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1.
目的探讨白细胞介素37b重组蛋白(rmIL-37b)通过调节CD39/ATP轴抑制树突状细胞(DC)诱导类风湿性关节炎(RA)大鼠炎症反应的机制。方法将SD大鼠随机分为空白对照组(CTL)、CIA模型组、rmIL-37b 5μg/kg组、rmIL-37b 10μg/kg组,每组各10只。除了空白对照组外,其余大鼠采用含有卡介苗的完全弗氏佐剂和牛Ⅱ型胶原混合乳液免疫刺激,建立CIA模型。确定建模成功当天(D0),rmIL-37b组分别尾静脉注射5μg/kg、10μg/kg rmIL-37b;CTL组和CIA模型组注射相同体积的(1 ml/kg)生理盐水,连续给药15 d。免疫组化法检测滑膜组织Nod样受体蛋白3(NRPL3)炎症小体的表达,流式细胞术检测DC表型,另外试剂盒检测血清三磷酸腺苷(ATP)和免疫学指标。结果与CIA模型组相比,rmIL-37b 10μg/kg组大鼠足容积、AI值、NLRP3炎症小体表达量、血清ATP、IL-1β、IL-18、肿瘤坏死因子α(TNF-α)、抗Ⅱ型胶原抗体亚型(anti-ColⅡ-IgG、anti-ColⅡ-IgG2a)水平均降低,同时DC表面CD... 相似文献
2.
《Vaccine》2022,40(6):934-944
Respiratory Syncytial Virus (RSV) remains a leading cause of severe respiratory disease for which no licensed vaccine is available. We have previously described the derivation of an RSV Fusion protein (F) stabilized in its prefusion conformation (preF) as vaccine immunogen and demonstrated superior immunogenicity in naive mice of preF versus wild type RSV F protein, both as protein and when expressed from an Ad26 vaccine vector. Here we address the question if there are qualitative differences between the two vaccine platforms for induction of protective immunity. In naïve mice, both Ad26.RSV.preF and preF protein induced humoral responses, whereas cellular responses were only elicited by Ad26.RSV.preF. In RSV pre-exposed mice, a single dose of either vaccine induced cellular responses and strong humoral responses. Ad26-induced RSV-specific cellular immune responses were detected systemically and locally in the lungs. Both vaccines showed protective efficacy in the cotton rat model, but Ad26.RSV.preF conferred protection at lower virus neutralizing titers in comparison to RSV preF protein. Factors that may contribute to the protective capacity of Ad26.RSV.preF elicited immunity are the induced IgG2a antibodies that are able to engage Fcγ receptors mediating Antibody Dependent Cellular Cytotoxicity (ADCC), and the induction of systemic and lung resident RSV specific CD8 + T cells. These data demonstrate qualitative improvement of immune responses elicited by an adenoviral vector based vaccine encoding the RSV preF antigen compared to the subunit vaccine in small animal models which may inform RSV vaccine development. 相似文献
3.
Seulbi Lee Hyesook Park Soontae Kim Eun-Kyung Lee Jiyoung Lee Young Sun Hong Eunhee Ha 《International journal of hygiene and environmental health》2019,222(3):533-540
Background
It has been reported that particulate matter (PM) is associated with cardiovascular diseases (CVD) while metabolic syndrome is also an important risk factor for CVD. However, few studies have investigated the epidemiological association between PM and metabolic syndrome.Objective
To investigate the association between one-year exposure to PM with an aerodynamic diameter <2.5?μm (PM2.5) and the risk of metabolic syndrome in Korean adults without CVD.Methods
Exposure to PM2.5 was assessed using a Community Multiscale Air Quality (CMAQ) model. Metabolic syndrome was defined by National Cholesterol Education Program Adult Treatment Panel III. Andersen and Gill model with time-varying covariates, considering recurrent events, was used to investigate the association between one-year average PM2.5 and the risk of incident metabolic syndrome in 119,998 adults from the national health screening cohort provided by Korea National Health Insurance from 2009 to 2013.Results
Higher risk of metabolic syndrome, waist-based obesity, hypertension, hypertriglyceridemia, low HDL cholesterol, and hyperglycemia were significantly associated with a 10-μg/m3 increase in PM2.5 [adjusted hazard ratio (HR): 1.070, 1.510, 1.499, 1.468, 1.627 and 1.380, respectively]. In addition, the risk of metabolic syndrome associated with PM2.5 exposure was significant in the consistently obese group (obese at baseline and endpoint).Conclusion
Exposure to one-year average PM2.5 is associated with an increased risk of metabolic syndrome and its components in adults without CVD. These associations are particularly prominent in the consistently obese group (obese at baseline and endpoint). Our findings indicate that PM2.5 affects the onset of MS and its components which may lead to increase the risk of CVD. 相似文献4.
