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101.
Populations of leatherside chub ( Gila copei ), a little-known species native to the eastern Great Basin, have declined and their distribution has become fragmented. To determine habitat requirements and possible factors responsible for population decline, we quantified macrohabitats and microhabitats occupied by leatherside chub. Macrohabitat was surveyed at 59 sites in the Sevier River drainage of south central Utah, and microhabitats occupied by leatherside chub were measured at 3 locations spanning the species latitudinal range. Characteristics of points in the stream where leatherside chub occurred were compared to points where they did not occur. Abundance of brown trout ( Salmo trutta ) and elevation were weakly negatively correlated with leatherside chub distribution on a macrohabitat scale. Microhabitats occupied by leatherside chub were characterized by low water velocities (2.5-45 cm sec -1 ), intermediate water depths (25-65 cm), and low percent composition of sand-silt or gravel substrates. This study suggests that the presence of introduced brown trout may have led to the decline of leatherside chub.  相似文献   
102.
The practice of the transcendental meditation technique in subjects eliciting this state regularly for 3--5 years is correlated with acute decline of adrenocortical activity not associated with sleep during the practice.  相似文献   
103.
Most human tumours have genetic mutations in their Rb and p53 pathways, but retinoblastoma is thought to be an exception. Studies suggest that retinoblastomas, which initiate with mutations in the gene retinoblastoma 1 (RB1), bypass the p53 pathway because they arise from intrinsically death-resistant cells during retinal development. In contrast to this prevailing theory, here we show that the tumour surveillance pathway mediated by Arf, MDM2, MDMX and p53 is activated after loss of RB1 during retinogenesis. RB1-deficient retinoblasts undergo p53-mediated apoptosis and exit the cell cycle. Subsequently, amplification of the MDMX gene and increased expression of MDMX protein are strongly selected for during tumour progression as a mechanism to suppress the p53 response in RB1-deficient retinal cells. Our data provide evidence that the p53 pathway is inactivated in retinoblastoma and that this cancer does not originate from intrinsically death-resistant cells as previously thought. In addition, they support the idea that MDMX is a specific chemotherapeutic target for treating retinoblastoma.  相似文献   
104.
Wilson SD  Dai P  Li S  Chi S  Kang HJ  Lynn JW 《Nature》2006,442(7098):59-62
In conventional superconductors, the interaction that pairs the electrons to form the superconducting state is mediated by lattice vibrations (phonons). In high-transition-temperature (high-T(c)) copper oxides, it is generally believed that magnetic excitations might play a fundamental role in the superconducting mechanism because superconductivity occurs when mobile 'electrons' or 'holes' are doped into the antiferromagnetic parent compounds. Indeed, a sharp magnetic excitation termed 'resonance' has been observed by neutron scattering in a number of hole-doped materials. The resonance is intimately related to superconductivity, and its interaction with charged quasi-particles observed by photoemission, optical conductivity, and tunnelling suggests that it might play a part similar to that of phonons in conventional superconductors. The relevance of the resonance to high-T(c) superconductivity, however, has been in doubt because so far it has been found only in hole-doped materials. Here we report the discovery of the resonance in electron-doped superconducting Pr0.88LaCe0.12CuO4-delta (T(c) = 24 K). We find that the resonance energy (E(r)) is proportional to T(c) via E(r) approximately 5.8k(B)T(c) for all high-T(c) superconductors irrespective of electron- or hole-doping. Our results demonstrate that the resonance is a fundamental property of the superconducting copper oxides and therefore must be essential in the mechanism of superconductivity.  相似文献   
105.
Foster DJ  Wilson MA 《Nature》2006,440(7084):680-683
The hippocampus has long been known to be involved in spatial navigational learning in rodents, and in memory for events in rodents, primates and humans. A unifying property of both navigation and event memory is a requirement for dealing with temporally sequenced information. Reactivation of temporally sequenced memories for previous behavioural experiences has been reported in sleep in rats. Here we report that sequential replay occurs in the rat hippocampus during awake periods immediately after spatial experience. This replay has a unique form, in which recent episodes of spatial experience are replayed in a temporally reversed order. This replay is suggestive of a role in the evaluation of event sequences in the manner of reinforcement learning models. We propose that such replay might constitute a general mechanism of learning and memory.  相似文献   
106.
