An MXene–graphene field-effect transistor (FET) sensor for both influenza virus and 2019-nCoV sensing was developed and characterized. The developed sensor combines the high chemical sensitivity of MXene and the continuity of large-area high-quality graphene to form an ultra-sensitive virus-sensing transduction material (VSTM). Through polymer linking, we are able to utilize antibody–antigen binding to achieve electrochemical signal transduction when viruses are deposited onto the VSTM surface. The MXene–graphene VSTM was integrated into a microfluidic channel that can directly receive viruses in solution. The developed sensor was tested with various concentrations of antigens from two viruses: inactivated influenza A (H1N1) HA virus ranging from 125 to 250,000 copies/mL and a recombinant 2019-nCoV spike protein ranging from 1 fg/mL to 10 pg/mL. The average response time was about ∼50 ms, which is significantly faster than the existing real-time reverse transcription-polymerase chain reaction method (>3 h). The low limit of detection (125 copies/mL for the influenza virus and 1 fg/mL for the recombinant 2019-nCoV spike protein) has demonstrated the sensitivity of the MXene–graphene VSTM on the FET platform to virus sensing. Especially, the high signal-to-viral load ratio (∼10% change in source-drain current and gate voltage) also demonstrates the ultra-sensitivity of the developed MXene–graphene FET sensor. In addition, the specificity of the sensor was also demonstrated by depositing the inactivated influenza A (H1N1) HA virus and the recombinant 2019-nCoV spike protein onto microfluidic channels with opposite antibodies, producing signal differences that are about 10 times lower. Thus, we have successfully fabricated a relatively low-cost, ultrasensitive, fast-responding, and specific inactivated influenza A (H1N1) and 2019-nCoV sensor with the MXene–graphene VSTM.

SARS-CoV-2 infection begins with the association of its spike 1 (S1) protein with host angiotensin-converting enzyme-2 (ACE2). Targeting the interaction between S1 and ACE2 is a practical strategy against SARS-CoV-2 infection. Herein, we show encouraging results indicating that human cathelicidin LL37 can simultaneously block viral S1 and cloak ACE2. LL37 binds to the receptor-binding domain (RBD) of S1 with high affinity (11.2 nM) and decreases subsequent recruitment of ACE2. Owing to the RBD blockade, LL37 inhibits SARS-CoV-2 S pseudovirion infection, with a half-maximal inhibitory concentration of 4.74 μg/mL. Interestingly, LL37 also binds to ACE2 with an affinity of 25.5 nM and cloaks the ligand-binding domain (LBD), thereby decreasing S1 adherence and protecting cells against pseudovirion infection in vitro . Intranasal administration of LL37 to C57 mice infected with adenovirus expressing human ACE2 either before or after pseudovirion invasion decreased lung infection. The study identified a versatile antimicrobial peptide in humans as an inhibitor of SARS-CoV-2 attachment using dual mechanisms, thus providing a potential candidate for coronavirus disease 2019 (COVID-19) prevention and treatment.

Background Syphilis self-testing may help expand syphilis testing among men who have sex with men (MSM). China has rapidly scaled up human immunodeficiency virus (HIV) self-testing, creating an opportunity for integrated syphilis self-testing. However, there is a limited literature on implementing syphilis self-testing. Methods A cross-sectional online survey was conducted among Chinese MSM in 2018. Participants completed a survey instrument including sociodemographic characteristics, sexual behaviors, syphilis self-testing, and HIV self-testing history. Multivariable logistic regression was conducted to identify correlates of syphilis self-testing. We also recorded potential harms associated with syphilis self-testing. Results Six hundred ninety-nine MSM from 89 cities in 21 provinces in China completed the study. A total of 361/699 (51.7%) men tested for syphilis, of whom 174/699 (24.9%) men used syphilis self-testing. Among 174 who had self-tested, 90 (51.7%) reported that the self-test was their first syphilis test and 161 (92.5%) reported that they undertook syphilis self-testing together with HIV self-testing. After adjusting for covariates, syphilis self-testing was correlated with disclosure of sexual orientation to family or friends (adjusted odds ratio [aOR], 1.90; 95% confidence interval [CI], 1.32–2.73), reporting 2–5 male sexual partners (aOR, 1.81; 95% CI, 1.04–3.16), HIV self-testing (aOR, 39.90; 95% CI, 17.00–93.61), and never tested for syphilis in the hospital (aOR, 2.96; 95% CI, 1.86–4.72). Self-reported harms associated with syphilis self-testing were minimal. Conclusions Scaling up syphilis self-testing could complement facility-based testing in China among MSM. Self-testing may increase first-time testing and has limited harms. Our findings suggest that syphilis self-testing could be integrated into HIV self-testing services.

Pruning that selectively eliminates unnecessary axons/dendrites is crucial for sculpting the nervous system during development. During Drosophila metamorphosis, dendrite arborization neurons, ddaCs, selectively prune their larval dendrites in response to the steroid hormone ecdysone, whereas mushroom body γ neurons specifically eliminate their axon branches within dorsal and medial lobes. However, it is unknown which E3 ligase directs these two modes of pruning. Here, we identified a conserved SCF E3 ubiquitin ligase that plays a critical role in pruning of both ddaC dendrites and mushroom body γ axons. The SCF E3 ligase consists of four core components Cullin1/Roc1a/SkpA/Slimb and promotes ddaC dendrite pruning downstream of EcR-B1 and Sox14, but independently of Mical. Moreover, we demonstrate that the Cullin1-based E3 ligase facilitates ddaC dendrite pruning primarily through inactivation of the InR/PI3K/TOR pathway. We show that the F-box protein Slimb forms a complex with Akt, an activator of the InR/PI3K/TOR pathway, and promotes Akt ubiquitination. Activation of the InR/PI3K/TOR pathway is sufficient to inhibit ddaC dendrite pruning. Thus, our findings provide a novel link between the E3 ligase and the InR/PI3K/TOR pathway during dendrite pruning.

Autologous platelet membrane camouflage improves the bioavailability of mesoporous silica-coated bismuth sulfide nanorods in tumor radio-photothermal synergistic therapy.

The ongoing COVID-19 pandemic worldwide necessitates the development of therapeutics against SARS-CoV-2. ACE2 is the main receptor of SARS-CoV-2 S1 and mediates viral entry into host cells. Herein, membrane nanoparticles (NPs) prepared from ACE2-rich cells were discovered to have potent capacity to block SARS-CoV-2 infection. The membranes of human embryonic kidney-239T cells highly expressing ACE2 were applied to prepare NPs using an extrusion method. The nanomaterials, termed ACE2-NPs, contained 265.1 ng mg –1 ACE2 on the surface and acted as baits to trap S1 in a dose-dependent manner, resulting in reduced recruitment of the viral ligand to HK-2 human renal tubular epithelial cells. Aside from affecting receptor recongnition, S1 translocated to the cytoplasm and induced apoptosis by reducing optic atrophy 1 expression and increasing cytochrome c release, which was also inhibited by ACE2-NPs. Further investigations revealed that ACE2-NPs efficiently suppressed SARS-CoV-2 S pseudovirions entry into host cells and blocked viral infection in vitro and in vivo . This study characterizes easy-to-produce memrbane nanoantagonists of SARS-CoV-2 that enrich the existing antiviral arsenal and provide possibilities for COVID-19 treatment.

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