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.

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.

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.

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.

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.

Adhesion molecule and proinflammatory cytokine gene expression in hepatic sinusoidal endothelial cells following cecal ligation and puncture

INTRODUCTIONMultiple organ dysfunction syndrome (MODS) isthought to be a frequent consequence of sepsis[1-3].Despite substantial advances in our knowledge and understanding of the basic pathophysiologic mechanisms[4-7], in critically ill patients infections and sepsis are still associated with a high mortality[8,9].

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.

Ubiquitin Reduces Expression of Intercellular Adhesion Molecules and Tumor Necrosis Factor-α in Lung Tissue of Experimental Acute Lung Injury

Background Intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) are two important cytokines in inflammatory response, which may induce rolling and adhesion of both leukocytes and lymphocytes, while modulating vascular permeability at the same time. These adhesion molecules usually serve as surrogate markers of activation and injury of vascular endothelial cells. Tumor necrosis factor-α (TNF-α) is a key factor to induce the expression and production of the above cell adhesion molecules. However, it remains to be elucidated whether exogenous ubiquitin exerts any effect on the cytokines in sepsis-induced ALI. Methods Sixty mice were devided randomly into five groups with twelve mice in each group, i.e. CLP group, SHAM group, UB1 group (10 mg/kg), UB2 group (5 mg/kg) and UB3 group(1 mg/kg). Mice of SHAM group underwent sham operation, and other four groups underwent CLP. Six hours after surgery, mice of three UB groups received ubiquitin by caudal vein injection while CLP and SHAM group received vehicle. Seven hours after surgery, blood and lungs of all mice were collected. ICAM-1, VCAM-1 and TNF-α level of 9% lung homogenate and serum TNF-α level were measured by ELISA. Results Pulmonary ICAM-1, VCAM-1 and TNF-α level of three UB groups were lower than CLP and SHAM group, and there were several comparisons with a statistically significant difference. Serum TNF-α level of three UB groups were slightly lower than CLP group, but far higher than SHAM group. Pulmonary ICAM-1 level, VCAM-1 level and serum TNF-α level of UB3 group were lower than UB1 and UB2 group, and there was a significant difference in VCAM-1 between UB3 and UB1 group. Pulmonary TNF-α level of UB3 group was slightly higher than UB1 and UB2 group.

精神分裂症患者神经细胞黏附分子、视锥蛋白样蛋白-1表达与认知功能障碍的相关性分析

目的:分析精神分裂症患者神经细胞黏附分子(nerve cell adhesion molecule,NCAM)、视锥蛋白样蛋白-1(cone-like protein-1,VILIP-1)表达与认知功能障碍的相关性分析。方法:选取进行治疗的精神分裂症患者65例为疾病组,进行健康体检的人员60名为健康组。检测白细胞介素-1β(interleukin-1β,IL-1β)、肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、白细胞介素-6(IL-6)、NCAM、VILIP-1;采用阳性与阴性症状量表(positive and negative syndrome scale,PANSS)对患者精神分裂症严重情况进行评定;蒙特利尔认知评估量表(Montreal cognitive assessment,MoCA)对患者自身认知功能情况进行评估。结果:与健康组相比,疾病组NCAM表达水平降低,VILIP-1升高(P均<0.05);NCAM与PANSS评分之间呈负相关性,NCAM与MoCA评分之间呈正相关性(P均<0.05);VILIP-1与PANSS评分之间呈正相关性,VILIP-1与MoCA评分之间呈负相关性(P均<0.05);受试者工作曲线(receiver operation characteristic,ROC)分析显示,与NCAM、VILIP-1单项诊断相比,联合检测对精神分裂症的诊断价值较高(P均<0.05)。结论:精神分裂症患者机体内NCAM和VILIP-1表达水平的异常升高或降低是精神分裂症的风险预测因子,可能与病情的诊断、发展及认知功能等具有紧密关联。

