Objectives:Glioma,as the most lethal primary brain malignancy with poor prognosis,requires further elucidation on the functional role of long noncoding RNA(lncRNA)DDX11 antisense RNA 1(DDX11-AS1)in its pathogenesis,de...Objectives:Glioma,as the most lethal primary brain malignancy with poor prognosis,requires further elucidation on the functional role of long noncoding RNA(lncRNA)DDX11 antisense RNA 1(DDX11-AS1)in its pathogenesis,despite its established oncogenic functions in other cancers.Therefore,this study sought to characterize the oncogenic role and molecular mechanism of DDX11-AS1 in glioma.Methods:DDX11-AS1 expression levels were analyzed in clinical surgical glioma specimens and publicly available datasets.The functional roles of DDX11-AS1 on glioma cell proliferation and migration were investigated using in vitro knockdown and overexpression assays.In vivo tumor growth was assessed using orthotopic glioma-bearing mouse models.To elucidate the regulatory axis involving DDX11-AS1,miR-1183,and E2F transcription factor 7(E2F7),we performed competitive endogenous RNA(ceRNA)analysis and conducted functional rescue experiments via miR-1183 inhibition.Results:DDX11-AS1 expression was markedly upregulated in clinical glioma specimens.Functionally,DDX11-AS1 knockdown significantly suppressed glioma cell proliferation and migration in vitro,while its overexpression exacerbated these malignant phenotypes.Orthotopic glioma-bearingmouse models confirmed that DDX11-AS1 drives in vivo glioma tumor growth.Mechanistically,DDX11-AS1 functions as a ceRNA by competitively interacting with miR-1183.Critically,inhibition of miR-1183 rescued the suppressive effects of DDX11-AS1 knockdown on glioma tumorigenic phenotypes and restored E2F7 expression levels.Conclusions:This study demonstrates that lncRNA DDX11-AS1 promotes glioma progression by regulating the miR-1183/E2F7 axis,indicating a potential therapeutic target for glioma.展开更多
When observing China＇s income distribution problems .from an international perspective, we find that China＇s income inequality is not much different from developed countries after primary distribution. The real diff...When observing China＇s income distribution problems .from an international perspective, we find that China＇s income inequality is not much different from developed countries after primary distribution. The real difference between China and developed countries is that income inequality in developed countries will reduce greatly after income redistribution while the income inequality remains the same for China. Therefore, one can conclude that income inequality in China derives from the ineffectiveness of redistribution. However, a large income gap is not the main reason for skewed income distribution in China. In fact, the problem lies in unfair distribution resulting from factor capitalization. A handful of people have taken proceeds from public assets at the expense of all the people, which has led to social poIarization. To remove unfair distribution, China should improve its means of redistribution to narrow its income gap in order to develop a fair and reasonable pattern of income distribution.展开更多
[ Objective ] The study aimed to explore the release conditions for the conidia of Botryosphaena berengeriana and understand the release dynamic of conidia. [Method] The systematical survey on the release conditions f...[ Objective ] The study aimed to explore the release conditions for the conidia of Botryosphaena berengeriana and understand the release dynamic of conidia. [Method] The systematical survey on the release conditions for the conidia of B. berengeriana were conducted in two growing seasons in 2008 and 2009, combined with the collection of meteorological data around conidia release period, the weather conditions causing large amount release of B. berengedana were analyzed. [ Result] During a growing season, the conidia of pathogen appeared several large release peaks. Under the suitable temperature, when the precipitation lasted for 4 h, the conidia of B. berengeriana began to release with large amount, the amount of conidia reached the peak after release and trended to be stable during 4 - 12 h, which significantly reduced after 24 h, tended to dis- appear after 36 h, and completely disappeared after 72 h. [Conclusion] The dominant factor affecting B. berengeriana conidia release in large a- mount was precipitation, while the lasting time of precipitation played a decisive role.展开更多
