Project description:Acute compartment syndrome (ACS) is a disease in which local circulation is affected due to increased pressure within the compartment. We previously found in patients with calf fractures, the pressure of fascial compartment could be sharply reduced upon the appearance of tension blisters. Deep fascia, as the important structure for compartment, might play key role in this process. Therefore, the aim of the present study was to examine the differences in gene profile in deep fascia tissue in fracture patients of the calf with or without tension blisters, and to explore the role of fascia in pressure improvement in ACS. Patients with lower leg fracture were enrolled and divided into without tension blister control group (CON group, n=10), and with tension blister group (TB group, n=10). Deep fascia tissues were collected and LC-MS/MS label-free quantitative proteomics were performed. Genes involved in fascia structure and fibroblast function were further validated by Western blot. The differentially expressed proteins were found to be mainly enriched in pathways related to protein synthesis and processing, stress fiber assembly, cell-substrate adhesion, leukocyte mediated cytotoxicity, and cellular response to stress. Compared with the CON group, the expression of Peroxidasin homolog (PXDN), which promotes the function of fibroblasts, and Leukocyte differentiation antigen 74 (CD74), which enhances the proliferation of fibroblasts, were significantly upregulated, while the expression of Matrix metalloproteinase-9 (MMP9), which is involved in collagen hydrolysis, and Neutrophil elastase (ELANE), which is involved in elastin hydrolysis, were significantly reduced in the TB group (p all <0.05), indicating fascia tissue underwent microenvironment reconstruction during ACS.In summary, the ACS accompanied by blisters is associated with the enhanced function and proliferation of fibroblasts and reduced hydrolysis of collagen and elastin. The adaptive alterations in the stiffness and elasticity of the deep fascia might be crucial for pressure release of ACS.
Project description:Fibrosis is a common and integral pathological feature in various chronic diseases, capable of affecting any tissue or organ. Fibrosis within deep fascia is implicated in many myofascial disorders, including gluteal muscle contracture (GMC), Dupuytren’s disease, plantar fasciitis, iliotibial band syndrome, and chronic muscle pain. In this study, we performed scRNA seq analysis on fibrotic fascia associated with GMC and compared them to nonfibrotic control fascial samples. Our findings show that fibroblast and macrophage cells play a role in pathological tissue remodeling within fibrotic deep fascia. We observed an upregulation of various collagens, proteoglycans, and extracellular matrix (ECM) glycoproteins in contracture deep fascia, attributed to the widespread activation of fibroblast subclusters. Additionally, two pro fibrotic macrophage subpopulations, SPP1+ MP and ECM like MP, appear to facilitate ECM deposition in fibrotic deep fascia by either regulating fibroblast activation or directly contributing to ECM production. SPP1+ MP and ECM like MP cells, as well as the signal interaction between SPP1+ MP and fibroblast cells, present novel and potential therapeutic target for treating GMC and other related myofascial disorders.
Project description:Wound infections are traditionally thought to occur when microbial burden exceeds the innate clearance capacity of host immune system. Here we introduce the idea that the wound environment itself plays a significant contributory role to wound infection. We developed a clinically relevant murine model of soft tissue infection to explore the role of activation of microbial virulence in response to tissue factors as a mechanism by which pathogenic bacteria cause wound infections. Mice underwent abdominal skin incision and light muscle injury with a crushing forceps versus skin incision alone followed by topical inoculation of Pseudomonas aeruginosa. Pseudomonas aeruginosa whole genome transcriptional profiling demonstrated that fascia induced the activation of multiple genes responsible for the synthesis of the iron scavenging protein pyochelin. Ex-vivo murine fascia homogenates were prepared and Pseudomonas aeruginosa MPAO1 was incubated with an inoculum of the fascia homogenate solution. Pseudomonas aeruginosa MPAO1 incubated under the same condtions without the homogenate was used as the control group. Three biological replicates in each group was used.
Project description:Wound infections are traditionally thought to occur when microbial burden exceeds the innate clearance capacity of host immune system. Here we introduce the idea that the wound environment itself plays a significant contributory role to wound infection. We developed a clinically relevant murine model of soft tissue infection to explore the role of activation of microbial virulence in response to tissue factors as a mechanism by which pathogenic bacteria cause wound infections. Mice underwent abdominal skin incision and light muscle injury with a crushing forceps versus skin incision alone followed by topical inoculation of Pseudomonas aeruginosa. Pseudomonas aeruginosa whole genome transcriptional profiling demonstrated that fascia induced the activation of multiple genes responsible for the synthesis of the iron scavenging protein pyochelin.
Project description:Analysis of perirenal adipose tissue from healthy kidney donors (age 44±9 years, BMI 25.8±3.3 kg/m2, mean±SD). The samples were taken bylaparoscopic technique beneath the incision plane that was created in the renal fascia (Greotas fascia) close to the renal vein.
Project description:Interventions: Bilateral transverse abdominal fascia block combined with general anesthesia group (DTAP):Rectus abdominis sheath nerve block based on surgical incision combined with general anesthesia;Incision-based rectus sheath nerve block combined with general anesthesia group (MSRA):Rectus abdominis sheath nerve block combined with general anesthesia based on surgical incision
Primary outcome(s): the dose of remifentanil
Study Design: Parallel