Objective To investigate the effect of wogonin on ethology and its possible mechanisms in chronic cerebral ischemia in rats.Methods Rats were randomly divided into a sham operation group,a wogonin intervention group,and a phosphate buffered solution (PBS) control group.A rat model of chronic cerebral ischemia was induced by the two-vessel occlusion method.Six weeks after modeling,the rats in the wogonin intervention group and the PBS control group were intragastric administrated with wogonin (50 μmol/L,10 ml/kg,once a day) and PBS with equal volume for 14 days.Morris water maze test was used to evaluate the spatial learning and memory function.Laser confocal three-dimensional vascular imaging was used to detect the vascular proliferation of ischemic brain tissue.5-Bromo-2-deoxyuridine (BrdU)immunochemical staining was used to detect the cell proliferation in ischemic brain tissue.Transmission electron microscope was used to observe the morphological changes of neural cells in cerebral ischernic region.Results The Morris water maze (n =8) showed that the trains of escape latency from the second to the fifth day in the wogonin intervention group were 43.45 ± 8.64 s,37.12 ± 1.31 s,34.75 ± 5.36 s,and 24.36 ± 5.43 s,respectively.They were significantly shorter than 51.69 ± 5.32 s,43.65 ± 9.21 s,50.19 ± 10.31 s,and 53.65 ± 7.15 s in the PBS control group (all P ＜ 0.05).The first quadrant swimming time of the wogonin intervention group was significantly longer than that of the PBS control group (26.16 ±3.29 s vs.14.38 ±2.16 s; P＜0.01).Laser confocal three-dimensional vascular imaging (n=4) showed that the capillary inner diameter in cerebral ischemia region of the wogonin intervention group was reduced significantly compared to the PBS control group (3.02 ±0.21 μm vs.3.35 ±0.18 μm; P ＜0.05),vascular density was increased significantly (205.80 ± 12.70/0.002 mm3vs.158.42 ± 10.92/0.002 mm3; P＜0.01),and total microvascular area was increased significantly (83 389 ± 4 026 μm2/0.002 mm3 vs.73 349 ±3 986 μm2/0.002 mm3; P＜0.01).Immunohistochemical staining (n =6) showed that the number of BrdU positive cells in the ischemic brain tissue of the wogonin intervention group was increased significantly compared to the PBS control group (24.62 ±3.25/HPF vs.9.87 ±2.89/HPF; P＜0.01).The observation of transmission electron microscope showed that the inflammatory edema in the intercellular spaces of the wogonin intervention group was significantly reduced compare to the PBS control group.Conclusions Wogonin can significantly improve the spatial learning and memory ability of chronic cerebral ischemia in rats,and its possible mechanisms may include the promotion of proliferation and angiogenesis in ischemic region and angiogenesis,and reduce inflammatory response.

Objective To analyze the clinical features of intestinal infection in patients with acute leukemia (AL) after chemotherapy. Methods The data of 103 cases of AL patients after chemotherapy from January 2014 to April 2016 were retrospectively analyzed, and categorical variables were compared by using chi-square test. Results A total of 364 cycles of chemotherapy was conducted among 103 patients, of which 66 times (18.13 %) in 59 cycles occurred intestinal infections, including twice intestinal infections in one cycle of chemotherapy in 7 cases. The incidence of intestinal infection was 27.48%(36/131) in group without complete remission (CR), and 9.87%(23/233) in CR group. There was a statistical difference between the two groups (P<0.01). Repeated intestinal infections were found in 46.67%of the patients who accepted multiple cycles of chemotherapy. In the same cycle of chemotherapy, the probability of recurrence of intestinal infection after chemotherapy was 3.7 times than patients without intestinal infection occurred during chemotherapy. The incidence of intestinal infection of patients with acute lymphoblastic leukemia (ALL) after primary inducing chemotherapy was higher than that of patients with acute myelogenous leukemia (AML) (P= 0.019). The incidence of intestinal infection combined with neutropenic was 9.89 % (36/364), and the incidence of intestinal infection was 8.24 % (30/364) in neutrophils > 0.5 × 109/L. There was no significant difference (P> 0.05). After chemotherapy, some patients with intestinal infection occurred acute abdomen, with high mortality rate. Conclusions Intestinal infection may occur in the procession of chemotherapy and myelosuppression. Special attention should be paid on intestinal infection, including reduction of blood stream infection and risk factors, as well as timely intervention.

