Background Esophageal squamous cell carcinoma (ESCC), accounting for approximately 90 % of esophageal cancer (EC) cases globally, is characterized by aggressive metastasis and poor prognosis. PANoptosis, an integrated form of pyroptosis, apoptosis, and necroptosis, has emerged as a potential predictor of cancer survival and therapy response. However, its role in ESCC remains unclear. Methods Using univariate and LASSO Cox regression analyses, we identified prognostic PANoptosis-related genes (PRGs) to construct a risk model that stratified patients into high- and low-risk groups. The model's accuracy was validated using Kaplan-Meier analysis, receiver operating characteristic (ROC) curves, and nomograms. Differential pathways were investigated using gene set enrichment analysis (GSEA), while the significance of genes was highlighted through single-cell RNA sequencing (scRNA-seq) analysis. In vitro experiments validated the tumor-suppressive effects of AZD4547, an FGFR inhibitor. This study elucidates the PANoptosis-driven mechanisms underlying the prognosis and therapeutic strategies for ESCC. Results Thirteen PRGs (CCNE1, CEACAM1, CR2, CRYAB, ERBB3, GAST, HELLS, IFT57, KLF5, MAPK13, PLAU, SAP18, SPATA4) associated with survival were identified and formed the foundation of a robust prognostic model. The model was validated in one external microarray cohort and an independent RNA-seq cohort. Immune microenvironment analysis revealed distinct differences in immune infiltration patterns and checkpoint expression levels between high-risk and low-risk groups. GSEA indicated that the activation of EMT, MYC signaling, E2F targets, and G2M checkpoints might contribute to adverse clinical outcomes in high-risk patients. Furthermore, AZD4547 demonstrated significant suppression of tumor proliferation and inhibition of EMT progression in cells with high-risk scores. Conclusion This study developed and validated the first prognostic model for ESCC based on PANoptosis, highlighting FGFR inhibitors as potential therapeutic strategies for targeting specific subtypes through the suppression of EMT and modulation of the MYC/E2F pathways.

BackgroundPrevious studies have reported abnormal expression of WNT1-inducible signaling pathway protein 1 (WISP1)/Cellular Communication Network Factor 4 (CCN4) in esophageal squamous cell carcinoma (ESCC). However, its specific significance remains unclear. To date, no in-depth research has been conducted to explore the role and importance of WISP1 in ESCC.MethodsIn this study, we downloaded the expression data of WISP1 (CCN4), Single-Cell RNA Sequencing (scRNA) data, and clinical information from public databases. A combination of bioinformatics analyses and experimental approaches was employed to comprehensively investigate the correlation between WISP1 expression and clinical prognosis, tumor microenvironment (TME), drug resistance, and response to immunotherapy. Additionally, the role of WISP1 in cancer-associated fibroblasts (CAFs) and its underlying mechanisms were explored.ResultsOur findings revealed that WISP1 exhibited differential expression in most analyzed cancers. In ESCC, WISP1 was upregulated and associated with TME characteristics, immune suppression, and drug resistance. Further analysis indicated that ESCC patients with higher WISP1 expression had relatively poorer prognoses. Moreover, it was confirmed that WISP1 is predominantly highly expressed in CAFs. Knockdown of WISP1 in CAFs significantly inhibited their proliferation, migration, and invasion capabilities, as well as markedly reduced the expression of extracellular matrix (ECM) proteins collagen type I alpha 1 chain (COL1A1) and matrix metallopeptidase 14 (MMP14). Notably, co-culture experiments of CAFs with knocked-down WISP1 and ESCC cancer cells demonstrated that the migration and invasion abilities of ESCC cancer cells were also significantly impaired.ConclusionIn summary, WISP1 is intricately involved in the pathogenesis of ESCC, exhibiting multifaceted roles. WISP1 can modulate the activities of CAFs and cancer cells in ESCC, as well as the process of ECM remodeling, thereby influencing the pathological progression of this malignancy. Based on the aforementioned research findings, WISP1 holds promise as a prognostic molecular marker and a potential therapeutic target for ESCC.

