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Biomedical subjects

M Yamaguchi

Publications and source records attributed to M Yamaguchi.

At least 649 records · Page 36Linked to original sources
PubMed1997

[Hemodynamic effects of amrinone in children during cardiopulmonary bypass and postoperative 12 hours].

Hemodynamic effects of amrinone in children during cardiopulmonary bypass (CPB) and postoperative 12 hours were studied. In 10 patients undergoing open heart surgery, 1 mg/kg of amrinone was infused as the initial CPB dose and 5 - 10 micrograms/kg/min of amrinone was continuously administered as the maintenance dose during CPB and postoperative 12 hours. Amrinone levels ranged from 0.9 to 1.4 micrograms/ml during CPB and postoperative 12 hours. After infusion of amrinone, mean arterial blood pressure decreased significantly, but other parameters did not show remarkable change. The administration of amrinone during CPB showed enough vasodilating effect and decreased the need of conventionally used other vasodilators (nitroglycerin or prostaglandin E1). The postoperative course of 10 patients was clinically uneventful. The administration of amrinone in 10 patients did not produce thrombocytopenia compared with the control group (5 patients) in the postoperative period. In conclusion, the administration of amrinone during CPB and postoperative 12 hours in children was useful in producing enough vasodilating effect without major side effect.

Amrinone↗
PubMed1997

[Effects of aprotinin on blood loss reduction in children undergoing repair of tetralogy of Fallot].

The effect of aprotinin on the blood loss reduction was studied in children undergoing repair of tetralogy of Fallot. We administered aprotinin to consecutive 21 patients during the repair of tetralogy of Fallot and examined the blood loss and operative time in comparison with that in a control group of 20 patients. 30,000 KIU/kg of aprotinin was infused as the initial cardiopulmonary bypass (CPB) dose and 10,000 KIU/kg/hr was continuously administered as the maintenance dose during CPB. There was no resternotomy case due to bleeding and no operative death in both groups. Blood loss after CPB during operation and total blood loss during operation were significantly lower in aprotinin group than in control group. There were no differences between two groups in the volume of chest tube drainage in the postoperative 24 hours and the duration of chest tube drainage. Time from cessation of CPB to skin closure and total operative time were significantly shorter in aprotinin group than in control group. In conclusion, aprotinin was effective on the reduction of blood loss and the shortening of operative time in children undergoing repair of tetralogy of Fallot.

Aprotinin↗
PubMed1997

Superoxide generation in neutrophils from hepatic vein in patients undergoing hepatectomy.

The present study was carried out to determine whether neutrophils could be activated to increase superoxide and myeloperoxidase production during liver surgery in clinical settings. We measured superoxide production in polymorphonuclear leukocytes (PMNs) obtained from the radial artery and hepatic vein during hepatectomy. We also determined plasma myeloperoxidase (MPO) as a marker of activation of the neutrophil. Blood samples were obtained from radial artery and from hepatic vein before operation and immediately after hepatectomy. Superoxide generation in PMNs from radial artery showed no significant change during hepatectomy, while oxidant generation in PMNs from hepatic vein increased after hepatectomy (from 40.5 +/- 4.20 to 44.8 +/- 4.80 nmol/10(6) cells/30 min; p < 0.05). MPO in the plasma obtained from hepatic vein also increased significantly after hepatectomy (from 166.6 +/- 23.0 to 225.4 +/- 26.2 micrograms/L; p < 0.05). The results show that neutrophils are activated locally in the liver for enhanced release of superoxide during hepatectomy, suggesting that these oxidant species may be involved in post hepatectomy liver damage.

Adult↗
PubMed1996

The 5' end sequences and exon organization in rat regucalcin gene.

The 5'-flanking region of the gene for a Ca(2+)-binding protein regucalcin was cloned from a rat genomic library which was constructed in lambda EMBL3 SP6/T7 vector. The genomic library was screened by using the radiolabeled probe with the 5' region (0.5 kb) of rat regucalcin complementary deoxyribonucleic acid (cDNA). Positive clone had the 5.5 kb fragment which was hybridized with the 5'-probe. This fragment contained three exons (I-III) of the gene coding for a rat regucalcin. The nucleotide sequence of exons completely agreed with that of a rat regucalcin cDNA clone. A supposed translational initiation site existed in the exon II. Homology analysis showed that a putative transcription start site in the rat regucalcin gene was located at position 26 downstream from a TATA-box. Another upstream element, a CCAAT box-like sequence, was located at -170. Moreover, there were many regulatory elements (Hox, AP-1, AP-2 and AP-4) in the 5'-flanking region of the rat regucalcin gene. The organization of rat regucalcin gene seemed to be about 18 kb in size and consisted of seven exons and six introns.

