Explore the vast range of titles available.

Current thermochemical methods to generate H 2 include gasification and steam reforming of coal and natural gas, in which anthropogenic CO 2 emission is inevitable. If biomass is used as a source of H 2 , the process can be considered carbon-neutral. Seaweeds are among the less studied types of biomass with great potential because they do not require freshwater. Unfortunately, reaction pathways to thermochemically convert salty and wet biomass into H 2 are limited. In this study, a catalytic alkaline thermal treatment of brown seaweed is investigated to produce high purity H 2 with substantially suppressed CO 2 formation making the overall biomass conversion not only carbon-neutral but also potentially carbon-negative. High-purity 69.69 mmol-H 2 /(dry-ash-free)g-brown seaweed is produced with a conversion as high as 71%. The hydroxide is involved in both H 2 production and in situ CO 2 capture, while the Ni/ZrO 2 catalyst enhanced the secondary H 2 formation via steam methane reforming and water-gas shift reactions. While biomass may serve as a renewable source of carbon-neutral hydrogen, it is challenging both to utilize as-found bio-resources and to suppress CO 2 formation. Here, authors convert wet, salty seaweed using alkaline thermal treatment to produce high-purity hydrogen and suppress carbon emission.

Development of materials that deliver more energy at high rates is important for high-power applications, including portable electronic devices and hybrid electric vehicles. For lithium-ion (Li⁺) batteries, reducing material dimensions can boost Li⁺ ion and electron transfer in nanostructured electrodes. By manipulating two genes, we equipped viruses with peptide groups having affinity for single-walled carbon nanotubes (SWNTs) on one end and peptides capable of nucleating amorphous iron phosphate(a-FePO₄) fused to the viral major coat protein. The virus clone with the greatest affinity toward SWNTs enabled power performance of a-FePO₄ comparable to that of crystalline lithium iron phosphate (c-LiFePO₄) and showed excellent capacity retention upon cycling at 1C. This environmentally benign low-temperature biological scaffold could facilitate fabrication of electrodes from materials previously excluded because of extremely low electronic conductivity.

The use of porous three-dimensional (3D) composite scaffolds has attracted great attention in bone tissue engineering applications because they closely simulate the major features of the natural extracellular matrix (ECM) of bone. This study aimed to prepare biomimetic composite scaffolds via a simple 3D printing of gelatin/hyaluronic acid (HA)/hydroxyapatite (HAp) and subsequent biomineralization for improved bone tissue regeneration. The resulting scaffolds exhibited uniform structure and homogeneous pore distribution. In addition, the microstructures of the composite scaffolds showed an ECM-mimetic structure with a wrinkled internal surface and a porous hierarchical architecture. The results of bioactivity assays proved that the morphological characteristics and biomineralization of the composite scaffolds influenced cell proliferation and osteogenic differentiation. In particular, the biomineralized gelatin/HA/HAp composite scaffolds with double-layer staggered orthogonal (GEHA20-ZZS) and double-layer alternative structure (GEHA20-45S) showed higher bioactivity than other scaffolds. According to these results, biomineralization has a great influence on the biological activity of cells. Hence, the biomineralized composite scaffolds can be used as new bone scaffolds in bone regeneration.

Industry 4.0 requires high-speed data exchange that includes fast, reliable, low-latency, and cost-effective data transmissions. As visible light communication (VLC) can provide reliable, low-latency, and secure connections that do not penetrate walls and are immune to electromagnetic interference; it can be considered a solution for Industry 4.0. The non-orthogonal multiple access (NOMA) technique can achieve high spectral efficiency using the same frequency and time resources for multiple users. It means that smaller amounts of resources will be used compared with orthogonal multiple access (OMA). Therefore, handling multiple data transmissions with VLC-NOMA can be easier for factory automation than OMA. However, as the transmit power is split, the reliability is reduced. Therefore, this study proposed a deep neural network (DNN)-based power-allocation algorithm (DBPA) to improve the reliability of the system. Further, to schedule multiple nodes in VLC-NOMA system, a priority-based user-pairing (PBUP) scheme is proposed. The proposed techniques in VLC-NOMA system were evaluated in terms of the factory automation scenario and showed that it improves reliability and reduces missed deadlines.

