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

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《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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Keratin 5-Cre-driven deletion of

Jun Yang, Lianqing Wang, Yingzhi Huang, Keqiang Liu, Chaoxia Lu, Nuo Si, Rongrong Wang, Yaping Liu, Xue Zhang

《医学前沿（英文）》 2020年第14卷第3期页码 305-317 doi: 10.1007/s11684-019-0722-8

摘要： Familial acne inversa (AI) is an autoinflammatory disorder that affects hair follicles and is caused by loss-of-function mutations in -secretase component genes. We and other researchers showed that ( ) is the most frequently mutated gene in familial AI. In this study, we generated a keratin 5-Cre-driven epidermis-specific conditional knockout mutant in mice. We determined that this mutant recapitulated the major phenotypes of AI, including hyperkeratosis of hair follicles and inflammation. In mice, the IL-36a expression level markedly increased starting from postnatal day 0 (P0), and this increase occurred much earlier than those of TNF- , IL-23A, IL-1 and TLR4. RNA-Seq analysis indicated that Sprr2d, a member of the small proline-rich protein 2 family, in the skin tissues of the mice was also upregulated on P0. Quantitative reverse-transcription polymerase chain reaction showed that other genes had a similar expression pattern. Our findings suggested that IL-36a might be a key inflammatory cytokine in the pathophysiology of AI and involved in the malfunction of the skin barrier in the pathogenesis of AI.

关键词： acne inversa mouse model interleukin 1 family member 6 small proline rich protein 2D key inflammatory cytokine

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

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《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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Cytokine storm and translating IL-6 biology into effective treatments for COVID-19

《医学前沿（英文）》 doi: 10.1007/s11684-023-1044-4

摘要： As of May 3, 2023, the coronavirus disease 2019 (COVID-19) pandemic has resulted in more than 760 million confirmed cases and over 6.9 million deaths. Several patients have developed pneumonia, which can deteriorate into acute respiratory distress syndrome. The primary etiology may be attributed to cytokine storm, which is triggered by the excessive release of proinflammatory cytokines and subsequently leads to immune dysregulation. Considering that high levels of interleukin-6 (IL-6) have been detected in several highly pathogenic coronavirus-infected diseases, such as severe acute respiratory syndrome in 2002, the Middle East respiratory syndrome in 2012, and COVID-19, the IL-6 pathway has emerged as a key in the pathogenesis of this hyperinflammatory state. Thus, we review the history of cytokine storm and the process of targeting IL-6 signaling to elucidate the pivotal role played by tocilizumab in combating COVID-19.

关键词： SARS-CoV-2 COVID-19 cytokine storm interleukin-6 tocilizumab

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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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Inflammation and liver tumorigenesis

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《医学前沿（英文）》 2013年第7卷第2期页码 242-254 doi: 10.1007/s11684-013-0256-4

摘要：

Inflammation has been considered as one of the hallmarks of cancer, and chronic hepatitis is a major cause of liver cancer. This review will focus on the pathogenic role of inflammation in hepatocarcinogenesis and will discuss recent advances in understanding the chronic hepatitis-liver cancer link based on hot spots in liver cancer research, including cellular interaction, cytokines, microRNA and stem cells. All of these mechanisms should be taken into consideration because they are crucial for the development of more efficacious therapeutic strategies for preventing and treating human chronic hepatitis and hepatocellular carcinoma.

关键词： hepatocellular carcinoma hepatitis cytokine stem cell miRNA

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High-affinity T cell receptors redirect cytokine-activated T cells (CAT) to kill cancer cells

Synat Kang, Yanyan Li, Yifeng Bao, Yi Li

《医学前沿（英文）》 2019年第13卷第1期页码 69-82 doi: 10.1007/s11684-018-0677-1

摘要：

Cytokine-activated T cells (CATs) can be easily expanded and are widely applied to cancer immunotherapy. However, the good efficacy of CATs is rarely reported in clinical applications because CATs have no or very low antigen specificity. The low-efficacy problem can be resolved using T cell antigen receptor-engineered CAT (TCR-CAT). Herein, we demonstrate that NY-ESO-1_157–165 HLA-A*02:01-specific high-affinity TCR (HAT)-transduced CATs can specifically kill cancer cells with good efficacy. With low micromolar range dissociation equilibrium constants, HAT-transduced CATs showed good specificity with no off-target killing. Furthermore, the high-affinity TCR-CATs delivered significantly better activation and cytotoxicity than the equivalent TCR-engineered T cells (TCR-Ts) in terms of interferon-g and granzyme B production and in vitro cancer cell killing ability. TCR-CAT may be a very good alternative to the expensive TCR-T, which is considered an effective personalized cyto-immunotherapy.

