MiR-488-3p facilitates wound healing through CYP1B1-mediated Wnt/ß-catenin signaling pathway by targeting MeCP2.

INTRODUCTION: Diabetic wounds are difficult to heal, but the pathogenesis is unknown. MicroRNAs (miRNAs) are thought to play important roles in wound healing. The effect of miR-488-3p in wound healing was studied in this article. MATERIALS AND METHODS: The gene methylation was measured by methylation specific PCR (MSP) assay. A dual-luciferase reporter assay was adopted to analyze the interaction between miR-488-3p and MeCP2. RESULTS: Cytochrome P450 1B1 (CYP1B1) is a monooxygenase belonging to the cytochrome P450 family that aids in wound healing. Our findings showed that the miR-488-3p and CYP1B1 expression levels were much lower in wound tissues of diabetics with skin defects, but the methyl-CpG-binding protein 2 (MeCP2) level was significantly higher than that in control skin tissues. MiR-488-3p overexpression increased cell proliferation and migration, as well as HUVEC angiogenesis, while inhibiting apoptosis, according to function experiments. In vitro, MeCP2 inhibited wound healing by acting as a target of miR-488-3p. We later discovered that MeCP2 inhibited CYP1B1 expression by enhancing its methylation state. In addition, CYP1B1 knockdown inhibited wound healing. Furthermore, MeCP2 overexpression abolished the promoting effect of miR-488-3p on wound healing. It also turned out that CYP1B1 promoted wound healing by activating the Wnt4/ß-catenin pathway. Animal experiments also showed that miR-488-3p overexpression could accelerate wound healing in diabetic male SD rats. CONCLUSIONS: MiR-488-3p is a potential therapeutic target for diabetic wound healing since it improved wound healing by activating the CYP1B1-mediated Wnt4/-catenin signaling cascade via MeCP2.

HI-MViT: A lightweight model for explainable skin disease classification based on modified MobileViT.

Objective: To develop an explainable lightweight skin disease high-precision classification model that can be deployed to the mobile terminal. Methods: In this study, we present HI-MViT, a lightweight network for explainable skin disease classification based on Modified MobileViT. HI-MViT is mainly composed of ordinary convolution, Improved-MV2, MobileViT block, global pooling, and fully connected layers. Improved-MV2 uses the combination of shortcut and depth classifiable convolution to substantially decrease the amount of computation while ensuring the efficient implementation of information interaction and memory. The MobileViT block can efficiently encode local and global information. In addition, semantic feature dimensionality reduction visualization and class activation mapping visualization methods are used for HI-MViT to further understand the attention area of the model when learning skin lesion images. Results: The International Skin Imaging Collaboration has assembled and made available the ISIC series dataset. Experiments using the HI-MViT model on the ISIC-2018 dataset achieved scores of 0.931, 0.932, 0.961, and 0.977 on F1-Score, Accuracy, Average Precision (AP), and area under the curve (AUC). Compared with the top five algorithms of ISIC-2018 Task 3, Marco's average F1-Score, AP, and AUC have increased by 6.9%, 6.8%, and 0.8% compared with the suboptimal performance model. Compared with ConvNeXt, the most competitive convolutional neural network architecture, our model is 5.0%, 3.4%, 2.3%, and 2.2% higher in F1-Score, Accuracy, AP, and AUC, respectively. The experiments on the ISIC-2017 dataset also achieved excellent results, and all indicators were better than the top five algorithms of ISIC-2017 Task 3. Using the trained model to test on the PH2 dataset, an excellent performance score is obtained, which shows that it has good generalization performance. Conclusions: The skin disease classification model HI-MViT proposed in this article shows excellent classification performance and generalization performance in experiments. It demonstrates how the classification outcomes can be applied to dermatologists' computer-assisted diagnostics, enabling medical professionals to classify various dermoscopic images more rapidly and reliably.

Application of septal extension grafts with auricular cartilage in rhinoplasty. / 耳廓软骨鼻中隔延伸支架移植物在鼻整形术中的应用.

