Imaging features and deep learning for prediction of pulmonary epithelioid hemangioendothelioma in CT images.

Background: Pulmonary epithelioid hemangioendothelioma (PEH) is a rare vascular tumour, and its early diagnosis remains challenging. This study aims to comprehensively analyse the imaging features of PEH and develop a model for predicting PEH. Methods: Retrospective and pooled analyses of imaging findings were performed in PEH patients at our center (n=25) and in published cases (n=71), respectively. Relevant computed tomography (CT) images were extracted and used to build a deep learning model for PEH identification and differentiation from other diseases. Results: In this study, bilateral multiple nodules/masses (n=19) appeared to be more common with most nodules less than 2 cm. In addition to the common types and features, the pattern of mixed type (n=4) and isolated nodules (n=4), punctate calcifications (5/25) and lymph node enlargement were also observed (10/25). The presence of pleural effusion is associated with a poor prognosis in PEH. The deep learning model, with an area under the receiver operating characteristic curve (AUC) of 0.71 [95% confidence interval (CI): 0.69-0.72], has a differentiation accuracy of 100% and 74% for the training and test sets respectively. Conclusions: This study confirmed the heterogeneity of the imaging findings in PEH and showed several previously undescribed types and features. The current deep learning model based on CT has potential for clinical application and needs to be further explored in the future.

Blastic Plasmacytoid Dendritic Cell Neoplasm Presenting as a Mammary Gland Tumor in a Pediatric Patient: A Case Report.

Emanating from a discrete category within the lympho-hematopoietic tumor system, as established by the World Health Organization in 2008, the blastic plasmacytoid dendritic cell neoplasm constitutes an uncommon malignant hematological disorder. It is routinely misidentified on account of its conspicuous dermatological manifestation, yet may insidiously permeate bone marrow and lymph nodes, involving peripheral blood and diverse extra-nodal tissues. Instances of mammary gland encroachment are extraordinarily infrequent. The current document delineates a case of a 14-year-old female patient contending with blastic plasmacytoid dendritic cell neoplasm, whose primary symptom was a mammary nodule, and whose breast and bone marrow/blood involvement were synchronous, in attempt to increase clinical vigilance.

Enhancement of efferocytosis through biased FPR2 signaling attenuates intestinal inflammation.

Efficient clearance of dying cells (efferocytosis) is an evolutionarily conserved process for tissue homeostasis. Genetic enhancement of efferocytosis exhibits therapeutic potential for inflammation resolution and tissue repair. However, pharmacological approaches to enhance efferocytosis remain sparse due to a lack of targets for modulation. Here, we report the identification of columbamine (COL) which enhances macrophage-mediated efferocytosis and attenuates intestinal inflammation in a murine colitis model. COL enhances efferocytosis by promoting LC3-associated phagocytosis (LAP), a non-canonical form of autophagy. Transcriptome analysis and pharmacological characterization revealed that COL is a biased agonist that occupies a part of the ligand binding pocket of formyl peptide receptor 2 (FPR2), a G-protein coupled receptor involved in inflammation regulation. Genetic ablation of the Fpr2 gene or treatment with an FPR2 antagonist abolishes COL-induced efferocytosis, anti-colitis activity and LAP. Taken together, our study identifies FPR2 as a potential target for modulating LC3-associated efferocytosis to alleviate intestinal inflammation and highlights the therapeutic value of COL, a natural and biased agonist of FPR2, in the treatment of inflammatory bowel disease.

Promoter cloning and activities analysis of JmLFY, a key gene for flowering in Juglans mandshurica.

