被建构的身体景观:“BM风”流行下青年女性审美异化现象研究

新媒介时代开启了网络审美的新纪元,大众媒介与消费主义合力构建了当代审美新景观。在众多美丽元素中,女性的身体成为备受关注的焦点。近年来,一种主打“短紧露”风格的“BM式”小码穿搭流行于各大社交媒体平台,并受到千万年轻女性追捧与效仿。这种穿搭时尚实则反映了一种审美异化现象。主要表现在当代青年女性因追求理想化的身体在身材焦虑与安全感缺失心理下对“BM”式审美产生误同心理,进而在社交媒体平台上进行异化的身体展演。青年女性的审美异化主要源于大众媒介与消费社会的合谋:大众媒介建构的拟态审美环境为公众提供的美的身体范式,消费主义下的资本逻辑又将美进行量化与符号化。二者的合谋导致单一、病态的“BM”审美应运而生。这种畸形的审美不仅导致女性主体性的缺失,也有碍和谐网络空间和良好社会审美风尚的建设。因此,应致力于发扬多元、流动的美,建立一种合乎公序良俗的社会审美机制,还女性一份纯粹的美丽与自由。

Lnc-BM通过FASTK/MT-ND6轴调节线粒体呼吸功能促进胃癌进展

目的探究Lnc-BM在胃癌发生发展中的作用及分子机制。方法收集36例胃癌患者的胃癌组织及配对的癌旁正常组织,RT-qPCR检测胃癌组织和癌旁正常组织中Lnc-BM的表达水平。构建Lnc-BM过表达或敲低细胞,平板克隆形成实验和CCK-8实验分析Lnc-BM对胃癌细胞增殖能力的影响,Transwell实验分析Lnc-BM对胃癌细胞迁移和侵袭能力的影响。RNA Pull-down实验分析Lnc-BM与FASTK蛋白的结合,Western blot检测Lnc-BM的表达对FASTK蛋白水平的影响。Western blot实验和Seahorse细胞能量代谢分析检测Lnc-BM过表达或敲降的胃癌细胞中线粒体相关蛋白的表达变化以及线粒体能量代谢的改变。裸鼠荷瘤实验进一步观察Lnc-BM对胃癌细胞体内生长的影响。结果Lnc-BM在胃癌组织中表达明显高于对应的癌旁正常组织。实验结果显示,过表达Lnc-BM促进胃癌细胞增殖、迁移和侵袭,敲低Lnc-BM抑制胃癌细胞增殖、迁移和侵袭(均P˂0.05)。RNA Pull-down结果显示,Lnc-BM可直接结合FASTK蛋白。Western blot实验结果显示,过表达Lnc-BM后FASTK蛋白水平升高,敲低Lnc-BM抑制FASTK蛋白表达(均P˂0.05)。与对照组相比,过表达Lnc-BM后,线粒体相关蛋白MT-ND6和TOM20表达升高(均P˂0.05)。Seahorse细胞能量代谢分析结果显示,Lnc-BM过表达显著提高细胞的线粒体呼吸能力(均P˂0.05)。在Lnc-BM稳定过表达细胞中敲低FASTK,可有效抑制Lnc-BM过表达细胞中增强的线粒体呼吸能力(均P˂0.05)。裸鼠皮下荷瘤实验显示,过表达Lnc-BM显著促进肿瘤生长(均P˂0.05)。结论Lnc-BM可通过FASTK/MT-ND6轴调节线粒体呼吸功能,促进胃癌进展。

RARRES2 regulates lipid metabolic reprogramming to mediate the development of brain metastasis in triple negative breast cancer

