《SCI论文投稿常见句型和优美句子1000句2.doc》由会员分享，可在线阅读，更多相关《SCI论文投稿常见句型和优美句子1000句2.doc（43页珍藏版）》请在三一办公上搜索。
1、1. impede/hamper./blockrescue/revert/reverse/inhibit/prevent/abrogate/ablate/abolish /impair reduce/suppress/halt/blunt/militate/impede/depletion/ diminution diminutionattenuate/diminish/increment/rescue.exaggerate Exacerbates vs ameliorate/ enhanced/ elevated/augment/potentiate.Markedly/ substantia
2、lly/ strikingly/ notably/ greatly/2. may play a critical role in atherogenesis and illuminate important targets for disease intervention.3. We evaluated gene expression ofcontrarily the gene expression profile.did not show any apparent difference between, questioning the involvement of 4. The presen
3、t study demonstrates for the first time that increasedexpression is associated with enhanced., suggesting thereby a role for LOX-1, that of mediating.5. It is widely believed that.Although the quantitative contribution of.is unknown, in has been shown that.6. Consistent with this idea, one recent st
4、udy fail to demonstrate a key role of LOX-1 in the progression of.7. Nevertheless, exploration of in vitro results to the in vivo situation is hazardous, and additional studies are warranted to assess the functional significance of increased LOX-1 expression on foam cell formation and plaque progres
5、sion and plaque stability in vivo.8. The underlying mechanisms that contribute to .dysfunction in patients with are incompletely understood, we therefore sought to quantify.9. adversely affect.have important implication for patient management.10. increaseinduce.enhanced.increment.augmented11. althou
6、gh clinical data suggest that.were paradoxically negative12. significantlymarkedly.robust.ostensibly.13. exhibit significant.with robust activation of .and up-regulation of14. Compared with , TNFR1/ HF exhibited (1) improved remodeling, hypertrophy, and contractile function; (2) less apoptosis; and
7、(3) diminished NF-B, p38 mitogen-activated protein kinase, and JNK2 activation and cytokine expression. In contrast, TNFR2/ HF showed exaggerated remodeling and hypertrophy, increased border zone fibrosis, augmented NF-B and p38 mitogen-activated protein kinase activation, higher IL-1 and IL-6 gene
8、expression, greater activated macrophages, and greater apoptosis.15. In H9c2 cardiomyocytes, sustained NF-B activation was proapoptotic, an effect dependent on TNFR1 signaling, whereas TNFR2 overexpression attenuated TNF-induced NF-B activation. 16. . have disparate and opposing effects on remodelin
9、g, hypertrophy, NF-B, inflammation, and apoptosis in HF: TNFR1 exacerbates, whereas TNFR2 ameliorates, these events. However, signaling through both receptors is required to. TNFR-specific effects in HF should be considered when therapeutic anti-TNF strategies are developed. 16. Cardiac hypertrophy,
10、 the clinical hallmark of hypertrophic cardiomyopathy (HCM), is a major determinant of morbidity and mortality not only in HCM but also in a number of cardiovascular diseases. There is no effective therapy for HCM and generally for cardiac hypertrophy. Myocardial oxidative stress and thiol-sensitive
11、 signaling molecules are implicated in pathogenesis of hypertrophy and fibrosis. We posit that treatment with N-acetylcysteine, a precursor of glutathione, the largest intracellular thiol pool against oxidative stress, could reverse cardiac hypertrophy and fibrosis in HCM. 17. Treatment with N-acety
12、lcysteine, a safe prodrug against oxidation, reversed established cardiac phenotype in a transgenic rabbit model of human HCM. Because there is no effective pharmacological therapy for HCM and given that hypertrophy, fibrosis, and cardiac dysfunction are common and major predictors of clinical outco
13、mes, the findings could have implications in various cardiovascular disorders18. The objective of the present study was to describe the relative19. Epidemiological data demonstrate that regular dietary intake of plant-derived foods and beverages reduces the risk of coronary heart disease and stroke2
14、0. Although still debated, a range of potential mechanisms through which cocoa might exert its benefits on cardiovascular health have been proposed, including activation of nitric oxide and antioxidant and antiinflammatory effects 21. This review summarizes the available data on the cardiovascular e
15、ffects of cocoa, outlines potential mechanisms involved in the response to cocoa, and highlights the potential clinical implications associated with its consumption22. Consequently, the role of.remains obscure.23. Its precise role in pathophysiological processes is controversial but our work and tha
16、t of others has shown that24. In contrast to, administration ofto.has consistently resulted in robust increase at the levels of.at the activity, mRNA and protein levels.25. This is consistent with the observation by.et al that.26. Although in most observational studies, .therapy with statins has sig
17、nificantly reduce.27. in .treated groups, whereashalted this increase, resulting in a significant treatment difference of 28. Plasma Lp-PLA(2) was measured at baseline and after the interventions.29. .is an emerging independent risk factor for cardiovascular disease (CVD). 30. Data regarding the ass
18、ociation between lipoprotein-associated phospholipase A2 (Lp-PLA(2) level and incidence of cardiovascular (CV) events are conflicting31. elevated levels of LDL is a well-documented risk factor for CVD and its sequelae32. attempts to improve have been frustrated by.technical difficulties.33. within t
