Ti3+/Ti4+ and Co2+/Co3+ redox couples in Ce-doped Co-Ce/TiO2 for enhancing photothermocatalytic toluene oxidation.

Cerium and cobalt loaded Co-Ce/TiO2 catalyst prepared by impregnation method was investigated for photothermal catalytic toluene oxidation. Based on catalyst characterizations (XPS, EPR and H2-TPR), redox cycle between Co and TiO2 (Co2+ + Ti4+ ↔ Co3+ + Ti3+) results in the formation of Co3+, Ti3+ and oxygen vacancies, which play important roles in toluene catalytic oxidation reaction. The introduction of Ce brings in the dual redox cycles (Co2+ + Ti4+ ↔ Co3+ + Ti3+, Co2+ + Ce4+ ↔ Co3+ + Ce3+), further promoting the elevation of reaction sites amount. Under full spectrum irradiation with light intensity of 580 mW/cm2, Co-Ce/TiO2 catalyst achieved 96% of toluene conversion and 73% of CO2 yield, obviously higher than Co/P25 and Co/TiO2. Co-Ce/TiO2 efficiently maintains 10-hour stability test under water vapor conditions and exhibits better photothermal catalytic performance than counterparts under different wavelengths illumination. Photothermal catalytic reaction displays improved activities compared with thermal catalysis, which is attributed to the promotional effect of light including photocatalysis and light activation of reactive oxygen species.

Differential Immunoregulation by Human Surfactant Protein A Variants Determines Severity of SARS-CoV-2-induced Lung Disease.

COVID-19 remains a significant threat to public health globally. Infection in some susceptible individuals causes life-threatening acute lung injury (ALI/ARDS) and/or death. Human surfactant protein A (SP-A) is a C-type lectin expressed in the lung and other mucosal tissues, and it plays a critical role in host defense against various pathogens. The human SP-A genes ( SFTPA1 and SFTPA2 ) are highly polymorphic and comprise several common genetic variants, i.e., SP-A1 (variants 6A 2 , 6A 4 ) and SP-A2 (variants 1A 0 , 1A 3 ). Here, we elucidated the differential antiviral and immunoregulatory roles of SP-A variants in response to SARS-CoV-2 infection in vivo . Six genetically-modified mouse lines, expressing both hACE2 (SARS-CoV-2 receptor) and individual SP-A variants: (hACE2/6A 2 (6A 2 ), hACE2/6A 4 (6A 4 ), hACE2/1A 0 (1A 0 ), and hACE2/1A 3 (1A 3 ), one SP-A knockout (hACE2/SP-A KO (KO) and one hACE2/mouse SP-A (K18) mice, were challenged intranasally with 10 3 PFU SARS-CoV-2 or saline (Sham). Infected KO and 1A 0 mice had more weight loss and mortality compared to other mouse lines. Relative to other infected mouse lines, a more severe ALI was observed in KO, 1A 0 , and 6A 2 mice. Reduced viral titers were generally observed in the lungs of infected SP-A mice relative to KO mice. Transcriptomic analysis revealed an upregulation in genes that play central roles in immune responses such as MyD88 , Stat3 , IL-18 , and Jak2 in the lungs of KO and 1A 0 mice. However, Mapk1 was significantly downregulated in 6A 2 versus 1A 0 mice. Analysis of biological pathways identified those involved in lung host defense and innate immunity, including pathogen-induced cytokine, NOD1/2, and Trem1 signaling pathways. Consistent with the transcriptomic data, levels of cytokines and chemokines such as G-CSF, IL-6 and IL-1ß were comparatively higher in the lungs and sera of KO and 1A 0 mice with the highest mortality rate. These findings demonstrate that human SP-A variants differentially modulate SARS-CoV-2-induced lung injury and disease severity by differentially inhibiting viral infectivity and regulating immune-related gene expressions.

Enhancement of Mineralization Ability and Water Resistance of Vanadium-Based Catalysts for Catalytic Oxidation of Chlorobenzene by Platinum Loading.

