橄榄—桥脑—小脑萎缩的研究进展

过去对橄榄 桥脑 小脑萎缩 (OPCA)的诊断 ,主要依据临床表现及病理改变 ,CT与MRI在临床广泛应用以来 ,尤其是MRI,能对OPCA作出较准确的诊断。近几年国外学者经遗传连锁分析确定此病基因位于 6p2 2 2 3 ,并成功地克隆了该基因 ,通过对OPCA患者作基因突变检测 ,可开展OPCA的基因诊断。本文对OPCA的临床特征、分型、影像学特征及基因定位的研究进展作一综述。     

交接性逸搏—心室夺获—反复心搏三联律1例

患者男 ,82岁。临床诊断 :肝硬化失代偿期。图示Ⅱ、Ｖ1导联。各导联可见延迟出现之ＱＲＳ波 ,时限 >0 12ｓ,其前无Ｐ(或Ｐ′)波 ,呈完全性右束支阻滞 (ＣＲＢＢＢ)图形 ,为交接性逸搏 (ＪＥ) ,每个ＪＥ后均伴有一窦性Ｐ -ＱＲＳ -Ｔ ,其ＱＲＳ波形态时限与ＪＥ相同。除Ⅱ导、Ｐ3-Ｒ间期为 0 19ｓ外 ,其余所有窦性ＰＲ间期均明显延长达 0 2 6ｓ ;且于该长ＰＲ心搏后均伴有逆行型Ｐ- -ＱＲＳ -Ｔ。Ｐ- 后ＱＲＳ形态时限与其它ＱＲＳ相同 ,形成“ＱＲＳ -Ｐ -ＱＲＳ -Ｐ- -ＱＲＳ -Ｔ”序列 ,重复出现形成三联律。心电图诊断 :窦缓、ＣＲＢ…     

Laurence—Moon—Biedl综合征一例报告

<正> 本病世界罕见。自Laurence—Moon(1866)报道以来,我国项坤三及王宗根(1983)分别共报告三例外,尚未发现国内文献有更多报遭。就笔者所见一例(注)报道如下: 患者。男,30岁,自幼发育差,弱智。10年前发现耳聋及视网膜色素变性,双眼白内障,1982年2月失明     

湖北省人群G—6—PD活性抽样调查

在湖北省６个县市抽样调查人群葡萄糖－６－磷酸脱氢酶（Ｇ－６－ＰＤ）缺乏情况，以例为疟防工作使用伯喹提供资料。共调查１６３１例中小学生，有显著缺乏，轻度缺乏及可疑缺乏者３３例，占调查总数的２．０２％。Ｇ－６－ＰＤ缺乏症在性别和民族间有明显差异。     

5—Aza—CdR在白血病治疗中的应用

在真核生物中 ,DNA甲基化作为 DNA合成后修饰的重要方式 ,可以影响基因的表达。DNA甲基化模式的改变 ,尤其是某些抑癌基因 (如 HIC1基因、CT基因、p1 5与 p1 6基因等 )局部甲基化水平的异常增高 ,在肿瘤的发生和发展过程中起到了不容忽视的作用。这一改变的原因 ,多数学者认为应归结于 DNA甲基转移酶 ( MTase)活性的增高。因此 ,抑制甲基转移酶活性以恢复抑癌基因的表达 ,可能干扰肿瘤的发生和发展过程。核苷酸类似物作为甲基转移酶抑制剂特别引起人们的关注。此类药物包括 5 -氮杂胞苷 ( 5 - Aza- CR)、5 -氮杂 - 2′-脱氧胞苷 ( …     