19、he context of this findings and current models ofwe proposed a refined model of.which may be useful to understanding how34. are important regulators of vascular physiology and contribute to the pathogenesis of vascular diseases, however, are poorly defined.35. The salient findings of the present stu
20、dy are as follows: (1); (2)., and (3)36. Although recent studies have demonstrated that., a possible link between these alternations and vascular diseases remains unclear.37. Because accumulating evidence supports the role of enhanced MMP-9 activity in AS, we evaluated the.further implicating an ess
21、ential role of.38. Therefore, with the increasing evidence for a role in AS, MMP-9.39. In addition to the implicated role of.in plaque rupture,.the observed increase inmay have important consequences foe the development of.40. Accumulating evidence indicates that oxidative stress may play an importa
22、nt role in the pathogenesis of AS41. In addition, recent data fromet al. , coupled with.is largely responsible for enhanced.42. previous findings indicating thatoffer a potential mechanism by which43. However, the elevated vascular expression ofmay set the stage for enhanced activation 44. a central
23、 role for .in the activation ofhas been assumed because.45. recent data demonstrating the interaction of andmay offer some explanation.46. Similarly, in the present study,intracellular signal transduction cascades/ intracellular signaling events.47. In summary, we have demonstrated that, indicating
24、a novel mechanism by whichFurthermore, oxidative stress appears to play a primary role in .induced activity, suggesting a possible beneficial effect of anti-oxidant therapy in the vascular complications of DM.48. Furthermore, MMP activity has been correlated with clinical manifestations of UAP, plaq
25、ue rupture and AAA. Because the prevalence of ACS is significantly greater in diabetic patients than non-diabetic subjects, we hypothesized thatmay be preferentially activated in the setting of DM. We firstly studiedin two well-established rodent models of DM. In addition, we investigated the possib
26、leOur findings indicate thatThis effect is partly due to the increased transcription of.via a redox sensitive mechanism.49. Which in accordance with published data.50. the upregulation of .is pronounced, and the stimulation for.was less prominent. 51. Stimulation could be demonstrated at both protei
27、n and mRNA levels as reflected by ELISA, Zymography and Northern Blot analysis. To explore the signaling transduction pathways for the.effect ofon, we studied the expression of both52. as reflected by/ as assessed by/ as evidenced by/ as revealed by/ as mirrored byAs demonstrated by/ as manifested b
28、y/ as determined by/ was evaluated by53. These data suggest the role ofin mediating stimulated expression in.cells.The physiological relevance ofwas studied by examining.54. our result indicates thattreatment acceleratedand this response was blocked by.MMP inhibition, which supports a permissive rol
29、e ofin55. these data are the first to demonstrate a direct effect of 56. The mechanism of this effect is under investigation.57. However, limited information exists on the comparison ofand58. We sought evidence ofby examining the association of 59. Our study contributes compelling evidence thatcauti
30、on is warranted when interpreting analysis that attributesto60. is a multifunctional cytokine known to regulate cellular functions in contexts of61. herein, we demonstrated thatour data suggest thatmay be important in regulatingand may play a role in the pathogenesis of62. to better understand the m
31、echanism of we performed a gene array63. the mechanism is demonstrated to include.stimulation ofwith subsequent activation of. These findings suggest a role for.HDL-rasing therapies beyond As to address T2DM.64. These results, taken in aggregate with other large-scale clinical trails of statins, dem
32、onstrate compellingly the benefit of reducing LDL and increasing HDL across a broad range of baseline cholesterol levels.65. was designed and powered to investigate whether.66. the procedures for.have been described in detail previously67. An exploratory, hypothesis-generating analysis was conducted
33、 to examine the effects of treatment with. may represent an important additional consideration inthe decision to intervene.68. has been proposed as.Nevertheless, criticisms have been voiced based on observation indicating that69. additional data on the relationship between .andis urgently required a
34、nd currently in progress.70. measurements have increasingly been used in observational and intervention studies.71. In conclusion, multiple lines of evidence have beeen supportive of assessment of72. the possibility.deserves further investigation in a clinical setting.73. the role of.have been exten
35、sively investigated.are now increasingly appreciated as74. The potential mechanisms of action for the observed effects ofon.may include a pleiotropic anti-inflammatory effects (due to reduction in macrophage number), which in turn abrogatesrendering a beneficial effect on A and B, all of which are c
36、rucial components of the progression of AS. Two independent groups have formally demonstrated the impact of inhibiting.75. Compelling evidence on the importance of. .inflammation on the pathogenesis of As has been accumulated over the last decades.76. Recent data emphasize the possible influence of.