Negative Association of Circulating MicroRNA-126 with High-sensitive C-reactive Protein and Vascular Cell Adhesion Molecule-1 in Patients with Coronary Artery Disease Following Percutaneous Coronary Intervention

Background： Percutaneous coronary intervention （PCI） causes endothelial damage, resulting in an inflammatory response with elevation of markers such as high-sensitive C-reactive protein （hs-CRP） and vascular cell adhesion molecule-1（VCAM-1）, which are associated with restenosis after PCI. Evidence suggests that microRNA-126 （miR-126） plays an important role in vascular inflammation, but its correlation with PCl-mediated inflammation has not been investigated. In this study, we investigated the effect of PCI on circulating miR-126 and inflammation markers such as hs-CRP and VCAM-1. Methods： We enrolled 130 patients with coronary artery disease （CAD） in the Second Hospital of Jilin University from October 2015 to December 2015. Among them, 82 patients with CAD, defined as at least one major epicardial vessel with 〉70% stenosis who planned to undergo PCI, were divided into acute coronary syndrome （ACS） group （46 patients） and stable angina （SA） group （36 patients）. Forty-eight patients confirmed by coronary angiography without PCI were used as controls. The plasmas of all patients were collected prior to PCI and at 30 min, 24 h, and 72 h after PCI. The plasma VCAM-1 and hs-CRP were detected by enzyme-linked immunosorbent assay, and the miR-126 was evaluated by quantitative reverse transcription-polymerase chain reaction. Results： Plasma concentrations of hs-CRP and VCAM-I in patients with either ACS （n = 46） or SA （n = 36） were significantly higher than in controls （n = 48） （P 〈 0.01） prior to PCI, and increased further at 24 h and 72 h after PCI, compared with prior PCI. Moreover, VCAM-1 was positively correlated with balloon time and pressure. In contrast, the plasma concentration of miR-126 was significantly lower in patients with CAD than in controls, and further decreased with time post-PCl. A negative correlation was observed between miR-126 and hs-CRP and VCAM-1 at 72 h after PCI. Conclusion： There was a negative correlation of miR-126 with the PCI-induced markers of inflammation such as hs-CRP and VCAM-1.

Expression of platelet-endothelial cell adhesion molecule-1 in human umbilical vein endothelial cells by exposure to advanced glycosylation end products and inflammatory mediators

Objective To determine whether advanced glycosylation end products modified bovine serum albumin (AGEs-BSA) affects endothelial cell lateral junction protein, platelet-endothelial cell adhesion molecule-1 (PECAM-1) in the presence or absence of inflammatory mediators.Methods Cultured human umbilical vein endothelial cells (HUVECs) were exposed to AGEs-BSA for 6, 12, 24, and 36 hours, and exposed to AGEs-BSA glycosylated with different concentrations of glucose, tumor necrosis factord-α (TNF-α), interferon (IFN-γ), TNF-α + IFN-y and AGEs-BSA + TNF-α for 24 hours, respectively. Expression of PECAM-1 mRNA was measured by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) with β-actin as an internal standard, and sequencing of RT-PCR products was performed to confirm the specificity of amplification for PECAM-1 gene. The endothelial cell surface expression of PECAM-1 was determined by flow cytometry (FCM).Results There were no significant changes in the expression of PECAM-1 mRNA and protein when the cells were exposed to AGEs-BSA with different concentrations or periods ( P>0. 05). However, PECAM-1 expression was reduced in the cells treated with TNF-α, IFN-y, TNF-α + IFN-γ and AGEs-BSA + TNF-α. The level of PECAM-1 treated with AGEs-BSA + TNF-α was lower than that of TNF-α treated alone (P<0. 01).Conclusions AGEs-BSA had no effect on the expression of PECAM-1 mRNA and protein in cultured HUVEC. With the presence of inflammatory mediator TNF-α, AGEs-BSA decreased the level of PECAM-1, which might reduce the adhesion interaction between adjacent endothelial cells, enhance the permeability of endothelial cells, and might be implicated in the endothelial dysfunction and pathogenesis of atherosclerosis in patients with diabetes mellitus. The significance of this phenomenon in intracellular signal transduction remains to be determined.