Background Triple negative breast cancer(TNBC),the most aggressive subtype of breast cancer,is characterized by a high incidence of brain metastasis(BrM)and a poor prognosis.As the most lethal form of breast cancer,BrM remains a major clinical challenge due to its rising incidence and lack of effective treatment strategies.Recent evidence suggested a potential role of lipid metabolic reprogramming in breast cancer brain metastasis(BCBrM),but the underlying mechanisms are far from being fully elucidated.Methods Through analysis of BCBrM transcriptome data from mice and patients,and immunohistochemical validation on patient tissues,we identified and verified the specific down-regulation of retinoic acid receptor responder 2(RARRES2),a multifunctional adipokine and chemokine,in BrM of TNBC.We investigated the effect of aberrant RARRES2 expression of BrM in both in vitro and in vivo studies.Key signaling pathway components were evaluated using multi-omics approaches.Lipidomics were performed to elucidate the regulation of lipid metabolic reprogramming of RARRES2.Results We found that downregulation of RARRES2 is specifically associated with BCBrM,and that RARRES2 deficiency promoted BCBrM through lipid metabolic reprogramming.Mechanistically,reduced expression of RARRES2 in brain metastatic potential TNBC cells resulted in increased levels of glycerophospholipid and decreased levels of triacylglycerols by regulating phosphatase and tensin homologue(PTEN)-mammalian target of rapamycin(mTOR)-sterol regulatory element-binding protein 1(SREBP1)signaling pathway to facilitate the survival of breast cancer cells in the unique brain microenvironment.Conclusions Our work uncovers an essential role of RARRES2 in linking lipid metabolic reprogramming and the development of BrM.RARRES2-dependent metabolic functions may serve as potential biomarkers or therapeutic targets for BCBrM.

电动汽车BMS从控板热分析及散热优化

针对电动汽车电池管理系统从控板服役过程中因温度过高和不均影响整车动力性、安全性问题,本文基于CFD理论,采用Icepak软件建立并验证了某商用BMS从控板热分析模型。首次在车载服役条件下,基于热分析模型开展了温度场分析和热均匀性优化研究。BMS从控板热仿真分析表明,均衡模块及供电模块因局部积热温度均超过BMS的设计温度限值60℃,整个BMS从控板最大温差为21.0℃。为此,进一步开展了BMS从控板散热路径分析,并通过改变均衡电阻间距、布局、PCB基材以及增设导热硅胶垫进行散热优化设计。提高了BMS从控板的散热能力,使BMS从控板的最高温度控制在设计规定值60℃以下,同时整个电路板的温差降为6.9℃,提高了BMS从控板在实际车载服役条件下的安全性和可靠性,可望为BMS从控板热设计与优化提供理论方法。

Biological factors driving colorectal cancer metastasis

Approximately 20%of colorectal cancer(CRC)patients present with metastasis at diagnosis.Among Stage I-III CRC patients who undergo surgical resection,18%typically suffer from distal metastasis within the first three years following initial treatment.The median survival duration after the diagnosis of metastatic CRC(mCRC)is only 9 mo.mCRC is traditionally considered to be an advanced stage malignancy or is thought to be caused by incomplete resection of tumor tissue,allowing cancer cells to spread from primary to distant organs;however,increa-sing evidence suggests that the mCRC process can begin early in tumor development.CRC patients present with high heterogeneity and diverse cancer phenotypes that are classified on the basis of molecular and morphological alterations.Different genomic and nongenomic events can induce subclone diversity,which leads to cancer and metastasis.Throughout the course of mCRC,metastatic cascades are associated with invasive cancer cell migration through the circulatory system,extravasation,distal seeding,dormancy,and reactivation,with each step requiring specific molecular functions.However,cancer cells presenting neoantigens can be recognized and eliminated by the immune system.In this review,we explain the biological factors that drive CRC metastasis,namely,genomic instability,epigenetic instability,the metastatic cascade,the cancer-immunity cycle,and external lifestyle factors.Despite remarkable progress in CRC research,the role of molecular classification in therapeutic intervention remains unclear.This review shows the driving factors of mCRC which may help in identifying potential candidate biomarkers that can improve the diagnosis and early detection of mCRC cases.