Juglans mandshurica (Manchurian walnut) is a precious timber and woody grain and oil species in Northeast China. The heterodichogamous characteristic phenomenon resulted in the non-synchronous flowering and development of male and female flowers, which limited the mating and the yield and quality of fruits. LFY is a core gene in the flowering regulatory networks, which has been cloned in J. mandshurica, and the function has also been verified preliminarily. In this study, the JmLFY promoter sequence with different lengths of 5'-deletion (pLFY1-pLFY6) were cloned and conducted bioinformatics analysis, the promoter activities were analyzed by detecting their driving activity to GUS gene in the tobacco plants that transformed with different promoter sequence stably or transiently. After that, the interaction between JmSOC1 and JmLFY gene promoter was also analyzed via yeast single-hybrid. The results showed that the promoter sequence contains core cis-acting elements essential for eukaryotic promoters, hormone response elements, defense- and stress-responsive elements, flowering-related elements, etc. Transgenic tobacco plants with pLFY1 were obtained by Agrobacterium infection using the pCAMBIA1301 expression vector, and the GUS gene driven by the JmLFY promoter was detected to express in the leaf, stem, flower, and root of the transformed tobacco plant, which indicated that the obtained JmLFY promoter had driving activity. GUS histochemical staining and enzyme activity detection showed that promoter fragments with different lengths had promoter activity and could respond to the induction of long photoperiod, low temperature, salicylic acid (SA), IAA, GA3, and methyl jasmonate (MeJA). The core regulatory region of JmLFY gene promoter in J. mandshurica was between -657 bp and -1,904 bp. Point-to-point validation of yeast single-hybrid confirmed the interaction between JmSOC1 and JmLFY gene promoter, which indicated that JmLFY gene is the downstream target of JmSOC1. These results reveal relevant factors affecting JmLFY gene expression and clarify the molecular mechanism of JmLFY gene regulation in the flower developmental partially, which will provide a theoretical basis for regulating the flowering time by regulating JmLFY gene expression in J. mandshurica.

Immunotherapy in combination with neoadjuvant anthracycline­free chemotherapy for triple­negative early breast cancer: A case report.

Immunotherapy is a promising anticancer strategy. In the present report, the case of a 36-year-old female patient with pathologically diagnosed, left triple-negative breast cancer and axillary lymph node involvement is reported. The patient received immunotherapy in combination with neoadjuvant anthracycline-free chemotherapy for six cycles, before undergoing left mastectomy and left axillary lymph node dissection. The postoperative pathology was a complete response to treatment, involving eradication of tumor from both the breast and the relevant lymph nodes. However, thyroid dysfunction occurred after two cycles of neoadjuvant treatment. The clinical presentation of the thyroid disorder was transient hyperthyroidism for 4 weeks and subsequent hypothyroidism, which required hormone replacement therapy.

Anti-breast cancer-induced cardiomyopathy: Mechanisms and future directions.

With the progression of tumor treatment, the 5-year survival rate of breast cancer is close to 90%. Cardiovascular toxicity caused by chemotherapy has become a vital factor affecting the survival of patients with breast cancer. Anthracyclines, such as doxorubicin, are still some of the most effective chemotherapeutic agents, but their resulting cardiotoxicity is generally considered to be progressive and irreversible. In addition to anthracyclines, platinum- and alkyl-based antitumor drugs also demonstrate certain cardiotoxic effects. Targeted drugs have always been considered a relatively safe option. However, in recent years, some random clinical trials have observed the occurrence of subclinical cardiotoxicity in targeted antitumor drug users, which may be related to the effects of targeted drugs on the angiotensin converting enzyme, angiotensin receptor and ß receptor. The use of angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers and beta-blockers may prevent clinical cardiotoxicity. This article reviews the toxicity and mechanisms of current clinical anti-breast cancer drugs and proposes strategies for preventing cardiovascular toxicity to provide recommendations for the clinical prevention and treatment of chemotherapy-related cardiomyopathy.

Mitochondria-Targeted Nanosystem with Reactive Oxygen Species-Controlled Release of CO to Enhance Photodynamic Therapy of PCN-224 by Sensitizing Ferroptosis.

The apoptosis-resistant mechanism of photodynamic therapy (PDT) usually results in limited therapeutic efficacy. The development of new strategies for sensitizing targeted ferroptosis that bypass apoptosis resistance is of great significance to improve the antitumor efficacy of PDT. In this study, a novel amphiphilic copolymer whose main chain contains reactive oxygen species (ROS)-responsive groups and the end of side chains contains triphenylphosphine is synthesized, to encapsulate porphyrinic metal-organic framework PCN-224 via self-assembly which are hydrothermally synthesized by coordination of zirconium (IV) with tetra-kis(4-caboxyphenyl) porphyrin, and loaded carbon monoxide releasing molecule 401 (CORM-401) by their hollow structures (PCN-CORM), and finally, surface-coated with hyaluronic acid. The nanosystem can sequentially localize to mitochondria which is an important target to induce apoptosis and ferroptosis in cancer cells. Upon excitation with near-infrared light, PCN-224 is activated to produce amounts of ROS, and simultaneously triggers the rapid intracellular release of CO. More importantly, the released CO can sensitize ferroptosis and promote apoptosis to significantly enhance the antitumor efficacy of PCN-224 both in vitro and in vivo. These results illustrate that the mitochondria-targeted drug delivery system combined PDT with CO leads to an effective antitumor efficacy, which maybe a promising way to enhance the treatment efficiency of PDT.