Current studies have reported a high association between the Hashimoto’s thyroiditis (HT) and papillary thyroid cancer (PTC). However, studies on the characteristics of central lymph node metastasis (CLNM) in PTC patients with HT are scarce. Therefore, this study aims to evaluate the risk factors of CLNM in PTC and HT patients. We retrospectively collected clinical data from 933 PTC patients with HT who underwent thyroid surgery. Of these, 653 patients were categorized into a training cohort for constructing the nomogram, and 280 patients formed a validation cohort to verify the performance of the model. Least absolute shrinkage and selection operator (LASSO) regression and multivariate logistic regression analyses were used to select risk factors. A nomogram model for predicting CLNM was developed and internally validated. We subsequently evaluated thyroid function within 3 years after surgery and estimated the prevalence and incidence of postoperative complications between the CLNM ( +) and CLNM (-) groups. LASSO regression revealed that 19 nonzero variables were associated with CLNM. Multivariate logistic regression analysis revealed that younger, patients of low body mass index (BMI), drinking, intranodular hyperechoic (IH) status, diameter ≥ 1 cm, multifocality, extrathyroidal extension (ETE), enlarged central lymph nodes (ECLNs) and lateral lymph node metastasis (LLNM) were at higher risk of CLNM (P < 0.05). A nomogram to predict CLNM in PTC patients with HT was constructed and internally validated on the basis of risk factors. The areas under the ROC curve (AUCs) of nomogram were 0.768 (95

Trace metal zinc is involved in key processes of solid tumors by its antioxidant properties, while the role of zinc at the onset of esophageal squamous cell carcinoma (ESCC) remains controversial. This study aimed to determine whether zinc is associated with the ESCC and underlying molecular events involving malignant progression. Based on a case-control study, we found serum and urine zinc were decreased and correlated with ESCC progression. Thus, an in vitro model for zinc deficiency (ZD) was established, and we found that ZD contributed to the proliferation, migration, and invasion of EC109 cells. Untargeted metabolomics identified 59 upregulated metabolites and 6 downregulated metabolites, among which glycolysis and ferroptosis-related oxidation of chain fatty acids might play crucial steps in ZD-treated molecular events. Interestingly, ZD disrupted redox homeostasis and enhanced cytosolic Fe2+ of EC109 cells, while lipid peroxidation, the key marker of ferroptosis occurrence, was decreased after ZD treatment. The mechanism underlying these changes may involve ZD-enhanced ESCC glycolysis and lactate production, which confer ferroptosis resistance by inhibiting of p-AMPK and leading to the upregulation of SREBP1 and SCD1 to enhance the production of anti-ferroptosis monounsaturated fatty acids.

IntroductionMycoplasma pneumoniae (MP) is the major cause of respiratory infections that threaten the health of children and adolescents worldwide. Therefore, an early, simple, and accurate detection approach for MP is critical to prevent outbreaks of MP-induced community-acquired pneumonia.MethodsHere, we explored a simple and accurate method for MP identification that combines loop-mediated isothermal amplification (LAMP) with the CRISPR/Cas12b assay in a one-pot reaction.ResultsIn the current study, the whole reaction was completed within 1 h at a constant temperature of 57°C. The limit of detection of this assay was 33.7 copies per reaction. The specificity of the LAMP-CRISPR/Cas12b method was 100%, without any cross-reactivity with other pathogens. Overall, 272 clinical samples were used to evaluate the clinical performance of LAMP-CRISPR/Cas12b. Compared with the gold standard results from real-time PCR, the present method provided a sensitivity of 88.11% (126/143), specificity of 100% (129/129), and consistency of 93.75% (255/272).DiscussionTaken together, our preliminary results illustrate that the LAMP-CRISPR/Cas12b method is a simple and reliable tool for MP diagnosis that can be performed in resource-limited regions.

BACKGROUND:Esophageal cancer (ESCA) is a common malignant tumor of the digestive tract, and its poor prognosis is mainly attributed to the occurrence of invasion and metastasis. Z-DNA binding protein 1 (ZBP1), as a mRNA regulatory factor, plays an important role in the occurrence and development of various tumors. However, the role of ZBP1 in ESCA is not yet understood.AIMS:This study aims to explore the expression of ZBP1 in ESCA and its role in the development of ESCA.METHODS:Using bioinformatics analysis and immunohistochemistry staining, we detected the expression of ZBP1 in ESCA and normal tissues. The potential mechanism of ZBP1 in ESCA was analyzed from the aspects of genetic mutations, protein interaction networks, and pathway enrichment. We performed functional experiments in vitro to elucidate the effect of ZBP1 on ESCA cells.RESULTS:ZBP1 was found to be significantly upregulated in ESCA compared to adjacent noncancerous tissues, and its expression is closely related to gender, age, and lymph node metastasis. In ESCA, the genetic variation rate of ZBP1 is 8%, and its expression is positively correlated with immune cell infiltration. The ZBP1 co-expressed gene is mainly involved in processes such as lymph node proliferation and intercellular adhesion. In vitro experiments have confirmed that downregulation of ZBP1 significantly inhibited the proliferation, migration, and invasion of ESCA cells.CONCLUSION:This research proves that downregulation of ZBP1 can inhibit the progression of ESCA. This finding indicates that ZBP1 may be a novel biomarker to improve the diagnosis and treatment of ESCA.

