Idiopathic pulmonary fibrosis (IPF) is a fatal interstitial lung disease with limited therapies and poorly defined cross-tissue immune mechanisms. We performed single-cell RNA sequencing and TCR profiling of paired lung, lymph node, and peripheral blood samples from patients with IPF, combined with functional coculture assays and mouse model. We identified GZMK-high CD8⁺ T cells enriched in fibrotic lungs, displaying inflammatory but low-cytotoxic features. TCR and trajectory analyses indicated that these cells originate from lymph-node CD8_HSPA1A cells and migrate to the lung. Higher GZMK⁺CD8⁺ T-cell levels correlated with impaired lung function and worse outcomes. Mechanistically, GZMK-overexpressing CD8⁺ T cells promoted fibroblast-to-myofibroblast differentiation and proliferation through TGF-β1 signalling, while GZMK inhibition reduced fibroblast activation and collagen deposition. Pharmacological blockade of TGFβR1/ALK4 with TEW suppressed fibroblast activation in vitro and significantly attenuated pulmonary fibrosis in vivo. Together, these findings identify a lymph node-to-lung migration axis of GZMK⁺CD8⁺ T cells that drives fibroblast activation through TGFβR1/ALK4 signalling, highlighting GZMK as a potential biomarker and therapeutic target in IPF. ### Competing Interest Statement The authors have declared no competing interest. ### Funding Statement This study was supported by National Key R&D Program of China (Noncommunicable Chronic Diseases-National Science and Technology Major Project; 2023YFC2507100 to Jingyu Chen) and Leading Talents Program of Zhejiang Province (2024C03185 to Man Huang), Nature Science Foundation of China (82470431 to Jun Yang). ### Author Declarations I confirm all relevant ethical guidelines have been followed, and any necessary IRB and/or ethics committee approvals have been obtained. Yes The details of the IRB/oversight body that provided approval or exemption for the research described are given below: This study was approved by the Ethics Committee of The Second Affiliated Hospital Zhejiang University School of Medicine (ID: 2024-1416). I confirm that all necessary patient/participant consent has been obtained and the appropriate institutional forms have been archived, and that any patient/participant/sample identifiers included were not known to anyone (e.g., hospital staff, patients or participants themselves) outside the research group so cannot be used to identify individuals. Yes I understand that all clinical trials and any other prospective interventional studies must be registered with an ICMJE-approved registry, such as ClinicalTrials.gov. I confirm that any such study reported in the manuscript has been registered and the trial registration ID is provided (note: if posting a prospective study registered retrospectively, please provide a statement in the trial ID field explaining why the study was not registered in advance). Yes I have followed all appropriate research reporting guidelines, such as any relevant EQUATOR Network research reporting checklist(s) and other pertinent material, if applicable. Yes The scRNA-seq and scTCR-seq data supporting the findings of this study have been deposited at GSA-Human (HRA013103) under accession code PRJCA032809.

Pulmonary veno-occlusive disease (PVOD) is a fatal disease characterized by the remodelling of pulmonary veins and haemosiderin accumulation in macrophages. Although (General Control Nonderepressible 2) GCN2 deficiency has been reported in PVOD patients, the underlying mechanism by which GCN2 deficiency affects the pulmonary venous cells and the surrounding cells, remains unclear. Here, we perform immunohistochemistry and scRNA-sequencing analyses to show that macrophages are the major population affected by GCN2 deficiency and ferroptosis pathway-related genes are upregulated in lung macrophages of PVOD patients. Treatment with the specific ferroptosis inhibitor ferrostatin-1 (Fer-1) reverses the changes in haemodynamic indices observed in Eif2ak4K1488X/K1488X hypoxia mice and PVOD model rats. Furthermore, GCN2 deficiency increases HMOX1 and iron levels to facilitate ferroptosis in macrophages, and enhances arterial marker expression in venous endothelial cells (VECs). Specifically, spatial transcriptome analysis shows increased expression of NRP1, KDR and EFNB2 through ETS1 in VECs from PVOD patients. Our findings suggest the potential of targeting macrophage ferroptosis as a therapeutic strategy for treating related vascular diseases, and of using NRP1/KDR/EFNB2 expression as a specific marker set for venous arterialization.

