Objective To systematically review the literature evaluating efficacy and adverse events of propranolol for infantile hemangiomas (IHs).Methods We searched the Cochrane,Medline,Wiley,CNKI and Wanfang Databases for all studies on the response of IHs to propranolol only which were published between June 2008 and May 2013.Results A total of 23 studies were collected,including 14 case reports and 2 follow-up studies which were without random and control;another 6 studies were clinical controlled trials and 1 study was RCT.Total 716 patients were included,and never received other treatments before propranolol.Propranolol was initiated at a mean age of (4.5 ± 0.5)months at a mean dose of 2.1 mg/kg/day and for a mean treatment duration of (9.7±9.2) months.The effective rate for patients with IHs treated with propranolol was 97％ (691/716),and patients after treatment completion reported IHs recurred in 8.6 ％ of patients.The adverse effects rate was 31％(223/7167) which most common adverse events were changes in sleep (n=35),gastrointestinal reaction (n =52) and decreased heart rate (n =73),and 5 patients discontinued the treatment because of the serious adverse events.Conclusions This systematic review of 716 patients treated with propranolol for IHs show a high rate of efficacy and a low rate of serious adverse events,and it is a better treatment of infantile hemangioma,but we should pay more attention to the serious adverse events and strictly select indications.

Aim To explore the proteomics mechanism of the differentiation induction effect of 4-amino-2-trif-luoromethyl-phenyl retinate(ATPR)on human leukemi-a K562 cells. Methods Human leukemia K562 cells were incubated with the same concentration (1 × 10 - 6 mol·L - 1 ) of ATPR or ATRA for 48 hours. The total cell proteins were collected, purified and digested by trypsin, solid phase extraction, and the peptides were detected by ESI-LC-MS / MS. The difference of the pro-tein expression between the cells treated with ATPR and ATRA was compared by using the Discoverer Pro-teome 1. 2 software, and the molecular function, the biological process and other information of those pro-teins were analyzed based on the DAVID, KEGG, STRING databases. Results 120 specific proteins were identified only in the ATPR group, 143 only in the ATRA group, and 422 other proteins in both groups. Results of DAVID analysis showed that ATPR-induced specific proteins were mainly involved in 39 biological processes of proteins and macromolecules metabolism, protein transport and localization and so on. Results of KEGG analysis revealed that ATPR-in-duced proteins participated in signal pathways, mainly metabolic pathways, PI3K-Akt signal pathway, TGF-beta signal pathway and other pathways in cancer. String protein interaction network analysis displayed that ATPR-induced proteins, like EIF3A, EIF6, RPL3, RPL8, RPL13, RPL7A, RPL21, RPS3, RPS14, NACA, BTF3, NHP2L1, PPP2CA proteins had direct interactions with more than or equal to 10 associated proteins. Conclusion The differentiation induction effect of ATPR on K562 cells might be as-cribed to the ATPR-induced proteins interaction net-work and the specific central proteins it induced, which are involved in the regulation of cell prolifera-tion, differentiation and apoptosis.

