Publications by authors named "Shun Xu"

124 Publications

CircRNA_141539 can serve as an oncogenic factor in esophageal squamous cell carcinoma by sponging miR-4469 and activating CDK3 gene.

Aging (Albany NY) 2021 Jan 27;13. Epub 2021 Jan 27.

Department of Thoracic Surgery, The First Affiliated Hospital of China Medical University, He-Ping, Shen-Yang 110001, Liao-Ning Province, China.

The abnormal expression and regulation of circular RNA (circRNA) is involved in the occurrence and development of a variety of tumors. The current study aimed to determine the role of circRNA_141539 in esophageal squamous cell carcinoma (ESCC). CircRNA_141539 expression in ESCC was detected via circRNA chip analysis and verified via reverse transcription-quantitative PCR. Associations between circRNA_141539, patient clinicopathological characteristics and prognosis were also statistically analyzed. Additionally, the effects of circRNA_141539 on ESCC cell proliferation and invasion were assessed. A dual-luciferase assay was performed to analyze the interaction between circRNAs, microRNAs (miRs) and mRNAs. The results revealed that circRNA_141539 was significantly up-regulated in patients with ESCC. Furthermore, high circRNA_141539 expressions were significantly associated with TNM stage, differentiation and poor prognosis, revealing high diagnostic value (P<0.05). Furthermore, circRNA_141539 overexpression promoted cell proliferation and invasion, while circRNA_141539 silencing inhibited cell proliferation and invasion (P<0.05). The dual-luciferase reporter assay identified that circRNA_141539 directly binds to miR-4469 and also revealed that cyclin-dependent kinase-3 (CDK3) was negatively regulated by miR-4469. The results indicated that circRNA_141539 served as an oncogenic factor in ESCC by sponging miR-4469 and activating CDK3 expression. circRNA_141539 may present as a novel diagnostic and prognostic biomarker and a therapeutic target for patients with ESCC.
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http://dx.doi.org/10.18632/aging.103071DOI Listing
January 2021

Expert Consensus on Clinical Practice of Burn Units in Shanghai during the COVID-19 Epidemic.

J Burn Care Res 2021 Jan 23. Epub 2021 Jan 23.

Department of Burn Surgery, Changhai Hospital, Navy Military Medical University, Shanghai, China.

In response to coronavirus disease (COVID-19), the Shanghai Burn Clinical Quality Control Center organized experts to formulate and implement a set of rapid, simple, and effective prevention and control measures, and there have not been any cases of healthcare professionals or inpatients in burn units suspected or confirmed with COVID-19. This article elaborates on the specific measures in burn units in response to the epidemic, including the implementation of standardized procedures, remote consultations, strengthened follow-up, exchange of experience, and popular science, among others. We share experience from Shanghai to benefit related disciplines in other countries and regions.
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http://dx.doi.org/10.1093/jbcr/irab010DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7928907PMC
January 2021

CD73 alleviates GSDMD-mediated microglia pyroptosis in spinal cord injury through PI3K/AKT/Foxo1 signaling.

Clin Transl Med 2021 Jan;11(1):e269

Department of Orthopedics, Shanghai Fifth People's Hospital, Fudan University, Shanghai, China.

Background: Neuroinflammation-induced secondary injury is an important cause of sustained progression of spinal cord injury. Inflammatory programmed cell death pyroptosis executed by the pore-forming protein gasdermin D (GSDMD) is an essential step of neuroinflammation. However, it is unclear whether CD73, a widely accepted immunosuppressive molecule, can inhibit pyroptosis via mediating GSDMD.

Methods: C57BL/6J CD73 deficient mice and wild-type mice, Lipopolysaccharide (LPS)-induced primary microglia and BV2 cells were respectively used to illustrate the effect of CD73 on microglia pyroptosis in vivo and in vitro. A combination of molecular and histological methods was performed to assess pyroptosis and explore the mechanism both in vivo and in vitro.

Results: We have shown molecular evidence for CD73 suppresses the activation of NLRP3 inflammasome complexes to reduce the maturation of GSDMD, leading to decreased pyroptosis in microglia. Further analysis reveals that adenosine-A adenosine receptor-PI3K-AKT-Foxo1 cascade is a possible mechanism of CD73 regulation. Importantly, we determine that CD73 inhibits the expression of GSDMD at the transcriptional level through Foxo1. What's more, we confirm the accumulation of HIF-1α promotes the overexpression of CD73 after spinal cord injury (SCI), and the increased CD73 in turn upregulates the expression of HIF-1α, eventually forming a positive feedback regulatory loop.

Conclusion: Our data reveal a novel function of CD73 on microglia pyroptosis, suggesting a unique therapeutic opportunity for mitigating the disease process in SCI.
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http://dx.doi.org/10.1002/ctm2.269DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7774461PMC
January 2021

Advances in Risk Factors for Recurrence of Common Bile Duct Stones.

Int J Med Sci 2021 1;18(4):1067-1074. Epub 2021 Jan 1.

Sir Run Run Hospital, Nanjing Medical University, Nanjing, 211100, China.

Choledocholithiasis is a chronic common disease. The incidence of cholelithiasis is 5%-15%, of which 5%-30% are combined with Choledocholithiasis. Although endoscopic cholangiopancreatography (ERCP) + endoscopic sphincterotomy (EST) is the most common treatment procedure, which clearance rate is up to 95%, the incidence of recurrent choledocholithiasis was 4%-25%. The risk factors of recurrence after choledocholithiasis clearance are the focuses of current researches, which are caused by multiple factors. We first systematically summarize the risk factors of common bile duct stones (CBDS) recurrence into five aspects: first-episode stone related factors, congenital factors, biological factors, behavioral intervention factors, and the numbers of stone recurrence.
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http://dx.doi.org/10.7150/ijms.52974DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7807200PMC
January 2021

Gefitinib Versus Vinorelbine Plus Cisplatin as Adjuvant Treatment for Stage II-IIIA (N1-N2) EGFR-Mutant NSCLC: Final Overall Survival Analysis of CTONG1104 Phase III Trial.

J Clin Oncol 2021 Mar 17;39(7):713-722. Epub 2020 Dec 17.

Guangdong Lung Cancer Institute, Guangdong Provincial People's Hospital, and Guangdong Academy of Medical Sciences, Guangzhou, China.

