VKC患儿与正常儿童泪液中细胞因子表达的比较

目的：比较VKC患儿与正常儿童泪液中细胞因子白细胞介素-4（IL-4）,白细胞介素-5（IL-5）和白细胞介素-13（IL-13）的表达量的变化,以及分析两组之间有无统计学差异。方法：收集10例春季角结膜炎（VKC）患儿与16例正常受试者（CT）的泪液;采用液体芯片技术测量两组泪液中IL-4,IL-5,IL-13的浓度,使用U检验来比较两组之间的差异有无统计学意义。结果：VKC组泪液中IL-4的浓度为1.09±0.73 pg/mL,IL-5的浓度为1.68±1.43 pg/mL,IL-13的浓度为1.90±1.59 pg/mL;与正常受试者（CT）相比,明显升高,两组之间比较差异均有统计学意义（P〈0.05）。结论：分析VKC患儿泪液中的细胞因子在了解VKC的发病机制中可能可以起到重要的作用,以及可以提供新的治疗方向。     

手足口病脑炎患儿脑脊液中细胞因子水平的比较

目的探讨不同病原体(CV-A6、CV-A16、EV-A71)所致手足口病脑炎患儿脑脊液中IL-6、IL-10、TNF-α、IFN-γ水平及意义。方法采用随机抽样的方法选取2018年3—5月在医院感染科收治的HFMD患儿,其中EV-A71组90例,CV-A6组77例,CV-A16组65例,选择同期高热惊厥患儿20例作为对照(高热惊厥组)。患儿入院后1～2 d行腰椎穿刺术,收集脑脊液2 mL,用流式细胞检测术分别检测细胞因子IL-6、IL-10、TNF-α、IFN-γ水平。结果 EV-A71组、CV-A6组、CV-A16组IL-6水平均明显高于高热惊厥组(t分别为6.224、7.579、6.667,P!0.05),且组间差异有统计学意义(F=18.631,P<0.05)。EV-A71组、CV-A6组、CV-A16组IL-10水平均高于高热惊厥组,差异具有统计学意义(t分别为5.387、3.227、3.084,P!0.05),且组间差异有统计学意义(F=17.480,P<0.05)。EV-A71组、CV-A6组、CV-A16组TNF-α水平与高热惊厥组差异均无统计学意义(t=-1.071、1.498、0.400,P>0.05),组间差异有统计学意义(F=6.069,P<0.05)。EV-A71组、CV-A6组、CV-A16组IFN-γ水平均高于高热惊厥组,差异具有统计学意义(t分别为4.718、7.303、8.919,P!0.05),且组间差异有统计学意义(F=16.566,P<0.05)。结论 EV-A71、CV-A6、CV-A16所致重症HFMD患儿脑脊液中IL-6、IL-10、IFN-γ均升高,表明在这3种不同病原体所致HFMD患儿脑炎中,IL-6、IL-10、IFN-γ均起到重要作用。其中,IL-6、IFN-γ明显升高,可作为疾病严重程度的评价指标。     

手足口病患儿细胞因子水平及免疫球蛋白的变化及其临床意义

目的 探讨不同病情的手足口病患儿（HFMD）主要细胞因子及免疫球蛋白IgM、IgG、IgA的表达水平及其变化的临床意义。方法 收集HFMD患儿50例,根据病情分为重症组12例,轻症组38例,另外选取同龄健康者15例为对照组。应用液相芯片分析平台检测IL-4、IL-6、IL-10、IL-17A、TNF-α、TGF-β水平;实时荧光定量PCR检测上述细胞因子mRNA表达水平;免疫比浊法检测免疫球蛋白IgM、IgG、IgA的水平。结果 重症组患儿血清各细胞因子水平显著高于轻症组及对照组（P0.05）。结论 HFMD患儿存在细胞因子水平的改变,体液免疫功能低下,这些变化可能参与HFMD病情的发展。     

