增血素口服液对麻醉犬脑血流量和血液粘度的影响

增血素１ｍｌ／ｋｇ时，对麻醉犬脑血流量（ＣＢＦ）和１０Ｓ－１下的全血粘度（ＢＶ）均无明显影响。增血素２ｍｌ／ｋｇ时，使ＣＢＦ显著增加，也使１０Ｓ－１下的ＢＶ明显降低。增血素１ｍｌ／ｋｇ和２ｍｌ／ｋｇ均可使１００Ｓ－１下的ＢＶ显著降低。结果提示，增皿素增加ＣＢＦ作用似与ＢＶ降低有关。

增血素口服液对苯肼致家兔溶血性贫血的影响

目的：研究增血素口服液对苯肼所致家兔溶血性贫血的影响。方法：家兔背部皮下注射盐酸苯肼 ００１ｇ／ｋｇ，造成溶血性贫血模型，增血素口服液连续灌胃 １２ 天。结果：外周血中红细胞数、血红蛋白含量回升速度及网织红细胞数升高速度均显著高于对照组，同时血清超氧化物歧化酶活力明显增加，丙二醛含量下降。结论：增血素有加速红细胞和血红蛋白回升的作用。

增血素对家兔白细胞减少症的疗效观察

家兔皮下注射苯1ml／kg，造成白细胞减少症模型。增血素口服液连续用胃一周后，周围血中白细胞总数、粒细胞数及非粒细胞数的回升速度均显著高于对照组，而对细红胞数及血红蛋白含量无明显影响。结果表明：增血素有加速白细胞回升的作用。

增血素口服液对动物体内氧自由基的影响

目的：观察增血素口服液对苯肼中毒的家兔和正常小鼠体内氧自由基的影响。方法：用黄嘌呤氧化法测定超氧化物歧化酶（ Ｓ Ｏ Ｄ），用硫代巴比妥酸法测定丙二醛（ Ｍ Ｄ Ａ）含量。结果：增血素口服液可使苯肼中毒家兔血清 Ｓ Ｏ Ｄ 活力和 Ｍ Ｄ Ａ 含量恢复正常；使正常小鼠血清 Ｓ Ｏ Ｄ 活力增强， Ｍ Ｄ Ａ 含量明显下降。结论：增血素口服液能增强机体清除氧自由基的能力。

增血素口服液对家兔免疫功能影响的初步研究

用增血素口服液０．９４ｍｌ／ｋｇ、１．８８ｍｌ／ｋｇ给家兔连续灌胃１５天，取血液测定其淋巴细胞转化率及血清溶血素含量。结果表明：淋巴细胞转化率无显著改变，血清溶血素含量明显降低。提示增血素口服液对家兔细胞免疫功能无明显影响。

仔猪使用增血素、血多素效果分析

给初生仔猪补铁避免了缺铁性贫血的出现,促进了仔猪的生长发育。注射增血素、血多素20日龄各实验组与对照组的平均体重为4.8、4.74、3.93kg。经方差分析,组间差异极显著。不同的注射时间,产生不同效益,但初生～24h内注射效益最为理想。

注射增血素补铁对仔猪生长的影响

用注射增血素的方法对出生３天后的仔猪实施补铁。分试验组和对照组。结果表明：在相同饲养条件下，试验组仔猪生长速度、抗病能力、成活率明显高于对照组。

补铁剂对仔猪增重的影响

本文报导了两种补铁剂,即增血素和牲血素,对不同年龄仔猪增重的影响。结果如下:在处理组,在21日龄前或45日龄前,仔猪平均日增重显著高于对照组,然而,在增血素组和牲血素组,没有显著差异。因此,这两种补铁剂均可推荐在仔猪饲养中采用。

Insulin promotes sinusoidal endothelial cell proliferation mediated by upregulation of vascular endothelial growth factor in regenerating rat liver after partial hepatectomy

