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医学 1

发酵乳杆菌 1

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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

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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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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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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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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

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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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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宫内节育器表面的细菌生物膜研究

张向卉,曲雯雯,黄薇,方婕,吴凡子,周辛璇

《中国工程科学》 2015年第17卷第6期页码 21-27

摘要：

目的：宫内节育器（IUD）是目前常用的长效避孕措施之一，然而众多研究认为IUD的应用增加了盆腔炎性疾病（PID）的发生率。近年研究发现细菌生物膜（BF）与感染性疾病的发生息息相关，本研究拟探究无盆腔炎疾病妇女的不同类型宫内节育器表面是否存在BF，了解IUD是否为BF形成提供平台，是否增加盆腔炎性疾病的易感性。方法：不同类型IUD标本，根据表面清洁程度分别进行单独电子扫描电镜（SEM）观察，单独需氧、厌氧细菌培养，以及SEM观察+培养了解IUD表面是否存在BF。结果：共纳入IUD标本86例，85例非PID女性的IUD，同期1例盆腔感染性疾病患者的IUD。25例进行单独SEM观察，阳性1例，其余标本未见典型BF结构。单独细菌培养47例，需氧细菌培养阳性1例，见大面积菌苔覆盖，考虑污染可能性大，其余标本未见细菌生长。SEM联合培养14例，细菌培养阳性，电镜无阳性发现。其余培养及SEM观察阴性。结论：不论IUD的类型如何，非PID女性体内的IUD表面无BF存在，不同与其他体内医疗装置，BF的形成不能成为限制IUD应用的理由。

关键词：宫内节育器；盆腔炎性疾病；细菌生物膜；SEM

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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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Francisco Schofer：发展硝基脂肪酸以治疗炎症和纤维化疾病（2019年9月18日）

2021年08月12日

关键词：医学

血清鸟氨酸水平下降与类风湿关节炎缓解情况密切相关——从青藤碱的一项随机双盲临床试验中得到的启示 Article

石颖, 潘胡丹, 伍建林, 邹庆华, 谢昕怡, 李红刚, 周华, 卞西清, 冷文飞, 王灿坚, 王亚峰, 方勇飞, 刘良

《工程（英文）》 2022年第16卷第9期页码 93-99 doi: 10.1016/j.eng.2021.04.014

摘要：

青藤碱（SIN）是中国类风湿关节炎（RA）治疗的常用药物，但目前尚无SIN单药治疗疗效的文献报道。本研究旨在探讨SIN治疗RA的有效性和安全性，并分析鸟氨酸水平与RA患者疾病活动情况的相关性。本项目设计为24周的多中心、随机、安慰剂对照、双盲临床试验，轻中度活动度的RA患者按照1∶1∶1随机分配接受SIN（120 mg，每日两次）、甲氨蝶呤（MTX）（每周10 mg）或SIN + MTX治疗。项目以24周达到ACR50标准的受试者比例，以及根据临床疾病活动指数(CDAI)显示改善的受试者比例为主要疗效指标，并进一步分析24周治疗后的RA受试者疾病活动变化是否与血清鸟氨酸水平相关。在135名受试者中，38名、39名和36名分别接受了SIN、MTX和SIN + MTX的治疗。在SIN治疗组中，52.63%的受试者在治疗24周后达到ACR50标准，与MTX治疗组和SIN + MTX治疗组的结果相当。患者不良反应以肝功能损害和胃肠功能紊乱为主，但SIN组肝功能损害的发生率（1/38）明显低于MTX组（10/39）和SIN + MTX组（8/36）。采用超高效液相-四极杆飞行时间质谱仪（UHPLC-Q-TOF/MS），测定了三个治疗组4个随访时间点共计221份血清样本中的鸟氨酸、瓜氨酸和精氨酸的含量。治疗24周后，血清鸟氨酸水平随着疾病活动度的降低而下降，敏感度为80%，提示鸟氨酸水平可一定程度上预测治疗应答情况。综上所述，SIN对RA患者的疗效与MTX相当，副作用更少，且首次发现血清鸟氨酸水平与类风湿关节炎的缓解密切相关，提示鸟氨酸具有成为类风湿关节炎疗效评价指标的潜在价值。

关键词：类风湿关节炎青藤碱有效性安全性炎性因子