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The oil-free dry air compressor plays a crucial role in the fuel cell system, particularly in commercial buses where twin-screw air compressors have proven effective. A novel rotor profile of the twin-screw dry air compressors has been developed, which simplifies the profile curve and yields excellent performance results with a volume flow of 11.99 m³/min and corrected specific power of 3.54 kW/(m³/min).

Semen persicae is the dried mature seeds of Prunus persica (L.) Batsch and P. davidiana (Carr.) Franch and is commonly used in traditional Chinese medicine (TCM) formulations because of its variety of biological effects. The present study aimed to evaluate the antioxidant activity and toxicity profiles of semen persicae extract (SPE) after determining the amygdalin content (4.95%) using HPLC. Regarding the in vitro antioxidant activity, SPE with 2 mg/mL concentration scavenged 1,1-diphenyl-2-picrylhydrazyl (DPPH), hydroxyl, and ABTS free radicals with rates of 51.78%, 55.47%, and 57.16%, respectively. The same concentration of SPE chelated 30.76% Fe2+. The in vitro cytotoxicity study revealed that SPE induced 92.45% cell viabilities of HEPG2 even at 2000 μg/mL. In the acute toxicity study, oral administration of SPE did not provoke mortality or any toxic signs at doses up to 2000 mg/kg bw. Repeated oral administration for 28 days at doses of 100, 300, and 600 mg/kg per day in rats did not show any toxicity signs or gross pathological abnormalities. The results of the present research provide basic reference data for SPE with a moderate effect on antioxidant activity and low toxicity for future screening of biological and pharmacological properties.

The insights into how genome topology couples with epigenetic states to govern the function and identity of the corneal epithelium are poorly understood. Here, we generate a high-resolution Hi-C interaction map of human limbal stem/progenitor cells (LSCs) and show that chromatin multi-hierarchical organisation is coupled to gene expression. By integrating Hi-C, epigenome and transcriptome data, we characterize the comprehensive 3D epigenomic landscapes of LSCs. We find that super-silencers mediate gene repression associated with corneal development, differentiation and disease via chromatin looping and/or proximity. Super-enhancer (SE) interaction analysis identified a set of SE interactive hubs that contribute to LSC-specific gene activation. These active and inactive element-anchored loop networks occur within the cohesin-occupied CTCF-CTCF loops. We further reveal a coordinated regulatory network of core transcription factors based on SE-promoter interactions. Our results provide detailed insights into the genome organization principle for epigenetic regulation of gene expression in stratified epithelia. Genome topology provides a structural basis for epigenome-mediated transcriptional regulation in eukaryotes. Here the authors characterized the 3D genome of stratified squamous epithelia. They generated a Hi-C map of human limbal stem/progenitor cells (LSCs) and integrated these data with epigenomics, transcription factor binding maps, and transcriptome data.

Patients with cancer are a high-risk population in the COVID-19 pandemic. We aimed to describe clinical characteristics and outcomes of patients with cancer and COVID-19, and examined risk factors for mortality in this population. We did a retrospective, multicentre, cohort study of 205 patients with laboratory-confirmed severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and with a pathological diagnosis of a malignant tumour in nine hospitals within Hubei, China, from Jan 13 to March 18, 2020. All patients were either discharged from hospitals or had died by April 20, 2020. Clinical characteristics, laboratory data, and cancer histories were compared between survivors and non-survivors by use of χ2 test. Risk factors for mortality were identified by univariable and multivariable logistic regression models. Between Jan 13 and Mar 18, 2020, 205 patients with cancer and laboratory-confirmed SARS-CoV-2 infection were enrolled (median age 63 years [IQR 56–70; range 14–96]; 109 [53%] women). 183 (89%) had solid tumours and 22 (11%) had haematological malignancies. The median duration of follow-up was 68 days (IQR 59–78). The most common solid tumour types were breast (40 [20%] patients), colorectal (28 [14%]), and lung cancer (24 [12%]). 54 (30%) of 182 patients received antitumour therapies within 4 weeks before symptom onset. 30 (15%) of 205 patients were transferred to an intensive care unit and 40 (20%) died during hospital admission. Patients with haematological malignancies had poorer prognoses than did those with solid tumours: nine (41%) of 22 patients with haematological malignancies died versus 31 (17%) of 183 patients with solid tumours (hazard ratio for death 3·28 [95% CI 1·56–6·91]; log rank p=0·0009). Multivariable regression analysis showed that receiving chemotherapy within 4 weeks before symptom onset (odds ratio [OR] 3·51 [95% CI 1·16–10·59]; p=0·026) and male sex (OR 3·86 [95% CI 1·57–9·50]; p=0·0033) were risk factors for death during admission to hospital. Patients with cancer and COVID-19 who were admitted to hospital had a high case-fatality rate. Unfavourable prognostic factors, including receiving chemotherapy within 4 weeks before symptom onset and male sex, might help clinicians to identify patients at high risk of fatal outcomes. National Natural Science Foundation of China.