关键词： cytokine-activated T cells high-affinity T cell receptor cancer immunotherapy TCR-CAT

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Molecular characterization of two suppressor of cytokine signaling 1 genes (

Xue XU,Jiannan ZHANG,Juan LI,Yajun WANG

《农业科学与工程前沿（英文）》 2015年第2卷第1期页码 73-83 doi: 10.15302/J-FASE-2015044

摘要： Suppressor of cytokine signaling 1 (SOCS1) protein can inhibit the signal transduction triggered by some cytokines or hormones and thus are important in many physiological/pathological processes, including innate and adaptive immunity, inflammation, and development in mammals. However, there is sparse information about their structure, tissue expression, in birds, where their biological functions remain unknown. In this study, we cloned and characterized two genes (named and ) from chickens. is predicted to encode a 207-amino acid protein, which shares high amino acid sequence identity (64%–67%) with human and mouse SOCS1. Besides , a novel gene was also identified in chickens and other non-mammalian vertebrates including . Chicken is predicted to encode a 212-amino acid protein, which shares only 30%–32% amino acid sequence identity with human SOCS1 and cSOCS1a. RT-PCR assay revealed that both and are widely expressed in all chicken tissues. Using a luciferase reporter assay system, we further demonstrated that transient expression of and can significantly inhibit chicken growth hormone (GH)- or prolactin (PRL)-induced luciferase activities of Hep G2 cells expressing cGH receptor (or cPRL receptor), indicating that SOCS1a and SOCS1b proteins can negatively regulate GH/PRL signaling. Taken together, these data suggest that both cSOCS1a and cSOCS1b may function as negative regulators of cytokine/hormone actions, such as modulation of GH/PRL actions in chickens.

关键词： chicken SOCS1a SOCS1b growth hormone prolactin

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Management of cytokine release syndrome related to CAR-T cell therapy

Hongli Chen, Fangxia Wang, Pengyu Zhang, Yilin Zhang, Yinxia Chen, Xiaohu Fan, Xingmei Cao, Jie Liu, Yun Yang, Baiyan Wang, Bo Lei, Liufang Gu, Ju Bai, Lili Wei, Ruili Zhang, Qiuchuan Zhuang, Wanggang Zhang, Wanhong Zhao, Aili He

《医学前沿（英文）》 2019年第13卷第5期页码 610-617 doi: 10.1007/s11684-019-0714-8

摘要： Chimeric antigen receptor T (CAR-T) cell therapy is a novel cellular immunotherapy that is widely used to treat hematological malignancies, including acute leukemia, lymphoma, and multiple myeloma. Despite its remarkable clinical effects, this therapy has side effects that cannot be underestimated. Cytokine release syndrome (CRS) is one of the most clinically important and potentially life-threatening toxicities. This syndrome is a systemic immune storm that involves the mass cytokines releasing by activated immune cells. This phenomenon causes multisystem damages and sometimes even death. In this study, we reported the management of a patient with recurrent and refractory multiple myeloma and three patients with acute lymphocytic leukemia who suffered CRS during CAR-T treatment. The early application of tocilizumab, an anti-IL-6 receptor antibody, according to toxicity grading and clinical manifestation is recommended especially for patients who suffer continuous hyperpyrexia, hypotensive shock, acute respiratory failure, and whose CRS toxicities deteriorated rapidly. Moreover, low doses of dexamethasone (5–10 mg/day) were used for refractory CRS not responding to tocilizumab. The effective management of the toxicities associated with CRS will bring additional survival opportunities and improve the quality of life for patients with cancer.

