[Intracranial epidural abscess: radiologic features and therapy. Report of two cases].
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Biomedical subjects
Publications and source records attributed to T Kuwata.
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A case of growing skull fracture with rapid growth is presented. A 4-month-old male fell and struck the right side of his head. Skull X-ray just after injury showed a right parietotemporal linear skull fracture with the maximum width of 4 mm. The width of the fracture line increased to 9 mm 7 hours after injury. Serial CT scan demonstrated growth of contusional hematoma just beneath of the fracture. Six days later, a pulsatile mass was palpated beneath the scalp, although neurological state was normal. The width of the fracture line was demonstrated to increase up to 11 mm on X-ray at that time. CT scan revealed subgaleal cerebral herniation surrounded by brain edema. He was operated 11 days after injury. It is thought that the contusional hematoma and following brain edema played an important role in the genesis of rapid growth of the skull fracture.
We examined the sensitivity of four human germ-cell-tumor cell lines exhibiting different stages of differentiation to human interferons (IFNs) in vitro. The cell lines were derived from two embryonal carcinomas (NEC 8 and NEC 14), a choriocarcinoma (IMa), and a yolk-sac tumor (HUOT). Treatment with poly I:C induced IFN production in IMa and HUOT cells, but not in NEC-8 and NEC-14 cells. In the two embryonal-carcinoma cell lines, the addition of IFN-alpha, IFN-beta, and IFN-gamma did not prevent infection by vesicular stomatitis virus and encephalomyocarditis virus. Also, in these two lines, 2-5A synthetase was not induced by the addition of IFN-alpha. In contrast, both IMa and HUOT showed sensitivity to the antiviral action of IFN-alpha and IFN-beta against the two viruses, and 2-5A synthetase was induced by IFN-alpha. IFNs added at doses of up to 1000 IU/ml had no antiproliferative effect on NEC 8, NEC 14, and HUOT, whereas colony formation by IMa cells was greatly suppressed by all three forms of IFN. These results indicate that the production of and sensitivity to IFN are developmentally regulated and are related to the level of differentiation of human germ-cell stem cells.
A case of T cell type primary lymphoma of the CNS is reported. A 50-year-old man was admitted because of speech and memory disturbance and dyscalculia. He had suffered from uveitis of both eyes two years before admission. Neurological examination revealed motor aphasia, finger agnosia, dyscalculia and memory disturbance. CT scan showed a mass lesion which was enhanced irregularly by the contrast medium in the left temporoparietal region. CAG confirmed the presence of a left temporoparietal avascular mass. Total removal of the tumor was performed through the left temporoparietal craniotomy. Histopathological diagnosis of the tumor was malignant lymphoma (diffuse, large cell type). Immunological study with tumor cells in the cerebrospinal fluid revealed that the tumor was T cell type malignant lymphoma. After postoperative whole CNS irradiation and intrathecal methotrexate injection, his preoperative symptoms disappeared. No evidence of the tumor recurrence is seen under CT scan one year and two months after the tumor resection. Relationship between the cell type of the tumor and CT findings is discussed.
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Three kinds of human choriocarcinoma cell lines (BeWo, HCCM-5, and NUC-1) were used for examining the antiviral and antiproliferative activities of human interferons (IFNs) in vitro and in vivo. All of the cell lines showed only low sensitivity to the antiviral action of every IFN-alpha, IFN-beta, and IFN-gamma against vesicular stomatitis virus infection. However, 2-5A synthetase was normally induced by IFN-alpha in all of the cell lines. The [3H]thymidine incorporation of both BeWo and HCCM-5 cells was suppressed in dose-dependent manner at 48 hr after treatment with 1 to 1,000 units (U)/ml of IFN-alpha or IFN-beta and the growth of them was also slightly inhibited when treated continuously with 1,000 U/ml for 6 days in vitro. Another cell line NUC-1 was the least sensitive to these IFNs among the three cell lines. IFN-gamma did not show any antiproliferative effect on these cell lines. The intraperitoneal administration of 5000 or 10,000 U of IFN-beta suppressed the growth of xenografts developed in hamster cheek pouches and subcutis of nude mice when its administration was initiated on the first day of cell inoculation. These results indicate that although some heterogeneities exist among the cell lines choriocarcinoma cells are weakly sensitive to the antiproliferative activity of human IFNs.
