Objective:To evaluate anti-diabetic effect of Caulrpa kntillifera(C.lentillifera).Methods:The inhibitory effect of C.lentillifera extract on dipeptidyl peptidase-IV and a-glucosidase enzyme was measured in a cell free...Objective:To evaluate anti-diabetic effect of Caulrpa kntillifera(C.lentillifera).Methods:The inhibitory effect of C.lentillifera extract on dipeptidyl peptidase-IV and a-glucosidase enzyme was measured in a cell free system.Then,interleukin-1βand interferon-γinduced cell death and insulin secretion were measured in rat insulinoma(RIN)cells by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and ELISA kit,respectively.Glucose uptake and glucose transporter expression were measured by fluorometry and western blotting,using 3T3-Ll adipocytes.Results:C.lentillifera extract significantly decreased dipeptidyl peptidase-IV and a-glucosidase enzyme activities,and effectively inhibited cell death and iNOS expression in interleukin-1βand interfcron-γinduced RIK cells.Furthermore,C.lntillifera extract significantly enhanced insulin secretion in RTN cells and glucose transporter expression and glucose uptake in 3T3-L1adipocytes.Conclusions:Thus,our results suggest that C.lentillifera could be used as a potential antidiabetic agenl.展开更多
In the perifused fura-2 loaded exocrine pancreatic acinar cell line AR4-2J pulses of high potassium induced repetitive increases in intracellular calcium. Attached cells when stimulated with high potassium secreted la...In the perifused fura-2 loaded exocrine pancreatic acinar cell line AR4-2J pulses of high potassium induced repetitive increases in intracellular calcium. Attached cells when stimulated with high potassium secreted large amount of amylase. High potassium-induced secretion was dependent both on the concentration of potassium and duration of stimulation. High potassium induced increases in intracellular calcium were inhibited by voltage-dependent calcium channel antagonists with an order of potency as follows: nifedipine > ω-agatoxin IVA > ω-conotoxin GVIA. In contrast, the L-type calcium channel antagonist nifedipine almost completely inhibited potassium-induced amylase secretion, whereas the N-type channel antagonist ω-conotoxin GVIA was without effect. The P-type channel antagonist ω-agatoxin IVA had a small inhibitory effect, but this inhibition was not significant at the level of amylase secretion. In conclusion, the AR4-2J cell line possesses different voltage-dependent calcium channels (L, P,N) with the L-type predominantly involved in depolarization induced amylase secretion.展开更多
In this paper, a successfully studied and developed master - slave muld - microcomputers control system based on PC - BUS for hollow spindle fancy yarn spinning machine, mainly Its overall scheme, software and hardwar...In this paper, a successfully studied and developed master - slave muld - microcomputers control system based on PC - BUS for hollow spindle fancy yarn spinning machine, mainly Its overall scheme, software and hardware construction, is introduced. Spinning experiments show that the system achieves satisfactory result. This system can solve the diftkultles of mechatronical fusion between domestic hollow splndk fancy yarn spuming muchine and its microcomputer control technology.展开更多
OBJECTIVE To identify the role of GSK3 isoform inhibition on inflammasome activation.METHODS The NLRP3 inflammasome was activated by typical LPS/ATP and host-derived metabolites in primary mouse macrophages.The pharma...OBJECTIVE To identify the role of GSK3 isoform inhibition on inflammasome activation.METHODS The NLRP3 inflammasome was activated by typical LPS/ATP and host-derived metabolites in primary mouse macrophages.The pharmacological inhibition of GSK3 isoforms on inflammasome activation was assayed by quantifying IL-1βin the supernatant,and activated caspase-1in cell lysates using highly selective inhibitors.Further molecular mechanisms were investigated by protein pulldown assay,confocal imaging using forced gene expression system and endogenous protein tagged mouse macrophages.RESULTS Pharmacological inhibition of GSK3-β,but not GSK3-αisoform suppressed NLRP3 inflammasome activation in response to ATP,urate crystal and the microbial alkaloid toxin staurosporine.GSK3-βinhibition did not inhibit melanoma 2(AIM2)inflammasome activation in response to double-stranded DNA(dsDNA)and did not affect non-canonical caspase-11 inflammasome activation.GSK3-βinhibition suppressed high glucose mediated NLRP3 inflammasome activation.Mechanistically,GSK3-βinhibition blocked NLRP3 inflammasome by preventing pro IL-1βtranscription,reducing caspase-1 activation and ASC speck formation.GSK3-βinhibition blocked NLRP3 inflammasome activation without affecting the level of reactive oxygen species(ROS)which is a crucial component in initialing inflammasome activation.Further studies revealed that GSK3-βdirectly binds to ASC by both co-forced expression and endogenous protein level.Interestingly,we found ASC can be glycosylated in response to inflammasome activation,and GSK3-βinhibition reduced ASC glycosylation.Consistently,the O-Glc NAc transferase(OGT)deficient mouse macrophages showed the significant reduction of mature IL-1βsecretion in response to NLRP3 inflammasome activation.CONCLUSION Our results demonstrate a critical role of metabolism-sensing GSK3-βpathway in mediating NLRP3 inflammasome activation,thus defining a new therapeutic target for sterile inflammation.展开更多