Lung transplantation(LT)has emerged as a crucial life-saving option for critically ill patients with severe coronavirus disease 2019(COVID-19)-related acute respiratory distress syndrome(ARDS)or irreversible lung injury.[1]Intensive care unit-acquired weakness(ICU-AW)is a prevalent complication in critically ill patients.[2]The recovery of recipients undergoing LT for COVID-19-related respiratory failure may face impediments due to ICU-AW,which negatively affects early mobilization and functional improvement.This study describes two cases of successful bilateral LT for severe COVID-19-related ARDS with the occurrence of ICU-AW and subsequent successful discharge.

Background:Carbapenem-resistant Acinetobacter baumannii (CRAB) infections were associated with higher mortality and significant healthcare burden. Novel antibiotics provided a powerful weapon against CRAB. This study aimed to describe the effectiveness of eravacycline for the treatment of CRAB infections in lung transplant recipients. Methods:This was a single-center, retrospective study that enrolled lung transplant recipients with CRAB infections who received eravacycline for over 72 hours between August 2023 and December 2024. The primary outcome was 28-day survival rate. Secondary outcomes included 14-day survival and clinical failure rate. Results:A total of 24 lung transplant recipients were enrolled, with a median age of 60.5 years and a predominance of male patients. Nearly half had interstitial lung disease as the primary pulmonary condition. These recipients in our study mainly had pulmonary infections attacked by CRAB, with six individuals suffering septic shock. The median duration of eravacycline therapy was 10 days, with most patients receiving combination therapy. The primary outcome, the 28-day survival rate, was 83.3%, while the secondary outcomes showed a 14-day survival rate of 100% and a clinical failure rate of 37.5%. The median ICU and hospital lengths of stay were 12.5 and 55 days, respectively. A comparison between patients with and without clinical failure showed that those with clinical failure were older, had a higher incidence of septic shock, a higher proportion of continuous renal replacement therapy, and a longer ICU stays. Additionally, these patients exhibited an elevated heart rate, higher levels of ALT and AST, lower protein levels (total protein, albumin), prolonged PT and APTT, and increased level of CRP and PCT at the end of treatment. Conclusion:This study presented the clinical efficacy of eravacycline in lung transplant recipients with CRAB infections, providing valuable evidence and clinical experience for its use in organ transplant populations.

The integration of artificial intelligence in medical imaging has shown tremendous potential, yet the relationship between pre-trained knowledge and performance in cross-modality learning remains unclear. This study investigates how explicitly injecting medical knowledge into the learning process affects the performance of cross-modality classification, focusing on Chest X-ray (CXR) images. We introduce a novel Set Theory-based knowledge injection framework that generates captions for CXR images with controllable knowledge granularity. Using this framework, we fine-tune CLIP model on captions with varying levels of medical information. We evaluate the model's performance through zero-shot classification on the CheXpert dataset, a benchmark for CXR classification. Our results demonstrate that injecting fine-grained medical knowledge substantially improves classification accuracy, achieving 72.5% compared to 49.9% when using human-generated captions. This highlights the crucial role of domain-specific knowledge in medical cross-modality learning. Furthermore, we explore the influence of knowledge density and the use of domain-specific Large Language Models (LLMs) for caption generation, finding that denser knowledge and specialized LLMs contribute to enhanced performance. This research advances medical image analysis by demonstrating the effectiveness of knowledge injection for improving automated CXR classification, paving the way for more accurate and reliable diagnostic tools.