This paper presents a new proof of a charaterization of fractional (g, f)-factors of a graph in which multiple edges are allowed. From the proof a polynomial algorithm for finding the fractional (g, f)-factor can be i...This paper presents a new proof of a charaterization of fractional (g, f)-factors of a graph in which multiple edges are allowed. From the proof a polynomial algorithm for finding the fractional (g, f)-factor can be induced.展开更多
Let G be a bipartite graph with vertex set V(G) and edge set E(G), and let g and f be two positive integer-valued functions defined on V(G) such that g(x) ≤ f(x) for every vertex x of V(G). Then a (g, f)-factor of G ...Let G be a bipartite graph with vertex set V(G) and edge set E(G), and let g and f be two positive integer-valued functions defined on V(G) such that g(x) ≤ f(x) for every vertex x of V(G). Then a (g, f)-factor of G is a spanning subgraph H of G such that g(x) ≤ dH(x) 5 f(x) for each x ∈ V(H). A (g, f)-factorization of G is a partition of E(G) into edge-disjoint (g, f)-factors. Let F = {F1, F2,…… ， Fm } and H be a factorization and a subgraph of G, respectively. If F, 1 ≤ i ≤ m， has exactly one edge in common with H, then it is said that ■ is orthogonal to H. It is proved that every bipartite (mg + m - 1, mf - m + 1 )-graph G has a (g, f)-factorization orthogonal to k vertex disjoint m-subgraphs of G if 2-k ≤ g(x) for all x ∈ V(G). Furthermore, it is showed that the results in this paper are best possible.展开更多
BACKGROUND MicroRNA 34c(miR-34c)has been reported to be associated with malignant types of cancer,however,it remains unknown whether miR-34c is involved in chemoresistance in gastric cancer(GC).AIM To investigate the ...BACKGROUND MicroRNA 34c(miR-34c)has been reported to be associated with malignant types of cancer,however,it remains unknown whether miR-34c is involved in chemoresistance in gastric cancer(GC).AIM To investigate the effect of miR-34c and its upstream transcription factor E2F1 on paclitaxel combined with cisplatin resistance in GC cells.METHODS Paired GC tissues and adjacent normal tissues were randomly sampled from 74 GC patients.miR-34c and E2F1 were detected by real-time quantitative PCR(qPCR)and Western blot.In addition,the drug resistance of GC cells to paclitaxel and cisplatin was induced by concentration gradient increasing methods,and changes in miR-34c and E2F1 during this process were measured.Furthermore,E2F1 and miR-34c overexpression or underexpression vectors were constructed and transfected into drug-resistant GC cells.MTT was employed to test the sensitivity of cells to paclitaxel combined with cisplatin,qPCR was adopted to detect the expression of miR-34c,Western blot was applied to detect the expression levels of E2F1,drug resistance-related proteins and apoptosis-related proteins,and flow cytometry was used for the determination of cell apoptosis and cell cycle status.RESULTS E2F1 was overexpressed while miR-34c was underexpressed in GC.After inducing GC cells to be resistant to paclitaxel and cisplatin,E2F1 expression increased while miR-34c expression decreased.Both silencing E2F1 and overexpressing miR-34c could increase the sensitivity of drug-resistant GC cells to paclitaxel combined with cisplatin,promote cell apoptosis and inhibit cell proliferation.Among which,silencing E2F1 could reduce the expression of drug resistance-related proteins and apoptosis-related proteins,while over-expression of miR-34c could upregulate the expression of apoptosis-related proteins without affecting the expression of MDR-1,MRP and other drug resistance-related proteins.Rescue experiments demonstrated that inhibiting miR-34c could significantly weaken the sensitization of drug resistant cells,and Si E2F1 to paclitaxel combined with cisplatin.CONCLUSION E2F1 inhibits miR-34c to promote the proliferation of GC cells and enhance the resistance to paclitaxel combined with cisplatin,and silencing E2F1 is conducive to improving the efficacy of paclitaxel combined with cisplatin in GC cells.展开更多