37、indicating a more direct involvement .favor/ facilitate the recruitment of.77. perpetuate the inflammatory milieu within the atheromatous plaqueis postulated a trigger of.78. our study is the first one reporting the effects ofa major advantage of the present study is that.a limitation of the present
38、 study is that it does not provide a precise mechanistic explanation for the anti-AS effects of.Hence there are many questions remain unanswered. Could the observed regression of AS be extrapolated to otherinterventions as recently suggested or is the anti-AS effects conferred by this agent explaine
39、d solely by itsinhibition activity? In spite of the limitation, we believe this study open new paths of investigation in the pathogenesis of As and may eventually modify the manner in which we understand the beneficial effects oftherapy.79. In conclusion, based on the results of histopathology, ICH
40、analysis, it can be concluded that.the compound have a potential anti-AS and plaque stabilizing effect. The possibility of combiningwith.through administration of could have very important clinical implications, and therefore deserve further investigation in clinical setting.80. A growing body of ev
41、idence suggest that81. However, there are several important questions remain unanswered.82. This results strongly support recent experimental evidence of mediated inflammation leading to acceleration and vulnerability of atherosclerotic plaques.83. .plays a central role in orchestrating the cytokine
42、 cascade and accelerates atherosclerosis and plaque vulnerability in animal models. However, epidemiological data evaluating the role of IL-18 levels in atherosclerosis are lacking.84. more recently,.lend support to the idea that.85. In conclusion, our findings prove that this combination of drugs i
43、s neuroprotective and suppress the severity of atherogenesis furthermore, this pharmacological approach appears to be promising as a future therapeutic strategy to control AS.86. Our finding provides a novel explanation for the pleiotropic effects of statins on the cardiovascular system87. have conc
44、lusively shown that.a plethora of studies 88. improve/promote plaque stability/ reduce plaque vulnerability/ plaque destabilizaton89. However, several caveats have to be kept in mind.90. As indicated in, in vivo evidence for genuine pleiotropic effects of statins is sparse, the present study offers
45、no additional insights into the mechanisms actually responsible for plaque stability.91. This assumption is strengthened by the observation that92. Observational evidence has consistently linked increased fruit and vegetable consumption with reduced cardiovascular morbidity; however, there is little
46、 direct trial evidence to support the concept that fruit and vegetable consumption improves vascular function93. Little evidence is available on the molecular mechanisms underlying the role of.94. More recently, reports have begun to emerge that95has been extensively reviewed elsewhere and we don no
47、t intend to recapitulate this work here.96. concomitantly / concurrently / simultaneously /synchronously伴随地,并发地97. These findings are in accordance with studies of98. culminate inthese appearances are highly suggestive of. are interpreted as indicative of.99. We can assert with confidence that. This
48、 refutes the argument that.100. These data provide further support for the idea thatThese data are irreconcilable with the idea that101. It is not a tenable argument to suggestin parallel with102. This stipulation is made to exclude the possibility of.nicely illustrate the way in which.103. bear witness to104. Despite the accumulating circumstantial evidence pointing to Lp-PLA2 as a culprit in unstable plaque formation, definitive proof has been lacking.105an effect that