Background:As a member of m6A methylated binding protein, RNA binding motif protein X-linked (RBMX) has been reported to be associated with tumor invasion, metastasis and prognosis. However, the prognostic significance of RBMX expression in esophageal cancer (ESCA) remains unclear.Methods:Based on the TIMER database, GEPIA database, cBioPortal database, CIBERSORT deconvolution algorithm, String-DB database, LinkedOmics database, etc., the RBMX expression level, mRNA expression level, prognostic relationship, genetic mutation, immune cell infiltration level, protein interaction network, differential co-expression genes and functional enrichment in esophageal carcinoma were analyzed. Immunohistochemistry was used to detect the expression of RBMX in 53 cases of esophageal carcinoma and adjacent esophageal tissues.Results:The RBMX expression in ESCA tissue was significantly higher than that in the normal tissues. The overall survival (OS) of patients with high RBMX expression was significantly lower than that of patients with low expression (P=0.04). The protein encoded by the RBMX gene appeared to copy number amplification, mutation and deep deletion. The expression level of RBMX was positively correlated with the levels of follicular helper T cells, eosinophils and initial B cells (P<0.05). Genes significantly and positively correlated with RBMX expression included HNRNPA1L2, SFRS13A, HNRNPA1, etc., which were mainly enriched in biological processes (BPs) such as cell division, mRNA splicing, RNA binding and mRNA 3'-UTR binding.Conclusions:RBMX may be as a biomarker of poor prognosis of ESCA. RBMX is closely related to the survival and prognosis, genetic mutation and immune cell infiltration of patients with ESCA.

Protein disulfide isomerase A3 (PDIA3) is a kind of thiol oxidoreductase with a wide range of functions, and its expression is elevated in a variety of tumors, which is closely related to the invasion and metastasis of tumor cells, and has a significant impact on the immunogenicity of tumor cells. Although more and more studies have shown that PDIA3 plays an important role in the occurrence and development of many tumors, there is no systematic pan-cancer study on PDIA3. Therefore, in this study, the differential expression of PDIA3 in 33 kinds of tumors was analyzed to explore its ability to regulate tumor immunity as a biomarker and evaluate its role in different cancer onset stages or clinical prognosis. In this paper, by analyzing the multilevel data including 33 kinds of cancers in the databases of Cancer Genome Atlas (TCGA), UCSC Xena, Cancer Cell Encyclopedia (CCLE), Genotypic Tissue Expression (GTEx), Human Protein Atlas (HPA), cBioPortal, and GDC; the differential expression level of PDIA3 in different types of malignant tumors and its relationship with prognosis and the potential correlation between PDIA3 expression and microsatellite instability (MSI), tumor mutation load (TMB), mismatch repair gene (MMR), DNA methylation level, and immune infiltration level were analyzed with bioinformatics. The results showed that PDIA3 was highly expressed in 19 types of cancers, but downregulated only in THCA. Next, PDIA3 in different tumors was positively or negatively correlated with patient outcome, Kaplan-Meier survival analysis showed that PDIA3 plays an important role in the prognosis of patients with KIRP, KICH, and CESC and may be used as a prognostic biomarker, and the methylation level of PDIA3 promoter region was closely related to patient outcome in eight tumors. The expression level of PDIA3 was correlated with TMB in 13 tumors and MSI in 9 tumors. Among them, the expression level of PDIA3 in THYM has the strongest correlation with TMB, and the expression level of PDIA3 in READ has the strongest correlation with MSI. In addition, the expression of PDIA3 in eight kinds of tumors, including BRCA, HNSC, THYM, LGG, LUAD, LUSC, PRAD, and THCA, had the highest correlation with the infiltration degree of immune cells, and the expression of PDIA3 had the highest correlation with the infiltration degree of 11 kinds of immune cells, including regulatory T cell and macrophages. And LGG is the tumor most likely to be affected by the tumor microenvironment to affect its development and prognosis. To sum up, this study suggests that PDIA3 plays an important role in the occurrence and development of KIRP, KICH, and CESC and in the immunotherapeutic response of THYM, READ, and LGG and can be used as a prognostic biomarker for these tumors.