Mahsa Noroozzadeh Samira Behboudi-Gandevani Nariman Mosaffa Maryam Tohidi 《Gynecological endocrinology》2019,35(8):679-684
Polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders in reproductive-age women. Significant associations between PCOS and benign breast diseases (BBD) and a possibly potential association between PCOS and breast cancer have been reported. The etiology of these events of mammary glands in PCOS remains unclear. Animal models that show BBD and breast cancer may contribute to further understanding about these diseases. We aimed to examine the spontaneous occurrence of mammary tumors, their prevalence, and type in our rat model of PCOS. Prenatal androgen-induced PCOS rats and controls were examined in later life. Benign mammary tumors were observed in 75% and 33.33% of PCOS rats and controls during the postmenopausal period, respectively (p?=?.0158). Mammary tumors were non-invasive, margins of excision were normal and tumors were freely movable, in both groups. After microscopic evaluations of tumors, proliferative breast lesions and adenomas with a tubular growth pattern were observed in both groups. However, in PCOS rats, of benign tumors two had a mixed pattern of fibroadenoma/fibroma and cysts. High prevalence of benign mammary tumors was observed in our rat model of PCOS during the postmenopausal period, possibly due to hormonal imbalances during their reproductive lifespan; this model may contribute to current data available regarding the events of mammary glands in PCOS. 相似文献
5.
6.
Amine Riahi Claude Kauffmann Eric Therasse Florence Morin-Roy Stephane Elkouri Patrick Gilbert Marie-France Giroux Pierre Perreault Louis Bouchard Vincent L. Oliva Gilles Soulez 《Journal of vascular and interventional radiology : JVIR》2019,30(4):523-530
Purpose
To compare automated measurements of maximal diameter (Dmax) of abdominal aortic aneurysm (AAA) orthogonal to luminal or outer wall envelope centerline for endovascular repair (EVAR) follow-up.Material and Methods
Eighty-three consecutive patients with AAA treated by EVAR who had at least 1 computed tomography (CT) scan before and 2 CT scans after EVAR with at least 5 months’ interval were included. Three-dimensional reconstruction of the AAA was achieved with dedicated segmentation software. Performances of automated calculation algorithms of Dmax perpendicular to lumen or outer wall envelope centerlines were then compared to manual measurement of Dmax on double-oblique multiplanar reconstruction (gold standard). Accuracy of automated Dmax measurements at baseline, follow-up, and progression over time was evaluated by calculation of mean error, Bland-Altman plot, and regression models.Results
Disagreement in Dmax measurements between outer wall envelope algorithm and manual method was insignificant (mean error: baseline, -0.07 ± 1.66 mm, P = .7; first follow-up, 0.24 ± 1.69 mm, P = .2; last follow-up, -0.41 ± 2.74 mm, P = .17); whereas significant discrepancies were found between the luminal algorithm and the manual method (mean error: baseline, -1.24 ± 2.01 mm, P < .01; first follow-up, -1.49 ± 3.30 mm, P < .01; last follow-up, -1.78 ± 3.60 mm, P < .01). Dmax progression results were more accurate with AAA outer wall envelope algorithm compared to luminal method (P = .2).Conclusions
AAA outer wall envelope segmentation is recommended to enable automated calculation of Dmax perpendicular to its centerline during EVAR follow-up. 相似文献7.
8.
《Clinical breast cancer》2022,22(6):507-514
Breast cancer (BC) is a highly metastatic, pathological cancer that significantly affects women worldwide. The mortality rate of BC is related to its heterogeneity, aggressive phenotype, and metastasis. Recent studies have highlighted that the tumor microenvironment (TME) is critical for the interplay between metastasis mediators in BC. BC stem cells, tumor-derived exosomes, circulatory tumor cells (CTCs), and signaling pathways dynamically remodel the TME and promote metastasis. This review examines the cellular and molecular mechanisms governing the epithelial to mesenchymal transition (EMT) that facilitate metastasis. This review also discusses the role of cancer stem cells (CSCs), tumor-derived exosomes, and CTs in promoting BC metastasis. Furthermore, the review emphasizes major signaling pathways that mediate metastasis in BC. Finally, the interplay among CSCs, exosomes, and CTCs in mediating metastasis have been highlighted. Therefore, understanding the molecular cues that mediate the association of CSCs, exosomes, and CTCs in TME helps to optimize systemic therapy to target metastatic BC. 相似文献
9.
目的:研究大鼠腹侧被盖区(VTA)多巴胺能神经元是否介导食欲素(orexin)的促进全麻后觉醒效应。方法:将兴奋性光遗传病毒注射至Hcrt-cre大鼠的orexin阳性神经元所在的下丘脑外侧穹隆周区(PeFLH),同时在VTA区注射抑制性化学遗传病毒及带有酪氨酸羟化酶(TH)-cre的混合病毒抑制多巴胺能神经元,并在VTA区植入光纤。观察通过化学遗传抑制VTA区多巴胺能神经元后,光遗传兴奋VTA区的orexin阳性神经投射终末是否仍能引起促进异氟醚麻醉后觉醒的效应。结果:与对照组相比,用化学遗传技术预先抑制VTA区多巴胺能神经元,阻断了光遗传兴奋VTA区orexin阳性神经投射终末所产生的缩短大鼠1.4%异氟醚麻醉后觉醒时间的作用;并阻断了光遗传兴奋VTA区orexin阳性神经投射终末所产生的降低大鼠1.4%异氟醚麻醉中脑电图爆发抑制率(BSR)效应。用Fos染色法验证了化学遗传法抑制多巴胺能神经元的可靠性。结论:抑制VTA区的多巴胺能神经元能够阻断兴奋大鼠VTA区orexin阳性神经末梢所产生的促进大鼠异氟醚后觉醒的效应,提示VTA区的多巴胺神经神经元介导了orexin调控VTA区产生的促进觉醒效应。 相似文献
10.