Objective:To compare the therapeutic efficacy of the dual anteromedial and anterolateral approaches versus that of the anterior midline approach in the treatment of Wahlquist type C medial tibial plateau fractures accompanied by posterior column collapse.Methods:A retrospective study was conducted to analyze the 21 patients who had been treated for Wahlquist type C medial tibial plateau fractures plus posterior column collapse at The Fourth Orthopedic Ward, The 72nd Group Army Hospital of PLA between January 2019 and August 2023. The cohort included 13 males and 8 females, with an age of (43.3±6.7) years. The left side was involved in 14 fractures and the right side in 7 ones. The patients were divided into 2 groups based on their surgical approaches: a dual-approach group ( n=13) undergoing fixation via the dual anteromedial and anterolateral approaches, and a single-approach group ( n=8) undergoing fixation via the anterior midline approach. Comparative parameters included operative time, intraoperative blood loss, fracture healing time, quality of fracture reduction, medial proximal tibial angle (MPTA), incision complications, postoperative bone mass reduction quality (evaluated according to the Rasmussen anatomical criteria for tibial condyle fracture reduction), lateral tibial plateau instability, incidence of genu varum, and post-traumatic arthritis. Functional recovery of the lower limb joints was assessed at the final follow-up using the Merchant criteria. Results:No statistically significant differences were observed in the baseline characteristics between the 2 groups preoperatively, indicating comparability ( P>0.05). All patients were followed up for a mean duration of (38.1±11.3) months. The postoperative MPTA in the dual-approach group (86.8°±0.8°) was significantly larger than that in the single-approach group (85.5°±0.9°) ( P<0.05). Genu varum occurred in 1 patient in the dual-approach group and in 4 patients in the single-approach group, while lateral tibial plateau instability was observed in 1 patient in the dual-approach group and in 4 patients in the single-approach group, showing statistically significant differences between the 2 groups ( P<0.05). No statistically significant differences were found between the 2 groups regarding operative time, intraoperative blood loss, fracture healing time, quality of fracture reduction, incidence of incision complications, or incidence of post-traumatic arthritis ( P>0.05). At the final follow-up, no statistically significant difference was observed in the functional recovery of the lower limb joints assessed by the Merchant criteria between the 2 groups ( P>0.05). Conclusion:In the treatment of Wahlquist type C medial tibial plateau fractures accompanied by posterior column collapse, compared with the single anterior midline approach, the dual anteromedial and anterolateral approaches can restore more effectively the MPTA, and reduce the incidences of genu varum and lateral tibial plateau instability.

Objective:To compare the therapeutic efficacy of the dual anteromedial and anterolateral approaches versus that of the anterior midline approach in the treatment of Wahlquist type C medial tibial plateau fractures accompanied by posterior column collapse.Methods:A retrospective study was conducted to analyze the 21 patients who had been treated for Wahlquist type C medial tibial plateau fractures plus posterior column collapse at The Fourth Orthopedic Ward, The 72nd Group Army Hospital of PLA between January 2019 and August 2023. The cohort included 13 males and 8 females, with an age of (43.3±6.7) years. The left side was involved in 14 fractures and the right side in 7 ones. The patients were divided into 2 groups based on their surgical approaches: a dual-approach group ( n=13) undergoing fixation via the dual anteromedial and anterolateral approaches, and a single-approach group ( n=8) undergoing fixation via the anterior midline approach. Comparative parameters included operative time, intraoperative blood loss, fracture healing time, quality of fracture reduction, medial proximal tibial angle (MPTA), incision complications, postoperative bone mass reduction quality (evaluated according to the Rasmussen anatomical criteria for tibial condyle fracture reduction), lateral tibial plateau instability, incidence of genu varum, and post-traumatic arthritis. Functional recovery of the lower limb joints was assessed at the final follow-up using the Merchant criteria. Results:No statistically significant differences were observed in the baseline characteristics between the 2 groups preoperatively, indicating comparability ( P>0.05). All patients were followed up for a mean duration of (38.1±11.3) months. The postoperative MPTA in the dual-approach group (86.8°±0.8°) was significantly larger than that in the single-approach group (85.5°±0.9°) ( P<0.05). Genu varum occurred in 1 patient in the dual-approach group and in 4 patients in the single-approach group, while lateral tibial plateau instability was observed in 1 patient in the dual-approach group and in 4 patients in the single-approach group, showing statistically significant differences between the 2 groups ( P<0.05). No statistically significant differences were found between the 2 groups regarding operative time, intraoperative blood loss, fracture healing time, quality of fracture reduction, incidence of incision complications, or incidence of post-traumatic arthritis ( P>0.05). At the final follow-up, no statistically significant difference was observed in the functional recovery of the lower limb joints assessed by the Merchant criteria between the 2 groups ( P>0.05). Conclusion:In the treatment of Wahlquist type C medial tibial plateau fractures accompanied by posterior column collapse, compared with the single anterior midline approach, the dual anteromedial and anterolateral approaches can restore more effectively the MPTA, and reduce the incidences of genu varum and lateral tibial plateau instability.

