The sulfonated poly(α-methyl styrene-b-isobutylene-b-α-methyl styrene)copolymers(S-ASIBS)with the average molar percentage of sulfonic acid(-SO_(3)H)groups(SP)ranging from 3.6 mol%to 14.3 mol%could be synthesized by...The sulfonated poly(α-methyl styrene-b-isobutylene-b-α-methyl styrene)copolymers(S-ASIBS)with the average molar percentage of sulfonic acid(-SO_(3)H)groups(SP)ranging from 3.6 mol%to 14.3 mol%could be synthesized by sulfonation of ASIBS with acetyl sulfate.The hydrophilic ionic channels were generated for proton exchange membranes(PEMs)by ion aggregation of-SO_(3)H groups and microphase separation between hydrophobic polyisobutylene and hydrophilic sulfonated poly(α-methyl styrene)segments in S-ASIBS.The proton transport ability was improved while oxidative stability was decreased by increasing SP in S-ASIBS.The appropriate SP of about 12.7 mol%in S-ASIBS provides the available PEMs with high proton transport ability,low methanol permeability and good oxidative stability.The absence of active tertiary hydrogen atoms along S-ASIBS copolymer chains avoids their attack by peroxy radicals.The residual rates of weight(RW)and proton conductivity(Rσ)of S-ASIBS-12.7 membrane after oxidation treatment for 916 h were 84.3%and 88.1%respectively,near to those of commercial Nafion 117(RW=87.9%,Rσ=90.3%).The membrane electrode assembly(MEA)could be prepared by using various S-ASIBS as PEMs for direct methanol fuel cell.The single cell with S-ASIBS-12.7 MEA behaves high performance of open circuit voltage(OCV)of 548 mV and peak power density(Pmax)of 36.1 mW·cm^(-2),which is similar to those of Nafion 117(OCV=506 mV,P_(max)=35.6 mW·cm^(-2)).To the best of our knowledge,this is the first example of advanced S-ASIBS membrane with high proton conductivity,excellent fuel barrier property and remarkable oxidative stability for promising PEMs.展开更多
BACKGROUND Colorectal cancer(CRC)is a major cause of cancer-related mortality,with limited therapeutic options for advanced stages.Simvastatin,primarily used to lower cholesterol,has shown potential as an anticancer a...BACKGROUND Colorectal cancer(CRC)is a major cause of cancer-related mortality,with limited therapeutic options for advanced stages.Simvastatin,primarily used to lower cholesterol,has shown potential as an anticancer agent.It may exert its effects by inhibiting SERPINE1,a protein implicated in CRC progression,and activating the cyclic guanosine monophosphate-protein kinase G(cGMP/PKG)signaling pathway.Given these findings,this study hypothesizes that simvastatin inhibits CRC cell proliferation and migration by downregulating SERPINE1 and activating the cGMP/PKG pathway,offering a novel therapeutic strategy for CRC management.AIM To study the effects of simvastatin on the function of colon cancer cells and to uncover the underlying mechanisms.METHODS NCM460,HCT-116,and SW620 cell lines were used for in vitro experiments with simvastatin at doses of 20μM,40μM,and 80μM.The Stitch database was used to analyze the target genes of simvastatin,whereas STRING was used to investigate SERPINE1 and its related pathways.HCT-116 and SW620 cells were transfected with single-cell RNA sequencing reveals SERPINE1 with or without Rp-8-Br-cGMP(a PKG inhibitor).Cell toxicity,proliferation,and migration were evaluated using the cell counting kit-8,colony formation,and Transwell assays,respectively.Apoptosis was analyzed via flow cytometry,and levels of reactive oxygen species(ROS),malondialdehyde(MDA),glutathione(GSH),and ferrous ion(Fe^(2+))were detected using commercial kits.Real-time polymerase chain reaction and western blotting were used to analyze gene expression.RESULTS Simvastatin dose-dependently inhibited the proliferation and migration of HCT-116 and SW620 cells while promoting apoptosis.It downregulated Ki-67,proliferating cell nuclear antigen,MMP2,and MMP9,and upregulated Bax,particularly at higher doses.Simvastatin