Amino Acid Sequence↗
PubMed1996

Calcium-binding protein regucalcin inhibits deoxyribonucleic acid synthesis in the nuclei of regenerating rat liver.

The effect of regucalcin, a Ca(2+)-binding protein isolated from rat liver cytosol, on deoxyribonucleic acid (DNA) synthesis in the nuclei of regenerating rat liver was investigated. At 1 day after partial hepatectomy, the liver weight was increased about 50% of that of sham-operated rats, and it reached to the same levels as sham operation at 3 days after hepatectomy. Nuclear DNA synthesis was markedly increased at 1 day after hepatectomy, and this increase was also seen at 3 days. Nuclear DNA synthesis was clearly enhanced in the presence of EGTA (0.4 mM) in the incubation mixture. The presence of Ca2+ (1.0-25 microM) caused a significant decrease in the nuclear DNA synthesis of normal rat liver. Regucalcin (0.25 and 0.5 microM) clearly inhibited the nuclear DNA synthesis of normal rat liver. This inhibition was also seen in the presence of Ca2+ (1.0 microM). Moreover, in the liver nuclei obtained at 1 day after partial hepatectomy, the presence of regucalcin (0.05-0.5 microM) caused a remarkable inhibition of nuclear DNA synthesis. This effect was also revealed in the presence of EGTA (0.4 mM). Thus, the inhibitory effect of regucalcin was remarkable in regenerating rat liver nuclei in comparison with that of normal rat liver. The present results demonstrate that regucalcin can suppress nuclear DNA synthesis in regenerating rat liver. We suppose that regucalcin may have a role in the regulation of nuclear DNA synthesis in liver cell proliferation.

Animals↗
PubMed1996

Enhancement of plasma membrane (Ca(2+)-Mg2+)-ATPase activity in regenerating rat liver: involvement of endogenous activating protein regucalcin.

The alteration of (Ca(2+)-Mg2+)-ATPase activity in the plasma membranes of regenerating rat liver after a partial hepatectomy was investigated. Liver was surgically removed about two thirds of that of sham-operated rats. The reduced liver weight by partial hepatectomy was restored about 50% at 24 h after the surgery, and it was completely restored at 72 h. Regenerating liver significantly increased calcium content and plasma membrane (Ca(2+)-Mg2+)-ATPase activity between 12-48 h after hepatectomy. Those increases were maximum at 24 h after the surgery. The regenerating liver-induced increase in hepatic plasma membrane (Ca(2+)-Mg2+)-ATPase activity was completely abolished by the presence of anti-regucalcin IgG (1.0-4.0 micrograms/ml). The regenerating liver-induced increase in hepatic plasma membrane (Ca(2+)-Mg2+)-ATPase activity was clearly inhibited by N-ethylmaleimide (2.5 and 5.0 mM) addition into the enzyme reaction mixture. This NEM effect was also seen for the activatory effect with regucalcin (0.25 microM) addition on the enzyme activity in the plasma membranes from normal rat liver. The endogenous regucalcin may play a cell physiological role in the activation of the plasma membrane (Ca(2+)-Mg2+)-ATPase to maintain the intracellular calcium level in regenerating rat liver.

Animals↗
PubMed1996

Calcium-binding protein regucalcin mRNA expression in the kidney cortex is suppressed by saline ingestion in rats.

The effect of adrenalectomy (ADX) or saline ingestion, which is a hypertensive factor, on the expression of calcium-binding protein regucalcin mRNA in the kidney cortex of rats was investigated. The change of regucalcin mRNA levels was analyzed by Northern blotting using rat liver regucalcin complementary DNA (0.9 kb of open-reading frame). Regucalcin mRNA was expressed in the kidney cortex but not the medulla. Rats were adrenalectomized, and 48 h later they were sacrificed. ADX caused a reduction of regucalcin mRNA levels in the kidney cortex, suggesting that adrenal glands participate in the regulation of the mRNA expression. This reduction was not restored by the subcutaneous administration of dexamethasone with an effective dose (1 mg/kg body weight), which can stimulate kidney regucalcin mRNA expression. Regucalcin mRNA levels in the kidney cortex of rats were markedly suppressed by the ingestion of saline for 7 days. The ADX-induced decrease of renal cortex regucalcin mRNA levels was not appreciably restored by saline ingestion. Moreover, regucalcin mRNA levels in the kidney cortex of spontaneous hypertensive rats (SHR) were clearly decreased as compared with that of control (Wistar-Kyoto) rats. Meanwhile, calcium content in the kidney cortex was not significantly decreased by ADX or saline ingestion. The present study suggests that the expression of regucalcin mRNA in the kidney cortex of rats is suppressed by saline administration.