Porous ceramics have been widely used in heat insulation, filtration, and as a catalyst carrier. Ceramics with high porosity and high strength are desired; however, this high porosity commonly results in low strength materials. In this study, porous alumina with high porosity and high strength was prepared by a popular direct foaming method based on particle-stabilized wet foam that used ammonium polyacrylate (PAA) and dodecyl trimethyl ammonium chloride (DTAC) as the dispersant and hydrophobic modifier, respectively. The effects of the dispersant and surfactant contents on the rheological properties of alumina slurries, stability of wet foams, and microstructure and mechanical properties of sintered ceramics were investigated. The microstructure of porous ceramics was regulated using wet foams to achieve high strength. For a given PAA content, the wet foams exhibited increasing stability with increasing DTAC content. The most stable wet foam was successfully obtained with 0.40 wt% PAA and 0.02 wt% DTAC. The corresponding porous alumina ceramics had a porosity of 82%, an average grain size of 0.7 µm, and a compressive strength of 39 MPa. However, for a given DTAC content, the wet foams had decreasing stability with increasing PAA content. A possible mechanism to explain these results is analyzed.

Adult stem cell identity, plasticity, and homeostasis are precisely orchestrated by lineage-restricted epigenetic and transcriptional regulatory networks. Here, by integrating super-enhancer and chromatin accessibility landscapes, we delineate core transcription regulatory circuitries (CRCs) of limbal stem/progenitor cells (LSCs) and find that RUNX1 and SMAD3 are required for maintenance of corneal epithelial identity and homeostasis. RUNX1 or SMAD3 depletion inhibits PAX6 and induces LSCs to differentiate into epidermal-like epithelial cells. RUNX1, PAX6, and SMAD3 (RPS) interact with each other and synergistically establish a CRC to govern the lineage-specific cis -regulatory atlas. Moreover, RUNX1 shapes LSC chromatin architecture via modulating H3K27ac deposition. Disturbance of RPS cooperation results in cell identity switching and dysfunction of the corneal epithelium, which is strongly linked to various human corneal diseases. Our work highlights CRC TF cooperativity for establishment of stem cell identity and lineage commitment, and provides comprehensive regulatory principles for human stratified epithelial homeostasis and pathogenesis. Corneal epithelium shares similar molecular signatures to other stratified epithelia. Here, the authors map super-enhancers and accessible chromatin in corneal epithelium, identifying a transcription regulatory circuit, including RUNX1, PAX6, and SMAD3, required for corneal epithelial identity and homeostasis.

ObjectivesGiven the increased ageing population and frequent epidemic challenges, it is vital to have the nurse workforce of sufficient quantity and quality. This study aimed to demonstrate the trends, composition and distribution of nurse workforce in China.DesignSecondary analysis using national public datasets in China from 2003 to 2018.Setting/participantsNational population, nurse workforce and physician workforce.Primary and secondary outcome measuresFrequency and proportion were used to demonstrate: (1) the longitudinal growth of nurse workforce; (2) the diversity of nurse workforce in gender, age, work experience and education level; and (3) the distribution of nurse workforce among provinces, rural–urban areas and hospital/community settings. The Gini coefficient and Theil L index were used to measure the inequality trends of nurse workforce.ResultsThe total number of nurses increased from 1.3 million to 4.1 million and the density increased from 1 to 2.94 per 1000 population over 2003–2018. The nurses to physician ratio changed from 0.65:1 to 1.14:1. The majority of the nurse workforce was female, under 35 years old, with less than 30 years of work experience, with an associate’s degree and employed within hospitals. Central and eastern regions had more nurses and there were 5.08 nurses per 1000 population in urban areas while less than two in rural areas in 2018. The Gini coefficient and between-provincial Theil index experienced a consistent decline. Within-province inequality accounted for overall inequality has risen from 52.38% in 2010 to 71.43% in 2018 suggested that the differences of distribution are mainly reflected in urban and rural areas.ConclusionChinese nurse workforce has been changed significantly in the past 15 years that may be associated with the reformations of policy, nursing education in China. Our study suggests current features in the nurse workforce and can be used to strengthen future health services.

