Quercetin exerts anti-inflammatory effects via inhibiting tumor necrosis factor-α-induced matrix metalloproteinase-9 expression in normal human gastric epithelial cells

BACKGROUND Gastric injury is the most common digestive system disease worldwide and involves inflammation,which can lead to gastric ulcer or gastric cancer(GC).Matrix metallopeptidase-9[MMP-9(gelatinase-B)]plays an important role in inflammation and GC progression.Quercetin and quercetin-rich diets represent potential food supplements and a source of medications for treating gastric injury given their anti-inflammatory activities.However,the effects and mechanisms of action of quercetin on human chronic gastritis and whether quercetin can relieve symptoms remain unclear.AIM To assess whether tumor necrosis factor-α(TNF-α)-induced MMP-9 expression mediates the anti-inflammatory effects of quercetin in normal human gastric mucosal epithelial cells.METHODS The normal human gastric mucosa epithelial cell line GES-1 was used to establish a normal human gastric epithelial cell model of TNF-α-induced MMP-9 protein overexpression to evaluate the antiinflammatory effects of quercetin.The cell counting Kit-8 assay was used to evaluate the effects of varying quercetin doses on cell viability in the normal GES-1 cell line.Cell migration was measured using Transwell assay.The expression of proto-oncogene tyrosine-protein kinase Src(cSrc),phospho(p)-c-Src,extracellular-signal-regulated kinase 2(ERK2),p-ERK1/2,c-Fos,p-c-Fos,nuclear factor kappa B(NF-κB/p65),and p-p65 and the effects of their inhibitors were examined using Western blot analysis and measurement of luciferase activity.p65 expression was detected by immunofluorescence.MMP-9 m RNA and protein levels were measured by quantitative reverse transcription polymerase chain reaction(q RT–PCR)and gelatin zymography,respectively.RESULTS q RT-PCR and gelatin zymography showed that TNF-αinduced MMP-9 m RNA and protein expression in a dose-and time-dependent manner.These effects were reduced by the pretreatment of GES-1 cells with quercetin or a TNF-αantagonist(TNFR inhibitor)in a dose-and timedependent manner.Quercetin and TNF-αantagonists decreased the TNF-α-induced phosphorylation of c-Src,ERK1/2,c-Fos,and p65 in a dose-and time-dependent manner.Quercetin,TNF-αantagonist,PP1,U0126,and tanshinone IIA(TSIIA)reduced TNF-α-induced c-Fos phosphorylation and AP-1–Luciferase(Luc)activity in a dose-and time-dependent manner.Pretreatment with quercetin,TNF-αantagonist,PP1,U0126,or Bay 11-7082 reduced TNF-α-induced p65 phosphorylation and translocation and p65–Luc activity in a dose-and timedependent manner.TNF-αsignificantly increased GES-1 cell migration,and these results were reduced by pretreatment with quercetin or a TNF-αantagonist.CONCLUSION Quercetin significantly downregulates TNF-α-induced MMP-9 expression in GES-1 cells via the TNFR-c-Src–ERK1/2 and c-Fos or NF-κB pathways.

S Phase Cell Percentage Normalized BrdU Incorporation Rate, a New Parameter for Determining S Arrest

In this study, a new parameter, S phase cell percentage （S fraction） normalized BrdU （SFN-BrdU） incorporation rate, was introduced to detect $ arrest. The results showed a positive linear correlation between the BrdU incorporation rate and the S fraction in unperturbed 16HBE cells. Theoretical analysis indicated that only S arrest could result in a decrease in the SFN-BrdU incorporation rate. Additionally, the decrease in SFN-BrdU incorporation rate and the activation of DNA damage checkpoints further demonstrated that S arrest was induced by diethyl sulfate treatment of 16HBE cells. In conclusion, $FN-BrdU incorporation rate can be used to detecting S arrest.

