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2022 3

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细胞因子 2

临床试验 1

单克隆抗体 1

发酵乳杆菌 1

安全性 1

宫内节育器；盆腔炎性疾病；细菌生物膜；SEM 1

左炔诺孕酮宫内系统；胰岛素样生长因子；盆腔炎 1

抗体应答 1

抗免疫球蛋白E 1

抗炎 1

新冠病毒肺炎 1

有效性 1

死亡率 1

比较基因组分析 1

炎性因子 1

病毒载量 1

类风湿关节炎 1

系统发育分析 1

结肠炎 1

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Bioactive hyaluronic acid fragments inhibit lipopolysaccharide-induced inflammatory responses via the

Na You, Sasa Chu, Binggang Cai, Youfang Gao, Mizhou Hui, Jin Zhu, Maorong Wang

《医学前沿（英文）》 2021年第15卷第2期页码 292-301 doi: 10.1007/s11684-020-0806-5

摘要： The high- and the low-molecular weight hyaluronic acids (HMW-HA and LMW-HA, respectively) showed different biological activities in inflammation. However, the role of LMW-HA in inflammatory response is controversial. In this study, we aimed to investigate the effect of bioactive hyaluronan (B-HA) on lipopolysaccharide (LPS)-induced inflammatory responses in human macrophages and mice. B-HA was produced from HA treated with glycosylated recombinant human hyaluronidase PH20. Human THP-1 cells were induced to differentiate into macrophages. THP-1-derived macrophages were treated with B-HA, LPS, or B-HA+LPS. The mRNA expression and the production of inflammatory cytokines were determined using quantitative real-time PCR and enzyme-linked immunosorbent assay. The phosphorylation levels of proteins in the nuclear factor- B (NF- B), mitogen-activated protein kinase (MAPK), and IRF-3 signaling pathways were measured using Western blot. The efficacy of B-HA was assessed in a mouse model of LPS-induced inflammation. Results showed that B-HA inhibited the expression of TNF-α, IL-6, IL-1, and IFN-β, and enhanced the expression of the anti-inflammatory cytokine IL-10 in LPS-induced inflammatory responses in THP-1-derived macrophages and . B-HA significantly suppressed the phosphorylation of the TLR4 signaling pathway proteins p65, IKKα/β, I Bα, JNK1/2, ERK1/2, p38, and IRF-3. In conclusion, our results demonstrated that the B-HA attenuated the LPS-stimulated inflammatory response by inhibiting the activation of the TLR4 signaling pathway. B-HA could be a potential anti-inflammatory drug in the treatment of inflammatory disease.

关键词： bioactive hyaluronan lipopolysaccharide inflammatory cytokines TLR4 human macrophages

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Critical roles of chemokines and cytokines in antiviral innate immune responses during rabies virus infection

Ying HUANG, Clement Wesley GNANADURAI, Zhenfang FU

《农业科学与工程前沿（英文）》 2017年第4卷第3期页码 260-267 doi: 10.15302/J-FASE-2016116

摘要： The innate immune response is the first line of defense against viral invasion and pro-inflammatory chemokines and cytokines have a critical function in the innate immune responses against virus infections. The ability of a rabies virus (RABV) to induce the expression of chemokines and cytokines can lead to viral clearance from the central nervous system (CNS), whereas the ability to evade such expression and activation contributes to virulence and pathogenicity. In this review, the crucial contribution of chemokines/cytokines to clearing RABV from the CNS is discussed, including recruiting leukocytes into the CNS, enhancement of blood brain barrier permeability and activation of various immune cells that are essential for viral clearance. In addition, recombinant RABV expressing cytokines and chemokines can induce elevated innate and adaptive immune responses which result in clearing an established wild-type RABV infection in the CNS.

