Expression of IL-17 and estrogen and its receptor in HPV16 continuously infected patients / 局解手术学杂志

Objective To understand the role of estrogen,estrogen receptor and IL-17 in human papillomavirus (HPV) infection and clearance.Methods We selected the clinic or the hospitalized patients in People' s Hospital of Pudong New District hospital with HPV negative or single-HPV16 positive during the period of August 2014 to January 2017.Cervical exfoliated cells were harvested by Thinprep cytologic test (TCT).The reverse spot hybridization technique was carried out for HPV subtype analysis.RT-PCR was employed for HPV16 DNA viral load.The levels of E2 and IL-17 were detected by ELISA.Immunohistochemical was used to detect ER expression.The experiments were repeated every three months.According to the difference in the outcome of human papilloma virus 16 infection,the experiment was divided into three groups.The first group was HPV negative,which was negative for one year.The second group was HPV16 positive,but within one year the difference was gradually cleared.The third group was HPV16 positive,but the HPV16 persistently existed after one year.Results The results of the last test were compared with the first test results.We found that There was no significant difference among the three groups in the expression of E2 and ER.Also,there was no significant difference between the HPV negative group and the HPV16 persistently infected group in variation of IL-17 concentration.But the difference between the HPV16 cleared group and the anyone of the two groups above was significantly.The variation of IL-17 concentration was significantly higher in the HPV16 cleared group.Conclusion In normal cytology,and only HPV16 infected stage,endogenous E2 and ER of cervix may not play a role in HPV infection,or they may have little effect on HPV infection.Local immune factor IL-17 plays an important role in the process of HPV16 removal,and the increase of IL-17 concentration can help to eliminate HPV16.

MicroRNA-34a contributes to the protective effects of glucagon-like peptide-1 against lipotoxicity in INS-1 cells / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Glucagon-like peptide-1 (GLP-1) reduces fatty acid-induced beta-cell lipotoxicity in diabetes; however, the explicit mechanisms underlying this process are not fully understood. This study was designed to investigate the involvement of microRNA, which regulates gene expression by the sequence-specific inhibition of mRNA transcription in the GLP-1 mediation of beta-cell function.</p><p><b>METHODS</b>The cell viability and apoptosis were determined using an methyl thiazoleterazolium (MTT) assay and flow cytometry. The expression of genes involved in beta-cell function, including microRNA-34a and sirtuin 1, were investigated using real-time PCR. The underlying mechanisms of microRNA-34a were further explored using cell-transfection assays.</p><p><b>RESULTS</b>A 24-hours incubation of INS-1 cells with palmitate significantly decreased cell viability, increased cell apoptosis and led to the activation of microRNA-34a and the suppression of sirtuin 1. A co-incubation with GLP-1 protected the cells against palmitate-induced toxicity in association with a reduction in palmitate-induced activation of microRNA-34a. Furthermore, palmitate-induced apoptosis was significantly increased in cells that were infected with microRNA-34a mimics and decreased in cells that were infected with microRNA-34a inhibitors.</p><p><b>CONCLUSION</b>MicroRNA-34a is involved in the mechanism of GLP-1 on the modulation of beta-cell growth and survival.</p>

Changes of proteomic spectra of total flavones of Hippophae rhamnoides on myocardial protection / 中国中药杂志

<p><b>OBJECTIVE</b>To study the mechanisms of the anti-myocardial ischemia of total flavones of Hippophae rhamnoides (TFH) at the level of proteome.</p><p><b>METHOD</b>Surface enhanced laser desorption/ionization (SELDI) mass spectrometry with protein chip IMAC3, SAX2 and NP20 was performed to compare the differentially expressed protein in myocardial ischemia in the TFH-treated groups with the 0.9% sodium chloride groups. Protein chips were examined in PBS II - C protein chip reader (ciphergen ciosystem inc) and the protein profiling was analyzed by Proteinchip Software 3. 0. 2.</p><p><b>RESULT</b>The revealed six peaks had significant difference between the TFH-treated groups and the control groups, one of which were up-regulated in the TFH-treated groups, and the other were down-regulated. And in these six distinct proteins, there were four proteins on the IMAC3 chips and one protein on the SAX2 chips.</p><p><b>CONCLUSION</b>The TFH could prevent the myocardium from ischemia via regulating expression of different proteins.</p>

Comparing the actions of the three flavone ingredients in choerospondias axillaris on arrhythmias induced by aconitine / 中国中药杂志