Differential expression of genes involved in the epigenetic regulation of cell identity in normal human mammary cell commitment and differentiation

The establishment and maintenance of mammary epithelial cell identity depends on the activity of a group of proteins, collectively called maintenance proteins, that act as epigenetic regulators of gene transcription through DNA methylation, histone modification, and chromatin remodeling. Increasing evidence indicates that dysregulation of these crucial proteins may disrupt epithelial cell integrity and trigger breast tumor initiation. Therefore, we explored in silico the expression pattern of a panel of 369 genes known to be involved in the establishment and maintenance of epithelial cell identity and mammary gland remodeling in cell subpopulations isolated from normal human mammary tissue and selectively enriched in their content of bipotent progenitors, committed luminal progenitors, and differentiated myoepithelial or differentiated luminal cells. The results indicated that, compared to bipotent cells, differentiated myoepithelial and luminal subpopulations were both characterized by the differential expression of 4 genes involved in cell identity maintenance: CBX6 and PCGF2, encoding proteins belonging to the Polycomb group, and SMARCD3 and SMARCE1, encoding proteins belonging to the Trithorax group. In addition to these common genes, the myoepithelial phenotype was associated with the differential expression of HDAC1, which encodes histone deacetylase 1, whereas the luminal phenotype was associated with the differential expression of SMARCA4 and HAT1, which encode a Trithorax protein and histone acetylase 1, respectively. The luminal compartment was further characterized by the overexpression of ALDH1A3 and GATA3, and the down-regulation of NOTCH4 and CCNB1, with the latter suggesting a block in cell cycle progression at the G2 phase. In contrast, myoepithelial differentiation was associated with the overexpression of MYC and the down-regulation of CCNE1, with the latter suggesting a block in cell cycle progression at the G1 phase.

Differential Proteomics in Malignant and Normal Liver Cell Lines

Objective： To detect differential protein expression in malignant and normal liver cell lines in vitro using the SELDI ProteinChip platform, for investigating the pathogenesis of liver cancer. Methods： Two cell lines, human normal liver cell line L02 and hepatoma cell line SMMC-7721 were cultured routinely, harvested in good condition and lysed. After quantification, the supernatant of the lysate was tested by IMAC3 （Immobilized Mental Affinity Capture） and WCX2 （Weak Cation Exchange） chips on the SELDI-TOF-MS ProteinChip reader. Results： Protein expression differed between the malignant and normal liver cell lines. A total of 20 differentially expressed proteins were found, among which, 7 were captured by the IMAC3 chip and 14 by the WCX2 chip. Peaks at 5,419, 7,979 and 11,265 Da were higher and at 8,103, 8,492, 10,160 and 11,304 Da lower in SMMC-7721 cells by the IMAC3 chip; peaks at 7,517, 7,945 and 7,979 Da were higher and at 5,061, 5,551, 5,818, 7,439, 9,401,10,100, 10,312, 11,621, 11,662, 11,830 and 12,772 Da lower in SMMC-7721 cells by the WCX2 chip. Interestingly, both chips captured the 7,979 Da peak. In addition, the 11,081 Da peak corresponded precisely with the molecular mass of the calcium binding protein S100A10, which may participate in the formation of liver cancer in association with p36. Conclusion： Detecting differential protein expression in malignant and normal liver cell lines using the SELDI ProteinChip platform was simple, sensitive and repeatable. The results we obtained can serve as a basis for investigating the pathogenesis of liver cancer and aid the discovery of new therapeutic targets.

Basic Investigations EXPRESSION OF GAP JUNCTION PROTEIN Cx43 IN CULTURED HUMAN NORMAL AND MALIGNANT LUNG CELLS

Gap junctional intercellular communicationexchange of small molecules and ions between contiguous cells through membranous gap junctional channelsis essential for growth control and tissue homecotasis. This work concerns the functional expression of gap junction protein connexin 43 (Cx43) in normal human lung cells and the changes in lung carcinoma cells. By. using Northern blot hybridization analysis and Cx43 immunocytochemical methods, it was otherved that cultured normal human embryonic lung cells expressed a high level of Cx43 in both mRNA and protein levels.The Cx43 immunofluorescence was localized at cell membrane regions corresponding to the location of gap junctions. These normal lung cells were competent of intercellular communication function as detected by Lucifer yellow dye transfer. In contrast to normal celis, Cx43 mRNA and protein was not detectable in the carcinoma PG cell line. These tumor cells were defective of intercellular communication function. These results demonstrate that Cx43 is expressed in normal cultured human embryonic lung cells but not in lung tumor cells. The lack of intercellular communication in the lung tumor cell line correlates with dysfunctional intercellular communication. The suggestive role of Cx as a tumor suppersor gene is discussed.

