Role of secreted frizzled-related protein 5 in granulosa cells of hu sheep ovaries.

The objective of this study was to examine the expression patterns of secreted frizzled-related protein 5 (SFRP5) in the ovaries of Hu sheep and to explore the key downstream factors of SFRP5 in sheep granulosa cells (GCs) using RNA-seq. In the present study, SFRP5 was widely expressed in the ovary and localized to GCs and oocytes during various stages of follicular development. In addition, the expression of SFRP5 increased with follicular diameter. In contrast to the negative control, SFRP5 knockdown promoted the EdU-positive cell rate with an increase in PCNA mRNA and protein levels, whereas SFRP5 overexpression had the opposite effect. In addition, the cell cycle was propelled from the G0/G1 phase to the S phase with the upregulation of CCNB1, CCND1, CDK1, and CDK4 after SFRP5 knockdown. Moreover, SFRP5 overexpression enhanced the apoptosis of GCs with increased Caspase3 protein levels. Following SFRP5 knockdown, differentially expressed genes were mainly enriched in the PI3K/AKT, MAPK, Wnt, and Hippo signaling pathways, and several related candidate genes such as MMP1, MMP3, SFRP4, INHA, TGFA, and CASP3 were screened. In general, this study enhances our understanding of the expression of SFRP5 in the GCs of Hu sheep, along with its functions in follicular development.

Disruption of pulmonary microvascular endothelial barrier by dysregulated claudin-8 and claudin-4: uncovered mechanisms in porcine reproductive and respiratory syndrome virus infection.

The pulmonary endothelium is a dynamic and metabolically active monolayer of endothelial cells. Dysfunction of the pulmonary endothelial barrier plays a crucial role in the acute lung injury (ALI) and acute respiratory distress syndrome (ARDS), frequently observed in the context of viral pneumonia. Dysregulation of tight junction proteins can lead to the disruption of the endothelial barrier and subsequent leakage. Here, the highly pathogenic porcine reproductive and respiratory syndrome virus (HP-PRRSV) served as an ideal model for studying ALI and ARDS. The alveolar lavage fluid of pigs infected with HP-PRRSV, and the supernatant of HP-PRRSV infected pulmonary alveolar macrophages were respectively collected to treat the pulmonary microvascular endothelial cells (PMVECs) in Transwell culture system to explore the mechanism of pulmonary microvascular endothelial barrier leakage caused by viral infection. Cytokine screening, addition and blocking experiments revealed that proinflammatory cytokines IL-1ß and TNF-α, secreted by HP-PRRSV-infected macrophages, disrupt the pulmonary microvascular endothelial barrier by downregulating claudin-8 and upregulating claudin-4 synergistically. Additionally, three transcription factors interleukin enhancer binding factor 2 (ILF2), general transcription factor III C subunit 2 (GTF3C2), and thyroid hormone receptor-associated protein 3 (THRAP3), were identified to accumulate in the nucleus of PMVECs, regulating the transcription of claudin-8 and claudin-4. Meanwhile, the upregulation of ssc-miR-185 was found to suppress claudin-8 expression via post-transcriptional inhibition. This study not only reveals the molecular mechanisms by which HP-PRRSV infection causes endothelial barrier leakage in acute lung injury, but also provides novel insights into the function and regulation of tight junctions in vascular homeostasis.

Response of bacterial ecological and functional properties to anthropogenic interventions during maturation of mine sand soil.