Purpose: ADJUVANT-CTONG1104 (ClinicalTrials.gov identifier: NCT01405079), a randomized phase III trial, showed that adjuvant gefitinib treatment significantly improved disease-free survival (DFS) versus vinorelbine plus cisplatin (VP) in patients with epidermal growth factor receptor () mutation-positive resected stage II-IIIA (N1-N2) non-small-cell lung cancer (NSCLC). Here, we report the final overall survival (OS) results.

Methods: From September 2011 to April 2014, 222 patients from 27 sites were randomly assigned 1:1 to adjuvant gefitinib (n = 111) or VP (n = 111). Patients with resected stage II-IIIA (N1-N2) NSCLC and -activating mutation were enrolled, receiving gefitinib for 24 months or VP every 3 weeks for four cycles. The primary end point was DFS (intention-to-treat [ITT] population). Secondary end points included OS, 3-, 5-year (y) DFS rates, and 5-year OS rate. Post hoc analysis was conducted for subsequent therapy data.

Results: Median follow-up was 80.0 months. Median OS (ITT) was 75.5 and 62.8 months with gefitinib and VP, respectively (hazard ratio [HR], 0.92; 95% CI, 0.62 to 1.36; = .674); respective 5-year OS rates were 53.2% and 51.2% ( = .784). Subsequent therapy was administered upon progression in 68.4% and 73.6% of patients receiving gefitinib and VP, respectively. Subsequent targeted therapy contributed most to OS (HR, 0.23; 95% CI, 0.14 to 0.38) compared with no subsequent therapy. Updated 3y DFS rates were 39.6% and 32. 5% with gefitinib and VP ( = .316) and 5y DFS rates were 22. 6% and 23.2% ( = .928), respectively.

Conclusion: Adjuvant therapy with gefitinib in patients with early-stage NSCLC and mutation demonstrated improved DFS over standard of care chemotherapy. Although this DFS advantage did not translate to a significant OS difference, OS with adjuvant gefitinib was one of the longest observed in this patient group compared with historic data.
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http://dx.doi.org/10.1200/JCO.20.01820DOI Listing
March 2021

Quality of life with adjuvant gefitinib versus vinorelbine plus cisplatin in patients with completely resected stage II-IIIA (N1-N2) EGFR-mutant non-small-cell lung cancer: Results from the ADJUVANT (CTONG1104) study.

Lung Cancer 2020 12 8;150:164-171. Epub 2020 Oct 8.

Department of Thoracic Surgery, The First Affiliated Hospital of Suzhou University, Suzhou, China.

Objectives: Health-related quality of life (HRQoL) data complement conventional clinical endpoints when comparing adjuvant gefitinib with chemotherapy in patients with early-stage non-small-cell lung cancer (NSCLC) and epidermal growth factor receptor (EGFR) mutations. This study aimed to assess changes in HRQoL with adjuvant gefitinib vs chemotherapy in this patient group.

Materials And Methods: In the phase III ADJUVANT trial, patients with completely resected, stage II-IIIA (N1-N2), EGFR-mutant NSCLC were randomized (1:1) to receive either gefitinib for 24 months or vinorelbine plus cisplatin (VP) every 3 weeks for four cycles. HRQoL was assessed as a secondary endpoint using the Functional Assessment of Cancer Therapy-Lung Cancer (FACT-L), Lung Cancer Symptom Scale (LCSS) questionnaires, and Trial Outcome Index (TOI) composite score. HRQoL dynamics, improvements, and time to deterioration were compared between groups.

Results: At baseline, 104 of 106, and 80 of 87 patients receiving gefitinib and VP, respectively, completed two questionnaires (FACT-L and LCSS). Baseline scores were balanced between groups. Although HRQoL fluctuated and gradually improved in both groups, longitudinally higher scores were reported with gefitinib than VP (FACT-L, odds ratio 418.16, 95 % confidence interval [CI] 2.75-63509.05, p =  0.019; LCSS, 1.13, 1.04-1.22, p =  0.003; TOI, 88.39, 4.40-1775.05, p =  0.003). Time to deterioration in HRQoL was delayed with gefitinib compared with VP (FACT-L, median 69 vs 6 weeks, hazard ratio 0.62, 95 % CI 0.42-0.90, p =  0.013; LCSS, median 45 vs 6 weeks, 0.63, 0.43-0.93, p =  0.020; TOI, median 164 vs 9 weeks, 0.51, 0.33-0.77, p =  0.001).

Conclusion: Adjuvant gefitinib is associated with improved HRQoL over VP, supporting its use in patients with stage II-IIIA (N1-N2), EGFR-mutant NSCLC.
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http://dx.doi.org/10.1016/j.lungcan.2020.09.027DOI Listing
December 2020

Sarcopenia affects clinical efficacy of immune checkpoint inhibitors in non-small cell lung cancer patients: A systematic review and meta-analysis.

Int Immunopharmacol 2020 Nov 18;88:106907. Epub 2020 Sep 18.

Department of Thoracic Surgery, The First Hospital of China Medical University, No.155, North Nanjing Street, Shenyang 110001, Liaoning, China. Electronic address:

Background: The clinical impact of sarcopenia on the immune checkpoint inhibitor's (ICI) efficacy and immune-related adverse events in non-small cell lung cancer (NSCLC) patients is unclear. Therefore, the purpose of this study is to evaluate the association between sarcopenia and clinical outcomes of ICI immunotherapy.

Methods: A systematic literature search of PubMed, Embase, Cochrane CENTRAL, and conference databases was conducted for the relevant studies. The primary outcomes were progression-free survival (PFS) and overall survival (OS) measured by hazard ratio (HR) with 95% confidence interval (CI), and the secondary outcomes were disease control rate, overall response rate, and immune-related adverse events measured by relative risk (RR) with 95% CI. Subgroup and sensitivity analysis were performed.

Results: Pre-immunotherapy sarcopenia was significantly associated with worse OS (HR = 1.61, 95% CI = 1.24-2.10) and PFS (HR = 1.98, 95% CI = 1.32-2.97). Development or worsening of sarcopenia during immunotherapy also predicted worse OS and PFS. Both pre-immunotherapy sarcopenia (RR = 0.70, 95% CI = 0.56-0.86) and development or worsening of sarcopenia (RR = 0.62, 95% CI = 0.40-0.96) resulted in a lower disease control rate. Sarcopenia tended toward a lower overall response rate, although there was no significant difference (RR = 0.54, 95% CI = 0.19-1.53). Moreover, sarcopenia did not increase immune-related adverse events (RR = 0.99, 95% CI = 0.21-4.67).

