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341.
342.
Stephen T. Buckland Andrew J. Plumptre Len Thomas Eric A. Rexstad 《International journal of primatology》2010,31(3):485-499
Line transect sampling is widely used for estimating abundance of primate populations. Researchers commonly use animal-to-observer
distances (AODs) in analysis, in preference to perpendicular distances from the line, which is in marked contrast with standard
practice for other applications of line transect sampling. We formalize the mathematical shortcomings of approaches based
on AODs, and show that they are likely to give strongly biased estimates of density. We review papers that claim good performance
for the method, and explore this performance through simulations. These confirm strong bias in estimates of density using
AODs. We conclude that AOD methods are conceptually flawed, and that they cannot in general provide valid estimates of density. 相似文献
343.
Megan K. Houseweart Len A. Pennacchio Alex Vilaythong Christoph Peters Jeffrey L. Noebels Richard M. Myers 《Developmental neurobiology》2003,56(4):315-327
The inherited epilepsy Unverricht‐Lundborg disease (EPM1) is caused by loss‐of‐function mutations in the cysteine protease inhibitor, cystatin B. Because cystatin B inhibits a class of lysosomal cysteine proteases called cathepsins, we hypothesized that increased proteolysis by one or more of these cathepsins is likely to be responsible for the seizure, ataxia, and neuronal apoptosis phenotypes characteristic of EPM1. To test this hypothesis and to identify which cysteine cathepsins contribute to EPM1, we have genetically removed three candidate cathepsins from cystatin B‐deficient mice and tested for rescue of their EPM1 phenotypes. Whereas removal of cathepsins L or S from cystatin B‐deficient mice did not ameliorate any aspect of the EPM1 phenotype, removal of cathepsin B resulted in a 36–89% reduction in the amount of cerebellar granule cell apoptosis depending on mouse age. The incidence of an incompletely penetrant eye phenotype was also reduced upon removal of cathepsin B. Because the apoptosis and eye phenotypes were not abolished completely and the ataxia and seizure phenotypes experienced by cystatin B‐deficient animals were not diminished, this suggests that another molecule besides cathepsin B is also responsible for the pathogenesis, or that another molecule can partially compensate for cathepsin B function. These findings establish cathepsin B as a contributor to the apoptotic phenotype of cystatin B‐deficient mice and humans with EPM1. They also suggest that the identification of cathepsin B substrates may further reveal the molecular basis for EPM1. © 2003 Wiley Periodicals, Inc. J Neurobiol 56: 315–327, 2003 相似文献