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Pure BiFeO3 and heterostructured BiFeO3/BiFe0.95Mn0.05O3 (5% Mn-doped BiFeO3) thin films have been prepared by a chemical deposition method. The band structures and photosensitive properties of these films have been investigated elaborately. Pure BiFeO3 films showed stable and strong response to photo illumination (open circuit potential kept −0.18 V, short circuit photocurrent density was −0.023 mA·cm−2). By Mn doping, the energy band positions shifted, resulting in a smaller band gap of BiFe0.95Mn0.05O3 layer and an internal field being built in the BiFeO3/BiFe0.95Mn0.05O3 interface. BiFeO3/BiFe0.95Mn0.05O3 and BiFe0.95Mn0.05O3 thin films demonstrated poor photo activity compared with pure BiFeO3 films, which can be explained by the fact that Mn doping brought in a large amount of defects in the BiFe0.95Mn0.05O3 layers, causing higher carrier combination and correspondingly suppressing the photo response, and this negative influence was more considerable than the positive effects provided by the band modulation.

Idiopathic pulmonary fibrosis (IPF) is a prevalent interstitial lung disease with high mortality. CD38 is a main enzyme for intracellular nicotinamide adenine dinucleotide (NAD + ) degradation in mammals. It has been reported that CD38 participated in pulmonary fibrosis through promoting alveolar epithelial cells senescence. However, the roles of endothelial CD38 in pulmonary fibrosis remain unknown. In the present study, we observed that the elevated expression of CD38 was related to endothelial-to-mesenchymal transition (EndMT) of lung tissues in IPF patients and bleomycin (BLM)-induced pulmonary fibrosis mice and also in human umbilical vein endothelial cells (HUVECs) treated with BLM. Micro-computed tomography (MCT) and histopathological staining showed that endothelial cell-specific CD38 knockout (CD38 EndKO ) remarkably attenuated BLM-induced pulmonary fibrosis. In addition, CD38 EndKO significantly inhibited TGFβ-Smad3 pathway-mediated excessive extracellular matrix (ECM), reduced Toll-like receptor4-Myeloid differentiation factor88-Mitogen-activated protein kinases (TLR4-MyD88-MAPK) pathway-mediated endothelial inflammation and suppressed nicotinamide adenine dinucleotide phosphate oxidases1 (NOX1)-mediated oxidative stress. Furthermore, we demonstrated that 3-TYP, a SIRT3-specific inhibitor, markedly reversed the protective effect of HUVECs CD38KD cells and 78 C, a CD38-specific inhibitor, on BLM-induced EndMT in HUVECs. Therefore, we concluded that CD38 EndKO significantly ameliorated BLM-induced pulmonary fibrosis through inhibiting ECM, endothelial inflammation and oxidative stress, further alleviating EndMT in mice. Our findings suggest that endothelial CD38 may be a new therapeutic target for the prevention and treatment of pulmonary fibrosis clinically. Graphical Abstract Protective role and the underlying mechanism of endothelial CD38 in bleomycin-induced pulmonary fibrosis in mice. Endothelial cells-specific CD38 knockout (CD38 EndKO ) inhibited TGFβ-Smad3-mediated ECM, ROS-mediated oxidative stress and TLR4-mediated inflammation, and in turn, suppressed endothelial-to-mesenchymal transition (EndMT), eventually, alleviated pulmonary fibrosis induced by bleomycin in mice, suggesting endothelial CD38 may be a therapeutic target for the prevention and the treatment of pulmonary fibrosis clinically

Fe-based and Fe/Mo composite amorphous coatings were deposited on the surface of plain carbon steel substrates by atmospheric plasma spraying （APS）. With increasing the Mo alloy content, the microstructure of the coatings revealed more dense structure. The porosities of composite coating were all less than those of Fe-based coat- ing due to Mo alloy self-bonding performance. The ML10 friction and wear tester was employed to investigate the wear behaviors of the coatings under dry sliding conditions. It was found that the mass loss of the resultant coatings decreased with increasing Mo-based powders into the feedstock. This was attributed to the reduction of the delamina- tions resulting from improved intersplat bond with Mo addition.

The Cu1.8Se/CuAgSe nanostructure was synthesized by a simple two-step process. Starting with the template of cubic Cu1.8Se nanoplate by precipitation method, Cu1.8Se/CuAgSe nanostructure and ternary CuAgSe were prepared through a rapid ion exchange reaction using various amount of AgNO3 at room temperature. The as-prepared samples were analyzed by XRD, SEM and DRS. It was found that Cu1.8Se/CuAgSe heterostructure and the pure CuAgSe phase were formed without changing the morphology, and these samples had efficient light absorption from UV light to near-infrared light region. Photocatalytic properties of these samples were evaluated by the degradation of Congo red under visible and near-infrared light. The Cu1.8Se/CuAgSe nanostructure showed enhanced photocatalytic activity due to the lower recombination of charge-carrier in the photodegradation process.

Low-dimensional nanostructures are a promising class of ideal high-performance candidates for energy storage and conversion owing to their unique structural, optical, and chemical properties. Low-dimensional nanostructured photocatalysts have attracted ever-growing research attention. In this review, we mainly emphasize on summarizing the 0-, 1-, and 2-dimensional nanostructured photocatalysts systematically, including their photocatalytic performance, synthesis methods, and theoretical analysis. From the viewpoint of dimension, we try to figure out the way to design more high-efficiency photocatalysts towards numerous applications in the field of solar energy conversion, hoping to promote efficient control and rational development of photocatalysts.