The design of a catalyst with multifunctional sites is one of the effective methods for low-temperature catalytic oxidation of chlorinated volatile organic compounds (CVOCs). The loss of redox sites and competitive adsorption of H2O prevalent in the treatment of industrial exhaust gases are the main reasons for the weak mineralization ability and poor water vapor resistance of V-based catalysts. In this work, platinum (Pt) is selected to combine with the V/CeO2 catalyst, which provides more redox sites and H2O dissociative activation sites and further enhances its catalytic performance. The results show that PtV/CeO2 achieves 90% of the CO2 yield at 318 °C and maintains excellent catalytic activity rather than continuous deactivation within 15 h after water vapor injection. The formation of Pt-O-V bonds enhances the redox ability and promotes deep oxidation of polychlorinated intermediates, accounting for the significantly improved mineralization ability of PtV/CeO2. The dissociative activation effect of Pt on H2O molecules strengthens the migration and activation of V-adsorbed H2O, precluding V-poisoning and notably improving water resistance. This study lays a solid foundation for the efficient degradation of chlorobenzene under humid conditions.

Human birth tissue products as a non-opioid medicine to inhibit post-surgical pain.

Pain after surgery causes significant suffering. Opioid analgesics cause severe side effects and accidental death. Therefore, there is an urgent need to develop non-opioid therapies for managing post-surgical pain. Local application of Clarix Flo (FLO), a human amniotic membrane (AM) product, attenuated established post-surgical pain hypersensitivity without exhibiting known side effects of opioid use in mice. This effect was achieved through direct inhibition of nociceptive dorsal root ganglion (DRG) neurons via CD44-dependent pathways. We further purified the major matrix component, the heavy chain-hyaluronic acid/pentraxin 3 (HC-HA/PTX3) from human AM that has greater purity and water solubility than FLO. HC-HA/PTX3 replicated FLO-induced neuronal and pain inhibition. Mechanistically, HC-HA/PTX3 induced cytoskeleton rearrangements to inhibit sodium current and high-voltage activated calcium current on nociceptive neurons, suggesting it is a key bioactive component mediating pain relief. Collectively, our findings highlight the potential of naturally derived biologics from human birth tissues as an effective non-opioid treatment for post-surgical pain. Moreover, we unravel the underlying mechanisms of pain inhibition induced by FLO and HC-HA/PTX3.

Oleanolic acid improved intestinal immune function by activating and potentiating bile acids receptor signaling in E. coli-challenged piglets.

BACKGROUND: Infection with pathogenic bacteria during nonantibiotic breeding is one of the main causes of animal intestinal diseases. Oleanolic acid (OA) is a pentacyclic triterpene that is ubiquitous in plants. Our previous work demonstrated the protective effect of OA on intestinal health, but the underlying molecular mechanisms remain unclear. This study investigated whether dietary supplementation with OA can prevent diarrhea and intestinal immune dysregulation caused by enterotoxigenic Escherichia coli (ETEC) in piglets. The key molecular role of bile acid receptor signaling in this process has also been explored. RESULTS: Our results demonstrated that OA supplementation alleviated the disturbance of bile acid metabolism in ETEC-infected piglets (P < 0.05). OA supplementation stabilized the composition of the bile acid pool in piglets by regulating the enterohepatic circulation of bile acids and significantly increased the contents of UDCA and CDCA in the ileum and cecum (P < 0.05). This may also explain why OA can maintain the stability of the intestinal microbiota structure in ETEC-challenged piglets. In addition, as a natural ligand of bile acid receptors, OA can reduce the severity of intestinal inflammation and enhance the strength of intestinal epithelial cell antimicrobial programs through the bile acid receptors TGR5 and FXR (P < 0.05). Specifically, OA inhibited NF-κB-mediated intestinal inflammation by directly activating TGR5 and its downstream cAMP-PKA-CREB signaling pathway (P < 0.05). Furthermore, OA enhanced CDCA-mediated MEK-ERK signaling in intestinal epithelial cells by upregulating the expression of FXR (P < 0.05), thereby upregulating the expression of endogenous defense molecules in intestinal epithelial cells. CONCLUSIONS: In conclusion, our findings suggest that OA-mediated regulation of bile acid metabolism plays an important role in the innate immune response, which provides a new diet-based intervention for intestinal diseases caused by pathogenic bacterial infections in piglets.

