The biological incompatibility of traditional peritoneal dialysis fluids(PDF) is the main reason for the poor outcomes of long-term peritoneal dialysis and the high rate of technical failure.Recently,two-compartment PDF has been applied in the treatment of peritoneal dialysis patients,and reportedly has lots of clinical advantages due to its better biocompatibility.This paper presents an overview of recent advances in the studies of two-compartment PDF.

AIM: To investigate the effect of heme oxygenase on vascular remodeling in renal hypertension. METHODS: Male Wistar rats were randomly divided into sham-operated, 2K1C (two-kidney one-clip) and hemin-induced groups. Four weeks after the treatments, the thickness of aortic media and HO enzymatic activity of the aorta were determined. Immunohistochemical staining was carried out to detect protein of HO-1 in the aorta. RESULTS: The blood pressure in 2K1C renal hypertension rats started to increase two weeks after the surgery and stabled at a high level at the 4th week. Hemin, an inducer of HO-1, markedly inhibited the increase in blood pressure. Aortic medium thickness of the 2K1C rats at 4th week was 27 5% thicker than that in the sham-operated rats. The thickness of aortic medium of the hemin-induced rats was 16 1% less than that in 2K1C group. At the 4th week after operation, protein level and enzymatic activity of HO-1 in aorta were higher than that in 2K1C group compared to those in the sham-operated group. CONCLUSION: Renal hypertension caused vascular remodeling and the activation of HO-1. HO-1 induction decreased the blood pressure of renal hypertension and reduced vascular remodeling.

Objective To observe the destructive and scavenging effect of ambroxol (AMB) on the biofilm (BF) of Pseudomonas aeruginosa (P.a).To evaluate the synergistically bactericidal effect of AMB along with levofloxacin (LFX) on BF of P.a.Methods The early model (cultured for 3 d) and mature model (cultured for 7 d) of P.a wild strain (PAO1) BF were established,in vitro,respectively.The models were randomly (random number) divided into control group,AMB group and AMB + LFX group.The concentrations of AMB were 256 μg/ml and 512 μg/ml,respectively.When the early BF model and mature BF model were made,different concentrations of AMB were added in AMB group and AMB + LFX (1μg/ml) was added in AMB + LFX group.The number of viable P.a on the BF carrier was counted with the continuous dilution method 24 h after AMB or/and LFX added.Then,the BF morphological changes on the carrier surface were observed by using scanning electron microscopy (SEM).Measured data were analyzed with single factor analysis of variance (One-Way ANOVA).Results Both in the early BF model and in the mature BF model,the SEM examination showed that the BF in AMB group was significantly reduced compared to the control group,and this reduction of BF was in dose-dependent manner.LFX 1 μg/ml could reduce the number of viable bacterial in BF in both early model and mature model (P ＜ 0.05).LFX with addition of different concentrations of AMB showed stronger bactericidal effect than LFX used alone identified by more significant reduction in the number of colonv within the BF (P ＜ 0.05).Furthermore,the LFX combined with 512 μg/ml AMB reduced more significant number of colony apparently than the LFX combined with 256 μg/ml AMB (P ＜ 0.05).Conclusions AMB can destroy the early BF or mature BF partly,and LFX alone can partly reduce the number of viable P.a within BF.When LFX combined with AMB,they exert a synergistically bactericidal effect.

The defense mechanism of tumor immune response is triggered spontaneously with the onset of oncogenesis in hemato-logical malignancy. However, the presence of activated immune cells and effector cytokines activates multiple immunosuppressive pathways prior to clinical diagnosis of tumors,which synergize with each other and cause dysfunction of tumor antigen-specific T cells, ultimately leading to a state of immune tolerance in hematological malignancies.Indoleamine-2,3-dioxygenase(IDO)is an important member of these immunosuppressive pathways,which induces counter-regulation to limit the inflammatory response and triggers T cell-acquired tolerance,eventually inhibiting the tumor immune response.Considering the role of IDO in immunosuppression,IDO in-hibitors constitute an important part of the immunotherapeutic arsenal against various tumors,especially hematological malignancies, and have been studied extensively in recent years.This review discusses the significance of IDO and its inhibitors in the treatment and prognosis of hematological malignancies.

Objective: To investigate the causes and management of enteral feeding intolerance in patients with severe acute pancreatitis (SAP). Methods: The clinical data were retrospectively analyzed of 128 SAP patients who underwent enteral feeding treatment during the period from January 2006 to January 2008. Results: The rate of enteral feeding intolerance was significantly higher in the group of patients who didn' t use Flocare 800 pump, single-use enteral feeding tube and heater (10/50 or 20.0%) than that in the group of patients who used Flocare 800 pump, single-use enteral feeding tube and heater (5/78 or 6.4%). Conclusion: The possible risk factors of enteral feeding intolerance may be transfusional speed, temperature and concentration of nutritional fluid. Severity of acute pancreatitis is another important factor. Intestinal dysfunction should be noticed during the enteral nutritional support.

