Indirect immunofluorescence (IIF) staining imaging on human epithelial cell (HEp-2) is a standard technique for anti-nuclear antibodies (ANA) screening. The application of deep neural networks for automated IIF image processing has led to remarkable progress in ANA pattern recognition. However, existing research has predominantly focused on coarse-grained and single-pattern recognition, despite the fact that the International Consensus on Antinuclear Antibody Patterns (ICAP) has defined 29 fine-grained patterns and IIF images often present multiple concurrent ANA patterns. In this study, we contribute a large scale IIF image dataset for fine-grained and multi-pattern recognition, which comprises up to 40 thousand high-resolution images and precise annotations of 17 ICAP recommended basic patterns and 5 pattern combinations from technologists with >10 years ANA experience. In addition, we introduce a neural network based recognition framework for this task, which consists of a mitotic detection network and a pattern classification network. To enhance the effectiveness and robustness of the recognition framework, we employ multiple strategies, including dataset resampling, automatic image augmentation and prediction aggregation. Our model achieved an F-score of 0.883 on the test dataset, significantly outperforming human technologists. Furthermore, with the assistance of the developed model, we observed a significant and consistent improvement in human performance. This approach enables scalable, automated and multi-pattern ANA reading aligned with ICAP standards.

Gastric cancer (GC), one of the most common and heterogeneous malignancies, is the second leading cause of cancer death worldwide and is closely related to dietary habits. Fatty acid is one of the main nutrients of human beings, which is closely related to diabetes, hypertension and other diseases. However, the correlation between fatty acid metabolism and the development and progression of GC remains largely unknown. Here, we profiled the genetic alterations of fatty acid anabolism-related genes (FARGs) in gastric cancer samples from the TCGA cohort and GEO database to evaluate the possible relationships and their internal regulatory mechanism. Through consistent clustering and functional enrichment analysis, three distinct fatty acid anabolism clusters and three gene subtypes were identified to participate in different biological pathways, and correlated with the characteristics of immune cell infiltration and clinical prognosis. Importantly, a distinctive FA-score was constructed through the principal component analysis to quantify the characteristics of fatty acid anabolism in each GC patient. Further analysis showed patients grouped in the high FA-score group were characterized with greater tumor mutational burden (TMB) and higher microsatellite stability (MSI-H), which may be more aeschynomenous to immunotherapy and had a favorable prognosis. Altogether, our bioinformatics analysis based on FARGs uncovered the potential roles of fatty acid metabolism in GC, and may provide newly prognostic information and novel approaches for promoting individualized immunotherapy in patients with GC.

The clinical application of the therapeutic approach in myelodysplastic syndromes (MDS) remains an insurmountable challenge for the high propensity for progressing to acute myeloid leukemia and predominantly affecting elderly individuals. Thus, the discovery of molecular mechanisms underlying the regulatory network of different programmed cell death holds great promise for the identification of therapeutic targets and provides insights into new therapeutic avenues. Herein, we found that disulfiram/copper (DSF/Cu) significantly repressed the cell viability, increased reactive oxygen species (ROS) accumulation, destroyed mitochondrial morphology, and altered oxygen consumption rate. Further studies verified that DSF/Cu induces cuproptosis, as evidenced by the depletion of glutathione (GSH), aggregation of lipoylated DLAT, and induced loss of Fe-S cluster-containing proteins, which could be rescued by tetrathiomolybdate and knockdown of ferredoxin 1 (FDX1). Additionally, GSH contributed to the tolerance of DSF/Cu-mediated cuproptosis, while pharmacological chelation of GSH triggered ROS accumulation and sensitized cell death. The xCT-GSH-GPX4 axis is the ideal downstream component of ferroptosis that exerts a powerful protective mechanism. Notably, classical xCT inhibitors were capable of leading to the catastrophic accumulation of ROS and exerting synergistic cell death, while xCT overexpression restored these phenomena. Simvastatin, an inhibitor of HMG-CoA (3-hydroxy-3-methylglutaryl-coenzyme A) reductase, has beneficial effects in repurposing for inhibiting GPX4. Similarly, the combination treatment of DSF/Cu and simvastatin dramatically decreased the expression of GPX4 and Fe-S proteins, ultimately accelerating cell death. Moreover, we identified that the combination treatment of DSF/Cu and simvastatin also had a synergistic antitumor effect in the MDS mouse model, with the reduced GPX4, increased COX-2 and accumulated lipid peroxides. Overall, our study provided insight into developing a novel synergistic strategy to sensitize MDS therapy by targeting ferroptosis and cuproptosis.