Glycosylated and non-glycosylated quantum dot-displayed peptides trafficked indiscriminately inside lung cancer cells but discriminately sorted in normal lung cells: An indispensable part in nanoparticle-based intracellular drug delivery

Difference in sub-cellular trafficking of glycosylated and naked peptides, between normal and lung cancer cells, was established. Normal lung tissue discriminately sorted glycosylated from non-glycosylated peptides by allowing golgi localization of the glycosylated peptides while restricting golgi entry of the naked peptides. This mechanism was surprisingly not observed in its cancer cell counterpart. Lung cancer cells tend to allow unrestricted localization of both glycosylated and naked peptides in the golgi apparatus. This newly discovered difference in sub-cellular trafficking between normal and lung cancer cells could potentially be used as an effective strategy in targeted intracellular delivery, especially targeting golgi-resident enzymes for possible treatment of diseases associated with glycans and glycoproteins, such as, congenital disease of glycosylation(CDG). This very important detail in intracellular trafficking inside normal and cancer cells is an indispensable part in nanoparticle-based intracellular drug delivery.

Antigen presenting cells may be able to distinguish between normal and radiatedSchistosoma japonicum cercaria:anin vitro observation

Objective： To observe the discrepancies of responses induced by Schistosoma japonicum （S. japonicum） normal cercaria antigen （NCA） and ultraviolet （UV） -radiation-attenuated cercaria antigen （UVACA） in an in vitro system. Methods： S. japonicum cercariae were collected and UVACA and NCA were prepared. Mouse macro- phage model cells （RAW 264.7） were treated with medium, NCA （40 μg/mL） or UVACA （40 μg/mL） in the presence or absence of recombinant mouse interferon gamma （rmIFN-γ; 4 ng/mL） for 48 h. Cell surface staining and flow cytometry were used to assess the major histocompatibility complex （MHC） Ⅱ expression, and data were expressed as mean fluorescence intensities （MFI）. Interleukin （IL） -10, IL-6 and prostaglandin E2 （PGE2） in cell culture supernatant were evaluated by commercial enzyme-linked immunosorbent assays. Results： NCA significantly suppressed IFN-7-induced MHC Ⅱ expression on RAW 264.7 cells. In the presence of 1FN-7, NCA significantly promoted IL-6, IL-10 and PGE2 secretion from RAW 264.7 cells. In the presence of IFN-γ, UVACA significantly promoted IL-10 but not IL-6 and PGE2 secretion from RAW 264.7 cells and showed no effect on IFN-γ-induced MHC Ⅱ expression. Compared with UVACA, NCA significantly suppressed IFN-γ-induced MHC Ⅱ expression and significantly promoted IL-6, PGE2 and IL-10 secretion from RAW 264.7 cells. Conclusion： RAW 264.7 cells respond differently to NCA and UVACA. NCA can significantly suppress IFN-γ-induced MHC Ⅱ expression and significantly promote IL-6, IL-10 and PGE2 secretion from RAW 264.7 cells compared with UVACA.

Selection of Reference Genes in Equine White Blood Cells for Real Time PCR Normalization Following Extracorporeal Shock Wave Therapy

