By Karl Maramorosch
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A brief, systematic and logical method of diagnosing and treating temporomandibular problems (TMD), this newest publication within the Dental replace sequence is a necessary scientific spouse for dental scholars and training dentists. beginning with an summary of the fundamental ideas of TMD, corresponding to the anatomy of the temporomandibular joint and its body structure and pathology with regards to scientific remedy, the ebook is going directly to current the realities of coping with sufferers, utilizing a case-based method of aid readers comprehend and have interaction with the knowledge.
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Extra info for Advances in cell culture. Volume 2
This suggests t h a t the altered template activity is an effect rather t h a n a cause of aging. , 1980). Bowman et al. (1976a) have reported t h a t the age-related decline in RNA synthesis in WI-38 cells is due entirely to decreased synthesis of nucleolar RNA. However, in resting, nongrowing embryonic lung fibroblast lines, including the WI-38 line, the amount of rRNA and mRNA were both reduced nearly 2-fold in comparison to growing cultures while polysome-associated RNA was reduced about 4-fold (Meedel and Levine, 1977).
In any case, a number of phenotypic differences including an indefinite life span characterize h u m a n cells transformed by SV40 (Sack, 1981). Unfortunately, the mechanism by which "immortality" is achieved is still obscure. At first glance it would appear t h a t transformation is unlikely to shed light on the mechanisms of senescence since the transformed cells have acquired abnormal characteristics. On the other hand, SV40 transformation probably represents a potentially powerful probe for understanding the mechanisms regulating senescence.
Ove and Coetzee (1978) have found t h a t bleomycin, a stimulator of DNA repair, caused a 2-fold higher incorporation of tritiated thymidine triphosphate in liver cell nuclei from middle-age rats as compared to old suggesting diminished repair capacity in old rats. Likewise, Epstein et al. (1973,1974) have reported that normal human skin fibroblasts show decreased repair of 7-ray-induced DNA chain breaks with increasing in vitro age. A similar finding of decreased repair in progeria cells by this group has not been confirmed (Regan and Setlow, 1974).