Determination and developmental changes in carbonic anhydrase III in swine liver.

1. CA-III was measured by enzyme-immunoassay in the livers of male and female swine aged from the fetus to 5 years old. 2. No sexual dimorphism in porcine liver could be detected at 6 months, but stag showed twice as much as swine of the same age. 3. The concentration of CA-III in the liver increased during development up to 6 months of age, followed by decline due to senescence.

Effects of combination therapy with low-dose aspirin and warfarin on platelet functions after heart valve replacement.

To evaluate the efficacy and safety of combination therapy with aspirin and warfarin for preventing the development of thromboembolism, we compared the effects of low-dose aspirin (81 mg/day) on platelet functions to those of ticlopidine (300 mg/day) in heart valve replacement patients. Experiments were performed in two groups; the first group within 1 month after operation (the unstable period) and the second group between 3 months and 3 years after operation (the stable period). At the stable period, low-dose aspirin inhibited platelet aggregation induced by ADP, collagen, or arachidonic acid, and suppressed the increase in intracellular Ca2+ concentration [( Ca2+]i) induced by thrombin significantly. On the other hand, ticlopidine inhibited platelet aggregation induced by ADP or collagen, but did not suppress arachidonic acid-induced aggregation and the thrombin-induced [Ca2+]i increase. At the unstable period, the combination therapy of low-dose aspirin plus warfarin did not prolong the bleeding time compared to ticlopidine plus warfarin. And low-dose aspirin inhibited platelet aggregation induced by ADP, collagen or epinephrine, and especially blocked arachidonic acid-induced aggregation. Ticlopidine inhibited ADP-, collagen- or U-46619-induced aggregation, but did not affect on the increase in [Ca2+]i induced by thrombin. From the results in this study, we suggest that the combination therapy with low-dose aspirin (81 mg/day) and warfarin is safe as an antithrombotic medication in heart valve replacement, and results in the inhibition of platelet functions without any side effect calling for special mention at the early unstable period after operation.

Growth of measles virus in continuous cell lines derived from the nervous tissues of human and rat.

Growth of two measles virus strains, the TYCSA and CAM, was compared in three continuous cell lines derived from the nervous tissues, human neuroblastoma IMR-32, human glioma 118MGC, and rat glioma C-6. The two human neural cells were shown to support the growth of both measles virus strains as efficiently as in the non-neural Vero cells. Different types of cytopathic effect (CPE) between the two virus strains were noticed in IMR-32 cells; the CAM strain induced strand-forming type CPE and the TYCSA strain giant-cell type CPE. As a difference of growth pattern between IMR-32 and 118MGC cells, virus antigen was demonstrated in both the nucleus and cytoplasm of 118MGC cells whereas virus antigen was present only in the cytoplasm of IMR-32 cells. In contrast to the productive infection in human neural cells, growth of both virus strains was restricted in rat glioma C-6 cells without showing CPE although the prolonged presence of virus antigens was demonstrated by the immunofluorescent technique.

Lysis of RSV-transformed Japanese quail cells by a factor from normal quail serum.

Normal sera of Japanese quails caused lysis of tumor cells from a Rous sarcoma virus (RSV)-induced quail tumor (QT cells). Other tumor cell lines, including RSV-transformed quail embryo cells and methylcholanthrene-induced quail tumors, were not lysed. This naturally occurring cytolytic factor (NCLF) was sensitive to heating at 56 degrees C, zymosan, and inulin, and it required magnesium but not calcium for the expression of its activity. These results suggested that NCLF activity was mediated by complement activated through an alternative pathway. This possible complement activation occurred in the absence of specific antibodies to the target cells.

Encephalomyelitis induced by canine distemper virus in non-human primates.

A strain of canine distemper virus was shown to be highly neuro-virulent in non-human primates. Intracerebral inoculation induced in monkeys histological lesions of encephalomyelitis, i.e., degenerative changes consisting mainly of neuronal damage and inflammatory changes such as perivascular cuffings and glial proliferation, in wide areas in the brain and spinal cord. In one monkey observed for 70 days, lesions with a tendency of subacute sclerosing were also noticed. Immunosuppression with cyclophosphamide or antithymocyte serum was found to aggravate the clinical course and to modify the histological lesions in the central nervous system as well as the level of antibody response to the virus in cerebrospinal fluid. Possible application of distemper encephalomyelitis in monkeys as a primate model for analysis of the immune mechanism involved in paramyxovirus-induced encephalomyelitis was discussed.

Growth of measles virus in nervous tissues. IV. Neurovirulence of wild measles and SSPE viruses in monkeys.

Neurovirulence of in vivo-passed wild measles virus and that of the cell-associated SSPE virus were compared by intracerebral inoculation into monkeys. The wild measles virus was found to lack neutrovirulence without producing neurological signs or significant histological changes in the brains, whereas the virus was confirmed to preserve the properties characteristic of the wild virus. In contrast, inoculation of the SSPE virus induced rapid onset of neurological signs with mild but definite histological changes including degeneration of nerve cells. The fact that SSPE virus exhibited neurovirulence in monkeys indicated importance of the current assay system for neurovirulence of measles vaccine by intracerebral inoculation into monkeys.