SARS死亡病例肺组织中细胞因子的表达及意义

目的研究重症SARS患者肺组织内细胞因子TNF,IL-1α,IL-1β,IL-6,IL-8和IL-10的表达及定位,探讨重症SARS患者弥漫性肺泡损伤的发病机制。方法应用免疫组织化学染色(SABC法)和定量分析方法对8例SARS死亡病例肺组织中TNF,IL-1α,IL-1β,IL-6,IL-8和IL-10进行检测。结果TNF,IL-1α,IL-1β,IL-6,IL-8和IL-10在8例SARS死亡病例肺组织中均有阳性表达,多种细胞均可表达这些细胞因子;与普通肺炎组比较,SARS死亡病例肺组织中细胞因子水平显著升高;SARS死亡病例细胞因子水平在病程不同阶段间的表达有差异。结论TNF,IL-1α,IL-1β,IL-6,IL-8和IL-10可能参与重症SARS患者弥漫性肺泡损伤的发生与发展。     

低智儿童与正常儿童中氨基酸的比较研究

我们对 30例低智儿童血清中TAU ,SER ,GLU ,GLY ,ALA ,VAL ,CYS ,MET ,ILE ,LEU ,TYR ,PHE ,TRP ,HIS ,ORN ,LYS ,ARG ,PRO ,18种游离氨基酸进行了测定。研究结果显示 :患儿血清中 11种游离氨基酸降低分别为 :TAU ,SER ,VAL ,MET ,ILE ,LEU ,TRY ,PHE ,ORN ,LYS ,TRP .氨基酸的失衡 ,儿童的蛋白质合成就将会受到严重的影响 ,因此将导致大脑的分化 ,发育受阻 ,引起智力低下。     

推进早期胚胎发育正常调控过渡的输卵管细胞因子的初步研究

本研究对勉输卵管上皮细胞分泌蛋白的特征及功能能作了初步研究和分析。ＲＯＳｓ分子量介于１３５－４４ｋＤ,可分为３组,其中第２,３组为酸性糖蛋白。经糖苷酶消化,第３组ＲＯＰＳ显著地降解为分子量接近３０ｋＤ的蛋白。利用制备的抗总ＲＯＰｓ多抗以及针对不同分子量ＲＯＰ的抗血清,分别进行功能分析发现,Ａｒｏｐ－Ｔ和Ａｒｏｐ－Ⅰ能使受精卵发育完全阻断．     

轮状病毒感染性腹泻患儿血清中CD4+T细胞相关细胞因子水平及意义

通过检测轮状病毒感染性腹泻儿童感染早期血清中的CD4+T细胞相关细胞因子IL-17、IL-6、IFN-γ、IL-4和TGF-β水平,探讨CD4+T细胞相关细胞因子在儿童轮状病毒感染性腹泻疾病中的作用.采用ELISA法定量检测了56例轮状病毒感染性腹泻儿童和30例正常对照儿童血清中的上述细胞因子水平.实验结果显示,轮状病...     

抗生素相关性腹泻患儿肠道菌群变化与血清细胞因子的关系

目的 研究抗生素相关性腹泻(AAD)患儿肠道菌群变化与血清细胞因子的相关性及其临床意义。 方法 选择2018年5月至2019年5月在我院儿科住院且使用过抗生素治疗的儿童,根据是否发生AAD分为AAD组和非AAD组。另取同期进行体检的健康儿童作为对照组。检测各组对象粪便中双歧杆菌、乳杆菌、肠球菌和肠杆菌的数量,血清中肿瘤坏死因子|α(TNF|α)、白介素|6(IL|6)的含量,并采用Logistics回归分析AAD的相关因素。 结果 AAD组儿童粪便中双歧杆菌、乳杆菌的数量低于非AAD组及对照组,而粪便中肠球菌、肠杆菌的数量及血清中TNF|α、IL|6的水平高于非AAD组及对照组(均P结论 肠道菌群紊乱与AAD的发病有关并且能够增加患者炎症因子的释放,其中益生菌的减少是AAD发生的主要独立危险因素。     

