Metformin accelerates bone fracture healing by promoting type H vessel formation through inhibition of YAP1/TAZ expression.

Due to increasing morbidity worldwide, fractures are becoming an emerging public health concern. This study aimed to investigate the effect of metformin on the healing of osteoporotic as well as normal fractures. Type H vessels have recently been identified as a bone-specific vascular subtype that supports osteogenesis. Here, we show that metformin accelerated fracture healing in both osteoporotic and normal mice. Moreover, metformin promoted angiogenesis in vitro under hypoxia as well as type H vessel formation throughout fracture healing. Mechanistically, metformin increased the expression of HIF-1α, an important positive regulator of type H vessel formation, by inhibiting the expression of YAP1/TAZ in calluses and hypoxia-cultured human microvascular endothelial cells (HMECs). The results of HIF-1α or YAP1/TAZ interference in hypoxia-cultured HMECs using siRNA further suggested that the enhancement of HIF-1α and its target genes by metformin is primarily through YAP1/TAZ inhibition. Finally, overexpression of YAP1/TAZ partially counteracted the effect of metformin in promoting type H vessel-induced angiogenesis-osteogenesis coupling during fracture repair. In summary, our findings suggest that metformin has the potential to be a therapeutic agent for fractures by promoting type H vessel formation through YAP1/TAZ inhibition.

Post-traumatic distal ulnar bifurcation in children: a case report.

BACKGROUND: Galeazzi fracture dislocation is a compound injury that encompasses fractures of the distal third of the radius and dislocation of the distal radial ulnar joint (DRUJ). Clinically, this condition is rare and often leads to distal ulnar bifurcation. In previous similar reports, patients were effectively managed through surgery. CASE PRESENTATION: In this case report, we describe an 11-year-old male child who presented with an ulnar bifida following trauma to the hand, and was treated with manipulation and conservative treatment without surgery. A follow-up performed over the years demonstrated that the patient recovered well, and had normal wrist movements without significant pain, and the patient expressed great satisfaction. CONCLUSIONS: Ulnar diaphyseal fracture may occur in children or adolescents due to injuries, and may be accompanied with manipulation and repositioning. Conservative treatment can be applied to avoid the trauma associated with surgery especially in the absence of severe joint mobility impairment with good outcomes.

MiR-19b-3p regulates osteogenic differentiation of PDGFRα+ muscle cells by specifically targeting PTEN.

Heterotopic ossification (HO) is a common disturbing complication of intra-articular fractures. Its prevention and treatment are still difficult as its pathogenesis is unclear. It was reported that PDGFRα+ muscle cells in skeletal muscle may participate in the formation of HO; however, the specific mechanism is still unknown. This study investigated the function of miR-19b-3p in osteogenic differentiation of PDGFRα+ muscle cells. MiR-19b-3p was upregulated during PDGFRα+ muscle cell osteogenic differentiation. The exogenous expression of miR-19b-3p led to an increase in osteogenic marker gene transcription and translation during the osteogenic differentiation of PDGFRα+ muscle cells. Furthermore, both alkaline phosphatase and alizarin red staining increased in miR-19b-3p mimic transfected cells. Over-expression of miR-19b-3p led to the down-regulation of gene of phosphate and tension homology deleted on chromosome ten (PTEN). Additionally, the dual luciferase reporter assay demonstrated that PTEN was a direct target of miR-19b-3p. The increase of osteocalcin, osteopontin, and Runt-related transcription factor 2 protein levels induced by ectopic miR-19b-3p expression could be partially reversed by PTEN over-expression. In conclusion, our results suggested that miR-19b-3p may be a promising target in inhibiting PDGFRα+ muscle cell osteogenic differentiation and treatment of HO.

Comparison of the Efficacy of Tenofovir Versus Tenofovir plus Entecavir in the Treatment of Chronic Hepatitis B in Patients With Poor Efficacy of Entecavir: A Systematic Review and Meta-analysis.