Objective To investigate the clinical effects of alprostadil combined with butylphthalide in treatment of cerebral infarction. Methods Ninety-four patients with cerebral infarction treated in our hospital from November 2011 to January 2014 were selected as the study subjects and randomly divided into the control group with 47 patients and the observation group with 47 patients. The control group received alprostadil treatment and the observation group re-ceived alprostadil combined with butylphthalide treatment. The changes of treatment efficacy and NIHSS scores, im-provement of quality of life, changes of laboratory parameters and safety of the two groups were observed. Results The observation group had significantly higher total effective treatment rate than the control group (P<0.05). The two groups were not significantly different in the NIHSS score before treatment (P>0.05); both groups improved gradually after 7 days of treatment and recovered well after 2 weeks; the observation group had significantly better recovery effect than the control group(P<0.05). After treatment, the quality of life of both groups was evaluated, which showed that the obser-vation group had significantly higher quality of life than the control group(P<0.05). The two groups were not significantly different in PT (P>0.05), and the observation group had significantly higher APTT and PLT and significantly lower Fb than the control group, with statistically significant differences (P<0.05). The incidence of complications of the observa-tion group was 8.51%, which was significantly lower than the 19.15% of the control group, with statistically significant difference (P<0.05). Conclusion Both alprostadil and butylphthalide have good treatment effects on cerebral infarction and their combination generates a synergistic effect, which can rapidly improve neurological function, enhance efficacy and help improve the patients' quality of life, thereby worthy of clinical promotion.

Cholestatic hepatopathy is a hepatobiliary system disease caused by abnormal bile excretion.It is common in infants.And its incidence varies with region and cause.The incidence of cholestatic jaundice in full-term infants is about 1/2 500.The etiology of infantile cholestatic hepatopathy involves many factors including abnormal liver or bile ducts structure, genetic metabolic diseases, infections, endocrine diseases and parenteral nutrition-associated cholestasis.The disease needs to be treated according to the primary disease.If there is a clear etiology, etiological treatment is necessary.Usually symptomatic and comprehensive treatment is adopted due to inconclusive diagnosis.The artical mainly states the present therapy methods.

Objective:To illustrate the effect and mechanism of ibrutinib,a Bruton's tyrosine kinase(BTK)inhibitor that inhibits diffuse large B-cell lymphoma(DLBCL)cell survival.Methods:DLBCL cell lines SUDHL-10 and HBL-1 were treated with ibrutinib at different concentrations.A MTT assay was used to detect the inhibition of cell proliferation.Cell apoptosis was analyzed by Annexin V-binding assay,as well as flow cytometry and DAPI staining.The expression of phosphorylated BTK,AKT and ERK was detected by Western blot. DLBCL cells were co-cultured with MSC.The inhibitory effect of ibrutinib on DLBCL cells in tumor microenvironment was assessed in clonogenicity in vitro and in a tumor-bearing non-obese diabetic/severe combined immunodeficient mice in vivo.Results:Up to 2.5 μmol/L and high concentrations of ibrutinib significantly inhibited the proliferation of DLBCL cells in a dose-dependent manner.Approx-imately 1 and 2.5 μmol/L ibrutinib was added on SUDHL-10 cells for 24 h,and the cell apoptotic rates were(21.73±3.64)% and(34.71± 2.36)%,respectively.Both were superior to that of the control group(3.55±1.89)%(P<0.05).Both two DLBCL cell lines pretreated with 5 and 10 μmol/L ibrutinib for 24 h and exhibited nuclear shrinkage at 5 μmol/L and nuclear fragmentation at 10 μmol/L.The expres-sion of phosphorylated BTK,AKT,and ERK decreased significantly after ibrutinib treatment.Ibrutinib inhibited clonogenicity in vitro(P<0.01)and cell proliferation and growth in vivo of DLBCL cells in co-culture system.The differences were statistically significant.Conclu-sion:Ibrutinib can inhibit the proliferation and induce apoptosis of SUDHL-10 and HBL-1 cell lines through a mechanism of blocking the AKT and ERK signaling pathways,as well as the proliferation of DLBCL cells in tumor microenvironment.This finding can significant-ly benefit DLBCL treatment.

