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Considering their superior charge-transfer characteristics, easy tenability of energy levels, and low production cost, organic semiconductors are ideal for photoelectrochemical (PEC) hydrogen production. However, organic-semiconductor-based photoelectrodes have not been extensively explored for PEC water-splitting because of their low stability in water. Herein, we report high-performance and stable organic-semiconductors photoanodes consisting of p -type polymers and n -type non-fullerene materials, which is passivated using nickel foils, GaIn eutectic, and layered double hydroxides as model materials. We achieve a photocurrent density of 15.1 mA cm −2 at 1.23 V vs. reversible hydrogen electrode (RHE) with an onset potential of 0.55 V vs. RHE and a record high half-cell solar-to-hydrogen conversion efficiency of 4.33% under AM 1.5 G solar simulated light. After conducting the stability test at 1.3 V vs. RHE for 10 h, 90% of the initial photocurrent density are retained, whereas the photoactive layer without passivation lost its activity within a few minutes. While organic semiconductors may be useful in photoelectrochemical water-splitting materials, they show low stability in water. Here, the authors report high-performance and stable organic-semiconductor-based photoanodes passivated using nickel foils, GaIn eutectic, and layered double hydroxides.

Chalcogenides are promising materials for photoelectrochemical (PEC) water splitting owing to their suitable band gaps, favourable band alignments, and efficient charge transport properties. However, their practical application has been limited by poor stability in aqueous environments, as they are prone to self-oxidation prior to water oxidation. This instability typically necessitates the use of sacrificial agents to scavenge photogenerated holes, thereby restricting long-term device operation and real-world implementation. Here we report a metal-encapsulated PbS quantum dot (PbS-QD) solar cell-based photoelectrode that simultaneously achieves high photocurrent and long-term operational stability for PEC water splitting without sacrificial agents. The optimised PbS-QD-based photoanode delivers a photocurrent density of 18.6 mA cm –2 at 1.23 V versus the reversible hydrogen electrode in 1.0 M NaOH, retaining 90% of its initial performance over 24 h. These values are comparable to those reported for chalcogenide-based photoelectrodes operating in the presence of sacrificial agents. This study reports a metal-encapsulated PbS quantum dot photoanode that delivers high photocurrent and long-term stability for PEC water splitting without sacrificial agents, advancing sustainable clean energy.

Efficient and robust bifunctional electrocatalysts for oxygen evolution reaction (OER) and oxygen reduction reaction (ORR) are critical for high‐performance zinc‐air batteries (ZABs). However, balancing OER and ORR activity in a single catalyst remains challenging due to the different mechanisms during charging and discharging. Here, a scalable strategy is presented for enhancing both reactions by integrating two‐dimensional OER‐ and ORR‐active components onto a carbon‐based conductive substrate with abundant anchoring sites, via high‐shear exfoliation. The heterostructure catalyst demonstrates exceptional bifunctionality, achieving an extremely low overpotential difference of 0.63 V. First‐principles calculations confirm a strong chemical compatibility between the active components and substrate. In scaled‐up ZAB applications, the catalyst delivers a high peak power density of 1569 mW cm−2, and an outstanding cycling stability over 300 h (1800 cycles). This work highlights a versatile approach for designing multifunctional electrocatalysts, advancing scalable energy conversion and storage technologies. A scalable nanocomposite synthesis is reported for a high‐performance bifunctional electrocatalyst by combining exfoliated layered materials—each active for OER and ORR—with a porous conductive substrate via high‐shear exfoliation. The electrocatalyst exhibits the lowest potential gap among reported transition metal‐based bifunctional catalysts. In a scaled‐up zinc‐air battery, the system demonstrates outstanding stability over 300 h.

Organic semiconductor-based photoelectrodes are gaining significant attention in photoelectrochemical (PEC) value-added chemical production systems, which are promising architectures for solar energy harvesting. Organic semiconductors consisting of conjugated carbon–carbon bonds provide several advantages for PEC cells, including improved charge transfer, tunable band positions and band gaps, low cost, and facile fabrication using organic solvents. This review gives an overview of the recent advances in emerging single organic semiconductor-based photoelectrodes for PEC water splitting and the various strategies for enhancing their performance and stability. It highlights the importance of photoelectrodes based on donor–acceptor bulk heterojunction (BHJ) systems for fabricating efficient organic semiconductor-based solar energy-harvesting devices. Furthermore, it evaluates the recent progress in BHJ organic base photoelectrodes for producing highly efficient PEC value-added chemicals, such as hydrogen and hydrogen peroxide. Finally, this review highlights the potential of organic-based photoelectrodes for bias-free solar-to-chemical production, which is the ultimate goal of PEC systems and a step toward achieving reliable commercial technology.

