Emerging evidence suggests that cancer survivors who have undergone anthracycline therapy frequently experience late-onset atherosclerosis. However, the mechanisms underlying this phenomenon and potential preventive strategies remain largely unexplored. In this study, we developed a mouse model to replicate doxorubicin (Dox)-induced atherosclerotic lesions. Given the established role of the RNA methyltransferase METTL3 in both atherogenesis and tumorigenesis, we conducted a comprehensive investigation to assess whether targeting METTL3 could mitigate Dox-induced atherosclerosis and enhance the efficacy of Dox in inhibiting tumor progression. Our findings reveal that Dox administration promotes vascular endothelial premature senescence and atherosclerosis, to a large extent by upregulating the expression of METTL3 and its substrate genes, particularly those encoding senescence-associated secreted proteins. To translate METTL3 as a therapeutic target, we developed and characterized an endothelium-targeted (achieved by coating with CD31 antibodies) nanoparticle loaded with the METTL3 inhibitor STM2457 (endothelium-targeted METTL3 nano-inhibitor, ETMN). As anticipated, ETMN effectively protects murine blood vessels against Dox-aggravated endothelial senescence and inflammation, as well as atheroma formation. Furthermore, ETMN, with enhanced enrichment in tumor allografts, significantly potentiates Dox's tumoricidal activity by attenuating METTL3 oncogenic signaling. In summary, our work offers a practical solution for addressing Dox therapy-related atherosclerosis, providing dual benefits and advancing the treatment and management of cancer patients undergoing anthracycline therapy.

Elevated levels of low-density lipoprotein cholesterol (LDL-C) play a critical role in the onset and progression of cardiovascular disease (CVD). Inhibitors or monoclonal antibody drugs targeting pro-protein convertase subtilisin/kexin type 9 (PCSK9) are novel cholesterol-lowering medications that can effectively reduce serum LDL-C levels. However, these drugs are usually expensive and require injections, which can reduce patient compliance and increase the financial burden. In this study, we constructed an engineered probiotic strain containing a prokaryotic expression element and a high-affinity fragment of the human PCSK9 nanobody (PCSK9nb). The engineered bacterium was evaluated in vitro and in vivo for its ability to express and release PCSK9nb, as well as for its biocompatibility and stability. The therapeutic potential of the engineered probiotics was confirmed using mouse models of hyperlipidemia and atherosclerosis. We analyzed differences in mouse gut microbiota using high-throughput sequencing and compared the therapeutic efficacy of the engineered bacteria with that of atorvastatin in a mouse model of hyperlipidemia. The engineered bacteria were found to express and release PCSK9nb in vivo after oral administration, achieving the effect of lowering serum cholesterol levels, alleviating atherosclerosis, and reducing body weight. In vivo, PCSK9nb was found to increase hepatic LDL receptor (LDLR) expression levels, decrease serum LDL-C content, regulate the diversity and community structure of gut microbiota, reduce lipid accumulation in the liver, and decrease systemic inflammation. By comparing their efficacy with that of statins, the engineered probiotics demonstrated similar therapeutic effects. The research results provide a new strategy for the development of orally delivered PCSK9 antibody drugs, reducing healthcare costs and minimizing statin drug tolerance.

IntroductionNumerous studies have demonstrated acute myeloid leukemia (AML) is one of the malignancies with high mortality worldwide. Immunogenic cell death (ICD) is a form of cell death that is specialised in that it triggers the body’s immune response, particularly the adaptive immune response. Recent evidence has confirmed that pseudogenes are implicated in multiple human tumorigenesis and progression although lacking the function of coding protein. However, the roles of ICD-associated genes in AML remain largely unascertained.MethodsTCGA-AML and GSE71014 cohorts were picked out and we combined them into a merged dataset by removing the batch effect using the sva package in the R project. A consensus clustering analysis of the ICD genes in AML was performed to define subgroups. Based on the expression of 15 prognostic-related pseudogenes, we developed a prognostic model and categorized AML samples into low and high-risk groups.ResultsAML was differentiated into two subgroups (C1 and C2 clusters). Most ICD-related genes were significantly up-regulated in the C2 cluster. The single sample gene set enrichment analysis (ssGSEA) revealed that the immune cell infiltration and immune checkpoint gene expression of the C2 cluster was strongly high, suggesting that the C2 population responded well to immune checkpoint blockade (ICB) therapy and had better survival. The C1 group was sensitive to chemotherapy, including Cytarabine, Midostaurin, and Doxorubicin. On the other hand, 15 ICD-related pseudogenes were identified to be associated with AML prognosis. The receiver operator curve (ROC) analysis and nomogram manifested that our prognostic model had high accuracy in predicting survival. However, the high-risk group was sensitive to ICB therapy and chemotherapy such as Methotrexate, Cytarabine, and Axitinib while the low-risk group benefited from 5-Fluorouracil, Talazoparib, and Navitoclax therapy.DiscussionIn summary, we defined two subgroups relying on 33 ICD-related genes and this classification exerted a decisive role in assessing immunotherapy and chemotherapy benefit. Significantly, a prognostic signature identified by critical ICD-related pseudogene was created. The pseudogene prognostic signature had a powerful performance in predicting prognosis and therapeutic efficacy, including immunotherapy and chemotherapy to AML. Our research points out novel implications of ICD in cancer prognosis and treatment approach choice.

