BACKGROUND Diabetic intracerebral hemorrhage(ICH)is a serious complication of diabetes.The role and mechanism of bone marrow mesenchymal stem cell(BMSC)-derived exosomes(BMSC-exo)in neuroinflammation post-ICH in patie...BACKGROUND Diabetic intracerebral hemorrhage(ICH)is a serious complication of diabetes.The role and mechanism of bone marrow mesenchymal stem cell(BMSC)-derived exosomes(BMSC-exo)in neuroinflammation post-ICH in patients with diabetes are unknown.In this study,we investigated the regulation of BMSC-exo on hyperglycemia-induced neuroinflammation.AIM To study the mechanism of BMSC-exo on nerve function damage after diabetes complicated with cerebral hemorrhage.METHODS BMSC-exo were isolated from mouse BMSC media.This was followed by transfection with microRNA-129-5p(miR-129-5p).BMSC-exo or miR-129-5poverexpressing BMSC-exo were intravitreally injected into a diabetes mouse model with ICH for in vivo analyses and were cocultured with high glucoseaffected BV2 cells for in vitro analyses.The dual luciferase test and RNA immunoprecipitation test verified the targeted binding relationship between miR-129-5p and high-mobility group box 1(HMGB1).Quantitative polymerase chain reaction,western blotting,and enzyme-linked immunosorbent assay were conducted to assess the levels of some inflammation factors,such as HMGB1,interleukin 6,interleukin 1β,toll-like receptor 4,and tumor necrosis factorα.Brain water content,neural function deficit score,and Evans blue were used to measure the neural function of mice.RESULTS Our findings indicated that BMSC-exo can promote neuroinflammation and functional recovery.MicroRNA chip analysis of BMSC-exo identified miR-129-5p as the specific microRNA with a protective role in neuroinflammation.Overexpression of miR-129-5p in BMSC-exo reduced the inflammatory response and neurological impairment in comorbid diabetes and ICH cases.Furthermore,we found that miR-129-5p had a targeted binding relationship with HMGB1 mRNA.CONCLUSION We demonstrated that BMSC-exo can reduce the inflammatory response after ICH with diabetes,thereby improving the neurological function of the brain.展开更多
Objective Endometrial carcinoma(EC)is a prevalent gynecological malignancy characterized by increasing incidence and mortality rates.This underscores the critical need for novel therapeutic targets.One such potential ...Objective Endometrial carcinoma(EC)is a prevalent gynecological malignancy characterized by increasing incidence and mortality rates.This underscores the critical need for novel therapeutic targets.One such potential target is cell division cycle 20(CDC20),which has been implicated in oncogenesis.This study investigated the effect of the CDC20 inhibitor Apcin on EC and elucidated the underlying mechanism involved.Methods The effects of Apcin on EC cell proliferation,apoptosis,and the cell cycle were evaluated using CCK8 assays and flow cytometry.RNA sequencing(RNA-seq)was subsequently conducted to explore the underlying molecular mechanism,and Western blotting and coimmunoprecipitation were subsequently performed to validate the results.Animal studies were performed to evaluate the antitumor effects in vivo.Bioinformatics analysis was also conducted to identify CDC20 as a potential therapeutic target in EC.Results Treatment with Apcin inhibited proliferation and induced apoptosis in EC cells,resulting in cell cycle arrest.Pathways associated with apoptosis and the cell cycle were activated following treatment with Apcin.Notably,Apcin treatment led to the upregulation of the cell cycle regulator p21,which was verified to interact with CDC20 and consequently decrease the expression of downstream cyclins in EC cells.In vivo experiments confirmed that Apcin treatment significantly impeded tumor growth.Higher CDC20 expression was observed in EC tissue than in nonmalignant tissue,and increased CDC20 expression in EC patients was associated with shorter overall survival and progress free interval.Conclusion CDC20 is a novel molecular target in EC,and Apcin could be developed as a candidate antitumor drug for EC treatment.展开更多