The occurrence and development of tumors involve a series of life activities of cells, among which cell death has always been a crucial part in the research of tumor mechanisms and treatment methods. Ferroptosis is a non-apoptotic form of cell death, which is characterized by lipid peroxidation accumulation and further cell membrane rupture caused by excessive production of intracellular oxygen free radicals dependent on iron ions. Esophageal cancer is one of the common digestive tract tumors. Patients in the early stage are mainly treated with surgery, and the curative effect is awe-inspiring. However, surgery is far from enough for terminal patients, and it is the best choice to combine radiotherapy and chemotherapy before the operation or during the perioperative period. Although the treatment plan for patients with advanced esophageal cancer is constantly being optimized, we are disappointed at the still meager 5-year survival rate of patients and the poor quality of life. A series of complex problems, such as increased chemotherapy drug resistance and decreased radiotherapy sensitivity of esophageal cancer cells, are waiting for us to tackle. Perhaps ferroptosis can provide practical and feasible solutions and bring new hope to patients with advanced esophageal cancer. The occurrence of ferroptosis is related to the dysregulation of iron metabolism, lipid metabolism, and glutamate metabolism. Therefore, these dysregulated metabolic participant proteins and signaling pathways are essential entry points for using cellular ferroptosis to resist the occurrence and development of cancer cells. This review first introduced the main regulatory mechanisms of ferroptosis. It then summarized the current research status of ferroptosis in esophageal cancer, expecting to provide ideas for the research related to ferroptosis in esophageal cancer.

The clinical efficacy of continuous subcutaneous insulin infusion (CSII) therapy combined with six classes of oral glucose-lowering drugs (GLDs) (TZDs/metformin/acarbose/GLP-1 receptor agonist/SGLT-2 inhibitor/DPP-4 inhibitor) was evaluated by a network meta-analysis to provide an evidence-based reference in making a clinical decision on CSII combined with drugs in the treatment of type 2 diabetes. Data were retrieved from eight databases: the Chinese Journal Full-Text Database (CNKI), VIP Chinese Science and Technology Periodicals Full-Text Database (VP-CSFD), Wanfang Data Journal Paper Resource (WANFANG), China Biomedical Database (CBM), PubMed, Embase, Cochrane Library, and Web of Science. The retrieval period dated from the library's construction to 27 June 2021. The search was for randomized, controlled trial studies (RCT) on insulin infusion (CSII) combined with oral hypoglycemic drugs (TZDs/metformin/acarbose/GLP-1 receptor agonist/SGLT-2 inhibitor/DPP-4 inhibitor) in the treatment of type 2 diabetes. Quality evaluation and data extraction were performed on the studies included, and network meta-analysis was performed with R4.0.1 software. A total of 56 publications was included in the final network meta-analysis, with a total sample size of 4395. Results based on the network meta-analysis were that CSII combined with a metformin works best on fasting blood glucose (FBG) and 2 h postprandial blood glucose (2hPG) and improves insulin resistance (lower HOMA-IR levels). CSII combined with a DPP-4 inhibitor had the best clinical effect in reducing glycosylated hemoglobin levels. Treatment with CSII combined with a DPP-4 inhibitor was the fastest way to achieve the blood glucose standard. In terms of insulin dosage, an insulin pump (CSII) combined with the GLP-1 receptor agonist can significantly reduce insulin dosage. Network meta-analysis evidence suggests that an insulin infusion (CSII) combined with oral hypoglycemic drugs can improve clinical efficacy in controlling blood sugar and improving insulin resistance, insulin dosage, and standard time. However, the most outstanding performance was that of insulin infusion (CSII) combined with metformin, which had the best clinical effect in controlling blood sugar and improving insulin resistance.