Conclusion: Sarcopenia was associated with worse treatment response and shorter long-term efficacy in NSCLC patients treated with ICI immunotherapy. Moreover, sarcopenia does not increase the rate of immune-related adverse events.
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http://dx.doi.org/10.1016/j.intimp.2020.106907DOI Listing
November 2020

[Erratum] circRNA_001275 upregulates Wnt7a expression by competitively sponging miR‑370‑3p to promote cisplatin resistance in esophageal cancer.

Int J Oncol 2020 Dec 21;57(6):1382. Epub 2020 Oct 21.

Department of Thoracic Surgery, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning 11000, P.R. China.

Following the publication of the above article, the authors have realized that certain intended corrections were not carried over to the published version of the article. First, the description of the results of Figs. 5 and 6 did not match the figures; Edu and Transwell invasion assays were intended to have been excluded from the manuscript during the proofreading stage, although these data were presented in the description of the results for Figs. 5 and 6. Consequently, the text for the "circRNA_001275 promotes cell proliferation" subsection of the Results section towards the end of p. 153 should have read as follows: "MTT assay was used to detect the effects of circRNA_001275 on cell proliferation. The results showed that cell viability was significantly increased in the circRNA_001275 OE group, and significantly decreased in the si circRNA_001275 group (both P<0.05, Fig. 5A and B), compared with the corresponding control groups." Furthermore, the text in the subsequent subsection ("circRNA_001275 inhibits cell apoptosis") should have read as follows: "Hoechst 33258 staining was used to detect the effects of circRNA_001275 on apoptosis. The apoptosis rate was significantly decreased in the circRNA_001275 OE group, and significantly increased in the si circRNA_001275 group (both P<0.05; Fig. 6), compared with the corresponding control group. Secondly, Fig. 5B was omitted from Fig. 5 in the published article; and thirdly, a higher‑resolution version of Fig. 6 was submitted during the revision stages, although the version of this figure that was deemed to have been too low in quality was the one that appeared in the final proofs. The corrected / updated versions of Figs. 5 and 6 are shown opposite. The Editor of International Journal of Oncology regrets that certain of these errors were introduced into the article during the production stages, and apologizes both to the authors and to the readership. [the original article was published in International Journal of Oncology 57: 151‑160, 2020; DOI: 10.3892/ijo.2020.5050].
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http://dx.doi.org/10.3892/ijo.2020.5137DOI Listing
December 2020

Unprecedented Uniform 3D Growth Integration of 10-Layer Stacked Si Nanowires on Tightly Confined Sidewall Grooves.

Nano Lett 2020 Oct 1;20(10):7489-7497. Epub 2020 Oct 1.

National Laboratory of Solid State Microstructures/School of Electronics Science and Engineering/Collaborative Innovation Centre of Advanced Microstructures, Nanjing University, 210093 Nanjing, P. R. China.

Bottom-up catalytic growth offers a high-yield, versatile, and powerful tool for the construction of versatile 3D nanocomplexes, while the major challenge is to achieve a precise location and uniformity control, as guaranteed by top-down lithography. Here, an unprecedented uniform and reliable growth integration of 10-layer stacked Si nanowires (SiNWs) has been accomplished, for the very first time, via a new groove-confined and tailored catalyst formation and guided growth upon the truncated sidewall of SiO/SiN multilayers. The SiNW array accomplishes a narrow diameter of = 28 ± 2.4 nm, NW-to-NW spacing of = 40 nm, and extremely stable growth over > 50 μm and bending locations, which can compete with or even outperform the top-down lithography and etching approaches, in terms of stacking number, channel uniformity at different levels, fabrication cost, and efficiency. These results provide a solid basis to establish a new 3D integration approach to batch-manufacture various advanced electronic and sensor applications.
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http://dx.doi.org/10.1021/acs.nanolett.0c02950DOI Listing
October 2020

Long non‑coding RNA LUCAT1 contributes to cisplatin resistance by regulating the miR‑514a‑3p/ULK1 axis in human non‑small cell lung cancer.

Int J Oncol 2020 Oct 7;57(4):967-979. Epub 2020 Aug 7.

Department of Thoracic Surgery, The First Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China.

Drug resistance is a major obstacle in the therapy of malignant tumors, including non‑small cell lung cancer (NSCLC). Long non‑coding RNAs (lncRNAs) have been demonstrated to be involved in chemoresistance. The present study aimed to investigate the role of lung cancer‑associated transcript 1 (LUCAT1) in cisplatin (DDP) resistance in NSCLC. By using reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR), it was found that the expression of LUCAT1 was elevated and that of microRNA‑514a‑3p (miR‑514a‑3p) was decreased in DDP‑resistant NSCLC tissues and cells. Functionally, LUCAT1 upregulation enhanced cisplatin resistance by promoting the viability, autophagy and metastasis, and inhibiting the apoptosis of NSCLC cells, as demonstrated by Cell Counting kit‑8 (CCK‑8) assay, western blot analysis, Transwell assay and flow cytometric analysis. LUCAT1 was identified as a sponge of miR‑514a‑3p and uncoordinated‑51‑like kinase 1 (ULK1) was proven to be a target gene of miR‑514a‑3p by bioinformatics analysis, dual‑luciferase reporter assay and RNA immunoprecipitation (RIP) assay. The enhancing effect of miR‑514a‑3p on cisplatin sensitivity was reversed by the elevation of LUCAT1. ULK1 knockdown suppressed cisplatin resistance, while this effect was attenuated by miR‑514a‑3p inhibition. Moreover, LUCAT1 positively regulated ULK1 expression by targeting miR‑514a‑3p. In addition, LUCAT1 knockdown suppressed tumor growth in vivo. On the whole, the findings of the present study demonstrate that LUCAT1 contributes to the resistance of NSCLC cells to cisplatin by regulating the miR‑514a‑3p/ULK1 axis, elucidating a novel regulatory network in cisplatin resistance in NSCLC.
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http://dx.doi.org/10.3892/ijo.2020.5106DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7473752PMC
October 2020

LINC01503/miR-342-3p facilitates malignancy in non-small-cell lung cancer cells via regulating LASP1.

Respir Res 2020 Sep 16;21(1):235. Epub 2020 Sep 16.

Thoracic Surgery, The First Hospital of China Medical University, No.155 North Nanjing Road, Heping Area, Shenyang, 110001, China.

