Objective To explore the effect of plasma-activated gas(PAG)in promoting wound healing.Methods The pro-healing effect of PAG was explored by testing the effectiveness of PAG in promoting cell proliferation and healing of infected wounds.Cell proliferation assay:five different cells(i.e.,HSF,IHSMC,WPMY-1,HaCaT,and HFF)in logarithmic growth phase were inoculated into culture plates.After the cells grew adherently to the wall,the different cells were each grouped experimentally using a suitable time gradient.After the cells were treated with PAG for different time,their activity was detected by CCK-8 method.Animal infected wound healing assay:a wound of about 1.5 cm × 1.5 cm in size was created on the back of SD rats with sterile tweezers and scissors,and then the wound was infected with P.Aeruginosa with A600nm=6.5.After the infection was completed,the wounds were treated with PAG at regular intervals,and the experiment groups were subdivided according to the different treatment durations.Wound healing photographs and changes in relative wound area were used as indicators of healing performance.Results Cell proliferation assay:PAG treatment was effective in promoting cell proliferation for a reasonable period of time,while overdose led to cell death.Therefore,the dose of cells treated with plasma activation gas was defined as=W/N(J/cell),where W is the work consumed by the activation gas device during the treatment process and N is the number of cells.The three indexes(starting dose,optimal dose and safe dose range)were used to characterize the proliferative effect of PAG.Animal infected wound healing assay:the experimental groups all showed accelerated wound healing,so the optimal treatment time was used to characterize the pro-healing effect of PAG.The sterilization mode played a primary role,with an optimal treatment time of 2 min,and the pro-healing mode played a secondary role.The treatment conditions with the best overall healing effect were 2 min for the sterilization mode and 1 min for the pro-healing mode.Conclusion PAG has the effect of promoting cell proliferation and infected wound healing,and indicators can be summarized to quantitatively describe its effect,which is conducive to further standardization of PAG research and clinical utility.

A 42-year-old male patient developed mild allergic symptoms after the use of cisatracurium besylate in laparoscopic left renal tumor resection,which was relieved by symptomatic treatment.When the drug was added again intraoperatively,the patient's blood pressure decreased sharply from 120/71 mmHg to 50/30 mmHg,and the airway resistance increased from 16 cmH2O to 38 cmH2O,and the patient developed typical signs of anaphylactic shock.After immediate intravenous injection of epinephrine,calcium chloride and other drugs,the patient's blood pressure rose to 95/57 mmHg,airway resistance decreased to 20 cmH2O,and vital signs tended to be stable.The Naranjo's Assessment Scale was used to evaluate and analyze the correlation of suspected drugs.The score was 9 points,indicating that the association between anaphylactic shock and cisatracurium besylate in this patient was judged to be"definitely related".This article suggests that cisatracurium besylate carries an allergic risk and should be used with caution,and the monitoring of vital signs and allergic reactions should be strengthened for early identification and timely treatment to ensure the safety of patients during the perioperative period.

A 42-year-old male patient developed mild allergic symptoms after the use of cisatracurium besylate in laparoscopic left renal tumor resection,which was relieved by symptomatic treatment.When the drug was added again intraoperatively,the patient's blood pressure decreased sharply from 120/71 mmHg to 50/30 mmHg,and the airway resistance increased from 16 cmH2O to 38 cmH2O,and the patient developed typical signs of anaphylactic shock.After immediate intravenous injection of epinephrine,calcium chloride and other drugs,the patient's blood pressure rose to 95/57 mmHg,airway resistance decreased to 20 cmH2O,and vital signs tended to be stable.The Naranjo's Assessment Scale was used to evaluate and analyze the correlation of suspected drugs.The score was 9 points,indicating that the association between anaphylactic shock and cisatracurium besylate in this patient was judged to be"definitely related".This article suggests that cisatracurium besylate carries an allergic risk and should be used with caution,and the monitoring of vital signs and allergic reactions should be strengthened for early identification and timely treatment to ensure the safety of patients during the perioperative period.

Objective: Neuronal apoptosis is considered to be a critical process in spinal cord injury (SCI). Despite growing evidence of the antiapoptotic, anti-inflammatory, and modulation of ischemic injury tolerance effects of extracellular ubiquitin (eUb), existing studies have paid less attention to the impact of eUb in neurological injury disorders, particularly in SCI. This study aimed to investigate whether eUb can play a protective role in neurons, both in vitro and in vivo, and explores the underlying mechanisms. Methods: By utilizing an oxygen glucose deprivation cellular model and a SCI rat model, we firstly investigated the therapeutic effects of eUb on SCI and further explored its effects on neuronal autophagy and mitochondria-dependent apoptosis-related indicators, as well as the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mechanical target of rapamycin (mTOR) signaling pathway. Results: In the SCI models both in vivo and in vitro, early intervention with eUb enhanced neuronal autophagy and inhibited mitochondrial apoptotic pathways, significantly mitigating SCI. Further studies had shown that this protective effect of eUb was mediated through its receptor, CXC chemokine receptor type 4 (CXCR4). Additionally, eUb-enhanced autophagy and antiapoptotic effects were possibly associated with inhibiting the PI3K/Akt/mTOR pathway. Conclusion In summary, the study demonstrates that early eUb intervention can enhance autophagy and inhibit mitochondrial apoptotic pathways via CXCR4, protecting neurons and promoting SCI repair.