Selection of proper reference genes (RGs) is an essential step needed for accurate normalization of results from genomic studies. Expression of RGs is regulated by many factors such as species, age, gender, type of tissue, the presence of disease, and the administration of therapeutic treatment. The aim of the present study was to identify optimal RGs in a set of blood samples collected at different time points (0, 24, 48, 72 h) from horses following administration of extracorporeal shock wave therapy (ESWT). The mRNA expression of twelve RGs: HPRT1, ACTB, HSP90A, SDHA, GUSB, B2M, UBC, NONO, TBP, H6PD, RPL32, GAPDH was determined using real time quantitative polymerase chain reaction (qPCR). An SAS program developed on the algorithm of geNorm, SASqPCR, was used to determine stability of the expression and the number of optimal RGs. The results showed that the range of quantification cycle (Cq) values of the evaluated genes varied between 17 and 26 cycles, and that one optimal RG, ACTB, was sufficient for normalization of gene expression. Results of stability of expression demonstrated that ACTB was the optimal choice for all the samples studied. Notably, in samples collected at 72 h post ESWT, TBP showed a significant change in the expression level, and was not suitable for use as a RG. These results substantiate the importance of validating and selecting an appropriate RG.

COMPARATIVE STUDY OF PHOSPHOTYROSYL PROTEIN PHOSPHATASE OF MICE NORMAL LIVER, REGENERATING LIVER, AND MICE H22A HEPATOMA ASCITES CELL

In regenerating liver of mice, marked increase of the activity of phosphotyrosyl protein phosphatase (PTPP) in cytosol was observed. The PTPP activity varied with time and reached the highest level between 24 to 48 hours after partial hepatectomy. In H22a cells the PTPP activity found in every subcellular fraction was lower than that of the normal liver. The PTPP activity was mostly concentrated in lysosomes of normal liver, but mainly distributed in nucleus, cytosol and microsome of regenerating liver. In H22a cells PTPP activity seemed distribute evenly. Five similar major PTPP peaks (I-V) were obtained on DEAE cellulose chromatography of cytosols from all three of liver cells studied. However, two additional PTPP peaks, a and b, were also obtained from cytosol of liver.

Differential Expression of Genes Involved in Cell Polarity, EMT and Cell-Fate in Breast Cancer and Corresponding Normal Tissue

Objectives: Cell polarity and epithelial morphology are peculiar features of cells forming the terminal ductal lobular unit, and they are early lost during neoplastic transformation because of an epithelial-mesenchymal transition (EMT). To understand these early events we analyzed a set of 125 genes related to cell polarity, EMT and cell-fate decision in 26 breast cancer specimens and corresponding patient-matched normal tissue. Methods: The difference of gene expression was explored by t-paired test. In addition, to evidence latent variables accounting for genes correlations, a Factor Analysis was applied as exploratory technique. Results: Among the 90 differentially expressed genes, those coding for cell polarity complexes, apical-junctional components and luminal cytokeratins were overexpressed in tumor samples (suggesting a terminally differentiated phenotype) whereas those coding for stemness-associated features or related with EMT were expressed in normal tissues but not in tumor samples, suggesting the persistence of stem/progenitor cells. Factor analysis confirmed these findings and indicated that the difference between tumors and normal tissues can be synthesized in three main features representative of specific molecular/morphological alterations. Conclusions: The a priori definition of a selected panel of genes and the application of an exploratory statistical approach, greatly contribute to reduce the intrinsic biological complexity of tumor specimens and to describe the difference between tumor specimens and corresponding histologically normal tissues.

基于课程思政的融合教学模式探索--以细胞生物学课程为例

立德树人是高等教育的根本任务,而将课程思政融入课堂教学是实现“三全育人”的重要途径。以杭州师范大学生物科学专业细胞生物学教学为例,构建思政视域下的课内外、校内外、线上线下资源充分混合,并将任务驱动教学、案例教学、实践教学等不同形式融合其中的教学模式。结合该校师范专业人才培养方案和教学大纲,将立德树人和“三位一体”的教育理念融入细胞生物学课重要知识点,有助于培养学生严谨科学作风和爱国情怀,与思政教育同向同行,形成协同效应。