关键词： antiviral blood brain barrier chemokines and cytokines innate immunity rabies virus

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Improved dissolution and anti-inflammatory effect of ibuprofen by solid dispersion

null

《医学前沿（英文）》 2012年第6卷第2期页码 195-203 doi: 10.1007/s11684-012-0189-3

摘要：

The purpose of this study was to improve the dissolution rate and anti-inflammatory effect of ibuprofen by a solid dispersion (SD) method. Initial screening was developed based on drug solubility in carriers in the liquid state to select a suitable water-soluble carrier system for the preparation of SDs. The dissolution of ibuprofen in urea was higher than in PEG4000 or mannitol. Thus, urea was selected as the carrier for the preparation of SDs. SDs were characterized in terms of dissolution, differential scanning calorimetry (DSC), X-ray diffraction (XRD), scanning electron microscopy (SEM), and Fourier transform infrared (FTIR) spectroscopy. Solid dispersion-based (SDBT) and conventional (CT) tablets were prepared by the wet granulation method. The anti-inflammatory effect of SDBT was evaluated using the mouse ear edema test with xylene. In vitro release results indicated that the ibuprofen dissolution rate was improved by the SD. SD characterization results suggested that ibuprofen partly precipitates in crystalline and amorphous forms after SD preparation and that ibuprofen and urea do not interact. SDBT displayed more significant anti-inflammatory effects than CT. The dissolution rate and anti-inflammatory effect of ibuprofen were significantly enhanced by the ibuprofen-urea SD.

关键词： ibuprofen solid dispersion physical mixture dissolution anti-inflammatory effect

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Cytokines and inflammation in adipogenesis: an updated review

Ning Jiang, Yao Li, Ting Shu, Jing Wang

《医学前沿（英文）》 2019年第13卷第3期页码 314-329 doi: 10.1007/s11684-018-0625-0

摘要： The biological relevance of cytokines is known for more than 20 years. Evidence suggests that adipogenesis is one of the biological events involved in the regulation of cytokines, and pro-inflammatory cytokines (e.g., TNF and IL-1 ) inhibit adipogenesis through various pathways. This inhibitory effect can constrain the hyperplastic expandability of adipose tissues. Meanwhile, chronic low-grade inflammation is commonly observed in obese populations. In some individuals, the impaired ability of adipose tissues to recruit new adipocytes to adipose depots during overnutrition results in adipocyte hypertrophy, ectopic lipid accumulation, and insulin resistance. Intervention studies showed that pro-inflammatory cytokine antagonists improve metabolism in patients with metabolic syndrome. This review focuses on the cytokines currently known to regulate adipogenesis under physiological and pathophysiological circumstances. Recent studies on how inhibited adipogenesis leads to metabolic disorders were summarized. Although the interplay of cytokines and lipid metabolism is yet incompletely understood, cytokines represent a class of potential therapeutic targets in the treatment of metabolic disorders.

关键词： cytokines inflammation adipogenesis type 2 diabetes mellitus metabolic disorder

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Beneficial metabolic activities of inflammatory cytokine interleukin 15 in obesity and type 2 diabetes

null

《医学前沿（英文）》 2015年第9卷第2期页码 139-145 doi: 10.1007/s11684-015-0377-z

摘要：

In obesity, chronic inflammation is believed to induce insulin resistance and impairs adipose tissue function. Although this view is supported by a large body of literature, it has been challenged by growing evidence that pro-inflammatory cytokines may favor insulin sensitivity through induction of energy expenditure. In this review article, interleukin 15 (IL-15) is used as a new example to explain the beneficial effects of the pro-inflammatory cytokines. IL-15 is secreted by multiple types of cells including macrophages, neutrophils and skeletal muscle cells. IL-15 expression is induced in immune cells by endotoxin and in muscle cells by physical exercise. Its transcription is induced by transcription factor NF-κB. IL-15 binds to its receptor that contains three different subunits (α, β and γ) to activate JAK/STAT, PI3K/Akt, IKK/NF-κB and JNK/AP1 pathways in cells. In the regulation of metabolism, IL-15 reduces weight gain without inhibiting food intake in rodents. IL-15 suppresses lipogenesis, stimulates brown fat function, improves insulin sensitivity through weight loss and energy expenditure. In human, circulating IL-15 is negatively associated with body weight. In the immune system, IL-15 stimulates proliferation and differentiation of T cells, NK cells, monocytes and neutrophils. In the anti-obesity effects of IL-15, T cells and NK cells are not required, but leptin receptor is required. In summary, evidence from human and rodents supports that the pro-inflammatory cytokine IL-15 may enhance energy expenditure to protect the body from obesity and type 2 diabetes. The mechanism of IL-15 action remains to be fully uncovered in the regulation of energy expenditure.