Temperature- and pH-responsive injectable chitosan hydrogels loaded with doxorubicin and curcumin as long-lasting release platforms for the treatment of solid tumors.

The efficacy of treating solid tumors with chemotherapy is primarily hindered by dose-limiting toxicity due to off-target effects and the heterogeneous drug distribution caused by the dense extracellular matrix. The enhanced permeability and retention (EPR) effect within tumors restricts the circulation and diffusion of drugs. To overcome these obstacles, hydrogels formed in situ at the tumor site have been proposed to promote drug accumulation, retention, and long-lasting release. We developed a thiolated chitosan (CSSH) hydrogel with a gelation point of 37°C. Due to the pH-sensitive characteristics of disulfides, the prepared hydrogel facilitated drug release in the acidic tumor environment. A drug release system composed of hydrophilic doxorubicin (Dox) and hydrophobic liposome-encapsulated curcumin (Cur-Lip) was designed to enhance the long-lasting therapeutic impacts and reduce adverse side effects. These composite gels possess a suitable gelation time of approximately 8-12 min under physiological conditions. The cumulative release ratio was higher at pH = 5.5 than at pH = 7.4 over the first 24 h, during which approximately 10% of the Dox was released, and Cur was released slowly over the following 24-120 h. Cell assays indicated that the Cur-Lip/Dox/CSSH gels effectively inhibited the growth of cancer cells. These in situ-formed Cur-Lip/Dox gels with long-term drug release capabilities have potential applications for tumor suppression and tissue regeneration after surgical tumor resection.

PCSK9 Inhibition: From Current Advances to Evolving Future.

Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a secretory serine protease synthesized primarily by the liver. It mainly promotes the degradation of low-density lipoprotein receptor (LDL-R) by binding LDL-R, reducing low-density lipoprotein cholesterol (LDL-C) clearance. In addition to regulating LDL-R, PCSK9 inhibitors can also bind Toll-like receptors (TLRs), scavenger receptor B (SR-B/CD36), low-density lipoprotein receptor-related protein 1 (LRP1), apolipoprotein E receptor-2 (ApoER2) and very-low-density lipoprotein receptor (VLDL-R) reducing the lipoprotein concentration and slowing thrombosis. In addition to cardiovascular diseases, PCSK9 is also used in pancreatic cancer, sepsis, and Parkinson's disease. Currently marketed PCSK9 inhibitors include alirocumab, evolocumab, and inclisiran, as well as small molecules, nucleic acid drugs, and vaccines under development. This review systematically summarized the application, preclinical studies, safety, mechanism of action, and latest research progress of PCSK9 inhibitors, aiming to provide ideas for the drug research and development and the clinical application of PCSK9 in cardiovascular diseases and expand its application in other diseases.

Cu-Hemin Nanosheets and Indocyanine Green Co-Loaded Hydrogel for Photothermal Therapy and Amplified Photodynamic Therapy.

Near-infrared (NIR) organic small molecule indocyanine green (ICG) could respond well to 808 nm laser to promote local high temperature and ROS generation for realizing photothermal therapy (PTT)/photodynamic therapy (PDT). However, the high content of GSH in the tumor microenvironment (TME) limited the further therapeutic performance of ICG. Herein, injectable agarose in situ forming NIR-responsive hydrogels (CIH) incorporating Cu-Hemin and ICG were prepared for the first time. When CIH system was located to the tumor tissue through local injection, the ICG in the hydrogel could efficiently convert the light energy emitted by the 808 nm laser into thermal energy, resulting in the heating and softening of the hydrogel matrix, which releases the Cu-Hemin. Then, the over-expressed GSH in the TME could also down-regulated by Cu-Hemin, which amplified ICG-mediated PDT. In vivo experiments validated that ICG-based PDT/PTT and Cu-Hemin-mediated glutathione depletion could eliminate cancer tissues with admirable safety. This hydrogel-based GSH-depletion strategy is instructive to improve the objective response rate of PDT.

Extracellular vesicles in pancreatic cancer immune escape: Emerging roles and mechanisms.

