Purpose:Immunocompromised patients are at increased risk for severe outcomes from COVID-19 due to their altered immune responses, yet their inflammatory profiles and the interplay between immunosuppression remain poorly understood. We aimed to illustrate the inflammation profile and clinical outcomes of hospitalized immunocompromised patients with COVID-19. Methods:We conducted a retrospective study using a multicenter database and included adult hospitalized patients with Corona virus disease 2019 (COVID-19) in China's late 2022 COVID-19 wave. Crude and adjusted 28- and 60-day mortality was compared between the two groups. Inflammatory phenotypes were evaluated by serum interleukin-6 (IL-6) and C-reactive protein (CRP) level. The interplay between overt inflammation and immunosuppression was analyzed. Results:Among the 4078 included patients, 348 (8.5%) were immunocompromised. Immunocompromised patients had lower crude mortality but higher adjusted mortality at 28-day (hazard ratio [HR] = 1.55; 95% CI 1.08 to 2.23) and 60-day (HR = 1.47; 95% CI 1.05 to 2.06). Besides, immunocompromised patients had a higher risk of developing hyperinflammation (odd ratio [OR] =1.92; 95% CI 1.47 to 2.50, p <0.001). Moreover, hyperinflammation mediated a major part of the deleterious survival effect of immunosuppression on COVID-19. Conclusion:Immunodeficiency not only increases short-term mortality risk but also predisposes patients to hyperinflammation. The complex interplay between immunosuppression, hyperinflammation, and COVID-19 outcomes warrants more detailed profiling of inflammation and immunity in this population.

Seawater-drowning-induced acute lung injury (SD-ALI) is a life-threatening disorder characterized by increased alveolar–capillary permeability, an excessive inflammatory response, and refractory hypoxemia. Perfluorocarbons (PFCs) are biocompatible compounds that are chemically and biologically inert and lack toxicity as oxygen carriers, which could reduce lung injury in vitro and in vivo. The aim of our study was to explore whether the vaporization of PFCs could reduce the severity of SD-ALI in canines and investigate the underlying mechanisms. Eighteen beagle dogs were randomly divided into three groups: the seawater drowning (SW), perfluorocarbon (PFC), and control groups. The dogs in the SW group were intratracheally administered seawater to establish the animal model. The dogs in the PFC group were treated with vaporized PFCs. Probe-based confocal laser endomicroscopy (pCLE) was performed at 3 h. The blood gas, volume air index (VAI), pathological changes, and wet-to-dry (W/D) lung tissue ratios were assessed. The expression of heme oxygenase-1 (HO-1), nuclear respiratory factor-1 (NRF1), and NOD-like receptor family pyrin domain containing-3 (NLRP3) inflammasomes was determined by means of quantitative real-time polymerase chain reaction (qRT-PCR) and immunological histological chemistry. The SW group showed higher lung injury scores and W/D ratios, and lower VAI compared to the control group, and treatment with PFCs could reverse the change of lung injury score, W/D ratio and VAI. PFCs deactivated NLRP3 inflammasomes and reduced the release of caspase-1, interleukin-1β (IL-1β), and interleukin-18 (IL-18) by enhancing the expression of HO-1 and NRF1. Our results suggest that the vaporization of PFCs could attenuate SD-ALI by deactivating NLRP3 inflammasomes via the HO-1/NRF1 pathway.

