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Myocardial infarction (MI), known to be rapidly progressed and fatal, necessitates a timely and effective intervention particularly within golden 24 h. The crux is to develop a therapeutic agent that can early target the infarct site with integrated therapeutic capacity. Finding the AT 1 receptor being most over-expressed at 24 h after MI, we developed a nanovector (AT 1 -PEG-DGL) anchored with AT 1 targeting peptide, and simultaneously armed it with specific microRNA-1 inhibitor (AMO-1) to attenuate cardiomyocyte apoptosis. In vivo imaging after IV administration demonstrated that AT 1 -PEG-DGL quickly accumulated in the MI heart during the desired early period, significantly outperforming the control group without AT 1 targeting. Most importantly, a pronounced in-vivo anti-apoptosis effect was observed upon a single IV injection. Apoptotic cell death in the infarct border zone was significantly decreased and the myocardial infarct size was reduced by 64.1% as compared with that in MI control group, promising for early MI treatment. [ABSTRACT FROM AUTHOR]

Infection resulting from carbapenem-resistant Klebsiella pneumoniae (CRKP) is an intractable clinical problem. Outer membrane vesicles (OMVs) from CRKP are believed to be potential vaccine candidates. However, their immune response remains elusive due to low structural stability and poor size homogeneity. In this study, hollow OMVs were reinforced internally by size-controlled BSA nanoparticles to obtain uniform and stable vaccines through hydrophobic interaction. The result showed that the BSA-OMV nanoparticles (BN-OMVs) were homogenous with a size around 100 nm and exhibited a core-shell structure. Remarkably, subcutaneous BN-OMVs vaccination mediated significantly higher CRKP specific antibody titers. The survival rate of the mice infected with a lethal dose of CRKP was increased significantly after BN-OMV immunization. The adoptive transfer experiment demonstrated that the protective effect of BN-OMVs was dependent on humoral and cellular immunity. This study demonstrated that the structure optimization improved the immune efficacy of OMVs for vaccine development against CRKP. To synthesize BN, BSA molecules were first treated with DTT. Subsequently, SDS and MES were carefully added into the reduced BSA solution. After homogenous dispersion, the assembly process was performed in water bath at 65 °C under rigorous stirring (750 rpm). The BSA molecules were then assembled into NPs. The bacterial outer-membrane was collected in the form of outer membrane vesicles (OMVs) and then mixed with BNs with a diameter of approximately 70 nm. Through an extrusion process, the bacterial outer-membrane was coated with BN and translocated onto the BN surfaces to form bacterial outer-membrane-coated BN. Unlabelled Image [ABSTRACT FROM AUTHOR]

• The monoclonal antibodies against S protein of COVID-19 have cross-reaction with HCoV-OC43, HCoV-NL63 and HCoV-HKU1. • The N protein Ag-mAb system is more specific and accurate, suitable for immunoassay. • N protein strips we prepared can quickly and easily screen the swab samples within 11 min with 93.33 % accuracy rate. The SARS-CoV-2 virus responsible for coronavirus 2019 (COVID-19) poses a significant challenge to healthcare systems worldwide. According to the World Health Organization (WHO), the outbreak of COVID-19 has been a pandemic that infected more than 25.32 million people and caused more than 848.25 thousand deaths worldwide at the time of 1st September 2020. Despite governmental initiatives aimed to contain the spread of the disease, several countries are experiencing unmanageable increases in medical equipment and larger testing capacity. The current diagnosis based on nuclear acid requires specialized instruments, time-consuming, and laborious, the low-cost and convenient technologies were still urgently needed. Both spike and nucleocapsid are key structural proteins of COVID-19 with good immunogenicity, can serve as primary targets for immunoassay. After comparative research, we certified nucleocapsid antigen-monoclonal antibody (mAbs) system was more suitable for the COVID-19 immunodetection. Subsequently, we designed a rapid test strip based on it that can be used in large-scale screening of COVID-19 in population and more suitable for some remote and special needs areas were restricted by a medical condition or for quick and large quantities of screenings. [ABSTRACT FROM AUTHOR]

Animal studies have demonstrated that multiple exposures to sevoflurane during the postnatal period lead to impaired synaptogenesis and cognitive deficits in adulthood. However, the underlying mechanisms remain unclear. Histone deacetylase 6 (HDAC6), a unique isoform of class II histone deacetylases (HDACs), mediates diverse cellular processes such as cell survival, inflammation, intracellular trafficking and protein degradation. Varieties of literature suggest the importance of HDAC6 in memory formation and abnormal neurodegenerative diseases. The aim of this study was to investigate potential roles of HDAC6 in sevoflurane-induced developmental neurotoxicity. Postnatal day 7 (P7) rat pups were randomly assigned to control group and sevoflurane group (n = 6 for each group). They were exposed to 60% oxygen and 40% nitrogen with or without 3% sevoflurane for 2 h daily for three consecutive days (P7, P8 and P9). Immediately after the last exposure, both hippocampi were harvested for detection of HDAC6 expression and activity. Next, P7 rat pups were divided into control group, sevoflurane group, sevoflurane + Tubastatin A, and Tubastatin A groups (n = 6 for each group in molecular experiments; n = 16 for each group in behavioral testing). A dose of 25 mg/kg body weight of Tubastatin A (a selective HDAC6 inhibitor) were administrated intraperitoneally 30 min prior to each sevoflurane exposure. After treatments, expression levels of synaptophysin and postsynaptic density 95 protein (PSD95) were quantified using Western blot, and synaptic ultrastructure was evaluated by transmission electron microscopy. Additional pups were raised until P49 to measure cognitive performance using the Morris water maze test. Our results demonstrated that multiple sevoflurane exposures enhanced HDAC6 expression and activity in hippocampi of the developing brain. Tubastatin A ameliorated sevoflurane-induced decreases in synaptophysin and PSD95 expression during development, as well as synaptic ultrastructural damage and cognitive deficits in adulthood. In conclusion, HDAC6 is involved in the developmental neurotoxicity caused by multiple sevoflurane exposures and its inhibition may prevent related damage. • Multiple sevoflurane exposures enhance HDAC6 expression and activity in hippocampi of the developing brain. • HDAC6 is involved in the sevoflurane-induced impaired synaptogenesis and memory decline in adulthood. • HDAC6 inhibition has the potential to prevent developmental neurotoxicity of sevoflurane. [ABSTRACT FROM AUTHOR]