Despite advances in cancer therapy, the clinical outcome of patients with gastric cancer remains poor, largely due to tumor heterogeneity. Thus, finding a hidden vulnerability of clinically refractory subtypes of gastric cancer is crucial. Here, we report that chemoresistant gastric cancer cells rely heavily on endocytosis, facilitated by caveolin-1, for survival. caveolin-1 was highly upregulated in the most malignant stem-like/EMT/mesenchymal (SEM)-type gastric cancer cells, allowing caveolin-1-mediated endocytosis and utilization of extracellular proteins via lysosomal degradation. Downregulation of caveolin-1 alone was sufficient to induce cell death in SEM-type gastric cancer cells, emphasizing its importance as a survival mechanism. Consistently, chloroquine, a lysosomal inhibitor, successfully blocked caveolin-1-mediated endocytosis, leading to the marked suppression of tumor growth in chemorefractory gastric cancer cells in vitro, including patient-derived organoids, and in vivo. Together, our findings suggest that caveolin-1-mediated endocytosis is a key metabolic pathway for gastric cancer survival and a potential therapeutic target. Caveolin-1: Survival Mechanism in Gastric Cancer Cells A new study reveals that Caveolin-1 (CAV1) is specifically expressed in the most malignant SEM-type gastric cancer (GC), and CAV1-driven endocytosis is a critical survival mechanism of malignant GC. Researchers found that chloroquine (CQ), an anti-malarial drug known to block endocytosis, effectively induced cell death in CAV1-positive SEM-type GC cells by impairing lysosomal activity and extracellular nutrient uptake. In patient-derived organoids and mouse models, CQ treatment significantly reduced tumor growth and improved survival rates, suggesting its potential as a therapeutic alternative for chemo-resistant SEM-type GC patients. The study highlights the importance of targeting endocytosis in cancer treatment and provides new insights into the development of personalized therapies for GC patients.

Stroke is a neurological complication that can occur in patients admitted to the intensive care unit (ICU) for non-neurological conditions, leading to increased mortality and prolonged hospital stays. The incidence of stroke in ICU settings is notably higher compared to the general population, and delays in diagnosis can lead to irreversible neurological damage. Early diagnosis of stroke is critical to protect brain tissue and treat neurological defects. Therefore, we developed a machine learning model to diagnose stroke in patients with acute neurological manifestations in the ICU. We retrospectively collected data on patients’ underlying diseases, blood coagulation tests, procedures, and medications before neurological symptom onset from 206 patients at the Chungbuk National University Hospital ICU (July 2020–July 2022) and 45 patients at Chungnam National University Hospital between (July 2020–March 2023). Using the Categorical Boosting (CatBoost) algorithm with Bayesian optimization for hyperparameter selection and k-fold cross-validation to mitigate overfitting, we analyzed model-feature relationships with SHapley Additive exPlanations (SHAP) values. Internal model validation yielded an average accuracy of 0.7560, sensitivity of 0.8959, specificity of 0.7000, and area under the receiver operating characteristic curve (AUROC) of 0.8201. External validation yielded an accuracy of 0.7778, sensitivity of 0.7500, specificity of 0.7931, and an AUROC of 0.7328. These results demonstrated the model’s effectiveness in diagnosing stroke in non-neurological ICU patients with acute neurological manifestations using their electronic health records, making it valuable for the early detection of stroke in ICU patients.

Creeping fat (CrF) is an extraintestinal manifestation observed in patients with Crohn’s disease (CD). It is characterized by the accumulation of mesenteric adipose tissue (MAT) that wraps around the intestinal wall. Although the role of CrF in CD is still debated, multiple studies have highlighted a correlation between CrF and inflammation, as well as fibrostenosais of the intestine, which contributes to the worsening of CD symptoms. However, the mechanism underlying the potential role of CrF in the development of Crohn’s fibrosis remains an enigma. This study aimed to analyze CrF comprehensively using single-cell RNA sequencing analysis. The data was compared with transcriptomic data from adipose tissue in other disease conditions, such as ulcerative colitis, lymphedema, and obesity. Our analysis classified two lineages of preadipocyte (PAC) clusters responsible for adipogenesis and fibrosis in CrF. Committed PACs in CrF showed increased cytokine expression in response to bacterial stimuli, potentially worsening inflammation in patients with CD. We also observed an increase in fibrotic activity in PAC clusters in CrF. Co-analyzing the data from patients with lymphedema, we found that pro-fibrotic PACs featured upregulated pentraxin-3 expression, suggesting a potential target for the treatment of fibrosis in CrF. Furthermore, PACs in CrF exhibited a distinct increase in cell-to-cell communication via cytokines related to inflammation and fibrosis, such as CCL, LIGHT, PDGF, MIF, and SEMA3. Interestingly, these interactions also increased in PACs of the lymphedema, whereas the increased MIF signal of PACs was found to be a distinct characteristic of CrF. In immune cell clusters in CrF, we observed high immune activity of pro-inflammatory macrophages, antigen-presenting macrophages, B cells, and IgG + plasma cells. Finally, we have demonstrated elevated IgG + plasma cell infiltration and increased pentraxin-3 protein levels in the fibrotic regions of CrF in CD patients when compared to MAT from both UC patients and healthy individuals. These findings provide new insights into the transcriptomic features related to the inflammation of cells in CrF and suggest potential targets for attenuating fibrosis in CD.

