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Biomedical subjects

Y Takeyama

Publications and source records attributed to Y Takeyama.

At least 73 records · Page 4Linked to original sources
PubMed1994

A family with pericentric inversion of chromosome 12.

A heterozygous pericentric inversion of chromosome 12 (inv(12)) was prenatally diagnosed. The breakpoints were localized to p12.3 and q14, resulting in more than one-third of the total length of the chromosome being inverted. The inversions was transmitted from the father whose phenotype was completely normal. The newborn also showed normal phenotype and grew without any clinical problems. The parents had no history of infertility. Based on these facts, it is indicated that pericentric inv(12)(p12.3q14) does not affect phenotype.

Adult↗
PubMed1994

Small vessel pathology and coronary hemodynamics in patients with microvascular angina.

We studied the ultrastructure of cardiac myocytes and small blood vessels obtained by endomyocardial biopsy from 21 patients with microvascular angina. Ischemic ST segment depression during atrial pacing was recognised in all the patients who had normal coronary arteriograms and biopsy tissues were examined by light and electron microscopy. In patients with microvascular angina, insufficient increases in coronary sinus blood flow and in myocardial oxygen consumption measured with a Webster's catheter were apparent during atrial pacing. Biopsy samples under the light microscope showed evidence of myocardial hypertrophy and sclerosis of small arteries and arterioles with perivascular fibrosis in 18 of 19 (95%) patients. Electron microscopy revealed that many endothelial nuclei in capillaries were swollen and that lumina of small arteries and arterioles were irregularly narrowed with proliferated and deformed medial smooth muscle cells. These findings suggest that disturbances in the coronary microcirculation in these patients is responsible for the ischemic changes in electrocardiograms.

Aged↗
PubMed1994

Atrial and brain natriuretic peptides in cardiovascular diseases.

The human heart secretes both atrial natriuretic peptide and brain natriuretic peptide. This study attempts to clarify the pathophysiological significance of the peptides in cardiovascular diseases. Using immunoradiometric assay, plasma brain natriuretic peptide and atrial natriuretic peptide levels in essential hypertension, various secondary hypertension, chronic renal failure, chronic heart failure during cardiac pacing, and acute myocardial infarction were determined. Mean plasma brain natriuretic peptide and atrial natriuretic peptide levels in healthy subjects were 3.7 +/- 0.3 and 5.7 +/- 0.3 pmol/L, respectively, and increased as a function of age. Plasma brain natriuretic peptide levels showed a larger increase than atrial natriuretic peptide levels in various cardiovascular diseases. In chronic renal failure, whereas plasma atrial natriuretic peptide levels decreased significantly after hemodialysis and were correlated with the changes in body weight, changes in plasma brain natriuretic peptide levels were less prominent and did not show such a correlation. In chronic heart failure, both basal plasma brain natriuretic peptide and atrial natriuretic peptide levels were also significantly elevated. However, in response to acute ventricular or atrial pacing, brain natriuretic peptide levels did not show any increase in contrast to the marked increase of atrial natriuretic peptide levels. In acute myocardial infarction, brain natriuretic peptide levels showed more prominent changes than atrial natriuretic peptide levels and were correlated with serum levels of creatine kinase and cardiac myosin light chain I in most patients. These results suggest that both brain and atrial natriuretic peptides play an important role in the regulation of cardiovascular homeostasis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Gland Neoplasms↗
PubMed1994

Cardiac sympathetic innervation in patients with dilated cardiomyopathy--immunohistochemical study using anti-tyrosine hydroxylase antibody.

Depletion of norepinephrine in the left ventricular myocardium in cases of dilated cardiomyopathy (DCM) has been suggested. However, there have been few histological studies of the sympathetic nerves, in which myocardial norepinephrine is believed to exist. We performed an immunohistological study of the density of tyrosine hydroxylase (TH, a marker of sympathetic nerves)-positive nerve fiber in endomyocardial biopsy specimens in cases of DCM using antibody against TH. TH-positive nerves were stained brown along with the myocardium, and they were more dense in the right ventricle than in the left ventricle in both the DCM and control groups. The density of TH-positive nerves in cases of DCM was significantly less than that in the control group in the subendocardial myocardium of the right and left ventricles, but especially in the left ventricle. A correlation was observed in the DCM group between the density of TH-positive nerves and the ejection fraction in the right ventricle, but not in the left ventricle. In the failing human heart, a decrease in subendocardial sympathetic nerve density may be one of the causes of myocardial norepinephrine depletion.

Adrenergic Fibers↗
PubMed1994

[Possible involvement of activation of pulmonary macrophages in respiratory failure with acute pancreatitis].

