To solve the problems in restoring sedimentary facies and predicting reservoirs in loose gas-bearing sediment,based on seismic sedimentologic analysis of the first 9-component S-wave 3D seismic dataset of China,a four...To solve the problems in restoring sedimentary facies and predicting reservoirs in loose gas-bearing sediment,based on seismic sedimentologic analysis of the first 9-component S-wave 3D seismic dataset of China,a fourth-order isochronous stratigraphic framework was set up and then sedimentary facies and reservoirs in the Pleistocene Qigequan Formation in Taidong area of Qaidam Basin were studied by seismic geomorphology and seismic lithology.The study method and thought are as following.Firstly,techniques of phase rotation,frequency decomposition and fusion,and stratal slicing were applied to the 9-component S-wave seismic data to restore sedimentary facies of major marker beds based on sedimentary models reflected by satellite images.Then,techniques of seismic attribute extraction,principal component analysis,and random fitting were applied to calculate the reservoir thickness and physical parameters of a key sandbody,and the results are satisfactory and confirmed by blind testing wells.Study results reveal that the dominant sedimentary facies in the Qigequan Formation within the study area are delta front and shallow lake.The RGB fused slices indicate that there are two cycles with three sets of underwater distributary channel systems in one period.Among them,sandstones in the distributary channels of middle-low Qigequan Formation are thick and broad with superior physical properties,which are favorable reservoirs.The reservoir permeability is also affected by diagenesis.Distributary channel sandstone reservoirs extend further to the west of Sebei-1 gas field,which provides a basis to expand exploration to the western peripheral area.展开更多
目的检测帕金森病(PD)患者血清视锥蛋白样蛋白1(VILIP-1)、补体Clq肿瘤坏死因子相关蛋白9(CTRP9)和纤维蛋白原样蛋白2(FGL2)表达水平,分析三者与PD患者疾病分期、认知功能的关系。方法选取2022年3月~2024年3月监利市人民医院收治的103...目的检测帕金森病(PD)患者血清视锥蛋白样蛋白1(VILIP-1)、补体Clq肿瘤坏死因子相关蛋白9(CTRP9)和纤维蛋白原样蛋白2(FGL2)表达水平,分析三者与PD患者疾病分期、认知功能的关系。方法选取2022年3月~2024年3月监利市人民医院收治的103例PD患者作为研究对象(PD组),依据Hoehn-Yahr(H-Y)分级系统将PD患者分为早期组(n=48),中/晚期组(n=55);依据蒙特利尔认知评估表(MoCA)将PD患者分为认知正常组(n=38)和认知障碍组(n=65)。另随机选择同期体检健康人105例作为对照组。采用酶联免疫吸附试验(ELISA)法测定血清VILIP-1、CTRP9和FGL2表达水平;采用Logistic回归分析影响PD患者发生认知功能障碍的影响因素;采用Pearson法分析血清VILIP-1、CTRP9、FGL2水平与疾病分期、认知障碍相关性;采用受试者工作特征(ROC)曲线分析血清VILIP-1、CTRP9、FGL2联合检测对PD患者疾病分期、认知功能障碍的诊断价值。结果PD组血清VILIP-1(7.16±1.28ng/ml)、FGL2(94.27±12.42ng/ml)水平高于对照组(4.67±0.95ng/ml,72.15±9.68ng/ml),CTRP9(0.53±0.07pg/ml)水平低于对照组(1.02±0.14pg/ml),差异具有统计学意义(t=15.952、14.342、31.831,均P<0.001)。中/晚期组血清VILIP-1(7.86±0.95ng/ml)、FGL2(102.21±13.04ng/ml)水平高于早期组(6.36±0.81ng/ml,85.17±10.35ng/ml),CTRP9(0.46±0.08pg/ml)水平低于早期组(0.62±0.14pg/ml),差异具有统计学意义(t=8.556、7.271、7.233,均P<0.001)。与认知正常组相比,认知障碍组血清VILIP-1(7.72±1.03ng/ml vs 6.21±0.92ng/ml)、FGL2(102.54±16.53ng/ml vs 80.12±13.27ng/ml)水平及UPDRS评分(54.17±7.68分vs 50.64±7.42分),SCOPA-AUT评分(15.27±3.82分vs 12.39±3.48分)升高,CTRP9(0.47±0.09pg/ml vs 0.65±0.13pg/ml)水平降低,差异具有统计学意义(t=2.279~7.537,均P<0.05)。Logistic分析显示,UPDRS、VILIP-1、FGL2是PD患者发生认知功能障碍的危险因素(Waldχ^(2)=5.041、6.127、7.414,均P<0.05),CTRP9是PD患者发生认功能障碍的保护因素(Waldχ^(2)=5.775,P<0.05)。Pearson相关分析显示,血清VILIP-1、FGL2水平与疾病分期、认知障碍呈正相关(r=0.524~0.637,均P<0.05),血清CTRP9水平与疾病分期、认知障碍呈负相关(r=-0.501、-0.595,均P<0.001)。ROC曲线分析显示,血清VILIP-1、CTRP9、FGL2三者联合预测PD患者疾病分期的AUC优于单独检测(Z=2.625、2.568、2.251,均P<0.05);三者联合预测PD患者认知功能障碍的AUC优于单独检测(Z=2.910、2.008、2.096,均P<0.05)。结论PD患者血清VILIP-1、FGL2呈高水平,CTRP9呈低水平,且均与PD患者疾病分期、认知功能密切相关。展开更多