Wheat is a major food crop used in producing bread, noodles, and cookies. Kernel vitreousness, closely related to protein content, is key to determining wheat's processing purpose. Traditionally, vitreousness is visually assessed, but studies on classifying vitreous and starchy kernels to improve quality are limited. This study expands the use of a commercial color sorter to classify kernel vitreousness by G value, distinguishing vitreous from starchy kernels. The system improved protein content and bread-making quality by classifying vitreous kernels, while reducing variability across 23 samples collected over four years. An industrial field test confirmed its applicability at scale. Genetic and environmental factors were also examined, revealing that varietal differences and flowering time were not significant contributors to variations in vitreousness. The findings suggest that color sorting is a reliable tool for enhancing wheat quality until more environmentally stable cultivars are developed, providing economic benefits through improved and consistent product quality.

Recently, hepatic peroxisome proliferator-activated receptor (PPAR)γ has been implicated in hepatic lipid accumulation. We found that the C3H mouse strain does not express PPARγ in the liver and, when subject to a high-fat diet, is resistant to hepatic steatosis, compared with C57BL/6 (B6) mice. Adenoviral PPARγ2 injection into B6 and C3H mice caused hepatic steatosis, and microarray analysis demonstrated that hepatic PPARγ2 expression is associated with genes involved in fatty acid transport and the triglyceride synthesis pathway. In particular, hepatic PPARγ2 expression significantly increased the expression of monoacylglycerol O -acyltransferase 1 (MGAT1). Promoter analysis by luciferase assay and electrophoretic mobility shift assay as well as chromatin immunoprecipitation assay revealed that PPARγ2 directly regulates the MGAT1 promoter activity. The MGAT1 overexpression in cultured hepatocytes enhanced triglyceride synthesis without an increase of PPARγ expression. Importantly, knockdown of MGAT1 in the liver significantly reduced hepatic steatosis in 12-wk-old high-fat–fed mice as well as ob/ob mice, accompanied by weight loss and improved glucose tolerance. These results suggest that the MGAT1 pathway induced by hepatic PPARγ is critically important in the development of hepatic steatosis during diet-induced obesity.

Cancer is heterogeneous among patients, requiring a thorough understanding of molecular subtypes and the establishment of therapeutic strategies based on its behavior. Gastric cancer (GC) is adenocarcinoma with marked heterogeneity leading to different prognoses. As an effort, we previously identified a stem-like subtype, which is prone to metastasis, with the worst prognosis. Here, we propose FNBP1 as a key to high-level cell motility, present only in aggressive GC cells. FNBP1 is also up-regulated in both the GS subtype from the TCGA project and the EMT subtype from the ACRG study, which include high portions of diffuse histologic type. Ablation of FNBP1 in the EMT-type GC cell line brought changes in the cell periphery in transcriptomic analysis. Indeed, loss of FNBP1 resulted in the loss of invasive ability, especially in a three-dimensional culture system. Live imaging indicated active movement of actin in FNBP1-overexpressed cells cultured in an extracellular matrix dome. To find the transcription factor which drives FNBP1 expression in an EMT-type GC cell line, the FNBP1 promoter region and DNA binding motifs were analyzed. Interestingly, the Sp1 motif was abundant in the promoter, and pharmacological inhibition and knockdown of Sp1 down-regulated FNBP1 promoter activity and the transcription level, respectively. Taken together, our results propose Sp1-driven FNBP1 as a key molecule explaining aggressiveness in EMT-type GC cells.