Background:The evaluation of immune reactivity within both the tumor microenvironment (TME) and the peripheral system has become a cornerstone in assessing the efficacy of cancer therapies. Pathological complete response (pCR) is widely recognized as a key prognostic indicator following neoadjuvant treatment, yet the immune-related biomarkers predictive of pCR remain incompletely characterized. This study aims to identify and validate specific systemic and local immunological factors associated with pCR in patients undergoing antitumor therapy, thereby facilitating more precise and individualized treatment strategies. Methods:A total of 216 patients with lung adenocarcinoma scheduled to undergo radical resection of pulmonary carcinoma were retrospectively enrolled. Among them, 19 attained pCR, whereas the other 197 did not (non-pCR). A detailed evaluation of clinicopathological features via a logistic regression model identified the predictors of pCR. Hematoxylin and eosin (HE) staining, multiplex immunofluorescence (mIF), and immunohistochemistry (IHC) were performed to analyze the local immune response, in particular the tertiary lymphoid structure (TLS) features. Results:Multivariate regression results revealed that low systemic inflammation, which could be derived from a combination of decreased systemic immune-inflammation index (SII) and neutrophil-to-lymphocyte ratio (NLR), was significantly associated with pCR [odds ratio (OR): 3.26; 95% confidence interval (CI): 1.79-6.58; P=0.04]. Increased TLS density and decreased PD1+ and CD8+ cell proportions in the TLS of tumor bed were closely associated with pCR. Conclusions:The local and systemic immune responses are linked to pCR. In addition, a decrease in the SII + NLR level can independently predict pCR, and certain TLS features are also associated with pCR. Immune responses should be carefully studied to optimize the preoperative treatment of patients with advanced lung adenocarcinoma.

Human adenovirus (HAdV) infection is a major cause of respiratory disease, yet no antiviral drugs have been approved for its treatment. Herein, we evaluated the antiviral and anti-inflammatory effects of cyclin-dependent protein kinase (CDK) inhibitor indirubin-3′-monoxime (IM) against HAdV infection in cells and a transgenic mouse model. After evaluating its cytotoxicity, cytopathic effect reduction, antiviral replication kinetics, and viral yield reduction assays were performed to assess the anti-HAdV activity of IM. Quantitative real-time polymerase chain reaction (qPCR), quantitative reverse transcription PCR (qRT-PCR), and western blotting were used to assess the effects of IM on HAdV DNA replication, transcription, and protein expression, respectively. IM significantly inhibited HAdV DNA replication as well as E1A and Hexon transcription, in addition to significantly suppressing the phosphorylation of the RNA polymerase II C-terminal domain (CTD). IM mitigated body weight loss, reduced viral burden, and lung injury, decreasing cytokine and chemokine secretion to a greater extent than cidofovir. Altogether, IM inhibits HAdV replication by downregulating CTD phosphorylation to suppress viral infection and corresponding innate immune reactions as a promising therapeutic agent.

Rationale: Primary spontaneous pneumothorax (PSP) is a manifestation of Vascular Ehlers-Danlos syndrome (vEDS) caused by heterozygous mutations in the COL3A1 gene. vEDS is a rare inherited disorder with an prevalence of one in 150,000. It can causes PSP and severe fragility of connective tissues with arterial but it remains poorly defined on clinical grounds and diagnose. Through this report, we hoped to help clinicians further understand the characteristics of vEDS.Patient concerns: A 22-year-old man presented with recurrent pneumothorax, hemoptysis, and chest pain. Physical examination revealed remarkable hypermobility of the small joints and translucent skin with visible veins. Chest computed tomography (CT) showed pneumothorax and multiple pulmonary cavities.Intervention and outcome: Genomic deoxyribonucleic acid (DNA) was extracted from patients. Heterozygosity was observed in all 3 novel variants. The main variant is COL3A1, c.3256-43T > G(NM_000090.3), which represents a missense mutation in collagen type III alpha 1 that can lead to vEDS. The other 2 mutations were FLNB c.4814G > A(NM_001457.3) and TSC2 c.3145G > A (NM_000548.3). These variants were validated by Sanger sequencing of their parents. COL3A1was not detected in either of the parent strains. FLNB and TSC2 were detected in his mother.Diagnoses: Vascular Ehlers-Danlos syndrome.Lessons: Both COL3A1 and TSC2 gene mutations can cause PSP; however, to the best of our knowledge, there are no reports on these 2 gene mutations in 1 patient at the same time.