OBJECTIVES: Rhinoplasty is one of the most common cosmetic surgeries in China. Septal extension grafts (SEG) have been widely used in rhinoplasty, but there are few reports on SEG derived from ear cartilage. This study aims to explore the effectiveness and stability of auricular cartilage nasal SEG transplantation in Chinese rhinoplasty. METHODS: A retrospective analysis of 35 rhinoplasty patients admitted from September 2019 to March 2022 has been conducted. Among them, 29 patients underwent rhinoplasty for the first time and 6 patients underwent rhinoplasty with the age of 18-32 (average 22.4) years old. The postoperative follow-up was 3-28 (average 18.5) months. The improvement of the nose shape was observed. The changes of the nose tip angle, nasolabial angle, and nasofrontal angle were compared between before and after the operation, and the complications were recorded. RESULTS: All patients who underwent rhinoplasty with a septal extension grafts constructed from the concha cavity and concha cartilage showed significant improvement in nasal contour. The preoperative nasal tip angle, nasolabial angle, and nasofrontal angle were significantly improved compared with 3 months after operation (all P<0.001), and there was no significant difference between 3 months and 14 months after operation (all P>0.05). The appearance of nasal cavity was satisfactory in 32 patients after operation. Columella deviation occurred in 2 patients and 1 patient complained of downward rotation of the nasal tip, which was satisfied after readjustment of the graft. CONCLUSIONS: The simplified SEG derived from auricular cartilage can provide stable support for the nasal tip, the nasal shape is natural after operation, and minimal trauma of unilateral auricle cartilage transplantation remains.

LncRNA-ZNF252P-AS1/miR-15b-5p promotes the proliferation of keloid fibroblast by regulating the BTF3-STAT3 signaling pathway.

BACKGROUND: JAK2/STAT3 signaling pathway plays an important role in keloid formation, but the upstream mechanism of their activation remains unclear. OBJECTIVE: This study aims to investigate the possible mechanism of lncRNA-ZNF252P-AS1 in keloid. METHODS: The differentially expressed genes in keloid and their upstream regulatory miRNAs and long non-coding RNAs (lncRNAs) were analyzed by bioinformatics database, and the targeting relationship was further verified by dual-luciferase reporter gene assay. LncRNA function as competitive endogenous RNA (ceRNA) in keloid was further verified by in keloid fibroblasts (KFs) and in nude mice with subcutaneous keloids. RESULTS: BTF3 expression was up-regulated in keloid tissues. The targeting relationship between BTF3 and miR-15b-5p was confirmed by dual-luciferase reporter gene assay. miR-15b-5p overexpression inhibited BTF3, Bcl-2, Cyclin D1, C-myc, Collagen I, MMP2, MMP9, N-cadherin, and ZEB2 expressions in KFs, inhibited cell proliferation and migration, while promoted E-cadherin levels. BTF3 overexpression reversed miR-15b-5p effects on KFs. Bioinformatics analysis as well as clinical and cellular experiments confirmed that the lncRNA ZNF252P-AS1 was highly expressed in keloid/KFs. Dual-luciferase reporter gene assays confirmed the targeting relationship between lncRNA ZNF252P-AS1 and miR-15b-5p. LncRNA ZNF252P-AS1 overexpression inhibited miR-15b-5p and E-cadherin levels, upregulated BTF3, Bcl-2, Cyclin D1, C-myc, Collagen I, MMP2, MMP9, N-cadherin, and ZEB2 expressions, increased cell proliferation and migration, and activated JAK2/STAT3 pathway, while miR-15b-5p overexpression reversed this effect. The in vivo results were consistent with in vitro results. In vivo experiments further confirmed that lncRNA ZNF252P-AS1 reduced keloid volume and weight. CONCLUSION: lncRNA ZNF252P-AS1 is a potential target for keloid treatment.

LINC00467, Driven by Copy Number Amplification and DNA Demethylation, Is Associated with Oxidative Lipid Metabolism and Immune Infiltration in Breast Cancer.

Breast cancer (BRCA) is a malignant tumor with a high incidence and poor prognosis in females. However, its pathogenesis remains unclear. In this study, based on bioinformatic analysis, we found that LINC00467 was highly expressed in BRCA and was associated with tumor metastasis and poor prognosis. The genomic and epigenetic analysis showed that LINC00467 may also be regulated by copy number amplification (CNA), chromatin openness, and DNA methylation. In vitro experiments showed that it could promote the proliferation, migration, and invasion of BRCA cells. Competitive endogenous RNA (ceRNA) regulatory network analysis and weighted gene coexpression network analysis (WGCNA) suggested that LINC00467 may play a role in signaling pathways of peroxisomal lipid metabolism, immunity, and others through microRNAs (miRNAs) targeting transforming growth factor beta 2 (TGFB2). In addition, copy number amplification and high expression of LINC00467 were associated with the low infiltration of CD8+ and CD4+ T cells. In conclusion, we found that LINC00467, driven by copy number amplification and DNA demethylation, may be a potential biomarker for the diagnosis and prognosis of BRCA and a tumor promoter acting as a potential therapeutic target for BRCA as well.

