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81.
The Meaning of Life in a Developing Universe 总被引:4,自引:4,他引:0
John E. Stewart 《Foundations of Science》2010,15(4):395-409
The evolution of life on Earth has produced an organism that is beginning to model and understand its own evolution and the
possible future evolution of life in the universe. These models and associated evidence show that evolution on Earth has a
trajectory. The scale over which living processes are organized cooperatively has increased progressively, as has its evolvability.
Recent theoretical advances raise the possibility that this trajectory is itself part of a wider developmental process. According
to these theories, the developmental process has been shaped by a yet larger evolutionary dynamic that involves the reproduction
of universes. This evolutionary dynamic has tuned the key parameters of the universe to increase the likelihood that life
will emerge and produce outcomes that are successful in the larger process (e.g. a key outcome may be to produce life and
intelligence that intentionally reproduces the universe and tunes the parameters of ‘offspring’ universes). Theory suggests
that when life emerges on a planet, it moves along this trajectory of its own accord. However, at a particular point evolution
will continue to advance only if organisms emerge that decide to advance the developmental process intentionally. The organisms
must be prepared to make this commitment even though the ultimate nature and destination of the process is uncertain, and
may forever remain unknown. Organisms that complete this transition to intentional evolution will drive the further development
of life and intelligence in the universe. Humanity’s increasing understanding of the evolution of life in the universe is
rapidly bringing it to the threshold of this major evolutionary transition. 相似文献
82.
Gramm F Baerlocher C McCusker LB Warrender SJ Wright PA Han B Hong SB Liu Z Ohsuna T Terasaki O 《Nature》2006,444(7115):79-81
Many industrially important materials, ranging from ceramics to catalysts to pharmaceuticals, are polycrystalline and cannot be grown as single crystals. This means that non-conventional methods of structure analysis must be applied to obtain the structural information that is fundamental to the understanding of the properties of these materials. Electron microscopy might appear to be a natural approach, but only relatively simple structures have been solved by this route. Powder diffraction is another obvious option, but the overlap of reflections with similar diffraction angles causes an ambiguity in the relative intensities of those reflections. Various ways of overcoming or circumventing this problem have been developed, and several of these involve incorporating chemical information into the structure determination process. For complex zeolite structures, the FOCUS algorithm has proved to be effective. Because it operates in both real and reciprocal space, phase information obtained from high-resolution transmission electron microscopy images can be incorporated directly into this algorithm in a simple way. Here we show that by doing so, the complexity limit can be extended much further. The power of this approach has been demonstrated with the solution of the structure of the zeolite TNU-9 (|H9.3|[Al9.3Si182.7O384]; ref. 10) with 24 topologically distinct (Si,Al) atoms and 52 such O atoms. For comparison, ITQ-22 (ref. 11), the most complex zeolite known to date, has 16 topologically distinct (Si,Ge) atoms. 相似文献
83.
84.
Enanga B Burchmore RJ Stewart ML Barrett MP 《Cellular and molecular life sciences : CMLS》2002,59(5):845-858
Recent progress in understanding the neuro-pathological mechanisms of sleeping sickness reveals a complex relationship between
the trypanosome parasite that causes this disease and the host nervous system. The pathology of late-stage sleeping sickness,
in which the central nervous system is involved, is complicated and is associated with disturbances in the circadian rhythm
of sleep. The blood-brain barrier, which separates circulating blood from the central nervous system, regulates the flow of
materials to and from the brain. During the course of disease, the integrity of the blood-brain barrier is compromised. Dysfunction
of the nervous system may be exacerbated by factors of trypanosomal origin or by host responses to parasites. Microscopic
examination of cerebrospinal fluid remains the best way to confirm late-stage sleeping sickness, but this necessitates a risky
lumbar puncture. Most drugs, including many trypanocides, do not cross the blood-brain barrier efficiently. Improved diagnostic
and therapeutic approaches are thus urgently required. The latter might benefit from approaches which manipulate the blood-brain
barrier to enhance permeability or to limit drug efflux. This review summarizes our current understanding of the neurological
aspects of sleeping sickness, and envisages new research into blood-brain barrier models that are necessary to understand
the interactions between trypanosomes and drugs active against them within the host nervous system.
Received 10 October 2001; received after revision 29 November 2001; accepted 5 December 2001 相似文献
85.
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87.
A progeroid syndrome in mice is caused by defects in A-type lamins 总被引:21,自引:0,他引:21
Numerous studies of the underlying causes of ageing have been attempted by examining diseases associated with premature ageing, such as Werner's syndrome and Hutchinson-Gilford progeria syndrome (HGPS). HGPS is a rare genetic disorder resulting in phenotypes suggestive of accelerated ageing, including shortened stature, craniofacial disproportion, very thin skin, alopecia and osteoporosis, with death in the early teens predominantly due to atherosclerosis. However, recent reports suggest that developmental abnormalities may also be important in HGPS. Here we describe the derivation of mice carrying an autosomal recessive mutation in the lamin A gene (Lmna) encoding A-type lamins, major components of the nuclear lamina. Homozygous mice display defects consistent with HGPS, including a marked reduction in growth rate and death by 4 weeks of age. Pathologies in bone, muscle and skin are also consistent with progeria. The Lmna mutation resulted in nuclear morphology defects and decreased lifespan of homozygous fibroblasts, suggesting premature cell death. Here we present a mouse model for progeria that may elucidate mechanisms of ageing and development in certain tissue types, especially those developing from the mesenchymal cell lineage. 相似文献
88.
Biofilms are surface-attached microbial communities with characteristic architecture and phenotypic and biochemical properties distinct from their free-swimming, planktonic counterparts. One of the best-known of these biofilm-specific properties is the development of antibiotic resistance that can be up to 1,000-fold greater than planktonic cells. We report a genetic determinant of this high-level resistance in the Gram-negative opportunistic pathogen, Pseudomonas aeruginosa. We have identified a mutant of P. aeruginosa that, while still capable of forming biofilms with the characteristic P. aeruginosa architecture, does not develop high-level biofilm-specific resistance to three different classes of antibiotics. The locus identified in our screen, ndvB, is required for the synthesis of periplasmic glucans. Our discovery that these periplasmic glucans interact physically with tobramycin suggests that these glucose polymers may prevent antibiotics from reaching their sites of action by sequestering these antimicrobial agents in the periplasm. Our results indicate that biofilms themselves are not simply a diffusion barrier to these antibiotics, but rather that bacteria within these microbial communities employ distinct mechanisms to resist the action of antimicrobial agents. 相似文献
89.
90.
Auwerx J Avner P Baldock R Ballabio A Balling R Barbacid M Berns A Bradley A Brown S Carmeliet P Chambon P Cox R Davidson D Davies K Duboule D Forejt J Granucci F Hastie N de Angelis MH Jackson I Kioussis D Kollias G Lathrop M Lendahl U Malumbres M von Melchner H Müller W Partanen J Ricciardi-Castagnoli P Rigby P Rosen B Rosenthal N Skarnes B Stewart AF Thornton J Tocchini-Valentini G Wagner E Wahli W Wurst W 《Nature genetics》2004,36(9):925-927
The European Mouse Mutagenesis Consortium is the European initiative contributing to the international effort on functional annotation of the mouse genome. Its objectives are to establish and integrate mutagenesis platforms, gene expression resources, phenotyping units, storage and distribution centers and bioinformatics resources. The combined efforts will accelerate our understanding of gene function and of human health and disease. 相似文献