PURPOSE: This study aimed to compare the efficacy between tenofovir disoproxil fumarate (TDF) and TDF plus entecavir (ETV) combination therapy in patients with chronic hepatitis B (CHB) with a poor response to ETV. METHODS: We searched the China National Knowledge Infrastructure (CNKI), PubMed, EMBASE, and SCOPE libraries for articles using the keywords chronic hepatitis B virus or CHB or HBV, entecavir or ETV, and tenofovir or TDF. FINDINGS: Five studies (from CNKI and PubMed) with a total of 408 patients met the inclusion criteria: 212 patients in the TDF group and 196 patients in the TDF plus ETV group. The rates of viral suppression between the 2 groups were comparable at weeks 24 and 48 of treatment (P = 0.546 vs P = 0.818). In addition, the subanalysis revealed that no significant differences were observed in the rates of viral suppression between the 2 groups at week 24 (subgroup 1 [partial response to ETV]: P = 0.822; subgroup 2 [resistance to ETV]: P = 0.294) and week 48 (subgroup 1: P = 0.797; subgroup 2: P = 0.545). No significant differences were found in alanine aminotransferase normalization, hepatitis B e antigen loss, hepatitis B e antigen seroconversion, virologic breakthrough, and tolerability between the 2 groups at weeks 24 and 48. Therefore, the results suggest that TDF monotherapy should be chosen for patients with CHB with a poor response to ETV for reasons of economy and convenience. IMPLICATIONS: We conclude that TDF monotherapy is comparable to TDF-ETV combination therapy for patients with a poor response to ETV; thus, TDF monotherapy may be a better choice for these patients. However, because of the limited citations in this meta-analysis, complete and systematic evidence is needed to evaluate the differences in efficacy and tolerability between TDF and TDF-ETV. Larger and longer randomized clinical trials and further studies should be conducted to verify the results.

The efficacy of a multimodal analgesia protocol in preventing heterotopic ossification after acetabular fractures surgery.

Background Heterotopic ossification (HO) after joint surgery is always a disturbing problem for patients and surgeons. Prophylaxis is the most effective therapy. Objective To assess the efficacy and safety of a multimodal analgesia protocol that included parecoxib and celecoxib in preventing HO after acetabular fracture surgery. Setting Selecting patients from trauma registry of our hospital. Method We identified 259 patients who had acetabular fracture surgery between January 2008 and December 2014. Hundredsixty-three patients received parecoxib and celecoxib (Group A) and 96 patients received no prophylaxis (Group B). The presence of HO was assessed according to the classification of Brooker et al. at the 12 month postoperative visit. Main outcome measure The differences in HO incidence and severity between the two groups. Results 49 patients (30.0%) developed HO in the Group A and 44(45.8%) in Group B. The difference in total HO incidence between the two groups was significant (P = 0.011 < 0.05, χ2 = 6.530, OR 0.508, 95% CI (0.301-0.857). Severe HO (Brooker grade III or IV) developed in 15 patients (9.2%) in Group A and 17 patients (17.7%) in Group B. Brooker grade I + II was 34(20.9%) and 27(28.1%) in each group. The difference in the severity of HO between the two Groups was significant (P = 0.008 < 0.05). Conclusion A short-term administration of parecoxib and celecoxib aids in the prevention of HO after acetabular fractures surgery.

Helicobacter pylori infection may increase the risk of progression of chronic hepatitis B disease among the Chinese population: a meta-analysis.

