Biomedical subjects

M Miyazaki

Publications and source records attributed to M Miyazaki.

At least 613 records · Page 34Linked to original sources

PubMed1991

Development of the brainstem: assessment by MR imaging.

The morphological development of the brainstem was studied by means of MR imaging. The subjects were 74 cases ranging in age from 4 months to 16 years, and 6 adult cases. The brainstem development was rapid until 4-6 years of age and thereafter it slowed down. That is the brainstem showed exponential growth (w', t', v and u). The relationship between brainstem growth and the cranium size was divided into 4 types as follows: 1) linear increase with development (s/T-O), 2) plateau (w/T-I and v/RTP-LTP), 3) down and up (u/RTM-LTM and z/RTM-LTM) and 4) exponential (t/T-P). In the values of v, z (the size of the brainstem in axial view) and t/T-P (the ratio of the midbrain and the cranium size in sagittal view), there were significant sex differences for cases of 10-16 years old. These values in male subjects were greater than those in female subjects (v, p less than 0.05, z, p less than 0.01, and t/T-P, p less than 0.05). That is the brainstem in male subjects was greater than that in female subjects.

Adolescent↗

PubMed1991

Congenital myotonic dystrophy associated with a chromosome pericentric inversion.

We report two cases of congenital myotonic dystrophy (CMyD) associated with a chromosome abnormality of pericentric inversion. Case 1 was a two-month-old boy, presented with 46 XY, inv (9) (p 11q 13). His father had the same chromosome abnormality without any clinical manifestations. His mother had clinical manifestations of myotonic dystrophy (MyD) but had no chromosomal aberration. Case 2 is a one-month-old girl, presented with 46 XX, inv (4) (p15.31q25). Her mother had clinical manifestations of MyD and the same chromosome abnormality as Case 2, but her father was normal. Our case report may be of value in adding further information on the pathogenesis of CMyD.

Chromosome Inversion↗

PubMed1991

Changes in gene expression of the renin-angiotensin system in two-kidney, one clip hypertensive rats.

To investigate the molecular mechanism of sustained hypertension in two-kidney, one clip (2K1C) hypertensive rats, possible changes in renin gene expression in the kidney and angiotensinogen in the liver were studied. In 2K1C rats 4 weeks after clipping, the plasma renin and angiotensin II levels were significantly higher than those in sham-operated rats, but the plasma angiotensinogen levels were similar in the two groups. At this time, expression of the renin gene in the ischaemic kidney of 2K1C rats was 2.6-times that in sham-operated rats (P less than 0.05), but expressions of the angiotensinogen gene were similar in the two groups. Sixteen weeks after clipping, the plasma renin and angiotensin II levels in 2K1C rats were not significantly higher than those in sham-operated controls, but expression of the renin gene in the kidney was still 2.2-times higher in 2K1C rats than in controls (P less than 0.05). The plasma angiotensinogen level was significantly higher in 2K1C rats than in controls (P less than 0.05), and expression of the angiotensinogen gene in the liver was 2.9-times higher in 2K1C rats than in controls (P less than 0.01). These results indicate that the roles of the renin-angiotensin system in maintenance of hypertension in 2K1C rats differ in the acute and chronic phases: in the acute phase, over-expression of the renal renin gene coupled to increased renin secretion plays the major role in elevating the blood pressure; in the chronic phase, a counter-regulatory mechanism may affect the post-transcriptional fate of renin.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensinogen↗

PubMed1991

N1-methylnicotinamide level in the blood after nicotinamide loading as further evidence for malignant tumor burden.