The group-contribution (GC) methods suffer from a limitation concerning to the prediction of process-related indexes, e.g., thermal efficiency. Recently developed analytical models for thermal efficiency of organic Ra...The group-contribution (GC) methods suffer from a limitation concerning to the prediction of process-related indexes, e.g., thermal efficiency. Recently developed analytical models for thermal efficiency of organic Rankine cycles (ORCs) provide a possibility of overcoming the limitation of the GC methods because these models formulate thermal efficiency as functions of key thermal properties. Using these analytical relations together with GC methods, more than 60 organic fluids are screened for medium-low temperature ORCs. The results indicate that the GC methods can estimate thermal properties with acceptable accuracy (mean relative errors are 4.45%-11.50%);the precision, however, is low because the relative errors can vary from less than 0.1% to 45.0%. By contrast, the GC-based estimation of thermal efficiency has better accuracy and precision. The relative errors in thermal efficiency have an arithmetic mean of about 2.9% and fall within the range of 0-24.0%. These findings suggest that the analytical equations provide not only a direct way of estimating thermal efficiency but an accurate and precise approach to evaluating working fluids and guiding computer-aided molecular design of new fluids for ORCs using GC methods.展开更多
Opioids,such as morphine,are the most potent drugs used to treat pain.Long-term use results in high tolerance to morphine.High mobility group box-1(HMGB1) has been shown to participate in neuropathic or inflammatory p...Opioids,such as morphine,are the most potent drugs used to treat pain.Long-term use results in high tolerance to morphine.High mobility group box-1(HMGB1) has been shown to participate in neuropathic or inflammatory pain,but its role in morphine tolerance is unclear.In this study,we established rat and mouse models of morphine tolerance by intrathecal injection of morphine for 7 consecutive days.We found that morphine induced rat spinal cord neurons to release a large amount of HMGB1.HMGB1 regulated nuclear factor κB p65 phosphorylation and interleukin-1β production by increasing Toll-like receptor 4receptor expression in microglia,thereby inducing morphine tolerance.Glycyrrhizin,an HMGB1 inhibito r,markedly attenuated chronic morphine tole rance in the mouse model.Finally,compound C(adenosine 5’-monophosphate-activated protein kinase inhibitor) and zinc protoporphyrin(heme oxygenase-1 inhibitor)alleviated the morphine-induced release of HMGB1 and reduced nuclear factor κB p65 phosphorylation and interleukin-1β production in a mouse model of morphine tolerance and an SH-SY5Y cell model of morphine tole rance,and alleviated morphine tolerance in the mouse model.These findings suggest that morphine induces HMGB1 release via the adenosine 5’-monophosphate-activated protein kinase/heme oxygenase-1 signaling pathway,and that inhibiting this signaling pathway can effectively reduce morphine tole rance.展开更多
ABSTRACT: This paper, with Milanggouwan stratigraphic section as a typical section of the Salawusu River Basin, explores the relation between CaCO3 content distribution and climate change since 150 ka B. P. and conclu...ABSTRACT: This paper, with Milanggouwan stratigraphic section as a typical section of the Salawusu River Basin, explores the relation between CaCO3 content distribution and climate change since 150 ka B. P. and concludes that: 1) The low-high changes of CaCO3 content in the section has a remarkable corresponding relation with the sedimentary cycles of ancient aeolian sand and overlying fluviolacustrine facies or palaeosols. 2) CaCO3 distribution in aeolian sand is relatively meagre, ranging from 0. 8% - 7. 18%, or on an average 2. 50% but relatively enriches in the fluviolacustrine faceis and palaeosols, ranging from 2. 20% - 14. 9% , or on an average 5. 74%. This implies that they have different climatic backgrounds. The former was the product of erosion, transport and deposition by wind under arid and cold climatic conditions, whereas the latter was related to its special low-lying geomorphic position between the Ordos Plateau and Loess Plateau and warm-humid climatic environment. When the climatic became warm and humid, fluviolacustrine and swamp facies developed, soil-forming action strengthened, and low-lying catchment condition was favorable to CaCO3 accumulation. 3) The basic cause responsible for the multicycle of CaCO3 migration and accumulation in the Milanggouwan section may be the multiple alterations of winter and summer monsoons over the Mu Us Desert under the influences of climatic fluctuation of glacial and interglacial periods in the Northern Hemisphere since 150ka B. P. .展开更多
