Objective To evaluate the value of 3.0T susceptibility-weighted magnetic resonance imaging (SWI) in the diagnosis of cerebrovascular malformations. Methods Forty-six patients with cerebrovascular malformations, admitted to our hospital fiom May 2008 to December 2010, were examined with a 3.0T MR scanner. All patients were examined with MRI conventional sequences T1WI,T2WI, 3DTOF, and their results were compared with SWI sequence so as to evaluate the value of SWI in the diagnosis of cerebrovascular malformations.Results Twenty-five patients had arteriovenous malformation (AVM), 10 with cavernous hemangioma, 8 with venous malformations, and 3 with telangiectasis in the 46 patients with cerebrovascular malformations. SWI could delineate all the cerebrovascular malformation lesions, especially small lesions, but could not display all supplying artery in AVM. 3DTOF was a better technique in delineating large AVM lesions. Conclusion SWI is much more sensitive in showing small cerebrovascular malformations; and combined with other MR sequences,clear diagnosis of cerebral vascular malformations can be made by SWI.

The fine structure of enoxaparin sodium samples with different degree of 1,6-anhydro derivatives were analyzed with polyacrylamide gel electrophoresis, high performance liquid chromatography, ultraviolet spectroscopy, infrared spectroscopy and nuclear magnetic resonance spectroscopy. A further study of anticoagulation activity of enoxaparins was performed, including those on their inhibition activities of coagulation factor Xa (FXa) and thrombin (FIIa). The results showed that the anti-FXa and -FIIa activities of enoxaparins with different degree of 1,6-anhydro derivatives (20.0%-39.7%) with similar structure characteristics, had decreasing tendency when the degree of 1,6-anhydro derivatives increased. Especially, the anti-FXa activity was sensitive to the change of the degree of 1,6-anhydro derivatives.
Anticoagulants ; chemistry ; Enoxaparin ; chemistry ; Factor Xa Inhibitors ; chemistry ; Thrombin ; antagonists & inhibitors

This study is to evaluate the therapeutic effect of fibroblast growth factor 21 (FGF21) on NAFLD in MSG-IR mice and to provide mechanism insights into its therapeutic effect. The MSG-IR mice with insulin resistance were treated with high dose (0.1 micromol.kg-1d-1) and low dose (0.025 micromol.kg-1d-1) of FGF21 once a day for 5 weeks. Body weight was measured weekly. At the end of the experiment, serum lipids, insulin and aminotransferases were measured. Hepatic steatosis was observed. The expression of key genes regulating energy metabolism were detected by real-time PCR. The results showed that after 5 weeks treatment, both doses of FGF21 reduced body weight (P<0.01), corrected dyslipidemia (P<0.01), reversed steatosis and restored the liver morphology in the MSG model mice and significantly ameliorated insulin resistance. Additionally, real-time PCR showed that FGF21 significantly reduced transcription levels of fat synthetic genes, decreased fat synthesis and promoted lipolysis and energy metabolism by up-regulating key genes of lipolysis, thereby liver fat accumulation was reduced and liver function was restored to normal levels. In conclusion, FGF21 significantly reduces body weight of the MSG-IR mice, ameliorates insulin resistance, reverses hepatic steatosis. These findings provide a theoretical support for clinical application of FGF21 as a novel therapeutics for treatment of NAFLD.
Animals ; Body Weight ; drug effects ; Dose-Response Relationship, Drug ; Dyslipidemias ; metabolism ; Energy Metabolism ; drug effects ; Fatty Liver ; chemically induced ; complications ; Female ; Fibroblast Growth Factors ; administration & dosage ; pharmacology ; therapeutic use ; Insulin Resistance ; Lipolysis ; drug effects ; Liver ; metabolism ; pathology ; Male ; Mice ; Non-alcoholic Fatty Liver Disease ; drug therapy ; Sodium Glutamate

OBJECTIVETo investigate the changes of guinea pig heart electrophysiological properties caused by increasing left ventricular preload, and to assess the effects of tetradrine on these changes.

