The concentration preprocessing and fan-out(CPPF) system is one of the electronic subsystems of the upgraded Compact Muon Solenoid(CMS) Level-1 trigger system. It includes, in hardware, eight specially designed CPPF c...The concentration preprocessing and fan-out(CPPF) system is one of the electronic subsystems of the upgraded Compact Muon Solenoid(CMS) Level-1 trigger system. It includes, in hardware, eight specially designed CPPF cards, one CMS card called AMC13, one commercial Micro-TCA Carrier HUB(MCH) card, and a MicroTCA shelf. Powerful online software is needed for the system, including providing reliable configuration and monitoring for the hardware, and a graphical interface for executing all actions and publishing monitoring messages.Further, to control and monitor the large amount of homogeneous hardware, the SoftWare Automating conTrol of Common Hardware(SWATCH) concept was proposed and developed. The SWATCH provides a generic structure and is flexible for customization. The structure includes a hardware access library based on the IPbus protocol, which assumes a virtual 32-bit address/32-bit data bus and builds a simple hardware access layer. Furthermore, the structure provides a graphical user interface, which is based on modern web technology and is accessible by web page. The CPPF controlling and monitoring online software was also customized from a common SWATCH cell, and provides afinite state machine(FSM) for configuring the entire CPPF hardware, and five monitoring objects for periodically collecting monitoring data from five main functional modules in the CPPF hardware. This paper introduces the details of the CPPF SWATCH cell development.展开更多
Objective To investigate whether Tuina alleviates fibrotic symptoms in myofascial trigger points(MTrPs)by regulating transforming growth factor(TGF)-β1/Smad3 signaling pathway,thereby deactivating these points.Method...Objective To investigate whether Tuina alleviates fibrotic symptoms in myofascial trigger points(MTrPs)by regulating transforming growth factor(TGF)-β1/Smad3 signaling pathway,thereby deactivating these points.Methods This study comprised two experimental phases.In phase 1,27 specific pathogenfree(SPF)grade female Sprague-Dawley(SD)rats were randomized into three groups:control 1,model 1,and Tuina 1 groups.Model 1 and Tuina 1 groups underwent an 8-week MTrPs modeling protocol involving blunt impact and eccentric exercise.After successful modeling,rats in Tuina 1 group received manual pressing on nodules or cord-like taut bands on the medial aspect of the left hindlimb.Pain sensitivity and tissue stiffness were evaluated via pressure pain threshold(PPT)and soft tissue tension(STT).Muscle histopathology and fibrosis were observed using hematoxylin and eosin(HE)and Masson staining.Inflammatory factors in muscle were measured by enzyme-linked immunosorbent assay(ELISA),while immunofluorescence(IF)and Western blot(WB)were used to detect the expression levels ofα-smooth muscle actin(α-SMA),collagenⅢ,and TGF-β1.In phase 2,45 SPF female SD rats were randomized into five groups:control 2,model 2,Tuina 2,TGF-β1 inhibitor(TI),and Tuina+TGF-β1 agonist(Tuina+TA)groups.All groups except control 2 underwent standardized MTrPs modeling.Rats in Tuina 2 group received consistent pressing manipulation.TI group received intraperitoneal injections of oxymatrine,while Tuina+TA group received intraperitoneal injections of SRI-011381 hydrochloride followed by the same pressing protocol as Tuina 2 group.WB was used to detect the expression of collagen I,collagen III,TGF-β1,and phosphorylated-Smad3(p-Smad3)/Smad3.Results In phase 1,Tuina significantly improved PPT and STT in MTrPs of rats(P<0.01),reversed pathological damages including disorganized muscle fiber arrangement,abnormal myocyte morphology,and exacerbated fibrosis.In addition,in MTrPs of rats in model 1 group,expression levels of nuclear factor kappa-light-chain-enhancer of activated B cells(NF-κB),interleukin(IL)-1β,IL-6,tumor necrosis factor(TNF)-α,and fibrosis markers(α-SMA,collagen I,and collagen III)were upregulated,and all exhibited a significant downward trend after Tuina intervention(P<0.05 or P<0.01).This indicates that the therapeutic effects of Tuina are directly associated with reduced local inflammation and fibrosis in MTrPs.In phase 2,compared with model 2 group,rats in TI and Tuina 2 