The clinical course and manifestations of subepithelial lesions (SEL) patients tend to vary from different pathological types, therefore the accurate diagnosis of SEL would undoubtedly be beneficial to the treatment and prognosis of SEL patients. Based on the decision tree method, we developed a novel classification model for SELs by combining endoscopy with endoscopic ultrasound (EUS). We retrospectively collected data from 469 patients hospitalized in the Affiliated Hospital of Qingdao University between January 2017 to November 2021 for endoscopic resection. Chi-square test (P < 0.05), independence test (P < 0.001), and Pearson correlation analysis (|r|<0.8) were performed to identify significant variables among endoscopic and EUS features, which were subsequently incorporated into decision tree analysis. Finally, a hierarchical diagnostic model based on multiple decision trees was constructed. The predictive performance of the model was obtained through a five-fold cross-validation, and each decision tree model was evaluated by the area under the curve (AUC) and F1. A total of 13 variables were included in the construction of the model. The overall accuracy of this hierarchical model was 75.12

Endoscopic procedures and surgery are common treatments for early colorectal cancer (CRC). However, only approximately 10

ObjectivesEndoscopic full‐thickness resection (EFTR) for submucosal tumors (SMTs) has been technically challenging. This retrospective study aimed to evaluate the feasibility, safety, and efficacy of EFTR for upper gastrointestinal (GI) SMTs, including extraluminal lesions.MethodsWe retrospectively investigated 232 patients with SMTs who underwent EFTR from January 2014 to August 2023. Clinicopathologic characteristics, procedure‐related parameters, adverse events (AEs), and follow‐up outcomes were assessed in all patients.ResultsThe en‐bloc resection and en‐bloc with R0 resection rates were 98.7% and 96.1%, respectively. The average endoscopic tumor size measured 17.2 ± 8.7 mm, ranging from 6 to 50 mm. The resection time and suture time were 49.0 ± 19.4 min and 22.5 ± 11.6 min, respectively. In all, 39 lesions (16.8%) exhibited predominantly extraluminal growth. Gastrointestinal stromal tumors (GISTs) were the predominant pathology, accounting for 78.4% of the cases. Twenty‐one patients (9.1%) encountered complications, including pneumothorax (1/232, 0.43%), hydrothorax (1/232, 0.43%), localized peritonitis (3/232, 1.29%), and fever (16/232, 6.9%). Although the incidence of postoperative fever was notably higher in the predominantly extraluminal group (7/39, 17.9%) compared to the predominantly intraluminal group (9/193, 4.7%, P = 0.008), there were no significant differences in outcomes of the EFTR procedure. No instances of recurrence were observed during the mean follow‐up period of 3.7 ± 2.3 years.ConclusionEFTR was found to be feasible, safe, and effective for resecting upper GI SMTs, including lesions with predominantly extraluminal growth. Further validation in a prospective study is warranted.

PDF File - 4550K, Photographs of immunostaining of MyD88 and CD68 in serial sections from HCC tissue samples were taken for further analyses.

PDF File - 656K, Inhibition of MEK-ERK pathway reduced promotion of MyD88 in the migration of HCC cells. And inhibition of IL-6 also reduced promotion of MyD88 in the migration of HCC cells, but not in one's proliferation.

PDF File - 154K, Description of materials and methods in supplementary data

PDF File - 868K, MyD88 regulated the expression of several tumor modifiers in HCC-LM3 cells. And inhibition of PI3K/Akt, p38 and MEK-ERK pathway decreased NF-B signal activities upregulated by overexpressing MyD88 in HCC-LM3 as analyzed by the luciferase activities.

PDF File - 1518K, The level of MyD88 in HL7702 was markedly elevated by the stimulation of LPS, IL-1 or IL-1 and MyD88 was overexpressed or depleted significantly compared to their controls after transfected with pMyD88 or shMyD88.

The clinicopathologic characteristics of 110 cases of HCC, relationship between MyD88 expression and survival rate, Lenti-Virus shMyD88 inhibit tumorigenesis and metastasis of MHCC-PDF File - 194K, LM3 cells in nude mice, primers used in this study and antibodies used in this study.

随着我国老龄化进程的加快,老年医学的重要性日益凸显,老年科患者中肿瘤患者占据了较大比例,亟需专业的老年肿瘤学医生来保障老年肿瘤患者的健康.我国老年学专科化起步较晚,老年肿瘤学是一个年轻的学科,同时具备扎实的肿瘤学以及老年医学专科知识及丰富实践经验的医生非常少.重视老年肿瘤学青年医师的培养对于老年肿瘤学的发展具有重大意义.在培养过程中,应当施行具有针对性的专业培养模式,鼓励青年医生参加多学科合作讨论.强化整合医疗思维,扎实共病管理,实践缓和医疗.制定合理的培训制度,注重培养过程及结果考核,全面提高老年肿瘤学青年医生的综合素质.

