Objectives:To investigate the clinical efficacy of the smiley face rod(SFR)technique in treating lumbar spondylolysis with grade Ⅰ spondylolisthesis.Methods:A total of 22 patients(18 males,4 females)with lumbar spondylolysis and grade Ⅰ spondylolisthesis treated with the SFR segmental fixation technique in our department from January 2019 to December 2024 were retrospectively analyzed.The age of the patients was 12-55(28.7±12.6)years old,the body mass index(BMI)was 18-29kg/m2(22.7±3.4kg/m2),and preoperative symptom duration was 6-60(12.3±14.3)months.The patients were followed up for 6-19(9.1±4.5)months.The operative time and intraoperative blood loss volume were recorded.Before opearation,at 3 months and 6 months after operation,visual analogue scale(VAS)for low back pain,Oswestry disability index(ODI),and Japanese Orthopaedic Association(JOA)scores were recorded to evaluate the clinical outcomes.Imaging exami-nations(X-ray,CT)were performed before operation and at 6 months after operation to measure preoperative and postoperative disc height(DH),slip distance(SD),slip rate,lumbar lordosis angle,and range of motion(ROM)at the surgical and adjacent segments to assess the improvement of spondylolisthesis and ROM,as well as the pars defect healing status.The correlations between age,BMI,preoperative disease duration and isthmus bone healing rate were studied.Results:The operative time was 131.8±32.8min(range:86-200min),and intraoperative blood loss was 86.4±41.4mL(range:50-150mL).Significant improvements in VAS,ODI and JOA scores were observed at 3 months and 6 months versus preoperative values(P＜0.05).Slip distance,slip percentage,and lumbar lordosis angle significantly decreased at 6 months versus preoperatively(P＜0.05).No significant differences were observed in DH ratio or ROM between the surgical and adjacent segments preoperatively and at 6 months(P＜0.05).At 6-month follow-up,complete bilateral pars bony union was achieved in 18 cases(81.82％),partial union(including unilateral or other types)in 3 cases(13.63％),and nonunion in 1 case(4.55％).Age,BMI,and preoperative symptom duration showed potential influence on bone healing.Conclusions:In the treatment of lumbar spondylolysis with grade Ⅰ spondylolisthesis,SFR can effectively enhance postoperative lumbar stability,significantly alleviate low back pain symptoms,preserve lumbar mobility,and mitigate disc height collapse to a certain extent.

Objectives:To investigate the clinical efficacy of the smiley face rod(SFR)technique in treating lumbar spondylolysis with grade Ⅰ spondylolisthesis.Methods:A total of 22 patients(18 males,4 females)with lumbar spondylolysis and grade Ⅰ spondylolisthesis treated with the SFR segmental fixation technique in our department from January 2019 to December 2024 were retrospectively analyzed.The age of the patients was 12-55(28.7±12.6)years old,the body mass index(BMI)was 18-29kg/m2(22.7±3.4kg/m2),and preoperative symptom duration was 6-60(12.3±14.3)months.The patients were followed up for 6-19(9.1±4.5)months.The operative time and intraoperative blood loss volume were recorded.Before opearation,at 3 months and 6 months after operation,visual analogue scale(VAS)for low back pain,Oswestry disability index(ODI),and Japanese Orthopaedic Association(JOA)scores were recorded to evaluate the clinical outcomes.Imaging exami-nations(X-ray,CT)were performed before operation and at 6 months after operation to measure preoperative and postoperative disc height(DH),slip distance(SD),slip rate,lumbar lordosis angle,and range of motion(ROM)at the surgical and adjacent segments to assess the improvement of spondylolisthesis and ROM,as well as the pars defect healing status.The correlations between age,BMI,preoperative disease duration and isthmus bone healing rate were studied.Results:The operative time was 131.8±32.8min(range:86-200min),and intraoperative blood loss was 86.4±41.4mL(range:50-150mL).Significant improvements in VAS,ODI and JOA scores were observed at 3 months and 6 months versus preoperative values(P＜0.05).Slip distance,slip percentage,and lumbar lordosis angle significantly decreased at 6 months versus preoperatively(P＜0.05).No significant differences were observed in DH ratio or ROM between the surgical and adjacent segments preoperatively and at 6 months(P＜0.05).At 6-month follow-up,complete bilateral pars bony union was achieved in 18 cases(81.82％),partial union(including unilateral or other types)in 3 cases(13.63％),and nonunion in 1 case(4.55％).Age,BMI,and preoperative symptom duration showed potential influence on bone healing.Conclusions:In the treatment of lumbar spondylolysis with grade Ⅰ spondylolisthesis,SFR can effectively enhance postoperative lumbar stability,significantly alleviate low back pain symptoms,preserve lumbar mobility,and mitigate disc height collapse to a certain extent.

