Carrier Proteins ; metabolism ; Humans ; Microfilament Proteins ; metabolism ; Neoplasm Proteins ; metabolism ; Thyroid Neoplasms ; metabolism ; pathology

AIM:To observe the expression of chemokine fractalkine,and its receptor,CX3CR1,in kidneys of lupus-prone BXSB mice,and their changes after treatment with prednisone. The role of fractalkine and CX3CR1 in the pathogenesis of lupus nephritis was also discussed. METHODS:Twelve 12-week-old male BXSB mice were randomly divided into two groups,the prednisone treatment group (BXSB-prednisone group,n=6) and the experimental control group (BXSB group,n=6). Six male C57BL/6J mice at the same weeks of age served as a normal control group (C57BL/6J group). Both the C57BL/6J and the BXSB group of mice received a daily intragastric administration of 0.5 mL normal saline. The BXSB-prednisone group of mice was given a daily intragastric administration of prednisone (0.18 mg/20 g BW) dissolved in 0.5 mL normal saline. All treatments lasted for 10 weeks. The mRNA and protein expressions of fractalkine and CX3CR1 in kidneys of mice were detected by reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting analysis respectively. The changes of laboratory index and the kidney histopathology of mice were also investigated. RESULTS:The mRNA and protein expressions of fractalkine and CX3CR1 in kidneys of BXSB mice were significantly higher than those in C57BL/6J mice. The expressions of fractalkine and CX3CR1 in BXSB-prednisone group of mice were much lower than those in BXSB group of mice,accompanied by the lower serum IgG,IgM and anti-dsDNA antibody levels as well as blood urea nitrogen,serum creatinine and urine protein. The glomerular immune complex deposition and the kidney histopathology were also significantly improved in BXSB-prednisone group of mice. CONCLUSION:These results indicate that fractalkine and CX3CR1 participate in the pathogenesis of lupus nephritis in BXSB mice,and the effect of glucocorticoids treatment may be attributed,in part,to its ability to inhibit the expression of fractalkine in kidney.

AIM: To investigate the effects of interleukin-13(IL-13) on the inflammatory reaction of glomerular mesangial cells. METHODS: TNF-? protein in the supernatant of cultured mesangial cells was determined with ELISA. ICAM-1 expression on the mesangial cells was determined with flow cytometry. The expression of TNF-? mRNA and ICAM-1 mRNA were semiquantatively tested with RT-PCR. RESULTS: Mesangial cells did not constitutively express TNF-? mRNA and TNF-? protein. Induced by LPS(10 mg/L) for 24 h, mesangial cells expressed TNF-? mRNA and TNF-? protein at a high level. At the concentration of 1 ?g/L and 10?g/L, IL-13 markedly inhibited LPS-induced TNF-? mRNA and protein expression in mesangial cells. At the concentration of 100?g/L, IL-13 completely inhibited LPS-induced TNF-? mRNA and protein expression in mesangial cells. ICAM-1 constitutively expressed on the surface of mesangial cells at very low level. Induced by TNF-?(100?g/L), mesangial cells expressed ICAM-1 mRNA and ICAM-1 cell surface molecule at high level. Costimulated mesangial cells with IL-13(10?g/L) and TNF-?(100?g/L), IL-13 inhibited TNF-?-induced ICAM-1 mRNA and cell surface molecule expression at every time course. CONCLUSION: IL-13 not only inhibits LPS-induced TNF-? expression but also inhibits TNF-?-induced ICAM-1 expression in mesangial cells. These data suggest that IL-13 inhibits the inflammatory reaction in mesangial cells.

AIM: To find new gene function associate with active lupus nephritis (LN) through study on the difference in gene expression of peripheral blood mononuclear cells between LN patients and healthy controls by gene chip. METHODS: The CSC-GE-80 chip containing 8 000 spots of cDNAs were used to investigate the difference of the expression. Both the total RNA from peripheral blood mononuclear cells of active LN patients and healthy donors were reversely transcribed to cDNA with the incorporation of fluorescent( cy3 and cy5) labeled dCTP to prepare the hybridization probes. After hybridization, the gene chip was scanned for the fluorescent intensity. The differentially expressed genes were screened. We repeated that in three groups of LN patients and healthy controls, respectively, and only the genes that have differential expression in all three chips were considered associated with LN. RESULTS: 75 genes were identified to be differently expressed in all three groups of LN patients as compared with healthy controls, including 42 up-regulated genes and 33 down-regulated ones. CONCLUSION: The present study represents a global view of gene expression of LN and provides important clues for further study of LN related genes. And it also suggests defensin ? 1, S100A8, S100A9 may be involved in the pathogenesis of LN.

