Synovial tuberculosis in the wrist is a rare disease that is usually misdiagnosed at the early stage. In this case, we presented a 67-year-old male with wrist joint tuberculosis who presented repeated left wrist joint edema for more than 2 years. The patient received surgery twice. During the second surgery, the combination of metagenomic next-generation sequencing (mNGS) and pathological analysis contributed to the detection of Mycobacterium tuberculosis in lesion tissues. Conventional anti-tubercular therapy confirmed the diagnosis of synovial tuberculosis in the wrist joint. In conclusion, mNGS contributed to the rapid and accurate detection of tubercle bacillus.
{"title":"Synovial tuberculosis in wrist diagnosed based on metagenomic next-generation sequencing: A case report","authors":"Meimei Wu, Xianfeng Lan, Shibei Lin, T. Lai, Wei-Sha Lin, Haomin Wu","doi":"10.1177/20587392221075507","DOIUrl":"https://doi.org/10.1177/20587392221075507","url":null,"abstract":"Synovial tuberculosis in the wrist is a rare disease that is usually misdiagnosed at the early stage. In this case, we presented a 67-year-old male with wrist joint tuberculosis who presented repeated left wrist joint edema for more than 2 years. The patient received surgery twice. During the second surgery, the combination of metagenomic next-generation sequencing (mNGS) and pathological analysis contributed to the detection of Mycobacterium tuberculosis in lesion tissues. Conventional anti-tubercular therapy confirmed the diagnosis of synovial tuberculosis in the wrist joint. In conclusion, mNGS contributed to the rapid and accurate detection of tubercle bacillus.","PeriodicalId":55162,"journal":{"name":"European Journal of Inflammation","volume":" ","pages":""},"PeriodicalIF":0.7,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46282255","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-01-01DOI: 10.1177/1721727X221095378
Lin Wang, Yuan Ma, Jinfang Shi, Yang Zhang, J. Tong, Q. Han
Objectives: Bacterial peptidoglycan (PGN) is an essential ligand of TLR2 inducing inflammatory damage by boosting MyD88 overexpression in pathogen invasion, such as Methicillin-resistant Staphylococcus aureus (MRSA) infection. CP-PGN is a novel PGN from an adjuvant bacterium, displaying anti-infection immune regulation. This study aimed to clarify the unique moderation of MyD88 expression by CP-PGN. Methods: Compared with other ligands of TLR2, high expression of MyD88 in macrophages was established by MRSA and virus to investigate the immunomodulation of CP-PGN. Results: Compared with PGN derived from MRSA (M-PGN) and chemosynthetic Pam3CSK4 of model agonists of TLR2, CP-PGN could inhibit overexpression of MyD88 in a time- and dose-dependent way in infected macrophages by MRSA or Abelson leukemia virus. CP-PGN also promoted more anti-inflammatory IL-10 and less pro-inflammatory TNF-α in immature primary macrophages. Furthermore, IL-10 secretion induced by CP-PGN was reduced most significantly by blocking the dimer formation of MyD88 with ST2825 and lowering down expression by si-MyD88. Conclusion: CP-PGN could inhibit MyD88 overexpression by infection to moderate inflammatory cytokines. Therefore, CP-PGN is a novel potential ligand of TLR2 to induce inflammatory balance in the process of host defense against invading pathogens.