Objective:To explore the effects of bariatric metabolic surgery on body composition.Methods:The retrospective cohort study was conducted. The clinicopathological data of 66 patients with metabolic diseases who were admitted to the Third Xiangya Hospital of Central South University from January 2013 to December 2014 were collected. There were 42 males and 24 females, aged (40±11)years, with a range from 17 to 63 years. Of the 66 patients, 27 undergoing laparoscopic sleeve gastrectomy (LSG) and 39 undergoing laparoscopic Roux-en-Y gastric bypass (LRYGB) were allocated into LSG group and LRYGB group, respectively. The body composition of all patients was determined by dual-energy X-ray absorptiometry at preoperation and postoperative 6 months. Observation indicators: (1) the changes of anthropometric parameters, glucolipid metabolism, body fat mass percentage (BF%) and the ratio of Android BF% and Gynoid BF% (A/G ratio) from preoperation to postoperative 6 months; (2) the changes of whole and local body composition from preoperation to postoperative 6 months; (3) analysis of the correlation between BF% and anthropometric parameters, glucolipid metabolism. (4) Follow-up. Follow-up was conducted using outpatient or hospitalization examination to detect the changes of body composition at the time of postoperative 6 month. The follow-up time was up to July 2015. Measurement data with normal distribution were represented as Mean± SD, paired-samples t test was used for intra-group comparison, and independent-samples t test when baseline data were consistency or covariance analysis when baseline data were not consistency was used for inter-group comparison. Measurement data with skewed distribution were represented as M ( P25, P75), and comparison between groups was analyzed using Wilcoxon signed rank test. The correlation test was undertaken with the Pearson bivariate analysis. Results:(1) The changes of anthropometric parameters, glucolipid metabolism, BF% and A/G ratio from preoperation to postoperative 6 months: for patients in the LSG group, the body mass, body mass index (BMI), waist circumference (WC), waist-to-hip ratio (WHR), diastolic blood pressure (DBP), systolic blood pressure (SBP), fasting plasma glucose (FPG), HbA1c, high density lipoprotein cholesterol (HDL-C), triglyceride (TG), whole BF%, arms BF%, legs BF%, trunk BF%, Android BF%, Gynoid BF% and A/G ratio at preoperation and postoperative 6 months were (102±17)kg, (37±5)kg/m 2, (118±14)cm, 1.01±0.06, (94±14)mmHg(1 mmHg=0.133 kPa), (137±15)mmHg, (8.1±4.2)mmol/L, 7.3%±2.4%, (1.11±0.26)mmol/L, 2.14 mmol/L(1.73 mmol/L, 2.59 mmol/L), 40%±6%, 46%±10%, 36%±8%, 42%±6%, 45%±6%, 37%±7%, 1.23±0.18 and (82±15)kg, (29±4)kg/m 2, (101±13)cm, 0.95±0.08, (76±10)mmHg, (118±16)mmHg, (7.2±1.2)mmol/L, 5.4%±0.8%, (1.26±0.32)mmol/L, 1.21 mmol/L(0.88 mmol/L, 1.55 mmol/L), 36%±8%, 41%±9%, 34%±10%, 38%±8%, 41%±8%, 35%±10%, 1.20±0.17, respectively. There was no significant difference in the intra-group comparison of the Gynoid BF% and A/G ratio ( t=1.903, 1.730, P>0.05) and there were significant differences in the intra-group comparison of the rest of above indicators ( t=12.748, 13.283, 9.013, 3.804, 6.031, 6.226, 2.393, 4.287, -2.900, 3.193, 2.932, 5.198, 2.167, 3.357, 3.116, P<0.05). For patients in the LRYGB group, the body