Adrenalectomy↗
PubMed1996

Hormone-induced apoptosis by Fas-nuclear receptor fusion proteins: novel biological tools for controlling apoptosis in vivo.

We have created fusion proteins between Fas and the ligand-binding domain of the estrogen or retinoic acid receptor. Murine fibrosarcoma L929 cells and human cervical carcinoma HeLa cells expressing the fusion proteins demonstrated apoptotic phenotypes in a tightly estrogen- or retinoic acid-dependent manner in vitro. Moreover, the fusion protein-expressing L929 cells transplanted into nude mice were also killed through apoptosis after injection of an estrogen agonist. This represents a novel system, "cell targeting," that can eliminate cells not only in vitro but also in vivo through the activation of a natural suicide machinery, i.e., apoptosis, by currently used hormones. This system implies wide applications not only in developmental biology and neurobiology but also in medicine, especially for cancer gene therapy.

Amino Acid Sequence↗
PubMed1996

Formation of crossline as a fluorescent advanced glycation end product in vitro and in vivo.

Crossline is one of the major advanced glycation end products resulting the reaction mixture of free amino group(s) such as epsilon-one in lysine with D-glucose in vitro. To study crossline formation on proteins in vitro and in vivo, polyclonal antiserum to the crossline hapten was prepared. This antiserum reacted with bovine and human serum albumin that had been modified by prolonged incubation with glucose as well as with crossline itself. Antisera did not react with unmodified serum albumin or the other Maillard-related compounds. Crossline was formed in a time-dependent manner when a mixture of six different proteins was incubated with glucose at pH 7.2 or 9.0. Crossline levels could be measured in rat lens proteins and the levels increased with age. The crossline content of lens proteins in diabetic rats was more than two-fold higher than that of age-matched controls. Results of this study suggest that most proteins containing advanced glycation end products have crossline-like structures. Measurement of crossline-like structures in biological specimens may provide an index of aging and of the development of diabetic complications.

Animals↗
PubMed1996

Role of ascorbic acid in the metabolism of S-nitroso-glutathione.

Although nitric oxide (NO) has been known to generate S-nitroso-thiols (RSNOs), dynamic aspects of their metabolism remain to be elucidated. The present work reports the reactivity of S-nitroso-glutathione (GS-NO) with various compounds with reducing activity. Kinetic analysis revealed that among various reagents tested, ascorbic acid showed a potent activity to decompose GS-NO to glutathione and oxidized products of NO. During the reaction of GS-NO and ascorbic acid, monodehydroascorbate was found to appear as an intermediate. These results suggest that ascorbic acid might be an important modulator for RS-NO metabolism.

Ascorbic Acid↗
PubMed1996

Role of cytokines in leukemic type growth of myelodysplastic CD34+ cells.

The clonal growth of progenitor cells from myelodysplastic syndromes (MDS) can be subdivided into four growth patterns: (1) normal, (2) no growth or low plating efficiency, (3) low colony and high cluster number, and (4) normal or high colony number with a large number of clusters. The former two (1 and 2) can be referred to as nonleukemic patterns and latter two (3 and 4) as leukemic. In a search for a role for cytokines in leukemic-type growth of MDS progenitor cells, marrow CD34+ cells were purified up to 94% for 8 normal individuals and 88% for 12 MDS patients, using monoclonal antibodies and immunomagnetic microspheres (MDS CD34+ cells). The purified CD34+ cells were cultured for 14 days with various combinations of cytokines, including recombinant human macrophage colony-stimulating factor (rM-CSF), granulocyte-CSF (rG-CSF), granulocyte-macrophage-CSF (rGM-CSF), interleukin-3 (rIL-3), and stem cell factor (SCF; a ligand for c-kit) in serum-free medium. The clonal growth of MDS CD34+ cells supported by a combination of all of the above cytokines was subdivided into the two patterns of leukemic or nonleukemic, and then the role of individual or combined cytokines in proliferation and differentiation of MDS CD34+ cells was analyzed in each group. Evidence we obtained showed that SCF plays a central role in the leukemic-type growth of MDS CD34+ cells and that G-CSF, GM-CSF; and/or IL-3 synergize with SCF to increase undifferentiated blast cell colonies and clusters over that seen in normal CD34+ cells. SCF is present in either normal or MDS plasma at a level of nanograms per milliliter, and this physiologic concentration of SCF can stimulate progenitor cells. This means that progenitor cells are continuously exposed to stimulation by SCF in vivo and that MDS leukemic cells have a growth advantage over normal blast cells. This depends, at least in part, on cytokines such as G-CSF, GM-CSF, IL-3, and SCF.

