Expression of platelet endothelial cell adhesion molecule-1 between pancreatic microcirculation and peripheral circulation in rats with acute edematous pancreatitis

OBJECTIVE: To study the ehanges of platelet endothelial cell adhesion molecule-1 (PECAM-1) expression on polymorphonuclear leukocytes (PMNs) in peripheral circulation anti pancreatic microcirculation in rats with acute edematous pancreatitis (AEP). METHODS: The model of AEP was established with 50 Wistar rats, and the changes of PECAM-1 expression on PMNs from the splenic vein and inferior vena cava were determined by flow cytometry. RESULTS: PECAM-I expression on PMNs showed no significant difference between pancreatic microcirculation and peripheral circulation at AEP2h and AEP4h time points. From the AEP4h to the AEP8h time point, PECAM-1 expression in peripheral circulation was up-regulated, but PECAM-1 expression in pancreatic microcirculation was down-regulated. PECAM-1 expression had a significant difference between pancreatic microcirculation and peripheral circulation at the AEP8h time point (P<0.05). CONCLUSION: PECAM-1 expression on PMNs is in a converse way between pancreatic microcirculation and peripheral circulation in AEP.

Effects of TCMP-1 on the changes of platelet endothelial cell adhesion molecule-1 expression in acute edematous pancreatitis

BACKGROUND: Traditional Chinese medicine is a potent agent in the management of clinical and experimental acute pancreatitis (AP), but the molecular mechanism of its the- rapeutic action is unclear. Numerous experimental and clinical studies have shown that platelet endothelial cell ad- hesion molecule-1 (PECAM-1) is pivotal to leukocyte re- cruitment, which results in microcirculatory injury during inflammation, but its role in acute pancreatitis is poorly un- derstood. We investigated the effects of a compound of tra- ditional Chinese medicine pancreatitis-1 (TCMP-1) on the changes of platelet endothelial cell adhesion molecule-1 (PECAM-1) expression on polymorphonuclear leukocytes (PMNs) in acute edematous pancreatitis (AEP). METHODS: The model of acute pancreatitis was estab- lished by subcutaneous injection of caerulein, and TCMP-1 treated groups were given TCMP-1 by catheterization from mouth to stomach (20 ml/kg) immediately after first time subcutaneous injection of caerulein. The changes of expres- sion of PECAM-1 on leukocytes from the blood of the splenic vein and inferior vena cava were determined by flow cytometry. RESULTS: In the AEP group, expression of PECAM-1 on PMNs was not significantly different between pancreatic microcirculation and systemic circulation at AEP2h and AEP4h time point. Then from AEP4h time point to AEP8h time point, expression of PECAM-1 was up-regulated in systemic circulation while it was down-regulated in pancre- atic microcirculation and was significantly different be- tween pancreatic microcirculation and systemic circulation at AEP8h time point (P<0.05). In the TCMP-1 treated group, compared with the AEP group, expression of PE-CAM-1 on PMNs decreased in different levels between pan- creatic microcirculation and systemic circulation and was of significant difference at AEP8h time point (P <0.05). CONCLUSION: Inhibition of PECAM-1 expression on PMNs may prevent PMNs from transmigration through the endo- thelium and may be one of the treatment mechanisms of TCMP-1 decoction on AEP.

The relationship between platelet endothelial cell adhesion molecule-1 and paraquat-induced lung injury in rabbits

