Effects of initial periodontal therapy on the formation of neutrophil extracellular traps in gingival crevicular fluid in patients with severe periodontitis.

Objectives: This study aimed to observe the effects of initial periodontal therapy on the level of neutrophil extracellular traps (NETs) in gingival crevicular fluid (GCF) of patients with severe periodontitis and to analyze the factors related to the formation of NETs.

Methods: Thirty-one patients with stage Ⅲ-Ⅳ periodontitis were recruited. Clinical periodontal parameters, including plaque index (PLI), gingival index (GI), probing depth (PD), and clinical atta-chment loss (CAL), were recorded before and 6-8 weeks after initial periodontal therapy.

The emerging progress on wound dressings and their application in clinic wound management.

Background: In addition to its barrier function, the skin plays a crucial role in maintaining the stability of the body's internal environment and normal physiological functions. When the skin is damaged, it is important to select proper dressings as temporary barriers to cover the wound, which can exert significant effects on defence against microbial infection, maintaining normal tissue/cell functions, and coordinating the process of wound repair and regeneration. It now forms an important approach in clinic practice to facilitate wound repair.

Excessive neutrophil extracellular trap formation induced by lipopolysaccharide exacerbates inflammatory responses in high glucose microenvironment.

Introduction: Neutrophil extracellular trap (NET) is a novel defense strategy of neutrophils and found to be induced by Porphyromonas gingivalis (P. gingivalis) lipopolysaccharide (LPS) or high glucose. The aim of this study was to investigate the roles and mechanisms of NET formation in high glucose inflammatory microenvironment.

MicroRNAs in the Pathogenesis of Ankylosing Spondylitis and their Clinical Implication.

Ankylosing spondylitis (AS) is a chronic and progressive immunoinflammatory disease, which mainly affects the spine and sacroiliac joints and shows a high rate of late disability. Inflammation, bone destruction, and new bone formation are typical pathological changes of AS. AS is dominated by inflammation at the early stage.

KR‑12‑a6 promotes the osteogenic differentiation of human bone marrow mesenchymal stem cells via BMP/SMAD signaling.

Considering the increased resistance to antibiotics in the clinic and the ideal antibacterial properties of KR‑12, the effects of KR‑12‑a6, an important analogue of KR‑12, on the osteogenic differentiation of human bone marrow mesenchymal stem cells (hBMSCs) were investigated. Osteogenic differentiation‑associated experiments were conducted in hBMSCs, and KR‑12‑a6 was used as an additional stimulating factor during osteogenic induction. Quantitative analysis of alkaline phosphatase (ALP) and alizarin red staining, and reverse transcription‑quantitative PCR analysis of the expression of osteogenesis‑associated genes were performed to determine the effects of KR‑12‑a6 on the osteogenic differentiation of hBMSCs.

Disruption of the association between drug transporter and actin cytoskeleton abolishes drug resistance in hypertrophic scar.

Hypertrophic scar is characterized by the overgrowth of fibroblasts and often considered as a kind of benign skin tumor, thus chemotherapeutic drugs have been used to treat scars. In view of the similarity, this study aims to investigate whether drug resistance in cancer that contributes to the failure of chemotherapy also exists in hypertrophic scar, and what is the possible mechanism. Fibroblasts derived from hypertrophic scar and normal skin tissues were first compared for their resistance to verapamil and etoposide phosphate.

Loss of CAR promotes migration and proliferation of HaCaT cells, and accelerates wound healing in rats via Src-p38 MAPK pathway.

The coxsackie and adenovirus receptor (CAR) is a cell adhesion molecule mostly localized to cell-cell contacts in epithelial and endothelial cells. CAR is known to regulate tumor progression, however, its physiological role in keratinocyte migration and proliferation, two essential steps in re-epithelialization during wound healing, has less been investigated. Here we showed that CAR was predominantly expressed in the epidermis of human skin, CAR knockdown by RNAi significantly accelerated HaCaT cell migration and proliferation.