植物多肽激素研究概况

目前发现的植物多肽多达9种.基于配基-受体的胞间互作模式,目前公认的植物多肽激素包括4种:系统素(Systemin)、植物硫肽激素(Phytosulfokine)、SCR/SP11和CLV3,分别参与了植食性昆虫防御反应、细胞增殖、自交不亲和的识别,以及茎分生组织干细胞分裂与分化平衡的维持.本文对四种植物多肽激素基因家族的研究进展做了较为详尽的综述,并结合本试验室的研究进展做了展望.     

Hormones in mammalian evolution.

Animals that produced increased levels of prolactin and dehydroepiandrosterone (DHEA) survived the period of mass extinctions at the end of the Cretaceous period. DHEA increases thermogenesis and supported existence through the extended episode of cold and dark. Further increases in DHEA and prolactin produced continual physiological and anatomical changes which eventually produced all of the characteristics of mammals.     

Hormones and cancer in humans

Hormones play a major role in the aetiology of several of the commonest cancers worldwide, including cancers of the endometrium, breast and ovary in women and cancer of the prostate in men. It is likely that the main mechanisms by which hormones affect cancer risk are by controlling the rate of cell division, the differentiation of cells and the number of susceptible cells. Hormones have very marked effects on cell division in the endometrium; oestrogens stimulate mitosis whereas progestins oppose this effect. The risk for endometrial cancer increases with late menopause, oestrogen replacement therapy and obesity, and decreases with parity and oral contraceptive use; thus risk increases in proportion to the duration of exposure to oestrogens unopposed by progestins, probably because unopposed oestrogens stimulate endometrial cell division. The effects of hormones on breast epithelial cell division in non-pregnant women are much less clear-cut than their effects on the endometrium, but both oestrogens and progestins appear to stimulate mitosis. Breast cancer risk increases with early menarche, late menopause and oestrogen replacement therapy, probably due to increased exposure of the breasts to oestrogen and/or progesterone. Early first pregnancy and multiparity reduce the risk for breast cancer, probably due to the hormonally-induced differentiation of breast cells and the corresponding reduction in the number of susceptible cells. Hormones do not have marked direct effects on the epithelial cells covering the ovaries, but hormones stimulate ovulation which is followed by cell division during repair of the epithelium. Risk for ovarian cancer increases with late menopause and decreases with parity and oral contraceptive use, suggesting that the lifetime number of ovulations may be a determinant of risk. For all three of these cancers risk changes within a few years of changes in exposure to sex hormones and some of the changes in risk persist for many years, indicating that hormones can affect both early and late stages of carcinogenesis. Understanding of the role of sex hormones in the aetiology of prostate cancer and of some rarer cancers is less complete.