Purpose: Adenosine A_2A receptor agonist polydeoxyribonucleotide (PDRN) possesses an anti-inflammatory effect and suppress apoptotic cell death in several disorders. In this current study, the effect of PDRN on inflammation and apoptosis in rats with Achilles tendon injury was investigated.Methods: von Frey filament test and plantar test were conducted for the determination of pain threshold. Analysis of histological alterations was conducted by hematoxylin and eosin staining. Immunohistochemistry for cleaved caspase-3-positive cells and cleaved caspase-9-positive cells was done. Enzyme-linked immunoassay was used to detect the concentrations of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and cyclic adenosine-3’,5’-monophosphate (cAMP). Western blot was conducted to detect the protein levels of cAMP response element-binding protein (CREB), protein kinase A (PKA), Bcl-2-associated X (Bax), and B-cell lymphoma 2 (Bcl-2).Results: PDRN treatment relieved mechanical allodynia and alleviated thermal hyperalgesia after Achilles tendon injury. TNF-α and IL-6 concentrations were decreased by PDRN application. PDRN injection significantly enhanced cAMP concentration and phosphorylated CREB versus CREB ratio, showing cAMP-PKA-CREB pathway was activated by PDRN application. PDRN treatment inhibited percentages of cleaved caspase-3-positive cells and caspase-9-posiive cells and the suppressed Bax versus Bcl-2 ratio in Achilles tendon injury rats.Conclusions: PDRN is probably believed to have a good effect on pain and inflammation in the urogenital organs. PDRN may be used as a new treatment for Achilles tendon injury.

The selective α2-adrenergic receptor agonist dexmedetomidine acts as an analgesic, sedative, and anesthetic adjuvant. The most common consequence of sleep deprivation is memory impairment. We investigated whether dexmedetomidine can counteract memory impairment caused by sleep deprivation and suppress the production of inflammatory factors. For inducing sleep deprivation, adult male mice were placed inside a water cage containing 15 platforms immersed in water up to 1 cm for 7 days. One day after sleep deprivation, dexmedetomidine at the respective dosage (5, 10, and 20 μg/kg) and α 2-adrenoceptor antagonist atipamezole (250 μg/kg) were intraperitoneally injected into the mice, once per day for six days. The step-down avoidance task and the Morris water maze test were performed. Western blot analysis was performed to determine the levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-6, brain-derived neurotrophic factor (BDNF), tyrosine kinase B (TrkB), nuclear transcription factor-κB (NF-κB), inhibitor of κBα (IκBα), and ionized calcium binding adapter molecule I (Iba-1) in the hippocampus. Immunohistochemistry was performed for the determination of Ki-67 and glial fibrillary acidic protein (GFAP) expression in the hippocampal dentate gyrus. Dexmedetomidine ameliorated sleep deprivation-induced deterioration of short-term memory and spatial learning ability. Dexmedetomidine inhibited production of inflammatory mediators caused by sleep deprivation. Dexmedetomidine also prevented the decrease in BDNF, TrkB expression, and cell proliferation induced by sleep deprivation. Dexmedetomidine could be used to counteract the neuropathological effects of sleep deprivation.

Preoperative hypoalbuminemia from malnutrition is associated with increased morbidity and mortality after geriatric hip fracture surgery. However, little is known regarding the correlation between postoperative hypoalbuminemia and mortality. This study aimed to evaluate whether postoperative hypoalbuminemia could predict 1-year mortality after intertrochanteric femoral fracture surgery in elderly patients. The medical records of 263 geriatric patients (age ≥65 years) who underwent intertrochanteric femoral fracture surgery between January 2013 and January 2016 in a single hospital were reviewed retrospectively. The patients were allocated to 2 groups based on lowest serum albumin levels within 2 postoperative days (≥3.0 g/dL [group 1, n = 46] and <3.0 g/dL [group 2, n = 217]. Data between the non-survival and survival groups were compared. Multivariable logistic regression analysis was conducted to identify the independent predictor for 1-year mortality. The 1-year mortality rate was 16.3% after intertrochanteric femoral fracture surgery. Multivariable logistic regression analysis revealed that postoperative hypoalbuminemia was significantly associated with 1-year mortality (adjusted odds ratio, 8.03; 95% confidence interval, 1.37-47.09; P = .021). The non-survival group showed a significantly increased incidence of postoperative hypoalbuminemia (95.4% vs 80.0%, P = .015) and intensive care unit admission (11.6% vs 2.7%, P = .020), older age (82.5 ± 5.8 years vs 80.0 ± 7.2 years, P = .032), lower body mass index (20.1 ± 3.2 kg/m 2 vs 22.4 ± 3.8 kg/m 2 , P < .001), and increased amount of transfusion of perioperative red blood cells (1.79 ± 1.47 units vs 1.43 ± 2.08 units, P = .032), compared to the survival group. This study demonstrated that postoperative hypoalbuminemia is a potent predictor of 1-year mortality in geriatric patients undergoing intertrochanteric femoral fracture surgery. Therefore, exogenous albumin administration can be considered to improve postoperative outcomes and reduce the risk of mortality after surgery for geriatric hip fracture.

Background Lumbar spinal stenosis is a common degenerative disease that causes low back and lower‐extremity pain that increases with age. The treatment of lumbar spinal stenosis is either conservative or surgical. ESI is a commonly performed conservative treatment, but evidence of its effectiveness in lumbar spinal stenosis is limited. Case series We encountered the three patients with back pain and claudication due to lumbar spinal stenosis, which could not be controlled by conservative therapy including ESIs. Trimacinolone acetonide was injected into the patients' ligamentum flavum. All patients experienced dramatic improvement in their symptoms. Conclusions Trimacinolone acetonide injection into the ligamentum flavum may be effective for lumbar spinal stenosis that does not improve with ESIs.