[Intracranial venous blood flow velocities in infants].
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Biomedical subjects
Publications and source records attributed to M Tatsuno.
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The structural abnormality of mRNA for argininosuccinate synthetase (ASS) and the structure of immune cross-reactive material for ASS (ASS-CRM) in the liver of a patient with type III citrullinemia were analyzed using dot and Northern blot hybridization, S1 nuclease analysis, and a sensitive enzyme-linked immunosorbent assay. The patient's liver contained no detectable ASS activity, the ASS-CRM content was about 0.5% of that in the control and the ASS mRNA content was almost normal. The ASS mRNA of the case was found to have an apparent structural abnormality; approximately 1.57 kb in length caused by a defect of about 0.1 kb near the 3' end of the coding region. Furthermore, gel filtration analysis revealed that the ASS-CRM had a molecular weight indistinguishable from the control ASS. These results indicate that the abnormal mRNA of the patient was translated in vivo to an immune-cross-reactive protein that was able to form a quaternary structure.
This paper deals with enzymological, immunochemical and molecular genetic analyses of citrullinemia and argininosuccinic aciduria. Citrullinemia has been classified by Saheki et al. [J. inher. Metab. Dis. 8: 155-156, 1985] into three types from the properties of the deficient argininosuccinate synthetase (ASS) of the patients. Analysis of hepatic mRNA coding for ASS revealed certain characteristics in type II and III citrullinemic patients whose hepatic ASS protein was low. A newly developed enzyme-linked immunosorbent assay (ELISA) of argininosuccinate lyase (ASL) protein showed that 8 out of ten cases of argininosuccinic aciduria had no detectable ASL protein in the liver, erythrocytes, cultured skin fibroblasts or cultured amniocytes.
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We studied 4 very low birth weight infants with secondary cystic lesions in the cerebellum by serial cranial ultrasound and computed tomography. These infants presented severe respiratory distress, asphyxia at birth and intraventricular hemorrhage. In the neonatal period, cranial ultrasound examination showed significant intraventricular hemorrhage and posthemorrhagic ventricular dilatation with intraparenchymal hemorrhage. However, a cerebellar cyst was not seen in any of the infants. We found evidence of cerebellar hemorrhage by ultrasound in only one patient. Follow-up ultrasound examinations and CT scans showed progressive posthemorrhagic ventriculomegaly in three of the infants and large cystic lesions in the infratentorial area from 3 to 6 months old in all 4 infants. We conclude that the cystic lesions were caused by hemorrhagic and hypoxic-ischemic insults which occurred in very low birth weight infant.
A recently described herpes simplex virus (HSV) type 2 (HSV-2)-specific glycoprotein (gG-2) was purified on an immunoaffinity column prepared with monoclonal antibody. This purified antigen was used in an immunodot enzymatic assay on nitrocellulose paper for the detection of HSV-2 antibodies in human serum. The test was very sensitive in that HSV-2 antibodies were detected in the convalescent sera of 132 of 134 patients with recurrent genital infections in which HSV-2 had been isolated earlier. Antibodies to gG-2 were detected in 17% of sera obtained within 10 days after the onset of a primary HSV infection and in 95% of sera obtained more than 10 days after onset. The specificity of the immunodot assay was demonstrated by testing sera from 245 HSV-seronegative adults, 344 children, 29 nuns, and 13 patients with primary genital HSV-1 infections. None of these 631 sera was reactive with the gG-2 antigen. When compared with a microneutralization test, the immunodot assay was found to be more specific in detecting HSV-2 antibodies. Reproducibility of the gG-2 assay, obtained by retesting 391 sera, was 95%. Thus, this assay has the sensitivity, specificity, and reproducibility necessary for the measurement of HSV-2 antibodies in seroepidemiological studies.