BM-MSCs延缓CD8^(+)初始T细胞衰老

目的验证骨髓间充质干细胞(BM-MSCs)缓解免疫衰老的作用,探究其衰老改善的主要免疫细胞群体。方法分离获得小鼠脾淋巴细胞,刺激增殖7d构建复制性衰老细胞模型。利用流式细胞测量术检测年轻对照组、复制性衰老对照组和BM-MSCs共培养组T细胞亚群衰老标志物p16ink4a(p16)和p21cip1(p21)的表达水平。结果T淋巴细胞复制性衰老模型中观察到持续增殖后CD8^(+)T细胞较CD4^(+)T细胞衰老显著,在CD8^(+)T细胞的初始细胞、效应细胞亚群中,效应细胞衰老最显著;BM-MSCs共培养对衰老的效应细胞没有明显影响,主要通过延缓初始T细胞的衰老,达到缓解CD8^(+)T细胞衰老的作用(P<0.01,P<0.001)。结论与BM-MSCs共培养可以缓解T细胞的复制性衰老表型,对CD8^(+)T细胞的抗衰作用更显著,主要通过抑制初始T细胞的衰老实现。

Mucosal esophageal carcinoma following endoscopic submucosal dissection with giant gastric metastasis:A case report and review of literature

BACKGROUND Esophageal carcinoma is a highly aggressive digestive cancer responsible for a notable proportion of cancer-related deaths worldwide.Its elevated metastatic rate contributes to a poor prognosis in affected patients.In this case review,we aim to summarize the metastatic characteristics of intramural gastric metastasis(IGM)in mucosal esophageal squamous carcinoma.CASE SUMMARY A 56-year-old man was admitted to our hospital because of a dry cough with an esophageal sensation for one year.Endoscopic examination revealed a 2.0 cm 1.0 cm,superficial esophageal squamous cell carcinoma,and the patient underwent endoscopic submucosal dissection(ESD).Fifteen months after ESD,positron emission tomography/computed tomography revealed that the metabolism of the stomach cardia wall had increased slightly.However,the mucosa of the gastric cardia was smooth under gastroendoscopy.Two years after ESD,endoscopic examination revealed a giant gastric cardia carcinoma,while the esophageal mucosa was smooth,and no advanced cancer was found.A biopsy of the gastric cardia indicated squamous-cell carcinoma.The patient received immunochemotherapy and radiotherapy for esophageal cancer for 8 mo and is currently under follow-up.CONCLUSION Early-stage esophageal carcinoma with IGM is rare.Despite the ESD of the primary lesion,IGM may still occur and should be closely monitored after ESD.

一种基于BM3D算法改进的图像去噪方法

在图像处理领域中,三维块匹配算法(BM3D)算法结合了空间域与频率域的相关特性,是当前图像去噪效果最好的算法之一。由于该算法存在计算耗时长、相似块提取不够准确、分割块内分布不同的相似特征无法提取等问题,论文提出基于Radon变换进行图像信息降维,并通过求解降维函数的方差值、以及方差最大值坐标定位进行相似块信息的判断,再计算各相似块相对参考块的像素均值比例,并放缩再用于去噪。实验结果显示,优化算法去噪图像相较于原算法去噪图像运行时间减短,图像质量提升。

基于改进BM3D的乳腺超声图像去噪算法研究

低噪声、高对比度的超声图像能极大提高医生对病情诊断的准确率。为解决乳腺超声图像在采集和传输过程中引入散斑噪声而导致图像质量恶化从而影响乳腺癌早期诊断的问题,提出一种基于改进BM3D的乳腺超声图像去噪算法。首先引入基于DBSCAN的超像素分割方法,对原图进行超像素分割得到相应的超像素标签矩阵;然后利用超像素标签矩阵引导BM3D算法中的块匹配过程,一方面可以减少待匹配块的搜索时间,另一方面可以给相似块度量提供辅助信息,进而提高块匹配的准确性;最后改进BM3D算法中的硬阈值滤波,采用自适应噪声参数估计进一步提升去噪效果。实验结果表明,改进BM3D算法的等效视数相较传统BM3D算法提高了1.75%,边缘保持指数提高了2.56%,而算法处理时间却减少了51.26%,说明其是一种兼顾去噪效果与运行时间的实用方法。

Solitary extraovarian primary peritoneal carcinoma with direct invasion into the liver,diaphragm and lung without peritoneal dissemination or distant metastasis

To the Editor:Extraovarian primary peritoneal carcinoma(EOPPC)is an uncommon malignancy with many similarities to epithelial ovarian carcinoma in histological,clinical,and etiological aspects[1].This phenomenon is explained by their common embryonal origin,in which both develop from the coelomic epithelium in the early embryological stage.Despite their similarities,the incidence of EOPPC is significantly lower than that of epithelial ovarian carcinoma(6.78 cases per million vs.120.5 cases per million)[1].

