Biomedical subjects

S Matsukawa

Publications and source records attributed to S Matsukawa.

At least 19 recordsLinked to original sources

PubMed1995

Increased nitric oxide biosynthesis in leukotoxin,9,10-epoxy-12-octadecenoate injured lung.

We measured effluent nitric oxide levels using a chemiluminescence method from leukotoxin (Lx, a linoleate epoxide) injured isolated rat lungs perfused with physiological salt solution. Nitric oxide production from Lx-injured lung promptly increased and lasted for 20 min. Pretreatment with NG-monomethyl-L-arginine (LNMMA) significantly suppressed Lx-induced production of nitric oxide. Effluent from control lungs showed trace levels of nitric oxide. The wet to dry lung weight (WLW/DLW) after termination of the experiments was significantly elevated in Lx-treated lungs compared with that of LNMMA pretreated lungs or control lungs. There was a correlation between nitric oxide levels (at 10 min) and lung edema (WLW/DLW). Thus, nitric oxide plays a role in the pathogenesis of Lx-induced lung injury.

Animals↗

PubMed1995

Leukotoxin, 9,10-epoxy-12-octadecenoate inhibits mitochondrial respiration of isolated perfused rat lung.

To investigate how mitochondrial function was affected in leukotoxin (Lx)-,9,10-epoxy-12-octadecenoate-induced lung injury, lung mitochondria were extracted from isolated perfused rat lung with or without Lx-induced edematous injury. In the lung treated with 30 mumol of Lx, the mitochondrial respiration rate in states 3 and 4 significantly decreased (without mitochondrial uncoupling) concomitantly with increased release of lactate dehydrogenase (LDH), a parameter for cellular damage, into the perfusate and decreased ATP content in the lung tissue compared with those of untreated lung. Moreover, 30 mumol of Lx resulted in significant inhibition of cytochrome-c oxidase activity (vs. vehicle control). In contrast, lower doses of Lx (10 mumol) caused lung edema and cellular damage without evidence for mitochondrial dysfunction. We also examined cellular and mitochondrial damage in hydrostatic lung edema. Such edema showed neither suppressed mitochondrial respiration nor elevated LDH activity in perfusate, although lung wet weight increased as much as it did after 30 mumol Lx treatment. Our results suggest that the ex vivo mitochondrial dysfunction is one of the secondary (vs. initial augmented permeability) but specific manifestations of toxicity of Lx, and together with the previous reports, the ex vivo damaging effect of Lx against mitochondria may be ascribed not to its direct action on mitochondria but to Lx-derived cellular mechanism(s).

Adenine Nucleotides↗

PubMed1995

Effect of ovarian steroid hormones and the presence of the fetus on oxytocin gene expression in the uterus.

Oxytocin (OT) is a neurohypophysial hormone with potent stimulating activity of the pregnant uterus, but its physiological role in parturition is still unclear. Recently, OT was found to be synthesized in the pregnant uterus, indicating that OT originating from the uterus, not from the posterior pituitary gland, may trigger the onset of labour. In order to define the factors responsible for the induction of uterine OT, the effect of ovarian steroid hormones and conceptus on the induction of OT mRNA in the rat uterus was examined by Northern and dot blot hybridization analysis. OT mRNA in the uterus started to increase on day 14 of pregnancy and showed very high levels at the time of parturition. Uterine OT mRNA was not altered by any steroid treatment, oestradiol-17 beta (0.2 microgram), progesterone (4 mg) or both in combination, for 6 days. The gravid horn of the uterus had 3.6-fold as much OT mRNA as the non-gravid horn on day 21 of pregnancy in hemipregnant rats with one ligated oviduct. The ovarian steroid hormones could not induce accumulation of OT mRNA in the uterus of ovariectomized rats, at least under the conditions used, but the presence of a conceptus may be critical for the very high levels of OT mRNA.

Animals↗

PubMed1994

Development of high-toughness resin for dental applications.

