Objective To explore the multiple risk factors for family lifestyle of children with congenital heart defects (CHDs) in Shaanxi Province, China. children and their parents. The univariate and multivariable logistic regression models were used to analyze the influence of risk factors related to parents' lifestyle on CHDs. Results Several possible risk factors were found for CHDs, including fever (OR=4.465, P=0.017), pesticides contact (OR=2.234, P=0.083), passive smoking during pregnancy (OR=20.529, P=0.007) and father's smoking (OR=3.342, P=0.005); fever (OR=2.428, P=0.012) and passive smoking during pregnancy (OR=1.201, P=0.037) were also correlated with ventricular sepal defect (VSD). Conclusion Fever, pesticides contact and passive smoking are associated with CHDs during pregnancy. We should focus our attention on health care during pregnancy to avoid the above-mentioned risk factors and call on parents to hold on to a good healthy lifestyle.

Objective To investigate the clinical feature of fibercolonscopy in children.Methods Olympus PCF-20 and Olympus(PSD-20) were used for all examinations and treatments after bowel preparation and anesthesia.Pathological change was observed,then took pictures,and biopsy was done.Intestine polyps underwent electrocision.Results Fibercoloscopy was performed on 243 children(male 177,female 66).Age ranged from 1 to 18 years,with an average of 6.74 years.The cecum was reached in 232 of 243 cases.Abnormal findings were seen in 116(47.74%) of the cases.There were large intestine polyps in 87(35.80%) cases.All cases underwent electrocision.One hundred and fifty-seven polyps were removed with satisfactory results.Conclusion Fibercoloscopy is effective and safe in diagnosis and treatment in children with intestine diseases.

Objective To determine the effect of photochemotherapy on the expression of gelatinases. Methods Reverse transcription-polymerase chain reaction and gelatine zymography were employed to detect the effect of photochemotherapy on the expression and bioactivity of gelatinases at mRNA and protein levels respectively. Results Combination of ultraviolet A(UVA,0.8-2.0 J/cm2) and 8-methoxypsoralen(8-MOP,100 ng/mL) resulted in a decrease in the expression and bioactivity of gelatinases. Conclusion Photochemotherapy can inhibit the angiogenesis of endothelial cells through downregulating the expression and bioactivity of gelatinases.

To investigate the role of signaling pathway in the effect of endoplasmic reticulum stress (ER stress) in endothelial cells stimulated with cigarette smoke extract (CSE).Human umbilical vein endothelial cells (HUVECs) were cultured and divided into 3 groups:CSE-stimulated group,CSE-stimulated with 4-PBA group,and negative control group.HUVECs were cultured and stimulated with CSE at concentrations of 5％,10％ and 20％,respectively,mRNA of CXCL-8 and GRP78 was detected by real-time PCR.ELISA was performed to test the expression of CXCL-8 protein,and neutrophils migration was detected by Transwell board test.The NF-κB,ERK,p38MAPK and transforming growth factor beta (TGF-β) were detected by flow cytometry.The mRNA of CXCL-8 and GRP78 increased in CSE-stimulated HUVECs (P＜0.05).Furthermore,it was concentration-dependent.4-PBA significantly reduced the expression of CXCL-8 protein (P＜0.05) and neutrophil migration (P＜0.05).The TGF-β,rather than the NF-κB,ERK and P38MAPK pathway might be involved in ER stress stimulated by CSE.CSE induced neutrophils migration by increasing the expression of CXCL-8 in endothelial cells.ER stress might play a role in the effect of neutrophils migration stimulated with CSE,and TGF-β pathway may contribute to the ER stress in HUVECs.

