We surveyed morphotectonic markers along the central part of the Gurvan Bulag thrust, a fault that ruptured with the Bogd fault during the Gobi‐Altay earthquake (1957, M 8.3), to document climatic ...and tectonic processes along the fault for the late Pleistocene‐Holocene period. The markers were dated using 10Be produced in situ. Two major periods of alluviation ended at 131 ± 20 and 16 ± 4.8 ka. These appear to be contemporaneous with global climatic changes at the terminations of marine isotope stages (MIS) 6 and 2. The vertical slip rates, determined from offset measurements and surfaces ages, are 0.14 ± 0.03 mm/yr over the late Pleistocene‐Holocene and between 0.44 ± 0.11 and 1.05 ± 0.25 mm/yr since the end of the late Pleistocene. The higher of these slip rates for the last ∼16 kyr is consistent with paleoseismic investigations along the fault Prentice et al., 2002, and suggests that, at the end of late Pleistocene, the fault evolved from quiescence to having recurrence intervals of 4.0 ± 1.2 kyr for surface ruptures with ∼4 m vertical offset (similar to that of 1957). The inferred recurrence interval is comparable to that of the Bogd fault (3.7 ± 1.3 kyr) suggesting that the two faults may have ruptured together also earlier during the last ∼16 kyr.
The shaker-1 (Myo7a) mouse deafness locus is encoded by an unconventional myosin gene: myosin VIIA Gibson, Walsh, Mburu, Varela, Brown, Antonio, Biesel, Steel and Brown (1995) Nature (London) 374, ...62-64. The myosin VIIA gene is expressed in hair cells in the cochlea, where it is thought to function in the development of the critical neuroepithelium where auditory transduction takes place. In order to understand better the function of myosin VIIA, we have determined the complete sequence of the mouse myosin VIIA cDNA and employed the wild-type sequence for mutational analysis of a number of shaker-1 alleles. Analysis of the mouse myosin VIIA tail sequence demonstrates a large internal repeat with regions of similarity to myosins IV, X and XII as well as members of the band 4.1 family. In addition, the myosin VIIA repeats are similar along their entire length to a tail domain from a plant kinesin. The mouse myosin VIIA tail also contains a putative Src homology 3 (SH3) domain. Along with three previously reported shaker-1 mutations, mutations for seven shaker-1 alleles in total have now been identified. The mutational changes have been analysed in terms of their predicted effect on both myosin motor head and tail domain function and the predictions related to the known phenotypes of the shaker-1 alleles. Five of the mutations lie in the motor head, and analysis of their likely effect on myosin head structure correlates well with the known severity of the shaker-1 alleles. Of the two mutations in the tail, one is a missense mutation within the kinesin and myosin IV, X and XII homology domains that substitutes a conserved amino acid and leads to a severe deafness phenotype. This and other data suggest that myosin VIIA may have properties of a myosin-motor-kinesin-tail hybrid and be involved in membrane turnover within the actin-rich environment of the apical hair cell surface.
With advances in the Human Genome Project, the implications of genetic technology in disease prevention should be assessed. The paradigm suggested in The Future of Public Health--assessment, policy ...development, and assurance--was used to examine the continuum from genetic technology to public health practice. First, important public health functions are to (1) assess the impact of genes and their interactions with modifiable disease risk factors on the health status of the population and (2) assess the impact and safety of genetic testing on the population. Second, given the many implications of genetic testing, the public health community should participate in policy development related to the timing and use of genetic testing in disease prevention. Third, whenever appropriate, the public health community needs to ensure the development of public health genetics programs (e.g. newborn screening) and evaluate the quality and effectiveness of the use of genetic testing in disease prevention. Although most current genetic tests are not ready for disease prevention, there is an important role for the public health community in translating genetic technology into disease prevention.