mass, BMI, WC, WHR, DBP, SBP, FPG, HbA1c, HDL-C, TG, whole BF%, arms BF%, legs BF%, trunk BF%, Android BF%, Gynoid BF% and A/G ratio at preoperation and postoperative 6 months were (80±12)kg, (28±4)kg/m 2, (98±9)cm, 0.96±0.05, (85±10)mmHg, (134±17)mmHg, (8.6±2.8)mmol/L, 8.3%±1.7%, (1.13±0.26)mmol/L, 2.06 mmol/L(1.15 mmol/L, 3.30 mmol/L), 30%±8%, 29%±11%, 23%±9%, 37%±7%, 40%±7%, 29%±8%, 1.42±0.26 and (69±9)kg, (24±3)kg/m 2, (91±8)cm, 0.93±0.05, (80±9)mmHg, (129±18)mmHg, (7.4±1.8)mmol/L, 7.0%±1.5%, (1.18±0.29)mmol/L, 1.29 mmol/L(0.85 mmol/L, 2.02 mmol/L), 25%±8%, 23%±12%, 20%±9%, 29%±9%, 32%±10%, 25%±9%, 1.29±0.25, respectively. There was no significant difference in the intra-group comparison of the SBP and HDL-C ( t=1.733, -1.073, P>0.05) and there were significant differences in the intra-group comparison of the rest of above indicators ( t=10.525, 10.200, 7.129, 2.887, 2.805, 2.517, 3.699, 2.608, 7.997, 8.018, 6.029, 8.342, 8.069, 5.813, 6.391, P<0.05). There were significant differences in DBP, SBP, HbA1c, trunk BF%, Android BF% and A/G ratio at postoperative 6 months between LSG group and LRYGB group ( F=6.408, t=2.641, F=20.673, 5.140, 5.735, 4.714, P<0.05). (2) The changes of whole and local body composition from preoperation to postoperative 6 months: for patients in the LSG group, the whole fat mass, muscle mass, fat-free mass at preoperation and postoperative 6 months were (38.74±9.68)kg, (57.71±11.62)kg, (60.14±11.95)kg and (26.64±8.29)kg, (48.65±13.80)kg, (51.00±14.27)kg, respectively, showing significant differences in the intra-group comparison of the above indicators ( t=5.256, 5.413, 5.315, P<0.05); the arms fat mass, muscle mass, fat-free mass were (5.19±1.67)kg, (5.78±1.58)kg, (6.10±1.64)kg and (3.73±1.19)kg, (5.10±1.53)kg, (5.43±1.57)kg, respectively, showing significant differences in the intra-group comparison of the above indicators ( t=7.564, 5.405, 5.363, P<0.05); the legs muscle mass and fat-free mass were (19.05±4.19)kg, (19.93±4.35)kg and (15.93±4.71)kg, (16.81±4.87)kg, respectively, showing significant differences in the intra-group comparison of the above indicators ( t=5.623, 5.568, P<0.05); the trunk fat mass and fat-free mass were (21.93±4.90)kg, (29.7±5.94)kg and (14.69±4.79)kg, (24.78±7.02)kg respectively, showing significant differences in the intra-group comparison of the above indicators ( t=8.903, 5.421, P<0.05); the Android fat mass and fat-free mass were (4.16±1.19)kg, (5.01±1.12)kg and (2.57±0.90)kg, (3.83±1.20)kg respectively, showing significant differences in the intra-group comparison of the above indicators ( t=8.288, 7.637, P<0.05); the Gynoid fat mass and fat-free mass were (5.51±1.42)kg, (9.27±1.86)kg and (3.85±1.16)kg, (7.65±2.31)kg, respectively, showing significant differences in the intra-group comparison of the above indicators ( t=7.461, 5.672, P<0.05); the skeletal muscle index were (8.86±1.38)kg/m 2 and (7.49±1.71)kg/m 2, respectively, showing a significant differences in the intra-group comparison ( t=5.724, P<0.05). For patients in the LRYGB group, the whole fat mass, muscle mass, bone mineral content, fat-free mass at preoperation and postoperative 6 months were (23.58±7.80)kg, (51.76±8.35)kg, (2.55±0.48)kg, (54.31±8.63)kg and (16.88±6.86)kg, (49.41±7.70)kg, (2.47±0.50)kg, (51.88±8.05)kg, respectively, showing