[Clinical survey of spontaneous pneumothorax in patient aged 40 or over].
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Biomedical subjects
Publications and source records attributed to H Tada.
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Glutamic acid decarboxylase (GAD) activity in the cerebrospinal fluid (CSF) of normal infants (n:14) and children (n:28) was determined by measuring the amount of 14CO2 released from L-[1-14C]-glutamic acid. The mean GAD activity in CSF of infants and children was 5.2 +/- 2.5 pmol CO2 formed/hr/ml. Dividing these subjects into 4 groups according to age, GAD activities in CSF were 5.4 +/- 1.6 pmol CO2 formed/hr/ml in neonates (0-1 m), 3.6 +/- 1.6 pmol CO2 formed/hr/ml in infants (2-12 m), 3.9 +/- 1.1 pmol CO2 formed/hr/ml in young children (2-6 yr) and 7.1 +/- 2.3 pmol CO2 formed/hr/ml in school children (7-16 yr), respectively. In neonates and school children, GAD activities were significantly higher (p less than 0.001) than those in the other age groups. In infants under 6 months of age, a significantly negative correlation between GAD activity in CSF and their ages was recognized (r = -0.52, p less than 0.001). In infants and children ranging from 6 months to 16 years of age, a significantly positive correlation between GAD activity in CSF and their ages was found (r = 0.67, p less than 0.001). These data suggest that high GAD activity in neonates may be due to hypoxia at birth and the activity gradually increases from 6 months to 15 years of age.
Glutamic acid decarboxylase (GAD) activity in cerebrospinal fluid (CSF) was determined in 53 patients with neurological diseases as follows: Epilepsy (n:17), febrile convulsions (n:3), meningoencephalitis (n:17), encephalopathies (n:10), CNS leukemia (n:3), congenital hydrocephalus (n:2) and pseudoileus neonatorum (n:1). Compared with the mean normal value (5.2 +/- 2.5 pmol CO2 formed/hr/ml) reported in Part I, a significant increase of GAD activity in CSF was demonstrated in patients with uncontrolled epileptic seizures (11.4 +/- 3.9 pmol CO2 formed/hr/ml), febrile convulsions (13.5 +/- 8.7), viral meningitis with or without encephalitis (20.3 +/- 13.6), encephalopathies (30.0 +/- 25.9), CNS leukemia (11.1 +/- 5.0), congenital hydrocephalus (20.5 +/- 7.3) and pseudoileus neonatorum (28.6). Markedly high GAD activity was found in patients with CNS leukemia several days after intrathecal injection of methotrexate (39.8 +/- 18.0). On the other hand, significantly low GAD activity was shown in patients with bacterial meningitis or brain abscess (1.3 +/- 1.2). This suggests that some bacterial factors may be inhibitory toward GAD activity in CSF. High GAD activity in CSF may be useful as an indicator of aseptic brain dysfunction, although it was not always correlated with the severity of symptoms.
Effects of acetazolamide (AZA) on the serum elimination and brain distribution of barbital (BA), phenobarbital (PHB), pentobarbital (PEB) and hexobarbital (HB) were studied in mice. When the barbiturates were administered intraperitoneally to mice, the pretreatment of AZA reduced the serum BA and PHB levels, and significantly increased these brain levels. While relatively small and no effects of AZA were observed for the PEB and HB levels, respectively. After the intravenous administration, the serum elimination of these barbiturates were described by the two compartment model. Although the pretreatment of AZA tended to increase the volumes of central compartment and decrease the elimination rate constants for BA, PHB and PEB, the elevated brain levels of the barbiturates could not be explained as the simulated peripheral concentrations. However, it appeared that the prolongation effect of AZA on the BA, PHB and PEB sleeps in mice was associated with the elevated brain barbiturate levels with AZA.
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Prevention of perinatal transmission of hepatitis B virus carrier state in neonates at high risk was attempted by a combined passive and active immunization. Immediately after delivery, ten babies born to mothers who were asymptomatic carriers of hepatitis B surface antigen (HBsAg) and seropositive for hepatitis B e antigen received an intravenous injection of F(ab')2 fragments (200 IU) derived from hepatitis B immune globulin (HBIG). On the following day, none of them revealed detectable levels of the antibody to HBsAg in their sera, and received an intramuscular injection of HBIG (200 IU) which was repeated at 2 and 4 months of age. Vaccination with 40 micrograms of purified, formalin-inactivated HBsAg particles was given to the nine babies at three months and repeated at 4, 5, and 7 months after birth. All of them maintained detectable levels of the antibody and escaped infection throughout the first 12 months of their lives. The one baby who did not have detectable F(ab')2 in serum for 24 hours developed persistent HBs antigenemia which was noticed as early as seven days after birth.
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The distribution of 2,4-dinitrophenyl (DNP) groups in the draining lymph nodes of guinea pigs 12 h after painting the skin with 2,4-dinitrochlorobenzene (DNCB) was examined by a peroxidase labelled antibody method using antibody against DNP groups. DNP groups were detected on cells that were found mainly in the subcapsular sinus of the lymph nodes. Electron microscopic examination showed DNP groups distributed on the surface of lymphocytes. The significance of these findings is discussed.
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