慢性乙型肝炎中医证型与IL—2、IL—10、IL—12、IFN—γ水平的关系初探

目的：探讨慢性乙型肝炎（以下简称慢乙肝）中医证型与血清白细胞介素－2（IL－2）、白细胞介素－10（IL－10）、白细胞介素－12（IL－12）、干扰素－γ（IFN－γ）含量的关系。方法：将50例慢乙肝患者按照中医辨证分型标准分为湿热中阻、肝郁脾虚、肝肾阴虚、瘀血阻络、脾肾阳虚5型。采用双抗体夹心ELISA方法检测血清IL－2、IL－10、IL－12、IFN－γ水平。同时与20例体检健康者的检测水平相比较。结果：除脾肾阳虚型的IL－10和瘀血阻络型的IL－12低于正常对照组外,其余的证型其检测结果均高于正常对照组,P＜0．05;中医辨证分型各组总体差异明显,P＜0．05）;中医证型各组间比较,湿热中阻、肝郁脾虚、瘀血阻铬及脾肾阳虚的IL－2差异明显,P＜0．05,IL－10在各组间无明显差异,肝郁脾虚的IL－12与湿热中阻和肝肾阴虚差异明显,P＜0．05）,肝郁脾虚的IFN－γ与肝肾阴虚、瘀血阻络、脾肾阳虚差异明显,P＜0．05。结论：慢乙肝细胞因子水平与其中医辨认分型有一定的相关性,可作为慢乙肝中医辨证分型的客观依据之一。     

104例高血压病Q—Td,J—Td分析

Devey等研究认为左心室肥厚患者Q-T离散度(Q-Td)明显增大。本文通过对104例有或无左室肥厚(LVH)的高血压患者的Q-Td、J-Td进行测定,探讨Q-Td、J-Td与高血压病LVH、高血压病分期、高血压病左室肥厚各肥厚部位及心功能损害程度的关系。 1 资料与方法 随机选择1998年1月～1999年2月符合WHO诊断标准的高血压病患者104例,男56例,女48例,年龄(62.72±11.89)岁,经心脏超声诊断LVH 60例,左室正常44例。高血压病按靶器官     

C—erbB—2与肺癌

本综述了Ｃ－ｅｒｂＢ－２与肺癌的关系，认为Ｃ－ｅｒｂＢ－２基因转录水平的上游调节在肺癌Ｐ１２５＾ｎｅｔ过表达中起重要作用，Ｐ１８５＾ｎｅｕ可做为肺癌分型及预后的可靠指标，Ｃ－ｅｒｂＢ－２与肺癌转移及多重耐药性有关，并对Ｃ－ｅｒｂＢ－２在肺癌诊断及治疗方面的应用前景做了介绍。     

慢性乙型肝炎血清TNF—α,IL—1B,IL—4和IL—6测定及意义

一般认为乙型病毒性肝炎的肝脏损害是由于免疫引起免疫损伤和免疫紊乱所致.为探讨一些重要细胞因子在慢性乙型肝炎(CHB)中的作用,本文对69例不同临床类型CHB患者血清联合进行TNF-α、IL-Lb、IL-2、IL-4和IL-6测定.现报告如下.     

比较血清标记物KL—6、SP—A、SP—D和MCP—1对间质性肺疾病的诊断意义

单性生殖细胞是指在缺少精子的情况下,卵子发育成胚胎的过程。在非人类的灵长目中此过程已有某种程度的研究,然而至今还未获得单性生殖胚胎干(ES)细胞系。人们也未能成功的获得整个鼠或牛的单性生殖个体,然而从双亲衍生的胚胎组织的单性生殖细胞的嵌合体已经繁殖稳定的后代。此处我们的研究证实了通过单性生殖衍生的灵长类多能干     

Effect of cis—9,trans—11—conjugated linoleic acid on cell cycle of gastric adenocarcinoma cell line（SGC—7901）

