Overexpression of ETS-1 is associated with malignan＇ biological features of prostate cancer

E26 transformation-specific-1 （ETS-1）, an ETS family transcription factor, has been reported to play an important role in a variety of physiological and pathological processes, but clinical implications of ETS-1 expression in prostate cancer （PCa）, particularly high-risk cases, including response to androgen-deprivation therapy （ADT） have yet to be elucidated. We examined the expression of ETS- 1 using immunohistochemical staining of paraffin-embedded prostate carcinoma tissue obtained by needle biopsy from 69 mostly advanced PCa patients. ETS-1 expression was compared with the clinicopathological characteristics of the 69 patients, including 25 who underwent ADT as a primary treatment. As a result, PCa patients with higher expression of ETS-1 were significantly more likely to be of high stage and high Gleason score （P〈O.05）. There was no significant association between ETS-1 expression and the initial prostate-specific antigen （PSA） level. In the 25 patients treated by ADT, the staining score for ETS-1 was significantly associated with rapid development of castration-resistant disease within 24 months （P〈O.05）, whereas the Gleason score and PSA level were not. In conclusion, increased ETS-1 expression was associated with a higher stage, higher Gleason score and shorter time to castration-resistant progression. These data suggest that immunostaining for ETS-1 could be a molecular marker for predicting a poor clinical outcome for PCa patients, oarticularlv those with hi^h-risk disease.

α-Vitamin E derivative, RRR-α-tocopheryloxybutyric acid inhibits the proliferation of prostate cancer cells

Aim： To investigate the activity of RRR-α-tocopheryloxybutyric acid （TOB）, an ether analog of RRR-α-tocopheryl succinate （VES）, in prostate cancer cells. Methods： VES and TOB were used to treat prostate cancer LNCaP, PC3, and 22Rvl cells and primary-cultured prostate fibroblasts. The proliferation rates were determined by MTT assay, the cell viabilities were determined by trypan blue exclusion assay, and the cell deaths were evaluated by using Cell Death Detection ELISA kit. The protein expression levels were determined by Western blot analysis. Results： The MTT growth assay demonstrated that TOB could effectively suppress the proliferation of prostate cancer cells, but not normal prostate fibroblasts. Mechanism dissections revealed that TOB reduced cell viability and induced apoptosis in prostate cancer cells similar to VES. In addition, both TOB and VES suppressed prostate-specific antigen （PSA） at the transcriptional level leading to reduced PSA protein expression. Furthermore, vitamin D receptor （VDR） expression increased after the addition of TOB. Conclusion： Our data suggests that the VES derivative, TOB, is effective in inhibiting prostate cancer cell proliferation, suggesting that TOB could be used for both chemopreventive and chemotherapeutic purposes in the future.

Immunoscreening of Alpha-Tocopherol in Breast, Prostate Cancers and in Gestational Choriocarcinoma Tissues

Background: Many literature reviews report vitamin E supplementation as a benefit chemopreventive and adjuvant therapy in breast and prostate cancers. We investigated in the present work, alpha-tocopherol (α-T) expression (the current active form of vitamin E) from tissues of Congolese patients neither smokers nor alcohol drinkers and without intake antioxidant vitamins supplement. Methods: α-T was analysed in one normal placenta of nine weeks of gestation and in nineteen cancerous tissues, including seven breast cancers, six prostate cancers, and six gestational choriocarcinomas. The study was performed by immunohistochemistry method after diagnosis confirmation by histological analysis. Results: α-T staining in membrane cells and collagen fibers presented a moderate expression in healthy sections of tissues (positive control), but the labelling was strong in breast, prostate adenocarcinomas, and in choriocarcinomas. Conclusion: Tumors immunohistochemistry of α-tocopherol in breast, prostate cancers and in choriocarcinoma show elevated immunostaining suggesting a probable oncogenic effect of the micronutrient.

