BACKGROUND: Different pretreatments of the tendon allograft for repairing hand tendon defect due to traumatic injuries have received much attention in the study of tissue engineering for hand surgeries.OBJECTIVE:To explore the characteristics of deep-frozen glutaraldehyde-treated tendon allograft for repairing hand tendon defect.DESIGN: A self-controlled study.SETTING:Ward of Orthopedic Department, Huizhou People's Central Hospital.PARTICIPANTS:Fifteen patients (aged 20-35 years) with 17 defected tendons were hospitalized in the Department of Orthopedics of Huizhou People's Central Hospital between January 1997 and August 2001. Among the 17 defected tendons, 8 were extensor tendons and 9 flexor tendons,with the length of defects varying from 2 to 9 cm.METHODS:The allogenic tendon grafts were obtained from young donors died in accidents or non-replantable amputated limbs due to traumatic injuries with informed consent obtained from the donors or their family members. These grafts were stored at -80 ℃ and immersed in 3.5 g/L glutaraldehyde solution before transplantation. Surgical operation was conducted following standard microsurgical procedures. According to the assessment criteria for total rang of motion (ROM) recommended by International Hand Surgery Association, the outcome of the surgically repaired hands was graded as excellent, good, acceptable and poor.MAIN OUTCOME MEASURES:Total ROM of the digits and graft rejection.RESULTS:None of the 15 patients was lost for analysis. The follow-up lasted for 8 months, during which 4 transplanted tendons had excellent, 6good, 4 acceptable and 3 poor functions, with a total effective rate of 82.36% (14/17). Neither cortical hormone nor immunosuppressants were used in these cases and no acute graft rejection or rupture of the tendons occurred.CONCLUSION: The antigenicity of the tendon allografts can be lowered after deep freezing of the grafts at -80 ℃ with preoperative glutaraldehyde treatment, which also increases the strength and tenacity of the tendons and decreases the risk for infection. The treated grafts provide a good alternative for autologous tendon graft but the complication of tendon adhesion still awaits to be tackled.

Objective To prepare the immunoconjugate composed of Adriamycin nanoparticles and VEGFR 2 monoclonal antibody(conjugate of ADM-NP and VEGFR 2-MAb) and study its pharmacokinetics property. Methods Adriamycin nanoparticles were prepared by using double emulsion method, with PLA and O-CMC as materials. Conjugate of ADM-NP and VEGFR 2-MAb was prepared by using molecule conjugate technology. Immunoreactivity of the conjugate with type IV collagenase and H 22 cell were analyzed by using ELISA. Pharmacokinetics parameters of the immunoconjugate were obtained by using SD rats as study objects. Results The prepared ADM-NP was sphere particles under SEM, which diameters were (160±34) nm. The drug loading rate and entrapment rate were (30.15±3.5)% and (80.56±4.24)% respectively. Conjugate of ADM-NP and VEGFR 2-MAb was successfully prepared, which had immunoreactivity with type IV collagenase and H 22 cell. The immunoconjugate showed good ADM control-release ability and could prolong the retention time of ADM in vivo. Conclusion Conjugate of ADM-NP and VEGFR 2-MAb keeps the immunoreactivity of VEGFR 2-MAb and shows good ADM control-release ability.

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: 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: 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.