Kinesin 26B modulates M2 polarization of macrophage by activating cancer-associated fibroblasts to aggravate gastric cancer occurrence and metastasis

BACKGROUND The regulatory effects of KIF26B on gastric cancer(GC)have been confirmed,but the specific mechanism still needs further exploration.Pan-cancer analysis shows that the KIF26B expression is highly related to immune infiltration of cancerassociated fibroblasts(CAFs),and CAFs promote macrophage M2 polarization and affect cancers’progression.AIM To investigate the regulatory functions of KIF26B on immune and metastasis of GC.METHODS We analyzed genes’mRNA levels by quantitative real-time polymerase chain reaction.Expression levels of target proteins were detected by immunohistochemistry,ELISA,and Western blotting.We injected AGS cells into nude mice for the establishment of a xenograft tumor model and observed the occurrence and metastasis of GC.The degree of inflammatory infiltration in pulmonary nodes was observed through hematoxylin-eosin staining.Transwell and wound healing assays were performed for the evaluation of cell invasion and migration ability.Tube formation assay was used for detecting angiogenesis.M2-polarized macrophages were estimated by immunofluorescence and flow cytometry.RESULTS KIF26B was significantly overexpressed in cells and tissues of GC,and the higher expression of KIF26B was related to GC metastasis and prognosis.According to in vivo experiments,KIF26B promoted tumor formation and metastasis of GC.KIF26B expression was positively associated with CAFs’degree of infiltration.Moreover,CAFs could regulate M2-type polarization of macrophages,affecting GC cells’migration,angiogenesis,invasion,and epithelial-mesenchymal transition process.CONCLUSION KIF26B regulated M2 polarization of macrophage through activating CAFs,regulating the occurrence and metastasis of GC.

增强光催化产氢的TiO_(2)/BMS复合材料的制备及评价

利用改进的溶胶-凝胶法合成了TiO_(2)/BMS复合材料,并以这些复合材料为光催化剂,研究了其光催化产氢的性能。结果显示,在最优条件下,TiO_(2)/BMS复合材料光催化产氢速率是TiO_(2)的3.7倍。研究表明,TiO_(2)/BMS复合材料是一种优秀的光催化剂,可用于光催化水分解产氢。

Anal metastasis in esophageal cancer:A case report

BACKGROUND Esophageal cancer is the sixth leading cause of cancer-related death and eighth most common cancer,affecting>450000 people worldwide.Esophageal squamous cell carcinoma is the most common histological type,whereas esophageal adenoid cystic carcinoma(EACC)is rare.The liver is the most common distant metastatic site in esophageal cancer.Anal metastasis is rare and has not been reported in clinical practice before.Here,we report anal metastases in a patient with EACC after regular chemotherapy and surgical resection.CASE SUMMARY A 61-year-old esophageal cancer patient was found to have lung and brain metastases during standardized treatment.The patient’s treatment plan was continuously adjusted according to the latest treatment guidelines.However,the patient subsequently noticed rectal bleeding and itching,and after obtaining pathology results at the local hospital,anal metastasis of esophageal cancer was diagnosed.CONCLUSION Postoperative pathology and immunohistochemistry confirmed EACC with rare anal metastasis.More exploration of EACC diagnosis and treatment is needed.