OBJECTIVES: Helicobacter pylori is a bacterium that infects over 50% of the human population worldwide. An increasing number of studies have demonstrated that H. pylori may cause liver diseases, and the underlying relationship between H. pylori infection and chronic hepatitis B has attracted much attention. This study aimed to examine the association between H. pylori infection and the progression of chronic hepatitis B in the Chinese population. METHODS: A search was performed of the PubMed/MEDLINE, Web of Science, and Cochrane Central Register of Controlled Trials (CENTRAL) databases, as well as the Chinese databases, China National Knowledge Infrastructure and Wanfang Data, for studies published between January 1, 1994 and November 1, 2015. RESULTS: In total, 2977 patients were included in the chronic hepatitis B group, while 1668 participants were included in the healthy control group. The prevalence of H. pylori among patients with chronic hepatitis B was significantly higher than that among those without chronic hepatitis B. The pooled odds ratio was 3.17. In the subgroup analysis, the odds ratio was 4.28 for hepatitis B virus (HBV)-related cirrhosis and 6.02 for hepatocellular carcinoma. CONCLUSION: These results indicate a strong relationship between H. pylori and chronic hepatitis B, particularly during HBV progression.

The Association between Helicobacter pylori Infection and Chronic Hepatitis C: A Meta-Analysis and Trial Sequential Analysis.

Purpose. Helicobacter pylori is a common gastric disease-inducing pathogen. Although an increasing number of recent studies have shown that H. pylori is a risk factor for liver disease, the potential association between H. pylori infection and chronic hepatitis C still remains controversial. The aim of our meta-analysis was to evaluate a potential association between H. pylori infection and chronic hepatitis C. Methods. We searched the PubMed, Embase, CNKI, Web of Science, and the Cochrane Central Register of Controlled Trials (CENTRAL) databases between January 1, 1994, and May 1, 2015. Results. This study included a total of 1449 patients with chronic hepatitis C and 2377 control cases. The prevalence of H. pylori was significantly higher in patients with chronic hepatitis C than in those without chronic hepatitis C. The pooled odds ratio was 2.93. In a subgroup analysis, the odds ratios were 4.48 for hepatitis C virus- (HCV-) related cirrhosis and 5.45 for hepatocellular carcinoma. Conclusion. Our study found a strong association between H. pylori and chronic hepatitis C, particularly during the HCV progression stage; thus, we recommend active screening for H. pylori in patients with chronic hepatitis C.

Comparison of the efficacy of Lamivudine plus adefovir versus entecavir in the treatment of Lamivudine-resistant chronic hepatitis B: a systematic review and meta-analysis.

BACKGROUND: Hepatitis B virus infection remains 1 of the major health threats worldwide. Currently, lamivudine plus adefovir combination therapy or entecavir monotherapy is usually used for the treatment of patients with lamivudine-resistant chronic hepatitis B (CHB). However, there are few systematic comparisons between the efficacy of lamivudine plus adefovir and the efficacy of entecavir in the treatment of these patients. OBJECTIVE: The goal of this systematic study and meta-analysis was to assess the efficacy of lamivudine plus adefovir compared with entecavir for the treatment of patients with lamivudine-resistant CHB. METHODS: A comprehensive literature search of PUBMED, Web of Science, WANFANG database, the Cochrane Central Register of Controlled Trials, and the Cochrane Database of Systematic Review, were screened to obtain citations from January 1990 to January 2012 in this study. Data analysis was done by using the Review Manager Software 5.1. RESULTS: Eight studies were suitable for analysis. A total of 696 patients with lamivudine-resistant CHB were studied and grouped according to treatment: 341 patients in the entecavir group and 355 patients in the lamivudine plus adefovir group. The results found that the rates of undetectable hepatitis B virus DNA levels, alanine aminotransferase normalization, hepatitis B e antigen loss, and hepatitis B e antigen seroconversion were not significantly different between the lamivudine plus adefovir group and the entecavir group. Moreover, the rate of adverse reactions was also not significantly different between the 2 groups. However, virologic breakthrough for the patients with lamivudine resistance was higher in the entecavir group than in the lamivudine plus adefovir group. CONCLUSIONS: For these CHB patients with lamivudine resistance, lamivudine plus adefovir was a better treatment option than entecavir alone.

HMGB1 release by human liver L02 and HepG2 cells induced by lipopolysaccharide.