Soil formation is a complex process that starts from the biological development. The ecological principles and biological function in soil are of great importance, whereas their response to anthropogenic intervention has been poorly understood. In this study, a 150-day microcosmic experiment was conducted with the addition of sludge and/or fermented wood chips (FWC) to promote the soil maturation. The results showed that, compared to the control (natural development without anthropogenic intervention), sludge, FWC, and their combination increased the availability of carbon, nitrogen, and potassium, and promoted the soil aggregation. They also enhanced the cellulase activity, microbial biomass carbon (MBC) and bacterial diversity, indicating that anthropogenic interventions promoted the maturation of sand soil. Molecular ecology network and functional analyses indicated that soil maturation was accomplished with the enhancement of ecosystem functionality and stability. Specifically, sludge promoted a transition in bacterial community function from denitrification to nitrification, facilitated the degradation of easily degradable organic matter, and enhanced the autotrophic nutritional mode. FWC facilitated the transition of bacterial function from denitrification to ammonification, promoted the degradation of recalcitrant organic matter, and simultaneously enhanced both autotrophic and heterotrophic nutritional modes. Although both sludge and FWC promoted the soil functionality, they showed distinct mechanistic actions, with sludge enhancing the physical structure, and FWC altering chemical composition. It is also worth emphasizing that sludge and FWC exhibited a synergistic effect in promoting biological development and ecosystem stability, thereby providing an effective avenue for soil maturation.

Association Between Vitamin B12 Intake and Mortality in Patients with Colorectal Cancer: The US National Health and Nutrition Examination Survey, 1999-2018.

Vitamin B12 plays a role in DNA methylation, influencing the 1-carbon cycle; However, its effect on colorectal cancer (CRC) mortality remains uncertain. This study assessed the relationship between vitamin B12 intake and all-cause and cancer-specific mortality among CRC patients. We analyzed data from the NHANES from 1999 to 2018, using multivariable Cox regression, competing risk model, Kaplan-Meier survival curves, and stratified analysis with interaction effects. The studied involved 4,554 cancer patients (mean age 65.8 years, 47.6% males). Results from multivariate Cox regression indicated that each additional 1 mcg/day of dietary vitamin B12 independently increased the risk of all-cause (HR, 1.07; 95% CI: 1.04-1.09, p < 0.001) and cancer-specific mortality (HR, 1.04; 95% CI, 1.02-1.06; p < 0.001). Kaplan-Meier curves indicated a higher risk of all-cause mortality with increased vitamin B12 intake (Log rank p = 0.01). Subgroup analysis suggested that higher vitamin B12 intake correlated with increased all-cause mortality risk, especially in individuals with higher protein (HR, 1.04; 95% CI, 1.02-1.06; p = 0.019) or carbohydrate intake (HR, 1.03; 95% CI, 1.01-1.05; p = 0.04). Thus, higher vitamin B12 intake correlates with increased all-cause and cancer-specific mortality in CRC patients, particularly those with higher protein or carbohydrate intake.

Formation, stability, and antimicrobial efficacy of eutectic nanoemulsions containing thymol and glycerin monolaurate.

In this study, based on the discovery of thymol/glycerol monolaurate (GML) eutectic solvent, we studied the effect of GML as a multi-functional component (ripening inhibitor and antibacterial agent) on the formation, stability and antibacterial activity of eutectic nanoemulsions, and investigated the preservation of nanoemulsion in fresh pork. These results indicated that the formation of eutectic solvent was due to the hydrogen bonding between thymol and GML in the molten state. And eutectic nanoemulsions prepared with medium GML concentrations (20%, 40%, and 60%) of eutectic solvents as oil phases had small droplet diameters (<150 nm), exhibited sustained-release characteristics, and had excellent physicochemical stability. Moreover, the addition of GML enhanced the antibacterial activity of thymol nanoemulsion against S. aureus. as seen by their ability to inhibit affect formation more effectively. Treatment of fresh pork with optimized eutectic nanoemulsions (40% thymol/60% GML) extended its shelf life during refrigeration, which was mainly attributed to the ability of the encapsulated essential oil to inhibit microbial growth and lipid oxidation. These results provide a novel strategy to control Ostwald ripening and maintain the high antibacterial activity of thymol in nanoemulsion-based delivery systems.

The distinction of area postrema syndrome between MOGAD and NMOSD.

