PubMed · 9828535
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D W Foerster. 1998. Changing insurance.. https://pubmed.ncbi.nlm.nih.gov/9828535/
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Patients with polyglutamine expansion diseases, like Huntington's disease or several spinocerebellar ataxias, first present with neurological symptoms that can occur in the absence of neurodegeneration. Behavioral symptoms thus appear to be caused by neuronal dysfunction, rather than cell death. Pathogenesis in polyglutamine expansion diseases is largely viewed as a cell-autonomous process in neurons. It is likely, however, that this process is influenced by changes in glial physiology and, at least in the case of DRPLA glial inclusions and glial cell death, seems to be an important part in the pathogenesis. To investigate these aspects in a Drosophila model system, we expressed polyglutamine proteins in the adult nervous system. Glial-specific expression of a polyglutamine (Q)-expanded (n=78) and also a nonexpanded (n=27) truncated version of human ataxin-3 led to the formation of protein aggregates and glial cell death. Behavioral changes were observed prior to cell death. This reveals that glia is susceptible to the toxic action of polyglutamine proteins. Neuronal expression of the same constructs resulted in behavioral changes similar to those resulting from glial expression but did not cause neurodegeneration. Behavioral deficits were selective and affected two analyzed fly behaviors differently. Both glial and neuronal aggregates of Q78 and Q27 appeared early in pathogenesis and, at the electron microscopic resolution, had a fibrillary substructure. This shows that a nonexpanded stretch can cause similar histological and behavioral symptoms as the expanded stretch, however, with a significant delay.
Recently, a non-random transmission of BRCA1 mutant alleles to the off-spring of carriers has been suggested. If confirmed by further studies, the finding will have important implications both for risk assessment and the understanding of BRCA1 biology. However, these kind of analysis are not easy to perform due to several ascertainment biases inherent to the identification of BRCA1 carriers. In this report we propose different approaches to overcome such biases and we present additional data supporting a non-random transmission of BRCA1 mutant alleles.
Vertical climbing has played an important role in theories about the evolution of habitual bipedalism in early hominids and of locomotor specialization in hominoids. However, empirical data on vertical climbing in nonhuman primates are scarce, especially regarding kinematics. In this paper, the kinematics of flexed-elbow vertical climbing of four hominoid species are reported: western lowland gorillas (Gorilla gorilla gorilla), bonobos (Pan paniscus), Sumatran orangutans (Pongo pygmaeus abelii), and yellow-cheeked crested gibbons (Hylobates concolor gabriellae). The climbing sequences were recorded simultaneously by four digital video cameras in European zoos. Analyzed parameters include intersegmental flexion/extension angles of the shoulder, elbow, hip, and knee joints, horizontal abduction/adduction angles of the upper arm and thigh, and distance of the body center of gravity from the substrate. Analyses reveal that differences in climbing kinematics between individuals of different age/sex classes of one species are mostly size-related, whereas interspecific differences reflect specific locomotor adaptations. The climbing kinematics of bonobos and gorillas are more similar to each other than to those of orangutans or gibbons. The range of motion of the major limb joints in adult orangutans is larger than in African apes, although the hip is not more extended. Gibbons horizontally abduct the arm more and the thigh less during climbing than any of the great apes. These results allow us to question some qualitative descriptions of vertical climbing kinematics reported in the literature, and to discuss implications for the evolution of locomotor adaptations in hominoids.