Background: Non-small cell lung cancer (NSCLC) is one of the major types of lung cancer, which is a prevalent human disease all over the world. LncRNA LINC01503 is a super-enhancer-driven long non-coding RNA that is dysregulated in several types of human cancer. However, its role in NSCLC remains unknown.

Methods: Thirty NSCLC patients were recruited between April 2012 and April 2016. Luciferase reporter assay, qRT-PCR, Cell Counting Kit-8 (CCK-8), Transwell migration assay, RNA pull-down assay, western blotting, 5-ethynyl-29-deoxyuridine (EdU) assays, and flow cytometry were utilized to characterize the roles and relationships among LINC01503, miR-342-3p, and LASP1 in NSCLC. The transplanted mouse model was built to examine their biological functions in vivo.

Results: We demonstrated that the expression of lncRNA LINC01503 and LIM and SH3 domain protein 1 (LASP1) were upregulated and miR-342-3p was downregulated in NSCLC samples and cell lines. Functional experiments revealed that inhibiting the expression of LINC01503 or over-expression of miR-342-3p inhibited NSCLC growth and metastasis both in vitro and in vivo. In addition, LINC01503 could bind to miR-342-3p and affect the expression of LASP1.

Conclusion: These results provide a comprehensive analysis of the roles of LINC01503 as a competing endogenous RNA (ceRNA) in NSCLC progression.
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http://dx.doi.org/10.1186/s12931-020-01464-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7493870PMC
September 2020

Role of major histocompatibility complex II antigen-presentation pathway genes in orange-spotted grouper infected with Cryptocaryon irritans.

J Fish Dis 2020 Dec 13;43(12):1541-1552. Epub 2020 Sep 13.

School of Biology and Biological Engineering, Guangzhou Higher Education Mega Center, South China University of Technology, Guangzhou, China.

Cryptocaryon irritans, a pathogen model for fish mucosal immunity, causes skin mucosal and systematic humoral immune response. Where and how MHC II antigen presentation occurs in fish infected with C. irritans remain unknown. In this study, the full-length cDNA of the grouper cysteine protease CTSS was cloned. The expression distributions of six genes (CTSB, CTSL, CTSS, GILT, MHC IIA and MHC IIB) involved in MHC II antigen presentation pathway were tested. These genes were highly expressed in systematic immune tissues and skin and gill mucosal-associated immune tissues. All six genes were upregulated in skin at most time points. Five genes expected CTSS was upregulated in spleen at most time points. CTSB, CTSL and MHC IIA were upregulated in the gill and head kidney at some time points. These results indicate that the presentation of MHC II antigen intensively occurred in local infected skin and gill. Spleen, not head kidney, had the most extensive systematic antigen presentation. In skin, six genes most likely peaked at day 2, earlier than in spleen (5-7 days), marking an earlier skin antibody peak than any recorded in serum previously. This significant and earlier mucosal antigen presentation indicates that specific immune response occurs in local mucosal tissues.
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http://dx.doi.org/10.1111/jfd.13256DOI Listing
December 2020

Advances in personalized neoantigen vaccines for cancer immunotherapy.

Authors:
Changbo Sun Shun Xu

Biosci Trends 2020 Nov 10;14(5):349-353. Epub 2020 Sep 10.

Department of Thoracic Surgery, the First Hospital of China Medical University, Shenyang, Liaoning, China.

Immunotherapy, which targets T cell inhibitory receptors (immune checkpoints), is now being widely used to treat a variety of types of cancer combined with surgery, chemotherapy, or radiotherapy. However, immune checkpoint inhibitors are highly dependent on the ability to present diverse tumor antigens to T cells. Neoantigens, arising from somatic mutations and specifically targeting tumor cells, have the potential to stimulate a highly specific immune anti-tumor response. Technological advances such as genomic sequencing and bioinformatics algorithms for epitope prediction have directly facilitated the development of neoantigen vaccines for individual cancers. Currently, several preclinical studies and early clinical trials using neoantigen in combination with checkpoint inhibitors have resulted in robust T cell responses and antitumor action. In the future, efforts will be made to optimize effective personalized neoantigen vaccines targeting individual tumors and to elucidate the immune mechanisms underlying tumor evolution.
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http://dx.doi.org/10.5582/bst.2020.03267DOI Listing
November 2020

Immune Checkpoint Inhibitor Therapy Achieved Complete Response for Drug-Sensitive Mutation-Negative Metastatic Pulmonary Large-Cell Neuroendocrine Carcinoma with High Tumor Mutation Burden: A Case Report.

Onco Targets Ther 2020 19;13:8245-8250. Epub 2020 Aug 19.

The Department of Thoracic Surgery, The First Hospital of China Medical University, Shenyang 110001, Liaoning Province, People's Republic of China.

Large-cell neuroendocrine lung carcinoma (LCNELC) is classified into lung neuroendocrine tumors according to WHO 2015 classification guidelines and represents approximately 3% of all lung cancer. Because of the rarity of LCNELC, there is a lack of prospective studies guiding treatment. Here, we report a case of a patient with pT2aN2M0 stage IIIA LCNELC (drug-sensitive EGFR/ALK mutation-negative, PD-L1-negative but tumor mutation burden (TMB) high), who progressed rapidly after surgery but achieved a complete response to subsequent immune checkpoint inhibitor (ICI) therapy. The concentration of circulating tumor DNA (ctDNA) following the treatment course strongly reflects the response to ICI therapy. This report highlights the efficacy of ICI treatment in metastatic LCNELC patients with a high TMB and suggests that ctDNA analysis in detecting molecular residual disease may facilitate the personalization of ICI therapy.
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http://dx.doi.org/10.2147/OTT.S259893DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7443410PMC
August 2020

Pneumothorax in 2019 novel coronavirus pneumonia needs to be recognized.

Infection 2020 Sep 2. Epub 2020 Sep 2.

Department of Surgical Oncology, The First Hospital of China Medical University, No. 155 Nanjing North Road, Shenyang, 110001, Liaoning, China.

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http://dx.doi.org/10.1007/s15010-020-01518-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7463101PMC
September 2020

Exosome-Transported circRNA_0000253 Competitively Adsorbs MicroRNA-141-5p and Increases IDD.

Mol Ther Nucleic Acids 2020 Sep 31;21:1087-1099. Epub 2020 Jul 31.