关键词： inflammation obesity cytokine energy expenditure insulin resistance

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The relationship between progesterone and Th-related cytokines in plasma during early pregnancy in cows

Lei CHENG,Youdong XIN,Xiaohua LIU,Xiuzhong HU,Min XIANG,Dingfa WANG,Shuhong ZHAO

《农业科学与工程前沿（英文）》 2016年第3卷第2期页码 147-152 doi: 10.15302/J-FASE-2016099

摘要： In cows, progesterone (P4) is essential for the maintenance of pregnancy and successful embryo development is dependent on the maternal immunomodulation of Th-related cytokines. However, investigation of the relationship between P4 and Th immunity in cattle remains incomplete. Therefore, we evaluated plasma P4 concentrations and expressions of three Th-related cytokines, interleukins IL-1β, IL-4 and IL-6, in 15 pregnant and 11 non-pregnant cows 0, 14, 18, 21, and 28 d post artificial insemination. Pregnant cows had significantly higher plasma P4 levels and pregnant cows with higher P4 on 14 d tended to have higher P4 in the subsequent period of pregnancy. There was no difference in IL-4 and IL-6 expression between pregnant cows and non-pregnant cows, whereas plasma IL-1β was temporally upregulated on 21 d. The cytokines measured were not affected in either the high-P4 group (>11.1 ng·mL ) or the low-P4 group (<11.1 ng·mL ) in pregnant cows. A weak negative correlation between IL-1β and IL-6 was observed, but none of the cytokines was associated with a change in plasma P4. In conclusion, there was no clear relationship between P4 and Th immunity in maternal plasma in the pregnant cows, which differs from what occurs in humans and mice during early pregnancy.

关键词： dairy cow progesterone pregnancy cytokine

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Advances in immunopathogenesis of adult immune thrombocytopenia

null

《医学前沿（英文）》 2013年第7卷第4期页码 418-424 doi: 10.1007/s11684-013-0297-8

摘要：

Primary immune thrombocytopenia (ITP) is an autoimmune disorder characterized by immune-mediated accelerated platelet destruction and/or suppressed platelet production. Although the development of autoantibodies against platelet glycoproteins remains central in the pathophysiology of ITP, several abnormalities involving the cellular mechanisms of immune modulation have been identified, and the pathways behind the immune-mediated destruction of platelets have opened new avenues for the design of specific immunotherapies in an attempt to reduce the platelet destruction. This review is primarily focused on the recent literature with respect to immunopathological mechanisms in patients with ITP.

关键词： primary immune thrombocytopenia B lymphocytes T lymphocytes antigen-presenting cells cytokines

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Predictive values of plasma TNFα and IL-8 for intracranial hemorrhage in patients with acute promyelocytic leukemia

《医学前沿（英文）》 2022年第16卷第6期页码 909-918 doi: 10.1007/s11684-021-0890-1

摘要： In patients with acute promyelocytic leukemia (APL), intracranial hemorrhage (ICH), if not identified promptly, could be fatal. It is the leading cause of failure of induction and early death. Thus, biomarkers that could promptly predict severe complications are critical. Here, cytokine differences between patients with APL with and without ICH were investigated to develop predictive models for this complication. The initial cytokine profiling using plasma samples from 39 patients and 18 healthy donors found a series of cytokines that were remarkedly different between patients with APL and healthy controls. The APL patients were subsequently divided into high and low white blood cell count groups. Results showed that tumor necrosis factor α and interleukin 8 (IL-8) were vital in distinguishing patients with APL who did or did not develop ICH. In addition, verification in 81 patients with APL demonstrated that the two cytokines were positively correlated with the cumulative incidence of ICH. Finally, in-vitro and in-vivo experimental evidence were provided to show that IL-8 influenced the migration of APL-derived NB4 cells and impaired the blood–brain barrier in PML/RARα positive blast-transplanted FVB/NJ mice. These assessments may facilitate the early warning of ICH and reduce future mortality levels in APL.

