慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD,慢阻肺)是一种由气道炎症和气道重塑(airway remodeling, AR)引起的一种常见的慢性呼吸系统疾病。其中,气道重塑与COPD的进展之间存在的正反馈环显示了气道重塑在COPD进...慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD,慢阻肺)是一种由气道炎症和气道重塑(airway remodeling, AR)引起的一种常见的慢性呼吸系统疾病。其中,气道重塑与COPD的进展之间存在的正反馈环显示了气道重塑在COPD进展中的重要性。目前气道重塑的具体机制不明。临床上通过胸部CT发现的气道异常常提示患者已经发生了气道重塑,因此,寻找识别早期气道重塑的方法至关重要。研究表明,基质金属蛋白酶-9 (matrix metalloproteinase-9, MMP-9)、金属蛋白酶组织抑制剂-1 (tissue inhibitor of metalloproteinase-1, TIMP-1)、及MMP-9/TIMP-1比值之间的失衡参与COPD的气道重塑过程,本文叙述了MMP-9、TIMP-1及MMP-9/TIMP-1比值作为非侵入性诊断标志物在COPD气道重塑方面的研究进展,期待能提高人们对早期气道重塑的认知,希望能为将来气道重塑靶向药的问世尽一份绵薄之力。Chronic obstructive pulmonary disease (COPD) is a common chronic respiratory disease caused by airway inflammation and airway remodeling (AR). Among them, the positive feedback loop between airway remodeling and the progression of COPD shows the importance of airway remodeling in the progress of COPD. At present, the specific mechanism of airway remodeling is unknown. Airway abnormalities found by chest CT often indicate that airway remodeling has occurred in patients. Therefore, it is very important to find a method to identify early airway remodeling. Studies have shown that the imbalance between matrix metalloproteinase-9 (MMP-9), tissue inhibitor of metalloproteinase-1 (TIMP-1) and MMP-9/TIMP-1 ratio is involved in the airway remodeling of COPD. This paper describes the research progress of MMP-9, TIMP-1 and MMP-9/TIMP-1 ratio as non-invasive diagnostic markers in airway remodeling of COPD. It is expected to improve people’s understanding of early airway remodeling and make a modest contribution to the development of targeted drugs for airway remodeling in the future.展开更多
目的研究血清基质金属蛋白酶-9(MMP-9)、基质金属蛋白酶-26(MMP-26)、基质金属蛋白酶抑制剂-4(TIMP-4)与弥漫大B细胞淋巴瘤(Diffuse large B celllymphoma,DLBCL)病理分期及预后的相关性。方法选取2021年1月1日至2022年4月1日于上海交...目的研究血清基质金属蛋白酶-9(MMP-9)、基质金属蛋白酶-26(MMP-26)、基质金属蛋白酶抑制剂-4(TIMP-4)与弥漫大B细胞淋巴瘤(Diffuse large B celllymphoma,DLBCL)病理分期及预后的相关性。方法选取2021年1月1日至2022年4月1日于上海交通大学医学院附属瑞金医院治疗的75例DLBCL患者为研究组,另选取75例淋巴结反应性增生患者作为对照组,观察研究组与对照组及研究组不同分期、不同发病部位血清MMP-9、MMP-26及TIMP-4水平;采用Spearman分析DLBCL患者血清MMP-9、MMP-26与TIMP-4间的相关性;绘制Kaplan-Meier生存曲线,分析MMP-9、MMP-26、TIMP-4水平与DLBCL患者预后的关系。结果研究组血清MMP-9、MMP-26水平均高于对照组,血清TIMP-4水平均低于对照组,差异有统计学意义(P<0.05)。研究组Ⅰ~Ⅱ期患者血清MMP-9、MMP-26水平低于Ⅲ~Ⅳ期患者,血清TIMP-4水平高于Ⅲ~Ⅳ期患者,差异有统计学意义(P<0.05)。研究组不同发病部位患者血清MMP-9、MMP-26、TIMP-4水平比较差异均无统计学意义(P>0.05)。DLBCL患者血清MMP-9、MMP-26水平与TIMP-4水平呈负相关(P<0.05);血清MMP-9水平与MMP-26水平正相关(P<0.05)。MMP-9和MMP-26高表达、TIMP-4低表达组患者累积生存率低于其他组患者,差异具有统计学意义(P<0.05)。结论血清MMP-9、MMP-26及TIMP-4水平与DLBCL病理分期及患者预后密切相关,检测血清MMP-9、MMP-26及TIMP-4水平有助于明确DLBCL病理分期及评价患者预后。展开更多
