Magdi Mohamed Mashly

The effectiveness of six commercially available mouthwashes against common buccal organisms was studied. The minimum inhibitory concentrations (MIC) for two of the studied mouthwashes (Corsodyl and Oraldene) against buccal organisms were determined in Todd Hewitt medium with or without 5% serum. The concentration of the active substance in these two mouthwashes was in excess of the corresponding MIC. When the medium was supplemented with serum, lower MIC values were observed. Kill-time determinations, used at half the concentration of the normal preparation, revealed a rapid lethal effect for all tested mouthwashes. The slowest lethal effect was observed with Fluocaril mouthwash. When mouthwashes were tested in volunteers, an immediate significant fall in salivary bacterial counts was produced by all except Fluocaril. With the latter mouthwash the decrease was significant 2-30 minutes after rinsing. The bacterial levels returned to pre-rinse levels after 30 minutes for Listerine, after 90 minutes for both Oraldene and Mint and after 180 minutes for Corsodyl, Fluocaril and Sansilla mouthwashes. The results indicate that there is a good correlation between in vivo efficacy and in vitro determination of all mouthwash preparations.

Chemical and histological indices of liver fibrosis were measured after eight, 18 and 28 weeks in mice infected with Schistosoma mansoni and treated at eight weeks with oxamniquine, in mice infected with S. mansoni and not treated and in mice not infected with S. mansoni. Total worm burdens and liver egg counts were determined in the infected mice to determine severity of infection. Treatment with oxamniquine resulted in near total eradication of S. mansoni worms after 10 weeks and in their complete killing and marked reduction of eggs in the liver at 10 and 20 weeks. Liver fibrosis 10 weeks after oxamniquine treatment was not significantly different than in the untreated, infected group but there was no progression between 10 and 20 weeks after oxamniquine treatment. Fibrosis did however increase between 10 and 20 weeks in the untreated infected group. In the murine model, oxamniquine is an effective treatment for S. mansoni and prevents progression of liver fibrosis.

Chemical and histological indices of liver fibrosis were measured after eight, 18 and 28 weeks in mice infected with Schistosoma mansoni and treated at eight weeks with oxamniquine, in mice infected with S. mansoni and not treated and in mice not infected with S. mansoni. Total worm burdens and liver egg counts were determined in the infected mice to determine severity of infection. Treatment with oxamniquine resulted in near total eradication of S. mansoni worms after 10 weeks and in their complete killing and marked reduction of eggs in the liver at 10 and 20 weeks. Liver fibrosis 10 weeks after oxamniquine treatment was not significantly different than in the untreated, infected group but there was no progression between 10 and 20 weeks after oxamniquine treatment. Fibrosis did however increase between 10 and 20 weeks in the untreated infected group. In the murine model, oxamniquine is an effective treatment for S. mansoni and prevents progression of liver fibrosis.

Chemical and histological indices of liver fibrosis were measured after eight, 18 and 28 weeks in mice infected with Schistosoma mansoni and treated at eight weeks with oxamniquine, in mice infected with S. mansoni and not treated and in mice not infected with S. mansoni. Total worm burdens and liver egg counts were determined in the infected mice to determine severity of infection. Treatment with oxamniquine resulted in near total eradication of S. mansoni worms after 10 weeks and in their complete killing and marked reduction of eggs in the liver at 10 and 20 weeks. Liver fibrosis 10 weeks after oxamniquine treatment was not significantly different than in the untreated, infected group but there was no progression between 10 and 20 weeks after oxamniquine treatment. Fibrosis did however increase between 10 and 20 weeks in the untreated infected group. In the murine model, oxamniquine is an effective treatment for S. mansoni and prevents progression of liver fibrosis.

Sulphadimidine was administered to chickens via the intracrop route to determine plasma concentrations of the unchanged sulphonamide and its acetylated derivatives, kinetic disposition, tissue residues and acetylation. The sulphadimidine was given alone (group 1) at a dose of 200 mg kg-1 bodyweight. Pantothenic acid was given via the intracrop route at a dose of 100 mg kg-1 bodyweight one hour before (group 2) and six hours after (group 3) sulphadimidine administration (200 mg kg-1 bodyweight intracrop). The highest plasma concentrations of sulphadimidine in groups 1, 2 and 3 were reached in 1.73, 1.62 and 1.71 hours, respectively, following intracrop administration. In birds of groups 1, 2 and 3 no sulphadimidine was detected at 72, 24 and 48 hours, respectively, following its administration. Estimation of sulphadimidine in most of the body tissues revealed that all tissues examined had lower concentrations than plasma. In chickens given pantothenic acid (groups 2 and 3) before and after sulphadimidine administration, an increase in the concentration of N4 acetylated derivatives of sulphadimidine was observed compared with birds given sulphadimidine alone (group 1).