Objective:To discuss the effect of ligustilide on the cardiac function and angiogenesis in the rats with heart failure,and to clarify its regulatory effect on protein kinase D1(PKD1)/hypoxia-inducible factor-1α(HIF-1α)/vascular endothelial growth factor(VEGF)pathway.Methods:The SD rats were randomly divided into sham operation group,model group,ligustilide group,PKD1/HIF-1α/VEGF signaling pathway inhibitor CID755673(CID)group,and ligustilide+CID group.The heart failure rat model was established by ligation of the left anterior descending coronary artery.The rats in ligustilide group were injected intravenously with 20 mg·kg-1 ligustilide,the rats in CID group were injected intraperitoneally with 50 mg·kg-1 CID,and the rats in ligustilide+CID group were injected intraperitoneally with 50 mg·kg-1 CID followed by intravenous injection of 20 mg·kg-1 ligustilide,once per day for 4 consecutive weeks.The cardiac function indexes of the rats in various groups were detected by echocardiography;the percentages of myocardial infarction areas of the rats in various groups were detected by 2,3,5-triphenyltetrazolium chloride(TTC)staining;the pathomorphology of myocardium tissue of the rats in various groups was observed by HE staining;the expression levels of PKD1,HIF-1α,CD31,and VEGF mRNA and proteins in ischemic area of myocardium tissue of the rats in various groups were detected by real-time fluorescence quantitative PCR(RT-qPCR)and Western blotting methods.Results:Compared with sham operation group,the rats in model group and CID group had altered myocardial cell morphology,increased intercellular gaps,disorganized arrangement,visible muscle fiber breaks and inflammatory cell infiltration;the rats in ligustilide group and ligustilide+CID group had relatively orderly myocardial fiber arrangement,fewer myocardial fiber breaks and decreased number of inflammatory cells.Compared with sham operation group,the left ventricular ejection fraction(LVEF)and left ventricular fractional shortening(LVFS)of the rats in model group were decreased(P<0.05),the left ventricular end-systolic diameter(LVESD)and left ventricular end-diastolic diameter(LVEDD)were increased(P<0.05),and the expression levels of PKD1,HIF-1α,CD31,and VEGF mRNA and proteins in myocardium tissue were decreased(P<0.05).Compared with model group,the LVEF and LVFS of the rats in ligustilide group were increased(P<0.05),the LVESD and LVEDD were decreased(P<0.05),the percentage of myocardium infarction area was decreased(P<0.05),and the expression levels of PKD1,HIF-1α,CD31,and VEGF mRNA and proteins in myocardium tissue were increased(P<0.05);compared with model group,the LVEF and LVFS of the rats in CID group were decreased(P<0.05),the LVESD and LVEDD were increased(P<0.05),the percentage of myocardium infarction area was increased(P<0.05),and the expression levels of PKD1,HIF-1α,CD31,and VEGF mRNA and proteins in myocardium tissue were decreased(P<0.05);compared with ligustilide group,the LVEF and LVFS of the rats in ligustilide+CID group were decreased(P<0.05),the LVESD and LVEDD were increased(P<0.05),the percentage of myocardium infarction area was increased(P<0.05),and the expression levels of PKD1,HIF-1α,CD31,and VEGF mRNA and proteins in myocardium tissue were decreased(P<0.05);compared with CID group,the LVEF and LVFS of the rats in ligustilide+CID group were increased(P<0.05),the LVESD and LVEDD were decreased(P<0.05),the percentage of myocardium infarction area was decreased(P<0.05),and the expression levels of PKD1,HIF-1α,CD31,and VEGF mRNA and proteins in myocardium tissue were increased(P<0.05).Conclusion:Ligustilide can promote the angiogenesis,reduce the myocardium infarction area,and improve the cardiac function in the rats with heart failure;it works through activation of the PKD1/HIF-1α/VEGF pathway.

Objective:To investigate the protective role of Yes-associated protein(YAP)in intestinal epithelial barrier injury.Methods:The intestinal epithelial barrier model was established by culturing human colorectal adenocarcinoma cell line Caco-2 cells, which were divided into four groups: control group, Caco-2 monolayers did not receive any treatment; recombinant human tumor necrosis factor-α(rhTNF-α)group, 100 μg/L of rhTNF-α was added to Caco-2 monolayers; vector+ rhTNF-α group, Caco-2 monolayers were first added with control plasmid pcDNA3.1-vector, and 100 μg/L rhTNF-α was added 24 hours later; YAP+ rhTNF-α group, Caco-2 cells with barrier construction were first added with pcDNA3.1-YAP, and 100 μg/L rhTNF-α was added 24 hours later.Realtime-PCR and Western blot were used to evaluate YAP mRNA and protein expression level.Epithelial permeability was assayed by trans-epithelial electrical resistance(TEER)and fluorescein isothiocyanate-dextran 40(FD-40 flu). Cellular distribution of F-actin was assayed by immunofluorescence staining.Results:Compared with control group[(607.3±29.3)Ω·cm 2], TEER of rhTNF-α group[(265.3±32.7)Ω·cm 2] decreased, while TEER of YAP+ rhTNF-α group[(387.0±18.7)Ω·cm 2]increased compared with rhTNF-α group, the differences were statistically significant( P<0.001). The FD-40 flux of rhTNF-α(22.7%±0.5%) group was higher than that of the control group(6.3%±0.9%), while the FD-40 flux of Yap + rhTNF-α group(12.2%±0.8%) was lower than that of rhTNF-α group, the differences were statistically significant( P<0.001). Immunofluorescence staining showed that compared with the control group, the cytoskeletal F-actin fiber dense spot decreased in rhTNF-α group, and some cells showed obvious trans-cellular stress fiber structure, while the peripheral actin band was clear in YAP+ rhTNF-α group, and the intracellular stress fiber decreased.YAP+ TNF-α group appeared as a clear, peripheral actin ribbon with a decrease in cytoplasmic stress fibres. Conclusion:YAP overexpression significantly inhibits TNF-α induced decline of TEER, and increases of FD-40 flux and F-actin rearrangement of Caco-2.YAP could ameliorate TNF-α induced intestinal epithelial barrier injury by regulating cytoskeleton F-actin.