Preoperative MRI Classification May Not Predict Symptom Relief after Uterine Artery Embolization in Patients with Adenomyosis.

OBJECTIVE: To investigate the association between magnetic resonance imaging (MRI) classification and symptom relief after uterine artery embolization (UAE) in patients with adenomyosis. METHODS: Totally, 73 patients with symptomatic adenomyosis who underwent UAE were retrospectively analyzed. Preoperative MRI classification was defined as: type I, high signal on both T2-weighted images (T2WI) and T1-weighted images (T1WI); type III, high signal only on T2WI, and type II, high signal on neither T1WI nor T2WI. Dysmenorrhea was measured with the visual-analog scales and the degree of menorrhagia was measured according to the number of sanitary pads used in one menstrual cycle. Dysmenorrhea and menorrhagia were measured before UAE and 12 months after UAE. RESULTS: The number of the type I, II, III cases was 23, 37, and 13, respectively. The baseline characteristics of the three groups exhibited no significant difference. The alleviation rates of dysmenorrhea among type I, II, III cases were 73.9%, 89.2%, and 84.6%, respectively (P=0.455). The alleviation rates of menorrhagia for type I, II, III were 69.6%, 78.4%, and 92.3%, respectively (P=0.714). CONCLUSION: Pre-procedure MRI classification and symptom relief after UAE exhibited no significant association. UAE has a favorable mid-term control on dysmenorrhea and menorrhagia among patients with adenomyosis. Preoperative MRI classification might not indicate symptom relief. More research is needed before changing clinical practice.

Co-circulation of coxsackieviruses A-6, A-10, and A-16 causes hand, foot, and mouth disease in Guangzhou city, China.

BACKGROUND: Hand, foot, and mouth disease (HFMD) is a common infectious disease occurring in children under 5 years of age worldwide, and Enterovirus A71 (EV-A71) and Coxsackievirus A16 (CVA-16) are identified as the predominant pathogens. In recent years, Coxsackievirus A6 (CVA-6) and Coxsackievirus A10 (CVA-10) have played more and more important role in a series of HFMD outbreaks. This study aimed to understand the epidemic characteristics associated with HFMD outbreak in Guangzhou, 2018. METHODS: The clinical and laboratory data of 1220 enterovirus-associated HFMD patients in 2018 were analysed in this study. Molecular diagnostic methods were performed to identify its serotypes. Phylogenetic analyses were depicted based on the complete VP1 gene. RESULTS: There were 21 enterovirus serotypes detected in Guangzhou in 2018. Three serotypes of enterovirus, CVA-6 (364/1220, 29.8%), CVA-10 (305/1220, 25.0%), and CVA-16 (397/1220, 32.5%), were identified as the causative pathogens and accounted for 87.3% among all 1220 HFMD patients. In different seasons, CVA-6 was the predominant pathogen of HFMD during autumn, and CVA-10 as well as CVA-16 were more prevalent in summer. Patients infected by CVA-6, CVA-10 or CVA-16 showed similar clinical features and laboratory characteristics, and the ratios of severe HFMD were 5.8, 5.9, and 1.5% in the three serotypes. Phylogenetic analyses of VP1 sequences showed that the CVA-6, CVA-10, and CVA-16 sequences belonged to the sub-genogroup E2, genogroup E, and genogroup B1, respectively. CONCLUSIONS: CVA-6, CVA-10, and CVA-16 were the predominant and co-circulated serotypes in Guangzhou China, 2018, which should be the new target for prevention and control of HFMD. Our findings provide useful information for diagnosis, treatment, and prevention of HFMD.

[Interaction between stress granules and viruses].

Stress granule (SG) formation is a primary mechanism through which gene expression is rapidly modulated when the eukaryotic cells undergo cellular stresses (including heat shock, oxidative stress, starvation, viral infection). SGs have been proposed to affect mRNA translation and stability, as well as being linked to apoptosis and nuclear processes. Formation of SGs after viral infection result in blockade of viral protein synthesis and viral replication. Not surprisingly, viruses from diverse families have been found to modulate SG formation in infected cells by associating with important SG effector proteins. Here we provide a summary of the current understanding of the mechanism of SG formation, describe the current knowledge on viruses induce and/or modulate SGs in infected cells via phosphorylation of eIF2α, and regulation of SGs in virus systems. Further, we summarize recent progresses in understanding the relationship between viruses and stress granules in mammalian cells, and suggest that SG formation is an important aspect of the antiviral innate immune response.

