Nonlinear association between visceral adipose tissue area and remnant cholesterol in US adults: a cross-sectional study.

BACKGROUND: Excessive visceral adipose tissue (VAT) is associated with a spectrum of diseases, including diabetes, cancer, and cardiovascular diseases. Remnant cholesterol (RC), denoting cholesterol within triglyceride-rich lipoproteins and their metabolic byproducts, has been identified as a key contributor to cardiovascular diseases and related mortality. However, the association between the VAT and RC remains unclear. In this study, the objective is to provide new evidence regarding the association between VAT and RC concentrations. METHODS: 4727 individuals aged 18-59 were selected from the National Health and Nutrition Examination Survey conducted between 2011 and 2018 as study participants. This study utilized several weighted linear regression models and a restricted cubic spline (RCS) to explore the association and potential nonlinearities between VAT and RC. Subgroup analyses were performed to determine the consistency of findings. RESULTS: The mean VAT value was 103.82 ± 1.42 cm2, and the median RC value was 18 mg/dl. VAT demonstrated a positive association with RC in a fully adjusted model, with a ß and 95% confidence interval (CI) of 0.09 (0.08, 0.11) after adjustment for potential confounders. Analysis using RCS revealed a nonlinear association between the VAT area and RC (P < 0.001 for nonlinearity). Adjusted two-piecewise regression models demonstrated ß coefficients of 0.13 (95%CI: 0.11 ~ 0.16, P < 0.001) for RC in individuals with VAT < 143 cm2, and 0.02 (95%CI: -0.01 ~ 0.06, P = 0.15) for those with VAT ≥ 143 cm2. Interactions were observed among the body mass index (BMI) subgroup; the ß coefficients for RC were 0.14 (95%CI: 0.12 ~ 0.16) in those with BMI < 30 kg/m2 and 0.05 (95%CI:0.04 ~ 0.07) in those with BMI ≥ 30 kg/m2, with a P-value of < 0.001 for interaction. CONCLUSIONS: This study identified a nonlinear association between VAT and RC in American adults. Reducing the VAT area may be beneficial in lowering RC concentration, particularly when VAT is < 143 cm2 and those with a BMI < 30 kg/m2.

Composite Dietary Antioxidant Index is inversely associated with visceral adipose tissue area among U.S. adults: A cross-sectional study.

Obesity is becoming a global health problem. Visceral adiposity is the main cause of metabolic and cardiovascular diseases. Dietary improvement is the key to controlling obesity. We hypothesized that a higher Composite Dietary Antioxidant Index (CDAI) was associated with a lower visceral adipose tissue (VAT) area. In this cross-sectional study, 10,389 adults were selected from the National Health and Nutrition Examination Survey 2011-2018. CDAI was calculated based on 6 micronutrients: zinc, selenium, total carotenoids, vitamin A, vitamin C, and vitamin E. VAT area was determined by the dual-energy X-ray absorptiometry scan. Linear regression models were constructed to evaluate the association between CDAI and VAT area. Subgroup analyses were also performed. The mean age of participants was 39.68 years, 5240 were male, and 3841 of those were non-Hispanic White. The inverse associations were observed in all models. In model 3, CDAI was inversely associated with VAT area as a continuous variable, ß (95% confidence interval), -0.56 (-0.85 to -0.27). When compared with the first tertile, the third tertile of CDAI was also inversely associated with VAT area, ß (95% confidence interval), -6.72 (-10.44 to -2.99). No interactions were found in the subgroup analyses. In conclusion, an inverse association between CDAI and VAT area was found among U.S. adults aged 20 to 59 years. These results suggest the possible benefit of an antioxidant diet in relieving visceral obesity. More prospective studies are needed to identify this dietary benefit.

Comprehensive analysis reveals potential therapeutic targets and an integrated risk stratification model for solitary fibrous tumors.

Solitary fibrous tumors (SFTs) are rare mesenchymal tumors with unpredictable evolution and with a recurrence or metastasis rate of 10-40%. Current medical treatments for relapsed SFTs remain ineffective. Here, we identify potential therapeutic targets and risk factors, including IDH1 p.R132S, high PD-L1 expression, and predominant macrophage infiltration, suggesting the potential benefits of combinational immune therapy and targeted therapy for SFTs. An integrated risk model incorporating mitotic count, density of Ki-67+ cells and CD163+ cells, MTOR mutation is developed, applying a discovery cohort of 101 primary non-CNS patients with negative tumor margins (NTM) and validated in three independent cohorts of 210 SFTs with the same criteria, and in 36 primary CNS SFTs with NTM. Compared with the existing models, our model shows significantly improved efficacy in identifying high-risk primary non-CNS and CNS SFTs with NTM for tumor progression.Our findings hold promise for advancing therapeutic strategies and refining risk prediction in SFTs.

