GB/T 5310-2023《高压锅炉用无缝钢管》国家标准概述

简要介绍了《高压锅炉用无缝钢管》(GB/T 5310—2023)修订的背景,重点解析修改的主要技术内容,对比分析国内外相关标准主要技术指标,并提出实施新版标准的建议,对企业执行标准具有指导意义。分析认为:新版GB/T 5310在标准的适用范围、钢管的尺寸精度、钢的化学成分、钢管的力学性能均与国外先进标准相当;在钢管的检验项目及指标要求方面,如无损检测、低倍、非金属夹杂物、显微组织、晶粒度和脱碳层要求等,新版GB/T 5310比国外先进标准规定项目多,部分指标要求严。

1+X证书制度下的书证融通:诉求、困境与破解

1+X证书制度是我国职业教育的一项具有时代与类型特征的制度创新,这与我国高校长期倡导的书证融通具有相同的价值诉求。然而在当前推行的1+X证书制度试点改革中,存在书证融通形式单一、教师书证融通破壁与重构能力不足、X职业技能证书社会认可与认知度不高、学生考证意愿不强等现实困境。职业院校应该积极联动企业、培训评价组织,努力融通“岗课赛证”,创新育人模式;对接产业技能标准,优化课程体系;提高教师“双师”素质,打造高水平师资队伍;以学习成果为导向,助力学生成长成才。

PpERF3 positively regulates ABA biosynthesis by activating PpNCED2/3 transcription during fruit ripening in peach

The plant hormone ethylene regulates ripening in climacteric fruits.The phytohormone abscisic acid(ABA)affects ethylene biosynthesis,but whether ethylene influences ABA biosynthesis is unknown.To explore this possibility,we investigated the interactions between the ABA biosynthesis genes PpNCED2/3 and the ethylene response transcription factor PpERF3 in peach fruit.The ABA content increased during fruit maturation and reached a peak at stage S4 III.The increase was greatly inhibited by the ethylene inhibitor 1-MCP,which also suppressed PpERF3 expression.PpERF3 shared a similar expression profile with PpNCED2/3,encoding a rate-limiting enzyme involved in ABA biosynthesis,during fruit ripening.A yeast one-hybrid assay suggested that the nuclear-localized PpERF3 might bind to the promoters of PpNCED2/3.PpERF3 increased the expression of PpNCED2/3 as shown by dual-luciferase reporters,promoter-GUS assays and transient expression analyses in peach fruit.Collectively,these results suggest that ethylene promotes ABA biosynthesis through PpERF3’s regulation of the expression of ABA biosynthesis genes PpNCED2/3.

Application of an antibody chip for screening differentially expressed proteins during peach ripening and identification of a metabolon in the SAM cycle to generate a peach ethylene biosynthesis model

Peach(Prunus persica)is a typical climacteric fruit that produces ethylene rapidly during ripening,and its fruit softens quickly.Stony hard peach cultivars,however,do not produce large amounts of ethylene,and the fruit remains firm until fully ripe,thus differing from melting flesh peach cultivars.To identify the key proteins involved in peach fruit ripening,an antibody-based proteomic analysis was conducted.A mega-monoclonal antibody(mAb)library was generated and arrayed on a chip(mAbArray)at a high density,covering~4950 different proteins of peach.Through the screening of peach fruit proteins with the mAbArray chip,differentially expressed proteins recognized by 1587 mAbs were identified,and 33 corresponding antigens were ultimately identified by immunoprecipitation and mass spectrometry.These proteins included not only important enzymes involved in ethylene biosynthesis,such as ACO1,SAHH,SAMS,and MetE,but also novel factors such as NUDT2.Furthermore,protein–protein interaction analysis identified a metabolon containing SAHH and MetE.By combining the antibody-based proteomic data with the transcriptomic and metabolic data,a mathematical model of ethylene biosynthesis in peach was constructed.Simulation results showed that MetE is an important regulator during peach ripening,partially through interaction with SAHH.

