The role of FGF-21 in promoting diabetic wound healing by modulating high glucose-induced inflammation.

Background: Wound healing is a complex biological process that can be impaired in individuals with diabetes. Diabetic wounds are a serious complication of diabetes that require promoting diagnosis and effective treatment. FGF-21, a member of the endocrine FGF factors family, has caught the spotlight in the treatment of diabetes for its beneficial effects on accelerating human glucose uptake and fat catabolism. However, the therapeutic efficacy of FGF-21 in promoting diabetic wounds remains unknown. This study aims to evaluate the therapeutic potential of FGF-21 in promoting diabetic wound healing. Methods: we investigated the effects of FGF-21 on wound healing related-cells under high-glucose conditions using various assays such as CCK8, scratch assay, flow cytometry analysis, endothelial tube-formation assay, and transmission electron microscopy. Furthermore, we used db/db mice to verify the healing-promoting therapeutic effects of FGF-21 on diabetic wounds. We also conducted qRT-PCR, Western blot, and immunofluorescence staining analyses to elucidate the underlying mechanism. Result: Our results indicate that FGF-21 treatment restored hyperglycemic damage on endothelial cell proliferation, migration, and tube-forming ability. It also reduced endothelial cell death rates under high-glucose conditions. TEM analysis showed that FGF-21 treatment effectively restored mitochondrial damage and morphological changes in endothelial cells caused by glucose. Additionally, qRT-PCR and Western blot analysis indicated that FGF-21 treatment restored inflammatory responses caused by hyperglycemic damage. Animal experiments confirmed these findings, suggesting that FGF-21 may be a promising candidate for the treatment of non-healing diabetic wounds due to its effectiveness in stimulating angiogenesis and anti-inflammatory function. Conclusion: Our study provides evidence that FGF-21 is an essential regulator of wound-related cells under high-glucose conditions and has the potential to be a novel therapeutic target for accelerating diabetic wound healing.

The implication of pyroptosis in cancer immunology: Current advances and prospects.

Pyroptosis is a regulated cell death pathway involved in numerous human diseases, especially malignant tumors. Recent studies have identified multiple pyroptosis-associated signaling molecules, like caspases, gasdermin family and inflammasomes. In addition, increasing in vitro and in vivo studies have shown the significant linkage between pyroptosis and immune regulation of cancers. Pyroptosis-associated biomarkers regulate the infiltration of tumor immune cells, such as CD4+ and CD8+ T cells, thus strengthening the sensitivity to therapeutic strategies. In this review, we explained the relationship between pyroptosis and cancer immunology and focused on the significance of pyroptosis in immune regulation. We also proposed the future application of pyroptosis-associated biomarkers in basic research and clinical practices to address malignant behaviors. Exploration of the underlying mechanisms and biological functions of pyroptosis is critical for immune response and cancer immunotherapy.

The Roles of Drug Metabolism-Related ADH1B in Immune Regulation and Therapeutic Response of Ovarian Cancer.

Background: The different pharmacological effects of drugs in different people can be explained by the polymorphisms of drug metabolism-related genes. Emerging studies have realized the importance of drug metabolism-related genes in the treatment and prognosis of cancers, including ovarian cancer (OV). In this study, using comprehensive bioinformatics and western blot, we identified that the drug metabolism-related gene, ADH1B, was significantly down-regulated in OV cells and tissues. The patients with a high level of ADH1B presented a good prognosis. We also found a negative correlation between ADH1B expression and the activity of chemotherapeutic agents, such as cyclophosphamide. In addition, positive correlations were observed between ADH1B expression and multiple immune checkpoints, including LAG3 and HAVCR2. The immune infiltration analysis further indicated that aberrantly expressed ADH1B might have important roles in regulating the infiltration of macrophages and neutrophils in OV tissues. Then, the co-expression analysis was conducted and the top three enriched KEGG pathways were spliceosome, RNA transport, and DNA replication. In conclusion, the drug metabolism-related gene ADH1B and its interactive network play an essential role in the immune regulation and therapeutic response and maybe identified as promising therapeutic targets for OV patients.

Identification of m6A-Associated Gene DST as a Prognostic and Immune-Associated Biomarker in Breast Cancer Patients.