关键词： acute promyelocytic leukemia intracranial hemorrhage cytokines biomarker

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Non-genetic mechanisms of diabetic nephropathy

null

《医学前沿（英文）》 2017年第11卷第3期页码 319-332 doi: 10.1007/s11684-017-0569-9

摘要：

Diabetic nephropathy (DN) is one of the most common microvascular complications in diabetes mellitus patients and is characterized by thickened glomerular basement membrane, increased extracellular matrix formation, and podocyte loss. These phenomena lead to proteinuria and altered glomerular filtration rate, that is, the rate initially increases but progressively decreases. DN has become the leading cause of end-stage renal disease. Its prevalence shows a rapid growth trend and causes heavy social and economic burden in many countries. However, this disease is multifactorial, and its mechanism is poorly understood due to the complex pathogenesis of DN. In this review, we highlight the new molecular insights about the pathogenesis of DN from the aspects of immune inflammation response, epithelial–mesenchymal transition, apoptosis and mitochondrial damage, epigenetics, and podocyte–endothelial communication. This work offers groundwork for understanding the initiation and progression of DN, as well as provides ideas for developing new prevention and treatment measures.

关键词： diabetic nephropathy immune inflammatory response epithelial–mesenchymal transition apoptosis mitochondrial damage epigenetics podocyte–endothelial communication

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Metformin and metabolic diseases: a focus on hepatic aspects

null

《医学前沿（英文）》 2015年第9卷第2期页码 173-186 doi: 10.1007/s11684-015-0384-0

摘要：

Metformin has been widely used as a first-line anti-diabetic medicine for the treatment of type 2 diabetes (T2D). As a drug that primarily targets the liver, metformin suppresses hepatic glucose production (HGP), serving as the main mechanism by which metformin improves hyperglycemia of T2D. Biochemically, metformin suppresses gluconeogenesis and stimulates glycolysis. Metformin also inhibits glycogenolysis, which is a pathway that critically contributes to elevated HGP. While generating beneficial effects on hyperglycemia, metformin also improves insulin resistance and corrects dyslipidemia in patients with T2D. These beneficial effects of metformin implicate a role for metformin in managing non-alcoholic fatty liver disease. As supported by the results from both human and animal studies, metformin improves hepatic steatosis and suppresses liver inflammation. Mechanistically, the beneficial effects of metformin on hepatic aspects are mediated through both adenosine monophosphate-activated protein kinase (AMPK)-dependent and AMPK-independent pathways. In addition, metformin is generally safe and may also benefit patients with other chronic liver diseases.

关键词： metformin diabetes hepatic steatosis inflammatory response insulin resistance

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左炔诺孕酮宫内释放系统对胰岛素样生长因子-1的影响与预防盆腔炎的相关性研究

吴晓杰,刘霞,陶跃平,王洁

《中国工程科学》 2015年第17卷第6期页码 4-7

摘要：

目的：研究左炔诺孕酮宫内释放系统对子宫内膜组织胰岛素样生长因子-1（IGF-1）的影响及预防盆腔炎疗效分析。方法：选取2010―2013年在嘉兴市妇幼保健院行宫腔镜下子宫内膜息肉切除术患者450例进行随机分组，研究组术后子宫内即时放置左炔诺孕酮宫内释放系统，而对照组不予放置。分别对术前及术后6个月子宫内膜组织IGF-1的表达情况进行对比，且随访2年，了解患者盆腔炎发生情况。结果：所有手术均成功，研究组子宫内膜组织IGF-1表达术后明显低于术前，对照组术前及术后子宫内膜组织IGF-1表达变化无差异，二组相比，术后IGF-1表达差异有显著性。随访2年对照组224例患者中39例发生盆腔炎，复发率为10.89 %，而研究组184例发生盆腔炎12例，差异有显著性；研究组子宫内膜厚度术后明显小于术前，差异有显著性，对照组子宫内膜厚度术后与术前变化无差异性。结论：左炔诺孕酮宫内释放系统对子宫内膜的IGF-1表达存在抑制作用，可能是其抑制子宫内膜增生并减少盆腔炎发生的机制之一。