Downregulation of the inwardly rectifying potassium channel Kir4.1 is a key step for inducing retinal Müller cell activation and interaction with other glial cells,which is involved in retinal ganglion cell apopt...Downregulation of the inwardly rectifying potassium channel Kir4.1 is a key step for inducing retinal Müller cell activation and interaction with other glial cells,which is involved in retinal ganglion cell apoptosis in glaucoma.Modulation of Kir4.1 expression in Müller cells may therefore be a potential strategy for attenuating retinal ganglion cell damage in glaucoma.In this study,we identified seven predicted phosphorylation sites in Kir4.1 and constructed lentiviral expression systems expressing Kir4.1 mutated at each site to prevent phosphorylation.Following this,we treated Müller glial cells in vitro and in vivo with the m Glu R I agonist DHPG to induce Kir4.1 or Kir4.1 Tyr^(9)Asp overexpression.We found that both Kir4.1 and Kir4.1 Tyr^(9)Asp overexpression inhibited activation of Müller glial cells.Subsequently,we established a rat model of chronic ocular hypertension by injecting microbeads into the anterior chamber and overexpressed Kir4.1 or Kir4.1 Tyr^(9)Asp in the eye,and observed similar results in Müller cells in vivo as those seen in vitro.Both Kir4.1 and Kir4.1 Tyr^(9)Asp overexpression inhibited Müller cell activation,regulated the balance of Bax/Bcl-2,and reduced the m RNA and protein levels of pro-inflammatory factors,including interleukin-1βand tumor necrosis factor-α.Furthermore,we investigated the regulatory effects of Kir4.1 and Kir4.1 Tyr^(9)Asp overexpression on the release of pro-inflammatory factors in a co-culture system of Müller glial cells and microglia.In this co-culture system,we observed elevated adenosine triphosphate concentrations in activated Müller cells,increased levels of translocator protein(a marker of microglial activation),and elevated interleukin-1βm RNA and protein levels in microglia induced by activated Müller cells.These changes could be reversed by Kir4.1 and Kir4.1 Tyr^(9)Asp overexpression in Müller cells.Kir4.1 overexpression,but not Kir4.1 Tyr^(9)Asp overexpression,reduced the number of proliferative and migratory microglia induced by activated Müller cells.Collectively,these results suggest that the tyrosine residue at position nine in Kir4.1 may serve as a functional modulation site in the retina in an experimental model of glaucoma.Kir4.1 and Kir4.1 Tyr^(9)Asp overexpression attenuated Müller cell activation,reduced ATP/P2X receptor–mediated interactions between glial cells,inhibited microglial activation,and decreased the synthesis and release of pro-inflammatory factors,consequently ameliorating retinal ganglion cell apoptosis in glaucoma.展开更多
基金Supported by the CNPC Science and Technology Projects(2022-N/G-47808,2023-N/G-67014)RIPED International Cooperation Project(19HTY5000008).
