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《Studies in History and Philosophy of Science Part B: Studies in History and Philosophy of Modern Physics》2004,35(3):377-396
This paper describes a long-standing, though little known, debate between Dirac and Heisenberg over the nature of scientific methodology, theory change, and intertheoretic relations. Following Heisenberg's terminology, their disagreements can be summarized as a debate over whether the classical and quantum theories are “open” or “closed.” A close examination of this debate sheds new light on the philosophical views of two of the great founders of quantum theory. 相似文献
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《Studies in History and Philosophy of Science Part B: Studies in History and Philosophy of Modern Physics》2004,35(3):397-405
Rohrlich claims that “the problem of the arrow of time in classical dynamics has been solved”. The solution he proposes is based on the equations governing the motion of extended particles. Rohrlich claims that these equations, which must take self-interaction into account, are not invariant under time reversal. I dispute this claim, on several grounds. 相似文献
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δ-Protocadherins constitute a group of cadherins characterized by several conserved motifs in their cytoplasmic domains. We
present a phylogenetic analysis that further divides this group into δ1-protocadherins (comprising protocadherin-1, −7, −9
and −11 or -X/Y) and δ2-protocadherins (comprising protocadherin-8, −10, −17, −18 and −19). The δ-protocadherin genes, which
are located on different chromosomes in man and mouse, have a similar gene structure. They are expressed as multiple splice
forms, differing mostly in their cytoplasmic domains. Some δ-protocadherins were reported to mediate weak cell-cell adhesion
in vitro and cell sorting in vivo. In addition, individual δ-protocadherins might play important roles in signaling pathways,
as they bind to proteins such as TAF1/Set, protein phosphatase-1α and the Frizzled 7 receptor. The spatiotemporally restricted
expression of δ-protocadherins in different tissues and species and the results of their functional analysis, mainly in Xenopus, suggest that they play multiple, tightly regulated roles in vertebrate development.
Received 18 July 2005; received after revision 26 August 2005; accepted 2 September 2005 相似文献
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The correct repair of double-strand breaks (DSBs) is essential for the genomic integrity of a cell, as inappropriate repair
can lead to chromosomal rearrangements such as translocations. In many hematologic cancers and sarcomas, translocations are
the etiological factor in tumorigenesis, resulting in either the deregulation of a proto-oncogene or the expression of a fusion
protein with transforming properties. Mammalian cells are able to repair DSBs by pathways involving homologous recombination
and nonhomologous end-joining. The analysis of translocation breakpoints in a number of cancers and the development of model
translocation systems are beginning to shed light on specific DSB repair pathway(s) responsible for the improper repair of
broken chromosomes.
Received 19 June 2001; received after revision 6 September 2001; accepted 11 September 2001 相似文献
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G. F. Van Went 《Cellular and molecular life sciences : CMLS》1978,34(3):324-325
Summary Using the micronucleus test as a screening method for mutagenic activity, no significant increase in the number of micronuclei was found when LSD, psilocybin or 9-THC were administered in 3 logarithmically increasing doses to mice. Azathioprine (Imuran®), given as a positive control, caused a statistically significant increase in micronucleated cells.Acknowledgment. The expert technical assistance of Mr Joop Branger is greatfully acknowledged. We thank Prof. Dr C. A. Salemink, University of Utrecht, for the supply of the THC, and Dr J. Fokkens, National Institute of Public Health, for preparing the solutions. 相似文献
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《Studies in History and Philosophy of Science Part B: Studies in History and Philosophy of Modern Physics》2000,31(3):371-404
This paper explores the history of a unique assemblage of researchers in the geodetic and allied sciences organised at Ohio State University (OSU) in 1947 at the beginning of the Cold War. From about 1950 to 1970, the OSU geodetic sciences group was the most significant group of geodetic researchers in the world. Funded almost entirely by military and intelligence agencies, they pioneered the technologies, organised the research initiatives, ordered the data sets, and trained the generation of geodesists who eventually created the Cold War Figure of the Earth to both prosecute and prevent global nuclear war. They devised elaborate mechanisms to pursue in secrecy and isolation research that had hitherto been performed collaboratively and globally. They invented methods to maintain professional associations and protocols, both to distribute—and disguise—the fruits of their geodetic research. In accomplishing this, their work also undermined the basic hypothesis of isostasy that had been foundational to geodesy for the previous century.Fundamental progress in the geosciences and military and intelligence directives were inextricably linked during the Cold War, although the extent of their convergence has been masked by the security protocols organised to disguise it. With the declassification of key programmes underway, it is now both possible and necessary to substantially revise the history of Cold War-era geosciences and their associated technologies. 相似文献
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Peroxisomes are single-membrane-bound organelles present in virtually all eukaryotic cells. They are involved in numerous
metabolic processes, both catabolic and anabolic, including β-oxidation of very long chain fatty acids, metabolism of hydrogen
peroxide, plasmalogen biosynthesis and bile acid synthesis. In several genetic diseases, there is either isolated deficiency
of a specific peroxisomal protein (single-protein deficiencies) or a defect in the formation of the organelle with loss of
multiple peroxisomal functions (peroxisome biogenesis disorders). X-linked adrenoleukodystrophy is an example of the former,
and the Zellweger spectrum of the latter. Peroxisome biogenesis disorders are inherited in an autosomal recessive manner and
result from mutations in any of at least 12 PEX genes that encode peroxins. This article reviews the peroxisomal system, the clinical, biochemical and molecular aspects
of peroxisomal disorders, and discusses recent scientific advances in the understanding of peroxisome biogenesis.
