目的 总结儿童传染性单核细胞增多症(IM)合并肝损害的临床特点及相关因素。 方法 对2000年1月－2012年1月入院收治48例合并肝损害IM与120例无肝损害IM的患儿年龄、性别、主要症状和体征、系统损害、实验室检查等资料进行回顾性分析。 结果 合并肝损害IM患儿血小板减少、异形淋巴细胞增加、丙氨酸氨基转换酶和天门冬氨酸氨基转移酶等血清酶学异常、持续发热、中重度肝脾肿大，以及多系统损害发生率较高；而咽峡炎、皮疹和浅表淋巴结肿大发生率较低；IM合并肝损害与发病年龄、性别无明显相关（r=0.127，0.075，P＜0.05）。 结论 IM合并肝损害表现为持续发热、肝脾肿大、肝酶异常、血小板减少、异形淋巴细胞增加较常见。及时作肝功能等辅助检查，及早发现和干预IM肝损害，有助于减少重症IM的发生。
目的:研究CC亚族趋化因子单核细胞趋化蛋白-4(MCP-4/CCL13)在类风湿关节炎(RA)患者外周血的表达水平,并分析MCP-4的水平与疾病活动性的关系,以探讨MCP-4在RA发病机制中的作用。 方法:应用酶联免疫吸附实验(ELISA)定量方法测定40例RA患者、20例其它自身免疫性疾病患者和20例正常健康对照者血清MCP-4水平。分析RA组血清MCP-4水平是否与ESR、CRP、RF及双手放射学检查等指标具有相关性。结果:RA组血清MCP-4水平为(203.79±18.64)pg/mL,其它自身免疫性疾病对照组血清MCP-4水平为(207.76±40.37)pg/mL,正常健康对照组血清MCP-4水平为(125.13±11.08)pg/mL。RA组、其它自身免疫性疾病对照组血清MCP-4水平与正常健康对照组相比均有统计学意义(Plt;0.05),RA组与其它自身免疫性疾病对照组间无统计学意义(P=0.787),RA活动期患者血清MCP-4水平(214.86±24.46)pg/mL和非活动期患者血清MCP-4水平(190.27±29.11)pg/mL比较无统计学意义(P=0.065)。RA组血清MCP-4水平与ESR、CRP、RF及双手X片分期无相关性。结论:RA组的血清MCP-4水平高于正常健康对照组,但与ESR、CRP、RF及双手X片分期无相关性。MCP-4可能参与了RA的发病过程。
Objective To investigate the expressions of monocyte chemoattractant protein-1 (MCP-1) and vascular endothelial growth factor (VEGF) in gastric cancer tissues and normal gastirc mucosa tissues and the situation of helicobacter pylori (HP) infection, and detect their relationships and clinicopathologic significances. Methods Expressions of MCP-1 and VEGF were detected by immunohistochemistry in gastric cancer tissues and normal gastric mucosa tissues (5-10 cm from the mass), and HP was detected in specimen from gastric antrum by Giemsa dyeing method. Results MCP-1 and VEGF expressions in gastric cancer tissues were significantly higher than those in normal gastric mucosa tissues (P＜0.05), but there was no difference in HP positive and negative tissues included the cancer and the normal tissues （P＞0.05）. The expressions of MCP-1 and VEGF in carcinoma with tumordiameter ＞5 cm, poorly differentiated， lymph node metastasis， distant metastasis and Ⅲ+Ⅳ stage of TNM were significantly higher than those with tumor diameter ≤5 cm, well and moderately differentiated， non-lymph node metastasis， non-distant metastasis and Ⅰ+Ⅱ stage of TNM (P＜0.05). Conclusion The high expressions of MCP-1 and VEGF in gastric cancer may relate to tumor angiogenesis and metastasis, but HP infection may be irrelevant.
Objective To investigate the correlation between monocyte-lymphocyte ratio (MLR) and intensive care unit (ICU) results in ICU hospitalized patients. Methods Clinical data were extracted from Medical Information Mart for Intensive Care Ⅲ database, which contained health data of more than 50000 patients. The main result was 30-day mortality, and the secondary result was 90-day mortality. The Cox proportional hazards model was used to reveal the association between MLR and ICU results. Multivariable analyses were used to control for confounders. Results A total of 7295 ICU patients were included. For the 30-day mortality, the hazard ratio (HR) and 95% confidence interval (CI) of the second (0.23≤MLR<0.47) and the third (MLR≥0.47) groups were 1.28 (1.01, 1.61) and 2.70 (2.20, 3.31), respectively, compared to the first group (MLR<0.23). The HR and 95%CI of the third group were still significant after being adjusted by the two different models [2.26 (1.84, 2.77), adjusted by model 1; 2.05 (1.67, 2.52), adjusted by model 2]. A similar trend was observed in the 90-day mortality. Patients with a history of coronary and stroke of the third group had a significant higher 30-day mortality risk [HR and 95%CI were 3.28 (1.99, 5.40) and 3.20 (1.56, 6.56), respectively]. Conclusion MLR is a promising clinical biomarker, which has certain predictive value for the 30-day and 90-day mortality of patients in ICU.
