A novel siphon-based divide-and-conquer(SbDaC)policy is presented in this paper for the synthesis of Petri net(PN)based liveness-enforcing supervisors(LES)for flexible manufacturing systems(FMS)prone to deadlocks or l...A novel siphon-based divide-and-conquer(SbDaC)policy is presented in this paper for the synthesis of Petri net(PN)based liveness-enforcing supervisors(LES)for flexible manufacturing systems(FMS)prone to deadlocks or livelocks.The proposed method takes an uncontrolled and bounded PN model(UPNM)of the FMS.Firstly,the reduced PNM(RPNM)is obtained from the UPNM by using PN reduction rules to reduce the computation burden.Then,the set of strict minimal siphons(SMSs)of the RPNM is computed.Next,the complementary set of SMSs is computed from the set of SMSs.By the union of these two sets,the superset of SMSs is computed.Finally,the set of subnets of the RPNM is obtained by applying the PN reduction rules to the superset of SMSs.All these subnets suffer from deadlocks.These subnets are then ordered from the smallest one to the largest one based on a criterion.To enforce liveness on these subnets,a set of control places(CPs)is computed starting from the smallest subnet to the largest one.Once all subnets are live,this process provides the LES,consisting of a set of CPs to be used for the UPNM.The live controlled PN model(CPNM)is constructed by merging the LES with the UPNM.The SbDaC policy is applicable to all classes of PNs related to FMS prone to deadlocks or livelocks.Several FMS examples are considered from the literature to highlight the applicability of the SbDaC policy.In particular,three examples are utilized to emphasize the importance,applicability and effectiveness of the SbDaC policy to realistic FMS with very large state spaces.展开更多
Neutrophil extracellular traps(NETs)have emerged as key mediators of cardiovascular diseases(CVDs),linking innate immune activation to vascular injury,thrombosis,and maladaptive remodeling.This review synthesizes rece...Neutrophil extracellular traps(NETs)have emerged as key mediators of cardiovascular diseases(CVDs),linking innate immune activation to vascular injury,thrombosis,and maladaptive remodeling.This review synthesizes recent insights into the molecular and cellular pathways driving NET formation,including post-translational modifications,metabolic reprogramming,inflammasome signaling,and autophagy.It highlights the role of NETs in atherosclerosis,thrombosis,myocardial ischemia-reperfusion injury,and hypertension,emphasizing common control points such as peptidylarginine deiminase 4(PAD4)-dependent histone citrullination and nicotinamide adenine dinucleotide phosphate oxidases 2(NOX2)-mediated oxidative stress.Mechanistic interpretation of circulating biomarkers,includingmyeloperoxidase(MPO)-DNA complexes,citrullinated histoneH3,and cell-free DNA,provides a translational bridge between NET biology and patient stratification.Therapeutic strategies targeting NETs are examined through three main approaches:inhibition of NET initiation,enhancement of chromatin clearance,and neutralization of toxic extracellular components,with attention to both established and emerging interventions.In contrast to previous reviews,this study highlights the novelty of a mechano-therapeutic framework by providing a mechanistic roadmap linking NET formation pathways to therapeutic targeting in cardiovascular disease.Moving forward,integrating mechanistic information with biomarker discovery,precision profiling,and targeted therapies offers innovative strategies to reduce vascular inflammation and improve outcomes in cardiovascular disease.展开更多
基金The authors extend their appreciation to King Saud University,Saudi Arabia for funding this work through the Ongoing Research Funding Program(ORF-2025-704),King Saud University,Riyadh,Saudi Arabia.
文摘A novel siphon-based divide-and-conquer(SbDaC)policy is presented in this paper for the synthesis of Petri net(PN)based liveness-enforcing supervisors(LES)for flexible manufacturing systems(FMS)prone to deadlocks or livelocks.The proposed method takes an uncontrolled and bounded PN model(UPNM)of the FMS.Firstly,the reduced PNM(RPNM)is obtained from the UPNM by using PN reduction rules to reduce the computation burden.Then,the set of strict minimal siphons(SMSs)of the RPNM is computed.Next,the complementary set of SMSs is computed from the set of SMSs.By the union of these two sets,the superset of SMSs is computed.Finally,the set of subnets of the RPNM is obtained by applying the PN reduction rules to the superset of SMSs.All these subnets suffer from deadlocks.These subnets are then ordered from the smallest one to the largest one based on a criterion.To enforce liveness on these subnets,a set of control places(CPs)is computed starting from the smallest subnet to the largest one.Once all subnets are live,this process provides the LES,consisting of a set of CPs to be used for the UPNM.The live controlled PN model(CPNM)is constructed by merging the LES with the UPNM.The SbDaC policy is applicable to all classes of PNs related to FMS prone to deadlocks or livelocks.Several FMS examples are considered from the literature to highlight the applicability of the SbDaC policy.In particular,three examples are utilized to emphasize the importance,applicability and effectiveness of the SbDaC policy to realistic FMS with very large state spaces.
文摘Neutrophil extracellular traps(NETs)have emerged as key mediators of cardiovascular diseases(CVDs),linking innate immune activation to vascular injury,thrombosis,and maladaptive remodeling.This review synthesizes recent insights into the molecular and cellular pathways driving NET formation,including post-translational modifications,metabolic reprogramming,inflammasome signaling,and autophagy.It highlights the role of NETs in atherosclerosis,thrombosis,myocardial ischemia-reperfusion injury,and hypertension,emphasizing common control points such as peptidylarginine deiminase 4(PAD4)-dependent histone citrullination and nicotinamide adenine dinucleotide phosphate oxidases 2(NOX2)-mediated oxidative stress.Mechanistic interpretation of circulating biomarkers,includingmyeloperoxidase(MPO)-DNA complexes,citrullinated histoneH3,and cell-free DNA,provides a translational bridge between NET biology and patient stratification.Therapeutic strategies targeting NETs are examined through three main approaches:inhibition of NET initiation,enhancement of chromatin clearance,and neutralization of toxic extracellular components,with attention to both established and emerging interventions.In contrast to previous reviews,this study highlights the novelty of a mechano-therapeutic framework by providing a mechanistic roadmap linking NET formation pathways to therapeutic targeting in cardiovascular disease.Moving forward,integrating mechanistic information with biomarker discovery,precision profiling,and targeted therapies offers innovative strategies to reduce vascular inflammation and improve outcomes in cardiovascular disease.
