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261.
262.
Role of sulphuric acid, ammonia and galactic cosmic rays in atmospheric aerosol nucleation 总被引:1,自引:0,他引:1
Kirkby J Curtius J Almeida J Dunne E Duplissy J Ehrhart S Franchin A Gagné S Ickes L Kürten A Kupc A Metzger A Riccobono F Rondo L Schobesberger S Tsagkogeorgas G Wimmer D Amorim A Bianchi F Breitenlechner M David A Dommen J Downard A Ehn M Flagan RC Haider S Hansel A Hauser D Jud W Junninen H Kreissl F Kvashin A Laaksonen A Lehtipalo K Lima J Lovejoy ER Makhmutov V Mathot S Mikkilä J Minginette P Mogo S Nieminen T Onnela A Pereira P Petäjä T Schnitzhofer R Seinfeld JH Sipilä M Stozhkov Y 《Nature》2011,476(7361):429-433
Atmospheric aerosols exert an important influence on climate through their effects on stratiform cloud albedo and lifetime and the invigoration of convective storms. Model calculations suggest that almost half of the global cloud condensation nuclei in the atmospheric boundary layer may originate from the nucleation of aerosols from trace condensable vapours, although the sensitivity of the number of cloud condensation nuclei to changes of nucleation rate may be small. Despite extensive research, fundamental questions remain about the nucleation rate of sulphuric acid particles and the mechanisms responsible, including the roles of galactic cosmic rays and other chemical species such as ammonia. Here we present the first results from the CLOUD experiment at CERN. We find that atmospherically relevant ammonia mixing ratios of 100 parts per trillion by volume, or less, increase the nucleation rate of sulphuric acid particles more than 100-1,000-fold. Time-resolved molecular measurements reveal that nucleation proceeds by a base-stabilization mechanism involving the stepwise accretion of ammonia molecules. Ions increase the nucleation rate by an additional factor of between two and more than ten at ground-level galactic-cosmic-ray intensities, provided that the nucleation rate lies below the limiting ion-pair production rate. We find that ion-induced binary nucleation of H(2)SO(4)-H(2)O can occur in the mid-troposphere but is negligible in the boundary layer. However, even with the large enhancements in rate due to ammonia and ions, atmospheric concentrations of ammonia and sulphuric acid are insufficient to account for observed boundary-layer nucleation. 相似文献
263.
Stephen J. Leybourne Brendan P. M. McCabe Terence C. Mills 《Journal of forecasting》1996,15(3):253-270
This paper considers the problems of statistically analysing the levels of financial time series rather than their differences, which are often equivalent to returns and which are traditionally analysed in econometric modelling. This focus on differences is a consequence of the inherent nonstationarity of the levels, and hence analysing the latter requires introducing an alternative framework for modelling nonstationary behaviour. We do this by considering randomized unit root processes, arguing that these can have a natural interpretation in the financial context. The paper thus develops methods for testing for randomized unit roots and for modelling such processes. It then applies these techniques to various financial time series, so as to ascertain their potential usefulness, particularly for forecasting. 相似文献
264.
该文应用连续介质力学理论建立了与蒸汽注入过程相关的热-流-变形耦合问题的基本数学模型;应用全隐式顺序Galerkin有限元数值解方案,对注蒸汽井的热-流体-变形耦合过程进行了数值模拟。结果表明,由于低渗透页岩地层流体高温膨胀导致的超高孔隙压力,有可能产生拉张应力,严重时会导致地层破裂。 相似文献
265.
I. Campia E. Gazzano G. Pescarmona D. Ghigo A. Bosia C. Riganti 《Cellular and molecular life sciences : CMLS》2009,66(9):1580-1594
Digoxin and ouabain are steroid drugs that inhibit the Na+/K+-ATPase, and are widely used in the treatment of heart diseases. They may also have additional effects, such as on metabolism
of steroid hormones, although until now no evidence has been provided about the effects of these cardioactive glycosides on
the synthesis of cholesterol. Here we report that digoxin and ouabain increased the synthesis of cholesterol in human liver
HepG2 cells, enhancing the activity and the expression of the
3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR), the rate-limiting enzyme of the cholesterol synthesis. This effect
was mediated by the binding of the sterol regulatory element binding protein-2 (SREBP-2) to the HMGCR promoter, and was lost
in cells silenced for SREBP-2 or loaded with increasing amounts of cholesterol. Digoxin and ouabain competed with cholesterol
for binding to the SREBP-cleavage-activating protein, and are critical regulators of cholesterol synthesis in human liver
cells.
Received 10 January 2009; received after revision 11 February 2009; accepted 6 March 2009 相似文献
266.
B. C. Yoo S-H. Hong J-L. Ku Y-H. Kim Y-K. Shin S-G. Jang I-J. Kim S-Y. Jeong J-G. Park 《Cellular and molecular life sciences : CMLS》2009,66(2):350-364
Comparative analysis of proteomes using 5-fluorouracil (5-FU)-resistant human colon cancer cell line revealed that decreased
galectin-3 expression was significantly associated with retarded proliferation. However, in the presence of 5-FU proliferation
rate of cells with suppressed galectin-3 expression did not differ from that of cells with normal galectin-3 expression, even
galectin-3 suppression augmented apoptosis. Mechanism by which galectin-3 regulates cancer cell proliferation has been identified
in immunoprecipitates of the anti-galectin-3 antibody. Heterogeneous nuclear ribonucleoprotein Q (hnRNP Q) was identified
as a protein interacting with galectin-3. Interestingly, while galectin-3 protein was not affected by the hnRNP Q level, its
suppression was accompanied by a decrease in hnRNP Q expression. The present study demonstrates that galectin-3 stabilizes
hnRNP Q via complex formation, and reduction in the hnRNP Q level leads to slow proliferation and less susceptibility to 5-FU.