A Novel Fat Making Strategy With Adipose-Derived Progenitor Cell-Enriched Fat Improves Fat Graft Survival.

BACKGROUND: A low survival rate is one of the main challenges in fat grafting. OBJECTIVES: This study aimed to evaluate whether microfat obtained by a novel strategy promoted the survival and retention of fat grafts. METHODS: A 5-mm-diameter blunt tip cannula with large side holes (~30 mm2/hole) was used to obtain macrofat. A novel strategy based on a newly invented extracorporeal cutting device was then used to cut the macrofat into microfat, which was named adipose-derived progenitor cell enrichment fat (AER fat); Coleman fat was used as the control. Aliquots (0.5 mL) of both types of fat were transplanted into 10 nude mice and analyzed 10 weeks later. Western blotting, flow cytometry, and immunofluorescence were performed to assess the AER fat characteristics and underlying mechanisms. RESULTS: The retention rate of fat grafts in AER fat-treated animals was significantly higher than that in the Coleman group (mean [standard deviation] 54.6% [13%] vs 34.8% [9%]; P < 0.05) after 10 weeks. AER fat contained more dipeptidyl peptidase-4-expressing progenitor cells (3.3 [0.61] × 103 vs 2.0 [0.46] × 103 cells/mL; P < 0.05), adipose-derived plastic-adherent cells (6.0 [1.10] × 104 vs 2.6 [0.17] × 104 cells/mL; P < 0.001), and viable adipocytes than Coleman fat. Moreover, histologic analysis showed that AER fat grafts had better histologic structure and higher capillary density. CONCLUSIONS: AER fat transplantation is a potential strategy to improve the survival and long-term retention of fat grafts. AER fat contained more dipeptidyl peptidase-4-expressing progenitor cells.

lncRNA PAPPA-AS1 Induces the Development of Hypertrophic Scar by Upregulating TLR4 through Interacting with TAF15.

Hypertrophic scar (HTS) is a complicated pathological process induced mainly by burns and wounds, with abnormal proliferation of fibroblasts and the transformation of fibroblasts to myofibroblasts. PAPPA-AS1, a differentially expressed long noncoding RNA (lncRNA) in the HTS tissues, attracted our interests in its potential role and mechanism in the development and process of HTS. In the present study, the regulatory effect of lncRNA PAPPA-AS1 on the Toll-like receptor 4 (TLR4) signal pathway, as well as the molecular mechanism, was investigated. Bioinformatics analysis was utilized to screen the differentially expressed lncRNAs in HTS tissues. PAPPA-AS1 was significantly upregulated in both HTS tissues and hypertrophic scar fibroblast (HTsFb) cells. The expression levels of TLR4, MyD88, TGF-ß1, collagen I, collagen III, and α-SMA were greatly elevated in HTsFb cells. By knocking down PAPPA-AS1, the proliferation of HTsFb cells, TLR4, and TGF-ß1 signal pathway and the expression of fibrosis markers both in HTsFb cells and HTS tissues were suppressed. It was accompanied by the alleviated pathological state in the HTS tissues, which were significantly reversed by cotransfecting with the pcDNA3.1-TLR4 vector. Positive correlation and interaction were observed between PAPPA-AS1 and TAF15 and between TAF15 and the promoter of TLR4, respectively. In conclusion, lncRNA PAPPA-AS1 might induce the development of HTS by upregulating TLR4 through interacting with TAF15.

Downregulation of long noncoding RNA DLEU1 attenuates hypersensitivity in chronic constriction injury-induced neuropathic pain in rats by targeting miR-133a-3p/SRPK1 axis.

