Objective To explore the expression and clinical value of major histocompatibility complex class-Ⅰ related chain A (sMICA) molecule in serum of patients with renal tumor.Methods From March 2013 to July 2013,60 patients with renal tumor,including 37 male patients and 23 female patients were enrolled in this study as experimental group.The mean age was 46 years (range 34-76 years).The pathological diagnosis included renal cell carcinoma in 48 cases and renal angiomyolipoma in 12 cases.The stage classification included T1 stage in 20 cases,T2 stage in 14 cases,T3 stage in 10 cases and T4 stage in 4 cases.Lymphatic metastases were found in 11 cases and metastases in other organs were found in 4 cases.Another 20 healthy volunteers were enrolled as control group,including 10 male and 10 female.The mean age was 31 years (range 24-50 years).The ELISA method was used to detect the soluble MICA's (sMICA) level in serum.And the results were compared with tumor's malice,TNM pathology stages,metastasis.In 15cases with renal cell carcinoma,the expression of MICA molecule in tumor masses and paraneoplastic masses was measured by immunohistochemical (IHC) method.The quantitative expression of MICA-mRNA was detected by RT-PCR in 9 tumor masses and 3 paraneoplastic masses.Results The level of sMICA in renal malignant tumor group was (348.5±32.5) pg/ml,while the sMICA's level in benign renal tumor groups was (289.3±30.4) pg/ml and that in the control group was (168.4±43.2) pg/ml.The level of sMICA in malignant group is statistically higher than that in benign group and control group (P＜0.05).The level of sMICA in T1 、T2 、T3 and T4 stage was (304.3±27.4),(308.4±26.8),(368.3±33.4),(378.4±43.4) pg/ml,respectively.Insignificant difference only demonstrated between T1 and T2 stage.The level of sMICA in those patients with and without lymphatic metastasis was (326.2±32.4),(319.4±32.5) pg/ml,respectively (P＞0.05).Significant difference in the sMICA level could also be observed between patients with other organ metastasis (373.4±45.4) pg/ml and those without metastasis (346.4±31.5) pg/ml (P＜0.05).The IHC results revealed that high expression of MICA molecule in tumor cell.However,this oppsite result was demonstrated in cells located in paraneoplastic tissues.In the results of RT-PCR,the MICA-mRNA level (2.03) in tumor masses was significantly higher than that in pareneoplastic masses (0.77) (P＜0.05).Conclusions MICA highly expressed in renal tumor,and its expression correlates with tumor's malice,TNM pathologic stages,and metastasis.

Objective To investigate the treatment of recipients carrying hepatic virus after renal transplantation. Methods Of the 14 patients, 8 carried HBV and 4 HCV, and the other 2 both HBV and HCV. HBV DNA or RNA was negative before transplantation.Results During the follow-up period of 3 to 20 months, 10 patients had liver dysfunction with higher ALT and AST, but negative for HBV DNA and/or HCV RNA. After adjusting the dosage of immunosuppressants and treatment of liver protection, liver function of these patients all restored to normal level.Conclusion In the hepatic virus carriers receiving renal transplantation, liver dysfunction caused by drug-induced liver damage or hepatic viral injury should be distinguished and corresponding treatment should be given in time.

Objective To explore the significance of complement split product C4d in monitoring chronic rejection of renal allografts in rats.Methods Healthy closed population rats were used as donors and SD rats as recipients. The Wistar to SD model of graft rejection was developed. All the 42 recipients were randomly divided into 2 groups: group A receiving nothing except CsA (5mg?kg~ -1 ? d~ -1 ) in the first 10 days after operation, and group B receiving MMF (10 mg/kg) and CsA after operation. On the 3rd, 5th and 10th week, all the allografts were tested by light microscopy and immunofluorescence. Pathological changes of the kidneys and the expression of C4d in allograft tissue were observed.Results From the 3rd week, the rats in group A showed light pathological changes of chronic rejection and they became more and more obvious as time increased. Pathological changes occurred in group B at the 5th week and lighter than in group A. At the same time, C4d deposition in PTC was obviously observed on the 3rd week in group A, and on the 10th week C4d widespread deposition in allografts.Conclusion The deposition of complement split product C4d in allografts appears earlier than pathological change of chronic rejection, which can be regarded as a significant indicator to predict chronic rejection of renal allografts.