Doxorubicin (DOX), a potent antineoplastic agent, is commonly associated with cardiotoxicity, necessitating the development of strategies to reduce its adverse effects on cardiac function. Previous research has demonstrated a strong correlation between DOX-induced cardiotoxicity and the activation of oxidative stress pathways. This work introduces a novel antioxidant therapeutic approach, utilizing libraries of tannic acid and N-acetyl-L-cysteine-protected bimetallic cluster nanozymes. Through extensive screening for antioxidative enzyme-like activity, an optimal bimetallic nanozyme (AuRu) is identified that possess remarkable antioxidant characteristics, mimicking catalase-like enzymes. Theoretical calculations reveal the surface interactions of the prepared nanozymes that simulate the hydrogen peroxide decomposition process, showing that these bimetallic nanozymes readily undergo OH⁻ adsorption and O₂ desorption. To enhance cardiac targeting, the atrial natriuretic peptide is conjugated to the AuRu nanozyme. These cardiac-targeted bimetallic cluster nanozymes, with their anchoring capability, effectively reduce DOX-induced cardiomyocyte ferroptosis and PANoptosis without compromising tumor treatment efficacy. Thus, the therapeutic approach demonstrates significant reductions in chemotherapy-induced cardiac cell death and improvements in cardiac function, accompanied by exceptional in vivo biocompatibility and stability. This study presents a promising avenue for preventing chemotherapy-induced cardiotoxicity, offering potential clinical benefits for cancer patients.

Gut microbiota have been linked to immune thrombocytopenia (ITP) and Henoch–Schönlein purpura (HSP) in recent studies, but a cause-and-effect relationship is unclear. We used Mendelian randomization (MR) to assess causal relationships between gut microbiota and HSP/ITP using summary statistics from the GWAS dataset of the international MiBioGen and FinnGen consortium. The IVW method was used as the main evaluation indicator. MR analysis of 196 intestinal flora and HSP/ITP/sTP phenotypes showed that 12 flora were potentially causally associated with ITP, 6 with HSP, and 9 with sTP. The genes predicted that genus Coprococcus3 (p = 0.0264, OR = 2.05, 95

The cardiotoxicity caused by Dox chemotherapy represents a significant limitation to its clinical application and is a major cause of late death in patients undergoing chemotherapy. Currently, there are no effective treatments available. Our analysis of 295 clinical samples from 132 chemotherapy patients and 163 individuals undergoing physical examination revealed a strong positive correlation between intestinal barrier injury and the development of cardiotoxicity in chemotherapy patients. We developed a novel orally available and intestinal targeting protein nanodrug by assembling membrane protein Amuc_1100 (obtained from intestinal bacteria Akkermansia muciniphila), fluorinated polyetherimide, and hyaluronic acid. The protein nanodrug demonstrated favorable stability against hydrolysis compared with free Amuc_1100. The in vivo results demonstrated that the protein nanodrug can alleviate Dox-induced cardiac toxicity by improving gut microbiota, increasing the proportion of short-chain fatty acid-producing bacteria from the Lachnospiraceae family, and further enhancing the levels of butyrate and pentanoic acids, ultimately regulating the homeostasis repair of lymphocytes in the spleen and heart. Therefore, we believe that the integrity of the intestinal barrier plays an important role in the development of chemotherapy-induced cardiotoxicity. Protective interventions targeting the intestinal barrier may hold promise as a general clinical treatment regimen for reducing Dox-induced cardiotoxicity.

