Biomedical subjects
N Matsuo
Publications and source records attributed to N Matsuo.
Transesophageal echocardiography for detection of mitral regurgitation due to papillary muscle rupture or dysfunction associated with acute myocardial infarction: a report of five cases.
Severe mitral regurgitation was associated with cardiogenic shock in five (0.8%) of 623 patients with acute myocardial infarction who were urgently admitted to the authors' hospitals between 1994 and 1996. The infarct was located in the inferior wall in four patients and in the inferoposterior wall in one patient. Severe mitral valve regurgitation occurred concurrently with cardiogenic shock between one and six days after the onset of myocardial infarction. A mitral regurgitant murmur was not audible in four of five patients. Similarly, mitral regurgitant Doppler signals were not detected in four patients by transthoracic echocardiographic examination, while transesophageal echocardiographic examination detected mitral regurgitant signals clearly in all patients. Thus, when cardiogenic shock is unexpectedly associated with inferior or inferoposterior wall acute myocardial infarction, severe mitral regurgitation should be suspected, even when a mitral regurgitant murmur is not audible. Furthermore, mitral regurgitant flow signals may not always be detected by transthoracic echocardiography. Thus, examination for mitral regurgitation by transesophageal echocardiography should be considered.
Bond strength of brackets cemented with light-cured glass-ionomer cements to contaminated enamel.
PURPOSE: To examine the effect of contamination on the bond strength of orthodontic brackets cemented with either a commercial (Fuji Ortho LC) or an experimental light-cured glass-ionomer cement to enamel, and the effect of etching times on the bond strength. MATERIALS & METHODS: Simulated metal brackets were applied with the cements to bond polished and etched (37% phosphoric acid) bovine enamel with and without contamination by water, human saliva, and blood. After 1-day water immersion, the shear bond strengths were measured. The fractured surfaces were examined using SEM. Additional tests were conducted on: (1) the Knoop hardness of the contaminated cements, (2) the HEMA composition of the cements, (3) the viscosity of the cements, and (4) the intensity of transmitted visible light through the contaminants. The results were compared by ANOVA and Duncan's tests at P=0.05. RESULTS: Water and saliva reduced the bond strength to polished and etched enamel, except for the bond strength of Fuji Ortho LC to polished enamel. The blood contamination produced poor bond strengths to polished and etched enamel. The experimental cement showed higher bond strengths to polished enamel with water and saliva contamination than Fuji Ortho LC. The bond strength of the experimental cement to etched enamel with and without contamination were comparable to those of Fuji Ortho LC. SEM micrographs revealed that the specimens exhibiting high bond strengths to polished and etched enamel mainly had cement-enamel interface failure and cement-metal mesh interface failure, respectively. Fuji Ortho LC had higher HEMA concentration than the experimental cement. The highest viscosity was measured with blood, followed by saliva and water. Blood contamination, showing the highest attenuation of the light intensity, reduced Knoop hardness of the experimental cement and Fuji Ortho LC.
Digynic triploid infant surviving for 46 days.
We report on a triploid infant who survived for 46 days. She had severe intrauterine growth retardation, relative macrocephaly, and a small, noncystic placenta, which are manifestations compatible with type II phenotype. Cultured amniotic fluid cells, skin fibroblasts, cord blood, and peripheral blood lymphocytes all showed a nonmosaic 69,XXX karyotype. Analysis of chromosomal heteromorphisms and microsatellite DNA polymorphisms in the infant and her parents indicated that the extra haploid set in the infant resulted from nondisjunction at maternal second meiosis. Postzygotic, mitotic nondisjunction was ruled out because of the presence of both homozygous and heterozygous markers of maternal origin. A search of the literature demonstrated five triploid infants, including the girl we described, who survived 4 weeks or more, and the parental origin of whose triploidy was studied: four were digynic and one was diandric. These findings support the notion that type II triploids are digynic in parental origin and that they survive longer than type I, diandric triploids.
Mammalian ELAV-like neuronal RNA-binding proteins HuB and HuC promote neuronal development in both the central and the peripheral nervous systems.
