Recombinant tissue plasminogen activator is commonly used for hematoma evacuation in minimally invasive surgery following intracerebral hemorrhage.However,during minimally invasive surgery,recombinant tissue plasminog...Recombinant tissue plasminogen activator is commonly used for hematoma evacuation in minimally invasive surgery following intracerebral hemorrhage.However,during minimally invasive surgery,recombinant tissue plasminogen activator may come into contact with brain tissue.Therefore,a thorough assessment of its safety is required.In this study,we established a mouse model of intracerebral hemorrhage induced by type VII collagenase.We observed that the administration of recombinant tissue plasminogen activator without hematoma aspiration significantly improved the neurological function of mice with intracerebral hemorrhage,reduced pathological damage,and lowered the levels of apoptosis and autophagy in the tissue surrounding the hematoma.In an in vitro model of intracerebral hemorrhage using primary cortical neurons induced by hemin,the administration of recombinant tissue plasminogen activator suppressed neuronal apoptosis,autophagy,and endoplasmic reticulum stress.Transcriptome sequencing analysis revealed that recombinant tissue plasminogen activator upregulated the phosphoinositide 3-kinase/RAC-alpha serine/threonine-protein kinase/mammalian target of rapamycin pathway in neurons.Moreover,the phosphoinositide 3-kinase inhibitor LY294002 abrogated the neuroprotective effects of recombinant tissue plasminogen activator in inhibiting excessive apoptosis,autophagy,and endoplasmic reticulum stress.Furthermore,to specify the domain of recombinant tissue plasminogen activator responsible for its neuroprotective effects,various inhibitors were used to target distinct domains.It has been revealed that the epidermal growth factor receptor inhibitor AG-1478 reversed the effect of recombinant tissue plasminogen activator on the phosphoinositide 3-kinase/RAC-alpha serine/threonineprotein kinase/mammalian target of rapamycin pathway.These findings suggest that recombinant tissue plasminogen activator exerts a direct neuroprotective effect on neurons following intracerebral hemorrhage,possibly through activation of the phosphoinositide 3-kinase/RAC-alpha serine/threonine-protein kinase/mammalian target of rapamycin pathway.展开更多
AIM:To evaluate visual outcomes of pars plana vitrectomy(PPV)combined with tissue plasminogen activator(tPA)-induced clot lysis and pneumatic displacement for submacular hemorrhage(SMH)in a cohort of closed-globe trau...AIM:To evaluate visual outcomes of pars plana vitrectomy(PPV)combined with tissue plasminogen activator(tPA)-induced clot lysis and pneumatic displacement for submacular hemorrhage(SMH)in a cohort of closed-globe trauma patients.METHODS:A retrospective,multicenter interventional case series involving 7 eyes of 7 patients who underwent PPV with subretinal tPA administration for SMH secondary to closed-globe injury were conducted.The primary outcome measure was the change in Snellen visual acuity.RESULTS:The mean age of patients was 32y(range:21-51y),with a mean follow-up duration of 4.6mo(range:1.1-14.9mo).The average best-corrected visual acuity(BCVA)was 20/1020 at baseline and 20/114 at the final visit,respectively(P=0.025).Preoperative BCVA was not a significant predictor of final BCVA(r=0.102,P=0.827).Final BCVA did not differ significantly between patients who underwent PPV within 14d of symptom onset and those who underwent surgery after 14d(P=0.57).All eyes received SF6 or C3F8 gas tamponade.CONCLUSION:Surgical intervention involving tPAmediated clot lysis and pneumatic displacement may yield visual benefits in trauma-induced SMH without underlying retinal vascular disease;however,larger prospective studies are warranted to confirm these findings.展开更多
BACKGROUND In vivo degradation of bone scaffolds is significantly influenced by osteoclast(OC)activity,which is orchestrated by the interplay between receptor activator of nuclear factor-kappa B ligand(RANKL)and osteo...BACKGROUND In vivo degradation of bone scaffolds is significantly influenced by osteoclast(OC)activity,which is orchestrated by the interplay between receptor activator of nuclear factor-kappa B ligand(RANKL)and osteoprotegerin(OPG).The ratio of RANKL/OPG is a crucial determinant of OC-mediated bone resorption,which plays an integral role in bone remodeling and scaffold degradation.Elevated levels of RANKL relative to OPG enhance osteoclastogenesis,thereby accelerating the degradation process essential for integrating bone scaffolds into the host tissue.AIM To elucidate the effects of OPG gene