Objective To evaluate the therapeutic effect with peter-williams intramedullary nail on children with humerus deformity due to osteogenesis imperfecta.Methods Data of 9 patients with humerus deformity due to osteogenesis imperfecta were retrospectively analyzed from Jun.2009 to Dec.2012.There were 7 males and 2 females,aged from 6 years to 10 years and 7 months(average 8 years and 3 months).There were 7 unilateral humerus deformity and 2 bilateral humerus deformity with severe radius and ulna deformity.The humerus fracture frequency was from 4 to 13 times (average,7.9 times)There were 2-3 deformity points in 9 patients (average 2.09 deformity points).The deformity angle ranged from 20°-100° (average 57.3°).The Constant-Murley scores were 16-24 scores (average 20.44).According to revised Sillence classifications,there were 6 cases of Type Ⅲ and 3 cases of Type Ⅳ.Eleven humerus of 9 patients were osteotomied and fixed with peter-williams intramedullary nail.Results All of 9 children were followed up for 12-66 months(average 22 months).The bone healing time were 8-12 weeks (average 9.5 weeks).Parents of 9 children were satisfied with surgical operation effect and deformity correction.The Constant-Murley scores ranged from preoperative average of (20.44 ± 2.79) points (16-24 points) to postoperative average of (35.56 ± 2.60) points(30-38 points) at the latest follow-up of patients,there was a statistically significant in score before and after treatment(t =0.20,P ＜0.05).Number 4 patient,one patient was found suffering from dorsal thumb numbness postoperatively after 3 days back stretching limitation.Considering the radial nerve stretching injury,treatment with neurotrophic drug for 3 months,symptoms disappeared.There was no infection,or osteomyelitis,no vascular damages.Epiphyseal plate injury or premature closure and affecting growth were not found in all of the patients at the latest follow-up examination.Conclusions Treatment with osteotomy and peter-williams intramedullary nail fixation on children with humerus deformity due to osteogenesis imperfecta is advantaged.It gets less damages,no intruding shoulder joint,less bleeding.The greatest degree of correction of the deformity can be achieved,and the shoulder joint function and the quality of life can be improved.

AIM: To investigate the potential inhibitory effect of pterostilbene on the endothelial-to-mesenchymal transition(EndMT)induced by high glucose conditions in human retinal microvascular endothelial cells(HRMECs).METHODS: The optimal concentration of pterostilbene for treating HRMECs was determined using the CCK-8 assay, with 12.5 and 25 μmol/L concentrations selected for subsequent experiments. Four experimental groups were established: control group, high glucose group, high glucose combined with 12.5 μmol/L pterostilbene treatment group, and high glucose combined with 25 μmol/L pterostilbene treatment group. The expression levels of HDAC7 and EndMT-associated markers were detected via Western blot analysis. Cell migration ability was assessed using Transwell migration assays and scratch wound healing tests, while vasculogenic capability was evaluated through tube formation assays.RESULTS: The CCK-8 assay revealed that pterostilbene at a concentration of 22.07 μmol/L inhibited 50% of cell viability in HRMECs. Western blot analysis demonstrated that compared with the control group, the expression levels of HDAC7, ZEB1, Vimentin, and Snail were significantly upregulated in HRMECs cultured in high glucose(all P<0.01), while the expressions of VE-cadherin and CD31 were significantly reduced(all P<0.01). Compared to the high glucose group, the treatment with 12.5 and 25 μmol/L pterostilbene significantly reduced the expression of HDAC7, ZEB1, Vimentin, and Snail under high glucose conditions(all P<0.01). Notably, 25 μmol/L pterostilbene enhanced the expression of VE-cadherin and CD31(all P<0.01). Scratch wound healing tests revealed that HRMECs treated with high glucose exhibited a significantly increased cell migration rate compared to the control group(P<0.05), while the application of 25 μmol/L pterostilbene significantly suppressed HRMECs migration under high glucose conditions(P<0.01). Transwell migration assays demonstrated that the cell migration rate in the high glucose group was significantly higher than that in the control group(P<0.01), with cell migration rate markedly reduced following treatment with both of 12.5 and 25 μmol/L pterostilbene(all P<0.01). The tube formation assay revealed that the ability of HRMECs to form tubular structures was significantly enhanced under high glucose conditions(P<0.01), and both 12.5 and 25 μmol/L of pterostilbene effectively inhibited this effect(all P<0.01).CONCLUSION: Pterostilbene can inhibit HDAC7 expression, suppress EndMT-mediated migration of HRMECs, and impair tube formation under high-glucose conditions.

AIM: To investigate the potential inhibitory effect of pterostilbene on the endothelial-to-mesenchymal transition(EndMT)induced by high glucose conditions in human retinal microvascular endothelial cells(HRMECs).METHODS: The optimal concentration of pterostilbene for treating HRMECs was determined using the CCK-8 assay, with 12.5 and 25 μmol/L concentrations selected for subsequent experiments. Four experimental groups were established: control group, high glucose group, high glucose combined with 12.5 μmol/L pterostilbene treatment group, and high glucose combined with 25 μmol/L pterostilbene treatment group. The expression levels of HDAC7 and EndMT-associated markers were detected via Western blot analysis. Cell migration ability was assessed using Transwell migration assays and scratch wound healing tests, while vasculogenic capability was evaluated through tube formation assays.RESULTS: The CCK-8 assay revealed that pterostilbene at a concentration of 22.07 μmol/L inhibited 50% of cell viability in HRMECs. Western blot analysis demonstrated that compared with the control group, the expression levels of HDAC7, ZEB1, Vimentin, and Snail were significantly upregulated in HRMECs cultured in high glucose(all P<0.01), while the expressions of VE-cadherin and CD31 were significantly reduced(all P<0.01). Compared to the high glucose group, the treatment with 12.5 and 25 μmol/L pterostilbene significantly reduced the expression of HDAC7, ZEB1, Vimentin, and Snail under high glucose conditions(all P<0.01). Notably, 25 μmol/L pterostilbene enhanced the expression of VE-cadherin and CD31(all P<0.01). Scratch wound healing tests revealed that HRMECs treated with high glucose exhibited a significantly increased cell migration rate compared to the control group(P<0.05), while the application of 25 μmol/L pterostilbene significantly suppressed HRMECs migration under high glucose conditions(P<0.01). Transwell migration assays demonstrated that the cell migration rate in the high glucose group was significantly higher than that in the control group(P<0.01), with cell migration rate markedly reduced following treatment with both of 12.5 and 25 μmol/L pterostilbene(all P<0.01). The tube formation assay revealed that the ability of HRMECs to form tubular structures was significantly enhanced under high glucose conditions(P<0.01), and both 12.5 and 25 μmol/L of pterostilbene effectively inhibited this effect(all P<0.01).CONCLUSION: Pterostilbene can inhibit HDAC7 expression, suppress EndMT-mediated migration of HRMECs, and impair tube formation under high-glucose conditions.