Acute Disease↗
PubMed1996

DNA replication-related elements cooperate to enhance promoter activity of the drosophila DNA polymerase alpha 73-kDa subunit gene.

An analysis was carried out on the promoter region of the Drosophila DNA polymerase alpha 73-kDa subunit gene and the factor(s) activating the promoter. Transcription initiation sites were newly identified in the region downstream of the previously determined sites. Full promoter activity resided within the region from -285 to +129 base pairs with respect to the newly determined major site. Within this region, we found three sequences identical or similar to the DNA replication-related element (DRE), 5'-TATCGATA, which is known as a common promoter-activating element for the Drosophila DNA polymerase alpha 180-kDa subunit gene and the proliferating cell nuclear antigen gene. These sites were located at positions -77 to -70 (DREalpha-I), -44 to -37 (DREalpha-II), and +3 to +10 (DREalpha-III). Footprinting analysis using the recombinant DRE-binding factor (DREF) or Kc cell nuclear extract demonstrated that DREF can bind to all three DRE-related sites. Introduction of mutation in even one of the three DRE-related sequences caused extensive reductions of the promoter activity and also the DREF-binding activity of the promoter-containing fragment. The results indicate that the three DREF-binding sites cooperate to enhance promoter activity of the DNA polymerase alpha 73-kDa subunit gene.

Animals↗
PubMed1996

Comprehensive care for hemophiliacs--activities of North Kyushu Hemophilia Center at the University Hospital of Occupational and Environmental Health, Japan.

One of our objectives in establishing the Hemophilia Center was to create a model of a total care system for chronic diseases which develop in the childhood and continue through adulthood. We also believe that the comprehensive medical care system should be introduced not only for the care of hemophiliacs but also for those with every chronic refractory disease. It may be a surprise that in a university hospital, which is likely to lack cooperation between departments, this kind of cross sectional support system, even extending to activities outside the hospital, has been continued. This success owes much to the understanding and consideration by successive Directors of the Hospital and the Professors (Directors) of every department, the enthusiastic efforts by members of the Center who have continued their volunteer work for the purpose of improving the QOL of patients, and the cooperation by students of the Volunteer Study Club. We also have to mention the advice and guidance by Dr. Minoru Inagaki (now at the National Children's Hospital) who established the first substantial hemophilia center in Ogikubo Hospital, and Dr. Kaneo Yamada, present Visiting Professor in the Faculty of Medicine, St. Marianna University. We would like to thank every one who has supported the activities of the Center. Finally, we strongly hope that this total care system will become popular among those responsible for caring of patients with other chronic refractory diseases.

Adolescent↗
PubMed1996

Zinc compounds inhibit osteoclast-like cell formation at the earlier stage of rat marrow culture but not osteoclast function.

The effect of zinc compounds on osteoclast-like cell formation in rat marrow culture in vitro was investigated. The bone marrow cells were cultured for 7 days in alpha-minimal essential medium containing a well-known bone resorbing hormone (1, 25-dihydroxyvitamin D3 and parathyroid hormone [1-34]). Osteoclast-like cell formation was estimated by staining for tartrate-resistant acid phosphatase (TRACP), a marker enzyme of osteoclasts. The presence of 1, 25-dihydroxyvitamin D3 (10(-8) M) or parathyroid hormone (PTH; 10(-8) M) induced a remarkable increase in osteoclast-like multinucleated cells (MNC). These increases were clearly inhibited by the presence of zinc sulfate or zinc-chelating dipeptide (beta-alanyl-L-histidinato zinc; AHZ) in the concentration range of 10(-7) to 10(-5) M. The inhibitory effect was seen at the earlier stage of osteoclast-like MNC formation. However, zinc compounds (10(-6) M) did not have an effect on PTH (10(-8) M)-induced osteoclast-like cell formation in the presence of EGTA (5 x 10(-4) M), dibucaine (10(-5) M) or staurosporine (10(-9) M). Moreover, when osteoclasts isolated from rat femoral-diaphyseal tissues were cultured for 24 h in the presence of zinc compounds (10(-7) to 10(-5) M), the compounds did not have an effect on cell numbers or lysosomal enzymes activity (acid phosphatase and beta-glucuronidase) in the cells. The present study clearly demonstrates that zinc compounds inhibit osteoclast-like cell formation at the earlier stage with differentiation of marrow cells.

