In the spring of 1993, hantavirus pulmonary syndrome (HPS) "emerged" in the southwestern United States, where a multiagency investigation led to the rapid description of this new clinical entity and its etiology. Analysis of the first 100 US cases identified showed that the disease was distributed in 21 states, had gone unrecognized since at least 1959, and had a distinct spring-early summer seasonality. Of the infected persons, 54% were male; 63% were Caucasian, 35% were Native American, and 2% were African American. The average age of case-patients was 34.9 years, and 8 were children or adolescents aged < or = 16 years. The overall case-fatality rate was 52%. There was a 91% concordance among serologic, immunohistochemical, and molecular results. HPS in the United States is caused by at least three newly described pathogenic hantaviruses, each of which has a distinct rodent host, and cases of HPS have been recently recognized in Canada and South America. National surveillance of this sporadic disease remains essential for further defining the epidemiology and clinical spectrum.
The objective of this research was to investigate skeletal muscle response to a chronic administration of stretch-shortening cycles (SSCs) in young and old rats. Dorsiflexor muscles of old (30 months, n = 5) and young (12 weeks, n = 6) rats were exposed 3 times/week for 4.5 weeks to a protocol of 80 maximal SSCs per exposure in vivo. Skeletal muscle response was characterized by isometric and dynamic performance, as well as by muscle wet mass and quantitative morphological analyses following the exposure period. The performance of the young and old groups was not statistically different at the start of the exposure. By the end of the exposure, however, a statistical difference was noted, as performance increased significantly in the young animals and decreased significantly in the old animals. Muscle wet mass of the left tibialis anterior (TA) in the treated limb was significantly greater in the youngthan in the old animals (p < 0.001), whereas there was no difference in the contra-lateral TA. No degenerative myofibers or changes in non-cellular interstitium were noted in either age group, but a significant increase was observed in the volume of the cellular interstitium in the exposed limb of the old animals (p = 0.01), which is indicative of an inflammatory response. Thus, a chronic exposure of SSCs results in significant performance increase and muscle hypertrophy in young animals, and a significant performance decrease and an increased cellular interstitial response in old animals. These findings suggest that age may impair the ability of skeletal muscle to adapt to repetitive mechanical loading, even in the absence of degeneration.
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