{"title":"Corynebacterium pyruviciproducens-peptidoglycan: A novel bacterial peptidoglycan inhibiting overexpression of MyD88 in macrophages","authors":"Lin Wang, Yuan Ma, Jinfang Shi, Yang Zhang, J. Tong, Q. Han","doi":"10.1177/1721727X221095378","DOIUrl":"https://doi.org/10.1177/1721727X221095378","url":null,"abstract":"Objectives: Bacterial peptidoglycan (PGN) is an essential ligand of TLR2 inducing inflammatory damage by boosting MyD88 overexpression in pathogen invasion, such as Methicillin-resistant Staphylococcus aureus (MRSA) infection. CP-PGN is a novel PGN from an adjuvant bacterium, displaying anti-infection immune regulation. This study aimed to clarify the unique moderation of MyD88 expression by CP-PGN. Methods: Compared with other ligands of TLR2, high expression of MyD88 in macrophages was established by MRSA and virus to investigate the immunomodulation of CP-PGN. Results: Compared with PGN derived from MRSA (M-PGN) and chemosynthetic Pam3CSK4 of model agonists of TLR2, CP-PGN could inhibit overexpression of MyD88 in a time- and dose-dependent way in infected macrophages by MRSA or Abelson leukemia virus. CP-PGN also promoted more anti-inflammatory IL-10 and less pro-inflammatory TNF-α in immature primary macrophages. Furthermore, IL-10 secretion induced by CP-PGN was reduced most significantly by blocking the dimer formation of MyD88 with ST2825 and lowering down expression by si-MyD88. Conclusion: CP-PGN could inhibit MyD88 overexpression by infection to moderate inflammatory cytokines. Therefore, CP-PGN is a novel potential ligand of TLR2 to induce inflammatory balance in the process of host defense against invading pathogens.","PeriodicalId":55162,"journal":{"name":"European Journal of Inflammation","volume":" ","pages":""},"PeriodicalIF":0.7,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43018978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Objective This study aimed to investigate the effects of hypoxia-inducible factor-1α (HIF-1α), hypoxia-inducible factor-2α (HIF-2α), and erythroferrone (ERFE) on hepcidin in patients with chronic kidney disease (CKD) stages 3–5 and renal anemia. Methods A total of 90 patients with CKD stages 3–5 and renal anemia were selected for the study at the Nephrology Department of Fujian Provincial People’s Hospital and divided into three groups, according to CKD stage, while another 30 healthy subjects who underwent a physical examination at the hospital during the same period were selected as the normal group. The serum levels of hepcidin, HIF-1α, HIF-2α, ERFE, and furin were measured using an avidin biotin peroxidase complex enzyme-linked immunosorbent assay to compare the differences between the groups in the related indicators. Results ① Serum HIF-2α, HIF-1α, ERFE, and furin levels increased gradually in the patients with CKD stages 3–5 (p < 0.05, p < 0.01). ②Simple correlation analysis:Serum hepcidin was positively correlated with HIF-2α, ERFE, and HIF-1α in the CKD patients (p < 0.01). ③Serum hepcidin was positively correlated with HIF-2α, HIF-1α, and ERFE in the CKD patients injected with erythropoietin (EPO) (p < 0.01), while serum hepcidin was positively correlated with HIF-2α and HIF-1α (p < 0.01) in the patients not injected with EPO. ④ Multivariate linear regression analysis showed that HIF-1α, (β = 4.36, p < 0.01), serum ferritin(SF) (β = 0.13, p < 0.01), and HIF-2α (β = 0.66, p < 0.01) were significantly correlated with hepcidin. Conclusion HIF-1α, HIF-2α, and SF are factors which have an effect on hepcidin in patients with CKD stages 3–5 and renal anemia. The increase of HIF-1α, HIF-2α, and ERFE does not seem to inhibit the increase of hepcidin.
目的探讨低氧诱导因子-1α (HIF-1α)、低氧诱导因子-2α (HIF-2α)和红细胞铁酮(ERFE)对慢性肾病(CKD) 3-5期及肾性贫血患者hepcidin的影响。方法选择福建省人民医院肾内科CKD 3 ~ 5期合并肾性贫血患者90例，按CKD分期分为3组，同期在该院体检的健康受试者30例为正常组。采用亲和素生物素过氧化物酶复合物酶联免疫吸附法测定血清hepcidin、HIF-1α、HIF-2α、ERFE和furin水平，比较各组间相关指标的差异。结果①CKD 3 ~ 5期患者血清HIF-2α、HIF-1α、ERFE、furin水平逐渐升高(p < 0.05, p < 0.01)。②简单相关分析:CKD患者血清hepcidin与HIF-2α、ERFE、HIF-1α呈正相关(p < 0.01)。③注射促红细胞生成素(EPO)的CKD患者血清hepcidin与HIF-2α、HIF-1α、ERFE呈正相关(p < 0.01)，未注射EPO的CKD患者血清hepcidin与HIF-2α、HIF-1α呈正相关(p < 0.01)。④多元线性回归分析显示，HIF-1α (β = 4.36, p < 0.01)、血清铁蛋白(SF) (β = 0.13, p < 0.01)和HIF-2α (β = 0.66, p < 0.01)与hepcidin呈极显著相关。结论HIF-1α、HIF-2α和SF是影响CKD 3-5期肾性贫血患者hepcidin水平的因素。HIF-1α、HIF-2α和ERFE的升高似乎并没有抑制hepcidin的升高。
