抗原变异可使得多种致病微生物易于逃避宿主免疫应答。表达在感染红细胞表面的恶性疟原虫红细胞表面蛋白1（PfPMP1）与感染红细胞、内皮细胞、树突状细胞以及胎盘的单个或多个受体作用，在黏附及免疫逃避中起关键的作用。每个单倍体基因组var基因家族编码约60种成员，通过启动转录不同的var基因变异体为抗原变异提供了分子基础。

疟原虫var基因转换速率变化导致抗原变异[英]／Paul H, Robert P, Christodoulou Z, et al//Proc Natl Acad Sci U S A

Lipid peroxidation can be described generally as a process under which oxidants such as free radicals attack lipids containing carbon-carbon double bond(s), especially polyunsaturated fatty acids (PUFAs). Over the last four decades, an extensive body of literature regarding lipid peroxidation has shown its important role in cell biology and human health. Since the early 1970s, the total published research articles on the topic of lipid peroxidation was 98 (1970–1974) and has been increasing at almost 135-fold, by up to 13165 in last 4 years (2010–2013). New discoveries about the involvement in cellular physiology and pathology, as well as the control of lipid peroxidation, continue to emerge every day. Given the enormity of this field, this review focuses on biochemical concepts of lipid peroxidation, production, metabolism, and signaling mechanisms of two main omega-6 fatty acids lipid peroxidation products: malondialdehyde (MDA) and, in particular, 4-hydroxy-2-nonenal (4-HNE), summarizing not only its physiological and protective function as signaling molecule stimulating gene expression and cell survival, but also its cytotoxic role inhibiting gene expression and promoting cell death. Finally, overviews of in vivo mammalian model systems used to study the lipid peroxidation process, and common pathological processes linked to MDA and 4-HNE are shown.

/pdf/lipid-peroxidation-production-metabolism-and-signaling-234bwmyps5.pdf

Lipid peroxidation: production, metabolism, and signaling mechanisms of malondialdehyde and 4-hydroxy-2-nonenal.

http://basicmed.med.ncku.edu.tw/admin/up_img/990319-2.pdf

Matrix Crosslinking Forces Tumor Progression by Enhancing Integrin Signaling

Riboflavin/ultraviolet-a-induced collagen crosslinking for the treatment of keratoconus.

The attainment of both strength and toughness is a vital requirement for most structural materials; unfortunately these properties are generally mutually exclusive. Although the quest continues for stronger and harder materials, these have little to no use as bulk structural materials without appropriate fracture resistance. It is the lower-strength, and hence higher-toughness, materials that find use for most safety-critical applications where premature or, worse still, catastrophic fracture is unacceptable. For these reasons, the development of strong and tough (damage-tolerant) materials has traditionally been an exercise in compromise between hardness versus ductility. Drawing examples from metallic glasses, natural and biological materials, and structural and biomimetic ceramics, we examine some of the newer strategies in dealing with this conflict. Specifically, we focus on the interplay between the mechanisms that individually contribute to strength and toughness, noting that these phenomena can originate from very different lengthscales in a material's structural architecture. We show how these new and natural materials can defeat the conflict of strength versus toughness and achieve unprecedented levels of damage tolerance within their respective material classes.

/pdf/the-conflicts-between-strength-and-toughness-2cr075f2ul.pdf

Allen J. Bailey

Papers

Mechanisms of maturation and ageing of collagen

Collagen cross-links in mineralizing tissues: A review of their chemistry, function, and clinical relevance

Molecular mechanisms of ageing in connective tissues

Changes in metabolism of collagen in genitourinary prolapse

Glycation of collagen: the basis of its central role in the late complications of ageing and diabetes