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Blackbody‐sensitive uncooled infrared photodetectors with ultra‐broadband and ultrafast photoresponse have a profound impact on many areas of modern science and technology. However, it is a big challenge for both traditional photodetectors and emerging low‐dimensional ones to simultaneously have all the above characteristics. Here, this challenge is addressed by establishing a Te/WTe2 heterostructure photodetector. The built‐in field of the heterostructure and the crossing conduction and valence bands of WTe2 jointly result in a high responsivity and a visible‐to‐long‐wavelength‐infrared photoresponse range. The peak responsivity (at the 3.3 µm wavelength) reaches 914 mA W−1 at zero bias and 8.51 A W−1 at 2 V bias. Further, the joint action coupled with the high mobility of Te and WTe2 promotes the 3‐dB bandwidth to 153 kHz. The self‐powered blackbody responsivity and specific detectivity reach 235.7 mA W−1 and 1.1 × 108 cm Hz1/2 W−1, respectively. The former increases to 5.82 A W−1 at 1 V bias. Moreover, this device is polarization‐sensitive with a contrast ratio of 2. This work reveals the potential of the Te/WTe2 heterostructure for high‐performance room‐temperature infrared photodetectors. [ABSTRACT FROM AUTHOR]

Cholestatic liver disease is characterized by disturbances in the intestinal microbiota and excessive accumulation of toxic bile acids (BA) in the liver. Melatonin (MT) can improve liver diseases. However, the underlying mechanism remains unclear. This study aimed to explore the mechanism of MT on hepatic BA synthesis, liver injury, and fibrosis in 3,5‐diethoxycarbonyl‐1,4‐dihydrocollidine (DDC)‐fed and Mdr2–/– mice. MT significantly improved hepatic injury and fibrosis with a significant decrease in hepatic BA accumulation in DDC‐fed and Mdr2–/– mice. MT reprogramed gut microbiota and augmented fecal bile salt hydrolase activity, which was related to increasing intestinal BA deconjugation and fecal BA excretion in both DDC‐fed and Mdr2–/– mice. MT significantly activated the intestinal farnesoid X receptor (FXR)/fibroblast growth factor 15 (FGF‐15) axis and subsequently inhibited hepatic BA synthesis in DDC‐fed and Mdr2–/– mice. MT failed to improve DDC‐induced liver fibrosis and BA synthesis in antibiotic‐treated mice. Furthermore, MT provided protection against DDC‐induced liver injury and fibrosis in fecal microbiota transplantation mice. MT did not decrease liver injury and fibrosis in DDC‐fed intestinal epithelial cell‐specific FXR knockout mice, suggesting that the intestinal FXR mediated the anti‐fibrosis effect of MT. In conclusion, MT ameliorates cholestatic liver diseases by remodeling gut microbiota and activating intestinal FXR/FGF‐15 axis‐mediated inhibition of hepatic BA synthesis and promotion of BA excretion in mice. [ABSTRACT FROM AUTHOR]

Cell enrichment is a powerful tool in many kinds of cell research, especially in applications with low abundance cell types. In this work, we developed a microfluidic fluorescence activated cell sorting device that was able to perform on‐demand, low loss cell detection, and sorting. The chip utilizes three‐dimensional acoustic standing waves to position all cells in the same fluid velocity regime without sheath. When the cells pass through a laser interrogation region, the scattering and fluorescent signals are detected, translated and transported to software. The target cells are then identified by gating on the plots. Short bursts of standing acoustic waves are triggered by order from PC to sort target cells within predefined gating region. For very low abundance and rare labeled lymphocytes mixed with high concentration unlabeled white blood cells (WBCs), (1–100 labeled lymphocytes are diluted in 106 WBCs in 1 ml volume fluid), the device is able to remove more than 98% WBCs and recover labeled lymphocytes with efficiency of 80%. We further demonstrated that this device worked with real clinical samples by successfully isolating fetal nucleated red blood cells (FNRBCs) in the blood samples from pregnant women with male fetus. The obtained cells were sequenced and the expressions of (sex determining region Y) SRY genes were tested to determine fetal cell proportion. In genetic analysis, the proportion of fetal cells in the final picked sample is up to 40.64%. With this ability, the device proposed could be valuable for biomedical applications involving fetal cells, circulating tumor cells, and stem cells. [ABSTRACT FROM AUTHOR]