BACKGROUND:The limited donor lung pool for lung transplantation (LTx) is largely due to concerns over ischaemia-reperfusion injury (IRI), a major cause of primary graft dysfunction (PGD). NLRP3 inflammasome activation is known to play a pivotal role in the onset of IRI. While human umbilical cord mesenchymal stromal cell-derived extracellular vesicles (hucMSC-EVs) have shown potential in reducing acute lung injury, their effects on NLRP3 activation in the context of LTx remain unclear. METHODS:In this study, engineered hucMSC-EVs were delivered via nebulisation to mitigate IRI in rat LTx models. We utilised both a rat orthotopic LTx model and a cell cold preservation reperfusion model to evaluate the therapeutic efficacy of hucMSC-EVs. Bulk-RNA sequencing, single-cell sequencing analysis, immunofluorescence and Western blot techniques were employed to assess NLRP3 inflammasome activation and inflammation. RESULTS:Nebulised hucMSC-EVs were efficiently internalised by alveolar macrophages (AMs), significantly reducing lung injury and improving oxygenation in the LTx models. Mechanistically, the engineered hucMSC-EVs, which enhance the expression of miR-146a, can more effectively suppress the activation of the NLRP3 inflammasome by targeting the IRAK1/TRAF6/NF-κB pathway, resulting in decreased levels of IL-1β, IL-18 and other inflammatory cytokines. These findings highlight the potential of miR-146a-modified EVs in modulating innate immune responses to alleviate IRI. CONCLUSION:Our results demonstrate that nebulised delivery of engineered hucMSC-EVs effectively mitigates IRI in LTx by inhibiting NLRP3 inflammasome activation. This innovative approach presents a promising strategy for enhancing donor lung preservation and improving post-transplant outcomes in LTx. HIGHLIGHTS:Nebulized Delivery of miR-146a Engineered hucMSC-EVs Mitigates Ischemia-Reperfusion Injury (IRI) in Lung Transplantation. This study demonstrates the therapeutic potential of nebulized, engineered human umbilical cord mesenchymal stromal cell-derived extracellular vesicles (hucMSC-EVs) modified with miR-146a to alleviate IRI in rat lung transplantation models. The treatment significantly improved lung oxygenation and reduced inflammation, highlighting the efficacy of this novel approach in enhancing donor lung preservation. Mechanistic Insights: Inhibition of NLRP3 Inflammasome Activation. Engineered hucMSC-EVs efficiently targeted alveolar macrophages and suppressed NLRP3 inflammasome activation through the IRAK1/TRAF6/NF-κB pathway. This modulation of innate immune responses played a crucial role in reducing IRI-induced lung injury and inflammation, offering a promising strategy to manage primary graft dysfunction in lung transplantation. Superior Efficacy of miR-146a-Modified EVs in Reducing Inflammatory Cytokines. The miR-146a modification enhanced the anti-inflammatory properties of hucMSC-EVs, leading to a more significant reduction in pro-inflammatory cytokines (IL-1β, IL-18, and TNF-α) compared to unmodified EVs. This targeted intervention presents a potential therapeutic avenue for improving lung transplant outcomes and mitigating IRI. Innovative Therapeutic Approach: Non-Invasive Nebulization for Direct Lung Delivery. The use of nebulized EVs for direct delivery to donor lungs represents a non-invasive and efficient method for lung-targeted therapy. This strategy could expand the applicability of MSC-EV-based treatments for improving lung transplantation outcomes, particularly in enhancing donor lung preservation during the procurement process.

We describe in detail a novel surgical technique for repairing donor anterior left atrial wall defect in vivo by rotating the posterior atrial flap during lung transplantation. This method can safely and effectively address the most common type of donor left atrial cuff defect: the anterior wall defect, with the intact posterior wall, typically retained when the donor heart is also used. During atrial cuff anastomosis in lung transplantation, the excess donor posterior atrial wall is trimmed into an atrial flap. After the posterior wall anastomosis is completed, the atrial flap is rotated 180° and used as a patch for anterior wall reconstruction anastomosis. After restoring blood flow, the flow rate of the pulmonary vein is normal and smooth as confirmed by transesophageal echocardiography. Compared with the traditional patch reconstruction method, the new method effectively reduces the atrial cuff anastomosis time. Our results showed no significant difference in pulmonary vein obstruction after reconstruction. Pulmonary artery systolic blood pressure was significantly lower and pulmonary function improved postoperatively in all groups, with no significant differences among the groups. The new technique provides a feasible strategy for the reconstruction of left atrial cuff defects and can improve the effective utilization rate of donor lungs.