不稳定型心绞痛患者血浆RANTES和MST1水平与冠状动脉斑块负荷的相关性

目的:探讨不稳定型心绞痛(UA)患者血浆调节活化正常T细胞表达和分泌因子(RANTES)水平和哺乳动物不育系20-样激酶1(MST1)与冠状动脉斑块负荷的相关性。方法:选择2018年1月至2021年1月在承德医学院附属医院心内科诊断UA且接受冠状动脉造影的住院患者,采用酶联免疫吸附实验法检测入院时血浆RANTES和MST1水平。应用SYNTAX评分和Gensini评分量化冠状动脉斑块负荷的程度。依据SYNTAX评分分为低SYNTAX评分组(≤22)和中/高SYNTAX评分组(>22),分别依据RANTES和MST1三分位数分为低RANTES组、中RANTES组和高RANTES组以及低MST1组、中MST1组和高MST1组。结果:本研究纳入321例UA患者,中/高SYNTAX评分组血浆RANTES和MST1水平高于低SYNTAX评分组,差异有统计学意义(P<0.05)。高RANTES组SYNTAX评分(18.91±6.57)高于中RANTES组(13.69±3.05)和低RANTES组(10.66±6.12)(P<0.05)。高MST1组SYNTAX评分(15.75±6.13)高于中MST1组(14.43±7.51)和低MST1组(13.06±5.28)(P<0.05)。多因素Logistic回归分析提示,RANTES最高三分位数(OR=2.672,95%CI1.173~6.090,P<0.05)和MST1最高三分位数(OR=5.274,95%CI1.769~15.722,P<0.05)是中/高SYNTAX评分的独立危险因素。RANTES和MST1以及两者联合预测中/高SYNTAX评分的ROC曲线下面积(AUC)分别为0.69(95%CI0.586~0.795,P<0.05)、0.625(95%CI0.553~0.696,P<0.05)以及0.786(95%CI0.705~0.866,P<0.001)。结论:血浆RANTES、MST1水平升高是UA患者较高冠状动脉斑块负荷的独立危险因子。

中国健康成人外周血自然杀伤细胞及其亚群的正常值范围流式细胞学分析

目的:研究中国健康人外周血中自然杀伤(natural killer, NK)细胞及其亚群的比例和数量,初步确定其正常值范围作为临床检验的参考数值。方法:选取200例健康成年人,年龄范围为18~87岁,所有受试者被分成6个年龄组:18~30、31~40、41~50、51~60、61~70、71~87岁,收集外周血,以CD16、CD56、CD3、CD19等作为表面标记,使用流式细胞术检测NK细胞及亚群的相对比例及绝对计数。采用SPSS 27.0软件分析数据,计量资料用均数±标准差表示,同时进行t检验、方差分析或秩和检验比较各年龄组和性别组的差异,检验水准α=0.05,以P<0.05为差异有统计学意义。结果:200例健康成人受试者CD3^(-)CD56^(+)NK细胞的范围为(13.14±7.56)×10^(6)/L,CD56^(dim)CD16^(+)NK细胞的范围为(5.23±3.12)×10^(6)/L,CD56^(bright)NK细胞的范围为(85.61±7.40)×10^(6)/L,NK T细胞的范围为(4.16±3.34)×10^(6)/L,NK B细胞的范围为(0.46±0.24)×10^(6)/L。CD3^(-)CD56^(+)NK和NK T细胞在和年龄的相关性方面差异无统计学意义(P=0.417,P=0.217);随着年龄的增长,NK B和CD56^(dim)CD16~+NK细胞的数量有一定的下降趋势(r=0.234,P<0.001;r=0.099,P<0.001),尤其是在50岁以后更加明显;CD56^(bright)NK则随着年龄增长有上升趋势(r=0.143,P<0.001)。结论:NK细胞及其亚群的检测对于自身免疫病、感染性疾病和肿瘤的诊断、治疗和预后分析具有重要参考价值;本研究为临床检测NK细胞亚群提供了初步的参考范围,但尚需扩大例数,进行多中心试验以进一步明确。