Microbiota in colorectal cancer related to liver metastasis

The prevalence of colorectal cancer(CRC) is increasing annually and metastasis is the principal cause of death in patients with CRC, with the liver being the most frequently affected site. Many studies have shown a strong interplay between the gut flora, particularly Fusobacterium nucleatum(F. nucleatum), Escherichia coli, and Bacteroides fragilis, and the development of gut tumors. Some strains can induce gut inflammation and produce toxins that directly harm gut epithelial cells, ultimately accelerating the onset and progression of CRC. However,little clinical evidence exists on the specific interplay between the gut microflora and colorectal cancer liver metastasis(CRLM). Some research showed the existence of viable F. nucleatum in distant metastasis of CRC.Subsequently, gut microbiota products, such as lipopolysaccharides, sodium butyrate, and protein cathepsin K, were also found to affect the development of CRC. This article summarizes the mechanism and research status of the interplay between gut microflora and CRLM, discusses the importance of gut microflora in the treatment of CRLM, and proposes a new approach to understanding the mechanism of CRLM and potential treatments for the microbiome. It is anticipated that the gut microbiota will be a formidable therapeutic and prophylactic tool for treating and preventing CRLM.

Game-changing insights on vertebral skeletal stem cells in bone metastasis and therapeutic horizons

Greenblatt and his team have unveiled vertebral skeletal stem cells(vSSCs)as a critical player in the landscape of bone metastasis.This commentary delves into the transformative discoveries surrounding vSSCs,emphasizing their distinct role in bone metastasis compared to other stem cell lineages.We illuminate the unique properties and functions of vSSCs,which may account for the elevated susceptibility of vertebral bones to metastatic invasion.Furthermore,we explore the exciting therapeutic horizons opened by this newfound understanding.These include potential interventions targeting vSSCs,modulation of associated signaling pathways,and broader implications for the treatment and management of bone metastasis.By shedding light on these game-changing insights,we hope to pave the way for novel strategies that could revolutionize the prognosis and treatment landscape for cancer patients with metastatic bone disease.

Chemoradiotherapy plus tislelizumab for mismatch repair proficient rectal cancer with supraclavicular lymph node metastasis:A case report

BACKGROUND According to the latest report,colorectal cancer is still one of the most prevalent cancers,with the third highest incidence and mortality worldwide.Treatment of advanced rectal cancer with distant metastases is usually unsatisfactory,especially for mismatch repair proficient(pMMR)rectal cancer,which leads to poor prognosis and recurrence.CASE SUMMARY We report a case of a pMMR rectal adenocarcinoma with metastases of multiple lymph nodes,including the left supraclavicular lymph node,before treatment in a 70-year-old man.He received full courses of chemoradiotherapy(CRT)followed by 4 cycles of programmed death 1 inhibitor Tislelizumab,and a pathologic complete response(pCR)was achieved,and the lesion of the left supraclavicular lymph node also disappeared.CONCLUSION pMMR advanced rectal cancer with preserved intact distant metastatic lymph nodes may benefit from full-course CRT combined with immunotherapy.

NUDT5 promotes the growth,metastasis,and Warburg effect of IDH wild-type glioblastoma multiforme cells by upregulating TRIM47

Objective:To explore the regulatory mechanism of NUDT5 in glioblastoma multiforme(GBM).Methods:GEPIA database was used to predict the expressions of NUDT5 and tripartite motif family proteins 47(TRIM47)in GBM patients.RT-qPCR and Western blot analyses were performed to examine NUDT5 expression in GBM cells.LN-229 cell proliferation,migration as well as invasion were estimated by CCK-8,colony formation,wound healing,and Transwell assays following interference with NUDT5.ECAR assay,L-lactic acid kit,glucose detection kit,and ATP detection kit were applied for the detection of glycolysis-related indexes.Co-immunoprecipitation experiment was carried out to verify the relationship between NUDT5 and TRIM47.Results:GEPIA database showed that NUDT5 expression was significantly increased in GBM patients.Inhibiting the expression of NUDT5 in GBM cells significantly suppressed the viability,proliferation,invasion,migration,and glycolysis of GBM cells.Moreover,TRIM47 was highly expressed in GBM cells and interacted with NUDT5.Overexpression of TRIM47 partially reversed the inhibitory effect of NUDT5 downregulation on the proliferation,metastasis,and glycolysis of GBM cells.Conclusions:NUDT5 promotes the growth,metastasis,and Warburg effect of GBM cells by upregulating TRIM47.Both NUDT5 and TRIM47 can be used as targets for GMB treatment.