Objecfive To study the effects of some cytokines such as TNF-α,IL-6 and IFN-γ as well as lipopolysaccharide on CD68 expression in HaCaT cells.Methods Human HaCaT keratinocytes were randomly divided into natural proliferation group (without stimulation),IFN-γ-stimulated group,TNF-α-stimulated group,LPS-stimulated group and IL-6 stimulated group.The work concentration of TNF-α,IL-6,IFN-γ and LPS was 50 mg/L.HaCaT cells were collected after 24-hour treatment with the cytokines followed by the examination of CD68 expression with flow cytometry,immunohistochemistry and reverse transcription(RT)-PCR,respectively.Results Compared with untreated HaCaT cells,the count of CD68-positive cells was elevated in cells stimulated by TNF-α(t=3.60,P<0.01),IL-6(t=3.93,P<0.01),IFN-γ(t=2.38,P<0.05)and LPS(t=2.52,P<0.05),and the effect of TNF-α and IL-6 was stronger than that of IFN-γ and LPS.Among the four cytokines,only IL-6 enhanced the mean fluorescence intensity of CD68-positive cells (t=8.34,P<0.01).After 24-hour treatment with TNF-α,IFN-γ and IL-6,CD68 expression was observed in the cytoplasm and on the membrane of HaCaT cells and was stronger in cells treated with TNF-α and IL-6 than in those with the other cytokines.A significant increase was observed in the CD68 mRNA expression after 24-hour treatment with TNF-α (t=4.34,P<0.01),IL-6 (t=7.52,P<0.01)and IFN-γ (t=2.81,P<0.05);TNF-α and IL-6showed a stronger promotive effect than IFN-γ.Conclusion IL-6,TNF-α,IFN-γ and LPS can upregulate the CD68 expression in HaCaT cells.

ObjectiveTo analyze the distribution and density of Langerhans cells and dermal CD68 positive histiocytes in lesions of secondary keloid.MethodsTissue specimens were resected from the lesions of 30 patients with secondary keloid and normal skin of 14 human controls.Immunohistochemistry was performed to observe the expressions of CD68 and CD1a in these specimens.A micrometer was used to count the number of positively stained cells per unit area.The Student's t test was conducted for data analysis by using the SPSS software.ResultsThe density of CD1a+ Langerhans cells was (61 ± 49) cells/mm2 in the epidermis of secondary keloid lesions, (258 ± 61 ) cells/mm2 in the control epidermis,and(40 ± 65) cells/mm2 in the dermis of keloid lesions.CD68+ cells were absent in the epidermis of keloid lesions.Significant differences were observed in the density of CD1a+ Langerhans cells between the lesional and normal control epidermis(t =9.88,P ＜ 0.001 ) and in the percentage of CD68+ cells in nucleated cells between the superficial dermis of lesions and control skin(62％ ± 12％ vs.70％ ± 14％,t =2.66,P ＜ 0.05).The density of dermal CD68+ histiocytes was similar between the lesions and control skin ((287 ± 73) cells/mm2 vs.(290 ± 22) cell/mm2,t =0.02,P ＞ 0.05).Conclusions In keloid lesions,Langerhans cells decrease in the epidermis but increase in the dermis,CD68+ histiocytes are absent in the epidermis,and reduced in the dermis with a declined percentage in nucleated cells.

Objective To compare the intensity and isotype of anticardiolipin(ACL)antibodies in the sera from patients with syphilis and SLE.Methods IgG and IgM type of ACL antibodies were examined by ELISA in99syphilis patients and75SLE patients.Results Although similar positive percentage of IgG ACL antibodies was shown in syphilis and SLE patients,stronger absorbance(A value)was seen in syphilis patients(P

Objective:To study the effect of astragalus polysacchrides on anticardiolipin, antiphosphatidyl choline, antiphosphatidyl serine, antiphospha-tidyl inositol, antiphosphatidic acid and antiphosphatidyl ethanolamine antibodies (aCL, aPC, aPS, aPI, aPA, aPE) in SLE mice. Methods:19 NZB?NZW F1 female mice were divided randomly into 3 groups: group PG2I (25 mg/kg/d), group PG2II (50 mg/kg/d), group NS (0.2 ml/d). Select BXSB and C57BL/6 female mice as control. The level of antiphospholipid antibodies in these mice were examined by ELISA. Results:Compared with group NS, the A value in group PG2II were decreased significantly, however, A value in group PG2I were elevated slightly. There were no difference among group PG2II, BXSB and C57BL/6. The level of antiphospholipid antibodies in group NS and PG2I were increased significantly compared with that of BXSB and C57BL/6 mice. Conclusion:The generation of antiphospholipid antibodies can be improved by low dose of PG2 and inhibited by high dose of PG2.