Department of Orthopaedics, Huashan Hospital, Fudan University, Shanghai 200040, China. Electronic address:

The pathogenesis of intervertebral disc degeneration (IDD) is complex, and a better understanding of IDD pathogenesis may provide a better method for the treatment of IDD. Exosomes are 40-100 nm nanosized vesicles that are released from many cell types into the extracellular space. We speculated that exosome-transported circular RNAs (circRNAs) could regulate IDD. Exosomes from different degenerative grades were isolated and added to nucleus pulposus cells (NPCs), and indicators of proliferation and apoptosis were detected. Based on the previous circRNA microarray results, the top 10 circRNAs were selected. PCR was performed to determine the circRNA with the maximum upregulation. Competing endogenous RNA (ceRNA) analysis was carried out, and the sponged microRNA (miRNA) was identified. Further functional verification of the selected circRNA was carried out in vivo and in vitro. NPCs of different degenerative grades secreted exosomes, which could regulate IDD. circRNA_0000253 was selected as having the maximum upregulation in degenerative NPC exosomes. ceRNA analysis showed that circRNA_0000253 could adsorb miRNA-141-5p to downregulate SIRT1. circRNA_0000253 was confirmed to increase IDD by adsorbing miRNA-141-5p and downregulating SIRT1 in vivo and in vitro. Exosomal circRNA_0000253 owns the maximum upregulation in degenerative NPC exosomes and could promote IDD by adsorbing miRNA-141-5p and downregulating SIRT1.
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http://dx.doi.org/10.1016/j.omtn.2020.07.039DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7473879PMC
September 2020

TLR4 promotes microglial pyroptosis via lncRNA-F630028O10Rik by activating PI3K/AKT pathway after spinal cord injury.

Cell Death Dis 2020 08 10;11(8):693. Epub 2020 Aug 10.

Department of Orthopedics, Shanghai Fifth People's Hospital, Fudan University, Shanghai, 200240, China.

Neuroinflammation plays a crucial role in the secondary phase of spinal cord injury (SCI), and is initiated following the activation of toll-like receptor 4 (TLR4). However, the downstream mechanism remains unknown. Pyroptosis is a form of inflammatory programmed cell death, which is closely involved in neuroinflammation, and it can be regulated by TLR4 according to a recent research. In addition, several studies have shown that long non-coding RNAs (lncRNAs) based mechanisms were related to signal transduction downstream of TLR4 in the regulation of inflammation. Thus, in this study, we want to determine whether TLR4 can regulate pyroptosis after SCI via lncRNAs. Our results showed that TLR4 was activated following SCI and promoted the expression of lncRNA-F630028O10Rik. This lncRNA functioned as a ceRNA for miR-1231-5p/Col1a1 axis and enhanced microglial pyroptosis after SCI by activating the PI3K/AKT pathway. Furthermore, we determined STAT1 was the upstream transcriptional factor of IncRNA-F630028O10Rik and was induced by the damage-responsive TLR4/MyD88 signal. Our findings provide new insights and a novel therapeutic strategy for treating SCI.
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http://dx.doi.org/10.1038/s41419-020-02824-zDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7443136PMC
August 2020

Immunomodulatory Effects of -Acetyl Chitooligosaccharides on RAW264.7 Macrophages.

Mar Drugs 2020 Aug 12;18(8). Epub 2020 Aug 12.

School of Biology and Biological Engineering, South China University of Technology, Guangzhou Higher Education Mega Center, Panyu District, Guangzhou 510006, China.

The ongoing development of new production methods may lead to the commercialization of -acetyl chitooligosaccharides (NACOS), such as chitosan oligosaccharides (COS). The bioactivity of NACOS, although not well detailed, differs from that of COS, as they have more acetyl groups than COS. We used two enzymatically produced NACOS with different molecular compositions and six NACOS (NACOS1-6) with a single degree of polymerization to verify their immunomodulatory effects on the RAW264.7 macrophage cell line. We aimed to identify any differences between COS and various NACOS with a single degree of polymerization. The results showed that NACOS had similar immune enhancement effects on RAW264.7 cells as COS, including the generation of reactive oxygen species (ROS), phagocytotic activity, and the production of pro-inflammation cytokines (IL-1β, IL-6, and TNF-α). However, unlike COS and lipopolysaccharide (LPS), NACOS1 and NACOS6 significantly inhibited nitric oxide (NO) production. Besides their immune enhancement effects, NACOS also significantly inhibited the LPS-induced RAW264.7 inflammatory response with some differences between various polymerization degrees. We confirmed that the NF-κB pathway is associated with the immunomodulatory effects of NACOS on RAW264.7 cells. This study could inform the application of NACOS with varying different degrees of polymerization in human health.
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http://dx.doi.org/10.3390/md18080421DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7460392PMC
August 2020

Conditional survival rate estimates of lobectomy, segmentectomy and wedge resection for stage IA1 non-small cell lung cancer: A population-based study.

Oncol Lett 2020 Aug 9;20(2):1607-1618. Epub 2020 Jun 9.

Department of Thoracic Surgery, First Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China.

Conditional survival rate (CSR) is defined as the dynamic possibility of survival, considering the changes in the survival risk over time. The present study aimed to compare the CSR of the surgical procedures for stage IA1 non-small cell lung cancer (NSCLC). Overall, data for 2,535 patients with stage IA1 NSCLC after lobectomy, segmentectomy or wedge resection were obtained from the Surveillance, Epidemiology and End Results database, and the overall survival (OS) rates were subsequently compared. CSR estimates, the possibility of patients who had already survived × years, to survive further y years, was calculated as CSR=S(x+y)/S(x), where S is the survival rate at a particular point in time. A Cox regression model and propensity-score matching were used to adjust confounding factors. There were no statistical differences in the OS among the three surgical procedures, except that OS of patients who underwent a lobectomy was improved compared with the wedge resection. The CSR of surviving to the 5th year after operation improved gradually over time. The 3-year CSR of lobectomy or segmentectomy was higher compared with that of the wedge resection. Moreover, the 3-year CSR of segmentectomy was higher compared with that of lobectomy from the 3rd year after surgery, particularly in some specific situations, such as female sex, patients ≥66 years old, patients with squamous cell carcinoma or patients with poor tumor differentiation. The present study is the first report to compare CSR following lobectomy, segmentectomy and wedge resection for patients with stage IA1 NSCLC, to the best of our knowledge. These findings indicated that lobectomy is the most conservative surgical procedure for stage IA1 NSCLC and raises questions regarding improved long-term prognosis of segmentectomy in some subsets of patients.
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http://dx.doi.org/10.3892/ol.2020.11713DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7377117PMC
August 2020

LncRNA LINC00467 acted as an oncogene in esophageal squamous cell carcinoma by accelerating cell proliferation and preventing cell apoptosis via the miR-485-5p/DPAGT1 axis.