BACKGROUND: Neuropathic pain belongs to chronic pain and is caused by the primary dysfunction of the somatosensory nervous system. Long noncoding RNAs (lncRNAs) have been reported to regulate neuronal functions and play significant roles in neuropathic pain. DLEU1 has been indicated to have close relationship with neuropathic pain. Therefore, our study focused on the significant role of DLEU1 in neuropathic pain rat models. METHODS: We first constructed a chronic constrictive injury (CCI) rat model. Paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) were employed to evaluate hypersensitivity in neuropathic pain. RT-qPCR was performed to analyze the expression of target genes. Enzyme-linked immunosorbent assay (ELISA) was conducted to detect the concentrations of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and IL-1ß. The underlying mechanisms of DLEU1 were investigated using western blot and luciferase reporter assays. RESULTS: Our findings showed that DLEU1 was upregulated in CCI rats. DLEU1 knockdown reduced the concentrations of IL-6, IL-1ß and TNF-α in CCI rats, suggesting that neuroinflammation was inhibited by DLEU1 knockdown. Besides, knockdown of DLEU1 inhibited neuropathic pain behaviors. Moreover, it was confirmed that DLEU1 bound with miR-133a-3p and negatively regulated its expression. SRPK1 was the downstream target of miR-133a-3p. DLEU1 competitively bound with miR-133a-3p to upregulate SRPK1. Finally, rescue assays revealed that SRPK1 overexpression rescued the suppressive effects of silenced DLEU1 on hypersensitivity in neuropathic pain and inflammation of spinal cord in CCI rats. CONCLUSION: DLEU1 regulated inflammation of the spinal cord and mediated hypersensitivity in neuropathic pain in CCI rats by binding with miR-133a-3p to upregulate SRPK1 expression.

Clinical application of the 6th autogenous costal cartilage in the treatment of severe saddle nose deformity after trauma. / 第6自体肋软骨在外伤后重度鞍鼻畸形修复中的临床应用.

OBJECTIVES: Saddle nose deformity is a common clinical nose deformity. This study aimed to evaluate the effectiveness of the 6th autogenous costal cartilage in the treatment of severe saddle nose deformity after trauma. METHODS: A retrospective analysis was conducted on 15 patients with severe post-traumatic saddle nose deformity from March, 2016 to March, 2019. The nasal tip and dorsum were reconstructed with autogenous costal cartilage. All patients were followed up for 6 to 13 months and changes in nasal appearance were evaluated. The changes in dorsum sag, nasolabial angle, nasal dorsal angle, and dorsum length were measured. RESULTS: Fourteen patients were basically satisfied with post-operative outcome. Only one patient developed infection afterwards, which was improved by the revised rhinoplasty 2 months after active treatment. The immediate nasal dorsal depression [(1.19±0.94) mm] and nasolabial angle [(94.06±1.52)°] after operation decreased compared with those before surgery [(8.28±0.24) mm, (109.42±2.78)°, respectively; all P<0.05]. The immediate nasal dorsal length [(44.18±1.02) mm] and nasal dorsal angle [(132.84±2.33)°] increased compared with those before operation [(31.73±1.86) mm, (122.87±2.42)°, respectively; all P<0.05]. The data at follow-ups showed no statistical difference compared with the immediate data after operation. CONCLUSIONS: Rhinoplasty with the 6th autogenous costal cartilage is an effective method for the correction of severe saddle nose deformity after trauma.

Promotion effects of mono-2-ethyhexyl phthalate (MEHP) on migration and invasion of human melanoma cells via activation of TGF-ß signals.

Malignant melanoma is one of the most leading forms of skin cancer associated with a low patient survival rate. There is an urgent need to illustrate risk factors that can trigger the motility of melanoma cancer cells. Our present study revealed that mono-(2-ethylhexyl)phthalate (MEHP) exposure can significantly increase the in vitro migration and invasion of WM983A and A375 cells. Among the tested cytokines, MEHP can increase the expression of transforming growth factor ß (TGF-ß). Inhibition of TGF-ß via its neutralization antibody can attenuate MEHP-induced cell migration and invasion. Further, upregulation of TGF-ß mediated MEHP-induced activation of Smad signals and upregulation of Snail in melanoma cells. Blocking the TGF-ß/Smad signal pathway can attenuate MEHP-induced cell migration. Estrogen receptor α (ERα) was essential for MEHP-induced expression of TGF-ß. In addition, MEHP can increase the expression of ERα in melanoma cells. Collectively, our study found that MEHP can stimulate the progression of melanoma via TGF-ß signals. SIGNIFICANCE: Mono-(2-ethylhexyl)phthalate (MEHP) is the active and most toxic metabolite of di(2-ethylhexyl)phthalate (DEHP). Our present study revealed that MEHP can trigger the in vitro migration and invasion of melanoma cells via upregulation of TGF-ß/Snail signals. It revealed that daily exposure to MEHP might be a risk factor for melanoma patients.

