FYN kinase is highly expressed in the testis and has been implicated in testis and sperm function, yet specific roles for this kinase in testis somatic and germ cells have not been defined. The purpose of the present investigation was to identify aspects of spermatogenesis, spermiation, or sperm fertilizing capacity that required FYN for normal reproductive function. Matings between Fyn-null males and wild-type females resulted in normal litter sizes, despite the fact that Fyn-null males exhibited reduced epididymal size and sperm count. Morphological analysis revealed a high frequency of abnormal sperm morphology among Fyn-null sperm, and artificial insemination competition studies demonstrated that Fyn-null sperm possessed reduced fertilizing capacity. Fyn-null sperm exhibited nearly normal motility during capacitation in vitro but reduced ability to undergo the acrosome reaction and fertilize oocytes. The typical pattern of capacitation-induced protein tyrosine phosphorylation was slightly modified in Fyn-null sperm, with reduced abundance of several minor phosphoproteins. These findings are consistent with a model in which FYN kinase plays an important role in proper shaping of the head and acrosome within the testis and possibly an additional role in the sperm acrosome reaction, events required for development of full fertilizing capacity in sperm.
A477indices were 1.72 (1.69-1.74), and 2.95 (2.92-2.99) from two databases respectively. Average sensitivity for individual Charlson categories was 0.321 (range: 0.100-0.710), and 0.374 (0.070-0.802) for Elixhauser categories. Conditions with low sensitivity were cerebrovascular, liver disease, AIDS/HIV, cancer, and psychosis. Average specificity was 0.999 for Charlson, and 0.997 for Elixhauser categories. ConClusions: Comorbidity indices were underestimated by 57% for Charlson and 42% for Elixhauser when calculated from hospital billing data. Individual comorbidity categories had high specificity, but low sensitivity.
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