And Migration
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2021 ◽  
Vol 144 ◽  
pp. 112325
Cheng Wang ◽  
Baojun Huang ◽  
Linxiao Sun ◽  
Xi Wang ◽  
Baofeng Zhou ◽  

2021 ◽  
pp. 001139212110485
Michaela Benson

In this article, the author advances understandings of the coloniality of British citizenship through the close examination of the status of the people of Hong Kong in Britain’s immigration and nationality legislation. This is a case that has been overlooked in most social scientific analysis of Britain’s citizenship–migration nexus. The article responds to Gurminder Bhambra’s call to recognise the connected sociologies and histories of citizenship, and the analysis is informed by the close reading of historical changes in legislation – from decolonisation and the making of the British nation-state to the post-Brexit construction of ‘Global Britain’ – and what these have meant for the people of Hong Kong. In dialogue with scholarship focused on the enduring colonial ties in present-day citizenship and migration regimes, the article offers an analysis inspired by Manuela Boatcă’s coloniality of citizenship and Ann Laura Stoler’s understanding of exception by design: imperial forms of governance producing differential rights within national populations that position some populations as ambiguous. Conceptualising the status of Hong Kongers in British legislation past and present as ambiguous by design, the author questions what the rhetoric of the Hong Kongers as ‘good migrants’ for ‘Global Britain’, the narrative at the heart of the promotion of the bespoke Hong Kong British Nationals (Overseas) (HK BN(O)) visa launched in early 2021, conceals from view. As the author argues, rather than a case apart in the context of increasingly restrictive immigration controls, the renewal of Britain’s obligations, commitments and responsibilities to the people of Hong Kong through this visa scheme provides further evidence of the enduring colonial entanglements in the formation of ‘Global Britain’ and its citizenship–migration nexus.

2021 ◽  
Vol 11 ◽  
Lijun Wang ◽  
Jing Li ◽  
Rongli Wang ◽  
He Chen ◽  
Ruiqi Wang ◽  

Nerve growth factor (NGF) is increasingly implicated in cervical cancer progression, but its mechanism in cervical cancer is unclear. Here, studies demonstrate that NGF inhibits the Hippo signaling pathway and activates Yes-associated protein (YAP) to induce cervical cancer cell proliferation and migration. Our results suggested that stimulation of NGF promoted cell growth and migration and activated YAP in HeLa and C-33A cell lines. The expression of YAP target genes (CTGF and ANKRD1) was upregulated after NGF treatment. The NGF inhibitor Ro 08-2750 and siRNA-mediated NGF receptor gene silencing suppressed HeLa and C-33A cells proliferation and migration, activated large suppressor kinase 1 (LATS1) kinase activity, and suppressed YAP function. In addition, the expression of YAP target genes (CTGF and ANKRD1) was suppressed by Ro 08-2750 treatment in HeLa and C-33A cells. Interestingly, proliferation was significantly higher in NGF-treated cells than in control cells, and this effect was completely reversed by the YAP small molecule inhibitor-verteporfin. Furthermore, the mouse xenograft model shows that NGF regulates YAP oncogenic activity in vivo. Mechanistically, NGF stimulation inactivates LATS1 and activates YAP, and NGF inhibition was found to induce large suppressor kinase 1 (LATS1) phosphorylation. Taken together, these data provide the first direct evidence of crosstalk between the NGF signaling and Hippo cancer pathways, an interaction that affects cervical cancer progression. Our study indicates that combined targeting of the NGF signaling and the Hippo pathway represents a novel therapeutic strategy for treatment of cervical cancer.

