Background: The development of new treatment strategies to improve peripheral nerve repair after injury, especially those that accelerate axonal nerve regeneration, is very important. The aim of this study is to elucidate the molecular mechanisms of how bone marrow stromal cell (BMSC)-derived exosomes (EXOs) participate in peripheral nerve regeneration and whether the regenerative effect of EXOs is correlated with dose. Method: BMSCs were transfected with or without an siRNA targeting Ago2 (SiAgo2). EXOs extracted from the BMSCs were administered to dorsal root ganglion (DRG) neurons in vitro. After 48 h of culture, the neurite length was measured. Moreover, EXOs at four different doses were injected into the gastrocnemius muscles of rats with sciatic nerve crush injury. The sciatic nerve functional index (SFI) and latency of thermal pain (LTP) of the hind leg sciatic nerve were measured before the operation and at 7, 14, 21, and 28 days after the operation. Then, the number and diameter of the regenerated fibers in the injured distal sciatic nerve were quantified. Seven genes associated with nerve regeneration were investigated by qRT-PCR in DRG neurons extracted from rats 7 days after the sciatic nerve crush. Results: We showed that after 48 h of culture, the mean number of neurites and the length of cultured DRG neurons in the SiAgo2-BMSC-EXO and SiAgo2-BMSC groups were smaller than that in the untreated and siRNA control groups. The average number and diameter of regenerated axons, LTP, and SFI in the group with 0.9 × 10 10 particles/ml EXOs were better than those in other groups, while the group that received a minimum EXO dose (0.4 × 10 10 particles/ml) was not significantly different from the PBS group. The expression of PMP22, VEGFA, NGFr, and S100b in DRGs from the EXO-treated group was significantly higher than that in the PBS control group. No significant difference was observed in the expression of HGF and Akt1 among the groups.

Dog owners are usually in close contact with dogs. Whether dogs can affect the gut microbiota of elderly dog owners is worth studying. Data from 54 elderly (over 65 years of age) dog owners were screened from the American Gut Project. Owning a dog did not affect the α-diversity of the gut microbiota of the dog owner. Dog ownership significantly modulated the composition of the gut microbiota of the dog owner. The abundance of Actinobacteria was significantly increased. The abundances of Bifidobacteriaceae and Ruminococcaceae were significantly increased, while the abundance of Moracellaceae was significantly suppressed. In general, dog ownership can regulate the composition of gut microbiota and has a more significant effect on elderly males.

This study aimed to investigate the effect of upregulated peroxisome proliferator-activated receptor-gamma (PPAR-c) activity on cyclooxygenase 2 (COX-2) expression and N-methyl-Daspartic acid (NMDA)-induced excitatory neurotoxicity in primary cultured cortical neurons. Rat cortical neurons were cultured for 8 days in vitro, and divided into control, NMDA, MK-801 (selective NMDA antagonist), rosiglitazone (ROSI, PPAR-c agonist), GW9662 (PPAR-c antagonist), NS398 (selective COX-2 antagonist) and NS398 þ ROSI groups. Two hours after treatment in each group, cell viability, intracellular Ca 2þ concentrations, PPAR-c and COX-2 protein expression were detected by CCK-8 assay, flow cytometry and western blot assay, respectively. The results showed that compared with the control group, 100 lmol/L of NMDA significantly decreased the neuronal cell viability, increased Ca 2þ concentrations, which also increased the COX-2 protein expression and decreased PPAR-c expression in neurons. Compared with the NMDA group, the cell viability was increased, Ca 2þ concentrations and COX-2 protein expression were significantly decreased, PPAR-c expression was significantly increased in the MK-801, ROSI, NS398 and ROSI þ NS398 groups (both P < 0.01). This finding suggested that upregulation of PPAR-c activity can inhibit COX-2 expression, decrease Ca 2þ concentrations in primary cultured cortical neurons, and protect neurons against NMDA-induced excitatory neurotoxicity.

Rationale:Myasthenia gravis (MG) is the most common cause of acquired neuromuscular junction disorder. Thymectomy has been established as an effective therapy for MG, as it attenuates the natural course of the disease and may result in complete remission.Patient concerns:We report the case of a 22-year-old female with a 6-year history of MG presented with bilateral ptosis, diplopia, and intermittent dysphagia. She denied shortness of breath, dysarthria, and fatigue.Diagnoses:She had been diagnosed with MG 6 years previously at the Neurology Department of our hospital. A computed tomography (CT) scan revealed thymic hyperplasiaInterventions:She was treated with modified unilateral VATET that minimized incision size.Outcomes:Unilateral VATET was performed using two 5-mm incisions to minimize pressure on intercostal soft tissues/nerves and reduce postoperative pain.Lessons:The lesson learnt from this case report is that this modified VATET method could be a useful approach to the management of non-thymomatous MG. The ability to achieve complete dissection with good cosmetic results may lead to wider acceptance of this technique by patients with MG and their neurologists for earlier thymectomy and improved outcomes. Additional studies are needed to determine the superiority of this approach to established methods.