The aim of this study was to investigate the neuroprotective effects of ketamine during acute spinal cord injury in rats. Sprague Dawley (SD) rats (N = 70) were randomly divided into three groups: sham-operated (N = 10), control (N = 30), and treatment (N = 30) groups. The moderate spinal cord injury model was established. After injury, the sham-operated group received no drug, the treatment group received intraperitoneal ketamine injections, and the control group received intraperitoneal normal saline injections.
Tumor necrosis factor-α
Recent data have indicated that inflammation may have an important correlation with obstructive sleep apnea (OSA). Studies have indicated a relationship between OSA and TNF-α gene polymorphisms. Zinc finger protein 36 (ZFP36) regulates TNF-α mRNAs. However, ZFP36 gene polymorphisms have not been investigated in OSA. Therefore, we conducted the present case-control study to assess whether variances in ZFP36 gene polymorphisms account for differences in TNF-α levels in patients with moderate-to-severe OSA.
The aim of this study was to explore the mRNA levels of tumor necrosis factor-α (TNF-α), vessel endothelial growth factor (VEGF), and matrix metalloproteinase-3 (MMP-3) in synovial tissues in ankylosing spondylitis (AS), and to analyze the functions of these proteins in the differentiation of AS synovial tissue fibroblasts into osteoblasts (OB) and osteoclasts. Synovial tissue samples from 22 AS patients and 22 normal individuals were collected.
The objective was to study peroxisome proliferator-activated receptor gamma (PPARγ) agonist pioglitazone regulation effect and its mechanism of expression of cytokines on acute gouty arthritis synovial in rats. Rats with unilateral ankle were injected with artificial monosodium urate (MSU) crystals to make the acute gouty arthritis model.
The dried roots of the plant Acanthopanax senticosus (AS) are used in traditional Oriental medicine and reportedly possess anti-inflammatory properties in vitro. However, whether AS has the same anti-inflammatory effect in vivo and the underlying mechanisms of this action remain unknown.
There is structural damage to myelin and secondary immune injury in the development of delayed encephalopathy after acute carbon monoxide (CO) poisoning (DEACMP). In order to assess the role of genetic factors in this mechanism, we studied the association between tumor necrosis factor-α308 (TNF-α308) and myelin basic protein (MBP) 5ꞌ-side tetranucleotide repetitive sequence (TGGA) n gene polymorphism and DEACMP.