OBJECTIVE To study the clinical diagnosis significance of the anti-ribosomal P0 protein antibodies in systemic Lupus Erythematosus(SLE).METHODS The ribosome protein zero(P0)of gene recombination and purified ribosome P protein were used as the antigens to detect the anti-ribosomal P0 protein antibodies and the anti-ribosomal P protein antibodies in 126 SLE sufferers and 145 non-SLE autoallergic disease sufferers.To detect the anti-dsDNA antibodies,the anti-SmD1 antibodies,the nuclear body antibodies and so on in 126 SLE sufferers by line immunoassay at the same time and to compare the significance of these antibodies in the clinical diagnosis of SLE.RESULTS The positive rate of the anti-ribosomal P0 protein antibodies was 38.89% in SLE sufferers vs 2.1% in non-SLE autoallergic disease sufferers.The difference of two groups had statistical significance(χ2=19.36,P0.001).The specificity of the anti-ribosomal P0 protein antibodies to diagnose SLE was 97.93%.The positive rate of the anti-ribosomal P0 protein antibodies,the anti-dsDNA antibodies,the anti-SmD1 antibodies and the nuclear body antibodies was 9.52% and 15.08% and 3.17% and 3.97%,respectively.CONCLUSIONS The anti-ribosomal P0 protein antibodies have significant clinical value in diagnosis of SLE.
Objective To study the effect of emodin on mRNA expression and extracellular release of high mobility group box 1(HMGB1)in endotoxin-stimulated macrophages.Methods The changes of HMGB1 and TNF-α levels in the culture medium and expression of HMGB1 mRNA were investigated after Emodin(5、20、50 μmol/L)was incubated with lipopolysaccharide-stimulated cultured mouse peritoneal macrophages.Results Emodin(50 μmol/L)markedly suppressed the release of HMGB1 and TNF-α,and expression of HMGB1 mRNA from lipopolysaccharide-stimulated macrophages(P﹤0.01).Conclusion Emodin confers inhibition onto extracellular release of HMGB1 and expression of HMGB1 mRNA from endotoxin-stimulated macrophages.
OBJECTIVE To discuss the application of Beckman Coulter LH750 blood corpuscle analyzer in analyzing stability of the related parameter.METHODS When the traceability of blood analyzer determination data was guaranteed,fluctuation average value analysis system provided by the analyzer software(X-B) analysis system) was applied.The MCV,MCH and MCHC,of the clinical specimen was examined,whose fluctuation average value tendency was determined.RESULTS When X-B was applied,many influencing factors which the material controls 5CPlus could not prompt may be discovered.On the other hand,when instrument was in good state,the average value of RBC,Hb,MCH,MCHC and MCV changes in the small scope,the XB analytic method quality control chart was basically consistent with the quality control chart change tendency of blood traceability quality control sample.CONCLUSION This method can be used as another approach to monitor the stability of traceability analyzed by LH750 blood corpuscle.
OBJECTIVE To establish the normal reference range of red blood cells parameters(RBC,HGB,MCV,MCH,MCHC and HCT) of healthy adults in Wuxi by analyzing the data measured by Beckman Coulter LH750 hematology analyzer.METHODS The healthy adults of male and female 1,000 in each group.The venous blood specimens were detected by using Beckman Coulter LH750 hematology analyzer.The reference rage was investigated.RESULTS All data was analyzed by the SPSS10.0 software,The parameters of red blood cells were RBC: the male(5.04±0.42)×1012/L,the female(4.40±0.38)×1012/L;HGB:the male(149.00±10.00)g/L,the female(130.2±11.2)g/L:MCV:the male(90.1±4.10)fL,the female(90.00±4.50)fL,HCT:the male(0.45±0.03)%,the female(0.38±0.04)%.CONCLUSION There are certain differences between the result and the reference range provided by the National Rules of Operation of Clinical Laboratory.Therefore,it is necessary to establish the local reference range of red blood cell in laboratories.
