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Biomedical subjects

M Segawa

Publications and source records attributed to M Segawa.

At least 127 records · Page 7Linked to original sources
PubMed1989

[An intensification therapy of adults acute leukemia].

Between January 1980 and March 1983, a study was conducted on the effects of intensification therapy in 20 adult acute leukemia patients who had achieved complete remission with induction therapy. Intensification therapy consisted of cyclic administration of six combination therapies given at gradually longer intervals, using daunorubicin, cytosine arabinoside, 6-mercaptopurine and prednisolone (DCMP), cyclocytidine (DCyMP), vincristine (DCVP), behenoyl-ara-c (BHAC-DMP), aclacinomycin (BHAC-AMP) and (ACM-MP). Six combinations were given sequentially at one-month intervals, at 2-, 3-, 4-, 5- and eventually 6-month intervals, until 5-year survival. The median remission duration was 38 months for AML, and 17 months for ALL. The median survival was 66 months for AML, and 37 months for ALL. The five year survival rate was 50%. Nine of the 20 patients are still alive. Methotrexate and prednisolone were administered intrathecally for prophylaxis of CNS leukemia on Day 4 for each intensification therapy. There was no CNS leukemia. This intensification protocol was shown to be effective in improving the prognosis of adults acute leukemia.

Acute Disease↗
PubMed1989

[A neurologic model of early infantile autism].

Based on the abnormalities in sleep-wakefulness cycle of early infantile autism, the author discussed its pathophysiology focusing on its main lesion in the raphe nuclei. These neurons, located in the midline portion of the brainstem send their axons to various neurons of the upper and lower nervous systems, including the locus coeruleus and the dopamine neurons of the tegmentum, the former having a broad innervation and the latter a restricted area in the central nervous system. These monoaminergic neurons modulate the functions of the involved neurons and regulate their functional and structural maturation in the early developmental course. The early lesion of the raphe nuclei causes poor adaptation to environment which develops as abnormal circadian oscillation and pervasive lack of responsiveness. Combined hypofunction of the locus ceruleus, particularly of its dorsal bundle, results in the failure of extinction of acquired memory in mice which relates clinically to the excellent memory and resistance to change peculiar interests and attachments in humans. From early childhood, the disturbance of dopaminergic neurons becomes apparent clinically, and causes hyperkinesia and stereotyped activities. With the other two monoaminergic neurons, dopaminergic neurons cause occasional aggressiveness or self-mutilation. The latter behaviors are like those of pampered children and are simulated to "muricide" and "friendliness" observed in rats with these monoaminergic lesions. The particular language disturbance with echolalia is due to the right hemispheric dominance, which might have been caused by a delayed functional lateralization of the hemisphere resulting also from the delayed development of the circadian oscillation in infancy. The motor disturbances consisting of hypotonia and impaired locomotion might be due to decreased tonic innervations of the locus ceruleus and the raphe nuclei to the spinal locomotion center. CT examination of symptomatic autism showed the amygdala as one of the causative nuclei for the autistic behavior.

Animals↗
PubMed1988

Muscle pathology in cytochrome c oxidase deficiency.

Muscle biopsies from 16 patients with cytochrome c oxidase (CCO) deficiency were examined morphologically. Two siblings had the fatal infantile form. The muscle of the older sister at the age of 5 months had numerous ragged-red fibers (RRF) and increased numbers of lipid droplets; at 28 days the brother had no RRF suggesting that the RRF formed later than 28 days. The muscle pathology in two patients with the benign infantile form improved as they grew older; numbers of RRF, lipid droplets and glycogen particles decreased and CCO activity increased in the second biopsy. In the encephalomyopathic form, RRF were seen in 5 of 12 muscles mostly in patients more than 6 years of age. Muscle spindles and blood vessel walls in the biopsies from three patients with rapid clinical aggravation had no CCO activity, suggesting that enzyme activity differed from tissue to tissue (tissue specificity).

Adolescent↗
PubMed1988

The development of electroretinogram abnormalities and the possible role of polyol pathway activity in diabetic hyperglycemia and galactosemia.

This study examined the induction of electroretinogram abnormalities in hyperglycemia and the possible role of increased polyol pathway activity in the development of these changes. Both diabetic hyperglycemia and galactosemia caused the prolongation of peak latencies and in some cases a reduction in the amplitudes of oscillatory potentials on the b-wave. Diabetic hyperglycemia-associated abnormalities were prevented and normalized by insulin or ADN-138, an aldose reductase inhibitor. Galactosemia-induced abnormalities were inhibited by ADN-138, and were reversed either by ADN-138 treatment or by withdrawal of galactose from the diet. Polyol accumulation was prevented by insulin or ADN-138, and the elevated polyol level was reversed by insulin, ADN-138, or withdrawal of galactose in diabetic hyperglycemia and/or galactosemia. These results suggest that the increased polyol pathway activity in the hyperglycemia may be involved in the development of electroretinogram abnormalities similar to those in human diabetes; therefore, ADN-138 could be a useful drug for therapy of retinopathy in the early diabetic stage.

