Traumatic wounds inflict small- and large-fiber sensory nerve damage, causing neuropathic pain in scar tissue, thus impairing patients' quality of life and leading to the development of psychological disorders. Autologous fat grafting has been clinically shown to improve scar quality, but few studies have explored the effects of this technique on pain. The purpose of this study was to assess the effect of fat grafting on treating neuropathic scar pain. From February 2008 to January 2013, 13 patients who were identified using the Douleur Neuropathique 4 Questions (scores>4/10) were enrolled in this study. The Visual Analog Scale (VAS) and Neuropathic Pain Symptom Inventory (NPSI) were used to evaluate pain preoperatively and 1 week, 4 weeks, and 24 weeks postoperatively. The mechanism of trauma, scar location and size, duration of allodynia, fat graft volume, pharmacologic therapy duration, and total follow-up time were recorded. Thirteen patients experiencing neuropathic pain were enrolled in this study. The mean±SD age was 33.08±16.35 years. The mean duration of pain was 4.29±2.85 months. The mean VAS score before treatment was 7.54±1.05. The mean VAS scores decreased by 4.38±1.66 after 1 week of treatment (P=0.009), 5.38±2.06 after 4 weeks of treatment, and 5.62±2.18 after 24 weeks of treatment. The mean NPSI scores were 49.38±13.25 before treatment, 25±14.4 after 1 week of treatment (P=0.004), 21±17.78 after 4 weeks of treatment, and 14.62±16.88 after 24 weeks of treatment. The 13 patients followed a mean of 24 weeks; 10 (77%) of the patients had improvement of 5 or greater on the VAS score. The mean follow-up period was 19.3±12.26 months (range, 6-38 months). No surgical complications were noted in this series. In our study, both VAS and NPSI scores decreased significantly, revealing that the autologous fat grafting can alleviate neuropathic scar pain 1 week after operation and in the long term.

Adipose-derived stem cells (ADSCs) transplant has been reported to be a potential treatment for burn wounds. However, the effects of autogenicity and allogenicity of ADSCs on burn wound healing have not been investigated and the method for using ADSCs still needs to be established. This study compared the healing effects of autologous and allogenic ADSCs and determined an optimal method of using ADSCs to treat acute burn wounds. Experiments were performed in 20 male Wistar rats (weight, 176–250 g; age, 6–7 weeks). Two identical full-thickness burn wounds (radius, 4 mm) were created in each rat. ADSCs harvested from inguinal area and characterized by their high multipotency were injected into burn wounds in the original donor rats (autologous ADSCs group) or in other rats (allogenic ADSCs group). The injection site was either the wound center or the four corners 0.5 cm from the wound edge. The reduction of burn surface areas in the two experimental groups and in control group were evaluated with Image J software for 15 days post-wounding to determine the wound healing rates. Wound healing was significantly faster in the autologous ADSCs group compared to both the allogenic ADSCs group (p<0.05) and control group (p<0.05). Wound healing in the allogenic ADSC group did not significantly differ from that in control group. Notably, ADSC injections 0.5cm from the wound edge showed significantly improved healing compared to ADSCs injections in the wound center (p<0.05). This study demonstrated the therapeutic efficacy of ADSCs in treating acute burn wounds in rats. However, only autologous ADSCs improved healing in acute burn wounds; allogenic ADSCs did not. This study further determined a superior location of using ADSCs injections to treat burn wounds including the injection site. Future studies will replicate the experiment in a larger and long-term scale burn wounds in higher mammalian models to facilitate ADSCs therapy in burn wound clinical practice.

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L 1 0 granular FePt–SiO2 films with a (001) preferred orientation and well-separated grains of 5.14nm were obtained by depositing atomic-scale Fe∕Pt∕SiO2 multilayers (MLs) on glass substrates and subsequently annealing MLs at a temperature of 350°C. Large out-of-plane coercivity of 7700Oe and a high ordering factor of 0.83 were achieved. Alternate atomic-scale depositions promoted the formation of (001) textures. Furthermore, because of the low surface energy of SiO2 layers, SiO2 tended to diffuse into grain boundaries of FePt during annealing, which may accelerate diffusion of Fe and Pt atoms, resulting in the low-temperature ordering.