Abstract Background: Clinical effectiveness of Azvudine against coronavirus infection and optimal time for initiation of Azvudine treatment to hospitalized COVID-19 patients are not fully understood. Methods: This is a multi-center retrospective cohort study, and five clinical centers of the Chinese People’s Liberation Army General Hospital participated. From omicron pandemics, 6218 hospitalized patients confirmed with COVID-19 from December 10, 2022, to February 20, 2023, were retrieved for this study. After exclusions and propensity score matching , 428 Azvudine recipients and 428 controls were included with a follow-up of 28 days. The primary outcome was all-cause mortality during 28 days of hospitalization, and the secondary outcome was the proportion of patients with clinical improvement up to day 28. Results: The Azvudine group had a lower crude all-cause death rate when compared to the control group (2.82 per 1000 person-days vs. 4.52 per 1000 person-days; HR: 0.63, 95%CI: 0.40-1.00; P=0.038). Notably, the incidence rate of clinical improvement outcome was significantly higher in patients who received Azvudine within 5 days from the onset of symptoms, compared to the control group (Median days: 9 vs. 10; P=0.007). Subgroup analyses showed that chronic lung disease and corticosteroid treatment acted as protective factors (P=0.010; P=0.050). Conclusions: Clinical effectiveness of Azvudine in improving all-cause mortality in COVID-19 patients was seen, and initiation of Azvudine treatment within 5 days of the onset of symptoms was found to be significant. Additionally, the findings revealed the protective effect of Azvudine in COVID-19 patients with chronic lung disease.

背景 急性呼吸窘迫综合征(acute?respiratory?distress?syndrome,ARDS)是一种以高致死率为特点的临床常见危重症,缺乏有效治疗手段,因此深入研究与ARDS发生发展相关的作用机制,从而找到有效的治疗药物尤为迫切.目的 应用脂多糖(lipopolysaccharide,LPS)复制兔ARDS模型,探讨炎症介质在ARDS发生发展过程中的致病机制及姜黄素的保护作用.方法 28只新西兰白兔随机分为对照(control,C)组、模型(model,M)组、模型?+?溶媒(vehicle,V)组和治疗(treatment,T)组,每组7只.用一次性静注LPS(720?μg/kg)方法复制ARDS模型.建模后,M组经腹腔注射0.9％氯化钠注射液(0.8?mL/kg),V组经腹腔注射等量二甲基亚砜,T组经腹腔注射姜黄素溶液(0.8?mL/kg).于实验后6?h,采用ELISA检测支气管肺泡灌洗液(bronchoalveolar?lavage?fluid,BALF)和肺组织IL-17、IL-22含量变化.结果 M组、V组BALF内IL-17含量较C组增高(P<0.05),T组IL-17含量虽高于C组升,但差异无统计学意义(P>0.05).M组、V组BALF内IL-22含量较C组有所下降,而T组IL-22含量较C组升高,但差异均无统计学意义(P>0.05).M组、V组肺组织内IL-17含量较C组显著升高(P<0.05);T组较C组亦有升高,但差异无统计学意义(P>0.05).T组肺组织内IL-22含量较C组升高(P<0.05);M组、V组IL-22含量较C组有所下降,但差异无统计学意义(P>0.05).病理结果显示M组、V组可见明显肺损伤改变,而T组损伤程度明显轻于M组、V组.结论 姜黄素可对LPS诱导的ARDS产生保护作用,这些作用可能是通过减少炎性浸润、减少促炎细胞因子在肺气道中的产生与释放、上调抗炎因子的表达来实现.

Primary tracheobronchial schwannoma is extremely rare. A woman in her early 60 s was admitted to our department with a 2-month history of cough and expectoration. Chest computed tomography (CT) revealed a high-density nodule at the opening of the right main bronchus, accompanied by atelectasis in the middle and lower lobes. Flexible bronchoscopy revealed a tumor at the opening of the bronchus of the right middle lung lobe, which protruded into the main bronchus. A high-frequency electrosurgical snare, endobronchial cryosurgery, and argon plasma coagulation (APC) were used under rigid bronchoscopy. Histopathological examination diagnosed the tumor as schwannoma. The patient’s symptoms resolved after the operation. Follow-up chest CT showed that the right main bronchus was unobstructed, and the bronchus of the lower lobe was open. Bronchoscopic interventional therapy is an alternative treatment for tracheobronchial schwannoma.