groups had decreased expression levels of TGF-β1 and p-Smad3/Smad3 in MTrPs,alongside reduced levels of inflammatory factors(IL-1β,IL-6,NF-κB,and TNF-α)and fibrosis markers(α-SMA,collagen I,and collagen III)(P<0.05 or P<0.01).When co-administered with TGF-β1 agonist,the therapeutic effects of Tuina were significantly attenuated,with rebounded TGF-β1 expression and p-Smad3/Smad3 in local MTrPs,and fibrosis and inflammatory responses were re-exacerbated(P<0.05 or P<0.01).Conclusion Tuina can effectively reduce inflammatory responses and fibrosis in MTrPs tissue,and its mechanism is closely related to the inhibition of the TGF-β1/Smad3 signaling pathway,which plays a critical role in Tuina-mediated regulation of MTrPs fibrosis.展开更多
Intracerebral hemorrhage(ICH)is a common severe emergency in neurosurgery,causing tremendous economic pressure on families and society and devastating effects on patients both physically and psychologically,especially...Intracerebral hemorrhage(ICH)is a common severe emergency in neurosurgery,causing tremendous economic pressure on families and society and devastating effects on patients both physically and psychologically,especially among patients with poor functional outcomes.ICH is often accompanied by decreased consciousness and limb dysfunction.This seriously affects patients’ability to live independently.Although rapid advances in neurosurgery have greatly improved patient survival,there remains insufficient evidence that surgical treatment significantly improves long-term outcomes.With in-depth pathophysiological studies after ICH,increasing evidence has shown that secondary injury after ICH is related to long-term prognosis and that the key to secondary injury is various immune-mediated neuroinflammatory reactions after ICH.In basic and clinical studies of various systemic inflammatory diseases,triggering receptor expressed on myeloid cells 1/2(TREM-1/2),and the TREM receptor family is closely related to the inflammatory response.Various inflammatory diseases can be upregulated and downregulated through receptor intervention.How the TREM receptor functions after ICH,the types of results from intervention,and whether the outcomes can improve secondary brain injury and the long-term prognosis of patients are unknown.An analysis of relevant research results from basic and clinical trials revealed that the inhibition of TREM-1 and the activation of TREM-2 can alleviate the neuroinflammatory immune response,significantly improve the long-term prognosis of neurological function in patients with cerebral hemorrhage,and thus improve the ability of patients to live independently.展开更多
基金supported by the National Natural Science Foundation of China(No.11435013)the National Key Program for S&T Research and Development(No.2016YFA0400104)
文摘The concentration preprocessing and fan-out(CPPF) system is one of the electronic subsystems of the upgraded Compact Muon Solenoid(CMS) Level-1 trigger system. It includes, in hardware, eight specially designed CPPF cards, one CMS card called AMC13, one commercial Micro-TCA Carrier HUB(MCH) card, and a MicroTCA shelf. Powerful online software is needed for the system, including providing reliable configuration and monitoring for the hardware, and a graphical interface for executing all actions and publishing monitoring messages.Further, to control and monitor the large amount of homogeneous hardware, the SoftWare Automating conTrol of Common Hardware(SWATCH) concept was proposed and developed. The SWATCH provides a generic structure and is flexible for customization. The structure includes a hardware access library based on the IPbus protocol, which assumes a virtual 32-bit address/32-bit data bus and builds a simple hardware access layer. Furthermore, the structure provides a graphical user interface, which is based on modern web technology and is accessible by web page. The CPPF controlling and monitoring online software was also customized from a common SWATCH cell, and provides afinite state machine(FSM) for configuring the entire CPPF hardware, and five monitoring objects for periodically collecting monitoring data from five main functional modules in the CPPF hardware. This paper introduces the details of the CPPF SWATCH cell development.
基金Natural Science Foundation of China(82274676 and 82374613)Program of Hunan Provincial Natural Science(2023JJ30458).
