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Objective: To explore the effect of intermittent pneumatic compression(IPC) combined with 3M thermometer on the prevention of deep venous thrombosis(DVT) in patients with femoral intertrochanteric fracture., Methods: From March 2016 to August 2019, 127 patients with femoral intertrochanteric fractures who underwent proximal femoral nail antirotation(PFNA) were retrospectively analyzed. They were divided into two groups according to different methods of thrombus prevention and treatment. Among them, 63 patients in group A did not use IPC and 3M thermometer;64 cases in group B were treated with IPC combined with 3M thermometer. Color Doppler ultrasound was used to dynamically monitor the DVT and changes of lower limbs during perioperative period. The venous thrombosis of lower limbs was monitored at 0, 24, 72 h and > 72 h after operation(recheck every 3 days until discharge)., Results: Occurrence of DVT of lower limbs after PFNA operation in two groups:there were 5 cases (7.8%) in group B and 20 cases (31.7%) in group A, there was significant difference between two groups ( P =0.001). There was no significant difference in lower limb DVT between two groups at 0, 72 and > 72 h after operation( P >0.05), but the formation rate of group A was significantly higher than that of group B at 24 h after operation ( P =0.049). There was no significant difference in DVT formation between group A and group B( P >0.05). However, the formation of DVT in group A was significantly higher than that in group B( P =0.012)., Conclusion: Intraoperative IPC combined with 3M thermostat can effectively prevent DVT of lower limbs in patients undergoing PFNA surgery.

This study was purpose to investigate the role of reactive oxygen species (ROS) in apoptosis and autophagy induced by FTY720 in multiple myeloma cell line U266. U266 cells were treated by different concentrations of FTY720 for 24 h, the apoptotic rates were detected by flow cytometry, and the expression of LC3B was detected by Western blot. The results indicated that apoptosis and autophagy were induced by FTY720 in U266 cells. Autophagy induced by FTY720 could lead to cell death. Bafilomycin A1, the inhibitor of autophagy, could enhance the cell viability in U266 cells treated with FTY720. NAC or Tiron, ROS scavenger, could decrease the FTY720 induced apoptosis and the expression of LC3B-II was reduced in combination of FTY720 with NAC or Tiron as compared with treatment with FTY720 only. It is concluded that FTY720 can induce U266 cell apoptosis and autophagy. ROS is the mediator that regulates both the apoptosis and autophagy in multiple myeloma cells.

Objective: To investigate the effects of FTY720, a new immunosuppressive agent, on apoptosis and autophagy in multiple myeloma(MM) cell line U266 and to clarify its molecular mechanism., Methods: U266 cells were treated with 0, 2.5, 5.0, 10.0 and 20.0 µmol/L FTY720 for 24 hours, and the cell viability was assayed by CCK-8 method. Then U266 cells were treated with 20.0 µmol/L FTY720 for 0, 2, 6 and 24 hours, the cell viability was tested. The apoptotic rates induced by different doses and time points of FTY720 were tested by flow cytometry separately. The expression of LC3B was detected by Western blot after U266 cells treated with different doses of FTY720 to see autophagy. U266 cells were treated with FTY720 ± Bafilomycin A1, an inhibitor of autophagy, for 24 hours, then the cell viability and apoptotic rates were tested. Meanwhile the expression of survivin, anti-apoptotic factors, were tested by Western blot., Results: The cell viability and the apoptotic rates were inhibited significantly by FTY720 (P < 0.05) in time-dependent and dose-dependent manner. The expression of LC3B-II increased significantly in a dose-dependent manner, it indicated that the autophagy was induced by FTY720. Bafilomycin A1 could rescue the cell viability and apoptotic rates in U266 cells treated with FTY720, and it could also rescue the expression of survivin decreased by FTY720., Conclusions: FTY720 can cause apoptosis and autophagy of U266 cells. The autophagy promote the apoptosis, which maybe due to the degradation of anti-apoptotic factors such as survivin or their upstream factors in lysosomes through autophagy.

Objective: To study the mechanism of bortezomib inducing peripheral neuropathy and the reversing affection of reduced glutathione., Methods: Female Wistar rats were randomly divided into three groups. Group 1, treatment with bortezomib; Group 2, treatment with bortezomib and reduced glutathione; Group 3, saline control group. Drugs were administrated on the 1st, 4th, 7th and 11th day for the three groups. The amorphous of sciatic nerve and dorsal root ganglion (DRG) were observed by electron microscope on 14th and 42nd day. On 14th day, laser confocal microscopy was used to detect reactive oxygen species (ROS) of DRG neuron obtained from the rats by treated with DCFH-DA after primary culture., Results: On 14th day, morphology of sciatic nerve and DRG changed in both group 1 and 2. On 42nd day, the amorphous became normally in group 1. On 14th day, ROS releasing from DRG neuron was increased obviously in group 1 (P < 0.01), while decreased in both group 2 and 3, and the difference between the latter two groups had no statistical significance (P = 0.210)., Conclusion: Releasing ROS to injure mitochondrion and endoplasmic reticulum maybe involved in bortezomib induced peripheral neuropathy. Although reduced glutathione can inhibit ROS release, it has no obviously reversal effect for peripheral neuropathy.

