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The coronavirus disease 2019 (COVID-19) pandemic has reminded us of human infections with the H7N9 virus and has raised questions related to the clinical and molecular pathophysiological diversity between the two diseases. Here, we performed a proteomic approach on sera samples from patients with H7N9-virus or SARS-CoV-2-virus infection and healthy controls. Compared to SARS-CoV-2, H7N9-virus infection caused elevated neutrophil concentrations, T cell exhaustion, and increased cytokine/interleukin secretion. Cell-type deconvolution and temporal analysis revealed that T cells and neutrophils could regulate the core immunological trajectory and influence the prognosis of patients with severe H7N9-virus infection. Elevated tissue-enhanced proteins combined with alterations of clinical biochemical indexes suggested that H7N9 infection induced more severe inflammatory organ injury and dysfunction in the liver and intestine. Further mechanical analysis revealed that the high concentration of neutrophils might impact the intestinal enterocyte cells through cytokine-receptor interaction, leading to intestinal damage in patients with H7N9-virus infection. [Display omitted] • We portrayed the different host responses to two types of viral infection • We observed the diverse impacts of two types of virus on NF-κB and p38 signaling pathways • We found that neutrophils could impact the prognosis of patients with H7N9 infection • We found neutrophils might impact intestinal enterocyte cells and cause intestinal damage Wang et al. portrayed the proteomic alterations during either H7N9- or SARS-CoV-2-virus infections. Their data revealed the diverse impacts of H7N9 and SARS-CoV-2 virus on NF-κB and p38 signaling pathways. Meanwhile, neutrophil infiltration and decreased expression of ANXA1 were associated with the severe progression of H7N9 infection. [ABSTRACT FROM AUTHOR]

Obesity and type 2 diabetes cause a loss in brown adipose tissue (BAT) activity, but the molecular mechanisms that drive BAT cell remodeling remain largely unexplored. Using a multilayered approach, we comprehensively mapped a reorganization in BAT cells. We uncovered a subset of macrophages as lipid-associated macrophages (LAMs), which were massively increased in genetic and dietary model of BAT expansion. LAMs participate in this scenario by capturing extracellular vesicles carrying damaged lipids and mitochondria released from metabolically stressed brown adipocytes. CD36 scavenger receptor drove LAM phenotype, and CD36-deficient LAMs were able to increase brown fat genes in adipocytes. LAMs released transforming growth factor β1 (TGF-β1), which promoted the loss of brown adipocyte identity through aldehyde dehydrogenase 1 family member A1 (Aldh1a1) induction. These findings unfold cell dynamic changes in BAT during obesity and identify LAMs as key responders to tissue metabolic stress and drivers of loss of brown adipocyte identity. [Display omitted] • scRNA-seq reveals a massive increase of LAM in BAT of obese mice • Metabolically stressed brown adipocytes release EVs containing mitochondria • EVs prime LAM phenotype through lipid scavenger CD36 • LAMs drive brown adipocyte loss identity via TGF-β1-Aldh1a1 pathway Sciarretta et al. found obesity increases lipid-associated macrophages (LAMs) in BAT. Metabolically overloaded brown adipocytes release damaged lipids and mitochondria via EVs, cleared by BAT macrophages via CD36. EVs induce LAM identity. LAMs secrete TGF-β1, suppressing brown fat genes via Aldh1a1 induction, regulating brown-to-white fat conversion in obesity and type 2 diabetes. [ABSTRACT FROM AUTHOR]

• Network pharmacology showed that the targets of ciliary diseases regulated by naringenin were significantly enriched in inflammation and oxidative stress pathways. • Naringenin exerted its protective effect on ciliary structure and number in part via modulation of the IL-17 signaling pathway. • Naringenin alleviated CSE-induced decrease in cilia beat frequency by activating cAMP signaling pathway. Cigarette smoke impairs mucociliary clearance via mechanisms such as inflammatory response and oxidative injury, which in turn induces various respiratory diseases. Naringenin, a naturally occurring flavonoid in grapes and grapefruit, has exhibited pharmacological properties such as anti-inflammatory, expectorant, and antioxidant properties. However, it is still unclear whether naringenin protects airway cilia from injury caused by cigarette smoke. This study aimed to investigate the effect of naringenin on cigarette smoke extract (CSE)-induced structural and functional abnormalities in airway cilia and highlight the potential regulatory mechanism. Initially, network pharmacology was used to predict the mechanism of action of naringenin in ciliary disease. Next, HE staining, immunofluorescence, TEM, qRT-PCR, western blot, and ELISA were performed to assess the effects of naringenin on airway cilia in tracheal rings and air-liquid interface (ALI) cultures of Sprague Dawley rats after co-exposure to CSE (10% or 20%) and naringenin (0, 25, 50, 100 μM) for 24 h. Finally, transcriptomics and molecular biotechnology methods were conducted to elucidate the mechanism by which naringenin protected cilia from CSE-induced damage in ALI cultures. The targets of ciliary diseases regulated by naringenin were significantly enriched in inflammation and oxidative stress pathways. Also, the CSE decreased the number of cilia in the tracheal rings and ALI cultures and reduced the ciliary beat frequency (CBF). However, naringenin prevented CSE-induced cilia damage via mechanisms such as the downregulation of cilia-related genes (e.g., RFX3, DNAI1, DNAH5, IFT88) and ciliary marker proteins such as DNAI2, FOXJ1, and β-tubulin IV, the upregulation of inflammatory factors (e.g., IL-6, IL-8, IL-13), ROS and MDA. IL-17 signaling pathway might be involved in the protective effect of naringenin on airway cilia. Additionally, the cAMP signaling pathway might also be related to the enhancement of CBF by naringenin. In this study, we first found that naringenin reduces CSE-induced structural disruption of airway cilia in part via modulation of the IL-17 signaling pathway. Furthermore, we also found that naringenin enhances CBF by activating the cAMP signaling pathway. This is the first report to reveal the beneficial effects of naringenin on airway cilia and the potential underlying mechanisms. [Display omitted] [ABSTRACT FROM AUTHOR]