文摘To solve the problems in restoring sedimentary facies and predicting reservoirs in loose gas-bearing sediment,based on seismic sedimentologic analysis of the first 9-component S-wave 3D seismic dataset of China,a fourth-order isochronous stratigraphic framework was set up and then sedimentary facies and reservoirs in the Pleistocene Qigequan Formation in Taidong area of Qaidam Basin were studied by seismic geomorphology and seismic lithology.The study method and thought are as following.Firstly,techniques of phase rotation,frequency decomposition and fusion,and stratal slicing were applied to the 9-component S-wave seismic data to restore sedimentary facies of major marker beds based on sedimentary models reflected by satellite images.Then,techniques of seismic attribute extraction,principal component analysis,and random fitting were applied to calculate the reservoir thickness and physical parameters of a key sandbody,and the results are satisfactory and confirmed by blind testing wells.Study results reveal that the dominant sedimentary facies in the Qigequan Formation within the study area are delta front and shallow lake.The RGB fused slices indicate that there are two cycles with three sets of underwater distributary channel systems in one period.Among them,sandstones in the distributary channels of middle-low Qigequan Formation are thick and broad with superior physical properties,which are favorable reservoirs.The reservoir permeability is also affected by diagenesis.Distributary channel sandstone reservoirs extend further to the west of Sebei-1 gas field,which provides a basis to expand exploration to the western peripheral area.
文摘目的检测帕金森病(PD)患者血清视锥蛋白样蛋白1(VILIP-1)、补体Clq肿瘤坏死因子相关蛋白9(CTRP9)和纤维蛋白原样蛋白2(FGL2)表达水平,分析三者与PD患者疾病分期、认知功能的关系。方法选取2022年3月~2024年3月监利市人民医院收治的103例PD患者作为研究对象(PD组),依据Hoehn-Yahr(H-Y)分级系统将PD患者分为早期组(n=48),中/晚期组(n=55);依据蒙特利尔认知评估表(MoCA)将PD患者分为认知正常组(n=38)和认知障碍组(n=65)。另随机选择同期体检健康人105例作为对照组。采用酶联免疫吸附试验(ELISA)法测定血清VILIP-1、CTRP9和FGL2表达水平;采用Logistic回归分析影响PD患者发生认知功能障碍的影响因素;采用Pearson法分析血清VILIP-1、CTRP9、FGL2水平与疾病分期、认知障碍相关性;采用受试者工作特征(ROC)曲线分析血清VILIP-1、CTRP9、FGL2联合检测对PD患者疾病分期、认知功能障碍的诊断价值。结果PD组血清VILIP-1(7.16±1.28ng/ml)、FGL2(94.27±12.42ng/ml)水平高于对照组(4.67±0.95ng/ml,72.15±9.68ng/ml),CTRP9(0.53±0.07pg/ml)水平低于对照组(1.02±0.14pg/ml),差异具有统计学意义(t=15.952、14.342、31.831,均P<0.001)。中/晚期组血清VILIP-1(7.86±0.95ng/ml)、FGL2(102.21±13.04ng/ml)水平高于早期组(6.36±0.81ng/ml,85.17±10.35ng/ml),CTRP9(0.46±0.08pg/ml)水平低于早期组(0.62±0.14pg/ml),差异具有统计学意义(t=8.556、7.271、7.233,均P<0.001)。与认知正常组相比,认知障碍组血清VILIP-1(7.72±1.03ng/ml vs 6.21±0.92ng/ml)、FGL2(102.54±16.53ng/ml vs 80.12±13.27ng/ml)水平及UPDRS评分(54.17±7.68分vs 50.64±7.42分),SCOPA-AUT评分(15.27±3.82分vs 12.39±3.48分)升高,CTRP9(0.47±0.09pg/ml vs 0.65±0.13pg/ml)水平降低,差异具有统计学意义(t=2.279~7.537,均P<0.05)。Logistic分析显示,UPDRS、VILIP-1、FGL2是PD患者发生认知功能障碍的危险因素(Waldχ^(2)=5.041、6.127、7.414,均P<0.05),CTRP9是PD患者发生认功能障碍的保护因素(Waldχ^(2)=5.775,P<0.05)。Pearson相关分析显示,血清VILIP-1、FGL2水平与疾病分期、认知障碍呈正相关(r=0.524~0.637,均P<0.05),血清CTRP9水平与疾病分期、认知障碍呈负相关(r=-0.501、-0.595,均P<0.001)。ROC曲线分析显示,血清VILIP-1、CTRP9、FGL2三者联合预测PD患者疾病分期的AUC优于单独检测(Z=2.625、2.568、2.251,均P<0.05);三者联合预测PD患者认知功能障碍的AUC优于单独检测(Z=2.910、2.008、2.096,均P<0.05)。结论PD患者血清VILIP-1、FGL2呈高水平,CTRP9呈低水平,且均与PD患者疾病分期、认知功能密切相关。