J Gastroenterol Hepatol 2020 Jul 27. Epub 2020 Jul 27.

Department of Thoracic Surgery, First Affiliated Hospital of China Medical University, Shenyang, China.

Background And Aim: Esophageal carcinoma has been regarded as one of the top 10 common malignancies globally. Esophageal squamous cell carcinoma (ESCC) is an important subtype of esophageal carcinoma with approximately 20% survival rate. Long noncoding RNAs were documented to regulate the occurrence or progression of several tumors. However, neither the biological role nor the molecular mechanism of LINC00467 has been explored. This research is aimed to investigating the regulatory mechanism of LINC00467 in ESCC.

Methods: In this study, a series of experiments including reverse transcription-quantitative polymerase chain reaction, Cell Counting Kit-8, luciferase reporter, western blot, and RNA immunoprecipitation were designed and conducted to explore the potential function and mechanism of LINC00467 in ESCC.

Results: According to experimental results, we found out upregulated LINC00467 improved cell proliferation, but hindered cell apoptosis. In mechanism, miR-485-5p was predicted, screened out, and validated to combine with LINC00467, which displayed lower expression in ESCC. Additionally, miR-485-5p negatively regulated and directly targeted DPAGT1. Rescue assays suggested that DPAGT1 amplification was able to recover the influence of LINC00467 deficiency on cell proliferation and apoptosis. Furthermore, knockdown of LINC00467 suppressed tumor growth in vivo.

Conclusion: We proved that LINC00467 acted as an oncogene in ESCC by accelerating cell proliferation and preventing cell apoptosis via miR-485-5p/DPAGT1 axis. This may provide a potential diagnostic marker for ESCC treatment.
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http://dx.doi.org/10.1111/jgh.15201DOI Listing
July 2020

Comparison between radiofrequency ablation and sublobar resections for the therapy of stage I non-small cell lung cancer: a meta-analysis.

PeerJ 2020 21;8:e9228. Epub 2020 May 21.

Department of Thoracic Surgery, The First Hospital of China Medical University, Shenyang, China.

Background: Sublobar resection (SLR) and radiofrequency ablation (RFA) are the two minimally invasive procedures performed for treating stage I non-small cell lung cancer (NSCLC). This study aimed to compare SLR and RFA for the treatment of stage I NSCLC using the meta-analytical method.

Methods: We searched PubMed and Embase for articles published till December 2019 to evaluate the comparative studies and assess the survival and progression-free survival rates and postoperative complications (PROSPERO registration number: CRD42018087587). A meta-analysis was performed by combining the outcomes of the reported incidences of short-term morbidity and long-term mortality. The fixed or random effects model was utilized to calculate the pooled odds ratios (OR) and the 95% confidence intervals.

Results: Four retrospective studies were considered in the course of this study. The studies included a total of 309 participants; 154 were assigned to the SLR group, and 155 were assigned to the RFA group. Moreover, there were statistically significant differences between the one- and three-year survival rates and one- and three-year progression-free survival rates for the two groups, which were in favor of the SLR group. Among the post-surgical complications, pneumothorax and pleural effusion were more common for the SLR group, while cardiac abnormalities were prevalent in the RFA group. There was no difference in prevalence of hemoptysis between SLR and RFA groups, which might be attributed to the limited study sample size.

Conclusion: Considering the higher survival rates and disease control in the evaluated cases, surgical resection is the preferred treatment method for stage I NSCLC. RFA can be considered a valid alternative in patients not eligible for surgery and in high-risk patients as it is less invasive and requires shorter hospital stay.
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http://dx.doi.org/10.7717/peerj.9228DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7246024PMC
May 2020

Endogenous thrombopoietin promotes non-small-cell lung carcinoma cell proliferation and migration by regulating EGFR signalling.

J Cell Mol Med 2020 06 26;24(12):6644-6657. Epub 2020 Apr 26.

Department of Thoracic Surgery, The First Hospital of China Medical University, Shenyang, China.

Thrombopoietin (TPO) is a haematopoietic cytokine mainly produced by the liver and kidneys, which stimulates the production and maturation of megakaryocytes. In the past decade, numerous studies have investigated the effects of TPO outside the haematopoietic system; however, the role of TPO in the progression of solid cancer, particularly lung cancer, has not been well studied. Exogenous TPO does not affect non-small-cell lung cancer (NSCLC) cells as these cells show no or extremely low TPO receptor expression; therefore, in this study, we focused on endogenous TPO produced by NSCLC cells. Immunohistochemical analysis of 150 paired NSCLC and adjacent normal tissues indicated that TPO was highly expressed in NSCLC tissues and correlated with clinicopathological parameters including differentiation, P-TNM stage, lymph node metastasis and tumour size. Suppressing endogenous TPO by small interfering RNA inhibited the proliferation and migration of NSCLC cells. Moreover, TPO interacted with the EGFR protein and delayed ligand-induced EGFR degradation, thus enhancing EGFR signalling. Notably, overexpressing TPO in EGF-stimulated NSCLC cells facilitated cell proliferation and migration, whereas no obvious changes were observed without EGF stimulation. Our results suggest that endogenous TPO promotes tumorigenicity of NSCLC via regulating EGFR signalling and thus could be a therapeutic target for treating NSCLC.
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http://dx.doi.org/10.1111/jcmm.15314DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7299695PMC
June 2020

Identification of lung adenocarcinoma biomarkers based on bioinformatic analysis and human samples.

Oncol Rep 2020 May 28;43(5):1437-1450. Epub 2020 Feb 28.

Department of Thoracic Surgery, First Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China.

