotypic expression, DNA ploidy patterns and other clinico-pathological features of early gastric cancers accompanied by lymph node metastasis. Of 241 cases studied, 18 (7.5%) were lymph node-positive. Histologically, 4 were tub1, 7 tub2, 4 sig and 3 por. Seven of the 18 were differentiated type cancers with accompanying undifferentiated type cancer cells in a part of the cancer tissue. Mucin histochemistry showed that 15 of the 18 cancers were composed exclusively of gastric type cells, while the other 3 were composed of intestinal type cells. The incidence of gastric type cells in node-positive cancers was significantly higher (p < 0.05) than that in node-negative cancers. All node-positive mucosal cancers were composed mainly of gastric type cells. These findings indicate that there are many cancers which are originally gastric in type, and that gastric type cancers readily develop lymph node metastasis. On the other hand, a cytofluorometric study showed that 10 tumors were diploid and 8 were aneuploid. There was no statistically significant association between DNA ploidy patterns and the occurrence of lymph node metastasis.

Adult↗
PubMed1995

[Surgical treatment of lung cancer over 80 years of age: investigation from post operative complications].

Seventeen patients with lung cancer over 80 years were treated surgically from 1983 through 1993 in our department. Thirteen patients were male and four were female. The histology of the tumor was adenocarcinomas, squamous, large and small cell carcinomas, in 9, 6, 1 and 1 cases, respectively. More than single lobectomy was performed in each patient. Unilateral pulmonary occlusion test was applied in patients whose expected contralateral FEV1.0/BSA was less than 800 ml.m2, or expected residual FEV1.0/BSA was less than 850 ml.m-2. Postoperative cardiovascular complications, such as PAT, PAC, PVC or Af, were seen in 9 patients, respiratory problems, namely, sputa retention, retained secretions or atelectasis, in 7 patients. Blood chemistry and hematology were performed for about three weeks after operations, and found increases in serum transaminases, and leukocytosis. However, there were no operative death. We conclude that some patients over 80 years of age are candidates for surgery after careful cardiopulmonary preoperative evaluation.

Adenocarcinoma↗
PubMed1995

[Role of cyclooxygenase metabolites in the increase in pulmonary vascular permeability caused by mechanically activated white blood cells].

To study the role of cyclooxygenase metabolites in changes in the pulmonary vasculature induced by mechanically activated white blood cells (WBCs), the effects of activated and inactive WBCs, and of a cyclooxygenase inhibitor, were studied in isolated perfused lungs from Sprague-Dawley rats. WBCs were activated by gentle agitation in a glass container for 10s. Baseline measurements were made, and then activated or inactive WBCs were added to the perfusate. Perfusion was stopped for 90 minutes, and then started again. The effects of the cyclooxygenase inhibitor meclofenamate on the pulmonary vascular filtration coefficient and on pulmonary vascular resistance were also measured. In the group that received activated WBCs, the pulmonary vascular filtration coefficient and the pulmonary vascular resistance were about 2.5 times and 3.3 times higher, respectively, than those in the group that received inactive WBCs. However, this apparent increase in the filtration coefficient caused by activated WBCs was partly blocked by meclofenamate. Histological examination indicated that meclofenamate did not prevent the adhesion of WBCs to the pulmonary vascular endothelium. These date indicate that WBCs that have been made to adhere to vessel walls can induce pulmonary vascular injury via cyclooxygenase products.

Animals↗
PubMed1995

Ileoanal anastomosis and ileoanal canal anastomosis in Japan: comparative retrospective study.

A questionnaire survey of ten institutions in Japan revealed that restorative proctocolectomy accounted for 81.8% of the surgical procedures performed in patients with UC in the last 5 years (1989-1993); ileoanal anastomosis (IAA) and ileo-anal canal anastomosis (IACA) were performed in 63% and 33% of these patients, respectively. Comparison of the two series showed that IACA was technically simpler and yielded better continence, but that it entailed a potential risk of recurrence of the disease in the remaining anal canal mucosa. Although IACA seems to be a useful surgical option for UC, until the long-term outcome of the procedure can be elucidated. It may be better regarded as a very low variation of IRA rather than as an improved technical version of IAA.