silencing on osteoclastogenesis within rat bone marrow-derived mesenchymal stem cells(BMSCs).By investigating these effects,the study aimed to provide deeper insights into the regulatory mechanisms that influence bone scaffold degradation,potentially leading to improved bone repair and regeneration strategies.METHODS We employed recombinant lentiviral plasmids to silence the OPG gene in rat BMSCs to achieve the aims.The efficacy of gene silencing was assessed using quantitative reverse transcription polymerase chain reaction and western blot analysis to measure the expression levels of OPG and RANKL.Tartrate-resistant acid phosphatase staining was utilized to evaluate the formation of OCs.Additionally,co-immunoprecipitation assays were conducted to explore the interactions between RANKL and OPG proteins,further assessing the biochemical pathways involved in osteoclastogenesis.RESULTS The silencing of the OPG gene in BMSCs resulted in a significant increase in the RANKL/OPG ratio,evidenced by decreased expression levels of OPG and increased levels of RANKL.Enhanced osteoclastogenesis was observed through tartrate-resistant acid phosphatase staining,which indicated a substantial rise in OC formation in response to the altered RANKL/OPG balance.The co-immunoprecipitation assays provided concrete evidence of the direct interaction between RANKL and OPG proteins,substantiating their pivotal roles in regulating OC activity.CONCLUSION The findings from this study underscore the critical role of the RANKL/OPG axis in osteoclastogenesis.Silencing of the OPG gene in BMSCs effectively increases the RANKL/OPG ratio,promoting OC activity and potentially enhancing bone scaffold degradation.This regulatory mechanism offers a promising avenue for modulating bone remodeling processes,which is essential for effective bone repair and the successful integration of bone scaffolds into damaged sites.Future research might focus on optimizing the control of this axis to better facilitate bone tissue engineering and regenerative therapies.展开更多
Using cemented rockfill to replace coal pillars offers an effective solution for reducing solid waste while ensuring the safety of gob-side entries.However,achieving the balance among low cost,high waste recycling rat...Using cemented rockfill to replace coal pillars offers an effective solution for reducing solid waste while ensuring the safety of gob-side entries.However,achieving the balance among low cost,high waste recycling rates,and adequate strength remains a significant challenge for cemented rockfill.This study used a composite alkali activator to activate gangue cemented rockfill.The compressive strength,scanning electron microscopy,energy dispersive spectrometer,mercury intrusion porosimetry,X-ray diffraction,and thermogra-vimetric tests were carried out to investigate the effect of the composite alkali activator proportion on the compressive strength,micro-structure,and composition of the cemented rockfill.The calcium silicate hydrate(C–S–H)molecular model of cemented rockfill was con-structed to explore the fracture evolution of the nucleated molecular structure under tension.The results show that compressive strength initially increased and then decreased with the activator proportion,the optimal activator proportion of 1:2 resulted in a 31.25%increase in strength at 3 d.This reasonable activator proportion strengthens the pozzolanic effect of gangue,and consumes more calcium hydroxide to inhibit its agglomeration,ultimately achieving the densification of microstructure.The activator proportion inevitably substitutes calcium ions with sodium ions in the C–S–H molecular model.The 12%substitution of calcium ions increases the adhesion between silicon chain layers,which is beneficial to the interlayer stress transfer.This work proposes a method for preparing low-cost cemented rockfill from al-kali-activated gangue,which can be used for solid waste recycling and reducing cement consumption to achieve low-carbon goals.展开更多