{"title":"The effects of hypoxia-inducible factors-1α and -2α and erythroferrone on hepcidin in patients with chronic kidney disease stages 3–5 and renal anemia","authors":"Jianghuai Hong, Jing-Yang Lai, Xiaoying Chen, Yan Yan, Yanyan Hong, Hailun Ke, Jing Zheng","doi":"10.1177/1721727X221103468","DOIUrl":"https://doi.org/10.1177/1721727X221103468","url":null,"abstract":"Objective This study aimed to investigate the effects of hypoxia-inducible factor-1α (HIF-1α), hypoxia-inducible factor-2α (HIF-2α), and erythroferrone (ERFE) on hepcidin in patients with chronic kidney disease (CKD) stages 3–5 and renal anemia. Methods A total of 90 patients with CKD stages 3–5 and renal anemia were selected for the study at the Nephrology Department of Fujian Provincial People’s Hospital and divided into three groups, according to CKD stage, while another 30 healthy subjects who underwent a physical examination at the hospital during the same period were selected as the normal group. The serum levels of hepcidin, HIF-1α, HIF-2α, ERFE, and furin were measured using an avidin biotin peroxidase complex enzyme-linked immunosorbent assay to compare the differences between the groups in the related indicators. Results ① Serum HIF-2α, HIF-1α, ERFE, and furin levels increased gradually in the patients with CKD stages 3–5 (p < 0.05, p < 0.01). ②Simple correlation analysis:Serum hepcidin was positively correlated with HIF-2α, ERFE, and HIF-1α in the CKD patients (p < 0.01). ③Serum hepcidin was positively correlated with HIF-2α, HIF-1α, and ERFE in the CKD patients injected with erythropoietin (EPO) (p < 0.01), while serum hepcidin was positively correlated with HIF-2α and HIF-1α (p < 0.01) in the patients not injected with EPO. ④ Multivariate linear regression analysis showed that HIF-1α, (β = 4.36, p < 0.01), serum ferritin(SF) (β = 0.13, p < 0.01), and HIF-2α (β = 0.66, p < 0.01) were significantly correlated with hepcidin. Conclusion HIF-1α, HIF-2α, and SF are factors which have an effect on hepcidin in patients with CKD stages 3–5 and renal anemia. The increase of HIF-1α, HIF-2α, and ERFE does not seem to inhibit the increase of hepcidin.","PeriodicalId":55162,"journal":{"name":"European Journal of Inflammation","volume":" ","pages":""},"PeriodicalIF":0.7,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43289557","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-01-01DOI: 10.1177/1721727X221112271
Yanhui Li, Chunyan Shao, Mou Zhou, Linying Shi
Objectives Platelet-rich plasma (PRP) plays an important role at all stages of wound healing, including the inflammatory stage. Macrophage autophagy has been found to influence the inflammatory response process. However, it is unclear whether PRP can affect inflammatory responses via macrophage autophagy. In the present study, we explored the effect of PRP on inflammatory responses and researched the underlying mechanism. Methods RAW 264.7 macrophages were treated with PRP and/or lipopolysaccharide (LPS). The effects of PRP on the expression of inflammatory factors were determined by ELISA and qRT-PCR. Macrophage autophagosomes were also assessed by TEM and immunofluorescence. Autophagy and NLRP3-related proteins were investigated using Western blot analysis. Results PRP reduced the levels of inflammatory factors and increased autophagy in RAW 264.7 cells. Pretreatment with 3-MA, which is an autophagy inhibitor, abolished the impact of PRP on the inflammatory response. Moreover, PRP induced macrophage autophagy by activating the NLRP3 inflammasome. Conclusions These results show that PRP can attenuate LPS-induced inflammatory responses by enhancing autophagy via NLRP3. These study also provides a new perspective on the molecular mechanism of PRP therapy in wound healing.
