Feeding experiments were conducted to investigate the relationship between the requirement for tocopherol and dietary linoleate levels in carp. The results obtained in the feeding
Adjuvant arthritic rats are known to be more susceptible to gastric damage induced by non-steroidal anti-inflammatory drugs (NSAIDs) than are normal rats. We compared the relative gastric safety profile of etodolac with those of meloxicam, diclofenac sodium and indometacin in adjuvant arthritic rats and normal rats or mice. As a measure of the safety profiles of NSAIDs, we used the safety index, the ratio of the dose that elicits gastric mucosal lesions to the effective dose as an anti-inflammatory or analgesic compound. The anti-inflammatory or analgesic effects of NSAIDs were assessed by paw swelling in adjuvant arthritic rats, and either carrageenin-induced paw edema or brewer’s yeast-induced hyperalgesia, as well as acetic acid-induced writhing, in normal rats or mice. In addition, we also investigated the effects of these NSAIDs on human COX-1 and COX-2 activity. Etodolac and other NSAIDs inhibited paw swelling and caused gastric mucosal lesions in adjuvant arthritic rats in a dose-dependent manner. Etodolac showed the highest UD50 value and safety index among these NSAIDs in arthritic rats. In normal rats, etodolac also showed the highest UD50 value and safety index, except when its effects were assessed by acetic acid-induced writhing. Etodolac and meloxicam showed selectivity for human COX-2 over COX-1. In contrast, diclofenac sodium and indometacin were selective for COX-1. These results suggest that etodolac, a COX-2 selective NSAID, has anti-inflammatory effects with a better safety profile for the stomach than do non-selective NSAIDs, including diclofenac sodium and indometacin, in adjuvant arthritic as well as normal rats.
The interface of bone marrow and trabeeular endostal surface is realised by cells of bone turnover, blood vessels, bone marrow cells,adipocytes or fibroblasts. With the bone marrow agelng the extent of adipocytes increases. We have observed histomorphometricaly a varying peritrabecular concentration of adipoeytee in cases of osteoporosis. It was to prove histomorphometrically the relationship between the percentage of the adipocytes occupied endostal bone surface (AS) and the histomorphometrical signs of bone turnover. Material and methods: undecalcified sections from 238 bone bioptates of metabolic bone diseases were quantitatively analysed. Bone volume(BY), osteoid ca) and eroded surface(Eel, oseoblasts(ObS) and osteoclasts occupied surface(OcS), total labelled surface (LS) and mineral apposition ratelMAR) were determined.In addition, the percentage of the trabecular bone surface with a contact to adipocytes(AS) was estimated.
Resul~s:The adipocytes endost interface ranges from 0 to 100%, in the mean of the whole group 46%18. Negative correlations were detectabl~ between AS and the histomorphometric parameters of ES, OcS and ObS. In the subgroups of osteoporosis and of renal osteodystrophy(ROD) the results were different. In the osteoporosis (n=184) were detectable a mean AS of 50% and significant correlations between AS and ES, OcSObS but a low correlatiQn rate of AS to BV and to MAR. In ROD (n=29) We could detect a mean AS Of 31% and a significant correlation of AS to ES, OcS and ObS. Conclusions: A low cellular bone turnover activity is combined with a high percentage of adipecytes endost interface.In osteoporosis we found the highest percentage of adipocytes endost interface. In ROD seems to be possible by this way to determine and to quantify the process of adynamic renal bone disease. The change of osteoblasts into adipocytes could be a cause of the increasing AS.
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