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ObjectiveThis study aimed to investigate the clinical manifestations and prognosis of lung transplant (LTx) recipients infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) during the coronavirus disease (COVID-19) pandemic.MethodsThe research participants were LTx recipients who underwent surgery and were regularly followed up at our center. From 1 December 2022 to 28 February 2023, during the COVID-19 pandemic in China, research participants were interviewed either online or in person. SARS-CoV-2 nucleic acid or self-tested antigens were detected according to accessibility. Diagnosis and treatment were performed according to the Diagnosis and Treatment Plan for COVID-19 (10th edition) issued by the National Health Commission of the People's Republic of China. Hospitalized patients underwent chest imaging examinations, routine blood tests, biomarkers for infection and inflammation, and biochemical tests, all of which were taken and recorded. Data were analyzed to describe the features of COVID-19 in LTx recipients.ResultsIn total, 52 patients were enrolled in this study, comprising 48 men and 4 women, with a mean age of 51.71 ± 11.67 years. By 1 December 2022, the mean survival period was 33.87 ± 25.97 months, of which 84.61% of the patients (44/52) had a survival period longer than 12 months. The SARS-CoV-2 infection rate in these LTx recipients was 82.69% (43/52), with 3.85% (2/52) of the infected recipients being asymptomatic, 50.00% (26/52) of the infected recipients experiencing mild COVID-19, 11.54% (6/52) having moderate COVID-19, and 17.31% (9/52) having severe or critical COVID-19. The mortality rate among severe and critical patients was 66.67% (6/9).ConclusionLTx recipients in this cohort exhibited a notable susceptibility to SARS-CoV-2, with 82.69% of individuals diagnosed with COVID-19. Moreover, the mortality rate among critically ill patients was high.

Abstract Background A reasonable supply of nitrogen (N) fertilizer is essential for obtaining high-quality, high-level, and stable potato yields, and an improvement in the N utilization efficiency can effectively reduce N fertilizer use. It is important to use accurate, straightforward, and efficient transgenic breeding techniques for the identification of genes that can improve nitrogen use efficiency, thus enabling us to achieve the ultimate goal of breeding N-efficient potato varieties. In recent years, some of the mechanisms of miRNAs have been elucidated via the analysis of the correlation between the expression levels of potato miRNA target genes and regulated genes under conditions of stress, but the role of miRNAs in the inhibition/expression of key genes regulating N metabolism under N stress is still unclear. Our study aimed to identify the role played by specific enzymes and miRNAs in the responses of plants to N stress. Results The roots and leaves of the N-efficient potato variety, Yanshu4 ("Y"), and N-inefficient potato variety, Atlantic ("D"), were collected at the seedling and budding stages after they were exposed to different N fertilizer treatments. The miRNAs expressed differentially under the two types of N stress and their corresponding target genes were first predicted using miRNA and degradome analysis. Then, quantitative polymerase chain reaction (qRT-PCR) was performed to verify the expression of differential miRNAs that were closely related to N metabolism. Finally, the shearing relationship between stu-miR396-5p and its target gene StNiR was determined by analyzing luciferase activity levels. The results showed that NiR activity increased significantly with an increase in the applied N levels from the seedling stage to the budding stage, and NiR responded significantly to different N treatments. miRNA sequencing enabled us to predict 48 families with conserved miRNAs that were mainly involved in N metabolism, carbon metabolism, and amino acid biosynthesis. The differences in the expression of the following miRNAs were identified via screening (high expression levels and P

