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 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 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 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.

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.

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 investigate the correlation between the expression of adhesion molecule CD146 and the vulnerability of carotid atherosclerotic plaque.Methods The plaque samples were collected from 40 patients who underwent the carotid endarterectomy and were divided into the stable plaque group and the instable plaque group by ultrasound imaging.Five carotid artery samples were taken from the healthy donors as the control.Immunohistochemistry was applied to test the CD146 expression in all samples.Results Higher expression of CD146 was observed in the atherosclerotic plaques than in the healthy control.Moreover,statistical difference was found in the expression of CD146 in the plaques between the instable plaque group and the stable plaque group (0.31 ± 0.19 vs 0.17 ± 0.07,P ＜ 0.05).The expression of CD146 was positively correlated with the necrotic area (r =0.471 8,P =0.019 9) and the matrix metalloproteinase (MMP)-9 expression in the plaques (r =0.535 6,P =0.000 9).Conclusion The CD146 expression is correlated with the vulnerability of carotid atherosclerotic plaque.

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.

Objective To analyze the expression of peripheral blood CD13+CD4+CD25hi regulatory T cells (Treg cells) in patients with diffuse large B-cell lymphoma (DLBCL) and its clinical significance. Methods The expression of peripheral blood CD13+CD4+CD25hi Treg cells in 58 newly diagnosed patients with DLBCL and 30 healthy adults was detected by flow cytometry, and the relationship between its expression and the clinical indicators were analyzed statistically. Results The levels of peripheral blood CD13+CD4+CD25hi Treg cells in newly diagnosed DLBCL and healthy adults were different, with statistically significant difference [(36.37 ±11.89) % vs. (9.03 ±2.10) %, t = 7.168, P < 0.001]. The level of peripheral blood CD13+CD4+CD25hi Treg cells was significantly higher in patients with IPI score 3ˉ5 than that in patients with IPI score 0ˉ2[(44.28±10.10)%vs. (21.51±6.23)%, t=ˉ9.347, P=0.03]. The expression of peripheral blood CD13+ CD4+ CD25hi Treg cells in stages Ⅱ, Ⅲ and Ⅳ patients were (19.48 ±1.34) %, (33.98 ±8.03) % and (47.89±8.25) %respectively, and there were significant differences among three groups (F= 38.363, P<0.001). The levels of peripheral blood CD13+CD4+CD25hi Treg cells had no relationship with age, sex or LDH level (all P>0.05). Conclusion The levels of peripheral blood CD13+CD4+CD25hi Treg cells are higher in DLBCL patients, which has a close relationship between the expression of CD13+CD4+CD25hi Treg cells and clinical stage and prognosis.

Objective To investigate the real experiences of nurses participating in the treatment of patients with new respiratory infectious diseases. Method The semi-structural interview method was used to carry out in-depth interviews with 8 nurses who were involved in the whole process of treatments and cares of patients with SARS and H1N1 influenza to understand their real experiences. Result The nurses, who participated in the treatment and care to patients with new respiratory infectious diseases, experienced such emotions of nervousness, excitement, anxiety, fear, exhaustion, obtained support from their families, hospitals, society and meanwhile recognized their lack of professional knowledge and clinical skills. Conclusion The nurses participating in the treatment of patients with new respiratory infectious diseases should be given strengthened professional training , psychological and social support.