无礼回复
发表于 2025-3-27 00:37:03
Daniele L. R. Marinihic factor signalling, cellular differentiation, and cellular protection against β-amyloid-induced neurotoxicity. Recent studies on sigma-1 receptor chaperones and other ER proteins clearly suggest that cholesterol, in concert with those ER proteins, may regulate several important functions of the E
Anticoagulants
发表于 2025-3-27 01:39:55
Daniele L. R. Marinihermore, crystals in the interstitial space can be recognized as a foreign body by the innate immune system that then triggers an inflammatory response contributing to plaque destabilization. Following plaque rupture, CCs released into the circulation can scrape the endothelial surface causing arter
GROG
发表于 2025-3-27 08:54:35
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文艺
发表于 2025-3-27 09:56:33
Daniele L. R. Mariniduce an inflammatory response in the local circulation and distal tissues that typically progresses over a few days..The clinical consequences of athero-embolism depend on the volume of the debris, quantity of CCs released, the extent of its crystal content, the extent of athero-thrombotic response,
褪色
发表于 2025-3-27 15:27:53
Daniele L. R. Marinitical coherence tomography (OCT). Although OCT mostly detects large aggregates of CCs, this evidence provides clear support for the belief that CCs develop in vivo in stable plaques, and that their presence in the plaque core has prognostic significance over and above other morphologic features of a
淘气
发表于 2025-3-27 18:16:10
Daniele L. R. Marini risk of future injury, most such plaques remain stable..Together these observations indicate that the vulnerability of plaques is dynamic and raises the possibly that instability relates to ongoing changes in the physiochemistry of the lipid core that at times favors the formation of cholesterol cr
洞察力
发表于 2025-3-28 01:34:46
Daniele L. R. Mariniinjury in the vascular bed leads to sclerosis, calcification, and neovascularization of the arterial wall and predisposes to erosion and rupture of the plaque cap that lead to atherothrombotic events and CC embolization..Thus, inhibiting the formation of cholesterol crystals, dissolving them, and in
琐碎
发表于 2025-3-28 04:55:40
Daniele L. R. Marinirated to slow the degenerative process in previously normal valve leaflets but does not slow valvular sclerosis once it is in train. This suggests that over time the inflammatory processes induced by cholesterol crystals entrapped in the valve matrix become the main drivers of valvular degeneration,
主动脉
发表于 2025-3-28 07:29:35
Daniele L. R. Marinin the first part of this protocol, we describe how to synthesize and image CTL in living cells relative to caveolin, a structural component of caveolae. In the second part, we explain in detail how to perform time-lapse experiments of commercially available BODIPY-tagged cholesterol (TopFluor-choles
不在灌木丛中
发表于 2025-3-28 13:26:14
Daniele L. R. Marinidentical physiochemical properties as .cholesterol. Hence, if the biological effects of cholesterol result solely due to membrane effects, it is expected that there will be no difference between .cholesterol and .cholesterol. However, when direct binding with chiral proteins and lipids is involved,