Stathmin is a novel member of microtubule-destabilizing proteins that play a critical role in the regulation of the dynamic equilibrium of microtubules during different phases of the cell cycle.The overexpression of stathmin was found in different type of cancer.Inhibition of stathmin expression in malignant cells may interfere with their orderly progression through the cell cycle.Overexpression of stathmin can affect the action of antimicrotuble drugs by markedly decreasing binding of paclitaxel,and increasing binding of Vinca alkaloids.In addition,stathmin provides an attractive molecular target for cancer therapy.It may be possible to combine adenovirus-mediated anti-stathmin ribozyme therapy with a chemotherapeutic agent such as taxol to obtain a more potent antiproliferative and antitumor effect.

Objective To investigate the early neurotoxicity of rotenone on dopaminergic neurons and explore an ideal tissue model. Methods A long-term midbrain slice culture system of SD pup was established according to the interface tissue culture method.After rotenone was added for some time,its toxic effects on the whole slices and the dopaminergic neurons were identified through the measurements of lactate dehydrogenase(LDH) released into the medium from the slices and dopamine(DA) content from the cultured tissue,as well as the observations of immunohistochemistry for tyrosine hydroxylase(TH). Results In those cultures exposed to rotenone for 24 h,the level of DA in tissue dramatically decreased with the concentrations rising.The processes of TH-positive neurons in slices demonstrated some morphological changes,such as appearance of string of beads,reduce of numbers and even disappearance.The content of dopamine in tissue was dominantly decreased with 5 nmol/L rotenone for 14 days,although its cellular morphology was not seen to change.Conclusion Long-time stable midbrain slice culture system has been set up successfully.The neurotoxicity of rotenone on the whole slices and dopaminergic neurons shows a dose-dependent manner.The functional damages on the neurons may be earlier than their morphological changes,of which the injury in the processes of neurons seems to be an early characteristic.

Objective: To estimate the clinical efficacy of combination of chemotherapy with osteoblast promoting and anti-osteolys-is agents in bone metastatic carcinoma. Methods: Seventy-one patients with bone metastatic carcinoma were divided into 2groups and treated with protocol A or B, respectively. The protocol A was a combination of chemotherapy with osteoblastpromoting and anti-osteolysis agents, the protocol B was a combination of chemotherapy with antiosteolysis agent only. Theefficacies of the 2 protocols were compared and studied. Results:The effect of A was more remarkable than that of B in re-lieving bone pain and enhancing bone repair. No severe adverse effect of these agents was found in therapy. Conclusion: Theclinical efficacy of combination of chemotherapy with osteoblast promoting and anti-osteolysis agents in bone metastatic car-cinoma was definite, the osteoblast promoting agent as an effective adjtmctive agent can be used not only in osteoprosis butalso in bone metastatic carcinoma.

Objective:To study the direct effects of gradient concentration inteiferon-a(IFN-a) on lymphoma cells line Daudi and Jur-kat and a group of 15 cases refractory lymphoma. Methods: The effects of IFN-a on the growth of tumor cells were assayed by MTT, apoptosis were measured by flow cytometty, TUNEL and electron-microscope, 15 refractory lymphoma cases were treated by local injection of IFN-a combination chemotherapy.Results: Low-dose IFN-a did not have any significant effects on growth of Daudi and Jurkat cells, high-dose IFN-a (10 000U/ml) not only have significant anti-proliferative effects with dependence of time and dosage but also can induce apoptosis on both Daudi and Jurkat cells. 5 patients achieved a complete remission and 7 patients achieved a partial remission, the overall response rate was 80% .Conclusion:IFN-a( 10 000 U/ml) had significant anti-proliferative effects and inducing apoptosis on lymphoma cells.Local injection of IFN-a is one of effective therapy on refractory lymphoma.

