Objective: To investigate the effects of Interlukin- 4(IL-4) on the invasiveness and the expression of several cell surface antigens related to invasive and metastatic potentials of human hepatocellular carcinoma QGY-7701 cell line in vitro. Methods: QGY-7701 cells were incubated with high concentration of IL-4 or low concentration of IL-4 in different time. The expression of ICAM-1, CD44 and HLA-I was determined by fluorescence-activated cell sorter (FACS) analysis, the tumor cell binding affinity to extracellular matrix (ECM) components was measured by cell attachment assay, the degree of homotypic aggregation was quantified by cell aggregation assay. Results: IL-4 pretreatment can enhance the expression of ICAM-1 and HLA-I, suppress the expression of CD44 on hepatocellular carcinoma cell line and decrease the binding affinity to ECM components and the degree of homotypic aggregation of hepatocellular carcinoma cells. Conclusoin: IL-4 can inhibit the invasive and metastatic potentials of hepatocellular carcinoma cells.

Objective To assess the value of combined assays of anti Saccharomyces cerevisia antibody (ASCA) and perinuclear antineutrophil cytoplasmic antibody (pANCA) in differential diagnosis of inflammatory bowel disease (IBD). Methods Nineteen patients with IBD, including 9 patients with Crohn's disease(CD) and 10 patients with ulcerative colitis(UC), and 18 healthy subjects were enrolled into study. Serum levels of pANCA and ASCA (IgG and IgA) were measured by indirect immunofluorescence technique and a standardized ELISA, respectively. Results The serum levels of ASCA IgG and ASCA IgA in CD patients (18.51? 6.38 and 11.74 ? 5.46 ) were significantly higher than those in UC patients ( 6.98 ? 5.24 and 3.88 ? 3.52 ) and healthy subjects( 5.90 ? 4.12 and 4.62 ? 3.21 )respectively (P

Objective: To study the apoptosis and the expression of proliferating cell nuclear antigen (PCNA) in colorec-tal neoplasms and their relationship with neoplasm biological behavior. Methods: Apoptotic index (AI) and proliferative index (PI) were determined in paraffin-embedded tissues from 62 cases of colorectal carcinomas, 15 cases of colon adenomas and 10 cases of normal colon mucosa with immunohistochemistry S-P method and TUNEL technique. Results: The difference of PI and AI was significant in normal colon mucosa, colon adenomas and colorectal carcinomas (P

Objective To investigate the expression of CRKL in thyroid papillary micro-carcinoma and its clinical significance.Methods 120 patients with thyroid tissue specimens were collected,in which 30 cases of diam-eter >1 cm of papillary thyroid carcinoma,30 cases of thyroid papillary micro-carcinoma,30 cases of nodular goiter, 30 cases for specimen of thyroid disease patients without diabetes.Immunohistochemical(SP)method was used to de-tect samples in CRKL expression.Results In thyroid papillary micro-carcinoma and thyroid papillary cancer group, CRKL expression positive rates were 30.12% and 29.87% respectively,which were higher than that of nodular goiter and normal thyroid group 30.03% and 28.57%(χ2 =52.102,P <0.05);The average absorbance(A)value in thy-roid papillary micro-carcinoma and thyroid papillary carcinoma group which were respectively (0.516 ±0.100)and (0.496 ±0.201),were higher than that in nodular goiter and normal thyroid group (0.246 ±0.050)and (0.117 ±0.015),the difference was statistically significant(F =149.105,P <0.05).Conclusion CRKL is highly expressed in papillary thyroid micro-carcinoma and the clinical detection of CRKL is helpful to determine the surgical plan for papillary thyroid micro-carcinoma.

OBJECTIVEThe glucocorticoid dexamethasone (DEX) can induce palatal cleft; however, the mechanism involved remains unclear. E-cadherin is an important cell adhesion molecule, and it can significantly affect cell fate and embryonic development. Recent studies have indicated that E-cadherin expression in palatal epithelial cells is suppressed in normal palate fusion. This study aimed to determine whether the change in E-cadherin expression is related to the incidence of cleft palate in DEX-induced mice.