Aqueous/alcoholic extracts of Populus tremula, Solidago virgaurea and Fraxinus excelsior (components of Phytodolor N) were tested individually and in 3 different combinations for anti-inflammatory activity using carrageenan induced edema and/or adjuvant induced arthritis of the rat paw. The tested combinations as well as the individual extracts significantly reduced the paw edema to varying degrees and also dose dependently inhibited the arthritic paw volume. The anti-inflammatory activity of the combinations was respectively comparable to the tested doses of diclofenac.

Aqueous/alcoholic extracts of Populus tremula, Solidago virgaurea and Fraxinus excelsior (components of Phytodolor N) were tested individually and in 3 different combinations for anti-inflammatory activity using carrageenan induced edema and/or adjuvant induced arthritis of the rat paw. The tested combinations as well as the individual extracts significantly reduced the paw edema to varying degrees and also dose dependently inhibited the arthritic paw volume. The anti-inflammatory activity of the combinations was respectively comparable to the tested doses of diclofenac.

Aqueous/alcoholic extracts of Populus tremula, Solidago virgaurea and Fraxinus excelsior (components of Phytodolor N) were tested individually and in 3 different combinations for anti-inflammatory activity using carrageenan induced edema and/or adjuvant induced arthritis of the rat paw. The tested combinations as well as the individual extracts significantly reduced the paw edema to varying degrees and also dose dependently inhibited the arthritic paw volume. The anti-inflammatory activity of the combinations was respectively comparable to the tested doses of diclofenac.

Experimental infection of dogs with camel (Camelus dromedarius) meat resulted in infection of the dogs with Isospora canis, Hammondia heydorni and Sarcocystis cameli. The dogs fed sheep (Ovis aries) meat passed oocysts of Isospora canis, Isospora ohioensis and sporocyts of Sarcocystis spp. Extraintestinal stages were detected in the intestinal lymph node of a rabbit killed 4 days following inoculation with Isospora ohioensis oocysts. Dogs fed the rabbit (killed 4 days after inoculation with I. ohioensis) passed I. ohioensis oocysts in their faeces 8 days post-infection.

The pharmacokinetic data of nalidixic acid were investigated in normal and E. coli infected chickens. The highest serum concentration were reached after 2 hours with t0.5 (ab) of (1.706 +/- 0.1 min in normal and 2.030 +/- 0.11 min in diseased) and (1.72 +/- 0.11 min in normal and 1.416 +/- 0.044 in diseased chickens) following oral and intramuscular administration, respectively. The elimination half-life t0.5 (beta) were (2.514 in normal and 2.35 hr in diseased) and (2.567 hr in normal and 2.672 hr in diseased) respectively. Following intravenous injection the kinetic of nalidixic acid followed two compartments open model with t0.5 of (6.27 and 9.15 hr), Vd (0.45 and 0.79 L/kg), Cltot (8.86 and 13.32 ml/kg/min) in normal and E. coli infected chickens, respectively. Administration of nalidixic acid twice daily for 5 successive days in a dose level of 25 mg/kg b. wt. by oral and intramuscular routes showed a cumulative behaviour.

Dielectric relaxation data are reported at frequencies of 0.1 – 10000 kHz over a temperature range of 10–80°C on cellulose acetates of different degrees of substitution, and on saponified cellulose acetate. The acetyl substitution is found to remove the low‐frequency relaxation process, γ, previously observed in medicated cotton cellulose, and to affect the other higher‐frequency process, β, in different ways, depending on the acetyl content. Conversely, saponification of cellulose acetate leads to the reversion of these two processes but with different features. Analysis of the absorption bands is made, and an assessment of the results obtained is given. © 1992 Hüthig & Wepf Verlag, Basel

The effect of preheating at 140°C and 180°C on the dielectric relaxation of cellulose acetate of degree of substitution 1·90 has been investigated, together with the dependence on temperature over the range 80-200°C of the 'static' dielectric constant of variously acetylated cellulose samples. The results obtained are discussed in terms of progressive gain of compact structure, together with the initiation of crystallization at a temperature governed by the acetyl content in the fiber. Phase changes involving discontinuity in the first variation of the 'static' dielectric constant on heating, and irreversibility of the temperature dependence path on cooling are thus observed. © 1992.