{"title":"Platelet-rich plasma improves lipopolysaccharide-induced inflammatory response by upgrading autophagy","authors":"Yanhui Li, Chunyan Shao, Mou Zhou, Linying Shi","doi":"10.1177/1721727X221112271","DOIUrl":"https://doi.org/10.1177/1721727X221112271","url":null,"abstract":"Objectives Platelet-rich plasma (PRP) plays an important role at all stages of wound healing, including the inflammatory stage. Macrophage autophagy has been found to influence the inflammatory response process. However, it is unclear whether PRP can affect inflammatory responses via macrophage autophagy. In the present study, we explored the effect of PRP on inflammatory responses and researched the underlying mechanism. Methods RAW 264.7 macrophages were treated with PRP and/or lipopolysaccharide (LPS). The effects of PRP on the expression of inflammatory factors were determined by ELISA and qRT-PCR. Macrophage autophagosomes were also assessed by TEM and immunofluorescence. Autophagy and NLRP3-related proteins were investigated using Western blot analysis. Results PRP reduced the levels of inflammatory factors and increased autophagy in RAW 264.7 cells. Pretreatment with 3-MA, which is an autophagy inhibitor, abolished the impact of PRP on the inflammatory response. Moreover, PRP induced macrophage autophagy by activating the NLRP3 inflammasome. Conclusions These results show that PRP can attenuate LPS-induced inflammatory responses by enhancing autophagy via NLRP3. These study also provides a new perspective on the molecular mechanism of PRP therapy in wound healing.","PeriodicalId":55162,"journal":{"name":"European Journal of Inflammation","volume":" ","pages":""},"PeriodicalIF":0.7,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41643182","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-01-01DOI: 10.1177/20587392211066424
Yanqiu Xu, Ying Zhang, Hongming Hu, J. Tan, Bin Wu
The coexistence of systemic lupus erythematosus (SLE) and myasthenia gravis (MG) is rarely reported, especially the appearance of SLE before MG. In addition to the production of autoantibodies after thymectomy, gene mutation may be an important contributing factor to the overlap of SLE and MG. Here, we report a case of a female patient diagnosed with SLE before MG and found to carry the heterozygous variation COL6A1 c. 2608G>A. We propose that this gene variation weakens the function of COL6A1 and indirectly activates STAT1, resulting in the phenotype of these two autoimmune diseases. This report suggests that it is feasible to explore common pathogenic genes in SLE and MG through future large-scale research.
{"title":"Systemic lupus erythematosus after delivery and myasthenia gravis with COL6A1 gene mutation: A case report","authors":"Yanqiu Xu, Ying Zhang, Hongming Hu, J. Tan, Bin Wu","doi":"10.1177/20587392211066424","DOIUrl":"https://doi.org/10.1177/20587392211066424","url":null,"abstract":"The coexistence of systemic lupus erythematosus (SLE) and myasthenia gravis (MG) is rarely reported, especially the appearance of SLE before MG. In addition to the production of autoantibodies after thymectomy, gene mutation may be an important contributing factor to the overlap of SLE and MG. Here, we report a case of a female patient diagnosed with SLE before MG and found to carry the heterozygous variation COL6A1 c. 2608G>A. We propose that this gene variation weakens the function of COL6A1 and indirectly activates STAT1, resulting in the phenotype of these two autoimmune diseases. This report suggests that it is feasible to explore common pathogenic genes in SLE and MG through future large-scale research.","PeriodicalId":55162,"journal":{"name":"European Journal of Inflammation","volume":" ","pages":""},"PeriodicalIF":0.7,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42708587","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-01-01DOI: 10.1177/20587392211051115
Li Zhu, Chuanmeng Zhang, Guangyao Mao, Jie Xu, Jingyu Qian, Lin Jiang, Jun Ye
To analyze the diagnostic value of CD40 ligand (CD40L), soluble growth stimulating expression gene 2 protein (ST2), interleukin-6 (IL-6), and C-reactive protein (CRP) are used in patients with acute coronary syndrome (ACS). Serum samples were collected from 259 ACS patients admitted to our hospital. Additionally, 119 healthy individuals who received physical examination in the hospital at the same time period were included as normal control. The levels of CD40L, ST2, IL-6, and CRP in 259 patients with ACS and 119 healthy subjects were detected by ELISA. The levels of CD40L, ST2, IL-6, and CRP were significantly increased in unstable angina (UA) patients, while ST2, CRP, and IL-6 were significantly elevated in acute myocardial infarction (AMI) patients. Pearson correlation analysis showed that ST2 was also closely related to CRP in ACS patients, while ST2 was positively correlated with creatine kinase (CK), creatine kinase isoenzyme (CK-MB), and troponin I (cTnI) in AMI patients. The levels of glucose (GLU) and low-density lipoprotein cholesterol (LDL-c) were significantly decreased, while the levels of high-density lipoprotein cholesterol (HDL-c) were significantly increased in AMI patients treated with stent implantation. Furthermore, the level of serum CD40 L was significantly elevated in coronary heart disease (CHD) patients treated with stent implantation, while the levels of ST2 and IL-6 in AMI patients treated with the stent implantation decreased significantly. The levels of inflammatory factors significantly changed in patients with ACS. These inflammatory factors may involve in the pathological progression of ACS and can be used as diagnostic indexes for ACS.