Death due to scorpion envenoming syndrome is a common event in tropical and subtropical countries. Severe scorpion envenoming causes autonomic storm, massive release of catecholamines, counter-regulatory hormones, sup...Death due to scorpion envenoming syndrome is a common event in tropical and subtropical countries. Severe scorpion envenoming causes autonomic storm, massive release of catecholamines, counter-regulatory hormones, suppressed insulin/hyperinsulinemia, acute myocarditis, hyperglycemia, increased free fatty Acid levels, acute pancreatitis, disseminated intra-vascular coagulation, acute pulmonary oedema and death. Severe scorpion envenoming causes cardiac sarcolemmal defects displayed by alterations in Na+ - K+ ATPase, Mg++ ATPase and Ca2+ ATPase activities, inhibition of erythrocyte Na+ - K+ ATPase activities, hyperkalemia and may result in death. Based on our animal experiments in which insulin administration reversed the metabolic and ECG changes induced by scorpion envenoming and treating the poisonous scorpion sting victims with insulin, we consider that insulin has a primary metabolic role in preventing and reversing acute myocarditis, the cardiovascular, haemodynamic, and neurological manifestations and pulmonary oedema induced by scorpion envenoming. Administration of insulin-glucose infusion to scorpion sting victims appears to be the physiological basis for the control of the metabolic response when that has become a determinant to survival. Continuous infusion of regular crystalline insulin should be given at the rate of 0.3 U/g glucose and glucose at the rate of 0.1 g/kg body weight/hour, for 48 - 72 hours, with supplementation of potassium as needed and maintenance of fluid, electrolytes and acid-base balance. The observation of cardiac sarcolemmal defects and physiological basis of various patho-physiological mechanisms involved in the genesis of scorpion envenoming syndrome and its reversal (in the experimental animals and scorpion sting victims) by administration of insulin are reviewed.展开更多
We address the cryptographic topic of proxy re-encryption （PRE）, which is a special public-key cryptosystem. A PRE scheme allows a special entity, known as the proxy, to transform a message encrypted with the public...We address the cryptographic topic of proxy re-encryption （PRE）, which is a special public-key cryptosystem. A PRE scheme allows a special entity, known as the proxy, to transform a message encrypted with the public key of a delegator （say Alice）, into a new ciphertext that is protected under the public key of a delegatee （say Bob）, and thus the same message can then be recovered with Bob＇s private key. In this paper, in the identity-based setting, we first investigate the relationship between so called mediated encryption and unidirectional PRE. We provide a general framework which converts any secure identity-based unidirectional PRE scheme into a secure identity-based mediated encryption scheme, and vice versa. Concerning the security for unidirectional PRE schemes, Ateniese et al. previously suggested an important property known as the master secret security, which requires that the coalition of the proxy and Bob cannot expose Alice＇s private key. In this paper, we extend the notion to the identity-based setting, and present an identity-based unidirectional PRE scheme, which not only is provably secure against the chosen eiphertext attack in the standard model but also achieves the master secret security at the same time.展开更多
1,4-α-Glucan branching enzyme(GBE;EC 2.4.1.18),which plays an important role in starch modification,has been mostly expressed in Escherichia coli.The application of GBE in food industry is limited by the low yield of...1,4-α-Glucan branching enzyme(GBE;EC 2.4.1.18),which plays an important role in starch modification,has been mostly expressed in Escherichia coli.The application of GBE in food industry is limited by the low yield of enzyme and production of endotoxins in E.coli.In this study,we first found that GBE from Geobacillus thermoglucosidans STB02(Gt-GBE)could be highly expressed in the Bacillus subtilis which is a food grade strain.The pathway of secretion was non-classical independent of signal peptides and was related to cell lysis.Bioinformatics analysis combined with site-directed mutagenesis was used to explore the influence of the N-terminal structure on its secretion.We found that the extracellular activity of Gt-GBE was increased about 17.29%and the secretion rate was also greatly improved through truncating the loop structure at the N-terminus.Besides,it was found that there was an optimal hydrophobicity,which increased the extracellular activity of Gt-GBE by 12.90%through the substitution of N-terminal amino acids with hydrophobic residues.In summary,we achieved high-efficiency non-classical secretion of Gt-GBE in B.subtilis and found an important role of the N-terminus in this secretion pathway,which provides a new perspective for improving the expression of proteins in B.subtilis.展开更多