多参数流式细胞术识别与急性髓系白血病微小残留病具有类似表型的再生细胞

目的探讨如何利用多参数流式细胞术(MFC)鉴别与急性髓系白血病(AML)微小残留病(MRD)具有类似表型的正常细胞。方法回顾性分析2020年3月-2022年4月在我院利用MFC检测的AML患者MRD骨髓标本157例次,识别容易被误认为是MRD的正常细胞。结果AML患者治疗后再生的骨髓样本中会出现如下易误判为MRD的正常细胞群:CD117 dim CD56^(+)CD7^(+)CD45^(str)自然杀伤(NK)细胞、CD19 dim CD56^(+)CD7^(+)CD45^(str) NK细胞、CD300e^(+)HLA-DR^(+)CD14^(part) CD64^(part)非经典单核细胞;这些细胞群占骨髓有核细胞比例的中位值分别是0.084%(范围:0~0.6200%)、0%(范围:0~0.2134%)、0.1549%(范围:0~2.0940%)。结论MFC检测AML患者MRD过程中,应避免将治疗后骨髓再生的正常细胞,误判为残留病。

血清RANTES、IL-35对儿童急性阑尾炎伴穿孔的辅助诊断价值

目的探讨血清T淋巴细胞激活性低分泌因子(RANTES)、白细胞介素-35(IL-35)对儿童急性阑尾炎伴穿孔的辅助诊断价值。方法选取2021年8月至2023年8月在唐山市丰南区医院就诊的132例急性阑尾炎患儿作为研究对象,根据是否发生阑尾穿孔分为穿孔组43例,未穿孔组89例。采用酶联免疫吸附试验检测血清RANTES、IL-35水平。采用Pearson相关分析血清RANTES、IL-35水平之间的相关性;采用多因素Logistic回归分析急性阑尾炎患儿发生阑尾穿孔的影响因素。采用受试者工作特征(ROC)曲线分析血清RANTES、IL-35对急性阑尾炎患儿阑尾穿孔的诊断效能。结果与未穿孔组相比,穿孔组的白细胞计数(WBC)、血小板计数(PLT)、中性粒细胞计数(NEUT)明显升高(P<0.05)。与未穿孔相比,穿孔组的血清RANTES水平明显升高(P<0.05),IL-35水平明显降低(P<0.05)。Pearson相关分析结果显示,急性阑尾炎患儿血清RANTES水平与IL-35水平呈负相关性(r=-0.474,P<0.05)。多因素Logistic回归分析结果显示,血清RANTES水平、WBC、NEUT、PLT升高是急性阑尾炎患儿发生阑尾穿孔的危险因素(P<0.05),IL-35水平升高是急性阑尾炎患儿发生阑尾穿孔的保护因素(P<0.05)。血清RANTES、IL-35联合诊断急性阑尾炎患儿阑尾穿孔的曲线下面积(AUC)优于RANTES、IL-35单独诊断的AUC(P<0.05)。结论急性阑尾炎患儿血清RANTES水平升高及IL-35水平降低与阑尾穿孔有关,二者联合检测可更好地辅助诊断急性阑尾炎患儿是否发生阑尾穿孔。

血清sTREM-1、RANTES水平与病毒性心肌炎患者不良预后的关系

目的 探讨血清可溶性髓样细胞触发受体-1(sTREM-1)、激活调节正常T细胞表达和分泌因子(RANTES)水平与病毒性心肌炎患者(VM)不良预后的关系。方法 选取2019年8月至2022年8月北京市东城区第一人民医收治的200例VM患者作为研究对象,根据随访情况分为预后不良组86例,预后良好组114例。同时选取200例同期该院体检健康人员作为对照组。收集各组一般资料,并检测血清sTREM-1、RANTES、血清白细胞介素-18(IL-18)、血清高敏C反应蛋白(hs-CRP)、肌酸激酶同工酶(CK-MB)、肌酸激酶(CK)、心肌肌钙蛋白I(cTnI)水平。对VM患者预后随访12个月,比较预后良好组和预后不良组的一般资料及血清sTREM-1、RANTES水平。采用受试者工作特征(ROC)曲线分析血清sTREM-1、RANTES水平对VM患者发生不良预后的预测价值,Logistic回归分析影响VM患者发生不良预后的危险因素。结果 VM组sTREM-1、RANTES水平明显高于对照组(P<0.05),预后不良组CK-MB、cTnI、hs-CRP、CK、IL-18水平高于预后良好组(P<0.05)。ROC曲线结果显示,血清sTREM-1、RANTES的ROC曲线的下面积(AUC)分别为0.814、0.824,二者联合检测的AUC为0.905,高于sTREM-1、RANTES单独检测(Z=2.485、2.212,均P<0.05)。Logistic多因素回归分析显示,sTREM-1、RANTES水平是影响VM患者预后不良的危险因素(P<0.05)。结论 血清sTREM-1、RANTES水平对VM患者的不良预后具有重要的预测价值。

