Forty cases of nonbacterial prostatitis were treated by pricking therapy, and another 40 cases were treated by norfloxacin capsul and flavoxate hydrochloride tablets as the control. The result showed the effective rate was 100% in the former and 95% in the latter,and there was a statistical difference in therapeutic effect between two groups(P ＜ 0.05).Pricking therapy had a good effect on the nonbacterial prostatitis.

Objective To investigate the effect and mechanism of p38 MAPK inhibition in reducing the damage to rat's hippocampal neurons caused by kainic acid (KA) and observe the three-dimensional morphological changes on the cell surface. Methods The rat's hippocampal neurons cultured primarily for 10 days were pretreated with SB203580 (0.2 ?mol/L, a p38 MAPK inhibitor). Thirty minutes later, the hippocampal neurons were administered with KA at concentrations of 0, 25 and 250 ?mol/L for action for 10 and 100 minutes respectively. The cellular membrane structure was scanned and examined at nano-level by using atomic force microscope. Results Normal neurons displayed smooth membrane surface with homogeneous and regular undulation. In contrast, the neurons treated with KA showed coarse membrane surface with holes. Furthermore, the degree changes increased with the action time and the KA concentrations in a dose-effect dependent fashion. The above-mentioned changes were obviously mitigated by means of pretreatment with SB203580 (200 nmol/L). Conclusions Inhibition of p38 MAPK may, in certain degrees, protect the neurons against the impairments on cytomembrane resulted from the toxic effect of KA.

Aplastic anemia (AA) refers to a life-threatening bone marrow failure disorder.With respect to the precise pathophysiology of AA at present, it is still unclear.MicroRNA (miRNA), about 22 nucleotides in length, is a kind of small RNAs and it can regulate gene expression post-transcriptionally.According to domestic and foreign reports recently, there are abnormal expressions of several miRNAs in AA patients, suggesting that miRNAs may be involved in the development and progression of AA.This article reviews the study progress of miRNAs in AA.

Objective To explore the new method to prevent graft versus host disease (GVHD) by clearing T lymphocytes of bone marrow graft through Fas-FasL way. Methods FasL-cDNA was transfected into BALB/C mouse hematopoietic cells by liposomes. The transfected cells were cultured together with BAC mice bone marrow graft. The mixed bone marrow graft was injected into BALB/C mouse recipients after 60 Co-? ray irradiating. Then the mortality, manifestation and pathologic change of GVHD of recipient mice were observed. Results Compared with control group, the mortality of the recipients in the experimental group was markedly decreased in 60 days (20% vs 70%, P

0.05).Conclusions The expression of galetin-3 was obviously increased in liver metastasis from colon cancer,and MCP can effectively inhibit the development of liver metastasis of colon cancer.

Objective To investigate the effects of co-exposure to LPS and heat on plasma tumor necrosis factor-? (TNF-?), interleukin-6 (IL-6), malondialdehyde (MDA) and activity of superoxide dismutase (SOD) in rats. Methods Male pathogen-free Wistar rats were randomly assigned to the following groups: saline-injected normothermic control (Group C), saline-injected heat exposure (Group H), LPS-injected normothermic control (Group L), LPS-injected heat exposure (Group HL). Mean arterial pressure (MAP) was continually monitored. Plasma levels of TNF-?, IL-6, MDA and SOD were determined at 0, 40, 80, 120 min. Results The rats in Group HL displayed much lower MAP, higher MDA and lower SOD than the other 3 groups. The rats in Group HL displayed an early rise in plasma TNF-?, IL-6 at 40 min, the peak values of both at 80 min significantly higher than the other three groups at the same time piont. Conclusion Co-exposure to LPS and heat primes the rats to advance and augment systemic inflammatory response syndrome.

OBJECTIVE:To determine the content of C 3 F 8 in human albumin microspheres filling-with C 3 F 8 .METHODS:By Tekmar3000purge and trap concentrator coupled with a Hewlett-Packard5972GC/MSD.RESULTS:C 3 F 8 contents in samples were119.1～433.5?g/ml.CONCLUSION:The method is feasible and suitable for quality control.

OBJECTIVE:To study the preparation of 5% albumin microspheres by sonication and the possible mechanism of microsphere forming.METHODS:The preparation technic was optimized with orthogonal design.The microsphere diameter was measured with Coulter multisizer and the outward apperance was observed with light and electronic microscope.RESUL_TS:The optimal preparation technic was as follows:5% albumin in NS,ultrasound power at 9th grade and 60 seconds of sonication.CONCLUSION:The albumin microspheres filled with air can be successfully prepared with orthogonal design and can be effectively used in intravenous myocardial contrast echocardiography.

Objective To study the distribution of hemodynamics in carotid artery under the fluid-solid interaction at the typical point of time during a single cardiac cycle, and to explore the mechanism of the formation and development of carotid atherosclerotic plaque. Methods Numerical analysis the blood flow characteristics within a cardiac cycle in carotid artery was analyzed by using computational method of fluid dynamics. Based on the hemodynamic parameters, the influences of the cardiac systole and diastole on the blood flow distribution were analyzed. Results The distribution of blood flow in the carotid artery within a typical cardiac cycle was obtained. Compared with the findings in cardiac diastole, a larger area of blood stasis at the entrance of external carotid artery was observed. In this area, the flow velocity, the wall pressure and the wall shear stress were all lower, while the arterial wall deformation and von Mises equivalent stress were larger. Conclusion Under fluid-solid interaction, the low blood flow in carotid artery causes blood reflux, resulting in the deposition of lipid, fiber and other large molecular materials. The low wall pressure produced“negative pressure” effect, thus the normal blood flow is changed, the flow velocity becomes slow, and the blood supply of the brain becomes insufficient. The low wall shear stress destroys the blood flow near the wall, causing the increase of platelet activity and intimal hyperplasia. The larger arterial wall deformation variable and von Mises equivalent stress can cause stress concentration and increase vascular rupture risk.

Objective To study the two-phase flow dynamics distribution and red blood cell distribution under the fluid-solid coupling interaction in left coronary artery at the typical time point within one cardiac cycle,and to investigate the formation and development mechanisms of left coronary artery atherosclerotic plaque Methods The blood was regarded as a two-phase fluid.Based on fluid-solid interaction between blood and vascular wall,the computational fluid dynamics method was used to make the transient numerical simulation of two-phase flow in the left coronary artery under fluid-solid interaction;the distribution of blood flow in the left coronary artery at the typical time point within one cardiac cycle was studied,the relationship between hemodynamic parameters and the formation of atherosclerotic plaque was analyzed.Results A lowspeed eddy zone existed in an area between the distal segment of circumferential branch and the proximal outside of blunt-edge branch of the left coronary artery,where both internal wall shear stress and red blood cell volume fraction were very small and the blood flow pattern was very complicated.Conclusion At the lowspeed eddy zone that carries small wall shear stress,the lipid concentration polarization and macromolecular material deposition are easy to be produced.The area that has less red blood cells is liable to develop hypoxia,resulting in increased vascular wall permeability and intimal injury,which will activate the immune system,causing lipid accumulation in vascular wall and intimal hyperplasia and,thus,to induce the formation of atherosclerotic plaque.(J Intervent Radiol,2017,26:253-257)