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Hermann G. W. Burchard 《Foundations of Science》2011,16(1):67-99
Impressions, energy radiated by phenomena in the momentary environmental scene, enter sensory neurons, creating in afferent
nerves a data stream. Following Kant, by our inner sense the mind perceives its own thoughts as it ties together sense data
into an internalized scene. The mind, residing in the brain, logically a Language Machine, processes and stores items as coded
grammatical entities. Kantian synthetic unity in the linguistic brain is able to deliver our experience of the scene as we
appear to see it. Uniquely, the brain records its own history, synthesizing a Movie-in-the-Brain, called the Noumenal Cosmos.
Attempting thereby to represent the actual Universe, this makes for a sovereign brain that governs itself. The brain is domicile
of an Ego, with its selfhood at stake at all times. Yet, it can know itself only by its actions, in which it appears as an
actor in its own movie. Phenomena enter garbled, as confused apparitions, and must be put in good form using top–down feedback
control by Ego, so that each movie frame makes rational sense within the overall context of the Noumenal Cosmos. A stack of
frames is processed typically in 40 Hz rhythm with 300 ms process time each, for about 12 in the stack at any time. Successive
neural centers are processing the stack in the brain assembly line, based on data from increasingly global receptive fields.
Ego stitches together the movie frames, but only the top frame is in consciousness for 25 ms. The top frame contains the whole
scene where the Ego makes an appearance as the actor that imposes Kantian synthetic unity on the scene, merely an assembly
of grammatical texts, in a system-internal coded process language, fitting the scene into the Noumenal Cosmos. But Ego observes
Ego only to the extent permitted by the objectivity rule, only what it does and thinks, not its true face. From the Noumenal
Cosmos, the Ego receives grammatical messages in the internal sense code. They are integrated into a whole in the reaction
of the Ego to the momentary scene. The voluntary nature of Ego’s decisions is explained, based on its ability to code in advance
its own actions sequentially in time, as it sees fit with a view to an orderly Noumenal Cosmos, records of code being arranged
spatially in neural structures. 相似文献
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Sabine Gilch Christian Bach Gloria Lutzny Ina Vorberg Hermann M. Schätzl 《Cellular and molecular life sciences : CMLS》2009,66(24):3979-3991
The infectious agent in prion diseases consists of an aberrantly folded isoform of the cellular prion protein (PrPc), termed PrPSc, which accumulates in brains of affected individuals. Studies on prion-infected cultured cells indicate that cellular cholesterol
homeostasis influences PrPSc propagation. Here, we demonstrate that the cellular PrPSc content decreases upon accumulation of cholesterol in late endosomes, as induced by NPC-1 knock-down or treatment with U18666A.
PrPc trafficking, lipid raft association, and membrane turnover are not significantly altered by such treatments. Cellular PrPSc formation is not impaired, suggesting that PrPSc degradation is increased by intracellular cholesterol accumulation. Interestingly, PrPSc propagation in U18666A-treated cells was partially restored by overexpression of rab 9, which causes redistribution of cholesterol
and possibly of PrPSc to the trans-Golgi network. Surprisingly, rab 9 overexpression itself reduced cellular PrPSc content, indicating that PrPSc production is highly sensitive to alterations in dynamics of vesicle trafficking. 相似文献
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本文应用经典制片法和离体培养法。对沙枣体内、外胚胎发育的各阶段做比较研究。主要区别于原胚期:1)、形态发生:体内只有一种方式,即两极分化方式。而离体的有二种方式,即器官发生和胚状体发生途径。2)、胚性细胞起源:体内只一种起源(即起源于受精卵),离体的胚性细胞的起源有三种方式:a由紧邻表皮细胞的单个薄壁细胞产生;b由表皮细胞横分裂产生和c由表皮及其下的薄璧细胞共同参与产生。3)胚性细胞的细胞学特征:体内发生的合子具明显的极性分化,细胞质、淀粉粒和细胞核集中在合点端。它第一次分裂后,顶、基细胞在细胞学特征上具明显区别。而离体条件下的胚性细胞第一次分裂后无典型的顶、基细胞之分。故也缺乏典型的胚柄细胞。胚分化和成熟期、二者在形态学特征上基本相同 相似文献
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HIV-1 evades antibody-mediated neutralization through conformational masking of receptor-binding sites 总被引:54,自引:0,他引:54
Kwong PD Doyle ML Casper DJ Cicala C Leavitt SA Majeed S Steenbeke TD Venturi M Chaiken I Fung M Katinger H Parren PW Robinson J Van Ryk D Wang L Burton DR Freire E Wyatt R Sodroski J Hendrickson WA Arthos J 《Nature》2002,420(6916):678-682
The ability of human immunodeficiency virus (HIV-1) to persist and cause AIDS is dependent on its avoidance of antibody-mediated neutralization. The virus elicits abundant, envelope-directed antibodies that have little neutralization capacity. This lack of neutralization is paradoxical, given the functional conservation and exposure of receptor-binding sites on the gp120 envelope glycoprotein, which are larger than the typical antibody footprint and should therefore be accessible for antibody binding. Because gp120-receptor interactions involve conformational reorganization, we measured the entropies of binding for 20 gp120-reactive antibodies. Here we show that recognition by receptor-binding-site antibodies induces conformational change. Correlation with neutralization potency and analysis of receptor-antibody thermodynamic cycles suggested a receptor-binding-site 'conformational masking' mechanism of neutralization escape. To understand how such an escape mechanism would be compatible with virus-receptor interactions, we tested a soluble dodecameric receptor molecule and found that it neutralized primary HIV-1 isolates with great potency, showing that simultaneous binding of viral envelope glycoproteins by multiple receptors creates sufficient avidity to compensate for such masking. Because this solution is available for cell-surface receptors but not for most antibodies, conformational masking enables HIV-1 to maintain receptor binding and simultaneously to resist neutralization. 相似文献
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Pathways to neuronal injury and apoptosis in HIV-associated dementia 总被引:53,自引:0,他引:53
Human immunodeficiency virus-1 (HIV-1) can induce dementia with alarming occurrence worldwide. The mechanism remains poorly understood, but discovery in brain of HIV-1-binding sites (chemokine receptors) provides new insights. HIV-1 infects macrophages and microglia, but not neurons, although neurons are injured and die by apoptosis. The predominant pathway to neuronal injury is indirect through release of macrophage, microglial and astrocyte toxins, although direct injury by viral proteins might also contribute. These toxins overstimulate neurons, resulting in the formation of free radicals and excitotoxicity, similar to other neurodegenerative diseases. Recent advances in understanding the signalling pathways mediating these events offer hope for therapeutic intervention. 相似文献