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1.
Maria Luisa Dalla Chiara 《Foundations of Science》2002,7(1-2):1-9
In recent times, a particular attention has been devoted to thesignificance of Quantum Theory for other disciplines. The articlescollected in this issue discuss some interesting cases,characterized by an interaction between Quantum Theory andother fields. Some basic notrons of the mathematical formalismof the theory are here summarized. 相似文献
2.
This paper stresses the restrictive nature of the standard unit root/cointegration assumptions and examines a more general type of time heterogeneity, which might characterize a number of economic variables, and which results in parameter time dependence and misleading statistical inference. We show that in such cases ‘operational’ models cannot be obtained, and the estimation of time‐varying parameter models becomes necessary. For instance, economic processes subject to endemic change can only be adequately modelled in a state space form. This is a very important point, because unstable models will break down when used for forecasting purposes. We also discuss a new test for the null of cointegration developed by Quintos and Phillips (1993), which is based on parameter constancy in cointegrating regressions. Finally, we point out that, if it is possible to condition on a subset of superexogenous variables, parameter instability can be handled by estimating a restricted system. Copyright © 2002 John Wiley & Sons, Ltd. 相似文献
3.
H. Watanabe J. A. Menzies J. C. K. Loo 《Cellular and molecular life sciences : CMLS》1981,37(8):883-884
Summary Isonicotinic acid hydrazide (isoniazid) was shown to react readily with 17-ethinyl-17-hydroxyestr-4-en-3-one (norethindrone) to form the isonicotinyl hydrazone of the steroid under conditions likely to exist in the stomach. The hydrazone was detected in guinea-pig, but not rat, plasma following its oral administration. Rat liver tissue metabolized the compound more rapidly than guinea-pig liver in vitro which probably accounts for the failure to detect the hydrazone in rat plasma. 相似文献
4.
P. J. Müller P. Masner Maria Kälin W. S. Bowers 《Cellular and molecular life sciences : CMLS》1979,35(5):704-705
Summary Corpora allata fromOncopeltus fasciatus incubated in vitro in medium containing 10–5.35 M (1 g/ml) of precocene II lose their ability to secrete juvenile hormone when reimplanted into last instar larvae.Acknowledgments. We thank Mr K. Dorn, Mrs L. Dolezal, Mrs V. Nötzli-Graf, Mr K.H. Trautmann and Mr A. Schuler for technical help, Dr W. Vogel and Dr A. Dübendorfer for valuable discussions. 相似文献
5.
仓鼠妊娠期瘦素分泌及其调节机制 总被引:1,自引:0,他引:1
对妊娠期瘦素的分泌及其调节机制进行探讨. 将100只3月龄雌性金黄仓鼠分成16组, 每组6~7只, 每天采血样用于测定其妊娠期的瘦素分泌. 实验结果表明, 瘦素于妊娠第9天开始显著升高, 于妊娠第12天达到高峰. 为验证不同生殖阶段的血清是否对瘦素分泌有不同影响, 将不同生殖阶段抽提与未抽提类固醇激素的血清加入培养液中进行培养, 发现动情期及妊娠期的血清均可刺激体外培养的脂肪细胞瘦素分泌, 动情期抽提与未抽提类固醇激素的血清对脂肪细胞瘦素分泌的刺激作用没有显著差异(P > 0.05). 与动情期血清相比, 妊娠中后期未抽提类固醇激素的血清显著刺激脂肪细胞瘦素分泌(P < 0.01). 但妊娠中后期的血清在抽提类固醇激素后对瘦素分泌的刺激作用显著下降, 与动情期的血清对瘦素分泌的刺激作用已没有显著差异(P > 0.05). 妊娠不同阶段未抽提类固醇激素的血清对瘦素分泌的刺激作用有很大差异, 妊娠第15天的血清对瘦素分泌的刺激作用显著高于妊娠第8天(P < 0.0001)和妊娠第12天(P < 0.001)的血清. 体外研究进一步表明, 肾上腺皮质素、孕酮以及胰岛素均能刺激瘦素分泌, 而雌激素却能抑制体外瘦素分泌. 研究结果提示, 妊娠期血液类固醇激素水平的上升是引起妊娠期瘦素峰出现的重要因素. 相似文献
6.
Novel neurotrophic factor CDNF protects and rescues midbrain dopamine neurons in vivo 总被引:1,自引:0,他引:1
Lindholm P Voutilainen MH Laurén J Peränen J Leppänen VM Andressoo JO Lindahl M Janhunen S Kalkkinen N Timmusk T Tuominen RK Saarma M 《Nature》2007,448(7149):73-77
In Parkinson's disease, brain dopamine neurons degenerate most prominently in the substantia nigra. Neurotrophic factors promote survival, differentiation and maintenance of neurons in developing and adult vertebrate nervous system. The most potent neurotrophic factor for dopamine neurons described so far is the glial-cell-line-derived neurotrophic factor (GDNF). Here we have identified a conserved dopamine neurotrophic factor (CDNF) as a trophic factor for dopamine neurons. CDNF, together with its previously described vertebrate and invertebrate homologue the mesencephalic-astrocyte-derived neurotrophic factor, is a secreted protein with eight conserved cysteine residues, predicting a unique protein fold and defining a new, evolutionarily conserved protein family. CDNF (Armetl1) is expressed in several tissues of mouse and human, including the mouse embryonic and postnatal brain. In vivo, CDNF prevented the 6-hydroxydopamine (6-OHDA)-induced degeneration of dopaminergic neurons in a rat experimental model of Parkinson's disease. A single injection of CDNF before 6-OHDA delivery into the striatum significantly reduced amphetamine-induced ipsilateral turning behaviour and almost completely rescued dopaminergic tyrosine-hydroxylase-positive cells in the substantia nigra. When administered four weeks after 6-OHDA, intrastriatal injection of CDNF was able to restore the dopaminergic function and prevent the degeneration of dopaminergic neurons in substantia nigra. Thus, CDNF was at least as efficient as GDNF in both experimental settings. Our results suggest that CDNF might be beneficial for the treatment of Parkinson's disease. 相似文献
7.