Human surfactant protein A inhibits SARS-CoV-2 infectivity and alleviates lung injury in a mouse infection model.

Introduction: SARS coronavirus 2 (SARS-CoV-2) infects human angiotensin-converting enzyme 2 (hACE2)-expressing lung epithelial cells through its spike (S) protein. The S protein is highly glycosylated and could be a target for lectins. Surfactant protein A (SP-A) is a collagen-containing C-type lectin, expressed by mucosal epithelial cells and mediates its antiviral activities by binding to viral glycoproteins. Objective: This study examined the mechanistic role of human SP-A in SARS-CoV-2 infectivity and lung injury in vitro and in vivo. Results: Human SP-A can bind both SARS-CoV-2 S protein and hACE2 in a dose-dependent manner (p<0.01). Pre-incubation of SARS-CoV-2 (Delta) with human SP-A inhibited virus binding and entry and reduced viral load in human lung epithelial cells, evidenced by the dose-dependent decrease in viral RNA, nucleocapsid protein (NP), and titer (p<0.01). We observed significant weight loss, increased viral burden, and mortality rate, and more severe lung injury in SARS-CoV-2 infected hACE2/SP-A KO mice (SP-A deficient mice with hACE2 transgene) compared to infected hACE2/mSP-A (K18) and hACE2/hSP-A1 (6A2) mice (with both hACE2 and human SP-A1 transgenes) 6 Days Post-infection (DPI). Furthermore, increased SP-A level was observed in the saliva of COVID-19 patients compared to healthy controls (p<0.05), but severe COVID-19 patients had relatively lower SP-A levels than moderate COVID-19 patients (p<0.05). Discussion: Collectively, human SP-A attenuates SARS-CoV-2-induced acute lung injury (ALI) by directly binding to the S protein and hACE2, and inhibiting its infectivity; and SP-A level in the saliva of COVID-19 patients might serve as a biomarker for COVID-19 severity.

Effects of bile acid metabolism on intestinal health of livestock and poultry.

Bile acids are synthesised in the liver and are essential amphiphilic steroids for maintaining the balance of cholesterol and energy metabolism in livestock and poultry. They can be used as novel feed additives to promote fat utilisation in the diet and the absorption of fat-soluble substances in the feed to improve livestock performance and enhance carcass quality. With the development of understanding of intestinal health, the balance of bile acid metabolism is closely related to the composition and growth of livestock intestinal microbiota, inflammatory response, and metabolic diseases. This paper systematically reviews the effects of bile acid metabolism on gut health and gut microbiology in livestock. In addition, our paper summarised the role of bile acid metabolism in performance and disease control.

Lymphocyte-Activation Gene 3 Facilitates Pathological Tau Neuron-to-Neuron Transmission.

The spread of prion-like protein aggregates is a common driver of pathogenesis in various neurodegenerative diseases, including Alzheimer's disease (AD) and related Tauopathies. Tau pathologies exhibit a clear progressive spreading pattern that correlates with disease severity. Clinical observation combined with complementary experimental studies has shown that Tau preformed fibrils (PFF) are prion-like seeds that propagate pathology by entering cells and templating misfolding and aggregation of endogenous Tau. While several cell surface receptors of Tau are known, they are not specific to the fibrillar form of Tau. Moreover, the underlying cellular mechanisms of Tau PFF spreading remain poorly understood. Here, it is shown that the lymphocyte-activation gene 3 (Lag3) is a cell surface receptor that binds to PFF but not the monomer of Tau. Deletion of Lag3 or inhibition of Lag3 in primary cortical neurons significantly reduces the internalization of Tau PFF and subsequent Tau propagation and neuron-to-neuron transmission. Propagation of Tau pathology and behavioral deficits induced by injection of Tau PFF in the hippocampus and overlying cortex are attenuated in mice lacking Lag3 selectively in neurons. These results identify neuronal Lag3 as a receptor of pathologic Tau in the brain，and for AD and related Tauopathies, a therapeutic target.

Efficient Catalytic Elimination of Chlorobenzene Based on the Water Vapor-Promoting Effect within Mn-Based Catalysts: Activity Enhancement and Polychlorinated Byproduct Inhibition.

