Objective:To compare the conventional percutaneous minimally invasive plate fixation sparing pronator quadratus versus the 3-point positioning percutaneous minimally invasive palmar locking plate fixation sparing pronator quadratus for distal radial fractures.Methods:Between January 2015 and December 2017, 50 patients with distal radius fracture were treated surgically at Department of Orthopaedics, The Second Hospital of Fuzhou by percutaneous minimally invasive plate fixation sparing pronator quadratus. They were 24 males and 26 females, aged from 21 to 71 years. Conventional percutaneous minimally invasive plate fixation was conducted for 25 patients and 3-point positioning minimally invasive plate fixation for the other 25 patients. The 2 groups were compared in terms of fluoroscopic adjustments of the plate under the pronator quadratus, fracture healing time, visual analogue scale (VAS) on days 1, 3 and 7 postoperation, and wrist flexion and extension, forearm rotation and upper limb function by Disabilities of the Arm, Shoulder and Hand(DASH) scores and Gartland-Werley scores at 3 months postoperation.Results:There was no significant difference in the general data between the 2 groups, showing comparability between groups ( P>0.05). The fluoroscopic adjustments of the plate under the pronator quadratus for the conventional group (3.4±0.5) were significantly more than for the 3-point positioning group (1.1±0.3) ( P<0.05). The VAS scores on days 1, 3 and 7 postoperation for the conventional group were significantly higher than for the 3-point positioning group ( P<0.05). At 3 months postoperation, the wrist pronation was respectively 76.6°±1.9° and 82.3°±2.0°, and the Gartland-Werley scores were respectively 3.4±0.5 and 1.9±0.2 for the conventional and 3-point positioning groups, showing significant differences between the 2 groups ( P< 0.05). Conclusions:In the treatment of distal radial fractures, compared with conventional percutaneous minimally invasive plate fixation, the 3-point positioning minimally invasive plate fixation sparing pronator quadratus may minimize the damage to the pronator quadratus, be more minimally invasive, and lead to less early postoperative pain and faster functional recovery.

Objective:To investigate the clinical efficacy of proximal femoral nail anti-rotation (PFNA) assisted by the "3-2-1" surface positioning method in the treatment of femoral subtrochanteric fractures.Methods:A total of 97 patients with subtrochanteric fractures admitted to the Second Hospital of Fuzhou from January 2015 to December 2020 were retrospectively analyzed. They were divided into two groups according to whether the "3-2-1" surface positioning method (3 longitudinal axes, 2 preset incisions, and 1 auxiliary incision) was used. There were 44 patients in the surface positioning group, including 25 males and 19 females, aged 61.59±18.43 years (range, 22-90 years). According to the Seinsheimer classification, there were 13 cases of type II, 11 cases of type III, 6 cases of type IV, and 14 cases of type V. The mechanism of injury was low energy injury in 26 cases and high energy injury in 18 cases. There were 53 patients in the traditional positioning group, including 30 males and 20 females, aged 56.38±17.24 years (range, 24-90 years). According to the Seinsheimer classification, there were 9 cases of type II, 22 cases of type III, 9 cases of type IV, and 13 cases of type V. According to the mechanism of injury, there were 30 cases of low energy injury and 23 cases of high energy injury. The length of incision, operation time, and blood loss were recorded. At 1, 3, 6, and 12 months after operation, the anteroposterior and lateral X-ray films of the hip were taken to evaluate the imaging indicators (neck-shaft angle, anteroposterior and lateral displacement, and angulation), fracture healing, and complications (infection, malunion, loosening and breakage of the internal fixation, and periprosthetic fracture). The Harris hip score and EuroQol five dimensions questionnaire (EQ-5D) were evaluated.Results:All patients successfully completed the operation and were followed up for 15.12±1.54 months (range, 12-18 months). The operation time, incision length, dominant blood loss and hidden blood loss in the surface positioning group were 1.78(1.50, 2.00) h, 8(8, 9) cm, 300(200, 400) ml and 843(629, 1 130) ml, respectively, which were less than 2.10(1.69, 2.38) h, 10(9, 12) cm, 400(300, 500) ml and 1 030(954, 1 266) ml in the traditional positioning group, and the difference was statistically significant ( P<0.05). The neck-shaft angle in the surface positioning group was 135.54°±2.83°, which was larger than 132.33°±3.37° in the traditional positioning group, and the difference was statistically significant ( t=5.02, P<0.001). The anterolateral and lateral displacement and lateral image angle in the surface positioning group were 4.70±1.60 cm, 4.52±1.71 cm and 9.36°±2.94°, respectively, which were lower than 6.14±2.57 cm, 5.98±2.70 cm and 11.46°±4.68° in the traditional positioning group, and the difference was statistically significant ( P<0.05). One year after operation, the Harris hip score and EQ-5D score of the surface positioning group were 92(84, 99) points and 0.90(0.73, 1.00) points, respectively, which were higher than 88(74, 96) points and 0.81(0.72, 0.94) points of the traditional positioning group ( P<0.05). Conclusion:The "3-2-1" surface positioning method assisted PFNA internal fixation in the treatment of femoral subtrochanteric fracture can improve the quality of reduction, reduce intraoperative blood loss, and improve hip function and quality of life.

