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

Despite the concern that has been expressed about potential method biases, and the pervasiveness of research settings with the potential to produce them, there is disagreement about whether they really are a problem for researchers in the behavioral sciences. Therefore, the purpose of this review is to explore the current state of knowledge about method biases. First, we explore the meaning of the terms “method” and “method bias” and then we examine whether method biases influence all measures equally. Next, we review the evidence of the effects that method biases have on individual measures and on the covariation between different constructs. Following this, we evaluate the procedural and statistical remedies that have been used to control method biases and provide recommendations for minimizing method bias.

Sources of Method Bias in Social Science Research and Recommendations on How to Control It

I have developed "tennis elbow" from lugging this book around the past four weeks, but it is worth the pain, the effort, and the aspirin. It is also worth the (relatively speaking) bargain price. Including appendixes, this book contains 894 pages of text. The entire panorama of the neural sciences is surveyed and examined, and it is comprehensive in its scope, from genomes to social behaviors. The editors explicitly state that the book is designed as "an introductory text for students of biology, behavior, and medicine," but it is hard to imagine any audience, interested in any fragment of neuroscience at any level of sophistication, that would not enjoy this book. The editors have done a masterful job of weaving together the biologic, the behavioral, and the clinical sciences into a single tapestry in which everyone from the molecular biologist to the practicing psychiatrist can find and appreciate his or

Principles of Neural Science

This paper presents a critical appraisal of resilience, a construct connoting the maintenance of positive adaptation by individuals despite experiences of significant adversity. As empirical research on resilience has burgeoned in recent years, criticisms have been levied at work in this area. These critiques have generally focused on ambiguities in definitions and central terminology; heterogeneity in risks experienced and competence achieved by individuals viewed as resilient; instability of the phenomenon of resilience; and concerns regarding the usefulness of resilience as a theoretical construct. We address each identified criticism in turn, proposing solutions for those we view as legitimate and clarifying misunderstandings surrounding those we believe to be less valid. We conclude that work on resilience possesses substantial potential for augmenting the understanding of processes affecting at-risk individuals. Realization of the potential embodied by this construct, however, will remain constrained without continued scientific attention to some of the serious conceptual and methodological pitfalls that have been noted by skeptics and proponents alike.

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The Construct of Resilience: A Critical Evaluation and Guidelines for Future Work

The secretion of glucocorticoids (GCs) is a classic endocrine response to stress. Despite that, it remains controversial as to what purpose GCs serve at such times. One view, stretching back to the time of Hans Selye, posits that GCs help mediate the ongoing or pending stress response, either via basal levels of GCs permitting other facets of the stress response to emerge efficaciously, and/or by stress levels of GCs actively stimulating the stress response. In contrast, a revisionist viewpoint posits that GCs suppress the stress response, preventing it from being pathologically overactivated. In this review, we consider recent findings regarding GC action and, based on them, generate criteria for determining whether a particular GC action permits, stimulates, or suppresses an ongoing stressresponse or, as an additional category, is preparative for a subsequent stressor. We apply these GC actions to the realms of cardiovascular function, fluid volume and hemorrhage, immunity and inflammation, metabolism, neurobiology, and reproductive physiology. We find that GC actions fall into markedly different categories, depending on the physiological endpoint in question, with evidence for mediating effects in some cases, and suppressive or preparative in others. We then attempt to assimilate these heterogeneous GC actions into a physiological whole. (Endocrine Reviews 21: 55‐ 89, 2000)

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How do glucocorticoids influence stress responses? Integrating permissive, suppressive, stimulatory, and preparative actions.

To be useful, the concept of stress needs to be defined in biological terms linked to a broader framework of allostasis and its role in the adaptation of brain and body to positive and negative life experiences. A clear biological framework helps connect and organize animal and human research on stress. In particular, the concepts of "toxic stress" and "allostatic load and overload" highlight those experiences and situations that, as Kagan says, "compromise an organism's health and capacity to cope with daily challenges" (p. 442). A deeper understanding is needed of the epigenetic influences throughout the life course that contribute both to these negative outcomes and to positive ones.

Response to Jerome Kagan's Essay on Stress (2016).

This paper summarizes recent work from this laboratory concerning the interaction of radioactive testosterone and various estrogens with brains of newborn rats. Testosterone7-3H is shown to be converted in vivo to estradi Ol7-3Hand this product is retained by cell nuclei in hypothalamus and limbic structures to a degree which points to the existence of putative estrogen receptor sites in the neonatal brain. This inference has been verified by in vivo studies using 3H-estradiol, 3H-diethylstilbastrol (DES) and 3H-II(3-methoxy I7 oc-ethynyl 17 (3-estradiol (RU 285) Cell nuclear retention of radioactive estrogens is prevented by non-radioactive 17(3-estradiol and i7a-estradiol and by the non-steroidal anti-estrogen CI6 28, and is not significantly reduced by a variety of non-radioactive 5a-reduced androgens or by progesterone. Cell nuclear labeling is substantial in hypothalamus, amygdala, preoptic area, and much lower in cerebellum and midbrain and brainstem. Cerebral cortex is noteworthy because it lacks significant aromatization capability and yet retains 3H-estrogens in a manner similar in specificity and intensity of labeling to hypothalamus, amygdala and preoptic area. The developmental changes of estrogen binding capacity are described. The neonatal brain and blood also contains another estrogen binding protein (fEBP-fetoneonatal estrogen binding protein) which binds 3H-estradiol but to a far lesser extent binds synthetic estrogens like 3H-DES and 3H-RU 285. The ability of 3H-estrogens to bind in vivo to cell nuclear receptor sites appears to be inversely related to their binding to fEBP. Hence, the protective role for this fEBP against potentially deleterious effects of estradiol17 Pis strongly supported, and the potential dangers of certain synthetic estrogens are once again demonstrated. The relationship of these results to the process of sexual differentiation is discussed.

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Bruce S. McEwen

Papers

Response to Jerome Kagan's Essay on Stress (2016).

Interactions of testosterone and estradiol with the neonatal rat brain : protective mechanism and possible relationship to sexual differentiation

Danazol suppression of luteinizing hormone secretion: a role for danazol-androgen receptor interaction within the brain-pituitary complex

Commentary on PTSD discussion

Novelty-induced locomotor activity in Long-Evans rats pre-and post-chronic 'binge'-pattern cocaine treatment