BackgroundCardiac-resident or -enriched microRNAs (miRNAs) could be released into the bloodstream becoming circulating cardiac miRNAs, which are increasingly recognized as non-invasive and accessible biomarkers of multiple heart diseases. However, dilated cardiomyopathy (DCM)-associated circulating miRNAs (DACMs) and their roles in DCM pathogenesis remain largely unexplored. MethodsTwo human cohorts, consisting of healthy individuals and DCM patients, were enrolled for serum miRNA sequencing (10 vs. 10) and quantitative polymerase chain reaction validation (46 vs. 54), respectively. Rigorous screening strategy was enacted to define DACMs and their potentials for diagnosis. DCM mouse model, different sources of cardiomyocytes, adeno-associated virus 9 (AAV9), gene knockout, RNAscope miRNA in situ hybridization, mRFP-GFP-LC3B reporter, echocardiography and transmission electron microscopy were adopted for mechanistic explorations. ResultsSerum miRNA sequencing revealed a unique expression pattern for DCM circulating miRNAs. DACMs miR-26a-5p, miR-30c-5p, miR-126-5p and miR-126-3p were found to be depleted in DCM circulation as well as heart tissues. Their expressions in circulation and heart tissues were proven to be correlated significantly, and a combination of these miRNAs was suggested potential values for DCM diagnosis. FOXO3, a predicted common target, was experimentally demonstrated to be co-repressed within cardiomyocytes by these DACMs except miR-26a-5p. Delivery of a combination of miR-30c-5p, miR-126-5p and miR-126-3p into the murine myocardium via AAV9 carrying an expression cassette driven by cTnT promoter, or cardiac-specific knockout of FOXO3 (Myh6-Cre(ERT2), FOXO3 flox(+/+)) dramatically attenuated cardiac apoptosis and autophagy involved in DCM progression. Moreover, competitively disrupting the interplay between DACMs and FOXO3 mRNA by specifically introducing their interacting regions into murine myocardium crippled the cardioprotection of DACMs against DCM. ConclusionsCirculating cardiac miRNA-FOXO3 axis plays a pivotal role in safeguarding against myocardial apoptosis and excessive autophagy in DCM development, which may provide serological cues for DCM non-invasive diagnosis and shed light on DCM pathogenesis and therapeutic targets.

Radix Puerariae (RP), a dry root of Pueraria lobata (Willd.) Ohwi, is used to treat a variety of diseases, including cancer. Several in vitro and in vivo studies have demonstrated the efficacy of RP in the treatment of colon cancer (CC). However, the biological mechanism of RP in the treatment of colon cancer remains unclear. In this study, the active component of RP and its potential molecular mechanism against CC were studied by network pharmacology and enrichment analysis. The methods adopted included screening active ingredients of Chinese medicine, predicting target genes of Chinese medicine and disease, constructing of a protein interaction network, and conducting GO and KEGG enrichment analysis. Finally, the results of network pharmacology were further validated by molecular docking experiments and cell experiments. Eight active constituents and 14 potential protein targets were screened from RP, including EGFR, JAK2 and SRC. The biological mechanism of RP against CC was analysed by studying the relationship between active components, targets, and enrichment pathways. These findings provide a basis for understanding the clinical application of RP in CC.

Cold-inducible RNA-binding protein (CIRBP) is documented to be required for maintaining cardiac function, however, its role in chemotherapy-induced cardiotoxicity remains obscured.Herein, we report that CIRBP decreases cardiomyocyte apoptosis and attenuates cardiotoxicity through disrupting OGF-OGFR signal.CIRBP deficiency is involved in diverse chemotherapeutic agents induced cardiomyocyte apoptosis.Delivery of exogenous CIRBP to the mouse myocardium significantly mitigated doxorubicin-induced cardiac apoptosis and dysfunction.Specifically, OGFR was identified as a downstream core effector responsible for chemotherapy-induced cardiomyocyte apoptosis.CIRBP was shown to interact with OGFR mRNA and to repress OGFR expression by reducing mRNA stability.CIRBP-mediated cytoprotection against doxorubicin-induced cardiac apoptosis was demonstrated to largely involve OGFR repression by CIRBP.NTX as a potent antagonist of OGFR successfully rescued CIRBP ablation-rendered susceptibility to cardiac dyshomeostasis upon exposure to doxorubicin, whereas another antagonist ALV acting only on opioid receptors did not.Taken together, our results demonstrate that CIRBP confers myocardium resistance to chemotherapy-induced cardiac apoptosis and dysfunction by dampening OGF/OGFR axis, shedding new light on the mechanisms of chemo-induced cardiotoxicity and providing insights into the development of an efficacious cardioprotective strategy for cancer patients.

