人胚肺细胞对人冠状病毒的敏感性

人冠状病毒72-62和73-50干燥毒种,用人胚器官和原代人胚肾细胞合管培养未能引起细胞病变,而将病毒液接种到人胚器官细胞或人胚肺传代细胞第一代就能引起明显的细胞病变。新传代病毒经电镜及中和试验鉴定确属人冠状病毒。实验结果证明人胚肺传代细胞比原代人胚肾细胞敏感,为进一步研究人冠状病毒提供了一株敏感的细胞。     

胃癌病人NK细胞活性变化机理的初步研究

应用~(51)Cr释放试验和效靶结合试验,同时测定了正常人和胃癌病人外周血NK细胞活性与靶结合细胞数(TBC),研究了正常人及病人血浆对NK细胞功能的影响。发现正常人NK细胞活性与靶结合细胞数之间的关系呈直线正相关,但在NK活性降低的病人中靶结合细胞数却无明显改变,二者无相关性,而病人的血浆对正常人外周血NK活性则有明显的抑制作用(P<0.05),且抑制率与胃癌人NK细胞活性存有着负相关的关系,提示胃癌病人血浆具有抑制NK细胞活性的物质。     

辛伐他汀对CD40L介导的ECV-304细胞E选择素表达及粘附功能的影响

目的研究在人脐静脉内皮细胞中3-羟-3-甲基戊二酰辅酶A(HMG-CoA)还原酶对CD40/CD40L系统介导的粘附分子表达的影响,及对淋巴细胞与内皮细胞的粘附功能的影响。方法采用人脐静脉内皮细胞株ECV-304,CD40L干预,使之与其表面的CD40作用,用不同浓度辛伐他汀或辛伐他汀(5μmol.L-1)+甲羟戊酸干预,流式细胞术和RT-PCR检测干预前后E选择素(E-Selectin)的表达,流式细胞术检测CD40L介导的淋巴细胞与内皮细胞的粘附功能。结果不同浓度辛伐他汀可下调CD40L介导的E-Selectin的表达,并呈一定的剂量依赖性。甲羟戊酸(400μmol.L-1)抑制了辛伐他汀(5μmol.L-1)对E-Selectin表达的下调作用。辛伐他汀可降低CD40L介导的淋巴细胞与内皮细胞的粘附功能。结论他汀类药物的抗炎作用与抑制CD40-CD40L系统有关,其机制是通过抑制HMG-CoA还原酶而发挥作用的。     

Chronotropic and inotropic effects of histamine in developing chick heart: differential mechanisms before and after hatching

Chronotropic and inotropic effects of histamine were examined in isolated atrial and ventricular preparations from embryonic and hatched chicken hearts. Histamine produced positive chronotropic and inotropic responses both in embryonic and hatched hearts. The responses to histamine in middle embryonic myocardia, which were observed in the micromolar range, were antagonized by H₂ antagonists but not by H₁, H₃ antagonists and propranolol. Isobutylmethylxantine, an inhibitor of phosphodiesterase, produced a leftward shift of the concentration-response curve for the chronotropic effect of histamine in the embryo. The responses to histamine in myocardia from hatched chicks, which were observed in the milimolar range, appeared concurrently with the responses to tyramine during development and were antagonized by beta adrenoceptor antagonists but not by any of the histamine antagonists. The positive inotropic response to histamine in hatched ventricular preparations were greatly attenuated by reserpine pretreatment or in the presence of desipramine. Thus, we demonstrated that exogenously applied histamine produces positive chronotropic and inotropic responses in developing chicken hearts and that the mechanisms are different between embryonic and hatched chicks: direct action on H₂ receptors in the embryonic heart and release of norepinephrine from sympathetic nerve terminals in hatched hearts.     

核黄素等抗甲基苄基亚硝胺的致细胞突变作用

采用ＣＨＯ细胞ＨＧＰＲＴ位点突变测定系统观察了核黄素、尼克酰胺和锌等微量营养素对甲基苄基亚硝胺（ＭＢＮＡ）致细胞突变作用的影响。结果表明，在ＲＰＭＩ１６４０培养基中添加核黄素（２．６～１３．０μｍｏｌ／Ｌ）或尼克酰胺（４０～１２０μｍｏｌ／Ｌ）可显著抑制ＭＢＮＡ的致细胞突变作用。联合应用核黄素、尼克酰胺和锌效果更佳。提示：核黄素等微量营养素可能具有阻止细胞癌变的作用，为应用微量营养素干预治疗癌变过程提供了一定的理论依据。     