Animals↗
PubMed1987

Localization of Rh1(D), 2(C), 3(E), 4(c), 5(e) and 25(LW) antigens of human Rh blood groups in fetal erythrocyte membranes.

The fetal erythrocyte membranes were partially solubilized with Triton X-100 at the low concentration (0.5%). The localizations of Rh1(D), 2(C), 3(E), 4(c), 5(e) and 25(LW) were investigated. Using hemagglutination inhibition assay, Rh1(D) antigen activity was observed in the Triton-treated membrane (Triton shell) containing mainly band 1, 2 (spectrin), band 5 (actin), band 4.1 and a part of band 3, while Rh2(C), 3(E), 4(c), 5(e) and 25(LW) antigens were detected in the supernatant containing band 3, 6, 2.2, 2.3 and 4.2. It is suggested that: Rh1(D) antigen would associate with cytoskeleton matrix of fetal erythrocyte membranes; Rh1(D) and Rh25(LW) antigens might be integral membrane proteins, while Rh2(C), 3(E), 4(c) and 5(e) antigens would be surface membrane proteins which are easily released from membranes by EDTA, mercaptoethanol and alkaline treatments.

Antibodies↗
PubMed1987

Pathophysiology of Rett syndrome.

Rett syndrome is a distinct clinical entity with an unknown cause. In previous publications we stressed the age related sequential appearance of pathognomonic symptoms of Rett syndrome and suggested the early central monoaminergic deficiency disorder as the pathophysiology. In this report we present a series of cinefilms made of one patient at different ages which clearly show the age dependent changes of motor disturbances. Furthermore, the record of sleep-wakefulness rhythm and the series of polysomnography of another patient who was on L-DOPS are presented. The results of sleep studies again confirm the early involvement of the noradrenergic and serotonergic systems and relatively early development of postsynaptic supersensitivity of the dopaminergic system. The possibility of the involvement of the cholinergic system is also suggested. The summary of the sensory evoked potentials (SEP) performed on six patients is also presented and the pathomechanism of cortical involvement is discussed. Based on these new and past findings, we confirm our speculation on the pathophysiology. The basic mechanism is probably the deficient states of the monoaminergic systems occurring at a very early developmental stage. These derangements occurring at an early stage cause serious abnormality in the higher centers during development. The striking age dependent clinical manifestations and measurable physiological parameters are the reflexion of the underlying patho-physiology of Rett syndrome.

Age Factors↗
PubMed1987

[Effect of a hybrid artificial pancreas in totally pancreatectomized dogs].

This study was undertaken to estimate the effect of hybrid artificial pancreas (HAP) containing xenogeneic hamster islets in totally pancreatectomized dogs. HAP were attached either to the systemic circulation or to the portal circulation for 12 to 24 hours in totally pancreatectomized dogs. Following the systemic attachment of HAP containing 10,000 islets, in four out of 6 dogs the plasma glucose levels decreased to normoglycemic levels within 5.8 +/- 1.3 hours and thereafter maintained within normal range at least 12 hours until the removal of HAP. When HAP containing 10,000 islets were attached to the portal circulation, no decrease in the plasma glucose levels was observed in all four dogs. However, HAP containing 14,000 islets were able to restore normoglycemia in four out of 5 dogs within 7.0 +/- 1.6 hours after the portal attachment. No significant difference in the plasma glucose level was observed between the dogs with HAP containing 10,000 islets attached to the systemic circulation and those with HAP containing 14,000 islets attached to the portal circulation. Those results suggested that the systemic circulation, concerning with the quantity of the islets, was the superior site of the attachment of HAP to the portal circulation for controlling hyperglycemia in apancreatic dogs.

Animals↗
PubMed1987

Determination of ABO blood groups by radioimmunoassay using 125I-protein A.

Since the crystallizable fragment (Fc) portion of the immunoglobulin G (IgG) molecule is the binding site of Protein A, a radioimmunoassay procedure using 125I-Protein A was developed for identification of the ABO blood groups. The isotope level bound to Group A, B, or AB red cells decreased with the dilution of anti-A or -B, respectively. After sensitization by anti-A plus B in Group O serum, the isotope bindings were observed in Groups A, B, and AB cells, while no significant radioactive count appeared in Group O cells. Furthermore, there was little significant isotope binding in both Group A and B red cells sensitized by the serum from Group A or B blood containing mainly IgM anti-A or -B. A radioimmunoassay using 125I-Protein A is an excellent method for identifying ABO blood groups.

Blood Group Antigens↗