PAK4-relevant proliferation reduced by cell autophagy via p53/mTOR/p-AKT signaling.

Background: P21-activated kinase 4 (PAK4) involves in cell proliferation in cancer and mutually regulates with p53, a molecule is demonstrated to control cell autophagy by mammalian target of rapamycin (mTOR)/protein kinase B (AKT) signaling. Since the signaling exhibits an association with PAK family members in cell autophagy, it implies that PAK4-relevant proliferation may be impacted by autophagy via p53 with a lack of evidence in cancer cells. Methods: In this research, transient and stable PAK4-knockdown human hepatocarcinoma cell lines (HepG2) were constructed by transfection of PAK4-RNA interference (RNAi) plasmid and lentivirus containing PAK4-RNAi plasmid, respectively. We investigated cell proliferation using methyl thiazolyl tetrazolium (MTT) and Cell Counting Kit 8 (CCK8) assays, cell cycle by flow cytometry (FCM) and cell autophagy by monodansylcadaverine (MDC) staining and autophagic biomarker's expression, and detected the expressions of p53, mTOR, phosphorylated-AKT (p-AKT) and AKT by immunofluorescence and western blot to explore the mechanism. Results: We successfully constructed transient and stable PAK4-knockdown HepG2 cell lines, and detected dysfunction of the cells' proliferation. An increased expression of p53, as a molecule of cell-cycle-surveillance on G1/S phase, was demonstrated in the cells although the cell cycle blocked at G2/M. And then, we detected increased autophagosome and autophagic biomarker LC3-II, and decreased expressions in p-AKT and mTOR. Conclusions: The proliferation is reduced in PAK4-knockdown HepG2 cells, which is relative to not only cell cycle arrest but also cell autophagy, and p53/mTOR/p-AKT signaling involves in the cell progress. The findings provide a new mechanism on PAK4 block in cancer therapy.

Metagenomic insights into the changes in the rhizosphere microbial community caused by the root-knot nematode Meloidogyne incognita in tobacco.

Root-knot nematode (RKN) disease is a destructive soil disease that affects crop health and causes huge losses in crop production. To explore the relationships between soil environments, rhizobacterial communities, and plant health, rhizosphere bacterial communities were analyzed using metagenomic sequencing in tobacco samples with different grades of RKN disease. The results showed that the community structure and function of the plant rhizosphere were significantly correlated to the RKN disease. RKN density and urease content were key factors affecting the rhizosphere bacterial community. Urease accelerated the catabolism of urea and led to the production of high concentrations of ammonia, which directly suppressed the development of RKNs or by improving the nutritional and growth status of microorganisms that were antagonistic to RKNs. Further experiments showed that the suppression role of ammonia should be attributed to the direct inhibition of NH3. The bacterial members that were positively correlated with RKN density, contained many plant cell wall degrading enzymes, which might destroy plant cell walls and promote the colonization of RKN in tobacco roots. The analysis of metatranscriptome and metabolism demonstrated the role of these cell wall degrading enzymes. This study offers a comprehensive insight into the relationships between RKNs, bacteria, and soil environmental factors and provides new ideas for the biological control of RKNs.

Association of post-intervention pressure gradient with symptom-free at 6 months in idiopathic intracranial hypertension with venous sinus stenosis treated by stenting.

OBJECTIVE: This study aimed to identify the key factors that might affect the clinical outcome of patients with idiopathic intracranial hypertension (IIH) and Venous sinus stenting (VSS). METHODS: We performed an analysis of a prospectively collected database of patients with IIH and VSS who underwent stenting. The trans-stenotic pressure gradient was measured before and after intervention. In additional, patients' baseline characteristics, procedure details and clinical outcomes at 6-month follow-up (including changes in headache, visual impairment, papilledema, etc.) were recorded. The effects of post-intervention pressure gradient on symptom-free at 6 months were explored using logistic regression analysis, generalized additive model and receiver operator characteristic (ROC) curve. RESULTS: Of 101 patients included in this study, the median pressure gradient across stenosis decreased from 19 mmHg before intervention to 2 mmHg after intervention. At 6 months, symptom-free was observed in 58 cases (57.4%). Multivariable logistic analysis and generalized additive model showed that post-intervention pressure gradient (increased by 1 mmHg) was independently and linearly correlated with symptom-free (OR = 0.79, 95% CI = 0.67-0.94). Moreover, the post-intervention pressure gradient revealed moderate discrimination with an area under ROC curve of 0.68 (95% CI = 0.57-0.78). Similar associations were observed for the disappearance of headache and papilledema, but not for the visual recovery. CONCLUSION: The post-intervention pressure gradient may be a valid and reliable predictor of 6-month clinical outcome in patients with IIH and VSS treated by stenting. Nevertheless, external validation with blinded outcome is still needed to confirm its performance before clinical application.