Cardiotrophin-1 induces intercellular adhesion molecule-1 expression by nuclear factor κB activation in human umbilical vein endothelial cells

Background In addition to elevated concentrations of cytokines, patients with congestive endothelial dysfunction and increased plasma concentrations of adhesion molecules heart failure （CHF） show ke intercellular adhesion molecule-1 （ICAM-1）. Furthermore, the concentration of cardiotrophin-1 （CT-1） - a cytokine of the interleukin-6 superfamily - is increased in CHF. We tested the hypothesis whether CT-1 is able to induce ICAM-1 in human umbilical vein endothelial cells （HUVEC）. Furthermore we examined the signalling mechanisms of CT-1 mediated ICAM-1 expression. Methods Confluent layers of HUVEC were incubated with increasing concentrations of CT-1 （5 to 100 ng/ml） for different periods. ICAM-1 mRNA was determined by real-time polymerase chain reaction （PCR） and ICAM-1 surface expression by fluorescence-activated cell sorter （FACS） analysis and soluble ICAM-1 （slCAM-1） in the culture supernatant by enzyme linked immunosorbent assay （ELISA）. To clarify the signalling pathway of CT-1 induced ICAM-1 expression we used various inhibitors of possible signal transducing molecules, electromobility shift assay （EMSA） and Western blot analysis. Results CT-1 induced ICAM-1 mRNA （1.8±0.8 fold increase compared to unstimulated cells after 6 hours） and protein （1.4±0.2 fold increase compared to unstimulated cells after 48 hours） in HUVEC in a time- and concentration-dependent manner. EMSA experiments show that CT-1 causes nuclear factor （NF） κB activation. Because parthenolide could inhibit CT-1 induced ICAM-1 expression NFκB activation is required in this pathway. CT-1 did not activate extracellular signal regulated kinases （ERK）, c-Jun N-terminal kinase （JNK） and p38. Conclusion CT-1 is able to induce ICAM-1 in endothelial cells by NFκB activation. These results may explain in part elevated ICAM-1 concentrations in patients with CHF and endothelial dysfunction.

鼻息肉中细胞间黏附分子1和E-选择素的表达及意义

鼻息肉是耳鼻咽喉科常见病,严重危害人们身心健康。鼻息肉发病机制至今仍未完全阐明,众多研究表明嗜酸性粒细胞（eosinophils,Eos）浸润是鼻息肉最显著的病理特征。因此,探讨以Eos为代表的炎性细胞聚集和活化成为研究鼻息肉发病机制的热点。本文拟通过分析鼻息肉组织中细胞间黏附分子1（intercellular adhesion molecule-1,ICAM．1）、E-选择素的表达，探讨其与Eos浸润及鼻息肉形成的关系。

2型糖尿病血清可溶性血管细胞黏附分子-1水平与心率变异性关系

目的研究2型糖尿病患者血清可溶性血管细胞黏附分子-1与心率变异性的关系。方法随机选择2型糖尿病人60例、健康对照者59例,所有的研究者进行24 h动态心电图监测及空腹血清VCAM-1检测,并进行分析。结果DM组患者平均心率、最慢心率与对照组比较显著增加,P<0.01,糖尿病组心率变异指数与对照组比较显著降低,P<0.01;最快心率两组比较无明显差异;DM组的血清SCVAM-1水平比对照组明显升高,P<0.01;HRVI低于25的患者其血清SCVAM-1水平明显高于HRVI高于25的患者,P<0.01。结论血清SCVAM-1与2型糖尿病心脏自主神经病变关系密切,参与2型糖尿病自主神经病变的发生与发展。