Objective: This research explores the relationship between the immuno-suppression function of regulatory T cells (Treg) in the ascites of ovarian cancer (OC) patients, the clinico-pathologic features of these patients, and the correlation of the function of Treg with initial treatment and relapse status of the patients to further investigate the specific mechanism of immuno-regulatory func-tion of CD4+ CD25+ Treg in the ascites of OC. Methods: Immuno-magnetic activated cell sorting (MACS) was conducted to sort CD4+CD25+Treg and autologous CD4+CD25-Treg from the ascites of 28 OC patients. Carboxyfluorescein-diacetate succinimidyl ester (CFSE) was used to label the autologous CD4+CD25-Treg. These labeled cells were then used as controls and co-cultured with autologous CD4+CD25+Treg at the ratio of 1∶1 or 1∶2. The mean inhibition ratio of Treg in specimens to the proliferation of autolo-gous CD4+ CD25-Treg was calculated after the flow cytometry of the CFSE expression and Modfit software analysis of the CD4+CD25-Treg proliferation index (PI) were performed. Anti-IL-10 and/or anti-TGF-β1 antibodies were neutralized to investigate whether the CD4+CD25+Treg-mediated immuno-suppression escaped through the ascites can produce a marked effect by the inhibitory cyto-kine IL-10 or TGF-β1. Results: The mean inhibition ratio of CD4+ CD25- Treg in the ascites of stage Ⅲ to Ⅳ OC patients was (75.72±17.04)%, which is significantly higher than that of stageⅠtoⅡOC patients (59.61±16.97)%;P<0.05. In addition, Treg in the as-cites of OC patients with recurrent disease showed a significantly higher inhibition ratio than that of patients with primary disease;P<0.001. Moreover, Treg in groups added into neutralizing anti-IL-10 and/or anti-TGF-β1 antibodies displayed significantly lower depres-sant effect than the control group;P<0.05. Conclusion:The immuno-suppression of CD4+CD25+Treg in the ascites of OC patients is correlated with the tumor staging and status of the primary or recurrent diseases. Moreover, Treg may indicate a suppressor function by secreting cytokine IL-10 and TGF-β1.

Objective:CD4+CD25+regulatory T cells (Treg) may contribute to tumor progression by suppressing antitumor im-munity. The function of Treg in antitumor immunity regulation in the peritoneal microenvironment of ovarian cancer (OC) was investi-gated and compared with the circulating Treg to elucidate OC immune escape. Methods: Flow cytometry was used to determine the proportion of CD4+CD25+T cells in CD4+T cells in ascites of 27 patients with OC and in peripheral blood lymphocytes of 28 patients with OC. The samples were analyzed and classified in three stages:primary disease (PD), after chemotherapy (AC), and recurrence dis-ease (RD), according to the clinical conditions of the OC patients upon donating the samples. The percentage of Treg in the three groups was determined in ascites and blood. CD4+CD25+T cells were isolated from ascites and peripheral blood of patients with OC us-ing magnetic sorting (MACS) system. The cells were then tested for regulatory function through coculture with carboxyfluorescein diac-etate succinimidyl ester-labeled autologous CD4+ CD25- responder cells. Results:The proportion of CD4+ CD25+T cells in CD4+T cells significantly increased in ascites (28.25%± 14.06%) compared with that in blood (14.6%± 4.74%;P<0.0001). The Treg in ascites and blood in AC showed higher proportion (P<0.0001) than those in the PD and RD;the proportion in RD was higher than that in PD (P<0.0001). Moreover, the Treg in ascites mediated a significantly higher suppression compared with the Treg in peripheral blood (P<0.001). Conclusion:The frequency and suppressor function of Treg were significantly higher in ascites than in peripheral blood. This finding suggests more possibility for escape immune surveillance in the peritoneal microenvironment. Moreover, the proportion of Treg in AC was higher than that in PD or RD;the proportion in RD was higher than that in the PD. Chemotherapy may favor the expansion of Treg, which may promote the recurrence of cancer.

Objective:The objective of this research is to study the serum level of the high-mobility group protein B1 (HMGB1) in human ovarian tumor (OvCa) and in a healthy control. This study also aims to identify different HMGB1 levels before and after sur-gery and to explore the inhibitory effect of HMGB1 gene silencing in the proliferation and invasion ability of OvCa. Methods: En-zyme-linked immunosorbent assay was used to measure the serum level of HMGB1 in OvCa patients and healthy subjects. Lentivirus vector with HMGB1 shRNA was constructed and used to infect OvCa cells. The expressions of HMGB1 mRNA and protein were test-ed by real-time PCR and Western blot. Cell proliferation was detected using the Cell Counting Kit-8 assay, whereas cell invasion and migration were detected by Transwell assay. Results:The serum level of HMGB1 was more elevated in patients with malignant diseas-es compared with individuals with benign diseases and the control groups. In the malignant group, the serum level of HMGB1 de-creased noticeably after therapy. Down-regulation of HMGB1 expression resulted in the inhibition of the biological behavior and metas-tasis of ovarian cancer cells. Conclusion: HMGB1 is closely associated with clinicopathologic features of OvCa. Knockdown of HMGB1 expression can significantly inhibit cell proliferation, cell migration, and cell invasion of OvCa. These findings indicate that HMGB1 can function as a therapeutic target for ovarian neoplasm in the future.