BACKGROUND:Platelet endothelial cell adhesion molecule-1(PECAM-1),also known as CD31,is mainly distributed in vascular endothelial cells.Studies have shown that PECAM-1 is a very significant indicator of angiogenesis,and has been used as an indicator for vascular endothelial cells.The present study aimed to explore the relationship between the expression of PECAM-1 and the degree of acute lung injury(ALI) and fibrosis in paraquat(PQ) induced lung injury in rabbits.METHODS:Thirty-six adult New Zealand rabbits were randomly divided into three groups(12rabbits in each group) according to PQ dosage:8 mg/kg(group A),16 mg/kg(group B),and 32 mg/kg(group C).After PQ infusion,the rabbits were monitored for 7 days and then euthanized.The lungs were removed for histological evaluation.Masson staining was used to determine the degree of lung fibrosis(LF),and semi-quantitative immune-histochemistry analysis to determine the expression of PECAM-1.Pearson's product-moment correlation analysis was performed to evaluate the relationship between the expression of PECAM-1 and the extent of lung injuries expressed by ALI score and degree of LF.RESULTS:Rabbits in the three groups showed apparent poisoning.The rabbits survived longer in group A than in groups B and C(6.47±0.99 days vs.6.09±1.04 days vs.4.77±2.04 days)(P<0.05).ALI score was lower in group A than in groups B and C(8.33±1.03 vs.9.83±1.17 vs.11.50±1.38)(P<0.05),and there was statistically significant difference between group B and group C(P=0.03).LF was slighter in group A than in groups B and C(31.09%±2.05%vs.34.37%±1.62%vs.36.54%±0.44%)(P<0.05),and there was statistically significant difference between group B and group C(P=0.026).The PEACAM-1 expression was higher in group A than in groups B and C(20.31%±0.70%vs.19.34%±0.68%vs.18.37%±0.46%)(P<0.05),and there was statistically significant difference between group B and group C(P=0.017).Pearson's correlation analysis showed that the expression of PECAM-1 was negatively correlated to both ALI score(Coe=-0.732,P=0.001)and degree of LF(Coe=-0.779,P<0.001).CONCLUSIONS:The PECAM-1 expression significantly decreases in New Zealand rabbits after PQ poisoning,and the decrease is dose-dependent.The PECAM-1 expression is negatively correlated with ALI score and LF,showing a significant role in the development of lung injuries induced by PQ.

Differences in platelet endothelial cell adhesion molecule-1 expression between peripheral circulation and pancreatic microcirculation in cerulein-induced acute edematous pancreatitis

AIM: To investigate the changes of platelet endothelial cell adhesion molecule-1 (PECAM-1) expression on polymorphonuclear leukocytes (PMNs) in peripheral circulation and pancreatic microcirculation in cerulein-induced acute edematous pancreatitis (AEP).METHODS: Fifty Wistar rats were randomly divided into control group (n=10) and AEP group (n=40). A model of AEP was established by subcutaneous injection of cerulein 5.5 and 7.5 μg/kg at 0 and 1 h after the beginning of experiment respectively. PECAM-1 expression on PMNs from splenic vein and inferior vena cava was determined by RT-PCR at mRNA level and determined by flow cytometry at protein level.RESULTS: In experimental rats, an increased PECAM-1mRNA expression was seen from 4 to 8 h of AEP in peripheral circulation (0.77±0.25%, 0.76±0.28%, 0.89±0.30%,1.00±0.21% ), while in pancreatic microcirculation,expression decreased from 2 h and reached the lowest level at 6 h of AEP (0.78±0.29%, 0.75±0.26%, 0.62±0.28%,0.66±0.20%). There were significant differences at 8-h time point of AEP between peripheral circulation and pancreatic microcirculation (1.00±0.21% vs0.66±0.20%, P＜0.05).Meanwhile,the difference at protein level was also found.CONCLUSION: A reverse expression of PECAM-1 on PMNs was found between peripheral circulation and pancreatic microcirculation, suggesting that inhibition of PECAM-1expression may improve the pathological change of AEP.

Association of G+1688A Polymorphism of Platelet Endothelial Cell Adhesion Molecule-1 Gene with Myocardial Infarction in the Chinese Han Population

In order to investigate the association of G＋1688A （Ser563Asn） polymorphism of platelet endothelial cell adhesion molecule-1 （PECAM-1） gene with myocardial infarction （MI） in the Chinese Han population, the G＋1688A polymorphism in PECAM-1 gene was detected by polymerase chain reaction-restriction fragment-length polymorphism （PCR-RFLP） method among 502 subjects, including 218 patients with MI and 284 controls. The results showed that there was significant difference in AA frequencies of genotype G＋1688A polymorphism between case and control groups （39% vs 24%, P〈0.001）. A similar trend was observed on the allele frequencies （A/G： 62% vs 49%, P〈0.001）. Among the subjects with high serum total cholesterol level or high systolic blood pressure level, the variant AA genotype was associated with high risk of MI （adjusted OR, 2.13; 95% CI, 1.08 -4.41 and adjusted OR, 2.53; 95%CI, 1.63-3.63）. The single nucleotide polymorphism （SNP） at position ＋1688 in the exon 8 of PECAM-1 gene was associated with MI and the allele A might be a risk factor for MI in the Chinese Han population.