Received 16 October 2001; received after revision 2 January 2002; accepted 3 January 2002 相似文献
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Dyskeratosis congenita is an inherited skin and bone marrow failure syndrome. There are X-linked, autosomal dominant and autosomal recessive forms of the disease. The X-linked form is due to mutations in the DKC1 gene at Xq28. The encoded protein, dyskerin, is a component of both small nucleolar ribonuclear protein particles and the telomerase complex. Mutations in DKC1 mainly lead to amino acid substitutions. The autosomal dominant form of the disease is due to mutations in hTR, the RNA component of telomerase, making it likely that the disease is due to defective telomerase activity. Mutations in hTR are predicted to either disrupt secondary structure or alter the template region. The gene or genes involved in the recessive forms of the disease remain elusive, though genes whose products are required for telomere maintenance are strong candidates. 相似文献
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《Cellular and molecular life sciences : CMLS》1991,47(8):827-828
Science Policy News
The Second VDI-International Conference on Effects of Atmospheric Precipitations on Soils: Uptake, Assessment and Regulation (Lindau, Germany, 15–17 May 1990) 相似文献15.
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I. Palik P. Hadházy K. Magyar B. Malomvölgyi M. Wagner G. Pogátsa 《Cellular and molecular life sciences : CMLS》1981,37(8):863-864
Summary Contractile responses of isolated coronary arteries from healthy and alloxan-diabetic dogs to prostaglandin F2 were enhanced by indomethacin and inhibited by prostaglandin I2. The potentiation by indomethacin was more prominent in diabetic vessels than in normal arteries. 相似文献
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Apaf1 has been described as the core of the apoptosome. Deficiency in murine Apaf1 leads to embryonic lethality with a phenotype affecting many aspects of developmental apoptosis. In the developing brain,
Apaf1 is a death regulator of the neuronal founder cells. Combined intercrosses of mouse lines mutant for members of the mitochondrial
death pathway are providing us with some clues about the relative regulation existing among neuronal cell populations. Apaf1-deficient embryos display an interesting phenotype in the inner ear and in limb development, which involves different caspase-dependent
and -independent pathways. Moreover, APAF1 is mutated in human melanomas, and its depletion contributes to malignant transformation in a mouse model of cancer. This
review has a double aim: the analysis of the alternatives taken by the embryo to bring into the suicidal program different
cells at different stages, and the relevance of APAF1 in the onset and progression of cancer.
Received 5 March 2001; received after revision 19 April 2001; accepted 4 May 2001 相似文献
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Hu QD Lu H Huo K Ying K Li J Xie Y Mao Y Li YY 《Cellular and molecular life sciences : CMLS》2003,60(8):1725-1732
The Saccharomyces cerevisiae TPT1 gene plays a role in removing the 2-phosphate from ligated tRNA during the maturation of pre-tRNA. Here we reported the cloning and characterization of the human TRPT1 gene as a homolog of yeast TPT1. The TRPT1 gene is located at human chromosome 11q13 and encodes a polypeptide of 253 amino acids. BLAST searches with its amino acid sequence revealed the ubiquitous occurrence of TRPT1 homologs and their functional relationships with the presence of the DUF60/KptA domain. Northern analysis demonstrated that the gene is primarily expressed in heart and skeletal muscle, with lower or undetectable levels in other tissues studied. A plasmid-shuffling experiment showed that the human TRPT1 gene could complement the tpt1 mutation in S. cerevisiaeReceived 19 March 2003; received after revision 25 April 2003; accepted 22 May 2003 相似文献