Abstract Introduction Previous evidence realized the critical role of histone in disease control. The anti‐inflammatory function of estradiol (E2) in sepsis has been documented. We here intended to unveil the role of extracellular histone H3 in sepsis regarding cell ferroptosis and the role of E2 in a such mechanism. Methods Clinical sample, cecal ligation and puncture (CLP)‐induced animal models and lipopolysaccharides (LPS)‐induced cell models were prepared for testing relative expression of extracellular histone H3 and E2 as well as analyzing the role of extracellular histone H3 and E2 in sepsis concerning cell viability, reactive oxygen species (ROS), and ferroptosis. Results Under sepsis, we found increased ferroptosis and extracellular histone H3 content, but reduced E2 concentration. Extracellular histone H3 facilitated ferroptosis of human umbilical vein endothelial cells (HUVECs) induced by LPS through activating the ROS/c‐Jun N‐terminal kinase (JNK) pathway. Moreover, E2 antagonized the effect of extracellular histone H3 on LPS‐induced HUVEC ferroptosis and sepsis injury in CLP‐induced animal models. Conclusion We highlighted that extracellular histone H3 facilitated lipopolysaccharides‐induced HUVEC ferroptosis via activating ROS/JNK pathway, and such an effect could be antagonized by E2.

Abstract Background Oesophageal leiomyomas are one of the most common benign oesophageal tumours. This retrospective, observational study summarized and compared the clinical outcomes of thoracoscopic enucleation of oesophageal leiomyoma between single-lumen endotracheal intubation with a bronchial blocker and double-lumen endotracheal intubation. Methods A total of 36 patients who underwent thoracoscopic enucleation of oesophageal leiomyoma at Peking Union Medical College Hospital between 2014 and 2020 were retrospectively analysed. Fifteen patients received single-lumen endotracheal intubation combined with a right bronchial blocker (SLT-B group), and twenty-one patients received double-lumen endotracheal intubation (DLT group). Clinical data, surgical variables, and postoperative complications were analysed and compared. Results The average tumour size in all patients was 4.3 ± 2.0 cm. The average tumour size among symptomatic patients was significantly larger than that among asymptomatic patients (5.1 ± 2.0 cm vs 3.7 ± 1.7 cm, P

In recent years, increasing evidence indicates the significant roles of circRNAs in carcinogenesis. However, their roles in lung cancer remain largely unclear. We profiled the circRNA expression in 10 paired non-small cell lung cancer (NSCLC) and adjacent non-cancer tissues using high-throughput sequencing. A total of 183 up-regulated and 428 down-regulated circRNAs were identified in the NSCLC tissues (fold change ≥ 2, P < 0.05). Circ_0089823, an up-regulated circRNA (5.4-fold, P = 0.0017), was further investigated through loss-of-function and gain-of-function. The circ_0089823 level in NSCLC samples was related to the gender, tumor size, pathological type, TNM stage and smoking history. Knockdown of circ_0089823 suppressed cell proliferation, induced cell cycle arrest and apoptosis of NSCLC cells in vitro. Additionally, circ_0089823-silenced xenografts grew much slowly. On the contrary, its over-expression promoted the malignant behaviors of NSCLC cells. Furthermore, SOX4, a tumor-promoting transcription factor, was highly expressed in NSCLC tissues and positively regulated by circ_0089823. Bioinformatic analysis revealed several potential binding sites for miR-507, miR-557, miR-579-3p and miR-1287-5p in circ_0089823 and SOX4 3′-untranslated region, which was later confirmed by luciferase reporter assay. Interestingly, silencing SOX4 countervailed the effects of circ_0089823 over-expression on NSCLC cells. Here, we revealed that circ_0089823 might act as a sponge of microRNAs targeting SOX4, thus increasing the expression of SOX4, thereby reinforcing the malignant behaviors of NSCLC cells. This study indicates that circ_0089823 has the potential to become a candidate target for NSCLC treatment.