Abstract The long non-coding RNA (lncRNA) Small Nucleolar RNA Host Gene 4 (SNHG4) has been demonstrated to be significantly downregulated in various inflammatory conditions, yet its role in chronic obstructive pulmonary disease (COPD) remains elusive. This study aims to elucidate the biological function of SNHG4 in COPD and to unveil its potential molecular targets. Our findings reveal that both SNHG4 and Four and a Half LIM Domains 1 (FHL1) were markedly downregulated in COPD, whereas microRNA-409-3p (miR-409-3p) was upregulated. Importantly, SNHG4 exhibited a negative correlation with inflammatory markers in patients with COPD, but a positive correlation with forced expiratory volume in 1s percentage (FEV1%). SNHG4 distinguished COPD patients from non-smokers with high sensitivity, specificity, and accuracy. Overexpression of SNHG4 ameliorated cigarette smoke extract (CSE)-mediated inflammation, apoptosis, oxidative stress, and airway remodeling in 16HBE bronchial epithelial cells. These beneficial effects of SNHG4 overexpression were reversed by the overexpression of miR-409-3p or the silencing of FHL1. Mechanistically, SNHG4 competitively bound to miR-409-3p, mediating the expression of FHL1, and consequently improving inflammation, apoptosis, oxidative stress, and airway remodeling in 16HBE cells. Additionally, SNHG4 regulated the miR-409-3p/FHL1 axis to inhibit the activation of the mitogen-activated protein kinase (MAPK) pathway induced by CSE. In a murine model of COPD, knockdown of SNHG4 exacerbated CSE-induced pulmonary inflammation, apoptosis, and oxidative stress. In summary, our data affirm that SNHG4 mitigates pulmonary inflammation, apoptosis, and oxidative damage mediated by COPD through the regulation of the miR-409-3p/FHL1 axis. Graphical Abstract

BACKGROUND:Acute lung injury (ALI) involves severe lung damage and respiratory failure, which are accompanied by alveolar macrophage (AM) activation. The aim of this article is to verify the influence of paralemmin-3 (PALM3) on alveolar macrophage (AM) polarization in ALI and the underlying mechanism of action. METHODS:An ALI rat model was established by successive lipopolysaccharide (LPS) inhalations. The influence of PALM3 on the survival rate, severity of lung injury, and macrophage polarization was analyzed. Furthermore, we explored the underlying mechanism of PALM3 in regulating macrophage polarization. RESULTS:PALM3 overexpression increased mortality of ALI rats, augmented lung pathological damage, and promoted AM polarization toward M1 cells. Conversely, PALM3 knockdown had the opposite effects. Mechanistically, PALM3 might promote M1 polarization by acting as an adaptor to facilitate transduction of Notch signaling. CONCLUSION:PALM3 aggravates lung injury and induces macrophage polarization toward M1 cells by activating the Notch signaling pathway in LPS-induced ALI, which may shed light on ALI/ARDS treatments.

BackgroundThe effectiveness of nirmatrelvir-ritonavir has mainly been shown in non-hospitalized patients with mild-to-moderate coronavirus disease 2019 (COVID-19). The real-world effectiveness of nirmatrelvir-ritonavir urgently needs to be determined using representative in-hospital patients with COVID-19 during the Omicron wave of the pandemic.MethodsWe performed a multicentre, retrospective study in five Chinese PLA General Hospital medical centers in Beijing, China. Patients hospitalized with COVID-19 from 10 December 2022 to 20 February 2023 were eligible for inclusion. A 1:1 propensity score matching was performed between the nirmatrelvir-ritonavir group and the control group.Results1010 recipients of nirmatrelvir-ritonavir and 1010 matched controls were finally analyzed after matching. Compared with matched controls, the nirmatrelvir-ritonavir group had a lower incidence rate of all-cause death (4.6/1000 vs. 6.3/1000 person-days, p = 0.013) and a higher incidence rate of clinical improvement (47.6/1000 vs. 45.8/1000 person-days, p = 0.012). Nirmatrelvir-ritonavir was associated with a 22% lower all-cause mortality and a 14% higher incidence of clinical improvement. Initiation of nirmatrelvir-ritonavir within 5 days after symptom onset was associated with a 50% lower mortality and a 26% higher clinical improvement rate. By contrast, no significant associations were identified among patients receiving nirmatrelvir-ritonavir treatment more than 5 days after symptom onset. Nirmatrelvir-ritonavir was also associated with a 50% increase in survival days and a 12% decrease in days to clinical improvement.ConclusionAmong hospitalized patients with COVID-19 during the Omicron wave in Beijing, China, the early initiation of nirmatrelvir-ritonavir was associated with clinical benefits of lowering mortality and improving clinical recovery.