Liver cells release the high mobility group box-1 (HMGB1) protein when exposed to lipopolysaccharides (LPSs). However, the timing and levels of protein released remain unclear. The present study aimed to characterize the secretion of the late pro-inflammatory cytokine HMGB1 by liver L02 and HepG2 cells. The human mononuclear macrophage cell line U937 was used as a control. Various concentrations of LPS were added to human U937, L02 and HepG2 cells for different durations, and the cells were analyzed at different time-points following this addition. Reverse transcription polymerase chain reaction (RT-PCR) was used to measure cellular HMGB1 mRNA levels, western blotting was performed to detect HMGB1 in cellular supernatants and the translocation of HMGB1 from the nucleus to the cytosol was examined using immunofluorescence staining. L02 and HepG2 cells exhibited higher HMGB1 mRNA levels compared with the control U937 cells 20 and 24 h following continuous exposure to LPS. U937 cells exhibited higher HMGB1 mRNA levels compared with the corresponding L02 and HepG2 cells 16 h following LPS exposure. The phase of HMGB1 protein detected in the cellular supernatants of L02 and HepG2 cells (16 h) was later than that of U937 cells (8 h). For the three cell lines, HMGB1 levels demonstrated a time dependency; however, the protein level was the highest in U937 cells. In the three cell lines, translocation of HMGB1 from the nucleus to the cytosol occurred; however, the phases of HMGB1 translocation in L02 and HepG2 cells occurred later than in U937 cells. LPS-induced secretion of the late pro­inflammatory cytokine HMGB1 by liver cells is characterized by a late phase of release and smaller quantity, and the process of HMGB1 secretion appears to be associated with HMGB1 translocation.

Surgical management for thoracic spinal tuberculosis in the elderly: posterior only versus combined posterior and anterior approaches.

PURPOSE: To compare the clinical outcomes of surgical management by posterior only and combined posterior and anterior approaches for thoracic spinal tuberculosis in the elderly. MATERIALS AND METHODS: This was a retrospective cohort study. Thirty-six cases of thoracic spinal tuberculosis treated by two different surgical procedures in our center from January 2004 to June 2009 were studied. All the cases were divided into two groups: 20 cases in Group A underwent single-stage posterior debridement, transforaminal fusion and instrumentation, and 16 cases in Group B underwent posterior instrumentation, anterior debridement and bone graft in a single- or two-stage procedure. The operation time, blood loss, correction rate, recovery of neurological function, fusion time and complications were, respectively, compared between Group A and Group B. RESULTS: All patients were followed up for an average of 35.1 ± 5.8 months (range 26-45 months). It was obviously that the average operative duration, blood loss, hospitalization and complication rate of Group A was less than those of Group B. Spinal tuberculosis was completely cured and the grafted bones were fused in 10 months in all patients. There was no persistence or recurrence of infection and no differences in the radiological results in both groups. The kyphosis was significantly corrected after surgical management. However, loss of correction also occurred in both groups. CONCLUSION: Our study showed that the posterior approach only procedure obtained better clinical outcomes than combined posterior and anterior surgeries. It might be a better surgical treatment for thoracic spinal tuberculosis in aged patients with poor health status, especially for cases in early phase of bone destruction and/or mild and moderate kyphosis.

[Short-term clinical observation on compound Xiatianwu combined with methotrexate in treating rheumatoid arthritis].

