Search PubMed⌕ Search

Biomedical subjects

T Saitoh

Publications and source records attributed to T Saitoh.

At least 325 records · Page 18Linked to original sources

Comparison of endothelin-1 concentrations in normal and complicated pregnancies.

Endothelin-1 (ET-1) may be important in regulating vascular tone in humans. To understand the role of ET-1 during pregnancy, we measured the concentrations of plasma immunoreactive ET-1 in normal, toxemic (pre-eclamptic or eclamptic), and other complicated pregnancies. There were no significant differences between ET-1 concentrations in normal pregnancy and those in toxemic pregnancy, except in one case with IgA nephropathy and severe toxemia. There also was no significant difference between the ET-1 concentrations in pure toxemia of pregnancy compared with superimposed toxemia of pregnancy. Furthermore, there was no correlation between ET-1 concentrations, blood pressure, or renal function during toxemic pregnancy. Similarly, there were no significant differences between ET-1 plasma levels in normal pregnancies and other complicated pregnancies except for two cases in which much blood was lost due to uterine atony and abruptio placenta. Thus, plasma ET-1 concentrations showed no significant relationship to blood pressure or renal function during normal or toxemic pregnancy, and were not related to the type (pure or superimposed type), grade, or severity of toxemic pregnancy.

Adult↗

Cytomegalovirus DNA in the sera of patients with cytomegalovirus pneumonia.

We attempted to detect cytomegalovirus DNA (CMV-DNA) in the sera of four leukaemia patients who underwent an allogeneic bone marrow transplant (BMT), in six leukaemia patients who suffered from pneumonia and in 16 healthy subjects, using the polymerase chain reaction (PCR). Three of the four BMT patients subsequently developed CMV pneumonia. In two cases, CMV-DNA was detected in the sera at about the time the pneumonia occurred, and the amount of DNA increased with disease progression. The serum of the third patient became positive for CMV-DNA before he developed pneumonia. The fourth patient did not develop CMV pneumonia, but his urine became persistently positive for CMV-DNA soon after the BMT, whereas the serum was negative. A relationship was found between the occurrence of pneumonia and the serum level of CMV-DNA. CMV-DNA was also detected in three of six pneumonia patients whose anti-CMV IgM antibodies were elevated in the circulation. Sera from the 16 normal subjects were negative for CMV-DNA, regardless of their being seropositive or seronegative for CMV. While it had been previously thought that CMV did not exist in serum, we detected CMV-DNA in serum by PCR in the active disease stage. Our results suggest that PCR would be useful for the early diagnosis of CMV pneumonia and in monitoring its course.

Adolescent↗

Altered protein tyrosine phosphorylation in Alzheimer's disease.

The activity of protein tyrosine kinase was determined in extracts from Alzheimer's disease brains and age- and postmortem time-matched control brains at autopsy using the synthetic peptide substrate poly(Glu4Tyr1). The specific activity of protein tyrosine kinases in the particulate fraction decreased roughly twofold (p less than 0.02) in Alzheimer's disease frontal cortex relative to unaffected control cortex. Cytosolic protein tyrosine kinase activity in Alzheimer's disease tissue was not significantly different from that in control tissue. In contrast to reduced particulate protein tyrosine kinase activity, analysis of Western blots of cytosolic and particulate fractions revealed increases in cytosolic antiphosphotyrosine immunoreactive polypeptides with molecular masses of 55 and 60 kDa. Quantitative immunohistochemistry and morphometry of frontal cortex sections with the antiphosphotyrosine antibody indicated increased antiphosphotyrosine staining in the neurons, although the number of antiphosphotyrosine-positive neurons per square millimeter decreased. Also, increased antiphosphotyrosine staining was observed in the hippocampal neurons. These results suggest that altered protein tyrosine kinases and protein tyrosine phosphorylation are involved in the pathology of Alzheimer's disease.

Aged↗

Changes in the activity of protein kinase C and the differential subcellular redistribution of its isozymes in the rat striatum during and following transient forebrain ischemia.