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.

一名76 岁男性患者,2012 年诊断晚期左上肺低分化腺癌,外院予以全身化疗及局部放疗.2020年6月病灶进展,病理示低分化腺鳞癌,PD-L1(TPS 70％),EGFR基因突变(Exon-18 G719X).予以马来酸阿法替尼片治疗12 周后出现药物致间质性肺炎,经停药、氧疗及激素等治疗后恢复.之后查血T790 M突变,予以口服甲磺酸奥西替尼片,同时口服强的松片(逐渐减量)治疗.治疗12周后再次出现药物性间质性肺炎,患者最终因呼吸衰竭加重死亡.晚期非小细胞肺癌患者中存在驱动基因突变,同时PD-L1高表达情况,临床上尚无明确的统一方案,如何选择更适合的治疗方案,需要我们不断的积累和总结.

Background: Real-time assessment of high-altitude pulmonary edema (HAPE) remains a challenge. Probe-based confocal laser microscopy (pCLE) allows a real-time in vivo visualization of the alveoli. This study aimed to develop a new non-invasive method for analyzing microscopic images in a canine model of HAPE using pCLE. Materials and methods: This was a prospective, controlled animal study in adult male beagle dogs randomized to control and HAPE groups. The HAPE group was exposed to a high altitude of 6000 m for 48 h. The blood gas levels, lung morphological changes, infectious factors, and lung wet-to-dry ratio were analyzed in different groups. The pCLE images were described based on the volume air index (VAI), which applies an integral over specific signal intensities. Results: The lung wet-to-dry weight ratio and injury scores in the HAPE group were significantly increased compared with those of the control group. The levels of infectious factors interleukin-1 beta, tumor necrosis factor-alpha, and interleukin-6 were significantly increased in the HAPE group compared with those in the control group. VAI was significantly decreased in the HAPE group. Conclusion: pCLE is a potential adjudicative bronchoscopic imaging technique for assessing HAPE. VAI may be acquired from quantitative parameters in the analysis of images.

Objective To investigate the effect of probiotics on BODE index and expression of inflammatory cytokines in patients with stable chronic obstructive pulmonary disease(COPD).Methods A total of 112 patients with stable COPD treated in the Sixth Medical Center of the PLA General Hospital were enrolled in the study from June 2019 to June 2021.The subjects were randomly divided into control group and experimental group by random number table method,each group contained 56 samples.The control group was treated with conventional therapy,and the experimental group was treated with probiotics on the basis of the control group.The efficacy,BODE index,pulmonary function(FEV1,PEF,and FVC),immune function(CD3+,CD4+,CD8+,and CD4+/CD8+),inflammatory factors(CRP,IL-6,and Svcam-1),and adverse reactions were compared between the two groups.Results The total effective rate of experimental group was 96.43％,which was higher than that of control group(82.14％,P＜0.05),the BODE Index of experimental group was lower than that of control group after treatment(P＜0.05),the FEV1,PEF,FVC of experimental group were higher than that of control group after treatment(P＜0.05).After treatment,the levels of CRP,IL-6 and Svcam-1 in the experimental group were significantly lower than those in the control group(P＜0.05),there was no significant difference in the incidence of adverse drug reactions between the two groups(P＞0.05).Conclusion Probiotics as an adjunctive therapy for COPD patients in stable stage has a good clinical effect,which can relieve the symptoms,improve the immune function and lung function,and reduce the inflammation of the body,high security.