Astrocytes and microglia are brain‐resident glia that can establish harmful inflammatory environments in disease contexts and thereby contribute to the progression of neuronal loss in neurodegenerative disorders. Correcting the diseased properties of glia is therefore an appealing strategy for treating brain diseases. Previous studies have shown that serum/ glucocorticoid related kinase 1 (SGK1) is upregulated in the brains of patients with various neurodegenerative disorders, suggesting its involvement in the pathogenesis of those diseases. In this study, we show that inhibiting glial SGK1 corrects the pro‐inflammatory properties of glia by suppressing the intracellular NFκB‐, NLRP3‐inflammasome‐, and CGAS‐STING‐mediated inflammatory pathways. Furthermore, SGK1 inhibition potentiated glial activity to scavenge glutamate toxicity and prevented glial cell senescence and mitochondrial damage, which have recently been reported as critical pathologic features of and therapeutic targets in Parkinson disease (PD) and Alzheimer disease (AD). Along with those anti‐inflammatory/neurotrophic functions, silencing and pharmacological inhibition of SGK1 protected midbrain dopamine neurons from degeneration and cured pathologic synuclein alpha (SNCA) aggregation and PD‐associated behavioral deficits in multiple in vitro and in vivo PD models. Collectively, these findings suggest that SGK1 inhibition could be a useful strategy for treating PD and other neurodegenerative disorders that share the common pathology of glia‐mediated neuroinflammation. Synopsis Pathogenic involvement of SGK1 has been implicated in various neurodegenerative disorders. In this study, we show that inhibition of SGK1 in glia treats Parkinson disease (PD) via suppressing glial inflammation and potentiating glial neurotrophic functions. SGK inhibition reduces neuroinflammation and protects dopamine neurons from degeneration. PD – associated behavioral deficits are improved in PD mice after SGK inhibition. Inhibition of SGK1 could be a useful strategy for treating PD and other neurodegenerative disorders. Graphical Abstract Pathogenic involvement of SGK1 has been implicated in various neurodegenerative disorders. In this study, we show that inhibition of SGK1 in glia treats Parkinson disease (PD) via suppressing glial inflammation and potentiating glial neurotrophic functions.

NLRP3 is an intracellular sensor molecule that affects neutrophil functionality and infiltration in brain disorders such as experimental autoimmune encephalomyelitis (EAE). However, the detailed molecular mechanisms underlying the role of NLRP3 in these processes remain unknown. We found that NLRP3 is crucial for neutrophil infiltration, whereas dispensable for neutrophil priming. Notably, NLRP3 activation in neutrophils induced blood-brain barrier (BBB) disruption and neutrophil infiltration into the brain via CXCL1/2 secretion and subsequent activation of the CXCL1/2-CXCR2 signaling axis. Moreover, CXCL1 and CXCL2 in the inflamed brain directly reduced Claudin-5 expression, which regulates BBB permeability in brain endothelial cells. Furthermore, neutrophil-specific NLRP3 activation aggravated EAE pathogenesis by promoting CXCR2-mediated infiltration of both neutrophils and CD4 + T cells into the central nervous system at disease onset. Thus, the CXCL1/2-CXCR2 axis plays a role in EAE progression. Therefore, this chemokine axis could be a potential therapeutic target for attenuating neuroinflammatory diseases through modulating of neutrophil and CD4 + T cell infiltration and BBB disruption.

Blood-brain barrier (BBB) disintegration is a key contributor to neuroinflammation; however, the biological processes governing BBB permeability under physiological conditions remain unclear. Here, we investigate the role of NLRP3 inflammasome in BBB disruption following peripheral inflammatory challenges. Repeated intraperitoneal lipopolysaccharide administration causes NLRP3-dependent BBB permeabilization and myeloid cell infiltration into the brain. Using a mouse model with cell-specific hyperactivation of NLRP3, we identify microglial NLRP3 activation as essential for peripheral inflammation-induced BBB disruption. Conversely, NLRP3 and microglial gasdermin D (GSDMD) deficiency markedly attenuates lipopolysaccharide-induced BBB breakdown. Notably, IL-1β is not required for NLRP3-GSDMD-mediated BBB disruption. Instead, microglial NLRP3-GSDMD axis upregulates CXCL chemokines and matrix metalloproteinases around BBB via producing GDF-15, promoting the recruitment of CXCR2-containing neutrophils. Inhibition of neutrophil infiltration and matrix metalloproteinase activity significantly reduces NLRP3-mediated BBB impairment. Collectively, these findings reveal the important role of NLRP3-driven chemokine production in BBB disintegration, suggesting potential therapeutic targets to mitigate neuroinflammation. The biological mechanisms regulating blood-brain barrier integrity remain unclear. Here, the authors identify microglial NLRP3-gasdermin D signaling as a driver of blood-brain barrier disruption during peripheral inflammation in mice, mediated by CXCL-dependent neutrophil recruitment.