OBJECTIVE:To study the inhibitory effect and mechanism of Inula helenium ethyl acetate extract(IHE)on prolif-eration of human pancreatic cancer Capan-2 cells. METHODS:MTT was used to determine the cell proliferation inhibition rate af-ter treated by 0,0.5,1,2,4,8 μg/mL IHE;clone formation test was used to observe the effects of 0,1,2 μg/mL IHE treating for 1 week on cell clone formation;Hoechest 33342 staining was used to observe the changes of nuclear morphology after treated by 0,2,4 μg/mL IHE for 48 h;flow cytometry was used to detect the cell apoptosis rate after treated by 0,4,8,16 μg/mL IHE for 48 h;JC-1 staining was used to observe the changes of intracellular mitochondrial membrane potential after treated by 0,4,8, 16 μg/mL IHE for 24 h;Western blot was used to detect the expressions of mitochondrial apoptosis-related proteins Bcl-2,Bax, Mcl-1,p53 up-regulated modulator of apoptosis (PUMA),and polymerase (PARP) after treated by 0,4,8,16 μg/mL IHE for 48 h. RESULTS:2,4,8 μg/mL IHE had obvious inhibitory effect on cell proliferation,showing concentration-dependent relation-ship,with IC50 of 6.6 μg/mL;1,2 μg/mL IHE can obviously inhibit the clone formation of cells;4 μg/mL IHE can obviously cause cell nuclear condensation;8,16 μg/mL IHE can obviously promote the cell apoptosis,and the cell apoptosis rate reached 45.53% after treated by 16 μg/mL IHE for 48 h;16 μg/mL IHE treating for 24 h can cause the decrease of 82.47% cells'mito-chondrial membrane potential;8 μg/mL IHE can obviously down-regulate the protein expressions of Bcl-2,Mcl-1,PUMA and PARP,and 16 μg/mL IHE can obviously down-regulate the expressions of Mcl-1 and PUMA. CONCLUSIONS:IHE may show its inhibitory effect on proliferation of human pancreatic cancer Capan-2 cells by causing the decrease of mitochondrial mem-brane potential in cells and down-regulating the protein expres-sions of Mcl-1 and PUMA to cause cell apoptosis.

Objective: To investigate the effect of down-regulation of miR-221 on cell proliferation and apoptosis of chronic myeloid leukemia (CML) K562 cells and its related regulatory mechanism. Methods: K562 cells were divided into control group, miRNAnegative control (miR-NC) group, miR-221 inhibitor group, miR-221 inhibitor+ negative control siRNA(NC siRNA) group and miR-221 inhibitor+SOCS3 siRNA group. The cells in the control group received no additional treatment. Cells in miR-NC group and miR-221 inhibitor group were transfected with miR-NC and miR-221 inhibitor, respectively. Cells in miR-221 inhibitor+NC siRNA group and miR-221 inhibitor+SOCS3 siRNA group were transfected with NC siRNA and SOCS3 siRNA, respectively, on the basis of successful transfection with miR-221 inhibitor. The transfection efficiency of miR-221 inhibitor was identified by qPCR. Cell viability in each group was measured by CCK-8 assay. Apoptosis in each group was detected by Annexin V-FITC/PI staining using a flow cytometry. The protein expressions of SOCS3, p-JAK1, p-JAK2, p-STAT3 and survivin in each group were detected by WB. Results: Compared with the control group, miR-221 expression was significantly down-regulated in miR-221 inhibitor group (P<0.01), cell viability was significantly reduced at 48 and 72 h after transfection (P<0.05 or P<0.01), the number of apoptotic cells was significantly increased (P< 0.01), the expression of SOCS3 was significantly increased (P<0.01) and the expression levels of p-JAK1, p-JAK2, p-STAT3 and survivin were significantly reduced (all P<0.01). Compared with miR-221 inhibitor group, cell viability was significantly increased at 24, 48 and 72 h after transfection (P<0.05 or P<0.01), the number of apoptotic cells was significantly decreased (P<0.01) and the expression levels of p-JAK1, p-JAK2, p-STAT3 and survivin were significantly increased in miR-221 inhibitor+SOCS3 siRNA group (all P< 0.01). Conclusion: Down-regulation of miR-221 inhibits proliferation and promotes apoptosis of K562 cells, the mechanism of which may be related with up-regulating SOCS3 expression to suppress JAK-STAT3 signaling pathway.