OBJECTIVES: The purpose of this study was to develop a heat-cured resin with improved toughness. Polyurethane dimethacrylate (PUDMA) with hard and soft segments in the chemical structure was synthesized using polyurethane diisocyanate and 2-HEMA. METHODS: The bulk polymerization of PUDMA, Bis-GMA, TEGDMA and MMA was carried out in a glass tube with 0.5 wt% of BPO at 60 degrees C for 24 h and 110 degrees C for 3 h. The physical and mechanical properties of these polymers were measured, i.e., the polymerization shrinkage, water sorption, transverse strength, modulus of elasticity, deflection and Knoop hardness of these polymerized methacrylates were determined. RESULTS: The volume shrinkage and the water sorption values of PUDMA were lower than those of Bis-GMA. The transverse strength and the modulus of elasticity of PUDMA were close to those of PMMA. The deflection of PUDMA, as determined by a bending test, was higher than any of the other cured resins tested. SIGNIFICANCE: These results suggest that PUDMA is an excellent toughened polymer. The fracture toughness of PUDMA is sufficient for crown and bridge resins and dental composites.

Acrylic Resins↗

PubMed1994

Immunohistochemical demonstration of thyrotropin (TSH)-receptor in normal and diseased human thyroid tissues using monoclonal antibody against recombinant human TSH-receptor protein.

We performed an immunohistochemical analysis of TSH-receptor in normal and diseased human thyroid tissues using a monoclonal antibody (T3-356) against the C terminal region of human TSH receptor. In normal human thyroid tissues, a positive staining was observed exclusively along the basal cell surface of the flattened follicular cells. In the tissues from adenomatous nodules, adenomas, and papillary carcinomas, a positive staining was also found along the basal cell surface of the follicular cells. In addition, a considerable cytoplasmic staining was observed. The apical and lateral cell surfaces of the follicular cells showed no staining. The foci of squamous cell metaplasia of papillary carcinomas, anaplastic carcinoma, and medullary carcinoma did not show a positive staining. In Graves' thyroids, the positive staining was also observed along the basal cell surface of the follicular cells. The staining was obviously intense in the Graves' thyroids, and the most intense staining was noted in the foci of papillary projection of the columnar follicular cells. These findings indicate that TSH receptor is preserved essentially in the basal cell surface of the thyroid follicular cells in neoplastic conditions and that the amount of TSH receptor protein is increased in Graves' thyroid.

Adenoma↗

PubMed1994

[Clinical meaning of 123I-MIBG myocardial SPeCT in patients with dilated cardiomyopathy].

MIBG-myocardial SPECT was performed on patients with dilated cardiomyopathy (DCM) undergoing treatment with beta blocker (Nipradilol). The findings of MIBG-myocardial SPECT were compared with the changes in cardiac function obtained by echocardiograms. The patients enrolled in the study were seven males who has been diagnosed as definitely suffering from DCM according to diagnostic guidelines provided by the Ministry of Health and Welfare. The patients were aged 57.5 +/- 10.2 years. Following intravenous administration of 111 MBq (3 mCi) of MIBG, myocardial SPECT was taken 20 minutes, and 4 hours later. The washout rate of the left ventricular wall was higher in the unchanged group (40.7 +/- 1.2%) than in the improved group (30.3 +/- 6.1%). Both the early and delayed images showed higher extent and severity scores for the unchanged group than for the improved group. A correlation of LVEF with the washout rates was demonstrated (r = -0.819, p < 0.05). A correlation was also observed between the variations in LVEF before and after beta blocker therapy with the washout rates (r = -0.969, p < 0.01), MIBG-myocardial SPECT suggested possibility of the evaluation of severity and prognosis in the patients with DCM.

3-Iodobenzylguanidine↗

PubMed1993

Induction of programmed cell death (apoptosis) by influenza virus infection in tissue culture cells.

