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Biomedical subjects

K Oyanagi

Publications and source records attributed to K Oyanagi.

At least 109 records · Page 6Linked to original sources
PubMed1988

[Early development of cerebral blood vessels: on the relationship between cerebral histogenesis and internal vascularization].

The purpose of this study is to evaluate the morphological relevance to cerebral histogenesis and internal vascularization during early fetal development of rats. Using light and electron microscopes, fetal brains and spinal cords from embryonic day 11 (E11) to E 16 were observed with special attention to new blood vessel formation in the parenchyma. At stages of the neural groove and neural tube blood vessels were confined in the perineural mesenchyma around the matrix cell layer whose cytoarchitecture was arranged in a pseudostratified pattern and did not include the blood vessels. At the prosencephalic stage (E 13), primordium of the striatum which localized in the ventrolateral portion of the cerebral neopallium made up the migrating zone in outer most of the matrix cell layer and blood vessels firstly appeared in this area. Similarly, the blood vessels were also recognized at the ventro-lateral portion of the mesencephalon where the migrating zone was initially formed on E 13. In the cervical spinal cord, the blood vessels were initially recognized on E 12, when the migrating zone was formed at the area of anterior horn. At the early telencephalic stage during E 14-E 15, blood vessels were evenly distributed in the lateral cerebral neopallium, while the cerebral neopallium in the midline where took place later evolution than lateral neopallium was still remaining in the state of matrix cell layer only, and was also lacking the blood vessels. In this area, first appearance of the vessels was E 15 or E 16.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Selective involvement of large neurons in the neostriatum of Alzheimer's disease and senile dementia: a morphometric investigation.

In order to evaluate the quantitative changes in the neostriatum of Alzheimer type (SDAT), sections of the caudate head (CN) and putamen (PT) from 4 AD/SDAT and 6 age-matched control cases were stained with Klüver-Barrera, and the cell body and nuclear areas of the neurons were measured by a digitizer. This study revealed a significant decrease in the number of large neurons (nuclear area; greater than 101 micron 2) and good preservation of the number of small neurons (nuclear area; less than 100 micron 2) in CN and PT of AD/SDAT.

Aged↗
PubMed1987

An autopsy case of a syndrome with muscular atrophy, decreased subcutaneous fat, skin eruption and hyper gamma-globulinemia: peculiar vascular changes and muscle fiber degeneration.

This is the first autopsy case report of a syndrome with autosomal recessive inheritance, muscular atrophy, contracture, skin eruption, hyper gamma-globulinemia, decreased subcutaneous fat, mental retardation and abnormal ECG findings. Skeletal muscles showed severe, discrete, multifocal muscular fibrosis which replaced several primary fasciculi. The tongue, heart and extraocular muscles showed identical but less severe findings. In the involved muscle fasciculi, veins and venules as well as arteries and arterioles showed medial hyperplasia and luminal constriction. Degeneration of endothelial cells of arterioles and narrowing of the lumen of terminal arterioles by the debris were observed. The peripheral nerves in the muscles were relatively well preserved. The correlation and pathogenesis of these findings are discussed.

Central Nervous System↗
PubMed1987

Clinical, biochemical and enzymatic studies in type I hyperprolinemia associated with chromosomal abnormality.

A severe mentally retarded infant with type I hyperprolinemia associated with chromosomal abnormality is reported. The patient had a characteristic facial appearance of hyperprolinemia and suffered from convulsions after the age of 10 months. The child developed severe mental and motor retardation. The karyotype of the patient revealed partial duplication of the short arm in chromosome 10 using G banding techniques. The patient and her mother showed a fasting hyperprolinemia and an abnormal clearance curve after the proline load in the serum. The proline oxidase activities of the liver tissues obtained by biopsy in the patient was about 9% of those of controls. Kinetic studies and mixed experiments of the enzyme were with normal limits. Restriction of dietary proline at the age of 12 months revealed a prompt fall of the plasma levels of proline to the normal range, and a low proline diet was continued until the present time. During the period of dietary treatment, growth was satisfactory, but her mental development did not improve. From the developmental patterns of proline oxidase activities postnataldy, we speculated that restriction of dietary proline intake should be relieved with age.

Amino Acid Metabolism, Inborn Errors↗
PubMed1987

Immunoenzymatic studies of ornithine transcarbamylase (OTC) in liver of patients with OTC deficiency by enzyme linked immunosorbent assay (ELISA).

Antigen contents of ornithine transcarbamylase (OTC) protein in the liver of 5 patients with OTC deficiency and mutant mice were studied by ELISA. OTC activities in the liver tissues of 2 patients were 13.1% and 5.2% of the controls, respectively. The 2 patients' antigen contents of OTC protein were decreased in parallel with the enzyme activities. OTC antigen contents were not detected in the liver tissues of remaining 3 patients who had the complete type of OTC deficiency. Enzyme activities, kinetic properties and antigen contents of the OTC deficient mutant mice were the same as the results reported previously (Briand et al. 1982). The ELISA method for the assay of OTC antigen contents used in this study is more sensitive as compared with the radial immunodiffusion technique.