Adult↗
PubMed1995

[Contribution of oxidative stress to pulmonary hypertension induced by chronic hypoxia].

Chronic hypoxia causes pulmonary hypertension and right ventricular hypertrophy associated with media wall thickening of pulmonary arteries in rats. Platelet-activating factor plays an important role in the pulmonary vascular remodeling induced by chronic hypoxia, and reactive oxygen species are involved in tissue injury induced by platelet activating factor. We therefore hypothesized that reactive oxygen species contribute to the pulmonary hypertension induced by chronic hypoxia, and examined the effect of N-acetyl-L-cysteine (NAC), a free radical scavenger and the precursor of glutathione sulfhydryl (GSH), on hypoxia-induced pulmonary hypertension. We used a chemiluminescence-HPLC assay to measure the levels of phosphatidylcholine hydroperoxide (PCOOH) in the rat lungs exposed to hypoxia. Three weeks of normobaric hypoxia (FiO2 = 0.1) with NAC significantly reduced pulmonary hypertension, right ventricular hypertrophy, and media wall thickening of the pulmonary arteries. NAC had no effect on the hematocrit of normoxic or chronically normobaric hypoxic rats. Lung PCOOH levels were significantly higher in the hypoxic rats than in the control rats, and those in the NAC-treated rats were significantly lower than those in the hypoxic rats that were not given NAC. Lung PCOOH levels were significantly higher in the hypoxic rats than in the control rats, and those in the NAC-treated rats were significantly lower than those in the hypoxic rats that were not given NAC. These results indicate that hypoxia induces oxidative stress in the lung tissue, and that oxidative stress may have a role in the development of pulmonary hypertension induced by chronic hypoxia in rats.

Acetylcysteine↗
PubMed1995

Heterogeneous expression of glycoprotein Ib, IX and V in platelets from two patients with Bernard-Soulier syndrome caused by different genetic abnormalities.

Bernard-Soulier syndrome (BSS) is a rare inherited bleeding disorder, which is caused by deficiency or decrease of the platelet GPIb/IX/V complex. Analysis of two patients with BSS by flow cytometry of the blood revealed different expression patterns of the components of the GPIb/IX/V complex. In case 1, GPIX was completely absent but residual amounts of GPIb alpha and GPV were detectable; in case 2, GPIb alpha was completely absent. We amplified the coding regions of GPIb alpha, GPIb beta, GPV, and GPIX from the patients' genomic DNA with the polymerase chain reaction (PCR) and sequenced the PCR products. in case 1, we identified a point mutation in the GPIX coding region that changes the codon for tryptophan-126 (TGG) to a nonsense codon (TGA). In case 2, we found a deletion of nucleotide within seven adenine repeats at the position of 1932 to 1938 in the coding region of GPIb alpha, which causes a frame shift that results in 58 altered amino acids and a premature stop codon. These genetic changes alter the transmembrane domain of GPIX or GPIb alpha and, therefore, would prevent proper insertion of the proteins in the plasma membrane. Thus, abnormality of a single component protein (GPIX or GPIb alpha) alters the assembly of the GPIb/IX/V complex and causes heterogeneous surface expression of GPIb alpha, GPV and GPIX.

Adult↗
PubMed1995

[Role of peptide leukotrienes in monocrotaline-induced lung disease].

