Objective:We aimed to develop a novel visualized model based on nomogram to predict postoperative overall survival.Methods:This was a multicenter, retrospective, observational cohort study, including participants with histologically confirmed gastric and colorectal cancer who underwent radical surgery from 11 medical centers in China from August 1, 2015 to June 30, 2018. Baseline characteristics, histopathological data and nutritional status, as assessed using Nutrition Risk Screening 2002 (NRS 2002) score and the scored Patient-Generated Subjective Global Assessment, were collected. The least absolute shrinkage and selection operator regression and Cox regression were used to identify variables to be included in the predictive model. Internal and external validations were performed.Results:There were 681 and 127 patients in the training and validation cohorts, respectively. A total of 188 deaths were observed over a median follow-up period of 59 (range: 58 to 60) months. Two independent predictors of NRS 2002 and Tumor-Node-Metastasis (TNM) stage were identified and incorporated into the prediction nomogram model together with the factor of age. The model's concordance index for 1-, 3- and 5-year overall survival was 0.696, 0.724, and 0.738 in the training cohort and 0.801, 0.812, and 0.793 in the validation cohort, respectively.Conclusions:In this study, a new nomogram prediction model based on NRS 2002 score was developed and validated for predicting the overall postoperative survival of patients with gastric colorectal cancer. This model has good differentiation, calibration and clinical practicability in predicting the long-term survival rate of patients with gastrointestinal cancer after radical surgery.

Objective:To compare the resting energy expenditure(REE)characteristics among young men with different body mass indexes(BMI).Methods:Thirty young men[average age was(26.93± 4.16)years]were enrolled in this study.They underwent resting metabolism tests in the Department of Sports Medicine of Peking University Third Hospital from December 2017 to June 2021.The resting meta-bolic rate(RMR)was measured by indirect calorimetry,the body composition was measured by bioresis-tance antibody component analyzer.The REE characteristics were analyzed,and 11 predictive equations were used to estimate RMR and compared with the measured value.The differences were analyzed by paired t-test and intra-class correlation coefficient(ICC).Results:The RMR of the overall 30 young men was(1 960.17±463.11)kcal/d(1 kcal=4.186 8 kJ).Including(1 744.33±249.62)kcal/d in those with normal BMI,which was significantly lower than that in those who were overweight or obese[(2 104.06±520.32)kcal/d,P＜0.01],but the weight-corrected RMR in those with normal BMI was significantly higher than that in those who were overweight or obese[(24.02±2.61)kcal/(kg·d)vs.(19.98±4.38)kcal/(kg·d),P＜0.01].The RMR was significantly and positively correlated with body weight,adiposity,lean body mass,body surface area,and extracellular fluid in the subjects with diffe-rent BMI(all P＜0.05).The predicted values of the 11 prediction equations were not in good agreement with the measured values(all ICC＜0.75),with relatively high agreement between the pre-dicted and measured values of the World Health Organization(WHO)equation in overweight obese young men(ICC=0.547,P＜0.01).Conclusion:There were significant differences in RMR among young men with different BMI,and the RMR after weight correction should be considered for those who were overweight or obese.The consistency between the predicted values of different prediction equations and the actual measured values of RMR was relatively poor,and it is recommended to accurately measure RMR by indirect calorimetry.For overweight or obese young men,the WHO prediction equation can be considered to calculate RMR,but it is necessary to establish an RMR prediction equation applicable to different BMI populations.