Achieving no or low polychlorinated byproduct selectivity is essential for the chlorinated volatile organic compounds (CVOCs) degradation, and the positive roles of water vapor may contribute to this goal. Herein, the oxidation behaviors of chlorobenzene over typical Mn-based catalysts (MnO2 and acid-modified MnO2) under dry and humid conditions were fully explored. The results showed that the presence of water vapor significantly facilitates the deep mineralization of chlorobenzene and restrains the formation of Cl2 and dichlorobenzene. This remarkable water vapor-promoting effect was conferred by the MnO2 substrate, which could suitably synergize with the postconstructed acidic sites, leading to good activity, stability, and desirable product distribution of acid-modified MnO2 catalysts under humid conditions. A series of experiments including isotope-traced (D2O and H218O) CB-TPO provided complete insights into the direct involvement of water molecules in chlorobenzene oxidation reaction and attributed the root cause of the water vapor-promoting effect to the proton-rich environment and highly reactive water-source oxygen species rather than to the commonly assumed cleaning effect or hydrogen proton transfer processes (generation of active OOH). This work demonstrates the application potential of Mn-based catalysts in CVOCs elimination under practical application conditions (containing water vapor) and provides the guidance for the development of superior industrial catalysts.

Niobium Boride/Graphene Directing High-Performance Lithium-Sulfur Batteries Derived from Favorable Surface Passivation.

Efficient catalysts are needed to accelerate the conversion and suppress the shuttling of polysulfides (LiPSs) to promote the further development of lithium-sulfur (Li-S) batteries. Intermetallic niobium boride (NbB2) has indefinite potential due to superior catalytic activity. Nonetheless, the lack of a rational understanding of catalysis creates a challenge for the design of catalysts. Herein, a NbB2/reduced graphene oxide-modified PP separator (NbB2/rGO/PP) is rationally designed. Essential, an in-depth insight into the catalysis mechanism of NbB2 toward LiPSs is established based on experiments and multiperspective measurement characterization, ab initio molecular dynamics (AIMD), and density functional theory (DFT). It has been uncovered that the actual catalyst that interacts with LiPSs in NbB2 is the passivated surface with an oxide layer (O2-NbB2), which occurs through B-O-Li and Nb-O-Li bonds, rather than the clean NbB2 surface. And the decomposition barrier of Li2S is greatly reduced by a substantial margin, dropping from 3.390 to 0.93 and 0.85 eV on the Nb-O and B-O surfaces, respectively, with fast Li+ diffusivity. Consequently, the cell with NbB2/rGO/PP as a functional separator achieves a high discharge capacity of 873 mAh g-1 at 1C after 100 cycles. Moreover, the benefits of NbB2/rGO/PP can be effectively maintained even at a high sulfur loading of 7.06 mg cm-2 without significant reduction and with a low electrolyte/sulfur ratio of 8 µL mg-1s. This study enhances our understanding of the catalytic mechanism of Li-S systems and presents a promising approach for developing electrocatalysts that are resilient to poisoning.

Disclosing Support-Size-Dependent Effect on Ambient Light-Driven Photothermal CO2 Hydrogenation over Nickel/Titanium Dioxide.

The size of support in heterogeneous catalysts can strongly affect the catalytic property but is rarely explored in light-driven catalysis. Herein, we demonstrate the size of TiO2 support governs the selectivity in photothermal CO2 hydrogenation by tuning the metal-support interactions (MSI). Small-size TiO2 loading nickel (Ni/TiO2 -25) with enhanced MSI promotes photo-induced electrons of TiO2 migrating to Ni nanoparticles, thus favoring the H2 cleavage and accelerating the CH4 formation (227.7 mmol g-1 h-1 ) under xenon light-induced temperature of 360 °C. Conversely, Ni/TiO2 -100 with large TiO2 prefers yielding CO (94.2 mmol g-1 h-1 ) due to weak MSI, inefficient charge separation, and inadequate supply of activated hydrogen. Under ambient solar irradiation, Ni/TiO2 -25 achieves the optimized CH4 rate (63.0 mmol g-1 h-1 ) with selectivity of 99.8 %, while Ni/TiO2 -100 exhibits the CO selectivity of 90.0 % with rate of 30.0 mmol g-1 h-1 . This work offers a novel approach to tailoring light-driven catalytic properties by support size effect.