AIM:To investigate the morphological altering effect of transforming growth factor-β2(TGF-β2) on untransfected human corneal endothelial cells(HCECs)in vitro.METHODS:After untransfected HCECs were treated with TGF-...AIM:To investigate the morphological altering effect of transforming growth factor-β2(TGF-β2) on untransfected human corneal endothelial cells(HCECs)in vitro.METHODS:After untransfected HCECs were treated with TGF-β2 at different concentrations, the morphology,cytoskeleton distribution, and type IV collagen expression of the cells were examined with inverted contrast light microscopy, fluorescence microscopy,immunofluorescence or Western Blot.RESULTS:TGF-β2 at the concentration of 3-15 μg/L had obviously alterative effects on HCECs morphology in dose and time-dependent manner, and 9 μg/L was the peak concentration. TGF-β2(9 μg/L) altered HCE cell morphology after treatment for 36 h, increased the mean optical density(P 【0.01) and the length of F-actin,reduced the mean optical density(P 【0.01) of the collagen type IV in extracellular matrix(ECM) and induced the rearrangement of F-actin, microtubule in cytoplasm and collagen type IV in ECM after treatment for 72 h.·CONCLUTION: TGF-β2 has obviously alterative effect on the morphology of HCECs from polygonal phenotype to enlarged spindle-shaped phenotype, in dose and time-dependence manner by inducing more, elongation and alignment of F-actin, rearrangement of microtubule and larger spread area of collagen type IV.展开更多
Let G be a bipartite graph and g and f be two positive integer-valued functions defined on vertex set V(G) of G such that g(x)≤f(x).In this paper,some sufficient conditions related to the connectivity and edge-connec...Let G be a bipartite graph and g and f be two positive integer-valued functions defined on vertex set V(G) of G such that g(x)≤f(x).In this paper,some sufficient conditions related to the connectivity and edge-connectivity for a bipartite (mg,mf)-graph to have a (g,f)-factor with special properties are obtained and some previous results are generalized.Furthermore,the new results are proved to be the best possible.展开更多
In this paper the properties of some maximum fractional [0, k]-factors of graphs are presented. And consequently some results on fractional matchings and fractional 1-factors are generalized and a characterization of ...In this paper the properties of some maximum fractional [0, k]-factors of graphs are presented. And consequently some results on fractional matchings and fractional 1-factors are generalized and a characterization of fractional k-factors is obtained.展开更多
BACKGROUND A series of long non-coding RNAs(lncRNAs)have been reported to play a crucial role in cancer biology.Some previous studies report that lncRNA CDKN2B-AS1 is involved in some human malignancies.However,its ro...BACKGROUND A series of long non-coding RNAs(lncRNAs)have been reported to play a crucial role in cancer biology.Some previous studies report that lncRNA CDKN2B-AS1 is involved in some human malignancies.However,its role in hepatocellular carcinoma(HCC)has not been fully deciphered.AIM To decipher the role of CDKN2B-AS1 in the progression of HCC.METHODS CDKN2B-AS1 expression in HCC was detected by quantitative real-time polymerase chain reaction.The malignant phenotypes of Li-7 and SNU-182 cells were detected by the CCK-8 method,EdU method,and flow cytometry,respectively.RNA immunoprecipitation was executed to confirm the interaction between CDKN2B-AS1 and E2F transcription factor 1(E2F1).Luciferase reporter assay and chromatin immunoprecipitation were performed to verify the binding of E2F1 to the promoter of G protein subunit alpha Z(GNAZ).E2F1 and GNAZ were detected by western blot in HCC cells.RESULTS In HCC tissues,CDKN2B-AS1 was upregulated.Depletion of CDKN2B-AS1 inhibited the proliferation of HCC cells,and the depletion of CDKN2B-AS1 also induced cell cycle arrest and apoptosis.CDKN2B-AS1 could interact with E2F1.Depletion of CDKN2B-AS1 inhibited the binding of E2F1 to the GNAZ promoter region.Overexpression of E2F1 reversed the biological effects of depletion of CDKN2B-AS1 on the malignant behaviors of HCC cells.CONCLUSION CDKN2B-AS1 recruits E2F1 to facilitate GNAZ transcription to promote HCC progression.展开更多
Brachial plexus avulsion often results in massive motor neuron death and severe functional deficits of target muscles. However, no satisfactory treatment is currently available. Hypoxia-inducible factor 1α is a criti...Brachial plexus avulsion often results in massive motor neuron death and severe functional deficits of target muscles. However, no satisfactory treatment is currently available. Hypoxia-inducible factor 1α is a critical molecule targeting several genes associated with ischemia-hypoxia damage and angiogenesis. In this study, a rat model of brachial plexus avulsion-reimplantation was established, in which C5–7 ventral nerve roots were avulsed and only the C6 root reimplanted. Different implants were immediately injected using a microsyringe