The study was aimed to investigate the effects of bortezomib (BTZ) on the expression of ERK, JNK and P38 in daunorubicin (DNR)-resistant K562 cells (K562/DNR) and to clarify the molecular mechanism of BTZ in reversing the drug-resistance in leukemic cells. The K562/DNR cells and the cellular toxicity of BTZ was determined by MTT, then 4 µg/L of BTZ was chosen to do the experiment. The expression of ERK, JNK, p38 and P-gp of K562/DNR cells treated with DNR only or DNR combined with BTZ for 12, 24 and 36 hours was detected by Western blot. The apoptosis rate in each group was assayed by flow cytometry. The results showed that as compared with DNR group, the expression of P-ERK, P-P38 and P-gp was significantly suppressed (p < 0.05) and the expression of P-JNK was significantly enhanced (p < 0.05) in the cells treated with DNR combined with BTZ. There was no change in the expression of total ERK, P38 and JNK. The effect increased with the prolonging of time. Meanwhile, the apoptosis rate in cells treated with DNR combined with BTZ increased compared with DNR only. It is concluded that the BTZ can reverse the drug resistance in K562/DNR cells by MAPK signaling pathway and increase the apoptosis of leukemic cells. The effect shows the characteristics of time-dependent manner.

The aim of this study was to investigate the apoptosis effect of Jurkat cells induced by ursolic acid (UA) and its molecular mechanism so as to provide the theoretical basis for treatment of hematological malignancies by using UA. The cytotoxic effect of different concentration UA on Jurkat cells and inhibitory effect of caspase-9 inhibitor on cytotoxicity of UA were assayed by using WST-8 method; the Jurkat cells treated with 20 or 40 micromol/L UA for 2 or 4 hours were collected and were stained by Annexin/PI, then the apoptosis rate of Jurkat cells was detected by flow cytometry; the Jurkat cells in logarithmic growth phase were collected after treatment with different concentrations of UA for different times, the cell protein was extracted, then the activation of caspase-9, -3 and cytochrome C as well as phosphorylation level of Akt were determined by Western blot. The results indicated that the cytotoxic effect of UA on Jurkat cells was significant. UA induced apoptosis of Jurkat cells. Caspase-9, caspase-3 and cytochrome C were activated, and the phosphorylation of Akt was inhibited in the Jurkat cell apoptosis process induced by UA. It is concluded that the UA shows significant cytotoxic effect on Jurkat cells, UA can induce apoptosis of Jurkat cells through the mitochondria pathway. The mechanism may be associated with the inhibition of Akt phosphorylation.

The objective of this study was to investigate the immunophenotypic subtype profiles of 192 patients with acute myeloid leukemia (AML) and its association to cytogenetics and clinical features. Immunophenotyping of 192 patients was performed by flow cytometry using a panel of monoclonal antibodies. The karyotypes in 125 out of 192 cases were analyzed by G-banding technology. The results showed that CD33, CD13, myeloperoxidase (MPO) and CD117 were the most commonly expressed antigens in AML. CD117 expressed in 84.6% of AML-M3 cases. A combination of intensive autofluorescence, both CD34- and HLA-DR-, and high expression of CD13, CD33 and MPO had significant value for AML-M3 diagnosis. CD14 expressed only in AML-M4 and AML-M5, and both intensive positivity of CD64 and CD15 with high expression of HLA-DR may suggest great possibility for diagnosis of AML-M5. Lymphoid marker expression was documented in 47.9% of the 192 AML cases. CD56 (26.0%) and CD7 (20.8%) were the most commonly expressed lymphoid markers in AML patients, followed by CD19 (9.9%) and CD2 (7.3%). Abnormal karyotypes were detected in 76 out of 125 cases (60.8%). Correlation test showed that t(8;21) was found only in 17 cases of AML-M2 and strongly associated with the individual or combinational expressions of CD15/CD19/CD56. And 28 cases of t(15;17) were found in AML-M3; 2 cases of inv(16) were found in AML-M4EO. Higher CD34 positivity was found in LymAg+ group (77.2%) than that in LymAg- group (48.0%). It is concluded that immunophenotype analysis is useful for AML diagnosis and classification, and the immunophenotype has close relevance to the abnormal cytogenetic changes and clinical features in AML. The results suggested that a new prognostic scoring system that integrated the morphology, cytogenetic abnormalities and immunophenotype parameters would benefit the diagnosis, classification, and estimation of prognosis in AML patients.