The effect of Epsin 3 (EPN3) on non‐small cell lung cancer (NSCLC) has not yet been clearly elucidated. This study identified the exact function of EPN3 on NSCLC progression. EPN3 expression in NSCLC patients were analyzed based on the Cancer Genome Atlas database. Kaplan–Meier analysis was implemented to research the effect of EPN3 on patients' survival. EPN3 expression in clinical tissues of 62 NSCLC cases was monitored by real‐time quantitative reverse transcription polymerase chain reaction, immunohistochemistry and Western blot. A549 and H1299 cells were transfected with EPN3 shRNA and treated by RO8191 (20 μM). Proliferation was researched by cell counting kit‐8 and 5‐ethnyl‐2 deoxyuridine assays. Apoptosis was monitored by flow cytometry. Migration and invasion was assessed by Transwell experiment. EPN3 effect on A549 cell in vivo growth was researched using nude mice. RO8191 (200 μg) was intratumoral injected into mice. Immunohistochemistry and Western blot was implemented to monitor protein expression in cells and xenograft tumor tissues. EPN3 was abnormally up‐regulated in NSCLC patients and cells, indicating a lower overall survival. Loss of EPN3 weakened proliferation, migration and invasion, induced apoptosis, and repressed epithelial‐mesenchymal transition in NSCLC cells. Loss of EPN3 inactivated the JAK1/2‐STAT3 pathway in NSCLC cells. RO8191 treatment reversed the inhibition of EPN3 knockdown on the malignant phenotype of NSCLC cells. RO8191 intratumoral injection reversed the suppression of EPN3 silencing on NSCLC cell in vivo growth. EPN3 acted as an oncogene in NSCLC via activating the JAK1/2‐STAT3 pathway. EPN3 may be a promising target for NSCLC treatment.

Purpose: To investigate the protective effect of vitexin on smoke inhalation-induced acute lung injury (SI-ALI), and the underlying mechanism of action.Methods: The ALI rat model was established by inhalation of smoke in a closed smoke chamber. Survival rate, arterial blood gas analysis, wet-to-dry weight ratio of lung tissues, bronchoalveolar lavage fluid protein concentration, lung tissue histology, and oxidative stress and inflammation level were evaluated. Expressions of protein kinase C β (PKC β), p66Shc, and phosphorylated p66Shc were determined by western blot or quantitative reverse transcription-polymerase chain reaction.Results: Compared with smoke inhalation group, vitexin alleviated the decline in arterial partial pressure of oxygen (p < 0.05), reduced lung tissue exudation and pathological lung tissue damage, inhibited the expression of PKC β/p66Shc signaling pathway proteins, downregulated the level of oxidative stress and inflammation, and ultimately improved the survival rate in SI-ALI rats (p < 0.05).Conclusion: Vitexin attenuates SI-ALI in rats by alleviating oxidative stress via inhibition of PKC β/p66Shc signaling pathway. Thus, this compound is a potential agent for the treatment of SI-ALI.

IgG4相关性疾病是一种免疫介导的慢性炎症伴纤维化疾病，多种疾病或感染可出现类似的临床表现和血清IgG4浓度升高，导致误诊或漏诊。本文报道1例以肺内病变伴胸腔积液起病，之后发现合并纹带棒状杆菌肺部感染的IgG4 相关性疾病病例。