Hypoxia Inhibits Proliferation of Human Dermal Lymphatic Endothelial Cells via Downregulation of Carcinoembryonic Antigen-related Cell Adhesion Molecule 1 Expression

Objective:Lymphatic endothelial cell(LEC)proliferation is essential for lymphangiogenesis.Hypoxia induces lymphangiogenesis,but it directly inhibits LEC proliferation and the underlying mechanisms have not been fully understood.The aim of this study was to investigate the role of carcinoembryonic antigen-related cell adhesion molecule 1(CEACAM1)in hypoxia-repressed LEC proliferation.Methods:Human dermal lymphatic endothelial cells(HDLECs)were cultured under normoxic or hypoxic conditions,and cell proliferation was determined using MTT or CCK-8 assays.CEACAM1 expression was silenced by siRNA transfection.Activation of mitogen-activated protein kinases(MAPKs)was examined by Western blotting and blocked by specific inhibitors.Results:Under hypoxia,HDLECs proliferation was suppressed and CEACAM1 expression was downregulated.Silence of CEACAM1 in normoxia inhibited HDLECs proliferation and did not further decrease proliferation in HDLECs in response to hypoxia,suggesting that CEACAM1 may mediate hypoxia-induced inhibition of HDLECs proliferation.In addition,silence of CEACAM1 increased phosphorylation of MAPK molecules:extracellular signal-regulated kinase(ERK),p38 MAPK and Jun N-terminal kinase(JNK)in HDLECs.However,only inhibition of the JNK pathway rescued the reduction of HDLEC proliferation induced by CEACAM1 silence.Conclusion:Our results suggested that hypoxia downregulates CEACAM1 expression by activation of the JNK pathway,leading to inhibition of HDLEC proliferation.These findings may help to understand the mechanisms of LEC-specific response to hypoxia and develop novel therapies for pathological lymphangiogenesis.

Adhesion of different cell cycle human hepatoma cells to endothelial cells and roles of integrin β_1

AIM: To investigate the adhesive mechanical properties of different cell cycle human hepatoma cells (SMMC-7721) to human umbilical vein endothelial cells (ECV-304), expression of adhesive molecule integrinβ1 in SMMC-7721 cells and its contribution to this adhesive course. METHODS: Adhesive force of SMMC-7721 cells to endothelial cells was measured using micropipette aspiration technique. Synchronous G1 and S phase SMMC-7721 cells were achieved by thymine-2-deoxyriboside and colchicines sequential blockage method and double thymine-2-deoxyriboside blockage method, respectively. Synchronous rates of SMMC-7721 cells and expression of integrinβ1 in SMMC-7721 cells were detected by flow cytometer. RESULTS: The percentage of cell cycle phases of general SMMC-7721 cells was 11.01% in G2/M phases, 53.51% in G0/G1 phase, and 35.48% in S phase. The synchronous rates of G1 and S phase SMMC-7721 cells amounted to 74.09% and 98.29%, respectively. The adhesive force of SMMC-7721 cells to endothelial cells changed with the variations of adhesive time and presented behavior characteristics of adhesion and de-adhesion. S phase SMMC-7721 cells had higher adhesive forces than d phase cells [(307.65±92.10)×10-10N vs(195.42±60.72)×10-10N, P<0.01]. The expressive fluorescent intensity of integrinβ1 in G1 phase SMMC-7721 cells was depressed more significantly than the values of S phase and general SMMC-7721cells. The contribution of adhesive integrinβ1 was about 53% in this adhesive course. CONCLUSION: SMMC-7721 cells can be synchronized preferably in d and S phases with thymine-2-deoxyriboside and colchicines. The adhesive molecule integrinβ1 expresses a high level in SMMC-7721 cells and shows differences in various cell cycles, suggesting integrin β1 plays an important role in adhesion to endothelial cells. The change of adhesive forces in different cell cycle SMMC-7721 cells indicates that S phase cells play predominant roles possibly while they interact with endothelial cells.

