One of the impediments in the genetic improvement of cotton fiber is the paucity of information about genes associated with fiber development.Availability of chromosome arm substitution line CS-
By consideration of the characteristics of martensitic transformation and the derivation from the application of the group theory to martensitic transformation, it may be concluded that the shape memory effect (SME) c...By consideration of the characteristics of martensitic transformation and the derivation from the application of the group theory to martensitic transformation, it may be concluded that the shape memory effect (SME) can be attained in materials through a martensitic transformation and its reverse transformation. only when there forms single or nearly single variant of martensite, with an absence of the factors causing the generation of the resistance against SME. on this principle, various shape memory materials including nonferrous alloys. iron-based alloys and ceramics containjng zirconia are expected to be further developed. A criterion for thermoelastic martensitic transformation is presented, Factors which may act as the resistance against SME in various materials are briefly described展开更多
Although numerous studies have examined the neurotoxicity of acrylamide in adult animals,the effects on neuronal development in the embryonic and lactational periods are largely unknown.Thus,we examined the toxicity o...Although numerous studies have examined the neurotoxicity of acrylamide in adult animals,the effects on neuronal development in the embryonic and lactational periods are largely unknown.Thus,we examined the toxicity of acrylamide on neuronal development in the hippocampus of fetal rats during pregnancy.Sprague-Dawley rats were mated with male rats at a 1:1 ratio.Rats were administered 0,5,10 or 20 mg/kg acrylamide intragastrically from embryonic days 6–21.The gait scores were examined in pregnant rats in each group to analyze maternal toxicity.Eight weaning rats from each group were also euthanized on postnatal day 21 for follow-up studies.Nissl staining was used to observe histological change in the hippocampus.Immunohistochemistry was conducted to observe the condition of neurites,including dendrites and axons.Western blot assay was used to measure the expression levels of the specific nerve axon membrane protein,growth associated protein 43,and the presynaptic vesicle membrane specific protein,synaptophysin.The gait scores of gravid rats significantly increased,suggesting that acrylamide induced maternal motor dysfunction.The number of neurons,as well as expression of growth associated protein 43 and synaptophysin,was reduced with increasing acrylamide dose in postnatal day 21 weaning rats.These data suggest that acrylamide exerts dose-dependent toxic effects on the growth and development of hippocampal neurons of weaning rats.展开更多
This project is supported by the 2007 R & D Special Fund for Public Welfare by Ministry of Science and Technology and Ministry of Finance.Research tasks in this project are proposed based on the implementation plan o...This project is supported by the 2007 R & D Special Fund for Public Welfare by Ministry of Science and Technology and Ministry of Finance.Research tasks in this project are proposed based on the implementation plan of the"THORPEX(The Observing System Research and Predictability Experiment) Interactive Grand Global Ensemble(TIGGE)",a sub-project of the THORPEX international program.展开更多
The V-MYC avian myelocytomatosis viral-related onco- gene, a neuroblastoma-derived gene (MYCN, MIM: 164840) located on chromosome 2p24, was previously found to be associated with Feingold syndrome 1 (FGLDS1, MIM:...The V-MYC avian myelocytomatosis viral-related onco- gene, a neuroblastoma-derived gene (MYCN, MIM: 164840) located on chromosome 2p24, was previously found to be associated with Feingold syndrome 1 (FGLDS1, MIM: 164280) [1]. FGLDS1 is an autosomal dominant disorder characterized by variable combinations of microcephaly, limb malformations, esophageal and duodenal atresias, and learning disabilities. Cardiac and renal malformations, vertebral anomalies, and deafness have also been described in a minority of patients [2]. Despite the involvement of intellectual disability in FGLDS1, the molecular mechanisms of the MYCN gene in regulating brain development remain largely unclear.Some truncated mutations in the N terminus of the MYCN have been identified in FGLDS1 [1, 3].展开更多
文摘One of the impediments in the genetic improvement of cotton fiber is the paucity of information about genes associated with fiber development.Availability of chromosome arm substitution line CS-
文摘By consideration of the characteristics of martensitic transformation and the derivation from the application of the group theory to martensitic transformation, it may be concluded that the shape memory effect (SME) can be attained in materials through a martensitic transformation and its reverse transformation. only when there forms single or nearly single variant of martensite, with an absence of the factors causing the generation of the resistance against SME. on this principle, various shape memory materials including nonferrous alloys. iron-based alloys and ceramics containjng zirconia are expected to be further developed. A criterion for thermoelastic martensitic transformation is presented, Factors which may act as the resistance against SME in various materials are briefly described
基金supported by the Guangdong Provincial Department of Science and Technology in China,No.2016A020225007
文摘Although numerous studies have examined the neurotoxicity of acrylamide in adult animals,the effects on neuronal development in the embryonic and lactational periods are largely unknown.Thus,we examined the toxicity of acrylamide on neuronal development in the hippocampus of fetal rats during pregnancy.Sprague-Dawley rats were mated with male rats at a 1:1 ratio.Rats were administered 0,5,10 or 20 mg/kg acrylamide intragastrically from embryonic days 6–21.The gait scores were examined in pregnant rats in each group to analyze maternal toxicity.Eight weaning rats from each group were also euthanized on postnatal day 21 for follow-up studies.Nissl staining was used to observe histological change in the hippocampus.Immunohistochemistry was conducted to observe the condition of neurites,including dendrites and axons.Western blot assay was used to measure the expression levels of the specific nerve axon membrane protein,growth associated protein 43,and the presynaptic vesicle membrane specific protein,synaptophysin.The gait scores of gravid rats significantly increased,suggesting that acrylamide induced maternal motor dysfunction.The number of neurons,as well as expression of growth associated protein 43 and synaptophysin,was reduced with increasing acrylamide dose in postnatal day 21 weaning rats.These data suggest that acrylamide exerts dose-dependent toxic effects on the growth and development of hippocampal neurons of weaning rats.
文摘This project is supported by the 2007 R & D Special Fund for Public Welfare by Ministry of Science and Technology and Ministry of Finance.Research tasks in this project are proposed based on the implementation plan of the"THORPEX(The Observing System Research and Predictability Experiment) Interactive Grand Global Ensemble(TIGGE)",a sub-project of the THORPEX international program.
基金supported by grants from the National Natural Science Foundation of China(81701494)the Shanghai Municipal Commission of Health and Family Planning(2013ZYJB0015)the Science and Technology Commission of Shanghai Municipality(14411950402)
文摘The V-MYC avian myelocytomatosis viral-related onco- gene, a neuroblastoma-derived gene (MYCN, MIM: 164840) located on chromosome 2p24, was previously found to be associated with Feingold syndrome 1 (FGLDS1, MIM: 164280) [1]. FGLDS1 is an autosomal dominant disorder characterized by variable combinations of microcephaly, limb malformations, esophageal and duodenal atresias, and learning disabilities. Cardiac and renal malformations, vertebral anomalies, and deafness have also been described in a minority of patients [2]. Despite the involvement of intellectual disability in FGLDS1, the molecular mechanisms of the MYCN gene in regulating brain development remain largely unclear.Some truncated mutations in the N terminus of the MYCN have been identified in FGLDS1 [1, 3].