目的:探讨Th1/Th2细胞因子对血流感染及病原菌类型诊断的预测价值.方法:收集2018年1月至10月郑州大学第一附属医院呼吸科、感染科住院且有血培养阳性的患者170例(G+菌56例、G-菌84例、真菌30例),病毒感染者35例,选取健康体检者280例为对照组.利用流式微球分析技术检测各组患者血浆Th1(IL-2、IFN-γ、TNF-α)及Th2(IL-4、IL-6、IL-10)细胞因子水平,分析各组间的差异,绘制ROC曲线,评价各细胞因子对血流感染的诊断价值及其诊断的灵敏度、特异度.结果:血培养阳性组患者血浆中IFN-γ、TNF-α、IL-4、IL-6、IL-10的水平高于健康对照组(P<0.05),其中IL-6与IL-10具有较高的AUC、灵敏度、特异度,IL-6、IL-10联合的AUC为0.997,灵敏度、特异度分别为0.982、0.996.G-组患者血浆中IL-6的水平与G+组、真菌组之间差异有统计学意义(P<0.05),表达水平为:G-组>真菌组>G+组,其AUC为0.769,灵敏度、特异度分别为0.857、0.570.真菌组患者血浆中IFN-γ的水平与G+组、G-组之间差异有统计学意义(P<0.05),表达水平为真菌组>G+组、真菌组>G-组,其AUC为0.808,灵敏度、特异度分别为0.933、0.664.结论:血流感染患者存在Th1/Th2细胞因子表达失衡.IL-6可作为G-菌感染的诊断指标,IFN-γ对于真菌感染具有提示作用.

The process by which Trichinella spiralis muscle larvae are activated to infect the intestine after exposure to the host small intestinal milieu is crucial for the successful establishment of T. spiralis infection. However, the molecular mechanism underlying the invasion of intestinal epithelial cells by T. spiralis has not been elucidated. MicroRNAs are a class of small noncoding RNAs that participate in parasite growth and development, pathogenic processes, and host-parasite interactions. In the present study, the differential expression profile of miRNAs in T. spiralis after exposure to the mouse small intestinal milieu was analysed using Solexa high-throughput sequencing technology. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed to analyse the functions of miRNA target genes, and dual-luciferase reporter assays were subsequently applied to test the regulatory effects of one significantly decreased miRNA (let-7) on its four predicted target genes. In total, 2,000 known miRNAs (930 upregulated and 1070 downregulated) and 43 novel miRNAs (22 upregulated and 21 downregulated) were found to be differentially expressed in intestinal larvae, compared with muscle larvae. The KEGG pathway analysis showed that the predicted target genes of differentially expressed miRNAs were involved in 299 different pathways, and the top 10 pathways were metabolic pathways, biosynthesis of secondary metabolites, neuroactive ligand-receptor interaction, lysosome, focal adhesion, purine metabolism, starch and sucrose metabolism, tight junction, carbohydrate digestion and absorption, and pathways in cancer. As one of the most widely studied miRNA families, the expression of let-7 was significantly decreased in T. spiralis after exposure to host small intestinal milieu. A dual-luciferase reporter assay revealed that neuropeptide Y receptor type 6 and carboxypeptidase E were direct target genes of let-7, and were downregulated by binding with their 3' UTR. GO function analysis showed that carboxypeptidase E had multiple enzymatic activities, suggesting that it might participate in cell membrane damage and larval invasion. These data suggest that the differentially expressed miRNAs in T. spiralis might have a regulatory role in the invasion of host intestinal epithelial cells. This study provides a new insight into the molecular mechanisms of invasion by T. spiralis and the regulatory functions of miRNAs in host-Trichinella interactions.

OBJECTIVE:To explore the molecular basis for two brothers affected with globozoospermia.METHODS:Whole exome sequencing was carried out for both patients. Candidate variant was verified by Sanger sequencing and quantitative real-time PCR (qRT-PCR).RESULTS:Whole exome sequencing, Sanger sequencing and qRT-PCR verification revealed a heterozygous c.384dup (p.Glu129*) variant in the DPY19L2 gene in the two brothers and their mother. A large heterozygous deletion, spanning approximately 164.5 kb and encompassing the entire DPY19L2 gene, was detected on chromosome 12 of the two patients and their father.CONCLUSION:The c.384dup (p.Glu129*) variant and deletion of the DPY19L2 gene probably underlie the pathogenesis of globozoospermia in the two patients, which was in keeping with the autosomal recessive inheritance of disease in this pedigree.