2021 ◽  
Jianming Wei ◽  
Xibo Gao ◽  
Bingbing Ren ◽  
Daqing Sun ◽  
Tong Liu

Abstract Background: Longstanding type 2 diabetes mellitus (T2DM) is an increased risk of pancreatic cancer (PC) in western populations, and PC is also a cause of T2DM. However, the association of glucose metabolism between T2DM and PC remains unclear. Methods: Differentially expressed genes (DEGs) were identified by bioinformatic analysis from Gene Expression Omnibus (GEO) datasets GSE20966 and GSE16515, respectively. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway, Gene Set Enrichment Analysis (GSEA), the Kaplan-Meier (KM) Plotter and Tumor Immune Estimation Resource (TIMER) database were applied. Pancreatic cancer cell lines and primary PDAC samples were used. Cell culture, immunohistochemistry (IHC), siRNA transfection, Western blot, RT-PCR, and migration assay, animal xenograft model studies and statistical analysis were performed in this study. Results: We identified 64 DEGs in GSE20966 of T2DM, and 296 DEGs were identified in GSE16515 of pancreatic cancer, respectively. T2DM-DEGs were mainly enriched in synaptic vesicle cycle, protein export. KEGG pathways in pancreatic cancer included spliceosome, RNA transport. Here, ISG20L2 was identified as only a co-expressed gene between T2DM and PDAC. We found that the expression of ISG20L2 was associated with tumor immune cell infiltration. ISG20L2 was significantly upregulated in PDAC and associated with prognosis of PDAC patients. Moreover, ISG20L2 expression was regulated by GLUT1 , HK2 , LDHA , PKM1 and PKM2 related with glycolysis in PDAC. ISG20L2 promoted PDAC cell proliferation and migration both in vitro and in vivo. Conclusion: This study showed that ISG20L2 promoted the progression and ISG20L2 may be a potential therapeutic strategy in PDAC.

2021 ◽  
pp. 1-11
Dong-Sheng Lin ◽  
Chi-Yuan Zhang ◽  
Liang Li ◽  
Guo-Hong Ye ◽  
Lu-Ping Jiang ◽  

Atherosclerosis is the leading global cause of mortality. The occurrence of coronary artery disease (CAD) is regulated by a diversity of pathways, including circRNAs. However, the potential mechanisms of circRNAs in CAD remain unclear. Here, qRT-PCR was used to examine the expressions of miR-149 and circ_ROBO2. Their influences on cell proliferation, migration, and apoptosis were measured by CCK-8, trans­well, and flow cytometry assays, respectively. The protein levels of p-IκBα and NF-κB p65 were examined using western blot. The molecular interactions were validated using dual luciferase reporter and RNA pull-down assays. The expression patterns of circ_ROBO2 and miR-149 in CAD patients and PDGF-BB-treated human aortic smooth muscle cells (HASMCs) were upregulated and downregulated, respectively. Knockdown of circ_ROBO2 could markedly inhibit the capabilities of proliferation and migration, enhance the apoptotic rate, and suppress NF-κB signaling in PDGF-BB-treated HASMCs. Mechanistically, circ_ROBO2 acted as a sponge of miR-149 to activate TRAF6/NF-κB signaling. Rescue studies demonstrated that neither silencing miR-149 nor activation of NF-κB signaling obviously abolished the biological roles of circ_ROBO2 knockdown in PDGF-BB treated-HASMCs. This discovery elucidated a functional mechanism of circ_ROBO2 in CAD, suggesting that circRNAs serve a vital role in the progression of CAD.

2021 ◽  
Vol 22 (6) ◽  
Chuanli Zhang ◽  
Limin Zhu ◽  
Xun Liu ◽  
Meixia Jiang ◽  
Qin Tang ◽  

2021 ◽  
Vol 21 (1) ◽  
Yanhui Li ◽  
Yue Xiong ◽  
Zhen Wang ◽  
Jianjun Han ◽  
Sufang Shi ◽  

