Ultrasonic treatment of laryngeal papillomata.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to A White.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
New Zealand Black (NZB) mice develop after 16 weeks of age an autoimmune and lymphoproliferative disease which is a model for systemic lupus erythematosus and lymphoid malignancy in humans. At this age, the mice manifest a progressive decline in T lymphocyte (thymus-derived lymphocyte) functions and serum thymosin levels. Thymocytes from 8-week old NZB mice exhibit an abnormal DNA synthetic response when transplanted into lethally irradiated C57B1/6 recipients. DNA synthesis (measured as the incorporation of radioactively labeled 5-iodo-2'-deoxyuridine) is delayed in onset and still increasing 6 days after cell transfer. By contrast, 2-week old NZB thymocytes show a normal response which is rapid in onset and completed by day 6.NZB mice were injected with thymosin fraction 5 or with bovine serum albumin starting at 2 weeks of age. Thymocytes from 8-week old thymosin-treated mice showed a normal DNA synthetic response, whereas the albumin-treated controls showed the abnormal response expected at this age. The ability of thymosin to correct the DNA synthetic response was related to dose and duration of treatment. These results suggest that thymosin can induce a more normal state of thymocyte differentiation in NZB mice. If abnormal thymocyte differentiation is related to the subsequent emergence of autoimmunity and lymphoid malignancy, then continuous treatment with thymosin may have therapeutic potential. These experiments suggest that an endocrine disturbance may contribute to autoimmune and lymphoproliferative disease in NZB mice and possibly in humans.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Lysates of human leukocytes, prepared by ultrasonic disruption, contained heat-labile histamine-releasing factors. An inhibitor of histamine release was generated from such lysates during thermal inactivation of the histamine-releasing activity. Lysates inactivated at 38 degrees C for 60 min produced up to 90% inhibition of histamine release from human leukocytes. Heated lysates produced significant inhibition (P < 0.001) of leukocyte histamine release induced by goat antihuman IgE (51+/-3% inhibition), compound 48/80 (69+/-7% inhibition), and fresh leukocyte lysate (63+/-6% inhibition). Membrane ultrafiltration and gel-filtration chromatography suggested that the inhibitor was of less than 1,000 molecular weight. The partially purified inhibitor, eluted from Sephadex G-15 and lyophilized, contained no detectable protein or carbohydrate but produced 80-90% inhibition of histamine release at a concentration of only 10 ng/ml. The histamine-releasing factors from lysates of purified suspensions of lymphocytes and granulocytes were fractionated on Sephadex G-25. A single peak of histamine-releasing activity with an estimated molecular weight of 5,000 was detected from each cell type. Incubation of the partially purified histamine-releasing factors at 38 degrees C resulted in generation of an inhibitor of histamine release which was nearly identical to the inhibitor from crude lysates. This natural inhibitor of histamine release, derived from human leukocytes, may provide an endogenous mechanism for the control of histamine release in inflammation.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.