Objective:To investigate the influence of all-trans-retinoic acid (ATRA) on the proliferation and invasion of osteosarcoma 143B cells and its possible regulatory mechanism.Methods:Different concentrations of ATRA were used to treat human osteosarcoma 143B cells, and the optimal concentration and treatment time those affected cell proliferation were selected. The MTS method, Transwell migration and invasion experiments were used to detect the changes in the proliferation, migration and invasion of 143B cells after ATRA treatment. The real-time quantitative polymerase chain reaction (qRT-PCR) and Western blot were used to detect the expression changes of miRNA-34a (miR-34a), E2F1 and Eag1 in osteosarcoma 143B cells after ATRA treatment. Then miR-34a was interfered and E2F1 was overexpressed, and the abilities of cell proliferation, invasion and migration abilities as well as the expression changes of miR-34a, E2F1 and Eag1 in 143B cells were detected.Results:The proliferation inhibition of 143B cells was most obvious when 143B cells were treated with 10 μmol/L ATRA for 72 h. The cell migration and invasion numbers when 143B cells were treated with 10 μmol/L ATRA for 72 h were lower than those in the negative control group [(73±3) cells vs. (182±5) cells, t = 21.46, P<0.01; (94±3) cells vs. (203±7) cells, t = 13.70, P<0.01]. 10 μmol/L ATRA could promote the expression of miR-34a in 143B cells and inhibit the expressions of Eag1 and E2F1 (all P<0.01). Compared with ATRA group, the ability of cell proliferation in ATRA+miR-34a interference group was restored after 72 h of treatment [cell survival rate (41.0±2.2)% vs. (25.0±3.6)%, t = 108.68, P<0.01]. Compared with ATRA group, the abilities of cell migration and invasion in ATRA+miR-34a interference group were restored [(122±14) cells vs. (64±10) cells, t = 21.06, P<0.01; (103±10) cells vs. (59±8) cells, t = 24.27, P<0.01), and the mRNA and protein expressions of Eag1 and E2F1 in cells were promoted (both P<0.01). Compared with ATRA group, the ability of cell proliferation in ATRA+E2F1 overexpression group was restored [cell survival rate (40.0±3.4)% vs. (24.0±3.1)%, t = 108.74, P<0.01]; the abilities of cell migration and invasion in ATRA+E2F1 overexpression group were restored [(78±12) cells vs. (29±8) cells, t = 13.52, P<0.01; (75±12) cells vs. (49±10) cells, t = 6.28, P<0.01], and the mRNA and protein expressions of Eag1 and E2F1 in cells were promoted (both P<0.01). Conclusion:ATRA inhibits the proliferation and invasion of osteosarcoma cells via regulating miR-34a-E2F1-Eag1 signaling pathway, and it may become one of the effective treatment drugs for osteosarcoma.

Objective:To identify whether splenectomy for treatment of hypersplenism has any impact on development of hepatocellular carcinoma(HCC) among patients with liver cirrhosis and hepatitis.Methods:Patients who underwent splenectomy for hypersplenism secondary to liver cirrhosis and portal hypertension between January 2008 and December 2012 were included from seven hospitals in China, whereas patients receiving medication treatments for liver cirrhosis and portal hypertension (non-splenectomy) at the same time period among the seven hospitals were included as control groups. In the splenectomy group, all the patients received open or laparoscopic splenectomy with or without pericardial devascularization. In contrast, patients in the control group were treated conservatively for liver cirrhosis and portal hypertension with medicines (non-splenectomy) with no invasive treatments, such as transjugular intrahepatic portosystemic shunt, splenectomy or liver transplantation before HCC development. All the patients were routinely screened for HCC development with abdominal ultrasound, liver function and alpha-fetoprotein every 3 to 6 months. To minimize the selection bias, propensity score matching (PSM) was used to match the baseline data of patients among splenectomy versus non-splenectomy groups. The Kaplan-Meier method was used to calculate the overall survival and cumulative incidence of HCC development, and the Log-rank test was used to compare the survival or disease rates between the two groups. Univariate and Cox proportional hazard regression models were used to analyze the potential risk factors associated with development of HCC.Results:A total of 871 patients with liver cirrhosis and hypertension were included synchronously from 7 tertiary hospitals. Among