significant differences in the intra-group comparison of the above indicators ( t=9.001, 3.974, 4.354, 4.075, P<0.05); the arms fat mass were (2.72±2.37)kg and (1.73±1.02)kg, respectively, showing significant differences in the intra-group comparison of the above indicators ( t=3.470, P<0.05); the legs fat mass, muscle mass, fat-free mass were (5.21±2.46)kg, (16.68±3.50)kg, (17.60±3.66)kg and (4.01±2.12)kg, (15.63±2.90)kg, (16.54±3.05)kg, respectively, showing significant differences in the intra-group comparison of the above indicators ( t=6.592, 3.372, 3.319, P<0.05); the trunk fat mass were (14.87±4.11)kg and (10.38±4.00)kg, respectively, showing a significant difference in the intra-group comparison of the above indicators ( t=8.431, P<0.05); the Android fat mass and fat-free mass were (2.61±0.86)kg, (3.96±0.87)kg and (1.81±0.79)kg, (3.78±0.67)kg respectively, showing significant differences in the intra-group comparison of the above indicators ( t=8.032, 2.153, P<0.05); the Gynoid fat mass and fat-free mass were (3.14±1.17)kg, (7.89±1.58)kg and (2.44±0.96)kg, (7.43±1.26)kg, respectively, showing significant differences in the intra-group comparison of the above indicators ( t=6.112, 3.207, P<0.05); the skeletal muscle index were (8.04±1.22)kg/m 2 and (7.43±1.13)kg/m 2, respectively, showing significant differences in the intra-group comparison ( t=4.953, P<0.05). There were significant differences in whole muscle mass, whole fat-free mass, arms fat mass, legs muscle mass, legs fat-free mass, trunk fat-free mass, Android fat-free mass, Gynoid fat-free mass and skeletal muscle index at postoperative 6 months between LSG group and LRYGB group ( F=13.846, 13.614, 23.696, 7.100, 7.127, 15.243, 16.921, 8.625, 5.497, P<0.05). (3) Analysis of the correlation between BF% and anthropometric parameters, glucolipid metabolism: the whole BF% of 66 patients was positively correlated with body mass, BMI, WC and WHR ( r=0.405, 0.663, 0.625, 0.331, P<0.05); the arms BF% was positively correlated with body mass, BMI, WC and WHR ( r=0.432, 0.682, 0.639, 0.309, P<0.05); the legs BF% was positively correlated with body mass, BMI and WC ( r=0.366, 0.646, 0.564, P<0.05); the trunk BF% was positively correlated with body mass, BMI, WC and WHR ( r=0.332, 0.560, 0.554, 0.335, P<0.05); the Android BF% was positively correlated with body mass, BMI, WC and WHR ( r=0.327, 0.537, 0.543, 0.336, P<0.05); the Gynoid BF% was positively correlated with BMI and WC ( r=0.561, 0.488, P<0.05), and negatively correlated with FPG ( r=-0.491, P<0.05); the A/G ratio was negatively correlated with BMI ( r=-0.334, P<0.05), and positively correlated with FPG ( r=0.506, P<0.05); the skeletal muscle index was positively correlated with body mass, BMI, WC and WHR ( r=0.757, 0.641, 0.609, 0.519, P<0.05), and negatively correlated with HDL-C ( r=-0.369, P<0.05). (4) Follow-up: 66 patients were followed up at the time of postoperative 6 month. Conclusions:Both LSG and LRYGB significantly change body composition. LRYGB is superior to LSG in reducing trunk BF% and Android BF%. The effects of the two surgical methods on fat mass and bone mineral content are similar. LSG lead to a more significant decrease in whole muscle mass, and LRYGB lead to a more significant decrease in legs muscle mass and skeletal muscle index.