OBJECTIVE：To provide reference for promoting individualized medication in clinic. METHODS ：Information on external quality assessment （EQA）projects and approved kits for the guidance of chemical drug use were collected from the websites of National Center for Clinical Laboratories （NCCL） and National Medical Products Administration （NMPA） as of December 31，2019. The number of laboratories participating in each evaluation project was count. Taking EQA projects of clopidogrel and warfarin drug metabolism gene polymorphism detection as examples ，who was with the highest participation rate ， the methods and reagent kits of each laboratory were analyzed so as to analyze the current status of the clinical pharmacogenomics （PGx）in China. RESULTS ：The number of PGx genetic test EQA projects conducted by NCCL increased from 3（2014）to 9 （2019）. The total number of participating laboratories was 926 in 2018，and 1 249 in 2019. The number of laboratories of warfarin and clopidogrel drug metabolism gene polymorphism detection increased from 57 to 300.5 for warfarin and from 124 to 374.5 for clopidogrel. The more widely used methods were fluorescent PCR and PCR-chip hybridization. The number of reagent kits currently approved by NMPA was 7 for warfarin and 15 for clopidogrel ，respectively. But some of the laboratories participating in EQA used self-prepared reagents yet. CONCLUSIONS ：The clinical PGx is in its infancy ，and the awareness of laboratories about EQA is improving；the main method was fluorescence PCR ，but the use of self-made reagents in laboratories is still common ，regulations concerning the approval ，use and supervision still need to be further improved.

OBJECTIVE： To observe the inhibitory effects and possible mechanism of new small molecular kinase inhibitors Ibr-7 [Irutinil（Ibr） derivatives] on human pancreatic cancer Capan-2 cells. METHODS： Taking Capan-2 cells as objects， CCK-8 method was used to determine the proliferation of cells after treated with 1， 2， 4， 8 μmol/L Ibr/Ibr-7 for 48 h. The survival rates of cells were calculated. Sensitization effects of 1 μmol/L Ibr/Ibr-7 on different doses of gemcitabine/paclitaxel （0.062 5， 0.125， 0.25， 0.5， 1 μmol/L） were detected. Clone formation test was used to detect the situation of cell clone formation after treated with 1， 2， 4 μmol/L Ibr/Ibr-7 for 48 h. The number of cell colony formation was recorded. Flow cytometry or JC-1 method was used to detect the apoptosis of cells after treated with 2， 4， 8 μmol/L Ibr-7 for 24 or 16 h and the changes of mitochondrial transmembrane potential； total apoptotic rate and the percentage of mitochondrial membrane potential decrease were calculated. Western blotting was used to detect the expression of related apoptotic protein （PARP， Noxa， Bcl-2， Bax， Mcl-1， Bcl-xL）. RESULTS： After treated with 1， 2， 4， 8 μmol/L Ibr/Ibr-7 for 48 h， the survival rates of cells were decreased significantly； those of Ibr-7 groups were significantly lower than those of same-dose Ibr groups； IC50 of Ibr-7 was significantly lower than that of Ibr （P＜0.05 or P＜0.01）. After combined with Ibr/Ibr-7， the survival rate of cells was significantly lower than that of same-dose gemcitabine/paclitaxel alone group， and the Ibr-7 combination group was significantly lower than same-dose Ibr combination group （P＜0.05 or P＜0.01）. After treated with 2， 4 μmol/L Ibr and 1， 2， 4 μmol/L Ibr-7 for 48 h， the number of cell clone formation was decreased significantly， while Ibr-7 groups were significantly lower than same-dose Ibr groups （P＜0.01）. After treated with different doses of Ibr-7 for 24 or 16 h， total apoptosis rate of cells （2， 4， 8 μmol/L）， the proportion of cell mitochondrial membrane potential decrease （8 μmol/L）， the relative protein expression of Noxa （2， 4， 8 μmol/L） and Bax （8 μmol/L） were increased significantly， while the protein expression of PARP （8 μmol/L）， Bcl-2 （4 μmol/L）， Mcl-1 （2， 4， 8 μmol/L） were decreased significantly； above indexes （except for relative expression of PARP and Bcl-2） of 8 μmol/L Ibr-7 group were significantly better than same-dose Ibr group （P＜0.05 or P＜0.01）. There was no statistical significance in protein expression of Bcl-xL among those groups （P＞0.05）. CONCLUSIONS： Compared with Ibr， Ibr-7 has better inhibitory and apoptotic effects on human pancreatic cancer Capan-2 cells in vitro， and has stronger chemotherapeutic drug sensitization activity， the mechanism of which may be associated with reducing mitochondrial transmembrane potential， down-regulating the protein expression of PARP， Bcl-2 and Mcl-1 and up-regulating the protein expression of Noxa and Bax.