Periostin, a secreted extracellular matrix protein, is highly expressed in wound healing and in various types of human cancer and is involved in angiogenesis. Keloids, considered dermal benign tumors, are granulomatous lesions characterized by capillary proliferation. However, the underlying regulatory mechanism of angiogenesis in keloids remains to be elucidated. The present study aimed to examine the effect of periostin on angiogenesis in keloids. The expression of periostin was upregulated and the vessel density was higher in human keloids compared with normal tissue, observed following staining with CD31 and CD105. Periostin demonstrated a markedly positive correlation with blood vessel density, which was assessed using CD31 staining (r=0.711; P<0.01) and a weak correlation was observed using CD105 staining (r=0.251; P<0.01). Conditioned medium from keloid fibroblasts (KFs) promoted the migration and tube formation of human umbilical vein endothelial cells (HUVECs) compared with normal fibroblasts and this effect may have been abrogated by the short hairpin RNA knockdown of periostin. Treatment with recombinant human periostin promoted the migration and tube formation of HUVECs by activating the extracellular signal-regulated kinase 1/2 and focal adhesion kinase signaling pathway. In addition, periostin increased the secretion of vascular endothelial growth factor and angiopoietin-1 in the KFs. In conclusion, these data suggested that upregulation in the level of periostin may promote angiogenesis directly and indirectly in keloids and may be a key factor in keloid development. Periostin may, therefore, be a promising therapeutic target in the treatment of keloids and other angioproliferative diseases.

ObjectiveFollistatin-like protein 1 (FSTL1) is a well-known mediator of inflammation. Intervertebral disc disease is an inflammatory disorder. Here, we investigated the role of FSTL1 in the intervertebral discs inflammation.MethodsExpression of FSTL1 in nucleus pulposus tissues from rats and human was determined by immunohistochemistry staining and western blot analysis. The expression levels of tumor necrosis factor-α (TNF-α), interleukin1-β (IL-1β) and matrix metalloproteinase 13 (MMP-13) in human and rat nucleus pulposus tissues were measured by immunohistochemistry staining. The mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NFκB) signaling pathways were detected by western blotting.ResultsFSTL1 serum levels were significantly increased in lumbar disc herniation patients and had a positive correlation with Visual Analogue Scores. Additionally, FSTL1 expression was significantly increased in extrusion group compared with protrusion and control groups. Furthermore, FSTL1 expression was significantly increased in intervertebral disc degeneration models of rats. Immunohistochemistry staining demonstrated that the levels of TNF-α, IL-1β and MMP-13 were increased in the pathogenesis of intervertebral disc disease. Recombinant human FSTL1 significantly increased the production of proinflammatory cytokines in vitro. In addition, FSTL1 promoted inflammation by activating c-Jun N-terminal kinase (JNK), extracellular regulated protein kinases 1/2(ERK1/2) and NFκB signaling.ConclusionsThese data imply that FSTL1 expression was increased in the pathogenesis of intervertebral disc disease. Importantly, FSTL1 promoted inflammatory catabolism in the nucleus pulposus by activating JNK, ERK 1/2/MAPK and NFκB signaling.

Background Tuberculosis (TB) remains a significant global public health problem. China has the second highest TB burden in the world. With a growing TB population with diabetes mellitus (DM), the TB control system faces mounting challenges. To date, evidence remains inconclusive regarding the association between TB-DM co-morbidity and delayed diagnosis of TB patients. This study aims to assess the diagnostic delay of TB patients with known DM and identify the factors associated with this delay. Methods Data was collected from China’s Tuberculosis information management system in two counties of Zhejiang province, China. Patient delay, health system delay and total diagnostic delay are defined as follows: 1) the interval between the onset of TB symptoms and first visit to any health facility; 2) from the first visit to the health facility to the confirmed TB diagnosis in the designated hospital; 3) the sum of patient and health system’s respective delays. Comparison of these delays was made between TB patients with and without DM using Mann-Whitney U test and Chi-square test. Univariate and multivariate regression analysis was used to identify factors influencing delays among TB patients with DM. Results Of 969 TB patients, 67 (7%) TB patients had DM co-morbidity. Compared with TB patients without DM, TB patients with DM experienced significantly shorter health system delays (p < 0.05), and there was a significantly lower proportion of patients whose health system delayed> 14 days (7.0% vs. 18%, p < 0.05). However, no significant difference was observed between both patient categories regarding patient delay and total diagnostic delay. The multivariate regression analysis suggested that TB patients with DM who were aged < 60 years (AOR = 3.424, 95%CI: 1.008–11.627, p < 0.05) and non-severe cases (AOR = 9.725, 95%CI: 2.582–36.626, p < 0.05) were more likely to have a total diagnostic delay of> 14 days. Conclusions Our study suggests that DM does not contribute to further diagnostic delay as expected. Instead, we observed significantly improved health system delay among TB patients with DM. The findings indicate the importance of early screening and diagnosis for TB among diabetic patients and of strengthening the integrated control and management of TB and diabetic programs.

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The relationship between rheumatoid arthritis and risk of vertebral fracture has been reported by several observational studies. However, there is no higher-level evidence study, such as meta-analysis, that has investigated the relationship, and its mechanisms are not yet fully clear. This meta-analysis aimed to provide a summary of an observational study of the relationship between rheumatoid arthritis and the risk of vertebral fractures.Relevant studies were identified by searching PubMed and EMBASE databases (up to August 1, 2016). We included published observational studies (cohort or case-control design) evaluating the relationship between rheumatoid arthritis and the risk of vertebral fractures. Two reviewers searched and abstracted the data independently. Relative risks (RRs) with 95% confidence intervals (CIs) were used throughout the whole analysis.Seven observational studies (2 cohort studies, 2 nested case-control studies, and 3 case-control studies) were included in this meta-analysis. The results showed that the pooled RR of vertebral fracture for individuals with rheumatoid arthritis was 2.34 (95% CI 2.05–2.63, I2 = 35.4%, P for heterogeneity = 0.16). Further subgroup analysis by sex showed that the pooled RRs for both women and men, and only women were 2.14 (95% CI 1.47–2.8, I2 = 48.5%, P for heterogeneity = 0.12) and 2.39 (95% CI 2.07–2.70, I2 = 34%, P for heterogeneity = 0.22), respectively. Subgroup analysis by study design showed that the pooled RRs for cohort studies, nested case-control studies, and case-control studies were 2.31 (95% CI 1.95–2.67, I2 = 4.8%, P for heterogeneity = 0.31), 1.89 (95% CI 1.01–2.77, I2 = 72.1%, P for heterogeneity = 0.06), and 2.62 (95% CI 2.04–3.91, I2 = 26.1%, P for heterogeneity = 0.26), respectively.Based on our meta-analysis, rheumatoid arthritis should be regarded as an independent risk factor of vertebral fracture. Further studies are needed to institute prevention and treatment strategies.