Lung adenocarcinoma is one of the most common malignant tumors worldwide. Although efforts have been made to clarify its pathology, the underlying molecular mechanisms of lung adenocarcinoma are still not clear. The microarray datasets GSE75037, GSE63459 and GSE32863 were downloaded from the Gene Expression Omnibus (GEO) database to identify biomarkers for effective lung adenocarcinoma diagnosis and therapy. The differentially expressed genes (DEGs) were identified by GEO2R, and function enrichment analyses were conducted using the Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO). The STRING database and Cytoscape software were used to construct and analyze the protein‑protein interaction network (PPI). We identified 376 DEGs, consisting of 83 upregulated genes and 293 downregulated genes. Functional and pathway enrichment showed that the DEGs were mainly focused on regulation of cell proliferation, the transforming growth factor β receptor signaling pathway, cell adhesion, biological adhesion, and responses to hormone stimulus. Sixteen hub genes were identified and biological process analysis showed that these 16 hub genes were mainly involved in the M phase, cell cycle phases, the mitotic cell cycle, and nuclear division. We further confirmed the two genes with the highest node degree, DNA topoisomerase IIα (TOP2A) and aurora kinase A (AURKA), in lung adenocarcinoma cell lines and human samples. Both these genes were upregulated and associated with larger tumor size. Upregulation of AURKA in particular, was associated with lymphatic metastasis. In summary, identification of the DEGs and hub genes in our research enables us to elaborate the molecular mechanisms underlying the genesis and progression of lung adenocarcinoma and identify potential targets for the diagnosis and treatment of lung adenocarcinoma.
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http://dx.doi.org/10.3892/or.2020.7526DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7108011PMC
May 2020

circRNA_001275 upregulates Wnt7a expression by competitively sponging miR‑370‑3p to promote cisplatin resistance in esophageal cancer.

Int J Oncol 2020 Jul 22;57(1):151-160. Epub 2020 Apr 22.

Department of Thoracic Surgery, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning 11000, P.R. China.

Circular RNAs (circRNAs) are aberrantly expressed in various tumors and are associated with tumorigenesis. The present study aimed to determine the role of circRNA_001275 in cisplatin‑resistant esophageal cancer. Three pairs of cisplatin‑resistant tissues and corresponding adjacent tissues were collected and subjected to circRNA chip analysis. Additionally, the effect of circRNA_001275 on cisplatin‑resistant cells was investigated. The relationship between circRNA_001275, microRNAs (miRs) and target genes were analyzed using luciferase assays, and validated via reverse transcription‑quantitative PCR (RT‑qPCR) and western blotting. The results showed that circRNA_001275 was significantly upregulated in cisplatin‑resistant esophageal cancer tissues and cells (P<0.05). Overexpression of circRNA_001275 promoted the proliferation and invasion, and decreased the apoptosis of cisplatin‑resistant cells. On the other hand, circRNA_001275 silencing inhibited cell proliferation and invasion, and promoted cell apoptosis (P<0.05). Dual‑luciferase reporter assays revealed that circRNA_001275 directly binds to miR‑370‑3p, and that Wnt family member 7A (Wnt7a) is targeted by miR‑370‑3p. RT‑qPCR and western blotting further demonstrated that circRNA_001275 serves as an miR‑370‑3p sponge to upregulate Wnt7a expression. In conclusion, the present study revealed that circRNA_001275 was upregulated in cisplatin‑resistant esophageal cancer and promoted cisplatin resistance by sponging miR‑370‑3p to upregulate Wnt7a expression. Therefore, circRNA_001275 may serve as a potential diagnostic biomarker and therapeutic target for patients with cisplatin‑resistant esophageal cancer.
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http://dx.doi.org/10.3892/ijo.2020.5050DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7252462PMC
July 2020

Exosomes from Long Noncoding RNA-Gm37494-ADSCs Repair Spinal Cord Injury via Shifting Microglial M1/M2 Polarization.

Inflammation 2020 Aug;43(4):1536-1547

Department of Orthopedics, Huashan Hospital, Fudan University, Shanghai, 200040, China.

Spinal cord injury (SCI) may lead to severe motor and sensory dysfunction, causing high mortality and disability rates. Adipose tissue-derived mesenchymal stem/stromal cells (ADSCs), especially hypoxia-pretreated ADSCs, represent an effective therapy for SCI by promoting the secretion of exosomes (Exos). Here, we investigated the therapeutic efficacy of exosomes secreted by ADSCs under hypoxia (HExos) and explored potential target molecules. We utilized nanoparticle tracking analysis, electron microscopy, qRT-PCR, and western blotting to analyze differences between HExos and Exos groups. The expression of long noncoding RNAs (lncRNAs) was examined by high-throughput sequencing. The therapeutic effects of different Exos treatments were compared in vitro and in an SCI model in vivo. The interaction between lncRNAs, microRNAs, and mRNA was examined by luciferase reporter experiments. We employed enzyme-linked immunosorbent assay and immunofluorescence to measure inflammatory factor expression and microglial polarization. The results showed that HExos was more effective than Exos for repairing SCI by suppressing inflammatory factor expression, promoting functional recovery, and shifting microglia from M1 to M2 polarization. High-throughput sequencing showed that LncGm37494 expression was significantly higher in HExos than Exos, and its upregulation promoted microglial M1/M2 polarization by inhibiting miR-130b-3p and promoting PPARγ expression, as shown by luciferase reporter experiments. Exos from lncGm37494 overexpressing ADSCs showed a similar therapeutic effect than HExos. The results indicated that HExos repair SCI by delivering lncGm37494, advising that lncGm3749 functions importantly in microenvironmental regulation and shows possibility for SCI treatments.
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http://dx.doi.org/10.1007/s10753-020-01230-zDOI Listing
August 2020

A novel multiscale scheme to accelerate atomistic simulations of bio-macromolecules by adaptively driving coarse-grained coordinates.

J Chem Phys 2020 Mar;152(11):114115

School of Physical Sciences, University of Chinese Academy of Sciences, Beijing 100049, China.

All-atom molecular dynamics (MD) simulations of bio-macromolecules can yield relatively accurate results while suffering from the limitation of insufficient conformational sampling. On the other hand, the coarse-grained (CG) MD simulations efficiently accelerate conformational changes in biomolecules but lose atomistic details and accuracy. Here, we propose a novel multiscale simulation method called the adaptively driving multiscale simulation (ADMS)-it efficiently accelerates biomolecular dynamics by adaptively driving virtual CG atoms on the fly while maintaining the atomistic details and focusing on important conformations of the original system with irrelevant conformations rarely sampled. Herein, the "adaptive driving" is based on the short-time-averaging response of the system (i.e., an approximate free energy surface of the original system), without requiring the construction of the CG force field. We apply the ADMS to two peptides (deca-alanine and Ace-GGPGGG-Nme) and one small protein (HP35) as illustrations. The simulations show that the ADMS not only efficiently captures important conformational states of biomolecules and drives fast interstate transitions but also yields, although it might be in part, reliable protein folding pathways. Remarkably, a ∼100-ns explicit-solvent ADMS trajectory of HP35 with three CG atoms realizes folding and unfolding repeatedly and captures the important states comparable to those from a 398-µs standard all-atom MD simulation.
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http://dx.doi.org/10.1063/1.5135309DOI Listing
March 2020

Analysis of Segmental Lymph Node Metastasis and Clinical Features in cT1N0M0 Lung Adenocarcinoma.