趋化因子MCP-1和RANTES与不明原因复发性流产的关系研究

目的 分析不明原因复发性流产(URSA)的危险因素,观察单核细胞趋化蛋白-1(MCP-1)、调节活化正常T细胞表达和分泌因子(RANTES)与URSA的关系。方法 选择70例URSA患者作为URSA组,同期正常妊娠孕妇70例作为正常妊娠组。比较两组的临床资料,包括年龄、孕产次、家族遗传史、吸烟饮酒史、体质量指数(BMI)、从事职业、受教育程度等;采用酶联免疫吸附试验(ELISA)检测两组血清中的RANTES以及MCP-1水平。分析URSA发生的危险因素;比较两组血清MCP-1、RANTES水平, URSA组中不同胎龄、流产次数患者血清MCP-1、RANTES水平。结果 单因素分析显示, URSA组中年龄≥35岁、BMI≥24 kg/m^(2)、有吸烟史、有饮酒史、受教育程度初中及以下占比分别为62.9%、67.1%、61.4%、57.1%、65.7%,较正常妊娠组的30.0%、27.1%、18.6%、17.1%、37.1%更高(P<0.05)。多因素Logistic回归分析显示,患者BMI≥24 kg/m^(2)、年龄≥35岁、有吸烟及饮酒史、受教育程度初中及以下是导致URSA的危险因素(OR>1, P<0.05)。URSA组患者血清MCP-1、RANTES水平分别为(127.31±70.12)、(220.98±69.51)ng/L,低于正常妊娠组的(239.20±75.64)、(412.34±82.47)ng/L(P<0.05)。URSA组中,随流产次数增加,血清MCP-1、RANTES水平降低,比较差异具有统计学意义(P<0.05)。URSA组中,不同胎龄患者的血清MCP-1、RANTES水平比较,差异无统计学意义(P>0.05)。结论 BMI偏高、年龄偏大以及有吸烟及饮酒史、受教育程度低等因素是导致URSA的危险因素,血清RANTES以及MCP-1异常表达与URSA的发生关系密切。对于URSA患者,妊娠早期及时检测血清中RANTES和MCP-1水平,可能成为URSA胚胎丢失及免疫治疗效果的临床观察指标。

血清AAT、RANTES、Resistin水平与大动脉粥样硬化型急性缺血性卒中患者病情及预后的关系研究

目的探讨血清α-1抗胰蛋白酶(AAT)、受激活调节正常T细胞表达和分泌因子(RANTES)、抵抗素(Resistin)水平与大动脉粥样硬化(LAA)型急性缺血性卒中(AIS)患者病情及预后的关系。方法选取2022年1月—2023年1月延安大学咸阳医院神经内科收治的LAA型AIS患者159例纳入AIS组,根据入院时美国国立卫生研究院卒中量表(NIHSS)评分分为轻度亚组31例,中度亚组72例,重度亚组56例,另选取同期医院体检健康志愿者84例纳入健康对照组。随访90 d后,根据改良Rankin量表评分将LAA型AIS患者分为预后不良亚组61例和预后良好亚组98例。多因素Logistic回归分析LAA型AIS患者预后影响因素,受试者工作特征(ROC)曲线分析血清AAT、RANTES、Resistin水平预测LAA型AIS患者预后的价值。结果与健康对照组比较,AIS组血清AAT、RANTES、Resistin水平升高(t/P=16.897/<0.001、20.334/<0.001、17.775/<0.001);血清AAT、RANTES、Resistin水平在轻度亚组、中度亚组、重度亚组中依次升高(F/P=146.195/<0.001、192.910/<0.001、194.396/<0.001)。随访90 d,LAA型AIS患者159例预后不良发生率为38.36%(61/159)。影响LAA型AIS患者预后的独立危险因素为年龄增加、合并糖尿病、入院时NIHSS评分增加、AAT升高、RANTES升高、Resistin升高[OR(95%CI)=1.078(1.019~1.141)、2.774(1.010~7.622)、1.106(1.054~1.160)、1.597(1.057~2.414)、1.136(1.059~1.219)、1.097(1.035~1.163)];血清AAT、RANTES、Resistin水平及三者联合预测LAA型AIS患者预后不良的ROC曲线下面积分别为0.769、0.771、0.766、0.897,三者联合的曲线下面积大于单独预测(Z/P=3.484/0.001、3.416/0.001、3.230/0.001)。结论LAA型AIS患者血清AAT、RANTES、Resistin水平升高与病情加重和预后不良密切相关,血清AAT、RANTES、Resistin水平联合预测LAA型AIS患者预后不良的价值较高。