Identification of the transforming EML4-ALK fusion gene in non-small-cell lung cancer 总被引:1,自引:0,他引:1
8.
XinMiao Lü LiPing Zhu Mitsugu Nishimura Yoshimune Morita Takahiro Watanabe Toshio Nakamura Yong Wang 《科学通报(英文版)》2011,56(27):2931-2940
A 380-cm-long sediment core was acquired from the deep water area of Pumoyum Co, southern Tibet. Twenty-five plant residue
samples were selected, and organic carbon stable isotopes were obtained using the AMS 14C chronological method. The 14C age and carbon reservoir effect were calibrated with surface sedimentation rate measurements using 210Pb dating. Results showed that the core sediment deposited over 19 cal ka BP. Based on a multi-proxy analysis of TOC and IC
contents, grain size and pollen assemblage data, the palaeoclimatic evolution of Pumoyum Co was reconstructed since the last
glacial. Pumoyum Co was a shallow lake prior to 16.2 cal ka BP; although the glacier around the lake began to melt due to
increasing temperatures, climate was still cold and dry. In the interval of 16.2–11.8 cal ka BP, the sedimentary environment
fluctuated drastically and frequently. Two cold-events occurred at 14.2 and 11.8 cal ka BP, and these may correspond to the
Older Dryas and the Younger Dryas events, respectively. After 11.8 cal ka BP, Pumoyun Co developed into the deep lake as it
is now. The lake water temperature was relatively lower at that time because of influx of cold water from glacial meltwater
entering the lake. As a result, the multi-proxy indicators showed no sign of warm conditions. Comparisons between the sedimentary
record of Pumoyum Co with that of other lakes of the same age in southern Tibet indicate a warmer climate following the last
deglaciation influenced the southeastern Tibetan Plateau. These results imply that the southwest Asian monsoon gradually became
stronger since the deglaciation during its expansion to the inner plateau. The glacial-supplied water of the lake responded
sensitively to cold-events. The entire southern Tibet region was dominantly influenced climatically by the southwest Asian
monsoon during the Holocene. 相似文献
9.
10.
FADD prevents RIP3-mediated epithelial cell necrosis and chronic intestinal inflammation 总被引:2,自引:0,他引:2
Welz PS Wullaert A Vlantis K Kondylis V Fernández-Majada V Ermolaeva M Kirsch P Sterner-Kock A van Loo G Pasparakis M 《Nature》2011,477(7364):330-334
Intestinal immune homeostasis depends on a tightly regulated cross talk between commensal bacteria, mucosal immune cells and intestinal epithelial cells (IECs). Epithelial barrier disruption is considered to be a potential cause of inflammatory bowel disease; however, the mechanisms regulating intestinal epithelial integrity are poorly understood. Here we show that mice with IEC-specific knockout of FADD (FADD(IEC-KO)), an adaptor protein required for death-receptor-induced apoptosis, spontaneously developed epithelial cell necrosis, loss of Paneth cells, enteritis and severe erosive colitis. Genetic deficiency in RIP3, a critical regulator of programmed necrosis, prevented the development of spontaneous pathology in both the small intestine and colon of FADD(IEC-KO) mice, demonstrating that intestinal inflammation is triggered by RIP3-dependent death of FADD-deficient IECs. Epithelial-specific inhibition of CYLD, a deubiquitinase that regulates cellular necrosis, prevented colitis development in FADD(IEC-KO) but not in NEMO(IEC-KO) mice, showing that different mechanisms mediated death of colonic epithelial cells in these two models. In FADD(IEC-KO) mice, TNF deficiency ameliorated colon inflammation, whereas MYD88 deficiency and also elimination of the microbiota prevented colon inflammation, indicating that bacteria-mediated Toll-like-receptor signalling drives colitis by inducing the expression of TNF and other cytokines. However, neither CYLD, TNF or MYD88 deficiency nor elimination of the microbiota could prevent Paneth cell loss and enteritis in FADD(IEC-KO) mice, showing that different mechanisms drive RIP3-dependent necrosis of FADD-deficient IECs in the small and large bowel. Therefore, by inhibiting RIP3-mediated IEC necrosis, FADD preserves epithelial barrier integrity and antibacterial defence, maintains homeostasis and prevents chronic intestinal inflammation. Collectively, these results show that mechanisms preventing RIP3-mediated epithelial cell death are critical for the maintenance of intestinal homeostasis and indicate that programmed necrosis of IECs might be implicated in the pathogenesis of inflammatory bowel disease, in which Paneth cell and barrier defects are thought to contribute to intestinal inflammation. 相似文献