The combination of peripheral arterial intervention and free tissue transfer resulted in successful wound healing and limb salvage instead of amputation in select diabetic patients with difficult-to-heal wounds.

Mitochondrial dysfunction is associated with cardiovascular diseases and diabetes. Pulmonary arterial hypertension (PAH) is characterized by pulmonary vascular remodeling, and the abnormal proliferation, apoptosis and migration of pulmonary arterial smooth muscle cells (PASMCs). The glucagon-like peptide-1 (GLP-1) receptor agonist, liraglutide, has been shown to prevent pulmonary hypertension in monocrotaline-exposed rats. The aim of this study was to investigate the effect of liraglutide on autophagy, mitochondrial stress and apoptosis induced by platelet-derived growth factor BB (PDGF-BB). PASMCs were exposed to PDGF-BB, and changes in mitochondrial morphology, fusion-associated protein markers, and reactive oxygen species (ROS) production were examined. Autophagy was assessed according to the expressions of microtubule-associated protein light chain 3 (LC3)-II, LC3 puncta and Beclin-1. Western blot analysis was used to assess apoptosis, mitochondrial stress and autophagy markers. Liraglutide significantly inhibited PDGF-BB proliferation, migration and motility in PASMCs. PDGF-BB-induced ROS production was mitigated by liraglutide. Liraglutide increased the expression of α-smooth muscle actin (α-SMA) and decreased the expression of p-Yes-associated protein (p-YAP), inhibited autophagy-related protein (Atg)-5, Atg-7, Beclin-1 and the formation of LC3-β and mitochondrial fusion protein dynamin-related (Drp)1. Therefore, liraglutide can mitigate the proliferation of PASMCs via inhibiting cellular Drp1/nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOX) pathways and Atg-5/Atg-7/Beclin-1/LC3β-dependent pathways of autophagy in PAH.

Highly ordered single-crystalline (001) FePt nanoparticles (NPs) with controllable sizes and a well-aligned easy axis were obtained by tuning the layer numbers and the SiO2-layer thickness of atomic-scale [Fe/Pt/SiO2]n multilayers deposited on SiO2∥Si substrates. After 700 °C annealing, quasi-self-assembled NPs with ultrahigh areal density of 1.0×1013 dots/in.2 and large out-of-plane coercivity (Hc,⊥) of 31 kOe were achieved. All particles were embedded into the SiO2 substrates due to the low surface energy of SiO2, which significantly prevented the coarsening during annealing and resulted in a reduced particle size of 5.6 nm and small size distribution of 14.1%.

Adipose-derived stem cells (ADSCs) have been implicated in tumor growth and metastasis in breast cancer. ADSCs exhibit tumor tropism, and are of increasing clinical relevance due to the autologous fat grafting for breast reconstruction. Although we have previously shown that a high level of the adipocytokine visfatin in human breast cancer tissues correlated with tumor progression mediated by cAbl and STAT3, the effects of visfatin in the tumor microenvironment are unclear. To understand how visfatin modulates breast cancer within the tumor-stromal environment, we examined determinants of breast cancer progression using a visfatin-primed ADSCs-tumor co-culture model. ADSCs were isolated from tumor-free adipose tissue adjacent to breast tumors. ADSCs were treated with or without visfatin for 48 h and then collected for co-culture with breast cancer cell line MDA-MB-231 for 72 h in a transwell system. We found that the MDA-MB-231 cells co-cultured with visfatin-treated ADSCs (vADSCs) had higher levels of cell viability, anchorage independent growth, migration, invasion, and tumorsphere formation than that co-cultured with untreated ADSCs (uADSCs). Growth differentiation factor 15 (GDF15) upregulation was found in the co-culture conditioned medium, with GDF15 neutralizing antibody blocking the promoting effect on MDA-MB-231 in co-culture. In addition, a GDF15-induced AKT pathway was found in MDA-MB-231Cancers 2020, 12, 29 2 of 18 and treatment with PI3K/AKT inhibitor also reversed the promoting effect. In an orthotopic xenograft mouse model, MDA-MB-231 co-injected with vADSCs formed a larger tumor mass than with uADSCs. Positive correlations were noted between visfatin, GDF15, and phosphor-AKT expressions in human breast cancer specimens. In conclusion, visfatin activated GDF15-AKT pathway mediated via ADSCs to facilitate breast cancer progression.