关键词：左炔诺孕酮宫内系统；胰岛素样生长因子；盆腔炎

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Intestinal Epithelial Axin1 Deficiency Protects Against Colitis via Altered Gut Microbiota

Shari Garrett,Yongguo Zhang,Yinglin Xia,Jun Sun,

《工程（英文）》 doi: 10.1016/j.eng.2023.06.007

摘要： Intestinal homeostasis is maintained by specialized host cells and the gut microbiota. Wnt/β-catenin signaling is essential for gastrointestinal development and homeostasis, and its dysregulation has been implicated in inflammation and colorectal cancer. Axin1 negatively regulates activated Wnt/β-catenin signaling, but little is known regarding its role in regulating host–microbial interactions in health and disease. Here, we aim to demonstrate that intestinal Axin1 determines gut homeostasis and host response to inflammation. Axin1 expression was analyzed in human inflammatory bowel disease datasets. To explore the effects and mechanism of intestinal Axin1 in regulating intestinal homeostasis and colitis, we generated new mouse models with Axin1 conditional knockout in intestinal epithelial cell (IEC; Axin1^Δ^IEC) and Paneth cell (PC; Axin1^Δ^PC) to compare with control (Axin1^LoxP; LoxP: locus of X-over, P1) mice. We found increased Axin1 expression in the colonic epithelium of human inflammatory bowel disease (IBD). Axin1^Δ^IEC mice exhibited altered goblet cell spatial distribution, PC morphology, reduced lysozyme expression, and enriched Akkermansia muciniphila (A. muciniphila). The absence of intestinal epithelial and PC Axin1 decreased susceptibility to dextran sulfate sodium-induced colitis in vivo. Axin1^Δ^IEC and Axin1^Δ^PC mice became more susceptible to dextran sulfate sodium (DSS)-colitis after cohousing with control mice. Treatment with A. muciniphila reduced DSS-colitis severity. Antibiotic treatment did not change the IEC proliferation in the Axin1^Loxp mice. However, the intestinal proliferative cells in Axin1^Δ^IEC mice with antibiotic treatment were reduced compared with those in Axin1^Δ^IEC mice without treatment. These data suggest non-colitogenic effects driven by the gut microbiome. In conclusion, we found that the loss of intestinal Axin1 protects against colitis, likely driven by epithelial Axin1 and Axin1-associated A. muciniphila. Our study demonstrates a novel role of Axin1 in mediating intestinal homeostasis and the microbiota. Further mechanistic studies using specific Axin1 mutations elucidating how Axin1 modulates the microbiome and host inflammatory response will provide new therapeutic strategies for human IBD.

关键词： Axin1 Bacteria Microbiome inflammation Inflammatory bowel disease Immunity Microbiome Paneth cells Akkermansia muciniphila Wnt

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Recent advances in myeloid-derived suppressor cell biology

Mahmoud Mohammad Yaseen, Nizar Mohammad Abuharfeil, Homa Darmani, Ammar Daoud

《医学前沿（英文）》 2021年第15卷第2期页码 232-251 doi: 10.1007/s11684-020-0797-2

摘要： In recent years, studying the role of myeloid-derived suppressor cells (MDSCs) in many pathological inflammatory conditions has become a very active research area. Although the role of MDSCs in cancer is relatively well established, their role in non-cancerous pathological conditions remains in its infancy resulting in much confusion. Our objectives in this review are to address some recent advances in MDSC research in order to minimize such confusion and to provide an insight into their function in the context of other diseases. The following topics will be specifically focused upon: (1) definition and characterization of MDSCs; (2) whether all MDSC populations consist of immature cells; (3) technical issues in MDSC isolation, estimation and characterization; (4) the origin of MDSCs and their anatomical distribution in health and disease; (5) mediators of MDSC expansion and accumulation; (6) factors that determine the expansion of one MDSC population over the other; (7) the Yin and Yang roles of MDSCs. Moreover, the functions of MDSCs will be addressed throughout the text.

