Objective To compare the efficacy and safety between Chinese generic imatinib (Xinwei(R),Jiansu Hansoh Pharmaceutical Group Co.,Ltd.) versus branded imatinib (Glivec(R),Novartis) in patients with newly-diagnosed chronic myeloid leukemia in chronic phase (CML-CP).Methods Patients with newly diagnosed CML-CP were enrolled and assigned to receive either Xinwei or Glivec at an initial dose of 400 mg/d according to patients' financial capability.The efficacy and adverse effects were evaluated.Results From January 2014 to September 2015,145 eligible patients were assigned to Xinwei (n =89) or Glivec (n =56) group.All patients were treated and followed up at least 3 months.At 3 months,the complete response rates were 95.5％ (85/89) and 100％ (56/56),major cytogenetic response rates were 74.2％ (66/89) and 80.4％ (45/56),and the proportions of achieving BCR-ALBIS ≤ 10％ were 76.1％ (67/88) and 82.1％ (46/56) in Xinwei and Glivec groups respectively (all P ＞0.05).With a median follow-up of 12 months,2 patients in each group progressed to accelerate or blast phase.Hematologic and non-hematologic side effects were similar between the 2 groups.Conclusions Early hematological,cytogenetic and molecular responses between Xinwei and Glivec are comparable in newly-diagnosed CML-CP patients.The progression rate and side effects are also similar between the 2 groups.

Objective To observe functional changes of renal tubular epithelial cells stimulated by high mobility group protein box 1 (HMGB1) and associated mechanism.Methods Renal tubular epithelial cells (NRK52E) were divided into control group,HMGB1 group and HMGB1+ lipopolysaccharide from Rhodobactersphaeroides (LPS RS) group.Toll-like receptor 4 (TLR4) expression was detected by immunofluorescence and Western blotting.Apoptosis rate and cell cycle arrest were identified with flow cytometry.The activation of MAPK signaling pathway and NF-κB were detected by Western blotting.The IL-1,IL-6 and tissue inhibitor of metalloproteinases 2 (TIMP2) mRNA levels were measured by real-time PCR.The secretion levels of IL-1,IL-6 and TIMP2 were measured by protein chips assay.Results TLR4 was expressed by NRK52E cells.Compared with the control group,there were increased cell cycle G1 arrest,MAPK signaling pathway and NF-κB activation in HMGB1 group.Furthermore,IL-1,IL-6 and TIMP2 mRNA levels were increased and IL-1,IL-6 and TIMP2 were secreted by NRK52E when stimulated with HMGB1 (all P ＜0.05).However,effects mediated by HMGB1 stimulation could be inhibited by LPS RS (all P＜0.05).Conclusions Inflammatory activation of NRK52E cells can be mediated by the interaction of HMGB1 and TLR4.

Objective: To observe the effect of coxsackie virus B3 on airway tract and lung morphology, and to study the relation between CVB infection and asthma. Methods: We established CVB3 infective model: 5 d neonatal rats inhaled CVB3 by ultrasonic brume. CVB3-IgM was examined 10 d after inoculating of CVB3, and LW/BW, airway tract and lung pathological change 10 d and 30 d after inoculation of CVB3 were observed. Results: Rats from the virus group had higher D of CVB3-IgM than control's (+2s ) and had higher LW/BW 10 d after inoculation of CVB3 than control (P<0.01). Neonatal rats had acute inflammatory changes 10 d after inoculation of CVB3 and persistent changes in morphology and cytology. Conclusion: Neonatal rats virus model is established. Respiratory infection by CVB3 in neonatal rats has persistent changes in airway tract inflammatory and morphology.