Monocrotaline (MCT) causes lung inflammation and right ventricular hypertrophy associated with lung vascular thickening in rats. We hypothesized that peptide leukotrienes play a role in MCT-induced lung disease, and examined the effect of ONO 1078, a specific antagonist of LTC4, D4 and E4 receptors on MCT-induced right ventricular hypertrophy and on lung vascular thickening. Next, we measured leukotriene C4 (LTC4) levels in the lung tissue of MCT-treated rats. Within 3 weeks after the injection MCT had caused an increase in the ratio of right ventricular weight to left ventricle+septum weight (RV/(LV+S)) and an increase in media wall thickness of the muscular arteries of the lung. In rats given both ONO 1078 and MCT, these changes were significantly less severe than in rats given MCT only. The LTC4 levels in MCT-treated rats were significantly higher than in saline-treated control rats. These results indicate that this antagonist of peptide leukotriene receptors inhibits right ventricular hypertrophy induced by MCT, and suggest a role for peptide leukotrienes in the inflammatory process that contributes to lung vascular remodeling in MCT-treated rats.

Animals↗
PubMed1995

The recognition of DNA containing an AP site by E.coli endonuclease VI (exonuclease III).

The major apurinic/apyrimidinic (AP) DNA-repair endonuclease of Escherichia coli is the endonuclease VI (exonuclease III) protein. To elucidate the substrate specificity of the AP endonuclease, we used the double- and single-stranded oligo deoxyribonucleotides containing an AP residue such as 2-deoxyribosylformamide (1), 2-deoxyribose (2), 1,2-dideoxyribofuranose (3), and propanediol (4) as the substrate. The endonuclease VI cleaved the phosphodiester bond 5' at these AP sites of the duplexes. The endonucleolytic activity was not influenced by the kind of nucleotide residue on the opposite side of the AP site. Further, it was observed that the AP endonuclease cleaved single-stranded oligomers containing an AP site.

Base Sequence↗
PubMed1994

Membrane proteins with molecular masses of 88, 90 and 150 kDa are responsible for binding of human immunoglobulin G Fc fragment to the native cells of Mycoplasma salivarium.

Mycoplasma salivarium cells bound the Fc fragment of human immunoglobulin G. The activity was remarkably enhanced by Mn2+, but not by Mg2+ and Ca2+; significantly inhibited by D-mannose; and reduced by pronase treatment of the cells. About 90% of the cells treated with pronase were not disrupted. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of proteins of the cells treated with pronase indicated that proteins with molecular masses of 88, 90 and 150 kDa (88 kp, 90 kp and 150 kp) were specifically digested. The results presented suggest that 88 kp, 90 kp and 150 kp, located in the outer surface of the cell membrane, are responsible for the activity of the M. salivarium cells and interact with a carbohydrate-containing moiety (D-mannose) of the Fc fragment in a Mn(2+)-dependent manner.

Bacterial Outer Membrane Proteins↗
PubMed1994

Multiple receptor-like protein tyrosine phosphatases in the form of chondroitin sulfate proteoglycan.

The possibility that some of the brain proteoglycans are receptor-like protein tyrosine phosphatases (PTPases) was investigated. Membrane-bound proteoglycan fractions were prepared from the postnuclear membrane fraction of 8-day-old rat brain by DEAE ion-exchange chromatography and CsCl density gradient centrifugation. The isolated proteoglycan fractions showed high PTPase specific activities together with the typical PTPase characteristics. Renaturation experiments indicated that chondroitin sulfate proteoglycans with 380- and 170-kDa core proteins carried the PTPase activity. The proteoglycan with 380-kDa core protein was identified as RPTP beta/zeta bearing HNK-1 carbohydrate.

Animals↗
PubMed1994

HMG-X, a Xenopus gene encoding an HMG1 homolog, is abundantly expressed in the developing nervous system.

We used a PCR-based subtraction cloning procedure with Concanavalin A-treated and untreated animal caps from stage 9 Xenopus embryos to search for genes the expression of which is induced during neurogenesis. One of these genes was found to encode a homolog of mammalian HMG 1 and 2, hence named HMG-X. HMG-X mRNA was maternally transmitted, up-regulated in neuroectoderm-derived tissues throughout early development, and eventually down-regulated in all adult tissues examined except ovary. Our data suggest that we have identified a gene for a member of the HMG1/2 family that could have an important role in neurogenesis.