The process of cell death caused by influenza virus infection in cultured MDCK and HeLa cells was analysed. This infection gave rise to nuclear fragmentation and chromatin condensation accompanied by chromosomal DNA fragmentation into oligonucleosomes. Chromosomal DNA fragmentation progressed concomitantly with cell lysis of MDCK cells and HeLa cells, producing high and low yields of virus particles, respectively, indicating that the extent of cell lysis was not proportional to the virus production. The endonuclease inhibitor zinc blocked DNA fragmentation in MDCK cells. Cycloheximide inhibited DNA fragmentation as well as cell lysis. Inhibition occurred when the drug was added to the medium within 2 h after infection but not efficiently at 4 h or later. Infection induced the Fas Ag gene, which encodes a possible apoptosis-mediating molecule, in the early infectious stage followed by the expression of Fas Ag on the cell surface. These results suggested that influenza virus infection causes apoptotic death of cultured cells, and their fate might be determined at an early stage of the infection by induction of an apoptotic gene.

Animals↗

PubMed1993

Pharmacokinetics of succinylcholine in man.

The pharmacokinetics of succinylcholine (SCh) 1 or 2 mg/kg was studied in 14 anesthetized patients. Arterial blood concentrations of SCh were measured using a high-performance liquid chromatographic assay. The arterial concentration vs. time data were analyzed by log-linear regression and fitted to an one-compartment model. The pharmacokinetic parameters were (SCh 1, n = 8 and 2 mg/kg, n = 6): apparent volume of distribution (16.4 +/- 14.7 and 5.6 +/- 6.8 ml/kg, mean +/- S.D.), total body clearance (40.5 +/- 38.7 and 15.0 +/- 14.8 liter/min), area under the plasma concentration-time curve (124.3 +/- 163.2 and 695.3 +/- 1008.9 min.micrograms/ml), and elimination half-life (16.6 +/- 4.8 and 11.7 +/- 4.5 sec). The rapid disappearance of SCh from the blood may be due to diffusion out of the blood vessel.

Adult↗

PubMed1993

[Effect of continuous intravenous administration of midazolam and ketamine on respiratory pattern].

The purpose of the study was to investigate the effect of continuous IV administration of midazolam and ketamine on respiratory pattern in six adult volunteers. Midazolam 0.05 mg/kg and ketamine 0.5 mg/kg were given, and then 0.1 mg/kg/hr for midazolam and 1 mg/kg/hr for ketamine were administered continuously. We measured MV, RR and TV (OMR86036), and calculated duty ratio and mean inspiratory flow at the level of 0 and 5 cmH2O CPAP during spontaneous respiration of air with and without 5% CO2. Each parameter was obtained before and 1 hr after the start of IV administration of the drugs. With 5% CO2, MV decreased significantly from 15.5 +/- 1.5 l/min to 11.7 +/- 0.8 l/min at 0 cmH2O CPAP level and from 15.8 +/- 1.8 l/min to 12.6 +/- 1.5 l/min at 5 cmH2O CPAP level, and also mean inspiratory flow decreased significantly from 590 +/- 2 ml/sec to 421 +/- 30 ml/sec at 0 cmH2O CPAP level and from 606 +/- 53 ml/sec to 477 +/- 48 ml/sec at 5 cmH2O CPAP level. TV decreased significantly during sedation at both CPAP levels with or without 5% CO2, while RR and duty ratio tended to increase. It was thought that, when the respiration was stimulated with 5% CO2, the decrease in mean inspiratory flow greatly contributed to the fall in MV during administration of midazolam and ketamine.

Adult↗

PubMed1992

Cervical cord birth injury and subsequent development of syringomyelia: a case report.

A 2830 g full-term baby, born by breech delivery, exhibited weak crying and sucking and severe hypotonia of the extremities after birth. Magnetic resonance imaging (MRI) showed marked thinning of the cervical cord at the level of C4 and C5. This lesion evolved into focal syringomyelia by the fourth month after birth. In this patient, MRI was useful in detecting the initial spinal cord injury, which appeared as marked thinning, and the subsequent syringomyelia as well. The role of birth trauma in cervical spinal cord injuries is discussed.