Objective Innate lymphoid cells(ILCs)are a class of newly discovered immunocytes.Group 1 ILCs(ILC1s)are identified in the decidua of humans and mice.High mobility group box 1(HMGB1)is predicted to be one of the target...Objective Innate lymphoid cells(ILCs)are a class of newly discovered immunocytes.Group 1 ILCs(ILC1s)are identified in the decidua of humans and mice.High mobility group box 1(HMGB1)is predicted to be one of the target genes of miR-142-3p,which is closely related to pregnancy-related diseases.Furthermore,miR-142-3p and HMGB1 are involved in regulating the NF-κB signaling pathway.This study aimed to examine the regulatory effect of miR-142-3p on ILC1s and the underlying mechanism involving HMGB1 and the NF-κB signaling pathway.Methods Mouse models of normal pregnancy and abortion were constructed,and the alterations of ILC1s,miR-142-3p,ILC1 transcription factor(T-bet),and pro-inflammatory cytokines of ILC1s(TNF-α,IFN-γand IL-2)were detected in mice from different groups.The targeting regulation of HMGB1 by miR-142-3p in ILC1s,and the expression of HMGB1 in normal pregnant mice and abortive mice were investigated.In addition,the regulatory effects of miR-142-3p and HMGB1 on ILC1s were detected in vitro by CCK-8,Annexin-V/PI,ELISA,and RT-PCR,respectively.Furthermore,changes of the NF-κB signaling pathway in ILC1s were examined in the different groups.For the in vivo studies,miR-142-3p-Agomir was injected in the uterus of abortive mice to evaluate the abortion rate and alterations of ILC1s at the maternal-fetal interface,and further detect the expression of HMGB1,pro-inflammatory cytokines,and the NF-κB signaling pathway.Results The number of ILC1s was significantly increased,the level of HMGB1 was significantly upregulated,and that of miR-142-3p was considerably downregulated in the abortive mice as compared with the normal pregnant mice(all P<0.05).In addition,miR-142-3p was found to drastically inhibit the activation of the NF-κB signaling pathway(P<0.05).The number of ILC1s and the levels of pro-inflammatory cytokines were significantly downregulated and the activation of the NF-κB signaling pathway was inhibited in the miR-142-3p Agomir group(all P<0.05).Conclusion miR-142-3p can regulate ILC1s by targeting HMGB1 via the NF-κB signaling pathway,and attenuate the inflammation at the maternal-fetal interface in abortive mice.展开更多
Background:Nitrogen(N)deposition affects forest stoichiometric flexibility through changing soil nutrient availability to influence plant uptake.However,the effect of N deposition on the flexibility of carbon(C),N,and...Background:Nitrogen(N)deposition affects forest stoichiometric flexibility through changing soil nutrient availability to influence plant uptake.However,the effect of N deposition on the flexibility of carbon(C),N,and phosphorus(P)in forest plant-soil-microbe systems remains unclear.Methods:We conducted a meta-analysis based on 751 pairs of observations to evaluate the responses of plant,soil and microbial biomass C,N and P nutrients and stoichiometry to N addition in different N intensity(050,50–100,>100 kg·ha^(-1)·year^(-1)of N),duration(0–5,>5 year),method(understory,canopy),and matter(ammonium N,nitrate N,organic N,mixed N).Results:N addition significantly increased plant N:P(leaf:14.98%,root:13.29%),plant C:P(leaf:6.8%,root:25.44%),soil N:P(13.94%),soil C:P(10.86%),microbial biomass N:P(23.58%),microbial biomass C:P(12.62%),but reduced plant C:N(leaf:6.49%,root:9.02%).Furthermore,plant C:N:P stoichiometry changed significantly under short-term N inputs,while soil and microorganisms changed drastically under high N addition.Canopy N addition primarily affected plant C:N:P stoichiometry through altering plant N content,while understory N inputs altered more by influencing soil C and P content.Organic N significantly influenced plant and soil C:N and C:P,while ammonia N changed plant N:P.Plant C:P and soil C:N were strongly correlated with mean annual precipitation(MAT),and the C:N:P stoichiometric flexibility in soil and plant under N addition connected with soil depth.Besides,N addition decoupled the correlations between soil microorganisms and the plant.Conclusions:N addition significantly increased the C:P and N:P in soil,plant,and microbial biomass,reducing plant C:N,and aggravated forest P limitations.Significantly,these impacts were contingent on climate types,soil layers,and N input forms.The findings enhance our comprehension of the plant-soil system nutrient cycling mechanisms in forest ecosystems and plant strategy responses to N deposition.展开更多