Objective: To investigate the in vitro and in vivo effects of apatinib in esophageal squamous cell carcinoma and the underlying mechanisms. Methods: The esophageal cancer cells, KYSE-150 and ECA-109, were divided into control group and apatinib treatment group at the concentrations of 2.5, 5, 10, 20 and 40 μmol/L respectively. All of experiments were performed in triplicate. MTT and colony formation assays were used to measure cell proliferation. Transwell assay was used to determine the migration capacity. The effect of apatinib on cell cycle and apoptosis was analyzed by flow cytometry. The expression of VEGF and VEGFR-2 was measured by real-time quantitative PCR (qRT-PCR). The concentration of VEGF in the cell supernatant was assessed by enzyme-linked immunosorbent assay (ELISA). The expression levels of MEK, ERK, p-MEK, p-ERK, JAK2, STAT3 and p-STAT3 after VEGF stimulation were detected by Western blot. Furthermore, the nude mice xenograft model was established. The tumor-bearing mice were randomly divided into control group, apatinib low dose treatment group (250 mg) and apatinib high dose treatment group (500 mg), respectively. Tumor inhibition rates of different groups were calculated. And then the expressions of VEGF and VEGFR2 were detected in xenograft tissues by immunohistochemical staining. Results: In the presence of 20 μmol/L and 40 μmol/L of apatinib for 24 hours, the migration cell numbers of KYSE-150 and ECA-109 were 428.67±4.16 and 286.67±1.53 as well as 1 123.67±70.00 and 477.33±26.84, respectively, that were significantly lower than control group (P<0.05 for all). In addition, after treatment with 10 μmol/L, 20 μmol/L and 40 μmol/L of apatinib for 7 days on KYSE-150 and ECA-109, the colony formation rates were (65.12±25.48)%, (58.19±24.73)% and (29.10±22.40)% as well as (70.61±15.14)%, (61.12±17.21)% and (43.09±11.13)%, respectively. The colony formation rates of 20 μmol/L and 40 μmol/L of apatinib treatment groups were significantly lower than control group (100.00±0.00, P<0.05). The cell cycle ratio of G₂/M phase and apoptosis rate of control group and 20 μmol/L apatinib group in KYSE-150 cells were (12.14±2.13)% and (3.49±0.74)% as well as (26.27±3.30)% and (15.65±1.54)%, respectively. The corresponding ratios in ECA-109 cells were (3.44±0.57)% and (6.31±1.43)% as well as (22.64±2.36)% and (49.26±1.62)%, respectively. The results show that apatinib suppressed cell cycle progression at G₂/M phase and induced cell apoptosis in both KYSE-150 and ECA-109 cells (P<0.05 for all). In the presence of 20 μmol/L and 40 μmol/L of apatinib in KYSE-150 cells, the relative levels of VEGF mRNA were (42.57±10.43)% and (25.69±1.24)%, and those of VEGF-2 mRNA were (36.09±10.82)% and (13.99±6.54)%, which were all significantly decreased compared to control group (100.00±0.00, P<0.05 for all). For ECA-109 cells, the relative expression of VEGF and VEGFR2 showed similar tendency (P<0.05 for all). Moreover, after treatment with 20 μmol/L and 40 μmol/L of apatinib in KYSE-150 cells, the VEGF concentrations were (766.48±114.27) pg/ml and (497.40±102.18)pg/ml, which were significantly decreased compared to control group [(967.41±57.75) pg/ml, P<0.05)]. The results in ECA-109 were consistent (P<0.05). Furthermore, after treatment with 40 μmol/L of apatinib in KYSE-150 and ECA-109, the relative expression of p-MEK and p-ERK were 0.49±0.05 and 0.28±0.03 as well as 0.63±0.03 and 1.22±0.15, which were significantly lower than control group (1.23±0.19 and 0.66±0.07 as well as 1.03±0.20 