Humans ; Tinnitus ; diagnosis ; therapy

Autophagy ; Child ; Humans ; Kidney Diseases

Ear, Middle ; surgery ; Otologic Surgical Procedures

Animals ; Cytokines ; blood ; Humans ; Peripheral Vascular Diseases ; etiology ; physiopathology ; Rabbits ; Vibration ; adverse effects

Age-related macular degeneration(AMD)is a kind of degenerative diseases with complex pathogenesis and stimulation of multiple factors.It has become one of the major diseases causing-blindness in the elderly population in China.Recently,some epidemiological findings demonstrated that diabetes mellitus possibly is one of risk factors for AMD,and this will offers a new approach for the prevention and treatment of AMD.Thus,it is very important for US to strengthen the research of mechanism of AMD impacted by diabetes mellitus,pay more attention to the progress of AMD,search for a scientific and rational therapeutic way of improving the prognosis and elevate the quality of life in the patients with diabetes mellitus.

Objective To study the effect of Coxsackie virus B3 (CVB3) infection on islet cells in vitro, and to explore the mechanism of islet cells caused by CVB3. Methods Bone marrow mesenchymal stem cells( BMSCs) were separated from the bone marrow and cultured. Then they were induced to differentiate into islet-like cells using nicotinamide and mercaptoethanol. Differentiated cells were detected by morphology , special staining and RT-PCR. Observe CVB3 infection on islet cells under inverse microscope and detect the specific gene fragment by RT-PCR. Results BMSCs showed half suspended shape and gathered to form a cluster after induction. Cells became red brown by dithizone specific staining. RT-PCR also proved the existence of mRNA expressing insulin. Infected islet cells appeared typical pathological changes like shrinks, refraction decreases. RT-PCR detected the desired specific gene fragment of 299 bp in infected islet cells. Conclusion CVB3 can directly injury islet cells, and damage the function of islet cells of secreting insulin.

Objective To investigate the effect of rapamycin(RPM)on hepatic interleukin-10(IL-10)gene and acute liver injury in rats with postburn Staphylococcus aureus sepsis.Methods Fifty male Wistar rats were randomly divided into four groups:normal control group,scald control group,postburn sepsis group,and RPM treatment group.Tissue samples from liver and plasma were collected to determine IL-10 mRNA and protein expressions,and liver function parameters were also measured.Results Compared to postburn Staphylococcus aureus sepsis group,in RPM treatment group hepatic IL-10 mRNA expression and plasma IL-10 were significantly increased at 0.5 hour after RPM treatment(P

Objective To set up a simple method to measure the SR Ca2+ release function in skeletal muscle strips.Methods The time from peak tension to 75 % relaxation(TR75) during intermittent tetanic contraction(fatigue contraction) of isolated musculus soleus strips was analyzed.It was prolonged rapidly,and then shortened slowly.The ratio of maximal TR75 to initial TR75(R-TR75) indicated a balance between SR Ca2+ release and uptake.If the SR Ca2+-ATPase(SERCA) activity and inhibition extent of SERCA in fatigue contraction were identical,R-TR75 should be an index for SR Ca2+ release function.Results Higher stimulation voltage or 5 mmol/L caffeine perfusion which increased the SR Ca2+ release channel open probability induced an increase of R-TR75 from 2.5 in control to 3.0.On the contrary,inhibition of SR Ca2+ release with 5 mmol/L magnesium sulfate perfusion significantly decreased R-TR75.Inhibition of SR Ca2+ release by metabolites during fatigue contraction was recovered slowly.So R-TR75 at the second fatigued contraction was reduced after 5 or 10 min of recovery,but no significant difference after 60 min of recovery.During intermittent tetanic contraction R-TR75 was increased to be 2.9 times of normal in unloaded soleus.Conclusion The above results suggest that R-TR75 during muscle strip fatigue contraction without any change of SERCA activity can indirectly reflected SR Ca2+ release function.In 2-week unloaded soleus,the enhanced R-TR75 indicates an increase in SR Ca2+ release function.

K-ras gene is one of oncogenes,which promotes cells growth and differentiation.Ras protein loses the activity of GTP enzyme because of K-ras mutations,and that may cause abnormal growth,differentiation of cells and promote the occurrence of tumor.Patients with colorectal carcinoma that carry mutations in K-ras gene do not benefit from the administration of anti-epidermal growth factor receptor (EGFR) polyclonal antibodies.Different solid tumors of colorectal carcinoma have different K-ras mutation rates.Different genotypes of K-ras gene (wild-type or K-ras mutant type) affect significantly on treatment options and prognosis.The efficacy of mutant type patients with anti-EGFR antibodies is poor,and the therapeutic effects of 5-FU and FOLFOX are still unclear.