• The roles of extracellular vesicles (EVs) from alveolar macrophages were investigated in vivo and in vitro. • The EVs from cigarette smoke extract (CSE)-stimulated alveolar macrophage induced ferroptosis in pulmonary epithelial cells. • The most dramatically altered miRNA in alveolar macrophage-derived EVs from CSE and naringenin treatment was miR-23a-3p. • Naringenin-increased EV miR-23a-3p attenuated the mouse lung epithelial ferroptosis by targeting ACSL4. Alveolar macrophages are one of the momentous regulators in pulmonary inflammatory responses, which can secrete extracellular vesicles (EVs) packing miRNAs. Ferroptosis, an iron-dependent cell death, is associated with cigarette smoke-induced lung injury, and EVs have been reported to regulate ferroptosis by transporting intracellular iron. However, the regulatory mechanism of alveolar macrophage-derived EVs has not been clearly illuminated in smoking-related pulmonary ferroptosis. Despite the known anti-ferroptosis effects of naringenin in lung injury, whether naringenin controls EVs-mediated ferroptosis has not yet been explored. We explore the effects of EVs from cigarette smoke-stimulated alveolar macrophages in lung epithelial ferroptosis, and elucidate the EV miRNA-mediated pharmacological mechanism of naringenin. Differential and ultracentrifugation were conducted to extract EVs from different alveolar macrophages treatment groups in vitro. Both intratracheal instilled mice and treated epithelial cells were used to investigate the roles of EVs from alveolar macrophages involved in ferroptosis. Small RNA sequencing analysis was performed to distinguish altered miRNAs in EVs. The ferroptotic effects of EV miRNAs were examined by applying dual-Luciferase reporter assay and miRNA inhibitor transfection experiment. Here, we firstly reported that EVs from cigarette smoke extract-induced alveolar macrophages (CSE-EVs) provoked pulmonary epithelial ferroptosis. The ferroptosis inhibitor ferrostatin-1 treatment reversed these changes in vitro. Moreover, EVs from naringenin and CSE co-treated alveolar macrophages (CSE+Naringenin-EVs) markedly attenuated the lung epithelial ferroptosis compared with CSE-EVs. Notably, we identified miR-23a-3p as the most dramatically changed miRNA among Normal-EVs, CSE-EVs, and CSE+Naringenin-EVs. Further experimental investigation showed that ACSL4, a pro-ferroptotic gene leading to lipid peroxidation, was negatively regulated by miR-23a-3p. The inhibition of miR-23a-3p diminished the efficacy of CSE+Naringenin-EVs. Our findings firstly provided evidence that naringenin elevated the EV miR-23a-3p level from CSE-induced alveolar macrophages, thereby inhibiting the mouse lung epithelial ferroptosis via targeting ACSL4, and further complemented the mechanism of cigarette-induced lung injury and the protection of naringenin in a paracrine manner. The administration of miR-23a-3p-enriched EVs has the potential to ameliorate pulmonary ferroptosis. [Display omitted] [ABSTRACT FROM AUTHOR]

Given the mismatch in size and morphology of intestinal organoids with native intestine, their application in intestinal segment regeneration has yet to be achieved. By engrafting ileal organoids in epithelium-removed colon, Sugimoto et al. recently constructed transplantable colonic segments with functional ileal epithelium and a subepithelial lymphovascular system, providing hope for the treatment of short bowel syndrome. [ABSTRACT FROM AUTHOR]

