Fragile X expression in thymidine-prototrophic and auxotrophic human-mouse somatic cell hybrids under low and high thymidylate stress conditions

Expression of the fragile X site fra(X)(q27.3) was studied in thymidine-prototrophic and auxotrophic human-mouse somatic cell hybrids. In these cells, low thymidylate stress, achieved by 5-fluoro-2'-deoxyuridine (FdU) treatment and by limiting the exogenous supply of thymidine (dT), induced fragile X expression. High thymidylate stress, produced by supplying excess amounts of dT, was also effective in inducing fragile X expression, even in a hybrid clone that retained a fragile X chromosome as the only human chromosome; addition of deoxycytidine (dC) completely abolished this effect. In contrast, 5-bromo-2'-deoxyuridine (BrdU) did not induce fragile X expression. Cell-cycle analysis of BrdU-deprived thymidine-auxotrophic hybrid cells indicated that one round of DNA replication under thymidylate stress conditions is sufficient for fragile X expression. Our results suggest that the expression is an intrinsic property of the fragile site itself, which is believed to be composed of replicon clusters with pyrimidine-rich DNA sequence(s).     

The small hospital's role in poliomyelitis

Medical skills should be developed by the staffs of smaller hospitals for the differential study of patients with symptoms resembling those of poliomyelitis in order to provide the rudiments of care for the occasional patient with mild poliomyelitis, to recognize the indications which point to the necessity of superior technical assistance, and to decide when it is appropriate to move patients to better equipped centers. The impetuous acquisition of mechanical aids for the treatment of special problems will be effective in small communities only to the extent that this equipment is kept serviceable and is operated by persons of sufficient skill. Epidemic situations in a small community can be met only by mobilization of facilities under adequate direction and by integration of care with that provided by larger treatment centers.     

Ultrastructural study of enzymes in reactive astrocytes: Clarification of astrocytic activity

Summary Enzymes in reactive astrocytes of the corebral cortex were examined at the ultrastructural level in an attempt to resolve some conflicting aspects of astrocytic activity. Correlations between morphological and enzyme changes after injury established that the apparent increase in oxidative enzyme activity was exclusively mitochondrial and not an artefactual reaction product resulting from anoxic cellular damage. Pronounced glucose-6-phosphatase activity within cisternae of an increased amount of the granular endoplasnie reticulum was related to increased glycogen. Further evidence from acid phosphatase activity indieated that astrocytes played a minimal role in phagocytosis.