Abstract Background Breast cancer (BC) is one of the most common cancers and the leading cause of death in women. Previous studies have demonstrated that FAM49B is implicated in several tumor progression, however, the role and mechanism of FAM49B in BC remain to be explored. Therefore, in this study, we aimed to systematically study the role of FAM49B in the proliferation, metastasis, apoptosis, and chemoresistance of BC, as well as the corresponding molecular mechanisms and downstream target. Methods The ONCOMINE databases and Kaplan–Meier plotter databases were analyzed to find FAM49B and its prognostic values in BC. FAM49B expression in BC and adjacent non-tumor tissues was detected by western blot and IHC. Kaplan–Meier analysis was used to identify the prognosis of BC patients. After FAM49B knockdown in MCF-7 and MDA-MB-231 cells, a combination of co-immunoprecipitation, MTT, migration, and apoptosis assays, nude mouse xenograft tumor model, in addition to microarray detection and data analysis was used for further mechanistic studies. Results In BC, the results showed that the expression level of FAM49B was significantly higher than that in normal breast tissue, and highly expression of FAM49B was significantly positively correlated with tumor volume, histological grade, lymph node metastasis rate, and poor prognosis. Knockdown of FAM49B inhibited the proliferation and migration of BC cells in vitro and in vivo. Microarray analysis revealed that the Toll-like receptor signaling pathway was inhibited upon FAM49B knockdown. In addition, the gene interaction network and downstream protein validation of FAM49B revealed that FAM49B positively regulates BC cell proliferation and migration by promoting the Rab10/TLR4 pathway. Furthermore, endogenous FAM49B interacted with ELAVL1 and positively regulated Rab10 and TLR4 expression by stabilizing ELAVL1. Moreover, mechanistic studies indicated that the lack of FAM49B expression in BC cells conferred more sensitivity to anthracycline and increased cell apoptosis by downregulating the ELAVL1/Rab10/TLR4/NF-κB signaling pathway. Conclusion These results demonstrate that FAM49B functions as an oncogene in BC progression, and may provide a promising target for clinical diagnosis and therapy of BC.

Claudia Tanja Mierke

Krishna Amuluru ◽  
Fawaz Al-Mufti ◽  
Daniel H. Sahlein ◽  
John Scott ◽  
Andrew Denardo

The Woven EndoBridge (WEB) is an intrasaccular flow-disrupting device for the treatment of wide-necked saccular cerebral aneurysms. As with any neuroendovascular device, complications in the form of malpositioning and migration must be managed quickly and safely. Few studies have reported complication management techniques in instances of dislocated or migrated WEB devices. We retrospectively describe a case of a malpositioned WEB device that was successfully adjusted with the use of a gooseneck snare. Multiple other intra-procedural bailout strategies for management of WEB malposition and migration were considered, and are herein discussed. Operators should be aware of the causes of WEB malposition and a variety of bailout strategies.

O. Lyulyov ◽  
T. Pimonenko ◽  
H. Shvindina ◽  
D. Pudryk

Abstract. The paper is focused on identifying interlinks between migration growth and economic development indicators. The main idea is to check the statements that migrants move to the countries with high levels of urbanization, high export-import, and budget potential, social, economic, and infrastructural development, high rates of innovations, accessible and effective health care system, financial stability.The previous studies in the sphere of migration were analyzed in detail, and their outcomes became a starting point for selection of the parameters that may affect the net migration growth. The paper is designed as quantitative research, based on Fuzzy-Logic Cognitive Maps (FCM) modeling for mapping the most influential parameters of nine systems (concepts) of national economic development and migration growth. In this study the matrices of causality and directions of influence of parameters of the nineconceptsand 53 sub-concepts and migration growth were computed, and cognitive maps of causal links between net migration growth and chosen parameters of national development were visualized. It was found that the highest level of positive interaction exists between net migration growth and such indicators as «International Tourism», «Income», «Total Government Spending», «Birth rates», «GDP per capita». And negative interactions were found between migration growth and risk of not covering the expenditures of surgical care, including catastrophic non-coverage, and mortality. The recommendations for further improvements of migration policy, social policy and budgeting policy were offered. Keywords: migration, net migration growth, national development, fuzzy cognitive maps, FCM modelling, determinants. JEL Classification F22, J01, O15 Formulas: 3; fig.: 11; tabl.: 17; bibl.: 45.

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