Customized Titanium Mesh for Repairing Cranial Defects: A Method With Comprehensive Evaluation.

Titanium cranioplasty is one of the well-established and widely used techniques for repairing cranial defects. In this paper, we present an improved way to design and create titanium meshes with more evaluation process. Computed tomography scan data of patients were used to create three-dimensional virtual models. Implants were designed with NX ImageWare 13.2 (Siemens PLM Software, Plano, TX). Final titanium meshes were assessed by Geomagic Studio 12 (Geomagic, Inc., Morrisville, NC) and NX ImageWare 13.2.Titanium meshes were designed and applied to cranioplasty surgery on 8 patients. Postoperative results were evaluated by computed tomography scanning and further analyzed with rainbow difference tomography. All patients were satisfied with the outcome. With this method, surgeons, engineers, and patients work together to evaluate and edit implant design. Our method provides better communication and comprehensive evaluation, which result in a satisfying outcome.

MiR-138/peroxisome proliferator-activated receptor ß signaling regulates human hypertrophic scar fibroblast proliferation and movement in vitro.

Excessive scars affect a patient's quality of life, both physically and psychologically, by causing pruritus, pain and contractures. Because there is a poor understanding of the complex mechanisms underlying the processes of hypertrophic scar formation, most therapeutic approaches remain clinically unsatisfactory. In this study, we found that miR-138 was downregulated and peroxisome proliferator-activated receptor (PPARß) was inversely upregulated in hypertrophic scar tissues compared to in paired normal skin tissues. Using a dual-luciferase assay, we validated that miR138 directly targets PPARß and regulates its expression at the transcriptional and translational levels. In gain-and-loss experiments, we found that miR-138/PPARß signaling regulated human hypertrophic scar fibroblast proliferation and movement, and affected scarring-related protein expression, which suggests that miR-138/PPARß signaling is important for hypertrophic scarring. Thus, our study provides evidence to help determine whether miR-138/PPARß signaling may be a potential target for hypertrophic scarring management.

Evaluation of cross-protection against three topotypes of serotype O foot-and-mouth disease virus in pigs vaccinated with multi-epitope protein vaccine incorporated with poly(I:C).

Epitope-based vaccines are always questioned for their cross-protection against the antigenically variable foot-and-mouth disease virus (FMDV). In this study, we proved the cross-protection effect of a multi-epitope vaccine incorporated with poly(I:C) against three topotypes of O type FMDV. A total of 45 naïve pigs were vaccinated with different doses of multi-epitope protein vaccine incorporated with poly(I:C). At 28 days post-vaccination, 45 vaccinated and 6 unvaccinated control pigs (two pigs for each group) were challenged with three topotypes of virulent O type FMDV, namely, O/Mya/98 (Southeast Asia topotype), O/HN/CHA/93 (Cathay topotype) and O/Tibet/CHA/99 (PanAsia topotype) strains. All unvaccinated pigs developed generalised FMD clinical signs. Results showed that all pigs (n=15) conferred complete protection against the O/Mya/98 and O/HN/CHA/93 FMDV strains, 11 of which were protected against the O/Tibet/CHA/99 FMDV strain. The 50% protective dose values of the vaccine against the O/Mya/98, O/HN/CHA/93 and O/Tibet/CHA/99 FMDV strains were 15.59, 15.59 and 7.05, respectively. Contact challenge experiment showed that transmission occurred from the donors to the unvaccinated but not to vaccinated pigs. These results showed that vaccination with multi-epitope protein vaccine incorporated with poly(I:C) can efficiently prevent FMD in pigs.

[Effects of antisense p38 α mitogen-activated protein kinase on myocardial cells exposed to hypoxia and burn serum].