Hu proteins are mammalian embryonic lethal abnormal visual system (ELAV)-like neuronal RNA-binding proteins that contain three RNA recognition motifs. Although Drosophila ELAV is required for the correct differentiation and survival of neurons, the roles played by the Hu genes in the mammalian nervous system remain largely unknown. To explore the in vivo functions of mouse Hu proteins, we overexpressed them in rat pheochromocytoma PC12 cells, where they induced neuronal phenotype in the absence of nerve growth factor. We have characterized the functions of various forms of mHuB and mHuC bearing point mutations or deletions. Mutants of mHuC that had amino acid exchanges in the RNP1 domain of the first or second RNA recognition motifs (RRMs) lost biologic activity as well as RNA-binding activity. In addition, the mutants containing only the third RRM failed to induce the neuronal phenotype in PC12 cells and inhibited the biologic activity of cotransfected wild-type mHuB and mHuC, thus acting as a dominant-negative form. However, these mutants could not suppress the nerve growth factor-induced differentiation of PC12 cells. Further, we misexpressed wild-type and dominant-negative Hu in E9.5 mouse embryos, by using electroporation into the neural tube at the level of the rhombencephalon. mHuB and mHuC induced the ectopic expression of neuronal markers, whereas the dominant-negative forms of mHuB and mHuC suppressed the differentiation of central nervous system motor neurons. From these results, we suggest that Hu proteins are required for neuronal differentiation in the mammalian nervous system.
cDNA cloning and expression of human lactosylceramide synthase.
Lactosylceramide synthase is an enzyme that catalyzes the transfer of galactose from UDP-Gal to glucosylceramide, and thus participates in the biosynthesis of most glycolipids in mammals. We have isolated and sequenced the cDNA clone encoding human lactosylceramide synthase. The deduced amino acid sequence of the human lactosylceramide synthase showed 94.2% identity with rat lactosylceramide synthase. Northern blotting analysis revealed that lactosylceramide synthase mRNA was expressed in various tissues, with the highest level in brain and adrenal gland.
Treatment with a gonadotropin-releasing-hormone analog and attainment of full height potential in a male monozygotic twin with gonadotropin-releasing hormone-dependent precocious puberty.
UNLABELLED: We report on a pair of male monozygotic twins, one unaffected and the other affected with gonadotropin-releasing hormone (GnRH)-dependent precocious puberty, and discuss the role of treatment with a GnRH analog in the attainment of full height potential in GnRH-dependent precocious puberty. At 1.6 years of age, the affected twin was studied for tall stature (+3.8 SD), and was diagnosed as having GnRH-dependent precocious puberty due to a hypothalamic hamartoma of the tuber cinereum. He was treated with oral cyproterone acetate (110-170 mg/m(2) daily) from 1.8 through 5. 0 years of age, with oral cyproterone acetate and intranasal buserelin acetate (700-900 microg/m(2) daily) from 5.0 through 7.5 years, and with intranasal buserelin acetate alone (1100- 1400 microg/m(2) daily) from 7.5 through 12.6 years. He attained a final height of 171.0 cm at 14.9 years of age (+0.10 SD) and his twin 170. 0 cm at 15.3 years of age (-0.10 SD), with their target height being 174.5 +/- 9.0 cm. CONCLUSION: This study indicates that GnRH analog treatment may preserve near full height potential in some patients with GnRH-dependent precocious puberty.
White coat hypertension in two adolescents.
We describe two adolescent boys with white coat hypertension. Both patients had significantly high blood pressure documented on more than three occasions at clinic. No cause for hypertension or target organ damage was demonstrated. Twenty-four-hour mean ambulatory blood pressure values were normal for height and sex, which led to the diagnosis.
The role of intrapulmonary nitric oxide generation in the development of adult respiratory distress syndrome.