them, 407 patients had a history of splenectomy for hypersplenism (splenectomy group), whereas 464 patients who received medical treatment but not splenectomy (non-splenectomy group). After PSM,233 pairs of patients were matched in adjusted cohorts. The cumulative incidence of HCC diagnosis at 1,3,5 and 7 years were 1%,6%,7% and 15% in the splenectomy group, which was significantly lower than 1%,6%,15% and 23% in the non-splenectomy group ( HR=0.53,95% CI:0.31 to 0.91, P=0.028). On multivariable analysis, splenectomy was independently associated with decreased risk of HCC development ( HR=0.55, 95%CI:0.32 to 0.95, P=0.031). The cumulative survival rates of all the patients at 1,3,5,and 7 years were 100%,97%,91%,86% in the splenectomy group,which was similar with that of 100%,97%,92%,84% in the non-splenectomy group ( P=0.899). In total,49 patients (12.0%) among splenectomy group and 75 patients (16.2%) in non-splenectomy group developed HCC during the study period, respectively. Compared to patients in non-splenectomy group, patients who developed HCC after splenectomy were unlikely to receive curative resection for HCC (12.2% vs. 33.3%,χ2=7.029, P=0.008). Conclusion:Splenectomy for treatment of hypersplenism may decrease the risk of HCC development among patients with liver cirrhosis and portal hypertension.

Objective:To identify whether splenectomy for treatment of hypersplenism has any impact on development of hepatocellular carcinoma(HCC) among patients with liver cirrhosis and hepatitis.Methods:Patients who underwent splenectomy for hypersplenism secondary to liver cirrhosis and portal hypertension between January 2008 and December 2012 were included from seven hospitals in China, whereas patients receiving medication treatments for liver cirrhosis and portal hypertension (non-splenectomy) at the same time period among the seven hospitals were included as control groups. In the splenectomy group, all the patients received open or laparoscopic splenectomy with or without pericardial devascularization. In contrast, patients in the control group were treated conservatively for liver cirrhosis and portal hypertension with medicines (non-splenectomy) with no invasive treatments, such as transjugular intrahepatic portosystemic shunt, splenectomy or liver transplantation before HCC development. All the patients were routinely screened for HCC development with abdominal ultrasound, liver function and alpha-fetoprotein every 3 to 6 months. To minimize the selection bias, propensity score matching (PSM) was used to match the baseline data of patients among splenectomy versus non-splenectomy groups. The Kaplan-Meier method was used to calculate the overall survival and cumulative incidence of HCC development, and the Log-rank test was used to compare the survival or disease rates between the two groups. Univariate and Cox proportional hazard regression models were used to analyze the potential risk factors associated with development of HCC.Results:A total of 871 patients with liver cirrhosis and hypertension were included synchronously from 7 tertiary hospitals. Among them, 407 patients had a history of splenectomy for hypersplenism (splenectomy group), whereas 464 patients who received medical treatment but not splenectomy (non-splenectomy group). After PSM,233 pairs of patients were matched in adjusted cohorts. The cumulative incidence of HCC diagnosis at 1,3,5 and 7 years were 1%,6%,7% and 15% in the splenectomy group, which was significantly lower than 1%,6%,15% and 23% in the non-splenectomy group ( HR=0.53,95% CI:0.31 to 0.91, P=0.028). On multivariable analysis, splenectomy was independently associated with decreased risk of HCC development ( HR=0.55, 95%CI:0.32 to 0.95, P=0.031). The cumulative survival rates of all the patients at 1,3,5,and 7 years were 100%,97%,91%,86% in the splenectomy group,which was similar with that of 100%,97%,92%,84% in the non-splenectomy group ( P=0.899). In total,49 patients (12.0%) among splenectomy group and 75 patients (16.2%) in non-splenectomy group developed HCC during the study period, respectively. Compared to patients in non-splenectomy group, patients who developed HCC after splenectomy were unlikely to receive curative resection for HCC (12.2% vs. 33.3%,χ2=7.029, P=0.008). Conclusion:Splenectomy for treatment of hypersplenism may decrease the risk of HCC development among patients with liver cirrhosis and portal hypertension.