and 1.76±0.20; P<0.05). The relative expression of STAT3, p-STAT3 in control group and experimental group were 0.96±0.15 and 0.85±0.16 as well as 0.62±0.09 and 0.36±0.13, respectively. The results showed that the protein levels of STAT3 and p-STAT3 were significantly lower than the control group (P<0.05 for all). The inhibition rates of apatinib in xenograft nude mice were 29.25% and 19.96% for 250 mg and 500 mg treatment groups. The concentration of VEGF were (25.11±4.12) pg/ml, (16.40±2.81) pg/ml and (15.04±4.88)pg/ml for control, 250 mg and 500 mg treatment groups, respectively. Conclusions Apatinib can inhibit cell proliferation, induce apoptosis and suppress migration of esophageal cancer cells in vitro and in vivo. This effect was mainly mediated via the alterations of Ras/Raf/MEK/ERK pathway and JAK2/STAT3 pathway.

Objective To investigate the relationship between thyroid stimulating hormone(TSH) and uric acid (UA), blood pressure, blood glucose, blood lipid and body mass index (BMI) in patients with type 2 diabetes. Methods A total of 254 patients with type 2 diabetes and normal thyroid function who were admitted to the Shengjing Hospital Affiliated to China Medical University from 2017 to 2019 were selected. Height, weight, systolic blood pressure (SBP) and diastolic blood pressure (DBP) and test fasting blood glucose (FBG), glycated hemoglobin (HbA1c), total cholesterol (TC), triacylglycerol (TG), low density lipoprotein cholestorol (LDL-C), free triiodothyronine (FT3), free theroxine (FT4), TSH and UA was measured. The correlations between TSH and blood pressure, blood lipid, FBG, BMI and UA was analyzed. Results According to gender, there were two groups. The levels of FT3, UA and BMI of males were significantly higher than that of females (P<0.05). Age, course of disease, TSH and TC of females were significantly higher than that of males (P<0.05). According to the TSH values of males and females, 254 patients were divided into TSH < 2.5 mU/L group and TSH ≥ 2.5 mU/L group respectively. The levels of BMI, FBG and UA in TSH≥2.5 mU/L group were significantly higher than those in TSH<2.5 mU/L group within females:(26.38 ± 4.06)kg/m2 vs.(23.91 ± 2.79)kg/m2,(10.29 ± 4.52)mmol/L vs. (8.38 ± 2.72)mmol/L,(406.53 ± 79.48)μmol/L vs.(270.17 ± 17.15)μmol/L. The levels of BMI, DBP and UA in TSH≥2.5 mU/L group were significantly higher than those in TSH<2.5 mU/L group within males:(27.87 ± 3.85)kg/m2 vs.(25.09 ± 3.10)kg/m2,(85.98 ± 9.75)mmHg(1 mmHg＝0.133 kPa) vs. (80.79 ± 8.44)mmHg,(430.35 ± 101.01)μmol/L vs.(318.10 ± 65.25)μmol/L, and the differences were statistically significant (P<0.05). Pearson correlation analysis was used to analyze the correlation between TSH and various indexes of all selected subjects. Only BMI, UA, FT4 and TG were statistically significant, and the correlation coefficients were 0.297, 0.550, - 0.208 and 0.127, P < 0.05, respectively. BMI, FBG and UA levels of females were positively correlated with TSH (P < 0.05), and the correlation coefficients were 0.332, 0.219 and 0.632, respectively. BMI, DBP, HbA1c and UA of males were positively correlated with TSH (P<0.05), and the correlation coefficients were 0.316, 0.204, 0.176 and 0.541, respectively. FT4 was negatively correlated with TSH, with a correlation coefficient of 0.248, which was statistically significant (P < 0.05), and UA had a stronger correlation with TSH. Conclusions Even in type 2 diabetics with normal thyroid function, small changes in TSH can affect weight, UA, FBG in women and DBP in men.