Objective:Chronic kidney disease(CKD)is a progressive disorder characterized by intricate structural and functional alterations in the kidneys,attributable to diverse causative factors.Notably,the therapeutic promise ...Objective:Chronic kidney disease(CKD)is a progressive disorder characterized by intricate structural and functional alterations in the kidneys,attributable to diverse causative factors.Notably,the therapeutic promise of miR-145-5p in addressing renal pathologies has been discerned.This investigation seeks to elucidate the functional role of miR-145-5p in injured kidneys by subjecting human glomerular mesangial cells(HGMCs)to stimulation with Angiotensin II(AngII).Materials and Methods:Cellular viability and the levels of inflammatory mediators were evaluated utilizing Cell Counting Kit-8(CCK-8),quantitative real-time polymerase chain reaction(qRT-PCR),and western blot methodologies,both in the presence of AngII incubation and in scenarios of miR-145p overexpression and downregulation.Furthermore,the cell cycle dynamics were elucidated through Fluorescence-activated Cell Sorting(FACS)analysis.Results:AngII incubation induced an upregulation of miR-145-5p and inflammatory factors including Intercellular Adhesion Molecule 1(ICAM-1),Interleukin 6(IL-6),Interleukin 8(IL-8),and Interleukin 1β(IL-1β).Additionally,it elevated the expression of Cyclin A2,Cyclin D1,and the G2/M cell cycle ratio.Conversely,inhibition of miR-145-5p heightened the levels of inflammatory factors and cell cycle regulators induced by AngII incubation.Reduced expression of miR-145-5p correlated with a downregulation of Interleukin 10(IL-10)expression,concurrently promoting HGMC proliferation under AngII stimulation.Moreover,ectopic miR-145-5p expression demonstrated a reduction in inflammatory factors,cell cyclin regulators,G2/M cell cycle ratio,and overall proliferation.Conclusion:MiR-145-5p exhibited inhibitory effects on the inflammatory response and proliferation induced by Angiotensin II in HGMCs,showcasing its potential as a therapeutic avenue for the treatment of kidney injury.展开更多
基金Supported by the National Natural Science Foundation of China,No.81900743Heilongjiang Province Outstanding Young Medical Talents Training Grant Project,China,No.HYD2020YQ0007.
文摘BACKGROUND Diabetic intracerebral hemorrhage(ICH)is a serious complication of diabetes.The role and mechanism of bone marrow mesenchymal stem cell(BMSC)-derived exosomes(BMSC-exo)in neuroinflammation post-ICH in patients with diabetes are unknown.In this study,we investigated the regulation of BMSC-exo on hyperglycemia-induced neuroinflammation.AIM To study the mechanism of BMSC-exo on nerve function damage after diabetes complicated with cerebral hemorrhage.METHODS BMSC-exo were isolated from mouse BMSC media.This was followed by transfection with microRNA-129-5p(miR-129-5p).BMSC-exo or miR-129-5poverexpressing BMSC-exo were intravitreally injected into a diabetes mouse model with ICH for in vivo analyses and were cocultured with high glucoseaffected BV2 cells for in vitro analyses.The dual luciferase test and RNA immunoprecipitation test verified the targeted binding relationship between miR-129-5p and high-mobility group box 1(HMGB1).Quantitative polymerase chain reaction,western blotting,and enzyme-linked immunosorbent assay were conducted to assess the levels of some inflammation factors,such as HMGB1,interleukin 6,interleukin 1β,toll-like receptor 4,and tumor necrosis factorα.Brain water content,neural function deficit score,and Evans blue were used to measure the neural function of mice.RESULTS Our findings indicated that BMSC-exo can promote neuroinflammation and functional recovery.MicroRNA chip analysis of BMSC-exo identified miR-129-5p as the specific microRNA with a protective role in neuroinflammation.Overexpression of miR-129-5p in BMSC-exo reduced the inflammatory response and neurological impairment in comorbid diabetes and ICH cases.Furthermore,we found that miR-129-5p had a targeted binding relationship with HMGB1 mRNA.CONCLUSION We demonstrated that BMSC-exo can reduce the inflammatory response after ICH with diabetes,thereby improving the neurological function of the brain.
