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In 1957, Jacobson et al performed bilateral nephrectomies on rats and showed that these animals no longer responsed to phlebotomy or cobalt administration with increased Ep production. Rats that only had their ureters ligated and that developed similar elevations of the blood urea nitrogen still responded to cobalt or phlebotomy in the usual fashion .Similiar results were found in mice , rabbits , baboons , and dogs .In humans , Ep levels were found to be low in the serum of anemic patients with severe uremia , but after successful renal transplantation increases in blood Ep levels and hematocrit were observed. Furthermore , erythropoietic activity was detected in the perfusates from isolated rabbit kidneys and was produced by renal cell cultures in vitro . Although the evidence to support the renal origin of Ep was substantial , Ep had not been extracted from normal kidneys or from various normal kidney fractions until very recently. To explain this difficulty , three different hypotheses have been proposed . Current evidence indicates that the stimulation of Ep production by hypoxia or ischemia may be mediated via increases in renal prostaglandin and cyclic AMP levels . The administration of cyclic AMP to plethoric mice increased Ep production and led to and increased red cell mass in normal mice . prostaglandin raised the renal cyclic AMP concentration in isolated perfused dog kidneys as well as the amount of Ep in the perfusates ;the administration of prostaglandin to polycythemic mice increased both prostaglandin E and Ep blood levels in dogs . The effect on both these parameters as well as on hypoxia-induced Ep production was blocked by indomethacin, a known inhibitor of prostaglandin synthesis .Since prostaglandins are located mainly in the renal medulla , while Ep has been identified by fluorescent antibodies in the renal cortex , these observations are most consistent with the hypothesis that renal hypoxia or ischemia produces a medullary release of prostaglandin which in turn elevates renal corticla cyclic AMP levels. The newly formed cyclic AMP THEN may activate a protein kinase that leads to increased Ep production , possibly through phosphorylation of a precursor renal erythropoietic factor. Although the kidney is the major site controlling Ep formation , after bilateral nephrectomy the production of hormone and erythropoiesis continues in most species , but at a considerably lower level .Anephric mice and rats retain about 10%of their original capacity to increase Ep production in the presence of hypoxia , while anephric patients who become very anemic have Ep in their plasma .The extrarenal Ep of rats appears to be similar to Ep of renal origin since it stimulates heme synthesis by marrow cells and is neutralized by antiserum to urinary Ep . Several lines of study point to the liver as the primary site of