Objective : To understand the current situation and influencing factors of occupational burnout among vaccination personnels in Haining. Methods : The vaccination staffs of all vaccination clinics in Haining were investigated by the general questionnaire and Maslach Burnout Inventory. Logistic regression model was used to analyze the influencing factors for job burnout of vaccination personnels. Results : A total of 160 questionnaires were distributed and 158 valid questionnaires were collected. The effective rate of questionnaires was 98.75%. A total of 91 vaccination staffs suffered from occupational burnout,accounting for 57.59%. Among them,the median（inter-quartile range）of the scores of emotional exhaustion,depersonalization and personal achievement were 13.00（14.00）,4.00（6.00）and 26.50（17.00）,respectively,which were all lower than the normalized scores（22.19,7.12 and 36.53,P<0.05）. The results of logistic regression analysis showed that having confidence in vaccination was a protective factor for emotional failure（OR=0.175,95%CI：0.058-0.523）and low sense of achievement（OR=0.272,95%CI：0.079-0.937）in vaccination personnels;having experience in adverse event following immunization（AEFI）was a risk factor for depersonalization（OR=3.125,95%CI：1.472-6.633）and occupational burnout（OR= 2.391,95%CI：1.189-4.807）in vaccination personnels. Conclusion A certain proportion of vaccination staffs in Haining suffered from occupational burnout. The experience of AEFI was a risk factor for their occupational burnout.

Objective: To investigate the differences in the intake of macronutrients between boarders and resident students in China, and to provide a scientific reference for relevant policies and preventive measures. Methods: The difference of macronutrients level between boarders and resident students were analyzed with the multilevel model (MLM) by using the data from Chinese Health and Nutrition Survey and the indicators of Chinese Dietary Reference Intakes (DRIs) 2013. Results: The daily intake of energy, carbohydrate, fat and protein were (1 597.59±557.15)kcal, (216.2±84.66)g, (57.88±31.96)g, (52.69±21.2)g respectively, with a rate of meeting DRIs of 17.32%, 84.17%, 50.30% for energy, carbohydrate and protein. There were significant differences in amount of energy, carbohydrate between boarders and resident students, but no significant difference in rate of meeting DRIs (15.09%, 87.28%, 17.54%, 83.86%, P>0.05 ). No difference in the amount of fat and protein intake between boarders and resident students, but the protein rate of meeting DRIs among resident students was significantly lower than that in boarders(34.91% vs 51.82%, χ2=4.45, P<0.01). Conclusion The results revealed an imbalanced intake of macronutrients among primary and secondary school students, which highlight the insufficiency in energy intake and the worse meeting rate of DRIs for protein among resident-student. The nutritional education targeting at boarder-students should be strengthened.