Birth Injuries↗

PubMed1992

Renal nerves contribute to salt-induced hypertension in sinoaortic-denervated uninephrectomized rabbits.

The objective of this study was to investigate the role of the renal nerves in the pathogenesis of salt-induced hypertension in sinoaortic-denervated uninephrectomized rabbits. Twelve rabbits were divided into two groups. Sinoaortic-denervated uninephrectomized rabbits with intact renal nerves (sham group: n = 6) and without renal nerves (RDN group; n = 6). In both groups, 2 days of 154 meq/l NaCl loading was followed by 10 days of 1,700 meq/l NaCl loading. We administered 154 meq/l or 1,700 meq/l NaCl intravenously at every 8 h. Serial changes in mean arterial pressure (MAP) and heart rate (HR) were recorded using a microcomputer system. We chronologically measured hematocrit, serum osmolality, serum sodium, potassium, and chloride concentration, serum creatinine, plasma renin activity, plasma aldosterone, plasma norepinephrine, plasma arginine vasopressin, and plasma atrial natriuretic peptide. Urine volume and body weight were recorded every day, as were urinary concentrations of sodium, potassium, and chloride. The basal value of MAP in the sham group was significantly higher than that in the RDN group (on day -2, 111 +/- 1 mmHg for sham, 99 +/- 2 for RDN, P less than 0.001). Hypertonic saline loading induced an elevation of blood pressure in the sham group (126 +/- 2 mmHg on day 4, 127 +/- 2 on day 7, 124 +/- 4 on day 10). There were no significant changes in the response to salt loading in the RDN group. In the sham group, the retention of sodium was significant compared with that in the RDN group on day 5, and this difference was maintained until the end of the experiments.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Immunohistochemical detection of c-myc products in colorectal cancer and proliferative cell rate.

Expression of c-myc protein was studied immunohistochemically in colorectal cancers using a monoclonal antibody, MYC-1. Immunoblotting assays with cellular lysates demonstrated a band of the gene products at the level of 60 kDa. c-myc-protein-positive tumor cells were observed in 43 (43.4%) of 99 specimens of colorectal cancers. There was no significant correlation between the incidence of MYC-1-positive tumors and clinicopathological findings. The rate of MYC-1 proteins occurring in patients with liver metastasis was significantly higher than that in patients without the metastasis. The rate of occurrence of DNA polymerase-alpha-positive cells in MYC-1 protein-positive tumors was significantly higher than in MYC-1 negative ones. The results suggested that MYC-1 immunoreactivity might possibly be a useful prognostic marker of colorectal cancers.

Adenocarcinoma↗

PubMed1991

Enhancement of the antitumor effect of glucose oxidase by combined administration of hydrogen peroxide decomposition inhibitors together with an oxygenated fluorocarbon.

Glucose oxidase (GO) catalyzes the conversion of beta-D-glucose and molecular oxygen to D-glucono-delta-lactone and H2O2. H2O2 produced by GO was effective in preventing tumor growth in mice bearing not only ascites tumor but also solid tumor. The effect of GO was enhanced by the combined administration of catalase inhibitors such as 3-aminotriazole, hydroxylamine and sodium azide or the GSH synthesis inhibitor buthionine-(S,R)-sulfoximine in vivo. The cytolytic activity of GO against T-24 cultured cells in vitro was also enhanced by addition of these inhibitors together with GO. In the peritoneal cavity of mice the antitumor effect of GO seemed to be dependent on the amount of oxygen released from oxygenated fluorocarbon-43 (FC-O2), an oxygen-supplying substance. Furthermore, the combined administration of H2O2-decomposing enzyme inhibitors and FC-O2 synergistically enhanced the antitumor effect of GO. These results suggest that GO is suitable for antitumor chemotherapy and that the use of inhibitors of H2O2-decomposing enzymes and FC-O2 potentiated the GO therapy.

