Objective To investigate the effect of enteral nutrition (EN) on the T lymphocytes-mediated immune function in patients with acquired immune deficiency syndrome (AIDS). Methods Totally 79 AIDS patients were randomly divided into enteral nutrition ( EN ) group ( supported with EN daily in addition to conventional treatment; n = 46) and control group (underwent conventional treatment only; n = 33 ). T lymphocytes including CD3, CD4, and CD8 cells as well as blood biochemical parameters including alanine aminotransferase ( ALT), aspartate aminotransferase (AST), glucose ( Glu ), total protein (TP), albumin ( ALB ), blood urea nitrogen (BUN) , Cr, and prealbumin (PA) were determined immediately before management (T0) and on the 30th day(T1). Results ALT, AST, Glu, TP, ALB, BUN, Cr, and PA showed no significant differences between these two groups before management ( all P ＞ 0. 05 ). The levels of TP ( P = 0. 015), ALB ( P = 0. 007 ), and PA ( P =0. 022 ) were significantly higher in EN group than those in control group at T1. The cell counts of CD3, CD4, and CD8 were not significantly different at T0, while the cell count of CD4 was significantly higher in EN group than that in control group at T1 ( P ＜ 0. 05 ). Conclusion EN can improve the nutritional status and T lymphocytesmediated immune function in AIDS patients.

Objective:To explore the role of epithelial-mesenchymal transition(EMT) in fusion of the secondary palatal shelves to form the intact secondary palate induced by 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD).Methods:Twelve C57BL/6 J pregnant mice on gestation day (GD) 10.5 were divided into two groups: one group was conducted through gastric tubes with one dose of 28 μg/kg TCDD (experimental group) and the other group was operated through gastric tubes with equal volume corn oil (control group). Embryos were removed by cesarean section from pregnant mice during the palatal formation stage (GD 15.5) and the morphology of palatal tissue was observed. Primary media edge epithelial(MEE) were divided into experimental group and control group. MEE were treated with medium containing TCDD, 5 nmol/L, 10 nmol/L, 20 nmol/L and normal medium respectively. The expression of cytokeratin 19(CK-19) protein and vimentin protein in MEE were detected by immunofluorescence laser confocal microscopy and Western blotting after 72 hours. Statistical comparisons were made using one-way ANOVA.Results:A total of 36 fetuses were obtained in the experimental group, including 3 dead fetuses and absorbed fetuses. The incidence of cleft palate was 100% (33/33); the incidence of complete cleft palate was 84.8% (28/33), and the incidence of partial cleft palate was 15.2% (5/33); 40 fetuses were obtained in the control group, including 2 dead fetuses and resorbed fetuses, and the incidence of cleft palate was 0 (0/38). After 72 hours, the shape of MEE changed from uniform pebble-like to star-like or irregular shape with pseudopodia. The expressions of CK-19 protein were(0.739 ± 0.120, 0.483 ± 0.023, 1.007 ± 0.109, 1.086 ± 0.145) and fluorescence intensities were (53.384±5.785, 36.818 ± 8.250, 64.575±8.323, 76.898 ± 3.711) in control group and TCDD (5 nmol/L), TCDD (10 nmol/L) and TCDD (20 nmol/L) groups, respectively. The expressions of vimentin protein were (0.527 ± 0.112, 0.781 ± 0.095, 0.284 ± 0.046, 0.216 ± 0.040) and fluorescence intensities were (63.672±6.135, 82.632 ± 4.474, 52.608±7.525, 42.664 ± 7.659). Compared with the control group, the low-dose experimental group (5 nmol/L) had a decrease in CK-19 and an increase in vimentin; the high-dose experimental group (10 nmol/L, 20 nmol/L) had an increase in CK-19 and a decrease in vimentin, and the expression difference was statistically significant ( P<0.05), while there was no statistical significance among high-dose groups ( P>0.05). Conclusions:EMT process of MEE was identified in vitro and was a spontaneous procedure. TCDD-induced cleft palate may be related to the inhibition of the EMT process in MEE and with the increased dose of TCDD, the effects of EMT inhibiton were sustainable.

Objective:To explore the role of epithelial-mesenchymal transition(EMT) in fusion of the secondary palatal shelves to form the intact secondary palate induced by 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD).Methods:Twelve C57BL/6 J pregnant mice on gestation day (GD) 10.5 were divided into two groups: one group was conducted through gastric tubes with one dose of 28 μg/kg TCDD (experimental group) and the other group was operated through gastric tubes with equal volume corn oil (control group). Embryos were removed by cesarean section from pregnant mice during the palatal formation stage (GD 15.5) and the morphology of palatal tissue was observed. Primary media edge epithelial(MEE) were divided into experimental group and control group. MEE were treated with medium containing TCDD, 5 nmol/L, 10 nmol/L, 20 nmol/L and normal medium respectively. The expression of cytokeratin 19(CK-19) protein and vimentin protein in MEE were detected by immunofluorescence laser confocal microscopy and Western blotting after 72 hours. Statistical comparisons were made using one-way ANOVA.Results:A total of 36 fetuses were obtained in the experimental group, including 3 dead fetuses and absorbed fetuses. The incidence of cleft palate was 100% (33/33); the incidence of complete cleft palate was 84.8% (28/33), and the incidence of partial cleft palate was 15.2% (5/33); 40 fetuses were obtained in the control group, including 2 dead fetuses and resorbed fetuses, and the incidence of cleft palate was 0 (0/38). After 72 hours, the shape of MEE changed from uniform pebble-like to star-like or irregular shape with pseudopodia. The expressions of CK-19 protein were(0.739 ± 0.120, 0.483 ± 0.023, 1.007 ± 0.109, 1.086 ± 0.145) and fluorescence intensities were (53.384±5.785, 36.818 ± 8.250, 64.575±8.323, 76.898 ± 3.711) in control group and TCDD (5 nmol/L), TCDD (10 nmol/L) and TCDD (20 nmol/L) groups, respectively. The expressions of vimentin protein were (0.527 ± 0.112, 0.781 ± 0.095, 0.284 ± 0.046, 0.216 ± 0.040) and fluorescence intensities were (63.672±6.135, 82.632 ± 4.474, 52.608±7.525, 42.664 ± 7.659). Compared with the control group, the low-dose experimental group (5 nmol/L) had a decrease in CK-19 and an increase in vimentin; the high-dose experimental group (10 nmol/L, 20 nmol/L) had an increase in CK-19 and a decrease in vimentin, and the expression difference was statistically significant ( P<0.05), while there was no statistical significance among high-dose groups ( P>0.05). Conclusions:EMT process of MEE was identified in vitro and was a spontaneous procedure. TCDD-induced cleft palate may be related to the inhibition of the EMT process in MEE and with the increased dose of TCDD, the effects of EMT inhibiton were sustainable.