ading for group C and group A was not statistically significant. The relationship of morphological grading to DSCA was statistically significant for all three groups. CONCLUSION  DSCA, morphological grading, and sedimentation sign are good to excellent radiologic indicators differentiating patients with simple back pain from those with lumbar spinal stenosis. Clinically, ODI is an excellent indicator of the severity of stenosis. But ODI statistically has no significant correlation to any of these radiologic parameters. Georg Thieme Verlag KG Stuttgart · New York.Aquaporin 4 (AQP4), a water-specific channel protein locating on the astrocyte membrane, has been found to be antagonist, agonist and undergone closely related to epilepsy.  https://www.selleckchem.com/products/actinomycin-d.html  Our previous study showed that inhibition of an N-methyl-D-aspartate receptor (NMDAR) subunit NR2A can suppress epileptic seizures, suggesting that AQP4 is potentially involved in NR2A-mediated epilepsy treatment. In this study, we aimed to explore the relevance of AQP4 in NR2A-mediated seizures treatment in pentylenetetrazol (PTZ)-induced rat models. We performed electroencephalogram (EEG) recording and examined AQP4 expression at mRNA and protein levels, and the downstream molecules of AQP4 as well. It showed that AQP4 expression was increased after the induction of seizures. Lateral ventricle pretreatment of NR2A inhibitor could mitigate the PTZ-induced seizures severity and counterbalance the increase of AQP4 expression. In contrast, NR2A activator that resulted in seizures aggravation could further augment the seizure-related elevations of AQP4 expression. Pharmacological inhibition of AQP4 alone could also suppress the PTZ-induced seizure activities, with decreased expressions of NF-κB p65, interleukin (IL)-1, IL-6, and tumor necrosis factor (TNF)-α in the brain. The results indicated that increased expression of AQP4 might be an important mechanism involved in NR2A of NMDAR-mediated treatment for epileptic seizures, enlightening a potentially new target for seizures treatment.OBJECTIVE Pharmacological evaluation of the mu-opioid receptor (MOR) agonist properties of NKTR-181 in rodent models. METHODS Graded noxious stimulus intensities were used in rats to establish the antinociceptive potency and efficacy of NKTR-181 relative to morphine, fentanyl, and oxycodone. Characteristics of MOR agonist actions, as measured by antinociceptive tolerance and cross-tolerance, as well as opioid-induced hyperalgesia (OIH) and naloxone-precipitated withdrawal in NKTR-181- and morphine-dependent in mice, were compared. RESULTS NKTR-181 showed dose- and time-related antinociception with similar maximal effects to morphine in the rat and mouse hot-water tail-flick test. No sex or species differences were observed in NKTR-181 or morphine antinociception. Rats treated with NKTR-181 and morphine exhibited decreases in both potency and maximal efficacy as nociceptive stimulus intensity was increased from a water temperature of 50 °C to 54 °C. Evaluation of antinociception at a high stimulus intensity revealed that oxycodone and fentanyl exhibited greater efficacy than either NKTR-181 or morphine. The relative potency difference between NKTR-181 and morphine across all tail-flick studies was determined to be 7.6-fold (90% confidence interval, 2.6, 21.5). The peak antinociceptive effect of NKTR-181 was delayed compared to that of the other opioids and cumulative drug effects were not observed. Repeated treatment with escalating, approximately equi-analgesic doses of NKTR-181 or morphine, produced antinociceptive tolerance and cross-tolerance. Under these pharmacological conditions, OIH and naloxone-precipitated physical dependence were similar for NKTR-181 and morphine. CONCLUSIONS NKTR-181 had a slower onset, but similar efficacy, to morphine in the models studied supporting reduced abuse potential while maintaining analgesic effect in comparison with current opioids.Systemic inflammation is associated with poor outcome after stroke. Glucocorticoids (GCs) play a fundamental role in limiting inflammation. The aim of this study was to explore the associations between GC sensitivity, systemic inflammation, and outcome after ischemic stroke. The study population compised 246 ischemic stroke patients (median age 69.0 years; 41.1% female). To assess GC sensitivity, we incubated venous blood samples that were obtained at day 3 after stroke with lipopolysaccharide (10 ng/mL) and dexamethasone (10-6 mol/L). We defined the GC sensitivity index as the ratio of tumor necrosis factor α (TNFα) released after blood stimulation with lipopolysaccharide and dexamethasone to the amount of TNFα released after blood stimulation with lipopolysaccharide alone. A higher index indicates higher GC resistance. The patients with poor functional outcome had a higher GC sensitivity index than those with good outcome (median 16.1% vs. 13.5%, P  less then  0.01). In a logistic regression analysis adjusted for age, stroke severity, pneumonia, leukocyte count, plasma interleukin-6, and TNFα release ex vivo, a higher GC sensitivity index was associated with a higher risk of poor outcome after stroke (OR 2.32, 95% CI 1.21-4.45, P = 0.01). In conclusion, GC resistance is associated with poor functional outcome after stroke.While light is the basic element for inducing vision and modulating circadian rhythms, excessive light has been reported to have a negative effect on the survival of various types of retinal cells. Among them photoreceptors and retinal pigment epithelial (RPE) cells degeneration after light exposure is widely observed, but light-induced retinal ganglion cell (RGC) damage achieves relatively little attention. The purpose of this article is to summarize the experimental evidence for the possible negative effects of excessive light on RGCs. By searching the database, twenty-six related articles have been included. Taken together, excessive light may insult RGCs through the three main ways (i) directly action on RGC mitochondria, as well as DNA, resulting in an upregulation of reactive oxygen species (ROS) and subsequently caspase-dependent or -independent cell death; (ii) mediation in gliotransmitters or relevant receptors of retinal glial cells; and (iii) a secondary event to photoreceptors and RPE cells degeneration and subsequent retinal remodeling.