Trichinellosis is an important food-borne parasitic zoonosis throughout the world. At present, the mechanisms of Trichinella spiralis infection remain unclear. Acquiring detailed information on the host-Trichinella interaction would be beneficial for the development of new strategies for trichinellosis control. Circulating miRNAs are stably detectable in the blood of humans and animals infected with parasites. Circulating miRNAs might regulate the expression of target genes in pathological responses during infection and might be novel potential biomarkers of parasitic diseases. In the present study, a total of ten differentially expressed circulating mouse miRNAs with |log2(fold change)| ≥ 1.0 and FDR < 0.01 were found during T. spiralis infection, of which five were upregulated and five were downregulated. GO and KEGG analyses showed that the target genes of the ten miRNAs were enriched in many signalling pathways, especially focal adhesion, MAPK pathway, and so on. The results of qRT-PCR showed that among the five upregulated miRNAs, mmu-miR-467a-3p and mmu-miR-467d-3p expression in mouse serum reached a peak at 30 days post-infection (dpi). The expression of mmu-miR-376b-3p and mmu-miR-664-3p increased significantly at 18 dpi and then decreased at 30 dpi. The expression of mmu-miR-292a-5p gradually decreased from 12 to 30 dpi. Among the 5 downregulated miRNAs, mmu-miR-199a-5p expression was significantly downregulated at 30 dpi, while the expression levels of the other four miRNAs (mmu-miR-455-5p, mmu-miR-125b-5p, mmu-miR-125a-5p, and mmu-miR-615-3p) were significantly lower compared with the control, showing a steady downregulation at different phases of infection. These findings will help to further understand the host-Trichinella interaction and provide promising serum biomarkers for trichinellosis.

Background Lung squamous cell carcinoma (LUSC) is a major subtype of lung cancer with limited therapeutic options and poor clinical prognosis. Methods Three datasets (GSE19188, GSE33532 and GSE33479) were obtained from the gene expression omnibus (GEO) database. Differentially expressed genes (DEGs) between LUSC and normal tissues were identified by GEO2R, and functional analysis was employed using the Database for Annotation, Visualization and Integrated Discovery (DAVID) online tool. Protein–protein interaction (PPI) and hub genes were identified via the Search Tool for the Retrieval of Interacting Genes (STRING) and Cytoscape software. Hub genes were further validated in The Cancer Genome Atlas (TCGA) database. Subsequently, survival analysis was performed using the Kapla–Meier curve and Cox progression analysis. Based on univariate and multivariate Cox progression analysis, a gene signature was established to predict overall survival. Receiver operating characteristic curve was used to evaluate the prognostic value of the model. Results A total of 116 up-regulated genes and 84 down-regulated genes were identified. These DEGs were mainly enriched in the two pathways: cell cycle and p53 signaling way. According to the degree of protein nodes in the PPI network, 10 hub genes were identified. The mRNA expression levels of the 10 hub genes in LUSC were also significantly up-regulated in the TCGA database. Furthermore, a novel seven-gene signature (FLRT3, PPP2R2C, MMP3, MMP12, CAPN8, FILIP1 and SPP1) from the DEGs was constructed and acted as a significant and independent prognostic signature for LUSC. Conclusions The 10 hub genes might be tightly correlated with LUSC progression. The seven-gene signature might be an independent biomarker with a significant predictive value in LUSC overall survival.

目的 探讨长链非编码RNA DQ786243(LncRNA DQ786243)促进肝细胞癌细胞增殖的作用机制.方法 采用qRT-PCR法检测175例肝细胞癌癌组织及对应癌旁正常组织中LncRNA DQ786243的表达;在HepG2细胞中瞬时转染LncRNA DQ786243的小干扰RNA片段(si-DQ786243),CCK-8实验检测降低LncRNA DQ786243的表达对细胞增殖能力的影响,West-ern blot法检测降低LncRNA DQ786243表达对p18蛋白表达的影响;在HepG2细胞中瞬时共转染si-DQ786243、p18的小干扰RNA片段(si-p18),CCK-8法检测同时降低LncRNA DQ786243、p18的表达对细胞增殖能力的影响.结果 肝细胞癌组织中LncRNA DQ786243的表达增加(P<0.05);在HepG2细胞中降低LncRNA DQ786243的表达,细胞增殖减慢,p18表达增加(P均<0.05);降低p18表达可部分逆转LncRNA DQ786243表达下降导致的细胞增殖能力下降(P<0.05).结论 LncRNA DQ786243可通过下调p18的表达促进肝细胞癌细胞的增殖,进而促进肝细胞癌的发生、发展.