AIM: To determine the effect of cis -9, trans -11-conjugated linoleic acid (c9, t11-CLA) on the cell cycle of gastric cancer cells (SGC-7901) and its possible mechanism in inhibition cancer growth. METHODS: Using cell culture and immunocytochemical techniques, we examined the cell growth, DNA synthesis, expression of PCNA, cyclin A, B(1), D(1), p16(ink4a) and p21(cip/waf1) of SGC-7901 cells which were treated with various c9, t11-CLA concentrations (25, 50, 100 and 200 micromol.L(-1))of c 9, t 11-CLA for 24 and 48h, with a negative control (0.1% ethane). RESULTS: The cell growth and DNA synthesis of SGC-7901 cells were inhibited by c9, t11-CLA.SGC-7901 cells. Eight day after treatment with various concentrations of c9, t11-CLA mentioned above, the inhibition rates were 5.92%, 20.15%, 75.61% and 82.44%, respectively and inhibitory effect of c9, t11-CLA on DNA synthesis (except for 25 micromol.L, 24h) showed significantly less (3)H-TdR incorporation than that in the negative controls (P<0.05 and P<0.01). Immunocytochemical staining demonstrated that SGC-7901 cells preincubated in media supplemented with different c9, t11-CLA concentrations at various times significantly decreased the expressions of PCNA (the expression rates were 7.2-3.0%, 24h and 9.1-0.9% at 48h, respectively), Cyclin A (11.0-2.3%, 24h and 8.5-0.5%,48h), B(1) (4.8-1.8% at 24h and 5.5-0.6% at 48h)and D(1) (3.6-1.4% at 24h and 3.7%-0 at 48h) as compared with those in the negative controls(the expressions of PCNA, Cyclin A, B(1) and D(1) were 6.5% at 24h and 9.0% at 48h, 4.2% at 24h and 5.1% at 48h, 9.5% at 24h and 6.0% at 48h,respectively)(P<0.01), whereas the expressions of P16(ink4a) and P21(cip/waf1), cyclin-dependent kinases inhibitors(CDKI), were increased. CONCLUSION: The cell growth and proliferation of SGC-7901 cell is inhibited by c9, t11-CLA via blocking the cell cycle, with reduced expressions of cyclin A,B(1) and D(1) and enhanced expressions of CDKI(P16(ink4a) and p21(cip/waf1)).     

Inhibitory effects of c9, t11-conjugated linoleic acid on invasion of human gastric carcinoma cell line SGC-7901

AIM: To investigate the effect of c9, t1l-conjugated linoleic acid (c9, t11-CLA) on the invasion of human gastric carcinoma cell line and its possible mechanism of preventing metastasis.METHODS: Using reconstituted basement membrane invasion, chemotaxis, adhesion, PAGE substrate zymography and RT-PCR assays, we analyzed the abilities of invasion,direct migration, adhesion of intracellular matrix, as well as the activity of type IV collagenase and expression of tissue inhibitor of metalloproteinase (TIMP)-1 and TIMP-2 mRNA in SGC-7901 cells which were treated with gradually increased concentrations (25, 50, 100 and 200μmol/L) of c9,c11-CLA for 24 h.RESULTS: At the concentrations of 200μmol/L, 100μmol/L and 50μmol/L, c9,tll-CLA suppressed the invasion of SGC-7901 cells into the reconstituted basement membrane by 53.7 %, 40.9 % and 29.3 %, respectively, in comparison with the negative control. Only in the 200 μmol/L c9,tll-CLA group, the chemotaxis of SGC-7901 cells was inhibited by 16.0 % in comparision with the negative control. C9,tll-CLA also could inhibit the adhesion of SGC-7901 cells to laminin, fibronectin and Matrigel, increase the expression of TIMP-1 and TIMP-2 mRNA, and reduce type IV collegenase activities in the serum-free medium supernatant of SGC-7901 cells.CONCLUSION: c9,t11-C:LA can inhibit the invasion of SGC-7901 cells at multiple procedures in tumor metastasis cascade, which may be associated with the induction of TIMP-1 and TIMP-2 mRNA expression.     

Effects of c9,t11-conjugated linoleic acid on adhesion of human gastric carcinoma cell line SGC-7901