背景 血嗜酸性粒细胞(eosinophils,EOS)计数已成为慢性阻塞性肺疾病(chronic?obstructive?pulmonary?disease,COPD)患者应用吸入糖皮质激素(inhaled?corticosteroids,ICS)治疗的指征,但呼出气一氧化氮(fractional?exhaled?nitric?oxide,FeNO)在稳定期COPD患者诊断治疗中的应用价值仍不清楚.目的 观察不同特征的稳定期COPD患者外周血EOS与FeNO的相关性,探讨FeNO在稳定期COPD患者中的应用价值及局限性.方法 回顾性纳入2017年3月-?2020年3月在我中心接受FeNO和外周血嗜酸性粒细胞计数检测的稳定期COPD患者和哮喘患者,分别对两组患者FeNO与血EOS计数的相关性进行统计分析.对FeNO值升高的危险因素进行二元logistic回归分析.根据气道阻塞程度(FEV1pred％)、过度充气程度(RVpred％:150％及RVpred％:200％)进一步将COPD患者分为FEV1pred％>50％组及FEV1pred％≤50％组、RVpred％>150组及RVpred％≤150组、RVpred％>200组及RVpred％≤200组分别进行FeNO和血嗜酸性粒细胞相关性分析.分别对哮喘组及COPD组血嗜酸性粒细胞预测FeNO值升高的鉴别效能进行ROC分析.结果 共纳入COPD患者113例,其中男性90例,女性23例,平均年龄(69.04±9.59)岁;支气管哮喘患者43例,其中男性31例,女性12例,平均年龄(68.37±9.45)岁.哮喘组FeNO与血EOS计数呈中度相关(r=0.439,P<0.001);而COPD组FeNO水平与血EOS无相关性(r=0.104,P=0.272).二元logistic回归分析发现吸烟史为COPD组FeNO升高的危险因素,RVpred％为FeNO升高的保护性因素.对COPD患者进行亚组分析,发现FEV1pred％≤50％组外周血EOS与FeNO呈正相关(r=0.370,P=0.020).其余亚组血EOS与FeNO均无相关性(P>0.05).ROC分析发现COPD组中血嗜酸性粒细胞对FeNO值几乎无鉴别效能;FEV1pred％<50％?COPD组血嗜酸性粒细胞对FeNO值有一定的鉴别效能,AUC为0.688(95％?CI:0.444?～?0.931),敏感度为0.56,特异性为0.90.哮喘组血嗜酸性粒细胞对FeNO值有较好的鉴别效能,AUC为0.869(95％?CI:0.721?～?1.018),敏感度为0.83,特异性为0.90.结论 稳定期COPD患者FeNO与血EOS的相关性与哮喘患者不同,其FeNO水平与血EOS无相关性,但FEV1pred％≤50％的患者FeNO与血EOS存在一定的正相关.稳定期COPD患者FeNO不能代替血EOS用于评估ICS使用,FEV1pred％<50％?COPD组FeNO值在一定程度上可代替血EOS用于评估是否使用ICS治疗,而哮喘患者FeNO值可代替血EOS用于评估气道嗜酸性炎症.

Objective:To explore the effect of early lung rehabilitation training on mechanical ventilation in patients with AECOPD.Methods:72 patients with acute exacerbations of chronic obstructive pulmonary disease(AECOPD) hospitalized in the department of respiratory and critical care medicine of our hospital from May 2020 to October 2021 were randomly divided into observation group 37 cases and control group 35 cases. The control group was treated with anti infection, expectorant, antispasmodic and ventilator support. On this basis, the observation group was given limb training, inspiratory muscle resistance and active respiratory and circulatory training from mechanical ventilation. PaO2, PaCO2, pH and lactic acid were measured. The incidence of lower extremity venous thrombosis, mechanical ventilation time, average length of stay in ICU and the incidence of ventilator-associated pneumonia were observed.Results:The incidence of lower extremity venous thrombosis(5.76% vs. 20.00%), mechanical ventilation time(11.40±1.32 vs. 14.46±1.86)d, average length of stay in ICU (16.15±1.93 vs. 18.55±2.34)d and the incidence of ventilator-associated pneumonia (9.61% vs. 26.00%)in the observation group were better than those in the control group (P<0.05). On the 5 th day(44.07±11.00 vs. 52.89±5.52)mmHg and 10 th day(41.87±3.96 vs. 45.22±3.30)mmHg, the node PaCO2 of the observation group was lower than that of the control group, while the pH value, SaO2 and PaO2 were higher than those of the control group (P<0.05).Conclusion:Early pulmonary rehabilitation training for patients with AECOPD mechanical ventilation can significantly improve the blood gas indexes of patients with COPD. Reduce the occurrence of complications and promote the early recovery of patients.