白头翁汤对炎症性肠病中促炎细胞因子表达的影响

目的：探讨白头翁汤治疗炎症性肠病的分子机制。方法：40只Wistar雄性大鼠随机分为5组（n=8）：正常对照组、模型组、模型＋阳性药物对照组（美沙拉嗪）、模型＋白头翁中、高剂量治疗组。阳性对照组、中药治疗组分别灌胃给药。疗程结束后取大鼠结肠组织提取RNA,利用realtimePCR的方法检测白介素-1β（IL-1β）、白介素-6（IL-6）YL肿瘤坏死因子-α（TNF-α）在各组中的表达变化。结果：相对于模型组,阳性药物及白头翁汤治疗组尤其是高剂量组可有效抑制IL-1β、IL-6及TNF-α的表达。结论：白头翁汤可通过抑制促炎因子的表达从而发挥了在炎症性肠病中的治疗作用。     

肾间质纤维化相关信号通路的研究进展

肾间质纤维化是以正常的肾间质和肾小管结构被大量聚集的细胞外基质所替代为特征的病理过程,是多数慢性肾脏疾病进展为终末期肾衰竭共同的病变过程,其病理变化主要由多种细胞因子和多条信号通路控制,是众多关键信号通路的交互影响与共同作用的结果。深入了解信号通路的相互作用对进一步揭示肾间质纤维化的分子机制有重要意义。现综述肾间质纤维化病理变化中关键的信号通路,以期为肾间质纤维化分子机制的研究提供参考。     

Beneficial effects of ApoA-I on LPS-induced acute lung injury and endotoxemia in mice

High density lipoprotein (HDL) binds lipopolysaccharide (LPS) and neutralizes its toxicity. The aim of our study was to investigate the effects of Apolipoprotein (ApoA-I), the major apolipoprotein of HDL, on LPS-induced acute lung injury (ALI) and endotoxemia. BALB/c mice were challenged with LPS, followed by ApoA-I or saline administration for 24h. The mice were then sacrificed and histopathological analysis of the lung was performed. We found that ApoA-I could attenuate LPS-induced acute lung injury and inflammation. To investigate the mechanisms, we measured tumor necrosis factor alpha (TNF-alpha), interleukin-1beta (IL-1beta) and interleukin-6 (IL-6) levels in the serum and bronchoalveolar lavage (BAL) fluid and found that ApoA-I could significantly inhibit LPS-induced increases in the IL-1beta and TNF-alpha levels in serum (P<0.05, respectively), as well as in the IL-1beta, TNF-alpha, and IL-6 levels in BAL fluid (P<0.01 and P<0.05, P<0.05, respectively). Moreover, we evaluated the effect of ApoA-I on the mortality of L-929 cells which were attacked by LPS-activated peritoneal macrophages. We found that ApoA-I could significantly inhibit the LPS-induced cell death in a dose-dependent fashion. Furthermore, we investigated in vivo the effects of ApoA-I on the mortality rate and survival time after LPS administration and found that ApoA-I significantly decreased the mortality (P<0.05) and increased the survival time (P<0.05). In summary, the results suggest that ApoA-I could effectively protect against LPS-induced endotoxemia and acute lung damage. The mechanism might be related to inhibition of inflammatory cytokine release from macrophages.     

TNF-α、IL-1β及LPS对血管平滑肌细胞一氧化氮合酶基因表达的影响及作用机制研究

通过ＲＮＡ印迹分析和亚硝酸盐含量测定检查ＴＮＦ－α、ＩＬ－１β和ＬＰＳ对大鼠血管平滑肌细胞（ＶＳＭＣ）诱导型一氧化氮合酶（ｉＮＯＳ）基因表达及ＮＯ生成的影响．结果表明,ＴＮＦ－α、ＩＬ－１β和ＬＰＳ均能显著诱导ＶＳＭＣｉＮＯＳ基因表达和促进ＮＯ生成,其作用强度与浓度和作用时间有关;双因素（ＴＮＦ－α＋ＬＰＳ,ＬＰＳ＋ＩＬ－１β）对诱导ｉＮＯＳ基因表达及ＮＯ生成产生协同作用．ＰｏｌｙｍｙｘｉｎＢ和地塞米松可部分抑制ＴＮＦ－α对ｉＮＯＳ基因表达的诱导作用及ＮＯ生成     