Objective To explore the potential effects of endothelial progenitor cells (EPCs)-angiogenesis on mechanism of alleviating cognitive dysfunction in rats subjected to cerebral ischemia-reperfusion (I/R) injury. Methods A total of 121 male Sprague–Dawley (SD) rats were randomly divided into four groups:Sham group (n=31), focal I/R(MCAO, 0.9%saline 10μL, n=30) group, MCAO+Vehicle (sodium azide, 0.1%Vehicle 10μL, n=30) group and MCAO+HPX (1.86 g/L HPX 10μL, n=30) group. The modified neurological severity scores (mNSS) was carried out to determine neurological function deficit after I/R. Morris water maze (MWM) was carried out to assess learning and memory abilities after I/R. The circulating EPCs after I/R were counted by flowcytometry (FCM) combined with double-immunofluorescence staining of CD34 and CD133. Angiogenesis in rat penumbra cortex after I/R was assessed by immunohistochemical technique combined with immunofluorescent chromogenic detection of CD31 and vWF. Results Compared with sham group, the mNSS scores, the escape latency and the circulating EPCs count were increased after I/R, the time percentage spent in target quadrant was reduced, and the new vessel density in penumbra cortex was increased after I/R in MCAO group (P < 0.05 respectively). There were no significant differences in mNSS score, the escape latency, the time percentage spent in target quadrant, the circulating EPCs count and the new vessel density in penumbra cortex between MCAO group and MCAO+Vehicle group ( P>0.05). The mNSS score and the escape latency were significantly decreased, the circulating EPCs count and new vessel density in penumbra cortex were significantly increased after I/R in MCAO+HPX group compared with those of MCAO+Vehicle and MCAO group (P<0.05). Conclusion EPCs-angiogenesis signaling plays positive effects on HPX alleviating cognitive dysfunction in rats subjected to focal cerebral ischemia reperfusion injury.

Background Previous studies showed that the pathogenesis of uveitis is related to γδ T cells.However,it remains unclear that how these cells are involved in experimental autoimmune uveitis (EAU).Objective This study aimed to observe the dynamic changes of γδ T cells in EAU and explore the role of γδ T cells in the pathological process of EAU.Methods Forty-five C57BL/6(B6) mice were assigned to the normal control group (six mice) and EAU model group (thirty-nine mice).The mice were immunized subcutaneously at 6 spots on the footpads,tail base,and flank with emulsion containing human interphotoreceptor retinoid binding protein1-20 (IRBP1-20) emulsified in complete Freund's adjuvant.After immunization,the mice were examined for clinical signs of EAU by using a Genesis-D camera.The changes of histopathology were compared by hematoxylin and eosin staining.Mouse lymphocytes were isolated and purified from the spleens of IRBP1-20-immunized or normal B6 mice by using a γδ T-cell isolation kit.Flow cytometry was used to detect the changes of intracellular expression of interleukin-17A (IL-17A),and then transferred the activated γδ T cells into EAU models to analyze the changes of clinical signs and histopathology of EAU.Experimental study program as well as the use and feeding of the animals were authorized by the Animal Management and Use Committee of Shandong Traditional Chinese Medicine University.Results The inflammatory symptoms in mouse eyes appeared on day 12 after modeling.The initial changes were fundal blood vessel thickening and minimal inflammatory cell infiltration.Then,multifocal chorioretinal lesions,serious vasculitis and linear lesions were observed on days 16-20,along with abundant lymphocyte infiltration in the vitreous and retinal disorganization.The inflammation symptom scores and the pathological inflammation scores at different time points after modeling had statistically significant differences (F =51.399,P =0.000;F =47.342,P =0.000).The inflammatory symptoms in the eyes began to abate from day 28 onwards.The number of γδ T cells was obviously increased during the inflammation phase of EAU at day 16-20 after modeling,with the number of γδ T cells was (5.67 ±-0.49) ％ and (5.78 ±±0.55) ％,respectively,which was significantly higher than (1.53 ± 0.14) ％ before modeling,with significant differences between them (both at P＜0.05),meanwhile CD69 levels and the integrin lymphocyte function-associated antigen-1 (LFA-1) and secreted IL-17A were elavated.The secretion level of IL-17A was (13.40±0.50)％ and (17.80±2.37)％ on day 16 and day 20 after modeling,respectively,which was significantly higher than (1.53 ± 0.19) ％ before modeling,with significant differences between them (P =0.000,0.001).The activated γδ T cells were transferred into EAU model,the inflammation symptom scores were 1.00 (1.00,2.00) after activated γδ T cells were transferred into EAU model,which was significantly higher than 0.75 (0.05,1.00) of the untransferred group (Z =27.00,P =0.03),and the symptoms of EAU were aggravated.Conclusions The proportion of γδ T cells reaches peak in inflammation of EAU,and the cells are activated.The activated γδ T cells in the EAU model play a immune regulation role by secreting IL-17A.