BACKGROUND: N6-methyladenosine (m6A) is most common internal RNA modification in eukaryotic cells. Existing evidence shows that m6A is closely related to pathogenesis and progression in breast cancer (BRCA). Therefore, it is critical to investigate the key role of m6A target genes in BRCA. METHODS: M6A target genes in BRCA are acquired using RMVar online database. The differentially expressed genes (DEGs) from three microarray datasets (GSE5764, GSE22358, GSE9014) is processed by GEO2R. Oncomine, GEPIA, UALCAN and TNMplot were applied to validate the expression of DST. Survival analyses were performed via DRUGSURV and Kaplan-Meier Plotter database. Univariable survival and multivariate Cox analysis were completed to assess the prognostic value of DST and receiver operating characteristic (ROC) curve was performed to evaluate the diagnostic value of DST. We also investigated the correlation between DST and cancer immune infiltration via using CIBERSORT, TIMER and TISIDB. RESULTS: DST and COL11A1 were significantly expressed in both DEGs and m6A target genes set. COL11A1 show no significance on the patients' survival. However, high expression of DST was related to the favorable prognosis. Multivariate analysis revealed that the DST dysregulation is an independent prognostic factor and ROC indicated that the great diagnostic value of DST with AUC of 0.948. Subsequently, immunological analyses showed that DST was significantly associated with various immune infiltration cells, including NK cells, T helper cells and Mast cells. Furthermore, DST was also related with multiple immune checkpoints and chemokines, including LAG3, LMTK3 CD24, CXCL12, KDR and CX3CR1. These results indicated the potential roles of DST in the development of BRCA via altering the immune response. CONCLUSION: DST can influence the development and progression of BRCA by altering the immune microenvironment.

Integrative bioinformatics and experimental analysis revealed TEAD as novel prognostic target for hepatocellular carcinoma and its roles in ferroptosis regulation.

OBJECTIVE: Transcriptional enhanced associate domain (TEAD) family consists of four members TEAD1/2/3/4 that regulate cell growth, stem cell functions and organ development. As the downstream of Hippo signaling pathway, TEAD family is involved in the progression of several cancers. However, the precise biology functions of TEAD family in hepatocellular carcinoma (HCC) have not been reported yet. METHODS: We apply bioinformatics analysis based on databases including UALCAN, Oncomine, GEPIA, Kaplan-Meier plotter, WebGestalt, cBioPortal, TIMER2.0, and in vitro experimental evidence to identify the exact roles of TEAD family in HCC. RESULTS: The results indicated that TEAD2/4 were significantly upregulated in HCC compared with normal tissues. Downregulated of TEAD2 could promote the death of HCC cells through inducing ferroptosis by iron accumulation and subsequent oxidative damage. According to the Kaplan-Meier plotter database, we found that the high expression of TEAD2 was significantly associated with poor disease-specific survival, overall survival, progression-free survival and relapse-free survival. In aspect of cancer immunity, Tumor Immune Estimation Resource algorithm showed that the expression of TEAD family members was obviously related to multiple of infiltrating immune cells including macrophages, neutrophils, dendritic cells, B cells, CD8+ T cells and CD4+ T cells. Finally, we conducted the functional enrichment analysis including protein-protein interaction network, gene ontology enrichment analysis and Kyoto Encyclopedia of Genes and Genomes pathway based on the TEAD family-associated coexpression genes. CONCLUSION: The study provided deep insight information of TEAD family in the diagnostic and prognostic evaluation of HCC patients.

Knockdown of enhancer of rudimentary homolog expression attenuates proliferation, cell cycle and apoptosis of melanoma cells.

Early stage or localized melanoma can be surgically resected with satisfactory outcome, whereas advanced malignant melanoma responds to treatment poorly and has a negative prognosis even after surgery, radiotherapy and other comprehensive treatments. Gene therapy targeting various biological signaling pathways has become an increasingly popular area in melanoma research. However, for gene therapy success, it is important to reveal the molecular mechanisms of melanoma tumorigenesis and development. The present study examined the effects of downregulating enhancer of rudimentary homolog (ERH) expression on the proliferation, metastasis and cell cycle of melanoma cells. ERH expression levels in melanoma tissues and cells were determined. Then, ERH gene expression in melanoma cell lines was downregulated or overexpressed by the lentiviral RNA interference technique. Furthermore, we performed cell counting kit-8, clone formation, scratch, transwell migration, subcutaneous tumorigenesis and venous metastasis assays as well as carried out flow cytometry analysis to explore the effects of ERH expression on cell proliferation, cell cycle, apoptosis and metastasis. We found that ERH expression in melanoma tissues and cells was markedly higher than in normal melanin nevus. Suppressing ERH expression by RNA interference in melanoma A375, WM35 and SK28 cell lines inhibited their proliferation and induced cell apoptosis. The cell cycle was also found to be blocked in the G1 phase. However, the metastatic properties of melanoma cells in vitro and in vivo remained largely unaltered by ERH knockdown. Our results show that ERH expression is increased in melanoma. Meanwhile, the proliferation and cell cycle transformation abilities are impaired potentially by downregulating the ERH expression in melanoma cells. Therefore, targeting ERH might serve as a novel therapeutic approach for malignant melanoma.