Nicotinamide methyltransferase (Nmd CH3transferase) activity increased in the liver of mice after i.p. transplantation of Ehrlich ascites tumor (ascitic form), but not in the liver of mice with acute inflammation induced by the i.p. administration of D-galactosamine, and it rather showed a decrease together with necrosis after carbon tetrachloride administration. When Nmd CH3transferase activity of rat hepatocytes in primary culture was investigated with the addition of dexamethasone, epidermal growth factor, transforming growth factor-beta, tumor necrosis factor-alpha and N1-methylnicotinamide (1-CH3Nmd), changes in activity were not correlated with DNA synthesis, suggesting that the increase of this enzyme activity in the tumor host liver was not directly related to liver cell proliferation. Thus, in order to make use of the increase of this enzyme activity as a tumor burden marker, a procedure for its estimation by measuring the blood level of 1-CH3Nmd, a metabolite of Nmd produced by Nmd CH3transferase, was established. The 1-CH3Nmd level in the blood of mice bearing Ehrlich ascites tumor 4 h after s.c. loading of Nmd (500 mg/kg body weight) was closely correlated with this enzyme activity in the liver (r = 0.835, P less than 0.00001) from the early to the terminal stage of tumor development. Furthermore, similar correlations were seen in the animal groups bearing various other tumors, such as s.c. implanted Ehrlich ascites tumor (solid form) and i.p. implanted sarcoma S-180, hepatoma MH-134, Yoshida ascites sarcoma and leukemia L-1210, but not solid tumors such as Lewis lung carcinoma and melanoma B-16, although almost all of the animals bearing these tumors showed a higher enzyme activity than their control normal animals.

Animals↗

PubMed1991

Effect of long-term treatment with an angiotensin-converting enzyme inhibitor on the renin-angiotensin system in spontaneously hypertensive rats.

1. To obtain information on regulation of the brain renin-angiotensin system, the effect of long-term administration of angiotensin-converting enzyme (ACE) inhibitor on brain renin and angiotensinogen mRNA was studied. 2. Spirapril (3 mg/kg) was orally administered daily for 8 weeks to spontaneously hypertensive rats (SHR) from 12 weeks after birth. Renin and angiotensinogen mRNA in the brain and kidney were then quantitated by Northern blot analyses with [32P]-labelled rat renin and angiotensinogen cDNA as hybridization probes. Plasma renin activity (PRA), angiotensin II (AII) concentration, plasma ACE activity and brain tissue ACE activity were also measured. 3. Compared with the control group, the Spirapril-treated group had significantly lower blood pressure (P less than 0.01), significantly higher PRA (P less than 0.01), a not significantly different plasma AII concentration, and lower plasma and brain ACE activities (P less than 0.01). Interestingly, the brain renin and angiotensinogen mRNA levels of the two groups were similar, but the renal renin mRNA level was significantly higher in the Spirapril-treated group (P less than 0.01). 4. These results indicate that the mRNA levels of brain renin and angiotensinogen were not affected by chronic ACE inhibition in the circulation and suggest that AII in the brain might not be affected by systemic ACE inhibition.

Actins↗

PubMed1991

Pathogenetic role of vascular angiotensin-converting enzyme in the spontaneously hypertensive rat.

1. This study was undertaken to examine the possibility that the level of angiotensin-converting enzyme (ACE) increases in vascular tissue, and that this may participate in the pathogenesis of hypertension in spontaneously hypertensive rat (SHR). 2. In SHR, at the established hypertensive stage, the prolonged antihypertensive effect induced by a single oral dose of spirapril was closely correlated to the long-lasting inhibition of ACE in aortae and mesenteric arteries. In contrast, ACE in plasma, lung, heart and kidney recovered from inhibition faster than in vessels. 3. Prolonged daily oral treatment of SHR with spirapril, initiated at the age of 8 weeks and continued for 8 weeks, prevented the development of hypertension with concomitant decrease in aortic ACE activity. Blood pressure continued to be suppressed after the drug was withdrawn, as did the aortic ACE activity. 4. Spontaneously hypertensive rats developed hypertension with age as well as with the increase in aortic ACE activity which became higher with age than that of Wistar-Kyoto (WKY) normotensive control rats. On the contrary, ACE activity in plasma and lung of SHR was substantially lower than that of WKY at any age from 4 to 20 weeks old. Brain ACE activity of SHR did not differ from that of WKY at any age. Aged SHR showed the lower enzyme activity in the kidney compared with that of age-matched WKY. 5. Our results support the hypothesis that increased vascular ACE may play an essential role in the development and maintenance of hypertension in SHR.