Presence of G84E Allelic Heterogeneity of the European Prostate Cancer SNP Mutation of HOX13B-G84E Associated with the European R-Haplogroup of Y-Chromosome and Absence of Gene Flow into Moroccans Patients

SNP mutations in the HOXB13 gene associated with prostate cancer were determined in Moroccans prostate cancer patients (PCa). All PCa SNP mutations were new and belong to the SNP point-mutations located on the stop codon of HOXB13 exon 1 and 2 located in chromosome 17. The five mutations and their frequencies were as follows: rs1197613952 (12%), rs1597934612 (4%), rs1597933874 (4%), rs1597933837 (4%) and rs867793282 (4%). The European HOXB13-G84E (rs138213197) PCa mutation was not detected among Moroccan patients. The Y-chromosome genealogical haplotypes of the Western European (R1b1b2-M2G9) and the Eastern European (R191a-M-17) were not observed in Moroccans PCa patients. The patients have their own haplotypes E1b1 and J with a frequency of 55 and 35%, respectively. The results of the SNP mutations in the HOXB13, the absence of the HOXB13-G84E of the European in the Moroccans PCa patients, the absence of the European-lineage haplogroups (R1a1a-M17 and R1b1b2-M269) and the presence of E1b1b and J in Moroccans PCa patients would clearly indicate the absence of gene flow from European to Moroccans gene pool.

5-70 MicroRNA-16-5p Enhances Radiosensitivity through Modulating Cyclin D1/E1-pRb-E2F1 Pathway in Prostate Cancer Cells.

Recently, miRNAs have been recognized as an important regulator in cellular ionizing radiation (IR) responsesand closely correlated with radiosensitivity in many cancers, suggesting that miRNAs might offer new therapeutic possibilities in radiotherapy[1].

Reduced expression of α-tocopherol-associated protein is associated with tumor cell proliferation and the-increased risk of prostate cancer recurrence

Aim： To examine the impact and prognostic significance of α-tocopherol associated protein （TAP） expression in a series of prostate cancer patients. Methods： Tissues from 87 patients underwent radical prostatectomy were examined for TAP expression by immunohistochemistry. The relationships of the staining results, the clinic pathological characteristics and the recurrence times were analyzed. Results： Compared with the adjacent areas of normal and benign glands, immunoreactivity of TAP was reduced in areas of prostate cancer. A lower TAP-positive cell number per mm^2 of the largest cancer area （defined as TAP-PN） was associated with higher clinical stage （r = -0.248, P = 0.0322）. Inverse associations were found among the TAP-PN and positive lymph nodes （r = -0.231, P = 0.0325）, preoperative prostatespecific antigen （PSA） levels （r = -0.423, P = 0.0043）, tumor size （r = -0.315, P = 0.0210） and elevated tumor cell proliferation, which was indicated by the staining of Ki-67 （r = -0.308, P = 0.0026）. TAP-PN was a significant predictor of recurrence univariately （P = 0.0006）, as well as multivariately, adjusted for known markers including preoperative PSA, clinical stage, Gleason score, surgical margin, extra-prostatic extension, seminal vesicle invasion and lymph node metastasis （P = 0.0012）. Conclusion： Reduced expression of TAP was associated with the cell proliferation status of prostate cancer, adverse pathological parameters and the increased risk of recurrence.

RNase L Variants Do Not Appear to Impact on Clinical Features of Sporadic Prostate Cancer Patients

Introduction: Prostate cancer is the most common non-cutaneous male cancers, contributing to significant mortality rates globally. Mutations of RNase L, an enzyme involved in inflammatory and immunological pathways, have been speculated to predispose to cancer. This study assesses three different mutations of the RNase L gene in Irish prostate cancer patients, including one linked with general cancer susceptibility never investigated before in prostate cancer (rs3738579), and reports on links with aggressive cancer. Methods: 134 patients had their RNase L mutation status determined by polymerase chain reaction (PCR) of serum DNA. Complementary clinical details for each patient are statistically analysed. Results: No link to age of diagnosis, high grade disease or prostate specific antigen (PSA) level at diagnosis was demonstrated with any of the studied single nucleotide polymorphisms (SNP). The SNP variation was consistent with that of published international series. Conclusion: SNP genotypic frequencies in Ireland are consistent with international findings. The studied RNase L mutations including rs3738579 do not appear to have a significant impact on our patient population.