Pancreatic cancer (PC) is the most lethal malignancy worldwide due to its delayed diagnosis and limited treatment options. Despite great progress in clinical trials of immunotherapies for various cancers, their effectiveness in PC is very low, indicating that immune evasion is still a major obstacle to immunotherapy in PC. However, the mechanism of immune escape in PC is not fully understood, which substantially restricts the development of immunotherapy. As an important component of intercellular communication networks, extracellular vesicles (EVs) have attracted increasing attention in relation to immune escape. This review aims to provide a better understanding of the roles of EVs in tumor immune escape and the potential to expand their application in cancer immunotherapy. The relationship between PC and the tumor immune microenvironment is briefly introduced. Then, the mechanism by which EVs are involved in immune regulation is summarized, and the latest progress in determining the role of EVs in regulating PC immune escape is highlighted.

Engineered extracellular vesicles and their mimetics for cancer immunotherapy.

Extracellular vesicles (EVs) are heterogeneous membranous vesicles secreted by living cells that are involved in many physiological and pathological processes as intermediaries for intercellular communication and molecular transfer. Recent studies have shown that EVs can regulate the occurrence and development of tumors by transferring proteins, lipids and nucleic acids to immune cells as signaling molecules. As a new diagnostic biomarker and drug delivery system, EVs have broad application prospects in immunotherapy. In addition, the breakthrough of nanotechnology has promoted the development and exploration of engineered EVs for immune-targeted therapy. Herein, we review the uniqueness of EVs in immune regulation and the engineering strategies used for immunotherapy and highlight the logic of their design through typical examples. The present situation and challenges of clinical transformation are discussed, and the development prospects of EVs in immunotherapy are proposed. The goal of this review is to provide new insights into the design of immune-regulatory EVs and expand their application in cancer immunotherapy.

Homogeneous Polyporus Polysaccharide Inhibit Bladder Cancer by Resetting Tumor-Associated Macrophages Toward M1 Through NF-κB/NLRP3 Signaling.

Bladder cancer(BC)is one of the most common urinary system tumors, which characterized by a high incidence. Polyporus polysaccharide is the main active component of polyporus, which is clinically used in the treatment of bladder cancer, but the mechanism is not clear. In previous study, we isolated homogeneous polyporus polysaccharide(HPP) with high purity from polyporus. The goal of this study was to assess the polarization of macrophages induced by HPP in the bladder tumor microenvironment and explored its anti-bladder cancer mechanism through BBN bladder cancer rat model and Tumor associated macrophages(TAM). The results suggested that HPP regulates TAM polarization to improve the tumor inflammatory microenvironment, possibly through the NF-κB/NLRP3 signaling pathway. Our results suggested that HPP may be a potential therapeutic agent for bladder tumors.

Urinary concentrations of phenols, oxidative stress biomarkers and thyroid cancer: Exploring associations and mediation effects.

Phenols have been shown to influence the cellular proliferation and function of thyroid in experimental models. However, few human studies have investigated the association between phenol exposure and thyroid cancer, and the underlying mechanisms are also poorly understood. We conducted a case-control study by age- and sex-matching 143 thyroid cancer and 224 controls to investigate the associations between phenol exposures and the risk of thyroid cancer, and further to explore the mediating role of oxidative stress. We found that elevated urinary triclosan (TCS), bisphenol A (BPA) and bisphenol S (BPS) levels were associated with increased risk of thyroid cancer (all P for trends < 0.05), and the adjusted odds ratios (ORs) comparing the extreme exposure groups were 3.52 (95% confidence interval (CI): 2.08, 5.95), 2.06 (95% CI: 1.06, 3.97) and 7.15 (95% CI: 3.12, 16.40), respectively. Positive associations were also observed between urinary TCS, BPA and BPS and three oxidative stress biomarkers measured by 8-hydroxy-2'-deoxyguanosine (8-OHdG), 8-iso-prostaglandin F2α (8-isoPGF2α) and 4-hydroxy-2-nonenal-mercapturic acid (HNE-MA), as well as between urinary 8-isoPGF2α and HNE-MA and the risk of thyroid cancer. Mediation analysis showed that urinary 8-isoPGF2α mediated 28.95%, 47.06% and 31.08% of the associations between TCS, BPA and BPS exposures and the risk of thyroid cancer, respectively (all P < 0.05). Our results suggest that exposure to TCS, BPA and BPS may be associated with increased risk of thyroid cancer and lipid peroxidation may be an intermediate mechanism. Further studies are warranted to confirm the findings.