Objective:To investigate the antibacterial effect of iodophor on Staphylococcus aureus biofilm (BBF).Methods:Staphylococcus aureus were cultured in vitro and 480 pieces of titanium alloy plates were selected. On the surface of titanium plates, in vitro models of Staphylococcus aureus biofilms were established at days 7, 14, 21 and 28 respectively with 120 pieces of titanium plates at each time points. The biofilms at each time point were assigned to no iodophor immersion (PBS group), 5 g/L iodophor immersion for 5 minutes (5-min group) and 5 g/L iodophor immersion for 10 minutes (10-min group), according to the random number table method. FITC-ConA, propidium iodide (PI) and SYT09 were used to dye Staphylococcus aureus in PBS group. After dyeing, confocal laser scanning microscopy and scanning electron microscopy were used to observe the morphological structure of bacterial biofilms, and the Colony forming unit (CFU) was counted by the viable count method. In the other two groups, PI and SYT09 were applied to dye Staphylococcus aureus, and then confocal laser scanning microscopy and scanning electron microscopy were used to observe the changes of biofilms and bacterial viability after iodophor immersion. The antibacterial effect of iodophor was evaluated by the viable count method.Results:After dyeing Staphylococcus aureus with FITC-ConA and PI in PBS group, confocal laser scanning microscopy showed that the extracellular polymers of the bacteria increased gradually with the extension of culture time. The space structure of biofilm was gradually mature, changed significantly at day 21 and became mature at day 28. After staining Staphylococcus aureus with PI and SYT09 in PBS group, confocal laser scanning microscopy showed that the number of bacteria increased, and had a mountain-like shape. Scanning electron microscopy showed that the number of bacterial extracellular polymers increased gradually with the extension of culture time and a structured microenvironment was formed and gradually matured. In 5-min and 10-min groups, all bacteria were killed at days 7 and 14 [0(0, 0)CFU/ml], the antibacterial effect was weakened at 21 days, but the antibacterial effect of iodophor immersion in 10-min group [100 (100, 125)CFU/ml] was better than that in 5-min group [300 (275, 425)CFU/ml] ( P<0.05). There was no significant difference in iodophor immersion in 5-min group [500 (375, 700)CFU/ml] and 10-min group [250 (175, 400)CFU/ml] at 28 days ( P>0.05). Conclusions:The maturation of biofilm is the overall maturation of bacteria and bacterial extracellular polymers and the formation of a spatialized microenvironment. Bounded by the 21st day, biofilms are divided into young biofilms and mature biofilms. The main difference between them lies in the maturation of extracellular polymers and microenvironment. For the bacterial biofilm with culture time less than 21 days, the antibacterial effect of the iodophor immersion for 10 min is better than that of 5 min. However, for the bacterial biofilm with culture time greater than 21 days, there is no significant difference in the antibacterial effect of the bacterial biofilm of prolonged iodophor immersion time.