Paraquat (PQ) is an irreplaceable insecticide in many countries for the advantage of fast-acting and broad-spectrum. However, PQ was classified as the most prevailing poisoning substance for suicide with no specific antidote. Therefore, it is imperative to develop more effective therapeutic agents for the treatment of PQ poisoning. In the present study, both the RNA-Seq and the application of various cell death inhibitors reflected that ferroptosis exerts a crucial regulatory role in PQ poisoning. Moreover, we found PQ strengthens lipid peroxidation as evidenced by different experimental approaches. Of note, pretreatment of iron chelation agent DFO could ameliorate the ferroptotic cell death and alleviate the ferroptosis-related events. Mechanistically, PQ treatment intensively impaired mitochondrial homeostasis, enhanced phosphorylation of AMPK, accelerated the autophagy flux and triggered the activation of Nuclear receptor coactivator 4-ferritin heavy chain (NCOA4-FTH) axis. Importantly, the activation of autophagy was observed prior to the degradation of ferritin, and inhibition of autophagy could inhibit the accumulation of iron caused by the ferritinophagy process. Genetic and pharmacological inhibition of ferritinophagy could alleviate the lethal oxidative events, and rescue the ferroptotic cell death. Excitingly, in the mouse models of PQ poisoning, both the administration of DFO and adeno-associated virus-mediated FTH overexpression significantly reduced PQ-induced ferroptosis and improved the pathological characteristics of pulmonary fibrosis. In summary, the current work provides an in-depth study on the mechanism of PQ intoxication, describes a framework for the further understanding of ferroptosis in PQ-associated biological processes, and demonstrates modulation of iron metabolism may act as a promising therapeutic agent for the management of PQ toxicity.

Background:Gastric cancer (GC) is a malignancy with a grim prognosis, ranking as the second most common cause of cancer-related deaths globally. Various investigations have demonstrated the substantial involvement of ferroptosis and pyroptosis in the advancement of tumors. Nevertheless, the precise molecular mechanisms by which distinct genes associated with ferroptosis and pyroptosis influence the tumor microenvironment (TME) in GC remain elusive. Therefore, this study aims to elucidate the role of ferroptosis and pyroptosis in GC and provide insigths for GC therapy and prognosis evaluation. Methods:The data including gene expression, clinicopathological characteristics and survival information of GC samples from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) cohorts were collected, and the expression level of ferroptosis and pyroptosis genes (FPGs) in GC samples were analyzed. Consensus clustering analysis, Cox logistic regression, principal component analysis (PCA), and the "survival", "survminer", "limma", "ggplot2" and other packages in R were utilized to compare the differences among different groups. In the level of GC cells, cell viability experiments were conducted by Cell Counting Kit-8 (CCK-8) assay. Results:Through the analysis of the expression level of FPGs in GC samples from the TCGA and GEO cohorts, twenty-three prognostic-related and differentially expressed FPGs were collected for further analysis. Through consensus clustering analysis, three distinct patterns of FPGs were identified and found to be correlated with clinicopathological characteristics, immune cell infiltration, and prognosis in patients with GC. Subsequently, 684 prognostic-related genes from 1,082 pattern-related differentially expressed genes (DEGs) were screened for constructing the FPG_Score system to quantify FPGs patterns in individual GC patients and predict the prognosis. The analysis indicated that GC patients with high FPG_Score exhibited improved survival rates, increased tumor mutation burden (TMB), higher microsatellite instability (MSI), and elevated programmed cell death protein ligand 1 (PD-L1) expression. These patients with high FPG_Score were more likely to benefit from immunotherapy and had a more favorable prognosis. Conclusions:Our study innovatively provided a comprehensive analysis of FPGs in GC, and constructed the FPG_Score system for stratification of individual patients, so as to predict its benefit from immunotherapy and prognosis.