This study investigates Hip Hop rap and R&B artists' use of monsters and characterizations of monstrosities in their lyrics. It examines Hip Hop rap and R&B artists' lyrics to determine the presence ...or absence of Afrocentricity and cultural linguistic resignification. Using Afrocentric method and a qualitative interpretive analysis of lyric's contextual meaning, findings suggest Hip Hop rap and R&B artist's lyrics containing monsters and characterizations of monstrosities is Afrocentric and culturally resignified. A further in-depth review of data also suggests the first semantic shift of references to monsters and monstrosities occurred through White hegemony's resignification of the terms and their meanings as a tool for pejorative reference and oppression. Hence, the Hip Hop generation has reclaimed the references to monsters and characterizations of monstrosities as an affirmation of positive regard.
Emery-Dreifuss muscular dystrophy (EDMD) is an X-linked recessive muscular dystrophy characterized by early contractures of the elbows, Achilles tendons and spine, slowly progressive muscle wasting ...and weakness, and cardiomyopathy associated with cardiac conduction defects. The emerin gene has been mapped to Xq28 and encodes a 34-kDa serine-rich protein, emerin, which has been localized to the nuclear envelope in a wide variety of tissues, including skeletal and cardiac muscle. Mutations spanning the emerin gene have been identified in patients with EDMD. We present here the effect, on emerin protein expression, of two missense mutations identified in unrelated EDMD patients. These alterations predict the replacement of a proline residue at position 183 with either a histidine or a threonine. Biochemical analysis has demonstrated that the mobility and expression levels of the mutant forms of emerin are indistinguishable from that of wild-type emerin, but that they have weakened interactions with nuclear lamina components. In comparison with the usual EDMD phenotype, patients with P183 missense mutations have a later age at onset of first symptoms, elbow contractures, ankle contractures, upper limb weakness and lower limb weakness, but there is no difference for the age at onset of cardiac involvement. This is the first report of protein studies on patients with missense mutations resulting in the clinical features of EDMD. These studies demonstrate the importance of proline 183 for the proper structure/function of emerin.
We surveyed morphotectonic markers along the central part of the Gurvan Bulag thrust, a fault that ruptured with the Bogd fault during the Gobi-Altay earthquake (1957, M 8.3), to document climatic ...and tectonic processes along the fault for the late Pleistocene-Holocene period. The markers were dated using super 10Be produced in situ. Two major periods of alluviation ended at 131 +/- 20 and 16 +/- 4.8 ka. These appear to be contemporaneous with global climatic changes at the terminations of marine isotope stages (MIS) 6 and 2. The vertical slip rates, determined from offset measurements and surfaces ages, are 0.14 +/- 0.03 mm/yr over the late Pleistocene-Holocene and between 0.44 +/- 0.11 and 1.05 +/- 0.25 mm/yr since the end of the late Pleistocene. The higher of these slip rates for the last ~16 kyr is consistent with paleoseismic investigations along the fault Prentice et al. 2002, and suggests that, at the end of late Pleistocene, the fault evolved from quiescence to having recurrence intervals of 4.0 +/- 1.2 kyr for surface ruptures with ~4 m vertical offset (similar to that of 1957). The inferred recurrence interval is comparable to that of the Bogd fault (3.7 +/- 1.3 kyr) suggesting that the two faults may have ruptured together also earlier during the last ~16 kyr.
Emerin, the product of the gene responsible for X-linked Emery-Dreifuss muscular dystrophy (EDMD), has a ubiquitous tissue distribution and is localised to the nuclear envelope. We present here the ...relationship between emerin protein expression, nuclear localization and clinical phenotype for two distal mutations identified in unrelated EDMD patients. The first mutation predicts the replacement of the last eight amino acids of emerin with the addition of 101 amino acids, but no emerin expression is detected. The second mutation, 35 bp upstream from the first mutation, deletes six amino acids from the transmembrane region, but in this case emerin expression is seen. Emerin from this second patient is expressed at reduced levels, mistargeted and has altered biochemical properties compared to wild type emerin. In both cases the clinical phenotype was similar to patients with typical null mutations. We discuss these data in comparison with previous reports of other C-terminal mutations in the emerin gene and suggest that the efficiency of emerin's nuclear membrane localization is affected by the hydrophobicity (and possibly length) of its transmembrane region, and a longer C-terminal tail prevents nuclear localization.
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