Background Human adenovirus (HAdV) infection outbreak causes community-acquired pneumonia. Cellular immune dysfunction and hypercytokinemia play important roles in the pathogenesis of adenovirus respiratory infection. Some soluble factors in peripheral blood can assist in judging the virus-induced disease severity. The expression levels of inflammatory cytokines differ among patients with different disease severity. However, whether and how HAdV-7 infection influences the composition of blood immune cells and serum cytokine levels in patients at different disease stages, as well as the diagnosis values of these parameters, have rarely been intensively studied. We aimed to investigate lymphocytes profiles and cytokines levels in blood of patients at different disease stages upon human adenovirus type 7 (HAdV-7) infections, and explored the diagnosis values of the investigated parameters. Methods Patients from two outbreaks of HAdV-7 in military of China were categorized into upper respiratory infection (URI) group, common pneumonia (CP) group and severe pneumonia (SP) group according to disease severity. Peripheral blood samples were subjected to routine laboratory tests, while flow cytometry and ELISA were used to measure the lymphocyte subsets and cytokines in blood, respectively. The receiver operating characteristic (ROC) curves were performed to examine the diagnostic of these blood parameters. Results Signs of imbalanced lymphocytes composition and hypercytokinemia were observed in HAdV-7-infected patients. The percentages of CD3 + T cells and NK cells were significantly decreased along with the aggravation of the disease, particularly for NK cells and CD4 + T cells. The neutrophil to lymphocyte ratio (NLR) increased significantly in patients with more severe disease. In addition, the levels of serum CXCL10, IL-2 and TNF-α were positively correlated with disease severity, while reduced levels of IFN-γ and IL-10 were found in SP patients. Furthermore, analysis of ROC showed that multiple parameters including the percentage of blood CD3 + cells and serum CXCL10 level could predict the progression of HAdV-7 infection. Conclusion Imbalance of immune state with hypercytokinemia occurred during HAdV-7 infection. The percentages of blood immune cells such as CD3 + T cells and the levels of serum cytokines such as CXCL10 showed potential diagnosis values in HAdV-7 infection.

背景 55型人腺病毒(human adenovirus type 55,HAdV-B55)可引起呼吸道感染,严重者可发展为病毒性肺炎甚至危及生命.理想的HAdV-B55感染模型对发病机制、药物治疗以及多价疫苗的研制有重要价值.目的 建立HAdV-B55人源化受体桥粒芯糖蛋白 2(humanized receptor desmoglein-2,hDSG2)转基因小鼠肺感染动物模型.方法 雄性hDSG2转基因小鼠、野生型C57BL/6(C57)小鼠各 25只,按感染后 3 d、5 d、7 d、14 d和PBS对照随机分为 5组,每组 5只,感染小鼠用HAdV-B55(108 TCID50)滴鼻进行感染,对照组用相同剂量的PBS滴鼻,每日称重并观察小鼠活动情况,分别于感染后 3d、5 d、7 d、14 d取材,对照组滴鼻后 14d取材.测定各组的肺系数、肺组织病理、肺组织内HAdV-B55基因拷贝量、白细胞介素-6(interleukin-6,IL-6)和γ干扰素表达水平以及血清中IL-6浓度水平.结果 hDSG2转基因小鼠感染HAdV-B55病毒后一般状况较C57小鼠恢复慢,体质量增长较慢(P＜0.01),且表现出活动减少、蜷缩抱团等急性感染症状;hDSG2转基因小鼠的肺组织病理表现较C57小鼠重,主要为肺泡壁增厚和炎性细胞浸润,同时肺系数增高显著(P＜0.05),肺组织内HAdV-B55基因拷贝量显著增多(P＜0.05),肺组织内IL-6表达水平(P＜0.05)与血清中IL-6浓度显著升高(P＜0.01).结论 采用经鼻滴入HAdV-B55方法,可以建立hDSG2转基因小鼠肺感染的动物模型,该模型稳定性和持续致病性较好,具有进一步深入研究的价值.