Aging↗

PubMed1991

Diagnosis of atlantoaxial subluxation in Morquio's syndrome and spondyloepiphyseal dysplasia congenita.

Compression of the spinal cord due to atlantoaxial subluxation was diagnosed in a patient with Morquio's syndrome and in another with spondyloepiphyseal dysplasia (SED) congenita by cervical radiography and magnetic resonance imaging (MRI). The patient with Morquio's syndrome, a 15 year old boy, had no neurologic symptoms and his somatosensory evoked potential (SSEP) was normal. However, MRI demonstrated spinal cord compression at C1-C2. In contrast, the patient with SED congenita, an 11 year old girl, had neck pain, hyperreflexia and loss of vibration sense in both legs. These findings were explained by the absence of P3 and later waves in SSEP and by compression of the spinal cord observed on MRI. Both SSEP and MRI should be used for evaluating disorders in which atlantoaxial subluxation might be present.

Adolescent↗

PubMed1991

Reduced thyroid-stimulating hormone response to thyrotropin-releasing hormone in autistic boys.

The thyroid-stimulating hormone (TSH) and prolactin responses to thyrotropin-releasing hormone (TRH) were compared among four groups of boys--41 autistic, 12 mentally retarded (MR), 12 with minimal brain dysfunction (MBD) and five controls. The autistic boys were divided into two groups: DQ(IQ) greater than or equal to 80 and DQ(IQ) less than 80. Mean TSH basal and peak levels were significantly lower in both autistic groups than in the MR, MBD and control groups. Mean TSH peak value minus basal value (p-b) was significantly lower in both autistic groups than in the control group. Mean prolactin levels and p-b value did not differ among groups. It is suggested that there may be enhanced dopaminergic and/or reduced serotonergic activity in the central nervous system of autistic children, together with hypothalamic dysfunction.

Attention Deficit Disorder with Hyperactivity↗

PubMed1991

A biliary protein identified by immunoblotting stimulates proliferation of peripheral blood T lymphocytes in primary biliary cirrhosis.

The source of activation of T lymphocytes in primary biliary cirrhosis (PBC) is undefined. Hence, T-cell-mediated reactivity against a biliary tract antigenic protein from human bile was studied. The bile protein was fractionated by 30-50% saturated ammonium sulphate and gel-chromatography, and analysed by SDS-PAGE and Western immunoblotting using rabbit antisera to the bile protein. The antisera reacted specifically with human bile duct epithelium. Western blotting of bile proteins showed two major bands, the B1 and B2 antigens. B1 stained for sialoglycoprotein but not lipid, but B2 was negative for both. Cell-mediated reactivity was tested by proliferation of peripheral lymphocytes against B1. Taking the upper limit of the normal range for stimulation indices (S.I.) as less than 1.89 (= mean + 2 SD), a mitogenic response was detected in 14 of 16 patients with PBC (S.I.: 11.7 to 2.3), and in 4 of 15 patients with chronic active hepatitis, but in none of 12 patients with drug-induced intrahepatic cholestasis or obstructive jaundice. The B2 protein was non-stimulatory. Lymphocyte proliferation to B1 in PBC was confined to T cell fractions of peripheral blood leucocytes. There was no cross-antigenicity between B1 and the M2 antigens, according to Western blotting using the rabbit antisera and PBC sera with anti-M2 reactivity. Thus, the B1 biliary protein is a possible source of T cell activation in PBC and hence could be an immunological co-factor in the pathogenesis of this disease.

Aged↗

PubMed1991

Consistent activation of prorenin mRNA in renal hypertensive rats.