The prevalence of non-small cell lung cancer (NSCLC) is notably elevated in individuals diagnosed with idiopathic pulmonary fibrosis (IPF). Secreted phosphoprotein 1 (SPP1), known for its involvement in diverse physiological processes, including oncogenesis and organ fibrosis, has an ambiguous role at the intersection of IPF and NSCLC. Our study sought to elucidate the function of SPP1 within the pathogenesis of IPF and its subsequent impact on NSCLC progression. Four GEO datasets was analyzed for common differential genes and TCGA database was used to analyze the prognosis. The immune infiltration was analyzed by TIMER database. SPP1 expression was examined in human lung tissues, the IPF fibroblasts and the BLM-induced mouse lung fibrosis model. Combined with SPP1 gene gain- and loss-of-function, qRT-PCR, Western blot, EdU and CCK-8 experiments were performed to evaluate the effects and mechanisms of SPP1 in IPF progression. Effect of SPP1 on NSCLC was detected by co-cultured IPF fibroblasts and NSCLC cells. Through bioinformatics analysis, we observed a significant overexpression of SPP1 in both IPF and NSCLC patient datasets, correlating with enhanced immune infiltration of cancer-associated fibroblasts in NSCLC. Elevated levels of SPP1 were detected in lung tissue samples from IPF patients and bleomycin-induced mouse models, with partial colocalization observed with α-smooth muscle actin. Knockdown of SPP1 inhibits TGF-β1-induced differentiation of fibroblasts to myofibroblasts and the proliferation of IPF fibroblasts. Conversely, SPP1 overexpression promoted IPF fibroblast proliferation via PI3K/Akt/mTOR pathway. Furthermore, IPF fibroblasts promoted NSCLC cell proliferation and activated the PI3K/Akt/mTOR pathway; these effects were attenuated by SPP1 knockdown in IPF fibroblasts. Our findings suggest that SPP1 functions as a molecule promoting both fibrosis and tumorigenesis, positioning it as a prospective therapeutic target for managing the co-occurrence of IPF and NSCLC.

ObjectivesExtracorporeal membrane oxygenation (ECMO) has become an important life support technique during lung transplantation. We aimed to develop a rat model for lung transplantation using venoarterial (VA) ECMO support.MethodsAdult male Sprague-Dawley rats weighing 400 to 450 g were used in this study. ECMO circuits were created by obtaining venous access from the femoral vein with subsequent extracorporeal oxygen exchange, which was then returned to the circulatory system through the left carotid artery (ie, VA-ECMO). Simultaneously, the donor lungs were retrieved and immersed in cold, low-potassium dextran lung preservation solution. Orthotopic left lung transplantation supported by VA-ECMO was performed. Thereafter, a respiratory failure rat model was constructed using ventilation with a hypoxic and hypercapnic gas mixture, consisting of 6% oxygen, 8% carbon dioxide, and 86% nitrogen, before lung transplantation. Similarly, left lung transplantation supported by VA-ECMO was performed in rats with respiratory failure. Arterial blood gas levels were measured at designated time points throughout the experiment.ResultsWe found that VA-ECMO provided sufficient oxygenation and carbon dioxide removal to allow for smooth left lung transplantation in healthy rats and those with respiratory failure.ConclusionsWe established a rat model for lung transplantation using VA-ECMO. Left lung transplantation using VA-ECMO support is also feasible and safe in rat models of respiratory failure. These models provide efficient and economical models for translational medicine for lung transplantation using ECMO. Moreover, it will be invaluable to evaluate the physiological and pathophysiological roles of ECMO during lung transplantation.