AIM： To determine whether insulin could promote sinusoidal endothelial cell （SEC） proliferation mediated by upregulation of vascular endothelial growth factor （VEGF） in regenerating rat liver after partial hepatectomy （PHx）. METHODS： Adult male Sprague-Dawley rats undergoing 70% PHx were injected with insulin （300 MU/kg） or saline via the tail veins every 8 h after surgery for 7 d and killed at 0, 24, 48, 72, 96, 120, 144, and 168 h after surgery. Proliferation of both hepatocytes and SECs was monitored by evaluating the proliferating cell nuclear antigen （PCNA） labeling index （LI）. The expression of VEGF protein was evaluated by immunohistochemistJv. The mRNA expressions of VEGF and its receptors FIt-1 and FIk-1 were evaluated by semi-quantitative reverse transcription-PCR. RESULTS： Insulin markedly increased the expression of VEGF mRNA between 24 and 120 h after hepatectomy compared to controls. Similarly, insulin significantly increased the expression of Fit-1 between 24 and 96 h. However, insulin had no significant effect on FIk-1. Furthermore, the immunohistochemical staining revealed that expression of VEGF protein increased in the insulin groups. Insulin significantly increased the PCNA LI of hepatocytes and SECs compared to controls. CONCLUSION： Exogenous insulin may promote SEC proliferation with an enhanced expression of VEGF and its receptor Fit-1 in regenerating rat liver after PHx.

Cronkhite-Canada syndrome associated with myelodysplastic syndrome

We report a case of Cronkhite-Canada syndrome(CCS)associated with myelodysplastic syndrome(MDS).A 54-year-old woman,diagnosed as MDS the prior year after evaluation of anemia,visited our hospital with the chief complaint of epigastric discomfort.She also had dysgeusia,alopecia,atrophic nail change,and pigmentation of the palm,all of which began several months ago.Blood tests revealed severe hypoalbuminemia.Colonoscopy(CS)showed numerous,dense,red polyps throughout the colon and rectum.Biopsy specimens showed stromal edema,infi ltration of lymphocytes,and cystic dilatation of the crypt.Her clinical manifestations and histology were consistent with CCS.We prescribed corticosteroids,which dramatically improved her physical findings,laboratory data,and endoscopic fi ndings.This is the first report of CCS in a patient with MDS.

Effects of varied interferons in combination with all-trans retinoic acid ( ATRA ) on proliferation and differentiation of ATRA-resistent APL cell

Objective：To investigate the effects and mechanisms of interferon in combination with alltrans retinoic acid （ATRA） on proliferation and differentiation of ATRA-resistent APL cell. Methods ：After MR2 cells （ATRA-resistance cell line） were treated with IFN-α, IFN-γ and ATRA alone or IFN-α and IFN-γ in combination with ATRA respectively. The cell proliferation was tested by MTT test and the cell differentiation was tested through light microscope by NBT test and flow cytometry （FCM）. The expres sion of promyelocytic leukemia （PML） protein was observed by indirect immune fluorescent method. Results： Both IFN-α and IFN-γ could inhibit the proliferation and induce the differentiation of MR2 cells to some extent. The effects were more obvious after both interferons in combination with ATRA respectively （P〈0.05）. Moreover, the maturation of MR2 cells induced by IFN-γ＋ATRA group was more higher than that by IFN-α＋ATRA group （P〈0. 05）. Both interferons could induce the expressions of PML protein. Conclusion：Both interferons can inhibit MR2 cells proliferation, which may be related to the expression of PML protein induced by both interferons. The inducing differentiation effects of IFN-γ＋ATRA group on MR2 cells are more powerful than those of IFN-aq-ATRA group, which may be related to the different signal transduction pathway of both interferons.

