Dear Editor,Two cases of primary angle-closure glaucoma(PACG)with persistent shallow anterior chamber after phacoemulsification,intraocular lens(IOL)implantation and goniosynechialysis(GSL)were presented.PACG,which ma...Dear Editor,Two cases of primary angle-closure glaucoma(PACG)with persistent shallow anterior chamber after phacoemulsification,intraocular lens(IOL)implantation and goniosynechialysis(GSL)were presented.PACG,which mainly presents with mechanical obstruction of the trabecular meshwork,is clinically characterized by elevated intraocular pressure(IOP)secondary to the apposition of peripheral iris or a synechial closure of the angle[1].A previous study reported that angle-closure glaucoma eyes experienced widening and deepening of anterior chamber angles following cataract extraction and IOL implantation,which could probably normalize the IOP[2].A randomized controlled trial demonstrated that in comparison with laser peripheral iridotomy(LPI),clear-lens extraction showed greater advantages in efficacy and cost-effectiveness and could be proposed as the first-line initial treatment for PACG[3].展开更多
Acute kidney injury(AKI) is a significant clinical complication with a substantial impact on morbidity and mortality, for which therapeutic options remain limited. The Hippo signaling pathway is an evolutionarily cons...Acute kidney injury(AKI) is a significant clinical complication with a substantial impact on morbidity and mortality, for which therapeutic options remain limited. The Hippo signaling pathway is an evolutionarily conserved pathway implicated in cell proliferation, dedifferentiation, and apoptosis via phosphorylation and inactivation of its downstream effectorsYes-associatedprotein(YAP)/transcriptional co-activator with PDZ-binding motif(TAZ). Recent studies have revealed that the Hippo pathway plays a pivotal role in the pathogenesis and repair of AKI. The Hippo pathway can mediate renal dysfunction through modulation of mitochondrial apoptosis under AKI conditions. Transient activation of YAP/TAZ in the acute phase of AKI may benefit renal recovery and regeneration, whereas persistent activation of YAP/TAZ in severe AKI may lead to maladaptive repair and transition to chronic kidney disease. This review aims to summarize recent findings on the associations between the Hippo pathway and AKI and to identify new therapeutic targets and strategies for AKI.展开更多
Background: Clarifying the mechanisms underlying vascular smooth muscle cell (VSMC) proliferation is important for the prevention and treatment of vascular remodeling and the reverse of hyperplastic lesions. Previo...Background: Clarifying the mechanisms underlying vascular smooth muscle cell (VSMC) proliferation is important for the prevention and treatment of vascular remodeling and the reverse of hyperplastic lesions. Previous research has shown that the gaseous signaling molecule sulfur dioxide (SO2) inhibits VSMC proliferation, but the mechanism for the inhibition of the angiotensin Ⅱ (Angll)-induced VSMC proliferation by SO, has not been fully elucidated. This study was designed to investigate if SO2 inhibited VSMC proliferation in mice with hypertension induced by Angll. Methods: Thirty-six male C57 mice were randomly divided into control, Angll, and Angll + SO2 groups. Mice in Angll group and Angl I + SO2 group received a capsule-type Angll pump implanted under the skin of the back at a slow-release dose of 1000 ng-kg^-1min In addition, mice in Angll + SO2 received intraperitoneal injections of SO., donor. Arterial blood pressure of tail artery was determined. The thickness of the aorta was measured by elastic fiber staining, and proliferating cell nuclear antigen (PCNA) and phosphorylated-extracellular signal-regulated kinase (P-ERK) were detected in aortic tissues. The concentration of SO~ in serum and aortic tissue homogenate supernatant was measured using high-performance liquid chromatography with fluorescence determination. In the in vio'o study, VSMC of A7R5 cell lines was divided into six groups: control, Angll, Angll + SO2 PD98059 (an inhibitor of ERK phosphorylation), Angll + PD98059, and Angll + SO, + PD98059. Expression of PCNA, ERK, and P-ERK was determined by Western blotting. Results: In animal experiment, compared with the control group, Angll markedly increased blood pressure (P 〈 0.01 ) and thickened the aortic wall in mice (P 〈 0.05) with an increase in the expression of PCNA (P 〈 0.05). SO2 however, reduced the systemic hypertension and the wall thickness induced by AnglI (P 〈 0.05). It inhibited the increased expression of PCNA and P-ERK induced by AnglI (P 〈 0.05). In cell experiment, PD98059, an ERK phosphorylation inhibitor, blocked the inhibitory effect of SO, on VSMC proliferation (P 〈 0.05). Conclusions: ERK signaling is involved in the mechanisms by which SO, inhibits VSMC proliferation in Angll-induced hypertensive mice via ERK signaling.展开更多
A non-precious metal catalyst CoMe]C for the oxygen reduction reaction is prepared by heat-treating a mechanical mixture of carbon black, melamine and cobalt chloride at 600 under nitrogen atmosphere for 2 h. The cata...A non-precious metal catalyst CoMe]C for the oxygen reduction reaction is prepared by heat-treating a mechanical mixture of carbon black, melamine and cobalt chloride at 600 under nitrogen atmosphere for 2 h. The catalytic activity of CoMe/C is characterized by the electrochemical linear sweep voltammetry technique. The onset reduction potential of the catalyst is 0.55 V (vs. SCE) at a scanning rate of 5 mV/s in 0.5 mol/L H2SO4 solution. The formation of the ORR activity sites of CoMe/C is facilitated by metallic β- cobalt.展开更多
基金Supported by National Natural Science Foundation of China(No.61634006)the National Key R&D Program of China(No.2020YFC2008200)the Beijing Science and Technology Plan Project(No.Z191100007619045)。
文摘Dear Editor,Two cases of primary angle-closure glaucoma(PACG)with persistent shallow anterior chamber after phacoemulsification,intraocular lens(IOL)implantation and goniosynechialysis(GSL)were presented.PACG,which mainly presents with mechanical obstruction of the trabecular meshwork,is clinically characterized by elevated intraocular pressure(IOP)secondary to the apposition of peripheral iris or a synechial closure of the angle[1].A previous study reported that angle-closure glaucoma eyes experienced widening and deepening of anterior chamber angles following cataract extraction and IOL implantation,which could probably normalize the IOP[2].A randomized controlled trial demonstrated that in comparison with laser peripheral iridotomy(LPI),clear-lens extraction showed greater advantages in efficacy and cost-effectiveness and could be proposed as the first-line initial treatment for PACG[3].