To investigate the mechanism of maintaining hypertension in chronic two-kidney, one-clip (2K1C) rats, we studied the expression of the kidney renin gene. Total cellular RNA was extracted by the guanidine thiocyanate--CsCl method. Kidney renin messenger RNA was quantified by densitometric Northern blot analysis using 32P-labeled rat renin genomic DNA as a hybridization probe. Sixteen weeks after clipping, plasma renin concentration and plasma angiotensin II concentration did not differ between 2K1C and sham-operated rats (plasma renin activity, sham rats 16.2 +/- 4.2 vs. 2K1C rats 8.9 +/- 1.3 ng angiotensin I.mL-1.h-1; plasma angiotensin II, sham rats 14.7 +/- 7.5 vs. 2K1C rats 6.8 +/- 1.3 pg/mL), while plasma angiotensin concentration in 2K1C rats was higher than that of sham rats (p less than 0.05). Renin gene expression in the ischemic kidney was 2.2 times higher than that in the kidney of sham-operated rats (p less than 0.05), and decreased to 80% of those in the kidneys of sham-operated rats. These results suggest that overexpression of the kidney renin gene in the chronic phases of 2K1C rats may contribute to the sustained high blood pressure, and the kidney renin gene may be inhibited by posttranscriptional factors, i.e., suppressed activation of prorenin to renin.

Animals↗

PubMed1991

Significance of levels of circulating IgA-class immune complex in discriminant analysis of patients with IgA nephropathy before renal biopsy.

Discriminant analysis of clinical markers including circulating IgA-class immune complex (IgA-CIC) before renal biopsy in patients with IgA nephropathy is described. Fifty-six patients with IgA nephropathy (IgA nephropathy group) and 54 patients with other primary chronic glomerulonephritis (non-IgA nephropathy group) were examined. Discriminant analysis was applied to separate these two groups by using 21 clinical markers including levels of IgA-CIC. The levels of IgA-CIC in sera were measured by a solid-phase anti-C3 Facb enzyme immunoassay (EIA). Among these clinical markers, the levels of serum IgA, IgA-CIC and creatinine, and the degree of microhematuria in the IgA nephropathy group were significantly higher than those in the non-IgA nephropathy group. Contributions of IgA and IgA-CIC to the classification were very high and both had almost the same effect. The correct classification rate was 80.00% using five clinical markers: serum IgA, microhematuria, IgA-CIC, serum creatinine, and blood urea nitrogen. It was shown that the levels of serum IgA and IgA-CIC were major markers for the clinical diagnosis of patients with IgA nephropathy. It was concluded that discriminant analysis before renal biopsy was useful for the diagnosis of IgA nephropathy.

Adolescent↗

PubMed1991

Homozygous C3 deficiency associated with IgA nephropathy.

A 23-year-old male patient with homozygous C3 deficiency who developed asymptomatic proteinuria and hematuria was reported. Renal biopsy disclosed typical IgA nephropathy with deposition of early- and late-complement components except for C3 deposition. C9 and membrane attack complex were detected in the glomeruli despite the absence of C3. It was suggested that there might be some unknown complement activation mechanism which does not require C3 component.

Adult↗

PubMed1991

Thrombosis-inducing activity in plasma of patients with acute respiratory tract infection disappears after treatment.

Thrombosis-inducing activity (TIA) was identified in plasma from 16 of 27 patients (59%) with acute respiratory tract infections. On the other hand, it was present in only 9 of 79 subjects (11%) with chronic lung diseases and 4 of 49 healthy volunteers (8%). In the patients with acute respiratory tract infections, there were significant elevations in plasma fibrinogen, C-reactive protein and erythrocyte sedimentation rate in the TIA-positive group compared with the negative group. Plasma TIA disappeared in all of the 8 patients who were retested for TIA 2-5 weeks after they became disease free. Pneumonia was induced in rabbits by transbronchial injection of viable Escherichia coli. TIA was not present in plasma from normal rabbits, but it appeared in plasma collected 3 days after injection. It then disappeared after 1-2 weeks of treatment with antibiotics. TIA may serve as a marker for inflammatory responses and be a factor responsible for elevated blood coagulation activity in patients with acute infectious diseases.

Acute Disease↗

PubMed1991

Plasma thrombosis-inducing activity in 120 patients with primary lung cancer.