RANTES和STAT3在难治性支原体肺炎患儿外周血中的表达及意义

目的探究受激活调节正常T细胞表达和分泌因子(RANTES)、信号转导子和转录激活子3(STAT3)在儿童支原体肺炎外周血中的表达,并评估其对难治性支原体肺炎(RMPP)的预测价值。方法选取2023年8—10月在河南省儿童医院郑州儿童医院住院的儿童支原体肺炎患儿103例,患儿均接受全程治疗,根据患儿治疗1周后是否仍出现持续发热、病情加重情况将患儿分为MPP组和RMPP组,对两组患儿外周血中RANTES、STAT3表达情况进行检测,并分析两组患儿相关实验室指标情况。收集两组患儿的一般资料,对可能诱发RMPP的因素进行单因素和多因素分析。结果RMPP组RANTES水平及STAT3 mRNA相对表达水平均高于MPP组(P<0.05)。RMPP组中性粒细胞计数、白细胞计数、C反应蛋白、血小板计数、乳酸脱氢酶以及红细胞沉降率等实验室指标均高于MPP组(P<0.05)。经单因素及多因素分析,RANTES和STAT3水平、乳酸脱氢酶水平和抗生素使用均与RMPP的发生有关(P<0.05)。结论RANTES和STAT3表达水平升高可以提示儿童支原体肺炎预后不良。

急性脑梗死患者血清趋化因子CXCL12、RANTES、MIP-1α的动态表达及与神经功能缺损程度和预后的相关性分析

目的:探究急性脑梗死(ACI)患者CXC基序趋化因子配体12(CXCL12)、调节激活正常T细胞表达和分泌细胞因子(RANTES)、巨噬细胞炎性蛋白-1α(MIP-1α)的动态表达及与神经功能缺损程度和预后的相关性。方法:选取2021年7月—2022年7月赣州市第三人民医院收治的80例ACI患者作为ACI组,另选取同期脑神经功能正常的80例志愿者作为对照组。比较ACI组与对照组、不同神经功能缺损程度及预后情况患者的CXCL12、RANTES、MIP-1α水平;分析上述血清指标与神经功能缺损程度的相关性;绘制受试者操作特征(ROC)曲线分析各血清指标对ACI患者预后不良的预测价值。结果:ACI组CXCL12、RANTES、MIP-1α水平均高于对照组(P<0.05)。重度缺损组血清CXCL12、RANTES、MIP-1α水平高于轻、中度缺损组,且中度缺损组均高于轻度缺损组(P<0.05)。预后不良组血清CXCL12、RANTES、MIP-1α水平均高于预后良好组(P<0.05)。Kendall的tau-b相关性分析显示,ACI患者血清CXCL12、RANTES、MIP-1α水平与神经功能缺损程度均呈正相关(τ=0.566、0.678、0.752,P<0.001)。ROC曲线显示,血清CXCL12、RANTES、MIP-1α水平单一及联合检测预测ACI患者预后不良的曲线下面积(AUC)均>0.8,联合检测的价值更高。结论:ACI患者血清CXCL12、RANTES、MIP-1α水平均呈高表达,且水平越高,患者的神经功能缺损越严重、预后不良风险越高。