Eicosanoid pathway expression in bovine endometrial epithelial and stromal cells in response to lipopolysaccharide,interleukin 1 beta,and tumor necrosis factor alpha

During endometrial inflammation, bovine endometrium responds by increasing the production of pro-inflammatory mediators, such as interleukin 1 beta (IL-1β), tumor necrosis factor alpha (TNFα), and eicosanoids. The purpose of this study was to establish and characterize an in vitro model of endometrial inflammation using bovine endometrial epithelial (bEEL) and stromal (bCSC) cell lines. We evaluated the effects of the infectious agent (bacterial lipopolysaccharide; LPS) and pro-inflammatory mediators (IL-1β and TNFα) on eicosanoid biosynthesis pathway gene expression and production by bEEL and bCSC cells. Based on concentration-response experiments, the optimal concentrations for responses were 1?μg/mL LPS, 10?ng/mL IL-1β and 50?ng/mL TNFα. Real-time PCR results show that there was an upregulation of relative mRNA expression of PTGS2 when bEEL and bCSC were treated with LPS, IL-1β and TNFα. An increase in PTGES3 expression was observed when bEEL cells were treated with LPS and IL-1β and PTGES2 when treated with IL-1β. In bCSC cells, FAAH relative mRNA was decreased upon treatments. Rate of production of PGE₂, PGF_2α, PGE₂-EA and PGF_2α-EA were also determined using liquid chromatography tandem mass spectrometry. Our results show that eicosanoid production was increased in both cell lines in response to LPS, IL-1β, and TNFα. We suggest that the characteristics of bEEL and bCSC cell lines mimic the physiological responses found in mammals with endometrial infection, making them excellent in vitro models for intrauterine environment studies.     

Premature progesterone rise in ART-cycles

Premature rise of progesterone during the late follicular phase in stimulated IVF cycles is a frequent event and its effect on the endometrial receptivity and on the ART (Assisted Reproductive Technique) – outcome has become a matter of intense debate and research. An emerging body of evidence demonstrates that premature progesterone rise does have a negative impact on the outcome of the ART-success. Until now, the exact cause of progesterone elevation is not fully clear, however lately published studies points to the fact, that premature progesterone elevation might be caused by enhanced FSH stimulation. The impact of elevated peripheral progesterone levels seems to be mainly on the endometrium and the window of implantation, leading to an asynchrony between the endometrium and the developing embryo. Hence, new data show additional an influence on the embryo quality. This review aims to summarize the up-to-date knowledge on the causes of premature progesterone rise during hormonal stimulation, on its influence on endometrial receptivity and embryo quality, on the impact on pregnancy and live birth rates as well as on the possible strategies to prevent this event or to deal with premature progesterone elevation in case it could not be avoided.     

Upregulation of miR-582-5p regulates cell proliferation and apoptosis by targeting AKT3 in human endometrial carcinoma

The human endometrial carcinoma is one of the most common female malignancies, and there is an urgent requirement to explore new therapeutic strategies. There is accumulating evidence that microRNAs (miRNAs) can serve as potential diagnostic and prognostic biomarkers for various types of cancer, but the significance of miR-582-5p still remains largely unknown in the endometrial carcinoma. The aims of this study were to understand and identify the influence of miR-582-5p on the proliferation and apoptosis of human endometrial carcinoma and its relevant mechanism. First, quantitative real-time PCR (qRT-PCR) was used to detect miR-582-5p and AKT3 expression in human tissue samples and cells. Then, CyQuant assay and 2D colony assay were employed to evaluate cell proliferation. Western blotting was used to determine protein expression. Subsequently, the luciferase reporter assay was used to identify the target of miR-582-5p. Finally, Annexin V assay was used to detect cell apoptosis. We found that miR-582-5p expression was significantly decreased in human endometrial carcinoma tissues, and miR-582-5p upregulation in human endometrial carcinoma cells inhibit cell proliferation and promote apoptosis. Moreover, AKT3 was validated as a target of miR-582-5p and AKT3 expression was inversely correlated with miR-582-5p expression. Besides, AKT3 upregulation efficiently abrogates the effect of miR-582-5p on the cells. These results demonstrated that miR-582-5p regulates cell proliferation and apoptosis in human endometrial carcinoma via AKT3. Thus, miR-582-5p represents a potential therapeutic target in human endometrial carcinoma meriting further investigation.     