Non-freezing cold injury is a prevalent cause of peripheral nerve damage, but its pathogenic mechanism is poorly understood, and treatment remains inadequate. Glucocorticoids have anti-inflammatory and lipid peroxidation-inhibiting properties. We therefore examined whether dexamethasone, a synthetic glucocorticoid compound, would alleviate early-stage non-freezing cold injury of the sciatic nerve. We established Wistar rat models of non-freezing cold injury by exposing the left sciatic nerve to cold（3–5°C） for 2 hours, then administered dexamethasone（3 mg/kg intraperitoneally） to half of the models. One day after injury, the concentration of Evans blue tracer in the injured sciatic nerve of rats that received dexamethasone was notably lower than that in the injured sciatic nerve of rats that did not receive dexamethasone; neither Evans blue dye nor capillary stenosis was observed in the endoneurium, but myelinated nerve fibers were markedly degenerated in the injured sciatic nerve of animals that received dexamethasone. After dexamethasone administration, however, endoneurial vasculopathy was markedly improved, although damage to the myelinated nerve fiber was not alleviated. These findings suggest that dexamethasone protects the blood-nerve barrier, but its benefit in non-freezing cold injury is limited to the vascular system.

Measurement-device-independent quantum key distribution (MDI QKD) removes all detector side channels and enables secure QKD with an untrusted relay. It is suitable for building a star-type quantum access network, where the complicated and expensive measurement devices are placed in the central untrusted relay and each user requires only a low-cost transmitter, such as an integrated photonic chip. Here, we experimentally demonstrate a 1.25-GHz silicon photonic chip-based MDI QKD system using polarization encoding. The photonic chip transmitters integrate the necessary encoding components for a standard QKD source. We implement random modulations of polarization states and decoy intensities, and demonstrate a finite-key secret rate of31bit/sover 36-dB channel loss (or 180-km standard fiber). This key rate is higher than state-of-the-art MDI QKD experiments. The results show that silicon photonic chip-based MDI QKD, benefiting from miniaturization, low-cost manufacture, and compatibility with CMOS microelectronics, is a promising solution for future quantum secure networks.

There is emerging evidence that α1‐blockers can be safely used in the treatment of hypertension. These drugs can be used in almost all hypertensive patients for blood pressure control. However, there are several special indications. Benign prostatic hyperplasia is a compelling indication of α1‐blockers, because of the dual treatment effect on both high blood pressure and lower urinary tract symptoms. Many patients with resistant hypertension would require α1‐blockers as add‐on therapy. Primary aldosteronism screen is a rapidly increasing clinical demand in the management of hypertension, where α1‐blockers are useful for blood pressure control in the preparation for the measurement of plasma aldosterone and renin. Nonetheless, α1‐blockers have to be used under several considerations. Among the currently available agents, only long‐acting α1‐blockers, such as doxazosin gastrointestinal therapeutic system 4–8 mg daily and terazosin 2–4 mg daily, should be chosen. Orthostatic hypotension is a concern with the use of α1‐blockers especially in the elderly, and requires careful initial bedtime dosing and avoiding overdosing. Fluid retention is potentially also a concern, which may be overcome by combining an α1‐blocker with a diuretic.

Hypertensive nephropathy (HTN) is the second leading cause of end-stage renal disease (ESRD) and a chronic inflammatory disease. Persistent hypertension leads to lesions of intrarenal arterioles and arterioles, luminal stenosis, secondary ischemic renal parenchymal damage, and glomerulosclerosis, tubular atrophy, and interstitial fibrosis. Studying the pathogenesis of hypertensive nephropathy is a prerequisite for diagnosis and treatment. The main cause of HTN is poor long-term blood pressure control, but kidney damage is often accompanied by the occurrence of immune inflammation. Some studies have found that the activation of innate immunity, inflammation and acquired immunity is closely related to the pathogenesis of HTN, which can cause damage and dysfunction of target organs. There are more articles on the mechanism of diabetic nephropathy, while there are fewer studies related to immunity in hypertensive nephropathy. This article reviews the mechanisms by which several different immune cells and inflammatory cytokines regulate blood pressure and renal damage in HTN. It mainly focuses on immune cells, cytokines, and chemokines and inhibitors. However, further comprehensive and large-scale studies are needed to determine the role of these markers and provide effective protocols for clinical intervention and treatment.

Anisakis infections have become a significant public health concern primarily caused by consuming raw or undercooked seafood. This in is due to a shift in global eating habits, and seafood consumption is becoming increasingly popular. This study explores how body proteins (ABP) and glycoproteins affect macrophage polarization. The parasites collected from East China Sea hairtail fish ( ), with glycoproteins isolated from ABP via ConA magnetic beads. RAW264.7 macrophages were treated with ABP, glycoproteins, and co-incubated with LPS or IL-4, then analyzed by qPCR for TNF-α and Arg-1. Transcriptomic profiling and bioinformatics analyses also helped identify differentially expressed genes and pathways. This study showed that ABP with LPS greatly upregulated TNF-α, boosting inflammation. Conversely, glycoproteins suppressed TNF-α transcription and reduced IL-4-induced Arg-1 expression, displaying immunosuppression. Transcriptomics analysis found that ABP enriched TNF and hematopoietic pathways, with IL6 and IL1β as key pro-inflammatory genes. Glycoproteins activated cytokine-cytokine receptor interactions and hampered leukocyte migration by downregulating Ccl2 and H3c7. Notably, ABP and glycoproteins differentially regulated the JAK-STAT pathway. This study shows that induces a dual-pronged immune response: ABP exacerbates inflammation, while glycoproteins suppress it. This highlights glycoproteins' potential as therapeutic targets for modulating parasitic immunopathology and inflammatory diseases. The analysis of ABP and glycoprotein - induced immune responses provides key insights into Anisakiasis pathogenesis and may help develop new treatments.