基金Supported by the Ministry of Education.Science and Technology (Grant No.2012RTAL2009172)
文摘Objective:To evaluate anti-diabetic effect of Caulrpa kntillifera(C.lentillifera).Methods:The inhibitory effect of C.lentillifera extract on dipeptidyl peptidase-IV and a-glucosidase enzyme was measured in a cell free system.Then,interleukin-1βand interferon-γinduced cell death and insulin secretion were measured in rat insulinoma(RIN)cells by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and ELISA kit,respectively.Glucose uptake and glucose transporter expression were measured by fluorometry and western blotting,using 3T3-Ll adipocytes.Results:C.lentillifera extract significantly decreased dipeptidyl peptidase-IV and a-glucosidase enzyme activities,and effectively inhibited cell death and iNOS expression in interleukin-1βand interfcron-γinduced RIK cells.Furthermore,C.lntillifera extract significantly enhanced insulin secretion in RTN cells and glucose transporter expression and glucose uptake in 3T3-L1adipocytes.Conclusions:Thus,our results suggest that C.lentillifera could be used as a potential antidiabetic agenl.
文摘In the perifused fura-2 loaded exocrine pancreatic acinar cell line AR4-2J pulses of high potassium induced repetitive increases in intracellular calcium. Attached cells when stimulated with high potassium secreted large amount of amylase. High potassium-induced secretion was dependent both on the concentration of potassium and duration of stimulation. High potassium induced increases in intracellular calcium were inhibited by voltage-dependent calcium channel antagonists with an order of potency as follows: nifedipine > ω-agatoxin IVA > ω-conotoxin GVIA. In contrast, the L-type calcium channel antagonist nifedipine almost completely inhibited potassium-induced amylase secretion, whereas the N-type channel antagonist ω-conotoxin GVIA was without effect. The P-type channel antagonist ω-agatoxin IVA had a small inhibitory effect, but this inhibition was not significant at the level of amylase secretion. In conclusion, the AR4-2J cell line possesses different voltage-dependent calcium channels (L, P,N) with the L-type predominantly involved in depolarization induced amylase secretion.
文摘In this paper, a successfully studied and developed master - slave muld - microcomputers control system based on PC - BUS for hollow spindle fancy yarn spinning machine, mainly Its overall scheme, software and hardware construction, is introduced. Spinning experiments show that the system achieves satisfactory result. This system can solve the diftkultles of mechatronical fusion between domestic hollow splndk fancy yarn spuming muchine and its microcomputer control technology.
文摘OBJECTIVE To identify the role of GSK3 isoform inhibition on inflammasome activation.METHODS The NLRP3 inflammasome was activated by typical LPS/ATP and host-derived metabolites in primary mouse macrophages.The pharmacological inhibition of GSK3 isoforms on inflammasome activation was assayed by quantifying IL-1βin the supernatant,and activated caspase-1in cell lysates using highly selective inhibitors.Further molecular mechanisms were investigated by protein pulldown assay,confocal imaging using forced gene expression system and endogenous protein tagged mouse macrophages.RESULTS Pharmacological inhibition of GSK3-β,but not GSK3-αisoform suppressed NLRP3 inflammasome activation in response to ATP,urate crystal and the microbial alkaloid toxin staurosporine.GSK3-βinhibition did not inhibit melanoma 2(AIM2)inflammasome activation in response to double-stranded DNA(dsDNA)and did not affect non-canonical caspase-11 inflammasome activation.GSK3-βinhibition suppressed high glucose mediated NLRP3 inflammasome activation.Mechanistically,GSK3-βinhibition blocked NLRP3 inflammasome by preventing pro IL-1βtranscription,reducing caspase-1 activation and ASC speck formation.GSK3-βinhibition blocked NLRP3 inflammasome activation without affecting the level of reactive oxygen species(ROS)which is a crucial component in initialing inflammasome activation.Further studies revealed that GSK3-βdirectly binds to ASC by both co-forced expression and endogenous protein level.Interestingly,we found ASC can be glycosylated in response to inflammasome activation,and GSK3-βinhibition reduced ASC glycosylation.Consistently,the O-Glc NAc transferase(OGT)deficient mouse macrophages showed the significant reduction of mature IL-1βsecretion in response to NLRP3 inflammasome activation.CONCLUSION Our results demonstrate a critical role of metabolism-sensing GSK3-βpathway in mediating NLRP3 inflammasome activation,thus defining a new therapeutic target for sterile inflammation.