Salt stress is a major constraint to seed germination and early seedling growth in rice, affecting crop establishment and productivity. To understand the mechanisms underlying salt tolerance, we investigated two rice varieties with contrasting responses as follows: salt-tolerant sea rice 86 (SR86) and salt-sensitive P559. Germination assays under increasing NaCl concentrations (50–300 mM) revealed that 100 mM NaCl induced clear phenotypic divergence. SR86 maintained bud growth and showed enhanced root elongation under moderate salinity, while P559 exhibited significant growth inhibition. Transcriptomic profiling of buds and roots under 100 mM NaCl identified over 3724 differentially expressed genes (DEGs), with SR86 showing greater transcriptional plasticity, particularly in roots. Gene ontology enrichment revealed tissue- and genotype-specific responses. Buds showed enrichment in photosynthesis-related and redox-regulating pathways, while roots emphasized ion transport, hormonal signaling, and oxidative stress regulation. SR86 specifically activated genes related to photosystem function, DNA repair, and transmembrane ion transport, while P559 showed activation of oxidative stress-related and abscisic acid (ABA)-regulated pathways. Hormonal profiling supported transcriptomic findings as follows: both varieties showed increased gibberellin 3 (GA3) and gibberellin 4 (GA4) levels under salt stress. SR86 showed elevated auxin (IAA) and reduced jasmonic acid (JA), whereas P559 maintained stable IAA and JA levels. Ethylene precursor and salicylic acid levels declined in both varieties. ABA levels rose slightly but not significantly. These findings suggest that SR86’s superior salt tolerance results from rapid growth, robust transcriptional reprogramming, and coordinated hormonal responses. This study offers key insights into early-stage salt stress adaptation and identifies molecular targets for improving stress resilience in rice.

Background To explore the role of family with sequence similarity 13 member A (FAM13A) in TGF-β1-induced EMT in the small airway epithelium of patients with chronic obstructive pulmonary disease (COPD). Methods Small airway wall thickness and protein levels of airway remodeling markers, EMT markers, TGF-β1, and FAM13A were measured in lung tissue samples from COPD and non-COPD patients. The correlations of FAM13A expression with COPD severity and EMT marker expression were evaluated. Gain- and loss-of-function assays were performed to explore the functions of FAM13A in cell proliferation, motility, and TGF-β1-induced EMT marker alterations in human bronchial epithelial cell line BEAS-2B. Results Independent of smoking status, lung tissue samples from COPD patients exhibited significantly increased small airway thickness and collagen fiber deposition, along with enhanced protein levels of remodeling markers (collagen I, fibronectin, and MMP-9), mesenchymal markers (α-SMA, vimentin, and N-cadherin), TGF-β1, and FAM13A, compared with those from non-COPD patients. FAM13A expression negatively correlated with FEV 1 % and PO 2 in COPD patients. In small airway epithelium, FAM13A expression negatively correlated with E-cadherin protein levels and positively correlated with vimentin protein levels. In BEAS-2B cells, TGF-β1 dose-dependently upregulated FAM13A protein levels. FAM13A overexpression significantly promoted cell proliferation and motility in BEAS-2B cells, whereas FAM13A silencing showed contrasting results. Furthermore, FAM13A knockdown partially reversed TGF-β1-induced EMT marker protein alterations in BEAS-2B cells. Conclusions FAM13A upregulation is associated with TGF-β1-induced EMT in the small airway epithelium of COPD patients independent of smoking status, serving as a potential therapeutic target for anti-EMT therapy in COPD.

RNA-binding proteins (RBPs) are involved in the regulation of RNA splicing, stability, and localization. How RBPs control the development of atherosclerosis, is not fully understood. To explore the relevant RNA-binding proteins (RBPs) and alternative splicing events (ASEs) in atherosclerosis. We made a comprehensive work to integrate analyses of differentially expressed genes, including differential RBPs, and variable splicing characteristics related to different stages of atherosclerosis in dataset GSE104140. A total of 3712 differentially expressed genes (DEGs) were identified, including 2921 upregulated genes and 791 downregulated genes. Further analysis screened out 54 RBP genes, and 434 AS genes overlapped DEGs. We selected high expression ten RBP genes (SAMHD1, DDX60 L, TLR7, RBM47, MYEF2, RNASE6, PARP12, APOBEC3G, SMAD9, and RNASE1) for co-expression analysis. Meanwhile, we found seven regulated alternative splicing genes (RASGs) (ABI1, FXR1, CHID1, PLEC, PRKACB, BNIP2, PPP3CB) that could be regulated by RBPs. The co-expression network was used to further elucidate the regulatory and interaction relationship between RBPs and AS genes. Apoptotic process and innate immune response, revealed by the functional enrichment analysis of RASGs regulated by RBPs were closely related to atherosclerosis. In addition, 26 of the 344 alternative splicing genes regulated by the above 10 RBPs were transcription factors (TFs), We selected high expression nine TFs (TFDP1, RBBP7, STAT2, CREB5, ERG, ELF1, HMGN3, BCLAF1, and ZEB2) for co-expression analysis. The target genes of these TFs were mainly enriched in inflammatory and immune response pathways that were associated with atherosclerosis. indicating that AS abnormalities of these TFs may have a function in atherosclerosis. Furthermore, the expression of differentially expressed RBPs and the alternative splicing events of AS genes was validated by qRT-PCR in umbilical vein endothelial cells (HUVEC). The results showed that RBM47 were remarkedly difference in HUVEC treated with ox-LDL and the splicing ratio of AS in BCLAF1which is regulated by RBM47 significantly changed. In conclusion, the differentially expressed RBPs identified in our analysis may play important roles in the development of atherosclerosis by regulating the AS of these TF genes.