Nanomaterials incorporated ultrasound contrast agents for cancer theranostics

Nanotechnology provides various nanomaterials with tremendous functionalities for cancer diagnostics and therapeutics.Recently, theranostics has been developed as an alternative strategy for efficient cancer treatment through combination of imaging diagnosis and therapeutic interventions under the guidance of diagnostic results. Ultrasound(US) imaging shows unique advantages with excellent features of real-time imaging, low cost, high safety and portability, making US contrast agents(UCAs)an ideal platform for construction of cancer theranostic agents. This review focuses on the development of nanomaterials incorporated multifunctional UCAs serving as theranostic agents for cancer diagnostics and therapeutics, via conjugation of superparamagnetic iron oxide nanoparticles(SPIOs), Cu S nanoparticles, DNA, si RNA, gold nanoparticles(GNPs), gold nanorods(GNRs), gold nanoshell(GNS), graphene oxides(GOs), polypyrrole(PPy) nanocapsules, Prussian blue(PB) nanoparticles and so on to different types of UCAs. The cancer treatment could be more effectively and accurately carried out under the guidance and monitoring with the help of the achieved theranostic agents. Furthermore, nanomaterials incorporated theranostic agents based on UCAs can be designed and constructed by demand for personalized and accurate treatment of cancer, demonstrating their great potential to address the challenges of cancer heterogeneity and adaptation, which can provide alternative strategies for cancer diagnosis and therapeutics.

Understanding the pathogenic evolution of Zika virus

Unlike the previous circulating strains that were not associated with significant human pathology,recent circulating Zika virus(ZIKV)strains isolated during the 2015–2016Brazilian Outbreak are highly suspected to cause neuropathology,including disorders of fetal brain development and Guillain-Barrésyndrome(Broutet et al.,2016).Studies have revealed that recent ZIKV strains can be spread through maternal-fetal(Calvet et al.,2016)and sexual(Hills et al.,2016)transmission,in addition to the traditional

Type I IFN augments IL-27-dependent TRIM25 expression to inhibit HBV replication

Hepatitis B virus(HBV)can cause chronic hepatitis B,which may lead to cirrhosis and liver cancer.Type I interferon(IFN)is an approved drug for the treatment of chronic hepatitis B.However,the fundamental mechanisms of antiviral action by type I IFN and the downstream signaling pathway are unclear.TRIM25 is an IFN-stimulated gene(ISG)that has an important role in RIG-I ubiquitination and activation.Whether TRIM25 is induced in liver cells by type I IFN to mediate anti-HBV function remains unclear.Here we report that interleukin-27(IL-27)has a critical role in IFN-induced TRIM25 upregulation.TRIM25 induction requires both STAT1 and STAT3.In TRIM25 knockout HepG2 cells,type I IFN production was consistently attenuated and HBV replication was increased,whereas overexpression of TRIM25 in HepG2 cells resulted in elevated IFN production and reduced HBV replication.More interestingly,we found that TRIM25 expression was downregulated in HBV patients and the addition of serum samples from HBV patients could inhibit TRIM25 expression in HepG2 cells,suggesting that HBV might have involved a mechanism to inhibit antiviral ISG expression and induce IFN resistance.Collectively,our results demonstrate that type I IFN-induced TRIM25 is an important factor in inhibiting HBV replication,and the IFN-IL-27-TRIM25 axis may represent a new target for treating HBV infection.

程序性坏死在癌症中的复杂作用（英文）

细胞程序性坏死是一种受到严格调控的细胞坏死形式,其发生依赖于受体相互作用蛋白(RIP)激酶RIPK1和RIPK3以及RIPK3底物混合谱系激酶域样蛋白(MLKL)的活化。由于细胞膜破裂,发生程序性坏死的细胞会释放损伤相关分子模式(DAMPs)分子,进而引发炎症反应。越来越多的研究表明细胞程序性坏死参与调控癌症的发生、发展和转移。肿瘤细胞程序性坏死被认为是一种具有激活抗肿瘤免疫功能的免疫原性细胞死亡,从而抑制肿瘤生长。细胞程序性坏死也被发现能增强髓系细胞诱导的适应性免疫抑制,进而促进肿瘤发生。此外,内皮细胞和肿瘤细胞的程序性坏死会促进肿瘤细胞的转移。在这篇综述中,我们总结了细胞程序性坏死信号通路及其在癌症中的复杂作用机制,并讨论了靶向程序性坏死调控蛋白在癌症治疗中的作用。

Type III interferon-induced CBFβinhibits HBV replication by hijacking HBx

Hepatitis B virus(HBV)and its associated chronic infection remain serious health threats worldwide.However,there is still no impactful approach for clinical treatment of hepatitis B patients.Therefore,developing a better understanding of the interactions between HBV and its host is particularly important.HBV infection has been reported to induce type-III but not type-I or type-II interferon(IFN).In this study,we identified CBFβ,an HIV enhancer,as an HBV restriction factor that is specifically induced by type-III IFN in the early stages of HBV infection.Type-III IFN-induced IL-10 played an important role in the production of CBFβ.Interestingly,the interaction between CBFβ-and HBV-encoded regulatory protein X(HBx)enhanced the stability of CBFβ,but notably blocked HBx-mediated promotion of HBV replication.CBFβexpression was lower in HBV patients than in healthy persons,and the addition of serum from HBV patients inhibited CBFβexpression in HepG2 cells.On the contrary,HBV via HBsAg inhibited type-III IFN-induced CBFβexpression and decreased the anti-HBV activity of type-III IFN,suggesting that HBV inhibits antiviral interferon-stimulated gene(ISG)expression and induces IFN resistance.Collectively,our results demonstrate that type-III IFN-triggered and IL-10-induced CBFβare crucial factors for inhibiting HBV replication,and the HBx–CBFβ–HBsAg axis reveals a new molecular mechanism of interaction between HBV and its hosts.