Objective:To evaluate the role of hemopexin (HPX) in cerebral ischemia-reperfusion (I/R) injury in rats.Methods:One hundred and twenty healthy male Sprague-Dawley rats, aged 7-8 weeks, weighing 250-280 g, were divided into sham operation group (S group, n=36), cerebral I/R group (I/R group, n=36), vehicle group (V group, n=24), and HPX group ( n=24). The model of cerebral I/R injury was established by 120 min middle cerebral artery occlusion followed by reperfusion in anesthetized rats.At 6, 12 and 24 h of reperfusion, 4 rats in S group and I/R group were sacrificed, and the ischemic penumbra of the ipsilateral cerebral cortex was obtained to detect the expression of HPX by Western blot.In I/R, V and HPX groups, 0.9% normal saline 10 μl, 0.1% NaN 3 10 μl, and 1.86 mg/ml HPX 10 μl were injected into the lateral ventricle, respectively, immediately after reperfusion.Eight rats in each group were selected, and neurological deficit was scored at 1-7 days of reperfusion.Eight rats in each group were sacrificed at 1 and 7 days of reperfusion, brains were removed, and brain tissues were obtained for measurement of infarct size, and the percentage of infarct size was calculated. Results:Compared with S group, the expression of HPX in cerebral ischemic penumbra was significantly up-regulated at 24 h of reperfusion in I/R group, and the neurological deficit scores were significantly decreased at 1-7 days of reperfusion, and the percentage of cerebral infarct size was increased at 1 and 7 days of reperfusion in I/R, V and HPX groups ( P<0.05). Compared with I/R group, the neurological deficit scores were significantly increased at 1-7 days of reperfusion, and the percentage of cerebral infarct size was decreased at 1 and 7 days of reperfusion in HPX group ( P<0.05), and no significant change was found in the above indicators in V and I/R groups ( P>0.05). Conclusion:Up-regulation of HPX expression is the endogenous protective mechanism of cerebral I/R injury in rats.