基金supported by the National Natural Science Foundation of China (82070718,81770712)Shanghai Science and Technology Innovation Natural Foundation(20ZR1444700)。
文摘Acute kidney injury(AKI) is a significant clinical complication with a substantial impact on morbidity and mortality, for which therapeutic options remain limited. The Hippo signaling pathway is an evolutionarily conserved pathway implicated in cell proliferation, dedifferentiation, and apoptosis via phosphorylation and inactivation of its downstream effectorsYes-associatedprotein(YAP)/transcriptional co-activator with PDZ-binding motif(TAZ). Recent studies have revealed that the Hippo pathway plays a pivotal role in the pathogenesis and repair of AKI. The Hippo pathway can mediate renal dysfunction through modulation of mitochondrial apoptosis under AKI conditions. Transient activation of YAP/TAZ in the acute phase of AKI may benefit renal recovery and regeneration, whereas persistent activation of YAP/TAZ in severe AKI may lead to maladaptive repair and transition to chronic kidney disease. This review aims to summarize recent findings on the associations between the Hippo pathway and AKI and to identify new therapeutic targets and strategies for AKI.
文摘Background: Clarifying the mechanisms underlying vascular smooth muscle cell (VSMC) proliferation is important for the prevention and treatment of vascular remodeling and the reverse of hyperplastic lesions. Previous research has shown that the gaseous signaling molecule sulfur dioxide (SO2) inhibits VSMC proliferation, but the mechanism for the inhibition of the angiotensin Ⅱ (Angll)-induced VSMC proliferation by SO, has not been fully elucidated. This study was designed to investigate if SO2 inhibited VSMC proliferation in mice with hypertension induced by Angll. Methods: Thirty-six male C57 mice were randomly divided into control, Angll, and Angll + SO2 groups. Mice in Angll group and Angl I + SO2 group received a capsule-type Angll pump implanted under the skin of the back at a slow-release dose of 1000 ng-kg^-1min In addition, mice in Angll + SO2 received intraperitoneal injections of SO., donor. Arterial blood pressure of tail artery was determined. The thickness of the aorta was measured by elastic fiber staining, and proliferating cell nuclear antigen (PCNA) and phosphorylated-extracellular signal-regulated kinase (P-ERK) were detected in aortic tissues. The concentration of SO~ in serum and aortic tissue homogenate supernatant was measured using high-performance liquid chromatography with fluorescence determination. In the in vio'o study, VSMC of A7R5 cell lines was divided into six groups: control, Angll, Angll + SO2 PD98059 (an inhibitor of ERK phosphorylation), Angll + PD98059, and Angll + SO, + PD98059. Expression of PCNA, ERK, and P-ERK was determined by Western blotting. Results: In animal experiment, compared with the control group, Angll markedly increased blood pressure (P 〈 0.01 ) and thickened the aortic wall in mice (P 〈 0.05) with an increase in the expression of PCNA (P 〈 0.05). SO2 however, reduced the systemic hypertension and the wall thickness induced by AnglI (P 〈 0.05). It inhibited the increased expression of PCNA and P-ERK induced by AnglI (P 〈 0.05). In cell experiment, PD98059, an ERK phosphorylation inhibitor, blocked the inhibitory effect of SO, on VSMC proliferation (P 〈 0.05). Conclusions: ERK signaling is involved in the mechanisms by which SO, inhibits VSMC proliferation in Angll-induced hypertensive mice via ERK signaling.
基金supported by the Fundamental Research Funds for the Central Universities (No. CDJXS12220002)the Specialized Research Fund for the Doctoral Program of Sichuan University of Science and Engineering (No. 2012RC16)+2 种基金the Opening Project of Key Laboratory of Green Catalysis of Sichuan Institutes of High Education (No. LYJ1206)the National Undergraduate Innovation Training Project (No. 1110611046)Discipline Construction Project of Sichuan University of Science and Engineering
文摘A non-precious metal catalyst CoMe]C for the oxygen reduction reaction is prepared by heat-treating a mechanical mixture of carbon black, melamine and cobalt chloride at 600 under nitrogen atmosphere for 2 h. The catalytic activity of CoMe/C is characterized by the electrochemical linear sweep voltammetry technique. The onset reduction potential of the catalyst is 0.55 V (vs. SCE) at a scanning rate of 5 mV/s in 0.5 mol/L H2SO4 solution. The formation of the ORR activity sites of CoMe/C is facilitated by metallic β- cobalt.