查看更多>>摘要：The increasing demand for wastewater treatment has become a notable trend for addressing global water scarcity.However,fouling is a significant challenge for wastewater distribution engineering systems.This study provides an approach using nanobubbles(NBs)to control fouling.The antifouling capacities of three types of NBs,six oxygen concentrations,and two application procedures(prevention and removal)are investigated.The results show that NBs effectively mitigate composite fouling-including biofouling,inorganic scaling,and particulate fouling-in comparison with the non-NBs group.More specifically,hydroxyl radicals generated by the self-collapse of NBs oxidize organics and kill microorganisms in wastewater.The negatively charged surfaces of the NBs transform the crystalline form of CaCO3 from cal-cite to looser aragonite,which reduces the likelihood of ion precipitation.Furthermore,the NBs gas-liquid interfaces act as gas"bridges"between colloidal particles,enhancing the removal of particles from wastewater.Lastly,although the NBs inhibit the growth of fouling,they do not significantly remove the already adhered fouling in non-NBs treated groups.This study anticipates that the application of NBs will address the significant fouling issue for various wastewater distribution engineering systems in order to meet the global challenge of sustainable water supplies.
查看更多>>摘要：There is currently no effective targeted therapeutic strategy for the treatment of central nervous system acute lymphoblastic leukemia(CNS-ALL).Integrin α6 is considered a potential target for CNS-ALL diag-nosis and therapy because of its role in promoting CNS-ALL disease progression.The targeted peptide d(RWYD)(abbreviated RD),with nanomolar affinity to integrin α6 was identified by peptide scanning techniques such as alanine scanning,truncation,and D-substitution.Herein,we developed a therapeutic nanoparticle based on the integrin α6-targeted peptide for treating CNS-ALL.The self-assembled proapoptotic nanopeptide D(RWYD)-D(KLAKLAK)2-GD(FFY)(abbreviated RD-KLA-Gffy)contains the inte-grin α6-targeted peptide RD,the well-known proapoptotic peptide D(KLAKLAK)2(abbreviated KLA),and the self-assembling tetrapeptide GD(FFY)(abbreviated Gffy).The functional mechanism of RD-KLA-Gffy is clarified using different experiments.Our results demonstrate that RD-KLA-Gffy is highly enriched in CNS-ALL lesions and induces tumor cell apoptosis,thus reducing CNS-ALL disease burden and prolonging the survival of CNS-ALL mice without obvious toxicity.Moreover,the combined use of RD-KLA-Gffy and methotrexate(MTX)shows a potent antitumor effect in treating CNS-ALL,indicating that RD-KLA-Gffy plays an important role in suppressing CNS-ALL progression either as a single agent or in combination with MTX,which shows promise for application in CNS-ALL therapy.
查看更多>>摘要：Intestinal homeostasis is maintained by specialized host cells and the gut microbiota.Wnt/β-catenin signaling is essential for gastrointestinal development and homeostasis,and its dysregulation has been implicated in inflammation and colorectal cancer.Axin1 negatively regulates activated Wnt/β-catenin signaling,but little is known regarding its role in regulating host-microbial interactions in health and dis-ease.Here,we aim to demonstrate that intestinal Axin1 determines gut homeostasis and host response to inflammation.Axin1 expression was analyzed in human inflammatory bowel disease datasets.To explore the effects and mechanism of intestinal Axin1 in regulating intestinal homeostasis and colitis,we gener-ated new mouse models with Axin1 conditional knockout in intestinal epithelial cell(IEC;Axin1ΔIEC)and Paneth cell(PC;Axin1ΔPC)to compare with control(Axin1LoxP;LoxP:locus of X-over,P1)mice.We found increased Axin1 expression in the colonic epithelium of human inflammatory bowel disease(IBD).Axin1ΔIEC mice exhibited altered goblet cell spatial distribution,PC morphology,reduced lysozyme expression,and enriched Akkermansia muciniphila(A.muciniphila).The absence of intestinal epithelial and PC Axin1 decreased susceptibility to dextran sulfate sodium(DSS)-induced colitis in vivo.Axin1ΔIEC and Axin1ΔPC mice became more susceptible to DSS-colitis after cohousing with control mice.Treatment with A.muciniphila reduced DSS-colitis severity.Antibiotic treatment did not change the IEC proliferation in the Axin1Loxp mice.However,the intestinal proliferative cells in Axin1ΔIEC mice with antibiotic treatment were reduced compared with those in Axin1ΔIEC mice without treatment.These data suggest non-colitogenic effects driven by the gut microbiome.In conclusion,we found that the loss of intestinal Axin1 protects against colitis,likely driven by epithelial Axin1 and Axin1-associated A.mucini-phila.Our study demonstrates a novel role of Axin1 in mediating intestinal homeostasis and the micro-biota.Further mechanistic studies using specific Axin1 mutations elucidating how Axin1 modulates the microbiome and host inflammatory response will provide new therapeutic strategies for human IBD.
查看更多>>摘要：Non-alcoholic steatohepatitis(NASH)is a severe form of non-alcoholic fatty liver disease without effec-tive treatment.The traditional Chinese medicine formulation Pien Tze Huang(PTH)can suppress inflam-matory diseases.Here,we evaluate the effects of PTH on the evolution of NASH and its underlying mechanisms.We found that PTH prevented the development of steatohepatitis induced by various diet-ary models,including a high-fat high-cholesterol(HFHC)diet,choline-deficient high-fat diet(CD-HFD),and methionine-and choline-deficient(MCD)diet,along with significant suppression of liver injury,hepa-tic triglyceride,and lipid peroxidation.Moreover,ten days of PTH treatment after the onset of NASH sig-nificantly ameliorated MCD diet-induced steatosis and liver injury in mice.Through the metagenomic sequencing of stool samples,we found that PTH administration restored the gut microbiota with enrich-ment of probiotics including Lactobacillus acidophilus(L.acidophilus),Lactobacillus plantarum,Lactococcus lactis,and Bacillus subtilis.The enriched L.acidophilus prevented MCD diet-induced steatohepatitis.In addition,PTH restored the gut barrier function in mice with steatohepatitis,as evidenced by reduced intestinal permeability,decreased serum lipopolysaccharides(LPS)level,and increased epithelial tight-junction protein E-cadherin expression.Our metabolomic analysis via liquid chromatography-mass spec-trometry profiling identified the alteration in the metabolism of bile acids in the portal vein of PTH-treated mice.We further confirmed that an intact gut microbiota is necessary for PTH to exhibit anti-steatohepatitis effects.In conclusion,PTH protects against steatohepatitis development by modulating the gut microbiota and metabolites.PTH is a potential promising prophylactic and therapeutic option for patients with NASH.
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