It is a consensus to place stent after cutting bile duct in the hepatobiliary surgery in the past.However,as the development of bile physiological research and surgical technique,especially the raise of medical concepts of rapid recovery,the negative effects which are caused by the placement of stent have been taken seriously gradually.Up to now,whether the stent should be placed after the bile duct is cut has no definite answer yet.

Objective To discuss the value of vacuum sealing drainage combined with continuous fluid irrigation in deep second degree burn.Methods 33 patients with deep second degree burns in burn department of the Third Affiliated Hospital of Qiqihar Medical College were selected as study object.The observation group used vacuum sealing drainage combined with continuous fluid irrigation,while the control group used the traditional method of treatment.The rate of wound healing,wound healing time and pain conditions were compared between the two groups of patients.Results After 3 days in the observation group,there was dissolved necrotic tissue which were drained into the negative pressure bottles,wound necrosis dropped off and dissolved when changing VSD dressings after seven days,a large number of newborn epithelial tissue appeared on the wound after 14 days of treatment.The healing rate after 7 days and 14 days,total healing time and wound pain showed statistically significant differences between two groups.Conclusions VSD combined with continuous fluid irrigation can effectively improve local microcirculation of burn wounds,increase local blood flow,keep the wound stay at a moist environment,accelerate the exudate drainage,which will help reduce the damage caused by local inflammation,promote epithelial cell regeneration from multiple perspectives,promote wound healing,and improve local pain symptoms and the quality of life of patients.

Objective To observe the long-term effect of suramin on the inhibition of proliferation of human retinal pigment epithelial (RPE) cells in vitro. Methods RPE cells grown in 9 pieces of 96-well plate (12 wells each plate) were divided into experimental and control group, with 6 wells in each group. The concentration of 0.1 ml RPE cells in each well is 5?104 cells/ml. After the change of the medium, RPE cells were treated with suramin (250 ?g/ml) in experimental group while treated with nothing in the control group. The medium of the 2 groups were changed to the normal medium after 4 days. At the 1~st , 2~nd , and 4~th day after the addition of suramin and at the 1~st , 2~nd , 3~rd , 5~th , 6~th , 7~th , 9~th , 11~th and 13~th day after removing suramin, 1 plate was randomly selected to stop culturing, and the proliferation of RPE cells were detected by methyl thiazolyl tetrazolium (MTT) assay. Results Under reversed microscope, RPE cells in control group were fused completely at the 7~th day after inoculation. The extracellular space of RPE cells in experimental groups was larger than that in the control group, and remained unfused at the 13~th day after inoculation. The inhibitory rate of proliferation of RPE cells at the first day after treated with suramin was 14.85% and increased to the highest 25.79% at the 4~th day. The first day after the suramin-containing media was removed, the inhibitory rate decreased to 12.35%, and then raised gradually to over 20% at the 3~rd to 5~th day. Finally, the rate drop to 14.71%. Conclusion Suramin has the long-term effect on the inhibition of RPE cells induced by serum, especially the inhibitive effect after the remove of suramin, which indicates the specific double-peak inhibition during the whole process.

OBJECTIVE:To provide reference for drug consultation of Chinese patent medicine(CPM)in pregnancy. METH-ODS:Package inserts of CPM in our hospital during Jan.-Jun. 2016 were collected. Referring to the prohibited,contraindicated and caution materials and decoction pieces in Chinese Pharmacopoeia(part 1,2015 edition),based onnoteitem in Chinese Pharma-copoeia and Clinical Application Guidelines(2010 edition),problems existing in pregnancy contraindication labeling of package in-serts were compared and analyzed. RESULTS:There were 99 kinds of prohibited,contraindicated and caution materials and decoc-tion pieces in Chinese Pharmacopoeia. There were 210 package inserts of CPM except for the special medicine for children,in which 32 contained prohibited materials,61 contained caution materials,only 21 were in line with the contained materials. Among the package inserts of 93 CPM containing prohibited or caution materials,27 were included in Chinese Pharmacopoeia,13 in Clini-cal Application Guidelines only,17 in both,but only 6 had the same contraindication labeling. Among the package inserts of 32 CPM containing prohibited materials,6 were explicitly labeled prohibited,17 labeled contraindicated or caution,and 9 labeled none. Among the package inserts of 61 CPM containing caution materials,29 were labeled prohibited or contraindicated,15 la-beled caution,and 17 labeled none. Among the package inserts of 117 CPM containing no prohibited,contraindicated or caution materials,8 were labeled contraindicated in pregnancy,and 18 labeled prohibited in pregnancy. CONCLUSIONS:The pregnancy contraindications of most CPM are not normative,showing poor consistency with Chinese Pharmacopoeia or Clinical Application Guidelines. Except for providing drug consultation by complying with Chinese Pharmacopoeia,Clinical Application Guidelines and package insert,pharmacists can judge the CPM without labeled pregnancy contraindication by analyzing its classification of con-tained materials. Using TCM does not indicate safety drug use,in addition,some CPM contain western medicine ingredients. There-fore,pharmacists should conduct medication education for patients who used CPM in pregnancy. Considering the new and severe adverse reactions of TCM injections are more,its adverse reactions exist unpredictability,so that pregnant patients should be sug-gested to avoid using TCM injections by pharmacists.