Summary Background The biological mechanisms underlying the use of platelet‐rich plasma (PRP), as well as the efficacy and possible adverse effects of PRP, have not yet been fully elucidated. Prior studies have evaluated PRP for cutaneous ulceration. However, the benefits from PRP still remain controversial and few have assessed the effects of ulceration etiologies. The purpose of our study is to determine the efficacy and safety of PRP and which kind of ulcer is more suitable for PRP by analyzing the effects of PRP on ulcers with different causes. Methods A comprehensive search was performed to identify randomized controlled trials (RCTs) regarding the application of PRP from PubMed, EMBASE, Scopus, and the Cochrane Library. The data were analyzed using Review Manager 5.3. Results A total of nineteen RCTs (909 patients) were included. In contrast with conventional treatments, PRP achieved higher healing rate, higher percentage of area reduction, and smaller final area in vascular ulcers. However, the advantage disappeared in diabetic and pressure ulcers. Concerning adverse events, PRP showed lower incidence in the short term, but higher in the long term. No significant differences were found in ulcer closure velocity and healing time. Conclusion Platelet‐rich plasma effectiveness and safety in treating cutaneous ulceration depend on what is the ulceration etiology. For diabetic ulcers, PRP showed no satisfactory results suggesting that PRP may not be suitable for diabetic patients. However, PRP could be efficient and more beneficial for vascular ulcers and effects on pressure ulcers remain unclear. Thus, PRP option should be carefully considered for each patient in accordance with their ulceration etiologies.
To define the roles of endothelial-intrinsic nuclear factor κB (NF-κB) activity in host defense and multiple organ injury in response to sepsis, we generated double transgenic (TG) mice (EC-rtTA/I-κBαmt) that conditionally overexpress a degradation-resistant form of the NF-κB inhibitor I-κBα (I-κBαmt) selectively on vascular endothelium. The EC-rtTA/I-κBαmt mice had no basal, but a relatively high level of doxycycline-inducible, I-κBαmt expression. I-κBαmt expression was detected in endothelial cells, but not in fibroblasts, macrophages, and whole blood cells, confirming that transgene expression was restricted to the endothelium. When subjected to endotoxemia, EC-rtTA/I-κBαmt mice showed endothelial-selective blockade of NF-κB activation, repressed expression of multiple endothelial adhesion molecules, reduced neutrophil infiltration into multiple organs, decreased endothelial permeability, ameliorated multiple organ injury, reduced systemic hypotension, and abrogated intravascular coagulation. When subjected to cecal ligation and puncture–induced sepsis, the TG mice had less severe multiple organ injury and improved survival compared with wild-type (WT) mice. WT and EC-rtTA/I-κBαmt mice had comparable capacity to clear three different pathogenic bacteria. Our data demonstrate that endothelial NF-κB activity is an essential mediator of septic multiple organ inflammation and injury but plays little role in the host defense response to eradicate invading pathogenic bacteria.
Abstract Bacterial endotoxin [lipopolysaccharide (LPS)] stimulates macrophages to sequentially release early [tumor necrosis factor (TNF)] and late [high mobility group box 1 (HMGB1)] proinflammatory cytokines. The requirement of CD14 and mitogen-activated protein kinases [MAPK; e.g., p38 and extracellular signal-regulated kinase (ERK)1/2] for endotoxin-induced TNF production has been demonstrated previously, but little is known about their involvement in endotoxin-mediated HMGB1 release. Here, we demonstrated that genetic disruption of CD14 expression abrogated LPS-induced TNF production but only partially attenuated LPS-induced HMGB1 release in cultures of primary murine peritoneal macrophages. Pharmacological suppression of p38 or ERK1/2 MAPK with specific inhibitors (SB203580, SB202190, U0126, or PD98059) significantly attenuated LPS-induced TNF production but failed to inhibit LPS-induced HMGB1 release. Consistently, an endogenous, immunosuppressive molecule, spermine, failed to inhibit LPS-induced activation of p38 MAPK and yet, still significantly attenuated LPS-mediated HMGB1 release. Direct suppression of TNF activity with neutralizing antibodies or genetic disruption of TNF expression partially attenuated HMGB1 release from macrophages induced by LPS at lower concentrations (e.g., 10 ng/ml). Taken together, these data suggest that LPS stimulates macrophages to release HMGB1 partly through CD14- and TNF-dependent mechanisms.
Objective To investigate the extracellular release of high mobility group box 1(HMGB1) in bladder cancer T24 cells induced by lipopolysaccharide(LPS) and its possible mechanism.Methods The changes of HMGB1 concentration in the culture medium and HMGB1 mRNA expression were investigated after T24 cells were stimulated with 100 μg/L LPS for different hours.The HMGB1 concentration and the level of HMGB1 mRNA expression were deter mined by ELISA and real-time fluorescent quantitative PCR,respectively.Inhibitory effect of PI3K/AKT pathway in hibitor was observed on HMGB1 release.Results The HMGB1 concentration in the culture medium and the level of HMGB1 mRNA expression significantly increased in a time-dependent manner after T24 cells after induced by LPS for 12 h.LY294002 partly inhibited extracellular release of HMGB1 in LPS-induced T24 cells.Conclusion LPS induces bladder cancer cells to release HMGB1,which may be related to PI3K/AKT signaling pathway.
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