increased the ROS,MDA,and Fe^(2+)levels while decreasing the GSH levels.It downregulated SLC7A11 and ferroportin and upregulated TRF1.SERPINE1 was identified as a core target,with related genes enriched in the cGMP/PKG pathway.SERPINE1 knockdown increased GUCY1B1 and PRKG1 levels,decreased cell viability,and altered oxidative stress markers,with the effects being reversed by Rp-8-Br-cGMP.CONCLUSION Simvastatin effectively inhibited the proliferation and migration of colon cancer cells and promoted apoptosis through the modulation of key targets,such as SERPINE1 and the cGMP/PKG signaling pathway.展开更多
The enduring enigma surrounding the near-infrared(NIR)emission of Mn^(2+)continues to ignite intense academic discussions.Numerous hypotheses have emerged from extensive research endeavors to explain this phenomenon,s...The enduring enigma surrounding the near-infrared(NIR)emission of Mn^(2+)continues to ignite intense academic discussions.Numerous hypotheses have emerged from extensive research endeavors to explain this phenomenon,such as the formation of Mn^(2+)-Mn^(2+)ion pairs,Mn^(2+)occupying cubically coordinated sites,as well as conjectures positing the involvement of Mn3+oxidized from Mn^(2+)or defects.Despite these diverse and valuable insights,none of the hypotheses have yet achieved broad consensus.In this study,we have observed prolonged fluorescence lifetimes(~10ms)for the NIR emissions of Mn^(2+)ions,hinting at these ions occupying the high-symmetry octahedral sites inherent to the garnet lattice.This inference is supported by the corroborating results from X-ray absorption fine structure analysis and first-principles calculations.The intense crystal field of octahedral sites,similar to that of AlO6,facilitates the splitting of d-d energy levels,thereby inducing a red-shift in the emission spectrum to the NIR region due to the transition ^(4)T_(1)(4G)→ ^(6)A_(n)(6S)of isolated Mn^(2+).Our findings not only offer a plausible rationale for the NIR emission exhibited by other Mn^(2+)-activated garnet phosphors but also pave a definitive route towards understanding the fundamental mechanisms responsible for the NIR emission of Mn^(2+)ions.展开更多
基金financially supported by the National Natural Science Foundation of China (No. 21774006)
文摘The sulfonated poly(α-methyl styrene-b-isobutylene-b-α-methyl styrene)copolymers(S-ASIBS)with the average molar percentage of sulfonic acid(-SO_(3)H)groups(SP)ranging from 3.6 mol%to 14.3 mol%could be synthesized by sulfonation of ASIBS with acetyl sulfate.The hydrophilic ionic channels were generated for proton exchange membranes(PEMs)by ion aggregation of-SO_(3)H groups and microphase separation between hydrophobic polyisobutylene and hydrophilic sulfonated poly(α-methyl styrene)segments in S-ASIBS.The proton transport ability was improved while oxidative stability was decreased by increasing SP in S-ASIBS.The appropriate SP of about 12.7 mol%in S-ASIBS provides the available PEMs with high proton transport ability,low methanol permeability and good oxidative stability.The absence of active tertiary hydrogen atoms along S-ASIBS copolymer chains avoids their attack by peroxy radicals.The residual rates of weight(RW)and proton conductivity(Rσ)of S-ASIBS-12.7 membrane after oxidation treatment for 916 h were 84.3%and 88.1%respectively,near to those of commercial Nafion 117(RW=87.9%,Rσ=90.3%).The membrane electrode assembly(MEA)could be prepared by using various S-ASIBS as PEMs for direct methanol fuel cell.The single cell with S-ASIBS-12.7 MEA behaves high performance of open circuit voltage(OCV)of 548 mV and peak power density(Pmax)of 36.1 mW·cm^(-2),which is similar to those of Nafion 117(OCV=506 mV,P_(max)=35.6 mW·cm^(-2)).To the best of our knowledge,this is the first example of advanced S-ASIBS membrane with high proton conductivity,excellent fuel barrier property and remarkable oxidative stability for promising PEMs.