Abstract Background Ulcerative colitis (UC) is an important inflammatory phenotype in bowel disease (IBD), which is caused by multiple potential factors, including fungal dysbiosis. Candida albicans (C. albicans) was confirmed to be an important factor promoting the occurrence and development of UC. Sanhuang decoction (SHD) has been used for UC therapy in China for thousand of years, although its core active constituents and pharmacological mechanism remain undefined. Methods In this work, a murine model of UC with C. albicans colonization was established with dextran sodium sulfate (DSS) and C. albicans intragastric administration. The major bioactive constituents and potential mechanism of SHD against UC with fungal dysbiosis were comprehensively examined by combining systems pharmacology and in vivo transcriptomics. Results SHD attenuated C. albicans burden, reduced DAI, increased mucosal integrity and relived systemic inflammation in UC mice. Systems pharmacology analysis identified 9 core bioactive ingredients and 45 hub targets of SHD against UC. Transcriptomics analysis confirmed 370 differentially expressed genes (DEGs) after SHD treatment, which were mainly enriched in inflammatory and immune response related signaling pathways. Toll-like receptor and PI3K-Akt signaling pathway were screened out as the candidate targets involved in the action of SHD on fungal dysbiosis-associated UC, which were consistent with the findings in systems pharmacology. The expression of TLR4, IL-1β, NF-κB, PI3K and Akt proteins were stimulated by C. albicans, and partially reversed by SHD in UC mice. Conclusion These findings suggested SHD could be a candidate for the treatment of fungal dysbiosis-associated UC via TLR4-NF-κB and PI3K-Akt signaling pathways.

BackgroundKidney cancer (KC) is one of the most challenging cancers due to its delayed diagnosis and high metastasis rate. The 5-year survival rate of KC patients is less than 11.2%. Therefore, identifying suitable biomarkers to accurately predict KC outcomes is important and urgent.MethodsCorresponding data for KC patients were obtained from the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA) databases. Systems biology/bioinformatics/computational approaches were used to identify suitable biomarkers for predicting the outcome and immune landscapes of KC patients.ResultsWe found two ferroptosis- and immune-related differentially expressed genes (FI-DEGs) (Klotho (KL) and Sortilin 1 (SORT1)) independently correlated with the overall survival of KC patients. The area under the curve (AUC) values of the prognosis model using these two FI-DEGs exceeded 0.60 in the training, validation, and entire groups. The AUC value of the 1-year receiver operating characteristic (ROC) curve reached 0.70 in all the groups.ConclusionsOur present study indicated that KL and SORT1 could be prognostic biomarkers for KC patients. Whether this model can be used in clinical settings requires further validation.

Background: Ferroptosis and immunity are novel treatments that target several cancers, including kidney renal clear cell carcinoma (KIRC). Long noncoding RNAs (lncRNAs) are an important class of gene expression regulators that play fundamental roles in the regulation of ferroptosis and immunity. We aimed to identify ferroptosis- and immune-related lncRNAs as biomarkers in patients with KIRC.Methods: Corresponding data for each patient with KIRC were obtained from The Cancer Genome Atlas (TCGA) database. Univariate and multivariate Cox regression analyses were used to identify candidate biomarkers followed by least absolute shrinkage and selection operator (LASSO) regression analyses, weighted gene coexpression network analysis (WGCANA), and gene set enrichment analysis (GSEA).Results: Three ferroptosis- and immune-related differentially expressed lncRNAs (FI-DELs) (AC124854.1, LINC02609, and ZNF503-AS2) were markedly and independently correlated with the overall survival (OS) of patients with KIRC. The area under the curve (AUC) value of the prognostic model in the entire group using the three FI-DELs was > 0.70. The sensitivity and specificity of the diagnostic model using the three FI-DELs were 0.8586 and 0.9583, respectively.Conclusion: The present study found that AC124854.1, LINC02609, and ZNF503-AS2 were considerably and independently correlated with the OS of patients with KIRC, suggesting that the three FI-DELs could be used as prognostic and diagnostic biomarkers for patients with KIRC.