Endoplasmic reticulum stress promotes breast cancer cells to release exosomes circ_0001142 and induces M2 polarization of macrophages to regulate tumor progression.

Breast cancer (BC) has a high morbidity and mortality rate. It is imperative to explore the pathogenesis of BC in order to find potential prognostic biomarkers and therapeutic targets. This study screened and verified the differential expression of circ_0001142 in BC tissues and cell lines through bioinformatics and qRT-PCR. Perform dual luciferase reporter gene assay and pull-down detection to verify the correlation between circ_0001142 and miRNA-361-3p and between miR-361-3p and PIK3CB. QRT-PCR, flow cytometry and ELISA were used to study the regulatory effects and regulatory mechanisms of different treatment groups on macrophage polarization. The role of exosomes circ_0001142 in the tumor microenvironment and its influence on BC growth, metastasis and macrophage polarization were investigated through in vivo and in vitro studies. We first found that circ_0001142 is highly expressed in BC. In addition, ERs promote the secretion of tumor exosomes, enhance the entry of circ_0001142 into macrophages and interfere with the process of autophagy and polarization. Finally, it was found that the circ_0001142/miR-361-3p/PIK3CB pathway plays an important role in the polarization of macrophages.

Risk prediction for central lymph node metastasis in isolated isthmic papillary thyroid carcinoma by nomogram: A retrospective study from 2010 to 2021.

Background: Isthmic papillary thyroid carcinoma (IPTC) is an aggressive thyroid cancer associated with a poor prognosis. Guidelines elaborating on the extent of surgery for IPTC are yet to be developed. This study aims to construct and validate a model to predict central lymph node metastasis (CLNM) in patients with IPTC, which could be used as a risk stratification tool to determine the best surgical approach for patients. Methods: Electronic medical records for patients diagnosed with isolated papillary thyroid carcinoma who underwent surgery at Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, from January 2010 to December 2021 were reviewed. All patients who underwent thyroidectomy with central neck dissection (CND) for isolated IPTC were included. We conducted univariate and multivariate logistic regression analyses to assess risk factors for ipsilateral and contralateral CLNM and the number of CLNM in IPTC patients. Based on the analysis, the nomogram construction and internal validations were performed. Results: A total of 147 patients with isolated IPTC were included. The occurrence of CLNM was 53.7% in the patients. We identified three predictors of ipsilateral CLNM, including age, gender, and size. For contralateral CLNM, three identified predictors were age, gender, and capsular invasion. Predictors for the number of CLNM included age, gender, capsular invasion, tumor size, and chronic lymphocytic thyroiditis (CLT). The concordance index(C-index) of the models predicting ipsilateral CLNM, contralateral CLNM, 1-4 CLNM, and ≥5 CLNM was 0.779 (95%CI, 0.704, to 0.854), 0.779 (95%CI, 0.703 to 0.855), 0.724 (95%CI, 0.629 to 0.818), and 0.932 (95%CI, 0.884 to 0.980), respectively. The corresponding indices for the internal validation were 0.756 (95%CI, 0.753 to 0.758), 0.753 (95%CI, 0.750 to 0.756), 0.706 (95%CI, 0.702 to 0.708), and 0.920 (95%CI, 0.918 to 0.922). Receiver operating characteristic (ROC) curves, calibration, and decision curve analysis (DCA) results confirmed that the three nomograms could precisely predict CLNM in patients with isolated IPTC. Conclusion: We constructed predictive nomograms for CLNM in IPTC patients. A risk stratification scheme and corresponding surgical treatment recommendations were provided accordingly. Our predictive models can be used as a risk stratification tool to help clinicians make individualized surgical plans for their patients.

Tumor-derived biomimetic nanozyme with immune evasion ability for synergistically enhanced low dose radiotherapy.

High doses of radiation can cause serious side effects and efficient radiosensitizers are urgently needed. To overcome this problem, we developed a biomimetic nanozyme system (CF) by coating pyrite (FeS2) into tumor-derived exosomes for enhanced low-dose radiotherapy (RT). CF system give FeS2 with immune escape and homologous targeting abilities. After administration, CF with both glutathione oxidase (GSH-OXD) and peroxidase (POD) activities can significantly lower the content of GSH in tumor tissues and catalyze intracellular hydrogen peroxide (H2O2) to produce a large amount of ·OH for intracellular redox homeostasis disruption and mitochondria destruction, thus reducing RT resistance. Experiments in vivo and in vitro showed that combining CF with RT (2 Gy) can provide a substantial suppression of tumor proliferation. This is the first attempt to use exosomes bionic FeS2 nanozyme for realizing low-dose RT, which broaden the prospects of nanozymes.