Obesity is a major risk factor for many chronic diseases, including diabetes, fatty livers, and cancer. Expansion of the adipose mass has been shown to be related to adipogenic differentiation of adipose-derived mesenchymal stem cells (ASCs). However, the underlying mechanism of this effect has yet to be elucidated. We found that osteopontin (OPN) is downregulated in ASCs and adipose tissues of obese mice and overweight human beings because of methylation on its promoter, indicating that OPN may affect the development of obesity. Silencing of OPN in wild-type ASCs promotes adipogenic differentiation, while reexpression of OPN reduced adipogenic differentiation in OPN-/- ASCs. The role of extracellular OPN in ASC differentiation was further demonstrated by supplementation and neutralization of OPN. Additionally, OPN suppresses adipogenic differentiation in ASCs through the C/EBP pathways. Consistent with these in vitro results, by intravenous injection of OPN-expressing adenovirus to the mice, we found OPN can delay the development of obesity and improve insulin sensitivity. Therefore, our study demonstrates an important role of OPN in regulating the development of obesity, indicating OPN might be a novel target to attenuate obesity and its complications.

Inflammation and tubular cell death are the hallmarks of acute kidney injury. However, the precise mechanism underlying these effects has not been fully elucidated. Here we tested whether caspase-11, an inflammatory member of the caspase family, was increased in cisplatin or ischemia-reperfusion-induced acute kidney injury. Caspase-11 knockout mice after cisplatin treatment exhibited attenuated deterioration of renal functional, reduced tubular damage, reduced macrophage and neutrophil infiltration, and decreased urinary IL-18 excretion. Mechanistically, the upregulation of caspase-11 by either cisplatin or ischemia-reperfusion cleaved gasdermin D (GSDMD) into GSDMD-N, which translocated onto the plasma membrane, thus triggering cell pyroptosis and facilitated IL-18 release in primary cultured renal tubular cells. These results were further confirmed in GSDMD knockout mice that cisplatin-induced renal morphological and functional deterioration as well as urinary IL-18 excretion were alleviated. Furthermore, deficiency of GSDMD significantly suppressed cisplatin-induced IL-18 release but not the transcription and maturation level of IL-18 in tubular cells. Thus, our study indicates that caspase-11/GSDMD dependent tubule cell pyroptosis plays a significant role in initiating tubular cell damage, urinary IL-18 excretion and renal functional deterioration in acute kidney injury.

Spinel LiMn2O4 is one of the most important cathode materials but it still suffers from rapid capacity degradation during electrochemical cycling. Beside surface coating to improve the electrochemical performances, controlling the bulk morphology of LiMn2O4 ( LMO) is another effective strategy. In this work, porous LiMn2O4 microspheres composed of numerous primary nanoparticles are synthesized by micro-emulsion and coprecipitation methods. The porous structure and the primary nanoparticles size of LiMn2O4 are effected by the concentration of micro-emulsion and the precursor of Mn2+. The well-established porous LiMn2O4 microspheres with abundant ionic channels and good contact with electrolyte endow the spinel a remarkable electrochemical performance. After 300 cycles, 0.50 M-LMO sample presents excellent reversible capacity of 112.8 mAhg(-1) at 0.5 C rate. After 1000 cycles, 0.50 M-LMO sample presents the highest capacity of 97.9 mAhg(-1) and remains 54.2 mAhg(-1) at the current rate of 10 C. The porous spherical structure of cathode materials is essential to improve the rate performance due to the good contact between the active material and electrolyte.

正常组织中用于供能的脂肪酸主要来自饮食中的游离脂质,但在生长旺盛的肿瘤组织中,能量却来自于脂质的重新合成,所以在不同来源的肿瘤组织中见到脂质合成相关基因的变化,在原发肿瘤中和肿瘤发生相关的生脂基因功能已经基本明确.研究表明在肿瘤细胞中脂肪酸合成酶,硬脂酰辅酶A脱氢酶1、乙酰辅酶A羧化酶在肿瘤的生成和发展起非常重要的作用.脂肪酸的功能与能量贮存、生物膜的结构、信号转导和蛋白质的乙酰化有关,但是现在对脂肪重新生成进程在肿瘤转移中的作用尚不明确.由于耐药性的产生和化疗药物的毒副反应,恶性肿瘤的化疗效果一直不满意,为了寻找新的、选择性抗肿瘤方法,以脂代谢催化酶为靶点的抗肿瘤药物亟待进一步研究和应用.

Hepatocellular carcinoma (HCC) is the third leading cause of death in cancer patients worldwide. Understanding the molecular pathogenesis of HCC recurrence and chemoresistance is key to improving patients’ prognosis. In this study, we report that downregulation of ASPP2, a member of the ankyrin-repeat-containing, SH3-domain-containing, and proline-rich-region-containing protein (ASPP) family, bestowed HCC cells with stem-like properties and resistance to chemotherapy, including the expansion of side population fractions, formation of hepatospheroids, expression of stem cell-associated genes, loss of chemosensitivity, and increased tumorigenicity in immunodeficient mice. An expression profiling assay revealed that ASPP2 specifically repressed focal adhesion kinase (FAK)/Src/extracellular signal regulated kinase (ERK) signaling. ASPP2 does this by physically interacting with C-terminal Src kinase (CSK) and stimulating its kinase activity, which eventually leads to activator protein 1 (AP1)-mediated downregulation of Snail expression. In addition, pharmacologic inhibition of Src attenuated the effects of ASPP2 deficiency. Our findings present functional and mechanistic insight into the critical role of ASPP2 in the inhibition of HCC stemness and drug resistance and may provide a new strategy for therapeutic combinations to treat HCC.