目的 研究金诺芬对表皮葡萄球菌及其生物膜的作用.方法 利用微量稀释法药敏试验检测金诺芬对表皮葡萄球菌浮游菌生长的影响,并利用结晶紫染色和激光共聚焦显微镜观察金诺芬对表皮葡萄球菌生物膜形成的影响.结果 金诺芬对表皮葡萄球菌的MIC和MBC分别为0.125～0.250 μg/mL和2.000～4.000 μg/mL.同时,4μg/mL金诺芬还能显著抑制表皮葡萄球菌标准菌株和临床菌株生物膜的形成(P＜0.05).通过激光共聚焦显微镜观察发现金诺芬能有效抑制生物膜的形成,降低生物膜的聚集,并增加死亡细菌的比例.结论 金诺芬能显著抑制表皮葡萄球菌浮游菌的增殖和生物膜的形成.

目的 研究血清及其主要成分对铜绿假单胞菌生物膜形成的影响.方法 在96孔板中用结晶紫染色法检测血清、清蛋白和转铁蛋白对铜绿假单胞菌生物膜形成的影响;激光头聚焦显微镜观察血清处理后铜绿假单胞菌生物膜的形态.结果 马血清能显著促进PAO1生物膜的形成,使生物膜的形成量从2.26±0.42增加到3.42+0.08(t=4.71,P＜0.01);而人血清能抑制其生物膜的形成,使生物膜形成量减少至0.81±0.10(t =4.71,P＜0.01).马血清可显著增加生物膜的总量并使生物膜呈片状分布;而人血清可显著抑制生物膜的形成,并使其呈散在点状分布.马血清可促进部分临床菌株生物膜的形成,而人血清能显著抑制所有临床菌株生物膜的形成.2.5 g/L清蛋白可使PAO1生物膜形成量从1.96±0.22增加到2.54+0.18(t=3.55,P＜0.05),而5 g/L转铁蛋白可使PAO1生物膜形成量从1.85±0.36减少到0.84±0.24(t 4.03,P＜0.05).结论 马血清和清蛋白可显著促进铜绿假单胞菌生物膜的形成,而人血清和转铁蛋白可抑制生物膜的形成.

Objective To summarize the experiences of diagnosing and treating acute pancreatitis (AP) after kidney transplantation .Methods From September 2007 to December 2017 , clinical data were retrospectively analyzed for 12 AP patients after kidney transplantation .Results They were diagnosed as AP within 72 h after an onset of abdominal pain .Among 4 recurrent cases within 1 week post-transplantation ,the curative interventions included non-operative therapy (n=2) and peripancreatic puncture & drainage (n=2) .AP occurred at 1 year post-transplantation (n=8) . Three cases were cured non-surgically while another 5 cases underwent surgery . The procedures included laparoscopic cholecystectomy ( n = 1 ) , endoscopic retrograde cholangiopancreatography (ERCP) for cholelithiasis (n=1) and peripancreatic puncture & drainage (n= 2) .One patient died after surgical debridement for adjacent pancreatic tissue .Conclusions After kidney transplantation , the occurrence of AP may be associated with immunosuppressants interfering with triglyceride metabolism and pancreatic microcirculation .For those with cholelithiasis-related pancreatitis ,surgical removal of precipitating factor is required .Mini-invasive puncture and drainage are preferred for severe non-gallstone pancreatitis while surgery is performed whenever necessary .

目的:通过特异性IgE(sIgE)检测分析荨麻疹患者过敏原的分布特点.方法:采用ELISA法对1355例荨麻疹患者进行血清过敏原sIgE检测.结果:1355例荨麻疹患者过敏原sIgE阳性检出率为69.0％(935例),sIgE阳性检出率较高的吸入性过敏原主要为霉菌(21.5％)、螨(17.4％)和梧桐花粉(14.2％),食物性过敏原主要为鸡蛋(23.5％)和花生(13.1％).男性患者总IgE增高者检出率高于女性(P<0.001).13～18岁年龄段人群sIgE检出率达到峰值.结论:荨麻疹患者过敏原以霉菌、鸡蛋、尘螨为主,过敏情况存在性别、年龄差异.