Background: Most patients with type 1 diabetes (T1DM) do not reach the blood glucose goal with treatment of insulin. In our research, we intended to estimate the therapeutic effect and safety of additional different doses of dapagliflozin on insulin treatment in T1DM. Methods: We performed direct and indirect network meta-analysis using Bayesian models and graded different dosages of dapagliflozin by mixed therapy contrasts. We retrieved information from the PubMed, Embase, The Cochrane Library, Web of Science, China Biology Medicine (CBM) disc, China National Knowledge Infrastructure (CNKI), Wanfang Data, and WEIPU Data. Our research included randomized controlled trials (RCTs) including T1DM treated with insulin and additional dapagliflozin 5 mg or dapagliflozin 10 mg from January 2012 to June 2021. Thirteen RCTs with 10,701 participants were divided into three groups as below: insulin alone, dapagliflozin 5 mg + insulin, and dapagliflozin 10 mg + insulin. Results: Dapagliflozin dose-dependently exhibited reductions in glycated hemoglobin (HbA1c), total insulin daily dose (TDD), and body weight. Neither dapagliflozin 5 mg nor 10 mg could induce hypoglycemia or severe hypoglycemia. However, both doses of dapagliflozin increased the incidence of diabetic ketoacidosis (DKA) and genital infection. Conclusions: Dapagliflozin 10 mg could achieve a better outcome in efficacy and could not increase the risk of hypoglycemia. Although it may induce a higher risk of DKA and genital infection, there was no significant difference between dapagliflozin 10 mg and 5 mg. Our outcomes indicate that dapagliflozin 10mg has a high reliability of being graded prior as a supplementary treatment to insulin in T1DM.

BACKGROUND:Since the first appearance in Wuhan, China in December 2019, the novel coronavirus disease (COVID-19) has posed serious threats to the public health in many Chinese places and overseas. It is essential to quantify the transmissibility on real-time basis for designing public health responses.METHODS:We estimated the time-varying reproduction numbers in China, Hubei province and Wuhan city by using the renewable equation determined by the serial interval (SI) of COVID-19. We compare the average reproduction numbers in different periods of time to explore the effectiveness of the public health control measures against the COVID-19 epidemic.RESULTS:We estimated the reproduction numbers at 2.61 (95% CI: 2.47-2.75), 2.76 (95% CI: 2.54-2.95) and 2.71 (95% CI: 2.43-3.01) for China, Hubei province and Wuhan respectively. We found that the reproduction number largely dropped after the city lockdown. As of February 16, the three reproduction numbers further reduced to 0.98, 1.14 and 1.41 respectively.CONCLUSIONS:The control of COVID-19 epidemic was effective in substantially reducing the disease transmissibility in terms of the reproduction number in China reduced to 0.98 as of February 16. At the same time, the reproduction number in Wuhan was probably still larger than 1, and thus the enhancement in the public health control was recommended to maintain.

The novel coronavirus disease 2019 (COVID-19) infection broke out in December 2019 in Wuhan, and rapidly overspread 31 provinces in mainland China on 31 January 2020. In the face of the increasing number of daily confirmed infected cases, it has become a common concern and worthy of pondering when the infection will appear the turning points, what is the final size and when the infection would be ultimately controlled. Based on the current control measures, we proposed a dynamical transmission model with contact trace and quarantine and predicted the peak time and final size for daily confirmed infected cases by employing Markov Chain Monte Carlo algorithm. We estimate the basic reproductive number of COVID-19 is 5.78 (95%CI: 5.71-5.89). Under the current intervention before 31 January, the number of daily confirmed infected cases is expected to peak on around 11 February 2020 with the size of 4066 (95%CI: 3898-4472). The infection of COVID-19 might be controlled approximately after 18 May 2020. Reducing contact and increasing trace about the risk population are likely to be the present effective measures.

Modulation of dystrophin pre-mRNA splicing is an attractive strategy to ameliorate the severe phenotype of Duchenne muscular dystrophy (DMD), although this requires a better understanding of the mechanism of splicing regulation. Aberrant splicing caused by gene mutations provides a good model to study splicing regulatory cis-elements and binding proteins. In this study, we identified skipping of in-frame exon 25 induced by a nonsense mutation (NM_004006.2:c.3340A > T;p.Lys1114*) in the DMD gene. Site-directed mutagenesis study in minigenes suggested that c.3340A > T converts an exonic splicing enhancer sequence (ESE) to a silencer element (ESS). Indeed, RNA pull-down and functional study provided evidence that c.3340A > T abolishes the binding of the splicing enhancer protein Tra2β and promotes interactions with the repressor proteins hnRNP A1, hnRNP A2, and hnRNP H. By carefully analyzing the sequence motif encompassing the mutation site, we concluded that the skipping of exon 25 was due to disruption of a Tra2β-dependent ESE and the creation of a new ESS associated with hnRNP A1 and hnRNP A2, which in turn increased the recruitment of hnRNP H to a nearby binding site. Finally, we demonstrated that c.3340A > T impairs the splicing of upstream intron 24 in a splicing minigene assay. In addition, we showed that the correct splicing of exon 25 is finely regulated by multiple splicing regulators that function in opposite directions by binding to closely located ESE and ESS. Our results clarify the detailed molecular mechanism of exon skipping induced by the nonsense mutation c.3340A > T and also provide information on exon 25 splicing.