METHODWorking model preparation of guinea pig hearts in vitro was used, and the preload of left ventricle was increased by adjusting the prefusion pressure of left atria. The changes of heart electrophysiologic parameters including monophasic action potential duration (MAPD90), monophasic action potential amplitude (MAPA), effective refractory period (ERP) and ventricular fibrillation threshold (VFT) were observed before and after altering the preload of left ventricle, and compared in the absence and presence of tetradrine, streptomycin or verapamil.

RESULTThe rising of left ventricular preload led to shortening of MAPD90, ERP, and to descent of MAPA, VFT (all P<0.01). Both Tetradrine and streptomycin inhibited these changes of heart electrophysiologic parameters caused by elevation of left ventricular afterload (all P<0.01). In contrast, verapamil had no effects on the preload-related electrophysiological changes (all P>0.05).

CONCLUSIONElectrophysiologic changes caused by increasing left ventricular preload may be inhibited by tetrandrine, through inhibition of stretch-activated ion channels.

Action Potentials ; drug effects ; Alkaloids ; isolation & purification ; pharmacology ; Animals ; Anti-Arrhythmia Agents ; isolation & purification ; pharmacology ; Benzylisoquinolines ; isolation & purification ; pharmacology ; Calcium Channel Blockers ; pharmacology ; Drugs, Chinese Herbal ; isolation & purification ; pharmacology ; Female ; Guinea Pigs ; Heart ; physiology ; In Vitro Techniques ; Male ; Plants, Medicinal ; chemistry ; Refractory Period, Electrophysiological ; drug effects ; Stephania tetrandra ; chemistry ; Streptomycin ; pharmacology ; Ventricular Function, Left ; drug effects ; Verapamil ; pharmacology

The purpose of this study was to investigate the growth characteristics and the expression level of integrin mRNA of the cultured bone marrow mesenchymal stem cells (BMMSCs) from patients with chronic myeloid leukemia (CML) in myeloid crisis (MC), and explore the role of BMMSCs in pathogenesis of CML. Five CML patients were enrolled in experimental group, five healthy persons were used as control. BMMSCs were cultured in vitro. The morphology of BMMSCs was observed every day and the growth curve were portrayed, and the ability of cell proliferation were detected according to the daily results of cell counting. Total RNA was extracted from third and fourth passages of BMMSCs, The expression of integrins mRNA of BMMSCs were measured by real-time PCR. The results showed that the BMMSCs of experimental and control groups had no difference in growth characterisctics, but the expression of integrins mRNA of the BMMSCs was higher in CML patients than in normal control group (p < 0.05). It is concluded that the abnormally high expression of integrins of BMMSC from the CML patients take part in pathogenesis of CML.
Adult ; Blast Crisis ; metabolism ; Bone Marrow Cells ; metabolism ; pathology ; Cell Proliferation ; Female ; Humans ; Integrins ; genetics ; metabolism ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; metabolism ; pathology ; Male ; Mesenchymal Stromal Cells ; metabolism ; pathology ; Middle Aged ; RNA, Messenger ; genetics ; metabolism ; Tumor Cells, Cultured

The aim of this article was to investigate the dependence of ventricular wallstress-induced refractoriness changes on pacing cycle lengths and its mechanism in anaesthetized rabbits. The rabbit heart preparation was used. The left ventricular afterload was increased by partially clipping the root of the ascending aorta. The changes in effective refractory periods (ERP) induced by the left ventricular afterload rising were examined at different pacing cycle lengths (1000, 500, 300 and 200 ms). In addition, the effect of streptomycin on these changes was also observed. The results are as follows: (1) The rising of left ventricular afterload led to marked changes in ERP at rapidly pacing cycle lengths (300 ms, 21+/-5 ms, 17.0%; 200 ms, 19+/-3 ms, 18.8%. P<0.01) than at slow ones (1000 ms, 3+/-2 ms, 1.5%; 500 ms, 7+/-3 ms, 4.0%. P>0.05); (2) Streptomycin inhibited the changes caused by the left ventricular afterload rising at pacing cycle lengths 300 ms and 200 ms (P>0.05). It is suggested that ventricular wallstress-induced refractoriness changes are pacing cycle length-dependent, and the effect of streptomycin appears to be consistent with the inhibition of stretch-activated ion channels.
Animals ; Aorta ; Cardiac Pacing, Artificial ; Constriction ; Mechanoreceptors ; drug effects ; physiology ; Rabbits ; Refractory Period, Electrophysiological ; drug effects ; Streptomycin ; pharmacology ; Ventricular Function ; drug effects ; physiology