Synthesis and post-translational modification of the androgen receptor in LNCaP cells

Androgen receptor synthesis and modification were studied in the human LNCaP cell line. Immunoblotting with a specific polyclonal antibody showed that the androgen receptor migrated as a closely spaced 110–112 kDa doublet on sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) gels. Most of the receptor protein is present in the higher molecular mass form. Pulse labelling experiments with [³⁵S]methionine showed that the androgen receptor is synthesized as a single 110 kDa protein which is rapidly converted to a 112 kDa protein. Alkaline phosphatase treatment of cytosols from [³⁵S]methionine pulse labelled cells caused a gradual elimination of the 112 kDa isoform with a concomitant increase of the 110 kDa isoform. This indicates that the observed 110 to 112 kDa upshift of the newly synthesized androgen receptor reflects receptor phosphorylation. Both isoforms can bind hormone and can undergo a hormone dependent transformation to a tight nuclear binding form, indicating that the 110 to 112 kDa conversion is not an obligatory step for hormone binding or receptor transformation.     

血小板衍生生长因子在肺鳞癌及肺腺癌中的表达及意义

目的　探讨血小板衍生生长因子 (PDGF)在肺鳞癌和肺腺癌中的表达及意义。方法　应用免疫组织化学技术观察了PDGF -A链和PDGF -B链在 42例肺鳞癌和 1 5例肺腺癌中的表达 ,并测定了它们在肺非特异性炎症组织中的表达。结果　PDGF -A链和PDGF -B链的表达主要定位于肿瘤细胞胞浆、血管内皮细胞及平滑肌细胞 ,炎症组织的肺泡上皮细胞及血管平滑肌细胞少量表达。PDGF -A链和PDGF -B链在肺鳞癌及肺腺癌中均有显著表达 ;PDGF的过度表达与肿瘤细胞的分化程度无关。结论　PDGF -A链和PDGF -B链的过度表达与肺鳞癌和肺腺癌有关 ;PDGF -A链和PDGF -B链的生物学特征可能有所不同 ,PDGF -B链与肿瘤微血管增生的关系可能更密切     

In Vitro Growth of Thymic Tumor Cell Lines from Xenopus

A spontaneous lymphoid thymus tumor was discovered in a male Xenopus of the MHC ff genotype. The tumor cell can be transplanted in histocompatible larval ff hosts, but not in ff adults unless irradiated (3000 rad). The tumor is rejected by allogeneic hosts. The tumor cells express neither markers of the B-cell lineage nor MHC encoded molecules; they express only markers of the T-cell lineage. Its lymphoid population is clonal as revealed by the existence of a stable rearrangement pattern of the immunoglobulin genes. Cell lines growing continuously in vitro have been derived from the tumor.     

在无血清培养基中代谢副产物对杂交瘤细胞生长代谢的影响 I.乳酸的作用

研究了无血清批培养中乳酸对杂交瘤细胞生长代谢的影响，当乳酸浓度低于5．3mmol/L时，乳酸对细胞生长和代谢无明显影响，当乳酸浓度在10mmol/L-25mmol/L时，对杂交瘤细胞的生长代谢有弱抑制，当乳酸浓度高于34mmol/L时，对细胞生长代谢有较明显的抑制。     

Cytoprotective effect of epidermal growth factor on acid- and pepsininduced damage to rat gastric epithelial cells: Roles of Na+/H+ exchangers

We have previously established a cell damage model, with damage induced by either acid or pepsin treatment for 30 min, involving a rat gastric epithelial cell line (RGM1). In the present study, pretreatment of cells with epidermal growth factor (EGF; 0.1–10ng/mL) or sucralfate (0.1–3 mg/mL) for 4 h prevented such cell damage in a concentration-dependent manner. Protection of cells by these drugs was not affected by pretreatment with indomethacin (10⁻⁵ mol/L) for 4 h. Removal of Na⁻, but not Ca²⁺, from the acidified medium totally abolished the inhibitory effect of EGF, but not that of sucralfate. Genistein (a tyrosine kinase inhibitor) apparently reduced the inhibitory effect of EGF. DNA synthesis by RGM1 cells did not increase when cells were incubated with EGF for 4 h. We conclude that both EGF and sucralfate protect RGM1 cells from acid- and pepsin-induced damage and that the mechanism of protection by EGF against acid-induced damage seems to be via activation of Na⁺/H⁺ exchangers.