Maternal/fetal transmission of HBsAg negative hepatitis.
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Biomedical subjects
Publications and source records attributed to S Agarwal.
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The reactivity of normal and tumor host lymphocytes incubated with normal serum or with serum or malignant ascites fluid from tumor hosts was measured by the ability of the lymphocytes to synthesize ornithine decarboxylase after phytohemagglutinin stimulation. Each of three tumors tested (a solid fibrosarcoma, an ascites mammary carcinoma, and an ascites ovarian carcinoma) caused increasing unresponsiveness in the lymphocytes of mice with progressing syngeneic neoplastic growth. The sera and particularly the malignant ascites fluids from mice given implants of the ascites cancers became progressively inhibitory to the activation of lymphocytes from tumor hosts as well as from normal mice. The serum from mice carrying s.c. implants of the fibrosarcoma enhanced the activation of lymphocytes from tumor hosts and from normal mice during early tumor growth before it also became inhibitory.
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The use of serum transfusion to remedy radiation-induced damage to established antitumor resistance was investigated in female C3H mice. The mice, which had been actively immunized against a syngeneic mammary carcinoma, were injected i.v. and s.c. with suspensions of cells from the same tumor and were then given 300 R extensive-field irradiation to the abdomen two times. Tumor cells implanted outside the irradiated area grew better in irradiated mice than in unirradiated controls. Under these experimental conditions, protection could be transferred to radiation-impaired hosts with several injections of cell-free immune serum. Transfers of normal serum provided a detectable but low degree of protection. The corrective effect of serum transfers to radiation-impaired hosts was clearly expressed against pulmonary tumor growth (i.v. challenge), provided the transfusions were started no later than the first day after the injection of the tumor cells. Serum transfusions were ineffective against the growth of tumors implanted s.c. Transfers of serum from hosts carrying large (15 mm) s.c. tumor implants had a negative effect on the resistance of irradiated recipients. The results indicate that humoral resistance factors, both normal and immune, may act against metastatic spread of solid tumors.
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The effects of syngeneic tumor vaccine preparations on resistance against s.c. and pulmonary implants of a spontaneous C3H mouse mammary carcinoma have been compared during progressive primary tumor growth, after surgical cure, and during declining immune resistance following complete tumor removal. Concomitant antitumor immunity reached a higher level of effectiveness in the lungs than in s.c. tissue. The concomitant immune resistance in the lungs also remained effective longer than did s.c. resistance, which was the first to decline under the increasing antigen burden of a growing tumor implant. Resistance to challenge recovered quickly after the complete removal of a large tumor burden, but recovery was impeded if killed tumor tissue was reinjected too soon after tumor removal. If injections of killed tumor tissue were given 7 days after tumor removal, the completed recovery was not affected. If injections of killed tumor tissue were given 30 days after tumor removal, immune resistance to challenge, at this time much declined, was stimulated.
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