Objective To compare the transplant-related toxicity and the efficacy of busulfan/fludarabine (Bu/Flu) and busulfan/cyclophosphamide (Bu/Cy) as conditioning regimen in allogeneic hematopoietic stem cell transplantation (allo-HSCT) for acute myeloid leukemia(AML) in the first complete remission (CR1).Methods Totally 32 AML-CR1 patients underwent allo-HSCT were divided into Bu/Cy (Bu 3.2 mg· kg-1 · d-1,7-4 days before transplantation; Cy 60 mg · kg-1 · d-1,3-2 days before transplantation) and Bu/Flu (Bu 3.2 mg · kg-1 · d-1,5-2 days before transplantation; Flu 30 mg · m-2·d-1,6-2 days before transplantation) groups.The regimen-related toxicity (RRT),incidence and severity of graft-versus-host disease (GVHD),3-year cumulative relapse rate,non-relapse mortality (NRM),3-year event-free survival (EFS) rate and overall survival (OS) rate were compared between the two groups.Results The median follow-up duration was 617.5 (6-1261) days.All patients achieved successful engraftment on 30 day after transplantation.There were no significant differences in the median time to neutrophil engraftment (P =0.121) and platelet engraftment (P =0.171) between the two groups.The median duration of neutrophil count under 0.1 × 109/L and platelet count under 20 × 109/L in the Bu/Cy group were significantly longer than those in the Bu/Flu group (P =0.000 and P =0.047).The incidence of grades Ⅱ-Ⅳ RRT were 68.8％ and 25.0％ (P =0.032) in the Bu/Cy and the Bu/Flu groups,respectively.There were no significant differences in the incidence of acute GVHD (P =0.149),chronic GVHD (P =0.149),incidence of NRM (P =0.333),3-year cumulative relapse rates (P =0.834),3-year EFS rate (P =0.362) and OS rate (P =0.111) between the two groups.Conclusion Compared with Bu/Cy,Bu/Flu is a myeloablative condition regimen with milder bone marrow suppression and lower RRT incidence rate in allogeneic HSCT for AML-CR1 patients without compromising the efficacy.

Adolescent ; Child ; Collagen Type I ; metabolism ; Extracellular Matrix ; metabolism ; Female ; Fibrillin-1 ; Fibrillins ; Heart Defects, Congenital ; metabolism ; pathology ; Humans ; Male ; Microfilament Proteins ; metabolism

Enterohemorrhagic Escherichia coli ; Escherichia coli Infections ; epidemiology ; Germany ; epidemiology ; Humans

BACKGROUND/OBJECTIVES: The objectives of this study were to investigate the effects of lycopene on the migration, adhesion, tube formation capacity, and p38 mitogen-activated protein kinase (p38 MAPK) activity of endothelial progenitor cells (EPCs) cultivated with high glucose (HG) and as well as explore the mechanism behind the protective effects of lycopene on peripheral blood EPCs. MATERIALS/METHODS: Mononuclear cells were isolated from human peripheral blood by Ficoll density gradient centrifugation. EPCs were identified after induction of cellular differentiation. Third generation EPCs were incubated with HG (33 mmol/L) or 10, 30, and 50 microg/mL of lycopene plus HG. MTT assay and flow cytometry were performed to assess proliferation and apoptosis of EPCs. EPC migration was assessed by MTT assay with a modified boyden chamber. Adhesion assay was performed by replating EPCs on fibronectin-coated dishes, after which adherent cells were counted. In vitro vasculogenesis activity was assayed by Madrigal network formation assay. Western blotting was performed to analyze protein expression of both phosphorylated and non-phosphorylated p38 MAPK. RESULTS: The proliferation, migration, adhesion, and in vitro vasculogenesis capacity of EPCs treated with 10, 30, and 50 microg/mL of lycopene plus HG were all significantly higher comapred to the HG group (P < 0.05). Rates of apoptosis were also significantly lower than that of the HG group. Moreover, lycopene blocked phosphorylation of p38 MAPK in EPCs (P < 0.05). To confirm the causal relationship between MAPK inhibition and the protective effects of lycopene against HG-induced cellular injury, we treated cells with SB203580, a phosphorylation inhibitor. The inhibitor significantly inhibited HG-induced EPC injury. CONCLUSIONS: Lycopene promotes proliferation, migration, adhesion, and in vitro vasculogenesis capacity as well as reduces apoptosis of EPCs. Further, the underlying molecular mechanism of the protective effects of lycopene against HG-induced EPC injury may involve the p38 MAPK signal transduction pathway. Specifically, lycopene was shown to inhibit HG-induced EPC injury by inhibiting p38 MAPKs.
Apoptosis ; Blotting, Western ; Centrifugation, Density Gradient ; Ficoll ; Flow Cytometry ; Glucose* ; Humans ; p38 Mitogen-Activated Protein Kinases ; Phosphorylation ; Protein Kinases ; Signal Transduction ; Stem Cells*