Acute myeloid leukemia (AML) is a prevalent hematological malignancy that exhibits a wide array of molecular abnormalities. Although traditional treatment modalities such as chemotherapy and allogeneic stem cell transplantation (HSCT) have become standard therapeutic approaches, a considerable number of patients continue to face relapse and encounter a bleak prognosis. The emergence of immune escape, immunosuppression, minimal residual disease (MRD), and other contributing factors collectively contribute to this challenge. Recent research has increasingly highlighted the notable distinctions between AML tumor microenvironments and those of healthy individuals. In order to investigate the potential therapeutic mechanisms, this study examines the intricate transformations occurring between leukemic cells and their surrounding cells within the tumor microenvironment (TME) of AML. This review classifies immunotherapies into four distinct categories: cancer vaccines, immune checkpoint inhibitors (ICIs), antibody-based immunotherapies, and adoptive T-cell therapies. The results of numerous clinical trials strongly indicate that the identification of optimal combinations of novel agents, either in conjunction with each other or with chemotherapy, represents a crucial advancement in this field. In this review, we aim to explore the current and emerging immunotherapeutic methodologies applicable to AML patients, identify promising targets, and emphasize the crucial requirement to augment patient outcomes. The application of these strategies presents substantial therapeutic prospects within the realm of precision medicine for AML, encompassing the potential to ameliorate patient outcomes.

BACKGROUND:C-type lectin domain family 1 member B (CLEC1B, encoding the CLEC-2 protein), a member of the C-type lectin superfamily, is a type II transmembrane receptor involved in platelet activation, angiogenesis, and immune and inflammatory responses. However, data regarding its function and clinical prognostic value in hepatocellular carcinoma (HCC) remain scarce. METHODS:The expression of CLEC1B was explored using The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. RT-qPCR, western blot, and immunohistochemistry assays were employed to validate the downregulation of CLEC1B. Univariate Cox regression and survival analyses were used to evaluate the prognostic value of CLEC1B. Gene Set Enrichment Analysis (GSEA) was conducted to investigate the potential association between cancer hallmarks and CLEC1B expression. The TISIDB database was applied to search for the correlation between immune cell infiltration levels and CLEC1B expression. The association between CLEC1B and immunomodulators was conducted by Spearman correlation analysis based on the Sangerbox platform. Annexin V-FITC/PI apoptosis kit was used for the detection of cell apoptosis. RESULTS:The expression of CLEC1B was low in various tumors and exhibited a promising clinical prognostic value for HCC patients. The expression level of CLEC1B was tightly associated with the infiltration of various immune cells in the HCC tumor microenvironment (TME) and positively correlated with a bulk of immunomodulators. In addition, CLEC1B and its related genes or interacting proteins are implicated in multiple immune-related processes and signaling pathways. Moreover, overexpression of CLEC1B significantly influenced the treatment effects of sorafenib on HCC cells. CONCLUSIONS:Our results reveal that CLEC1B could serve as a potential prognostic biomarker and may be a novel immunoregulator for HCC. However, its function in immune regulation should be further explored.

COVID-19, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), emerged as a global health threat in 2019. An important feature of the disease is that multiorgan symptoms of SARS-CoV-2 infection persist after recovery. Evidence indicates that people who recovered from COVID-19, even those under the age of 65 years without cardiovascular risk factors such as smoking, obesity, hypertension, and diabetes, had a significantly increased risk of cardiovascular disease for up to one year after diagnosis. Therefore, it is important to closely monitor individuals who have recovered from COVID-19 for potential cardiovascular damage that may manifest at a later stage. Ferroptosis is an iron-dependent form of non-apoptotic cell death characterized by the production of reactive oxygen species (ROS) and increased lipid peroxide levels. Several studies have demonstrated that ferroptosis plays an important role in cancer, ischemia/reperfusion injury (I/RI), and other cardiovascular diseases. Altered iron metabolism, upregulation of reactive oxygen species, and glutathione peroxidase 4 inactivation are striking features of COVID-19-related cardiovascular injury. SARS-CoV-2 can cause cardiovascular ferroptosis, leading to cardiovascular damage. Understanding the mechanism of ferroptosis in COVID-19-related cardiovascular injuries will contribute to the development of treatment regimens for preventing or reducing COVID-19-related cardiovascular complications. In this article, we go over the pathophysiological underpinnings of SARS-CoV-2-induced acute and chronic cardiovascular injury, the function of ferroptosis, and prospective treatment approaches.