One hundred and twenty patients with primary lung cancer were examined for the presence of thrombosis-inducing activity (TIA) in their plasma. TIA was identified in plasma from 16 of 38 patients with stage 3 (42%) and 31 of 65 patients with stage 4 (48%) disease. On the other hand, only 1 of 17 patients with stages 1 and 2 (6%) showed TIA in their plasma. Cell type did not seem to correlate with the presence of plasma TIA, since TIA was identified in plasma from patients with all cell types. Survival of 32 patients with inoperable non-small cell lung cancer, all stage 4, was studied. The mean survival time was 7.2 months in the TIA-positive group and 10.3 months in the TIA-negative group. This difference was statistically significant.

Adult↗

PubMed1991

Dentin bond strength of light-cured glass-ionomer cements.

The purpose of this study was to investigate the influence of surface treatments and irradiation conditions on the bond strength of light-cured glass-ionomer cements to dentin. The light-cured glass-ionomer cements used in this study were Vitrabond, XR Ionomer, and Fuji Lining LC. Three experiments were designed to study the influence of the following factors on bond strength to dentin: (1) effect of the surface treatment of the dentin, (2) effect of the irradiation time, (3) effect of an increase in the interval between mixing of the cement and irradiation. Samples were stored in water for 24 hours, after which shear bond testing was performed at a cross-head speed of 1 mm/min. For Vitrabond, the Scotchprep and Gluma 2 treatments gave the greatest shear bond strengths. For XR Ionomer and Fuji Lining LC, the Scotchprep treatment gave the greatest shear bond strengths. The bond strengths for all cements increased with prolonged irradiation time. Bond strengths decreased with a longer elapsed time between mixing and light-curing. This means that light-curing should be done soon after the cement is placed. The failure mode was found to be cohesive in the ionomer.

Acid Etching, Dental↗

PubMed1991

[Interdigestive migrating complex (IMC) and effect of cisapride in patients with non-ulcer dyspepsia (NUD)].

The 24-hr gastric and duodenal pressure measurement was performed in 5 patients with non-ulcer dyspepsia (NUD). The reduction of incidence of IMC and prolongation of the first appearance of IMC after evening meal were observed in NUD patients. The gastroprokinetic agent, cisapride 5 mg, 3 times a day for 7 days significantly increased the incidence of IMC and shortened the time before the first appearance of IMC after evening meal. This result indicates that in NUD patients impaired gastrointestinal motility is present in fasting phases and cisapride may be useful for correcting motility disorders.

Aged↗

PubMed1991

Effects of antioxidants on survival of adult rat hepatocytes under various oxygen tensions in serum-free primary culture.

Effects of antioxidants, such as superoxide dismutase, vitamin C, vitamin E, 4-(0-benzylphenoxy)-N-methylbutylamine hydrochloride (bifemelane), and selenite on survival of adult rat hepatocytes were examined under normoxic and hyperoxic conditions in serum-free primary culture. The tested antioxidants, except for vitamin C, significantly increased the survival rate of hepatocytes under the normoxic condition (under air). Thus, even the normoxic culture condition is hyperoxic for hepatocytes. Elevation of oxygen tension (40% O2) caused severe morphologic degeneration of hepatocytes and remarkable decrease in the survival rate of the cells. Addition of the antioxidants effectively protected hepatocytes from the morphologic degeneration, and significantly improved the survival of the cells under the hyperoxic condition. These findings indicate that the antioxidants can maintain the long-term survival of hepatocytes in serum-free primary culture.

Animals↗

PubMed1991

AVDO2 and EEG as indicators for treatment of post-traumatic brain swelling--experimental study.

A cat model of compression ischemia using epidural balloon inflation investigated: 1) the relationship between postischemic cerebral blood flow (CBF) and metabolism and brain swelling, 2) the use of arteriovenous oxygen difference (AVDO2) and electroencephalographic (EEG) frequency band analysis for monitoring CBF and cerebral metabolism, and 3) indications for selecting the therapy. Global ischemia was induced by brain compression, followed by rapid decompression, and AVDO2, CBF, cerebral metabolic rate for oxygen, and EEG were monitored. The animals were divided into delayed brain swelling and no swelling groups. The severity of compression ischemia influenced the recovery of CBF and cerebral metabolism. The AVDO2 and EEG reflected the CBF and cerebral metabolism. These parameters are useful in selecting the therapy for focal brain injury.

Animals↗