Objective: To detect the effect and regulatory mechanism of human ether à go-go related gene 1 (Herg 1) knockdown on the proliferation and invasion of osteosarcoma (OS). Methods: We constructed a recombinant adenovirus vector (Ad5-Herg1-shRNA) expressing short hair RNA (shRNA) against Herg1 and tested the knockdown efficiency. Then, the effects of Herg 1 knockdown on the proliferation, growth and invasion of osteosarcoma were measured by using cell counting kit-8 (CCK-8), wound healing assay, Transwell assay and xenograft model of nude mice, respectively. Tandem affinity purification, mass spectrometry and dual luciferase reporter assay were used to find out the molecules interacted with Herg1. Western blot was used to detect the expressions of large tumor suppressor gene (LATS1), p-LATS1, Yes-associated protein (YAP) and p-YAP in cells after infection of Ad5-Herg1-shRNA. Results: Compared to Ad5-control-shRNA, Ad5-Herg1-shRNA dramatically inhibited the expression of Herg1 in OS cells. The result of CCK8 array demonstrated that 143B cell vitalities of Ad5-Herg1-shRNA1 and Ad5-Herg1-shRNA2 group were (65.47±3.90)% and (79.90±1.52)%, significantly lower than (100.00±6.14)% of Ad5-control-shRNA group. Meanwhile, U2OS cell vitality of Ad5-Herg1-shRNA1 and Ad5-Herg1-shRNA2 group were (69.69±1.36)% and (76.72±2.75)%, significantly lower than (100.00±3.01)% of Ad5-control-shRNA group (all P<0.001). The results of wound healing array showed that 143B cell migration rates of Ad5-Herg1-shRNA1 and Ad5-Herg1-shRNA2 group were (33.03±2.88)% and (36.47±4.16)%, significantly lower than (97.78±2.28)% of Ad5-control-shRNA group. Meanwhile, U2OS cell migration rates of Ad5-Herg1-shRNA1 and Ad5-Herg1-shRNA2 group were (68.07±0.90)% and (73.97±1.25)%, significantly lower than (96.50±1.12)% of Ad5-control-shRNA group (all P<0.001). The results of Transwell showed that 143B cell invasion numbers of Ad5-Herg1-shRNA1 and Ad5-Herg1-shRNA2 group were 36.50±12.15 and 44.83±7.62, significantly lower than 195.33±19.68 of Ad5-control-shRNA group. Meanwhile, U2OS cell migration rates of Ad5-Herg1-shRNA1 and Ad5-Herg1-shRNA2 group were 21.83±7.99 and 22.85±7.08, significantly lower than 83.33±12.36 of Ad5-control-shRNA group (all P<0.001). The results of xenograft model of OS showed that the tumor volume and weight of Ad5-Herg1-shRNA group were significantly smaller than of Ad5-control-shRNA group after 14 days and 5 weeks of inoculation, respectively (P<0.001). Moreover, knockdown of Herg1 inhibited the metastasis of OS cells. In mechanism, Herg1 protein interacted with NF2 protein. Knockdown of Herg1 significantly suppressed the expression levels of LATS1 and YAP protein, and promoted the phosphorylation of LATS1 and YAP in OS cells (all P<0.001). Conclusion Our findings suggest that Herg1 participates in the proliferation and motility of OS cells and may serve as a potential therapeutic target for osteosarcoma patients.

Objective To detect the effect and regulatory mechanism of human ether à go?go related gene 1 ( Herg 1) knockdown on the proliferation and invasion of osteosarcoma ( OS). Methods We constructed a recombinant adenovirus vector ( Ad5?Herg1?shRNA) expressing short hair RNA ( shRNA) against Herg1 and tested the knockdown efficiency. Then, the effects of Herg 1 knockdown on the proliferation, growth and invasion of osteosarcoma were measured by using cell counting kit?8 (CCK?8), wound healing assay, Transwell assay and xenograft model of nude mice, respectively. Tandem affinity purification, mass spectrometry and dual luciferase reporter assay were used to find out the molecules interacted with Herg1. Western blot was used to detect the expressions of large tumor suppressor gene (LATS1), p?LATS1, Yes?associated