Background and objectives: Both myelin oligodendrocyte glycoprotein-IgG associated disorders (MOGAD) and neuromyelitis optica spectrum disorder (NMOSD) are demyelinating diseases of the central nervous system. They present similar clinical manifestations such as optica neuritis, myelitis and area postrema syndrome (APS). The distinctions of optica neuritis (ON) and myelitis between them have been elaborated to great length while their differences in APS remain to be elucidated. We aim to report the frequency of APS in patients with MOGAD as well as NNOSD patients, and to compare the characteristics of APS between patients with MOGAD and those with NMOSD. Methods: Seven MOG-IgG positive APS patients were retrospectively identified between 2017 and 2022. APS phenotypes have been previously described. The similarities and differences between MOGAD and NMOSD patients with APS was compared, including the frequency and duration of APS between the two diseases, and their incidences of accompanied subtentorial lesions have also been described and compared. Results: We reviewed a cohort of 218 MOG-IgG-positive patients, and 396 patients with NMOSD. 200 MOGAD patients and 332 NMOSD patients were included in this study. In the cohort, seven patients with MOG-IgG-positive antibody presented with APS were analyzed, four of whom had disease onset with APS. Of the 332 patients with NMOSD, 47 had APS attacks while 31 had APS at disease onset. In patients with MOGAD, 2 had nausea, 3 had vomiting, 5 had hiccups, and 1 patient presented with all three symptoms above. In patients with NMOSD, 70.2 % had nausea, vomiting and hiccups at the same time during APS attacks. Apart from the medulla oblongata, other subtentorial regions were also affected in 6/7 MOGAD patients while 14/47 NMOSD patients had other subtentorial regions involved. During an APS attack, the incidence of concomitant lesions in the brainstem and other regions was significantly greater in MOGAD than in the NMOSD cohort (P = 0.008*). Conclusion: APS is a rare, but not isolated clinical manifestation of MOGAD. APS happened more frequently with other supratentorial and subtentorial lesions in MOGAD. The symptoms of NVH (nausea, vomiting, hiccups) tended to happen respectively in MOGAD compared with NMOSD. The phenotype or mechanism of APS in MOGAD may differ from that in NMOSD.

Epigenetic-related gene-based prognostic model construction and validation in prostate adenocarcinoma.

Prostate adenocarcinoma (PRAD), driven by both genetic and epigenetic factors, is a common malignancy that affects men worldwide. We aimed to identify and characterize differentially expressed epigenetic-related genes (ERGs) in PRAD and investigate their potential roles in disease progression and prognosis. We used PRAD samples from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) to identify prognosis-associated ERGs. Thirteen ERGs with two distinct expression profiles were identified through consensus clustering. Gene set variation analysis highlighted differences in pathway activities, particularly in the Hedgehog and Notch pathways. Higher epigenetic scores correlated with favorable prognosis and improved immunotherapeutic response. Experimental validation underscored the importance of CBX3 and KAT2A, suggesting their pivotal roles in PRAD. This study provides crucial insights into the epigenetic scoring approach and presents a promising prognostic tool, with CBX3 and KAT2A as key players. These findings pave the way for targeted and personalized interventions for the treatment of PRAD.

Primary lung adenocarcinoma with breast metastasis harboring the EML4­ALK fusion: A case report.

Pulmonary adenocarcinoma with breast metastasis is rarely encountered in clinical practice. Therefore, precise clinical diagnosis of patients with this disease is crucial when selecting subsequent treatment modalities and for overall prognosis assessment. The present study reported on a case of lung cancer with breast metastasis harboring the EML4-ALK fusion. The patient was initially diagnosed with triple-negative breast cancer with lung metastasis, but comprehensive breast cancer treatment was ineffective. Reevaluation of the patient's condition via lung biopsy revealed primary lung adenocarcinoma. In addition, the results of genetic testing revealed the EML4-ALK fusion protein in both lung and breast tissues. After treatment with ALK inhibitors, the patient's symptoms improved rapidly. This case highlights the prolonged diagnostic journey from presentation with a breast mass to ultimately being diagnosed with lung cancer with breast metastasis, underscoring the critical need for heightened awareness among clinicians regarding the possibility of rare metastatic patterns. Timely identification of lung cancer with breast metastasis, facilitated by comprehensive genetic testing, not only refines treatment decisions but also emphasizes the importance of interdisciplinary collaboration in navigating complex clinical scenarios. Such insight contributes to the ongoing development of personalized cancer care that guides clinicians toward more effective and tailored therapeutic strategies for patients with similar diagnostic challenges.