The degradation of organic pollutants in water is a critical environmental challenge.The iron-doped MoS_(2) catalysts have demonstrated potential in activating peroxymonosulfate(PMS)for environmental remediation,but t...The degradation of organic pollutants in water is a critical environmental challenge.The iron-doped MoS_(2) catalysts have demonstrated potential in activating peroxymonosulfate(PMS)for environmental remediation,but they face challenges such as poor conductivity,limited electron transfer efficiency,and a scarcity of active sites.To address these issues,we successfully synthesized a nano-flowers FeS/MoS_(2) composite derived from polyoxometalates(NH_(4))_(3)[Fe(III)Mo_(6)O_(24)H_(6)]⋅6H_(2)O(denoted as FeMo6)as the bimetallic precursors.This synthesis strategy enhances the interaction between FeS and MoS_(2),thereby facilitating electron transfer.Notably,the introduction of sulfur vacancies in FeS/MoS_(2) exposes additional Mo4t active sites,promoting the redox cycle of Fe^(2+)/Fe^(3+) and accelerating the regeneration of Fe^(2+),which in turn enhances PMS activation.Therefore,a catalytic oxidation system of FeS/MoS_(2)/PMS is presented that primarily relies on SO_(4)^(⋅-)and⋅OH,with ^(1)O_(2) as a supplementary oxidant.This system exhibits exceptional degradation efficiency for p-chlorophenol(4-CP),achieving 100% degradation within 10 min over a wide pH range of 2.4–8.4.The robust performance and wide applicability of FeS/MoS_(2) catalyst make it a promising candidate in advanced oxidation processes(AOPs)for environmental remediation.展开更多
BACKGROUND:Urokinase-type plasminogen activator(uPA) and urokinase-type plasminogen activator receptor(uPAR) are known as important factors,which mediate a variety of functions in terms of vascular homeostasis,inflamm...BACKGROUND:Urokinase-type plasminogen activator(uPA) and urokinase-type plasminogen activator receptor(uPAR) are known as important factors,which mediate a variety of functions in terms of vascular homeostasis,inflammation and tissue repair.However,their role in systemic inflammatory response syndrome(SIRS) has been less well studied.This study aimed to test the hypothesis that the abnormalities of fibrinolysis and degradation of extracellular matrix mediated by uPA and uPAR are directly related to the patients with SIRS.We therefore analyzed their role and clinicopathological significance in patients with SIRS.METHODS:A case-control study was conducted with 85 patients who were divided into two groups according to the diagnostic criteria of SIRS:SIRS group(n=50) and non-SIRS group(/7=35).The SIRS group was divided into MODS group(n=26) and non-MODS group(n=24) by their severity,and survival group(n=35) and non-survival group(n=15) by their prognosis.Another 30 healthy adults served as normal controls.uPA and uPAR in plasma were detected by commercial enzyme-linked immunosorbent assay(ELISA) kits.RESULTS:The plasma level of uPA was lower in the SIRS group than in the non-SIRS group and controls(P<0.001 and P<0.001).It was lower in sepsis patients and the MODS group than in the non-sepsis patients and the non-MODS patients(all P<0.05).However,there was no difference in uPA level between survivors and non-survivors(P>0.05).The plasma level of uPAR increased in the SIRS group compared with the non-SIRS group and controls(P<0.001 and P<0.001).There was a significant elevation of uPAR in sepsis patients,MODS patients and non-survivors as compared with non-sepsis patients,non-MODS patients and survivors respectively(all P<0.05).Plasma uPAR levels were positively correlated with APACHE Ⅱ score(r=0.575,P<0.001) and SOFA score(r=0.349,P=0.013).AUCs for the prediction of SIRS mortality were 0.67 and 0.51,respectively,for uPA and uPAR.CONCLUSION:uPAR could be a predictor of poor outcome in patients with SIRS.展开更多
AIMTo investigate the role of tissue plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI) in proliferative diabetic retinopathy (PDR) and to discuss the correlations among t-PA, PAI and vascular endo...AIMTo investigate the role of tissue plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI) in proliferative diabetic retinopathy (PDR) and to discuss the correlations among t-PA, PAI and vascular endothelial growth factor (VEGF) expressions.展开更多
Signal transducer and activator of transcription（STAT）is a unique protein family that binds to DNA,coupled with tyrosine phosphorylation signaling pathways,acting as a transcriptional regulator to mediate a variety ...Signal transducer and activator of transcription（STAT）is a unique protein family that binds to DNA,coupled with tyrosine phosphorylation signaling pathways,acting as a transcriptional regulator to mediate a variety of biological effects.Cerebral ischemia and reperfusion can activate STATs signaling pathway,but no studies have confirmed whether STAT activation can be verified by diffusion-weighted magnetic resonance imaging（DWI）in rats after cerebral ischemia/reperfusion.Here,we established a rat model of focal cerebral ischemia injury using the modified Longa method.DWI revealed hyperintensity in parts of the left hemisphere before reperfusion and a low apparent diffusion coefficient.STAT3 protein expression showed no significant change after reperfusion,but phosphorylated STAT3 expression began to increase after 30 minutes of reperfusion and peaked at 24 hours.Pearson correlation analysis showed that STAT3 activation was correlated positively with the relative apparent diffusion coefficient and negatively with the DWI abnormal signal area.These results indicate that DWI is a reliable representation of the infarct area and reflects STAT phosphorylation in rat brain following focal cerebral ischemia/reperfusion.展开更多