Objective:To observe the distribution,morphology and density of monocytes/macrophages and dendritic cells in the normal human dermis.Methods:Normal skin from 6 locations such as the face,trunk,proximal limbs,distal limbs,and palms and soles of 8 subjects were collected for the study.The horizontal and longitudinal sections of the skin were stained with an ABC immunoperoxidase procedure with anti-CD1a and anti-CD68 monoclonal antibodies.Results:In the superficial dermis CD68 positive monocytes/macrophages form a dense network with a density in a 6-micron section ranging from 361/mm~2 to 562/mm~2.These network of CD68 positive cells continued on to surround the blood vessels and skin appendages.Lower densities of CD68 positive dendritic cells were found in the deep(reticular) dermis,dispersed between collagen bundles.The CD68 positive cells were detected within the superficial dermis with variable densities: distal limbs 562/mm~2,trunk 517/mm~2,face 509/mm~2,palms 507/mm~2,proximal limbs,472/mm~2,and soles 361/mm~2.Conclusion:There exists in the superficial dermis a relatively dense network of CD68 positive monocytes/macrophages.Such a distribution might indicate the clear polarity of the dermal monocytes/macrophages,with their direction of defense towards to the dermal-epidermal junction.

Objective To investigate the distribution of antiphospholipid antibodies(APA) in patients with systematic lupus erythematosus (SLE) and normal controls and its significance. Methods Six kinds of APA were detected by enzyme linked immunosorbent assay(ELISA). The examined sera were collected from 82 cases of normal controls and 32 cases of SLE. Results ①The positivity rate of IgG type aCL, aPI, aPA, aPE, aPS and aPC in the serum from normal controls was 6.10%, 6.10%, 7.32%, 7.32%, 3.66% or 3.66%, respectively. ②The positivity rate of IgM type aCL, aPA, aPC, aPS, aPE aPI in serum from normal controls was 2.44%, 3.66%, 3.66%, 6.10%, 6.10% and 4.88%, respectively. ③Compared with normal controls, the A values and positivity rate of IgG type of aCL, aPA, aPS, aPC and aPI in SLE patients were significantly higher. ④Compared with normal controls, the A values and positivity rate of IgM type of aCL, aPA, aPS, aPE and aPC in SLE patients were significantly higher. ⑤The total positivity rate of IgG type and IgM type APA was 68.75% or 71.88%, respectively. Conclusion ①There is lower titer of APA in normal controls, with some relationships between different types of APA and they appear at the same time.②the measurment of APA in sera of SLE might be benefit to the diagnosis of antiphospholipid syndrome. [

Objective To study the changes in some important surface markers of Langerhans cell (LC) in the skin of SLE patients. Methods The normal-appearing skin and lesional skin of 9 SLE patients were studied. ABC immunohistochemistry and the monoclonal antibodies against HLA-DR, CD54, CD68, CD1a and CD4 were used. Results ①In SLE skin lesions decreased LC density was shown,and there were also changes in the morphology and surface markers of LC. ②HLA-DR expression on keratinocytes was shown in most lesional specimens and a few on non-lesional specimens. ③Neither CD4 nor CD54 expression was shown on both lesional epidermis and non-lesional epidermis, CD4+cells were only observed in the dermal infiltrates. ④Two types of CD68+dendritic cells were seen in lesional and non-lesional epidermis, and more CD68+dendritic cells were seen in the infiltrates of lesional skin. ⑤Fibrillar CD68+materials around the basal KC were observed, and some of such fibrillar materials were connected with epidermal dendritic cells while others were not. Conclusions There are some differences in LC surface marker expression on lesional skin and non-lesional skin of SLE patients, which need to be further studied.