The aim of this study is to identify and consolidate reliable endoscopic features associated with H. pylori infection in gastric mucosa, which is one of the major causes of gastric cancer. A total of 256 Chinese patients with symptomatic stomach disturbances were enrolled. Pathological examination was conducted using a light microscope and biopsy specimens stained with hematoxylin-eosin. Endoscopic examination was performed using a high resolution video endoscope. The association between endoscopic features and pathological H. pylori diagnosis was compared, and endoscopic features significantly associated with H. pylori infection were identified. A total of 14 endoscopic features were observed. Six of the 14 endoscopic features, including mucus on the gastric mucosa, diffuse redness, spotty redness of fundic mucosa, enlarged fold, mucosal edema, and RAC (type D and type I), were highly associated with H. pylori infection and were significantly sensitive and specific predictors for H. pylori diagnosis. The type R RAC was not significantly associated with H. pylori diagnosis. Our results indicate that conventional endoscopy features can be used to diagnose H. pylori in Chinese patients and can help determine the risk factor for gastric cancer.

Hepatocellular carcinoma (HCC) is a major health burden worldwide for its high incidence and mortality. Osteopontin (OPN) is a chemokine-like, matricellular phosphoglycoprotein whose expression is elevated in various types of cancer including HCC. OPN has been shown to be involved in tumorigenesis, chemo-resistance, metastasis and sustaining stem-like properties of cancer cells. Autophagy is a cellular process by which cytoplasmic components are degraded and recycled for maintaining cellular homeostasis. There is increasing evidence supports that autophagy plays a critical role for stem-like properties and chemo-resistance of cancer cells. However, the relationship between OPN and autophagy in maintaining cancer stem-like properties and chemo-resistance is yet to be clarified. Herein, we found that secreted OPN induced autophagy via binding with its receptor integrin αvβ3 and sustaining FoxO3a stability. OPN-elicited autophagy could promote cancer cell survival and resistance to chemotherapy drugs, as well as stem-like properties. Our findings indicated that OPN was capable of promoting chemo-resistance of HCCs via autophagy, which might provide a new strategy for the treatment of HCC.

Objective:To screen and identify the differential expression of miRNAs in rat serum post traumatic in-jury by the miRNA microarray technique. Methods:We chose partial hepatectomy(PH)as traumatic injury model. The serum ALT,AST,CRP and histological changes of the liver were measured to evaluate the severity of trauma. The miRNA microarray was used to assess the level and composition of serum miRNAs. The target genes of candidate miR-NA were predicted by bioinformatics software(MiRand and TargetScan). Results:There was significantly differential expression of miRNAs in rat serum post traumatic injury(24 miRNAs were more than 2 - fold up - regulated). Espe-cially,the expression of miR - 9 showed the highest up - regulated(more than 50 - fold). The results showed that CDH1,E - cadherin,MTHFD2,PDYN,MCPIP1,BCL2L11,CMA1,Map3k1 may be the target genes of miR - 9. Con-clusion:Injury caused by abdominal operation could make significant change in the spectra and levels of serum miR-NAs,suggesting that miRNAs may be involved in regulating the stress response post trauma.

Pancreatic ductal adenocarcinoma (PDAC) is known for its aggressive growth, and is characterized by early tissue invasion and metastasis with poor prognosis. Identifying prognostic markers and delineating the underlying mechanisms that promote progression of PDAC are important for the treatment of pancreatic cancer. TIP30, a newly identified tumor suppressor, appears to be involved in multiple processes during tumor development and metastasis. Here, we investigated the expression of TIP30 in PDAC and its prognostic value in PDAC patients. We examined the expression of TIP30 by immunohistochemistry in tissue microarrays containing 106 surgically resected PDAC. Kaplan–Meier analysis and Cox proportional hazards regression modeling analysis showed that TIP30 expression independently predicted better survival in pancreatectomy patients ( p < 0.01). Moreover, decreased TIP30 expression was associated with lymph node metastasis ( p < 0.05) and loss of E‐cadherin expression ( r = 0.329, p < 0.01). Suppression of TIP30 resulted in upregulation of Snail and subsequent downregulation of E‐cadherin in SW1990 cells containing high‐level of endogenous TIP30 . However, in the PANC‐1 cells containing low level of endogenous TIP30 , suppressing TIP30 caused upregulation of Slug instead of Snail, followed by upregulation of MMP9 rather than E‐cadherin. Taken together, our work reveals that decreased TIP30 expression is able to enhance invasion and metastasis of pancreatic cancer cells through upregulation of the Snail family members and may serve as an independent predictor for poor outcomes in PDAC patients.