into the avulsion-reimplantation site of the C6 root post-brachial plexus avulsion. Rats were randomly divided into five groups: phosphate-buffered saline, negative control of lentivirus, hypoxia-inducible factor 1α(hypoxia-inducible factor 1α overexpression lentivirus), gel(pluronic F-127 hydrogel), and gel + hypoxia-inducible factor 1α(pluronic F-127 hydrogel + hypoxia-inducible factor 1α overexpression lentivirus). The Terzis grooming test was performed to assess recovery of motor function. Scores were higher in the hypoxia-inducible factor 1α and gel +hypoxia-inducible factor 1α groups(in particular the gel + hypoxia-inducible factor 1α group) compared with the phosphate-buffered saline group. Electrophysiology, fluorogold retrograde tracing, and immunofluorescent staining were further performed to investigate neural pathway reconstruction and changes of neurons, motor endplates, and angiogenesis. Compared with the phosphate-buffered saline group, action potential latency of musculocutaneous nerves was markedly shortened in the hypoxia-inducible factor 1α and gel + hypoxia-inducible factor1α groups. Meanwhile, the number of fluorogold-positive cells and ChAT-positive neurons, neovascular area(labeled by CD31 around av ulsed sites in ipsilateral spinal cord segments), and the number of motor endplates in biceps brachii(identified by α-bungarotoxin) were all visibly increased, as well as the morphology of motor endplate in biceps brachil was clear in the hypoxia-inducible factor 1α and gel + hypoxia-inducible factor 1α groups. Taken together, delivery of hypoxia-inducible factor 1α overexpression lentiviral vectors mediated by pluronic F-127 effectively promotes spinal root regeneration and functional recovery post-brachial plexus avulsion. All animal procedures were approved by the Institutional Animal Care and Use Committee of Guangdong Medical University, China.展开更多
In this paper, the cosmological models of the universe are constructed in gravity with choice of the functional in the form ?and . The space-time considered here is Bianchi Type I and the energy momentum tensor is in ...In this paper, the cosmological models of the universe are constructed in gravity with choice of the functional in the form ?and . The space-time considered here is Bianchi Type I and the energy momentum tensor is in the form of perfect fluid. Two cosmological models are presented using a power form of exponential function and a hyperbolic form. The energy conditions along with the state finder diagnostic pair have been obtained and analyzed.展开更多
基金supported by Shenzhen Science and Technology Program(JCYJ20220530152614033,JCYJ20230807142213027)Funding Statement Special Fund for Economic and Technological Development in Longgang District,Shenzhen(LGKCYLWS2023028).
文摘Objectives:Glioma,as the most lethal primary brain malignancy with poor prognosis,requires further elucidation on the functional role of long noncoding RNA(lncRNA)DDX11 antisense RNA 1(DDX11-AS1)in its pathogenesis,despite its established oncogenic functions in other cancers.Therefore,this study sought to characterize the oncogenic role and molecular mechanism of DDX11-AS1 in glioma.Methods:DDX11-AS1 expression levels were analyzed in clinical surgical glioma specimens and publicly available datasets.The functional roles of DDX11-AS1 on glioma cell proliferation and migration were investigated using in vitro knockdown and overexpression assays.In vivo tumor growth was assessed using orthotopic glioma-bearing mouse models.To elucidate the regulatory axis involving DDX11-AS1,miR-1183,and E2F transcription factor 7(E2F7),we performed competitive endogenous RNA(ceRNA)analysis and conducted functional rescue experiments via miR-1183 inhibition.Results:DDX11-AS1 expression was markedly upregulated in clinical glioma specimens.Functionally,DDX11-AS1 knockdown significantly suppressed glioma cell proliferation and migration in vitro,while its overexpression exacerbated these malignant phenotypes.Orthotopic glioma-bearingmouse models confirmed that DDX11-AS1 drives in vivo glioma tumor growth.Mechanistically,DDX11-AS1 functions as a ceRNA by competitively interacting with miR-1183.Critically,inhibition of miR-1183 rescued the suppressive effects of DDX11-AS1 knockdown on glioma tumorigenic phenotypes and restored E2F7 expression levels.Conclusions:This study demonstrates that lncRNA DDX11-AS1 promotes glioma progression by regulating the miR-1183/E2F7 axis,indicating a potential therapeutic target for glioma.