文摘Objective Endometrial carcinoma(EC)is a prevalent gynecological malignancy characterized by increasing incidence and mortality rates.This underscores the critical need for novel therapeutic targets.One such potential target is cell division cycle 20(CDC20),which has been implicated in oncogenesis.This study investigated the effect of the CDC20 inhibitor Apcin on EC and elucidated the underlying mechanism involved.Methods The effects of Apcin on EC cell proliferation,apoptosis,and the cell cycle were evaluated using CCK8 assays and flow cytometry.RNA sequencing(RNA-seq)was subsequently conducted to explore the underlying molecular mechanism,and Western blotting and coimmunoprecipitation were subsequently performed to validate the results.Animal studies were performed to evaluate the antitumor effects in vivo.Bioinformatics analysis was also conducted to identify CDC20 as a potential therapeutic target in EC.Results Treatment with Apcin inhibited proliferation and induced apoptosis in EC cells,resulting in cell cycle arrest.Pathways associated with apoptosis and the cell cycle were activated following treatment with Apcin.Notably,Apcin treatment led to the upregulation of the cell cycle regulator p21,which was verified to interact with CDC20 and consequently decrease the expression of downstream cyclins in EC cells.In vivo experiments confirmed that Apcin treatment significantly impeded tumor growth.Higher CDC20 expression was observed in EC tissue than in nonmalignant tissue,and increased CDC20 expression in EC patients was associated with shorter overall survival and progress free interval.Conclusion CDC20 is a novel molecular target in EC,and Apcin could be developed as a candidate antitumor drug for EC treatment.
基金Project(51778626) supported by the National Natural Science Foundation of China
文摘The group-contribution (GC) methods suffer from a limitation concerning to the prediction of process-related indexes, e.g., thermal efficiency. Recently developed analytical models for thermal efficiency of organic Rankine cycles (ORCs) provide a possibility of overcoming the limitation of the GC methods because these models formulate thermal efficiency as functions of key thermal properties. Using these analytical relations together with GC methods, more than 60 organic fluids are screened for medium-low temperature ORCs. The results indicate that the GC methods can estimate thermal properties with acceptable accuracy (mean relative errors are 4.45%-11.50%);the precision, however, is low because the relative errors can vary from less than 0.1% to 45.0%. By contrast, the GC-based estimation of thermal efficiency has better accuracy and precision. The relative errors in thermal efficiency have an arithmetic mean of about 2.9% and fall within the range of 0-24.0%. These findings suggest that the analytical equations provide not only a direct way of estimating thermal efficiency but an accurate and precise approach to evaluating working fluids and guiding computer-aided molecular design of new fluids for ORCs using GC methods.
基金supported by the National Natural Science Foundation of ChinaNos.81971047 (to WTL) and 82073910 (to XFW)+2 种基金the Natural Science Foundation of Jiangsu Province,No.BK20191253 (to XFW)Key R&D Program (Social Development) Project of Jiangsu Province,No.BE2019 732 (to WTL)Jiangsu Province Hospital (the First Affiliated Hospital of Nanjing Medical University) Clinical Capacity Enhancement Project,No.JSPH-511B2018-8 (to YBP)。
文摘Opioids,such as morphine,are the most potent drugs used to treat pain.Long-term use results in high tolerance to morphine.High mobility group box-1(HMGB1) has been shown to participate in neuropathic or inflammatory pain,but its role in morphine tolerance is unclear.In this study,we established rat and mouse models of morphine tolerance by intrathecal injection of morphine for 7 consecutive days.We found that morphine induced rat spinal cord neurons to release a large amount of HMGB1.HMGB1 regulated nuclear factor κB p65 phosphorylation and interleukin-1β production by increasing Toll-like receptor 4receptor expression in microglia,thereby inducing morphine tolerance.Glycyrrhizin,an HMGB1 inhibito r,markedly attenuated chronic morphine tole rance in the mouse model.Finally,compound C(adenosine 5’-monophosphate-activated protein kinase inhibitor) and zinc protoporphyrin(heme oxygenase-1 inhibitor)alleviated the morphine-induced release of HMGB1 and reduced nuclear factor κB p65 phosphorylation and interleukin-1β production in a mouse model of morphine tolerance and an SH-SY5Y cell model of morphine tole rance,and alleviated morphine tolerance in the mouse model.These findings suggest that morphine induces HMGB1 release via the adenosine 5’-monophosphate-activated protein kinase/heme oxygenase-1 signaling pathway,and that inhibiting this signaling pathway can effectively reduce morphine tole rance.