Interleukin-15 Promotes the Commitment of Cord Blood CD34^+ Stem Cells into NK Cells

To explore the effect of rhIL-15 on CB-CD34 + stem cells committing to NK cells, CD34 + stem cells were obtained from cord blood (CB) by magnetic-assisted cell sorting (MACS) method. CD3, CD16 and CD56 molecules expressed on cell surface were detected by flow cytometer. MTT method was used to test the cytotoxicity of NK cells. The results were that stem cell factor (SCF) alone has no effect on CD34 + stem cells. IL-15 stimulated CD34 + stem cells commit to NK cells, and SCF showed strong synergistic effect with IL-15. It was concluded that IL-15 and SCF played different roles during NK cell development, IL-15 promoted CD34 + stem cells differentiate to NK cell precursor and SCF improved the effects of IL-15 on NK cell differentiation.

Endostatin inhibits fibrosis by modulating the PDGFR/ERK signal pathway:an in vitro study

Accumulating evidence indicates that endostatin inhibits fibrosis. However, the mechanism is yet to be clarified. The aim of this study is to evaluate the effect of endostatin on platelet-derived growth factor-BB （PDGF-BB）- or transforming growth factor β1 （TGF-β1）-induced fibrosis in cultured human skin fibroblasts, and to further examine the molecular mechanisms involved. Human dermal flbroblasts were cultured in Dulbecco＇s modified Eagle＇s medium （DMEM） and serum-starved for 48 h before treatment. Cells were grouped as follows： ＂PDGF-BB＂, ＂PDGF-BB＋ endostatin＂, ＂TGF-β1＂, ＂TGF-β1＋endostatin＂, ＂endostatin＂, and ＂blank control＂. The fibroblasts were stimulated with either TGF-β1 or PDGF-BB for 72 h in order to set up the fibrosis model in vitro. The cells were co-cultured with either TGF-β1 or PDGF-BB and endostatin and were used to check the inhibiting effect of endostatin. A blank control group and an endostatin group were used as negative control groups. The biomarkers of fibrosis, including the expression of collagen I, hydrroxyproline, and α-smooth muscle actin （a-SMA）, were evaluated using an enzyme-linked immune- sorbent assay （ELISA） and Western blot. The expression of phosphorylated PDGF receptor β （p-PDGFRβ）, PDGFRβ, phosphorylated extracellular signal-regulated kinase （p-ERK）, and ERK was detected using Western blot and im- munofiuorescent staining was used to explore the mechanisms. Both PDGF-BB and TGF-β1 significantly up-regulated the expression of collagen I, hydroxyproline, and a-SMA. Endostatin significantly attenuated both the PDGF-BB- and TGF-β1-induced over-expression of collagen I, hydroxyproline, and a-SMA. PDGF-BB and TGF-β1 both promoted the expression of PDGFR, ERK, and p-ERK. Endostatin inhibited the expression of PDGFR and p-ERK but did not affect the expression of total ERK. Endostatin inhibited hypertrophic scar by modulating the PDGFRI3/ERK pathway. En- dostatin could be a promising multi-target drug in future fibrosis therapy.

Cell cycle regulator geminin is dispensable for the proliferation of vascular smooth muscle cells

The proliferation of vascular smooth muscle cells(VSMCs) plays a major role in the pathogenesis of many cardiovascular diseases.Geminin regulates DNA replication and cell cycle progression and plays a key role in the proliferation of cancer cells.We therefore hypothesized that geminin regulates the proliferation of VSMCs.The present study demonstrates that the level of geminin expression was low in quiescent VSMCs(approximately 90% and 10% of cells in the G1 and in S/G2/M phases of the cell cycle,respectively),increased as more cells entered in S/G2/M,and then decreased as cells exited S/G2/M.Further,angiotensin II and norepinephrine stimulated expression of geminin in VSMCs.However,the DNA content,nuclear morphology,percentage of cells at different stages of the cell cycle,and rate of proliferation of VSMCs from which geminin was either depleted or overexpressed were all similar.These findings indicate geminin functions differently in VSMCs than it does in cancer cell lines and that it may provide a target for treating cancers without affecting normal cells.