MicroRNAs:A novel signature in the metastasis of esophageal squamous cell carcinoma

Esophageal squamous cell carcinoma(ESCC)is a malignant epithelial tumor,characterized by squamous cell differentiation,it is the sixth leading cause of cancer-related deaths globally.The increased mortality rate of ESCC patients is predominantly due to the advanced stage of the disease when discovered,coupled with higher risk of metastasis,which is an exceedingly malignant charac-teristic of cancer,frequently leading to a high mortality rate.Unfortunately,there is currently no specific and effective marker to predict and treat metastasis in ESCC.MicroRNAs(miRNAs)are a class of small non-coding RNA molecules,approximately 22 nucleotides in length.miRNAs are vital in modulating gene expression and serve pivotal regulatory roles in the occurrence,progression,and prognosis of cancer.Here,we have examined the literature to highlight the intimate correlations between miRNAs and ESCC metastasis,and show that ESCC metastasis is predominantly regulated or regulated by genetic and epigenetic factors.This review proposes a potential role for miRNAs as diagnostic and therapeutic biomarkers for metastasis in ESCC metastasis,with the ultimate aim of reducing the mortality rate among patients with ESCC.

Shedding light on pancreatic metastasis of clear cell sarcoma:An exceptional journey

This editorial comments on the study by Liu et al investigating pancreatic metastasis of clear cell sarcoma(CCS)published in the World Journal of Clinical Cases.CCS is a rare and aggressive melanocytic tumor,that typically arises from tendons and aponeuroses of the limbs,and metastasizes to the lungs,bones,and brain.However,pancreatic metastasis has rarely been reported,presenting unique diagnostic and therapeutic challenges.Elucidating the clinical characteristics,imaging features,prognostic factors,and treatment outcomes of patients with pancreatic CCS metastasis is crucial.Surgery remains an effective management strategy for CCS.However,the high recurrence rate and low effectiveness of traditional adjuvant treatments necessitate a shift towards more personalized and targeted treatment plans.Research is needed to investigate and validate novel therapeutic approaches specifically tailored to the distinct genetic and molecular characteristics of rare malignancies like CCS.Additionally,the development of late metastases after a long disease-free interval is common in CCS patients.Therefore,routine postoperative surveillance for metastasis using computed tomography,magnetic resonance imaging,bone scans,and positron emission tomography scans is crucial.Moving forward,enhanced collaboration,investigation,and creative thinking among scientists,medical professionals,and legislators are essential to gain a deeper understanding of these rare presentations.

Role of cancer stem cell ecosystem on breast cancer metastasis and related mouse models

Breast cancer metastasis is responsible for most breast cancer-related deaths and is influenced by many factors within the tumor ecosystem,including tumor cells and microenvironment.Breast cancer stem cells(BCSCs)constitute a small population of cancer cells with unique characteristics,including their capacity for self-renewal and differentiation.Studies have shown that BCSCs not only drive tumorigenesis but also play a crucial role in promoting metastasis in breast cancer.The tumor microenvironment(TME),composed of stromal cells,immune cells,blood vessel cells,fibroblasts,and microbes in proximity to cancer cells,is increasingly recognized for its crosstalk with BCSCs and role in BCSC survival,growth,and dissemination,thereby influencing metastatic ability.Hence,a thorough understanding of BCSCs and the TME is critical for unraveling the mechanisms underlying breast cancer metastasis.In this review,we summarize current knowledge on the roles of BCSCs and the TME in breast cancer metastasis,as well as the underlying regulatory mechanisms.Furthermore,we provide an overview of relevant mouse models used to study breast cancer metastasis,as well as treatment strategies and clinical trials addressing BCSC-TME interactions during metastasis.Overall,this study provides valuable insights for the development of effective therapeutic strategies to reduce breast cancer metastasis.