The changes in the levels of protein kinase C [PKC(alpha, beta II, gamma)] were studied in cytosolic and particulate fractions of striatal homogenates from rats subjected to 15 min of cerebral ischemia induced by bilateral occlusion of the common carotid arteries and following 1 h, 6 h, and 48 h of reperfusion. During ischemia the levels of PKC(beta II) and -(gamma) increased in the particulate fraction to 390% and 590% of control levels, respectively, concomitant with a decrease in the cytosolic fraction to 36% and 20% of control, respectively, suggesting that PKC is redistributed from the cytosol to cell membranes. During reperfusion the PKC(beta II) levels in the particulate fraction remained elevated at 1 h postischemia and decreased to below control levels after 48 h reperfusion, whereas PKC(gamma) rapidly decreased to subnormal levels. In the cytosol PKC(beta II) and -(gamma) decreased to 25% and 15% of control levels at 48 h, respectively. The distribution of PKC(alpha) did not change significantly during ischemia and early reperfusion. The PKC activity in the particulate fraction measured in vitro by histone IIIS phosphorylation in the presence of calcium, 4 beta-phorbol 13-myristate 12-acetate, and phosphatidylserine (PS) significantly decreased by 52% during ischemia, and remained depressed over the 48-h reperfusion period. In the cytosolic fraction PKC activity was unchanged at the end of ischemia, and decreased by 47% after 6 h of reperfusion. The appearance of a stable cytosolic 50-kDa PKC-immunoreactive peptide or an increase in the calcium- and PS-independent histone IIIS phosphorylation was not observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Adult T cell leukemia derived factor (ADF) in oral epithelial lesions.

To examine the distribution of adult T cell leukemia derived factor (ADF) in oral epithelial lesions, an immunohistochemical method using a polyclonal antibody against ADF C-terminal peptide was applied to formalin fixed and paraffin embedded tissues. All cases of periodontitis, epithelial hyperplasia, epithelial dysplasia and leukoplakia examined stained positively for ADF. Immunoreactive products were localized in the cytoplasm and/or nucleus of spinous and parakeratotic layers, but not in basal and keratinous layers. In addition, five out of nine papillomas stained positively for ADF, especially in koilocytotic cells. Eight out of 13 squamous cell carcinomas stained positively. Furthermore, ADF positive areas in oral epithelial lesions were included in the areas for protein bound SH-groups. Our results suggested that ADF may be a factor involved in the differentiation and proliferation of stratified squamous epithelium of the oral cavity.

Carcinoma, Squamous Cell↗

Inhibition of adenosine 3',5'-cyclic monophosphate phosphodiesterase by flavonoids from licorice roots and 4-arylcoumarins.

Isoliquiritigenin, glabridin, licoarylcoumarin and licoricidin were identified as strong inhibitors of adenosine 3',5'-cyclic monophosphate (cAMP) phosphodiesterase in waste materials which were obtained during the industrial extraction of glycyrrhizin from licorice roots. The structure-activity relationships of 12 flavonoids from licorice roots and 34 4-arylcoumarins were studied. In 4-arylcoumarins, 5,7-dihydroxy derivatives were generally highly inhibitory towards cAMP phosphodiesterase.

3',5'-Cyclic-AMP Phosphodiesterases↗

[A study on the prognostic significance of silent myocardial ischemia in angina pectoris and myocardial infarction patients].