基金This paper is a staged achievement of ＂Study on China＇s Income Distribution＂, a project supported by National Social Science Foundation.
文摘When observing China＇s income distribution problems .from an international perspective, we find that China＇s income inequality is not much different from developed countries after primary distribution. The real difference between China and developed countries is that income inequality in developed countries will reduce greatly after income redistribution while the income inequality remains the same for China. Therefore, one can conclude that income inequality in China derives from the ineffectiveness of redistribution. However, a large income gap is not the main reason for skewed income distribution in China. In fact, the problem lies in unfair distribution resulting from factor capitalization. A handful of people have taken proceeds from public assets at the expense of all the people, which has led to social poIarization. To remove unfair distribution, China should improve its means of redistribution to narrow its income gap in order to develop a fair and reasonable pattern of income distribution.
基金Supported by State Apple Industry Technology System Project(nybcytx-08-04-01)~~
文摘[ Objective ] The study aimed to explore the release conditions for the conidia of Botryosphaena berengeriana and understand the release dynamic of conidia. [Method] The systematical survey on the release conditions for the conidia of B. berengeriana were conducted in two growing seasons in 2008 and 2009, combined with the collection of meteorological data around conidia release period, the weather conditions causing large amount release of B. berengedana were analyzed. [ Result] During a growing season, the conidia of pathogen appeared several large release peaks. Under the suitable temperature, when the precipitation lasted for 4 h, the conidia of B. berengeriana began to release with large amount, the amount of conidia reached the peak after release and trended to be stable during 4 - 12 h, which significantly reduced after 24 h, tended to dis- appear after 36 h, and completely disappeared after 72 h. [Conclusion] The dominant factor affecting B. berengeriana conidia release in large a- mount was precipitation, while the lasting time of precipitation played a decisive role.
基金This work is supported by NNSF of ChinaRFDP of Higher Education
文摘This paper presents a new proof of a charaterization of fractional (g, f)-factors of a graph in which multiple edges are allowed. From the proof a polynomial algorithm for finding the fractional (g, f)-factor can be induced.
基金This work was supported by NNSF. RFDP and NNSF of shandong province(Z2000A02 ).
文摘Let G be a bipartite graph with vertex set V(G) and edge set E(G), and let g and f be two positive integer-valued functions defined on V(G) such that g(x) ≤ f(x) for every vertex x of V(G). Then a (g, f)-factor of G is a spanning subgraph H of G such that g(x) ≤ dH(x) 5 f(x) for each x ∈ V(H). A (g, f)-factorization of G is a partition of E(G) into edge-disjoint (g, f)-factors. Let F = {F1, F2,…… ， Fm } and H be a factorization and a subgraph of G, respectively. If F, 1 ≤ i ≤ m， has exactly one edge in common with H, then it is said that ■ is orthogonal to H. It is proved that every bipartite (mg + m - 1, mf - m + 1 )-graph G has a (g, f)-factorization orthogonal to k vertex disjoint m-subgraphs of G if 2-k ≤ g(x) for all x ∈ V(G). Furthermore, it is showed that the results in this paper are best possible.
