Objective To investigate the relationship between the methylation status of mucoprotein 3A (MUC3A)gene and the prognosis of children with neuroblastoma(NB).Methods A pathological section of 92 cases of NB from January 2013 to December 2015 in Department of Pathology,Children and Women′s Healthcare Hospital of Laiwu City,were co-llected.There were 43 males and 49 females;and their ages ranged from 3 months to 13 years old, in which 31 cases were less than 1 year old,and 61 cases were over 1 year old.Methylation specific polymerase chain reaction was used to detect the methylation status of MUC3A gene in 92 cases of NB,and the relationship between the methylation status of MUC3A gene and the clinicopathological features of NB were analyzed.According to the methyla-tion status of MUC3A gene,the 3-year survival rate and survival time of the MUC3A gene methylation positive group and the negative group were compared.Results For those over 1 year old,the pathological types were differentiated +undifferentiated and in clinical stage of stage Ⅲ+Ⅳ,their MYCN gene amplification,MUC3A gene methylation inci-dence(86.89%,91.80%,90.32%,81.82%)were significantly higher than those less than 1 year old,whose patho-logical types were well differentiated and in clinical stage of Ⅰ + Ⅱ,MYCN gene was not amplified(38. 71%, 29.03%,30. 00%,42.31%),and the differences were statistically significant(χ2= 23.007,39. 059,35. 480, 14.043,all P<0.001).The 3 year survival rate of MUC3A gene methylation positive children(26.15%)was signifi-cantly lower than that of MUC3A gene methylation negative children(66.67%),and the difference was statistically sig-nificant(χ2=13.283,P<0.001).The median survival time of MUC3A gene methylation positive children in 3-year old children was 19 months,significantly shorter than that of MUC3A gene methylation negative children(32 months), and the difference was statistically significant(log-rank:χ2=5.910,P=0.015).Conclusion The positive methyla-tion of MUC3A gene suggests that children with NB have poor prognosis.

Objective To investigate the pathological characteristics,diagnosis,treatment decision and short?term curative effect of abdominal desmoplastic small round cell tumor??Methods The clinical data of a case of desmoplastic small round cell tumor admitted to Gansu provincial people′s Hospital in April 2018 were analyzed retrospectively??The clinical manifestations, pathological features, diagnosis and differential diagnosis, treatment and prognosis of desmoplastic small round cell tumor were summarized and analyzed??Results The patient was successfully treated with maximum tumor reduction??The operation time was 360 minutes??The estimated blood loss during operation was 200 ml,and no blood was transfused during operation??The abdominal drainage tube was removed on the 8th day after operation and the liver function recovered well??Postoperative pathology: ( retroperitoneal) small round cell malignant tumor??Combined with clinical and immunohistochemical staining results: highly considered: desmoplastic small round cell tumor??The patient was discharged on the 16th day after operation??The patient was followed up for 4 months and the tumor recurred and liver metastasis??The follow?up period is now up to October 2018??Conclusion Desmoplastic small round cell tumor is a rare and highly malignant soft tissue small cell tumor with poor prognosis??Imaging examination and detection of tumor markers have no specificity and diagnose of it is difficult??Complete resection of the tumor and combined chemotherapy can improve the prognosis of the patients,but the prognosis is still not satisfactory, and more effective treatment decisions still need to be explored??

ObjectiveTo investigate the therapeutic effect of Baihe Wuyaotang （BWT） on non-alcoholic fatty liver disease （NAFLD） and elucidate its underlying mechanism. MethodC57BL/6J mice were randomly assigned to six groups： normal control， model， positive drug （pioglitazone hydrochloride 1.95×10^-3 g·kg^-1）， and low-， medium-， and high-dose BWT （1.3，2.5 and 5.1 g·kg^-1）. Following a 12-week high-fat diet （HFD） inducement， the mice underwent six weeks of therapeutic intervention with twice-daily drug administration. Body weight was monitored weekly throughout the treatment period. At the fifth week， glucose tolerance （GTT） and insulin tolerance （ITT） tests were conducted. Subsequently， the mice were euthanized for the collection of liver tissue and serum， and the subcutaneous adipose tissue （iWAT） and epididymal adipose tissue （eWAT） were weighed. Serum levels of total triglycerides （TG） and liver function indicators，such as alanine aminotransferase （ALT） and aspartate aminotransferase （AST）， were determined. Histological examinations， including oil red O staining， hematoxylin-eosin （HE） staining， Masson staining， and transmission electron microscopy， were performed to evaluate hepatic lipid deposition， pathological morphology， and ultrastructural changes， respectively. Meanwhile， Western blot and real-time quantitative polymerase chain reaction （Real-time PCR） were employed to analyze alterations， at both gene and protein levels， the insulin signaling pathway molecules， including insulin receptor substrate 1/2/protein kinase B/forkhead box gene O1 （IRS1/2/Akt/FoxO1）， glycogen synthesis enzymes phosphoenolpyruvate carboxy kinase （Pepck） and glucose-6-phosphatase （G6Pase）， lipid metabolism-related genes stearoyl-coA desaturase-1 （SCD-1） and carnitine palmitoyltransferase-1 （CPT-1）， fibrosis-associated molecules α-smooth muscle actin （α-SMA）， type Ⅰ collagen （CollagenⅠ）， and the fibrosis canonical signaling pathway transforming growth factor-β₁/drosophila mothers against decapentaplegic protein2/3（TGF-β₁/p-Smad/Smad2/3）， inflammatory factors such as interleukin（IL）-6， IL-8， IL-11， and IL-1β， autophagy markers LC3B Ⅱ/Ⅰ and p62/SQSTM1， and the expression of mammalian target of rapamycin （mTOR）. ResultCompared with the model group， BWT reduced the body weight and liver weight of NAFLD mice（P<0.05， P<0.01）， inhibited liver lipid accumulation， and reduced the weight of white fat： it reduced the weight of eWAT and iWAT（P<0.05， P<0.01） as well as the serum TG content（P<0.05， P<0.01）. BWT improved the liver function as reflected by the reduced ALT and AST content（P<0.05， P<0.01）. It improved liver insulin resistance by upregulating IRS2， p-Akt/Akt， p-FoxO1/FoxO1 expressions（P<0.05）. Besides， it improved glucose and lipid metabolism disorders： it reduced fasting blood glucose and postprandial blood glucose（P<0.05， P<0.01）， improved GTT and ITT（P<0.05， P<0.01）， reduced the expression of Pepck， G6Pase， and SCD-1（P<0.01）， and increased the expression of CPT-1（P<0.01）. The expressions of α-SMA， Collagen1， and TGF-β₁ proteins were down-regulated（P<0.05， P<0.01）， while the expression of p-Smad/Smad2/3 was downregulated（P<0.05）， suggesting BWT reduced liver fibrosis. BWT inhibited inflammation-related factors as it reduced the gene expression of IL-6， IL-8， IL-11 and IL-1β（P<0.01） and it enhanced autophagy by upregulating LC3B Ⅱ/Ⅰ expression（P<0.05）while downregulating the expression of p62/SQSTM1 and mTOR（P<0.05）. ConclusionBWT ameliorates NAFLD by multifaceted improvements， including improving IR and glucose and lipid metabolism， anti-inflammation， anti-fibrosis， and enhancing autophagy. In particular， BWT may enhance liver autophagy by inhibiting the mTOR-mediated signaling pathway.