AIM: To investigate the effect of c9, t11-conjugated linoleic acid (c9,t11-CLA) on the adhesion of human gastric carcinoma cell line (SGC-7901).METHODS: SGC-7901 cells were at first treated with different concentrations (25, 50, 100, 200 μmol/L) of c9,t111-CLA and 1 mL/L ethanol (as a negative control) for 24 h.Using adhesion assay and Western blot, we investigated the ability of SGC-7901 cells to adhere to intracellular matrix and examined the expression of E-cadherin (ECD), α-catenin,intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) in these cells.RESULTS: The attachment rate to laminin of SGC-7901 cells treated with different concentrations of c9,t11-CLA (0,25, 50, 100, and 200 μmol/L) was 100.0&#177;3.3, 95.7&#177;4.0,89.2&#177;4.6, 87.9&#177;6.1, and 65.9&#177;5.8, respectively. The attachment rate to fibronectin was 100.0&#177;4.7, 96.8&#177;3.8,94.5&#177;4.1, 76.5&#177;4.3, and 61.8&#177;4.8, respectively. The attachment rate to Matrigel was 99.9&#177;6.6, 91.4&#177;6.8,85.5&#177;7.4, 79.3&#177;5.6, and 69.6&#177;5.1, respectively. Besides,c9,t11-CLA could increase the level of ECD and α-catenin,and decrease the level of ICAM-1 and VCAM-1 in SGC-7901 cells.CONCLUSION: c9, t11-CLA can reduce the adhesion of human gastric carcinoma cells to laminin, fibronectin and Matrigel. c9,t11-CLA can increase the level of ECD and α-catenin, and decrease the level of ICAM-1 and VCAM-1 in human gastric carcinoma cells.     

Inhibitory effects of c9, t11-conjugated linoleic acid on invasion of human gastric carcinoma cell line SGC-7901

AIM: To investigate the effect of c9, t11-conjugated linoleic acid (c9, t11-CLA) on the invasion of human gastric carcinoma cell line and its possible mechanism of preventing metastasis.METHODS: Using reconstituted basement membrane invasion, chemotaxis, adhesion, PAGE substrate zymography and RT-PCR assays, we analyzed the abilities of invasion,direct migration, adhesion of intracellular matrix, as well as the activity of type IV collagenase and expression of tissue inhibitor of metalloproteinase (TIMP)-1 and TIMP-2 mRNA in SGC-7901 cells which were treated with gradually increased concentrations (25, 50, 100 and 200 μmol/L) of c9, t11-CLA for 24 h.RESULTS: At the concentrations of 200 μmol/L, 100 μmol/L and 50 μmol/L, cg, t11-CLA suppressed the invasion of SGC7901 cells into the reconstituted basement membrane by 53.7%, 40.9% and 29.3%, respectively, in comparison with the negative control. Only in the 200 μmol/L c9,t11CLA group, the chemotaxis of SGC-7901 cells was inhibited by 16.0% in comparision with the negative control. cg, t11CLA also could inhibit the adhesion of SGC-7901 cells to laminin, fibronectin and Matrigel, increase the expression of TIMP-1 and TIMP-2 mRNA, and reduce type IV collagenase activities in the serum-free medium supernatant of SGC7901 cells.CONCLUSION: c9, t11-CLA can inhibit the invasion of SGC7901 cells at multiple procedures in tumor metastasis cascade, which may be associated with the induction of TIMP-1 and TIMP-2 mRNA expression.     

Roles of Fas signaling pathway in vitamin E succinateinduced apoptosis in human gastric cancer SGC—7901 cells

AIM: To investigate the roles of Fas signaling pathway in vitamin E succinate-induced apoptosis in human gastric cancer SGC-7901 cells. METHODS: Human gastric cancer SGC-7901 cells were treated with VES at 5, 10, 20 mg x L(-1), succinic acid and vitamin E as vehicle control and condition media only as untreated (UT) control. Apoptotic morphology was observed by DAPI staining. Western blot analysis was applied to measure the expression of Fas, FADD and caspase-8 proteins. After the cells were transiently transfected with Fas and FADD antisense oligonucleotides, respectively, caspase-8 activity was determined by flurometric method. RESULTS: The morphologically apoptotic changes were observed after VES treatment by DAPI staining. 23.7 % and 89.6 % apoptosis occurred after 24 h and 48 h of 20 mg x L(-1) VES treatment, respectively. The protein levels of Fas, FADD and caspase-8 were evidently increased in a dose-dependent manner after 24 h of VES treatment. The blockage of Fas by transfection with Fas antisense oligonucleotides obviously inhibited the expression of FADD protein. After SGC-7901 cells were transfected with Fas and FADD antisense oligonucleotides, caspase-8 activity was obviously decreased (P<0.01), whereas Fas blocked more than FADD. CONCLUSION: VES-induced apoptosis in human gastric cancer SGC-7901 cells involves Fas signaling pathway including the interaction of Fas, FADD and caspase-8.     