甲状腺转录因子-1和细胞角蛋白7与神经细胞黏附分子CD56及p63蛋白在支气管针吸活检确诊肺癌标本中的表达及其诊断价值

目的探讨甲状腺转录因子-1和细胞角蛋白7与神经细胞黏附分子CD56及p63蛋白在支气管针吸活检确诊肺癌标本中的表达及其诊断价值。方法回顾性分析2018年1月至2021年1月本院收治的200例行支气管针吸活检的肺癌患者的临床资料。采用免疫组织化学染色SP法检测肺癌患者标本中甲状腺转录因子-1、细胞角蛋白7、神经细胞黏附分子CD56及p63蛋白的表达情况,比较甲状腺转录因子-1、细胞角蛋白7、神经细胞黏附分子CD56及p63蛋白在不同病理类型中的阳性表达率,分析甲状腺转录因子-1、细胞角蛋白7、神经细胞黏附分子CD56诊断小细胞肺癌、腺癌和p63蛋白诊断鳞癌的价值。结果不同病理类型中,小细胞肺癌中甲状腺转录因子-1阳性表达率高于腺癌和鳞癌,且腺癌中甲状腺转录因子-1阳性表达率高于鳞癌,差异有统计学意义(P<0.05);小细胞肺癌中神经细胞黏附分子CD56阳性表达率高于腺癌和鳞癌,差异有统计学意义(P<0.05);腺癌中细胞角蛋白7阳性表达率高于小细胞肺癌和鳞癌,差异有统计学意义(P<0.05);鳞癌中p63蛋白阳性表达率高于腺癌和小细胞肺癌,差异有统计学意义(P<0.05)。甲状腺转录因子-1单项检测小细胞肺癌的特异度、阳性预测值均低于神经细胞黏附分子CD56单项检测及联合检测,差异有统计学意义(P<0.05);甲状腺转录因子-1、神经细胞黏附分子CD56单项检测及联合检测小细胞肺癌的灵敏度、阴性预测值比较差异无统计学意义。甲状腺转录因子-1单项检测腺癌的灵敏度、特异度、阳性预测值、阴性预测值均低于细胞角蛋白7和联合检测,且细胞角蛋白7单项检测的特异度、阳性预测值均低于联合检测,差异有统计学意义(P<0.05)。p63蛋白诊断鳞癌的灵敏度为100.00%,特异度为86.00%,阳性预测值为70.42%,阴性预测值为100.00%。结论肺癌患者支气管针吸活检标本的甲状腺转录因子-1、细胞角蛋白7、神经细胞黏附分子CD56及p63蛋白免疫组织化学染色有助于肺癌的诊断及组织学分型,具有临床指导价值。

精神分裂症患者血清NCAM、IGF-1、Galectin-3表达水平及与认知功能的关系

目的探讨精神分裂症患者血清神经细胞黏附分子(NCAM)、胰岛素样生长因子-1(IGF-1)、半乳糖凝集素-3(Galectin-3)表达水平及与认知功能的关系。方法选取2018年1月至2020年1月在我科接受治疗的精神分裂症患者90例(观察组),另选取体检健康者90例(对照组)作为研究对象。采用酶联免疫吸附法检测血清NCAM、IGF-1、Galectin-3水平。应用阳性和阴性症状量表(PANSS)评估患者临床症状,采用MATRICS公认认知成套测验(MCCB)评估患者认知功能,根据患者有无认知功能损害分为认知功能障碍组(n=36)和认知功能正常组(n=54),分析血清NCAM、IGF-1、Galectin-3与患者认知功能的关系。结果观察组血清NCAM、IGF-1、Galectin-3水平低于对照组,差异有统计学意义(P<0.05)。认知功能障碍组血清NCAM、IGF-1、Galectin-3水平低于认知功能正常组,差异有统计学意义(P<0.05)。Pearson相关性分析结果显示,血清NCAM、IGF-1、Galectin-3分别与PANSS、MCCB呈正相关(P<0.05)。ROC曲线结果示,血清NCAM、IGF-1、Galectin-3及三者联合检测预测精神分裂症患者认知功能的AUC分别为0.828、0.790、0.765和0.913。结论精神分裂症患者血清NCAM、IGF-1、Galectin-3水平明显降低,其血清水平与患者认知功能状态密切相关,且对患者的认知功能改变具有一定预测价值。