OBJECTIVE: To observe the short-term clinical efficacy of compound Xiatianwu combined with methotrexate (MTX) in treating rheumatoid arthritis. METHOD: One hundred and four patients with rheumatoid arthritis were randomly divided into two groups: 64 cases in the combined treatment group who was treated with compound Xiatianwu combined with MTX, and the remaining 40 cases in the control group which was only treated with MTX. The changes in ACR20, ACR50, ACR70 and laboratory indexes including anti-cyclic citrulline polypeptide, rheumatoid factor, erythrocyte sedimentation rate, high sensitivity creative protein were compared before and after treatment. Adverse reactions in the two groups were observed as well. RESULT: After being treated for 3 months, the ACR20 improvement rate reached 59.4% in the combined treatment group, higher than 35% in the control group, with significant statistical difference (P <0.05); The ACR50 improvement rate reached 32. 8% the treated group, also higher than 17.5% in the control group, with significant statistical difference (P <0.05). After treatment for three months, both groups showed remarkable improvement in anti-cyclic citrulline polypeptide, rheumatoid factor, erythrocyte sedimentation rate and high sensitivity creative protein compared with that before treatment, demonstrating statistical significance (P <0. 05). The combined treatment group displayed more significant improvement in erythrocyte sedimentation rate and high sensitivity creative protein as well as much less adverse reactions than the MTX group. CONCLUSION: Compound Xiatianwu combined with MTX can effectively improve clinical symptoms of RA patients and laboratory indexes, and shows higher medication safety.

A nested case-control study of maternal-neonatal transmission of hepatitis B virus in a Chinese population.

AIM: To examine the determinants of maternal-neonatal transmission of hepatitis B virus (HBV). METHODS: A nested case-control study was conducted in Changsha, Hunan, People's Republic of China from January 1, 2005 to September 31, 2006. To avoid potential maternal blood contamination, we collected vein blood of newborns immediately after birth and before initial hepatitis B vaccination to determine the HBV infection status of the newborn. For each HBsAg-positive infant, one HBsAg-negative infant born to an HBsAg-positive mother was matched by hospital at birth (same), gender (same), and date of birth (within 1 mo). A face-to-face interview was conducted to collect clinical and epidemiological data. Conditional logistic regression analysis was used to estimate the independent effects of various determinants on maternal-neonatal transmission of HBV. RESULTS: A total of 141 HBsAg-positive infants and 141 individually matched HBsAg-negative infants were included in the final analysis. Maternal first-degree family history of HBV infection, intrahepatic cholestasis, and premature rupture of membranes were risk factors for perinatal transmission of HBV, whereas systematic treatment and HBV immunoglobulin injections for mothers with HBV infection were protective factors for maternal-neonatal transmission of HBV, after adjustment for potential confounding factors. CONCLUSION: For HBsAg-positive mothers, systematic treatment, HBV immunoglobulin administration, and controlling intrahepatic cholestasis and pregnancy complications may reduce the incidence of perinatal transmission of HBV.

Comparison of the efficacy of tenofovir and adefovir in the treatment of chronic hepatitis B: a systematic review.

Chronic viral hepatitis B remains a global public health concern. Currently, several drugs, such as tenofovir and adefovir, are recommended for treatment of patients with chronic hepatitis B. tenofovir is a nucleoside analog with selective activity against hepatitis b virus and has been shown to be more potent in vitro than adefovir. But the results of trials comparing tenofovir and adefovir in the treatment of chronic hepatitis B were inconsistent. However, there was no systematic review on the comparison of the efficacy of tenofovir and adefovir in the treatment of chronic hepatitis B. To evaluate the comparison of the efficacy of tenofovir and adefovir in the treatment of chronic hepatitis B we conducted a systematic review and meta-analysis of clinical trials. We searched PUBMED, Web of Science, EMBASE, CNKI, VIP database, WANFANG database, the Cochrane Central Register of Controlled Trials and the Cochrane Database of Systematic Review. Finally six studies were left for analysis which involved 910 patients in total, of whom 576 were included in tenofovir groups and 334 were included in adefovir groups. At the end of 48-week treatment, tenofovir was superior to adefovir at the HBV-DNA suppression in patients[RR = 2.59; 95%CI(1.01-6.67), P = 0.05]. While there was no significant difference in the ALT normalization[RR = 1.15; 95%CI(0.96-1.37), P = 0.14], HBeAg seroconversion[RR = 1.32; 95%CI(1.00-1.75), P = 0.05] and HBsAg loss rate[RR = 1.19; 95%CI(0.74-1.91), P = 0.48]. More high-quality, well-designed, randomized controlled, multi-center trails are clearly needed to guide evolving standards of care for chronic hepatitis B.