Objective To explore the relationship of depth of trophoblastic invasion with trophoblast cell activity and serum β-hCG according to the expression of proliferation antigen Ki-67 which viewed as an indicator of cell proliferation activity.Methods Fallopian tube specimens collected from 108 patients who underwent operation treatment for fallopian tubal pregnancy in our hospital were investigated by light microscopic examination.They were divided into three groups according to the depth of trophoblastic infiltration: Ⅰ group (stage): trophoblastic invasion of tubal mucosa,Ⅱ group(stage): trophoblastic invasion of the muscularis,Ⅲ group(stage): trophoblast invasion of serosa layer(muscularis penetration).The expression of Ki-67 was detected by SP method and blood β-hCG was detected within 2 hours of preoperative.The level of β-hCG,the expression of Ki-67 and the depth of trophoblast invasion were analyzed.Results Mean level of serumβ-hCG in Group Ⅰ,Ⅱ and Ⅲ were(1416.64 ± 859.94)U/L,(3380.33 ± 2392.36)U/L and(6999.33 ± 4949.90)U/L respectively.Positive expression rate of cell proliferation antigen Ki-67 in Group Ⅰ,Ⅱ and Ⅲ were 21.95％,53.66％ and 6.40％ respectively.There were significant difference on the expression of Ki-67 between group Ⅰ and group Ⅱ,group Ⅱ and Ⅲ group,group Ⅰ and group Ⅲ(x2 =3.94,4.07,4.35,respectively,P ＜ 0.05).The serumβ-hCG level also displayed statistics difference in the three groups(F =9.914,P ＜ 0.01).The positive expression of Ki-67 and serum β-hCG level were positively correlated with each other(r =0.678,P ＜ 0.05)Conclusion The high level of the serum β-hCG indicates high expression of Ki-67 and deeper trophoblast invasion of tubal wall.

Objective To evaluate the effects of Ang Ⅱ on the expression of IQ domain GTPase-activating protein1 (IQGAP1) and apoptosis of glomerular cells,and to explore the role of IQGAP1 in Ang Ⅱ-induced apoptosis of glomerular cells.Methods Thirty-six male Wistar rats were randomly assigned to receive either saline or Ang Ⅱ by osmotic mini-pump,or be used as normal control.The systolic blood pressure and proteinuria were measured at day 7,14,21,28.After the animals were sacrificed at day 14,28 respectively,the kidneys were collected.Renal pathological change,glomerular cell apoptosis were observed.The expression of glomerular IQGAP1 was assessed by immunohistochemistry,immunofluorescence and Western blotting.The activation of caspase-3 and phosphorylation of extracellular regulated protein kinases 1 and 2 (ERK1/2) were determined by Western blotting.Results Ang Ⅱ-infused rats developed significant hypertension and marked proteinuria.Mild glomerular mesangial cell proliferation and mesangial matrix increase were also observed in Ang Ⅱ-infused rats.The number of apoptotic glomerular cells in Ang Ⅱ-infused rats was significantly more than that in normal control (P ＜ 0.05).The expression of IQGAP1 in glomeruli distributed linearly along the capillary loops.Ang Ⅱ infusion up-regulated the expression of glomerular IQGAP1,which had an significantly positive correlation with activation of caspase-3(r =0.689,P ＜ 0.05) and phosphorylation of ERK1/2 (r =0.658,P ＜ 0.05).Conclusion The enhanced expression of IQGAP1 may be involved in Ang Ⅱ-induced glomerular cells apoptosis via activation of ERK1/2 signaling pathway.

BACKGROUND: Mesenchymal stem cells are the stem cells that possess the capability for self-renewal and multi-directional differentiation. Umbilical cord is the tissue outside the embryos and would be fallen off after parturition. In addition, it has wide source and no ethical restriction, so it is promising to be the first choice for mesenchymal stem cells. OBJECTIVE: To detect the surface markers CD29, CD44, CD49e, CD73, CD90, CD34, CD45, and CD271 of human umbilical cord-derived mesenchymal stem cells (hUCMSCs) prior to and after cryopreservation and resuscitation. METHODS: After isolation and culture, morphology of the primary, P4 and P8 hUCMSCs was observed prior to cryopreservation and after resuscitation. Surface markers CD29, CD44, CD49e, CD73, CD90, CD34, CD45, and CD271 of primary, P4, and P8 hUCMSCs were detected through the use of flow cytometry prior to cryopreservation and after resuscitation RESULTS AND CONCLUSION: hUCMSCs prior to cryopreservation and hUCMSCs of different passages after resuscitation present the same phenotype, i.e., positive for CD29, CD44, CD49e, CD73, and CD90, and negative for CD34, CD45, CD271. These findings suggest that primary hUCMSCs do not present changes in surface markers after cryopreservation and resuscitation.

Twenty-three patients with pain from osteoporotic vertebral fractures,aged 65-90 yr,weighing 51-78 kg,received an image intensifier-assisted nerve-root block with a 6-8 ml mixture of 0.5 ％ lidocaine,mecobalamine 0.5 mg and betamethasone sodium phosphate injection 5.26 mg in a prone or lateral position.The VAS scores before operation,at 0,1 week,1 and 3 months after operation were 8.6 ± 0.9,1.5 ± 0.7,2.8 ± 0.9,1.6 ± 0.5 and 2.5 ± 0.7,respectively.VAS scores were significantly lower at each time pint after operation than before operation (P ＜ 0.05).According to modified MacNab standard,the effectiveness of treatment was rated as excellent/good in 87％ of the patients.No complication such as bleeding,hematoma,infection,pneumothorax,hemopneumothorax,headache was found during or after operation.Selective nerve-root block is effective in the treatment of pain resulting from osteoporotic vertebral fractures in patients.