Comparison of microcatheter and pressure wire for venous sinus manometric evaluation of patients with idiopathic intracranial hypertension.

BACKGROUND: Venous sinus manometry performed by microcatheter to assess candidacy for venous sinus stenting in patients with idiopathic cranial pressure (IIH) can be tiring, time-consuming and unreliable. Pressure wire is widely used to measure coronary pressure and evaluate coronary stenosis severity, but venous sinus manometry using the pressure guide wire has only been reported in one case, and few studies have examined the accuracy of this approach. OBJECTIVE: To compare venous manometry performed by microcatheter with by pressure wire under awake setting in patients with IIH. METHODS: The manometry results of 30 patients with IIH were recorded by Rebar-27 microcatheter and a pressure wire under awake setting. The mean venous pressures (MVPs) and trans-stenosis pressure gradients were obtained and compared between microcatheter and pressure wire. Paired t-test) were used to evaluate the data between the two groups. RESULTS: MVPs in superior sagittal sinus (SSS) and torcula were slightly higher with microcatheter, though without statistically significant differences (p > 0.05). MVPs in transverse sinus (TS) and sigmoid sinus (SS) were significantly higher with microcatheter (p < 0.05). Trans-stenotic pressure gradient with microcatheter was significantly higher than with pressure wire (p＜0.001). CONCLUSIONS: Intracranial venous pressure measured with the microcatheter and pressure wire showed a moderate difference. Compared with the traditional microcatheter method，the pressure wire is safe, fast and effective method to identify the patient needing intervention.

Regulation of Hippo/YAP signaling and Esophageal Squamous Carcinoma progression by an E3 ubiquitin ligase PARK2.

Objective: Esophageal squamous cell carcinoma (ESCC) is one of the most commonly diagnosed cancer types in China. Recent genomic sequencing analysis indicated the over-activation of Hippo/YAP signaling might play important roles for the carcinogenic process and progression for ESCC patients. However, little is known about the molecular mechanisms that controls Hippo signaling activity in ESCC. Our previous studies indicated that PLCE1-an important risk factor for ESCC-linked to ESCC progression through snail signaling, during this period, we found PARK2 was an important downstream target of PLCE1-snail axis. PARK2 was decreased in ESCC human samples, and correlated with good prognosis in ESCC patients. Further research showed that PARK2 could inhibit YAP, which functions as key downstream effectors of the Hippo pathway. Here, we aim to reveal the molecular mechanisms of PARK2 modulated Hippo pathway in ESCC. Methods: To evaluate the function of PARK2 in ESCC, we used a tissue microarray (TMA) of 223 human ESCC patients and immunohistochemistry to analyze the correlation between PARK2 expression and clinicopathologic variables. Depletion of endogenous PARK2 and YAP from ESCC cells using CRISPR/Cas9 technologies. Flow cytometry and EdU cell proliferation assay were used to detect proliferation of ESCC cells. Nude mice subcutaneous injection and Ki-67 staining were used to evaluate tumor growth in vivo. Migration and invasion assays were performed. In addition, lung metastasis models in mice were used to validate the function of PARK2 in vivo. Identification of PARK2 involved in hippo pathway was achieved by expression microarray screening, double immunofluorescence staining and co-immunoprecipitation assays. The RNA-seq analysis results were validated through quantitative real-time PCR (qRT-PCR) analysis. The protein half-life of YAP was analyzed by Cycloheximide assay, and the TEAD activity was detected by Luciferase reporter assays. Results: Clinical sample of ESCC revealed that low PARK2 expression correlated with late tumor stage (P < 0.001), poor differentiation (P < 0.04), lymph node (P < 0.001) and distant metastasis (P = 0.0087). Multivariate Cox proportional regression analysis further revealed that PARK2 expression (P = 0.032) is an independent prognostic factor for the overall survival of ESCC patients. Besides, the immunohistochemistry results showed that PARK2 negatively correlated with YAP protein level (P < 0.001). PARK2 depletion promotes ESCC progression both through Hippo/YAP axis, while PARK2 overexpression suppresses ESCC tumor progression by Hippo signaling. Co-IP and ubiquitination assays revealed that PARK2 could interact with YAP in the cytosol and promotes YAP K48-linked ubiquitination at K90 sites. Conclusion: Clinical sample analysis and mechanistic study have validated PARK2 as a tumor suppressor for ESCC. Multivariate Cox proportional regression analysis further revealed that PARK2 is an independent prognostic factor for the overall survival of ESCC patients. Cellular and molecular mechanisms in this study showed that PARK2 associated with YAP protein in the cytosol, promoted YAP ubiquitination and proteasome-dependent degradation in ESCC cells. Therefore, as a novel modulator for Hippo signaling, modulation of PARK2 activity or gene expression level could be an appealing strategy to treat esophageal.