Objective To study the expression of c -Met protein in gastrointestinal stromal tumor(GIST) and to evaluate its clinicopathological significance.Methods The immunohistochemical technique,EnVision method was used to evaluate the expression of c -Met in 105 cases of GISTs.Results c -Met protein positive rate in GISTs was 9.52%(10 /105),its expression rate was significantly higher in GISTs with >10 /50HPF mitotic activity(P <0.05).c -Met protein expression rate was higher in GISTs which >5cm,moderate or high -risk,or mass located outside the stomach,but the difference was not statistically significant(P >0.05 ).Conclusion c -Met protein expression may related with risk of GISTs.We think that c -Met is worthy of further study for its potential usage as a evaluation indicators of GISTs clinicobiological behavior.

AIM: To explore the role of Akt/NF-?B pathway in immune-complexes-induced monocyte chemoattractant protein-1 (MCP-1) and colony stimulating factor-1 (CSF-1) expression in Mesangial Cells. METHODS: Primary murine glomerular mesangial cells were cultured in vitro and divided into control group, stimulation group and antisense, sense and mismatched oligodeoxynucleotide group. In control group, the cells were stimulated with monomeric IgG after treatment with 0.5% lipofectin for 8 h. In stimulation group, the cells, which had been treated with 0.5% lipofectin for 8 h, were stimulated with aggregated IgG. In antisense, sense and mismatched oligodeoxynucleotide group, being transduced antisense, sense and mismatched oligodeoxynucleotide respectively with 0.5% lipofectin 8 h, the cells were stimulated with AIgG. MCP-1 and CSF-1 in supernatant were deteced with ELISA. In addition, RT-PCR was used to determine MCP-1 and CSF-1 mRNA expression, and EMSA to investigated the activation of NF-?B. RESULTS: Mesangial cells cultured in vitro had a low level NF-?B activation and a low level constitutive expression of MCP-1 and CSF-1. Stimulated with AIgG, activation of NF-?B was markedly increased(0.35?0.06 vs 0.75?0.16, P

ObjectiveTo investigate the accuracy of automated breast volume scanning (ABVS) for the measurement of breast tumor size.MethodsSixty-two breast tumors in 59 patients were included in this study and were examined using conventional ultrasound and ABVS to measure the maximal diameters of the tumors. And the measurement results were compared with the pathological maximal diameters.Results There were 21 malignant and 41 benign tumors according to histopathological evaluation. There were no signifi cant differences between the maximal diameters on ABVS and on pathological measurements for both benign tumors and malignant tumors (Z=1.761, 0.262,P=0.078, 0.794). However, for malignant tumors, the maximal diameters on conventional ultrasound were significantly smaller than those on pathological measurements (Z=3.743,P=0.000). For benign tumors, the maximal diameters on conventional ultrasound were similar with those on pathological measurements (Z=1.935,P=0.053). The measurement values of conventional ultrasound and ABVS were both positively correlated with those on pathological values (r=0.935, 0.964,r=0.870, 0.964). And the correlation coeffi cients between ABVS and pathological measurement values were higher than those between conventional ultrasound and pathological measurement values for both benign and malignant tumors. ConclusionABVS can assess the size of breast tumor more accurately than conventional ultrasound, especially for the malignant tumors.

Objective To explore the expression and correlation of Fascin-1 and epidermal growth factor receptor (EGFR) in hormone receptor-positive breast cancer.Methods The immunohistochemical technique,EnVision method,was used to evaluate the expression of Fascin-1 and EGFR in 294 cases of hormone receptor-positive breast cancer,which contains 290 cases of estrogen receptor (ER) positive and 244 cases of progestrone receptor (PR) positive.According to ER,PR,Epidermal growth factor receptor 2 (HER2),and Ki-67 status,all cases of hormone receptor-positive breast cancer were categorized into 2 subtypes:160 cases of luminal A and 134 cases of luminal B.Results Fascin-1 and EGFR protein positive rates in hormone receptor-positive breast cancer was 13.9％ (41/294) and 30.6％ (90/294),respectively.Fascin-1 positive rate was significantly higher in EGFR positive cases (30.0％,27/90) than in EGFR negative cases (6.9％,14/204) (x2 =27.857,P =0.000).In the ER positive and PR positive cases,Fascin-1 positive rates were both significantly higher in EGFR positive cases than in EGFR negative cases (x2 =29.23,P =0.000;x2 =27.596,P =0.000,respectively).In the Luminal A and Luminal B subtype,Fascin-1 positive rates were also both significantly higher in EGFR positive cases than in EGFR negative cases (x2 =23.247,P=0.000;x2 =5.325,P=0.021,respectively).Conclusions EGFR signal pathway may positive regulate Fascin-1 expression in hormone receptor-positive breast cancer.