OBJECTIVETo investigate the risk factors of early death after lung transplantation in patients with idiopathic pulmonary fibrosis (IPF) complicated with pulmonary arterial hypertension (PAH).METHODSA retrospective cohort study was conducted. The clinical data of 134 patients with IPF and PAH who underwent lung transplantation at Wuxi People's Hospital Affiliated to Nanjing Medical University from January 2017 to December 2020 were collected. The donor's gender, age, duration of mechanical ventilation, and cold ischemia time, the recipient's gender, age, body mass index (BMI), smoking, history of hypertension and diabetes, preoperative usage of hormones, mean pulmonary arterial pressure (mPAP), cardiac echocardiography and cardiac function, serum creatinine (SCr), N-terminal pro-brain natriuretic peptide (NT-proBNP) as well as surgical type, extracorporeal membrane oxygenation (ECMO) treatment, duration of operation, and plasma and red blood cell infusion ratio were collected. The cumulative survival rates of patients at 30, 60, and 180 days after lung transplantation were calculated by Kaplan-Meier method. The univariate and multivariate Cox proportional hazards regression models were used to analyze the effects of donor, recipient, and surgical factors on early survival in donors after lung transplantation.RESULTSThe majority of donors were male (80.6%). There was 63.4% of the donors older than 35 years old, 80.6% of the donors had mechanical ventilation duration less than 10 days, and the median cold ischemia time was 465.00 (369.25, 556.25) minutes. The recipients were mainly males (83.6%). Most of the patients were younger than 65 years old (70.9%). Most of them had no hypertension (75.4%) or diabetes (67.9%). The median mPAP of recipients was 36 (30, 43) mmHg (1 mmHg ≈ 0.133 kPa). There were 73 patients with single lung transplantation (54.5%), and 61 with double lung transplantation (45.5%). The survival rates of 134 IPF patients with PAH at 30, 60, 180 days after lung transplantation were 81.3%, 76.9%, and 67.4%, respectively. Univariate Cox proportional risk regression analysis showed that recipient preoperative use of hormone [hazard ratio (HR) = 2.079, 95% confidence interval (95%CI) was 1.048-4.128], mPAP ≥ 35 mmHg (HR = 2.136, 95%CI was 1.129-4.044), NT-proBNP ≥ 300 ng/L (HR = 2.411, 95%CI was 1.323-4.392), New York Heart Association (NYHA) cardiac function classification III-IV (HR = 3.021, 95%CI was 1.652-5.523) were the risk factors of early postoperative death in patients with IPF complicated with PAH (all P < 0.05). In the multivariable Cox proportional risk regression analysis, recipient preoperative hormone usage (model 1: HR = 2.072, 95%CI was 1.044-4.114, P = 0.037; model 2: HR = 2.098, 95%CI was 1.057-4.165, P = 0.034), NT-proBNP ≥ 300 ng/L (HR = 2.246, 95%CI was 1.225-4.116, P = 0.009) and NYHA cardiac function classification III-IV (HR = 2.771, 95%CI was 1.495-5.134, P = 0.001) were independent risk factors of early postoperative death in patients with IPF.CONCLUSIONSPreoperative hormone usage, NT-proBNP ≥ 300 ng/L, NYHA cardiac function classification III-IV are independent risk factors for early death in patients with IPF and PAH after lung transplantation. For these patients, attention should be paid to optimize their functional status before operation. Preoperative reduction of receptor hormone usage and improvement of cardiac function can improve the early survival rate of such patients after lung transplantation.

Background. Primary graft dysfunction, which is directly related to cold ischemia–reperfusion (CI/R) injury, is a major obstacle in lung transplantation (LTx). Ferroptosis, a novel mode of cell death elicited by iron-dependent lipid peroxidation, has been implicated in ischemic events. This study aimed to investigate the role of ferroptosis in LTx-CI/R injury and the effectiveness of liproxstatin-1 (Lip-1), a ferroptosis inhibitor, in alleviating LTx-CI/R injury. Methods. LTx-CI/R-induced signal pathway alterations, tissue injury, cell death, inflammatory responses, and ferroptotic features were examined in human lung biopsies, the human bronchial epithelial (BEAS-2B) cells, and the mouse LTx-CI/R model (24-h CI/4-h R). The therapeutic efficacy of Lip-1 was explored and validated both in vitro and in vivo. Results. In human lung tissues, LTx-CI/R activated ferroptosis-related signaling pathway, increased the tissue iron content and lipid peroxidation accumulation, and altered key protein (GPX4, COX2, Nrf2, and SLC7A11) expression and mitochondrial morphology. In BEAS-2B cells, the hallmarks of ferroptosis were significantly evidenced at the setting of both CI and CI/R compared with the control, and the effect of adding Lip-1 only during CI was much better than that of only during reperfusion by Cell Counting Kit-8. Furthermore, Lip-1 administration during CI markedly relieved LTx-CI/R injury in mice, as indicated by significant improvement in lung pathological changes, pulmonary function, inflammation, and ferroptosis. Conclusions. This study revealed the existence of ferroptosis in the pathophysiology of LTx-CI/R injury. Using Lip-1 to inhibit ferroptosis during CI could ameliorate LTx-CI/R injury, suggesting that Lip-1 administration might be proposed as a new strategy for organ preservation.