Adolescent ; Child ; External Fixators ; utilization ; Female ; Fibula ; injuries ; Fractures, Open ; surgery ; Humans ; Male ; Tibia ; injuries

A first order system model is proposed for simulating the influence of stress stimulation on fracture strength during fracture healing. To validate the model, the diaphyses of bilateral tibiae in 70 New Zealand rabbits were osteotomized and fixed with rigid plates and stress-relaxation plates, respectively. Stress shielding rate and ultimate bending strength of the healing bone were measured at 2 to 48 weeks postoperatively. Ratios of stress stimulation and fracture strength of the healing bone to those of intact bone were taken as the system input and output. The assumed first order system model can approximate the experimental data on fracture strength from the input of stress stimulation over time, both for the rigid plate group and the stress-relaxation plate group, with different system parameters of time constant and gain. The fitting curve indicates that the effect of mechanical stimulus occurs mainly in late stages of healing. First order system can model the stress adaptation process of fracture healing. This approach presents a simple bio-mathematical model of the relationship between stress stimulation and fracture strength, and has the potential to optimize planning of functional exercises and conduct parametric studies.
Animals ; Biomechanical Phenomena ; Fracture Healing ; physiology ; Mathematics ; Models, Animal ; Models, Biological ; Rabbits

Adult ; Endoscopy ; Female ; Humans ; Male ; Maxillary Sinus ; surgery ; Nasal Septum ; injuries ; surgery ; Periosteum ; transplantation

OBJECTIVETo determine the safety and efficacy of local administration of lentivirus-mediated small interfering RNA (siRNA) targeting tumor necrosis factor-alpha (TNF-alpha) in murine air pouch model.

METHODSFrom May 2007 to April 2008 a siRNA targeting TNF-alpha and a missense siRNA were designed, and recombine lentivirus which coexpressed the green fluorescent protein (GFP) as a marker gene was constructed. Air pouches were established and stimulated by Ti-6Al-4V particles. Pouches were divided into 3 groups randomly. Lentivirus-mediated siRNA targeting TNF-alpha (TNF-alpha group) or lentivirus-mediated missense siRNA (MS group), or virus-free saline (control group) were injected into pouches respectively. Pouch membrane, peripheral blood, heart, liver, spleen, kidney, lung and brain were harvested at 28 d after transfection, and assayed for markers of inflammation using histological, molecular, immunological techniques and Xenogen in vivo imaging system (IVIS) 50 vivo bioluminescent assay system.

RESULTSXenogen IVIS 50 vivo image revealed strong expression of GFP localized in pouch areas and no expression in other parts of mice both in TNF-alpha group and MS group at 4 weeks after transfection, while no expression of GFP was found in control group. By RT-PCR and ELISA, the mRNA and protein levels of TNF-alpha in TNF-alpha group decreased by 81.6% and 82.6% respectively compared to control group (P < 0.01), and decreased by 78.9% and 84.0% respectively compared to MS group (P < 0.01), whereas TNF-alpha level in peripheral blood, heart, liver, spleen, kidney, lung and brain remained invariant (P > 0.05). Less inflammatory responses (thinner pouch membrane and decreased cellular infiltration) were observed in TNF-alpha group.

CONCLUSIONEfficient local delivery of lentivirus-mediated siRNA targeting TNF-alpha into modified murine air pouch can inhibit debris-induced inflammation effectively, with no systemic adverse effects.

Animals ; Disease Models, Animal ; Genetic Therapy ; Genetic Vectors ; genetics ; Inflammation ; therapy ; Lentivirus ; genetics ; Mice ; Mice, Inbred BALB C ; RNA, Small Interfering ; genetics ; Random Allocation ; Transfection ; Tumor Necrosis Factor-alpha ; genetics