Therapeutic mechanism of ginkgo biloba exocarp polysaccharides on gastric cancer

AIM: To study the therapeutic mechanism of Ginkgo biloba exocarp polysaccharides (GBEP) on gastric cancer. METHODS: Thirty patients with gastric cancer were treated with oral GBEP capsules. The area of tumors was measured by electron gastroscope before and after treatment, then the inhibitory and effective rates were calculated. The ultrastructures of tumor cells were examined by transmissional electron microscope. Cell culture, MTT, flow cytometry were performed to observe proliferation, apoptosis and changes of relevant gene expression of human gastric cancer SGC-7901 cells. RESULTS: Compared with the statement before treatment, GBEP capsules could reduce the area of tumors, and the effective rate was 73.4%. Ultrastructural changes of the cells indicated that GBEP could induce apoptosis and differentiation in tumor cells of patients with gastric cancer. GBEP could inhibit the growth of human gastric cancer SGC-7901 cells following 24-72 h treatment in vitro at 10-320 mg/L, which was dose- and time-dependent. GBEP was able to elevate the apoptosis rate and expression of c-fos gene, but reduce the expression of c-myc and bcl-2 genes also in a dose-dependent manner. CONCLUSION: The therapeutic mechanism of GBEP on human gastric cancer may relate to its effects on the expression of c-myc, bcl-2 and c-fos genes, which can inhibit proliferation and induce apoptosis and differentiation of tumor cells.     

Apoptosis of human gastric adenocarcinoma cells induced by β-ionone

AIM:To investigate the effect of β-ionone on the growth and apoptosis of gastric adenocarcinoma cell line SGC-7901.METHODS: Using M-IT, fluorescence dye (Hoechst-33258),transmission electron microscopy and the TUNEL assay,we examined growth and apoptosis of SGC-7901 cells treated with β-ionone at various concentrations (i.e. 25, 50, 100 and 200μmol/L) for 24h,48h.RESULTS:The growth of SGC-7901 cells was inhibited by β-ionone. Seven days after treatment with β-ionone at four concentrations, the inhibition rates were 12.04%, 30.59%,78.25% and 94.15%, respectively. The IC50 value of β-ionone for SGC-7901 cells was estimated to be 89μmol/L.The apoptotic morphology was demonstrated in SGC-7901 cells treated with β-ionone by Hoechst-33258 staining and electron microscopy. Apoptosis was also shown in β-iononetreated SGC-7901 cells by the TUNEL assay.CONCLUSION:β-ionone can inhibit cell proliferation and induce apoptosis of SGC-7901 cells.However, the mechanism needs to be further investigated.     

RRR—α—tocopheryl succinate inhibits human gastr cancer SGC—7901 cell growth by inducing apoptos and DNA synthesis arrest