extrarenal Ep production. Ep is produced primarily in the liver during fetal life .Hepatectomy abolishes hypoxia-stimulated hormone production in anephric rats , but not in animals with intact kidneys . In partially hepatectomized rats , the extrarenal Ep response to hypoxia correlates directly with liver regeneration and is most increased during the period of greatest proliferation . Administration of colloidal carbon or zymosan, which induces liver reticuloendothelial cell hyperplasia, enhances Ep production in nephrectomized rats exposed to hypoxia .This effect, which is also blocked by hepatectomy , suggests that the liver reticuloendothelial system may be and important factor in extrarenal Ep production . |
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3樓2011-03-05 21:04:18
wjmsicuan(金幣+1, 翻譯EPI+1): 很差勁，不過(guò)還是慰問(wèn)下��！ 2011-03-06 19:43:10
 在1957年，Jacobson 等人對(duì)大鼠首先進(jìn)行雙側(cè)腎切除，之后放血或用鈷處理，發(fā)現(xiàn)Ep不增高，然而，如果預(yù)先只是將大鼠輸尿管結(jié)扎，其血液尿素含量增高，之后放血或用鈷處理，其Ep，和正常鼠一樣，增高。在小鼠，家兔，狒狒和狗身上做相同的實(shí)驗(yàn)，獲得的結(jié)果相似。在人群中，伴有嚴(yán)重尿毒癥的白血病患者的血液Ep水平較低，但在腎移植手術(shù)成功后，血液Ep水平升高，且血細(xì)胞計(jì)數(shù)也有所增加。此外，對(duì)分離的家兔的腎灌流液，即體外培養(yǎng)的腎細(xì)胞的紅血球生成活性進(jìn)行檢測(cè)。雖然支持Ep 來(lái)源于腎的證據(jù)可靠，但直到現(xiàn)在，人們還沒(méi)能從正常的腎或不同的腎fractions提取出 Ep 。為了解釋這個(gè)難題，三個(gè)不同的假說(shuō)被提出。最新證據(jù)顯示，由組織缺氧和局部缺血誘導(dǎo)的 Ep的產(chǎn)生是通過(guò)上調(diào)腎臟前列腺素和cAMP水平來(lái)介導(dǎo)的。用cAMP處理多血癥小鼠可增加Ep的產(chǎn)生，處理正常小鼠可導(dǎo)致紅細(xì)胞塊的增加。前列腺可以上調(diào)體外灌流的狗腎臟的cAMP濃度，同時(shí)也可以上調(diào)灌流液中Ep含量。用前列腺素處理紅細(xì)胞增多小鼠，可以增加血液前列腺素E含量，也可以增加狗的血Ep含量。對(duì)這2個(gè)參數(shù)的影響和組織缺氧誘導(dǎo)的Ep增多可以被消炎藥茚甲新阻斷，茚甲新是前列腺素合成的抑制劑。由于前列腺素主要分布于腎髓，而Ep已通過(guò)熒光抗體被鑒定存在于腎皮質(zhì)， 這些觀察結(jié)果與假設(shè)一致，即腎缺氧或缺血誘導(dǎo)腎髓釋放前列腺素，而前列腺素反過(guò)來(lái)又上調(diào)腎皮質(zhì)的cAMP濃度。新生成的cAMP，接下來(lái)可能可以激活蛋白激酶增加Ep的產(chǎn)生，很可能是通過(guò)磷酸化腎紅血球生成因子前體來(lái)實(shí)現(xiàn)的。 雖然腎是控制Ep生成的主要場(chǎng)所，在大多數(shù)物種經(jīng)歷雙腎切除手術(shù)之后，激素和紅血球產(chǎn)生過(guò)程仍然繼續(xù)，只是以相當(dāng)?shù)偷乃俣�。無(wú)腎小鼠和無(wú)腎大鼠在缺氧條件下仍然保留約10%生產(chǎn)Ep的能力,但無(wú)腎的病人，常表現(xiàn)為嚴(yán)重貧血，在血漿中含有Ep。大鼠腎外的Ep和腎來(lái)源的Ep很相似，也可以刺激骨髓細(xì)胞生成亞鐵血紅素，可以被抗尿Ep的抗血清中和。一些研究團(tuán)隊(duì)認(rèn)為肝臟是腎外Ep產(chǎn)生的最初部位。在胎兒期 Ep主要在肝臟中產(chǎn)生。在無(wú)腎大鼠中，肝臟切除可以阻斷低氧誘導(dǎo)激素的產(chǎn)生，但在有完整腎的動(dòng)物中肝臟切除不可阻斷。在部分肝臟切除的大鼠中， 腎外Ep對(duì)低氧的反應(yīng)直接與肝再生相關(guān)，且在增殖最旺盛期腎外Ep增加最快。 用膠狀碳或酵母聚糖誘導(dǎo)肝網(wǎng)狀內(nèi)皮組織增生，可以促進(jìn)受低氧脅迫的腎切除大鼠的Ep的產(chǎn)生。這個(gè)效應(yīng)同樣可以被肝切除手術(shù)阻斷，提示肝網(wǎng)狀內(nèi)皮系統(tǒng) 可能是腎外Ep產(chǎn)生的重要因素。 第一次翻譯，湊活著看啊 |
2樓2011-03-05 20:56:56
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SP(side population)細(xì)胞 1996年, Goodell et al [2] 在用Hoechst33342熒光 染色對(duì)小鼠骨髓造血干細(xì)胞進(jìn)行檢測(cè)時(shí), 通過(guò) 紫外激發(fā)檢測(cè)雙波長(zhǎng)分別為450 nm的藍(lán)色熒光 和675 nm的紅色熒光, 發(fā)現(xiàn)不到0.1%的細(xì)胞發(fā) 出極弱的藍(lán)光和紅光, 在流式二維分析點(diǎn)陣圖 上, 這一小群細(xì)胞呈彗星狀分布在細(xì)胞主群的 一側(cè), 他們將這群細(xì)胞稱為SP(side population) 細(xì)胞. ;  |
4樓2011-03-06 21:18:12
5樓2011-03-07 17:18:26
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