Change of hs-CRP,sVCAM-1,NT-proBNP levels in patients with pregnancy-induced hypertension after therapy with magnesium sulfate and nifudipine

Objective:To investigate the change of the hs-CRP,sVC AM-1,NT-proBNP levels of the patients with pregnancy-induced hypertension(PIH) syndrome.Methods:A total of 200 patients with PIH were divided into mild,moderate and severe group,and 50 healthy pregnancy patients served as the control group.The serum sVCAM-1 levels were detected by enzyme-linked immunosorbent assay,hs-CRP were detected by immunity transmission turbidity,and NT-proBNP levels were determined by the colloidal gold method.Patients were treated with magnesium sulfate and nifudipine and the contrastive analysis was performed before and after treatment.And the pathological changes in placental of PIH patients were delected by hematoxylin-eosin staining at the same time.Results:The hs-CRP,sVCAM-l,NT-proBNP levels of patients in the mild, moderate and severe PHI group were significantly higher than that in the control group(P<0.05). The hs-CKP,sVCAM-l,NT-proBNP levels in the severe group were significantly higher than the mild group and the moderate group,the difference was statistically significant(P<0.05).The hsCRP,sVCAM-l,NT-proBNP of the moderate group were significantly higher than the mild group(P<0.05).There was a positive correlation between hs-CRP,sVCAM-1,NT-proBNP expression levels and the degree of the PIH.The expression of hs-CRP,sVCAM-1,NT-proBNP levels of the moderate and the severe group were significantly decreased(P<0.05).The number of placental villi and interstitial blood vessel in the moderate and severe PIH group were significantly less than the control group(P<0.05).Conclusions:The increased levels of serum hs-CRP,sVCAM-1, NT-proBNP may be involved in the process of vascular endothelial cell injury of the PIH,and the hs-CRP,sVCAM-1,NT-proBNP can be used as the auxiliary index for diagnosis of PIH and determination of PIH severity.

CT冠脉成像联合血清Sortilin、NCAM-1在冠心病诊断中的临床价值分析

目的探究CT冠脉成像联合血清Sortilin、NCAM-1在冠心病(CHD)诊断中的临床价值。方法选取2021年6月-2022年6月我院收治的疑似CHD患者138例为研究对象,经冠状动脉造影诊断为CHD的有96例即为CHD组,其中分急性心肌梗死(AMI组)30例,不稳定型心绞痛(UAP组)34例,稳定型心绞痛(SAP组)32例,同期正常体检健康志愿者88例为对照组。采用酶联免疫吸附测定法(ELISA)测定血清中Sortilin、NCAM-1表达水平;Pearson法分析CHD患者血清中Sortilin和NCAM-1的相关性;绘制受试者工作特征(ROC)曲线分析Sortilin、NCAM-1对CHD的诊断价值;采用四格表评估CT冠脉成像联合血清Sortilin、NCAM-1对CHD的诊断效能。结果与对照组相比,CHD组Sortilin的表达水平显著升高,NCAM-1水平显著降低(P<0.05)。与AMI组相比,UAP组和SAP组患者Sortilin的表达水平显著升高,SAP组显著高于UAP组;UAP组和SAP组患者NCAM-1的表达水平与AMI组相比显著降低,SAP组显著低于UAP组(P<0.05)。相关性分析显示,在CHD患者血清中Sortilin、NCAM-1表达水平呈负相关关系(r=-0.570,P<0.001)。CT冠脉成像联合血清Sortilin、NCAM-1诊断CHD的敏感度较高于CT冠脉成像、Sortilin、NCAM-1单独诊断的敏感度。结论CHD患者血清中Sortilin的表达水平显著升高,NCAM-1水平显著降低,CT冠脉成像联合血清Sortilin、NCAM-1可以提高CHD的诊断效能。