BackgroundBlood gas analyzers (BGAs) and dry biochemistry analyzers for potassium and sodium are based on direct electrode methods, and both involve glucose oxidase for glucose detection. However, data are lacking regarding whether the results of the two assay systems can be used interchangeably. In addition, there remains controversy over the consistency between BGA-measured hemoglobin and complete blood count analyzer data. Here, we compared the consistency of sodium, potassium, glucose, and hemoglobin levels measured by BGA and dry chemistry and complete blood count analyzers.MethodsData from two teaching hospitals, the Zhejiang Provincial People's Hospital (ZRY) and the Qianfoshan Hospital (QY), were retrospectively analyzed based on dry biochemistry and complete blood count analyzer results as the reference system (X) and BGA as the experimental system (Y). Plasma was used for biochemical analysis at the ZRY Hospital, and serum at the QY Hospital. Paired data from the respective hospitals were evaluated for consistency, and biases between methods were assessed by simple correlation, Passing–Bablok regression, and Bland–Altman analyses.ResultsThe correlations of potassium, sodium, glucose, and hemoglobin measured by BGA and dry biochemistry and complete blood count analyzers were high, at 0.9573, 0.8898, 0.9849, and 0.9883 for the ZRY Hospital and 0.9198, 0.8591, 0.9764, and 0.8666, respectively, for the QY Hospital. The results of Passing to Bablok regression analysis showed that the predicted biases at each medical decision level were within clinically acceptable levels for potassium, sodium, glucose, and hemoglobin at the ZRY Hospital. Only the predicted bias of glucose was below the clinically acceptable medical decision levels at the QY Hospital, while potassium, sodium, and hemoglobin were not. Compared with the reference system, the mean bias for BGA measurements at the ZRY Hospital was −0.08 mmol/L (95% confidence interval [CI] −0.091 to −0.069) for potassium, 1.2 mmol/L (95% CI 1.06 to 1.42) for sodium, 0.20 mmol/L (95% CI 0.167 to 0.228) for glucose, and −2.8 g/L for hemoglobin (95% CI −3.14 to −2.49). The mean bias for potassium, sodium, glucose, and hemoglobin at the QY Hospital were −0.46 mmol/L (95% CI −0.475 to −0.452), 3.7 mmol/L (95% CI 3.57 to 3.85), −0.36 mmol/L (95% CI −0.433 to −0.291), and −8.7 g/L (95% CI −9.40 to −8.05), respectively.ConclusionBGA can be used interchangeably with plasma electrolyte results from dry biochemistry analyzers but does not show sufficient consistency with serum electrolyte results from dry biochemistry analyzers to allow data interchangeability. Good consistency was observed between BGA and plasma or serum glucose results from dry biochemistry analyzers. However, BGA-measured hemoglobin and hematocrit assay results should be treated with caution.

霍乱弧菌(Vibrio cholerae)是一种致病性革兰阴性杆菌,是导致急性腹泻的病原体.根据其菌体脂多糖O抗原的不同,可将霍乱弧菌分为200多种血清型,其中O1群和O139群霍乱弧菌曾多次在世界范围内引起霍乱暴发性流行[1].非O1/非O139群霍乱弧菌(non-O1 non-O139 Vibrio cholerae,NOVC)菌株不产生霍乱毒素,因此不会引起霍乱.这些微生物的临床意义在很长一段时间内都被忽视.然而,在过去的几十年中,越来越多的报道显示NOVC与人类多种感染性疾病有关[2-3].最常见的NOVC感染是胃肠炎,中耳炎和软组织感染.目前估计发展中国家和发达国家急性腹泻发病率的1％～3.4％是由于NOVC引起的[3].NOVC菌血症是NOVC感染中病死率最高的一种,近年来报告数呈上升趋势.然而,一些临床医生对这种疾病知之甚少.本文描述了1例酒精性肝硬化肝性脑病并发NOVC菌血症的患者,血清凝集试验显示该NOVC血液分离株具有自凝性.这种现象在NOVC感染病例中非常罕见,现予以报道.同时本研究首次对国内NOVC菌血症相关的病例进行回顾性分析,以期对NOVC菌血症的临床特征和流行病学有更好的认识.