文摘Death due to scorpion envenoming syndrome is a common event in tropical and subtropical countries. Severe scorpion envenoming causes autonomic storm, massive release of catecholamines, counter-regulatory hormones, suppressed insulin/hyperinsulinemia, acute myocarditis, hyperglycemia, increased free fatty Acid levels, acute pancreatitis, disseminated intra-vascular coagulation, acute pulmonary oedema and death. Severe scorpion envenoming causes cardiac sarcolemmal defects displayed by alterations in Na+ - K+ ATPase, Mg++ ATPase and Ca2+ ATPase activities, inhibition of erythrocyte Na+ - K+ ATPase activities, hyperkalemia and may result in death. Based on our animal experiments in which insulin administration reversed the metabolic and ECG changes induced by scorpion envenoming and treating the poisonous scorpion sting victims with insulin, we consider that insulin has a primary metabolic role in preventing and reversing acute myocarditis, the cardiovascular, haemodynamic, and neurological manifestations and pulmonary oedema induced by scorpion envenoming. Administration of insulin-glucose infusion to scorpion sting victims appears to be the physiological basis for the control of the metabolic response when that has become a determinant to survival. Continuous infusion of regular crystalline insulin should be given at the rate of 0.3 U/g glucose and glucose at the rate of 0.1 g/kg body weight/hour, for 48 - 72 hours, with supplementation of potassium as needed and maintenance of fluid, electrolytes and acid-base balance. The observation of cardiac sarcolemmal defects and physiological basis of various patho-physiological mechanisms involved in the genesis of scorpion envenoming syndrome and its reversal (in the experimental animals and scorpion sting victims) by administration of insulin are reviewed.
基金partially supported by the National Natural Science Foundation of China under Grant No.60873229Shanghai Rising-Star Program under Grant No.09QA1403000the Office of Research,Singapore Management University
文摘We address the cryptographic topic of proxy re-encryption （PRE）, which is a special public-key cryptosystem. A PRE scheme allows a special entity, known as the proxy, to transform a message encrypted with the public key of a delegator （say Alice）, into a new ciphertext that is protected under the public key of a delegatee （say Bob）, and thus the same message can then be recovered with Bob＇s private key. In this paper, in the identity-based setting, we first investigate the relationship between so called mediated encryption and unidirectional PRE. We provide a general framework which converts any secure identity-based unidirectional PRE scheme into a secure identity-based mediated encryption scheme, and vice versa. Concerning the security for unidirectional PRE schemes, Ateniese et al. previously suggested an important property known as the master secret security, which requires that the coalition of the proxy and Bob cannot expose Alice＇s private key. In this paper, we extend the notion to the identity-based setting, and present an identity-based unidirectional PRE scheme, which not only is provably secure against the chosen eiphertext attack in the standard model but also achieves the master secret security at the same time.
基金This work was financially supported by National Key R&D Program of China(2021YFD2101001-2)the National Natural Science Foundation of China(No.31901628)+1 种基金the Fundamental Research Funds for the Central Universities(JUSRP121004)Science and Technology Support Program(Modern Agriculture)of Jiangsu Province(BE2022323).
文摘1,4-α-Glucan branching enzyme(GBE;EC 2.4.1.18),which plays an important role in starch modification,has been mostly expressed in Escherichia coli.The application of GBE in food industry is limited by the low yield of enzyme and production of endotoxins in E.coli.In this study,we first found that GBE from Geobacillus thermoglucosidans STB02(Gt-GBE)could be highly expressed in the Bacillus subtilis which is a food grade strain.The pathway of secretion was non-classical independent of signal peptides and was related to cell lysis.Bioinformatics analysis combined with site-directed mutagenesis was used to explore the influence of the N-terminal structure on its secretion.We found that the extracellular activity of Gt-GBE was increased about 17.29%and the secretion rate was also greatly improved through truncating the loop structure at the N-terminus.Besides,it was found that there was an optimal hydrophobicity,which increased the extracellular activity of Gt-GBE by 12.90%through the substitution of N-terminal amino acids with hydrophobic residues.In summary,we achieved high-efficiency non-classical secretion of Gt-GBE in B.subtilis and found an important role of the N-terminus in this secretion pathway,which provides a new perspective for improving the expression of proteins in B.subtilis.