Background: Idiopathic pulmonary fibrosis is a severe and deadly form of diffuse parenchymal lung disease and treatment options are few. Alveolar epithelial type 2 (AEC2) cell senescence is implicated in the pathogenies of IPF. A major bioactive compound from the traditional Chinese medicine Fructus arctii, arctiin (ARC) has robust anti-inflammatory, anti-senescence, and anti-fibrosis functions. However, the potential therapeutic effects of ARC on IPF and the underlying mechanisms involved are still unknown. Methods: First of all, ARC was identified as an active ingredient by network pharmacology analysis and enrichment analysis of F. arctii in treating IPF. We developed ARC-encapsulated DSPE-PEG bubble-like nanoparticles (ARC@DPBNPs) to increase ARC hydrophilicity and achieve high pulmonary delivery efficiency. C57BL/6 mice were used to establish a bleomycin (BLM)-induced pulmonary fibrosis model for assessing the treatment effect of ARC@DPBNPs on lung fibrosis and the anti-senescence properties of AEC2. Meanwhile, p38/p53 signaling in AEC2 was detected in IPF lungs, BLM-induced mice, and an A549 senescence model. The effects of ARC@DPBNPs on p38/p53/p21 were assessed in vivo and in vitro. Results: Pulmonary route of administration of ARC@DPBNPs protected mice against BLM-induced pulmonary fibrosis without causing significant damage to the heart, liver, spleen, or kidney. ARC@DPBNPs blocked BLM-induced AEC2 senescence in vivo and in vitro. The p38/p53/p21 signaling axis was significantly activated in the lung tissues of patients with IPF, senescent AEC2, and BLM-induced lung fibrosis. ARC@DPBNPs attenuated AEC2 senescence and pulmonary fibrosis by inhibiting the p38/p53/p21 pathway. Conclusion: Our data suggest that the p38/p53/p21 signaling axis plays a pivotal role in AEC2 senescence in pulmonary fibrosis. The p38/p53/p21 signaling axis inhibition by ARC@DPBNPs provides an innovative approach to treating pulmonary fibrosis in clinical settings.

Pediatric lung transplantation is an effective treatment for children with end-stage lung diseases. The indications include end-stage pulmonary vascular disease,bronchiolitis obliterans, interstitial lung disease, cystic fibrosis and so on. In recent years,with the development and maturity of lung transplantation technology,the number of pediatric lung transplantation has also increased year by year.This article summarizes the current status of pediatric lung transplantation in the treatment of different lung diseases in children in order to provide a reference for the lung transplantation evaluation, diagnosis and treatment of children with end-stage lung diseases.

Bronchiolitis obliterans (BO) is a severe complication of Castleman disease (CD), a rare lymphoproliferative disease with unclear pathogenesis. Currently, there are no reports on the safety or outcomes of bilateral lung transplantation in patients with BO due to CD. This study aimed to characterize the clinical manifestations and features of BO and CD. We retrospectively analyzed the medical records of six consecutive patients with BO and CD who underwent bilateral lung transplantation between December 2012 and December 2020. The average age of patients at lung transplantation was 33 +/- 15 years, and the age range of patients at diagnosis of CD was about 9-56 years. The body mass index was 15.2 +/- 1.9 kg/m(2). The average time from diagnosis to lung transplantation was 4.1 +/- 2.7 years. All the patients had unicentric CD (UCD); five had concomitant paraneoplastic pemphigus, and four received extracorporeal membrane oxygenation during surgery. The average hospital stay was 51 +/- 53 days. Infection was the most common postoperative complication. CD did not recur in any of the patients. Thus, bilateral lung transplantation is a viable and safe treatment for selected patients with CD and BO, which can improve the quality of life and prolong survival.