Acid Phosphatase↗
PubMed1996

Characterization of calcium accumulation in the brain of rats administered orally calcium: the significance of energy-dependent mechanism.

The characterization of calcium accumulation in the brain of rats administered orally calcium chloride solution was investigated. Rats received a single oral administration of calcium (15-50 mg/100 g body weight), and they were sacrificed by bleeding between 15 and 120 min after the administration. The administration of calcium (50 mg/100 g) produced a significant increase in serum calcium concentration and a corresponding elevation of brain calcium content, indicating that the transport of calcium into the brain is associated with the elevation of serum calcium levels. The increase in brain calcium content by calcium administration was not appreciably altered by the pretreatment with Ca2+ channel blockers (verapamil or diltiazem with the doses of 1.5 and 3.0 mg/100 g). In thyroparathyroidectomized rats, the administration of calcium (50 mg/100 g) caused a significant increase in brain calcium content, indicating that calcium-regulating hormones do not participate in the brain calcium transport. Now, brain calcium content was clearly elevated by fasting (overnight), although serum calcium level was not significantly altered. Calcium administration to fasted rats induced a further elevation of brain calcium content as compared with that of control (fasted) rats. The fasting-induced increase in brain calcium content was appreciably restored by refeeding. This restoration was also seen by the oral administration of glucose (0.4 g/100 g) to fasted rats. The present study demonstrates that serum calcium is transported to brain, and that the increased brain calcium is released promptly. The release of calcium from brain may be involved in energy metabolism, and this release may be weakened by the reduction of glucose supply into brain. The finding suggests a physiological significance of energy-dependent mechanism in the regulation of brain calcium.

Animals↗
PubMed1996

Activatory effect of regucalcin on hepatic plasma membrane (Ca(2+)-Mg2+)-ATPase is impaired by liver injury with carbon tetrachloride administration in rats.

The alteration of the plasma membrane (Ca(2+)-Mg2+)-ATPase activity in the liver of rats administered orally carbon tetrachloride (CCl4) solution was investigated. Rats received a single oral administration of CCl4 (10, 25 and 50%, 1.0 ml/100 g body weight), and 3 or 24 h later they were sacrificed. CCl4 administration caused a remarkable elevation of liver calcium content and a corresponding increase in liver plasma membrane (Ca(2+)-Mg2+)-ATPase activity, indicating that the increased Ca2+ pump activity is partly involved in calcium accumulation in liver cells. Moreover, the participation in regucalcin, which is an intracellular activating factor on the enzyme, was examined by using anti-regucalcin IgG. The plasma membrane (Ca(2+)-Mg2+)-ATPase activity increased by CCl4 administration was not entirely inhibited by the presence of anti-regucalcin IgG (1.0 and 2.5 ug/ml) in the enzyme reaction mixture. However, the effect of regucalcin (0.25-1.0 uM) to activate (Ca(2+)-Mg2+)-ATPase in the liver plasma membranes of normal rats was not revealed in the liver plasma membranes obtained from CCl4-administered rats. Also, the effect of regucalcin was not seen when the plasma membranes were washed with 1.0 mM EGTA, indicating that the disappearance of regucalcin effect is not dependent on calcium binding to the plasma membranes due to liver calcium accumulation. Now, the presence of dithiothreitol (5 mM) or heparin (20 ug/ml) caused a remarkable elevation of the plasma membrane (Ca(2+)-Mg2+)-ATPase activity in the liver obtained from CCl4-administered rats. Thus, the regucalcin effect differed from that of dithiothreitol or heparin. The present study suggests that the impairment of regucalcin effect on Ca2+ pump activity in liver plasma membranes is partly contribute to hepatic calcium accumulation induced by liver injury with CCl4 administration.

Animals↗