关键词： chimeric antigen receptor T cell cytokine release syndrome tocilizumab

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基于系统发育和比较基因组分析揭示与发酵乳杆菌缓解结肠炎相关的关键基因 Article

赵岩, 张程程, 于雷雷, 田丰伟, 赵建新, 张灏, 陈卫, 翟齐啸

《工程（英文）》 2022年第17卷第10期页码 170-182 doi: 10.1016/j.eng.2020.09.016

摘要：

越来越多的研究表明，发酵乳杆菌可以用于溃疡性结肠炎的预防和治疗。本研究中，我们从中国不同地区的人群粪便样本中分离出了105 株发酵乳杆菌，并对其基因组草图进行了测序。我们分析了这些菌株的泛基因组和系统发育特征，并对4 个模型菌株（发酵乳杆菌3872、CECT5716、IFO3956 和VRI003）也进行了分析。系统发育分析表明，发酵乳杆菌基因组的进化方向与宿主的地理位置、性别、族群和年龄没有明显的关系。我们挑选了3 株来自不同的系统发育支系的发酵乳杆菌（FWXBH115、FGDLZR121和FXJCJ61）和发酵乳杆菌模式菌株CECT5716，通过构建右旋糖酐硫酸钠（DSS）诱导的结肠炎小鼠模型，
探究这几株菌的抗炎和免疫调节活性。发酵乳杆菌FXJCJ61 和CECT5716 可以通过缓解所有结肠炎相关的组织学指标，保护黏膜完整性，增加肠道短链脂肪酸（SCFA），显著减轻结肠炎，而其他两株菌未能提供类似的保护作用。发酵乳杆菌FXJCJ61 和CECT5716 的抗炎机制与核转录因子kappa-B（NF-κB）信号通路激活以及促进白细胞介素10（IL-10）的产生有关。比较基因组分析结果表明，这些有益发酵乳杆菌的抗炎作用可能与一些特定基因有关。

关键词：发酵乳杆菌结肠炎抗炎系统发育分析比较基因组分析

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Non-genetic mechanisms of diabetic nephropathy

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《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

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《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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NEW ZEALAND DAIRY FARM SYSTEMS AND KEY ENVIRONMENTAL EFFECTS

《农业科学与工程前沿（英文）》 2021年第8卷第1期

摘要：

• NZ dairy farming systems are based on year-round grazing of perennial pasture (ryegrass/white clover).

• Milk production per hectare has increased by about 29% with increased use of externally-sourced feeds over the last two decades.

• Externally-sourced feeds with a low protein concentration can potentially reduce N₂O emissions and N leaching per unit of production.

• Systems analysis is important for evaluating mitigations to minimize trade-offs between environmental impacts.

This paper provides an overview of the range of dairy pasture grazing systems used in New Zealand (NZ), the changes with increased inputs over time and associated key environmental effects including nitrogen (N) leaching and greenhouse gas (GHG) emissions. NZ dairy farming systems are based on year-round grazing and seasonal milk production on perennial ryegrass/clover pasture where cows are rotationally grazed in paddocks. There was an increase in stocking rate on NZ dairy farms from 2.62 cows ha⁻¹ in 2000/2001 to 2.84 cows ha⁻¹ in 2015/2016. During the same period annual milk solids production increased from 315 to 378 kg·yr⁻¹per cow. This performance has coincided with an increase in N fertilizer use (by ~ 30%) and a twofold increase in externally-sourced feeds. Externally-sourced feeds with a low protein concentration (e.g., maize silage) can increase the efficiency of N utilization and potentially reduce N losses per unit of production. Off-paddock facilities (such as standoff or feed pads) are often used to restrict grazing during very wet winter conditions. A systems analysis of contrasting dairy farms in Waikato (largest NZ dairying region) indicates that the increased input would result in an increase in per-cow milk production but little change in efficiency of milk production from a total land use perspective. This analysis also shows that the increased inputs caused an 11% decrease in N footprint (i.e., N emissions per unit of milk production) and a 2% increase in C footprint (i.e., greenhouse gas (GHG) emissions per unit of milk production).jiafa.luo@agresearch.co.nz