Abstract Background Single-Stranded DNA Binding Protein 1(SSBP1) has been found closely related to the malignant biological process of the tumor. However, the functions of SSBP1 in lung adenocarcinoma (LUAD) are still unclear. The present study explored the prognosis of SSBP1 in LUAD. Methods Oncomine, TIMER, and UALCAN were used to analyze the difference of SSBP1 expression in normal and tumor tissues, and HPA was used to analyze the immunohistochemical staining in tumor tissues. We also used Kaplan-Meier analysis to evaluate the impact of SSBP1 on LUAD patients’ survival. In addition, we used the TIMER database to explore the correlation between the expression of SSBP1 and tumor-infiltrating immune cells (TILs). Furthermore, we used STRING and GeneMANIA to build a network of protein-protein interaction (PPI) and perform GO analysis. Finally, we used CARE to evaluate the relationship between the expression of SSBP1 and the response of the drug. Results The expression of SSBP1 was up-regulated in the patients with LUAD and was related to the worse overall survival (OS) probability. And, SSBP1 was negatively associated with ImmuneScore, ESTIMATEScore, and StromalScore. In addition, SSBP1 expression has a negative correlation with the infiltration level of B cells, dendritic cells, CD4 + T cells, and macrophages. And, the expression of SSBP1 in B cells, CD8 + T cells, and dendritic cells (DC) was related to OS. Furthermore, a positive correlation was found between the expression SSBP1 and CARE. Conclusion SSBP1 is a potentially poor prognostic biomarker of LUAD and correlated with immune infiltrates in LUAD.

背景 慢性阻塞性肺疾病(chronic?obstructive?pulmonary?disease,COPD)患者在达到流速指标第1秒用力呼气容积(forced?expiratory?volume?in?one?second,FEV1)/用力肺活量(forced?vital?capacity,FVC)<0.7之前已经存在肺功能指标的受损,但具体受损特点尚不明确,目前相关研究较少.目的 本研究通过比较FEV1/FVC≥0.7的吸烟者和不吸烟者肺功能指标的差异,探讨FEV1/FVC≥0.7的吸烟者肺功能受损特点及其影响因素,以期为早期识别COPD提供依据.方法 回顾性研究2017年3月-?2020年4月在我中心接受肺功能检查的FEV1/FVC≥0.7且无慢性气道疾病的吸烟者(吸烟指数>50)和不吸烟者共388例,其中男性223例,女性165例.依据年龄分为<50岁组(86例)、50?～?70岁组(197例)和>70岁组(105例),对各组吸烟者与不吸烟者肺功能指标进行比较.对这一人群各肺功能指标影响因素进行统计分析.结果 <50岁组中吸烟者肺功能容量指标FVCpred％、ICpred％较不吸烟者明显降低(P均<0.05).50?～?70岁组中吸烟者流速指标FEV1pred％、FEV1/FVC和容量指标FVC、FVCpred％、ICpred％均较不吸烟者降低(P均<0.05).>70岁组吸烟者FVCpred％、FEV1pred％、ICpred％低于不吸烟者(P均<0.05).以各肺功能指标为因变量,以性别、年龄、吸烟指数为自变量,分别对纳入的人群进行九次线性回归分析,结果发现FVC与性别(B=-0.756,95％?CI:-1.079?～?-0.432)、年龄(B=-0.032,95％CI:-0.040?～?-0.025)、吸烟指数(B=-0.001,95％CI:-0.001?～?0.000)独立关联;FEV1与性别(B=-0.586,95％?CI:-0.840?～-0.333)、年龄(B=-0.028,95％?CI:-0.034?～?-0.022)、吸烟指数(B=-0.001,95％CI:-0.001?～?0.000)独立关联;IC与性别(B=-0.530,95％?CI:-0.814?～?-0.247)、年龄(B=-0.018,95％?CI:-0.025?～?-0.011)、吸烟指数(B=-0.001,95％?CI:-0.001?～?0.000)独立关联.在肺功能指标中,仅与吸烟指数独立关联的指标包括FVCpred％(B=-0.027,95％CI:-0.034?～?-0.020)、FEV1pred％(B=-0.028,95％CI:-0.034?～?-0.022)、ICpred％(B=-0.033,95％CI:-0.041?～?-0.025),RV仅与年龄独立关联(B=0.013,95％?CI:0.003?～?0.024),而FEV1/FVC、RVpred％几乎不受性别、年龄和吸烟指数的影响.结论 在FEV1/FVC≥0.7吸烟人群中,吸烟对肺功能的损伤在各年龄组均可发现.但在<50岁组的年轻人群中,肺功能容量指标FVCpred％、ICpred％下降更明显.肺功能容量指标下降在吸烟导致的肺功能早期损害中需引起重视.