Objective To evaluate expression and significance of TLR4 and NF-κB on inflammatory injure after intracerebral hemorrhage in rats .Methods 60 Sprague Dawley maleness rats were randomly divided into Sham group ,12 h ,24 h ,72 h and 7 d af-ter ICH group(12 s) .The ICH was induced by injection of autologous blood in rats .The behavioral changes were detected by neu-rologic deficit score .The water content of the brain was used to evaluate brain edema changes .Number of TLR4 and NF-κB positive cells by Nissl staining and the expression of protein determined by immunohistochemistry and Western blot .Results After ICH 12 h ,expression of TLR4 and NF-κB positive cells around the hematoma were expressed ,with the extension of the time ,expression was gradually increasing ,and after ICH 72 h the expression of protein were the highest .Cerebral edema and severe neurological damage occurred .Western blot shows the amount of TLR4 expression and NF-κB were in line with the result .Conclusion After in-tracerebral hemorrhage in rat causing inflammatory injure of brain tissue around the hematoma .TLR4 may activate the expression of NF-κB involved in the secondary inflammatory injure after intracerebral hemorrhage in rats .

Objective To investigate the role of IQ domain GTPase-activating protein 1 (IQGAP1) in angiotensin Ⅱ (Ang Ⅱ)-induced podocyte apoptosis and the underlying mechanism.Methods Differentiated mouse podocytes were exposed to Ang Ⅱ at different concentrations for 6 h or at 10-8 mol/L for variable incubation time.Podocyte apoptosis was assessed by flow cytometry.Expression of IQGAP1 was analyzed by immunofluorescence and Western blotting.IQGAP1 siRNA and MAPK pathway inhibitors(10 μmol/L SB202190,25 μmol/L SP600125,10 μmol/L U0126) were further introduced to investigate the role of IQGAP1 and MAPK signalings in the process.And coimmunoprecipitation was used to evaluate the interaction between ERK1/2 and IQGAP1.Results (1)Ang]] promoted podocyte apoptosis in a dose-and time-dependent manner.(2) IQGAP1 was located in celluar membrane and cytoplasm of cultured podocytes.Exposure to Ang Ⅱ stimulated IQGAP1expression in a dose-and time-dependent manner,and elevated phosphorylation of p38,JNK,and ERK1/2 simultaneously.(3) Pretreatment with SB202190,SP600125,or U0126 dramatically prevented Ang Ⅱ-promoted podocyte apoptosis respectively (P ＜ 0.05).However,the protein level of IQGAP1 was not altered.(4) Knockdown of IQGAP1 with siRNA obviously prevented Ang]Ⅱ-induced apoptosis of podocytes(P ＜ 0.05) and reduced Ang Ⅱ-induced phosphorylation of ERK1/2(P ＜ 0.05),but not that of p38,JNK.This was accompanied by a reduced interaction between ERK1/2 and IQGAP1(P ＜ 0.05).Conclusion IQGAP1 contributes to Ang Ⅱ-induced podocyte apoptosis by interacting with the ERK1/2 signaling protein.

In the present study, the apoptotic mechanism and polyamine transporter recognition of WJH-6, a novel polyamine conjugate, were investigated in K562 and HL-60 cells. The cytotoxicity of WJH-6 was assessed by MTT assay; cell cycle distribution and apoptosis were measured by flow cytometry; the protein expression of Caspase-3, Caspase-8, Caspase-9, Bid and mitochondrial membrane potential (MMP) were evaluated by high content screening (HCS) analysis; the protein expression of cytochrome c was measured by Western blotting. The results showed that WJH-6 could be recognized and transported by polyamine transporter (PAT). Furthermore, WJH-6 was able to inhibit K562 and HL-60 cells proliferation and induce apoptosis. This apoptotic effect was relative to MMP loss, cytochrome c release from mitochondria to cytoplasm and the activation of Caspase-8, Caspase-9, Caspase-3 and Bid. These results suggested that WJH-6-induced K562 and HL-60 cells apoptosis was related with mitochondrial damage.