目的 评价连续性肾脏替代治疗在边缘性供肺维护中的应用价值.方法 2019年1月1日～2019年10月31日经无锡市人民医院肺移植中心维护的脑死亡边缘性供肺30例,根据维护方法 不同,将其分为两组,实验组12例,在获取前予以常规+持续性肾脏替代治疗(CRRT)联合方案维护48小时;对照组18例,仅进行常规方案维护.两组每24小时留取外周血样,行胸片及气道纤支镜检查,动态监测并对比两种维护方式在血流动力学、氧合指数、感染指标、气道黏膜水肿以及供肺最终使用情况等的差异.结果 经两种方法 维护后,两组供肺质量均较前有不同程度改善,实验组和对照组氧合指数增加分别为(93.58±16.92)％ 和(57.72±11.41)％,C-反应蛋白(CRP)下降分别为(36.04±22.30)mg/L和(18.01±6.78)mg/L,降钙素原(PCT)下降分别为1.09±0.45和0.59±0.82,两组比较,差异有统计学意义(P<0.05).实验组肺影像学的渗出改变、气道黏膜水肿程度改善显著.实验组中8例、对照组中5例达到供肺使用标准,实验组使用率显著高于对照组(P<0.05).结论 早期予以CRRT联合方案,能显著改善边缘性供肺肺功能,提高供体器官利用率.

Background: Destroyed lung can cause mediastinal displacement and asymmetric chest deformity. Reports on bilateral lung transplantation (LT) to treat destroyed lung and asymmetric chest deformity are rare. This study presents our surgical experience of bilateral LT among patients with destroyed lung and asymmetric chest deformity. Methods: Six patients with destroyed lung and asymmetric chest deformity who underwent bilateral LT at our center from 2005 to 2020 were included in the study. Demographic data, technical data, perioperative details, and short-term follow-up data were reviewed. Results: Three patients underwent bilateral LT via anterolateral incisions in the lateral position without sternal transection, while three patients underwent bilateral LT via clam-shell incisions in the supine position with sternal transection. Only one patient required intraoperative extracorporeal membrane oxygenation. Four patients underwent size-reduced LT. In the other two patients, we restored the mediastinum by releasing mediastinal adhesions to ensure maximal preservation of the donor lung function. Patients in the lateral position group had a higher volume of blood loss, longer operation time, and longer postoperative in-hospital stay than those in the supine position group. However, these differences were not statistically significant. Postoperative computed tomography in the supine position group revealed that the donor lungs were well expanded and the mediastina were in their original positions. Conclusions: Although bilateral LT in patients with destroyed lung and asymmetric chest deformity is high risk, with sufficient preoperative preparation and evaluation, it is safe and feasible to perform bilateral LT for selected patients. For patients without severe chest adhesions, releasing the mediastinal adhesions and restoring the mediastinum through a clam-shell incision in the supine position is a simple and effective method to maximally preserve the donor lung function without pneumonectomy or lobectomy.

Background: Lymphangioleiomyomatosis (LAM) is a rare systemic disease that generally leads to a progressive decline in pulmonary function. Experience, especially from the Asian population, including combined drug therapy before and after lung transplantation (LT) in LAM, is still limited. This study aimed to summarize the clinical data from patients with pulmonary LAM who underwent LT at centers in China.Methods: A retrospective review of all patients with LAM undergoing LT at the two largest centers in China between 2010 and 2018 was conducted. Pre- and posttransplant data were assessed and analyzed.Results: Overall, 25 patients with LAM underwent bilateral LT. The mean age was 35.0 ± 8.6 years at diagnosis and 36.8 ± 9.3 years at the time of transplant. Before LT, only six patients could complete pulmonary function test; the reachable mean forced expiratory volume in one second (FEV1) before LT was 15.9 ± 6.9%. Twenty-one patients (84%) had a recurrent pneumothorax, four (16.0%) of which required pleurodesis. Eight patients (32%) were treated with sirolimus pretransplant for 3.9 years (1–9 years). The average intra-surgery bleeding volume was 1,280 ± 730 ml in need of a transfusion of 1,316 ± 874 ml due to moderate-to-severe adhesion and pretransplant pleurodesis. The causes of death of four patients (16%) included primary graft dysfunction, bronchial dehiscence with long-term use of sirolimus, and uncontrollable infections. The median follow-up time from LT was 41.1 ± 25.0 months.Conclusions: LT for LAM patients from the Asian population has been reinforced from the data that we presented. Peri-transplantation use of sirolimus and LAM-related complications should be further defined and under constant surveillance.