Potato (Solanum tuberosum L.), a species of the family Solanaceae, is the fourth most important food crop worldwide. Solanum tuberosum L. cv. Shepody is a long, smooth, white-skinned potato cultivar with medium green leaves. It has good specific gravity and boils and bakes well. To support more molecular data for breeding of S. tuberosum, the complete chloroplast (cp) genome sequence of S. tuberosum L. cv. Shepody was determined using the next-generation sequencing. In leaves, the chloroplast genome accounts for 3.88% of the total genome. The entire cp genome was determined to be 155,296 bp in length. It contained large single-copy (LSC) and small single-copy (SSC) regions of 85,737 and 18,373 bp, respectively, which were separated by a pair of 25,593 bp inverted repeat (IR) regions. The genome contained 132 total genes, including 87 protein-coding genes, 37 tRNA genes, and 8 rRNA genes. The overall GC content of the genome is 37.9%. A phylogenetic tree reconstructed by 60 chloroplast genomes reveals that S. tuberosum L. cv. Shepody was closely related to S. tuberosum L. cv. Desiree with bootstrap support values of 100%.

Abstract Long noncoding RNAs (lncRNAs) possessed essential functions in the biological behaviors of various human cancers. SLCO4A1 antisense RNA 1 (SLCO4A1‐AS1) is a lncRNA that has been reported as a oncogenic regulator in colorectal cancer and bladder cancer. However, whether it exerted functions in the gene expression and cellular processes in lung adenocarcinoma (LUAD) remains still obscure. In the present research, we unveiled the high level of SLCO4A1‐AS1 in LUAD tissues and cells. Moreover, functional assays indicated that SLCO4A‐AS1 facilitated LUAD cell proliferation, motility, and cisplatin‐resistance. Besides, mechanism investigation revealed that miR‐4701‐5p could interact with SLCO4A1‐AS1 and directly target to NFE2L1. The expression correlation between miR‐4701‐5p and SLCO4A1‐AS1 or NFE2L1 was found to be negative. Moreover, NFE2L1 was expressed at a same tendency with SLCO4A1‐AS1 in LUAD tissues and cells. In addition, it was confirmed that NFE2L1 was involved in SLCO4A1‐AS1‐mediated activation of WNT pathway. According to rescue assays, NFE2L1 could involve in SLCO4A1‐AS1‐mediated LUAD cell growth. Conclusively, our study demonstrated that SLCO4A1‐AS1 facilitated cell growth and enhanced the resistance of LUAD cells to chemotherapy via activating WNT pathway through miR‐4701‐5p/NFE2L1 axis.

Abstract Background Mediastinal teratoma is a rare disease, many cases were reported before, but few articles focus on large case analyses. The objective of this article is to summarize the clinical characteristics of benign mediastinal teratoma and the experience of surgical treatment, especially thoracoscopic surgery for benign mediastinal teratoma. Methods The clinical data of 108 patients with benign mediastinal teratoma confirmed by operation and pathology from January 1992 to January 2018 were analyzed retrospectively. The clinical symptoms, imaging examination, surgical methods and prognosis of all patients were analyzed. We compared the difference of thoracoscopic surgery and thoracotomy surgery using 102 patients underwent only chest surgery. Normally distributed continuous variables were compared by independent sample t test. Categorical variables were analyzed by chi-square test. Results Imaging examination showed that all 108 cases of mediastinal teratoma were located in the anterior region of mediastinum. All cases underwent surgical resection, postoperative pathology confirmed that all cases were benign. 1 case was taken simple neck collar incision, 5 case was taken median thoracotomy combined with neck incision, other 102 cases were taken thoracoscopic surgery (22) or thoracotomy surgery (80). 4 cases were treated with partial pericardial resection due to adhesions, 12 cases underwent partial pericardial resection, 5 cases underwent lobectomy, 9 cases underwent wedge resection of lobe, and 2 patients underwent anonymous vein angioplasty. 1 case underwent second operation because of postoperative bleeding, 1 case of chylothorax, 1 case of recurrent laryngeal nerve injury, 2 cases of wound infection, 1 case of secondary pulmonary infection. 106 cases were followed up, period from 12 months to 10 years, no recurrence of tumor was found. Comparing to take thoracotomy surgery, patients underwent thoracoscopic surgery has strong advantage on intraoperative blood loss and hospital stay days after surgery (P