We examined the stimulatory state of pulmonary macrophages (Mø) in rats with caerulein-induced pancreatitis by measuring their activity for free radical production in vitro and in situ using nitroblue tetrazolium (NBT) under treatment of phorbol myristate acetate. The Mø from bronchoalveolar lavage were significantly activated 24 h after caerulein administration. The lung perfusion with NBT in the presence of PMA confirmed in situ that pulmonary Mø were also significantly activated in the same condition. Thereafter significant hypoxia was observed. These results indicate that the activation of pulmonary Mø may be involved in the respiratory failure in acute pancreatitis.

Acute Disease↗
PubMed1993

A radioimmunoassay for pancreatic elastase 1: use of alpha 1-antitrypsin-elastase 1 conjugate as both standard and tracer to eliminate the influence of anti-elastase 1 autoantibodies.

We have recently reported the occurrence of anti-elastase 1 autoantibodies in human sera (Asada et al., Biochim Biophys Acta, 1991;1080:34-39). The usual radioimmunoassay of elastase 1 in autoantibody-positive sera gave abnormally high levels of elastase 1 and low recoveries of elastase 1 added to the sera. Now we have established a new radioimmunoassay system for determining pancreatic elastase 1 in serum, in which alpha 1-antitrypsin elastase 1 conjugate, the major conjugation form of elastase 1 in serum, is used as standard and alpha 1-antitrypsin-[125I]elastase 1 as tracer, because we found that the conjugate could bind to the elastase 1 specific antiserum but not to the autoantibodies. Thus the new assay system completely eliminate the unfavorable effects of the autoantibodies. The elastase 1 levels determined by the new assay method exhibited a good correlation with those obtained by a commercial assay kit in the autoantibody-negative sera, while no correlation was observed in the autoantibody-positive sera.

Acute Disease↗
PubMed1993

A case of a female infant with simultaneous occurrence of de novo terminal deletions on chromosome 14q and 20p.

This is a case report on an infant with de novo terminal deletions on the long arm of chromosome 14 and on the short arm of chromosome 20 [46, XX, del(14)(q32)del(20)(p11)]. Examination revealed that the infant had a peculiar face, a cleft and high palate, abnormal dentition, butterfly-like vertebral defects, finger anomalies, a simian line on the left hand, talipes equinovarus, deep plantar furrows, abnormally high values of alkali phosphatase and lactate dehydrogenase, mild anemia and psychomotor retardation. Comparing the present case with previously reported cases of a single deletion on chromosome 14q or chromosome 20p, the infant showed some symptomatic and dysmorphic features of both deletions.

Abnormalities, Multiple↗
PubMed1993

[Activation of peritoneal macrophages in rats with caerulein-induced pancreatitis].

We examined the stimulatory state of peritoneal macrophages (M phi) in caerulein-induced pancreatitis. Edematous pancreatitis was developed by the intravenous continuous injection of caerulein (5 micrograms/kg/hr) for 4 hr. Thereafter peritoneal M phi were collected and the activity for free radical production was measured by the reduction of nitro blue tetrazorium in the presence of phorbol myristate acetate. The increase in free radical production reached a statistical significance at 12 hr and a maximum at 20 hr after the beginning of caerulein infusion. These results suggested that the peritoneal M phi are activated even in mild edematous pancreatitis, and that their activation is involved into the mechanism of the development of remote organ failure in acute pancreatitis.

Acute Disease↗
PubMed1992

Protective effect of a microtubule stabilizer taxol on caerulein-induced acute pancreatitis in rat.

The effect of taxol, which is a microtubule stabilizer, was examined in a model of acute edematous pancreatitis induced in rat by the administration of caerulein. Prophylactic administration of taxol ameliorated inhibition of pancreatic secretion, increased level of serum amylase, pancreatic edema, and histological alterations in this model. Immunofluorescence studies revealed that taxol stabilized the arrangement of microtubules by the action of promoting tubulin polymerization and prevented inhibition of pancreatic digestive enzyme secretion. In isolated rat pancreatic acini, taxol reversed the inhibition of amylase secretion induced by supramaximal concentrations of cholecystokinin octapeptide and did not affect the binding of cholecystokinin octapeptide to its receptor. The results obtained in this study suggest that microtubule disorganization is the initiating event in caerulein-induced pancreatitis and that the inhibition of pancreatic digestive enzyme secretion by interfering with intracellular vesicular transport due to microtubule disorganization causes caerulein-induced pancreatitis.

Acute Disease↗
PubMed1992

Pericentric inversion of chromosome 9 in prenatal diagnosis and infertility.