文摘BACKGROUND MicroRNA 34c(miR-34c)has been reported to be associated with malignant types of cancer,however,it remains unknown whether miR-34c is involved in chemoresistance in gastric cancer(GC).AIM To investigate the effect of miR-34c and its upstream transcription factor E2F1 on paclitaxel combined with cisplatin resistance in GC cells.METHODS Paired GC tissues and adjacent normal tissues were randomly sampled from 74 GC patients.miR-34c and E2F1 were detected by real-time quantitative PCR(qPCR)and Western blot.In addition,the drug resistance of GC cells to paclitaxel and cisplatin was induced by concentration gradient increasing methods,and changes in miR-34c and E2F1 during this process were measured.Furthermore,E2F1 and miR-34c overexpression or underexpression vectors were constructed and transfected into drug-resistant GC cells.MTT was employed to test the sensitivity of cells to paclitaxel combined with cisplatin,qPCR was adopted to detect the expression of miR-34c,Western blot was applied to detect the expression levels of E2F1,drug resistance-related proteins and apoptosis-related proteins,and flow cytometry was used for the determination of cell apoptosis and cell cycle status.RESULTS E2F1 was overexpressed while miR-34c was underexpressed in GC.After inducing GC cells to be resistant to paclitaxel and cisplatin,E2F1 expression increased while miR-34c expression decreased.Both silencing E2F1 and overexpressing miR-34c could increase the sensitivity of drug-resistant GC cells to paclitaxel combined with cisplatin,promote cell apoptosis and inhibit cell proliferation.Among which,silencing E2F1 could reduce the expression of drug resistance-related proteins and apoptosis-related proteins,while over-expression of miR-34c could upregulate the expression of apoptosis-related proteins without affecting the expression of MDR-1,MRP and other drug resistance-related proteins.Rescue experiments demonstrated that inhibiting miR-34c could significantly weaken the sensitization of drug resistant cells,and Si E2F1 to paclitaxel combined with cisplatin.CONCLUSION E2F1 inhibits miR-34c to promote the proliferation of GC cells and enhance the resistance to paclitaxel combined with cisplatin,and silencing E2F1 is conducive to improving the efficacy of paclitaxel combined with cisplatin in GC cells.
基金Supported by National High Technology Research and Development Program("863"Program)of China(No.2006AA02A132)Key Developing Discipline of Hebei Province(No.201221)
文摘AIM:To investigate the morphological altering effect of transforming growth factor-β2(TGF-β2) on untransfected human corneal endothelial cells(HCECs)in vitro.METHODS:After untransfected HCECs were treated with TGF-β2 at different concentrations, the morphology,cytoskeleton distribution, and type IV collagen expression of the cells were examined with inverted contrast light microscopy, fluorescence microscopy,immunofluorescence or Western Blot.RESULTS:TGF-β2 at the concentration of 3-15 μg/L had obviously alterative effects on HCECs morphology in dose and time-dependent manner, and 9 μg/L was the peak concentration. TGF-β2(9 μg/L) altered HCE cell morphology after treatment for 36 h, increased the mean optical density(P 【0.01) and the length of F-actin,reduced the mean optical density(P 【0.01) of the collagen type IV in extracellular matrix(ECM) and induced the rearrangement of F-actin, microtubule in cytoplasm and collagen type IV in ECM after treatment for 72 h.·CONCLUTION: TGF-β2 has obviously alterative effect on the morphology of HCECs from polygonal phenotype to enlarged spindle-shaped phenotype, in dose and time-dependence manner by inducing more, elongation and alignment of F-actin, rearrangement of microtubule and larger spread area of collagen type IV.
基金Supported by the National Natural Science Foundation of China( 60 1 72 0 0 3) NSF of Shandongprovince ( Z2 0 0 0 A0 2 )
文摘Let G be a bipartite graph and g and f be two positive integer-valued functions defined on vertex set V(G) of G such that g(x)≤f(x).In this paper,some sufficient conditions related to the connectivity and edge-connectivity for a bipartite (mg,mf)-graph to have a (g,f)-factor with special properties are obtained and some previous results are generalized.Furthermore,the new results are proved to be the best possible.
基金This work is supported by NSFC (10471078.10201019)RSDP (20040422004) of China
文摘In this paper the properties of some maximum fractional [0, k]-factors of graphs are presented. And consequently some results on fractional matchings and fractional 1-factors are generalized and a characterization of fractional k-factors is obtained.