Despite the soaring popularity of short video application (SVA) worldwide and its unique affordances provided for adolescent development, little is known about its potential impact on adolescent users' cognitive ability. This study aimed to examine whether and how adolescents' user behaviors regarding SVA, including daily usage and reliance on algorithmic recommendations, predict their cognitive functioning and academic performance. A sample of Chinese adolescents from two age cohorts (M age = 12.25, SD = 0.02, N = 454; M age = 15.21, SD = 0.02, N = 368) completed the survey on SVA user behavior and cognitive ability tests regarding academic delay of gratification (ADOG), working memory and verbal ability, with their academic performance assessed by final exam grades. The findings reveal that daily usage of SVA predicted lower ADOG and academic performance for both age cohorts. SVA daily usage also predicted lower working memory and verbal ability for the younger cohort only, which simultaneously mediated the associations between their user behaviors and poorer academic performance. And the dependency on algorithmic personalization predicted lower working memory for the younger cohort only. Regarding the age differences in SVA-related effects, the study further points out the higher susceptibility of younger adolescents to SVA use compared to their older counterparts, which should be noted by students, parents, educators and researchers so as to prevent the potentially negative impact of using SVA. • Short video use negatively predicts adolescents' cognitive functioning. • Recommender reliance negatively predicts younger adolescents' cognitive functioning. • Short video use negatively predicts adolescents' academic performance. • Younger adolescents show higher susceptibility to the potential negative impacts. [ABSTRACT FROM AUTHOR]

Gelatin-based inks have a broad range of applications in bioprinting for tissue engineering and regenerative medicine due to their biocompatibility, ease of modification, degradability, and rapid gelation induced by low temperature. However, gelatin-derived inks prepared through low-temperature treatment have poor mechanical properties that limit their applications. To solve this problem, we designed polyacrylamide/gelatin/silver nanoparticle (PAAm-GelatinAgNPs) ink to improve gelatin-based hydrogels. The ink is based on double networks, in which the physically cross-linked gelatin as the first network and covalently cross-linked PAAm as the second network. It was found that the presence of PAAm increased the tensile and compression strength of the gelatin-based ink. Moreover, silver nanoparticles endowed the antibacterial properties to the gelatin-based ink and were able to shield the UV irradiation and damages to rat skin. In addition, this ink showed the shear thinning property; Consequently it succeeded in printing complex 3D scaffolds such as the cube, five-pointed star, flower, and university logo of "SEU". In summary, this ink presents a new strategy for the modification of gelatin and offers new potential applications for customized therapy of antimicrobial and anti-UV damage to tissues. [ABSTRACT FROM AUTHOR]

• Attachment anxiety was positively associated with NSSI. • Rumination mediated the association between attachment anxiety and NSSI. • Meaning in life moderated the direct and indirect relationships between attachment anxiety and NSSI. Nonsuicidal self-injury (NSSI), which refers to the direct and deliberate destruction of one's body tissues without the intention of death, is a serious public health problem. Attachment anxiety is an important predictor of NSSI, but the underlying mechanisms between their relationship need to be further explored. This study examined the mediating role of rumination and the moderating role of meaning in life in the relationship between attachment anxiety and NSSI. The study was cross-sectional, and 2,716 Chinese junior high school students (53.3 % male; M age = 12.25 years, SD = 0.86) were measured by the attachment anxiety subscale of Experience of Close Relationships-Relationship Structures Scale, the Rumination Responses Scale, the Self-Injurious Behavior Assessment Questionnaire, and the Meaning in Life Questionnaire. The results showed: (1) attachment anxiety, rumination and NSSI were significantly and positively correlated; (2) rumination partially mediated the relationship between attachment anxiety and NSSI; (3) meaning in life moderated the pathways of attachment anxiety → NSSI and rumination → NSSI respectively. Findings of the study further reveal the mechanism underlying the relationship between attachment anxiety and NSSI from a cognitive perspective, and also help provide ideas for the prevention and intervention of adolescents NSSI (i.e., improving adolescents' meaning in life). [ABSTRACT FROM AUTHOR]

Based on a modification of a magnetohydrodynamic turbulence model, a numerical study was performed to investigate the effects of transverse uniform and gradient magnetic field on the turbulent flow and heat transfer characteristics of a low melting point molten salt in a stainless steel pipe. With the Hartmann number from 0 to 80, the numerical results showed that the fluid flow displayed anisotropic distributions under the magnetic field with decrease of velocity in the mainstream region, and decrease of turbulent intensity, whereas the flow velocity increased in the boundary layer near the Hartmann and Roberts wall. Especially, a velocity jet phenomenon was observed in the Roberts boundary layers at higher Hartmann number in the uniform magnetic field or the positive gradient magnetic field. Under the gradient magnetic field, the flow and heat transfer of molten salt displayed much more variations than under the uniform magnetic field. The magnetohydrodynamic calculation results proposed here might be helpful to the design of the composite heat transfer system for molten salt in actual industrial applications. • Both the uniform and non-uniform magnetic field were applied in pipe flow of molten salt for comparison. • A modified MHD turbulence model was established for turbulent flow of molten salt. • The characteristics of flow and heat transfer were numerically studied for a low melting point molten salt. • The complex influence of magnetic field to flow and heat transfer of molten salt was observed. [ABSTRACT FROM AUTHOR]