{"title":"Serum CD40L, ST2, IL-6, and CRP serving as biomarkers for acute coronary syndrome","authors":"Li Zhu, Chuanmeng Zhang, Guangyao Mao, Jie Xu, Jingyu Qian, Lin Jiang, Jun Ye","doi":"10.1177/20587392211051115","DOIUrl":"https://doi.org/10.1177/20587392211051115","url":null,"abstract":"To analyze the diagnostic value of CD40 ligand (CD40L), soluble growth stimulating expression gene 2 protein (ST2), interleukin-6 (IL-6), and C-reactive protein (CRP) are used in patients with acute coronary syndrome (ACS). Serum samples were collected from 259 ACS patients admitted to our hospital. Additionally, 119 healthy individuals who received physical examination in the hospital at the same time period were included as normal control. The levels of CD40L, ST2, IL-6, and CRP in 259 patients with ACS and 119 healthy subjects were detected by ELISA. The levels of CD40L, ST2, IL-6, and CRP were significantly increased in unstable angina (UA) patients, while ST2, CRP, and IL-6 were significantly elevated in acute myocardial infarction (AMI) patients. Pearson correlation analysis showed that ST2 was also closely related to CRP in ACS patients, while ST2 was positively correlated with creatine kinase (CK), creatine kinase isoenzyme (CK-MB), and troponin I (cTnI) in AMI patients. The levels of glucose (GLU) and low-density lipoprotein cholesterol (LDL-c) were significantly decreased, while the levels of high-density lipoprotein cholesterol (HDL-c) were significantly increased in AMI patients treated with stent implantation. Furthermore, the level of serum CD40 L was significantly elevated in coronary heart disease (CHD) patients treated with stent implantation, while the levels of ST2 and IL-6 in AMI patients treated with the stent implantation decreased significantly. The levels of inflammatory factors significantly changed in patients with ACS. These inflammatory factors may involve in the pathological progression of ACS and can be used as diagnostic indexes for ACS.","PeriodicalId":55162,"journal":{"name":"European Journal of Inflammation","volume":" ","pages":""},"PeriodicalIF":0.7,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46076682","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-01-01DOI: 10.1177/20587392211050805
Changgon Kim, Hyun-Sook Kim
Catastrophic antiphospholipid syndrome (CAPS) is a lethal disease that occurs suddenly and progresses to multi-organ failure. We present a case of CAPS successfully treated with the rituximab biosimilar CT-P10. A 38-year-old man was referred with a sustained fever and unexplained elevated creatinine levels. Cardiac arrest by ventricular fibrillation occurred upon arrival at the hospital. We diagnosed probable CAPS because of coronary thrombus, renal impairment, suspected diffuse alveolar hemorrhage, and positive anticardiolipin antibody immunoglobulin G. We performed percutaneous coronary intervention for the cardiac arrest, and treated him with extracorporeal membrane oxygenation, mechanical ventilation, and continuous renal replacement therapy. When CAPS was diagnosed, we administered CT-P10 after administering high-dose glucocorticoid. Our case suggests that the use of a rituximab biosimilar is economically efficient in the treatment of CAPS, as in other rheumatic diseases. The patient was cured without recurrence at the 2-year follow-up.
