Background:Disruption of intestinal epithelial tight junction and the followed barrier function play important roles in the pathogenesis of intestinal disorders. Curcumin could provide protection for the impaired barrier function. Aims:To investigate the protective effect of curcumin on ethanol-induced intestinal mucosal barrier disruption. Methods:Caco-2 cells were cultured to establish intestinal epithelial cell barrier model in vitro,and then were divided into control group, ethanol group and different concentrations of curcumin groups(5,20,80 μmol/ L curcumin). Trans-epithelial electrical resistance(TEER)and flux of sodium fluorescein for Caco-2 cell monolayers were measured to examine intestinal epithelial barrier function. Expression and localization of Occludin protein were measured by Western blotting and immunofluorescence,respectively. Cell structure was observed by transmission electron microscopy( TEM). Results:Compared with control group,TEER was significantly decreased and flux of sodium fluorescein was significantly increased (P < 0. 05),expression of Occludin protein was significantly decreased(P < 0. 05)in ethanol group. Immunofluorescence showed that Occludin protein expression was discontinuous and fluorescence intensity was low. TEM showed that brusher border was disorganized,and cell-cell junction was vague. When pretreated with curcumin,the above-mentioned indices were significantly improved,especially in 20 μmol/ L curcumin group( P < 0. 05). Conclusions:Curcumin protects ethanol-induced intestinal epithelial cell barrier disruption.

Teaching reform is the strong requirement of the times and social development.Immunology department inTaishan Medical College integrated teaching and a variety of extra-curricular teaching,broke the constraints of traditional teaching model in time and space,played the leading role of teachers and inspired students' independent learning,thus improving the teaching effectiveness in immunology.

The patient 1 was a 9-year-old boy of Hui nationality who presented with recurrent erythema over the face and auricles for 8 years.Telangiectasis and erythema developed on both cheeks 7 months after birth,which gradually spread to the auricles,forearms and both legs with a mild ichthyosiform appearance.At 5 years of age blisters and erosions appeared on the lips,which occurred and were aggravated after exposure to strong sunlight during summer and spontaneously subsided or disappeared in winter.The patient 2,a 3-year-old boy who was the younger brother of the patient 1,presented with recurrent erythema for 2 years.At 1 year of age,erythema began to appear on both cheeks and gradually spread to the buccal region,with mild pruritus and scaling.Meanwhile,the skin of both legs was dry and scaling and gave an ichthyosifonn appearance.The lesions usually appeared in early summer and gradually subsided in winter.No abnormality was found by systemic,laboratory,pathological or other auxiliary examination.Chromosomal abnormality was undetected.Body height was normal.The parents of the two siblings were first cousins.Both children were diagnosed with Bloom's syndrome.

OBJECTIVETo explore the secondary correction demand rule for unilateral cleft lip patients.

METHODSThe population in parts of Henan province were investigated by census method. The unilateral cleft lip patients underwent the primary correction were selected and be photographed, and 100 patients were selected randomly into study. The subjective satisfaction for the patients' facial appearance was evaluated by three groups: Professional group(cleft lip and palate specialist), non-professional group (the hospital administrative staff), and family members of patients group. The facial symmetry rate was measured for the patients with consistent subjective evaluation.

RESULTSThe rate of facial symmetry and subjective evaluation was not convergence. The subjective evaluation disaffect rates of profes-sional and non-professional groups were higher than that in family members of patients group (P<0.05).

CONCLUSIONThe rate of facial symmetry is not the most suitable method to evaluate the demand of the secondary correction for unilateral cleft lip patients.