Unlocking the potential of enzyme engineering via rational computational design strategies.

Enzymes play a pivotal role in various industries by enabling efficient, eco-friendly, and sustainable chemical processes. However, the low turnover rates and poor substrate selectivity of enzymes limit their large-scale applications. Rational computational enzyme design, facilitated by computational algorithms, offers a more targeted and less labor-intensive approach. There has been notable advancement in employing rational computational protein engineering strategies to overcome these issues, it has not been comprehensively reviewed so far. This article reviews recent developments in rational computational enzyme design, categorizing them into three types: structure-based, sequence-based, and data-driven machine learning computational design. Case studies are presented to demonstrate successful enhancements in catalytic activity, stability, and substrate selectivity. Lastly, the article provides a thorough analysis of these approaches, highlights existing challenges and potential solutions, and offers insights into future development directions.

Investigation of Nasal Mucosal IgA Responses in the Population Following COVID-19 Pandemic - China, September 2022-August 2023.

What is already known about this topic?: Mucosal IgA plays a crucial role in host immunity against respiratory viruses. Recent studies suggest that it has the potential to mitigate the transmission of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) Omicron variant. However, a comprehensive population-based analysis examining mucosal IgA levels following the winter 2022 wave of the coronavirus disease 2019 (COVID-19) pandemic is yet to be conducted. What is added by this report?: In our study involving 3,421 participants, we documented IgA responses subsequent to SARS-CoV-2 infection. A significant proportion of individuals sustained increased levels of IgA for over six months. These levels were also observed in individuals with prior infections who underwent asymptomatic reinfections, indicating an active production of IgA antibodies. Further, individuals with multiple vaccinations or severe symptoms tended to display elevated IgA levels after recovery. What are the implications for public health practice?: IgA in the nasal mucosa is crucial for defense against SARS-CoV-2 infection. These insights can enhance our knowledge of immune responses following infection and have provided certain reference values for disease prevention and control strategies.

Downregulated SPESP1-driven fibroblast senescence decreases wound healing in aged mice.

BACKGROUND: Human dermal fibroblasts (HDFs) are essential in the processes of skin ageing and wound healing. However, the underlying mechanism of HDFs in skin healing of the elderly has not been well defined. This study aims to elucidate the mechanisms of HDFs senescence and how senescent HDFs affect wound healing in aged skin. METHODS: The expression and function of sperm equatorial segment protein 1 (SPESP1) in skin ageing were evaluated via in vivo and in vitro experiments. To delve into the potential molecular mechanisms by which SPESP1 influences skin ageing, a combination of techniques was employed, including proteomics, RNA sequencing, immunoprecipitation, chromatin immunoprecipitation and liquid chromatography-mass spectrometry analyses. Clearance of senescent cells by dasatinib plus quercetin (D+Q) was investigated to explore the role of SPESP1-induced senescent HDFs in wound healing. RESULTS: Here, we define the critical role of SPESP1 in ameliorating HDFs senescence and retarding the skin ageing process. Mechanistic studies demonstrate that SPESP1 directly binds to methyl-binding protein, leading to Decorin demethylation and subsequently upregulation of its expression. Moreover, SPESP1 knockdown delays wound healing in young mice and SPESP1 overexpression induces wound healing in old mice. Notably, pharmacogenetic clearance of senescent cells by D+Q improved wound healing in SPESP1 knockdown skin. CONCLUSIONS: Taken together, these findings reveal the critical role of SPESP1 in skin ageing and wound healing, expecting to facilitate the development of anti-ageing strategies and improve wound healing in the elderly.

Investigation of crucial genes and mitochondrial function impairment in diabetic cardiomyopathy.