Objective: To test the effect of metastasis associated in lung adenocarcinoma transcript 1 (MALAT1) and/or osimertinib on the proliferation and apoptosis of HCC827 cells, and explore the potential mechanism of MALAT1 induced resistance to osimertinib. Methods: We transfected HCC827 cells with LV-vector or LV-over/MALAT1. Stable transfected cells (HCC827/Vector, HCC827/MALAT1) were selected by adding puromycin. HCC827/MALAT1 cells were further transfected with the shRNA-negative control (NC) or shRNA-human epidermal growth factor receptor 3 (ERBB3) plasmid. The effects of overexpression of MALAT1, knockdown of ERBB3 and/or osimertinib on the proliferation of HCC827 cells were evaluated by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2H tetrazolium bromide (MTT) assay. Cell apoptosis induced by MALAT1 overexpression, knockdown of ERBB3 and/or osimertinib treatment were analyzed by flow cytometry analysis. The expressions of EGFR and ERBB3 signal pathway related proteins in HCC827 cells treated with overexpression of MALAT1, knockdown of ERBB3 and/or osimertinib treatment were detected by western blot. Results: The MTT assay showed that sensitivity to osimertinib of HCC827/MALAT1 cells were significantly repressed. The 50% inhibitive concentration (IC₅₀) of osimertinib >4 000 nmol/L in HCC827/MALAT1 cells. However, knockdown of ERBB3 facilitated the anti-proliferation effect of osimertinib, and the IC₅₀ of osimertinib in shRNA-ERBB3 cells was (17.27±3.21) nmol/L. The results of flow cytometry analysis showed that the apoptotic rate of HCC827/MALAT1 cells induced by 10 nmol/L osimertinib was (8.38±0.92)%, significantly lower than (27.17±5.83)% of knockdown of ERBB3 (P<0.01). Western blotting showed that the expression of p-ERBB3, p-AKT and p-extracellular regulated protein kinases (ERK) in HCC827/MALAT1 cells was markedly up-regulated, while the expression of p-epithelial growth factor receptor (EGFR) was inhibited. The expressions of p-ERBB3, p-AKT and p-ERK were marginally affected by osimertinb. However, osimertinib downregulated the expressions of p-EGFR, p-ERBB3, p-AKT and p-ERK in ERBB3 deleted cells. Conclusions MALAT1 confers resistance to osimertinb in HCC827 cells by activating of the ERBB3/PI3K/AKT and ERBB3/MAPK/ERK signaling pathways.

Objective: To investigate the relationship of procollagen-lysine 2-oxoglutarate 5-dioxygenase 2 (PLOD2) expression and the clinical characteristics of osteosarcoma, and explore the potential mechanism of tumour metastasis promoted by PLOD2. Methods: The expression of PLOD2 in osteosarcoma tissues and paired adjacent tissues were detected by immunohistochemistry and qRT-PCR. Correlation of PLOD2 expression in osteosarcoma with the clinical pathologic features was analyzed by Chi square test and Kaplan-Meier analysis.Fibrillar collagen formation and collagen deposition in the tumor tissues were detected by picrosirius red staining. We transfected U-2OS cells with LV-vector, LV-over/PLOD2, sh-NC and sh-PLOD2. The expression of PLOD2 was detected by qRT-PCR. The impact of POLD2 on U-2OS cell invasion was determined by wound-healing assay and Transwell migration assay. The expressions of PLOD2/FAK/JAK2-STAT3 signal pathway related proteins were detected by western blotting. Results: The high expression level of PLOD2 in osteosarcoma tissues was 72.5%, significantly higher than 0% in paired adjacent noncancerous tissues (P<0.01), the expression of PLOD2 was positively correlated with lymph node metastasis, pulmonary metastasis and poor outcome (P<0.01). The same results were also observed in qRT-PCR assay. The median survival time of patients with high expression of PLOD2 protein was 13 months, significantly shorter than 32 months of patients with low expression of PLOD2 (P<0.05). The result of picrosirius red staining showed that the percentage of collagen fiber deposition in the osteosarcoma tissue with high level of PLOD2 was (74.43+ 9.63)%, significantly higher than (9.67±1.28)% in tissue with low expression of PLOD2 (P<0.001). The result of wound-healing and Transwell migration assay showed that over-expression of PLOD2 markedly promoted the invasion, however, knockdown of PLOD2 suppressed the invasion of U-2OS cells (both P<0.01). The result of western blotting showed that over-expression of PLOD2 significantly increased the expression levels of p-FAK, p-JAK2, p-STAT3, but knockdown PLOD2 decreased the levels of p-FAK, p-JAK2, p-STAT3 in U-2OS cells. Conclusions Up-regulation of PLOD2 in osteosarcoma is correlated with lymphatic and distant metastasis. PLOD2 promotes invasion and metastasis of osteosarcoma might through FAK/JAK2-STAT3 signal pathway.