Biomed Res Int 2020 18;2020:2842604. Epub 2020 Feb 18.

Thoracic Surgery, China Medical University First Hospital, Shenyang, LiaoNing, China.

The progression of lung adenocarcinoma through lymph node metastasis has been well established; however, the process of segmental lymph node (LSN) metastasis in cT1N0M0 lung adenocarcinoma remains unclear. We aimed to elucidate the markers of lymph node metastasis to different segments in early-stage lung adenocarcinoma and identify new indications for segmentectomy. A total of 200 patients were enrolled in this study. These patients were diagnosed with cT1N0M0 lung adenocarcinoma after positron emission tomography/computed tomography and received lobectomy and lymph node dissection surgeries. Lymph nodes retrieved from each station were sorted. The metastatic status of the isolated (i) LSNs and several characteristics were analyzed. Patients with ground-glass nodules (GGNs) (=0.025), AIS/MIA/lepidic adenocarcinoma (=0.038), nodules with a maximum diameter ≤1 cm (=0.017), maximum standardized uptake value (SUV) < 2.5 (=0.029), serum carcinoembryonic antigen (CEA) levels ≤4.5 ng/ml (=0.036), and no N1 lymph nodes metastasis (=0.036) had significantly lower iLSN metastasis rates than those without these characteristics. Pure GGNs, CEA levels ≤4.5 ng/ml, SUV < 2.5, tumors with a maximum diameter of ≤1 cm, or those confirmed to be adenocarcinoma , minimally invasive adenocarcinoma, or invasive lepidic-predominant adenocarcinoma by frozen section may indicate segmentectomy. However, segmentectomy is not suitable for patients with metastasis to the N1 lymph nodes.
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http://dx.doi.org/10.1155/2020/2842604DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7049444PMC
December 2020

Unlocking the catalytic activity of an eight-atom gold cluster with a Pd atom.

Nanoscale 2020 Mar 3;12(10):6020-6028. Epub 2020 Mar 3.

School of Chemistry and Chemical Engineering, Nanjing University, Nanjing 210093, China.

It remains elusive as to how exactly the site-specific atom in a catalyst can induce a chemical reaction mainly due to the observed catalytic performance from an ensemble average of all active atoms in the catalyst. In this work, we have reported the catalytic properties of four metal clusters (namely, AuPd, Au, AuPd and Au) for the oxidation of benzyl alcohol. It was found that the Pd atom in the AuPd cluster is likely to be a key to catalyze the oxidation reaction, in which the Pd atom can provide an active site to adsorb and activate O. Our calculation study suggests that the high catalytic activity of the AuPd cluster is due to the unique ability of AuPd to mediate the electrons and holes of the adsorbates. This work provides a feasible strategy to enable highly efficient chemical processes via precisely doping foreign atoms into catalysts with atomic precision.
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http://dx.doi.org/10.1039/c9nr10198eDOI Listing
March 2020

Deficiency Shortens the Replicative Lifespan of through Upregulation of .

Biomed Res Int 2020 12;2020:3858465. Epub 2020 Feb 12.

Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics, Institute of Aging Research, Guangdong Medical University, Dongguan, China.

The cytosolic isozyme of phosphoenolpyruvate carboxykinase () was the first rate-limiting enzyme in the gluconeogenesis pathway, which exerted a critical role in maintaining the blood glucose levels. has been established to be involved in various physiological and pathological processes, including glucose metabolism, lipid metabolism, diabetes, and tumorigenesis. Nonetheless, the association of with aging process and the detailed underlying mechanisms of on aging are still far to be elucidated. Hence, we herein constructed the -deficient (Δ) and overexpression () . The results unveiled that deficiency significantly shortened the replicative lifespan (RLS) in the , while overexpression of prolonged the RLS. Additionally, we noted that the ROS level was significantly enhanced in -deficient strain and decreased in strain. Then, a high throughput analysis by deep sequencing was performed in the Δ and wild-type strains, in an attempt to shed light on the effect of on the lifespan of aging process. The data showed that the most downregulated mRNAs were enriched in the regulatory pathways of glucose metabolism. Fascinatingly, among the differentially expressed mRNAs, was one of the most upregulated genes, which was involved in the glycolysis process and ROS generation. Thus, we further constructed the ΔΔ strain by deletion of in the -deficient strain. The results unraveled that ΔΔ strain significantly suppressed the ROS level and restored the RLS of Δ strain. Taken together, our data suggested that deficiency enhanced the ROS level and shortened the RLS of via .
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http://dx.doi.org/10.1155/2020/3858465DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7037958PMC
November 2020

Structural Relaxation Enabled by Internal Vacancy Available in a 24-Atom Gold Cluster Reinforces Catalytic Reactivity.

J Am Chem Soc 2020 Mar 24;142(9):4141-4153. Epub 2020 Feb 24.

School of Chemistry and Chemical Engineering, Nanjing University, Nanjing 210093, China.

Unveiling the mystery of the contribution of nonsurface or noninterface sites in a catalyst to its catalytic performance remains a great challenge because of the difficulty in capturing precisely structural information (surface plus inner) encoded in the catalyst. This work attempts to elucidate the critical role of the internal vacancy in an atomically precise 24-atom gold cluster in regulating the catalytic performance on the hydrogenation reaction of CO. The experiment results show that the Au cluster with internal vacancy can mitigate sintering and exhibit high catalytic activity under relatively harsh reaction conditions, in contrast to the structurally similar Au cluster without internal vacancy. Our computational study suggests that the internal vacancy in Au provides the cluster with much more structural flexibility, which may be crucial to resisting the aggregation of the cluster and further postponing the deactivation. The hydrogenation and coupling stages of the reaction intermediates are proposed to explain the potential reaction pathway of CO with H on the Au catalyst with internal vacancy.
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http://dx.doi.org/10.1021/jacs.9b07761DOI Listing
March 2020