Symptom development of a viral plant disease results from molecular interactions between the virus and its host plant. Tomato mosaic virus coat protein (ToMV CP) not only plays a major role in virion assembly and long-distance movement but is also responsible for symptom development in ToMV-infected plants. This study provides evidence that chloroplast ferredoxin I (Fd I) interacts with ToMV CP in a GAL4-based two-hybrid yeast system for screening a Nicotiana tabacum cDNA library. The interaction between CP and Fd I was confirmed by in vitro binding and bimolecular fluorescence complementation assays in plant cells. [ABSTRACT FROM AUTHOR]

During infrared detection, the thermal radiation from the background generates substantial photon noise and thus severely limit the capability of an infrared detector to identify a target. Going beyond this limitation has been a long‐standing challenge in the development of infrared detectors. This paper proposes to break this limitation by creating a narrow photoresponse band with a high peak responsivity to reject the background radiation and enhance the responsivity to the target with characteristic emission lines. This scheme is numerically demonstrated in a dimerized grating integrated quantum well infrared photodetector, based on critical coupling with a Brillouin zone folding induced quasi‐bound state in the continuum (BIC). The asymmetric deformation of the grating structure folds the photonic band and generates a quasi‐BIC with a tunable high radiation Q factor (QR) at the Γ point. By reducing the doping concentration of the quantum wells for a high absorption Q factor (QA) and tuning the QR to make QR = QA for critical coupling, a narrowband photoresponse with a high peak responsivity is achieved and the background‐limited specific detectivity of 4.55 × 1012 cm Hz1/2 W−1 is obtained for a 2π field of view, surpassing the ideal‐photoconductor limit by 92 times. [ABSTRACT FROM AUTHOR]

Cadmium (Cd) is a widespread environmental contaminant with high toxicity to human health. Melatonin has been shown to improve Cd-induced liver damage. However, its mechanism has not yet been elucidated. In this study, we aimed to investigate the effects of melatonin on Cd-induced liver damage and fibrosis. A combination of 16S rRNA gene sequencing and mass spectrometry-based metabolomics was adopted to investigate changes in the gut microbiome and its metabolites on the regulation of melatonin in Cd-induced liver injury and fibrosis of mice. Further, nonabsorbable antibiotics, a fecal microbiota transplantation (FMT) program and intestine-specific farnesoid X receptor (FXR) knockout mice were employed to explore the mechanism of melatonin (MT) on liver injury and fibrosis in Cd treated mice. MT significantly improved hepatic inflammation, bile duct hyperplasia, liver damage, and liver fibrosis, with a notable decrease in liver bile acid levels in Cd-exposed mice. MT treatment remodeled the gut microbiota, improved gut barrier function, and reduced the production of gut-derived lipopolysaccharide (LPS). MT significantly decreased the intestinal tauro-β-muricholic acid levels, which are known as FXR antagonists. Notably, MT prominently activated the intestinal FXR signaling, subsequently inhibiting liver bile acid synthesis and decreasing hepatic inflammation in Cd-exposed mice. However, MT could not ameliorate Cd-induced liver damage and fibrosis in Abx-treated mice. Conversely, MT still exerted a protective effect on Cd-induced liver damage and fibrosis in FMT mice. Interestingly, MT failed to reverse liver damage and fibrosis in Cd-exposed intestinal epithelial cell-specific FXR gene knockout mice, indicating that intestinal FXR signaling mediated the protective effect of MT treatment. MT improves Cd-induced liver damage and fibrosis through reshaping the intestinal flora, activating the intestinal FXR-mediated suppression of liver bile acid synthesis and reducing LPS leakage in mice., (© 2024 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)