Objective To explore the role of high mobility group box protein 1 ( HMGB1 ) and receptor for ad-vanced glycation endproducts( RAGE) in lupus nephritis( LN) . Methods The serum and urine levels of HMGB1 were detected by ELISA in SLE patients and normal controls, and intrarenal expressions of HMGB1 and RAGE were detected by immunohistochemistry in renal tissues of SLE patients and normal-appearing renal tissues. Results
The serum and urine levels of HMGB1 were significantly higher in SLE patients compared to healthy controls( P<0. 01 ) , in patients with active disease compared to those with inactive disease ( P <0. 05 ) , serum levels of HMGB1 were found to be significantly higher in patients with renal involvement compared to those without renal in-volvement(P<0. 05). In addition, the levels of serum HMGB1 showed positive correlation with SLEDAI,urine pro-tein(24 h) and lencocyte count (P <0. 05). The expression of urine HMGB1 showed positive correlation with SLEDAI ( P<0. 05 ) . Intermediate-intensity staining of HMGB1 and RAGE was detected in renal tubules in normal-appearing renal tissues, however, both renal tubules and glomerular cells had the strong expression of HMGB1 and RAGE in SLE patients. The intrarenal production of HMGB1 and RAGE in SLE patients was obviously higher than that in normal-appearing renal tissues(P<0. 05), and the expression levels of HMGB1 in SLE IV and IV+V were higher than those in SLE II ( P<0. 05 ) . The expression levels of RAGE in SLE IV were higher than those in SLE II(P<0. 05). Conclusion HMGB1 and RAGE may play key roles in the pathogenesis of LN and may associate with the pathology category of LN.

Objective:To assess the association between preoperative neutrophil–lymphocyte ratio (NLR), platelet-lymphocyte ratio (PLR), and red cell distribution width (RDW) and the tumor pathological features in gastric cancer (GC) patients. Methods: We re-viewed the records of 434 patients from 2012 to 2014 in Fujian Cancer Hospital. All patients were admitted to the hospital for the first time, and no patients received any cancer-specific pretreatment. For comparison, 309 age-and gender-matched healthy individuals who underwent annual physical examination at the hospital and 342 patients with chronic atrophic gastritis were enrolled. Results:GC patients had higher NLR, PLR, and RDW than the controls (P<0.000 1). Elevated NLR, PLR, and RDW were associated with the develop-ment of tumor stages as indicated by the Kruskal-Wallis analysis. However, no similar association was observed between the tumor dif-ferentiation grade and location and those three markers. Multivariate regression analysis further revealed that both NLR and PLR were independent predicting factors for either the tumor TNM or T stage (P<0.000 1). ROC curve analysis showed that NLR and PLR had a certain diagnostic effect on the preoperative T staging of GC. Conclusion:The preoperative NLR and PLR levels are closely correlated with the tumor TNM stages in GC patients. Both these parameters have potential values as markers to assist either in early diagnosis or preoperative tumor stage evaluation in GC.

Objective: To investigate the role of microRNA-375 (miR-375) in the occurrence of trastuzumab-resistance in human epidermal growth factor receptor 2 (HER2)-positive breast cancer cells through regulating epithelial-mesenchymal transition (EMT). Methods: The sensitivities of HER2-positive breast cancer cell lines SK-BR-3 (a parental sensitive cell line) and SK-BR-3R (a trastuzumab-resistant cell line) to trastuzumab were detected by MTT assay. The expression levels of miR-375 and EMT-associated proteins E-cadherin and vimentin in the two cell lines were detected by real-time fluorescent quantitative PCR and Western blotting, respectively. After miR-375 mimic was transfected into SK-BR-3R cells, the changes of miR-375, E-cadherin and vimentin expression levels were detected by real-time fluorescent quantitative PCR and Western blotting, and the change of trastuzumab sensitivity of SK-BR-3R cells was detected by MTT method. The potential target genes of miR-375 were predicted by bioinformatics software, and metadherin (MTDH) was selected as one of target genes. Luciferase reporter assay was conducted to verify the role of miR-375 in regulation of MTDH gene transcription. In addition, the changes of E-cadherin and vimentin expression levels in SK-BR-3R cells after transfection with MTDH siRNA were detected by Western blotting. Results: Compared to the sensitive SK-BR-3 cells, the sensitivity of SK-BR-3R cells to trastuzumab decreased significantly (P < 0.001), and the expression levels of miR-375 (P < 0.001) and vimentin (P < 0.05) were significantly down-regulated, but the level of EMT marker E-cadherin was significantly up-regulated (P < 0.05). After transfection with miR-375 mimic, the expression levels of miR-375 (P < 0.001) and vimentin (P < 0.01) were up-regulated, while the level of E-cadherin was down-regulated (P < 0.001); the trastuzumab sensitivity of SK-BR-3R cells was increased (P < 0.001). A negative regulatory effect of miR-375 on the transcription of MTDH gene was observed (P < 0.001). After MTDH-siRNA transfection, the expressions of MTDH and vimentin were down-regulated (both P < 0.001), while the expression of E-cadherin was up-regulated (P < 0.001). Conclusion: miR-375 plays a role in drug-resistance of HER2-positive breast cancer cells to trastuzumab through regulating EMT, which is related to the target regulation of MTDH gene expression.