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Correlation between susceptibility to the anticellular effect of human interferon (HuIFN) and ultraviolet (uv) lethality was examined in a set of isogeneous human cell lines (RSa and IFr cells), a human endometrial cancer cell line (HEC-1 cells), and a Xeroderma pigmentosum-derived fibroblast cell line ( CRL1200 cells). IFr cells, previously established as a HuIFN-alpha-resistant subline by exposing HuIFN-alpha- and uv-sensitive RSa cells to HuIFN-alpha preparations, appeared more refractory to uv than did the parent RSa cells in the cell proliferation and colony-formation studies. The extent of recovery from uv-inhibited total cellular DNA synthesis and uv-induced DNA-repair synthesis was enhanced to a greater extent in IFr cells than in RSa cells. The preexposure of RSa cells to HuIFN-alpha enhanced uv-induced DNA-repair replication activities. HEC-1 cells, which are reportedly totally refractory to HuIFN actions, appeared most resistant to uv, in all the tests. The uv-sensitive CRL1200 cells appeared highly susceptible to HuIFN-beta, in both cell proliferation and DNA-synthesis inhibition tests. These results support and extend our previous finding (N. Suzuki, J. Nishimaki , and T. Kuwata (1982). Mutat . Res. 106, 357-376) that susceptibility to the anticellular effect of HuIFN closely relates with uv lethality.
When human transformed RSa cells were treated simultaneously with potent tumor promoter 12-O-tetradecanoyl-phorbol-13 acetate (TPA) and interferon (IFN) (20-100 IU/ml) at the concentration which suppresses the multiplication of cells slightly, distinct synergistic suppression of cell growth was observed. Synthesis of DNA in these cells was reduced in proportion to the concentration of IFN and it was more strongly reduced by combined treatment with IFN and TPA. When IFN was pretreated with anti-IFN serum, such synergistic effect was not observed. Highly purified IFN (specific activity, 2 X 10(8) U/ml) together with TPA elicited almost the same synergistic effect on RSa cells. Similar concentration of phorbol-12,13-didecanoate (PDD) also produced synergistic effects with IFN on RSa cells. In contrast, phorbol (PHR), which lacks tumor promoting activity, did not produce such synergistic effects even at a concentration of as high as 500 ng/ml. In the case of HeLa cells and IFN-resistant IFr cells, only an additive effect was observed. Effect of TPA on the antiviral action of IFN against VSV was tested and there was almost no influence of TPA on IFN action. In accordance with these results, 2-5A synthetase activity was not induced by TPA treatment and the level of enzyme action did not change significantly by the combined treatment with TPA and IFN.
The anti-viral and anti-cell fusion actions of human gamma interferon (IFN) were examined on human rhabdomyosarcoma cells and compared with the actions of IFN-alpha. Treatment of A204 and RD114-C1 cells with IFN-gamma resulted in significant inhibition of retrovirus production and cell fusions which were induced by Sendai virus, but IFN-gamma did not induce 2'-5' oligoadenylate (2-5A) synthetase or dsRNA-dependent protein kinase, and failed to inhibit EMC virus replication in RD114-C1 cells as previously observed on IFN-alpha treatment (Tomita, Y. et al. (1982) Virology 120, 258-263). Although IFN-gamma induced 56K protein more strongly than IFN-alpha in human transformed HEp-2, HeLa, RSa, IFr, and A204 cells, no significant induction of this protein was observed in RD114-C1 cells after IFN-alpha or IFN-gamma treatment. Specific bindings of 125I-labeled human IFN-alpha A to HeLa, A204 and RD114-C1 cell surfaces showed that the numbers of the binding sites on RD114-C1 cells were reduced to less than 22% of those on A204 cells. These results suggest that RD114-C1 cells exhibit a reduced number of receptors for IFN on the cell surface and that the receptors are functional for the expression of the anti-retrovirus and anti-cell fusion actions of IFN, but are not enough in number for expression of the anti-EMC virus action of IFN.