The purpose of this study is to increase understanding of the prognosis of coronary artery disease (CAD) patients whose anginal symptoms have been removed by medical therapy, and to evaluate the prognostic and clinical significance of silent myocardial ischemia (SMI). Cardiac events including cardiac death, acute myocardial infarction, PTCA/CABG and unstable angina were examined in 253 CAD patients who underwent ambulatory Holter monitoring, treadmill exercise testing and coronary angiography. The subjects were classified into two groups: 93 patients with exertional angina (AP) without previous myocardial infarction and 160 patients with old myocardial infarction (MI). SMI was diagnosed by Holter monitoring. Cox's proportional hazard regression model and the survival curves using the Kaplan-Meier method were used to analyze 9 variables in patients with AP, including Holter monitoring parameters, exercise parameters and angiographic findings, and 12 variables in patients with MI, including the same parameters as in AP patients. The cardiac event rate was 19% in patients with AP and 18% in patients with MI. The independent and common predictors of unfavorable outcome in both groups were severe coronary lesion and SMI. The incidence of SMI was 30% in AP patients and 38% in MI patients, the same incidence as reported in previous studies. The cardiac event rate in patients with SMI was higher than in those without SMI for both groups (28% vs 9% and 32% vs 9%; p less than 0.05). However, the most frequent cardiac event was different in the groups with SMI: PTCA/CABG in AP patients and re-infarction in MI patients. The significant predictors of cardiac events in patients with SMI were severe coronary lesion, short exercise duration, severe asynergy and exercise-induced angina in patients with AP and lower ejection fraction and maximum ST depression on Holter monitoring in patients with MI. In conclusion, it was ascertained that SMI is a significant and independent marker of unfavorable outcome in patients with CAD and that the cardiac event rate in patients with SMI was significantly higher than in those without SMI. However, severe complications such as acute myocardial infarction were more frequent in MI patients than in AP patients. Therefore, it was suggested that the use of re-vascularization procedure (PTCA/CABG) should be considered as soon as possible in patients with SMI, regardless of whether anginal symptoms are present or not.(ABSTRACT TRUNCATED AT 400 WORDS)

Aged↗

Transplantable mononuclear cell leukemia in F344 rat with particular reference to nodular tumor developing at the transplant site.

A transplantable mononuclear cell leukemia (MCL) was established from spontaneous MCL in an F344 rat. In this work, we paid special attention to a nodular tumor, named MCL-YSK, developed at the subcutaneous transplant site. MCL-YSK was serially passaged in subcutaneous tissue of syngeneic rats up to the 19th generation. Transplants from MCL-YSK grew into nodules 3 cm in diameter and 11.3 g in weight 9 weeks after subcutaneous implantation. Neoplastic cells forming the nodules had azurophilic cytoplasmic granules, which ultrastructurally appeared to be lysosomes. The cells reacted positively for acid phosphatase and nonspecific esterase, but not for alkaline phosphatase, alpha-1 antitrypsin and lysozyme, nor reacted with anti-rat monocyte/macrophage monoclonal antibody and anti-rat CD-8 monoclonal antibody. They possessed Fc-receptor. Leukemic cells first appeared in the peripheral blood 6 weeks after transplantation when subcutaneous nodules reached an average diameter of one cm. Subsequently, leukemic changes progressed in recipients as MCL-YSK grew larger. The recipients died during the period from 8 to 12 weeks after transplantation, showing anemia, depression, splenohepatomegaly and lymph node enlargement. Diffuse or focal proliferation of sprinkled tumor cells was present in many organs. Hematologic changes suggestive of hemolytic anemia, elevated plasma enzymes and decreased drug-metabolizing enzymes, indicative of hepatic malfunction, were seen in transplant recipients. MCL-YSK was easily transplanted into athymic nude mice. The transplanted mice showed leukemic changes similar to those observed in rats with transplanted MCL-YSK.

Animals↗

[Effects of ethanol on acid secretion by isolated parietal cells from guinea pig].

We studied the effects of ethanol (0.1-10%) on acid secretion of parietal cell-rich fractions isolated from guinea pig gastric mucosa. Ethanol (0.1-3%) increased histamine-stimulated cAMP content, while over 1% ethanol decreased histamine-stimulated acid secretion. H+, K(+)-ATPase activity in microsomal fraction also decreased after treatment with 3% ethanol. Thus, ethanol may disturb the signalling process from cAMP to H+, K(+)-ATPase. On the other hand, carbachol-stimulated acid secretion was more sensitive to ethanol than that with histamine, and 0.1% ethanol suppressed the acid secretion. This effect was well correlated with the extent of the ethanol-induced increase of [Ca2+]i and with the attenuation of [Ca2+]i response following carbachol stimulation. The calcium response may be a primary target against ethanol in carbachol-dependent process. In conclusion, low-dose ethanol have multi-effects on these critical intermediary steps in acid secretion.