目的 比较抗SSA+/SSB+和抗SSA+/SSB-pSS患者临床及实验室特征,探讨抗SSB抗体在pSS患者中的价值.方法 选取2017年7月-2019年7月本院就诊的269例pSS患者为研究对象,分析抗SSA/SSB表达情况.将抗SSA+/SSB+作为观察组,抗SSA+/SSB-为对照组,比较其临床及实验室特点.结果 纳入的269例pSS患者中,抗SSA+/SSB+112例(占41.6％);抗SSA+/SSB-有114例(占42.4％).观察组和对照组间,年龄、性别、临床表现和系统性并发症的发生率差异均无统计学意义(P ＞0.05).观察组RF的阳性率高于对照组(P =0.008),其余免疫学指标(IgG、C3、C4和ANA)、血常规指标(WBC、NEUT、LY、HB 和PLT)以及生化指标(ALT、AST、TBIL、DBIL 和AFP)的变化差异均无统计学意义(P ＞0.05).结论 抗SSA+/SSB+的pSS患者更倾向于RF阳性,除此之外,抗SSA+pSS患者是否合并抗SSB+对其临床表现和实验室特征均无影响.

Objective Adenosine deaminase (ADA) associated with cell-mediated immune responses is involved in many diseases. But little is known about the value of ADA activity in the progression of different diabetes types. The purpose of this study was to compare the ADA level between latent autoimmune diabetes in adults (LADA), type 2 diabetes (T2D) patients, and healthy controls (HC) and analyze its correlation with glycemic parameters and systemic cytokines. Methods This hospital-based study included 28 LADA patients, 52 T2D patients, and 50 HC. Serum ADA activity and concentrations of inflammatory cytokines were measured. Correlations of ADA level with different indicators were assessed by using spearman’s correlation method. Results Serum ADA activity was significantly higher in T2D patients compared with LADA ( p = 0.008) and HC ( p < 0.001). Correlation analysis of ADA with HbA1c% ( r = 0.34, p = 0.003) and inflammatory cytokines (IL-6, r = 0.31, p = 0.007; IL-10, r = 0.22, p = 0.049) showed significant positive correlations. Conclusions Serum ADA activity may reflect the different immunopathogenesis between LADA and T2D patients.

Objective To detect the serum concentrations of interleukin-6 (IL-6) in patients with polymyositis (PM),and to explore its clinical relationships in order to investigate the pathogenesis and treatment of PM.Methods Thirty-six patients with polymyositis were enrolled from April,2010 to January,2014 in our study.Serum IL-6 and TNF-α were detected using a commercially available EILSA.The statistical differences between groups were evaluated by the analysis of variance (ANOVA).The Spearman's correlation test was used to evaluate the relationship of IL-6 and clinical and laboratory data.Results Serum IL-6 concentrations were (19.67 ± 7.16) pg/ml in active PM patients,and (15.81 ± 4.00) pg/ ml in remission,which were significantly higher thin those of controls [(8.14 ± 3.71)pg/ml,P ＜ 0.001].Furthermore,IL-6 concentrations in active PM patients were significantly higher than those in remission (P =0.043).TNFαconcentrations were (114.44 ± 36.04) pg/ml in active PM patients,and (97.65 ± 30.78) pg/ml in remission,which were significantly higher than those of controls [(55.43 ± 22.83) pg/ml,P ＜ 0.001].However,there was no significant deference between PM patients in active phase and in remission.The serum IL-6 levels were positively correlated TNF-α (r =0.709,P =0.000),and negatively correlated with current glucocorticoid dose (r =-0.573,P =0.000).Conclusion IL-6 could be used as a marker of hormone dosage when evaluating and treating PM disease.

