The effect of Ding's screws and tension band wiring for treatment of olecranon fractures: a biomechanical study.

Although tension band wiring (TBW) is popular and recommended by the AO group, the high rate of complications such as skin irritation and migration of the K-wires cannot be ignored. Ding's screw tension band wiring (DSTBW) is a new TBW technique that has shown positive results in the treatment of other fracture types. The objective of this study was to evaluate the stability of DSTBW in the treatment of olecranon fractures by biomechanical testing.

HIF-1α regulates DcR3 to promote the development of endometriosis.

Objective: The aim of this study was to investigate the expression and clinical significance of HIF-1α and DcR3 in endometriosis by analysing clinical case data. Tissue samples were collected for tissue chip analysis and staining, and human endometrial stromal cells were isolated and cultured for cell experiments. Additionally, experiments were conducted on collected peritoneal fluid to explore the association and role of HIF-1α and DcR3 in endometriosis.

A novel technique of a new cannulated screw for treatment of inferior pole patellar fractures: a finite element study.

Objective: We invented a new cannulated screw with holes on the tail, which called Ding's screw. The goal of this study was to evaluate the biomechanical outcomes of this new screw with tension band wiring for the treatment of inferior pole patellar fractures in a finite element model.

Methods: We conducted a finite element biomechanical study using two fixation methods: Ding's screw and tension band wiring (DSTBW) and cannulated screws and tension band wiring (CSTBW).

Identification and validation of FPR1, FPR2, IL17RA and TLR7 as immunogenic cell death related genes in osteoarthritis.

Immunogenic cell death (ICDs) has gained increasing attention for its significant clinical efficacy in various diseases. Similarly, more and more attention has been paid in the role of immune factors in the pathological process of osteoarthritis (OA). The objective of this study is to reveal the relationship between ICD-related genes and the process of OA at the gene level through bioinformatics analysis.

The effect of ding's screw and tension band wiring for treatment of olecranon fractures: a finite element study.

Background: Tension band wiring (TBW) is a common surgical intervention for olecranon fractures. However, high rate of complications such as loss of reduction, skin irritation, and migration of the K-wires were reported up to 80%. Ding's screw tension band wiring (DSTBW) is a new TBW technique that has shown positive results in the treatment of other fracture types.

Minimally invasive technique of monoaxial percutaneous screws and instrumentational maneuvers in thoracolumbar and lumbar fractures.

Objectives: Percutaneous pedicle screw fixation (PPSF) has been a common surgery for treating thoracolumbar and lumbar fractures. Many studies have reported PPSF is associated with poor reduction. We present a reliable method by using short-segment monoaxial percutaneous screws and instrumentational maneuvers to reduce the spine.

MMP2 promotes osteoblast differentiation and calcification of muscle-derived mesenchymal stem cells by interaction with miR-29b-3p.

Matrix metalloproteinase 2 (MMP2) was previously reported to play important role in the process of stem cell migration and various differentiation behaviors of muscle-derived mesenchymal stem cells (M-MSCs). However, its role and regulatory mechanism in the osteoblast differentiation and calcification of M-MSCs remain unclear. In the current study, we found that MMP2 could facilitate the osteoblast differentiation and calcification of muscle-derived mesenchymal stem cells by up-regulating the expression of some typical osteogenic differentiation phenotype markers, such as runt-related transcription factor 2 (Runx2), alkaline phosphatase (ALP), and osteocalcin (OCN).

Platelet-rich plasma enhances the repair capacity of muscle-derived mesenchymal stem cells to large humeral bone defect in rabbits.

Mesenchymal stem cell-based therapy is a highly attractive strategy that promotes bone tissue regeneration. The aim of the present study was to evaluate the combination effect of muscle-derived mesenchymal stem cells (M-MSCs) and platelet-rich plasma (PRP) on bone repair capacity in rabbits with large humeral bone defect. Precise cylindrical bone defects of 10 mm diameter and 5 mm depth were established in rabbit humeral bones, which were unable to be repaired under natural conditions.

MiR-135-5p promotes osteoblast differentiation by targeting HIF1AN in MC3T3-E1 cells.

Background: MicroRNAs (miRNAs or miRs) serve crucial roles in the progression of osteoporosis. This study investigated the role and specific molecular mechanism of miR-135-5p in regulating osteoblast differentiation and calcification.

Methods: Bone morphogenetic protein 2 (BMP2) was employed to interfere with the differentiation of MC3T3-E1.

Enhancing the Astrocytic Clearance of Extracellular α-Synuclein Aggregates by Ginkgolides Attenuates Neural Cell Injury.

The accumulation of aggregated forms of the α-Synuclein (α-Syn) is associated with the pathogenesis of Parkinson's disease (PD), and the efficient clearance of aggregated α-Syn represents a potential approach in PD therapy. Astrocytes are the most numerous glia cells in the brain and play an essential role in supporting brain functions in PD state. In the present study, we demonstrated that cultured primary astrocytes engulfed and degraded extracellular aggregated recombinant human α-Syn.

Ginkgolide B and bilobalide ameliorate neural cell apoptosis in α-synuclein aggregates.

The accumulation of aggregated forms of the α-Synuclein (α-Syn) is associated with the pathogenesis of Parkinson's disease (PD), a chronic progressive neurodegenerative disorder. Extensive evidences have shown the promising effects of Ginkgo biloba consumption on motor activity after PD. However, the mechanisms underline the α-Syn-induced cell damage and whether ginkgolides exert neuroprotection against this injury are unclear.

Atp13a2 Deficiency Aggravates Astrocyte-Mediated Neuroinflammation via NLRP3 Inflammasome Activation.

Aim: Atp13a2 (Park9) gene encodes a transmembrane lysosomal P5-type ATPase (ATP13A2), and its missense or truncation mutations leads to lysosomal dysfunction and consequently results in neuronal death in the pathogenesis of Parkinson's disease (PD). Nevertheless, the roles of ATP13A2 in the biological features of astrocytes, especially in the regulation of PD-related neuroinflammation, have not been investigated.

Methods: We cultured primary neurons and astrocytes from mouse midbrain to investigate the mechanisms for astrocyte ATP13A2-regulated lysosomal function and neuroinflammation following 1-methyl-4-phenylpyridinium (MPP(+) ) treatment.