基金supported by the National Natural Science Foundation of China,Nos.32271043(to ZW)and 82171047(to YM)the both Science and Technology Major Project of Shanghai,No.2018SHZDZX01 and ZJLabShanghai Center for Brain Science and Brain-Inspired Technology(to ZW)。
文摘Downregulation of the inwardly rectifying potassium channel Kir4.1 is a key step for inducing retinal Müller cell activation and interaction with other glial cells,which is involved in retinal ganglion cell apoptosis in glaucoma.Modulation of Kir4.1 expression in Müller cells may therefore be a potential strategy for attenuating retinal ganglion cell damage in glaucoma.In this study,we identified seven predicted phosphorylation sites in Kir4.1 and constructed lentiviral expression systems expressing Kir4.1 mutated at each site to prevent phosphorylation.Following this,we treated Müller glial cells in vitro and in vivo with the m Glu R I agonist DHPG to induce Kir4.1 or Kir4.1 Tyr^(9)Asp overexpression.We found that both Kir4.1 and Kir4.1 Tyr^(9)Asp overexpression inhibited activation of Müller glial cells.Subsequently,we established a rat model of chronic ocular hypertension by injecting microbeads into the anterior chamber and overexpressed Kir4.1 or Kir4.1 Tyr^(9)Asp in the eye,and observed similar results in Müller cells in vivo as those seen in vitro.Both Kir4.1 and Kir4.1 Tyr^(9)Asp overexpression inhibited Müller cell activation,regulated the balance of Bax/Bcl-2,and reduced the m RNA and protein levels of pro-inflammatory factors,including interleukin-1βand tumor necrosis factor-α.Furthermore,we investigated the regulatory effects of Kir4.1 and Kir4.1 Tyr^(9)Asp overexpression on the release of pro-inflammatory factors in a co-culture system of Müller glial cells and microglia.In this co-culture system,we observed elevated adenosine triphosphate concentrations in activated Müller cells,increased levels of translocator protein(a marker of microglial activation),and elevated interleukin-1βm RNA and protein levels in microglia induced by activated Müller cells.These changes could be reversed by Kir4.1 and Kir4.1 Tyr^(9)Asp overexpression in Müller cells.Kir4.1 overexpression,but not Kir4.1 Tyr^(9)Asp overexpression,reduced the number of proliferative and migratory microglia induced by activated Müller cells.Collectively,these results suggest that the tyrosine residue at position nine in Kir4.1 may serve as a functional modulation site in the retina in an experimental model of glaucoma.Kir4.1 and Kir4.1 Tyr^(9)Asp overexpression attenuated Müller cell activation,reduced ATP/P2X receptor–mediated interactions between glial cells,inhibited microglial activation,and decreased the synthesis and release of pro-inflammatory factors,consequently ameliorating retinal ganglion cell apoptosis in glaucoma.
