Biomedical subjects
F Hardt
Publications and source records attributed to F Hardt.
A low-dose immunization schedule for the production of ALG in rabbits.
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The fate of heterologous specific and non-specific antilymphocyte globulins in plasma and tissues studied by a paired-label technique.
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Quantitative studies on the decay of lymphoid cells during the development of casein-induced murine amyloidosis.
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The effect of syngeneic transfer of normal lymphoid cells on the development of casein-induced amyloidosis in mice.
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Studies on casein-induced amyloidosis in mice with congenital aplasia of the thymus.
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Occurrence of autoimmune phenomena during the development of casein-induced amyloidosis in C3H and NZB-BL mice.
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Induction of amyloidosis in germ-free NMRI-mice after prolonged stimulation with sterilized casein.
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Quantitative studies on the T cell populations in spleens from amyloidotic and non-amyloidotic mice.
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Transfer amyloidosis. Studies on the nature of the amyloid inducing factor in a murine transfer system.
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Graft-versus-host reactions mediated by spleen cells from amyloidotic and nonamyloidotic mice.
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Acceleration of casein induced amyloidosis in mice by immunosuppressive agents.
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In vitro evaluation of cell-mediated immunity in mice: experiments with soluble and cellular antigens in a spleen-thymus cell leucocyte migration test (LMT).
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Transfer amyloidosis. I. Studies on the transfer of various lymphoid cells from amyloidotic mice to syngeneic nonamyloidotic recipients. II. Induction of amyloidosis in mice with spleen, thymus and lymph node tissue from casein-sensitized syngeneic donors.
Lymphoid cells from various lymphoid organs were transferred from amyloidotic mice to normal syngeneic recipients. The recipients were treated with nitrogen mustard. Only the recipients of spleen cells developed amyloidosis. Furthermore, slices of spleen, thymus and lymph node from casein-sensitized mice were transplanted to kidneys of normal syngeneic mice. The recipients were treated with ten casein injections, and they all developed amyloidosis. The results from both experiments indicate that amyloid is formed by macrophages due to a stimulation of these cells with both antigen and an amyloid-inducing factor released from the pyroninophilic lymphoid cells.
Amyloidosis and tolerance.
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The influence of the hair follicle phase on the survival time of skin allografts in the mouse.
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The migration-inhibitory factor (MIF). Effect of antilymphocytic serum on formation and performance of MIF in murine in vitro experiments.
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Antihepatic cellular hypersensitivity in hepatic cirrhosis.
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