Objective To test the effect of metastasis associated in lung adenocarcinoma transcript 1 ( MALAT1) and／or osimertinib on the proliferation and apoptosis of HCC827 cells, and explore the potential mechanism of MALAT1 induced resistance to osimertinib. Methods We transfected HCC827 cells with LV?vector or LV?over／MALAT1. Stable transfected cells ( HCC827／Vector, HCC827／MALAT1) were selected by adding puromycin. HCC827／MALAT1 cells were further transfected with the shRNA?negative control ( NC) or shRNA?human epidermal growth factor receptor 3 ( ERBB3 ) plasmid. The effects of overexpression of MALAT1, knockdown of ERBB3 and／or osimertinib on the proliferation of HCC827 cells were evaluated by 3?(4,5?dimethyl?2?thiazolyl)?2,5?diphenyl?2H tetrazolium bromide ( MTT) assay. Cell apoptosis induced by MALAT1 overexpression, knockdown of ERBB3 and／or osimertinib treatment were analyzed by flow cytometry analysis. The expressions of EGFR and ERBB3 signal pathway related proteins in HCC827 cells treated with overexpression of MALAT1, knockdown of ERBB3 and／or osimertinib treatment were detected by western blot. Results The MTT assay showed that sensitivity to osimertinib of HCC827／MALAT1 cells were significantly repressed. The 50% inhibitive concentration (IC50 ) of osimertinib ＞4 000 nmol／L in HCC827／MALAT1 cells.However, knockdown of ERBB3 facilitated the anti?proliferation effect of osimertinib, and the IC50 of osimertinib in shRNA?ERBB3 cells was (17.27±3.21) nmol／L. The results of flow cytometry analysis showed that the apoptotic rate of HCC827／MALAT1 cells induced by 10 nmol／L osimertinib was (8.38±0.92)%, significantly lower than ( 27.17± 5.83)% of knockdown of ERBB3 ( P＜0.01). Western blotting showed that the expression of p?ERBB3, p?AKT and p?extracellular regulated protein kinases ( ERK) in HCC827／MALAT1 cells was markedly up?regulated, while the expression of p?epithelial growth factor receptor (EGFR) was inhibited. The expressions of p?ERBB3, p?AKT and p?ERK were marginally affected by osimertinb. However, osimertinib downregulated the expressions of p?EGFR, p?ERBB3, p?AKT and p?ERK in ERBB3 deleted cells. Conclusions MALAT1 confers resistance to osimertinb in HCC827 cells by activating of the ERBB3／PI3K／AKT and ERBB3／MAPK／ERK signaling pathways.