CXCR4和NF-κB在子宫内膜癌中的表达及其临床意义

目的:检测CXCR4和NF-κB在子宫内膜癌中的表达并探讨其在肿瘤发生发展中的作用机制。方法:用免疫组织化学SP法测定不同子宫内膜组织中CXCR4和NF-κB的蛋白质表达情况,并分析两者表达的相关性,所选标本包括20例正常子宫内膜蜡块、30例子宫内膜不典型增生石蜡标本、60例子宫内膜癌。结果:CXCR4的阳性表达率在子宫内膜癌中为73.33%、在不典型增生子宫内膜中为43.33%,在正常子宫内膜中为25.00%;NF-κB在子宫内膜癌、不典型增生子宫内膜和正常子宫内膜的阳性表达率依次为:63.33%、36.67%、15.00%,差异均具有统计学意义(P0.05)。CXCR4和NF-κB两个因子与淋巴结有无转移、年龄、肌层浸润情况无相关性,但与癌组织分化级别相关。两个因子在子宫内膜癌中的表达具有明显的相关性(r=0.341,P=0.008)。结论:CXCR4和NF-κB在子宫内膜癌组中的阳性表达率明显升高,且两者成正相关,两个因子在诱发子宫内膜癌的发生中可能起协同作用。     

经阴道超声与宫腔镜对子宫内膜病变患者的诊断价值比较研究

目的:探讨经阴道超声与宫腔镜检查诊断子宫内膜病变的临床价值,为临床诊断子宫内膜病变提供理论依据。方法:选取2011年3月-2014年3月间我院收治的158例疑似子宫内膜病变患者,分别采用经阴道超声和宫腔镜进行检查,并以病理诊断结果为"金标准",比较两种检查方法的诊断价值。结果:病理检查结果中,143例患者被确诊为子宫内膜病变,其中子宫内膜增生23例(16.08%),子宫内膜息肉31例(21.68%),子宫粘膜下肌瘤24例(16.78%),子宫内膜癌19例(13.29%),慢性非特异性子宫内膜炎46例(32.17%)。宫腔镜对子宫内膜病变诊断的准确率为94.41%,高于阴道超声的81.12%,差异有统计学意义(P0.05),其中阴道超声和宫腔镜对子宫粘膜下肌瘤、子宫内膜癌诊断的准确率比较差异无统计学意义(P0.05),阴道超声对子宫内膜增生、子宫内膜息肉及慢性非特异性子宫内膜炎的诊断准确率均较宫腔镜降低,差异有统计学意义(P0.05)。阴道超声对子宫内膜病变诊断的特异度较宫腔镜更低(P0.05),但两者灵敏度、AUC比较差异无统计学意义(P0.05)。结论:经阴道超声诊断子宫内膜病变简单、有效,而宫腔镜诊断子宫内膜病变具有准确率以及特异度较高的特点。     

子宫内膜癌组织中GDF-15和p-mTOR蛋白的表达及临床意义

目的:研究子宫内膜癌组织中生长分化因子15(GDF-15)和磷酸化哺乳动物雷帕霉素靶蛋白(p-mTOR)的表达,并分析其临床意义,为临床治疗提供依据。方法:选取2011年1月到2016年2月我院子宫内膜癌组织75例为研究组,另选取同期正常子宫内膜组织75例为对照组,应用免疫组化法检测GDF-15和p-mTOR蛋白的表达。结果:研究组GDF-15和p-mTOR蛋白的表达阳性率显著高于对照组,比较差异具有统计学意义(P0.05);子宫内膜癌分期Ⅲ-Ⅳ期、淋巴结转移者、病理分级G2+G3、肌层浸润深度≥1/2的GDF-15和p-mTOR蛋白的表达阳性率均较高(P0.05);子宫内膜癌组织GDF-15与p-mTOR蛋白表达呈正相关关系(P0.05)。结论:子宫内膜癌组织中GDF-15与p-mTOR蛋白表达升高,且与肿瘤转移、临床分期、肌层浸润深度有关。     