基金Under the auspices of the National Natural Science Foundation of China(No.49971009) State Key Laboratory ofLoess and Quaternary Geology,Institute of Earth Environment,the Chinese Academy of sciences(SKLLQG0088)and National KeyProject for Basic Re
文摘ABSTRACT: This paper, with Milanggouwan stratigraphic section as a typical section of the Salawusu River Basin, explores the relation between CaCO3 content distribution and climate change since 150 ka B. P. and concludes that: 1) The low-high changes of CaCO3 content in the section has a remarkable corresponding relation with the sedimentary cycles of ancient aeolian sand and overlying fluviolacustrine facies or palaeosols. 2) CaCO3 distribution in aeolian sand is relatively meagre, ranging from 0. 8% - 7. 18%, or on an average 2. 50% but relatively enriches in the fluviolacustrine faceis and palaeosols, ranging from 2. 20% - 14. 9% , or on an average 5. 74%. This implies that they have different climatic backgrounds. The former was the product of erosion, transport and deposition by wind under arid and cold climatic conditions, whereas the latter was related to its special low-lying geomorphic position between the Ordos Plateau and Loess Plateau and warm-humid climatic environment. When the climatic became warm and humid, fluviolacustrine and swamp facies developed, soil-forming action strengthened, and low-lying catchment condition was favorable to CaCO3 accumulation. 3) The basic cause responsible for the multicycle of CaCO3 migration and accumulation in the Milanggouwan section may be the multiple alterations of winter and summer monsoons over the Mu Us Desert under the influences of climatic fluctuation of glacial and interglacial periods in the Northern Hemisphere since 150ka B. P. .
基金supported by the National Key Research and Development Program of China(Nos.2018YFC1002804 and 2016YFC1000600)the National Natural Science Foundation of China(Nos.81771618 and 81971356)the Fundamental Research Funds for the Central Universities(No.2042023kf0028).
文摘Objective Innate lymphoid cells(ILCs)are a class of newly discovered immunocytes.Group 1 ILCs(ILC1s)are identified in the decidua of humans and mice.High mobility group box 1(HMGB1)is predicted to be one of the target genes of miR-142-3p,which is closely related to pregnancy-related diseases.Furthermore,miR-142-3p and HMGB1 are involved in regulating the NF-κB signaling pathway.This study aimed to examine the regulatory effect of miR-142-3p on ILC1s and the underlying mechanism involving HMGB1 and the NF-κB signaling pathway.Methods Mouse models of normal pregnancy and abortion were constructed,and the alterations of ILC1s,miR-142-3p,ILC1 transcription factor(T-bet),and pro-inflammatory cytokines of ILC1s(TNF-α,IFN-γand IL-2)were detected in mice from different groups.The targeting regulation of HMGB1 by miR-142-3p in ILC1s,and the expression of HMGB1 in normal pregnant mice and abortive mice were investigated.In addition,the regulatory effects of miR-142-3p and HMGB1 on ILC1s were detected in vitro by CCK-8,Annexin-V/PI,ELISA,and RT-PCR,respectively.Furthermore,changes of the NF-κB signaling pathway in ILC1s were examined in the different groups.For the in vivo studies,miR-142-3p-Agomir was injected in the uterus of abortive mice to evaluate the abortion rate and alterations of ILC1s at the maternal-fetal interface,and further detect the expression of HMGB1,pro-inflammatory cytokines,and the NF-κB signaling pathway.Results The number of ILC1s was significantly increased,the level of HMGB1 was significantly upregulated,and that of miR-142-3p was considerably downregulated in the abortive mice as compared with the normal pregnant mice(all P<0.05).In addition,miR-142-3p was found to drastically inhibit the activation of the NF-κB signaling pathway(P<0.05).The number of ILC1s and the levels of pro-inflammatory cytokines were significantly downregulated and the activation of the NF-κB signaling pathway was inhibited in the miR-142-3p Agomir group(all P<0.05).Conclusion miR-142-3p can regulate ILC1s by targeting HMGB1 via the NF-κB signaling pathway,and attenuate the inflammation at the maternal-fetal interface in abortive mice.