HMGB1 cytoplasmic translocation in patients with acute liver failure.

BACKGROUND: High-mobility group box 1 (HMGB1) is a late mediator of lethal systemic inflammation. Acute liver failure (ALF) has been shown to trigger systemic inflammation in clinical and animal studies. To evaluate the possibility of HMGB1 cytoplasmic translocation in ALF, we determined whether HMGB1 is released in hepatocytes and end organ in patients with liver failure/injury. METHODS: HepG2 cell were stimulated with LPS or TNF-α, the increase of HMGB1 extracellularly in the culture medium and intracellularly in various cellular fractions were determined by western blot or immunocytochemistry. To observe sub-cellular location of HMGB1 in hepatocytes, liver specimens were obtained from 6 patients with ALF caused by HBV infection, 10 patients with chronic viral hepatitis B, 6 healthy controls, as well as animals model of ALF by intraperitoneal administration of D-GalN (600 mg/kg) and LPS (0.5 mg/kg). RESULTS: In HepG2 cell culture, LPS or TNF actively induced HMGB1 cytoplasmic translocation and release in a time- and dose-dependent fashion. In animal model of ALF, cytoplasmic HMGB1 translocation was observed in hepatocyts as early as 3 hours post onset of ALF. In patients with ALF caused by HBV infection, cytoplasmic HMGB1 translocation was similarly observed in some hepatocytes of the liver specimen. CONCLUSIONS: Cytoplasmic HMGB1 translocation may occur during ALF, which may potentially contribute to the pathogenesis of liver inflammatory diseases.

[Expression of FOXP3 in CD4+ CD39+ T cells of patients with systemic lupus erythematosus and dynamic observation of treatment with glucocorticoid].

OBJECTIVE: To investigate the level of FOXP3 expressed in CD4+ CD39+ T cells in peripheral blood of patients with systemic lupus erythematosus (SLE) and observe the regulation of glucocorticoid on it. METHODS: Frequencies of CD4+ CD25+ CD39+, CD4 CD25+ FOXP3+ and CD4+ CD39+ FOXP3+ T cells and levels of FOXP3 protein were analyzed by flow cytometry of 47 SLE patients (including 29 untreated/active SLE) and 22 healthy controls. Meanwhile, correlations among three groups and influences of glucocorticoid were analyzed. RESULTS: Percents of CD4+ CD25+ CD39+ T cells expressed in active SLE, inactive SLE and healthy controls were (1.3 +/- 0.5)%, (1.9 +/- 0.8)% and (2.3 +/- 1.0)% respectively, the level decreased in active SLE compared with inactive SLE and healthy controls P < 0.05 in each group, but it had no significant difference between the latter two groups (P > 0.05). In active SLE, levels of FOXP3 protein expressed in CD4+ CD25+, CD4+ CD25high and CD4+ CD39+ T cells were (45 +/- 12)%, (65 +/- 14)% and (70 +/- 14)% respectively. Levels of FOXP3 expressed in CD4+ CD25high and CD4+ CD39+ T cells were higher than that expressed in CD4+ CD25+ T cells (P < 0.01), while it had no significant difference between CD4 CD25high T cells and CD4+ CD39+ T cells (P > 0.05). CONCLUSIONS: These results demonstrate that CD39 may be a better surface marker of regulatory T cells, and that deficiency of CD39+ Treg cells may play an important role in the pathogenesis of SLE.

The expressions of Toll-like receptor 9 and T-bet in circulating B and T cells in newly diagnosed, untreated systemic lupus erythematosus and correlations with disease activity and laboratory data in a Chinese population.