<p><b>OBJECTIVE</b>To compare the actions of the three flavone ingredients in choerospondias axillaris on arrhythmias Induced by aconitine.</p><p><b>METHOD</b>Langendorff perfuse was applied in the experiment, the antiarrhythmic action was to study by using aconitine on the the isolated heart; The antiarrhythmic action of the three flavone ingredients in choerospondias axillaris was to study by using i.v. aconitine in rat to induce arrhythmias.</p><p><b>RESULT</b>Compared with the NS group, sample 1 and sample 2 both significantly prolonged the beginning time of VF of isolated heart and increased the dosage of aconitine, sample 3 reduced the beginning time of VF of isolated heart and decreased the dosage of aconitine, sample 1 and sample 2 both greatly prolonged the beginning time of VE, VT, VF, HA; sample 3 greatly reduced the beginning time of VT,VF. The actions of the three samples were in a concentration-dependent way.</p><p><b>CONCLUSION</b>Sample 1 and sample 2 both resisted the occurrence of arrhythmias induced by aconitine, sample 3 markedly promoted the occurrence of arrhythmias induced by aconitine.</p>

Damaging effect of cigarette smoke extract on primary cultured human umbilical vein endothelial cells and its mechanism / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To investigate the cellular effects of cigarette smoke extract (CSE) on primarily cultured human umbilical vein endothelial cells (HUVEC).</p><p><b>METHODS</b>The effects of CSE (5%-20%) and nicotine (10(-4) mol/L) on HUVEC viability, proliferation, angiogenesis and apoptosis were observed.</p><p><b>RESULTS</b>CSE decreased HUVEC survival rate and angiogenesis after 24 h as well as its proliferation after 48 h in a dose-dependent manner. Moreover, CSE induced apoptosis of HUVEC as indicated in condensation of nuclear chromatin and the presence of hypodiploid DNA. HUVEC incubated with CSE for 24 h gave a significant decrease in the expression of Bcl-2 as well as the decline in the Bcl-2/Bax ratio accompanied with the loss of mitochondrial membrane potential and excess cytosolic calcium. Our study also observed that p53 protein level decreased, rather than increased in cells treated with CSE. Nicotine had no discernible inhibitory effects on the above indices of HUVEC.</p><p><b>CONCLUSION</b>Exposure to CSE other than nicotine causes inhibition of viability, proliferation and differentiation of HUVEC. CSE-induced HUVEC injury is mediated in partthrough accelerated apoptosis but independent of p53 pathway. It appears that mitochondria have played a key role in the apoptosis of HUVEC induced by CSE.</p>

Injury of mouse brain mitochondria induced by cigarette smoke extract and effect of vitamin C on it in vitro / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To investigate the toxicity of cigarette smoke extract (CSE) and nicotine on mouse brain mitochondria as well as the protective effect of vitamin C in vitro.</p><p><b>METHOD</b>Mouse brain mitochondria in vitro was incubated with CSE or nicotine in the absence or presence of vitamin C for 60 minutes, and the changes of mitochondrial function and structure were measured.</p><p><b>RESULTS</b>CSE inhibited mitochondrial ATPase and cytochrome C oxidase activities in a dose-dependent manner. However, no significant changes in the peroxidation indices were observed when mitochondrial respiratory enzymes activity was inhibited, and protection of mitochondria from CSE-induced injury by vitamin C was not displayed in vitro. The effect of CSE on mouse brain mitochondria swelling response to calcium stimulation was dependent on calcium concentrations. CSE inhibited swelling of mitochondria at 6.5 mumol/L Ca2+, but promoted swelling response at 250 mumol/L Ca2+. Nicotine, the major component of cigarette smoke, showed no significant damage in mouse brain mitochondria in vitro. The CSE treatment induced mitochondrial inner membrane damage and vacuolization of the matrix, whereas the outer mitochondrial membrane appeared to be preserved.</p><p><b>CONCLUSION</b>The toxic effect of CSE on brain mitochondria may be due to its direct action on enzymatic activity rather than through oxygen free radical injury. Nicotine is not the responsible component for the toxicity of CSE to brain mitochondria.</p>

Changes of Matrix Metalloproteinase in Serum and Cerebrospinal Fluid of Children with Purulent Meningitis and Those Clinical Significances / 实用儿科临床杂志

0.05,respectively).But most inte-restingly,the MMP-9 showed a positive relevance(r=0.686,P