基金supported by the National Natural Science Foundation of China,Nos.92148206,82071330(both to ZT)a grant from the Major Program of Hubei Province,No.2023BAA005(to ZT)+1 种基金a grant from the Key Research and Discovery Program of Hubei Province,No.2021BCA109(to ZT)the Research Foundation of Tongji Hospital,No.2022B37(to PZ)。
文摘Recombinant tissue plasminogen activator is commonly used for hematoma evacuation in minimally invasive surgery following intracerebral hemorrhage.However,during minimally invasive surgery,recombinant tissue plasminogen activator may come into contact with brain tissue.Therefore,a thorough assessment of its safety is required.In this study,we established a mouse model of intracerebral hemorrhage induced by type VII collagenase.We observed that the administration of recombinant tissue plasminogen activator without hematoma aspiration significantly improved the neurological function of mice with intracerebral hemorrhage,reduced pathological damage,and lowered the levels of apoptosis and autophagy in the tissue surrounding the hematoma.In an in vitro model of intracerebral hemorrhage using primary cortical neurons induced by hemin,the administration of recombinant tissue plasminogen activator suppressed neuronal apoptosis,autophagy,and endoplasmic reticulum stress.Transcriptome sequencing analysis revealed that recombinant tissue plasminogen activator upregulated the phosphoinositide 3-kinase/RAC-alpha serine/threonine-protein kinase/mammalian target of rapamycin pathway in neurons.Moreover,the phosphoinositide 3-kinase inhibitor LY294002 abrogated the neuroprotective effects of recombinant tissue plasminogen activator in inhibiting excessive apoptosis,autophagy,and endoplasmic reticulum stress.Furthermore,to specify the domain of recombinant tissue plasminogen activator responsible for its neuroprotective effects,various inhibitors were used to target distinct domains.It has been revealed that the epidermal growth factor receptor inhibitor AG-1478 reversed the effect of recombinant tissue plasminogen activator on the phosphoinositide 3-kinase/RAC-alpha serine/threonineprotein kinase/mammalian target of rapamycin pathway.These findings suggest that recombinant tissue plasminogen activator exerts a direct neuroprotective effect on neurons following intracerebral hemorrhage,possibly through activation of the phosphoinositide 3-kinase/RAC-alpha serine/threonine-protein kinase/mammalian target of rapamycin pathway.
基金Supportea by DeNardo Education and Research Foundation GrantJeffrey T.Fort Innovation Fund+3 种基金Siteman Retina Research FundResearch to Prevent Blindness IncGetahun H is supported by Washington University in St.Louis School of Medicine Dean’s Medical Student Research Fellowship for the MD5 Yearlong Research ProgramGetahun H is also a recipient of a Research to Prevent Blindness Medical Student Eye Research Fellowship.
文摘AIM:To evaluate visual outcomes of pars plana vitrectomy(PPV)combined with tissue plasminogen activator(tPA)-induced clot lysis and pneumatic displacement for submacular hemorrhage(SMH)in a cohort of closed-globe trauma patients.METHODS:A retrospective,multicenter interventional case series involving 7 eyes of 7 patients who underwent PPV with subretinal tPA administration for SMH secondary to closed-globe injury were conducted.The primary outcome measure was the change in Snellen visual acuity.RESULTS:The mean age of patients was 32y(range:21-51y),with a mean follow-up duration of 4.6mo(range:1.1-14.9mo).The average best-corrected visual acuity(BCVA)was 20/1020 at baseline and 20/114 at the final visit,respectively(P=0.025).Preoperative BCVA was not a significant predictor of final BCVA(r=0.102,P=0.827).Final BCVA did not differ significantly between patients who underwent PPV within 14d of symptom onset and those who underwent surgery after 14d(P=0.57).All eyes received SF6 or C3F8 gas tamponade.CONCLUSION:Surgical intervention involving tPAmediated clot lysis and pneumatic displacement may yield visual benefits in trauma-induced SMH without underlying retinal vascular disease;however,larger prospective studies are warranted to confirm these findings.
基金Supported by the National Natural Science Foundation of China,No.82160192and Guangxi Science and Technology Program,No.2023AB23037.