来曲唑片联合放疗对耐药性子宫内膜癌患者血清VEGF, IL-6及肿瘤标志物水平的影响

目的:探讨来曲唑片联合放疗对耐药性子宫内膜癌患者血清VEGF、IL-6及肿瘤标志物水平的影响及临床疗效。方法:选取前来我院就诊的已产生耐药性的术后子宫内膜癌患者68例,随机分为对照组和治疗组,每组34例。对照组在术后联合放射疗法进行治疗;治疗组在对照组基础上采用芙瑞来曲唑片治疗。比较两组患者治疗前后血清VEGF、IL-6、CA125、HE4水平及ROMA指数的变化,两组患者临床疗效及生存率。结果:对照组总有效率及八年后生存率均显著低于治疗组(P0.05)。治疗后,两组患者血清VEGF、IL-6、CA125、HE4水平及ROMA指数均较治疗前显著降低(P0.05);与对照组比较,治疗组患者血清VEGF、IL-6、CA125、HE4水平及ROMA指数较低(P0.05)。结论:来曲唑片联合放疗对耐药性子宫内膜癌术后患者的治疗效果良好,可能与其降低患者血清VEGF、IL-6、CA125及HE4水平有关。     

多西紫杉醇联合卡铂治疗老年子宫内膜癌的疗效及安全性

目的:探讨多西紫杉醇与卡铂联合化疗在老年子宫内膜癌患者中的疗效及安全性。方法:选择2010年1月至2016年1月我院收治的子宫内膜癌患者78例作为研究对象,其中年龄60岁的患者42例纳入非老年组,年龄≥60岁的患者36例纳入老年组,均给予多西紫杉醇与卡铂联合化疗。对两组患者一般情况、化疗实施情况、临床疗效以及毒副反应进行观察与比较。结果:两组患者组织学分型有明显差异(P0.05),其他一般资料无显著差别(P0.05)。老年组患者采用低剂量完成化疗的比例明显高于非老年组,差异有统计学意义(P0.05),化疗周期及中断率无显著差异(P0.05)。两组患者临床疗效、血液系统毒副反应及消化系统毒副反应发生率均差异不显著(P0.05)。结论:多西紫杉醇与卡铂联合化疗在老年子宫内膜癌患者中治疗效果与非老年患者类似,安全性尚可,值得临床推广应用。     

Calcification process dynamics in coral primary polyps as observed using a calcein incubation method

Calcification processes are largely unknown in scleractinian corals. In this study, live confocal imaging was used to elucidate the spatiotemporal dynamics of the calcification process in aposymbiotic primary polyps of the coral species Acropora digitifera. The fluorophore calcein was used as a calcium deposition marker and a visible indicator of extracellular fluid distribution at the tissue-skeleton interface (subcalicoblastic medium, SCM) in primary polyp tissues. Under continuous incubation in calcein-containing seawater, initial crystallization and skeletal growth were visualized among the calicoblastic cells in live primary polyp tissues. Additionally, the distribution of calcein-stained SCM and contraction movements of the pockets of SCM were captured at intervals of a few minutes. Our experimental system provided several new insights into coral calcification, particularly as a first step in monitoring the relationship between cellular dynamics and calcification in vivo. Our study suggests that coral calcification initiates at intercellular spaces, a finding that may contribute to the general understanding of coral calcification processes.     

Estrogens, phytoestrogens and colorectal neoproliferative lesions

Epidemiological and experimental studies suggest a protective role of estrogens against colorectal cancer. This effect seems to be mediated by their binding to estrogen receptor beta (ER-beta), one of the two estrogen receptors with high affinity for these hormones. Very recently, the demonstration of an involvement of ER-beta in the development of adenomatous polyps of the colon has also been documented, suggesting the use of selective ER-beta agonists in primary colorectal cancer prevention. Phytoestrogens are plant-derived compounds that structurally and functionally act as estrogen-agonists in mammals. They are characterized by a higher binding affinity to ER-beta as compared to estrogen receptor alpha (ER-alpha), the other estrogen receptor subtype. These biological characteristics explain why the administration of phytoestrogens does not produce the classical side effects associated to estrogen administration (cerebro- and cardio-vascular accidents, higher incidence of endometrial and breast cancer) and makes these substances ideal candidates for the prevention of colorectal cancer.