Selenium, an essential trace element for human health, mainly exerts its biological function through selenoproteins. Selenoprotein M (SelM) is one of the highly expressed selenoproteins in the brain, but its biological effect and molecular mechanism remain unclear. Thus, the interactive protein of SelM was investigated in this paper to guide further study. In order to avoid protein translational stop, the selenocysteine-encoding UGA inside the open reading frame of SelM was site-directly changed to the cysteine-encoding UGC to generate the SelM' mutant. Meanwhile, its N terminal transmembrane signal peptide was also cut off. This truncated SelM' was used to screen a human fetal brain cDNA library by the yeast two-hybrid system. A new interactive protein of SelM' was found to be galectin-1 (Gal-1). This protein-protein interaction was further verified by the results of fluorescence resonance energy transfer techniques, glutathione S-transferase pull-down and co-immunoprecipitation assays. As Gal-1 plays important roles in preventing neurodegeneration and promoting neuroprotection in the brain, the interaction between SelM' and Gal-1 displays a new direction for studying the biological function of SelM in the human brain.

A new pulse-dilated photomultiplier tube (PD-PMT) with sub-20 ps temporal resolution and associated drivers have been developed for use detection and signal amplification in the inertial confinement fusion (ICF) community. The PD-PMT is coupled to a transmission line output in order to provide a continuous time history of the input signal. Electron pulse dilation provides high-speed detection capabilities by converting incoming signals into a free-electron cloud and manipulating the electron signal with electric and magnetic fields. This velocity dispersion is translated into temporal separation after the electrons transit into a drift space. The free electrons are then detected by using conventional time-resolved methods and the effective temporal resolution is improved about 12 times. In order to accurately obtain the actual device input signal, we experimentally investigated the relationship between microchannel plate (MCP) gain and electron energy during the first collision. We report the measurements with the PD-PMT, and the error source of the amplitude of the compressed signal is analyzed, which provides a reference for subsequent accurate construction.

During the past decade, many diagnostic instruments have been developed that utilize electronic pulse dilation to achieve temporal resolution in the sub-10 ps range. The motivation behind these development efforts was the need for advanced diagnostics in high-density physics experiments around the world. This technology converts the signal of interest into a free electron cloud, which is accelerated into a vacuum drift space. The acceleration potential varies over time and causes axial velocity dispersion in the electron cloud. This velocity dispersion is converted into time separation after electrons pass through drift space. Then, traditional time resolved methods were used to detect free electrons, and the effective temporal resolution was magnified many times. A gated microchannel plate (MCP) X-ray framing camera based on pulse-dilation technology has been designed and manufactured in the paper. Here, we discuss design details and applications of these instruments. The temporal resolution measured without using broadening technology is approximately 78 ps. When the excitation pulse is applied to the PC, the pulse dilation technique is used to increase the measured temporal resolution to 9 ps. The propagation speed of gated pulses in MCP microstrip lines was measured using fiber bundle method, which is approximately 1.8 × 10⁸ m/s.

This study aimed to map the cerebrospinal fluid (CSF) molecular landscape across distinct stages of tuberculosis progression and to identify multi-omics signatures associated with tuberculous meningitis (TBM). Integrated proteomic and metabolomic profiling of CSF from 17 patients representing three disease stages: pulmonary tuberculosis (TB), hematogenous disseminated tuberculosis (HDTB), and disseminated tuberculosis with concomitant tuberculous meningitis (HDTB+TBM) were performed. Quantitative proteomics and non-targeted metabolomics were combined with pathway enrichment and network-based analyses to delineate stage-specific molecular alterations. CSF multi-omics profiling revealed modest molecular changes between TB and HDTB, but a marked and coordinated remodeling during the transition from HDTB to TBM. Compared with the HDTB+TBM group, the TB group exhibited 546 upregulated and 410 downregulated proteins, together with 80 differentially abundant metabolites. Integrated analyses converged on glycolysis/gluconeogenesis, pentose phosphate metabolism, and extensive O- and N-glycan biosynthesis pathways, indicating coupled metabolic and glycosylation rewiring during meningeal involvement. Six proteins (ENO2, LDHB, GALNT7, MAN1C1, PGD, and B4GALT1) emerged as a biologically coherent signature distinguishing TBM from non-meningeal tuberculosis. This study maps the molecular trajectory from tuberculosis to disseminated disease and tuberculous meningitis, identifying TBM as a distinct neuro-immune-metabolic state and providing a framework for mechanism-informed biomarker development.