Deep venous thrombosis (DVT) is initiated intraoperatively and may display symptoms postopera- tively following total hip or total knee arthroplasties. Pulmonary embolism (PE) and DVT cause morbidity and mortality. It has been established that patients who undergo a major lower-extremity joint replacement should receive prophylaxis due to the increased risk of DVT. Despite use of thrombo-prophylaxis, elective replacement surgery carries a high risk of venous thromboembolic complications. The early detection of DVT and treatment with systemic anticoagulation to pre- vent DVT are essential in the management of patients undergoing total joint arthroplasty. Extended medical throm- bo-prophylaxis is indicated for some high-risk patients. Routine postoperative duplex surveillance for DVT may be clinically useful. In the early post-operative phase, combined prophylaxis such as low-molecular-weight heparins and mechanical methods may be more effective than single intervention measures. However, the efficacy and safety of an- ticoagulation therapy, using various medicines administered after total arthroplasty of large joints are still undetermined and controversial.We should also be alert to the frequency and extent of postoperative hematomas. There are still many uncertainties in treatments to prevent DVT in terms of safety and cost-effectiveness. Therefore, prospective, ran- domised, controlled and multicenter studies may be necessary to obtain valuable information according to evidence based medicine.

Objective To investigate the regulatory effects of IFN-γon Treg cells from HIV/AIDS patients receiving highly active antiretroviral therapy (HAART) for one year.Methods Thirty HIV/A1DS patients whose CD4+T cells were below 350/μ1 were recruited for HAART therapy.Blood samples were collected at the time points of 0,24,48 weeks after HAART.PBMCs were isolated and randomly divided into two culture groups.One group was cultured directly in medium and another group was co-cultured with IFN-γ (40 pg/ml).The supernatants and cells were separated after 5 days of culture for analysis.The concentrations of IL-12 and CD4+CD25+Foxp3 Treg cells were measured by ELISA and flow cytometry,respectively.Results The levels of IL-12 in the supernatants from the culture without IFN-γ at time points of 0,24,48 weeks after HAART were lower than those from the co-cultured group [(37.02±12.76) vs (41.79± 15.02),t=2.336,P=0.03; (41.76±17.01) vs (47.2±14.26),t=2.702,P=0.014; (48.01± 11.84) vs (53.44± 11.30),t =3.14,P =0.003].The percentages of CD4+ CD25 + Foxp3 Treg cells in CD4+ T cells from the direct-cultured group were higher than those from the co-cultured group at the three time points [(10.41±1.10)％ vs (2.40±1.11)％,t=13.89,P=0.000; (8.33±2.03)％ vs (1.99± 0.86)％,t=12.93,P=0.000; (5.65±1.55)％ vs (1.32±0.73)％,t=10.61,P=0.000].Moreover,the results within the same group at the time points of 0,24,48 weeks upon HAART were also significantly different.Conclusion With the interference of HAART,IL-12 levels were increased,while CD4+CD25+ Foxp3 Treg cells were decreased in patients with HIV/AIDS.IFN-γ plays an important role in this process.