Animals↗

[Influence of respiratory frequency in measurement of specific airway conductance during non-panting breathing].

In order to investigate the influence of respiratory frequency in the measurement of specific airway conductance (sGaw) during non-panting breathing, we examined specific airway conductance using a body plethysmograph (BX-82, Minato) in 20 stable pulmonary emphysema patients and 19 normal control subjects. Our body plethysmograph device can measure sGaw automatically without panting by making various corrections using a 16-bit microcomputer. We measured sGaw first at a flow of 0.5 L/sec during both inspiratory and expiratory ventilatory phases, then the respiratory frequency was changed from 0.5 to 1.0, 1.5 and 2.0 Hz. In normal control subjects sGaw, tidal volume and mouth flow significantly changed by increasing respiratory frequency, and there was a significant correlation between sGaw and mouth flow. In pulmonary emphysema patients, tidal volume decreased significantly by increasing respiratory frequency, and there was a significant correlation between sGaw and tidal volume, but sGaw and mouth flow did not change significantly by increasing respiratory frequency. These results suggest that specific airway conductance is influenced by respiratory frequency, possibly due to the change in tidal volume and mouth flow. It is necessary to standardize respiratory frequencies and mouth flows in the measurement of specific airway conductance during non-panting breathing.

Aged↗

[Hyperkinésie volitionnelle following head injury].

A 13-year-old girl was struck by a car while riding her bicycle. She was comatose on her arrival at the hospital. Neurological examination revealed no focal sign except for right oculo-motor palsy. She became alert 15 days after the head injury when she first experienced a coarse tremor-like movement on the right arm. Neurological examination showed persistent oculo-motor palsy on the right side, decreased sensation of pain and touch on the left. There was no pyramidal deficit. Her gait and speech were normal and joint sensation was intact. A coarse tremor of the right arm was induced by volitional movements especially such as maintaining the arm in certain posture. It was not present at rest. Trajectory of finger-to-nose test was fairly well. However, the tremor became worse when the patient kept her finger near the target. Occasionally myoclonic-jerk and movement oppositionniste were mixed. Superficial EMG recordings of the tremor revealed 4 c/s rhythmic reciprocal grouping discharges, alternating flexor and extensor muscles. From these features, the abnormal movement should better be called tremor type of hyperkinésie volitionnelle (HV). The HV subsided spontaneously 4 months later. MRI of T2-weighted image showed high-intensity areas corresponding anatomically to the caudal part of right red nucleus and the right superior cerebellar peduncle just before its decussation. It is widely believed that lesions in cerebellar outflow pathway (i.e. dentate, red nucleus and thalamus) can cause HV.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

Protein kinase C alteration is an early biochemical marker in Alzheimer's disease.

Neuritic (senile) plaques are a hallmark of the pathology found in the brain of patients afflicted with Alzheimer's disease (AD). Neuritic plaques have been considered to be composed of an amyloid core surrounded by dilated neurites, although the use of anti-beta/A4-protein antibody revealed the presence of diffuse plaques without a nuclear-like central mass or surrounding paired helical filament (PHF)-containing neuritic components. The presence of diffuse plaques without PHF-containing neuritic components strongly suggests that the formation of amyloid precedes the degeneration of neurites that surround amyloid. Diffuse plaques are thus considered to be an early marker of AD pathology. In this article, we report that diffuse plaques, possible markers of early AD pathology, are immunostained with anti-protein kinase C(beta II) [anti-PKC(beta II)] antibodies. The PKC(beta II)-immunoreacting components of the diffuse plaques extend from neurons embedded in the plaques. Immunoelectron microscopy of diffuse and mature neuritic plaques shows that PKC(beta II)-like immunoreactivity in the plaques is closely associated with membranous structures of fine neuronal processes apposed to the amyloid fibers. These fine neuronal processes are distinct from classical neurites found typically in mature neuritic plaques. Furthermore, biochemical analysis demonstrates that PKC abnormalities, but not other AD markers (ubiquitin and A68), were found in the neocortex of clinically nondemented individuals with cortical plaques. Therefore, the PKC alteration in neurons might be involved in the early pathophysiology of AD.