METHODSMice were divided into the experimental group and the control group. Pregnant mice were injected with DEX on E10.0-E12.0, whereas mice in the control group were injected with normal saline. Hematoxylin and eosin (HE) staining, immunohistochemistry, and real-time quantitative polymerase chain reaction were employed to evaluate the effect of DEX on fetal mouse palatal processes, particularly the changes in E-cadherin and β-catenin expression levels in the phases of the experimental and control groups.

RESULTSData indicated that the incidence of cleft palate in the DEX group was 43.59% (17/39), whereas that in the control group was only 3.03% (1/33). The results of HE staining showed that the obviously shortened palatal processes could not contact and fuse with one another in the DEX-treated mice model compared with those in the control group. The ectopic expression of E-cadherin in embryonic palatal mesenchymal cells was also analyzed. The expression levels of E-cadherin and β-catenin in the experimental group were higher than those in the control group.

CONCLUSIONThese findings indicated that DEX could induce E-cadherin gene upregulation and ectopic expression, as well as high β-catenin expression, thereby inhibiting the growth of mesenchyme cells and cleft palate.

Animals ; Cadherins ; genetics ; metabolism ; Cleft Palate ; chemically induced ; embryology ; Dexamethasone ; adverse effects ; Disease Models, Animal ; Epithelial Cells ; Female ; Glucocorticoids ; Immunohistochemistry ; Mice ; Pregnancy ; beta Catenin ; metabolism

OBJECTIVE:Study regarding Smad3/transforming growth factor-β1(TGF-β1)signal transduction in pathological scars mainly focus on in vitro cultured fibroblasts,however,the correlation study was rare on keloid.The aim of this study is to detect the expressions of Smad3 and TGF-β1,and investigate their relationship in pathogenesis and development of pathological scars METHODS:Experimental samples were obtained frOm the patients who underwent burn and plastic surgery at the Department of Burn and Plastic Surgery,Workers'Hospital of Tangshan,Hebei Medical University,from June 2004 to June 2008,including 48 patients with Keloid,aged 16-52 years,and 40 patients with hypertrophic scars aged 18-56 years.Normal skins from additional 40 cases were served as controls The expressions of Smad3 and TGF-β1 protein in keloid,hypertrophic scars and normal skin were examined by flow cytometry.RESULTS:The expression of Smad3 and TGF-β1 were obviously greater in the experimental group than that of the control group (P＜0.05),but the difference between keloid and hypertrophic scars had no significance(P＞0.06).There was a positive correlation between Smad3 and TGF-β1 in keloid and hypertrophic scars(r=0 489 2,P=0.000 4:r=0.471 0,P=0.002 2).No notable correlation was found between Smad3 and TGF-β1 in normal skins(P=0.471 4).CONCLUSION:The expressions of Smad3 and TGF-β1 are up-regulated and the synergism of Smad3 and TGF-β1 may promote the development in pathological scars.

Objective: To assess the relationships between nutritional risks, nutritional support, and doctors' knowledge related to nutritional risks. Methods: 217 pre-operative patients and 41 doctors in the same general surgical wards were surveyed by using NRS2002 and self-developed questionnaires in a Beijing hospital. Results: The overall prevalence of pre-operative nutritional risks was 15.7%. Patients with gastrointestinal and/or malignant diseases had higher risks than others(P values were both less than 0.001). The nutritional support rates were 14.7% among patients with nutritional risks, and 2.2% among those without risks. The EN: PN ratio was 1∶ 2. A majority of doctors had misconceptions in nutritional risk screening and the effectiveness of nutritional supports. Their clinical practices were not consistent with their knowledge. Related trainings were required. Conclusions: Patients with gastrointestinal and/or malignant diseases have higher possibilities of nutritional risks. The nutritional supports rates are generally low. Doctors' knowledge related to nutritional risk screening is insufficient. More training opportunities are suggested to enhance the application of NRS2002 and appropriate nutritional supports.