Objective:To explore the characteristics and variation of lung function parameters of chronic obstructive pulmonary disease(COPD) patients complicated with lung cancer.Methods:This was a case-control study.By nonrandom sampling, we admitted 110 COPD patients complicated with lung cancer without operation and radiotherapy or chemotherapy from January 2016 to May 2021 in the Department of Pulmonary and Critical Care Medicine in the Sixth Medical Center of the Chinese People′s Liberation Army General Hospital as the experiment group, while 110 patients with simple COPD at the same period were admitted as the control group.The patients′ characteristics and lung function parameters of the two groups were compared.The lung functions of 22 patients during the surrounding period of lung cancer onset were further explored by pair tests.Results:The factors of the pack-year, the grade of a global initiative for chronic obstructive lung disease (GOLD), and the symptoms including hemoptysis, dyspnea, chest pain, marasmus, pulmonary atelectasis, and pleural effusion, etc.showed significant statistical differences when compared to the control group (all P<0.05).The forced expiratory volume in the first second in percent predicted values (FEV 1%pred) and the forced expiratory volume in the first second/forced vital capacity (FEV 1/FVC) of the experiment group vs control group were (64.33±16.93)% vs (50.18±18.37)% and (60.39±10.02)% vs (50.27±10.70)%, respectively ( t values were 5.94 and 7.24, respectively, both P<0.01).The carbon monoxide diffusing capacity in percent predicted values after hemoglobin adjusted (D LCOadj%pred) was declined in the experiment group compared to the control group, with the value of 73.05±12.01 vs 76.80±11.63 ( t=2.35, P=0.020).When we tested the lung functions of 22 COPD patients before and after the lung cancer onset, the FEV 1%pred, FEV 1/FVC, the carbon monoxide diffusing capacity in percent predicted values (D LCO%pred), and the D LCOadj%pred on the post-lung cancer period were declined ( t values were 3.02, 3.82, 3.21, and 3.65, respectively, all P<0.05), while the residual volume/total lung capacity (RV/TLC) was higher than the pre-lung cancer period ( t=2.43, P=0.024). Conclusions:The symptoms including hemoptysis, chest pain, and marasmus in COPD patients complicated with lung cancer had a significant difference compared to the control group.Although the lung function index of FEV 1%pred and FEV 1/FVC were better in the experiment group than in the control group, the ventilation function and diffusion function data both declined after lung cancer onset.