Alzheimer Disease↗

Genesis of pulmonary foam cells in rats with diet-induced hyper beta-lipoproteinaemia.

Hyper beta-lipoproteinaemia in rats was produced by feeding a standard diet to which was added excess cholesterol and cholic acid, with or without olive oil, for 4, 8, and 12 weeks. The beta-lipoprotein percentage in serum lipoprotein electrophoresis and lipid contents in very low density lipoprotein and low density lipoprotein fractions in these rats were significantly higher than in the control rats fed the standard diet only. The percentage of foamy monocytes (FMs) to the total number of blood monocytes (BMs) from mononuclear leucocyte fractions and percentage of pulmonary foam cells (PFCs) to the number of alveolar macrophages (AMs) from bronchopulmonary lavage fluids in the rats increased with the extension of the feeding period and were significantly higher than those in the controls. An increase in the percentage of PFCs was closely correlated with that of FMs in the rats. FMs and PFCs had cytoplasmic fine vacuoles proved to be neutral lipid and cholesterol. Histologically, PFCs made an appearance in the lungs of all the rats as early as 4 weeks after the start of feeding. The degree of the PFCs' development increased as the feeding period lengthened. When latex particles were injected intravenously into rats at feeding week 4, the percentage of latex-ingested AMs to the number of AMs in the rats was significantly higher than that of the controls at 4 and 8 days post-injection. The percentage of latex-ingested PFCs to the number of latex-ingested AMs increased with the lapse of a day after injection and was significantly higher than that of the controls at 2, 4, and 8 days post-injection. The present findings suggest that the foamy transformation of BMs and their migration into the pulmonary alveoli may be a potential mechanism of the PFCs' development in rats with hyper beta-lipoproteinaemia.

Animals↗

[A case of human tail].

A human tail is a rare anatomical curiosity. A case of a human tail associated with lipomyelomeningocele is reported. The made subject was born, by breech delivery, at the 39th-week with a 3,008 g body weight. He was admitted to our hospital because of the presence of a human tail and subcutaneous mass in the midline lumbosacral region. The tail was about 7.5 cm in length and 2 cm in diameter. It was elastic and covered by normal skin. No systemic anomaly was found. Spina bifida below L5 was revealed, and no bony shadow was found on the plain X-ray film. CT scan showed a low density area in the spinal canal between L3 and lower sacral region that extended into the tail through the spina bifida. MRI also revealed intraspinal long T2 mass which was attached to the spinal cord and extended into the tail. Myelogram indicated intradural extramedullary mass below the L3 level. Surgical treatment was performed on the 3rd month of life with a diagnosis of a human tail with lipomyelomeningocele. At surgery, the tail was found to consist mainly of lipomatous tissue which extended subcutaneously and entered the spinal canal through the spina bifida. The tail and subcutaneous lipomatous tissue were totally excised. The capsule of subcutaneous lipomatous tissue was followed circumferentially down into the spinal canal, and found to be transformed to arachnoid membrane. Intradural lipomatous tissue was excised piece by piece, leaving only a small remnant attached to the conus medullaris to preserve sacral nerve root function.(ABSTRACT TRUNCATED AT 250 WORDS)

Child, Preschool↗

[Analysis of factors affecting hepatic dysfunction during group health checks for local inhabitants].

