The ability of VITEK mass spectrometry (MS) in detection of bacterial resistance is currently under exploration and evaluation. In this study, we developed and validated a VITEK MS method to rapidly test carbapenemase-producing Klebsiella pneumoniae (CPKP). Solvents, antibiotic concentrations, crystal conditions and times, centrifugation speeds, and other factors were optimized to design a rapid sample pretreatment process for CPKP detection by VITEK MS. The related parameters of the mass spectrum were adjusted on the instrument to establish an CPKP detection mode. 133 clinically isolated strains of CPKP in the microbiology laboratory at the Shenzhen People\'s Hospital from 2004 to 2017 were selected for accuracy evaluation. The fresh suspected strains from the microbiology laboratory in 2020 were used to complete the clinical verification. Two antibiotics, meropenem (MEM) and imipenem (IPM), were used as substrates. These two substrates were incubated with suspected CPKP, and the results were obtained by VITEK MS detection. Using this method, different types of CPKP showed different detection results and all the CPKP strains producing KPC-2 and IMP-4 carbapenemase were detected by VITEK MS. Thus, VITEK MS can be used for rapid detection of CPKP, especially for some common types of CPKP. This method provides high accuracy and speed of detection. Combined with its cost advantages, it can be intensely valuable in clinical microbiology laboratories after the standard operating procedures are determined.

High corrosion kinetics and localised corrosion progress are the primary concerns arising from the clinical implementation of magnesium (Mg) based implantable devices. In this study, a binary Mg-lithium (Li) alloy consisting a record high Li content of 14% (in weight) was employed as model material aiming to yield homogenous and slow corrosion behaviour in a simulated body fluid, i.e. minimum essential medium (MEM), in comparison to that of generic Mg alloy AZ31 and biocompatible Mg-0.5Zn-0.5Ca counterparts. Scanning electron microscopy examination reveals single-phase microstructural characteristics of Mg-14Li (β-Li), whilst the presence of insoluble phases, cathodic to α-Mg matrix, in AZ31 and Mg-0.5Zn-0.5Ca. Though slight differences exist in the corrosion kinetics of all the specimens over a short-term time scale (no longer than 60 min), as indicated by potentiodynamic polarisation and electrochemical impedance spectroscopy, profound variations are apparent in terms of immersion tests, i.e. mass loss and hydrogen evolution measurements (up to 7 days). Cross-sectional micrographs unveil severe pitting corrosion in AZ31 and Mg-0.5Zn-0.5Ca, but not the case for Mg-14Li. X-ray diffraction patterns and X-ray photoelectron spectroscopy confirm that a compact film (25 μm in thickness) consisting of lithium carbonate (Li2CO3) and calcium hydroxide was generated on the surface of Mg-14Li in MEM, which contributes greatly to its low corrosion rate. It is proposed therefore that the single-phase structure and formation of protective and defect-free Li2CO3 film give rise to the controlled and homogenous corrosion behaviour of Mg-14Li in MEM, providing new insights for the exploration of biodegradable Mg materials.

Quinocetone, a new quinoxaline 1, 4-dioxide derivative, has been widely used as an animal feed additive in China. This study was conducted to explore the molecular mechanisms of apoptosis induced by quinocetone in HepG2 cells. MTT assay revealed that the viability of HepG2 cells was significantly inhibited by quinocetone in a dose- and time-dependent manner. Quinocetone-induced apoptosis in HepG2 cells was characterized by cell and nuclei morphology change, cell membrane phosphatidylserine translocation, DNA fragmentation, cleavage of poly (ADP-ribose) polymerase (PARP) and a cascade activation of caspase-8, caspase-9 and caspase-3. Simultaneously, quinocetone induced HepG2 cell cycle arrest, which was supported by overexpression of p21. Cytochrome c release was caused by the mitochondrial membrane potential dissipation, a process related to quinocetone-induced Bid cleavage and elevated Bax/Bcl-2 ratio. Moreover, quinocetone treatment caused the up-regulation of TNF-α and TNFR1 in HepG2 cells. Both soluble TNFR1 receptors and caspase inhibitors suppressed quinocetone-induced apoptosis. In addition, the protein levels of p53, p-p38 and p-JNK were increased in quinocetone-treated cells. Taken together, quinocetone induced apoptosis in HepG2 cells via activation of caspase, interaction of TNF-α and TNFR1 and modulation of the protein levels of Bid, Bax and Bcl-2, involving the participation of p53, p38 and JNK.

Amyloid-β (Aβ) peptides can exist in distinct forms including monomers, oligomers and fibrils, consisting of increased numbers of monomeric units. Among these, Aβ oligomers are implicated as the primary toxic species as pointed by multiple lines of evidence. It has been suggested that toxicity could be rendered by the soluble higher-molecular-weight (high-n) Aβ oligomers. Yet, the most culpable form in the pathogenesis of Alzheimer\'s disease (AD) remains elusive. Moreover, the potential interaction among the insoluble fibrils that have been excluded from the responsible aggregates in AD development, Aβ monomers and high-n oligomers is undetermined. Here, we report that insoluble Aβ fibrillar seeds can interact with Aβ monomers at the stoichiometry of 1:2 (namely, each Aβ molecule of seed can bind to two Aβ monomers at a time) facilitating the fibrillization by omitting the otherwise mandatory formation of the toxic high-n oligomers during the fibril maturation. As a result, the addition of exogenous Aβ fibrillar seeds is seen to rescue neuronal cells from Aβ cytotoxicity presumably exerted by high-n oligomers, suggesting an unexpected protective role of Aβ fibrillar seeds.