Objective To evaluate the preoperative undernutrition, nutritional risks, and nutritional support in general surgical wards. Methods The nutritional risks of 217 new in-patients in general surgical wards in a Beijing-based hospital were assessed using nutrition risk screening 2002 ( NRS 2002 ) and the medical records were reviewed. Results The overall prevalence of preoperative undernutrition and nutritional risks was 7.4% and 14.7% respectively, most of which occurred in patients with gastrointestinal diseases and malignant diseases. Nutritional supports were provided to 18.8% of patients with undernutrition, 12.5% of patients with nutritional risks,3.0% of patients without undernutrition, and 2.7% of patients without nutritional risks. The enteral nutrition:The application of nutritional support should be further improved in general surgical wards.

Objective To investigate the gene polymorphism of inhibitory killer cell immunoglobulin- like receptor (iKIR) in patients with inflammatory bowel disease (IBD) and whether the iKIR gene polymorphisms were associated with IBD.Methods Peripheral blood DNA samples were isolated from 100 patients with ulcerative colitis (UC),52 patients with Crohn's disease (CD) and 106 randomly ethnically matched healthy controls.The iKIR gene polymorphisms were analyzed by sequence specific primer polymerase chain reproduction (PCR-SSP).Phenotypic frequency and gene frequency of iKIR gene were calculated,and differences were compared between IBD patients and healthy controls.Results iKIR genes (including KIR2DL1,KIR2DL2,KIR2DL3,KIR2DL4,KIR2DL5,KIR3DL1,KIR3DL2, KIR3DL3) were found to be present in all subjects at different levels.Interestingly,phenotypic frequencies of KIR2DL1 and KIR2DL3 were significantly lower in UC patients than those in healthy controls (P = 0.001),while phenotypic frequencies of KIR2DL2,KIR2DL4,KIR2DL5,KIR3DL1, KIR3DL2 and KIR3DL3 were no difference between UC patients and healthy controls (P>0.05).The phenotype frequency of KIR2DL1 was significantly decreased in CD patients compared with healthy controls (P = 0.007),while phenotypic frequencies of other iKIR were observed to be no significant change between CD patients and healthy controls (P>0.05 ).Conclusions The KIR2DL1 and KIR2DL3 gene phenotype frequencies are decreased in UC patients,which suggests that these gene polymorphisms are associated with the susceptibility of UC,and the polymorphism of KIR2DL1 gene is involved in the susceptibility of CD.

Objective To eveluate the pancreatic injury induced by smoking alone or combined with alcohol consumption,and its possible mechanism.Methods The Wistar rats were divided into control group (n=10),smoking group (n=30),drinking group (n=42) and smoking combined with drinking group (combination group,n=48).Serum levels of interleukin (IL)-6,superoxide dismutase (SOD) activities,monocyte chemoattractant protein-1 (MCP-1) and hydroxyproline were determined at 4th-,8th- and 12th- week.The pathohistological changes of the pancreas were examined using HE staining and the expression of α-smooth muscle actin (α-SMA) were measured by immunohistochemistry.ResultsIn contrast to control group,pancreatic changes including cytoplasmic vacuolation and increased levels of α-SMA and hydroxyproline were found in both smoking and drinking groups at the 8th-week (P<0.01).Whereas these changes were aggravated in combination group (P<0.05).Serum level of IL-6 and MCP-1 expression in pancreatic tissue were significantly increased in smoking group when compared with control group.But MCP-1 expression was lower in drinking group than control group.Moreover,the SOD activity in pancreatic tissue decreased in smoking and drinking groups,especially in combination group.Conclusions Long-term smoking can induce cytoplasmic vacuolation in pancreatic acinar cells,enhance inflammatory factors and chemokine expression and aggravate oxidative stress response in pancreas.These changes are aggravated when smoking and drinking coexisted.The mechanism behind it may be associated with increased oxidative stress response in pancreas.