This study was conducted to investigate the role of nitric oxide (NO) in the development of adult respiratory distress syndrome (ARDS). An experimental model of endotoxemia-induced ARDS was prepared in guinea pigs and the following parameters were measured: pulmonary vascular permeability, the nitrate and nitrite concentrations in blood and bronchoalveolar lavage fluid (BALF), and the activities of constitutive and inducible NO synthase in lung tissue following the administration of lipopolysaccharide (LPS). Following the intravenous administration of 0.5 mg/kg LPS, the pulmonary vascular permeability increased, as did the concentrations of nitrate and nitrite in the BALF and blood. The activities of both constitutive and inducible NO synthase (NOS) increased significantly in the lung tissue 4 h after the intravenous administration of LPS, the constitutive form showing significantly higher activity than the inducible form. Furthermore, the increase of vascular permeability in the lungs after LPS injection was blocked by the subcutaneous administration of N(G)-monomethyl-l-arginine. These observations indicate that the intrapulmonary generation of NO may play an important role in the development of ARDS.
Structure-activity relationship of polyphenols on inhibition of chemical mediator release from rat peritoneal exudate cells.
The effect of phenolic compounds in foodstuffs on histamine and leukotriene B4 (LTB4) release from rat peritoneal exudate cells and their antioxidative activity were examined to assess their antiallergenic activities. Among them, triphenols such as pyrogallol and gallic acid inhibited histamine release from the cells, but diphenols did not. On the other hand, o- and p-diphenols such as catechol and hydroquinone with strong antioxidative activity inhibited LTB4 release as strongly as pyrogallol, but an m-derivative resorcinol with weak antioxidative activity did not. Though carboxylated compounds and their noncarboxylated counterparts were antioxidative, the former exerted a much weaker inhibitory effect on the LTB4 release than the latter. In flavonols, only myricetin with a triphenolic B ring strongly inhibited histamine release, but all flavonols strongly suppressed LTB4 release irrespective of the number of OH groups in the B ring. Among flavonoids with an o-diphenolic B ring, flavonol and flavone with a C4-carbonyl group strongly inhibited LTB4 release, whereas the activity of anthocyan without C4-carbonyl was much weaker than the above compounds. These results suggest that triphenolic structure is essential for the inhibition of histamine release. On the other hand, antioxidative activity and membrane permeability of phenolic compounds seemed to be essential for the inhibition of LTB4 release. In addition, the C4-carbonyl group seemed to be important for strongly inhibiting LTB4 release.
In vitro responses to antigen stimulation: comparison between human lung parenchyma resected from asthmatic patients and non-asthmatic patients.
BACKGROUND: The airway of asthmatic patients is hyperresponsive to various stimuli in vivo. There are, however, only a few reports that compared the in vivo responsiveness of asthmatic patients and non-asthmatic subjects to those of lung parenchyma in vitro. OBJECTIVES: To compare the contractile response, release of various chemical mediators, and responsiveness to drugs in samples of lung parenchyma excised from asthma patients with those of non-asthmatic subjects. METHODS: Human lung parenchymal strips were subjected to passive sensitization with sera of 5+ RAST titer to mites. The strip was suspended in a magnus bath containing a buffer solution. Parenchymal contraction was induced by PGF2 alpha. After washing, the baseline concentrations of thromboxane B2 (TXB2), leukotriene (LT), and histamine were measured in each bath and then contraction was induced by the addition of a mite antigen. The concentrations of TXB2, LT, and histamine were measured after contraction. The inhibitory effects of TXA2 synthetase inhibitor (DP-1904) and TXA2 receptor antagonist (AA-2414) were also evaluated in both tissue samples. RESULTS: There were no significant differences between lung parenchymal tissues of asthmatic and non-asthmatic patients with regard to PGF2 alpha-induced contraction, antigen-induced contraction, release of chemical mediators, and the response to drugs. CONCLUSION: Unlike the response in vivo, there are no differences in the response to stimuli in vitro between lung parenchymal tissues of asthmatic and non-asthmatic patients.
Sensitivity to the house dust mite and airway hyperresponsiveness in a young adult population.