Generation and characterization of a humanized ACE2 mouse model to study long-term impacts of SARS-CoV-2 infection.

Although the COVID-19 pandemic has officially ended, the persistent challenge of long-COVID or post-acute COVID sequelae (PASC) continues to impact societies globally, highlighting the urgent need for ongoing research into its mechanisms and therapeutic approaches. Our team has recently developed a novel humanized ACE2 mouse model (hACE2ki) designed explicitly for long-COVID/PASC research. This model exhibits human ACE2 expression in tissue and cell-specific patterns akin to mouse Ace2. When we exposed young adult hACE2ki mice (6 weeks old) to various SARS-CoV-2 lineages, including WA, Delta, and Omicron, at a dose of 5 × 105 PFU/mouse via nasal instillation, the mice demonstrated distinctive phenotypes characterized by differences in viral load in the lung, trachea, and nasal turbinate, weight loss, and changes in pro-inflammatory cytokines and immune cell profiles in bronchoalveolar lavage fluid. Notably, no mortality was observed in this age group. Further, to assess the model's relevance for long-COVID studies, we investigated tau protein pathologies, which are linked to Alzheimer's disease, in the brains of these mice post SARS-CoV-2 infection. Our findings revealed the accumulation and longitudinal propagation of tau, confirming the potential of our hACE2ki mouse model for preclinical studies of long-COVID.

Oleanolic acid attenuates hydrogen peroxide-induced apoptosis of IPEC-J2 cells through suppressing c-Jun and MAPK pathway.

Oleanolic acid (OA) is a natural triterpenoid with therapeutic potential for a multitude of diseases. However, the precise mechanism by which OA influences stress-induced apoptosis of intestinal epithelial cells remains elusive. Therefore, the effect of OA on intestinal diseases under stressful conditions and its possible mechanisms have been investigated. In a hydrogen peroxide (H2 O2 )-induced oxidative stress model, OA attenuated H2 O2 -induced apoptosis in a concentration-dependent manner. To investigate the underlying mechanisms, the gene expression profile of OA on IPEC-J2 cells was analyzed using an RNA sequencing system. Results from gene ontology and Kyoto encyclopedia of genes and genomes analysis confirmed that OA may mitigate the cytotoxic effects of H2 O2 by downregulating gene expression through the MAPK signaling pathway. Furthermore, Quantitative real-time polymerase chain reaction results validated the differentially expressed genes data. Western blot analysis further demonstrated that OA effectively suppressed the expression level of c-Jun protein induced by H2 O2 in IPEC-J2 cells. Collectively, our results indicate that OA pretreatment significantly attenuated H2 O2 -induced apoptosis in intestinal epithelial cells through suppressing c-Jun and MAPK pathway.

Monolithic Catalyst of Ni Foam-Supported MnOx for Boosting Magnetocaloric Oxidation of Toluene.

Catalytic oxidation has been considered an effective technique for volatile organic compound degradation. Development of metal foam-based monolithic catalysts coupling electromagnetic induction heating (EMIH) with efficiency and low energy is critical yet challenging in industrial applications. Herein, a Mn18.2-NF monolithic catalyst prepared by electrodeposition exhibited superior toluene catalytic activity under EMIH conditions, and the temperature of 90% toluene conversion decreased by 89 °C compared to that in resistance furnace heating. Relevant characterizations proved that the skin effect induced by EMIH encouraged activation of gaseous oxygen, leading to superior low-temperature redox properties of Mn18.2-NF under the EMIH condition. In situ Fourier transform infrared spectroscopy results showed that skin effect-induced activation of oxidizing species further accelerated the conversion of intermediates. As a result, the Mn18.2-NF monolithic catalyst under EMIH demonstrated remarkable performance for the toluene oxidation, surpassing the conventional nonprecious metal catalyst and other reported monolithic catalysts.

Discovery, validation, and prodrug design of an ACE2 activator for treating bacterial infection-induced lung inflammation.