Electronic supplementary material The online version of this article (doi:) contains supplementary material, which is available to authorized users.
B.C.Yoo; S-H.Hong; These two authors contributed equally to this work.
Received 10 September 2008; received after revision 19 October 2008; accepted 07 November 2008 相似文献
267.
J. Kim D. C. Han J. M. Kim S. Y. Lee S. J. Kim J. R. Woo J. W. Lee S.-K. Jung K. S. Yoon H. G. Cheon S. S. Kim S. H. Hong B.-M. Kwon 《Cellular and molecular life sciences : CMLS》2009,66(10):1766-1781
Indenone KR-62776 acts as an agonist of PPARγ without inducing obesity in animal models and cells. X-ray crystallography reveals
that the indenone occupies the binding pocket in a different manner than rosiglitazone. 2-Dimensional gel-electrophoresis
showed that the expression of 42 proteins was altered more than 2.0-fold between KR-62776- or rosiglitazone-treated adipocyte
cells and control cells. Rosiglitazone down-regulated the expression of ERK1/2 and suppressed the phosphorylation of ERK1/2
in these cells. However, the expression of ERK1/2 was up-regulated in KR-62776-treated cells. Phosphorylated ERK1/2, activated
by indenone, affects the localization of PPARγ, suggesting a mechanism for indenone-inhibition of adipogenesis in 3T3-L1 preadipocyte
cells. The preadipocyte cells are treated with ERK1/2 inhibitor PD98059, a large amount of the cells are converted to adipocyte
cells. These results support the conclusion that the localization of PPARγ is one of the key factors explaining the biological
responses of the ligands.
Received 04 March 2009; received after revision 13 March 2009; accepted 17 March 2009 相似文献
268.
Functions and pathologies of BiP and its interaction partners 总被引:1,自引:1,他引:0
J. Dudek J. Benedix S. Cappel M. Greiner C. Jalal L. Müller R. Zimmermann 《Cellular and molecular life sciences : CMLS》2009,66(9):1556-1569
The endoplasmic reticulum (ER) is involved in a variety of essential and interconnected processes in human cells, including
protein biogenesis, signal transduction, and calcium homeostasis. The central player in all these processes is the ER-lumenal
polypeptide chain binding protein BiP that acts as a molecular chaperone. BiP belongs to the heat shock protein 70 (Hsp70)
family and crucially depends on a number of interaction partners, including co-chaperones, nucleotide exchange factors, and
signaling molecules. In the course of the last five years, several diseases have been linked to BiP and its interaction partners,
such as a group of infectious diseases that are caused by Shigella toxin producing E. coli. Furthermore, the inherited diseases Marinesco-Sj?gren syndrome, autosomal dominant polycystic liver disease, Wolcott-Rallison
syndrome, and several cancer types can be considered BiP-related diseases. This review summarizes the physiological and pathophysiological
characteristics of BiP and its interaction partners.
Received 20 November 2008; received after revision 09 December 2008; accepted 12 December 2008 相似文献
269.
A. Beqqali W. van Eldik C. Mummery R. Passier 《Cellular and molecular life sciences : CMLS》2009,66(5):800-813
Studies on identification, derivation and characterization of human stem cells in the last decade have led to high expectations
in the field of regenerative medicine. Although it is clear that for successful stem cell-based therapy several obstacles
have to be overcome, other opportunities lay ahead for the use of human stem cells. A more immediate application would be
the development of human models for cell-type specific differentiation and disease in vitro. Cardiomyocytes can be generated from stem cells, which have been shown to follow similar molecular events of cardiac development
in vivo. Furthermore, several monogenic cardiovascular diseases have been described, for which in vitro models in stem cells could be generated. Here, we will discuss the potential of human embryonic stem cells, cardiac stem
cells and the recently described induced pluripotent stem cells as models for cardiac differentiation and disease.
Received 07 August 2008; received after revision 26 September 2008; accepted 03 October 2008 相似文献
270.
G. M. C. Janssen P. Schwertman T. A. T. Wanga R. S. Jahangir Tafrechi P. J. A. van den Broek A. K. Raap 《Cellular and molecular life sciences : CMLS》2009,66(4):721-730
Cytoplasmic translation is under sophisticated control but how cells adapt its rate to constitutive loss of mitochondrial
oxidative phosphorylation is unknown. Here we show that translation is repressed in cells with the pathogenic A3243G mtDNA
mutation or in mtDNA-less ρ0 cells by at least two distinct pathways, one transiently targeting elongation factor eEF-2 and the other initiation factor
eIF-2α constitutively. Under conditions of exponential cell growth and mammalian target of rapamycin (mTOR) activation, eEF-2
becomes transiently phosphorylated by an AMP-activated protein kinase (AMPK)-dependent pathway, especially high in mutant
cells. Independent of AMPK and mTOR, eIF-2α is constitutively phosphorylated in mutant cells, likely a signature of endoplasmic
reticulum (ER)-stress response induced by the loss of oxidative phosphorylation. While the AMPK/eEF-2K/eEF-2 pathway appears
to function in adaptation to physiological fluctuations in ATP levels in the mutant cells, the ER stress signified by constitutive
protein synthesis inhibition through eIF-2α-mediated repression of translation initiation may have pathobiochemical consequences.
Received 29 October 2008; received after revision 11 December 2008; accepted 16 December 2008 相似文献