Autologous chondrocyte implantation (ACI) is a promising treatment for articular cartilage degeneration and injury; however, it requires a large number of human hyaline chondrocytes, which often undergo dedifferentiation during in vitro expansion. This study aimed to investigate the effect of suramin on chondrocyte differentiation and its underlying mechanism. Porcine chondrocytes were treated with vehicle or various doses of suramin. The expression of collagen, type II, alpha 1 (COL2A1), aggrecan (ACAN); COL1A1; COL10A1; SRY-box transcription factor 9 (SOX9); nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX); interleukin (IL)-1β; tumour necrosis factor alpha (TNFα); IL-8; and matrix metallopeptidase 13 (MMP-13) in chondrocytes at both messenger RNA (mRNA) and protein levels was determined by quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) and western blot. In addition, the supplementation of suramin to redifferentiation medium for the culture of expanded chondrocytes in 3D pellets was evaluated. Glycosaminoglycan (GAG) and collagen production were evaluated by biochemical analyses and immunofluorescence, as well as by immunohistochemistry. The expression of reactive oxygen species (ROS) and NOX activity were assessed by luciferase reporter gene assay, immunofluorescence analysis, and flow cytometry. Mutagenesis analysis, Alcian blue staining, reverse transcriptase polymerase chain reaction (RT-PCR), and western blot assay were used to determine whether p67phox was involved in suramin-enhanced chondrocyte phenotype maintenance.Aims
Methods
Interleukin (IL)-1β is one of the major pathogenic regulators during the pathological development of intervertebral disc degeneration (IDD). However, effective treatment options for IDD are limited. Suramin is used to treat African sleeping sickness. This study aimed to investigate the pharmacological effects of suramin on mitigating IDD and to characterize the underlying mechanism. Porcine nucleus pulposus (NP) cells were treated with vehicle, 10 ng/ml IL-1β, 10 μM suramin, or 10 μM suramin plus IL-1β. The expression levels of catabolic and anabolic proteins, proinflammatory cytokines, mitogen-activated protein kinase (MAPK), and nuclear factor (NF)-κB-related signalling molecules were assessed by Western blotting, quantitative real-time polymerase chain reaction (qRT-PCR), and immunofluorescence analysis. Flow cytometry was applied to detect apoptotic cells. The ex vivo effects of suramin were examined using IDD organ culture and differentiation was analyzed by Safranin O-Fast green and Alcian blue staining.Aims
Methods
Proliferation, migration, and differentiation of anterior cruciate ligament (ACL) remnant and surrounding cells are fundamental processes for ACL reconstruction; however, the interaction between ACL remnant and surrounding cells is unclear. We hypothesized that ACL remnant cells preserve the capability to regulate the surrounding cells’ activity, collagen gene expression, and tenogenic differentiation. Moreover, extracorporeal shock wave (ESW) would not only promote activity of ACL remnant cells, but also enhance their paracrine regulation of surrounding cells. Cell viability, proliferation, migration, and expression levels of Collagen-I (COL-I) A1, transforming growth factor beta (TGF-β), and vascular endothelial growth factor (VEGF) were compared between ACL remnant cells untreated and treated with ESW (0.15 mJ/mm2, 1,000 impulses, 4 Hz). To evaluate the subsequent effects on the surrounding cells, bone marrow stromal cells (BMSCs)’ viability, proliferation, migration, and levels of Type I Collagen, Type III Collagen, and tenogenic gene (Aims
Methods
We evaluated the morphological changes to the ulnar nerve of both elbows in the cubital tunnel by sonography in a total of 237 children, of whom 117 were aged between six and seven years, 66 between eight and nine years, and 54 between ten and 11 years. We first scanned longitudinally in the extended elbow and then transversely at the medial epicondyle with the elbow extended to 0°. We repeated the scans with the elbow flexed at 45°, 90°, and 120°. There were no significant differences in the area of the ulnar nerve, but the diameter increased as the elbow moved from extension to flexion in all groups. More importantly, the ulnar nerve was subluxated anteriorly on to the medial epicondyle by 1.5% to 1.9% in extended elbows, by 5.9% to 7.9% in those flexed to 45°, by 40.0% to 44% in those flexed to 90°, and by 57.4% to 58.1% in those flexed to 120°, depending on the age group. Sonography clearly and accurately showed the ulnar nerve and was useful for localising the nerve before placing a medial pin. Because the ulnar nerve may translate anteriorly onto the medial epicondyle when the elbow is flexed to 90° or more, it should never be overlooked during percutaneous medial pinning.
The lumbar or sacral root compression is frequently associated with degenerative spinal diseases. It may be caused by the hypertrophic facets, hypertrophic ligamentum flavum, or protruding disc. Canal stenosis, epidural hematoma, the cyst of pseudo-joint from degenerative or lytic-type spondylolisthesis, or tumors are less common. We present one unusual case with the severe progressive symptom of bilateral S2-4 root compression. The 80-year-old active male suffered the intermittent claudication for 4 months and got the worse symptom including bilateral painful buttocks in recent one month. The bilateral radiation pain cannot be changed at any position and taking a rest. Plain x-ray showed the degenerative spondylolisthesis over L4-5 level. The magnetic resonance imaging showed the cyst-like mass indented the dura posteriorly. During the operation, one huge psudo-joint capsule created from the interspinous ligament compressed the dorsal side of the cauda equina. We performed the posterior decompression and removal of the pseudo-joint capsule and ligamentum flavum with posterolateral fusion. The patient was completely resolved from all the symptoms after surgery. Therefore we present the unusual case and discuss the differentiation from synovial or ganglion cysts of the spine.