Objective:To analyze the epidemiology, predisposing factors, and prognosis of mucormycosis, which were reported from 1980 to 2020 in China.Methods:This was a cross-sectional study.A total of 310 cases of mucormycosis reported from 1980 to 2020 were collected by using the following six databases: the Chinese National Knowledge Infrastructure, Wanfang Data, VIP Information for Biomedical Engineering and Clinical Medicine, China Hospital Knowledge Database, China Biology Medicine Disc, and Chinese Medical Association Full-text Database.The data collected include age, gender, onset time, underlying diseases, infection site, diagnostic method, treatment method and prognosis of the patients, and statistical analysis of the epidemiology was performed.Results:A total of 310 cases of mucormycosis were reported over the 40-year period with a mortality rate of 42.9%.The reported incidence showed an increasing trend annually.Among the cases, 59.7% had a long-term history of broad-spectrum antibiotic application, and this proportion increased annually.Diabetes was a common underlying disease, accounting for 33.5% of the cases, and was an independent risk factor for the death of patients with mucormycosis ( OR=2.22, 95% CI: 1.02-4.83). Pulmonary infection was common and found in 41.0% of all patients (127/310), with a mortality rate of 50.4% (64/127). Sinus infections accounted for 21% of cases, with a mortality rate of 41.5%.Amphotericin B and its liposomes reduced the risk of death in the patients ( OR=0.33, 95% CI: 0.17-0.64). Surgery also reduced the mortality rate ( OR=0.14, 95% CI: 0.06-0.32). Conclusions:In the recent years, the incidence of mucormycosis has significantly increased.The extensive application of broad-spectrum antibiotics, diabetes and the use of hormones were risk factors for mucormycosis.The mortality rate was affected by a variety of factors, including the underlying diseases, infection site and treatment.Surgery and amphotericin B with its liposomes were effective treatments that can improve the prognosis and reduce mortality in patients with mucormycosis.

目的 回顾性分析呼吸道人腺病毒7型(human adenovirus-7,HAdV-7)感染造成凝血筛查指标的变化及其对鉴别患者临床分型的诊断价值.方法 选取2015年1月20日-2月21日我院参与救治的82例呼吸道HAdV-7感染者作为研究对象,根据病情严重程度分为上呼吸道感染(upper respiratory infection,URI)组(42例),普通肺炎(common pneumonia,CP)组(30例)和重症肺炎(severe pneumonia,SP)组(10例),对比分析不同组别患者的一般资料、血常规、凝血筛查指标等.结果 82例患者均为青年男性,平均年龄为(18.8±1.5)岁.3组间凝血酶时间(thrombintime,TT)比较差异有统计学意义,两两比较,SP组较URI组和CP组均有明显延长(P均＜0.05)03组间D-二聚体(D-dimmer,DD)和纤维蛋白原降解产物(fibrinogen degradation product,FDP)比较差异均有统计学意义,两两比较,SP组DD和FDP较URI组和CP组均有显著升高(P均＜0.05).TT在鉴别诊断URI和SP时,AUC为0.855(95％CI:0.741～0.968,P＜0.05),在临界值为12.75 s时,其灵敏度为82.8％,特异度为60.4％;TT在鉴别诊断CP和SP时,AUC为0.853(95％CI:0.729～0.976,P＜0.05),在临界值为12.95 s时,其灵敏度为73.3％,特异度为70.0％.DD在鉴别诊断URI和SP时,AUC为0.924(95％CI:0.849～1.000,P＜0.05),在临界值为149.00 pg/L 时,其灵敏度为 88.9％,特异度为 86.5％;DD 在鉴别 CP 和 SP 时,AUC 为 0.913(95％CI:0.822～1.000,P＜0.05),在临界值为155.50ug/L时,其灵敏度为89.5％,特异度为82.4％.FDP在鉴别诊断URI和SP时,AUC为0.861(95％CI:0.755～0.993,P＜0.05),在临界值为2.25mg/L时,其灵敏度为77.8％,特异度为91.9％;FDP在鉴别诊断CP和SP时,AUC为0.875(95％CI:0.757～0.993,P＜0.05),在临界值为1.55 mg/L时,其灵敏度为84.2％,特异度为76.5％.结论 呼吸道HAdV-7感染可导致患者凝血和纤溶功能出现紊乱.评估、监测凝血筛查指标特别是DD、FDP和TT,对早期识别呼吸道HAdV-7感染高危病例和预测疾病进展,及时干预有重要意义.