A variety of markers combined use of clinical significance for diagnosis of prostate cancer

Objective:To explore the combined application of multiple markers for diagnosis of prostate cancer.Methods:To choose the hospital in September, 2015 to September 2012, initially determined both by serum PSA test for prostate cancer patients 117 cases, for patients with confirmed will be divided into three groups (39 cases further examination, compared with the pathological diagnosis of three groups of patients with prostate cancer diagnosis accuracy. Results: The detection rate in group A patients compared with the pathological diagnosis coincidence rate was 77.2%, B group was 90.3%, and 98.2% of group C, A, B two groups were lower in group C, group A and group B was higher than that that P504s inspection diagnosis rate is higher than about, CK34 beta E12 at 11:45, joint detection and diagnosis rate is highest. Three groups of patients were compared with difference had statistical significance . A group of 13 cases of benign specimen, 10 cases were negative, false positive in 3, coincidence rate was 76.9%, B group of 12 cases of benign specimens, the negative in 11 cases, false positives in 1 case, the coincidence rate is 91.7%, group C of 11 cases of benign specimens, negative in 11 cases, false positive 0 cases, coincidence rate was 100%. Combined detection of false positive diagnosis rate was lower than that in group A, B two patients, three groups of patients were compared with difference had statistical significance. Group A in 26 cases of prostate cancer, positive 22 cases, 4 cases were missed diagnosis coincidence rate was 84.6%. Group B in 27 cases of prostate cancer, positive 25 cases, 2 cases of misdiagnosis, the coincidence rate is 92.6%, group C in 27 cases of prostate cancer, 26 patients, positive, 1 case of misdiagnosis, the coincidence rate was 96.3%. Three groups of patients were compared with difference had statistical significance.Conclusion: Combination of P504s (AMACR), basal cell specific markers (about and CK34 beta E12 at 11:45) detection diagnosis can improve the early diagnostic rate of prostate cancer, have important significance on clinical.

Antibody-Cytokeratin Marker 34βE12 in Prostate Cancer Detection

Introduction:The histological diagnosis of prostate cancer is commonly based on morphological patterns.The presence of malignant tissue mixed with benign tissue,or the presence of carcinoma that mimics benignity may generate difficulty in the diagnostic elucidation.Therefore,the application of immunohistochemistry contributes its diagnostic value.Objectives:To evaluate the 34βE12 marker in the detection of adenocarcinoma(ADn),atypical small acinar proliferation(ASAp),regular prostatic tissue(RPT)and regular prostatic tissue alternated by atrophy spotlights(RPTa)in transrectal biopsy guided by ultrasonography of patients with suspected prostate cancer.Method:Analysis of 34 patients who underwent ultrasound-guided transrectal biopsy with subsequent analysis by H&E staining and 34βE12 labeling for elucidation of neoplasms or diseased tissues with doubtful diagnosis.Results:The marker 34βE12 showed negativity in 100%of the neoplasms ADn,positivity in 100%of the benign prostatic tissues(RPT and RPTa);the patients with ASAp presented positivity(20%)and negativity(80%).The chi-square test(χ2)showed that there is an association(χ2=29.55 and p<0.0001)between the groups,that is,the 34βE12 marker has a significant value(p<0.0001)in the elucidation of patients with prostatic neoplasia and benign prostatic tissues.Discussion and Conclusion:With the early screening of prostate cancer in the modern era,pathologists have become increasingly challenged to diagnose small outbreaks of cancer when only a few atypical glands are present in transrectal biopsy-guided ultrasonography.The 34βE12 marker becomes an important tool in elucidating diagnoses such as ADn and ASAp.

Evaluation of immunogenicity elicited from two DNA vaccine candidates that expresses the prM and E genes of the dengue-3 virus