Exacerbated inflammatory responses can be detrimental and pose fatal threats to the host, as exemplified by the global impact of the COVID-19 pandemic, resulting in millions of fatalities. Developing novel drugs to combat the damaging effects of inflammation is essential for both preventive measures and therapeutic interventions. Accumulating evidence suggests that Angiotensin Converting Enzyme 2 (ACE2) possesses the ability to optimize inflammatory responses. However, the clinical applicability of this potential is limited due to the lack of dependable ACE2 activators. In this study, we conducted a screening of an FDA-approved drug library and successfully identified a novel ACE2 activator, termed H4. The activator demonstrated the capability to mitigate lung inflammation caused by bacterial lung infections, effectively modulating neutrophil infiltration. Importantly, to improve the clinical applicability of the poorly water-soluble H4, we developed a prodrug variant with significantly enhanced water solubility while maintaining a similar level of efficacy as H4 in attenuating inflammatory responses in the lungs of mice exposed to bacterial infections. This finding highlights the potential of formulated H4 as a promising candidate for the treatment and prevention of inflammatory diseases, including lung-related conditions.

Efficient Solar-Driven CO2 Methanation and Hydrogen Storage Over Nickel Catalyst Derived from Metal-Organic Frameworks with Rich Oxygen Vacancies.

Solar-driven photothermal conversion of carbon dioxide (CO2 ) to methane (CH4 ) is a promising approach to remedy energy shortage and climate changes, where highly efficient photothermal catalysts for CO2 methanation urgently need to be designed. Herein, nickel-based catalysts (Ni/ZrO2 ) derived from metal-organic frameworks (MOFs) are fabricated and studied for photothermal CO2 methanation. The optimized catalyst 50Ni/ZrO2 achieves a stable CH4 production rate of 583.3 mmol g-1  h-1 in a continuous stability test, which is almost tenfold higher than that of 50Ni/C-ZrO2 synthesized via commercial ZrO2 . Physicochemical properties indicate that 50Ni/ZrO2 generates more tetragonal ZrO2 and possesses more oxygen vacancies (OVs) as well as enhanced nickel-ZrO2 interaction. As a result, 50Ni/ZrO2 exhibits the strong abilities of light absorption and light-to-heat conversion, superior adsorption capacities of reactants (H2 , CO2 ), and an intermediate product (CO), which finally boosts CH4 formation. This work provides an efficient strategy to design a photothermocatalyst of CO2 methanation through utilizing MOFs-derived support.

Human Surfactant Protein A Alleviates SARS-CoV-2 Infectivity in Human Lung Epithelial Cells.

SARS coronavirus 2 (SARS-CoV-2) infects human angiotensin-converting enzyme 2 (hACE2)-expressing lung epithelial cells through its spike (S) protein. The S protein is highly glycosylated and could be a target for lectins. Surfactant protein A (SP-A) is a collagen-containing C-type lectin, expressed by mucosal epithelial cells and mediates its antiviral activities by binding to viral glycoproteins. This study examined the mechanistic role of human SP-A in SARS-CoV-2 infectivity. The interactions between human SP-A and SARS-CoV-2 S protein and hACE2 receptor, and SP-A level in COVID-19 patients were assessed by ELISA. The effect of SP-A on SARS-CoV-2 infectivity was analyzed by infecting human lung epithelial cells (A549-ACE2) with pseudoviral particles and infectious SARS-CoV-2 (Delta variant) pre-incubated with SP-A. Virus binding, entry, and infectivity were assessed by RT-qPCR, immunoblotting, and plaque assay. The results showed that human SP-A can bind SARS-CoV-2 S protein/RBD and hACE2 in a dose-dependent manner (p<0.01). Human SP-A inhibited virus binding and entry, and reduce viral load in lung epithelial cells, evidenced by the dose-dependent decrease in viral RNA, nucleocapsid protein, and titer (p<0.01). Increased SP-A level was observed in the saliva of COVID-19 patients compared to healthy controls (p<0.05), but severe COVID-19 patients had relatively lower SP-A levels than moderate COVID-19 patients (p<0.05). Therefore, SP-A plays an important role in mucosal innate immunity against SARS-CoV-2 infectivity by directly binding to the S protein and inhibiting its infectivity in host cells. SP-A level in the saliva of COVID-19 patients might serve as a biomarker for COVID-19 severity.