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Monoclonal antibody panels selected in this and preceding studies were employed to begin to characterize the properties of human cytomegalovirus (CMV) glycoproteins. The results were as follows. (i) Four antigenically distinct CMV glycoproteins designated as gA, gB, gC, and gD have been identified. (ii) gA, gC, and gD each form several bands when immune precipitated from infected cell extracts by the corresponding monoclonal antibodies and electrophoretically separated in sodium dodecyl sulfate-polyacrylamide gels. In contrast, gB migrated at one broad band with an apparent molecular weight in the range of 116,000 to 123,000. Bands with different molecular weights were shown to share antigenic determinants by reactivity of monoclonal antibodies with electrophoretically separated polypeptides immobilized on nitrocellulose. (iii) A panel of 16 monoclonal antibodies to gA precipitated a family of glycoproteins 160,000-148,000, 142,000, 138,000, 123,000-107,000, 95,000, and 58,500 in apparent molecular weight designated as gA1 through gA6, respectively. (iv) To identify partially glycosylated precursors of gA, infected cells were treated with tunicamycin or deoxyglucose and reacted with different monoclonal antibodies. Tunicamycin-treated infected cells labeled for a short pulse or longer intervals contained only gA5. Whereas cells treated with deoxyglucose during a pulse contained gA4, those labeled for a longer interval contained gA6 and an additional band approximately 56,500 in apparent molecular weight designated gA7. (v) Precipitates of gA from infected cells labeled for a short pulse contained gA2 and gA3 which appear to be products of rapid glycosylation. After a chase, trace amounts of gA1 and gA6 were also precipitated suggesting that these are products of slow post-translational processing. (vi) Endo-beta-N-acetylglucosaminidase H was used to identify the forms of gA which contain high-mannose oligosaccharide chains. After treatment, the electrophoretic mobility of gA2, gA3, and gA6 increased significantly suggesting that these forms contain high-mannose chains cleaved by the enzyme. A hypothesis for processing gA is presented.
This report concerns 844 children with Down syndrome under 15 years of age. Of the 844 cases with Down syndrome, 1.4% have epilepsy at the present time. The types of seizures are as follows; infantile spasms in 4 cases (30.8%), generalized tonic-clonic convulsions in 6 (46.1%), Lennox-Gastaut syndrome in 1 (7.7%) and psychomotor seizure in 2 (15.4%). The onset of seizure was high in the first two years (73.7%). The occurrence of epilepsy in Down syndrome in childhood did not differ from that in the general population, but infantile spasms were prevalent in Down syndrome.
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The color Doppler flow imaging (CDFI) technique was used to study the dynamics of cerebrospinal fluid (CSF) flow in 13 infants with intracranial hemorrhage. CDFI was performed 46 times in 6 intraventricular hemorrhage (IVH) patients and 7 subarachnoid hemorrhage (SAH) patients with or without subdural hemorrhage during different stages. CSF flow was observed in 8 infants with IVH (5) or SAH (3) on CDFI. CSF flow in the aqueduct, third ventricle and foramen of Monro was visualized in both the upward and downward directions, primarily reflecting respiration and/or cardiac pulsation in the acute stage. It is suggested that CDFI may allow evaluation of the CSF flow dynamics and an early diagnosis of intracranial hemorrhage in infants.
Continuous monitoring of the cerebral blood flow, oxyhemoglobin, deoxyhemoglobin, total hemoglobin, oxidized cytochrome a, a3, and tissue pH during prolonged CO2 or N2 loading in 2-week-old rabbits was performed by near-infrared spectroscopy, the thermocouple method, and a tissue pH meter. Near-infrared spectroscopy demonstrated decreases in oxyhemoglobin and oxidized cytochrome a, a3 and increases in deoxyhemoglobin and total hemoglobin in the early stage within 5 min, which gradually lessened with time on both 10% concentration of inspired O2 with CO2 and N2. CBF increased with venous retention in the early stage and then slowly decreased in parallel with blood pressure and oxidized cytochrome a, a3 on abolition of autoregulation. These changes were more remarkable during the 10% concentration of inspired O2 with CO2 than N2 which may be caused by marked acidosis and hypotension associated with hypercarbia. Oxidized cytochrome a, a3, however, demonstrated a gradual decrease in 10% concentration of inspired O2 with N2 rather than CO2; therefore, the continuous monitorings demonstrated hemodynamic and oxygenation changes despite the same extent of prolonged hypoxic loading. These changes in prolonged hypoxic conditions may occur in human intrapartum asphyxia which develops into postnatal hypoxic-ischemic encephalopathy.