Background: Henoch Schonlein Purpura (HSP) is a systemic vasculitic disease which is common in children. It is very important to understand the clinical features of this disease for doctors and nurses. Objectives: To study the clinical characteristics of HSP in children. Methods: Collect the clinical data of the HSP children, and analyze the clinical characteristics of these HSP patients. Results: The ratio of M:F was 1.9:1. The mean age was 6.6 ± 1.6 years. The typical onset seasons were spring, winter and autumn. Infection and food allergy were the main etiological factors. The first symptom was skin purpura and these purpura mainly concentrated the lower extremities and buttocks. The dominant digestive clinical features were abdominal pains and vomiting. The knee joint and ankle joint were most frequently affected. The typical kidney symptoms were microscopic hematuria and albuminuria. An increased ESR was reported in 68 patients (56.7%). Serum C3 decreased in 13 cases (10.8%). ASO titer was higher in 57 children (47.5%). Conclusion: There were gender, season and area differences for the HSP patients. The etiological factors were diverse. HSP patients could have various clinical symptoms and rare complications.

There is emerging awareness that subchondral bone remodeling plays an important role in the development of osteoarthritis (OA). This review presents recent investigations on the cellular and molecular mechanism of subchondral bone remodeling, and summarizes the current interventions and potential therapeutic targets related to OA subchondral bone remodeling. The first part of this review covers key cells and molecular mediators involved in subchondral bone remodeling (osteoclasts, osteoblasts, osteocytes, bone extracellular matrix, vascularization, nerve innervation, and related signaling pathways). The second part of this review describes candidate treatments for OA subchondral bone remodeling, including the use of bone-acting reagents and the application of regenerative therapies. Currently available clinical OA therapies and known responses in subchondral bone remodeling are summarized as a basis for the investigation of potential therapeutic mediators.

ObjectivesOsteoarthritis (OA) is the most common degenerative joint disease in aged population and its development is significantly influenced by aberrant epigenetic modifications of numerous OA susceptible genes; however, the precise mechanisms that DNA methylation alterations affect OA pathogenesis remain undefined. This study investigates the critical role of epigenetic PPARγ (peroxisome proliferator–activated receptor-gamma) suppression in OA development.MethodsArticular cartilage expressions of PPARγ and bioactive DNA methyltransferases (DNMTs) from OA patients and mice incurred by DMM (destabilisation of medial meniscus) were examined. DNA methylation status of both human and mouse PPARγ promoters were assessed by methylated specific PCR and/or bisulfite-sequencing PCR. OA protections by a pharmacological DNA demethylating agent 5Aza (5-Aza-2'-deoxycytidine) were compared between wild type and PPARγ knockout mice.ResultsArticular cartilages from both OA patients and DMM mice display substantial PPARγ suppressions likely due to aberrant elevations of DNMT1 and DNMT3a and consequential PPARγ promoter hypermethylation. 5Aza known to inhibit both DNMT1 and DNMT3a reversed the PPARγ promoter hypermethylation, recovered the PPARγ loss and effectively attenuated the cartilage damage in OA mice. 5Aza also inhibited the OA-associated excessive inflammatory cytokines and deficit anti-oxidant enzymes, which were blocked by a specific PPARγ inhibitor in cultured chondrocytes. Further, 5Aza-confered protections against the cartilage damage and the associated abnormalities of OA-susceptible factors were significantly abrogated in PPARγ knockout mice.ConclusionEpigenetic PPARγ suppression plays a key role in OA development and PPARγ preservation via promoter demethylation possesses promising therapeutic potentials in clinical treatment of OA and the related joint diseases.

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mtDNA oxidative damage seems to be the "trigger" for cell dysfunction in high glucose-treated HRECs by setting in motion the vicious circle of mtDNA damage leading to ROS overproduction and further mtDNA damage, which may explain in part early vascular damage in diabetic retinopathy.