Cytokine-Induced Cell Surface Expression of Adhesion Molecules in Vascular Endothelial Cells In vitro

Regulation of the adhesion molecules expression by cytokine in vascular endothelial cells was investigated. Human umbilical vein endothelial cells (HUVEC) were stimulated with cytokines, TNF α (1-250 U/ml) or IL 1β (0.1-50 U/ml) for 24 h. HUVEC were also cultured with cytokines, TNF α (100 U/ml) or IL 1β (10 U/ml), for 4-72 h, cell surface expression of adhesion molecules (ICAM 1 and VCAM 1) were detected and quantitated by immunocytochemical methods and computerized imaging analysis technique. Adhesion molecules expression were up regulated by TNF α, IL 1β in a concentration and time dependent manner. Some significant differences were observed between the effects of cytokines on the ICAM 1 and on VCAM 1 expression. Cytokines might directly induce the expression of ICAM 1 and VCAM 1 in vascular endothelial cells. Our observations indicate differential functions of the two adhesion molecules during the evolution of inflammatory responses in stroke.

Nerve bundle formation during the promotion of peripheral nerve regeneration:collagenⅥ-neural cell adhesion molecule 1 interaction

The formation of nerve bundles,which is partially regulated by neural cell adhesion molecule 1(NCAM1),is important for neural network organization during peripheral nerve regeneration.However,little is known about how the extracellular matrix(ECM)microenvironment affects this process.Here,we seeded dorsal root ganglion tissue blocks on different ECM substrates of peripheral nerve ECM-derived matrixgel,Matrigel,laminin 521,collagen I,and collagen IV,and observed well-aligned axon bundles growing in the peripheral nerve ECM-derived environment.We confirmed that NCAM1 is necessary but not sufficient to trigger this phenomenon.A protein interaction assay identified collagen VI as an extracellular partner of NCAM1 in the regulation of axonal fasciculation.Collagen VI interacted with NCAM1 by directly binding to the FNIII domain,thereby increasing the stability of NCAM1 at the axolemma.Our in vivo experiments on a rat sciatic nerve defect model also demonstrated orderly nerve bundle regeneration with improved projection accuracy and functional recovery after treatment with 10 mg/m L Matrigel and 20μg/m L collagen VI.These findings suggest that the collagen VI-NCAM1 pathway plays a regulatory role in nerve bundle formation.This study was approved by the Animal Ethics Committee of Guangzhou Medical University(approval No.GY2019048)on April 30,2019.

Pingyangmycin-regulated Expressions of Adhesion Molecules in Human Venous Malformation Endothelial Cells

Pingyangmycin (bleomycin A5 hydrochloride,PYM) is one of the anti-neoplastic agents which have been commonly used to treat venous malformations.However,the underlying mechanism by which PYM treats venous malformations remains poorly understood.It was reported that venous endothelial cells could recruit neutrophils via adhesion molecules (E-selectin,ICAM-1,ICAM-3,VCAM-1) during the acute/chronic inflammation and subsequent histological fibrosis after sclerotherapy with PYM.This study explored if the expression of E-selectin,ICAM-1,ICAM-3 and VCAM-1 in human venous malformation endothelial cells could be affected by PYM.HVMECs were cultured from human venous malformation tissue.Expressions of E-selectin,ICAM-1,ICAM-3 and VCAM-1 on HVMECs in response to PYM were analyzed by cell ELISA.The relative levels of mRNA expression in the cells were semi-quantified.The results showed that PYM up-regulated the expressions of E-selectin,ICAM-3,VCAM-1 and ICAM-1 in both time-and concentration-dependent manner.Our findings suggested that PYM could induce the expression of adhesion molecules in HVMECs,which might be a possible mechanism by which sclerotherapy by intralesional injection of PYM treats venous malformations.