Microwatts continuous-wave pumped second harmonic generation in few- and mono-layer GaSe.

We demonstrate the first achievement of continuous-wave (CW) pumped second harmonic generation (SHG) in few- and mono-layer gallium selenide (GaSe) flakes, which are coated on silicon photonic crystal (PC) cavities. Because of ultrahigh second order nonlinearity of the two-dimensional (2D) GaSe and localized resonant mode in the PC cavity, SHG's pump power is greatly reduced to microwatts. In a nine-layer GaSe coated PC cavity, while the optical power inside the GaSe flake is only 1.5% of that in the silicon PC slab, the SHG in GaSe is more than 650 times stronger than the third harmonic generation in silicon slab, indicating 2D GaSe's great potentials to strengthen nonlinear processes in silicon photonics. Our study opens up a new view to expand 2D materials' optoelectronic applications in nonlinear regime and chip-integrated active devices.

[The application of CRISPR-Cas9 gene editing technology in viral infection diseases].

The RNA-guided Cas9 nuclease from microbial clustered regularly interspaced short palindromic repeats (CRISPR) adaptive immune system has been used to facilitate efficient genome engineering in eukaryotic cells. The specific targeted genome is recognized and cut by gRNA-directed CRISPR/Cas9 complex, specifically by the endonuclease Cas9. The targeted gene locus could be repaired either by homology-directed repair or nonhomologous end joining, thus achieving a desired editing outcome. Viruses infect cells through specific receptors, and then the viral genome is transcribed, replicated and translated to complete its life cycle. As a result, some DNA virus and retrovirus genomes are integrated into the cellular genome. Gene therapy is a new trend to treat viral infected diseases. Given its designable sequence-specific editing of the targeted genome, CRISPR/Cas9 has tremendous potential in treating persistent and latent viral infections. In this review, we summarize the mechanism and progresses of CRISPR/Cas9, and also highlight its therapeutic application in infectious diseases.

[Host factor Moloney leukemia virus 10 (MOV10) protein inhibits replication of the xenotropic murine leukemia virus-related virus (XMRV)].

We investigated inhibition of Moloney leukemia virus 10 (MOV10) upon xenotropic murine leukemia virus-related virus (XMRV) and made a preliminary study of the mechanism of action. Using transfection, infection, western blotting and real-time polymerase chain reaction, we found that MOV10 inhibited XMRV replication. Using MOV10 overexpressed in viral producer cells, MOV10 was shown to reduce the infectivity of XMRV. MOV10 could be incorporated into XMRV, suggesting that MOV10 could undergo encapsidation by XMRV during viral assembly. MOV10 could also restrict the DNA production of XMRV in target cells. We found that the putative RNA-helicase domain of MOV10 maintained most of its XMRV inhibition. These results suggest that MOV10 could be required during the retroviral lifecycle. Perturbation of MOV10 disrupts the generation of infectious viral particles, suggesting that MOV10 has broad antiretroviral activity. Hence, MOV10 could be actively involved in host defense against retroviral infection.

[Establishment of a high-throughput screening assay for interaction inhibitor between BST-2 and Vpu].

BST-2 plays an important role in host innate immune response via inhibiting the release of HIV-1. HIV-1 accessory protein Vpu can interact with BST-2 through its transmembrane domains, degrade BST-2, and decrease BST-2 that are transported to the cell surface, thus anti-virus function of BST-2 is antagonized. In our study, we constructed plasmid RB connecting Rluc to the N-termimal of BST-2, and plasmid VE connecting EYFP to the C-terminal of Vpu. The two fusion proteins were co-expressed in 293 cells, and the interaction between the two proteins was detected via BRET method. And we further established a stable 293 cell line of dual-expression. By using BRET method, and the interaction between BST-2 and Vpu transmembrane domain as the target, a high-throughput screening assay was created that was expected to seek novel interaction inhibitors.

[Inhibition of HIV virus-like particles production by BST-2].

Recently, BST-2 has been identified as an effective cellular factor that prevents the release of human immunodeficiency virus type 1 and other enveloped viruses by tethering virus particles to the cell surface. Here, we showed that the production of HIV-1 virus-like particles was markedly inhibited by BST-2. Both the transient and stable expressing of BST-2 had the same function and Vpu rescued the release of HIV-1 VLP in the presence of human BST-2. Consistent with a direct tethering mechanism, we confirmed that proteolysis releases restricted virions and further showed that this removed the ectodomain of BST-2 from the cell surface.