文摘Objective To investigate whether Tuina alleviates fibrotic symptoms in myofascial trigger points(MTrPs)by regulating transforming growth factor(TGF)-β1/Smad3 signaling pathway,thereby deactivating these points.Methods This study comprised two experimental phases.In phase 1,27 specific pathogenfree(SPF)grade female Sprague-Dawley(SD)rats were randomized into three groups:control 1,model 1,and Tuina 1 groups.Model 1 and Tuina 1 groups underwent an 8-week MTrPs modeling protocol involving blunt impact and eccentric exercise.After successful modeling,rats in Tuina 1 group received manual pressing on nodules or cord-like taut bands on the medial aspect of the left hindlimb.Pain sensitivity and tissue stiffness were evaluated via pressure pain threshold(PPT)and soft tissue tension(STT).Muscle histopathology and fibrosis were observed using hematoxylin and eosin(HE)and Masson staining.Inflammatory factors in muscle were measured by enzyme-linked immunosorbent assay(ELISA),while immunofluorescence(IF)and Western blot(WB)were used to detect the expression levels ofα-smooth muscle actin(α-SMA),collagenⅢ,and TGF-β1.In phase 2,45 SPF female SD rats were randomized into five groups:control 2,model 2,Tuina 2,TGF-β1 inhibitor(TI),and Tuina+TGF-β1 agonist(Tuina+TA)groups.All groups except control 2 underwent standardized MTrPs modeling.Rats in Tuina 2 group received consistent pressing manipulation.TI group received intraperitoneal injections of oxymatrine,while Tuina+TA group received intraperitoneal injections of SRI-011381 hydrochloride followed by the same pressing protocol as Tuina 2 group.WB was used to detect the expression of collagen I,collagen III,TGF-β1,and phosphorylated-Smad3(p-Smad3)/Smad3.Results In phase 1,Tuina significantly improved PPT and STT in MTrPs of rats(P<0.01),reversed pathological damages including disorganized muscle fiber arrangement,abnormal myocyte morphology,and exacerbated fibrosis.In addition,in MTrPs of rats in model 1 group,expression levels of nuclear factor kappa-light-chain-enhancer of activated B cells(NF-κB),interleukin(IL)-1β,IL-6,tumor necrosis factor(TNF)-α,and fibrosis markers(α-SMA,collagen I,and collagen III)were upregulated,and all exhibited a significant downward trend after Tuina intervention(P<0.05 or P<0.01).This indicates that the therapeutic effects of Tuina are directly associated with reduced local inflammation and fibrosis in MTrPs.In phase 2,compared with model 2 group,rats in TI and Tuina 2 groups had decreased expression levels of TGF-β1 and p-Smad3/Smad3 in MTrPs,alongside reduced levels of inflammatory factors(IL-1β,IL-6,NF-κB,and TNF-α)and fibrosis markers(α-SMA,collagen I,and collagen III)(P<0.05 or P<0.01).When co-administered with TGF-β1 agonist,the therapeutic effects of Tuina were significantly attenuated,with rebounded TGF-β1 expression and p-Smad3/Smad3 in local MTrPs,and fibrosis and inflammatory responses were re-exacerbated(P<0.05 or P<0.01).Conclusion Tuina can effectively reduce inflammatory responses and fibrosis in MTrPs tissue,and its mechanism is closely related to the inhibition of the TGF-β1/Smad3 signaling pathway,which plays a critical role in Tuina-mediated regulation of MTrPs fibrosis.
基金Supported by Shanxi Provincial Key Research and Development Plan Project,No.2020ZDLSF01-02Doctor Foundation of the Second Affiliated Hospital of Xi’an Medical University,No.X2Y-R11.
文摘Intracerebral hemorrhage(ICH)is a common severe emergency in neurosurgery,causing tremendous economic pressure on families and society and devastating effects on patients both physically and psychologically,especially among patients with poor functional outcomes.ICH is often accompanied by decreased consciousness and limb dysfunction.This seriously affects patients’ability to live independently.Although rapid advances in neurosurgery have greatly improved patient survival,there remains insufficient evidence that surgical treatment significantly improves long-term outcomes.With in-depth pathophysiological studies after ICH,increasing evidence has shown that secondary injury after ICH is related to long-term prognosis and that the key to secondary injury is various immune-mediated neuroinflammatory reactions after ICH.In basic and clinical studies of various systemic inflammatory diseases,triggering receptor expressed on myeloid cells 1/2(TREM-1/2),and the TREM receptor family is closely related to the inflammatory response.Various inflammatory diseases can be upregulated and downregulated through receptor intervention.How the TREM receptor functions after ICH,the types of results from intervention,and whether the outcomes can improve secondary brain injury and the long-term prognosis of patients are unknown.An analysis of relevant research results from basic and clinical trials revealed that the inhibition of TREM-1 and the activation of TREM-2 can alleviate the neuroinflammatory immune response,significantly improve the long-term prognosis of neurological function in patients with cerebral hemorrhage,and thus improve the ability of patients to live independently.