Expression changes of nerve cell adhesion molecules L1 and semaphorin 3A after peripheral nerve injury

The expression of nerve cell adhesion molecule L1 in the neuronal growth cone of the central nervous system is strongly associated with the direction of growth of the axon, but its role in the regeneration of the peripheral nerve is still unknown. This study explored the problem in a femoral nerve section model in rats. L1 and semaphorin 3A m RNA and protein expressions were measured over the 4-week recovery period. Quantitative polymerase chain reaction showed that nerve cell adhesion molecule L1 expression was higher in the sensory nerves than in motor nerves at 2 weeks after injury, but vice versa for the expression of semaphorin 3A. Western blot assay results demonstrated that nerve cell adhesion molecule L1 expression was higher in motor nerves than in the sensory nerves at the proximal end after injury, but its expression was greater in the sensory nerves at 2 weeks. Semaphorin 3A expression was higher in the motor nerves than in the sensory nerves at 3 days and 1 week after injury. Nerve cell adhesion molecule L1 and semaphorin 3A expressions at the distal end were higher in the motor nerves than in the sensory nerves at 3 days, 1 and 2 weeks. Immunohistochemical staining results showed that nerve cell adhesion molecule L1 expression at the proximal end was greater in the sensory nerves than in the motor nerves; semaphorin 3A expression was higher in the motor nerves than in the sensory nerves at 2 weeks after injury. Taken together, these results indicated that nerve cell adhesion molecules L1 and semaphorin 3A exhibited different expression patterns at the proximal and distal ends of sensory and motor nerves, and play a coordinating role in neural chemotaxis regeneration.

Re-expression of Cell Adhesion Molecule Inhibits Growth and Induces Apoptosis of Human Pancreatic Cancer Cell Line PANC-1

This study examined the expression of cell adhesion molecule 1 （CADM1） in pancreatic cancer and the possible mechanism. The expression of CADM 1 was detected by immunohistochemistry in tissues of pancreatic cancer, pancreatitis, and normal pancreas. The plasmid pcDNA3.1-Hy- gro（＋）/CADM1 was transfected into PANC-1 cells （a pancreatic cancer cell line）. The expression of CADM1 in the transfected cells was determined by RT-PCR and Western blotting. Cell growth was measured by the MTT method and cell apoptosis by flow cytometry. The results showed that CADM1 was weakly expressed in tissues of pancreatic cancer in contrast to its high expression in normal pancreatic and pancreatitis tissues. The expression level of CADM in pancreatic caner was intensely correlated with the differentiation degree, lymph node metastasis and TNM stages. The growth of CADMl-transfected PANC-1 cells was significantly suppressed in vitro by a G1 cell cycle arrest and apoptosis occurrence. It was concluded that re-expression of CADM1 inhibits the growth of pancreatic cancer cells and induces their apoptosis in vitro. As a tumor suppressor gene, CADM1 plays an important role in the occurrence, progression and metastasis of pancreatic cancer.

The law of anti-VCAM-1 targeted microbubbles adhesion to activated endothelial cells under controlled shear flow

Microbubbles can enhance the detection in noninvasive ultrasound imaging.Recently,targeted microbubbles have been developed to selectively adhere to specific and overexpressed p molecules in endothelial cells in some pathologic conditions.However,the law of

