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

This chapter suggests that delinquency conceals two distinct categories of individuals, each with a unique natural history and etiology: A small group engages in antisocial behavior of one sort or another at every life stage, whereas a larger group is antisocial only during adolescence. According to the theory of life-course-persistent antisocial behavior, children's neuropsychological problems interact cumulatively with their criminogenic environments across development, culminating m a pathological personality. According to the theory of adolescence-limited antisocial behavior, a contemporary maturity gap encourages teens to mimic antisocial behavior in ways that are normative and adjustive. There are marked individual differences in the stability of antisocial behavior. The chapter reviews the mysterious relationship between age and antisocial behavior. Some youths who refrain from antisocial behavior may, for some reason, not sense the maturity gap and therefore lack the hypothesized motivation for experimenting with crime.

/pdf/adolescence-limited-and-life-course-persistent-antisocial-52vil00qlw.pdf

Adolescence-limited and life-course-persistent antisocial behavior: A developmental taxonomy.

The emerging field of emotion regulation studies how individuals influence which emotions they have, when they have them, and how they experience and express them. This review takes an evolutionary perspective and characterizes emotion in terms of response tendencies. Emotion regulation is denned and distinguished from coping, mood regulation, defense, and affect regulation. In the increasingly specialized discipline of psychology, the field of emotion regulation cuts across traditional boundaries and provides common ground. According to a process model of emotion regulation, emotion may be regulated at five points in the emotion generative process: (a) selection of the situation, (b) modification of the situation, (c) deployment of attention, (d) change of cognitions, and (e) modulation of responses. The field of emotion regulation promises new insights into age-old questions about how people manage their emotions.

http://www.elaborer.org/cours/A13/lectures/Gross1998.pdf

The emerging field of emotion regulation: An integrative review.

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)

/pdf/how-do-glucocorticoids-influence-stress-responses-4egr3fa2k0.pdf

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

Over 60 years ago, Selye1 recognized the paradox that the physiologic systems activated by stress can not only protect and restore but also damage the body. What links these seemingly contradictory roles? How does stress influence the pathogenesis of disease, and what accounts for the variation in vulnerability to stress-related diseases among people with similar life experiences? How can stress-induced damage be quantified? These and many other questions still challenge investigators. This article reviews the long-term effect of the physiologic response to stress, which I refer to as allostatic load.2 Allostasis — the ability to achieve stability through change3 — . . .

/pdf/protective-and-damaging-effects-of-stress-mediators-34e0m747fy.pdf

Protective and Damaging Effects of Stress Mediators

AS RECENTLY as 1900, tuberculosis, influenza, and pneumonia were the leading causes of death in our country (1). For the most part, however, these infectious diseases, as well as those of poor hygiene or undernutrition, no longer plague us. Instead, we succumb most frequently to heart disease and cancer, diseases of slow degeneration (1). Most of all, unlike so many in the generations before us, we are in a position to age. Regardless of what else occurs, we age, we become more constrained by the discrepancy between what we were and what we have become, and each step becomes harder. The goal in the study of aging is not to halt the process, because we can no more be cured of aging than of birth. The goal, instead, is to slow and soften the sharpest edges of the biological unraveling that constitutes aging. Over the past 5 yr, we have examined some of the sharpest edges of the pathology of aging. We have studied the capacity of aged organisms to respond appropriately to stress and the capacity of stress to...

The Neuroendocrinology of Stress and Aging: The Glucocorticoid Cascade Hypothesis*

Over the past 5 yr, we have examined some of the sharpest edges of the pathology of aging. We have studied the capacity of aged organisms to respond appropriately to stress and the capacity of stre...

The Neuroendocrinology of Stress and Aging: The Glucocorticoid Cascade Hypothesis

An extensive literature stretching back decades has shown that prolonged stress or prolonged exposure to glucocorticoids-the adrenal steroids secreted during stress-can have adverse effects on the rodent hippocampus. More recent findings suggest a similar phenomenon in the human hippocampus associated with many neuropsychiatric disorders. This review examines the evidence for hippocampal atrophy in (1) Cushing syndrome, which is characterized by a pathologic oversecretion of glucocorticoids; (2) episodes of repeated and severe major depression, which is often associated with hypersecretion of glucocorticoids; and (3) posttraumatic stress disorder. Key questions that will be examined include whether the hippocampal atrophy arises from the neuropsychiatric disorder, or precedes and predisposes toward it; whether glucocorticoids really are plausible candidates for contributing to the atrophy; and what cellular mechanisms underlie the overall decreases in hippocampal volume. Explicit memory deficits have been demonstrated in Cushing syndrome, depression, and posttraumatic stress disorder; an extensive literature suggests that hippocampal atrophy of the magnitude found in these disorders can give rise to such cognitive deficits.

https://jamanetwork.com/journals/jamapsychiatry/articlepdf/481654/ynv20127.pdf

Robert M. Sapolsky

Papers

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

The Neuroendocrinology of Stress and Aging: The Glucocorticoid Cascade Hypothesis*

The Neuroendocrinology of Stress and Aging: The Glucocorticoid Cascade Hypothesis

Glucocorticoids and hippocampal atrophy in neuropsychiatric disorders.

Stress and cognitive function