Amino Acid Sequence↗
PubMed1994

Activated Ki-Ras complements erythropoietin signaling in CTLL-2 cells, inducing tyrosine phosphorylation of a 160-kDa protein.

We have previously shown that expression of erythropoietin (EPO) receptor (EPOR) alone failed to confer EPO responsiveness on the interleukin 2-dependent T-cell line CTLL-2, whereas the introduction of the EPOR into interleukin 3-dependent pro-B-cell lines, such as BAF-B03, allowed the cells to proliferate in response to EPO. Here, we report that additional expression of v-Ki-Ras conferred EPO-dependent growth on CTLL-2 cells expressing the EPOR, with additional formation of a high-affinity EPOR. To investigate possible mechanisms of EPOR downstream signaling induced by v-Ki-Ras expression in these CTLL-2-derived cells, we carried out anti-phosphotyrosine immunoblot analysis of the EPOR complex immunoprecipitated with anti-EPOR antibody from lysates of cells with and without cytokine stimulation, revealing two 160-kDa and 130-kDa phosphotyrosyl proteins. An anti-JAK2 antibody did not react with these proteins, suggesting that they may represent cellular components involved in an EPO-EPOR signaling pathway induced by v-Ki-Ras. Similar phosphotyrosyl proteins were present among Friend erythroleukemia cell lines, in which the Friend virus gp55/EPOR complex on the cell surface constitutively sends signals for cell growth.

Cell Division↗
PubMed1994

Differentiation of HL-60 cells is promoted by H-toxin of Clostridium septicum.

H-toxin of Clostridium septicum potentiated dimethyl sulfoxide (DMSO)-induced differentiation of human promyelocytic leukemia HL-60 cells which were monitored by nuclear morphology and production of oxidative radicals. But, H-toxin did not induce differentiation of HL-60 cells in the absence of DMSO. These phenomena were not observed by staphylococcal leukocidin, a cytotoxin affecting to HL-60 cells. In HL-60 cells, ADP-ribosylation of 118, 93, 75 and 58 kDa membrane proteins was observed, but the ADP-ribosylation was not detected either in differentiated HL-60 cells by DMSO or in normal polymorphonuclear leukocytes of human. When the membranes of HL-60 cells were incubated with H-toxin, ADP-ribosylation of the membrane proteins was inhibited. Such suppressive effects on ADP-ribosylation were not observed by DMSO or staphylococcal leukocidin. These data suggest that inhibition of the ADP-ribosylation by H-toxin may play an important role in potentiation of DMSO-induced differentiation of HL-60 cells.

Adenosine Diphosphate Ribose↗
PubMed1994

Priming effect of hydroxyapatite on the chemiluminescence response in human polymorphonuclear leukocytes.

In order to determine whether hydroxyapatite modulates the response of polymorphonuclear leukocyte (PMN) to oxidative stimuli, human PMNs were incubated with a non-activating concentration (1 or 10 micrograms/ml) of hydroxyapatite prior to stimulation with N-formyl-methionyl-leucyl-phenylalanine (FMLP; 0.1 or 1 microM), phorbol 12-myristate 13-acetate (PMA; 100 pg/ml), sodium fluoride (50 microM), zymosan (1 microgram/ml), or the calcium ionophore A23187 (0.1 microM). Chemiluminescence was measured with an automatic microcomputer-controlled luminescence analyzer at 37 degrees C. Hydroxyapatite alone did not stimulate chemiluminescence at concentrations below 10 micrograms/ml. Levels 300-400% higher than 'stimulus only' controls without preincubation with hydroxyapatite have been recorded. This synergism between hydroxyapatite and subsequent stimuli reveals a new activity of hydroxyapatite and suggests that particulate material may prepare PMNs for an exaggerated inflammatory response to other phlogistic mediators. This is the first report demonstrating PMNs primed with particulate material.

Calcimycin↗