子宫动脉血流多普勒超声联合血清PIGF、Vaspin、ESM-1诊断HDP价值

目的:探讨妊娠高血压疾病(HDP)患者子宫动脉血流多普勒超声、血清促血管生成因子(PIGF)、丝氨酸蛋白酶抑制剂(Vaspin)、内皮细胞特异分子-1(ESM-1)水平及其诊断价值。方法:回顾性收集2020年6月-2021年12月本院接诊的HDPL患者86例为病例组,产前检查健康孕妇75例为对照组,检测两组血清PIGF、Vaspin、ESM-1水平及子宫动脉血流参数,分析在诊断HDP价值。结果:病例组血清PIGF(271.56±45.56 pg/ml)低于对照组(330.15±50.35 pg/ml),Vaspin(0.46±0.04 ng/ml)、ESM-1(1.38±0.51μg/L)高于对照组(0.39±0.08 ng/ml、1.01±0.07μg/L),多普勒超声子宫动脉血流阻力指数(RI)(0.79±0.14)、搏动指数(PI)(0.83±0.21)、收缩期峰值流速与舒张末期血流速度比值(S/D)(2.26±0.74)均高于对照组(0.51±0.20、0.44±0.19、1.41±0.35),且病例组妊娠期高血压、轻度子痫前期、重度子痫前期患者上述各指标均有差异(均P<0.05)。受试者工作特征曲线分析,血清PIGF、Vaspin、ESM-1、RI、PI、S/D及各项联合,诊断HDP的曲线下面积分别为0.811、0.780、0.691、0.944、0.860、0.813、0.999,截断值分别为291.56 pg/ml、0.43 ng/ml、1.12μg/L、0.58、0.53、1.87,联合检测的特异度(96.5%)、准确度(93.4%)最高(均P<0.05)。结论:HDP患者血清PIGF、Vaspin、ESM-1、子宫动脉血流参数异常改变,且对HDP有较好诊断价值,本次研究也为靶向药物治疗HDP提供了新思路。

血清VCAM-1、PECAM-1水平与MMSE评分联合检测对老年全髋关节置换术患者术后谵妄的预测价值

目的探讨术前血清血管细胞黏附分子-1(VCAM-1)、血小板内皮细胞黏附分子-1(PECAM-1)水平与简易精神状态量表(MMSE)评分联合检测对老年全髋关节置换术(THA)患者术后谵妄(POD)的预测价值。方法选择住院并行手术治疗的髋部骨折老年患者200例作为研究对象,并根据术后3 d内是否发生POD分为POD组(44例)和非POD组(156例)。收集2组患者的临床资料,术前采用MMSE评估患者的认知状况,并检测术前、术后第1天和第3天血清VCAM-1、PECAM-1水平。对比2组患者上述指标的差异,并分析术前血清VCAM-1、PECAM-1水平与MMSE评分的相关性。应用多因素Logistic回归分析老年THA患者发生POD的影响因素。构建受试者工作特征(ROC)曲线评估术前血清VCAM-1水平、PECAM-1水平、MMSE评分单独及联合检测对老年THA患者并发POD的预测价值。结果POD组年龄、医院焦虑抑郁量表评分、术中低血压发生率、术后住院时间明显高于或长于非POD组,MMSE评分低于非POD组(P<0.05)。POD组术前、术后第1天和术后第3天血清VCAM-1、PECAM-1水平升高,且高于非POD组(P<0.05)。老年THA患者术前血清VCAM-1、PECAM-1水平分别与MMSE评分呈负相关(r分别为-0.390、-0.501,均P<0.01)。术前血清VCAM-1和PECAM-1水平升高以及术后住院时间延长为老年THA患者发生POD的独立危险因素,MMSE评分升高为独立保护因素(P<0.05)。术前血清VCAM-1(AUC=0.793,95%CI:0.730~0.847)、PECAM-1(AUC=0.799,95%CI:0.736~0.852)及MMSE评分(AUC=0.805,95%CI:0.744~0.858)对THA患者发生POD均有较高的预测价值,三项指标联合预测的效能更高。结论血清VCAM-1、PECAM-1水平升高与老年THA患者认知功能受损有关,且均为老年THA患者发生POD的独立预测因子,术前检测以上指标可能对POD的早期防治具有重要价值。