In this work, we report the evaluation of two DNA vaccines against dengue-3 virus (DENV-3). The first construction, called pVAC3DEN3, was engineered inserting the pre-membrane (prM) and envelope (E) gene of DENV-3 truncated with a restriction site between them, as previously described. The second construction was developed cloning the full gene sequence of prM and E from DENV-3 virus in pCI plasmid for mammalian expression and was denominated pVAC1WDEN3. The results showed that both constructions were capable of expressing the prM and E proteins, as demonstrated by ELISA and immunoblotting detection in cell culture transfected with the plasmids. After positive “in vitro” results, the vaccine candidates were used to immunize BALB/c mice and the elicited response was investigated. After immunization by intramuscular inoculation with three doses of each vaccinal clone the animals were sacrificed, the cytokine levels and T cell response were analyzed in the spleens, after three days of culture with stimulus, our analysis showed that the two constructions elicited T cell responses mea- sured by BrdU incorporation assay and high levels of IFN-γ, detected in the supernatant of the cultures. Moreover, both constructions induced detectable titers of neutralizing antibodies in mice. And finally the survival rate of the immunized animals after intracerebral challenge was analyzed, showing a better result in the pVAC3DEN3 group with an 80% survival compared with a 50% survival of the pVAC1 WDEN3. Thus, these data showed that our two constructions were able to induce specific immune response and protects mice against a lethal challenge with DENV-3, and these vaccine candidates can be employed to develop a viable dengue vaccine.

Oncogene goosecoid is transcriptionally regulated by E2F1 and correlates with disease progression in prostate cancer

Background:Although some well-established oncogenes are involved in cancer initiation and progression such as prostate cancer(PCa),the long tail of cancer genes remains to be defined.Goosecoid(GSC)has been implicated in cancer development.However,the comprehensive biological role of GSC in pan-cancer,specifically in PCa,remains unexplored.The aim of this study was to investigate the role of GSC in PCa development.Methods:We performed a systematic bioinformatics exploration of GSC using datasets from The Cancer Genome Atlas,Genotype-Tissue Expression,Gene Expression Omnibus,German Cancer Research Center,and our in-house cohorts.First,we evaluated the expression of GSC and its association with patient prognosis,and identified GSC-relevant genetic alterations in cancers.Further,we focused on the clinical characterization and prognostic analysis of GSC in PCa.To understand the transcriptional regulation of GSC by E2F transcription factor 1(E2F1),we performed chromatin immunoprecipitation quantitative polymerase chain reaction(qPCR).Functional experiments were conducted to validate the effect of GSC on the tumor cellular phenotype and sensitivity to trametinib.Results:GSC expression was elevated in various tumors and significantly correlated with patient prognosis.The alterations of GSC contribute to the progression of various tumors especially in PCa.Patients with PCa and high GSC expression exhibited worse progression-free survival and biochemical recurrence outcomes.Further,GSC upregulation in patients with PCa was mostly accompanied with higher Gleason score,advanced tumor stage,lymph node metastasis,and elevated prostate-specific antigen(PSA)levels.Mechanistically,the transcription factor,E2F1,stimulates GSC by binding to its promoter region.Detailed experiments further demonstrated that GSC acted as an oncogene and influenced the response of PCa cells to trametinib treatment.Conclusions:GSC was highly overexpressed and strongly correlated with patient prognosis in PCa.We found that GSC,regulated by E2F1,acted as an oncogene and impeded the therapeutic efficacy of trametinib in PCa.

Redox responsive polymeric nanoparticles enhance the efficacy of cyclin dependent kinase 7 inhibitor for enhanced treatment of prostate cancer

Traditional therapies such as surgery and endocrine therapy no longer meet the clinical needs in prostate cancer treatment,and more effective treatments are urgently required.Recent studies have reported that targeted inhibition of the transcription factor cyclin dependent kinase 7(CDK7)could effectively suppress prostate cancer progression.However,the toxicity of CDK7 inhibitors such as THZ1 is the main limitation of the clinical application.In this work,we synthesized Cys8E(C8E)nanoparticles(NPs)loaded with THZ1(C8E@THZ1),a novel GSH-targeting and stimuli-responsive nano-delivery platform,and investigated its anti-tumor potential and biosafety properties.In vitro,C8E@THZ1 potently inhibited the proliferation and promoted the apoptosis of prostate cancer cells.On tumor-bearing mice,C8E@THZ1 inhibited tumors by up to 85%,while the damage of THZ1 to liver function was effectively avoided.These results confirmed that inhibition of CDK7 can effectively block the progression of prostate cancer,and that Cys8E NPs is a highly prospective delivery platform to promote the clinical application of CDK7 inhibitors.