{"title":"Catastrophic antiphospholipid syndrome presented with coronary thrombosis, renal impairment, and suspected diffuse alveolar hemorrhage treated with rituximab biosimilar (CT-P10)","authors":"Changgon Kim, Hyun-Sook Kim","doi":"10.1177/20587392211050805","DOIUrl":"https://doi.org/10.1177/20587392211050805","url":null,"abstract":"Catastrophic antiphospholipid syndrome (CAPS) is a lethal disease that occurs suddenly and progresses to multi-organ failure. We present a case of CAPS successfully treated with the rituximab biosimilar CT-P10. A 38-year-old man was referred with a sustained fever and unexplained elevated creatinine levels. Cardiac arrest by ventricular fibrillation occurred upon arrival at the hospital. We diagnosed probable CAPS because of coronary thrombus, renal impairment, suspected diffuse alveolar hemorrhage, and positive anticardiolipin antibody immunoglobulin G. We performed percutaneous coronary intervention for the cardiac arrest, and treated him with extracorporeal membrane oxygenation, mechanical ventilation, and continuous renal replacement therapy. When CAPS was diagnosed, we administered CT-P10 after administering high-dose glucocorticoid. Our case suggests that the use of a rituximab biosimilar is economically efficient in the treatment of CAPS, as in other rheumatic diseases. The patient was cured without recurrence at the 2-year follow-up.","PeriodicalId":55162,"journal":{"name":"European Journal of Inflammation","volume":" ","pages":""},"PeriodicalIF":0.7,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48322439","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-01-01DOI: 10.1177/1721727X221095381
Yan-Ling Xie, Jian-Xun Li, Wei-Zhong Ji, Yong-Li Yao
Objective: To understand the distribution characteristics of the relative frequencies of apolipoprotein E (APOE) alleles in Tibetans of Qinghai province, to provide a basis for subsequent research. Method: Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was used to determine the APOE genotypes and analyze the distribution characteristics in 96 indigenous Tibetans randomly selected from the Medical Examination Center of Qinghai Provincial People’s Hospital, and the results of this study were compared with those of other ethnic groups in China. Results: The frequencies of E2, E3, and E4 alleles in the 96 subjects were 1.563%, 89.062%, and 9.375%, respectively, and the genotype frequencies were E2/E2 (0%), E2/E3 (3.125%), E2/E4 (0%), E3/E3 (78.125%), E3/E4 (18.750%), and E4/E4 (0%), respectively. The frequency distribution of the ε2 allele in the Tibetan population was lower than that of the Northern Han, Southern Hakka, Hui, Mongolian, and Dai populations of China. The frequency distribution of the ε4 allele in the Tibetan population was of no significant difference compared with that of the Northern Han, Southern Hakka, Hui, and Mongolian populations, but was higher than that of the Dai population. The frequency distribution of the ε3 allele in the Tibetan population was of no significant difference compared with that of the Northern Han, Mongolian, and Dai populations, but higher than that of the Southern Hakka and Mongolian populations. Conclusion: There are ethnic differences in the frequency distribution of the three common alleles of APOE.
{"title":"Distribution characteristics of ApoE gene polymorphism in the Tibetan population of Qinghai","authors":"Yan-Ling Xie, Jian-Xun Li, Wei-Zhong Ji, Yong-Li Yao","doi":"10.1177/1721727X221095381","DOIUrl":"https://doi.org/10.1177/1721727X221095381","url":null,"abstract":"Objective: To understand the distribution characteristics of the relative frequencies of apolipoprotein E (APOE) alleles in Tibetans of Qinghai province, to provide a basis for subsequent research. Method: Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was used to determine the APOE genotypes and analyze the distribution characteristics in 96 indigenous Tibetans randomly selected from the Medical Examination Center of Qinghai Provincial People’s Hospital, and the results of this study were compared with those of other ethnic groups in China. Results: The frequencies of E2, E3, and E4 alleles in the 96 subjects were 1.563%, 89.062%, and 9.375%, respectively, and the genotype frequencies were E2/E2 (0%), E2/E3 (3.125%), E2/E4 (0%), E3/E3 (78.125%), E3/E4 (18.750%), and E4/E4 (0%), respectively. The frequency distribution of the ε2 allele in the Tibetan population was lower than that of the Northern Han, Southern Hakka, Hui, Mongolian, and Dai populations of China. The frequency distribution of the ε4 allele in the Tibetan population was of no significant difference compared with that of the Northern Han, Southern Hakka, Hui, and Mongolian populations, but