OBJECTIVE: To summarize the study of bone marrow cell infusion-induced immune tolerance. METHODS: The Pubmed database was researched using the computer for articles published from January 2000 to December 2008 using the key words of "bone marrow cells, transplantation immune tolerance" in English. Simultaneously, Chinese Biomedical Literature Database and China Journal Full-text Database were retrieved for articles published from January 2000 to December 2008 using the key words of "bone marrow cells, immune tolerance" in Chinese. Besides, Organ Transplantation, Transplantation Immune Tolerance and Conference Proceedings of English and Chinese were retrieved by hand. Inclusion criteria: relevant mechanism of immune tolerance; scheme of bone marrow cell infusion-induced immune tolerance; advantages and disadvantages of bone marrow cell infusion-induced immune tolerance; articles in the same circle published in recent years or in authorized journals. Exclusion criteria: repetitive studies or irrelevant articles. RESULTS: Mechanism of immune tolerance comprised cleaning, inability, regulation or inhibition, and ignorance. The scheme of bone marrow cell infusion-induced immune tolerance mainly contained bone marrow cell infusion combined with myeloablative pretreatment, bone marrow cell infusion combined with non-myeloablative pretreatment, pretreatment with immunosuppressive drug or chemotherapeutics, pretreatment of costimulatory signaling blockage, bone marrow cell combined with mesenchymal stem cell infusion. Bone marrow cell infusion-induced immune toleranca could induce long-lasting stable specific immune tolerance by effective immune tolerance mechanism, and had been an effective main method for inducing transplanted tolerance. CONCLUSION: Up to now, clinical immune tolerance is still uncontrollable and facultative. Bone marrow cell infusion-induced stable immune tolerance can develop a new space for organ transplantation.

OBJECTIVE: To determine the expression and mechanism of osteoactivin (OA) in the kidney by establishing SD rat model of acute cyclosporine A (CsA) toxicity. METHODS: SD rats were fed with normal diet for a week, which they were then randomly divided into 3 groups: an experimental group (gavage with cycloporin A and olive oil), a vector group (gavage with olive oil), and a control group (gavage with normal saline). SD rats were killed 2 days, 1 week, or 2 weeks after the gavage to examine the serum creatinine (SCr) and body weight. HE staining was used to detect the kidney histopathological change. Immunohistochemistry was used to observe the staining degree and area of OA. Western blot was used to detect the OA protein.The mRNA expressions of the OA, matrix metalloproteinase-13(MMP-13), and collagen type III(Col III) were examined by RT-PCR. RESULTS: The body weight and SCr of the rats in the experimental group 1 week and 2 days after the gavage had no significant difference compared with the vector group or the control group (P>0.05).On the end of 2nd week, the rats' body weight was significantly reduced, and SCr significantly increased compared with the vector group or the control group (P<0.001).The main histopathological changes in the experimental group were inflammatory cell infiltration, vacuolar degeneration of interstitial cells, or tubular epithelial cell necrosis. Intense OA expression located in the tubular epithelium and interstitial fibroblasts in the kidney of the experimental group was observed by immunohistochemistry. After CsA gavage, the relative mRNA expressions of OA, MMP-13, and Col III significantly increased with time. Western blot did not find the expression of OA protein in the control and the vector group, which increased with time in the experimental group. CONCLUSION OA expresses in the kidney of SD rats after acute CsA toxicity and mainly expresses in the tubular epithelial cells and renal interstitium. OA is more sensitive to the damage of kidney tissue caused by CsA than by SCr. The early-phase up-regulation of OA expression in the tubular epithelium in response to renal injury caused by acute CsA toxicity might play a key role in triggering the renal interstitial fibrosis via activating expression of MMPs and collagen remodeling in SD rats.
Animals ; Collagen Type III ; genetics ; metabolism ; Cyclosporine ; toxicity ; Epithelial Cells ; metabolism ; pathology ; Immunosuppressive Agents ; toxicity ; Kidney Diseases ; chemically induced ; metabolism ; pathology ; Kidney Tubules ; metabolism ; pathology ; Male ; Matrix Metalloproteinase 13 ; genetics ; metabolism ; Membrane Glycoproteins ; genetics ; metabolism ; RNA, Messenger ; genetics ; metabolism ; Random Allocation ; Rats ; Rats, Sprague-Dawley

To explore roles of expressions of EHD2 and E-cadherin in clear cell renal cell carcinoma (ccRCC).
 Methods: Four couples of fresh ccRCC tissues and adjacent non-cancerous tissues were collected to evaluate the expression of EHD2 and E-cadherin protein by Western blotting. A total of 65 paraffin-embedded renal ccRCC tissues were collected, and immunohistochemical assay was used to detect the expression of EHD2 and E-cadherin in the samples. The correlation between their expression and clinical and pathological indicators of ccRCC was analyzed, and the relationship between EHD2 and E-cadherin proteins and prognosis for patients with ccRCC was also explored.
 Results: The results of Western blotting showed that the expression levels of EHD2 and E-cadherin were low in 4 ccRCC tissues compared with the adjacent noncancerous tissues. Immunohistochemical results revealed that the expressions of EHD2 and E-cadherin were higher in the localized ccRCC tissues than those in the metastatic ccRCC tissues; the expression levels of EHD2 and E-cadherin were decreased, while the TNM staging and Fuhrman grade were increased (P<0.05 or P<0.01). There was positive correlation between the expressions of EHD2 and E-cadherin in ccRCC (r=0.390, P<0.01). The progression-free survival in ccRCC patients with lower expression of both EHD2 and E-cadherin was better than that in ccRCC patients with higher expressions of EHD2 and E-cadherin (P<0.05). 
 Conclusion: The low expressions of EHD2 and E-cadherin are the potential indicators for the ccRCC patients with poor prognosis.
Cadherins ; Carcinoma, Renal Cell ; Carrier Proteins ; Humans ; Kidney Neoplasms ; Neoplasm Staging ; Prognosis

Objective：To analyze the expression and clinic significance of activity-dependent neuroprotective protein (ADNP) in bladder urothelial carcinoma. Methods: A total of 28 pairs of bladder cancer tissues and corresponding adjacent normal tissuesthat surgically resected at the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University from June 1, 2019 to July 15, 2019 were collected for this study. The mRNAexpression ofADNP in 20 pairs of tissue samples was detected by qPCR, and the protein expressionin the other 8 pairs was detected by WB. Mean while, the clinicopathological data of patients with bladder urothelial carcinoma treated in our hospital from January 1, 2005 to December 31, 2007 were retrospectively analyzed; and the expression of ADNP in the corresponding paraffin tumor sections were determined with immunohistochemical staining, and normal bladder tissue sections from patients who underwent surgery for other bladder diseases during the same period were collected for comparison. Chi-square test was used to analyze the correlation between ADNP expression and different clinicopathological features, Kaplan-Meier method was used for survival analysis, and Cox risk regression model was used forunivariate and multivariate analysis of prognosticfactors. Results: ThetranscriptionalandtranslationallevelsofADNPincancertissues were higher than those in adjacent normal tissues (all P<0.05), and the expression level ofADNP was correlated with the histological grade, clinical stages and survival status of patients with bladder cancer (P<0.05). Of all the 221 patients included in the study, 32 patients lost to follow-up,and patients with high ADNP expression had