Objective To investigate the in vitro and in vivo effects of apatinib in esophageal squamous cell carcinoma and the underlying mechanisms. Methods The esophageal cancer cells, KYSE?150 and ECA?109, were divided into control group and apatinib treatment group at the concentrations of 2.5, 5, 10, 20 and 40 μmol／L respectively. All of experiments were performed in triplicate. MTT and colony formation assays were used to measure cell proliferation. Transwell assay was used to determine the migration capacity. The effect of apatinib on cell cycle and apoptosis was analyzed by flow cytometry. The expression of VEGF and VEGFR?2 was measured by real?time quantitative PCR (qRT?PCR). The concentration of VEGF in the cell supernatant was assessed by enzyme?linked immunosorbent assay (ELISA). The expression levels of MEK, ERK, p?MEK, p?ERK, JAK2, STAT3 and p?STAT3 after VEGF stimulation were detected by Western blot. Furthermore, the nude mice xenograft model was established. The tumor?bearing mice were randomly divided into control group, apatinib low dose treatment group (250 mg) and apatinib high dose treatment group (500 mg), respectively.Tumor inhibition rates of different groups were calculated.And then the expressions of VEGF and VEGFR2 were detected in xenograft tissues by immunohistochemical staining. Results In the presence of 20 μmol／L and 40 μmol／L of apatinib for 24 hours, the migration cell numbers of KYSE?150 and ECA?109 were 428.67±4.16 and 286.67±1.53 as well as 1 123.67±70.00 and 477.33± 26.84, respectively, that were significantly lower than control group ( P＜0.05 for all). In addition, after treatment with 10 μmol／L, 20 μmol／L and 40 μmol／L of apatinib for 7 days on KYSE?150 and ECA?109, the colony formation rates were ( 65.12± 25.48)%, ( 58.19± 24.73)% and (29.10± 22.40)% as well as (70.61±15.14)%, (61.12±17.21)% and (43.09±11.13)%, respectively. The colony formation rates of 20 μmol／L and 40 μmol／L of apatinib treatment groups were significantly lower than control group (100.00±0.00, P＜0.05). The cell cycle ratio of G2／M phase and apoptosis rate of control group and 20 μmol／L apatinib group in KYSE?150 cells were (12.14±2.13)% and (3.49±0.74)% as well as (26.27±3.30)% and (15.65± 1.54)%, respectively. The corresponding ratios in ECA?109 cells were (3.44±0.57)% and (6.31±1.43)%as well as (22.64±2.36)% and (49.26± 1.62)%, respectively. The results show that apatinib suppressed cell cycle progression at G2／M phase and induced cell apoptosis in both KYSE?150 and ECA?109 cells (P＜0.05 for all). In the presence of 20 μmol／L and 40 μmol／L of apatinib in KYSE?150 cells, the relative levels of VEGF mRNA were (42.57± 10.43)% and ( 25.69± 1.24)%, and those of VEGF?2 mRNA were (36.09±10.82)% and (13.99±6.54)%, which were all significantly decreased compared to control group (100.00±0.00, P＜0.05 for all). For ECA?109 cells, the relative expression of VEGF and VEGFR2 showed similar tendency (P＜0.05 for all). Moreover, after treatment with 20 μmol／L and 40 μmol／L of apatinib in KYSE?150 cells, the VEGF concentrations were ( 766.48± 114.27) pg／ml and ( 497.40± 102.18) pg／ml, which were significantly decreased compared to control group [(967.41± 57.75) pg／ml, P＜0.05)]. The results in ECA?109 were consistent (P＜0.05). Furthermore, after treatment with 40 μmol／L of apatinib in KYSE?150 and ECA?109, the relative expression of p?MEK and p?ERK were 0.49±0.05 and 0.28±0.03 as well as 0.63±0.03 and 1.22±0.15, which were significantly lower than control group (1.23±0.19 and 0.66± 0.07 as well as 1.03±0.20 and 1.76±0.20; P＜0.05). The relative expression of STAT3, p?STAT3 in control group and experimental group were 0.96 ± 0.15 and 0.85 ± 0.16 as well as 0.62 ± 0.09 and 0.36 ± 0.13, respectively. The results showed that the protein levels of STAT3 and p?STAT3 were significantly lower than the control group (P＜0.05 for all). The inhibition rates of apatinib in xenograft nude mice were 29.25% and 19.96% for 250 mg and 500 mg treatment groups. The concentration of VEGF were (25.11±4.12) pg／ml, (16.40 ± 2.81) pg／ml and ( 15.04 ± 4.88) pg／ml for control, 250 mg and 500 mg treatment groups, respectively. Conclusions Apatinib can inhibit cell proliferation, induce apoptosis and suppress migration of esophageal cancer cells in vitro and in vivo. This effect was mainly mediated via the alterations of Ras／Raf／MEK／ERK pathway and JAK2／STAT3 pathway.