Animals↗
PubMed1987

Studies on the expression of liver-specific functions of human fetal hepatocytes in primary culture.

Biochemical functions of human livers were studied using fetal hepatocytes in primary culture. Immunocytochemical staining showed that albumin was not expressed in any fetal hepatocytes, whereas alpha-fetoprotein was detected in almost all the cells. Tryptophan 2,3-dioxygenase (TO, EC 1.13.11.11.) activity was not induced in the presence of 10(-7) M dexamethasone and 10(-7) M glucagon, but the activity of tyrosine aminotransferase (TAT, EC 2.6.1.5.) was elevated about 35 fold under the same conditions. These results suggest that the TAT and alpha-fetoprotein genes are activated in human fetal liver at 14 to 20 weeks of gestation.

Albumins↗
PubMed1987

Control of growth and amino acid transport of mature rat hepatocytes by human newborn serum.

DNA synthesis and system A-mediated amino acid transport were studied in primary culture of adult rat hepatocytes maintained as a monolayer. Potent growth promoting activity and inducibility of system A-mediated amino acid transport could be found in human newborn sera but not in human adult sera. The maximal activity to promote DNA synthesis was about the same level as insulin (10(-7) M) plus epidermal growth factor (EGF, 20 ng/ml). These results suggest the presence of a hepatocyte-specific growth factor in human newborn sera controlling the amino acid metabolism during the newborn period.

Amino Acids↗
PubMed1987

Cytotoxicities of sodium benzoate in primary culture of hepatocytes from adult rat liver.

The cytotoxicities of sodium benzoate was studied using primary culture of hepatocytes established from adult rat liver by a collagenase perfusion technique and maintained as a monolayer in serum-free culture medium. The activities of ornithine transcarbamylase (as a marker of mitochondria) and tyrosine aminotransferase (as a marker of cytosol) were clearly suppressed by sodium benzoate at concentration in excess of 500 micrograms/ml. Intracellular protein synthesis and DNA synthesis were also suppressed, and the suppression of DNA synthesis was observed even with a lower concentration of benzoate (100 micrograms/ml).

Animals↗
PubMed1987

[Selectivity of cell degeneration and histological peculiarities of the repair process in the developing rat spinal cord after ethylnitrosourea administration].

We observed the selectivity of cell degeneration and histological peculiarities of the repair process in the lesion of developing rat spinal cord. Each of the 21 pregnant rats was given a single injection of ethylnitrosourea (ENU), 60 mg/kg body weight, in the tail vein on embryonic day 16. Each fetus was removed surgically from the dam every 2 hours for 24 hours and every 24 hours for 5 days. These fetuses were fixed by the transcardial perfusion to observe them with light and electron microscope. Degeneration was induced selectively in certain cells of the proliferating phase of the matrix cell layer and in the migrating neuroblasts in the alar plate. Individually affected cells were eliminated by phagocytes in the pre-existing extracellular space. No reactive gliosis, fibrosis, abnormal vascularization or infiltration of granulocytes and lymphocytes was observed at any time.

Animals↗
PubMed1986

Absence of argininosuccinate lyase protein in the liver of two patients with argininosuccinic aciduria.

The enzyme defects in two cases of argininosuccinic aciduria were examined at the molecular level by enzymatic and immunological methods. No argininosuccinate lyase activity was detected in the liver or erythrocytes of either patient nor in the kidney or brain of one of the patients even in the presence of high concentrations of the substrate. The titration curve of antiserum to human argininosuccinate lyase with the liver extract from a control subject was not affected by the addition of the liver extracts from one of the patients. Double immunodiffusion analysis revealed a single precipitin line between the purified antiserum and the liver extract from a control, but no precipitin lines between the antisera and the liver extracts from the two patients. These results indicate a complete or almost complete defect of an immunologically cross-reactive material in the liver of the patients.

Amino Acid Metabolism, Inborn Errors↗
PubMed1986

The chronology of lesion repair in the developing rat brain: biological significance of the pre-existing extracellular space.