OBJECTIVE: To study the effects of antisense p38α mitogen-activated protein kinase (hereinafter referred to as p38α) on myocardial cells exposed to hypoxia and burn serum. METHODS: Thirty adult SD rats were inflicted with 40% TBSA full-thickness burn on the back to obtain burn serum. The myocardial cells were isolated from 80 neonatal SD rats and cultured, then they were divided into 4 groups according to the random number table: normal control group (N, ordinary culture without any treatment), hypoxia+burn serum group (HB, exposed to hypoxia after being treated with 10% burn rat serum), hypoxia+burn serum+infection group (HBI, exposed to hypoxia and 10% burn rat serum after being infected with antisense p38α gene-carrying adenovirus), hypoxia+burn serum+empty vector infection group (exposed to hypoxia and 10% burn rat serum after being infected with adenovirus empty vector). At post hypoxia hour (PHH) 1, 3, 6, and 12, mRNA and protein expression levels of p38α in the latter 3 groups were determined by RT-PCR and Western blotting, cell viability was determined by methylthianolyldiphenyl-tetrazolium bromide assay, and lactate dehydrogenase (LDH) activity was assayed at the same time point. At PHH 1, 6, and 12, apoptosis rate of myocardial cells was assessed by annexin V staining method. The indexes of group N were determined with the methods mentioned-above. Three wells were set at each time point in each group. Data were processed with one-way analysis of variance and LSD- t test. RESULTS: (1) At PHH 1, 3, and 6, the p38α mRNA level was higher in group HB than in group N and group HBI (with t values from 2.725 to 4.375, P values all below 0.05). (2) At PHH 1, 3, and 6, the p38α protein level was higher in group HB than those in group N and group HBI (with t values from 5.351 to 7.981, P values all below 0.01). (3) At PHH 3, 6, and 12, the cell viability in group HB (0.115 ± 0.007, 0.104 ± 0.006, 0.094 ± 0.005) was lower than that in group N (0.141 ± 0.014) and group HBI (0.136 ± 0.009, 0.124 ± 0.010, 0.112 ± 0.007, with t values from 2.357 to 6.812, P values all below 0.05). (4) The LDH activity was up-regulated in group HB as compared with that in group N and group HBI at each time point (with t values from 22.753 to 201.273, P values all below 0.01). (5) At PHH 1, 6, and 12, the apoptosis rate of myocardial cells in group HB [(5.4 ± 0.7)%, (8.7 ± 1.1)%, (13.6 ± 1.7)%] was higher than that of group N [(3.1 ± 0.3)%] and group HBI [(4.3 ± 0.5)%, (5.1 ± 0.7)%, (7.2 ± 0.9)%, with t values from 2.345 to 9.700, P < 0.05 or P < 0.01]. CONCLUSIONS: Antisense p38α can protect the myocardial cells from the injury of hypoxia and burn serum.

[Study on adenovirus mediated antisense p38α fragment gene in suppressing apoptosis of the myocardium of neonatal rat by burn serum and hypoxia].

OBJECTIVE: To investigate the relationship between the activation of p38 mitogen-activated protein kinase (p38MAPK) in the myocardium and the apoptosis in the presence of burn serum and hypoxia. METHODS: Ventricular myocardium isolated from neonatal rats were employed in this study, and they were divided into three groups as the normal control group, with the myocardium grew naturally; burn serum+ hypoxia group, in which the myocardium was stimulated by the serum collected from the rat 6 hours after burn injury involving 40% of total body surface area (TBSA), and at the same time exposed to 1%O(2), 5%CO(2), and 94%N(2); antisense blocking group, in which rats were pretreated by AD-antisense (AS) p38α, then exposed to the same conditions as burn serum+hypoxia group. The phosphorylation of p38 in the myocardium was determined by Western blotting. The level of myocardium apoptosis was determined by DNA ladder and flow cytometry. RESULTS: Compared with normal control group, the level of phosphorylation of p38 (gray value) was markedly increased (8.68±0.14 vs. 3.21±0.05, P<0.01) after being exposed to burn serum and hypoxia, and at the same time myocardium apoptosis was strikingly increased [(50.367±0.451)% vs. (2.063±0.111)%, P<0.01]. When the myocardium was transfected by AD-ASp38α, the phosphorylation of p38 (gray level) was decreased remarkably (5.46±0.16 vs. 8.68±0.14, P<0.01), the rate of the apoptosis was lowered remarkably [(13.200±0.121)% vs. (50.367±0.451)%, P<0.01]. CONCLUSION: Burn serum combined with hypoxia can induce apoptosis of the myocardium by activating p38MAPK; blockage of p38MAPK signal transduction pathway may lessen the damage of the myocardium in early period of severe burn.

[Anatomic basis of the accompanying pattern of the superficial temporal arterial branches and veins and its clinical application].