基金supported by the National Natural Science Foundation of China(Nos.31800369,32271686,U1904204)the State Scholarship Fund of Chinathe Innovation Scientists and Technicians Troop Construction Projects of Henan Province(No.182101510005)。
文摘Background:Nitrogen(N)deposition affects forest stoichiometric flexibility through changing soil nutrient availability to influence plant uptake.However,the effect of N deposition on the flexibility of carbon(C),N,and phosphorus(P)in forest plant-soil-microbe systems remains unclear.Methods:We conducted a meta-analysis based on 751 pairs of observations to evaluate the responses of plant,soil and microbial biomass C,N and P nutrients and stoichiometry to N addition in different N intensity(050,50–100,>100 kg·ha^(-1)·year^(-1)of N),duration(0–5,>5 year),method(understory,canopy),and matter(ammonium N,nitrate N,organic N,mixed N).Results:N addition significantly increased plant N:P(leaf:14.98%,root:13.29%),plant C:P(leaf:6.8%,root:25.44%),soil N:P(13.94%),soil C:P(10.86%),microbial biomass N:P(23.58%),microbial biomass C:P(12.62%),but reduced plant C:N(leaf:6.49%,root:9.02%).Furthermore,plant C:N:P stoichiometry changed significantly under short-term N inputs,while soil and microorganisms changed drastically under high N addition.Canopy N addition primarily affected plant C:N:P stoichiometry through altering plant N content,while understory N inputs altered more by influencing soil C and P content.Organic N significantly influenced plant and soil C:N and C:P,while ammonia N changed plant N:P.Plant C:P and soil C:N were strongly correlated with mean annual precipitation(MAT),and the C:N:P stoichiometric flexibility in soil and plant under N addition connected with soil depth.Besides,N addition decoupled the correlations between soil microorganisms and the plant.Conclusions:N addition significantly increased the C:P and N:P in soil,plant,and microbial biomass,reducing plant C:N,and aggravated forest P limitations.Significantly,these impacts were contingent on climate types,soil layers,and N input forms.The findings enhance our comprehension of the plant-soil system nutrient cycling mechanisms in forest ecosystems and plant strategy responses to N deposition.
基金This work was supported by Nantong Science and Technology Project(MS22022012,MS12021039,MS12018020,MS12018041,JC2020040)Jiangsu Provincial Laboratory Animal Association(DWXH202116)+1 种基金the Doctoral Scientific Research Foundation of Nantong University(135420505015,135422505037)National College Students’Innovation and Entrepreneurship Training Program(202110304036Z).
文摘Objective:Chronic kidney disease(CKD)is a progressive disorder characterized by intricate structural and functional alterations in the kidneys,attributable to diverse causative factors.Notably,the therapeutic promise of miR-145-5p in addressing renal pathologies has been discerned.This investigation seeks to elucidate the functional role of miR-145-5p in injured kidneys by subjecting human glomerular mesangial cells(HGMCs)to stimulation with Angiotensin II(AngII).Materials and Methods:Cellular viability and the levels of inflammatory mediators were evaluated utilizing Cell Counting Kit-8(CCK-8),quantitative real-time polymerase chain reaction(qRT-PCR),and western blot methodologies,both in the presence of AngII incubation and in scenarios of miR-145p overexpression and downregulation.Furthermore,the cell cycle dynamics were elucidated through Fluorescence-activated Cell Sorting(FACS)analysis.Results:AngII incubation induced an upregulation of miR-145-5p and inflammatory factors including Intercellular Adhesion Molecule 1(ICAM-1),Interleukin 6(IL-6),Interleukin 8(IL-8),and Interleukin 1β(IL-1β).Additionally,it elevated the expression of Cyclin A2,Cyclin D1,and the G2/M cell cycle ratio.Conversely,inhibition of miR-145-5p heightened the levels of inflammatory factors and cell cycle regulators induced by AngII incubation.Reduced expression of miR-145-5p correlated with a downregulation of Interleukin 10(IL-10)expression,concurrently promoting HGMC proliferation under AngII stimulation.Moreover,ectopic miR-145-5p expression demonstrated a reduction in inflammatory factors,cell cyclin regulators,G2/M cell cycle ratio,and overall proliferation.Conclusion:MiR-145-5p exhibited inhibitory effects on the inflammatory response and proliferation induced by Angiotensin II in HGMCs,showcasing its potential as a therapeutic avenue for the treatment of kidney injury.