SnFe2O4 Nanozyme Based TME Improvement System for Anti-Cancer Combination Thermoradiotherapy.

High doses of radiotherapy (RT) are associated with resistance induction. Therefore, highly selective and controllable radiosensitizers are urgently needed. To address this issue, we developed a tin ferrite (SFO)-based tumor microenvironment (TME)-improved system (SIS) that can be used in combination with low-dose radiation. The SIS was delivered via intratumoral injection directly to the tumor site, where it was stored as a ration depot. Due to the photothermal properties of SFO, SIS steadily dissolved under near-infrared (NIR) laser irradiation. Simultaneously, the dual glutathione oxidase (GSH-OXD) and catalase (CAT) activities of the SFO nanozyme significantly lowered the content of GSH in tumor tissues and efficiently catalyzed the conversion of intracellular hydrogen peroxide to produce a large amount of oxygen (O2) for intracellular redox homeostasis disruption, thus reducing radiotherapy resistance. Our in vivo and in vitro studies suggested that combining the SIS and NIR irradiation with RT (2Gy) significantly reduced tumor proliferation without side effects such as inflammation. To conclude, this study revealed that SFO-based nanozymes show great promise as a catalytic, radiosensitizing anti-tumor therapy.

A Novel H2O2 Generator for Tumor Chemotherapy-Enhanced CO Gas Therapy.

Carbon monoxide (CO) gas therapy is a promising cancer treatment. However, gas delivery to the tumor site remains problematic. Proper tunable control of CO release in tumors is crucial to increasing the efficiency of CO treatment and reducing the risk of CO poisoning. To overcome such challenges, we designed ZCM, a novel stable nanotechnology delivery system comprising manganese carbonyl (MnCO) combined with anticancer drug camptothecin (CPT) loaded onto a zeolitic imidazole framework-8 (ZIF-8). After intravenous injection, ZCM gradually accumulates in cancerous tissues, decomposing in the acidic tumor microenvironment, releasing CPT and MnCO. CPT acts as a chemotherapy agent destroying tumors and producing copious H2O2. MnCO can react with the H2O2 to generate CO, powerfully damaging the tumor. Both in vitro and in vivo experiments indicate that the ZCM system is both safe and has excellent tumor inhibition properties. ZCM is a novel system for CO controlled release, with significant potential to improve future cancer therapy.

The relationship of long non-coding RNA maternally expressed gene 3 with microRNA-21 and their correlation with acute ischemic stroke risk, disease severity and recurrence risk.

OBJECTIVE: Long non-coding RNA maternally expressed gene 3 (lnc-MEG3) directly targets microRNA-21 (miR-21) to regulate the vascular microenvironment, and is closely implicated in the pathology of acute ischemic stroke (AIS). However, no research regarding the interaction of lnc-MEG3 and miR-21 in AIS patients has been conducted, to the best of our knowledge. Therefore, we performed this study to evaluate the correlation of lnc-MEG3 with miR-21, and to explore their clinical role for AIS management. METHODS: A total of 170 AIS patients and 100 controls with at least two high-risk factors for stroke were enrolled. The expression of lnc-MEG3 and miR-21 in peripheral blood mononuclear cells was detected by reverse transcription-quantitative polymerase chain reaction. RESULTS: Lnc-MEG3 expression was increased in AIS patients and could differentiate AIS patients from controls using receiver operating characteristic (ROC) curve analysis with area under the curve (AUC) of 0.874 and a 95% confidence interval (CI) of 0.833-0.914. Lnc-MEG3 expression was positively correlated with tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-17A and the National Institutes of Health Stroke Scale (NIHSS) score, and its high expression was also correlated with elevated accumulating recurrence rate in AIS patients. In addition, lnc-MEG3 expression was negatively correlated with miR-21 expression in AIS patients. Regarding miR-21, it was reduced in AIS patients and could differentiate AIS patients from controls with AUC of 0.889 (95% CI: 0.850-0.927). Also, miR-21 expression was negatively correlated with TNF-α, IL-17A, NIHSS score and accumulating recurrence rate in AIS patients. CONCLUSION: Lnc-MEG3 is negatively correlated with miR-21, and both factors are related to disease risk, inflammatory cytokines, disease severity and recurrence risk of AIS.