RACO-1 modulates Hippo signalling in oesophageal squamous cell carcinoma.

Oesophageal cancer is one of the most lethal malignancies worldwide, whereas the 5-year survival is less than 20%. Although the detailed carcinogenic mechanisms are not totally clear, recent genomic sequencing data showed dysregulation of Hippo signalling could be a critical factor for oesophageal squamous cell carcinoma (ESCC) progression. Therefore, understanding of the molecular mechanisms that control Hippo signalling activity is of great importance to improve ESCC diagnostics and therapeutics. Our current study revealed RACO-1 as an inhibitory protein for YAP/TEAD axis. Depletion of RACO-1 increases the protein level of YAP and expression of YAP/TEAD target gene. Besides, RACO-1 silencing could promote ESCC cell invasion and migration, which effect could be rescued by YAP depletion in ESCC cells. Immunoprecipitation showed that RACO-1 associated with YAP and promote ubiquitination and degradation of YAP at k48 poly-ubiquitination site. Our research discovered a new regulator of Hippo signalling via modulating YAP stability. RACO-1 could be a promising factor, which serves cancer diagnostics and therapeutics in ESCC patients.

Germacrone protects against oxygen-glucose deprivation/reperfusion injury by inhibiting autophagy processes in PC12 cells.

BACKGROUND: Germacrone is an anti-inflammatory ingredient in the Chinese medicine zedoary turmeric. The purpose of this study was to explore the protective mechanism of germacrone against PC12 cells injury caused by oxygen-glucose deprivation/reperfusion (OGD/R). METHODS: OGD/R injury model of PC12 cells was established by using OGD/R (2 h/24 h). The cell viability was assessed by MTT assay and LDH release. The ultrastructure of cells was observed by transmission electron microscopy (TEM). The expression of autophagy related proteins in cells was determined by Western Blot. RESULTS: The results of ultrastructural observation showed that PC12 cells damaged by OGD/R showed typical autophagy characteristics. In addition, OGD/R observably up-regulated the expression of autophagy related proteins: the class III type phosphoinositide 3-kinase (PI3K III), light chain 3(LC3), and Beclin-1 in PC12 cells, and inhibited the expression of the class I type phosphoinositide 3-kinase (PI3K I), Protein kinase B (Akt), the mammalian target of rapamycin (mTOR), and B-cell lymphoma 2(Bcl-2) proteins. Furthermore, germacrone increased the cell viability of OGD/R-damaged PC12 cells by down-regulating the expression of LC3 protein in cells in a concentration-dependent manner. More importantly, germacrone significantly inhibited the expression of PI3K III, LC3, and Beclin-1 in OGD/R-injured PC12 cells, and up-regulated the expressionof PI3K I, Akt, mTOR, and Bcl-2 proteins in cells, and this inhibited or up-regulated effect was reversed by PI3K I inhibitor (ZSTK474). CONCLUSION: The above results indicated that germacrone could inhibit the autophagy effect in OGD/R injury model of PC12 cells, the mechanism of inhibition was regulated by PI3K III/Beclin-1/Bcl-2 and PI3K I/Akt/mTOR pathways, thereby improving the cell viability of PC12 cells and playing a neuroprotective role, which provided a new drug for the treatment of OGD/R.

SHARPIN Inhibits Esophageal Squamous Cell Carcinoma Progression by Modulating Hippo Signaling.