Abstract Background Human adenovirus (HAdV) infection outbreak causes community-acquired pneumonia. Cellular immune dysfunction and hypercytokinemia play important roles in the pathogenesis of adenovirus respiratory infection. Some soluble factors in peripheral blood can predict the virus-induced disease progression accurately. The expression levels of inflammatory cytokines differ among patients with different disease severity. However, whether and how HAdV-7 infection influences the composition of blood immune cells and serum cytokine levels in patients at different disease stages, as well as the diagnosis and prognosis values of these parameters, have rarely been intensively studied. We aimed to investigate lymphocytes profiles and cytokines levels in blood of patients at different disease stages upon human adenovirus type 7 (HAdV-7) infections, and explored the diagnosis and prognosis values of the investigated parameters. Methods Patients from two outbreaks of HAdV-7 in military of China were categorized into upper respiratory infection (URI) group, common pneumonia (CP) group and severe pneumonia (SP) group according to disease severity. Peripheral blood samples were subjected to routine laboratory tests, while flow cytometry and ELISA were used to measure the lymphocyte subsets and cytokines in blood, respectively. The receiver operating characteristic (ROC) curves were performed to examine the diagnostic and prognostic abilities of these blood parameters. Results Signs of imbalanced lymphocytes composition and hypercytokinemia were observed in HAdV-7-infected patients. The percentages of CD3+ T cells and NK cells were significantly decreased along with the aggravation of the disease, particularly for NK cells and CD4+ T cells. The neutrophil to lymphocyte ratio (NLR) increased significantly in patients with more severe disease. In addition, the levels of serum CXCL10, IL-2 and TNF-α were positively correlated with disease severity, while reduced levels of IFN-γ and IL-10 were found in SP patients. Furthermore, analysis of ROC showed that multiple parameters including the percentage of blood CD3+ cells and serum CXCL10 level could predict the progression of HAdV-7 infection. Conclusions Imbalance of immune state with hypercytokinemia occurred during HAdV-7 infection. The percentages of blood immune cells such as CD3+ T cells and the levels of serum cytokines such as CXCL10 showed potential diagnosis and prognosis values in HAdV-7 infection.

目的 研究白藜芦醇(resveratrol,Res)对内毒素的主要成分脂多糖(lipopolysacchride,LPS)诱导急性肺损伤(acute lung injury,ALI)兔内质网应激和细胞凋亡的影响.方法 24只雄性新西兰白兔随机分为对照组、急性肺损伤模型组(ALI组)、白藜芦醇干预组(Res组),每组8只;Res组在造模前7 d每早给予白藜芦醇(250 mg/kg)灌胃,ALI组和Res组均经耳缘静脉给予LPS(750μg/kg)构建急性肺损伤模型,对照组给予等量0.9％氯化钠注射液.苏木素-伊红(HE)染色病理检查观察肺组织损伤程度,判定建模是否成功;末端脱氧核苷酸转移酶介导的dUTP缺口末端标记测定法(TUNEL)染色观察细胞凋亡情况;蛋白免疫印迹法(Western blot)检测兔肺组织PERK、ATF4、CHOP、Caspase 9、Bax、Bcl-2蛋白表达,RT-PCR法检测PERK、ATF4、CHOP、Caspase 9、Bax、Bcl-2 mRNA的表达.结果 白藜芦醇可以减轻LPS诱导的ALI兔肺组织病理损伤;降低肺组织湿/干重比(P<0.05);减少肺泡间隔细胞凋亡指数(P<0.05);降低ALI兔肺组织PERK、ATF4、CHOP、Caspase9、Bax的蛋白水平和mRNA表达(P<0.05),增加Bcl-2的蛋白和mRNA表达水平(P<0.05).结论 白藜芦醇可能通过减轻内质网应激和细胞凋亡,发挥对LPS诱导兔ALI的保护作用.