体素内不相干运动扩散加权成像(IVIM-DWI)采用双指数模型,通过多个b值分析,无需使用对比剂即能获得水分子扩散运动和微循环灌注信息,可较准确地量化评估胰腺疾病的微观结构变化,为胰腺常见疾病的诊断、鉴别诊断、病理分级及分期、疗效评估提供了新思路.本文就IVIM-DWI在胰腺疾病中的应用进展做简要综述.

以转基因大豆的研发、生产和安全评估为例,对转基因作物的安全问题进行详细剖析,引导人们正确合理对待转基因产品.

The genetic diagnosis of Duchenne muscular dystrophy (DMD) has been complicated by the large size of the gene and its heterogeneous mutational spectrum. Multiplex PCR and multiplex ligation‐dependent probe amplification (MLPA) are two well‐established mutation screening methods. Here, we applied targeted next‐generation sequencing (NGS) to clarify discrepant results between multiplex PCR and MLPA in a Chinese patient with DMD.

Background: This study investigated the associations between lipoprotein-associated phospholipase A2 (Lp-PLA2) and the risks of coronary heart disease (CHD) and ischemic stroke (IS) in the general population.Methods: PubMed, Embase, and the Cochrane Library databases were searched for prospective cohort studies published prior to June 2016. Multivariate-adjusted hazard ratios (HRs) with 95% confidence intervals (Cis) for CHD and IS risks according to Lp-PLA2 activity or mass were extracted, pooled, and weighted using random effects modeling.Results: Twelve studies examining Lp-PLA2 activity or mass and long-term risks of CHD and IS were included. Combined HRs for CHD and IS risks for the highest category referring to lowest category of Lp-PLA2 were 1.46 (95% CI: 1.20-1.78, P < 0.001) and 1.58 (95% CI: 1.21-2.07, P = 0.001), respectively. The same patterns were observed for both mass and activity, with the exception of those for CHD. For every 1-standard deviation (SD) increase in Lp-PLA2 activity, CHD risk increased by 12% (HR: 1.12, 95% CI: 1.05-1.22, P = 0.002); no association between 1-SD increases in Lp-PLA2 activity and IS was observed. Lp-PLA2 mass was associated with CHD risk (HR: 1.02-1.24, 95% CI: 1.02-1.24, P = 0.021). Lp-PLA2 mass per 1-SD increase was not associated with IS risk.Conclusions: Greater Lp-PLA2 activity or mass was associated with an increased risk of CHD and IS; however, additional well-designed trials are warranted to confirm this association.

The fresh fruit of juicy peach is famous for its admirable taste and rich nutrient, which is widely recognized by the market and consumers. Because of its own respiratory peak and the production of strong seasonal, it is liable to decay with the rapid deterioration, resulting in huge economic losses. As the continuous development of agricultural industry and social economy, the peach preservation technology for multi-directional ways have been explored through the detection of important physiological indicators (weight loss, hardness, soluble solids content, relative conductivity, respiratory strength, malonaldehyde content, polyphenol oxidase content and decay index, etc.) with a gradual understanding of the mechanism of fruit and vegetable decay, which has formed some practical methods in the actual production. Those methods are divided into three categories according to technical principles, which are named physical preservation methods (temperature control, air conditioning, adsorption materials, ultraviolet radiation and ultrasound, etc.), chemical preservation methods (calcium regulator, fungicide, coating technology and growth regulators, etc.) and biological preservation methods (plant-source Chinese herbal medicine, microbial antagonism bacteria and biological enzyme preparations, etc.), which have their own characteristics in the effectiveness, safety and economy. On this basis, the combined preservation methods have been investigated and developed after integration and optimization, which have obvious advantages, and are becoming the important future research trends of antisepsis and preservation of peaches. In this paper, the status quo, analysis methods, practical techniques and effect evaluation of domestic juicy peach preservation were summarized, which can provide scientific evidences for continuously improving the postharvest storage and transportation quality and economic benefit of the fruit.