Esophageal cancer is one of the leading malignancies worldwide, while around sixty percent of newly diagnosed cases are in China. In recent years, genome-wide sequencing studies and cancer biology studies show that Hippo signaling functions a critical role in esophageal squamous cell carcinoma (ESCC) progression, which could be a promising therapeutic targets in ESCC treatment. However, the detailed mechanisms of Hippo signaling dys-regulation in ESCC remain not clear. Here we identify SHARPIN protein as an endogenous inhibitor for YAP protein. SHARPIN depletion significantly decreases cell migration and invasion capacity in ESCC, which effects could be rescued by further YAP depletion. Depletion SHARPIN increases YAP protein level and YAP/TEAD target genes, such as CTGF and CYR61 in ESCC. Immuno-precipitation assay shows that SHARPIN associates with YAP, promoting YAP degradation possibly via inducing YAP K48-dependent poly-ubiquitination. Our study reveals a novel post-translational mechanism in modulating Hippo signaling in ESCC. Overexpression or activation of SHARPIN could be a promising strategy to target Hippo signaling for ESCC patients.

TIPE2 sensitizes osteosarcoma cells to cis-platin by down-regulating MDR1 via the TAK1- NF-κB and - AP-1 pathways.

TIPE2 participates in multiple types of cancer development. However, its mechanism underlying chemoresistance in osteosarcoma has not been elucidated. Herein, we observed the expression of TIPE2 and MDR1 in cis-platin-resistant osteosarcoma tissues and cell lines. Compared to their matched sensitive cell lines and tissues, TIPE2 was downregulated while MDR1 expression was increased. Further investigation showed that overexpression of TIPE2 effectively inhibited MDR1 expression and greatly sensitized osteosarcoma cells to cis-platin, both in vivo and in vitro. Mechanistically, TIPE2 inhibited the transcription of the MDR1 promoter by interfering with the TAK1-NF-κB and -AP-1 pathways. Overall, our results elucidated for the first time that TIPE2 sensitizes osteosarcoma cells to cis-platin through downregulation of MDR1 and may be a novel target in osteosarcoma therapy.

Expression of E-prostanoid receptors in nasal polyp tissues of smoking and nonsmoking patients with chronic rhinosinusitis.

BACKGROUND: Different inflammatory reactions have been observed in the polyp tissues of nonsmokers and smokers with chronic rhinosinusitis (CRS). E-prostanoid (EP) receptors play a role in the inflammatory processes. Cigarette smoke (CS) exposure regulates EP-receptor expression levels promoting inflammatory mediator release from various inflammatory cells. In this study, we characterize the EP-receptor expression profiles in the polyps of nonsmoking and smoking CRS patients to explore the possible role of CS in the pathogenesis of chronic rhinosinusitis with nasal polyps (CRSwNP). METHODS: Polyp biopsies were obtained from 28 non-smoking and 21 smoking CRSwNP patients. Histopathological characteristics were observed under a light microscope. The prostaglandin E2 (PGE2), TNF-α, and IL-8 contents in polyp tissues were detected using enzyme-linked immunosorbent assay. Immunostaining was used to locate EP receptors in polyps. Messenger RNA and protein expression of EP receptors were examined using quantitative real-time polymerase chain reaction and Western blot, respectively. RESULTS: More severe inflammatory reactions occurred in polyp tissues of smoking CRSwNP patients. The PGE2, TNF-α, and IL-8 in tissue homogenate levels were significantly higher in smoking CRSwNP patients than those in nonsmoking CRSwNP patients. Moreover, the distribution of each EP receptor subtype was similar in both groups. Compared with the EP-receptor expression in nonsmokers, messenger RNA and protein of EP2 and EP4 receptor were significantly down-expressed in smoking patients, but EP1 and EP3 receptors did not show significant differences. CONCLUSION: CS exposure downregulates the expression levels of EP2 and EP4 receptors and stimulates the production of PGE2 and the proinflammatory cytokine IL-8 and TNF-α in polyp tissues of CRS patients. The down-expressed EP2 and EP4 receptors might be associated with severe inflammatory reactions in smoking CRSwNP patients.

Identification of CSF biomarkers by proteomics in Guillain-Barré syndrome.