Objective: Neuronal apoptosis is considered to be a critical process in spinal cord injury (SCI). Despite growing evidence of the antiapoptotic, anti-inflammatory, and modulation of ischemic injury tolerance effects of extracellular ubiquitin (eUb), existing studies have paid less attention to the impact of eUb in neurological injury disorders, particularly in SCI. This study aimed to investigate whether eUb can play a protective role in neurons, both in vitro and in vivo, and explores the underlying mechanisms. Methods: By utilizing an oxygen glucose deprivation cellular model and a SCI rat model, we firstly investigated the therapeutic effects of eUb on SCI and further explored its effects on neuronal autophagy and mitochondria-dependent apoptosis-related indicators, as well as the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mechanical target of rapamycin (mTOR) signaling pathway. Results: In the SCI models both in vivo and in vitro, early intervention with eUb enhanced neuronal autophagy and inhibited mitochondrial apoptotic pathways, significantly mitigating SCI. Further studies had shown that this protective effect of eUb was mediated through its receptor, CXC chemokine receptor type 4 (CXCR4). Additionally, eUb-enhanced autophagy and antiapoptotic effects were possibly associated with inhibiting the PI3K/Akt/mTOR pathway. Conclusion In summary, the study demonstrates that early eUb intervention can enhance autophagy and inhibit mitochondrial apoptotic pathways via CXCR4, protecting neurons and promoting SCI repair.

Objective This study aims to explore the correlation between the grade of testicular tissue damage and clinical features which is used to evaluate the viability of testicular tissue after the orchidopexy for testicular torsion.Methods We conducted a retrospective,multicenter analysis of pathological specimens obtained from patients who under-went unilateral orchiectomy due to testicular torsion.Tissue viability was reassessed by the Mikuz grading scale.The corre-lations among tissue viability,duration of torsion symptoms,the angle of torsion,preoperative Doppler ultrasound image and intraoperative testicular resuscitation methods were analyzed.Results Eighty-five pathological specimens were en-rolled from 4 medical centers.The age range was 18 years(IQR 14-33),with a median torsion angle of 480°(IQR 180°-1080°).The interval from the torsion onset to surgical intervention was 18 hours(IQR 9-84).In the subgroup analysis of different torsion durations,the distribution of Grade I injuries was as follows.The subgroup within 12 hours ac-counted for 37.5％.The subgroup between 12 to 24 hours accounted for 14.28％.And the subgroup between 24 to 48 hours ac-counted for 6.45％.The subgroup exceeding 48 hours only accounted for 3.13％.Four patients received orchiectomy due to pre-operative ultrasound image indicating necrosis,correlating with Mikuz grade 3 tissue damage.The decision was made based on the failure of color recovery of affected testis in 57 cases,revealing 12.28％with grade 1 and 35.89％with grade Ⅱ damage.Twenty-four cases were identified as an Arda score of 3,with 4.16％showing grade 1 and 20.83％showing grade Ⅱ Mikuz damage.The method of Arda's grading could be used to determine the vitality of testicular tissue more accurately compared to the post-resusci-tation color observation method(P=0.032).Conclusion Pathological reassessment provides a precise determination of tis-sue viability in the affected testis.In some instances,the testicular tissue damage can be found potentially reversible.

Objective: Neuronal apoptosis is considered to be a critical process in spinal cord injury (SCI). Despite growing evidence of the antiapoptotic, anti-inflammatory, and modulation of ischemic injury tolerance effects of extracellular ubiquitin (eUb), existing studies have paid less attention to the impact of eUb in neurological injury disorders, particularly in SCI. This study aimed to investigate whether eUb can play a protective role in neurons, both in vitro and in vivo, and explores the underlying mechanisms. Methods: By utilizing an oxygen glucose deprivation cellular model and a SCI rat model, we firstly investigated the therapeutic effects of eUb on SCI and further explored its effects on neuronal autophagy and mitochondria-dependent apoptosis-related indicators, as well as the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mechanical target of rapamycin (mTOR) signaling pathway. Results: In the SCI models both in vivo and in vitro, early intervention with eUb enhanced neuronal autophagy and inhibited mitochondrial apoptotic pathways, significantly mitigating SCI. Further studies had shown that this protective effect of eUb was mediated through its receptor, CXC chemokine receptor type 4 (CXCR4). Additionally, eUb-enhanced autophagy and antiapoptotic effects were possibly associated with inhibiting the PI3K/Akt/mTOR pathway. Conclusion In summary, the study demonstrates that early eUb intervention can enhance autophagy and inhibit mitochondrial apoptotic pathways via CXCR4, protecting neurons and promoting SCI repair.