Pemphigus is a severe chronic autoimmune mucocutaneous bullous disease. Glucocorticoids are considered as the first line of treatment for this disease. Dysfunctional uterine bleeding is also observed as a result of hypothalamic-pituitary-ovary axis dysfunction. This study reported one female patient with pemphigus vulgaris complicated with dysfunctional uterine bleeding upon systemic glucocorticoid usage. Before this disease was diagnosed, the patient experienced normal menstruation. The mechanism of dysfunctional uterine bleeding triggered by glucocorticoids is elucidated on the basis of case studies and literature review.
Female ; Glucocorticoids ; adverse effects ; Humans ; Metrorrhagia ; chemically induced ; Pemphigus ; drug therapy

Objective To investigate neuroprotective mechanisms of vinpocetine by observing the effects of vinpocetine injection on the expressions of peroxisome proliferators-activated receptor γ(PPARγ),nuclear factor (NF)-κB p65,cyclooxygenase-2 (COX-2) in the ischemic cortex,and infarct volume after focal cerebral ischemia-reperfusion in rats.Methods A focal cerebral ischemia-reperfusion injury model was induced by suture method.The rats were randomly divided into a normal control,a cerebral ischemiareperfusion and a vinpocetine groups.They were also divided into either a day 7 subgroup or a day 14 subgroup (n =6 in each subgroup) according to the reperfusion time.Western blot was used to detect the expression levels of PPARγand NF-κB P65 in the ischemic cortex.Triphenyl tetrazolium staining was used to detect the volume of cerebral infarction.Results Western blot showed that at day 7 and 14 after cerebral ischemia-reperfusion,expression levels of PPARκ (all P＜0.001) and NF-κB p65 (all P＜0.001) in the cerebral ischemia-reperfusion group were significantly higher than those in the sham operation group,the expression levels of PPARκ (all P ＜0.05) in the vinpocetine group were significantly higher than those in the cerebral ischemia-reperfusion group,but the expression levels of NF-κB p65 (all P ＜0.05) were significantly lower than those in the cerebral ischemia-reperfusion group.Reverse transcription polymerase chain reaction showed that COX-2 mRNA expression levels were upregulated significantly at day 7 and 14 after cerebral ischemia-reperfusion compared with the sham operation group (all P ＜ 0.001),the expression levels of COX-2 mRNA in the vinpocetine group were significantly downregulated compared with the cerebral ischemia-reperfusion group (all P＜ 0.05).The infarct volumes at day 7 (134.308± 9.954 mm3vs.185.543 ± 9.100 mm3;q=10.659,P＜0.001) and at day 14 (137.865 ± 9.094 mm3vs.183.210±4.368 mm3;q=11.166,P＜0.001) in the vinpocetine group were significantly less than those in the cerebral ischemia-reperfusion group.Conclusions Vimpocetine significantly reduces infarct vohme after focal cerebral ischemia-reperfusion,its mechanism may be associated with upreguhtion of PPARγexpression and downreguhtion of the expressions of NF-κB p65 and COX-2.

[ ABSTRACT] AIM: To investigate the protective effect of mesenchymal stem cell ( MSC)-conditioned medium (MSCCM) on myocardial cell line H9c2 and its mechanism.METHODS:Verification of MSC was performed by flow cy-tometry analysis, followed by MTT assay to determine the optimal incubation time of MSCCM with myocardial cells.The cells were divided into 4 groups:normal ( N) group, model ( M) group, M+MSCCM group and MSCCM group.The cells in M+MSCCM group and MSCCM group were pre-incubated with MSCCM for 24 h.The cells in M group and M+MSCCM group were treated with 300 μmol/L H2 O2 for 4 h to imitate oxidative injury of myocardial cells.Mitochondrial membrane potential and apoptotic rate of injured myocardial cells were detected by flow cytometry.The ROS production was measured by fluorescence microscopy.The nuclear translocation of Nrf2 and expression of HO-1 was examined by Western blot.RE-SULTS:No difference of mitochondrial membrane potential, apoptotic rate or ROS production between MSCCM group and N group was observed (P>0.05).The mitochondrial membrane potential depolarization, apoptotic rate and ROS produc-tion in M+MSCCM group were significantly lower than those in M group ( P<0.01 ) .The nuclear translocation of Nrf2 and expression of HO-1 in the myocardial cells were increased with MSCCM incubation time prolonged.CONCLUSION:MSCCM protects the myocardial cells against oxidative injury induced by H2 O2 .The anti-oxidative mechanism would be as-sociated with the activation of Nrf2/ARE pathway.