ObjectiveTo investigate whether the miR-33s negatively regulates LPS-induced production of inflammatory cytokines by targeting p38 MAPK. MethodsHuman monocytes THP-1 cells were cultured in vitro and transfected with miR-33s mimic (25 nmol/L) or miR-33s inhibitor (25 nmol/L)by TransIT-X2® Dynamic Delivery System for 24 h. Then the transfected THP-1 cells were stimulated by LPS of 10.0 ng/mL for 24 h. The expression of miR-33s and p38 MAPK protein were measured by semi-quantitative RT-PCR. The concentrations of TNF-α,IL-6 and IL-1β in the cultured supernatant were assessed by ELISA. ResultsThe transfection of miR-33s mimic significantly increased the release of TNF-α,IL-6 and IL-1β(P<0.05). The expression of p38 MAPK protein was also significantly reduced(P<0.05). However,the pre-treatment of miR-33s inhibitor reversed the LPS-induced release of TNF-α,IL-6,and IL-1β,and the expression of p38 MAPK protein of THP-1 cells. ConclusionmiR-33s may play an important role in the regulation in inflammatory factors released from THP-1 cells by targeting p38 MAPK.
ObjectiveTo determine the nuclear factor kappa B (NFkB) activity in peripheral blood mononuclear cells (PBMC) in patients with acute cholangitis of severe type (ACST) and correlate the degree of NFkB activation with severity of biliary tract infection and clinical outcome.MethodsTwenty patients with ACST were divided into survivor group (14 cases) and nonsurvivor group (6 cases). Other 10 patients undergoing elective gastrectomy or inguinal hernia repair were selected as control group. Peripheral blood samples were taken 24 hours after operation, PBMC was separated and nuclear proteins were isolated from PBMC, and NFkB was determined with electrophoretic mobility shift assay (EMSA). The levels of TNFα, IL6 and IL10 in plasma were determined by using an enzymelinked immunoassay (ELISA). ResultsThe NFkB activity was 5.02±1.03, 2.98±0.51 and 1.02±0.34 respectively in three groups. It was increased in all patients with ACST, versus the control group (P＜0.05), and the patients of nonsurvivor group had higher levels of NFkB activation than those of survivor group (P＜0.05). The levels of TNFα and IL6 were (496.28±52.35) ng/L and (578.13±67.72) ng/L in nonsurvivor group; (284.47±39.41) ng/L and (318.67±34.92) ng/L in survivor group; (89.43±10.39) ng/L and (101.27±13.47) ng/L in control group. All patients with ACST had increased levels of TNFα and IL6, which were many fold greater than that of control group, and there was an evidence of significantly higher levels in nonsurvivor group than in survivor group (P＜0.05). All patients had also increased levels of IL10 as compared to control group (P＜0.05), but the IL10 concentrations in plasma were not significantly higher in nonsurvivors than that of in those survivors (Pgt;0.05). ConclusionNFkB activation in PBMCs in patients with ACST
ObjectiveTo investigate the role of Krüppel-like factor 4 (KLF4) mediated monocyte/macrophage subtype switch in the pathological progression of pulmonary fibrosis.MethodsThirty-six patients with interstitial pneumonia were recruited from Characteristic Medical Center of the Chinese People's Armed Police Force between May 2015 and January 2017. Peripheral venous blood and bronchoalveolar lavage fluid were collected in the morning. Pulmonary function and arterial blood gas were tested after admission. Flow cytometry was used to test monocyte subtypes of peripheral blood and macrophage subtypes of bronchoalveolar lavage fluid. KLF4 of peripheral blood was detected by enzyme linked immunosorbent assay. Thirty normal subjects were selected as control group of peripheral blood mononuclear cell subtypes and KLF4 (control group A), and 10 patients without pulmonary fibrosis who needed bronchoscopy were selected as control group of macrophage subtypes in alveolar lavage fluid (control group B). The relationship between the expression of KLF4 and the differentiation of monocytes and macrophages were observed. Furthermore, the relationship between the differentiation of monocytes subtypes, macrophages subtypes and lung function were observed.ResultsMonocyte of CD14++CD16– subtype in pulmonary fibrosis group was significantly lower than that in control group A (P<0.05). Monocyte of CD14++CD16+ subtype in pulmonary fibrosis group was significantly higher than that in control group A (P<0.05). No significant difference was found between the two groups regarding CD14+CD16++. No correlation was found between three subtypes of monocyte and DLCO of patients and between three subtypes of monocyte and PaO2 of patients. M1 macrophage in pulmonary fibrosis group was significantly lower than that in control group B (P<0.05). M2 macrophage in pulmonary fibrosis group was significantly higher than that in control group B (P<0.05). Negative correlation was found between the ratio of M2 subtypes and DLCO of patients and between the ratio of M2 subtypes and PaO2 of patients (P<0.05). KLF4 protein of blood in pulmonary fibrosis group was significantly higher than that in control group A (P<0.05). Positive correlation was found between the ratio of M2 subtypes and KLF4 protein (P<0.05).ConclusionsCD16+ monocyte plays a role in the occurrence and development of pulmonary fibrosis, but no evidence is found there is a direct correlation between monocyte subtypes of peripheral blood and fibrosis degree of lung tissue. M2 macrophage subtype plays an important role in the development of interstitial pneumonia. The number of M2 macrophages is positively correlated with the severity of pulmonary fibrosis. Monocyte/macrophage subtype differentiation by KLF4 may play a role in the pathological progression of pulmonary fibrosis.