OBJECTIVE: To study the course of branches of the superficial temporal artery (BSTA) and the accompanying pattern of their veins in order to provide anatomic basis for flap design. METHODS: Head and facial part of ten adult corpses (19 sides) were dissected and photographed. The coordinate system was set up with external auditory foramen as the point of origin, aided by the graph analysis software Digimizer. The course of the frontal branch and parietal branch of the superficial temporal artery (STA), and the accompanying pattern between the BSTA and the veins were measured and analyzed. The STA and its branches were located by Ultrasonic Doppler, and the corresponding branches of the superficial temporal vein (BSTV) were disclosed by bowing patient's head with breath holding or cerclaging the basement of the patient's skull. And then 10 sides of transposition (fascia) flaps with axis at the angular bisector between BSTA and BSTV were devised to repair wounds of 9 patients that hospitalized from February 2008 to December 2009. Data were processed with test of variance homogeneity. RESULTS: Frontal BSTV absence was found in 6 head sides, and the maximum distance between artery and vein was (2.1 ± 1.2) cm. Parietal BSTV absence was found in 3 head sides, and the maximum distance was (1.4 ± 0.7) cm. The distance between frontal BSTA and BSTV was larger than that between parietal BSTA and BSTV, and the dispersion degree of the former was higher than that of the latter (F = 0.0404, P = 0.0475). All the (fascia) flaps survived without congestion or necrosis. CONCLUSIONS: When branch of the superficial temporal vessel was selected as the axial vessel of flap, the flap design shall depend on the accompanying pattern of BSTV to avoid the flap necrosis due to poor venous return after surgery. The superficial temporal vein and its branches can be well disclosed by bowing head or cerclaging skull. The approach is simple, useful, safe, and reliable.

[Application of latissimus dorsi flap in different forms in repair of skin and soft tissue defects in lower extremities].

OBJECTIVE: To explore repair methods of skin and soft tissue defects in lower extremities with free latissimus dorsi flaps. METHODS: Forty-two patients with wounds and soft tissue defects in lower extremities, including 4 cases on knee, 22 cases on leg, 15 cases on ankle and foot, 1 case with extensive avulsion from knee to dorsum of foot, were hospitalized in our unit from February 1996 to February 2008. Wounds or soft tissue defects were respectively repaired with latissimus dorsi musculocutaneous flaps, latissimus dorsi muscle flaps, latissimus dorsi perforator flaps with preserved vascular sleeves, 2 double-leaf segmental latissimus dorsi compound flaps after debridement. The flaps ranged from 18 cm x 8 cm to 40 cm x 18 cm in size. The donor sites were covered by skin grafting in 19 cases. RESULTS: All wounds were healed primarily except vascular crisis occurred in 3 cases, partial necrosis of skin at donor site in 2 cases, and graft site (1 case). Follow-up for 3 to 24 months of 31 patients showed: six cases received two-stage plastic operation on account of bulkiness with trouble in wearing shoes, and mild contraction of muscular flap in 3 cases. CONCLUSIONS: Latissimus dorsi flap in various forms can be satisfactory for repair of large skin and soft tissue defects in lower extremities.

[Repair of nose and adjacent tissue defect deformities after burn].

OBJECTIVE: To look for the best method of repairing nose and adjacent tissue defect after burn and observe the effect. METHODS: Twelve patients with post-burn nose and adjacent tissue defect deformities hospitalized from January 1999 to December 2008 were repaired with expanded forehead flap, pedicled upper-arm flap, axial post-auricular reversed flow island flap, and nasolabial groove flap. Among them, 4 cases with total nasal defect, 8 cases with partial nasal defect; and 3 cases were accompanied with scars on cheek, 5 cases accompanied with scars on forehead, 5 cases accompanied with upper lip ectropion and subtotal upper lip defect. The skin flap size ranged from 3.0 cm x 1.5 cm to 10.0 cm x 8.0 cm. RESULTS: Five cases were repaired with expanded forehead flap, 3 cases with pedicled upper-arm flap, 1 case with axial post-auricular reversed flow island flap, and 3 cases with nasolabial groove flap respectively. All the 12 flaps survived. Patients were followed up for 1 to 7 years, and nasal function and appearance were obviously improved. CONCLUSIONS: Optimal repairing method shall be chosen to repair nasal defect after burn according to its extent, and forehead flap is preferred. Pedicled upper-arm flap and reversed flow axial post-auricular island flap can be employed if local flap and ortho-position skin flap are unavailable when obvious scar is present on face as a result of severe burn.