was higher than that of the Dai population. The frequency distribution of the ε3 allele in the Tibetan population was of no significant difference compared with that of the Northern Han, Mongolian, and Dai populations, but higher than that of the Southern Hakka and Mongolian populations. Conclusion: There are ethnic differences in the frequency distribution of the three common alleles of APOE.","PeriodicalId":55162,"journal":{"name":"European Journal of Inflammation","volume":" ","pages":""},"PeriodicalIF":0.7,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44642640","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Introduction: Sepsis can cause acute lung injury (ALI), one of the leading causes of death in critically ill patients. The underlying mechanisms of sepsis-induced acute lung injury include excessive inflammation, oxidative stress, cell apoptosis, pulmonary edema, and lung tissue dysfunction. Recent studies have shown that miRNA-21 (miR-21) plays a vital role in sepsis-induced acute kidney injury. Relatively few studies have focused on the protective effects of ALI. This study aimed to determine the potential role of miR-21 in sepsis-induced ALI. Methods: We performed quantitative real-time polymerase chain reaction in a septic mouse model induced by cecal ligation and puncture (CLP) and found that miR-21 expression was upregulated. We then transfected the miR-21 precursor to upregulate miR-21 expression and miR-21 inhibitor to downregulate miR-21 expression. The sham group was exposed only to the cecum. ALI was induced by CLP, and the pre-miR-21+ALI and anti-miR-21+ALI groups were treated with miR-21 precursor or miR-21 inhibitor in the caudal vein before CLP. Pre-miR-21+ALI+PTEN inhibition (Pre-miR-21+ALI+PI) and anti-miR-21+ALI+PTEN inhibition (Anti-miR-21+ALI+PI) groups were treated with PTEN inhibition into the caudal vein after miR-21 transfection. Inflammatory cytokines, oxidative stress indicators, lung tissue cell apoptosis, oxygenation index (OI), lung wet/dry weight ratio, and lung pathological changes in the lung were observed in each group. Results: Compared with ALI mice, inflammatory response, oxidative stress indicators, lung tissue cell apoptosis, and the degree of lung injury were remarkably alleviated in Pre-miR-21+ALI mice and aggravated in Anti-miR-21+ALI mice. Western blot analysis showed that phosphatase and tensin homolog (PTEN) protein expression was decreased in CLP-treated mics. PTEN protein expression was decreased in the Pre-miR-21+ALI group but increased in the Anti-miR-21+ALI group. Moreover, the effect of miR-21 on anti-inflammatory, anti-oxidative stress, and anti-apoptosis enhanced after PTEN inhibition. Conclusion: This study revealed that miR-21 has a protective effect in sepsis-induced ALI by regulating PTEN in mice.
{"title":"MicroRNA-21 protects against sepsis-induced acute lung injury by targeting phosphatase and tensin homolog in mice","authors":"Chen Ge, Junhang Liu, You Fu, Lijing Jia, Ling Long, Shimin Dong","doi":"10.1177/1721727X221120978","DOIUrl":"https://doi.org/10.1177/1721727X221120978","url":null,"abstract":"Introduction: Sepsis can cause acute lung injury (ALI), one of the leading causes of death in critically ill patients. The underlying mechanisms of sepsis-induced acute lung injury include excessive inflammation, oxidative stress, cell apoptosis, pulmonary edema, and lung tissue dysfunction. Recent studies have shown that miRNA-21 (miR-21) plays a vital role in sepsis-induced acute kidney injury. Relatively few studies have focused on the protective effects of ALI. This study aimed to determine the potential role of miR-21 in sepsis-induced ALI. Methods: We performed quantitative real-time polymerase chain reaction in a septic mouse model induced by cecal ligation and puncture (CLP) and found that miR-21 expression was upregulated. We then transfected the miR-21 precursor to upregulate miR-21 expression and miR-21 inhibitor to downregulate miR-21 expression. The sham group was exposed only to the cecum. ALI was induced by CLP, and the pre-miR-21+ALI and anti-miR-21+ALI groups were treated with miR-21 precursor or miR-21 inhibitor in the caudal vein before CLP. Pre-miR-21+ALI+PTEN inhibition (Pre-miR-21+ALI+PI) and anti-miR-21+ALI+PTEN inhibition (Anti-miR-21+ALI+PI) groups were treated with PTEN inhibition into the caudal vein after miR-21 transfection. Inflammatory cytokines, oxidative stress indicators, lung tissue cell apoptosis, oxygenation index (OI), lung wet/dry weight ratio, and lung pathological changes in the lung were observed in each group. Results: Compared with ALI mice, inflammatory response, oxidative stress indicators, lung tissue cell apoptosis, and the degree