BACKGROUND: The pathogenic mechanisms of airway hyperresponsiveness (AHR) in asthma are unknown and only a few studies have examined the importance of sensitivity to antigens in AHR in young adults. OBJECTIVE: We investigated the correlation between AHR and sensitivity to specific antigens, atopy, history of childhood asthma and spirometry in a young adult population. METHODS: Based on the results of interviews with 447 students at our university, 308 non-smoker students were classified into six groups. Group 1 comprised subjects with intermittent mild bronchial asthma; group 2, subjects with history of childhood asthma; group 3, subjects with atopic disease, and a RAST score for Dermatophagoides farinae (Def) of > or = 2; group 4, normal subjects with a RAST score for Def of > or = 2; group 5, subjects with cedar pollinosis; and group 6, normal subjects. We measured AHR to methacholine (MCh), spirometry, immunoglobulin E-radioimmunosorbent test (IgE-RIST), IgE-radioallergosorbent test to six common antigens, eosinophil cationic protein (ECP), and eosinophil count in peripheral blood in each subject. RESULTS: Airway hyperresponsiveness to MCh did not correlate with IgE-RIST, eosinophil count, or ECP. The highest AHR to MCh was present in groups 1 and 2 and lowest in groups 5 and 6. Multiple regression analysis showed that sensitivity to Def was the only factor that significantly influenced AHR to MCh. Airway hyperresponsiveness to MCh of groups with a RAST score for Def of 0/1 was lower than groups with a RAST score of 2 to 6. Airway hyperresponsiveness to MCh did not correlate with the degree of positivity to Def antigen among positive sensitized groups (RAST score 2 to 6). CONCLUSIONS: Sensitivity to mite antigen may be important in the pathogenesis of AHR and Def is a major contributing antigen in young adults in Japan. Once asthma occurs, AHR remains positive for a long time even after the disappearance of asthma-related symptoms.
Corticosteroid resistance in mild asthma: markers of persistent inflammation.
BACKGROUND: Bronchial hyperresponsiveness (BHR) is an important feature of asthma. Glucocorticosteroids (GCS) reduce BHR, probably by suppressing allergic inflammation. There are, however, two groups of asthmatics with either GCS-responsive or non-responsive BHR to methacholine. We investigated the mechanism of non-GCS-responsive BHR in mild asthma. METHODS: Non-GCS-responsive BHR asthma was defined as failure of reduction of BHR to methacholine after a 2-week course of oral prednisolone (30 mg/day). The expression of interleukin (IL)-4, IL-5, IFN-gamma mRNA in peripheral blood mononuclear cells, eosinophil count, serum cortisol, eosinophilic cationic protein (ECP), and spirometry were measured in five non-GCS-responsive BHR asthmatics and six patients with GCS-responsive BHR asthma before and after prednisolone therapy. RESULTS: With the exception of serum ECP and expression of IL-5 mRNA, no significant differences were observed between GCS-responsive BHR and non-GCS-responsive BHR asthma. The mean ECP level was significantly higher in non-GCS-responsive BHR than in GCS-responsive BHR asthma before and after prednisolone therapy. Interleukin-5 mRNA was detected in all asthmatics before prednisolone therapy; however, after prednisolone therapy, IL-5 mRNA was only detected in non-GCS-responsive BHR asthmatics. CONCLUSIONS: Our findings suggest that activation of eosinophils appears to persist in some asthmatics with non-GCS-responsive BHR due to continuous IL-5 production by lymphocytes.
Sodium cromoglycate inhibits antigen-induced cytokine production by peripheral blood mononuclear cells from atopic asthmatics in vitro.
BACKGROUND: Several anti-allergic anti-inflammatory drugs are used for the treatment of asthma including glucocorticosteroids (GCS), sodium cromoglycate (SCG), leukotriene (LT) inhibitors, and LT receptor antagonists. The major mechanism of the anti-inflammatory action of GCS is inhibition of cytokine production by T-lymphocytes: however, the mechanisms of anti-inflammatory effects of SCG are still unclear. OBJECTIVE: We elucidated the anti-inflammatory effects of SCG by investigating its effects on cytokine production by peripheral blood mononuclear cells (PBMCs) obtained from atopic asthmatics. METHODS: Peripheral blood mononuclear cells were obtained from seven atopic asthmatics and sensitized with Dermatophagoides farinae (DJ) or concanavalin A (ConA). We compared the effects of SCG on interleukin (IL)-5 and interferon (IFN)-gamma production by sensitized PBMCs with that of dexamethasone (Dex). Based on their clinical concentrations, we compared the effects of 10(-6) to 10(-4) M of SCG to those of 10(-6) M Dex. RESULTS: Stimulation with ConA increased the production of IL-5 and IFN-gamma. Dex significantly inhibited the production of both cytokines but SCG showed no inhibitory effects. On the other hand, Df stimulation increased IL-5 production only. Dermatophagoides farinae-induced overproduction of IL-5 was inhibited by SCG and Dex. CONCLUSIONS: Our results suggested that SCG has antigen-specific anti-allergic inflammatory effects.