基金Supported by the Jiangsu Province Key Research and Development Plan(Social Development)Project,No.BE2021611。
文摘BACKGROUND Colorectal cancer(CRC)is a major cause of cancer-related mortality,with limited therapeutic options for advanced stages.Simvastatin,primarily used to lower cholesterol,has shown potential as an anticancer agent.It may exert its effects by inhibiting SERPINE1,a protein implicated in CRC progression,and activating the cyclic guanosine monophosphate-protein kinase G(cGMP/PKG)signaling pathway.Given these findings,this study hypothesizes that simvastatin inhibits CRC cell proliferation and migration by downregulating SERPINE1 and activating the cGMP/PKG pathway,offering a novel therapeutic strategy for CRC management.AIM To study the effects of simvastatin on the function of colon cancer cells and to uncover the underlying mechanisms.METHODS NCM460,HCT-116,and SW620 cell lines were used for in vitro experiments with simvastatin at doses of 20μM,40μM,and 80μM.The Stitch database was used to analyze the target genes of simvastatin,whereas STRING was used to investigate SERPINE1 and its related pathways.HCT-116 and SW620 cells were transfected with single-cell RNA sequencing reveals SERPINE1 with or without Rp-8-Br-cGMP(a PKG inhibitor).Cell toxicity,proliferation,and migration were evaluated using the cell counting kit-8,colony formation,and Transwell assays,respectively.Apoptosis was analyzed via flow cytometry,and levels of reactive oxygen species(ROS),malondialdehyde(MDA),glutathione(GSH),and ferrous ion(Fe^(2+))were detected using commercial kits.Real-time polymerase chain reaction and western blotting were used to analyze gene expression.RESULTS Simvastatin dose-dependently inhibited the proliferation and migration of HCT-116 and SW620 cells while promoting apoptosis.It downregulated Ki-67,proliferating cell nuclear antigen,MMP2,and MMP9,and upregulated Bax,particularly at higher doses.Simvastatin increased the ROS,MDA,and Fe^(2+)levels while decreasing the GSH levels.It downregulated SLC7A11 and ferroportin and upregulated TRF1.SERPINE1 was identified as a core target,with related genes enriched in the cGMP/PKG pathway.SERPINE1 knockdown increased GUCY1B1 and PRKG1 levels,decreased cell viability,and altered oxidative stress markers,with the effects being reversed by Rp-8-Br-cGMP.CONCLUSION Simvastatin effectively inhibited the proliferation and migration of colon cancer cells and promoted apoptosis through the modulation of key targets,such as SERPINE1 and the cGMP/PKG signaling pathway.
基金supported by the National Natural Science Foundation of China(Grant No.12104231,12364051,22303031)Innovation Training Program for College Students in Nanjing Forestry University(Grant No.202410298184Y)。
文摘The enduring enigma surrounding the near-infrared(NIR)emission of Mn^(2+)continues to ignite intense academic discussions.Numerous hypotheses have emerged from extensive research endeavors to explain this phenomenon,such as the formation of Mn^(2+)-Mn^(2+)ion pairs,Mn^(2+)occupying cubically coordinated sites,as well as conjectures positing the involvement of Mn3+oxidized from Mn^(2+)or defects.Despite these diverse and valuable insights,none of the hypotheses have yet achieved broad consensus.In this study,we have observed prolonged fluorescence lifetimes(~10ms)for the NIR emissions of Mn^(2+)ions,hinting at these ions occupying the high-symmetry octahedral sites inherent to the garnet lattice.This inference is supported by the corroborating results from X-ray absorption fine structure analysis and first-principles calculations.The intense crystal field of octahedral sites,similar to that of AlO6,facilitates the splitting of d-d energy levels,thereby inducing a red-shift in the emission spectrum to the NIR region due to the transition ^(4)T_(1)(4G)→ ^(6)A_(n)(6S)of isolated Mn^(2+).Our findings not only offer a plausible rationale for the NIR emission exhibited by other Mn^(2+)-activated garnet phosphors but also pave a definitive route towards understanding the fundamental mechanisms responsible for the NIR emission of Mn^(2+)ions.
