SAID SHEHATA

requirements are evolved, not predetermned: requirements design

n/a

The anti-inflammatory activity of piroxicam was assessed after whole body irradiation in rats. Two models of inflammation, the carrageenan-induced oedema and the adjuvant-induced arthritis in rats have been utilised. Piroxicam at doses of 1, 5 & 10 mg kg-1 i.p. was effective in inhibiting the paw oedema produced in both models of inflammation. The inflammatory response in irradiated was significantly higher than that produced in normal animals and was dependent on the radiation dose level used (0.5-2 Gy). The effect of piroxicam on the late inflammatory response produced by exposure to 2 Gy was studied by measuring the carrageenan-induced oedema 4 h after irradiation and on the third and seventh day thereafter. The increase in paw volume was significantly suppressed in animals receiving the drug. Administration of piroxicam (5 mg kg-1) one hour before irradiation of animals at 0.5 Gy, produced inhibition to the exaggerated inflammatory response in irradiated animals. This suggests that piroxicam possibly owes its protective value to prevention of the increase in cellular permeability induced by radiation. Alternatively, the drug may exert this effect by inhibiting PG synthesis, thereby reducing their potentiating influence on the other mediators of inflammation. Furthermore, the inhibition of lysosomal enzyme release possibly induced by the drug may contribute to the probable reduction in the release of inflammatory mediators.

The anti-inflammatory activity of piroxicam was assessed after whole body irradiation in rats. Two models of inflammation, the carrageenan-induced oedema and the adjuvant-induced arthritis in rats have been utilised. Piroxicam at doses of 1, 5 & 10 mg kg-1 i.p. was effective in inhibiting the paw oedema produced in both models of inflammation. The inflammatory response in irradiated was significantly higher than that produced in normal animals and was dependent on the radiation dose level used (0.5-2 Gy). The effect of piroxicam on the late inflammatory response produced by exposure to 2 Gy was studied by measuring the carrageenan-induced oedema 4 h after irradiation and on the third and seventh day thereafter. The increase in paw volume was significantly suppressed in animals receiving the drug. Administration of piroxicam (5 mg kg-1) one hour before irradiation of animals at 0.5 Gy, produced inhibition to the exaggerated inflammatory response in irradiated animals. This suggests that piroxicam possibly owes its protective value to prevention of the increase in cellular permeability induced by radiation. Alternatively, the drug may exert this effect by inhibiting PG synthesis, thereby reducing their potentiating influence on the other mediators of inflammation. Furthermore, the inhibition of lysosomal enzyme release possibly induced by the drug may contribute to the probable reduction in the release of inflammatory mediators.

The anti-inflammatory activity of piroxicam was assessed after whole body irradiation in rats. Two models of inflammation, the carrageenan-induced oedema and the adjuvant-induced arthritis in rats have been utilised. Piroxicam at doses of 1, 5 & 10 mg kg-1 i.p. was effective in inhibiting the paw oedema produced in both models of inflammation. The inflammatory response in irradiated was significantly higher than that produced in normal animals and was dependent on the radiation dose level used (0.5-2 Gy). The effect of piroxicam on the late inflammatory response produced by exposure to 2 Gy was studied by measuring the carrageenan-induced oedema 4 h after irradiation and on the third and seventh day thereafter. The increase in paw volume was significantly suppressed in animals receiving the drug. Administration of piroxicam (5 mg kg-1) one hour before irradiation of animals at 0.5 Gy, produced inhibition to the exaggerated inflammatory response in irradiated animals. This suggests that piroxicam possibly owes its protective value to prevention of the increase in cellular permeability induced by radiation. Alternatively, the drug may exert this effect by inhibiting PG synthesis, thereby reducing their potentiating influence on the other mediators of inflammation. Furthermore, the inhibition of lysosomal enzyme release possibly induced by the drug may contribute to the probable reduction in the release of inflammatory mediators.

The immunopharmacological properties of praziquantel were studied in mice infected with Schistosoma mansoni. Hepatic granuloma measurement was the main parameter of assessment. Delayed foot pad swelling as an in vivo correlate for the delayed granulomatous hypersensitivity reaction was also determined. Fluorescent direct antigen-antibody reaction in the granuloma together with the immediate foot pad swelling were used to test for the humoral immune response. Praziquantel administered at seven weeks after infection in two dose regimens (3 X 250 mg kg-1 for three consecutive days and 3 X 83 mg kg-1 given four hourly within the same day was more or less equally effective in reducing the size of hepatic granuloma by 37-41% two weeks after treatment and by 81-85% one month after treatment. Delayed foot pad swelling using soluble egg antigen (SEA) was significantly suppressed one month after treatment by 53%. At nine weeks after infection the fluorescent antigen-antibody reaction in the granuloma was positive in the untreated controls, but at the same time (i.e. two weeks after treatment) it was negative in the praziquantel-treated mice. One month after treatment positivity was less compared to infected control mice. Reduction in worm burden, hepatic shift of the worms and the reduced number of ova per gram of tissue denoted the efficacy of the drug in its two dose regimens against the Egyptian strain of S. mansoni.

The immunopharmacological properties of praziquantel were studied in mice infected with Schistosoma mansoni. Hepatic granuloma measurement was the main parameter of assessment. Delayed foot pad swelling as an in vivo correlate for the delayed granulomatous hypersensitivity reaction was also determined. Fluorescent direct antigen-antibody reaction in the granuloma together with the immediate foot pad swelling were used to test for the humoral immune response. Praziquantel administered at seven weeks after infection in two dose regimens (3 X 250 mg kg-1 for three consecutive days and 3 X 83 mg kg-1 given four hourly within the same day was more or less equally effective in reducing the size of hepatic granuloma by 37-41% two weeks after treatment and by 81-85% one month after treatment. Delayed foot pad swelling using soluble egg antigen (SEA) was significantly suppressed one month after treatment by 53%. At nine weeks after infection the fluorescent antigen-antibody reaction in the granuloma was positive in the untreated controls, but at the same time (i.e. two weeks after treatment) it was negative in the praziquantel-treated mice. One month after treatment positivity was less compared to infected control mice. Reduction in worm burden, hepatic shift of the worms and the reduced number of ova per gram of tissue denoted the efficacy of the drug in its two dose regimens against the Egyptian strain of S. mansoni.