BACKGROUND/OBJECTIVES: The objectives of this study were to investigate the effects of lycopene on the migration, adhesion, tube formation capacity, and p38 mitogen-activated protein kinase (p38 MAPK) activity of endothelial progenitor cells (EPCs) cultivated with high glucose (HG) and as well as explore the mechanism behind the protective effects of lycopene on peripheral blood EPCs. MATERIALS/METHODS: Mononuclear cells were isolated from human peripheral blood by Ficoll density gradient centrifugation. EPCs were identified after induction of cellular differentiation. Third generation EPCs were incubated with HG (33 mmol/L) or 10, 30, and 50 microg/mL of lycopene plus HG. MTT assay and flow cytometry were performed to assess proliferation and apoptosis of EPCs. EPC migration was assessed by MTT assay with a modified boyden chamber. Adhesion assay was performed by replating EPCs on fibronectin-coated dishes, after which adherent cells were counted. In vitro vasculogenesis activity was assayed by Madrigal network formation assay. Western blotting was performed to analyze protein expression of both phosphorylated and non-phosphorylated p38 MAPK. RESULTS: The proliferation, migration, adhesion, and in vitro vasculogenesis capacity of EPCs treated with 10, 30, and 50 microg/mL of lycopene plus HG were all significantly higher comapred to the HG group (P < 0.05). Rates of apoptosis were also significantly lower than that of the HG group. Moreover, lycopene blocked phosphorylation of p38 MAPK in EPCs (P < 0.05). To confirm the causal relationship between MAPK inhibition and the protective effects of lycopene against HG-induced cellular injury, we treated cells with SB203580, a phosphorylation inhibitor. The inhibitor significantly inhibited HG-induced EPC injury. CONCLUSIONS: Lycopene promotes proliferation, migration, adhesion, and in vitro vasculogenesis capacity as well as reduces apoptosis of EPCs. Further, the underlying molecular mechanism of the protective effects of lycopene against HG-induced EPC injury may involve the p38 MAPK signal transduction pathway. Specifically, lycopene was shown to inhibit HG-induced EPC injury by inhibiting p38 MAPKs.
Apoptosis ; Blotting, Western ; Centrifugation, Density Gradient ; Ficoll ; Flow Cytometry ; Glucose* ; Humans ; p38 Mitogen-Activated Protein Kinases ; Phosphorylation ; Protein Kinases ; Signal Transduction ; Stem Cells*

Orthodenticlehomeobox 1 (OTX1) overexpression had previously been associated with the progression of several tumors. The present study aimed to determine the expression and role of OTX1 in human hepatocellular carcinoma (HCC). The expression level of OTX1 was examined by quantitative real-time PCR (qRT-PCR) in 10 samples of HCC and paired adjacent non-cancerous tissues, and by immunohistochemistry (IHC) analysis in 128 HCC samples and matched controls. The relationship between OTX1 expression and the clinicopathological features werealso analyzed. Furthermore, the effects of OTX1 knockdown on cell proliferation and migration were determined in HCC cell lines. Axenograft mouse model was also established to investigate the role of OTX1 in HCC tumor growth. TheqRT-PCR and IHC analyses revealed that OTX1 was significantly elevated in HCC tissues compared with the paired non-cancerous controls. Expression of OTX1 was positively correlated with nodal metastasis status (P = 0.009) and TNM staging (P = 0.001) in HCC tissues. In addition, knockdown of OTX1 by shRNA significantly inhibited the proliferation and migration, and induced cell cycle arrest in S phase in vitro. Tumor growth was markedly inhibited by OTX1 silencing in the xenograft. Moreover, OTX1 silencing was causable for the decreased phosphorylation level of ERK/MAPK signaling. In conclusion, OTX1 contributes to HCC progression possibly by regulation of ERK/MAPK pathway. OTX1 may be a novel target for molecular therapy towards HCC.
Aged ; Animals ; Blotting, Western ; Carcinoma, Hepatocellular/metabolism/*pathology ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Disease Progression ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Immunohistochemistry ; Liver/metabolism/pathology ; Liver Neoplasms/metabolism/*pathology ; Lymphatic Metastasis ; MAP Kinase Signaling System ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Middle Aged ; Neoplasm Staging ; Otx Transcription Factors/antagonists & inhibitors/genetics/*metabolism ; Phosphorylation ; RNA Interference ; Real-Time Polymerase Chain Reaction ; S Phase Cell Cycle Checkpoints ; Transplantation, Heterologous