Back ground Superoxide anion produced by oxidative stress combined with nitric oxide(NO)released by cellular NO synthase(NOS)generates peroxynitrite(ONOO-)which was one of reactive oxygen species.Objective To study the role of peroxynitrite in the pathogenesis of myocardial stunning(MS)and the effects of aminoguanidine(AMD).Methods Twenty-four dogs were randomly divided into four groups:(1)Short-time myocardical stunning(MS)group:the animals underwent 15 min occlusion of left anterior descending coronary artery(LAD),followed by 120 min of reperfusion.(2)Long-time MS group:60 min of LAD occlusion,followed by 120 min of reperfusion.(3)AMD group:Dogs were subjected to the same ischemia/reperfusion management as Long-MS group,but AMD was administrated(total 100 mg/kg).(4)Sham-operation group.Left ventricular function was evaluated by echocardiography and blood samples were taken from coronary venous sinus for the examination of NO at different time points.The stunned myocardium was examined immunohistochemically and electronic microscope.Results(1)Systolic thickening of stunned myocardium region and left ventricular ejection fraction were markedly declined during LAD occlusion in the 3 experimental groups,but progressively improved with the time of reperfusion.The improvement was faster in short-MS and AMD groups than in long-MS group.(2)Plasma NO concentrations in coronary venous sinus were greatly increased during reperfusion in short-and long-MS group,while no significant elevation was found in AMD group.(3)A marked increase in the immunoreactivity to nitrotyrosine,a specific "footprint" of peroxynitrite,was shown in the stunned myocardium both in short-and long-MS group,with larger and stronger positive foci in long-MS group.The positive staining was located in myocardial cytoplasm,especially at myofibrils and contractile bands.Treatment with AMD significantly reduced the nitrotyrosine staining in the stunned myocardium.(4)No ultrastructural changes of myocardial cells were noted in stunned myocardium in short-MS group except a slight loss of mitochondrial granules.On the contrary,myocyte edema,myofilament fractures,granule loss and swelling of mitochondrias were significant in long-MS group.AMD significantly ameliorated the ultrastructural abnormalities.Conclusion Myocardial stunning was associated peroxynitrite with production which mainly deteriorate the contractile proteins of myofibrils.AMD significantly inhibit the peroxynitrite formation leading to attenuation of the ultrastructural and functional injuries of stunned myocardium.

Objective Establish an experimental model for primary subchondral bone osteoblasts culture of neonatal SD rat's condylar process. Methods Under the condition of sterile,24-hour SD rat was executed and its condylar process was isolated. Removing cartilage layer, the subchondral bone was exposed obviously, then it was cultured with modified repeating enzymatic digestion-adherent explants method. The cellular morphology was identified with invert microscope and immunohistochemistry staining, the osteoblasts were identified by alkaline phosphorase (ALP) staining and calcified nodules staining, and the proliferation of the acquired cells was examined by methyl thiazolyl tetrazolium (MTT) assay. Results A variety of cell morphologies were observed, such as spindle-shaped, triangular and irregular-shape, and their cell processes were significant. The alkaline phosphatase staining and calcified nodules staining of cultured osteoblasts with mineralized nodules were positive. Cells grew slowly in 1-3 days, and the cells growth reached the highest level at the 8th day. The cells growth trend has gradually slowed down after 8 days. Conclusion The method is an efficient way to culture and obtain purified neonatal SD rat's subchondral bone osteoblasts with typical characteristics.

Aim To investigate the protective effect of isorhamnetin on H9 C2 myocardial cell line and its mechanisms. Methods The toxicity and optimal pro-tective concentration of isorhamnetin were determined by MTT assay. The experimental subjects were divided into four groups:group N ( normal ) , group M ( mod-el) , group M + ISO ( model + isorhamnetin ) , and group ISO ( isorhamnetin only ) . Group M +ISO and ISO were pre-incubated with isorhamnetin for 12 hours while other groups with plain DMEM. Group M and M+ ISO were treated with 300μmol · L-1 H2 O2 for 4 hours after pre-incubation. Mitochondrial membrane potential depolarization of H9 C2 was measured by fluo-rescence microscope. Apoptotic rate and ROS produc-tion of injured myocardial cell line were detected using
flow cytometry. The oxidative indictors were measured by spectrophotometry. The expressions of cytoplasmic cytochrome C, caspase-9, caspase-3, Bcl-2, Bax, Nrf2 and HO-1 were examined by Western blot. Result There was no difference in mitochondrial membrane potential depolarization, apoptotic rate, ROS produc-tion, oxidative indictors production and expressions of cytoplasmic cytochrome C, caspase-9,caspase-3, Bcl-2 , Bax between groups ISO and N ( P>0. 05 ) . Apop-totic rate, ROS production, expressions of cytoplasmic cytochrome C, caspase-9, caspase-3, Bax, MDA pro-duction of group M+ISO were significantly lower than those of group M ( P < 0. 01 ) . And mitochondrial membrane potential, Bcl-2, CAT, SOD and GSH-Px of group M + ISO were increased compared to group M .
Nuclear translocation of Nrf2 and expression of HO-1 in myocardial cell line were increased with the prolonged isorhamnetin incubation time. Conclusion Isorham-netin could protect myocardial cell line against H2 O2-induced oxidative injury and apoptosis through the in-
terruption of mitochondrial dependent apoptotic path-way and activation of Nrf2/ARE pathway.