Ischemia-reperfusion injury is a common early complication after lung transplantation. It was reported that long non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is involved in ischemia-reperfusion injury and regulates inflammation. This study aimed to explore the role of MALAT1 in inflammatory injury following lung transplant ischemia-reperfusion (LTIR). A LTIR rat model was successfully established, with the expression of MALAT1 and interleukin-8 (IL-8) in lung tissues detected. Then, in vitro loss- and gain-of-function investigations were conducted to evaluate the effect of MALAT1 on pulmonary epithelial cell apoptosis and IL-8 expression. The relationship among MALAT1, p300, and IL-8 was tested. Moreover, a sh-MALAT1-mediated model of LTIR was established in vivo to examine inflammatory injury and chemotaxis infiltration. Both IL-8 and MALAT1 were highly expressed in LTIR. MALAT1 interacted with p300 to regulate the IL-8 expression by recruiting p300. Importantly, silencing of MALAT1 inhibited the chemotaxis of neutrophils by downregulating IL-8 expression via binding to p300. Besides, MALAT1 silencing alleviated the inflammatory injury after LTIR by downregulating IL-8 and inhibiting infiltration and activation of neutrophils. Collectively, these results demonstrated that silencing of MALAT1 ameliorated the inflammatory injury after LTIR by inhibiting chemotaxis of neutrophils through p300-mediated downregulation of IL-8, providing clinical insight for LTIR injury. Keywords: lung transplant ischemia-reperfusion, long non-coding RNA, metastasis-associated lung adenocarcinoma transcript 1, interleukin-8, p300, chemotaxis of neutrophils, pulmonary epithelial cells, inflammatory injury, H3K27 acetylation

Purpose: To determine the incidence and risk factors of bleeding events as well as assess the performance of the PRECISE-DAPT score in elderly patients (≥75 years) who underwent percutaneous coronary intervention (PCI) and one-year dual antiplatelet therapy (DAPT).Methods: A total of 940 patients (≥75 years) who received PCI and one-year DAPT were retrospectively enrolled into the study. The multivariable logistic regression analysis was conducted to identify risk factors of antiplatelet-related bleeding complications. The receiver operating characteristic (ROC) curve analysis and the Delong test were performed to obtain the optimized PRECISE-DAPT score.Results: It was observed that 89 (9.47%) patients suffered bleeding complications, while 37 (3.94%) of them had the Bleeding Academic Research Consortium (BARC, type ≥2) bleeding events. We stratified the PRECISE-DAPT score in tertiles (T1: ≤23; T2:24 to 32; T3: ≥33) and found that BARC ≥ 2 type bleeding occurred more frequently in T3 than in T1 and T2 (8.25 vs. 1.46% vs. 2.40%, p

Nitrogen (N) plays an important role in the growth cycle of the potato, and is an important guarantee of yield and quality. Rational N application is one of the key ways to improve a crop’s high and stable yield and economic and environmental benefits. The N nutrition level of potato regulates the gene expression of enzymes related to the N metabolism pathway, which shows the change of the activity of key enzymes in N metabolism, and finally realizes the regulation of N absorption and utilization. In this study, the key enzyme genes and enzyme activity of different genotypes of potato under different N supply treatments were identified, which laid a foundation for further exploration of the functions of each gene in the potato N metabolism pathway and provided theoretical basis for rational N application. The results showed that the relative expression levels of StNRT1.5, StNR, StNiR in leaves, StNRT2.5, StNRT2.4, StGS1-2 in roots and StNRT2.7, StGS1-3, StGS2, StGS1-4, StFd-GOGAT in leaves and roots showed that the levels of N-inefficient potato Atlantic (A) were higher than the N-efficient potato Yanshu 4 (Y), while the relative expression levels of StNRT2.5, StGS1-2 in leaves, StNRT1.5StNR, StNiR in roots and StGDH, StNADH-GOGAT in leaves and roots showed that levels in Yanshu 4 (Y) were higher than in Atlantic (A). At the same time, we especially found that the GDH activity in the leaves of the two genotypes of potato were higher at low N levels. Additionally, the activity of NR and NiR, and the activity of GS and GOGAT were correlated. In addition, the changes of key enzymes in different N metabolism showed a certain continuity with the advancement of growth and development, and some gene expression rules and enzyme activity changes also showed a certain consistency.