目的:观察肺磨玻璃结节(GGN)的胸部CT征象,分析其在结节良恶性诊断中的价值.方法:回顾性分析2019年1月至2019年9月解放军总医院收治的65例具有GGN的CT影像征象的患者,根据病理结果分为良性组(26例)、恶性组(39例),收集整理相关临床及影像资料,分析良、恶性GGN不同CT影像特点及诊断价值.结果:良、恶性肺GGN在病变直径、形状、边界、分叶征、毛刺征、空泡征、支气管充气征、血管集束征、胸膜凹陷征和密度具有差异,差异有统计学意义(P＜0.05).其中胸膜凹陷征的诊断灵敏度和特异度最高,分别为76.92％和73.08％;而粗糙边界的诊断灵敏度和特异度最低,分别为25.64％和26.92％.分叶征、胸膜凹陷征的AUC值分别为0.718、0.75,对恶性GGN有较高的预测价值.结论:肺GGN的胸部CT征象(病变直径、形状、边界、分叶征、毛刺征、空泡征、支气管充气征、血管集束征、胸膜凹陷征、密度)有助于鉴别诊断良、恶性肺GGN.

Objectives: To analyze the effect of berberine on acute respiratory distress syndrome (ARDS) and clarify the underlying mechanism. Background: ARDS is a common respiratory disease. There is no standard therapeutic drug for the disease. Berberine may attenuate lung injury via inhibiting inflammation. Methods: The ARDS model was established with lipopolysaccharide administration. The lung injury was evaluated by analyzing the pulmonary pathology, edema and blood oxygenation with hematoxylin and eosin staining, wet to dry ratios and arterial blood gas analysis. The levels of inflammatory factors were determined by ELISA. To clarify the underlying mechanism, western blot was used to analyze the expression of NF-kappa B and sirtuin-1. Results: Berberine significantly repressed disease progression in lipopolysaccharide-induced ARDS rats, which was indicated by reduced pulmonary neutrophil infiltration, decreased wet to dry ratios and improved blood oxygenation. The effect was comparable to meprednisone treatment. The expression of TNF-alpha, IL-6, IL-10, ICAM-1, IL-1 beta and IL-8 was also inhibited by berberine treatment. Further studies showed that the sirtuin-1 mediated NF-kappa B pathway might be responsible, as the addition of sirtuin-1 inhibitor blocked the effect of berberine, while the agonist simulated berberine treatment. Conclusion: Berberine protects against lipopolysaccharide-induced acute respiratory distress syndrome via the sirtuin-1 pathway.

吡嗪酰胺(pyrazinamide,PZA)是一种通过渗入含结核分枝杆菌的巨噬细胞内转变为吡嗪酸而起到杀菌作用的抗结核药物,是目前全程督导短程化学治疗(directly observed treatment short-course)中推荐与异烟肼、利福平联合应用的不可缺少的重要药物[1].其常见不良反应主要是高尿酸血症、关节痛、肝损害、食欲缺乏和恶心,而过敏性皮炎在国内目前报道相对少见.及早发现并意识到由吡嗪酰胺引起的过敏性皮炎,停用并更换其他一线抗结核药物,是保证这部分患者达到早期、规律、全程、联合、适量抗结核治疗原则的关键.本文报道解放军总医院第一医学中心收治的吡嗪酰胺引起过敏性皮炎1例,为临床治疗过程中药物不良反应的诊断和治疗提供新参考.

2019年12月武汉报道多起新型冠状病毒肺炎.引起该疾病的病毒是单股正链RNA病毒,具有较强传染性,可感染多种动物和人.其临床特征与严重急性呼吸综合征(SARS)、A/H5N1禽流感、腺病毒肺炎及甲型H1N1流感等病毒性肺炎类似,不易鉴别.本文综述了上述病毒性肺炎的流行病学、临床表现、实验室及影像学检查方面的共性与特异性,对临床病例诊断及鉴别有一定指导作用.