Distinct protein kinase A anchoring proteins direct prostaglandin E2 modulation of Toll-like receptor signaling in alveolar macrophages

Toll-like receptors (TLRs) direct a proinflammatory program in macrophages. One mediator whose generation is induced by TLR ligation is prostaglandin E(2) (PGE(2)), which is well known to increase intracellular cAMP upon G protein-coupled receptor ligation. How PGE(2)/cAMP shapes the nascent TLR response and the mechanisms by which it acts remain poorly understood. Here we explored PGE(2)/cAMP regulation of NO production in primary rat alveolar macrophages stimulated with the TLR4 ligand LPS. Endogenous PGE(2) synthesis accounted for nearly half of the increment in NO production in response to LPS. The enhancing effect of PGE(2) on LPS-stimulated NO was mediated via cAMP, generated mainly upon ligation of the E prostanoid 2 receptor and acting via protein kinase A (PKA) rather than via the exchange protein activated by cAMP. Isoenzyme-selective cAMP agonists and peptide disruptors of protein kinase A anchoring proteins (AKAPs) implicated PKA regulatory subunit type I (RI) interacting with an AKAP in this process. Gene knockdown of potential RI-interacting AKAPs expressed in alveolar macrophages revealed that AKAP10 was required for PGE(2) potentiation of LPS-induced NO synthesis. AKAP10 also mediated PGE(2) potentiation of the expression of cytokines IL-10 and IL-6, whereas PGE(2) suppression of TNF-α was mediated by AKAP8-anchored PKA-RII. Our data illustrate the pleiotropic manner in which G protein-coupled receptor-derived cAMP signaling can influence TLR responses in primary macrophages and suggest that AKAP10 may coordinate increases in gene expression.     

Role of desert annuals in nutrient flow in arid area of Northwestern China: a nutrient reservoir and provider

Previous studies have tested the “vernal dam” hypothesis of spring ephemeral herbs in hardwood forests. The desert annual is a component of the desert ecosystem that takes advantage of water resources and temperature conditions during the rainy season to rapidly complete its life cycle within several months. To understand the role desert annual/ephemeral plants play in nutrient flow, we studied vegetation cover, nitrogen content and litter production of annual plants and litter decomposition rate in plant communities dominated by four shrubs (Haloxlon ammodendron, Hedysarum scoparium, Calligonum mongolicum, and Nitraria tangutorum) and two dominant annuals (Agriophyllum squarrosum and Halogeton arachnoideus Moq) in Minqin, northwestern China. Results indicate that over half of the total vegetation cover was provided by annuals. Annuals also took up a large amount of nitrogen (0.46–3.78 g N m⁻²) along the oasis–desert ecotone. Litter production and nutrient content were higher in areas dominated by annual plants than in areas dominated by shrubs. Furthermore, the litter decomposition rate of the annuals was higher than that of the shrubs, except for the shrub H. ammodendron, although almost all of the litter’s carbon (C) and nitrogen (N) remained after 6 months of decomposition. Without the annuals, more nutrients and rainwater might be lost through leaching or dust transfer caused by the wind erosion. In addition, green twigs of the annuals are the food for some animals, we found some green twigs and litter from annuals left in front of gerbil and rabbit burrows, sometimes even blocking these burrows. Thus, desert summer annuals, like nutrient reservoirs and providers, take up nutrients during the rainy season, providing some animals and microbes with food, and finally release these nutrients after death. Bao-Ming Chen and Gen-Xuan Wang contributed equally to this work.