Objective To investigate the relationship of procollagen?lysine 2?oxoglutarate 5?dioxygenase 2 ( PLOD2 ) expression and the clinical characteristics of osteosarcoma, and explore the potential mechanism of tumour metastasis promoted by PLOD2. Methods The expression of PLOD2 in osteosarcoma tissues and paired adjacent tissues were detected by immunohistochemistry and qRT?PCR. Correlation of PLOD2 expression in osteosarcoma with the clinical pathologic features was analyzed by Chi square test and Kaplan?Meier analysis.Fibrillar collagen formation and collagen deposition in the tumor tissues were detected by picrosirius red staining. We transfected U?2OS cells with LV?vector, LV?over／PLOD2, sh?NC and sh?PLOD2. The expression of PLOD2 was detected by qRT?PCR. The impact of POLD2 on U?2OS cell invasion was determined by wound?healing assay and Transwell migration assay. The expressions of PLOD2／FAK／JAK2?STAT3 signal pathway related proteins were detected by western blotting. Results The high expression level of PLOD2 in osteosarcoma tissues was 72.5%, significantly higher than 0% in paired adjacent noncancerous tissues ( P＜0.01), the expression of PLOD2 was positively correlated with lymph node metastasis, pulmonary metastasis and poor outcome (P＜0.01). The same results were also observed in qRT?PCR assay. The median survival time of patients with high expression of PLOD2 protein was 13 months, significantly shorter than 32 months of patients with low expression of PLOD2 ( P＜0.05). The result of picrosirius red staining showed that the percentage of collagen fiber deposition in the osteosarcoma tissue with high level of PLOD2 was (74.43+9.63)%, significantly higher than ( 9.67± 1.28)% in tissue with low expression of PLOD2 (P＜0.001).The result of wound?healing and Transwell migration assay showed that over?expression of PLOD2 markedly promoted the invasion, however, knockdown of PLOD2 suppressed the invasion of U?2OS cells ( both P＜0.01).The result of western blotting showed that over?expression of PLOD2 significantly increased the expression levels of p?FAK, p?JAK2, p?STAT3, but knockdown PLOD2 decreased the levels of p?FAK, p?JAK2, p?STAT3 in U?2OS cells. Conclusions Up?regulation of PLOD2 in osteosarcoma is correlated with lymphatic and distant metastasis. PLOD2 promotes invasion and metastasis of osteosarcoma might through FAK／JAK2?STAT3 signal pathway.

Objective To test the effect of metastasis associated in lung adenocarcinoma transcript 1 ( MALAT1) and／or osimertinib on the proliferation and apoptosis of HCC827 cells, and explore the potential mechanism of MALAT1 induced resistance to osimertinib. Methods We transfected HCC827 cells with LV?vector or LV?over／MALAT1. Stable transfected cells ( HCC827／Vector, HCC827／MALAT1) were selected by adding puromycin. HCC827／MALAT1 cells were further transfected with the shRNA?negative control ( NC) or shRNA?human epidermal growth factor receptor 3 ( ERBB3 ) plasmid. The effects of overexpression of MALAT1, knockdown of ERBB3 and／or osimertinib on the proliferation of HCC827 cells were evaluated by 3?(4,5?dimethyl?2?thiazolyl)?2,5?diphenyl?2H tetrazolium bromide ( MTT) assay. Cell apoptosis induced by MALAT1 overexpression, knockdown of ERBB3 and／or osimertinib treatment were analyzed by flow cytometry analysis. The expressions of EGFR and ERBB3 signal pathway related proteins in HCC827 cells treated with overexpression of MALAT1, knockdown of ERBB3 and／or osimertinib treatment were detected by western blot. Results The MTT assay showed that sensitivity to osimertinib of HCC827／MALAT1 cells were significantly repressed. The 50% inhibitive concentration (IC50 ) of osimertinib ＞4 000 nmol／L in HCC827／MALAT1 cells.However, knockdown of ERBB3 facilitated the anti?proliferation effect of osimertinib, and the IC50 of osimertinib in shRNA?ERBB3 cells was (17.27±3.21) nmol／L. The results of flow cytometry analysis showed that the apoptotic rate of HCC827／MALAT1 cells induced by 10 nmol／L osimertinib was (8.38±0.92)%, significantly lower than ( 27.17± 5.83)% of knockdown of ERBB3 ( P＜0.01). Western blotting showed that the expression of p?ERBB3, p?AKT and p?extracellular regulated protein kinases ( ERK) in HCC827／MALAT1 cells was markedly up?regulated, while the expression of p?epithelial growth factor receptor (EGFR) was inhibited. The expressions of p?ERBB3, p?AKT and p?ERK were marginally affected by osimertinb. However, osimertinib downregulated the expressions of p?EGFR, p?ERBB3, p?AKT and p?ERK in ERBB3 deleted cells. Conclusions MALAT1 confers resistance to osimertinb in HCC827 cells by activating of the ERBB3／PI3K／AKT and ERBB3／MAPK／ERK signaling pathways.