文摘BACKGROUND In vivo degradation of bone scaffolds is significantly influenced by osteoclast(OC)activity,which is orchestrated by the interplay between receptor activator of nuclear factor-kappa B ligand(RANKL)and osteoprotegerin(OPG).The ratio of RANKL/OPG is a crucial determinant of OC-mediated bone resorption,which plays an integral role in bone remodeling and scaffold degradation.Elevated levels of RANKL relative to OPG enhance osteoclastogenesis,thereby accelerating the degradation process essential for integrating bone scaffolds into the host tissue.AIM To elucidate the effects of OPG gene silencing on osteoclastogenesis within rat bone marrow-derived mesenchymal stem cells(BMSCs).By investigating these effects,the study aimed to provide deeper insights into the regulatory mechanisms that influence bone scaffold degradation,potentially leading to improved bone repair and regeneration strategies.METHODS We employed recombinant lentiviral plasmids to silence the OPG gene in rat BMSCs to achieve the aims.The efficacy of gene silencing was assessed using quantitative reverse transcription polymerase chain reaction and western blot analysis to measure the expression levels of OPG and RANKL.Tartrate-resistant acid phosphatase staining was utilized to evaluate the formation of OCs.Additionally,co-immunoprecipitation assays were conducted to explore the interactions between RANKL and OPG proteins,further assessing the biochemical pathways involved in osteoclastogenesis.RESULTS The silencing of the OPG gene in BMSCs resulted in a significant increase in the RANKL/OPG ratio,evidenced by decreased expression levels of OPG and increased levels of RANKL.Enhanced osteoclastogenesis was observed through tartrate-resistant acid phosphatase staining,which indicated a substantial rise in OC formation in response to the altered RANKL/OPG balance.The co-immunoprecipitation assays provided concrete evidence of the direct interaction between RANKL and OPG proteins,substantiating their pivotal roles in regulating OC activity.CONCLUSION The findings from this study underscore the critical role of the RANKL/OPG axis in osteoclastogenesis.Silencing of the OPG gene in BMSCs effectively increases the RANKL/OPG ratio,promoting OC activity and potentially enhancing bone scaffold degradation.This regulatory mechanism offers a promising avenue for modulating bone remodeling processes,which is essential for effective bone repair and the successful integration of bone scaffolds into damaged sites.Future research might focus on optimizing the control of this axis to better facilitate bone tissue engineering and regenerative therapies.
基金supported by the Key Research and Development Special Tasks of Xinjiang,China (No.2022B01051-2)the National Natural Science Foundation of China (Nos.U23B2091,42372328,and 52478253)+1 种基金the Natural Science Foundation of Jiangsu Province,China (No.BK20240209)the Science and Technology Program Special Fund of Jiangsu Province (Frontier Leading Technology Basic Research) Major projects,China (No.BK 20222004)
文摘Using cemented rockfill to replace coal pillars offers an effective solution for reducing solid waste while ensuring the safety of gob-side entries.However,achieving the balance among low cost,high waste recycling rates,and adequate strength remains a significant challenge for cemented rockfill.This study used a composite alkali activator to activate gangue cemented rockfill.The compressive strength,scanning electron microscopy,energy dispersive spectrometer,mercury intrusion porosimetry,X-ray diffraction,and thermogra-vimetric tests were carried out to investigate the effect of the composite alkali activator proportion on the compressive strength,micro-structure,and composition of the cemented rockfill.The calcium silicate hydrate(C–S–H)molecular model of cemented rockfill was con-structed to explore the fracture evolution of the nucleated molecular structure under tension.The results show that compressive strength initially increased and then decreased with the activator proportion,the optimal activator proportion of 1:2 resulted in a 31.25%increase in strength at 3 d.This reasonable activator proportion strengthens the pozzolanic effect of gangue,and consumes more calcium hydroxide to inhibit its agglomeration,ultimately achieving the densification of microstructure.The activator proportion inevitably substitutes calcium ions with sodium ions in the C–S–H molecular model.The 12%substitution of calcium ions increases the adhesion between silicon chain layers,which is beneficial to the interlayer stress transfer.This work proposes a method for preparing low-cost cemented rockfill from al-kali-activated gangue,which can be used for solid waste recycling and reducing cement consumption to achieve low-carbon goals.
基金financially supported by the National Natural Science Foundation of China(52063024 and 51868052)the Natural Science Foundation of Jiangxi Province(20192ACBL21046)the National Science Foundation of State Key Laboratory of Structural Chemistry(20160013).