血清SIRT1、sICAM-1及PD-L1联合检测对难治性弥漫性大B细胞淋巴瘤患者预后的评估效能

目的探讨血清沉默信息调节因子1(SIRT1)、可溶性细胞间黏附分子-1(sICAM-1)及细胞程序性死亡-配体1(PD-L1)联合检测对难治性弥漫性大B细胞淋巴瘤(DLBCL)患者预后的评估效能。方法选取2022年1月至2023年10月在郑州大学第一附属医院诊治的84例难治DLBCL患者作为研究对象,根据治疗后1个月的疾病状态将患者分为预后良好组(57例)和预后不良组(27例),收集患者的一般临床资料;采用酶联免疫吸附法(ELISA)检测患者血清SIRT1、sICAM-1及PD-L1水平;分析血清SIRT1、sICAM-1及PD-L1水平与患者临床特征、治疗效果及预后的关系;采用多因素logistic回归分析,筛选出患者预后不良的影响因素。绘制受试者工作特征(ROC)曲线,计算曲线下面积(AUC),评价血清SIRT1、sICAM-1及PD-L1水平对难治DLBCL患者预后的预测能力。结果预后不良组血清SIRT1、sICAM-1及PD-L1水平均高于预后良好组(P<0.05)。多因素logistic回归分析显示,血清SIRT1、sICAM-1及PD-L1水平是影响难治性DLBCL患者预后不良的独立危险因素(P<0.05);ROC结果显示,血清SIRT1、sICAM-1及PD-L1单独及三者联合预测难治性DLBCL患者预后不良的AUC分别为0.851、0.843、0.924、0.980,且三者联合的预测价值高于单独预测(P<0.05)。结论血清SIRT1、sICAM-1及PD-L1水平可作为难治DLBCL患者预后评估的重要指标,且三者联合检测的效能优于单项检测,对指导临床治疗及监测疾病进展有重要意义。

冠心病患者血清VCAM-1、miR-145、Gal-3、SFRP5水平变化

目的探讨冠心病患者血清血管细胞黏附分子-1(VCAM-1)、miR-145、半乳糖凝集素-3(Gal-3)、分泌型卷曲蛋白5(SFRP5)水平变化及意义。方法选取冠心病患者80例为冠心病组,另收集健康志愿者40名为健康对照组。采集清晨空腹肘静脉血,酶联免疫吸附法测定血清VCAM-1、Gal-3、SFRP5浓度;RT-PCR检测血清miR-145表达水平。根据冠脉造影检查诊断的病变支数分为单支病变、双支病变、多支病变。收集两组受试者人口学特征及冠心病患者实验室指标;进行1 a随访,记录不良预后发生情况(病情加重再入院、死亡)。结果冠心病组患者血清VCAM-1、Gal-3水平明显高于健康对照组,miR-145、SFRP5水平明显低于健康对照组(均P<0.01)。急性心肌梗死组患者血清VCAM-1、Gal-3水平明显高于不稳定型心绞痛组、稳定型心绞痛组患者,血清miR-145、SFRP5水平明显低于不稳定型心绞痛组、稳定型心绞痛组患者(均P<0.05)。多支病变患者血清VCAM-1、Gal-3水平明显高于双支病变和单支病变患者,血清miR-145、SFRP5水平明显低于双支病变和单支病变患者(均P<0.05)。预后不良组患者血清VCAM-1、Gal-3水平明显高于预后良好组患者,miR-145、SFRP5水平明显低于预后良好组患者(均P<0.01)。VCAM-1、miR-145、Gal-3、SFRP5水平是冠心病患者预后的独立影响因素;ROC曲线分析显示,血清VCAM-1、miR-145、Gal-3、SFRP5水平联合检测对冠心病患者预后具有较高的预测价值(AUC=0.928)。结论冠心病患者血清VCAM-1、Gal-3水平高表达,miR-145、SFRP5水平低表达,且与冠心病分类、冠脉病变支数密切相关,联合检测对预后具有较高的预测价值。