Objective To investigate the relationship of procollagen?lysine 2?oxoglutarate 5?dioxygenase 2 ( PLOD2 ) expression and the clinical characteristics of osteosarcoma, and explore the potential mechanism of tumour metastasis promoted by PLOD2. Methods The expression of PLOD2 in osteosarcoma tissues and paired adjacent tissues were detected by immunohistochemistry and qRT?PCR. Correlation of PLOD2 expression in osteosarcoma with the clinical pathologic features was analyzed by Chi square test and Kaplan?Meier analysis.Fibrillar collagen formation and collagen deposition in the tumor tissues were detected by picrosirius red staining. We transfected U?2OS cells with LV?vector, LV?over／PLOD2, sh?NC and sh?PLOD2. The expression of PLOD2 was detected by qRT?PCR. The impact of POLD2 on U?2OS cell invasion was determined by wound?healing assay and Transwell migration assay. The expressions of PLOD2／FAK／JAK2?STAT3 signal pathway related proteins were detected by western blotting. Results The high expression level of PLOD2 in osteosarcoma tissues was 72.5%, significantly higher than 0% in paired adjacent noncancerous tissues ( P＜0.01), the expression of PLOD2 was positively correlated with lymph node metastasis, pulmonary metastasis and poor outcome (P＜0.01). The same results were also observed in qRT?PCR assay. The median survival time of patients with high expression of PLOD2 protein was 13 months, significantly shorter than 32 months of patients with low expression of PLOD2 ( P＜0.05). The result of picrosirius red staining showed that the percentage of collagen fiber deposition in the osteosarcoma tissue with high level of PLOD2 was (74.43+9.63)%, significantly higher than ( 9.67± 1.28)% in tissue with low expression of PLOD2 (P＜0.001).The result of wound?healing and Transwell migration assay showed that over?expression of PLOD2 markedly promoted the invasion, however, knockdown of PLOD2 suppressed the invasion of U?2OS cells ( both P＜0.01).The result of western blotting showed that over?expression of PLOD2 significantly increased the expression levels of p?FAK, p?JAK2, p?STAT3, but knockdown PLOD2 decreased the levels of p?FAK, p?JAK2, p?STAT3 in U?2OS cells. Conclusions Up?regulation of PLOD2 in osteosarcoma is correlated with lymphatic and distant metastasis. PLOD2 promotes invasion and metastasis of osteosarcoma might through FAK／JAK2?STAT3 signal pathway.

Objective: To explore the mechanism of Xuebijing injection in the treatment of acute paraquat poisoning by means of studying the expression of TNF-alpha, NF-kappa B, Caspase-3 and the changes of cell apoptosis rate detected by TUNEL in the lung tissue of acute paraquat-induced rats. Methods: On the base of random number table, 126 Wister rats weighing 220 g to 270 g were divided into 3 groups: (1) Control group: 42 rats, (2) Poisoned group: 42 rats, (3) Treatment group: 42 rats. On 1^st、3^rd、7^th、14^th、21^st、28^th、and 35^th day, six rats from each group were anaesthetized by intraperitoneal injection of chloral hydrate. To cut the chest and take the lung tissue samples. The expression levels of Tumor Necrosis Factor-alpha, Nuclear Factor-kappa B and Caspase-3 protein in lung tissue were detected by immunohistochemical staining, as well as apoptotic cell rate was detected by TUNEL staining. Results: The expression levels of Tumor Necrosis Factor-alpha, Nuclear Factor-kappa B, Caspase-3 protein and TUNEL staining in the lung tissue of the poisoned group was significantly higher than that of the control group (P<0.05) . Compared with the poisoned group, the expression of TNF-alpha, NF-kappa B, Caspase-3 and TUNEL in treatment group decreased significantly (P<0.05) , but they were still higher than those of the control group, and the difference was statistically significant compared with the control group (P<0.05) . Conclusion Apoptosis and TNF-alpha, NF-kappa B and Caspase-3 play an important role in lung injury of paraquat-induced rats. Xuebijing injection can inhibit the expression of TNF-alpha, NF-kappa B, Caspase-3 in lung tissue, reduce the apoptosis rate and alleviate the damage of lung tissue in paraquat-poisoning rats.