基于比亚迪e5 CAN线故障分析研究

文章主要对比亚迪e5 CAN线故障进行分析研究,主要对电池子网、电机控制器动力网、BMC动力网和DC-DC动力网的CAN线故障进行检测分析,通过采用电脑诊断仪读取故障码、数据流等方式确定故障部位,使用数字万用表检测电压及电阻数据方式来排除CAN线故障,最后通过电脑诊断仪及仪表显示方式验证故障是否清除。

27-Hydroxycholesterol/liver X receptor/apolipoprotein E mediates zearalenone-induced intestinal immunosuppression:A key target potentially linking zearalenone and cancer

Zearalenone(ZEN)is a mycotoxin that extensively contaminates food and feed,posing a significant threat to public health.However,the mechanisms behind ZEN-induced intestinal immunotoxicity remain unclear.In this study,Sprague-Dawley(SD)rats were exposed to ZEN at a dosage of 5 mg/kg/day b.w.for a duration of 14 days.The results demonstrated that ZEN exposure led to notable pathological alterations and immunosuppression within the intestine.Furthermore,ZEN exposure caused a significant reduction in the levels of apolipoprotein E(ApoE)and liver X receptor(LXR)(P<0.05).Conversely,it upregulated the levels of myeloid-derived suppressor cells(MDSCs)markers(P<0.05)and decreased the presence of 27-hydroxycholesterol(27-HC)in the intestine(P<0.05).It was observed that ApoE or LXR agonists were able to mitigate the immunosuppressive effects induced by ZEN.Additionally,a bioinformatics analysis highlighted that the downregulation of ApoE might elevate the susceptibility to colorectal,breast,and lung cancers.These findings underscore the crucial role of the 27-HC/LXR/ApoE axis disruption in ZEN-induced MDSCs proliferation and subsequent inhibition of T lymphocyte activation within the rat intestine.Notably,ApoE may emerge as a pivotal target linking ZEN exposure to cancer development.

Analysis of the potential biological value of pyruvate dehydrogenase E1 subunitβin human cancer

BACKGROUND The pyruvate dehydrogenase E1 subunitβ(PDHB)gene which regulates energy metabolism is located in mitochondria.However,few studies have elucidated the role and mechanism of PDHB in different cancers.AIM To comprehensive pan-cancer analysis of PDHB was performed based on bioinformatics approaches to explore its tumor diagnostic and prognostic value and tumor immune relevance in cancer.In vitro experiments were performed to examine the biological regulation of PDHB in liver cancer.METHODS Pan-cancer data related to PDHB were obtained from the Cancer Genome Atlas(TCGA)database.Analysis of the gene expression profiles of PDHB was based on TCGA and Genotype Tissue Expression Dataset databases.Cox regression analysis and Kaplan-Meier methods were used to assess the correlation between PDHB expression and survival prognosis in cancer patients.The correlation between PDHB and receiver operating characteristic diagnostic curve,clinicopathological staging,somatic mutation,tumor mutation burden(TMB),microsatellite instability(MSI),DNA methylation,and drug susceptibility in pan-cancer was also analyzed.Various algorithms were used to analyze the correlation between PDHB and immune cell infiltration and tumor chemotaxis environment,as well as the co-expression analysis of PDHB and immune checkpoint(ICP)genes.The expression and functional phenotype of PDHB in single tumor cells were studied by single-cell sequencing,and the functional enrichment analysis of PDHB-related genes was performed.The study also validated the level of mRNA or protein expression of PDHB in several cancers.Finally,in vitro experiments verified the regulatory effect of PDHB on the proliferation,migration,and invasion of liver cancer.RESULTS PDHB was significantly and differently expressed in most cancers.PDHB was significantly associated with prognosis in patients with a wide range of cancers,including kidney renal clear cell carcinoma,kidney renal papillary cell carcinoma,breast invasive carcinoma,and brain lower grade glioma.In some cancers,PDHB expression was clearly associated with gene mutations,clinicopathological stages,and expression of TMB,MSI,and ICP genes.The expression of PDHB was closely related to the infiltration of multiple immune cells in the immune microenvironment and the regulation of tumor chemotaxis environment.In addition,single-cell sequencing results showed that PDHB correlated with different biological phenotypes of multiple cancer single cells.This study further demonstrated that down-regulation of PDHB expression inhibited the proliferation,migration,and invasion functions of hepatoma cells.CONCLUSION As a member of pan-cancer,PDHB may be a novel cancer marker with potential value in diagnosing cancer,predicting prognosis,and in targeted therapy.