Early laparotomy and timely reconstruction for patients with abdominal electrical injury: Five Case Reports and Literature Review.

INTRODUCTION: High-tension electricity can cause devastating injuries that may result in abdominal wall loss, visceral damage, and sometimes major threat to life. The visceral organ may be exposed after debridement and require flap cover, but the tensile strength of abdominal wall may be lack even if flap transplanted. METHODS: From April 2007 through May 2015, 5 patients with severe abdominal electrical injury were treated at our hospital. Exploratory laparotomy was performed based on their clinical manifestations and debridement findings of abdominal wall at early stage, and decision regarding technique for reconstruction of abdominal wall was based on an assessment of the location and extent of the defect. Medical records were reviewed for these data. RESULTS: Clinical evaluation and debridement findings of the abdomen revealed 4 patients with suspicious visceral damage. Laparotomy was performed in 4 cases, and revealed obvious lesion in 3 cases, including segmental necrosis of small intestine, partial necrosis of diaphragm, left liver and gastric wall, and greater omentum. Five patients underwent abdominal wall reconstruction using island retrograde latissimus dorsi myocutaneous flap or free/island composite anterolateral thigh myocutaneous flap. All flaps survived, abdominal bulging occurred in 3 cases after follow-up of 12 to 36 months. CONCLUSIONS: The clinical manifestations and wound features of abdomen collectively suggest a possible requirement of laparotomy for severe abdominal electrical burns. Retrograde latissimus dorsi myocutaneous flap or composite anterolateral thigh myocutaneous flap is an effective option for reconstruction of abdominal wall loss, the long-term complication of abdominal bulging, however, remains a significant clinical challenge.

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.

Intrathecal lentivirus-mediated transfer of interleukin-10 attenuates chronic constriction injury-induced neuropathic pain through modulation of spinal high-mobility group box 1 in rats.

BACKGROUND: Neuropathic pain is a complex state of chronic pain that is usually accompanied by peripheral and central nervous system damage or dysfunction. Previous studies have indicated that neuroinflammation in the spinal cord is an important contributor to neuropathological and behavioral abnormalities. A series of early inflammatory markers, such as IL-1, TNF-α, and IFN-γ, and advanced inflammatory markers, such as high-mobility group box 1 (HMGB1), are involved in neuroinflammation. STUDY DESIGN: A randomized, double blind, controlled animal trial. OBJECTIVE: In this study, a lentivirus delivering human IL-10 (LV/hIL-10) was administered intrathecally to determine the effects of IL-10 on allodynia and hyperalgesia in a chronic constriction injury-induced (CCI) rat model of neuropathic pain. METHODS: Sprague-Dawley rats weighting 260 - 320 g were randomly divided into 4 groups. Group Sham (Sham), Group CCI±Normal Saline (NS), Group CCI±LV/hIL-10 (LV/hIL-10), and Group CCI±LV/control (vector). Rats in each group were intrathecally delivered with NS, LV/control, or recombinant vector LV/hIL-10 in a total volume of 10 µl. Paw withdrawal mechanical thresholds (PWMT) and paw withdrawal thermal latency PWTL were measured one day before CCI (baseline) and 0, 3, 7, 14, and 28 days after intrathecal administration. Cerebrospinal fluid (CSF) samples were collected during surgical plane anesthesia and the collected CSF samples were used to assay for human IL-10, rat IL-1ß, rat IL-6, and rat TNF-α by enzyme-linked immunosorbent assay (ELISA). Animals were sacrificed and the L4-5 lumbar segment of the spinal cord was removed for determination of green fluorescent protein (GFP) expression. Immunohistochemical analysis was performed using anti HMGB1 antibodies and the expression of HMGB1 protein in the spinal cord was determined by western blot analysis after intrathecal delivery (n = 8 each). RESULTS: The results show that intrathecal LV/hIL-10 reverses enhanced pain states. Moreover, the increased level of HMGB1 exhibited in a late stage of CCI was inhibited by exogenous overexpression of hIL-10 in the CCI model. Expression of HMGB1, RAGE, and pAkt were lower in CCI-induced rats treated with LV/hIL-10 than in those treated with LV/control (vector) or saline (NS). Our results showed that IL-10 inhibits activation of the inflammatory HMGB1-RAGE pathway in the CCI rat model. LIMITATIONS: Further experimental investigations are needed to clarify the specific biological roles played by HMGB1 in IL-10-mediated regulation of neuropathic pain. CONCLUSION: Our results indicate that intrathecal lentiviral-mediated transfer of IL-10 attenuates CCI-induced neuropathic pain in rats. The anti-thermal hyperalgesia and anti-mechanical allodynia may be partly attributable to the decreased expression of HMGB1 and inhibition of HMGB1-RAGE pathway.