中枢神经系统感染性疾病是病原微生物侵犯中枢神经系统(central nervous system, CNS)的实质、背膜及血管等引起的急性或慢性炎症(或非炎症性)疾病,这些病原微生物包括病毒、细菌、真菌、螺旋体、寄生虫、朊蛋白等。多种物质参与中枢神...中枢神经系统感染性疾病是病原微生物侵犯中枢神经系统(central nervous system, CNS)的实质、背膜及血管等引起的急性或慢性炎症(或非炎症性)疾病,这些病原微生物包括病毒、细菌、真菌、螺旋体、寄生虫、朊蛋白等。多种物质参与中枢神经系统感染性疾病的发生及发展。基质金属蛋白酶(matrix metalloproteinases, MMPs)是一个包括20多种蛋白在内的大家族。它参与胚胎发育、前体细胞或干细胞动员、创面重塑和愈合等生理反应,以及炎症、肿瘤进展和转移、血管内皮细胞损伤等病理反应。其中基质金属蛋白酶-9 (matrix metalloproteinase-9, MMP-9)在中枢神经系统疾病中发挥着重要的作用,无论是中枢神经系统感染性疾病还是肿瘤,目前的研究线索指向MMP-9与血脑屏障(blood brain barrier, BBB)的破坏相关。本文将就其研究现状进行综述和讨论。Infectious diseases of the central nervous system are acute or chronic inflammatory (or non- inflammatory) diseases caused by pathogenic microorganisms invading the substance, dorsal membrane and blood vessels of the central nervous system (CNS). These pathogenic microorganisms include viruses, bacteria, fungi, spirochetes, parasites, prions, etc. Many substances are involved in the occurrence and development of central nervous system infectious diseases. Matrix metalloproteinases (MMPs) are a large family that includes over 20 proteins. It participates in physiological reactions such as embryonic development, mobilization of precursor cells or stem cells, wound remodeling and healing, as well as pathological reactions such as inflammation, tumor progression and metastasis, and damage to vascular endothelial cells. Matrix metalloproteinase-9 (MMP-9) plays an important role in central nervous system diseases. Whether it is central nervous system infectious diseases or tumors, the current research clues point to the relationship between MMP-9 and the destruction of blood brain barrier (BBB). This article will review and discuss the current research status.展开更多
文摘慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD,慢阻肺)是一种由气道炎症和气道重塑(airway remodeling, AR)引起的一种常见的慢性呼吸系统疾病。其中,气道重塑与COPD的进展之间存在的正反馈环显示了气道重塑在COPD进展中的重要性。目前气道重塑的具体机制不明。临床上通过胸部CT发现的气道异常常提示患者已经发生了气道重塑,因此,寻找识别早期气道重塑的方法至关重要。研究表明,基质金属蛋白酶-9 (matrix metalloproteinase-9, MMP-9)、金属蛋白酶组织抑制剂-1 (tissue inhibitor of metalloproteinase-1, TIMP-1)、及MMP-9/TIMP-1比值之间的失衡参与COPD的气道重塑过程,本文叙述了MMP-9、TIMP-1及MMP-9/TIMP-1比值作为非侵入性诊断标志物在COPD气道重塑方面的研究进展,期待能提高人们对早期气道重塑的认知,希望能为将来气道重塑靶向药的问世尽一份绵薄之力。Chronic obstructive pulmonary disease (COPD) is a common chronic respiratory disease caused by airway inflammation and airway remodeling (AR). Among them, the positive feedback loop between airway remodeling and the progression of COPD shows the importance of airway remodeling in the progress of COPD. At present, the specific mechanism of airway remodeling is unknown. Airway abnormalities found by chest CT often indicate that airway remodeling has occurred in patients. Therefore, it is very important to find a method to identify early airway remodeling. Studies have shown that the imbalance between matrix metalloproteinase-9 (MMP-9), tissue inhibitor of metalloproteinase-1 (TIMP-1) and MMP-9/TIMP-1 ratio is involved in the airway remodeling of COPD. This paper describes the research progress of MMP-9, TIMP-1 and MMP-9/TIMP-1 ratio as non-invasive diagnostic markers in airway remodeling of COPD. It is expected to improve people’s understanding of early airway remodeling and make a modest contribution to the development of targeted drugs for airway remodeling in the future.