Toll-like receptor 9 (TLR9) plays a controversial role in the pathogenesis of systemic lupus erythematosus (SLE). T-bet may be involved in the processes between the initiation of TLR9 activation and the antibodies' production. To clarify the paradox of TLR9, we investigated the intracellular expressions of TLR9 and T-bet in B and T cells in peripheral blood samples from 35 newly diagnosed, untreated patients with SLE and 16 healthy subjects by flow cytometry (FCM). And we collected the clinic laboratory data obtained from the same individual blood sample tested by FCM each time. And the correlations among the expression levels of the two proteins and SLE laboratory data were calculated. We found the percentages of B cells expressing TLR9 and T-bet and of T cells expressing TLR9 were significantly elevated in SLE patients when compared with healthy controls. There was a significantly negative relationship between the proportion of B cells expressing TLR9 and SLE Disease Activity Index (SLEDAI) score. The serum levels of anti-dsDNA antibody reversely correlated with the mean fluorescence intensity (MFI) of B cells co-expressing T-bet and TLR9. The serum levels of anti-C1q antibody significantly associated with the proportion of B cells expressing T-bet. Also, the serum levels of IgM and IgA antibodies both significantly correlated with TLR9 and T-bet expressions in T and B cells. According to the immunological pathway knowledge and the mutually verified associations, the following conclusions are made. Expressions of TLR9 and T-bet were increased in patients with SLE. TLR9 may have a role to play in protecting against lupus. And the increase of the co-expression of TLR9 and T-bet may be of benefit to the protective antibodies' production and pathogenic antibodies' decline, and could be regarded as a good sign for lupus demission and/or treatment.

[Expression of CD4+ CD25+ CD127(low/-) T cells in patients with systemic lupus erythematosus].

OBJECTIVE: To detect the new and old surface markers of regulatory T cells (Treg cells) in the CD4+ T cells of the patients with systemic lupus erythematosus (SLE) in order to reveal the role of Treg cells in the pathogenesis of SLE. METHODS: Peripheral blood samples were collected from 29 newly diagnosed and treatment-naïve SLE patients, 3 males and 26 females, aged (34 +/- 13), and 24 sex and aged-matched healthy controls. Three-color flow cytometry was used to detect the CD4+CD25+ CD127(low/-) T cells, CD4+CD25high T cells, and CD4+CD25+FOXP3+ T cells. The serum anti-nuclear antibody (ANA), anti-ds-DNA antibody, anti-smooth muscle antibody, anti-nucleosome antibody, anti-C1q, C3, and C4 were detected. Blood and urine routine examinations were conducted. RESULTS: The proportion of blood CD4+ CD25+CD127(low/-) T cells of the SLE patients was not significantly different from that of the controls (P > 0.05), however, the proportions of CD4+CD25+FOXP3+ T cells and CD4+CD25high T cells of the SLE patients were 2.1 +/- 1.2 and 0.8 +/- 0.4 respectively, both significantly lower than those of the controls (4.0 +/- 1.4 and 1.8 +/- 0.8 respectively, both P <0.01). The ratios of the CD4+CD25+CD127(low/-) T cells, CD4+CD25high T cells, and CD4+CD25+FOXP3+ T cells to the CD4+CD25+ T cells of the SLE patients were 0.5 +/- 0.1, 0.1 +/- 0, and 0.3 +/- 0.1 respectively, all significantly lower than those of the controls (0.6 +/- 0.1, 0.2 +/- 0.1, and 0.5 +/- 0. respectively, all P <0.01). The level of CD4+CD25+CD127(low/-) T cell was positively correlated with the levels of CD4+CD25+FOXP3+ T cells and CD4+CD25high T cell (both P < 0.01). The levels of these 3 kinds of cells and their ratios to CD4+CD25+ T cells had no correlation with age, sex, course, IgG, IgA, IgM, urine protein, TIPU, anti-dsDNA, anti-C1q, anti-nuclear body antibody (all P > 0.05), however, were significantly associated negatively with SLE disease activity index, P < 0.05). Only the CD4+CD25+CD127(low/-) T cells/ CD4+CD25+ T cells was negatively correlated with C4 (P <0.01). CONCLUSION: The relative ratio of Treg cells to the activated CD4+ T cells may play an important role in the pathogenesis of SLE.