文摘The degradation of organic pollutants in water is a critical environmental challenge.The iron-doped MoS_(2) catalysts have demonstrated potential in activating peroxymonosulfate(PMS)for environmental remediation,but they face challenges such as poor conductivity,limited electron transfer efficiency,and a scarcity of active sites.To address these issues,we successfully synthesized a nano-flowers FeS/MoS_(2) composite derived from polyoxometalates(NH_(4))_(3)[Fe(III)Mo_(6)O_(24)H_(6)]⋅6H_(2)O(denoted as FeMo6)as the bimetallic precursors.This synthesis strategy enhances the interaction between FeS and MoS_(2),thereby facilitating electron transfer.Notably,the introduction of sulfur vacancies in FeS/MoS_(2) exposes additional Mo4t active sites,promoting the redox cycle of Fe^(2+)/Fe^(3+) and accelerating the regeneration of Fe^(2+),which in turn enhances PMS activation.Therefore,a catalytic oxidation system of FeS/MoS_(2)/PMS is presented that primarily relies on SO_(4)^(⋅-)and⋅OH,with ^(1)O_(2) as a supplementary oxidant.This system exhibits exceptional degradation efficiency for p-chlorophenol(4-CP),achieving 100% degradation within 10 min over a wide pH range of 2.4–8.4.The robust performance and wide applicability of FeS/MoS_(2) catalyst make it a promising candidate in advanced oxidation processes(AOPs)for environmental remediation.
文摘BACKGROUND:Urokinase-type plasminogen activator(uPA) and urokinase-type plasminogen activator receptor(uPAR) are known as important factors,which mediate a variety of functions in terms of vascular homeostasis,inflammation and tissue repair.However,their role in systemic inflammatory response syndrome(SIRS) has been less well studied.This study aimed to test the hypothesis that the abnormalities of fibrinolysis and degradation of extracellular matrix mediated by uPA and uPAR are directly related to the patients with SIRS.We therefore analyzed their role and clinicopathological significance in patients with SIRS.METHODS:A case-control study was conducted with 85 patients who were divided into two groups according to the diagnostic criteria of SIRS:SIRS group(n=50) and non-SIRS group(/7=35).The SIRS group was divided into MODS group(n=26) and non-MODS group(n=24) by their severity,and survival group(n=35) and non-survival group(n=15) by their prognosis.Another 30 healthy adults served as normal controls.uPA and uPAR in plasma were detected by commercial enzyme-linked immunosorbent assay(ELISA) kits.RESULTS:The plasma level of uPA was lower in the SIRS group than in the non-SIRS group and controls(P<0.001 and P<0.001).It was lower in sepsis patients and the MODS group than in the non-sepsis patients and the non-MODS patients(all P<0.05).However,there was no difference in uPA level between survivors and non-survivors(P>0.05).The plasma level of uPAR increased in the SIRS group compared with the non-SIRS group and controls(P<0.001 and P<0.001).There was a significant elevation of uPAR in sepsis patients,MODS patients and non-survivors as compared with non-sepsis patients,non-MODS patients and survivors respectively(all P<0.05).Plasma uPAR levels were positively correlated with APACHE Ⅱ score(r=0.575,P<0.001) and SOFA score(r=0.349,P=0.013).AUCs for the prediction of SIRS mortality were 0.67 and 0.51,respectively,for uPA and uPAR.CONCLUSION:uPAR could be a predictor of poor outcome in patients with SIRS.
基金Supported by Natural Science Foundation of Ningxia(No.NZ10129)
文摘AIMTo investigate the role of tissue plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI) in proliferative diabetic retinopathy (PDR) and to discuss the correlations among t-PA, PAI and vascular endothelial growth factor (VEGF) expressions.
文摘Signal transducer and activator of transcription（STAT）is a unique protein family that binds to DNA,coupled with tyrosine phosphorylation signaling pathways,acting as a transcriptional regulator to mediate a variety of biological effects.Cerebral ischemia and reperfusion can activate STATs signaling pathway,but no studies have confirmed whether STAT activation can be verified by diffusion-weighted magnetic resonance imaging（DWI）in rats after cerebral ischemia/reperfusion.Here,we established a rat model of focal cerebral ischemia injury using the modified Longa method.DWI revealed hyperintensity in parts of the left hemisphere before reperfusion and a low apparent diffusion coefficient.STAT3 protein expression showed no significant change after reperfusion,but phosphorylated STAT3 expression began to increase after 30 minutes of reperfusion and peaked at 24 hours.Pearson correlation analysis showed that STAT3 activation was correlated positively with the relative apparent diffusion coefficient and negatively with the DWI abnormal signal area.These results indicate that DWI is a reliable representation of the infarct area and reflects STAT phosphorylation in rat brain following focal cerebral ischemia/reperfusion.