In order to evaluate the relation between pericentric inversion of chromosome 9 (inv(9)) and clinical problems, the characteristics of inv(9) were investigated on the basis of chromosomal analyses of fetuses and infertile couples. The incidence of such inversion in fetuses with parents having an offspring who suffered from various clinical problems was significantly higher than the basic incidence obtained in fetuses karyotyped by reason of advanced maternal age. In the chromosomal examination of the parents whose fetuses were diagnosed as inv(9), it was revealed that either parent might be the carrier. Furthermore, in the inv(9) carrying fetuses, the number of females was significantly greater than that of males. Analysis of infertile couples revealed that the incidence of such inversion in males was significantly higher than the basic incidence mentioned above. Moreover, infertile couples with an inv(9) carrier showed a significantly higher incidence of intrauterine fetal death, compared with infertile couples with a translocation carrier or those in which the etiology was unknown. These results indicate that inv(9) may often cause clinical problems in offspring of the carrier and infertility with unknown mechanisms related to sex.

Chromosome Aberrations↗
PubMed1992

[Hematological values in fetal blood by cordocentesis].

Reference ranges for four hematological parameters--hemoglobin, hematocrit, white blood cell and platelet count--in each gestation were established from values for fetal blood samples obtained by cordocentesis from 72 pregnancies at 16-39 weeks gestation. These 72 fetuses turned out as normal or single malformations which should not affect fetal hematological values. Significant correlations were observed between hemoglobin, hematocrit and platelet counts and the number of weeks of gestation. No correlation was found between the white blood cell count and gestational age. Fetal anemia (hematocrit was below the lower limit of the 95% confidence interval) was found in 18 (7%) of all the fetuses that underwent cordocentesis, including nonimmune hydrops fetalis (8 cases), Rh isoimmunization (4 cases), twin-to-twin transfusion syndrome (3 cases), trisomy 18 (2 cases) and autoimmune thrombocytopenia (1 case). Of 26 hydropic fetuses, 8 (31%) were anemic. The prognosis of those fetuses depended on either the gestational age or the severity of the fetal anemia. Our results are useful in diagnosing fetal hematological disorders and to make decisions for fetal therapy.

Anemia↗
PubMed1992

[Analysis of pancreatic stone protein gene of hereditary pancreatitis].

To investigate the pathogenesis of hereditary pancreatitis we determined whether pancreatic stone protein (PSP) gene was structurally altered in two independent families diagnosed as hereditary pancreatitis. Because, it has been shown that a decrease in the activity of PSP which inhibits CaCO3 crystal formation in pancreatic juice is closely related to the development of chronic calcifying pancreatitis. Southern blot analysis revealed neither a rearrangement nor a gross deletion of PSP gene in genomic DNA of affected members of both families. Furthermore, six exons of PSP gene amplified by polymerase chain reaction from genomic DNA was directly sequenced, while no apparent base mutation was observed. The immunohistochemical study utilizing monoclonal antibody to PSP showed the presence of immunoreactive PSP in the section of pancreatic tissue obtained from a patient affected with hereditary pancreatitis. However, the level of immunoreactive PSP in the remaining acinar cells of the patient pancreas was not reduced when compared with that of normal pancreas. Results, therefore, indicate that genetic alteration of PSP gene may not be responsible for the pathogenesis of hereditary pancreatitis.

Adolescent↗
PubMed1991

Presence of human immunoglobulin G anti serum pancreatic elastase 1 autoantibodies and their influence on elastase 1 radioimmunoassay.

Human immunoglobulin G (IgG) anti human pancreatic elastase 1 autoantibodies were detected in sera of patients with pancreatic disorders. The characteristics of these anti elastase 1 autoantibodies and their influence on radioimmunoassay (RIA) for elastase 1 were investigated. They were placed in the IgG class by the double antibody method, and most were assumed to be of a monoclonal type from their elution profiles in gel filtration analysis. The presence of autoantibodies in serum caused an increase in apparent elastase 1 values and a decrease in the recovery of elastase 1 exogenously added to the serum. These results suggest that elastase 1 immunoassay data for autoantibody positive sera can cause misjudgement of clinical stages of patients.

Autoantibodies↗
PubMed1991

Molecular cloning and characterization of a ras p21-like GTP-binding protein (24KG) from rat liver.

We have isolated cDNA clones from a rat liver cDNA library that encode a ras p21-like small GTP-binding protein (24KG) which was purified from the microsomes-Golgi complex fraction of the rat liver. The cloning was accomplished using polymerase chain reaction amplified with a set of oligonucleotide primers which were designed from the partial amino acid sequences for 24KG. The cDNA contained an open reading frame encoding a 216 amino acid protein with a calculated Mr weight of 24,397. This Mr weight was similar to that of the purified 24KG estimated by sodium dodecyl sulfate polyacrylamide gel electrophoresis. The sequence analysis of 24KG revealed that a 24KG cDNA is the rat counterpart of a rab11 cDNA cloned from a Madin-Darby canine kidney cell cDNA library. The 1.0-kilobase 24KG mRNA corresponding to the isolated cDNA was also detected in various rat tissues, such as brain, testis, spleen, and heart.

Amino Acid Sequence↗