Phenotype-driven genetics can be used to create mouse models of human disease and birth defects. However, the utility of these mutant models is limited without identification of the causal gene. To ...facilitate genetic mapping, we developed a fixed single nucleotide polymorphism (SNP) panel of 394 SNPs as an alternative to analyses using simple sequence length polymorphism (SSLP) marker mapping. With the SNP panel, chromosomal locations for 22 monogenic mutants were identified. The average number of affected progeny genotyped for mapped monogenic mutations is nine. Map locations for several mutants have been obtained with as few as four affected progeny. The average size of genetic intervals obtained for these mutants is 43 Mb, with a range of 17-83 Mb. Thus, our SNP panel allows for identification of moderate resolution map position with small numbers of mice in a high-throughput manner. Importantly, the panel is suitable for mapping crosses from many inbred and wild-derived inbred strain combinations. The chromosomal localizations obtained with the SNP panel allow one to quickly distinguish between potentially novel loci or remutations in known genes, and facilitates fine mapping and positional cloning. By using this approach, we identified DNA sequence changes in two ethylnitrosourea-induced mutants.
The Authentic Text of Titus Andronicus Bolton, Joseph S. G.
PMLA : Publications of the Modern Language Association of America,
09/1929, Letnik:
44, Številka:
3
Journal Article
Recenzirano
It was in 1905 that Mr. Evald Ljunggren, Librarian of Lund University, collated the newly discovered copy of the first quarto of
Titus Andronicus
with the quarto of 1600, and published his list of ...variant readings. Forty-seven of his readings involved more than mere variations in spelling and punctuation, and, of these, fifteen had been anticipated by the ingenuity of earlier scholars. One variant was a misprint, and thirty-one offered material for the consideration of the textual critic. But although these readings have been available to the scholarly world for a quarter of a century, editors have shown a marked hesitancy in introducing them into the traditional text of the play. The Neilson text, published the following year, incorporates only four, although twenty-two are listed in the notes. In the Tudor edition of 1913 Professor Elmer E. Stoll adopted as many as twenty-one, and in his notes included five others. But in the Yale Shakespeare issued in 1926, Mr. A. M. Witherspoon accepts none of the recovered variants, and in his notes leaves twenty-seven unmentioned. Basing his text almost entirely upon the First Folio, Mr. Witherspoon, I take it, assumes either that the editors of one or more of the editions following the first quarto had had access to the original Shakespearean manuscript or Shakespearean annotations, or else that Shakespeare himself did the revising.
Millions of mild traumatic brain injuries (TBIs) occur every year in the United States, with many people subject to multiple head injuries that can lead to chronic behavioral dysfunction. We ...previously reported that mild TBI induced using closed head injuries (CHI) repeated at 24h intervals produced more acute neuron death and glial reactivity than a single CHI, and increasing the length of time between injuries to 48h reduced the cumulative acute effects of repeated CHI. To determine whether repeated CHI is associated with behavioral dysfunction or persistent cellular damage, mice receiving either five CHI at 24h intervals, five CHI at 48h intervals, or five sham injuries at 24h intervals were evaluated across a 10 week period after injury. Animals with repeated CHI exhibited motor coordination and memory deficits, but not gait abnormalities when compared to sham animals. At 10wks post-injury, no notable neuron loss or glial reactivity was observed in the cortex, hippocampus, or corpus callosum. Argyrophilic axons were found in the pyramidal tract of some injured animals, but neither silver stain accumulation nor inflammatory responses in the injury groups were statistically different from the sham group in this region. However, argyrophilic axons, microgliosis and astrogliosis were significantly increased within the optic tract of injured animals. Repeated mild CHI also resulted in microgliosis and a loss of neurofilament protein 200 in the optic nerve. Lengthening the inter-injury interval from 24h to 48h did not effectively reduce these behavioral or cellular responses. These results suggest that repeated mild CHI results in persistent behavioral dysfunction and chronic pathological changes within the visual system, neither of which was significantly attenuated by lengthening the inter-injury interval from 24h to 48h.
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