Objective To investigate the in vitro and in vivo effects of apatinib in esophageal squamous cell carcinoma and the underlying mechanisms. Methods The esophageal cancer cells, KYSE?150 and ECA?109, were divided into control group and apatinib treatment group at the concentrations of 2.5, 5, 10, 20 and 40 μmol／L respectively. All of experiments were performed in triplicate. MTT and colony formation assays were used to measure cell proliferation. Transwell assay was used to determine the migration capacity. The effect of apatinib on cell cycle and apoptosis was analyzed by flow cytometry. The expression of VEGF and VEGFR?2 was measured by real?time quantitative PCR (qRT?PCR). The concentration of VEGF in the cell supernatant was assessed by enzyme?linked immunosorbent assay (ELISA). The expression levels of MEK, ERK, p?MEK, p?ERK, JAK2, STAT3 and p?STAT3 after VEGF stimulation were detected by Western blot. Furthermore, the nude mice xenograft model was established. The tumor?bearing mice were randomly divided into control group, apatinib low dose treatment group (250 mg) and apatinib high dose treatment group (500 mg), respectively.Tumor inhibition rates of different groups were calculated.And then the expressions of VEGF and VEGFR2 were detected in xenograft tissues by immunohistochemical staining. Results In the presence of 20 μmol／L and 40 μmol／L of apatinib for 24 hours, the migration cell numbers of KYSE?150 and ECA?109 were 428.67±4.16 and 286.67±1.53 as well as 1 123.67±70.00 and 477.33± 26.84, respectively, that were significantly lower than control group ( P＜0.05 for all). In addition, after treatment with 10 μmol／L, 20 μmol／L and 40 μmol／L of apatinib for 7 days on KYSE?150 and ECA?109, the colony formation rates were ( 65.12± 25.48)%, ( 58.19± 24.73)% and (29.10± 22.40)% as well as (70.61±15.14)%, (61.12±17.21)% and (43.09±11.13)%, respectively. The colony formation rates of 20 μmol／L and 40 μmol／L of apatinib treatment groups were significantly lower than control group (100.00±0.00, P＜0.05). The cell cycle ratio of G2／M phase and apoptosis rate of control group and 20 μmol／L apatinib group in KYSE?150 cells were (12.14±2.13)% and (3.49±0.74)% as well as (26.27±3.30)% and (15.65± 1.54)%, respectively. The corresponding ratios in ECA?109 cells were (3.44±0.57)% and (6.31±1.43)%as well as (22.64±2.36)% and (49.26± 1.62)%, respectively. The results show that apatinib suppressed cell cycle progression at G2／M phase and induced cell apoptosis in both KYSE?150 and ECA?109 cells (P＜0.05 for all). In the presence of 20 μmol／L and 40 μmol／L of apatinib in KYSE?150 cells, the relative levels of VEGF mRNA were (42.57± 10.43)% and ( 25.69± 1.24)%, and those of VEGF?2 mRNA were (36.09±10.82)% and (13.99±6.54)%, which were all significantly decreased compared to control group (100.00±0.00, P＜0.05 for all). For ECA?109 cells, the relative expression of VEGF and VEGFR2 showed similar tendency (P＜0.05 for all). Moreover, after treatment with 20 μmol／L and 40 μmol／L of apatinib in KYSE?150 cells, the VEGF concentrations were ( 766.48± 114.27) pg／ml and ( 497.40± 102.18) pg／ml, which were significantly decreased compared to control group [(967.41± 57.75) pg／ml, P＜0.05)]. The results in ECA?109 were consistent (P＜0.05). Furthermore, after treatment with 40 μmol／L of apatinib in KYSE?150 and ECA?109, the relative expression of p?MEK and p?ERK were 0.49±0.05 and 0.28±0.03 as well as 0.63±0.03 and 1.22±0.15, which were significantly lower than control group (1.23±0.19 and 0.66± 0.07 as well as 1.03±0.20 and 1.76±0.20; P＜0.05). The relative expression of STAT3, p?STAT3 in control group and experimental group were 0.96 ± 0.15 and 0.85 ± 0.16 as well as 0.62 ± 0.09 and 0.36 ± 0.13, respectively. The results showed that the protein levels of STAT3 and p?STAT3 were significantly lower than the control group (P＜0.05 for all). The inhibition rates of apatinib in xenograft nude mice were 29.25% and 19.96% for 250 mg and 500 mg treatment groups. The concentration of VEGF were (25.11±4.12) pg／ml, (16.40 ± 2.81) pg／ml and ( 15.04 ± 4.88) pg／ml for control, 250 mg and 500 mg treatment groups, respectively. Conclusions Apatinib can inhibit cell proliferation, induce apoptosis and suppress migration of esophageal cancer cells in vitro and in vivo. This effect was mainly mediated via the alterations of Ras／Raf／MEK／ERK pathway and JAK2／STAT3 pathway.