Human milk oligosaccharides reduce necrotizing enterocolitis-induced neuroinflammation and cognitive impairment in mice.

Necrotizing enterocolitis (NEC) is the leading cause of morbidity and mortality in premature infants. One of the most devastating complications of NEC is the development of NEC-induced brain injury, which manifests as impaired cognition that persists beyond infancy and which represents a proinflammatory activation of the gut-brain axis. Given that oral administration of the human milk oligosaccharides (HMOs) 2'-fucosyllactose (2'-FL) and 6'-sialyslactose (6'-SL) significantly reduced intestinal inflammation in mice, we hypothesized that oral administration of these HMOs would reduce NEC-induced brain injury and sought to determine the mechanisms involved. We now show that the administration of either 2'-FL or 6'-SL significantly attenuated NEC-induced brain injury, reversed myelin loss in the corpus callosum and midbrain of newborn mice, and prevented the impaired cognition observed in mice with NEC-induced brain injury. In seeking to define the mechanisms involved, 2'-FL or 6'-SL administration resulted in a restoration of the blood-brain barrier in newborn mice and also had a direct anti-inflammatory effect on the brain as revealed through the study of brain organoids. Metabolites of 2'-FL were detected in the infant mouse brain by nuclear magnetic resonance (NMR), whereas intact 2'-FL was not. Strikingly, the beneficial effects of 2'-FL or 6'-SL against NEC-induced brain injury required the release of the neurotrophic factor brain-derived neurotrophic factor (BDNF), as mice lacking BDNF were not protected by these HMOs from the development of NEC-induced brain injury. Taken in aggregate, these findings reveal that the HMOs 2'-FL and 6'-SL interrupt the gut-brain inflammatory axis and reduce the risk of NEC-induced brain injury.NEW & NOTEWORTHY This study reveals that the administration of human milk oligosaccharides, which are present in human breast milk, can interfere with the proinflammatory gut-brain axis and prevent neuroinflammation in the setting of necrotizing enterocolitis, a major intestinal disorder seen in premature infants.

Suppressive Strong Metal-Support Interactions on Ruthenium/TiO2 Promote Light-Driven Photothermal CO2 Reduction with Methane.

Strong metal-support interactions (SMSI) have gained great attention in the heterogeneous catalysis field, but its negative role in regulating light-induced electron transfer is rarely explored. Herein, we describe how SMSI significantly restrains the activity of Ru/TiO2 in light-driven CO2 reduction by CH4 due to the photo-induced transfer of electrons from TiO2 to Ru. In contrast, on suppression of SMSI Ru/TiO2 -H2 achieves a 46-fold CO2 conversion rate compared to Ru/TiO2 . For Ru/TiO2 -H2 , a considerable number of photo-excited hot electrons from Ru nanoparticles (NPs) migrate to oxygen vacancies (OVs) and facilitate CO2 activation under illumination, simultaneously rendering Ruδ+ electron deficient and better able to accelerate CH4 decomposition. Consequently, photothermal catalysis over Ru/TiO2 -H2 lowers the activation energy and overcomes the limitations of a purely thermal system. This work offers a novel strategy for designing efficient photothermal catalysts by regulating two-phase interactions.

Unveiling the Position Effect of Ce within Layered MnO2 to Prolong the Ambient Removal of Indoor HCHO.

The position of Ce doping has a significant effect on ambient HCHO storage and catalytic oxidation on layered MnO2. By associating structure and performance, it is unveiled that doping Ce into the in-layered lattice of MnO2 is favorable to the generation of high-valence Mn cations, enhancing the oxidizing ability and capacity, but an opposite influence is displayed by interlayered Ce doping. From the aspect of energy minimization calculated by DFT, in-layered Ce doping is also recommended due to the decreased energies for molecule adsorption and oxygen vacancy formation. As a result, in-layered Ce-doped MnO2 displays exceptional activity in catalyzing the deep oxidation of HCHO and a fourfold higher capacity of ambient HCHO storage than pristine MnO2. The optimal oxide is combined with electromagnetic induction heating to complete the "storage-oxidation" cycle as a promising approach absolutely depending on non-noble oxides and household appliances to realize the long-acting removal of indoor HCHO at room temperature.