Animals↗

PubMed1991

Role of endogenous angiotensin II in the control of vasopressin secretion during hypovolemia and hypotension in conscious rabbits.

In order to investigate the physiological role of angiotensin II (ANG II) in the control of vasopressin (VP) secretion, the VP responses to hypotension induced by hemorrhage (20 ml/kg, n = 10) or nitroprusside infusion (1-10 micrograms/kg.min, n = 9) were studied with or without blockade of ANG II formation by the converting enzyme inhibitor captopril in conscious rabbits. Administration of captopril (5 mg/kg, iv) caused a small decrease in mean arterial pressure but did not enhance the hypotensive response to subsequent hemorrhage or nitroprusside infusion. The renin response to both stimuli was enhanced by captopril, whereas the increase in plasma ANG II concentration was attenuated. Plasma VP (PAVP) concentration increased during hemorrhage (2.0 +/- 0.2-113.6 +/- 47.7 pg/ml, P less than 0.01) and nitroprusside infusion (2.1 +/- 0.3-5.1 +/- 1.0 pg/ml, P less than 0.01). Captopril did not change basal plasma PAVP, nor did it attenuate the VP responses to hemorrhage or nitroprusside. Indeed, captopril tended to enhance the VP responses to hemorrhage (2.3 +/- 0.3-147.1 +/- 65.9 pg/ml) and nitroprusside infusion (1.9 +/- 0.2-15.4 +/- 6.0 pg/ml). The relationship between log PAVP and mean arterial pressure during hemorrhage and nitroprusside infusion in the presence of captopril was not different than in the absence of captopril. These results indicate that in conscious rabbits, the renin-angiotensin system does not contribute to the increase in VP secretion during hypotension induced by hemorrhage or nitroprusside infusion.

Angiotensin II↗

PubMed1991

The role of sex hormones and sodium intake in postmenopausal hypertension.

To determine the role of sex hormones and sodium intake in hypertension seen in postmenopausal woman, 12 women (aged 50 to 59 years) in whom blood pressure increased for the first time to above 150/90 mmHg after cessation of menstruation were examined in comparison with 7 age-matched postmenopausal normotensive women (118 +/- 2/62 +/- 3 mmHg). All subjects were admitted to the hospital and their sodium intake was maintained at 204 (normal), 306 (high), and 51 (low) mmol/day for 5 days each. In each period, body weight, blood pressure, heart rate, serum levels of sex hormones and vasoactive hormones, and urinary excretions of sodium, kallikrein and dopamine were determined. The plasma levels of prolactin, progesterone, oestrone, and oestradiol in the hypertensive women were all significantly lower than those in the normotensive women in all study periods. With a change in sodium intake from high to low, blood pressure in 8 out of 12 hypertensive patients decreased by more than 10% from 160 +/- 2/100 +/- 2 mmHg to 144 +/- 2/87 +/- 2 mmHg, while in the normotensive women, only 1 out of 7 patients responded to this change in sodium intake. The changes in sodium intake did not alter the plasma levels of sex hormones in the hypertensive and normotensive subjects. Among the hypertensive patients, three had a history of pregnancy-induced hypertension, while none of the normotensive subjects had such a history. The results of the present study suggest that decreases in sex hormones and increased sensitivity to sodium are important factors in the genesis of postmenopausal hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗

PubMed1990

Active oxygen-mediated cytotoxic and antitumor actions of streptococcal cytotoxic protein.

