Hypertrophic scar (HS) formation is a common complication that develops after skin injury; however, there are few effective and specific therapeutic approaches for HS. Emodin has previously been reported to inhibit mechanical stress-induced HS inflammation. Here, we investigated the molecular mechanisms underlying the inhibitory effects of emodin on HS formation. First, we conducted in vitro assays that revealed that emodin inhibited M1 and M2 polarization in rat macrophages. We subsequently established a combined rat model of tail HS and dorsal subcutaneous polyvinyl alcohol (PVA) sponge-induced wounds. Rats were treated with emodin or vehicle (DMEM). Tail scar specimens were harvested at 14, 28, and 42 days post-incision and subjected to H&E staining and Masson's trichrome staining. Histopathological analyses confirmed that emodin attenuated HS formation and fibrosis. Macrophages were separated from wound cells collected from the PVA sponge at 3 and 7 days after implantation. Flow cytometry analysis demonstrated that emodin suppressed in vivo macrophage recruitment and polarization at the wound site. Finally, we explored the molecular mechanisms of emodin in modulating macrophage polarization by evaluating the expression levels of selected effectors of the Notch and TGF-β pathways in macrophages isolated from PVA sponges. Western blot and qPCR assays showed that Notch1, Notch4, Hes1, TGF-β, and Smad3 were downregulated in response to emodin treatment. Taken together, our findings suggested that emodin attenuated HS formation and fibrosis by suppressing macrophage polarization, which is associated with the inhibition of the Notch and TGF-β pathways in macrophages.

OBJECTIVES: Parkinson’s disease (PD) and the parkinsonian variant of multiple system atrophy (MSA-P) are distinct neurodegenerative disorders that share similar clinical features of parkinsonism. The morphological alterations of these diseases have yet to be understood. The purpose of this study was to evaluate gray matter atrophy in PD and MSA-P using regions of interest (ROI)-based measurements and voxel-based morphometry (VBM). METHODS: We studied 41 patients with PD, 20 patients with MSA-P, and 39 controls matched for age, sex, and handedness using an improved T1-weighted sequence that eased gray matter segmentation. The gray matter volumes were measured using ROI and VBM. RESULTS: ROI volumetric measurements showed significantly reduced bilateral putamen volumes in MSA-P patients compared with those in PD patients and controls (p<0.05), and the volumes of the bilateral caudate nucleus were significantly reduced in both MSA-P and PD patients compared with those in the controls (p<0.05). VBM analysis revealed multifocal cortical and subcortical atrophy in both MSA-P and PD patients, and the volumes of the cerebellum and temporal lobes were remarkably reduced in MSA-P patients compared with the volumes in PD patients (p<0.05). CONCLUSIONS: Both PD and MSA-P are associated with gray matter atrophy, which mainly involves the bilateral putamen, caudate nucleus, cerebellum, and temporal lobes. ROI and VBM can be used to identify these morphological alterations, and VBM is more sensitive and repeatable and less time-consuming, which may have potential diagnostic value.

OBJECTIVES: To introduce a new laparoscopic splenectomy (LS) approach. METHODS: Sixteen patients underwent LS with general anaesthesia and carbon dioxide pneumoperitoneum. The details of the surgery are as follows: 1. The omentum was incised along the greater curvature and retracted as much as possible to expose the pancreatic body and tail. 2. The right arteriovenous root in the gastric omentum was ligated to sufficiently expose the pancreatic body and tail. 3. The pancreatic capsula was opened along the inferior margin of the pancreatic tail, elevated and separated until the superior margin of the pancreas was grasped. The entire splenic pedicle was retracted using a string. The branching blood vessels in the splenic hilus were ligated using clamps and separated. The splenogastric and splenophrenic ligaments were transected proximally using an ultrasonic knife, and the thick short gastric blood vessels were clamped. This procedure allows complete exposure of the area above the pancreatic tail where the splenic hilus is located. The splenoportal vasculature was suspended using a 7-0 silk suture to easily manipulate this tissue. The splenic portal vessels were dissected using an ultrasonic knife, and the portal vessels were isolated individually using vascular clamps and transected. The splenogastric and lienorenal ligaments were also transected. The spleen was then placed into a bag, and the surgical port was slightly enlarged. Finally, the spleen was sectioned for removal. RESULTS: Fifteen surgeries were successfully performed from March 2015 to January 2016. One patient underwent laparotomy. No patients developed postoperative intra-abdominal haemorrhage or infection. One patient developed subcutaneous emphysema, and one developed a wound infection. No deaths occurred. CONCLUSIONS: Active exposure of the area dorsal to the pancreatic tail is a safe and simple splenectomy method.