The purpose of the present study was to screen for differentially expressed proteins in the cerebrospinal fluid (CSF) of patients with Guillain-Barré syndrome (GBS). The identification of differentially expressed protein can provide new targets for understanding the pathogenic mechanism, early clinical diagnosis, prognosis and for measuring the effectiveness of interventions. We enrolled 50 GBS patients and 50 meningitis patients (control group) to compare protein expression in CSF. The GBS cases included 28 cases of acute inflammatory demyelinating polyneuropathy (AIDP) and 22 cases of acute motor axonal neuropathy (AMAN). We then performed two-dimensional differential in-gel electrophoresis combined with matrix-assisted laser desorption/ionization time-of-flight mass spectrometry to identify the differentially expressed proteins. The expression levels were validated by ELISA, and their accuracy, sensitivity, and specificity in GBS diagnosis were analyzed by the receiver operating characteristic curve. Three differentially expressed proteins were identified, including the upregulated haptoglobin (Hp) and heat shock protein 70 (Hsp70), and downregulated cystatin C. There were no significant differences between the AIDP and AMAN patients in the positive rates and quantitative expression levels of the three differentially expressed proteins. The accuracy of Hp in the diagnosis of GBS was 0.835, sensitivity was 86.7%, and specificity was 88.2%. The accuracy of cystatin C in the diagnosis of GBS was 0.827, sensitivity was 85.5%, and specificity was 89.7%. The accuracy of Hsp70 in the diagnosis of GBS was 0.841, its sensitivity was 87.8%, and its specificity was 92.3%. Hp and Hsp70 are significantly increased, and cystatin C is downregulated in CSF of GBS patients, which provides important biomarkers for early GBS diagnosis, although these proteins cannot distinguish AIDP and AMAN.

Expression of Prostaglandin E2 Receptors in Acquired Middle Ear Cholesteatoma.

OBJECTIVES: To investigate the expression of prostaglandin E2 receptor subtypes, E-prostanoid (EP) 1-4 receptors, in acquired cholesteatoma and its possible role in the pathologic process of this disorder. METHODS: Specimens of human acquired cholesteatoma were obtained from 29 patients and 19 skin biopsies of normal external auditory canal were as controls. The mRNA and protein expression of EP receptors was assessed by quantitative real-time polymerase chain reaction, immunohistochemistry and Western blot. RESULTS: In acquired cholesteatoma, EP1-EP4 receptors were mainly expressed on squamous epithelium and subepithelial infiltrated inflammatory cells. In external auditory canal skin, EP1-EP4 receptors were mainly expressed on squamous epithelium and glandular epithelium. The expression of EP4 receptor on mRNA and protein levels were significant lower in acquired cholesteatoma compared with controls. EP1-EP3 receptors had no significant difference between the experimental and control group. CONCLUSION: Low expression of EP4 may play a crucial role in the pathologic process of inflammation reaction and bone destruction in acquired cholesteatoma, but not EP1, EP2, or EP3 receptors.

Biomechanical characteristics investigation on long-term free graft with expanded porcine skin.

BACKGROUND: Free skin graft has to be used when the large area skin are burned. The objective of this study is to quantify the influence of free graft and expansion on the skin biomechanical remodeling. METHOD: Four white pigs (weighing from 17 kg to 23 kg) were used. Two 180 ml rectangle expanders were aseptically placed beneath the skin on the back of each pig. Four normal skin flaps and four expanded skin flaps were incised from the foreside back of each pig. Two normal skin flaps and two expanded skin flaps were then grafted to rearward back of the pig. Stress-strain relationship, stress relaxation and creep characters in normal skin: N(n=8), expanded skin without graft: E(n=8), normal skin with free graft after three months: NG(n=8) and expanded skin with free graft after three months: EG(n=8) were measured by using Instron material testing machine. FINDINGS: The strains at 3.5 MPa stress (mean (SD)) are 0.4436(0.1760), 0.4851(0.1401), 0.7750(0.1984) and 0.5854(0.0655) respectively in N, E, NG and EG groups. The maximum relaxations (mean (SD)) are 0.6324(0.0169), 0.6279(0.0401), 0.5630(0.0170) and 0.6057(0.0883) in N, E, NG and EG groups, respectively. The maximum creeps (mean (SD)) are 1.0876(0.0086), 1.1037(0.0116), 1.1948(0.0394) and 1.1328(0.0223) in N, E, NG and EG groups. INTERPRETATION: The biomechanical characteristics of free graft with expanded skin after three months have no significant difference with the normal skin, expansion skin and free graft with normal skin after three months (P>0.05). The free graft and expansion have no significant influence on the skin biomechanical remodeling.