We observed the histological peculiarities of the repair process in a destructive lesion of the developing rat brain during neurogenesis. Degeneration was induced selectively in certain cells of the proliferating phase in the rat fetal neopallium on embryonic day 16 by transplacental administration of ethylnitrosourea. Successive elimination of necrotic cells and the restoration process were observed. The repair process was divided into the following steps: elimination of individually affected cells by phagocytes in the pre-existing extracellular space; successive restoration of the disintegrated area by cells which differentiated from remaining matrix cells. No reactive gliosis, fibrosis, abnormal vascularization or infiltration of granulocytes and lymphocytes was observed at any time. The thinned neopallium on postnatal day 21 revealed only a small number and abnormal distribution of the cortical neurons. It may be assumed that the fetal brain owes its unique repair features to the presence of a vast extracellular space under normal conditions. In this pre-existing extracellular space, every kind of cell seems to exist separately without the intracellular adhesions characteristic of the adult brain. When degeneration occurs in certain cells the phagocytes would be able to eliminate the degenerate cells completely in this space without having to break intercellular adhesions. As a result, after the completion of cell elimination, the injured brain is restored to its original state with no cell reaction, giving the appearance of a small brain with normal-looking histological architecture, save only for the sparseness of cells.

Animals↗
PubMed1986

Citrullinemia: quantitative deficiency of argininosuccinate synthetase in the liver.

Two cases of citrullinemia were reported. Case 1 was an one month old female. Her clinical course and findings were different from the fulminant type of neonatal citrullinemia reported in predominantly Caucasian countries. Our patient was well controlled under a low protein diet and essential amino acids till 9 months of age, but unfortunately she died of Reye's like syndrome. Case 2 was 31 year old male (at the time of death). He was admitted to our hospital because of hyperammonemia and mental retardation. By subsequent laboratory investigations he was diagnosed as having adult type of citrullinemia and died of hepatoma. Enzymological analysis revealed that argininosuccinate synthetase (ASS) activities in the liver tissues of the patients decreased to 40% (Case 1), 20% (Case 2) compared with those in control liver tissues. The other urea cycle enzyme activities were all within normal range. ASS activities in the kidney and brains of the two cases were within normal range. The kinetic constant values of ASS for three substrates in the tissues of liver and kidney were all normal. Results of immunochemical analyses indicated that citrullinemia in our patients was caused by a quantitative deficiency of ASS associated proteins of the liver and kidney tissues as to the molecular weight.

Adenosine Triphosphate↗
PubMed1984

[Initial cellular damage in the developing rat brain caused by cytotoxicity of ethylnitrosourea].

Initial cellular degeneration in developing rat fetal brains were induced during the early cytogenetic period of neuroblasts by cytotoxic action of ethylnitrosourea (ENU). This was transplacentally administered. After a single intravenous administration of 60 mg/kg body weight ENU to 16th day-pregnant rats, each fetus was removed surgically from the uteri every hour for 24 hours and every day for 9 days. These were fixed by the transcardial perfusion method to observe them with light and electron microscopes. From 4 hours after the ENU-treatment, the degenerative alteration of cells, characterized ultrastructurally by cytoplasmic condensation and nuclear pyknosis, developed selectively in the matrix cell layer of the fetal cerebrum where active cell division was carried out to produce neuroblasts. Cellular degeneration was first noticed at the zone of DNA synthesis and then all the matrix cell layer including the mitotic phase. Furthermore, the cell processes of matrix cells, or so-called radical fibers, were also recognized to be in the same degenerative processes. These affected cells increased in number and became arranged in columns along the radial fibers through the process of time, and successively migrated to the migrating zone through the outer part of the matrix cell layer. At 10 hours after treatment, many cells were observed in the migrating zone and a few cells were noticed in the matrix cell layer. The degenerated neuroblasts reached the cortical plate about 3 hours after the development of initial degeneration. In contrast, the neuroblasts in the cerebral cortical plate which had already been formed at the time of ENU administration were not affected by the ENU and persisted for the following developments.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Revised pathophysiology on BBB damage: the edema as an ingeniously provided condition for cell motility and lesion repair.

Probably, the most important evidence concerning the breakdown of the BBB is a large inflow of hematogenous fluid into the extravascular spaces. Thus all parenchymal cell elements represent freely floating cells in this fluid medium called the edema fluid. These essential morphological alterations, such as extremely expanded extracellular space and freely floating cells within the fluid, were also observed in the developing normal fetal brain. Many neuroblasts were vigorously migrating in the fetal brain, as were the macrophages and reactive astrocytes in the edema fluid. Obviously, hematogenous cells and reactive astrocytes in the edematous lesion take part in its repair. Many astrocytes, GFAP positive, in the 3 or 4 day-old lesions, revealed mitosis. And in vitro, when we immersed these astrocytes in the protein and glucose rich medium, they demonstrated a remarkably changed morphology and were moved into the M and G1 phases, thus gaining the ability of cell motility. This was also true in the edema fluid. Brain edema is definitely a serious "pathological" condition. But it is also conceivable from a different biological aspect that as a result of BBB "opening", free extracellular space essential for cell motility and a source of their energy is ingeniously provided for these cells, and thus the lesion can be effectively repaired. The biological significance of the edema fluid was emphasized and stereotaxic morphology and cinematography, supporting the above evidence, have also been presented.

Animals↗