Abstract Background To investigate the early diagnostic and prognostic value of microRNA-1 in patients with acute chest pain. Methods This study enrolled 341 patients attacked by chest pain within 3 h, and another 100 volunteers as control group. Circulating microRNA-1 was collected and determined by real-time quantitative reverse transcription-polymerase chain reaction. The clinical follow-up period was 720 days. Results There were 174 patients in acute myocardial infarction (AMI) group, 167 in non-AMI group. The relative expression of microRNA-1 was significantly increased within 3 h in AMI group, and it continued rising within 12 h, lower at 24 h than that 12 h in AMI group without reperfusion therapy. Otherwise, microRNA-1 concentration was markedly low at 12 h after primary percutaneous coronary intervention in AMI group. The 95% reference range of circulating microRNA-1 was 0.171–0.653. It was significantly available for microRNA-1 to early diagnose AMI with an optimal cutoff value of 2.215 and diagnostic accuracy could be improved when combined with cardiac troponin I. It was not statistically significant for microRNA-1 to forecast future AMI but might prognose mortality of 720 days in chest pain patients. In patients with chest pain, microRNA-1 concentration was high with major adverse cardiac events within 30 days, low with high overall survival within 720 days. Conclusions Circulating microRNA-1 might diagnose early AMI and predict the prognosis of patients with chest pain.

Nitrogen (N2) is the most important source of mineral N for plant growth, which was mainly transported by nitrate transporters (NRTs). However, little is known about the NRT gene family in potato. In this study, StNRT gene family members were identified in potato. In addition, we performed StNRT subfamily classification, gene structure and distribution analysis, and conserved domain prediction using various bioinformatics tools. Totally, 39 StNRT gene members were identified in potato genome, including 33, 4 and 2 member belong to NRT1, NRT2, and NRT3, respectively. These 39 StNRT genes were randomly distributed on all chromosomes. The collinearity results show that StNRT members in potato are closely related to Solanum lycopersicum and Solanum melongena. For the expression, different members of StNRT play different roles in leaves and roots. Especially under sufficient nitrogen conditions, different members have a clear distribution in different tissues. These results provide valuable information for identifying the members of the StNRT family in potato and could provide functional characterization of StNRT genes in further research.

Background: Growing evidence from studies elsewhere have illustrated that microRNAs (miRNAs) play important roles in polymyositis and dermatomyositis (PM/DM). However, little has been reported on their relationship with regenerating islet-derived protein 3-alpha (REG3A) as well as their associative roles in macrophage migration. Therefore, this study sought to establish the association between miR-146a and REG3A as well as investigate their functional roles in macrophage migration and PM/DM pathogenesis.Methods: Peripheral blood mononuclear cells (PBMCs) were isolated from PM/DM patients and healthy controls through density centrifugation. Macrophages were obtained from monocytes purified from PBMCs via differentiation before their transfection with miRNA or plasmids to investigate cell migration with transwell assay. An experimental autoimmune myositis murine model was used to investigate PM/DM. Real-time PCR and Western blot analysis were conducted to determine the expression levels of miR-146a, interferon gamma (IFN-γ), interleukin (IL)-17A, and REG3A.Results: The messenger RNA (mRNA) expression level of miR-146a markedly decreased, while the mRNA level of REG3A, IFN-γ, and IL-17A expression increased substantially in PBMCs from PM/DM patients compared with the healthy controls. The levels of IFN-γ and IL-17A in serum from PM/DM patients was much higher than the healthy controls. Immunohistochemistry analysis showed that REG3A expression increased in muscle tissues from patients. Consistent with clinical data, the mRNA expression level of miR-146a also decreased, whereas the mRNA and protein level of REG3A, IFN-γ, and IL-17A significantly increased in the muscle tissues of experimental autoimmune myositis mice. Moreover, miR-146a inhibited monocyte-derived macrophage migration, and REG3A promoted macrophage migration. In addition, IL-17A induced REG3A expression, while miR146a inhibited expression of REG3A in monocyte-derived macrophages from the PBMCs of the healthy donors. Notably, inhibition of macrophage migration by miR-146a was via the reduction in REG3A expression.Conclusions: Reduced miR-146a expression in PM/DM leads to increased REG3A expression that increases inflammatory macrophage migration, which may be a possible underlying mechanism of DM/PM pathogenesis.