Cleft Lip ; Cleft Palate ; Humans

Background: Disruption of tight junctions between intestinal epithelial cells followed by loss of barrier function is crucial for the pathogenesis and progression of a variety of gastrointestinal disorders.Aims: To investigate the protective effect of ulinastatin on hydrogen peroxide (H2O2)-induced intestinal epithelial barrier disruption.Methods: Model of intestinal epithelial monolayer barrier was established with Caco-2 cells in vitro,and then divided into four groups: blank control group (without any intervention),H2O2 group (500 μmol/L H2O2),low-dose (500 U/mL) and high-dose (3 000 U/mL) ulinastatin groups (ulinastatin + H2O2).Level of malondialdehyde (MDA) and activity of superoxide dismutase (SOD) were detected;transepithelial electrical resistance (TEER) and flux of sodium fluorescein were measured to assess the barrier function;expression and localization of two tight junction proteins,ZO-1 and occludin were evaluated by Western blotting and immunofluorescence;ultrastructure of tight junctions was observed by transmission electron microscopy (TEM).Results: Compared with the blank control group,treatment of Caco-2 cell monolayers with H2O2 resulted in increase in level of MDA,flux of sodium fluorescein and decrease in activity of SOD,TEER and expressions of ZO-1 and occludin (P all ＜0.05).TEM and immunofluorescence showed that the brusher border of Caco-2 cells in H2O2 group was destroyed,the cell-cell junction was vague and the localization of ZO-1 and occludin was discontinuous and the fluorescence intensity was extremely low.While in ulinastatin groups,especially the high-dose group,all the indices above-mentioned were significantly improved (P all ＜0.05).Conclusions: Ulinastatin protects intestinal epithelial monolayer barrier against H2O2-induced disruption at least partially by its antioxidant activity and modulating expression and localization of tight junction proteins.

OBJECTIVETo observe the effect of livin gene suppression by genistein on apoptosis, cell cycle and proliferation of malignant melanoma LiBr cells.

METHODSRT-PCR was used to detect the expression of livin mRNA in LiBr cells 48 h after treatment with 40 µmol/L genistein. Flow cytometry with annexin V-FITC/PI double staining was employed to detect cell apoptosis, and the caspase-3 protein expression in the cells following genistein treatment was assayed using Western blotting. The changes in the cell cycle and proliferation of the cells after genistein treatment were examined with flow cytometry with PI staining and MTT colorimetric assay, respectively.

RESULTSGenistein can suppress the expression of Livin Gene (87.94% with 40 µmol/L genistein) and induce the apoptosis of LiBr effectively, both in the early and late phases (27.87∓5.38% and 11.87∓3.86% respectively). LiBr cells in phase G(0)/G(1) increases notably(G(0)/G(1)=72.11∓5.89%,S=14.53∓3.47%,G(2)/M=12.36∓2.64%). Genistein significantly reduced caspase-3 protein expression and inhibit cell proliferation.

CONCLUSIONGenistein can suppress Livin Gene expression, induce LiBr cell apoptosis, hinder cell generation cycle, restrain cell proliferation.

Adaptor Proteins, Signal Transducing ; genetics ; Apoptosis ; drug effects ; Cell Cycle ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Genistein ; pharmacology ; Humans ; Inhibitor of Apoptosis Proteins ; genetics ; Melanoma ; pathology ; Neoplasm Proteins ; genetics

Disrupted redox status primarily contributes to myocardial ischemia/reperfusion injury (MIRI). NRF2, the endogenous antioxidant regulator, might provide therapeutic benefits. Dihydrotanshinone-I (DT) is an active component in Salvia miltiorrhiza with NRF2 induction potency. This study seeks to validate functional links between NRF2 and cardioprotection of DT and to investigate the molecular mechanism particularly emphasizing on NRF2 cytoplasmic/nuclear translocation. DT potently induced NRF2 nuclear accumulation, ameliorating post-reperfusion injuries via redox alterations. Abrogated cardioprotection in NRF2-deficient mice and cardiomyocytes strongly supports NRF2-dependent cardioprotection of DT. Mechanistically, DT phosphorylated NRF2 at Ser40, rendering its nuclear-import by dissociating from KEAP1 and inhibiting degradation. Importantly, we identified PKC-δ-(Thr505) phosphorylation as primary upstream event triggering NRF2-(Ser40) phosphorylation. Knockdown of PKC-δ dramatically retained NRF2 in cytoplasm, convincing its pivotal role in mediating NRF2 nuclear-import. NRF2 activity was further enhanced by activated PKB/GSK-3β signaling via nuclear-export signal blockage independent of PKC-δ activation. By demonstrating independent modulation of PKC-δ and PKB/GSK-3β/Fyn signaling, we highlight the ability of DT to exploit both nuclear import and export regulation of NRF2 in treating reperfusion injury harboring redox homeostasis alterations. Coactivation of PKC and PKB phenocopied cardioprotection of DT in vitro and in vivo, further supporting the potential applicability of this rationale. Graphical abstract