IL-10 overexpression attenuated expression of TNF-α and IL-1ß activated by lipopolysaccharide in astrocytes.

OBJECTIVE: To investigate the intervention effect of lentivirus expressing human IL-10 (LV-hIL-10) on activated astrocytes. METHODS: DI TNC1 cell line was treated with different concentrations of lipopolysaccharide (LPS) and time points. The expression of proinflammatory cytokines tumor necrosis factor-α (TNF-α) and interleukinb-1ß (IL-1ß) was detected by RT-PCR and ELISA. Moreover, the effect on the expression of proinflammatory cytokines TNF-α and IL-1ß was analyzed in DI TNC1 cell lines infected with and without LV-hIL-10. RESULTS: The expression of TNF-α and IL-1ß was increased in DI TNC1 induced by LPS. The expression of IL-10 was upregulated in DI TNC1 infected with LV-hIL-10. TNF-α and IL-1ß were inhibited by IL-10 overexpression in DI TNC1 actived by LPS. CONCLUSION: DI TNC1 is activated by LPS and secretes proinflammatory cytokines TNF-α and IL-1ß as immune-like cells, and these activation is inhibited by hIL-10 overexpression.

[Construction and identification of RNAi lentiviral vector targeting at triggering receptors expressed on myeloid cells-1].

OBJECTIVE: To construct a lentiviral vector of RNA interference (RNAi) of murine triggering receptor expressed on myeloid cells-1(TREM-1) gene and to explore the effect of TREM-1 on the inflammatory response caused by Bacteroides fragilis. METHODS: Four target sequences were selected according to murine TREM-1 mRNA sequence, and then 4 pairs of double-strand DNA oligo according to these target sequences and one pair of negative control double-strand DNA oligo were designed and synthesized. These fragments were subcloned into pGCSIL-GFP/Lenti plasmid. After being identified by PCR and sequencing, these plasmids were cotransfected into 293T cells to package lentiviral particles. The lentiviral vector particles were transfected into Raw 264.7 cells and TREM-1 expression in the transfected cells was assayed by real-time PCR and ELISA. Different concentrations of Bacteroides fragilis lipopolysaccharide (LPS) were administered in the Raw264.7 cells, and the cells were stimulated with LPS for 12 h. TREM-1 expression was determined by real-time PCR and ELISA at the time points. RESULTS: PCR and sequencing confirmed that lentiviral vectors had the correct structure and could express high titer of virus. After being transfected into Raw264.7 cells, TREM-1 expression was knocked down significantly by all of these lentiviral vectors at both protein and mRNA levels, and the pGCSIL-GFP/Lenti-1 had the most efficient interference. TREM-1 was upregulated in the presence of Bacteroides fragilis LPS, and this increase was partly abrogated in the TREM-1 siRNA-treated cell models of endotoxemia, depending on the sequence. CONCLUSION: The lentivirus RNAi vector of TREM-1 was constructed successfully. The lentivirus RNAi vector of TREM-1 can inhibit the expression of TREM-1 in the murine endotoxemia model caused by Bacteroides fragilis LPS.

[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.

