Natural biocompatible nanomaterials such as self-assembled triterpene natural small molecule products with favorable anticancer activity show great potential for biomedical application. However, the mechanisms of their molecular self-assembled structures have not been investigated systematically, while there are still few reports of the natural active carrier for drug delivery. Herein, in this work, we further explored the molecular assembly mechanism and common regularity of tetracyclic triterpenes ergosterol, stigmasterol as well as pentacyclic triterpenes glycyrrhetinic acid and ursolic acid, which suggested that the coplanarity and orderliness of molecular arrangements which are speculated to be responsible for their self-assembly into the spherical, rod-like or lamellar nanostructure. Besides, ergosterol (ET) with better anticancer activity was chosen as a representative substance for construction of the synergistic antitumor nanodrug. By intermolecular hydrogen bonding and π-π stacking, chemotherapeutic drug paclitaxel (PTX) was encapsulated into ET-PTX NPs successfully. Then, the anti-cancer efficacy of the tumor-bearing mice was evaluated according to the protocol approved by the Experimental Animal Research Center of Harbin Medical University. The resulting nanodrug exhibited excellent biosafety and enhanced in vivo anticancer activity efficiency of 52.3%, higher than free PTX (29.4%) or ET NPs (32.5%) alone, further verifying the potential medical application value of triterpene natural products. This work provides not only a theoretical basis for exploring the self-assembly behavior of small molecule natural products, but also a promising perspective for the fabrication of active natural biocompatible nanodrug delivery systems for synergistic antitumor therapy and other biomedical applications.

Objective To evaluate the value of color Doppler flow imaging(CDFI) in the diagnosis of congenital coronary artery fistula (CAF).Methods Thirteen consecutive patients ranging in age from 8 to 68 years underwent conventional transthoracic echocardiography,which depicts their origin, course, and drainage site. Results Right CAFs were detected in 8 patients: four of them had drainages to the left ventricle, two to the main pulmonary artery, one to the right ventricle(RV) and the other to the right atrium(RA). CAFs arising from the left coronary artery were noted in five patients: three of them had drainages to the main pulmonary, and the other two to the RA and RV respectively. The origin and the course were precisely defined and the drainage site was clearly depicted in all thinteen patients. The diagnosis of the thirteen patients was confirmed by coronary angiography, and eight of them received surgical treatment. Conclusions CDFI offers a simple, useful and reliable technique in diagnosis of CAF.

0.05).However,the sex distribution was different between the two groups(P

Chronic Disease ; Constipation ; surgery ; Humans

Acute Disease ; Adult ; Bridged-Ring Compounds ; poisoning ; Female ; Humans ; Male ; Middle Aged ; Rodenticides ; poisoning

Objective To investigate the mechanism of disturbed immunological function induced by Epstein-Barr virus(EBV) infection through evaluating NKG2D expressions in NK cells and CD8+ T lymphocytes from children with infectious mononucleosis.Methods Twenty-nine children with infectious mononucleosis (IM) and twenty-five age-matched healthy children were enrolled in the study.NKG2D/NKG2A expressions in NK cells and CD8+T lymphocytes,and NKG2D ligand MHC Ⅰ chain-related molecules A(MICA) and UL-16binding proteins (ULBP-1) expressions on CD14+ mononuclear cells (MC) were analyzed by flow cytometry.The concentrations of cytokines such as IL-7,IL-12,IL-15,IFN-γ,TGF-β and soluble MICA(sMICA) in plasma were determined by enzyme-linked immunosorbent assay (ELISA).Results (1) Compared with the control group,NKG2D expression was significantly decreased in both NK cells and CD8+T lymphocytes from children with IM (P＜0.05),especially in the three cases of suspected EVB-HLH children.(2)There was no difference in the expression of MICA and ULBP-1 in CD14+ MC between the children with IM and the normal control(P＞0.05).(3)The concentrations of IL-15 and TGF-β in plasma were lower than those of the control group (P＜0.05),while the levels of IL-7,IL-12,IFN-γ and sMICA were up-regulated(P＜0.05) in children with IM.(4)NKG2A expression in NKcells in children with IM was significantly increased as compared with healthy controls(P＜0.05),however,there was no differences in the expression of NKG2A in CD8+ T lymphocytes between the two groups (P＞0.05).Conclusion Remarkable down-regulated expressions of NKG2D in NK cells and CD8+T lymphocytes might be one of the factors causing disturbed immunological function in children with EBV infection,which might have a close relationship with abnormal cytokine milieu of IL-15 and IL-12or high concentration of sMICA.

