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.

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

Cyclosporine ; pharmacokinetics ; therapeutic use ; Humans ; Treatment Outcome

ObjectiveTo explore the expression of EZH2 and p53 protein in primary prostate cancer (Pca) and its clinical significance.Methods High-throughput tissue microarray technique and immunohistochemistry was used to detect the expression of EZH2 and p53 protein in 48 human prostate cancer specimens without a history of chemo-radiation therapy and 15 cases of benign prostate hyperplasic (BPH) tissues. The pathological characteristics and the relationship of the expression of EZH2 and p53 protein in primary prostate cancer was analyzed. ResultsImmunohistochemical results showed that the positive rates of EZH2 and p53 protein in prostate cancer were 87.50 ％ (42/48) and 33.33 ％ (16/48), respectively, which were significantly higher than that in BPH tissues[13.33 ％ (2/15) and 0 (0/15)](x2=26.429, x2=5.058,P ＜0.05). The expression of EZH2 and p53 protein was significantly related to Gleason score, TNM stage (P ＜0.05), but not to age and serum prostate-specific antigen (PSA) level (P ＞0.05). The positive expression in patients with Gleason＞6 was higher than that with Gleason≤6(P ＜0.05).The positive expression in patients with T3-T4 stage was higher than that with T1-T2 stage(P ＜0.05).Spearman rank correlation showed a significantly positive correlation between EZH2 and p53 protein (r=0.294, P ＜0.05). ConclusionEZH2 and p53 protein may participate in the pathogenesis of prostate cancer.The overexpression of EZH2 and p53 protein could become an index for the evaluation of the level of malignancy and progression of prostate cancer.Furthermore,combining detection of EZH2 and p53 protein may provide a new theoretical basis for the treatment of prostate cancer.

Objective To analyse the tongue characteristics of cancer patients during chemotherapy ,in order to guide the TCM treatment. Methods 42 patients' tongue figure was collected respectively before and after chemotherapy by Canon digital camera, then to analyse the characteristics. Results Purple tongue was the most common in tongue color, account for 38.10%;meanwhile the tongue with stasis patch or with toothmark were common in tongue shape, account for respectively 26.19% and 21.43%;white thick or greasy tongue fur was the most common, especially in the central of tongue. Conclusion Deficience of Qi and blood stasis syndrome is common in cancer patients after chemotherapy, it is helpful to provide tasis for treatment of tonifying Qi and activating blood during chemotherapy.

Background Left ventricular hypertrophy(LVH) is a cardiovascular risk factor independent of the blood pressure. JAK/STAT pathway has been confirmed to participate in cardiac hypertrophy and hyperplasia. Our previous reports have shown that sodium tanshinone ⅡA sulfonate(STS) reversed LVH,inhibited the myocardial cells Ca2+ influx,lowered left ventricular myocardial tumor necrosis factor-?(TNF-?)and the proto-oncogene c-fos,Bcl-2,and p53 protein expression. Objective To study the effect of sodium tanshinone ⅡA sulfonate(STS) on JAK/STAT pathway in left ventricular hypertrophy(LVH) induced by abdominal aorta stenosis in rats. Methods Twenty-four 9-weeks-old rats submitted to abdominal aorta constriction,were randomized to receive STS 10 mg/(kg?d)(n=8)or sterilized distilled water (1 mL/d)(n=8),or valsartan 10 mg/(kg?d) by gavage(n=8),with age and sex matched sham operated rats(n=8) as control. HE,VG and immunohistonchemical staining were used to evaluate the myocardial fiber dimension(MFD). Expressions of JAK1 and STAT3 were assessed by using Western blot. Results Compared with the control group,pressure loaded rats had higher SBP[(117.3?8.3) vs LVH: (186.5?13.5)mmHg,P

Posterior capsular opacification (PCO) is the most common complication that leads to loss of vision after cataract surgery.Neodymium doped:Yttrium-Aluminum-Garnet (Nd:Yag) laser capsulotomy is a common treatment for PCO, but still associated with several complications.In the past decades, the prevention and treatment of PCO have always been a hot spot of research in ophthalmology.This review will address the advances in the prevention and treatment of PCO in the aspects of surgical techniques and types of intraocular lens (IOL).

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.

BACKGROUND:Demineralized bone can be used as the scaffolds of osteoblasts,and body tissue developed immunologic rejection to demineralized bone.OBJECTIVE:To investigate the histological changes of cyclosporin A(CSA) effect on ossification of demineralized bone,in addition,to explore the feasibility of demineralized bone served as ideal available bone substitute material.DESIGN,TIME AND SETTING:The randomized control experiment of animals was performed at the Experimental Center of Second Hospital of Dalian Medical University between March 2007 and April 2008.MATERIALS:Sixteen New Zealand rabbits were divided into the control and experimental group of homogenic decalcified bone,control and experimental group of heterogenous decalcified bone.CSA was produced by Beijing Novartis Pharmaceutical Co.,Ltd.METHODS:Decalcified bone prepared from rabbits was served as homogenic decalcified bone,and decalcified bone prepared from dogs were served as heterogenous decalcified bone.Sixteen rabbits were randomly divided into 4 groups:the control and experimental group of homogenic decalcified bone,control and experimental group of heterogenous decalcified bone,with 4 rabbits in each group.Each rabbit was implanted with homogenic or heterogenous decalcified bone,respectively,2 samples per side.2 mg/kg CSA or 2 mg/kg placebo was intramuscular injected in the experimental or control groups for 4 weeks.Samples were examined by hematoxylin-eosin staining and light microscope.MAIN OUTCOME MEASURES:The histological observation of decalcified bone in each group.RESULTS:Homogenic allogeneic bone induced formation in all implants.CSA did not induce morphological changes of homogenic allogeneic bone.In the heterogenous decalcified bone treated group,at 4 weeks,there was no bone formation or chondrocytes production in the control group,but there was cartilage and bone formation in the experimental group.CONCLUSION:CSA did not alter the morphology of bone induction by homogenic allogeneic bone.Immunologic reactions may inhibit bone induction by heterogenous decalcified bone,which can be counteracted by treatment with CSA.CSA can increase the rate of nonunion or bone defect using heterogenous decalcified bone.