Streptococcal cytotoxic protein (SCP), obtained from the cell-free extract of Streptococcus pyogenes, inhibited the uptake of [methyl-3H]thymidine by Ehrlich ascites carcinoma cells depending on the concentration of fetal calf serum (FCS) added to the culture medium. The same results were found using sera from different animals. The inhibitory activity of SCP was completely suppressed by catalase but not by hydroxyl radical scavengers or superoxide dismutase. The antitumor activity of SCP in tumor-bearing mice was inhibited by administration of catalase together with SCP. SCP enzymatically produced hydrogen peroxide in the presence of FCS as detected by the 2,2'-azino-di[3-ethyl-benzothiazoline-(6)-sulfonic acid]/horseradish peroxidase method. The kinetic parameters, Km and Vmax, for hydrogen peroxide production of SCP were 2.13% FCS and 0.53 nmol/min/micrograms SCP, respectively. These results indicate that SCP is an enzyme which produces hydrogen peroxide and exerts potent cytotoxic and antitumor effects using an active oxygen species, hydrogen peroxide, produced by the enzymatic reaction of SCP with an unknown substrate contained in FCS or sera from various animals and molecular oxygen.

Animals↗

PubMed1990

Flowcytometric analysis of DNA pattern of cells derived from xeroderma pigmentosum A--hypersensitivity to vincristine, etoposide and methotrexate.

Xeroderma pigmentosum complementation group A (XPA) is one of the DNA repair deficient syndromes. The cell biological features of XPA were examined by flowcytometry using Epstein Barr (EB) virus-transformed lymphoblastoid cells. Cellular sensitivity to vincristine (VCR), etoposide (VP-16) and methotrexate (MTX) were assayed by DNA pattern changes by flowcytometry. Recently, ataxia-telangiectasia (AT), one of the same kind of disorder, has been reported to have an increased sensitivity to VCR and VP-16. However, AT showed some resistance to MTX according to other reports. Our results showed that XPA had an increased sensitivity to VCR and also to VP-16. Moreover, different from AT, XPA showed some sensitivity to MTX. Thus there is some cell biological similarity between XPA and AT, as well as some difference of the abnormality in the DNA repair pathway.

Cell Line↗

PubMed1990

Role of renal nerves in regulation of vasopressin secretion and blood pressure in conscious rabbits.

The observation that electrical stimulation of the renal nerves increases vasopressin secretion raises the possibility that the renal nerves may participate in the control of vasopressin secretion. In the present investigation, the effects of renal denervation on the vasopressin response to two reflex stimuli (nitroprusside infusion and hemorrhage) and two osmotic stimuli (hypertonic saline infusion and water deprivation) were studied in conscious, chronically prepared rabbits. Nitroprusside infusion in 13 intact and 14 denervated rabbits caused similar decreases in mean arterial pressure (MAP) and the increase in plasma arginine vasopressin concentration (PAVP) in intact (2.6 +/- 0.3 to 5.8 +/- 0.9 pg/ml, P less than 0.01) and denervated (2.8 +/- 0.3 to 5.7 +/- 1.3 pg/ml, P less than 0.01) rabbits was not significantly different. Hemorrhage (20 ml/kg) in 15 intact and 14 denervated rabbits caused similar decreases in MAP. Again, the increase in PAVP from 2.7 +/- 0.3 to 159.0 +/- 37.1 pg/ml (P less than 0.01) in intact and from 5.0 +/- 1.7 to 115.4 +/- 45.6 pg/ml (P less than 0.01) in denervated rabbits was not significantly different, nor was the relationship between PAVP and MAP in the two groups. In seven intact rabbits, hypertonic saline infusion increased PAVP from 4.0 +/- 0.9 to 10.9 +/- 2.8 pg/ml (P less than 0.05). The change in six denervated rabbits was not significantly different, nor was the relationship between PAVP and plasma osmolality. During water deprivation (24 h) in six intact rabbits, PAVP increased from 4.0 +/- 0.7 to 6.9 +/- 0.6 pg/ml (P less than 0.05). Again, the increase in PAVP in six denervated rabbits was not significantly different from that in the intact rabbits. The change in MAP during water deprivation in the two groups was also not significantly different. Renal cortical norepinephrine concentration in denervated kidneys was less than 10 ng/g wet wt. These results indicate that, in conscious rabbits, renal denervation does not impair the osmotic or reflex regulation of vasopressin secretion, nor does it interfere with blood pressure regulation during hypovolemia or hypotension.

Animals↗