Objective To investigate the effects of exogenous hydrogen sulfide (H2S) on injury of rat hippocampus neurons induced by oxygen-glucose deprivation and restoration (OGD/R) and explore its mechanism.Methods Hippocampus neurons were isolated from embryonic day 16-18 (E16-18) rat embryos.Hippocampus was immediately removed and digested with 0.25％ trypsin.The neurons were isolated and cultured at 37 ℃ for 7 days and neuron-specific enolase (NSE) was detected by immunohistochemical staining method to identify neurons.At 8th day,the neurons were placed in deoxygenated glucose-free medium and exposed to 95％ N2-5％ CO2 in an air tight chamber for 1 hour,and then replaced the glucose-free medium with original medium,and returned the cultures to a standard incubator in 5％ CO2 at 37 ℃ and incubated for another 24 h.The neurons were divided into 3 groups:group Ⅰ control; group Ⅱ OGD/R,and group ⅢOGD + NaHS,the latter was further divided into 5 subgroups:groups Ⅲ1-5 with 25,50,100,200,400 μmol/L NaHS added,respectively.Then cell viability was quantified by MTT method,the level of lactate dehydrogenase (LDH) were detected,apoptosis was measured by Annexin V FITC/PI Apoptosis Kits,and RT-PCR was used to assay HIF-1 α mRNA in neurons in all groups.Results Compared with control group,the LDH level,apoptosis and expression of HIF-1α mRNA in group Ⅱ were significantly increased,the cell viability was significantly decreased (P ＜ 0.01).There were no significant differences in the LDH level,apoptosis and expression of HIF-1 α mRNA and the cell viability between group Ⅱ and group Ⅲ1 (P ＞ 0.05).Compared with group Ⅱ,the LDH level,apoptosis and expression of HIF-1α mRNA in group Ⅲ2-4 were significantly increased,the cell viability was significantly increased (P ＜ 0.01).Compared with group Ⅱ,the LDH level,apoptosis and expression of HIF-1 α mRNA in the group Ⅲ 5 were significantly decreased,the cell viability was significantly decreased (P ＜ 0.01).Conclusions H2S of low concentration has no significant effects on injury of rat hippocampus neurons induced by OGD/R.H2S of moderate doses can protect rat hippocampus neurons from OGD/R injury and H2S of high concentration can aggravate injury.The expression of HIF-1α mRNA in rat hippocampus neurons was increased after OGD/R,and the protective role of H2S is associated with increase in the expression of HIF-1α mRNA.

Objective To explore the effects of hydrogen sulfide (H2S) on apoptosis of cardiomyocytes after cardiopulmonary resuscitation (CPR) in rat models.Methods Forty-five male SD rats were randomly into sham group (n =15),CPR group (n =15) and NaHS group (n =15).Rats of CPR group and NaHS group were operated to induce cardiac arrest by transcutaneous electrical stimulation to epicardium.In NaHS group,NaHS (5 mg/kg) was administrated via the femoral venous line 1 min before CPR.Hemodynamic variables were monitored and obtained continuously.Survival rats were sacrificed at 24 h after restoration of spontaneous circulation and the hearts were removed for analysis by RT-PCR and TUNEL assays.Blood samples were collected and plasma content of cTnT was detected.Results Compared with the CPR group,animals treated with NaHS had improved left ventricular function (P ＜0.01),lower plasma cTnT levels (P ＜0.05) and decreased apoptosis index (P ＜ 0.01) 24 h after ROSC.The expressions of Caspase-3 mRNA,Bax mRNA and Bcl-2 mRNA in CPR group and NaHS group were higher compared with the control group (P ＜0.01).The NaHS group had lower expressions of Caspase-3 mRNA and Bax mRNA (P ＜0.01),but higher expression of Bcl-2 mRNA (P ＜0.05) compared with the CPR group.Conclusions Exogenous (H2S) regulated the expressions of Caspase-3,Bax and Bcl-2 mRNA,thereby preventing apoptosis of cardiomyocytes,inhibiting cTnT release and improving left ventricular function 24 h after CPR.

ving CQI(P＜0.05).Conclusion CQI program effectively reduces CRBSI incidenee in cancer patients with PICC.

Objective To find the possible pathogenesis of enteric nervous system, gut hormone and gastric Cajal interstitial cell ( ICC ) in gastritis related gastrointestinal ( GI ) motor disorders on the changes of protein gene product 9. 5 in neurons , mucosal expression of C-kit, gastrin and somatostatin from the gastric wall of gastritis rat. Methods 45 rats were divided into 3 groups which included gastritis group A, gastritis group B and control group. Rats in gastritis group A were fed with Hp Sydney Strain 1, the mixture of 2% aspirin and 0. 6N hydrochloric acid was fed in gastritis group B. The control group only received saline. All of the rats were killed and mucosal tissue was obtained from antrum and greater curvature of the gastric body. Pathological and Hp examination were performed in the tissue slides, and then it was stained to check PGP 9. 5, gastric body's mucosal expression of C-kit, antrium's mucosal expression of gastrin and somatostatin. The cell body, the maximum diameter (Dmax, μm), mean area( μm2) and optical density (nm), integral optical density of the gastrin and somatostatin in the C-kit expression positive neurons from the gastric wall were compared among the groups. Result The mean area and optical density of PGP 9. 5 expression in neurons from the gastric wall of rat in group A or B were obviously lower than that of the control group ( P ＜0. 01 ), while there was no difference between gastric group A and B ( P ＞0. 05). Gastric group A had higher GAS expression than control group, while SS expression was lower than control group( P＜0. 05). There was no difference between group B and the control group in the two variances( P ＞0. 05).By linear correlation analysis, it showed that SS was negatively correlated with GAS ( r = - 0. 333, P ＜0. 01 ). The distributive area and diameter of cells with C-kit expression in both group A and B were significantly smaller than that in the control group ( P ＜ 0. 05 ), while there was no obvious difference between group A and B ( P ＞ 0. 05 ). There was no difference of integral optical density of the C-kit expression positive neurons among the three groups. Conclusions Hp infection and NSAIDs might cause gastritis and had influence on the structural changes of neurons from gastric wall and ICC. Hp infection could obviously inhibit SS excretion from antrum mucosa while increase Gastrin excretion. NSAIDs induced gastritis had little influence on GAS and SS.

