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

The transforming growth factor beta (TGF-beta) family of growth factors control the development and homeostasis of most tissues in metazoan organisms. Work over the past few years has led to the elucidation of a TGF-beta signal transduction network. This network involves receptor serine/threonine kinases at the cell surface and their substrates, the SMAD proteins, which move into the nucleus, where they activate target gene transcription in association with DNA-binding partners. Distinct repertoires of receptors, SMAD proteins, and DNA-binding partners seemingly underlie, in a cell-specific manner, the multifunctional nature of TGF-beta and related factors. Mutations in these pathways are the cause of various forms of human cancer and developmental disorders.

TGF-beta signal transduction.

The neural basis of drug craving: An incentive-sensitization theory of addiction

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.

In response to a peripheral infection, innate immune cells produce pro-inflammatory cytokines that act on the brain to cause sickness behaviour. When activation of the peripheral immune system continues unabated, such as during systemic infections, cancer or autoimmune diseases, the ensuing immune signalling to the brain can lead to an exacerbation of sickness and the development of symptoms of depression in vulnerable individuals. These phenomena might account for the increased prevalence of clinical depression in physically ill people. Inflammation is therefore an important biological event that might increase the risk of major depressive episodes, much like the more traditional psychosocial factors.

/pdf/from-inflammation-to-sickness-and-depression-when-the-immune-maw2hn72o8.pdf

From inflammation to sickness and depression: when the immune system subjugates the brain

Urocortin stimulates placental adrenocorticotropin and prostglandin release and myometrical conctractily

Erratum: Cloning and structure of the human corticotrophin releasing factor-binding protein gene (CRHBP) (Genomics (1993) 16 (63-68))

The peptide having the following formula has a potent effect on the reproduction processes of fish and is termed Fish GnRH: pGlu-His-Trp-Ser-Tyr-Gly-Trp-Leu-Pro-Gly-NH2. Spawning of teleostei fish can be promoted by administration of effective amounts of the peptide.

Peptides affecting gonadal function

Synthetic TRF (pyroglutamylhistidyl-proline amide) was infused (1 ng/min) for 20 min (1) into the anterior pituitary of 10 rats by way of a cannulated hypophysial stalk portal vessel or (2) into a femoral vein of 10 rats. At the end of the 20-min infusion period, the plasma concentration of TSH in 8 of 10 rats given TRF via a cannulated portal vessel was significantly greater than the pre-infusion level. In contrast, in only 3 of 10 rats given TRF via a femoral vein was the plasma concentration of TSH significantly greater than the pre-infusion level of TSH (Endocrinology 89: 1054, 1971)

Release of TSH by TRF Infused Directly into a Pituitary Stalk Portal Vessel

Peptides have been synthesized which influence the secretion of gonadotropins by the pituitary gland of mammalians, including humans. Some of the peptides promote the release of gonadotropins, while other peptides inhibit the release.

LH-RH Analogs

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