BACKGROUND: Diabetic cardiomyopathy (DCM) is a special type of cardiovascular disease, termed as a situation of abnormal myocardial structure and function that occurs in diabetic patients. However, the most fundamental mechanisms of DCM have not been fully explicated, and useful targets for the therapeutic strategies still need to be explored. METHODS: In the present study, we combined bioinformatics analysis and in vitro experiments throughout the process of DCM. Differentially Expressed Genes (DEGs) analysis was performed and the weighted gene co-expression network analysis (WGCNA) was constructed to determine the crucial genes that were tightly connected to DCM. Additionally, Functional enrichment analysis was conducted to define biological pathways. To identify the specific molecular mechanism, the human cardiomyocyte cell line (AC16) was stimulated by high glucose (HG, 50 mM D-glucose) and used to imitate DCM condition. Then, we tentatively examined the effect of high glucose on cardiomyocytes, the expression levels of crucial genes were further validated by in vitro experiments. RESULTS: Generally, NPPA, IGFBP5, SERPINE1, and C3 emerged as potential therapeutic targets. Functional enrichment analysis performed by bioinformatics indicated that the pathogenesis of DCM is mainly related to heart muscle contraction and calcium (Ca2+) release activation. In vitro, we discovered that high glucose treatment induced cardiomyocyte injury and exacerbated mitochondrial dysfunction remarkably. CONCLUSION: Our research defined four crucial genes, as well as determined that mitochondrial function impairment compromises calcium homeostasis ultimately resulting in contractile dysfunction is a central contributor to DCM progression. Hopefully, this study will offer more effective biomarkers for DCM diagnosis and treatment.

Human Umbilical Cord Mesenchymal Stem Cells Promote Anti-Inflammation and Angiogenesis by Targeting Macrophages in a Rat Uterine Scar Model.

BACKGROUND: Human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) have demonstrated efficacy in repairing uterine scars, although the underlying mechanisms remain unclear. METHODS: Uterine injury was surgically induced in a rat model, followed by immediate transplantation of 5 × 10 ^ 5 hUC-MSCs to each side of the uterus. Uterine morphology was evaluated at days 14 and 30 using HE and Masson staining. Immunohistochemistry assessed macrophage polarization, angiogenesis and endometrial receptivity in the endometrium. Additionally, the regulatory effects of hUC-MSCs on macrophage polarization were explored through coculture. qRT-PCR quantified the expression of anti-inflammatory (IL10 and Arg1) and pro-inflammatory (iNOS and TNF-α) factors. Western blotting evaluated CD163 expression. RESULTS: Transplantation of hUC-MSCs promoted the healing of uterine injuries and tissue regeneration while inhibiting tissue fibrosis. Immunohistochemistry at days 14 and 30 post-transplantation demonstrated the polarization of macrophages toward the M2 phenotype in the uterine injury area in the presence of hUC-MSCs. Furthermore, hUC-MSC transplantation improved angiogenesis and endometrial receptivity in the uterine injury rat model, associated with increased IL10 expression. hUC-MSC-induced angiogenesis can be resisted by depleted macrophages. In vitro coculture experiments further demonstrated that hUC-MSCs promoted IL10 expression in macrophages while suppressing TNF-α and iNOS expression. Western blotting showed enhanced CD163 expression in macrophages following hUC-MSC treatment. CONCLUSIONS: hUC-MSCs contribute to the healing of uterine injuries by targeting macrophages to promote angiogenesis and the expression of anti-inflammatory factors.

Mitochondria-Targeted Nanoadjuvants Induced Multi-Functional Immune-Microenvironment Remodeling to Sensitize Tumor Radio-Immunotherapy.

It is newly revealed that collagen works as a physical barrier to tumor immune infiltration, oxygen perfusion, and immune depressor in solid tumors. Meanwhile, after radiotherapy (RT), the programmed death ligand-1 (PD-L1) overexpression and transforming growth factor-ß (TGF-ß) excessive secretion would accelerate DNA damage repair and trigger T cell exclusion to limit RT efficacy. However, existing drugs or nanoparticles can hardly address these obstacles of highly effective RT simultaneously, effectively, and easily. In this study, it is revealed that inducing mitochondria dysfunction by using oxidative phosphorylation inhibitors like Lonidamine (LND) can serve as a highly effective multi-immune pathway regulation strategy through PD-L1, collagen, and TGF-ß co-depression. Then, IR-LND is prepared by combining the mitochondria-targeted molecule IR-68 with LND, which then is loaded with liposomes (Lip) to create IR-LND@Lip nanoadjuvants. By doing this, IR-LND@Lip more effectively sensitizes RT by generating more DNA damage and transforming cold tumors into hot ones through immune activation by PD-L1, collagen, and TGF-ß co-inhibition. In conclusion, the combined treatment of RT and IR-LND@Lip ultimately almost completely suppressed the growth of bladder tumors and breast tumors.