MiRNA-145-5p inhibits gastric cancer progression via the serpin family E member 1-extracellular signal-regulated kinase-1/2 axis

BACKGROUND MicroRNAs(miRNAs)regulate gene expression and play a critical role in cancer physiology.However,there is still a limited understanding of the function and regulatory mechanism of miRNAs in gastric cancer(GC).AIM To investigate the role and molecular mechanism of miRNA-145-5p(miR145-5p)in the progression of GC.METHODS Real-time polymerase chain reaction(RT-PCR)was used to detect miRNA expression in human GC tissues and cells.The ability of cancer cells to migrate and invade was assessed using wound-healing and transwell assays,respectively.Cell proliferation was measured using cell counting kit-8 and colony formation assays,and apoptosis was evaluated using flow cytometry.Expression of the epithelial-mesenchymal transition(EMT)-associated protein was determined by Western blot.Targets of miR-145-5p were predicated using bioinformatics analysis and verified using a dual-luciferase reporter system.Serpin family E member 1(SERPINE1)expression in GC tissues and cells was evaluated using RT-PCR and immunohistochemical staining.The correlation between SERPINE1 expression and overall patient survival was determined using Kaplan-Meier plot analysis.The association between SERPINE1 and GC progression was also tested.A rescue experiment of SERPINE1 overexpression was conducted to verify the relationship between this protein and miR-145-5p.The mechanism by which miR-145-5p influences GC progression was further explored by assessing tumor formation in nude mice.RESULTS GC tissues and cells had reduced miR-145-5p expression and SERPINE1 was identified as a direct target of this miRNA.Overexpression of miR-145-5p was associated with decreased GC cell proliferation,invasion,migration,and EMT,and these effects were reversed by forcing SERPINE1 expression.Kaplan-Meier plot analysis revealed that patients with higher SERPINE1 expression had a shorter survival rate than those with lower SERPINE1 expression.Nude mouse tumorigenesis experiments confirmed that miR-145-5p targets SERPINE1 to regulate extracellular signal-regulated kinase-1/2(ERK1/2).CONCLUSION This study found that miR-145-5p inhibits tumor progression and is expressed in lower amounts in patients with GC.MiR-145-5p was found to affect GC cell proliferation,migration,and invasion by negatively regulating SERPINE1 levels and controlling the ERK1/2 pathway.

Cohort study on the treatment of BRAF V600E mutant metastatic colorectal cancer with integrated Chinese and western medicine

BACKGROUND Patients with BRAF V600E mutant metastatic colorectal cancer(mCRC)have a low incidence rate,poor biological activity,suboptimal response to conventional treatments,and a poor prognosis.In the previous cohort study on mCRC conducted by our team,it was observed that integrated Chinese and Western medicine treatment could significantly prolong the overall survival(OS)of patients with colorectal cancer.Therefore,we further explored the survival benefits in the population with BRAF V600E mutant mCRC.AIM To evaluate the efficacy of integrated Chinese and Western medicine in the treatment of BRAF V600E mutant metastatic colorectal cancer.METHODS A cohort study was conducted on patients with BRAF V600E mutant metastatic colorectal cancer admitted to Xiyuan Hospital of China Academy of Chinese Medical Sciences and Traditional Chinese Medicine Hospital of Xinjiang Uygur Autonomous Region from January 2016 to December 2022.The patients were divided into two cohorts.RESULTS A total of 34 cases were included,with 23 in Chinese-Western medicine cohort(cohort A)and 11 in Western medicine cohort(cohort B).The median overall survival was 19.9 months in cohort A and 14.2 months in cohort B,with a statistically significant difference(P=0.038,hazard ratio=0.46).The 1-3-year survival rates were 95.65%(22/23),39.13%(9/23),and 26.09%(6/23)in cohort A,and 63.64%(7/11),18.18%(2/11),and 9.09%(1/11)in cohort B,respectively.Subgroup analysis showed statistically significant differences in median OS between the two cohorts in the right colon,liver metastasis,chemotherapy,and first-line treatment subgroups(P<0.05).CONCLUSION Integrated Chinese and Western medicine can prolong the survival and reduce the risk of death in patients with BRAF V600E mutant metastatic colorectal cancer,with more pronounced benefits observed in patients with right colon involvement,liver metastasis,combined chemotherapy,and first-line treatment.