Objective To elucidate the clinical significance of macrophage migration inhibitory factor (MIF) serum concentration in patients with polymyositis. Methods Thirty-six patients with polymyositis were enrolled. Serum samples were obtained and stored to detect MIF and interleukin (IL)-6 using commercially available enzyme-linked immunosorbent assay kits. The relationships between these cytokines and clinical data were analyzed. Results The serum MIF concentration was significantly lower in patients in remission (34.74 ± 17.75) and in healthy controls (38.87 ± 9.30 ng/ml) than that in patients with active polymyositis (50.04 ± 23.84 ng/ml). There were no significant differences between healthy controls and patients in remission. The serum IL-6 concentration in patients with active polymyositis (19.67 ± 7.16 pg/ml) was significantly higher than that in patients in remission (15.81 ± 4.00 pg/ml) and controls (8.14 ± 3.71 pg/ml). The serum IL-6 concentration was negatively correlated with the serum MIF concentration (r = −0.283). No relationship was found between the serum MIF concentration and glucocorticoid dose. The MIF concentration peaked twice during treatment when the creatine kinase concentration was decreasing. Conclusion MIF and IL-6 play important roles in the inflammation associated with polymyositis. MIF might also be involved in the early stage of regeneration in polymyositis. MIF may thus serve as a biomarker of disease activity and outcome.

Previous studies suggested a pathological role for the death decoy receptor 3 (DcR3) in systemic lupus erythematosus (SLE) and rheumatic arthritis (RA). Herein, the expression of DcR3 in primary Sjögren’s syndrome (pSS) and the relationship with clinical characteristics were investigated. The serum DcR3 levels of pSS patients and healthy controls were measured by ELISA. Pearson’s correlation analysis was used to evaluate the relationship between the DcR3 levels with the clinical characterstics of pSS patients. Additionally, the DcR3 expression in salivary glands of pSS patients was investigated by the immunohistochemistry method. The serum DcR3 expression in pSS patients was significantly higher than healthy controls (p < 0.001), especially in new onset pSS patients (p = 0.036). Moreover, Pearson’s correlation analysis show that DcR3 levels were positively correlated with age (p = 0.013), platelet (PLT) (p = 0.002), hemoglobin (Hb) (p = 0.004), Sjögren’s syndrome disease damage activity index (SSDAI) score (p = 0.005), Sjögren’s syndrome disease damage index (SSDDI) score (p < 0.001) and EULAR Sjögren’s syndrome disease activity index (ESSDAI) score (p = 0.010). Furthermore, the DcR3 levels were significantly lower when the pSS patients were treated with the disease-modifying anti-rheumatic drugs. At last, DcR3 expression in salivary glands of pSS patients was significantly higher than healthy controls. The DcR3 expression was significantly elevated in the pSS patients and positively correlated with the clinical characteristics, and it might be an important factor involved in the progression of pSS patients and could be a potential therapeutic target.

目的 建立人SW1116结肠癌细胞中稳定过表达CXCR2稳定细胞株,分析过表达CXCR2基因对人结肠癌SW1116细胞迁移能力的影响.方法 分离健康人外周血单个核细胞,Trizol提取总RNA并反转录为cDNA,PCR扩增CXCR2的CDS序列,连接至慢病毒穿梭质粒pLVX-IRES-ZsGreen1多克隆位点,进行CXCR2基因的克隆,构建pLVX-IRES-ZsGreen1-CX-CR2重组质粒.重组质粒与包装质粒通过磷酸钙共转染法包装出慢病毒上清并对人SW1116结肠癌细胞进行感染.real-timePCR及Western blot方法分析转染pLVX-IRES-ZsGreen1-CXCR2重组质粒的人SW1116结肠癌细胞中CXCR2表达情况.Tr-answell实验分析过表达CXCR2对结肠癌细胞体外迁移的影响.结果 成功建立稳定表达CXCR2基因的SW1116结肠癌细胞株,并初步阐明CXCR2能够促进结肠癌细胞体外迁移.结论 成功建立过表达CXCR2基因的结肠癌细胞并能促进其体外迁移.