Objective To investigate the role of T follicular helper ( Tfh) cells in the immuno-pathogenesis of persistent immune thrombocytopenic purpura ( pITP) .Methods Twenty children with pITP and twenty healthy controls were enrolled in this study .The proportion of CD4+CXCR5+ICOShigh PD-1high T ( cTfh) cells and the expression of ICOSL on CD 19+B cells in peripheral blood of the patients and healthy subjects were analyzed by flow cytometry .The expressions of Bcl-6, c-Maf, IL-21 and ICOSL at mRNA level were detected by real-time PCR.The plasma concentrations of IL-2, IL-6 and IL-21 were determined by ELISA.Results (1) Compared with the healthy controls , the proportions of cTfh cells increased signifi-cantly in patients with pITP [(17.45±9.04) %vs.(7.57±2.57) %, P<0.05], but decreased with the treatment of dexamethasone (DEX) for 7 days [(5.93±1.64) %vs.(17.45±9.04) %, P<0.05].(2) The expression of Bcl-6, c-Maf and IL-21 at mRNA level in patients with pITP were higher than those in healthy controls (P<0.05).(3) Compared with healthy controls, the expression of ICOSL at mRNA and protein levels in CD19+B cells were significantly up-regulated in patients with pITP (P<0.05), which showed no significant changes after treatment with DEX (P>0.05).(4) The plasma concentration of IL-21 was remarkably elevated in patients with pITP , regardless of DEX treatment (P<0.05).But the plasma concentrations of IL-2 and IL-6 showed no significant changes compared with control group (P>0.05).Con-clusion The immunopathogenesis of persistent immune thrombocytopenic purpura might be associated with the hyper-activation of Tfh cells caused by excessive expression of ICOSL and IL-21.The persistent high expression of ICOSL and IL-21 might be one of the important factors resulting in the recurrence of pITP in children .

Objective To investigate whether transplantation of embryonic stem cell-derived cardiac myocytes (ESCMs) directly into the infarcted myocardium could improve the cardiac function in the rats.Methods Cell culture medium with or without ESCMs was injected into the borders of car- diac scar tissue one week after experimental infarction.Cardiac performance was evaluated 4 weeks later by means of echocardiography after ESCMs (n=16) or medium (n=12) injection.Results Im- munostaining confirmed the presence of?-actinin,?-MHC,and cTnI in the beating EBs.RT-PCR analysis of EBs revealed the expression of cardiac-specific genes,including cardiac Nkx 2.5,GATA-4 and?-MHC.ESCMs implantation significantly improved fractional shortening compared with medium- treated hearts (P

AIM: To investigate the contribution of angiotensin-converting enzyme inhibitor (ACEI) to the regulation of calpain system in infarcted myocardium. METHODS: Rat myocardial infarction (MI) model was established by permanent ligation of the left coronary artery. The treatment with the ACEI inhibitor rampril (1 mg?kg~-1 ?d~-1 ) was started 7 days prior to surgery. On day 1, 3, 7 and 14 after MI, protein levels of calpainⅠ, Ⅱ and calpastatin were determined in left ventricular free wall (LVFW), interventricular septum (IS) and right ventricule. RESULTS: CalpainⅠprotein level was increased in IS 14 d post MI, whereas the protein level of calpainⅡ was maximally increased in LVFW 3 d post MI. Rampril decreased protein up-regulation of calpainⅠ and Ⅱ, and reduced infarct size and interstitial fibrosis. Calpastatin protein expression was not affected by ACEI. CONCLUSIONS: CalpainⅠ is involved in cardiac remodelling in the late and calpainⅡ contributes to cardiac tissue damage in the early phase of MI. The heart protective effect of ACEI may be related to the inhibition of calpain system in the pathogenesis of myocardial infarction.

AIM: To investigate the protective effect of calcium antagonists on anoxia/reoxygenation (A/R) injury of cardiomyocytes. METHODS: Primary-cultured cardiomyocytes were divided into four groups, namely A/R, A/R+nifedipine(Nif), A/R+ruthenium red(Ru)+heparin (Hep) and control groups. The following parameters were measured in all groups: intracellular calcium concentration ([Ca 2+ ]i), cardiac cell viability, ATP content, lactate dehydrogenase (LDH) activity in the medium, PKC and MAPK activity and -Leucine(-Leu) incorporation. RESULTS: In comparison with A/R group, A/R+nifedipine(Nif) and A/R+ruthenium red(Ru)+heparin (Hep) groups showed a marked decrease in [Ca 2+ ]i and LDH content, and a significant increase in cell viability ,ATP content, activity of PKC and MAPK and -Leu incorporation(P