目的:本实验以脂多糖(LPS)静脉注射的方法复制兔急性呼吸窘迫综合征(ARDS)模型,通过观察模型动物的病理生理变化,探讨ARDS的发病机理及防治方法.方法.21只新西兰白兔被随机分成3组,分别为对照组(A组)、致伤组(B组)和干预组(C组).B组一次性静注脂多糖(剂量为720 μ.g/kg)建立实验动物模型;C组除同等剂量脂多糖外,同时给予复方苦参注射液(剂量为4 ml/kg)进行干预;A组静注同等容量0.9％ NaCl注射液.不同时间点观察PaO2、PaO2/FiO2变化,测定肺组织湿/干重比、肺组织髓样细胞触发性受体-1(TREM-1)及细胞间黏附因子-1(ICAM-1)的表达,光镜下观察各组肺组织病理变化.结果:A组各项指标基本正常;B组致伤后PaO2、PaO2/FiO2下降,湿/干重比增加,TREM-1及ICAM-1表达明显增加,光镜下可见肺泡间隔显著增厚、炎细胞浸润;C组损伤明显轻于B组.结论:一次性静注LPS(720 μg/kg)可复制兔ARDS动物模型,TREM-1和ICAM-1在模型动物损伤组中表达明显增加,复方苦参具有一定保护作用.

BACKGROUND The aim of this study was to characterize adenovirus-associated acute respiratory infection (ARI) and observe correlations between inflammatory markers and severity of human adenovirus type 7 (HAdV-7) infection, and to evaluate the potential of inflammatory markers to predict progression from upper-respiratory infection (URI) to adenovirus pneumonia (AdP). MATERIAL AND METHODS A total of 81 patients with adenovirus-associated ARI and confirmed HAdV-7 infection were enrolled. Cases were classified according to severity, as AdP and URI. Demographic and clinical data were collected retrospectively. Clinical features and serum inflammatory markers were evaluated and compared according to the severity of adenoviral infection. RESULTS We observed high-grade fever and strong inflammatory response in patients with HAdV-7-associated ARI. Procalcitonin (PCT), interleukin 6 (IL-6), and C-reactive protein concentrations were higher in patients with AdP than in those with URI. The mean erythrocyte sedimentation rate (ESR) was significantly higher in patients with AdP (p=0.008). Reduced serum prealbumin levels were observed in patients with HAdV-7 infection. In the analysis of URI to AdP prediction ability, areas under the curve (AUCs) for all inflammatory markers were <0.9. We found that 35.9% of pneumonia had ≥2 lobars of lung infiltrate and bilateral lung infiltrate, and 20% of patients with SP had pleural effusion and atelectasis. CONCLUSIONS IL-6 and ESR were associated with the severity of HAdV-7 respiratory infection. No inflammatory marker in our study predicted URI-to-AdP progression accurately. Lung infiltration and consolidation are common in HRCT in AdP. Multiple- or single-lobar/segment consolidation was most common in SP. SP progressed very quickly after onset.

Objective To investigate the mechanism of acute respiratory distress syndrome (ARDS) by measuring the changes of interleukin-23 (IL-23),IL-27,plasminogen activator inhibitor-1 (PAI-1) and tissue plasminogen activator (t-PA) in ARDS rabbit models.Methods 24 male Japanese flap eared white rabbits were randomly divided into three groups:control group (group A),endotoxin induced ARDS group (group B) and Xuebijing treatment group (group C).ARDS rabbit models were replicated by intravenous injection of endotoxin (750 μg/kg) in group B and group C,and Xuebijing (1.8 ml /kg)was administered intravenously in group C.IL-23,IL-27,PAI-1 and t-PA were measured.Results Compared with group A,the expression of IL 23 was increased and IL-27 was decreased in group B (P ＜0.05 or P ＜0.01).The level of IL-23 in group C was also increased than that in group A,but it was lower than that in group B (P ＜0.05 orP ＜0.01).The level of IL-27 in group C was lower than that in group A and group B (P ＜0.05 or P ＜0.01).The level of t-PA in group B was significantly higher than that in group A (P ＜0.01).There was no significant difference in the level of t-PA between group A and group C.The level of PAI-1 in group B was higher than that in group A (P ＜0.01) and group C (P ＜0.05 or P ＜0.01).The level of PAI-1 in group C was higher than that in group A (P ＜0.01).Conclusions ARDS has imbalance of inflammatory reaction,imbalance between proinflammatory and antiinflammatory reactions.Coagulation-fibrinolysis is abnormal,procoagulation and anticoagulation is imbalanced after injury induced by endotoxin.Xuebijing can antagonize the release of inflammatory mediators caused by endotoxin and improve the abnormal coagulation mechanism.