关键词： non-human primates (rhesus macaques) myeloid-derived pro-inflammatory cells (MDPCs) autoimmune disorders alloimmune responses pregnancy mature MDSCs multiple sclerosis Yin-Yang law of MDSCs

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Effect of IL-10 on formation of foam cell induced by ox-LDL

WANG Fei, DAI Yalei, XU Ting, XU Bo, WANG Kaifeng

《医学前沿（英文）》 2008年第2卷第3期页码 298-302 doi: 10.1007/s11684-008-0057-3

摘要： Atherosclerosis is a chronic disease that causes various cardiovascular complications. It has been realized that cellular and humoral immunity plays crucial roles in atherogenic lesion formation. In this study the effects of lipopolysaccharide (LPS) and interleukin-10 (IL-10) on the formation of foam cells during the early stages of atherosclerosis have been investigated. Macrophage was induced by phorbol myristate acetate (PMA) treatment on THP-1 cells. The cells were further stimulated by ox-LDL, ox-LDL plus LPS, ox-LDL plus IL-10 and LPS. By using an oil red O staining technique, the formation of foam cells was evaluated by lipid granules formation in the cells. The ratio of foam cell formation was increased from (9.77 ± 1.70)% to (16.27 ± 2.27)% after 24 h stimulation with ox-LDL, and the increase was observed with incubating time. The foam cells were significantly increased in the presence of LPS in a dose-dependent manner. The maximum increase of about 40% was observed. However, the significant elevation by LPS was abrogated when IL-10 was added. These results indicated that IL-10 can effectively prevent the formation of foam cells induced by ox-LDL with or without LPS. This study demonstrates that ox-LDL can cause foam cell formation from macrophages . LPS can significantly accelerate this event. IL-10, an anti-inflammatory cytokine, can inhibit the effect of ox-LDL and LPS. These results indicate that inflammatory effects in blood vessels can speed up foam cell formation. The inhibitive effect of IL-10 is an important factor for delaying atherosclerosis processes.

关键词： inflammatory presence interleukin-10 dose-dependent ox-LDL

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单克隆抗体治疗过敏性疾病的研究现状 Review

陈彦, 王炜, 袁慧慧, 李艳, 吕喆, 崔烨, 刘杰, 孙英

《工程（英文）》 2021年第7卷第11期页码 1552-1556 doi: 10.1016/j.eng.2020.06.029

摘要：

过敏性疾病是常见的慢性疾病之一，由变应原在不同器官上引发变态反应，在临床上以不同器官的疾病为主要表现形式，如哮喘、特应性皮炎、鼻-鼻窦炎等，常累及儿童和成人。由于其在世界范围内的广泛流行和对患者生活质量的影响，采用新型生物疗法治疗过敏性疾病的研究业已成为该领域的热点。已知多种因素可促进或触发Th2 型免疫应答，导致2 型细胞因子和免疫球蛋白E（IgE）的产生并参与过敏性疾病的发生发展，因此，开发针对2 型细胞因子和IgE 的单克隆抗体为治疗过敏性疾病提供了新的策略。此外，一些潜在的靶点，如上皮源性预警素-胸腺基质淋巴细胞生成素（TSLP）和白介素33（IL-33）业已进入临床研究阶段。这些新的和潜在的靶点极大地提高了变应性疾病的治疗机会。本文阐述了目前已开发的针对细胞因子、细胞因子受体和IgE 的单克隆抗体在过敏性疾病治疗中的作用，并对这些抗体的临床效果进行了讨论和分析。

关键词：过敏性疾病单克隆抗体抗免疫球蛋白E 细胞因子临床试验