USCANNER(E)尿沉渣分析仪参考区间建立及临床适用性探讨

目的建立USCANNER(E)尿沉渣分析仪(简称USE)常用参数参考区间;对其进行性能验证;分别比较USE和IQ200尿沉渣分析仪(简称IQ200)与人工镜检结果一致性。方法筛选331例健康标本进行检测,建立常用参数参考区间;测定USE携带污染率;另收集标本147例,同时用USE和IQ200检测,其中92例进行人工镜检。将USE分别与IQ200和人工镜检作一致性分析,评估USE诊断效能。结果在95%可信区间内USE参考区间为:红细胞:0~6个/μL(男),0~15个/μL(女);白细胞:0~13个/μL(男),0~22个/μL(女);鳞状上皮细胞:0~8个/μL(男),0~29个/μL(女);非鳞状上皮细胞:0~1个/μL(不分性别);管型、结晶、细菌及真菌为阴性。未检出携带污染。USE与IQ200经人工修饰后红细胞、白细胞的Kappa值均≥0.85,其余项目在0.54~0.72之间。USE人工修饰后与人工镜检相比,除了非鳞状上皮细胞和结晶外,其余项目Kappa值均≥0.77。USE各项目符合率均≥88%;红细胞、白细胞、鳞状上皮细胞的受试者工作特征曲线的曲线下面积为0.973、0.998、0.941。结论本研究建立的USE参考区间可供参考;USE对尿液有形成分的总体检测性能良好,适用于日常临床样本的初筛检查,但仍需配合人工镜检以提高结果的准确性。

人参皂苷Rg3通过调控E2F1对人胃癌SGC-7901细胞生物行为学的影响

目的探究人参皂苷Rg3通过调控E2F1对人胃癌SGC-7901细胞生物行为学的影响。方法MTT测定不同浓度人参皂苷Rg3(0、80、160、320μmol·L^(-1))对细胞增殖影响;流式细胞术测定不同浓度人参皂苷Rg3对细胞凋亡的影响;划痕愈合实验和Transwell实验测定不同浓度人参皂苷Rg3对细胞迁移及侵袭的影响;Western blot测定不同浓度人参皂苷Rg3对E2F1、MMP-2、MMP-9、BCL-2、Bax表达的影响。结果80、160、320μmol·L^(-1)人参皂苷Rg3组细胞存活率与空白对照组比较明显降低,且呈浓度依赖性(P<0.05)。80、160、320μmol·L^(-1)人参皂苷Rg3组细胞凋亡率与空白对照组比较明显增加,且呈浓度依赖性(P<0.05)。80、160、320μmol·L^(-1)人参皂苷Rg3组细胞迁移数目与空白对照组比较明显降低,且呈浓度依赖性(P<0.05)。80、160、320μmol·L^(-1)人参皂苷Rg3组细胞侵袭数目与空白对照组比较明显降低,且呈浓度依赖性(P<0.05)。80、160、320μmol·L^(-1)人参皂苷Rg3组E2F1 mRNA与E2F1蛋白表达量相较空白对照组明显减少且,呈浓度依赖性(P<0.05)。80、160、320μmol·L^(-1)人参皂苷Rg3组细胞中MMP-2、MMP-9、BCL-2蛋白表达量与空白对照组比较明显降低,BCL-2与空白对照组比较明显升高,且呈浓度依赖性(P<0.05)。结论人参皂苷Rg3能降低胃癌SGC-7901细胞增殖能力,抑制细胞迁移及侵袭能力,同时还促进SGC-7901细胞凋亡,且具有浓度依赖性,其作用机制可能通过E2F1因子下调MMP-2、MMP-9、BCL-2表达,上调Bax表达有关。