The prefrontal cortex (PFC) is responsible for executive functions, including planning, goal setting, problem solving, inhibitory control, monitoring, and action adjusting. Executive functions also include selective attention and the flexibility or switching of attention; therefore, attention is an executive function in which the PFC participates. Working memory (WM), which is the temporary maintenance and processing of particular information, is usually considered to be a basic neural mechanism underlying the executive functions. This review systematically discusses the relationship between the prefrontal WM and attention and emphasizes two forms of prefrontal attention. The first form occurs in the dlPFC, which encodes the location of objects with respect to the position of the head, thereby providing a frame of reference from which the focus of attention can be centered. The second occurs in the inferior convexity of the prefrontal cortex (IFC), which encodes the different attributes (shape, texture, color) of objects to enable the ability to focus on one or to switch attention between sensory attributes of objects.  相似文献   
107.
Urotensin-II (U-II) is a vasoactive 'somatostatin-like' cyclic peptide which was originally isolated from fish spinal cords, and which has recently been cloned from man. Here we describe the identification of an orphan human G-protein-coupled receptor homologous to rat GPR14 and expressed predominantly in cardiovascular tissue, which functions as a U-II receptor. Goby and human U-II bind to recombinant human GPR14 with high affinity, and the binding is functionally coupled to calcium mobilization. Human U-II is found within both vascular and cardiac tissue (including coronary atheroma) and effectively constricts isolated arteries from non-human primates. The potency of vasoconstriction of U-II is an order of magnitude greater than that of endothelin-1, making human U-II the most potent mammalian vasoconstrictor identified so far. In vivo, human U-II markedly increases total peripheral resistance in anaesthetized non-human primates, a response associated with profound cardiac contractile dysfunction. Furthermore, as U-II immunoreactivity is also found within central nervous system and endocrine tissues, it may have additional activities.  相似文献   
108.
基于在低速移动荷载或静力荷载作用下,多跨连续曲梁各跨峰值挠度相等的原则,给出了多跨连续曲梁在静力荷载作用下优化跨度及在动力荷载作用下近于优化跨度的取值,并对近于优化跨度的三跨连续曲梁,采用逆向搜索法首次获得其自由振动率及模态的解析解.对比试验曲梁的试验结果与计算结果,两者吻合十分良好,证明所得结果的正确性  相似文献   
109.
Nitric oxide and cellular respiration   总被引:7,自引:0,他引:7  
The role of nitric oxide (NO) as a signalling molecule involved in many pathophysiological processes (e.g., smooth muscle relaxation, inflammation, neurotransmission, apoptosis) has been elaborated during the last decade. Since NO has also been found to inhibit cellular respiration, we review here the available information on the interactions of NO with cytochrome c oxidase (COX), the terminal enzyme of the respiratory chain. The effect of NO on cellular respiration is first summarized to present essential evidence for the fact that NO is a potent reversible inhibitor of in vivo O2 consumption. This information is then correlated with available experimental evidence on the reactions of NO with purified COX. Finally, since COX has been proposed to catalyze the degradation of NO into either nitrous oxide (N2O) or nitrite, we consider the putative role of this enzyme in the catabolism of NO in vivo.  相似文献   
110.
The molecular mechanisms by which different mutations in the same gene can result in distinct disease phenotypes remain largely unknown. Truncating mutations of SOX10 cause either a complex neurocristopathy designated PCWH or a more restricted phenotype known as Waardenburg-Shah syndrome (WS4; OMIM 277580). Here we report that although all nonsense and frameshift mutations that cause premature termination of translation generate truncated SOX10 proteins with potent dominant-negative activity, the more severe disease phenotype, PCWH, is realized only when the mutant mRNAs escape the nonsense-mediated decay (NMD) pathway. We observe similar results for truncating mutations of MPZ that convey distinct myelinopathies. Our experiments show that triggering NMD and escaping NMD may cause distinct neurological phenotypes.  相似文献   
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