Objective To investigate the effect of different antiplatelet or anticoagulation therapy on postoperative pocket hematoma after electrophysiological devices placements (EPD). Methods The clinic data of 410 patients who took anti-platelet or anticoagulation therapy and needed to be implanted EPD from February 2012 to February 2015 were selected. According to the type of therapy, patients were divided into 4 groups:dual anti-platelet drug (DAP) treatment group (DAP group, 114 cases), low-molecular-weight heparin (LMWH) bridging treatment group (LMWH group, 98 cases), aspirin (ASA) alone group (ASA group, 94 cases) and warfarin group (104 cases). The incidence of pocket hematoma after electrophysiological devices placements was observed. The risk factors of pocket hematoma were analyzed. Results The incidence of pocket hematoma was higher in LMWH group than that in the other 3 groups: 18.4% (18/98) vs. 4.4% (5/114), 3.2% (3/94) and 2.9% (3/104), and there was statistical difference (P<0.05). But there were no significant differences in the incidence of pocket hematoma among DAP group, ASA group and warfarin group (P>0.05). The multiple Logistic regression analysis revealed that LMWH bridging therapy was an independent risk factor for the development of pocket hematoma (OR=7.105, 95%CI 1.872-17.283). Conclusions LMWH bridging therapy can increase the risk of development of pocket hematomas after electrophysiological devices placement.

Objective To investigate the role of NFIC on the stimulation effects of cAMP-induced differentiation of stem cells from the apical papilla ( SCAPs) in vitro. Methods SCAPs isolated from dental papilla of human imma-ture third molars were cultured by enzyme digestion. SCAPs were transfected with lentivirus that overexpressed NF-IC gene ( ov-NFIC) or an empty vector ( LV-empty) and co-treatment with Forskolin. Mineralized nodule formation of each group was measured by alizarin red staining. Quantitative real-time reverse-transcription polymerase chain reaction was performed to test the expressions of RUNX2,ALP,OCN mRNA. Results Forskolin increased the ex-pression of Runx2, ALP, OCN mRNA as well as matrix mineralization in SCAPs, and the stimulation effects of For-skolin were enhanced by overexpressing NFIC gene. Conclusion The results indicate that NFIC can promote cAMP-induced differentiation of SCAPs.

Objective To investigate the effects of propofol on death-associated protein kinase (DAPK) mRNA expression in a rat model of traumatic brain injury (TBI). MethodsSixty male Wistar rats with a mean age of 3-4 months and mean body weight of 250-300 g were randomly divided into 6 groups ( n = 10 each) : Ⅰ normal control;Ⅱ sham operation; Ⅲ TBI; Ⅳ normal saline (NS) +TBI;Ⅴ fat emulsinn+ TBI and Ⅵ propefol + TBI. TBI was produced according to Feeney et al. In group Ⅲ-Ⅵ the animals were killed and their brains were removed at 24 h after brain contusion. NS 2 ml·kg-1 · h-1 , 10% fat emulsion 2 ml · kg-1 · h-1 and propofol 2 ml·kg-1·h-1 were infused iv for 4 h after lead trauma in group Ⅳ, Ⅴ and Ⅵ respectively. DAPK mRNA expression in the brain tissue was determined by RT-PCR and neuronal apeptosis was assessed by TUNEL. Results The expression of DAPK mRNA and neuronal apoptosis were significantly increased in the TBI group as compared with normal control and sham operation groups. Propefol infusion significantly attenuated neuronal apoptosis and reduced DAPK mRNA expression as compared with TBI, NS and FE groups. ConclusionPropofol can protect the brain from traumatic injury by suppression of the expression of DAPK mRNA.

Humans ; Male ; Middle Aged ; Polycythemia ; etiology ; Sleep Apnea, Obstructive ; complications

Cyclosporine ; pharmacokinetics ; therapeutic use ; Humans ; Treatment Outcome

The tumor microenvironment is closely related to the occurrence and development of tumor. Hypoxia is considered to be one of the most important factors in tumor microenvironment.Formation of hypoxic microenvironment can be found in most of malignant tumors,which can inhibit the anti-tumor immune response. Recent studies have indicated that immunosuppressive cells,tumor stem cells and circulating tumor cells in hypoxic tumor microenvironment can mediate immune suppression and immune tolerance,and then promote development of tumor.The new immune therapy will focus on normalizing tumor vasculature,reconstructing the tumor microenvironment,avoiding immune suppression and averting tumor immune tolerance.