During health checks within the framework of the Geriatric Health Law, hepatic dysfunction was detected at a high incidence in inhabitants of K town. The factors affecting hepatic dysfunction in these cases were explored. The number of inhabitants who received health checks in 1989 in this town was 4,491 (78.5% of all inhabitants aged over 35 years). A diagnosis of hepatic dysfunction was made if GOT was equal to or higher than 41 IU/l or GPT was equal to or higher than 39 IU/l. On this basis, hepatic dysfunction was detected in 418 inhabitants (9.8%). The incidence of hepatic dysfunction was higher in males than in females. Inhabitants younger than 50 years had a higher incidence than those 50 years or older. The percentage of inhabitants with either a history of alcohol consumption or of receiving blood transfusion was significantly higher for inhabitants with hepatic dysfunction (29% and 10%, respectively) than for healthy inhabitants (10% and 3%, respectively). HBs antigen and anti HCV antibody positive rates for inhabitants with hepatic dysfunction were 3.3% and 36.1% respectively. These results suggest that the relatively high rate of hepatic dysfunction in this town is related to alcohol consumption, blood transfusion and hepatitis C virus (HCV) infection. Of these three factors, the influence of HCV infection seemed to be the most influential. The study additionally disclosed variations in the incidence of hepatic dysfunction among the different regions of the town probably related to regional differences in the anti-HCV antibody positive rate.

Adult↗

Altered amyloid beta-protein precursor processing in brains of patients with neuronal ceroid lipofuscinosis.

Our previous study disclosed strong immunostaining of brain tissue in neuronal ceroid lipofuscinosis (NCL) with antibodies against amyloid beta-protein and the presence of 31-kDa polypeptide in the storage material. In the present study, we investigated the immunoreactivity of the NCL brain tissue with anti-serum (anti-GID) raised against a synthetic peptide, based on the amyloid beta-protein precursor, with the 175-186 amino acid sequence. Immunocytochemistry was performed on autopsy brain material collected from 15 NCL cases, and from 8 age-matched normal controls. The results showed strong immunoreactivity of nerve cells in the NCL cases, which according to densitometry was 5 times more intense than in the control group (P less than 0.0001 by Student's t-test). Western blot analysis revealed that in protein fractions of NCL brain homogenates anti-GID recognized the protein band of 35 kDa. Thus our present and previously performed studies supplied for the first time data pointing to abnormal processing of amyloid beta-protein precursor in NCL. Moreover, the accumulation of both 31- and 35-kDa polypeptides that was demonstrated provides further support for postulated defective protein metabolism in this disorder.

Amyloid beta-Peptides↗

Depletion of CD8+ cells exacerbates organ-specific autoimmune diseases induced by CD4+ T cells in semiallogeneic hosts with MHC class II disparity.

Autoimmune diseases are known to be induced in some donor-recipient combinations of mice undergoing the graft-vs-host reaction (GVHR). In this paper, we report on the development of primary biliary cirrhosis (PBC)-like hepatic lesions and also on pancreatic insulitis in (B6 x bm12)F1 mice injected with B6 CD4+ T cells. At the sites of these lesions, cellular infiltration around ductal structure was observed. Immunohistochemical studies revealed that both CD4+ and CD8+ T cells were present in the lesions of the liver and pancreas. To clarify the role of the CD8+ T cells, which were probably of host origin, we used a mAb against the Lyt-2 molecule. Both the PBC-like hepatic lesions and pancreatic insulitis were exacerbated by eliminating CD8+ T cells from mice with MHC class II GVHR. Also, autoantibodies against the pyruvate dehydrogenase-E2 component, which has been recently found to contain an immunodominant site (autoepitope) for B cell reactivity in patients with PBC, were detected in the sera of these mice by ELISA and their presence was confirmed by immunoblotting procedures. Our findings suggest that similar mechanisms as in GVHR caused by MHC class II disparity are active in the development of PBC. It should also be noted that, in addition to the hepatic lesions, insulitis closely resembling that seen in the nonobese diabetic mouse was induced in our experimental system. The results suggest that our model provides a unique opportunity to study organ-specific autoimmune diseases. Because the effector in our experimental system was defined to be CD4+ T cells responding to Iabm12 Ag, our findings support the hypothesis that an excessive immune response directed against Ia Ag can produce autoimmune disease.

Animals↗