protein ( YAP ) and p?YAP in cells after infection of Ad5?Herg1?shRNA. Results Compared to Ad5?control?shRNA, Ad5?Herg1?shRNA dramatically inhibited the expression of Herg1 in OS cells. The result of CCK8 array demonstrated that 143B cell vitalities of Ad5?Herg1?shRNA1 and Ad5?Herg1?shRNA2 group were ( 65.47 ± 3.90)% and ( 79.90 ± 1.52)%, significantly lower than (100.00±6.14)% of Ad5?control?shRNA group. Meanwhile, U2OS cell vitality of Ad5?Herg1?shRNA1 and Ad5?Herg1?shRNA2 group were (69.69±1.36)% and (76.72±2.75)%, significantly lower than (100.00± 3.01)% of Ad5?control?shRNA group (all P＜0.001). The results of wound healing array showed that 143B cell migration rates of Ad5?Herg1?shRNA1 and Ad5?Herg1?shRNA2 group were (33.03± 2.88)% and (36.47±4.16)%, significantly lower than (97.78±2.28)% of Ad5?control?shRNA group. Meanwhile, U2OS cell migration rates of Ad5?Herg1?shRNA1 and Ad5?Herg1?shRNA2 group were ( 68.07 ± 0.90 )% and (73.97±1.25)%, significantly lower than (96.50± 1.12)% of Ad5?control?shRNA group ( all P＜0.001). The results of Transwell showed that 143B cell invasion numbers of Ad5?Herg1?shRNA1 and Ad5?Herg1?shRNA2 group were 36.50±12.15 and 44.83±7.62, significantly lower than 195.33±19.68 of Ad5?control?shRNA group. Meanwhile, U2OS cell migration rates of Ad5?Herg1?shRNA1 and Ad5?Herg1?shRNA2 group were 21.83±7.99 and 22.85±7.08, significantly lower than 83.33±12.36 of Ad5?control?shRNA group ( all P＜0.001). The results of xenograft model of OS showed that the tumor volume and weight of Ad5?Herg1?shRNA group were significantly smaller than of Ad5?control?shRNA group after 14 days and 5 weeks of inoculation, respectively (P＜0.001).Moreover, knockdown of Herg1 inhibited the metastasis of OS cells.In mechanism, Herg1 protein interacted with NF2 protein. Knockdown of Herg1 significantly suppressed the expression levels of LATS1 and YAP protein, and promoted the phosphorylation of LATS1 and YAP in OS cells ( all P＜0.001). Conclusion Our findings suggest that Herg1 participates in the proliferation and motility of OS cells and may serve as a potential therapeutic target for osteosarcoma patients.

Objective To detect the effect and regulatory mechanism of human ether à go?go related gene 1 ( Herg 1) knockdown on the proliferation and invasion of osteosarcoma ( OS). Methods We constructed a recombinant adenovirus vector ( Ad5?Herg1?shRNA) expressing short hair RNA ( shRNA) against Herg1 and tested the knockdown efficiency. Then, the effects of Herg 1 knockdown on the proliferation, growth and invasion of osteosarcoma were measured by using cell counting kit?8 (CCK?8), wound healing assay, Transwell assay and xenograft model of nude mice, respectively. Tandem affinity purification, mass spectrometry and dual luciferase reporter assay were used to find out the molecules interacted with Herg1. Western blot was used to detect the expressions of large tumor suppressor gene (LATS1), p?LATS1, Yes?associated protein ( YAP ) and p?YAP in cells after infection of Ad5?Herg1?shRNA. Results Compared to Ad5?control?shRNA, Ad5?Herg1?shRNA dramatically inhibited the expression of Herg1 in OS cells. The result of CCK8 array demonstrated that 143B cell vitalities of Ad5?Herg1?shRNA1 and Ad5?Herg1?shRNA2 group were ( 65.47 ± 3.90)% and ( 79.90 ± 1.52)%, significantly lower than (100.00±6.14)% of Ad5?control?shRNA group. Meanwhile, U2OS cell vitality of Ad5?Herg1?shRNA1 and Ad5?Herg1?shRNA2 group were (69.69±1.36)% and (76.72±2.75)%, significantly lower than (100.00± 3.01)% of Ad5?control?shRNA group (all P＜0.001). The results of wound healing array showed that 143B cell migration rates of Ad5?Herg1?shRNA1 and Ad5?Herg1?shRNA2 group were (33.03± 2.88)% and (36.47±4.16)%, significantly lower than (97.78±2.28)% of Ad5?control?shRNA group. Meanwhile, U2OS cell migration rates of Ad5?Herg1?shRNA1 and Ad5?Herg1?shRNA2 group were ( 68.07 ± 0.90 )% and (73.97±1.25)%, significantly lower than (96.50± 1.12)% of Ad5?control?shRNA group ( all P＜0.001). The results of Transwell showed that 143B cell invasion numbers of Ad5?Herg1?shRNA1 and Ad5?Herg1?shRNA2 group were 36.50±12.15 and 44.83±7.62, significantly lower than 195.33±19.68 of Ad5?control?shRNA group. Meanwhile, U2OS cell migration rates of Ad5?Herg1?shRNA1 and Ad5?Herg1?shRNA2 group were 21.83±7.99 and 22.85±7.08, significantly lower than 83.33±12.36 of Ad5?control?shRNA group ( all P＜0.001). The results of xenograft model of OS showed that the tumor volume and weight of Ad5?Herg1?shRNA group were significantly smaller than of Ad5?control?shRNA group after 14 days and 5 weeks of inoculation, respectively (P＜0.001).Moreover, knockdown of Herg1 inhibited the metastasis of OS cells.In mechanism, Herg1 protein interacted with NF2 protein. Knockdown of Herg1 significantly suppressed the expression levels of LATS1 and YAP protein, and promoted the phosphorylation of LATS1 and YAP in OS cells ( all P＜0.001). Conclusion Our findings suggest that Herg1 participates in the proliferation and motility of OS cells and may serve as a potential therapeutic target for osteosarcoma patients.

Objective To investigate the clinical efficacy of our self-designed adjustable weight-bearing brace for AO type B tibial shaft fractures managed by interlocking intramedullary nail.Methods A total of 68 consecutive patients with AO type 42-B tibial shaft fracture who had been managed from April 2013 to March 2015 hy interlocking intramedul]ary nail were recruited into our study.They were randomized into 2 equal groups (n =34).Group A received conventional therapy after operation while group B received auxiliary mauagement with our self-designed adjustable weight-bearing brace after conventional postoperative therapy for one week.The 2 groups were compared at postoperative 1,3 and 6 months and at the final follow-up in terms of visual analogue scale (VAS),weight-bearing status of the affected limb,time for fracture union,Radiographic Union Score for Tibial Fractures (RUST) and Johner-Wruhs scale.Results Of this series,62 cases were followed up for 12 to 18 months (average,14.7 months),5 ones were lost to the follow-up and one withdrew.The mean VAS scores at 3-month and 6-month follow-ups for group B were 2.5 ± 0.8 and 0.9 ± 0.6 respectively,significantly lower than those for group A (3.0 ± 0.9 and 1.4 ± 0.8 respectively) (P ＜ 0.05).In group A at 1-month,3-month and 6-month follow-ups,the weight-bearing status was 44.1％ ± 17.5％,72.0％ ±17.4％ and 86.4％ ±12.5％ while the mean RUST scores were 5.4±1.4,8.7±1.1 and 10.3 ± 1.1,respectively.In group B at 1-month,3-month and 6-month follow-ups,the weight-bearing status was 53.8％ ± 11.0％,84.1％ ± 12.2％ and 94.4％ ± 10.6％ while the mean RUST scores were 6.5 ± 0.8,9.9 ± 0.9 and 11.3 ± 0.8,respectively.There were significant differences between the 2 groups in the above indexes (all P ＜ 0.05).Group B achieved clinical fracture union after an average of 3.3 ±0.7 months,significantly faster than group A (3.9 ± 1.0 months) (P ＜ 0.05).According to the Johner-Wruhs scoring,group A had 19 excellent cases and 12 good ones while group B had 27 excellent ones and 4 good ones,showing a significant difference between the 2 groups (P ＜ 0.05).Conclusions Early application of our self-designed adjustable weight-bearing brace for patients with AO type B tibial shaft fracture managed by interlocking intramedullary nail can reduce postoperative pain,accelerate callus growth,shorten bony healing time and achieve satisfactory functional recovery.