EP-CAM、N-CAM1及C-KIT与原发性肝癌分级、转移及患者预后的关系

目的探讨上皮细胞黏附分子(EP-CAM)、神经细胞黏附分子1(N-CAM1)及C-KIT与原发性肝癌分级、转移及患者预后的关系。方法收集80例原发性肝癌患者作为观察组,选择同期行手术治疗的50例肝硬化及乙型肝炎患者作为对照组,均收集患者病理组织标本,采用免疫组化法测定肝癌组织EP-CAM、N-CAM1、C-KIT表达情况,分析EP-CAM、N-CAM1、C-KIT与原发性肝癌临床病理特点及患者预后的关系。结果观察组EP-CAM、N-CAM1、C-KIT阳性表达率均高于对照组(P<0.05);高AFP水平、无包膜或包膜不完整、低中分化肿瘤、临床分期为Ⅲ~Ⅳ期、病理类型为胆管上皮癌、混合型肝癌及出现肝内外转移的肝癌患者EP-CAM、N-CAM1、C-KIT阳性率较高(P<0.05);肝癌患者1年、2年、3年生存率分别为72.50%、53.75%、37.50%,随访3年存活患者,EP-CAM、N-CAM1、C-KIT阳性率低于1年及2年存活患者(P<0.05)。结论EP-CAM、N-CAM1、C-KIT表达水平与原发性肝癌患者AFP水平、肿瘤包膜情况、分化程度、临床分期、组织学类型及预后均有一定的关系,且参与肝癌侵袭、转移过程。

Effect of a cancer vaccine prepared by fusions of hepatocarcinoma cells with dendritic cells

AIM: To prepare a cancer vaccine (H(22)-DC) expressing high levels of costimulatory molecules based on fusions of hepatocarcinoma cells (H(22)) with dendritic cells (DC) of mice and to analyze the biological characteristics and induction of specific CTL activity of H(22)-DC. METHODS: DCs were isolated from murine spleen by metrizamide density gradient centrifugation, purified based on its characteristics of semi-adhesion to culture plates and FcR-,and were cultured in the medium containing GM-CSF and IL-4. A large number of DC were harvested. DCs were then fused with H(22) cells by PEG and the fusion cells were marked with CD11c MicroBeads. The H(22)-DC was sorted with Mimi MACS sorter. The techniques of cell culture, immunocytochemistry and light microscopy were also used to test the characteristics of growth and morphology of H(22)-DC in vitro. As the immunogen, H(22)-DC was inoculated subcutaneously into the right armpit of BALB/C mice, and their tumorigenicity in vivo was observed. MTT was used to test the CTL activity of murine spleen in vivo. RESULTS: DC cells isolated and generated were CD11c+ cells with irregular shape, and highly expressed CD80, CD86 and CD54 molecules. H22 cells were CD11c- cells with spherical shape and bigger volume, and did not express CD80, CD86 and CD54 molecules.H(22)-DC was CD11c+ cells with bigger volume, being spherical, flat or irregular in shape, and highly expressed CD80, CD86 and CD54 molecules, too. H(22)-DC was able to divide and proliferate in vitro, but its activity of proliferation was significantly decreased as compared with H(22) cells and its growth curve was flatter than H(22) cells. After subcutaneous inoculation over 60 days, H(22)-DC showed no tumorigenecity in mice, which was significantly different from control groups (P【0.01). The spleen CTL activity against H(22) cells in mice implanted with fresh H(22)-DC was significantly higher than control groups (P 【 0.01). CONCLUSION: H(22)-DC could significantly stimulate the specific CTL activity of murine spleen, which suggests that the fusion cells have already obtained the function of antigen presenting of parental DC and could present H(22)specific antigen which has not been identified yet, and H(22)-DC could induce antitumor immune response; although simply mixed H(22) cells with DC could stimulate the specific CTL activity which could inhibit the growth of tumor in some degree, it could not prevent the generation of tumor. It shows that the DC vaccine is likely to become a helpful approach in immunotherapy of hepatocarcinoma.