目的 应用受试者工作特征曲线(Receiver operating characteristics,ROC)分析死亡诱骗受体3(Death decoy receptor 3,DcR3)对类风湿性关节炎(Rheumatoid Arthritis,RA)的诊断价值.方法 用亲和素放大的酶联免疫吸附试验(ELISA)检测33例RA患者、10例硬化征患者及16例正常对照组血清可溶性DcR3浓度,分析不同组间DcR3表达的差异,以及RA患者DcR3与各临床指标的相关性.采用ROC曲线,评价DcR3对RA的诊断效能.结果 RA患者DcR3水平显著高于正常对照组(U =158.00,P＜0.05),与硬化征组比较差异无统计学意义(U =121.50,P＞0.05).RA患者DcR3水平与不同疾病分期(X线分期)、性别、年龄及各临床指标相关性差异无统计学意义(P＞0.05).通过ROC曲线分析,用DcR3诊断RA的曲线下面积(Area under the ROC curve)为0.701,曲线下95％可信区间(Asymptotic 95％ Confidence Interval)为0.553～0.849.最佳临界点为213 pg/ml,敏感度为51.5％,特异性为81.2％;阳性似然比为2.75,阴性似然比为0.60.结论 RA患者血清可溶性DcR3高表达,对RA具有良好的诊断价值.

Objective:To explore the expression of serum soluble decoy receptor 3(DcR3) in systemic lupus erythematosus(SLE) and relation with clinical medicine treatment.Methods: 51 patients with SLE and 19 healthy controls were collected.The levels of serum soluble DcR3 were detected by enzyme linked immunosorbent assay(ELISA).SLE disease activity index(SLEDAI) were used to assess the disease activity in SLE,and the relevance between the main medcine(prednisone,cyclophosphamide,azathioprine,hydroxychloroquine) in SLE treatment with serum soluble DcR3 and SLEDAI were analyzed.Results: The concentrations of serum soluble DcR3 were markedly higher in SLE group than those in the control group(t=2.42,P0.05),and it was positively correlated with SLEDAI(r=0.373,P0.01).In particular,serum soluble DcR3 levels of SLE patients treated with a regimen containing prednisone were significantly higher than those without using prednisone(P 0.05),while serum soluble DcR3 level was much lower in group treated with a regimen containing hydroxychloroquine.Furthermore,a regimen containing prednisone or cyclophosphamide showed a higher SLEDAI score than those not containing.Conclusion: Serum soluble DcR3 expression in SLE increased and positively correlated with SLEDAI.The influence of medication on serum soluble DCR3 is not obvious and it can serve as an indicator for SLE diagnosis and evaluation of SLE disease activity.

OBJECTIVE:To evaluate the value of plasma ProGRP, CYFRA 21-1 and CEA in patients with lung cancer.METHODS:The levels of plasma ProGRP, CYFRA 21-1 and CEA were detected in 85 healthy control, 49 benign lung diseases and 143 lung neoplasms. The levels of ProGRP in the patients with SCLC was monitored.RESULTS:The level of plasma ProGRP in SCLC (M 179.1 ng/ml) was significantly higher than adenocarcinoma (M 35.3 ng/ml), squamous-cell carcinoma (M 33.3 ng/ml), healthy control (M 35.6 ng/m) and benign lung diseases (M 33.3 ng/m), P < 0.001. The sensitivity and specificity for diagnosing SCLC by ProGRP were 60.6% and 95.0% respectively. In the effective treatment group, ProGRP reduced 45.9%, in the progression group, ProGRP increased 103.1%, P < 0.05. The level of CEA in the metastatic adenocarcinoma (M 10.22 ng/ml) was significantly higher than non-metastatic adenocarcinoma (M 3.85 ng/ml) and squamous cell carcinoma (M 2.56 ng/ml) (P < 0.01).CONCLUSION:The plasma ProGRP is a good indicator for diagnosing and evaluating cure effect in SCLC; the high expression of CEA is related to the metastatic adenocarcinoma.

干燥综合征(Sj(o)gren's syndrome,SS)是一种以侵犯泪腺、唾液腺等外分泌腺为主的慢性自身免疫性疾病.我国人群患病率为0.3%～0.7%,是自身免疫性疾病中极为常见的一种,但其临床研究远落后于系统性红斑狼疮(SLE)、类风湿关节炎(RA)等其他风湿性疾病[1],故对病因形成及临床特征进行探析性研究,为加强疾病的早期诊断和治疗非常必要。