Predictive value of plasma sICAM-1 and sP-Selectins in the risk of death in patients with acute respiratory distress syndrome.

Background: To evaluate the predictive value of sICAM-1 and sP-Selectins in the risk of death in a prospective cohort of adult acute respiratory distress syndrome (ARDS). Methods: Adult ARDS patients were included. Plasma sICAM-1, sP-Selectins, and inflammatory cytokines (TNF-α, IL-1b, IL-6, IL-8, and IL-17A) were detected in ARDS subjects. The correlation between different factors and the potential of sICAM-1 and sP-Selectins as endothelial markers to predict the risk of deathfrom ARDS was analyzed.

Spatial and functional targeting of intratumoral Tregs reverses CD8+ T cell exhaustion and promotes cancer immunotherapy.

Intratumoral regulatory T cells (Tregs) are key mediators of cancer immunotherapy resistance, including anti-PD-(L)1 immune checkpoint blockade (ICB). The mechanisms driving Treg infiltration into the tumor microenvironment (TME) and the consequence on CD8+ T cell exhaustion remains elusive. Herein, we report that heat shock protein gp96 (GRP94) is indispensable for Treg tumor infiltration, primarily through gp96's roles in chaperoning integrins. Among various gp96-dependent integrins, we found that only LFA-1 (αL integrin) but not αV, CD103 (αE) or ß7 integrin was required for Treg tumor homing. Loss of Treg infiltration into the TME by genetically deleting gp96/LFA-1 potently induces rejection of multiple ICB-resistant murine cancer models in a CD8+ T cell-dependent manner without loss of self-tolerance. Moreover, gp96 deletion impeded Treg activation primarily by suppressing IL-2/STAT5 signaling, which also contributes to tumor regression. By competing for intratumoral IL-2, Tregs prevent activation of CD8+ tumor-infiltrating lymphocytes (TILs), drive TOX induction and induce bona fide CD8+ T cell exhaustion. By contrast, Treg ablation leads to striking CD8+ T cell activation without TOX induction, demonstrating clear uncoupling of the two processes. Our study reveals that the gp96/LFA-1 axis plays a fundamental role in Treg biology and suggests that Treg-specific gp96/LFA-1 targeting represents a valuable strategy for cancer immunotherapy without inflicting autoinflammatory conditions.

Nardosinone relieves metabolic-associated fatty liver disease and promotes energy metabolism through targeting CYP2D6.

BACKGROUND: Nardosinone, a major extract of Rhizoma nardostachyos, plays a vital role in sedation, neural stem cell proliferation, and protection of the heart muscle. However, the huge potential of nardosinone in regulating lipid metabolism and gut microbiota has not been reported, and its potential mechanism has not been studied. PURPOSE: To explore the regulation of nardosinone on liver lipid metabolism and gut microbiota. METHODS: In this study, the role of nardosinone in lipid metabolism was investigated in vitro and in vivo by adding it to mouse feed and HepG2 cell culture medium. And 16S rRNA gene sequencing was used to explore its regulatory effect on gut microbiota. RESULTS: Results showed that nardosinone could improve HFD-induced liver injury and abnormal lipid metabolism by promoting mitochondrial energy metabolism in hepatocytes, alleviating oxidative stress damage, and regulating the composition of the gut microbiota. Mechanistically, combined with network pharmacology and reverse docking analysis, it was predicted that CYP2D6 was the target of nardosinone, and the binding was verified by cellular thermal shift assay (CETSA). CONCLUSIONS: This study highlights a novel mechanism function of nardosinone in regulating lipid metabolism and gut microbiota. It also predicts and validates CYP2D6 as a previously unknown regulatory target, which provides new possibilities for the application of nardosinone and the treatment of metabolic-associated fatty liver disease.