Effect of contamination and etching on enamel bond strength of new light-cured glass ionomer cements.
The effect of water and saliva contamination on the bond strength of metal orthodontic brackets cemented to etched (10% polyacrylic acid) and unetched human premolar enamel was investigated. Two bonding agents were used: one commercially available product (LC) and one experimental (EX) light-cured glass ionomer. Shear bond strength was measured after aging for 5 minutes, 15 minutes, and 24 hours. The results were compared by ANOVA and Scheffe's tests at p = 0.05. For LC, the bond strength of brackets bonded to etched enamel, with and without contamination, was statistically higher than that of brackets bonded to unetched enamel for all aging times. An exception was the bond strength to unetched enamel with saliva contamination after 24 hours; for EX, this value was statistically higher than that measured on unetched enamel with water contamination. Contamination by saliva did not reduce bond strength to unetched enamel. For both etched and unetched enamel, there was no significant difference between LC and EX after 24 hours for all contamination conditions.
Molecular defects in achondroplasia and the effects of growth hormone treatment.
Achondroplasia is a common skeletal dysplasia with severe growth retardation. Recently, mutations in the fibroblast growth factor receptor 3 (FGFR3) were identified in patients with achondroplasia. In the present study, 70 of 75 Japanese patients with achondroplasia were found to have a G1138A mutation in FGFR3, and two patients had a G1138C mutation. Growth hormone therapy was given to 145 patients with achondroplasia. Significant dose-dependent effects on skeletal growth were obtained, with no long-term adverse effects.
Skeletal features and growth patterns in 14 patients with haploinsufficiency of SHOX: implications for the development of Turner syndrome.
We report on clinical features in 14 Japanese patients (4 males and 10 females) with partial monosomy of the short arm pseudoautosomal region involving SHOX (n = 11) or total monosomy of the pseudoautosomal region with no involvement of disease genes on the sex-differential regions (n = 3). Skeletal assessment showed that three patients had no discernible skeletal abnormalities, one patient exhibited short 4th metacarpals and borderline cubitus valgus, and the remaining 10 patients had Madelung deformity and/or mesomelia characteristic of Léri-Weill dyschondrosteosis (LWD), together with short 4th metacarpals and/or cubitus valgus. Skeletal lesions were more severe in females and became obvious with age. Growth evaluation revealed that patients without LWD grew along by the -2 SD growth curve before puberty and showed a normal or exaggerated pubertal growth spurt, whereas those with LWD grew along by the standard growth curves before puberty but exhibited an attenuated pubertal growth spurt and resultant short stature. Maturational assessment indicated a tendency of relatively early maturation in patients with LWD. There was no correlation between the clinical phenotype and the deletion size. These findings suggest that haploinsufficiency of SHOX causes not only short stature but also Turner skeletal anomalies (such as short 4th metacarpals, cubitus valgus, and LWD) and that growth pattern is primarily dependent on the presence or absence of LWD. Because skeletal lesions have occurred in a female-dominant and age-influenced fashion, it is inferred that estrogens exert a maturational effect on skeletal tissues that are susceptible to premature fusion of growth plates because of haploinsufficiency of SHOX, facilitating the development of skeletal lesions.
Structure and sequence of the mouse V1a and V1b vasopressin receptor genes.
The structural organization and 5'-flanking region of the mouse V1a and V1b vasopressin receptor genes were determined. The mouse V1a receptor gene was located within an 8-kb XbaI fragment, and the mouse V1b receptor gene was located within a 14-kb EcoRV fragment. Both genes were comprised of two coding exons that were separated by a 2.3-kb and a 8.0-kb intron, respectively, located before the respective seventh transmembrane domain of the receptor sequence. The availability of these genes would allow us to study the functional role of V1a and V1b receptors by disrupting the gene in mice.