Objective To evaluate the radiosensitivity effects of apatinib on the esophageal cancer cell line ECA-109 and its cancer stem-like cells,and to investigate the underlying mechanism.Methods A serum-free medium (SFM) was used to culture esophageal cancer stem cell line ECA-109 and enrich the esophageal stem-like spheres.ECA-109 and its stem-like cells were divided into control group,drug treatment group,radiation group and drug plus radiation group.Cell proliferations of ECA-109 and its stem-like cells were detected with CCK-8 method.The concentration of vascular endothelial growth factor (VEGF) in the cell culture medium was determined by enzyme linked immunosorbent assay(ELISA).Cell cycle and apoptosis were detected by flow cytometry method.The expressions of CHK2 and P-STAT3 proteins were detected by Western blot assay.Results With the administration with apatinib for 24,48 and 72 h,the half of the inhibitory concentration (IC50) of ECA-109 stem-like cells was significantly higher than that of the parent cells (t =8.17,9.29,18.85,P ＜ 0.05) in a time dependent manner (parental cells:r2 =0.94-0.97,P ＜0.05;stem-like cells:r2 =0.94-0.98,P ＜0.05).After administration with different concentrations of apatinib (parental cells:10 and 20 μmol/L;stem-like cells:30 and 40 μmol/L) combined with different dose of X-rays (6 and 8 Gy),the proliferations of ECA-109 and its stem-like cells were significantly (t =5.20-39.68,P ＜ 0.05) inhibited compared with radiation alone group.VEGF secretion from both ECA-109 cells and its stem like cells were significantly decreased in different manner (t =7.45,P ＜ 0.05).Compared with control group,the cell apoptosis rate and the percentages of cells in G2/M phase were significantly increased in drug plus radiation group (t =8.83,11.59,P ＜ 0.05),and the expressions of CHK2 and P-STAT3 were decreased in drug group (t =3.36,4.10,P ＜ 0.05).Compared with radiation group,the expressions of CHK2 and P-STAT3 were decreased in drug plus radiation group (t =9.05,2.36,P ＜ 0.05).Conclusions Apatinib enhanced the radiosensitivity of ECA-109 cells and its stem-like cells,which was much more effective on ECA-109 cells and may be related to the radiation-induced inhibition of VEGF signal pathway that can further inhibit cell proliferation,promote cell apoptosis and induce cell cycle redistribution.The higher intrinsic level of VEGF protein may contribute to radioresistance of ECA-109 stem-like cells.

Objective To evaluate the radiosensitization effect of apatinib on esophageal cancer cell line Kyse-150, and to investigate the underlying mechanism. Methods Cells were divided into four groups:control group, apatinib treatment group, X-ray radiation group, and the combination group treated with X-rays plus apatinib. The effect of apatinib with different concentrations on the cell proliferative and radiosensitivity were evaluated by CCK-8 kit and colony formation assay. Flow cytometry method was adopted to detect the effect of apatinib on cell cycle progress and apoptosis induction. Results Apatinib inhibited the proliferation of Kyse-150 cells in time-and dose-dependent manners (r=0. 89-0. 96, P<0. 05). With the increase of apatinib concentration, D0, Dq and SF2 value of Kyse-150 cells decreased and SERD0 value increased. Compared with control group, apatinib alone group, and radiation alone group, the cell apoptosis rate significantly increased in the combination group (t=12. 36, 5. 99, 15. 47,P<0. 05). Compared with control group, the percentages of cells in G2/M phase were all significantly increased in apatinib group, radiation group and combination group (t=8. 81, 39. 69, 20. 61,P<0. 05). Compared with radiation alone group and control group, the percentage of cells in S phase significantly increased in apatinib alone group and combination group(t = 6.06, 3.82,8.81,6.24,P < 0.05). Conclusions Apatinib can increase radiosensitivity of esophageal cancer cell line Kyse-150 possibly by inhibiting cell proliferation, inducing cell apoptosis and causing redistribution of cell cycle.