F-IFr cells, which are more resistant to the anticellular and antiviral action of human alpha and beta interferons (IFN-alpha and IFN-beta) than the parental RSa cells, were also found to be more resistant to both the anticellular and antiviral effect of IFN-gamma. A high level of 2-5A synthetase was induced by treatment with IFN-alpha or -beta, but induction of 2-5A synthetase was not detected after IFN-gamma treatment of the cells. F-IFr cells had less than half the number of specific binding sites for IFN-alpha than the parental RSa cells.
Iodinated human interferon alpha A (HuIFN-alpha A) was found to bind specifically to IFN-sensitive RSa cells: the dissociation constant was 8.7 X 10(-10)M and the estimated number of receptor sites per cell was 1110. Seven cell lines that were either insensitive or of low sensitivity to the antiproliferative effect of IFN were found to contain a much smaller (3- to 4-fold) number of receptor sites, but the dissociation constants of these binding sites were of the same order of magnitude as those of receptors on RSa cells. Under the present experimental conditions, cell resistance to the antiproliferative effect of IFN is closely associated with the number of receptor sites.
Two cell lines derived from human choriocarcinomas (HCCM-5 and BeWo) are resistant to several biological effects of human interferon such as inhibition of VSV multiplication and inhibition of cell growth, but they develop a normal antiviral activity against EMCV. Nevertheless, in both cell lines, 2-5A synthetase and protein kinase are induced by IFN. 2-5A-dependent endonuclease can be measured by two independent methods and 2-5A itself is detected at least in poly(rI):poly(rC)- and IFN-treated BeWo cells. This is another example of two cell lines that are partially, with respect to the antiviral effect toward VSV, and totally, with respect to the anticellular effect, refractory to IFN treatment, although all the known elements of the 2-5A system are present.
Two cloned cell lines, HEC-IC and HEC-ID, derived from the human endometrial adenocarcinoma cell line HEC-I, were found to be as resistant to the antiviral and anticellular activities of interferon (IFN) as were the parental cells, and 2'-5' oligoadenylate (2-5A) synthetase was not induced in these clones by IFN treatment. They were sensitive to the cytotoxicity of natural killer (NK) cells but their sensitivity was not changed by treatment of the cell lines with IFN. Binding of [3H]-leucine-labelled IFN-alpha to HEC-IC cells was examined, and Scatchard plot analysis showed that HEC-IC cells did not have any high-affinity binding sites for IFN-alpha. The cells had hyperploid chromosomes. HEC-IC had three copies of chromosome 21 while HEC-ID had only one copy of chromosome 21. The results suggest that these clones may have the structural gene for the IFN receptor but that functional receptor sites may be absent.
A human nongestational choriocarcinoma cell line of ovarian origin (IMa) was established in vitro. This cell line had been subcultured serially more than 22 times over 18 months. Small polygonal cells with a prominent nucleus were dominant and a sparsity of cytoplasmic organelles was an ultrastructural characteristic of the IMa cells. The production and secretion of human chorionic gonadotropin and its subunits were identified by radioimmunoassay. The IMa cells were transplantable in the hamster cheek pouch and the histological diagnosis was choriocarcinoma. A newly established ovarian choriocarcinoma cell line can be considered useful for clarifying the biological differences between nongestational and gestational choriocarcinoma cells.
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Human alpha interferon (IFN-alpha) and beta interferon (IFN-beta) showed antiviral and anticellular effects on human lymphoblastoid Daudi and P3HR-1 cells, but up to 1,000 units/ ml of gamma interferon (IFN-gamma) showed no such effect. Though a fairly high level of dsRNA-dependent 2'-5'-oligoadenylate synthetase (2-5A synthetase) was found in Daudi cells, treatment of these cells with IFN-alpha and beta enhanced the enzyme level in cells at least four-fold, but IFN-gamma did not show any such effect. Lymphoblastoid Raji cells were insensitive to the antiviral and anticellular activities of IFN-alpha, beta and gamma, but 2-5A synthetase was induced in cells by the treatment with IFN-alpha and beta, though the enzyme level was lower than that found in interferon-treated Daudi cells. Human leukemic K562 cells were completely insensitive to IFN-alpha, beta and at the same time to IFN-gamma with regard to the antiviral, anticellular activities and to the induction of 2-5A synthetase.