of lung injury were remarkably alleviated in Pre-miR-21+ALI mice and aggravated in Anti-miR-21+ALI mice. Western blot analysis showed that phosphatase and tensin homolog (PTEN) protein expression was decreased in CLP-treated mics. PTEN protein expression was decreased in the Pre-miR-21+ALI group but increased in the Anti-miR-21+ALI group. Moreover, the effect of miR-21 on anti-inflammatory, anti-oxidative stress, and anti-apoptosis enhanced after PTEN inhibition. Conclusion: This study revealed that miR-21 has a protective effect in sepsis-induced ALI by regulating PTEN in mice.","PeriodicalId":55162,"journal":{"name":"European Journal of Inflammation","volume":" ","pages":""},"PeriodicalIF":0.7,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49132718","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
It is difficult to diagnose necrotizing fasciitis early. In addition, untimely or incorrect treatment worsens the disease, which may then develop into severe necrotizing fasciitis. A retrospective analysis of the clinical data of 35 patients with severe necrotizing fasciitis admitted to the Burn Department of Gansu Provincial Hospital from 1 January 2015, to 1 January 2020, and the etiology, causes and diagnosis of their aggravated conditions was performed. Thirty cases were directly or indirectly related to trauma, 4 cases were pressure sores caused by long-term paraplegia, and 1 case was from mosquito bites on the left side of the chest. The preliminary diagnosis of 24 patients was unclear, and these cases were misdiagnosed as cellulitis or skin infections; 11 patients were diagnosed at the early stage, but due to the incorrect treatment or failure of timely treatment, their condition was further aggravated and developed into critical necrotizing fasciitis. 1. The diagnosis of necrotizing fasciitis mainly depends on clinical manifestations, and early diagnosis is key; 2. When the patient has local trauma accompanied by local inflammation, fever or hypothermia, necrotizing fasciitis should be highly suspected, and a differential diagnosis should be made between necrotizing fasciitis and cellulitis. The affected tissue should be thoroughly debrided and drained to avoid necrosis spreading to the distal limb along the fascial space. 3. Necrotizing fasciitis should be treated with systemic comprehensive treatment, rational use of antibiotics, correction of water and electrolyte disturbance, early active and thorough debridement and effective wound closure.
{"title":"Clinical analysis of diagnosis and treatment of necrotizing fasciitis","authors":"Xiaoping Yu, Zheng Guo, Miaomiao Zhang, Qianqian Fu, Junli Zhou","doi":"10.1177/1721727X221141822","DOIUrl":"https://doi.org/10.1177/1721727X221141822","url":null,"abstract":"It is difficult to diagnose necrotizing fasciitis early. In addition, untimely or incorrect treatment worsens the disease, which may then develop into severe necrotizing fasciitis. A retrospective analysis of the clinical data of 35 patients with severe necrotizing fasciitis admitted to the Burn Department of Gansu Provincial Hospital from 1 January 2015, to 1 January 2020, and the etiology, causes and diagnosis of their aggravated conditions was performed. Thirty cases were directly or indirectly related to trauma, 4 cases were pressure sores caused by long-term paraplegia, and 1 case was from mosquito bites on the left side of the chest. The preliminary diagnosis of 24 patients was unclear, and these cases were misdiagnosed as cellulitis or skin infections; 11 patients were diagnosed at the early stage, but due to the incorrect treatment or failure of timely treatment, their condition was further aggravated and developed into critical necrotizing fasciitis. 1. The diagnosis of necrotizing fasciitis mainly depends on clinical manifestations, and early diagnosis is key; 2. When the patient has local trauma accompanied by local inflammation, fever or hypothermia, necrotizing fasciitis should be highly suspected, and a differential diagnosis should be made between necrotizing fasciitis and cellulitis. The affected tissue should be thoroughly debrided and drained to avoid necrosis spreading to the distal limb along the fascial space. 3. Necrotizing fasciitis should be treated with systemic comprehensive treatment, rational use of antibiotics, correction of water and electrolyte disturbance, early active and thorough debridement and effective wound closure.","PeriodicalId":55162,"journal":{"name":"European Journal of Inflammation","volume":" ","pages":""},"PeriodicalIF":0.7,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45920438","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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