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The experiments were carried out on mice (Balb/c, 6 weeks old) exposed to restraint stress. Animals were restrained for 12 h per day at nighttime and released at daytime for 2 consecutive days. Some mice were immunized i.p. immediately before the stress with 4xl08 sheep red blood cell (SRBC). Sodium diethyldithiocarbamate (DTC, 20 mg/kg) was administered i.p. twice e.g. 4 and 2 days prior to restraint stress. Calf thymus extract (TFX, 10 mg/kg) was injected i.p. four times at 24 h intervals prior to exposure to stress. It was found that restraint stress led to thymic atrophy which was reflected in the decreased total number of thymocytes, weight index of the thymus, and caused depletion of thymocytes. In addition, it was found that restraint stress reduced humoral response to SRBC which was reflected in the decreased number of splenocytes producing anti-SRBC antibodies (PFC) and serum haemagglutynin titres (19S+7S and 7S). The total number of spleen cells and weight index of the spleen in stressed mice were also diminished. The suppressing effect of stress was observed for 10 days. Pretreatment with DTC or TFX partially counteracted the immunosuppresive effects of restraint stress. Administration of DTC or TFX retarded the stress-induced thymic atrophy and promoted the restoration of the synthesis of anti-SRBC haemagglutinins and the number of PFC. Regeneration of the thymus gland occured more rapidly in stressed mice previously treated with TFX. On the other hand, the stronger effect of restoring the humoral response to SRBC was observed for DTC.
 Three monoclonal antibodies specific to the central cell-binding and the C- and N-terminal domains of fibronectin (FN) were used to test antigenic epitope accessibility on human plasma and cerebrospinal fibronectins. In the plasma group, the mean N-terminal FN domain immunoreactivity was about one fourth that of the cell-binding and C-terminal domains, whereas in cerebrospinal fluid they were nearly equal. In the presence of 0.5-6 M urea N-terminal domain immunoreactivity in the plasma increased 3-6-fold, but it decreased 0.7-3-fold in the cerebrospinal fluid. Analysis of fibronectin domain immunoreactivities of the cell-binding and N-terminal domains by a panel of specific monoclonal antibodies may reveal N-terminal fibronectin domain accessibility for reaction with biological partner ligand(s) and/or processes in which FN could be implicated. Such determinations may have important clinical implications.
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