Deaf Studies on the English Curriculum

What do we mean by Deaf Studies ? Where is its place in the schools and classes for the deaf? How do we teach it? Before we attempt to answer these questions, let us consider some of the more salient trends in contemporary education and the problem of teaching our multi-cultured society

Deaf characters and deafness in science fiction

Through the years, many individual reports have been published which review the treatment of deafness and deaf characters in various literary works. More recently, comprehensive anthologies have also addressed this topic. The authors add a new dimension to this area of Deaf Studies with their review of science fiction literature. Selected nineteenth and twentieth-century works of science fiction are discussed, and several deaf writerd in this genre are introduced

NTID Focus

COMMUNICATION: The Job of IRLColloquium Features Larry StewartNTID National Advisory Group Confers at RIT CampusNTID Profiles: Marilyn Ware, Counseling SpecialistNTID Student Cited at ConventionNational Theatre of the Deaf Invites NTID StudentsSeminar Draws Wide Audienc

Selective cyclo-oxygenase-2 inhibitors and their influence on the protective effect of a mild irritant in the rat stomach

1. The effects of the non-selective cyclo-oxygenase (COX) inhibitor indomethacin and the selective COX-2 inhibitors, N-[2-(cyclohexyloxy)-4-nitrophenyl] methanesulphonamide (NS-398), 5-methanesulphonamido-6-(2,4-difluorothio-phenyl)-1-indanone (L-745,337) and 5,5-dimethyl-3-(3-fluorophenyl)-4-(4-methylsulphonyl) phenyl-2(5H)-furanone (DFU), on the protection induced by the mild irritant 20% ethanol were investigated in the rat stomach. 2. Instillation of 20% ethanol (1 ml, p.o.) effectively protected against gastric mucosal injury induced by subsequent instillation of 70% or 96% ethanol (1 ml, p.o.). 3. Oral administration of indomethacin (1.25–20 mg kg(−1)) dose-dependently counteracted the protective effect of 20% ethanol (ID(50): 3.5 mg kg(−1)). 4. Likewise, NS-398 (0.1–1 mg kg(−1)), L-745,337 (0.2–2 mg kg(−1)) and DFU (0.02–0.2 mg kg(−1)) inhibited the protective effect of 20% ethanol in a dose-dependent manner with ID(50) values of 0.3 mg kg(−1), 0.4 mg kg(−1) and 0.06 mg kg(−1), respectively. 5. Inhibition of mild irritant-induced protection was also found when NS-398 (1 mg kg(−1)) was administered s.c. or when 96% ethanol was used to damage the mucosa. 6. Pretreatment with 16,16-dimethyl-prostaglandin (PG)E(2) at 4 ng kg(−1), a dose that did not protect against ethanol (70%)-induced mucosal damage when given alone, completely reversed the effect of the selective COX-2 inhibitors on the mild irritant-induced protection. 7. Pretreatment with dexamethasone (3 mg kg(−1), 24 and 2 h before instillation of 20% ethanol) did not affect the protective activity of the mild irritant, indicating that enzyme induction is not involved. 8. Indomethacin (20 mg kg(−1), p.o.) did not prevent the protection conferred by sodium salicylate (100 mg kg(−1)), dimercaprol (30 μg kg(−1)), iodoacetamide (50 mg kg(−1)) and lithium (20 mg kg(−1)). Likewise, the protective effect of these agents was not counteracted by NS-398 (1 mg kg(−1), p.o.). 9. Whereas indomethacin (20 mg kg(−1), p.o.) near-maximally inhibited gastric mucosal formation of PGE(2), 6-keto-PGF(1α) and thromboxane (TX) B(2) as well as platelet TXB2 release, the selective COX-2 inhibitors were ineffective. 10. The findings show that selective COX-2 inhibitors, although lacking in ulcerogenic activity, prevent the protection conferred by a mild irritant. Prostaglandis generated by a constitutive COX-2 could thus contribute to physiological functions involved in gastric homeostasis, although at present a non-COX-2-related mechanism underlying the effect of the selective COX-2 inhibitors tested on mild irritant-induced protection cannot be completely excluded