Prominin-1 (PROM1), also known as CD133, is expressed in hepatic progenitor cells (HPCs) and cholangiocytes of the fibrotic liver. In this study, we show that PROM1 is upregulated in the plasma membrane of fibrotic hepatocytes. Hepatocellular expression of PROM1 was also demonstrated in mice ( Prom1 CreER ; R26 TdTom ) in which cells expressed TdTom under control of the Prom1 promoter. To understand the role of hepatocellular PROM1 in liver fibrosis, global and liver-specific Prom1 -deficient mice were analyzed after bile duct ligation (BDL). BDL-induced liver fibrosis was aggravated with increased phosphorylation of SMAD2/3 and decreased levels of SMAD7 by global or liver-specific Prom1 deficiency but not by cholangiocyte-specific Prom1 deficiency. Indeed, PROM1 prevented SMURF2-induced SMAD7 ubiquitination and degradation by interfering with the molecular association of SMAD7 with SMURF2. We also demonstrated that hepatocyte-specific overexpression of SMAD7 ameliorated BDL-induced liver fibrosis in liver-specific Prom1- deficient mice. Thus, we conclude that PROM1 is necessary for the negative regulation of TGFβ signaling during liver fibrosis. Liver disease: Preventing progression of fibrosis Progression of liver fibrosis is kept in check by a regulatory protein that switches off a signaling pathway responsible for cell death and subsequent scar tissue formation. Liver fibrosis is a common outcome of alcoholism, viral infection, and hepatitis. Researchers led by Young-Gyu Ko at Korea University, Seoul, South Korea, determined that a protein called PROM-1 is highly expressed in fibrotic liver tissue from mice and humans, and set out to uncover its function. They found that PROM-1 exerts a protective role, as PROM-1-deficient mice experienced accelerated liver degeneration in response to bile duct injury. PROM-1 acts by blocking the effects of transforming growth factor-β, a signaling protein which promotes cell death. These results are consistent with evidence linking PROM-1 to anti-fibrotic activity in other organ systems.

This study aimed to investigate the potential of Bacillus licheniformis-fermented products (BLFP) and their derived antimicrobial lipopeptide, surfactin, for the prevention of coccidiosis in broilers. Broilers were fed BLFP at 1.25 and 5 g/kg under Eimeria tenella challenge. At the end of experiment (35 days), the growth performance, survival rate, cecal morphology, cecal lesion scores, oocyst-count index, and anti-coccidial index were analyzed. The effects of the BLFP-derived surfactin on oocyst sporulation and sporozoite morphology in Eimeria species were also investigated in vitro. Results showed that BLFP supplementation at 1.25 and 5 g/kg improved cecal morphology and increased the survival rate of broilers under E. tenella challenge. Supplementation with 1.25 g/kg of BLFP reduced the lesion scores in the cecum of E. tenella-challenged broilers, while the oocyst-count index was reduced in broilers given 5 g/kg of BLFP. The anti-coccidial index of the 1.25 g/kg of BLFP-treated group was greater than 160, compared with the E. tenella-challenge-only group. Furthermore, surfactin inhibited Eimeria oocyst sporulation and disrupted sporozoite morphology. These results demonstrate that BLFPs and their derived antimicrobial lipopeptide, surfactin, exhibit anti-coccidial activity in vitro and in vivo. BLFP may be used as a natural feed additive for the prevention of coccidiosis in broilers, and 1.25 g/kg can be considered the optimum dosage.

Osteoporosis is one of the most common chronic metabolic diseases, but detection and treatment rates are low. The aim of the current study was to evaluate the correlation between frontal skull Hounsfield unit (HU) values from brain computed tomography (CT) scans and T-scores of the lumbar spine and femoral neck from dual-energy X-ray absorptiometry (DXA) scans. Patients with < 1 year between brain CT and DXA scans were included in the study. The average frontal skull HU value used for analysis was defined as the average of four HU values of the frontal bone. A receiver operating characteristic curve was generated, and area under the curve (AUC) was used to determine the HU values of the frontal skull for predicting osteoporosis. The frontal skull HU value with the highest sensitivity and specificity was considered the optimal cutoff value. In total, 899 patients who underwent both brain CT and DXA scans at a single institution were enrolled. Average skull HU values differed significantly among patients in different bone mineral density categories (p < 0.001). There was a positive correlation between skull HU value and T-score (β = 105.06, p < 0.001, R2 = 0.343). The mean HU value in subjects with osteoporosis was 515, and the optimal cutoff value for the prediction of osteoporosis was 610 HU (AUC = 0.775, 95% CI 0.744-0.806, p < 0.001). Clinical brain CT scans can assist in the detection of osteoporosis, and patients with an HU value < 610 as determined via brain CT may be considered for further evaluation for possible osteoporosis.