血清IL-8、ESM-1、VAP-1在慢性阻塞性肺疾病临床诊断及病情评估中的应用

目的探讨慢性阻塞性肺疾病(COPD)患者血清白细胞介素-8(IL-8)、内皮特异性分子-1(ESM-1)、血管黏附蛋白-1(VAP-1)表达水平,分析其与病情程度相关性及其对COPD的诊断价值。方法选取2021年11月至2022年8月郑州大学第一附属医院收治的153例COPD患者为研究对象,其中COPD稳定期42例(设为SCOPD组)、COPD急性加重期111例(设为AECOPD组),同时选取同期于医院体检的健康志愿者51例为对照组。比较两组临床资料及血清IL-8、ESM-1、VAP-1水平。对比不同病情程度患者血清IL-8、ESM-1、VAP-1水平。分析血清各指标与肺功能、生化指标、病情程度相关性。评价血清各指标对SCOPD、AECOPD的诊断价值。结果AECOPD组、SCOPD组血清IL-8、ESM-1、VAP-1水平高于对照组,且AECOPD组高于SCOPD组(P<0.05);IL-8、ESM-1、VAP-1与生化指标、COPD评估测试表(CAT)、病情程度呈正相关,与肺功能呈负相关(P<0.05);血清各指标联合诊断SCOPD与AECOPD的曲线下面积(AUC)大于单独指标诊断(P<0.05)。结论血清IL-8、ESM-1、VAP-1与COPD病情严重程度相关,联合检测其水平对COPD具有一定诊断价值,可能作为疾病诊断、病情评估的重要指标。

膝关节置换术后患者血清RANKL、sVCAM-1、ESR表达水平及其与预后的相关性

目的 探讨膝关节置换术后患者血清核因子-κB受体活化因子配基(RANKL)、可溶性血管细胞黏附分子-1(sVCAM-1)、红细胞沉降率(ESR)的表达意义及其与预后的关系。方法 回顾性分析2020年1月至2022年9月安阳市人民医院收治的118例膝关节置换手术患者的临床资料,根据术后6个月Lysholm评分将患者分为预后不良组(总分<70分,27例)和预后良好组(总分≥70分,91例)。比较两组术后1、3个月血清RANKL、sVCAM-1、ESR表达水平,分析其与Lysholm评分的相关性,评估上述血清学指标联合检测对患者术后预后不良的预测价值。结果 术后1、3个月预后不良组血清RANKL、sVCAM-1、ESR水平高于预后良好组(P <0.05),术后1、3个月血清RANKL、sVCAM-1、ESR水平与Lysholm评分呈负相关(P <0.05),联合预测患者术后预后不良的曲线下面积(AUC)优于各血清指标单独预测(P <0.05)。结论 血清RANKL、sVCAM-1、ESR水平升高可提示膝关节置换术患者预后不良风险的增加,联合检测可作为预测预后不良、判断病情转归的参考依据。

2型糖尿病下肢血管病变患者介入治疗后血清NLRP3及sVCAM-1水平对再狭窄的意义

目的探讨2型糖尿病下肢血管病变患者介入治疗后血清NOD样受体蛋白3(NLRP3)及可溶性血管细胞黏附分子-1(sVCAM-1)水平对再狭窄的意义。方法回顾性分析2022年1月~2023年1月于河北省邯郸市中心医院血管介入科104例成功行血管介入治疗的2型糖尿病下肢血管病变患者的临床资料。根据介入后再狭窄发生情况分为再狭窄组(n=20)和无再狭窄组(n=84),比较两组患者一般资料及介入后24 h血清NLRP3、sVCAM-1水平,采用多因素Logistic回归模型分析再狭窄发生的影响因素;创建受试者工作特征(ROC)曲线,分析血清NLRP3、sVCAM-1检测对再狭窄的预测价值。结果与无再狭窄组相比,再狭窄组患者2型糖尿病病程、下肢动脉病变长度更长,Fontaine分期Ⅳ期占比、下肢动脉完全闭塞占比及血清糖化血红蛋白(HbA1c)、超敏C反应蛋白(hs-CRP)、NLRP3、sVCAM-1水平更高(P<0.05);多因素Logistic回归分析显示,下肢动脉完全闭塞、下肢动脉病变长度、HbA1c、NLRP3及sVCAM-1是2型糖尿病下肢血管病变患者介入后再狭窄发生的影响因素(P<0.05);ROC曲线显示,血清NLRP3、sVCAM-1联合检测对2型糖尿病下肢血管病变患者介入后再狭窄发生的预测价值较高,敏感度为95.00%,特异度为71.43%,ROC曲线下面积为0.929。结论血清NLRP3、sVCAM-1水平高表达均是2型糖尿病下肢血管病变患者介入治疗后再狭窄发生的危险因素,二者联合检测能提高2型糖尿病下肢血管病变患者介入治疗后再狭窄预测的准确性。