Y-shaped shunt for the treatment of Dandy-Walker malformation combined with giant arachnoid cysts:A case report

BACKGROUND Dandy-Walker malformation(DWM)was first reported in 1914.In this case report,a pediatric case was complicated with giant and isolated arachnoid cysts in the right cerebellar hemisphere along with the typical DWM.CASE SUMMARY The patient was at 20 mo old boy,with the complaint of staggering for more than 2 mo.He was admitted to the hospital due to high intracranial pressure and staggering.At admission,the patient had typical manifestations of high intracranial pressure,including vomiting,poor appetite and feeding difficulty.Physical examination revealed increased head circumference,closed anterior fontanelle,unstable standing,staggering,leaning right while walking and ataxia.After admission,he was diagnosed with DWM accompanied by giant isolated arachnoid cysts in the posterior fossa.He underwent Y-shaped three-way valve repair for treating differential pressure between the supratentorial hydrocephalus and the subtentorial arachnoid cysts at once.The child recovered well after the surgery.CONCLUSION In this case,supratentorial and subtentorial shunts were placed,which solved the problem of differential pressure between the supratentorial and subtentorial parts simultaneously.This provides useful information regarding treatment exploration in this rare disease.

BIR repeat-containing ubiquitin conjugating enzyme (BRUCE) regulation of β-catenin signaling in the progression of drug-induced hepatic fibrosis and carcinogenesis

BACKGROUND BIR repeat-containing ubiquitin conjugating enzyme(BRUCE)is a liver tumor suppressor,which is downregulated in a large number of patients with liver diseases.BRUCE facilitates DNA damage repair to protect the mouse liver against the hepatocarcinogen diethylnitrosamine(DEN)-dependent acute liver injury and carcinogenesis.While there exists an established pathologic connection between fibrosis and hepatocellular carcinoma(HCC),DEN exposure alone does not induce robust hepatic fibrosis.Further studies are warranted to identify new suppressive mechanisms contributing to DEN-induced fibrosis and HCC.AIM To investigate the suppressive mechanisms of BRUCE in hepatic fibrosis and HCC development.METHODS Male C57/BL6/J control mice[loxp/Loxp;albumin-cre(Alb-cre)-]and BRUCE Alb-Cre KO mice(loxp/Loxp;Alb-Cre+)were injected with a single dose of DEN at postnatal day 15 and sacrificed at different time points to examine liver disease progression.RESULTS By using a liver-specific BRUCE knockout(LKO)mouse model,we found that BRUCE deficiency,in conjunction with DEN exposure,induced hepatic fibrosis in both premalignant as well as malignant stages,thus recapitulating the chronic fibrosis background often observed in HCC patients.Activated in fibrosis and HCC,β-catenin activity depends on its stabilization and subsequent translocation to the nucleus.Interestingly,we observed that livers from BRUCE KO mice demonstrated an increased nuclear accumulation and elevated activity ofβ-catenin in the three stages of carcinogenesis:Pre-malignancy,tumor initiation,and HCC.This suggests that BRUCE negatively regulatesβ-catenin activity during liver disease progression.β-catenin can be activated by phosphorylation by protein kinases,such as protein kinase A(PKA),which phosphorylates it at Ser-675(pSer-675-β-catenin).Mechanistically,BRUCE and PKA were colocalized in the cytoplasm of hepatocytes where PKA activity is maintained at the basal level.However,in BRUCE deficient mouse livers or a human liver cancer cell line,both PKA activity and pSer-675-β-catenin levels were observed to be elevated.CONCLUSION Our data support a“BRUCE-PKA-β-catenin”signaling axis in the mouse liver.The BRUCE interaction with PKA in hepatocytes suppresses PKA-dependent phosphorylation and activation ofβ-catenin.This study implicates BRUCE as a novel negative regulator of both PKA andβ-catenin in chronic liver disease progression.Furthermore,BRUCE-liver specific KO mice serve as a promising model for understanding hepatic fibrosis and HCC in patients with aberrant activation of PKA andβ-catenin.

Loss of IKB kinase βpromotes myofibroblast transformation and senescence through activation of the ROS-TGFβ autocrine loop

Using forward and reverse genetics and global gene expression analyses, we explored the crosstalk between the IKB kinase β （IKKβ） and the transforming growth factor β （TGFβ） signaling pathways. We show that in vitro ablation of Ikkβ in fibroblasts led to progressive ROS accumulation and TGFβ activation, and ultimately accelerated cell migration, fibroblast-myofibroblast transformation and senescence. Mechanistically, the basal IKKβ activity was required for anti-oxidant gene expression and redox homeostasis. Lacking this activity, IKKβ-null cells showed ROS accumulation and activation of stress-sensitive transcription factor AP-1/c- Jun. AP-1/c-Jun activation led to up-regulation of the Tgfβ2 promoter, which in turn further potentiated intracellular ROS through the induction of NADPH oxidase （NOX）. These data suggest that by blocking the autocrine amplification of a ROS-TGFβ loop IKKβ plays a crucial role in the prevention of fibroblast-myofibroblast transformation and senescence.