文摘目的研究血清基质金属蛋白酶-9(MMP-9)、基质金属蛋白酶-26(MMP-26)、基质金属蛋白酶抑制剂-4(TIMP-4)与弥漫大B细胞淋巴瘤(Diffuse large B celllymphoma,DLBCL)病理分期及预后的相关性。方法选取2021年1月1日至2022年4月1日于上海交通大学医学院附属瑞金医院治疗的75例DLBCL患者为研究组,另选取75例淋巴结反应性增生患者作为对照组,观察研究组与对照组及研究组不同分期、不同发病部位血清MMP-9、MMP-26及TIMP-4水平;采用Spearman分析DLBCL患者血清MMP-9、MMP-26与TIMP-4间的相关性;绘制Kaplan-Meier生存曲线,分析MMP-9、MMP-26、TIMP-4水平与DLBCL患者预后的关系。结果研究组血清MMP-9、MMP-26水平均高于对照组,血清TIMP-4水平均低于对照组,差异有统计学意义(P<0.05)。研究组Ⅰ~Ⅱ期患者血清MMP-9、MMP-26水平低于Ⅲ~Ⅳ期患者,血清TIMP-4水平高于Ⅲ~Ⅳ期患者,差异有统计学意义(P<0.05)。研究组不同发病部位患者血清MMP-9、MMP-26、TIMP-4水平比较差异均无统计学意义(P>0.05)。DLBCL患者血清MMP-9、MMP-26水平与TIMP-4水平呈负相关(P<0.05);血清MMP-9水平与MMP-26水平正相关(P<0.05)。MMP-9和MMP-26高表达、TIMP-4低表达组患者累积生存率低于其他组患者,差异具有统计学意义(P<0.05)。结论血清MMP-9、MMP-26及TIMP-4水平与DLBCL病理分期及患者预后密切相关,检测血清MMP-9、MMP-26及TIMP-4水平有助于明确DLBCL病理分期及评价患者预后。
文摘中枢神经系统感染性疾病是病原微生物侵犯中枢神经系统(central nervous system, CNS)的实质、背膜及血管等引起的急性或慢性炎症(或非炎症性)疾病,这些病原微生物包括病毒、细菌、真菌、螺旋体、寄生虫、朊蛋白等。多种物质参与中枢神经系统感染性疾病的发生及发展。基质金属蛋白酶(matrix metalloproteinases, MMPs)是一个包括20多种蛋白在内的大家族。它参与胚胎发育、前体细胞或干细胞动员、创面重塑和愈合等生理反应,以及炎症、肿瘤进展和转移、血管内皮细胞损伤等病理反应。其中基质金属蛋白酶-9 (matrix metalloproteinase-9, MMP-9)在中枢神经系统疾病中发挥着重要的作用,无论是中枢神经系统感染性疾病还是肿瘤,目前的研究线索指向MMP-9与血脑屏障(blood brain barrier, BBB)的破坏相关。本文将就其研究现状进行综述和讨论。Infectious diseases of the central nervous system are acute or chronic inflammatory (or non- inflammatory) diseases caused by pathogenic microorganisms invading the substance, dorsal membrane and blood vessels of the central nervous system (CNS). These pathogenic microorganisms include viruses, bacteria, fungi, spirochetes, parasites, prions, etc. Many substances are involved in the occurrence and development of central nervous system infectious diseases. Matrix metalloproteinases (MMPs) are a large family that includes over 20 proteins. It participates in physiological reactions such as embryonic development, mobilization of precursor cells or stem cells, wound remodeling and healing, as well as pathological reactions such as inflammation, tumor progression and metastasis, and damage to vascular endothelial cells. Matrix metalloproteinase-9 (MMP-9) plays an important role in central nervous system diseases. Whether it is central nervous system infectious diseases or tumors, the current research clues point to the relationship between MMP-9 and the destruction of blood brain barrier (BBB). This article will review and discuss the current research status.