背景 既往研究发现最大中期呼气流量(maximal?mid-expiratory?flow,MMEF)与用力肺活量(forced?vital?capacity,FVC)的比值可反映慢性阻塞性肺疾病(chronic?obstructive?pulmonary?disease,COPD)患者小气道功能,而在COPD患者中MMEF/FVC、呼出气一氧化氮(fractional?exhaled?nitric?oxide,FeNO)和血清标志物的相关性及意义尚不清楚.目的 探索COPD患者MMEF/FVC、FeNO和血清标志物之间的相关性及意义.方法 纳入2020年1月-?2021年1月解放军总医院第六医学中心149例患者,其中COPD组58例,COPD风险组44例,健康对照组47例.比较三组受试者MMEF/FVC、FeNO、白细胞介素-6(interleukin-6,IL-6)、C反应蛋白(C-reactive?protein,CRP)、肺泡表面蛋白D(surface?protein?D,SP-D)的表达水平及之间的相关性,并分析MMEF/FVC、FeNO联合不同血清标志物在COPD诊断中的预测价值.结果 MMEF/FVC值在COPD组、COPD风险组、健康对照组依次升高,差异有统计学意义(P均<0.05);而FeNO水平依次降低,差异有统计学意义(P均<0.05);COPD组血清IL-6、SP-D水平高于COPD风险组和健康对照组(P均<0.05);三组患者中FeNO、血清标志物(IL-6、CRP、SP-D)与MMEF/FVC均低度负相关(FeNO:r=-0.289,P<0.001;IL-6:r=-0.296,P<0.001;CRP:r=-0.255,P=0.002;SP-D:r=-0.177,P=0.031).血清标志物(IL-6、CRP)与FeNO呈中度正相关(分别为IL-6:r=0.323,P<0.001;CRP:r=0.434,P<0.001).MMEF/FVC联合FeNO与血清标志物诊断COPD风险的受试者工作曲线下面积为0.696,95％?CI为0.588～0.804.结论 MMEF/FVC、FeNO和血清标志物之间存在一定的相关性,可作为反映COPD患者疾病严重程度的指标,联合筛查的方式可提高COPD高风险人群的识别能力.

目的 探讨免疫球蛋白辅助治疗老年脓毒症患者的疗效,研究死亡患者的临床特征,分析临床指标对患者预后的预测价值.方法 选取2017年1月-2020年5月解放军总医院第六医学中心诊治的140例老年脓毒症患者,常规治疗+免疫球蛋白治疗70例为研究组,常规治疗70例为对照组,评估免疫球蛋白治疗效果及治疗前后临床指标情况.根据患者28 d预后情况分为存活及死亡两亚组,采用受试者工作曲线(ROC)评价临床指标对患者预后的预测价值.结果 研究组与对照组患者一般情况差异无统计学意义(P>0.05);研究组28 d死亡率下降,但与对照组比较差异无统计学意义(P>0.05);免疫球蛋白辅助治疗能更好的降低C反应蛋白(CRP)等炎性指标,差异有统计学意义(P<0.05);存活和死亡亚组患者临床指标单因素分析,结果示SOFA、APACHEⅡ、乳酸(Lac)、降钙素原(PCT)和血小板差异有统计学意义(P<0.05);多因素logistic分析示SOFA、APACHEⅡ和Lac是影响预后的独立危险因素;将预测值纳入受试者工作曲线(ROC),结果显示曲线下面积(AUC)为0.854,95％置信区间为(0.789～0.919).结论 免疫球蛋白辅助治疗老年脓毒症患者的死亡率下降,但差异无统计学意义;SOFA、APACHEⅡ和Lac对患者预后预测效能较好.

Lung cancer is a global disease and a major cause of cancer-related mortality worldwide. Accumulated studies have confirmed the essential role of long non-coding RNAs (lncRNAs) in the occurrence and development of cancers. Meanwhile, there have been reports concerning the role of Small Nucleolar RNA Host Gene 3 (SNHG3) in various cancers. However, there are so far few studies on the function and mechanism of SNHG3 in lung cancer. In the present study, SNHG3 was found to be highly expressed in lung cancer tissues and cells. Downregulation of SNHG3 could inhibit cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) process. In addition, SNHG3 was found to have the ability to bind to miR-515-5p. Furthermore, Small Ubiquitin Like Modifier 2 (SUMO2) was identified to be the downstream target of miR-515-5p, which was negatively correlated with miR-515-5p expression. SNHG3 could positively regulate SUMO2 expression by sponging miR-515-5p. In addition, the rescue experiment showed that simultaneous transfection of miR-515-5p or SUMO2 siRNA could reverse the effect of SNHG3 expression on cell proliferation and metastasis. Collectively, our study demonstrates that SNHG3 can act on miR-515-5p in the form of competitive endogenous RNA (ceRNA) to regulate SUMO2 positively and thus affect the proliferation and metastasis of NSCLC cells. Findings in our study support that SNHG3/miR-515-5p/SUMO2 regulatory axis may become a potential therapeutic target for lung cancer.