A resting-state EEG dataset for sleep deprivation.

To investigate the impact of sleep deprivation (SD) on mood, alertness, and resting-state electroencephalogram (EEG), we present an eyes-open resting-state EEG dataset. The dataset comprises EEG recordings and cognitive data from 71 participants undergoing two testing sessions: one involving SD and the other normal sleep. In each session, participants engaged in eyes-open resting-state EEG. The Psychomotor Vigilance Task (PVT) was employed for alertness measurement. Emotional and sleepiness were measured using Positive and Negative Affect Scale (PANAS) and Stanford Sleepiness Scale (SSS). Additionally, to examine the influence of individual sleep quality and traits on SD, Pittsburgh Sleep Quality Index (PSQI) and Buss-Perry Aggression Questionnaire (BPAQ) were utilized. This dataset's sharing may contribute to open EEG measurements in the field of SD.

Aspherical interferometric probe with wave-plate-array detection: system design and nonlinearity analysis.

Optical probes are the preferred choice for high-precision surface metrology, necessitating improved flexibility and a broader range of motion to adapt to the increasing complexity of surfaces. This study introduces an interferometric probe designed for measuring aspheric surfaces, utilizing a wave-plate-array detection component. By integrating splitter elements into the detector, the probe improves integration and dynamic scanning performance, while maintaining high-precision measurement capability. The system design and working principle are explored, and comprehensive nonlinear models based on the Jones matrix theory are established. These models focus on the nonlinear errors arising from alignment errors in various cases. Moreover, rigorous numerical simulations and optical experiments are conducted to validate the proposed models. When the alignment error reaches 10°, it results in a maximum nonlinear error of 3.02 nm. The experimental results demonstrate the effectiveness of the models in capturing nonlinear errors induced by alignment errors, providing a theoretical foundation for error reduction and compensation.

NLRC4 inflammasome-dependent cell death occurs by a complementary series of three death pathways and determines lethality in mice.

Inflammasome is an innate immune defense mechanism, but its overactivation can lead to host death. Here, we show that cell death dictates mouse death caused by NLRC4 inflammasome overactivation. To execute NLRC4-dependent cell death, three death pathways complement each other in a specific order: Pyroptosis pathway requiring caspase-1 and GSDMD is the default path; impairment of it initiates ASC-mediated caspase-8­dependent apoptosis; when these two pathways are blocked, caspase-1 triggers intrinsic apoptotic pathway. Blocking one or two of these death pathways inhibits induction of various cytokines and lipid mediators, but mice still succumb, and only genetic deletions that block all death paths prevent NLRC4-mediated cell death, tissue damage, and mice death. In addition, infection of nonpropagative Salmonella-caused mice death is attenuated by blocking these death pathways. Thus, to reduce the lethality of infection-related diseases, preventing cell death might be necessary when propagation of infected pathogen was controlled by other means.

Mechanical insight into the formation of H2S from thiophene pyrolysis: The influence of H2O.

The thermal utilization of waste rubber is accompanied by the release of sulfur, and the release of H2S to the gas phase is one of the crucial issues. In this work, density functional theory (DFT) calculations and wave function analysis were employed to explore the possible formation pathways of H2S and its precursor (·SH radical) during the pyrolysis of thiophene in the presence of H2O. It indicates that H2O affects the decomposition of thiophene and the formation of H2S in two patterns. First, H2O can participate in the hydrogen transfer process by acting as a catalyst or generating weak hydrogen bonds with thiophene. In this way, the hydrogen transfer reactions are promoted with lower energy barriers, and thus the formation of H2S is facilitated by H2O without changing the pyrolysis pathways. Secondly, H2O can saturate the thiophene ring by addition reactions and alter the generation pathways of H2S significantly. The energy barriers can be decreased with one or two CC bonds of thiophene being saturated. The completely saturated thiophene results in a greater decline of the overall energy barriers for H2S formation. H2O provides the H atom for H2S in the second pattern. Due to the combination of the two influence patterns, the release of H2S can be promoted greatly in the presence of H2O. The present study aims to lay a foundation for the clean thermal utilization of thiophene/rubber and to inspire the advance of desulfurization techniques.

SAMD4 family members suppress human hepatitis B virus by directly binding to the Smaug recognition region of viral RNA.

HBV infection initiates hepatitis B and promotes liver cirrhosis and hepatocellular carcinoma. IFN-α is commonly used in hepatitis B therapy, but how it inhibits HBV is not fully understood. We screened 285 human interferon-stimulated genes (ISGs) for anti-HBV activity using a cell-based assay, which revealed several anti-HBV ISGs. Among these ISGs, SAMD4A was the strongest suppressor of HBV replication. We found the binding site of SAMD4A in HBV RNA, which was a previously unidentified Smaug recognition region (SRE) sequence conserved in HBV variants. SAMD4A binds to the SRE site in viral RNA to trigger its degradation. The SAM domain in SAMD4A is critical for RNA binding and the C-terminal domain of SAMD4A is required for SAMD4A anti-HBV function. Human SAMD4B is a homolog of human SAMD4A but is not an ISG, and the murine genome encodes SAMD4. All these SAMD4 proteins suppressed HBV replication when overexpressed in vitro and in vivo. We also showed that knocking out the Samd4 gene in hepatocytes led to a higher level of HBV replication in mice and AAV-delivered SAMD4A expression reduced the virus titer in HBV-producing transgenic mice. In addition, a database analysis revealed a negative correlation between the levels of SAMD4A/B and HBV in patients. Our data suggest that SAMD4A is an important anti-HBV ISG for use in IFN therapy of hepatitis B and that the levels of SAMD4A/B expression are related to HBV sensitivity in humans.