In Vitro Gastrointestinal Digestion of Various Sweet Potato Leaves: Polyphenol Profiles, Bioaccessibility and Bioavailability Elucidation.

The chemical composition discrepancies of five sweet potato leaves (SPLs) and their phenolic profile variations during in vitro digestion were investigated. The results indicated that Ecaishu No. 10 (EC10) provided better retention capacity for phenolic compounds after drying. Furthermore, polyphenols were progressively released from the matrix as the digestion process proceeded. The highest bioaccessibility of polyphenols was found in EC10 intestinal chyme at 48.47%. For its phenolic profile, 3-, 4-, and 5-monosubstituted caffeoyl quinic acids were 9.75%, 57.39%, and 79.37%, respectively, while 3,4-, 3,5-, and 4,5-disubstituted caffeoyl quinic acids were 6.55, 0.27 and 13.18%, respectively. In contrast, the 3,4-, 3,5-, 4,5-disubstituted caffeoylquinic acid in the intestinal fluid after dialysis bag treatment was 62.12%, 79.12%, and 62.98%, respectively, which resulted in relatively enhanced bioactivities (DPPH, 10.51 µmol Trolox/g; FRAP, 8.89 µmol Trolox/g; ORAC, 7.32 µmol Trolox/g; IC50 for α-amylase, 19.36 mg/g; IC50 for α-glucosidase, 25.21 mg/g). In summary, desirable phenolic acid release characteristics and bioactivity of EC10 were observed in this study, indicating that it has potential as a functional food ingredient, which is conducive to the exploitation of the sweet potato processing industry from a long-term perspective.

Atmosphere teleconnections from abatement of China aerosol emissions exacerbate Northeast Pacific warm blob events.

During 2010 to 2020, Northeast Pacific (NEP) sea surface temperature (SST) experienced the warmest decade ever recorded, manifested in several extreme marine heatwaves, referred to as "warm blob" events, which severely affect marine ecosystems and extreme weather along the west coast of North America. While year-to-year internal climate variability has been suggested as a cause of individual events, the causes of the continuous dramatic NEP SST warming remain elusive. Here, we show that other than the greenhouse gas (GHG) forcing, rapid aerosol abatement in China over the period likely plays an important role. Anomalous tropospheric warming induced by declining aerosols in China generated atmospheric teleconnections from East Asia to the NEP, featuring an intensified and southward-shifted Aleutian Low. The associated atmospheric circulation anomaly weakens the climatological westerlies in the NEP and warms the SST there by suppressing the evaporative cooling. The aerosol-induced mean warming of the NEP SST, along with internal climate variability and the GHG-induced warming, made the warm blob events more frequent and intense during 2010 to 2020. As anthropogenic aerosol emissions continue to decrease, there is likely to be an increase in NEP warm blob events, disproportionately large beyond the direct radiative effects.

Metal-organic frameworks-based moisture responsive essential oil hydrogel beads for fresh-cut pineapple preservation.

The preservation of fresh-cut fruits and vegetables has attracted attention to the shelf-life reduction caused by high humidity. Herein, alginate/copper ions cross-linking, in-situ growth and self-assembly techniques of metal-organic frameworks (MOFs) were utilized to prepare a moisture responsive hydrogel bead (HKUST-1@ALG). As the multistage porous structure formation, tea tree essential oil (TTO) load capacity in hydrogel bead (TTO-HKUST-1@ALG) was increased from 6.1% to 21.6%. TTO-HKUST-1@ALG had excellent moisture response performance, and the release rates of TTO increased from 33.89% to 70.98% with moisture increasing from 45% to 95%. Besides, TTO-HKUST-1@ALG exhibited excellent antimicrobial, antioxidant capacity, and biocompatibility. During storage, TTO-HKUST-1@ALG effectively improved the cell membrane integrity by maintaining the balance of reactive oxygen species metabolism. The degradation of cell wall structure and tissue softening were delayed by inhibiting the cell wall-degrading enzymes activity. Briefly, TTO-HKUST-1@ALG improved the storage quality and extended shelf-life of fresh-cut pineapple, which was a promising preservative.