Background: Primary graft dysfunction (PGD) is a known acute lung injury (ALI) and a major cause of fatality post-lung transplantation. Though some long non-coding RNAs (lncRNAs) have been studied in ALI through regulation of microRNAs (miRNAs), their effects on PGD remain undefined. The present study aims to explore the underlying mechanism of lncRNA X-inactive specific transcript (XIST) in PGD after lung transplantation. Methods: Initially, the expression of miR-21, IL-12A and XIST was determined by RT-qPCR and western blot analysis. The dual luciferase reporter assay, RNA pull-down and RIP assay were performed to identify the targeting relationship between miR-21 and IL-12A and the binding relationship between miR-21 and XIST. Loss- and gain-of-function investigations were conducted in rats treated with prolonged cold ischemia and polymorphonuclear neutrophils (PMNs). Findings: miR-21 was decreased, whilst XIST and IL-12A were increased in the bronchoalveolar lavage fluid of PGD patients after lung transplantation. Enhanced miR-21 expression in rats and PMNs resulted in downregulated expression of pro-inflammatory factors and chemokines, and enhanced the apoptosis of PMNs. XIST was found to upregulate IL-12A expression in a miR-21-dependent manner. Additionally, XIST silencing enhanced the apoptosis of PMNs and inhibited the neutrophil extracellular trap (NET) formation through upregulation of miR-21 but downregulation of IL-12A in vivo. Interpretation: In summary, lncRNA XIST upregulates IL-12A by binding to miR-21, thereby inducing NET formation and accelerating PGD after lung transplantation. This suggests that inhibition of XIST and NET may be beneficial for the treatment of PGD. Keywords: Long non-coding RNA, X-inactive specific transcript, Primary graft dysfunction, Interleukin-12A, MicroRNA-21, Neutrophil extracellular trap, Competing endogenous RNA

The immunosuppressive role of regulatory T (Treg) cells largely depends on their virtue of expressing the transcription factor FOXP3. Here the authors show that the E3 deubiquitinase USP21 stabilizes FOXP3 by mediating its deubiquitination and helps to maintain the expression of Treg signature genes and Treg lineage stability in mice.

Non–small cell lung cancer is one of the most common types of cancer, and the prognosis of non–small cell lung cancer is still poor. Recent evidence has proved that long noncoding RNA is involved in tumorigenesis. For non–small cell lung cancer, the expression profile of long noncoding RNA has been studied. Here, we identified a novel long noncoding RNA TRPM2-AS from published dataset and found TRPM2-AS is widely upregulated in non–small cell lung cancer tissues compared with adjacent non-tumor tissues. Higher expression level of TRPM2-AS was correlated with higher TNM stages and larger tumor size. Patients with high TRPM2-AS expression level had poor survival than those with low TRPM2-AS level. We silenced TRPM2-AS by small interfering RNA and found that cell proliferation was significantly inhibited after knockdown of TRPM2-AS. Annexin V/propidium iodide staining and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay confirmed that cell apoptosis increased after TRPM2-AS knockdown. Further experiments showed that silence of TRPM2-AS upregulated SHC1 and silence of SHC1 partially reversed cell apoptosis after TRPM2-AS knockdown. In summary, the novel long noncoding RNA TRPM2-AS upregulated in non–small cell lung cancer, and downregulation of TRPM2-AS promotes apoptosis in vitro.