Objective:To study the expression of Resistin protein in breast cancer and to evaluate its significance to clinicopathology.Methods:The immunohistochemical technique, EnVision method, was used to evaluate the expression of Resistinin in 42 cases of normal breast tissues and 145 cases of breast cancer, and to analyze the relationship between Resistin protein expression and clinicopathological characteristics and molecular typing of invasive breast cancer patients.Results:The positive rate and strong positive rate of Resistin protein in normal breast tissue were 23.8% (10/42) and 0.0% (0/42) , respectively, while the positive rate and strong positive rate in invasive breast cancer were 88.3% (128/145) and 24.8% (36/145) . The positive rate and strong positive rate of Resistin protein in invasive breast cancer tissues were significantly higher than those in normal breast tissues (both P=0.000) . The positive rate of Resistin protein in invasive breast cancer was significantly higher in estrogen receptor (ER) -negative patients than in ER-positive patients ( P=0.006) , and it was higher in histological grade III and progesterone receptor (PR) -negative subjects than that of I-II and PR-positive, but the difference was not statistically significant ( P=0.053 and P=0.058, respectively) . The strong positive rate of Resistin protein in histological grade III, ER negative, PR negative and human epidermal growth factor receptor 2 (HER2) positive was significantly higher than that in histological grade I-II, ER positive, PR positive and HER2 negative ( P=0.001, P=0.001, P=0.001, and P=0.015, respectively) .The positive rate and strong positive rate of Resistin protein in triple negative breast cancer (TNBC) were significantly higher than those in other breast cancer subtypes ( P=0.048 and P=0.003, respectively) . Conclusion:Resistin plays an important role in the development of breast cancer and is expected to be a potential anti-cancer therapy biologic marker.

OBJECTIVETo study the expression of fascin-1 protein in breast cancer and to evaluate its correlation with clinicopathologic features of the tumor.

METHODSImmunohistochemical EnVision method was performed to evaluate the expression of fascin-1 in 23 cases of normal breast tissues, 69 cases of benign breast lesions, 58 cases of usual ductal hyperplasia (UDH), 61 cases of ductal carcinoma in situ (DCIS) and 221 cases of breast cancer from March 2007 to December 2011.

RESULTSFascin-1 protein expression rates in normal breast tissues, benign breast lesions, UDH, DCIS and breast cancer were 100.0% (23/23), 89.9% (62/69), 13.8% (8/58), 19.7% (12/61), and 42.1% (93/221), respectively. Fascin-1 expression in normal breast tissues and benign breast lesions was significantly higher than those in UDH, DCIS and breast cancer (P < 0.01); Fascin-1 expression in breast cancer was significantly higher than those in UDH and DCIS (P < 0.01). There was a tendency of increased fascin-1 expression in DCIS compared to UDH, but the difference was not statistically significant (P > 0.05). Fascin-1 positive rates in patients with DCIS grade III (26.8%, 11/41) was significantly higher than that in patients with DCIS grade I-II (1/20, P < 0.05). Fascin-1 protein expression in breast cancer increased with increasing histologic grade and clinical stage (P < 0.01). Fascin-1 protein expression was also significantly higher in tumors with negative estrogen receptor (ER) and progestone receptor (PR) status and > 3 axillary lymph node metastases compared to tumors that were ER and PR positive and ≤ 3 axillary lymph node metastases (P < 0.01 and P < 0.05, respectively). Logistic regression analysis showed that fascin-1 expression correlated positively with high clinical stage (OR = 1.568, 95% CI = 1.029-2.387, P < 0.05) , but negatively with ER expression (OR = 0.149, 95% CI = 0.079-0.281, P < 0.01) .

CONCLUSIONSFascin-1 is highly expressed in normal breast tissues and benign breast lesions, suggesting that it may be a biological marker of mature mammary ductal epithelium. Fascin-1 protein expression shows a significantly increasing trend from UDH, DCIS to invasive breast cancer, suggesting that fascin-1 plays an important role in breast carcinogenesis and may be a potential target for therapy.

Axilla ; Breast ; metabolism ; pathology ; Breast Neoplasms ; metabolism ; pathology ; Carcinoma in Situ ; metabolism ; pathology ; Carcinoma, Ductal, Breast ; metabolism ; pathology ; Carrier Proteins ; metabolism ; Estrogen Receptor alpha ; metabolism ; Female ; Humans ; Hyperplasia ; metabolism ; Lymph Nodes ; metabolism ; Lymphatic Metastasis ; Microfilament Proteins ; metabolism ; Receptors, Estrogen ; metabolism