AIM: To investigate the effects of growth inhibition of human gastric cancer SGC-7901 cell with RRR-alpha-tocopheryl succinate (VES), a derivative of natural Vitamin E, via inducing apoptosis and DNA synthesis arrest. METHODS: Human gastric cancer SGC-7901 cells were regularly incubated in the presence of VES at 5, 10 and 20mg x L(-1) (VES was dissolved in absolute ethanol and diluted in RPMI 1640 complete condition media correspondingly to a final concentration of VES and 1 mL x L(-1) ethanol), succinic acid and ethanol equivalents as vehicle (VEH) control and condition media only as untreated (UT) control. Trypan blue dye exclusion analysis and MTT assay were applied to detect the cell proliferation. Cells were pulsed with 37kBq of tritiated thymidine and (3H) TdR uptake was measured to observe DNA synthesis. Apoptotic morphology was observed by electron microscopy and DAPI staining. Flow cytometry and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay were performed to detect VES-triggered apoptosis.RESULTS: VES inhibited SGC-7901 cell growth in a dose-dependent manner. The growth curve showed suppression by 24.7%, 49.2% and 68.7% following 24h of VES treatment at 5, 10 and 20 mg x L(-1), respectively, similar to the findings from MTT assay. DNA synthesis was evidently reduced by 35%, 45% and 98% after 24h VES treatment at 20mg x L(-1) and 48 h at 10 and 20mg x L(-1), respectively. VES induced SGC-7901 cells to undergo apoptosis with typically apoptotic characteristics, including morphological changes of chromatin condensation, chromatin crescent formation/margination, nucleus fragmentation and apoptotic body formation, typical apoptotic sub-G1 peak by flow cytometry and increase of apoptotic cells by TUNEL assay in which 90% of cells underwent apoptosis after 48 h of VES treatment at 20 mg x L(-1). CONCLUSION: VES can inhibit human gastric cancer SGC-7901 cell growth by inducing apoptosis and DNA synthesis arrest. Inhibition of SGC-7901 cell growth by VES is dose- and time-dependent. Therefore VES can function as a potent chemotherapeutic agent against human gastric carcinogenesis.     

Apoptosis of human gastric adenocarcinoma cells induced by β-ionone

AIM: To investigate the effect of β-ionone on the growthMETHODS: Using MTT, fluorescence dye (Hoechst-33258),transmission electron microscopy and the TUNEL assay, we examined growth and apoptosis of SGC-7901 cells treated with β-ionone at various concentrations (i.e. 25, 50, 100 and 200 μmol/L) for 24 h, 48 h.RESULTS: The growth of SGC-7901 cells was inhibited by β-ionone, Seven days after treatment with β-ionone at four concentrations, the inhibition rates were 12.04%, 30.59%,78.25% and 94.15%, respectively. The IC50 value of β-ionone for SGC-7901 cells was estimated to be 89 μmol/L. The apoptotic morphology was demonstrated in SGC-7901 cells treated with β-ionone by Hoechst-33258 staining and electron microscopy. Apoptosis was also shown in β-iononetreated SGC-7901 cells by the TUNEL assay.CONCLUSION: β-ionone can inhibit cell proliferation and induce apoptosis of SGC-7901 cells. However, the mechanism needs to be further investigated.     

Tributyrin inhibits human gastric cancer SGC-7901 cell growth by inducing apoptosis and DNA synthesis arrest

AIM: To evaluate the effects of tributyrin, a pro-drug of natural butyrate and a neutral short-chain fatty acid triglyceride, on the growth inhibition of human gastric cancer SGC-7901 cell.METHODS: Human gastric cancer SGC-7901 cells were 24-72 h. MTT assay was applied to detect the cell proliferation.[3H]-TdR uptake was measured to determine DNA synthesis.Apoptotic morphology was observed by electron microscopy and Hoechst-33258 staining. Flow cytometry and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay were performed to detect tributyrin-triggered apoptosis. The expressions of PARP, Bcl-2 and Bax were examined by Western blot assay.RESULTS: Tributyrin could initiate growth inhibition of SGC7901 cell in a dose- and time-dependent manner. [3H]-TdR uptake by SGC-7901 cells was reduced to 33.6% after 48 h control (P＜0.05). Apoptotic morphology was detected by TUNEL assay. Flow cytometry revealed that tributyrin could induce apoptosis of SGC-7901 cells in dose-dependent manner. After 48 hours incubation with tributyrin at 2 mmol.L-1, the level of Bcl-2 protein was lowered, and the level of Bax protein was increased in SGC-7901, accompanied by PARP cleavage.CONCLUSION: Tributyrin could inhibit the growth of gastric cancer cells effectively in vitro by inhibiting DNA synthesis and inducing apoptosis, which was associated with the downregulated Bcl-2 expression and the up-regulated Bax expression. Therefore, tributyrin might be a promising chemopreventive and chemotherapeutic agent against human gastric carcinogenesis.