Objective:To evaluate the role of heme oxygenase-1 (HO-1) in hemopexin (HPX)-induced reduction of cerebral ischemia-reperfusion (I/R) injury in rats.Methods:One hundred and eighty male Sprague-Dawley rats, aged 7-8 weeks, weighing 250-280 g, were divided into 5 groups ( n=36 each) using a random number table method: sham operation group (group SH), I/R group, vehicle group (group V), HPX group, and HPX plus HO-1 specific inhibitor ZnPPIX(HZ group). Local cerebral I/R was produced by middle cerebral artery occlusion for 120 min followed by reperfusion in anesthetized rats.In I/R, V, HPX and HZ groups, 0.9% normal saline 10 μl, 0.1% NaN 3 10 μl, 1.86 g/L HPX (diluted to 10 μl in 0.1% NaN 3 solution), and 1.86 g/L+ ZnPPIX 20 μmol/L (diluted to 10 μl in 0.1% NaN 3 solution) were injected through the lateral ventricle, respectively, immediately after onset of reperfusion.Morris water maze test was used to detect the cognitive function on day 1 before ischemia and day 2 of reperfusion.Rats were sacrificed, brains were removed and brain tissues were obtained for determination of the permeability ratio of Evans blue (EB), brain water content, expression of VE-cadherin in ischemic penumbra (by Western blot), and expression of angiopoietin-1 (Ang1) mRNA and Ang2 mRNA (by real-time polymerase chain reaction). Ang1 mRNA/Ang2 mRNA ratio was calculated.CD31/vWF double labeling immunofluorescence was used to detect the density of neovascularization in hippocampal tissues in the ischemic penumbra. Results:Compared with SH group, the escape latency was significantly prolonged at 2-7 days of reperfusion, the percentage of time of staying at the target quadrant was decreased, the frequency of crossing the platform was decreased, the permeability ratio of EB in brain tissues was increased at day 7 of reperfusion, and the brain water content, Ang1 mRNA/Ang2 mRNA ratio, expression of VE-cadherin and density of neovascularization were decreased in I/R, V, HPX and HZ groups ( P<0.05). Compared with I/R group, the escape latency was significantly shortened at 2-7 days of reperfusion, the percentage of time of staying at the target quadrant was increased, the frequency of crossing the platform was increased, the permeability ratio of EB in brain tissues was decreased at day 7 of reperfusion, and the brain water content, Ang1 mRNA/Ang2 mRNA ratio, expression of VE-cadherin and density of neovascularization were increased in HPX group ( P<0.05), and no significant change was found in the parameters mentioned above in V and HZ groups ( P>0.05). Compared with HPX group, the escape latency was significantly prolonged at 2-7 days of reperfusion, the percentage of time of staying at the target quadrant was decreased, the frequency of crossing the platform was decreased, the permeability ratio of EB in brain tissues was increased at day 7 of reperfusion, and the brain water content, Ang1 mRNA/Ang2 mRNA ratio, expression of VE-cadherin and density of neovascularization were decreased in HZ group ( P<0.05). Conclusion:HO-1 is involved in HPX-induced reduction of cerebral I/R injury in rats.