Objective To build experimental animal model of cerebral alveolar echinococcosis disease of sheep,in order to study of human alveolar hydatid disease of the brain.Methods Experiment animal models of ten Xinjiang big-tail sheep were performed by, direct skull puncture,intracerebral inoculation of echinococcus multilocularis.MRI was used to observe the growth status of cerebral alveolar echinococcosis disease of sheep after 8 months,and morphological and pathological characteristics after autopsy were ana-lysed.Results 4 sheep models (40%)were successful built which were confirmed by pathology and MRI.On MRI,4 cases all were single lesion,on T2 WI there was multiple follicles bubbles under the background of low signal in one case,and low signal in other three cases.Under the microscope,a large number of lymphocytes,eosinophils and plasma cells infiltrated the lesion area,around which small blood vessels were blocked and had inflammatory reaction were showed.Conclusion The method using artificial inocula-tion rat alveolar echinococcosis to establish experimental model of cerebral alveolar echinococcosis disease of sheep has the character-istic of feasibility,simplicity and repeatability.

Objective To investigate the management of external iliac artery mycotic hemorrhage after kidney transplantation. Methods A case of external iliac artery mycotic hemorrhage after kidney transplantation managed by the use of hypogastric artery autograft was reported with review of the literature.The massive blooding occurred 3 times after kidney transplantation in a male patient 25 years of age on the 22nd,24th and 38th day after transplantation.The blooding amounted to 800 ml,2500 ml and 3800 ml respectively.The blood loss was replaced and prompt surgical exploration was carried out with the blooding site at the anastomosis sutured up on the 1st and 2nd episode of bleeding.On the 3rd occurrence of bleeding, the diseased external iliac artery segment, about 2cm in length, was resected and the gap was replaced by a 3cm long hypogastric artery autograft. Results The blood flow through the repaired external iliac artery and the blood supply to the lower extremity was adequate.Periodic hemodialysis had been restored and the patient waited for reimplantation. Conclusions External iliac artery mycotic hemorrhage after kidney transplantation is a serious and fatal complication.Simple arterial repair is usually noneffective.Resection of the diseased mycotic segment of the external iliac artery with repairing of the gap with a hypogastric artery autograft is rational,feasible and simple.The procedure is highly recommended.

Objective: To explore the sensitization effects of resveratrol on CNE2 nasopharyngeal carcinoma cell line with hypoxia-induced chemotherapy resistance and the potential mechanism. Methods: Human CNE2 nasopharyngeal carcinoma cell line was cultured under hypoxic conditions (37 degrees centigrade, 5% CO(2), 2% O(2)) in vitro. The cultured cells were treated with different concentrations of resveratrol for 48 h. Reversal fold (RF) of reseratrol to chemotherapeutic drugs in CNE2 cells was measured by methyl thiazolyl tetrazolium (MTT) assay. Apoptotic rate of CNE2 cells was observed by flow cytometry. Reverse transcription-polymerase chain reaction (RT-PCR) method and Western blotting were used to investigate the expressions of multidrug resistance gene 1 (mdr1), multidrug resistance-associated protein 1 (MRP1) and hypoxia inducible factor 1alpha (HIF-1alpha) in CNE2 cells. Results: Resveratrol combined with chemotherapeutics produced a synergistic effect. The RF of 200 alphamol/L resveratrol to paclitaxel was 2.58. Combined with paclitaxel, 25, 50, 100 and 200 alphamol/L of resveratrol increased the apoptotic rate of CNE2 cells from (22.14+/-1.09)% to (23.24+/-1.37)%, (27.57+/-2.01)%, and (30.36+/-2.31)%, respectively. Resveratrol could down-regulate the expressions of HIF-1alpha, mdr1 and MRP1 significantly. After being treated with resveratrol at different concentrations separately, the expressions of HIF-1alpha, mdr1 and MRP1 in CNE2 cells decreased significantly as compared with paclitaxel alone or paclitaxel plus verapamil (P<0.01). Conclusion: Resveratrol can enhance the sensitivity of CNE2 cells to chemotherapeutic drugs under hypoxia. The potential mechanism is partly attributed to inhibiting the gene expressions of HIF-1alpha, mdr1 and MRP1.