Objective: Neuronal apoptosis is considered to be a critical process in spinal cord injury (SCI). Despite growing evidence of the antiapoptotic, anti-inflammatory, and modulation of ischemic injury tolerance effects of extracellular ubiquitin (eUb), existing studies have paid less attention to the impact of eUb in neurological injury disorders, particularly in SCI. This study aimed to investigate whether eUb can play a protective role in neurons, both in vitro and in vivo, and explores the underlying mechanisms. Methods: By utilizing an oxygen glucose deprivation cellular model and a SCI rat model, we firstly investigated the therapeutic effects of eUb on SCI and further explored its effects on neuronal autophagy and mitochondria-dependent apoptosis-related indicators, as well as the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mechanical target of rapamycin (mTOR) signaling pathway. Results: In the SCI models both in vivo and in vitro, early intervention with eUb enhanced neuronal autophagy and inhibited mitochondrial apoptotic pathways, significantly mitigating SCI. Further studies had shown that this protective effect of eUb was mediated through its receptor, CXC chemokine receptor type 4 (CXCR4). Additionally, eUb-enhanced autophagy and antiapoptotic effects were possibly associated with inhibiting the PI3K/Akt/mTOR pathway. Conclusion In summary, the study demonstrates that early eUb intervention can enhance autophagy and inhibit mitochondrial apoptotic pathways via CXCR4, protecting neurons and promoting SCI repair.

Objective To explore the effect of plasma-activated gas(PAG)in promoting wound healing.Methods The pro-healing effect of PAG was explored by testing the effectiveness of PAG in promoting cell proliferation and healing of infected wounds.Cell proliferation assay:five different cells(i.e.,HSF,IHSMC,WPMY-1,HaCaT,and HFF)in logarithmic growth phase were inoculated into culture plates.After the cells grew adherently to the wall,the different cells were each grouped experimentally using a suitable time gradient.After the cells were treated with PAG for different time,their activity was detected by CCK-8 method.Animal infected wound healing assay:a wound of about 1.5 cm × 1.5 cm in size was created on the back of SD rats with sterile tweezers and scissors,and then the wound was infected with P.Aeruginosa with A600nm=6.5.After the infection was completed,the wounds were treated with PAG at regular intervals,and the experiment groups were subdivided according to the different treatment durations.Wound healing photographs and changes in relative wound area were used as indicators of healing performance.Results Cell proliferation assay:PAG treatment was effective in promoting cell proliferation for a reasonable period of time,while overdose led to cell death.Therefore,the dose of cells treated with plasma activation gas was defined as=W/N(J/cell),where W is the work consumed by the activation gas device during the treatment process and N is the number of cells.The three indexes(starting dose,optimal dose and safe dose range)were used to characterize the proliferative effect of PAG.Animal infected wound healing assay:the experimental groups all showed accelerated wound healing,so the optimal treatment time was used to characterize the pro-healing effect of PAG.The sterilization mode played a primary role,with an optimal treatment time of 2 min,and the pro-healing mode played a secondary role.The treatment conditions with the best overall healing effect were 2 min for the sterilization mode and 1 min for the pro-healing mode.Conclusion PAG has the effect of promoting cell proliferation and infected wound healing,and indicators can be summarized to quantitatively describe its effect,which is conducive to further standardization of PAG research and clinical utility.

Objective: Neuronal apoptosis is considered to be a critical process in spinal cord injury (SCI). Despite growing evidence of the antiapoptotic, anti-inflammatory, and modulation of ischemic injury tolerance effects of extracellular ubiquitin (eUb), existing studies have paid less attention to the impact of eUb in neurological injury disorders, particularly in SCI. This study aimed to investigate whether eUb can play a protective role in neurons, both in vitro and in vivo, and explores the underlying mechanisms. Methods: By utilizing an oxygen glucose deprivation cellular model and a SCI rat model, we firstly investigated the therapeutic effects of eUb on SCI and further explored its effects on neuronal autophagy and mitochondria-dependent apoptosis-related indicators, as well as the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mechanical target of rapamycin (mTOR) signaling pathway. Results: In the SCI models both in vivo and in vitro, early intervention with eUb enhanced neuronal autophagy and inhibited mitochondrial apoptotic pathways, significantly mitigating SCI. Further studies had shown that this protective effect of eUb was mediated through its receptor, CXC chemokine receptor type 4 (CXCR4). Additionally, eUb-enhanced autophagy and antiapoptotic effects were possibly associated with inhibiting the PI3K/Akt/mTOR pathway. Conclusion In summary, the study demonstrates that early eUb intervention can enhance autophagy and inhibit mitochondrial apoptotic pathways via CXCR4, protecting neurons and promoting SCI repair.