文摘BACKGROUND A series of long non-coding RNAs(lncRNAs)have been reported to play a crucial role in cancer biology.Some previous studies report that lncRNA CDKN2B-AS1 is involved in some human malignancies.However,its role in hepatocellular carcinoma(HCC)has not been fully deciphered.AIM To decipher the role of CDKN2B-AS1 in the progression of HCC.METHODS CDKN2B-AS1 expression in HCC was detected by quantitative real-time polymerase chain reaction.The malignant phenotypes of Li-7 and SNU-182 cells were detected by the CCK-8 method,EdU method,and flow cytometry,respectively.RNA immunoprecipitation was executed to confirm the interaction between CDKN2B-AS1 and E2F transcription factor 1(E2F1).Luciferase reporter assay and chromatin immunoprecipitation were performed to verify the binding of E2F1 to the promoter of G protein subunit alpha Z(GNAZ).E2F1 and GNAZ were detected by western blot in HCC cells.RESULTS In HCC tissues,CDKN2B-AS1 was upregulated.Depletion of CDKN2B-AS1 inhibited the proliferation of HCC cells,and the depletion of CDKN2B-AS1 also induced cell cycle arrest and apoptosis.CDKN2B-AS1 could interact with E2F1.Depletion of CDKN2B-AS1 inhibited the binding of E2F1 to the GNAZ promoter region.Overexpression of E2F1 reversed the biological effects of depletion of CDKN2B-AS1 on the malignant behaviors of HCC cells.CONCLUSION CDKN2B-AS1 recruits E2F1 to facilitate GNAZ transcription to promote HCC progression.
基金financially supported by the National Natural Science Foundation of China,No.81371366(to HFW)the Natural Science Foundation of Guangdong Province of China,No.2015A030313515(to HFW)+1 种基金the Dongguan International Science and Technology Cooperation Project,No.2013508152010(to HFW)the Key Project of Social Development of Dongguan of China,No.20185071521640(to HFW)
文摘Brachial plexus avulsion often results in massive motor neuron death and severe functional deficits of target muscles. However, no satisfactory treatment is currently available. Hypoxia-inducible factor 1α is a critical molecule targeting several genes associated with ischemia-hypoxia damage and angiogenesis. In this study, a rat model of brachial plexus avulsion-reimplantation was established, in which C5–7 ventral nerve roots were avulsed and only the C6 root reimplanted. Different implants were immediately injected using a microsyringe into the avulsion-reimplantation site of the C6 root post-brachial plexus avulsion. Rats were randomly divided into five groups: phosphate-buffered saline, negative control of lentivirus, hypoxia-inducible factor 1α(hypoxia-inducible factor 1α overexpression lentivirus), gel(pluronic F-127 hydrogel), and gel + hypoxia-inducible factor 1α(pluronic F-127 hydrogel + hypoxia-inducible factor 1α overexpression lentivirus). The Terzis grooming test was performed to assess recovery of motor function. Scores were higher in the hypoxia-inducible factor 1α and gel +hypoxia-inducible factor 1α groups(in particular the gel + hypoxia-inducible factor 1α group) compared with the phosphate-buffered saline group. Electrophysiology, fluorogold retrograde tracing, and immunofluorescent staining were further performed to investigate neural pathway reconstruction and changes of neurons, motor endplates, and angiogenesis. Compared with the phosphate-buffered saline group, action potential latency of musculocutaneous nerves was markedly shortened in the hypoxia-inducible factor 1α and gel + hypoxia-inducible factor1α groups. Meanwhile, the number of fluorogold-positive cells and ChAT-positive neurons, neovascular area(labeled by CD31 around av ulsed sites in ipsilateral spinal cord segments), and the number of motor endplates in biceps brachii(identified by α-bungarotoxin) were all visibly increased, as well as the morphology of motor endplate in biceps brachil was clear in the hypoxia-inducible factor 1α and gel + hypoxia-inducible factor 1α groups. Taken together, delivery of hypoxia-inducible factor 1α overexpression lentiviral vectors mediated by pluronic F-127 effectively promotes spinal root regeneration and functional recovery post-brachial plexus avulsion. All animal procedures were approved by the Institutional Animal Care and Use Committee of Guangdong Medical University, China.
文摘In this paper, the cosmological models of the universe are constructed in gravity with choice of the functional in the form ?and . The space-time considered here is Bianchi Type I and the energy momentum tensor is in the form of perfect fluid. Two cosmological models are presented using a power form of exponential function and a hyperbolic form. The energy conditions along with the state finder diagnostic pair have been obtained and analyzed.
