Apocynin Improves Insulin Resistance through Suppressing Inflammation in High-Fat Diet-Induced Obese Mice

We investigated the effects of apocynin on high-fat diet- (HFD-) induced insulin resistance in C57BL/6 mice. After 12 weeks of HFD, the mice that exhibited insulin resistance then received 5 weeks of apocynin (2.4 g/L, in water). Following apocynin treatment, fasting glucose, insulin, and glucose tolerance test showed significant improvement in insulin sensitivity in HFD-fed mice. We demonstrated that serum levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and leptin were remarkably reduced with apocynin treatment. We also found that mRNA expression of TNF-α, IL-6, and monocyte chemoattractant protein-1 (MCP-1) in the liver and mRNA expression of TNF-α, IL-6, MCP-1, and leptin in adipose tissue were suppressed by apocynin. Furthermore, the activity of transcription factor NF-κB in the liver was significantly suppressed with apocynin treatment. These results suggest that apocynin may reduce inflammatory factors in the blood, liver, and adipose tissue, resulting in amelioration of insulin resistance in HFD-fed mice

Symmetries and Lie algebra of the differential-difference Kadomstev-Petviashvili hierarchy

By introducing suitable non-isospectral flows we construct two sets of symmetries for the isospectral differential-difference Kadomstev-Petviashvili hierarchy. The symmetries form an infinite dimensional Lie algebra.Comment: 9 page

Coseeded Schwann cells myelinate neurites from differentiated neural stem cells in neurotrophin-3-loaded PLGA carriers

Biomaterials and neurotrophic factors represent promising guidance for neural repair. In this study, we combined poly-(lactic acid-co-glycolic acid) (PLGA) conduits and neurotrophin-3 (NT-3) to generate NT-3-loaded PLGA carriers in vitro. Bioactive NT-3 was released stably and constantly from PLGA conduits for up to 4 weeks. Neural stem cells (NSCs) and Schwann cells (SCs) were coseeded into an NT-releasing scaffold system and cultured for 14 days. Immunoreactivity against Map2 showed that most of the grafted cells (>80%) were differentiated toward neurons. Double-immunostaining for synaptogenesis and myelination revealed the formation of synaptic structures and myelin sheaths in the coculture, which was also observed under electron microscope. Furthermore, under depolarizing conditions, these synapses were excitable and capable of releasing synaptic vesicles labeled with FM1-43 or FM4-64. Taken together, coseeding NSCs and SCs into NT-3-loaded PLGA carriers increased the differentiation of NSCs into neurons, developed synaptic connections, exhibited synaptic activities, and myelination of neurites by the accompanying SCs. These results provide an experimental basis that supports transplantation of functional neural construction in spinal cord injury

Therapeutic Effect of Large Channel Endoscopic Decompression in Lumbar Spinal Stenosis

Background: Percutaneous endoscopic decompression (PED) is a minimally invasive surgical technique that is now used for not only disc herniation but also lumbar spinal stenosis (LSS). However, few studies have reported endoscopic surgery for LSS. Therefore, we conducted this study to evaluate the outcomes and safety of large channel endoscopic decompression.Methods: Forty-one patients diagnosed with LSS who underwent PED surgery were included in the study. The estimated blood loss, operative time, length of hospital stay, hospital costs, reoperations, complications, visual analogue scale (VAS) score, Oswestry Disability Index (ODI) score, Japanese Orthopaedic Association (JOA) score and SF-36 physical-component summary scores were assessed. Preoperative and postoperative continuous data were compared through paired-samples t-tests. The significance level for all analyses was defined as p < 0.05.Results: A total of 41 consecutive patients underwent PED, including 21 (51.2%) males and 20 (48.8%) females. The VAS and ODI scores decreased from preoperatively to postoperatively, but the JOA and SF-36 physical component summary scores significantly increased. The VAS (lumbar) score decreased from 5.05 ± 2.33 to 0.45 ± 0.71 (P = 0.000); the VAS (leg) score decreased from 5.51 ± 2.82 to 0.53 ± 0.72 (P = 0.000); the ODI score decreased from 52.80 ± 20.41 to 4.84 ± 3.98 (P = 0.000), and the JOA score increased from 11.73 ± 4.99 to 25.32 ± 2.12 (P = 0.000). Only 1 patient experienced an intraoperative complication (2.4%; dural tear), and 1 patient required reoperation (2.4%).Conclusions: Surgical treatment for LSS is to sufficiently decompress and minimize the trauma and complications caused by surgery. This study did not reveal any obvious shortcomings of PED and suggested PED is a safe and effective treatment for LSS

Antigen retrieval pre-treatment causes a different expression pattern of Cav3.2 in rat and mouse spinal dorsal horn

Cav3 channels consist of three isoforms, Cav3.1 (α1G), Cav3.2 (α1H), and Cav3.3 (α1I), which produce low-threshold spikes that trigger burst firings in nociceptive neurons of the spinal dorsal horn (SDH) and dorsal root ganglion (DRG). Although Cav3.2 plays a crucial role in pathological pain, its distribution in SDH still remains controversial. One study showed that Cav3.2 is ubiquitously expressed in neurons, but another study implied that Cav3.2 is expressed restricted to astrocytes. To unravel these discrepancies, we used methods of immunohistochemistry either with or without antigen retrieval (AR) pre-treatment to detect Cav3 in SDH and DRG from both rats and mice. Moreover, Cav3.2 mRNA was detected in mice SDH using in situ hybridization. We found that the expression pattern of Cav3.2 but not Cav3.1 and Cav3.3 in SDH were largely different with or without AR pre-treatment, which showed a neuron-like and an astrocyte-like appearance, respectively. Double staining further demonstrated that Cav3.2 was mainly co-stained with the neuronal marker NeuN in the presence of AR but was with glial fibrillary acidic protein (GFAP, marker for astrocytes) in the absence of AR pre-treatment. Importantly, Cav3.2 mRNA was mainly co-localized with Cav3.2 but not GFAP. Together, our findings indicate that AR pre-treatment or not impacts the expression pattern of Cav3.2, which may make a significant contribution to the future study of Cav3.2 in SDH