[Effect of lentiviral vector encoding on triggering receptor expressed on myeloid cells 1 on expression of inflammatory cytokine in septic mice infected by Bacteroides fragilis].

OBJECTIVE: To investigate the effect of triggering receptor expressed on myeloid cells 1 (TREM-1) vshRNA vector on expression of inflammatory cytokines and survival rate in septic mice infected by Bacteroides fragilis. METHODS: (1) TREM-1 vshRNA vector was constructed. Bacteroides fragilis (2.5 x 10(9) CFU/mL, 0.5 mL) was intraperitoneally injected in each mouse, and septic model was reproduced after 12 hours. (2) One hundred and fifteen mice were divided into healthy control group (n = 3, HC), sepsis group (n = 28, S), TREM-1 vshRNA group (n = 28, T), TREM-1 vshRNA hd group (n = 28, Th), GFP group (n = 28, G) according to random number table. Mice in S, T, Th, G groups were firstly injected with isotonic saline, TREM-1 vshRNA 2 x 10(8) TU, TREM-1 vshRNA 1 x 10(8) TU, GFP siRNA through tail vein, and then sepsis was induced after 1 hour. Mice in HC group were injected with equal volume of isotonic saline through tail vein. Three mice in each group were sacrificed after 12 hours for determination of plasma level of TNF-alpha, IL-1 beta and IL-6, and level of TREM-1mRNA and its protein in hepatic tissue. The survival rate of other mice in each group was monitored for 72 hours. (3) In 125 mice sepsis was reproduced, among them 100 mice were injected with TREM-1 vshRNA 2 x 10(8) TU after 1, 2, 4, 6 hours through tail vein (25 mice at each time point), other 25 mice were injected with equal volume of isotonic saline as control. The survival rate of mice in each group was recorded 72 hours after injection. RESULTS: (1) Compared with those in S group, the plasma level of TNF-alpha, IL-1 beta and IL-6 lowered in T and Th groups (P < 0.05), especially in T group, while those in G group showed no obvious difference (P > 0.05). (2) Compared with those in G group, the level of TREM-1mRNA and its protein in hepatic tissue in T and Th groups decreased (P < 0.01), especially in T group. (3) The survival rate of mice in S and G group was 16%, which was obviously lower than that in T and Th groups (76%, 44%, respectively, P < 0.05 or P < 0.01). (4) The survival rate of mice at 1, 2, 4, 6 hours after injection was 72%, 56%, 40%, 16%, respectively, while all that except at 6 hour after injection were higher significantly than that of control (P < 0.05 or P < 0.01). CONCLUSIONS: The intervention with TREM-1 vshRNA can effectively decrease hepatic level of TREM-1 in septic mice induced by Bacteroides fragilis, inhibit inflammatory response, and improve the survival rate.

[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.

The role of peroxisome proliferator-activated receptor-beta/delta in epidermal growth factor-induced HaCaT cell proliferation.

Epidermal growth factor (EGF) has been shown to be a potent mitogen for epidermal cells both in vitro and in vivo, thus contributing to the development of an organism. It has recently become clear that peroxisome proliferator-activated receptor-beta/delta (PPARbeta/delta) expression and activation is involved in the cell proliferation. However, little is known about the role of PPARbeta/delta in EGF-induced proliferation of HaCaT keratinocytes. In this study, HaCaT cells were cultured in the presence and absence of EGF and we identified that EGF induced an increase of PPARbeta/delta mRNA and protein level expression in time-dependent and dose-dependent manner, and AG1487, an EGF receptor (EGFR) special inhibitor, caused attenuation of PPARbeta/delta protein expression. Electrophoretic mobility shift assay (EMSA) revealed that EGF significantly increased PPARbeta/delta binding activity in HaCaT keratinocytes. Antisense phosphorothioate oligonucleotides (asODNs) against PPARbeta/delta caused selectively inhibition of PPARbeta/delta protein content induced by EGF and significantly attenuated EGF-mediated cell proliferation. Treatment of the cells with L165041, a specific synthetic ligand for PPARbeta/delta, significantly enhanced EGF-mediated cell proliferation. Finally, c-Jun ablation inhibited PPARbeta/delta up-regulation induced by EGF, and chromatin immunoprecipitation (ChIP) showed that c-Jun bound to the PPARbeta/delta promoter and the binding increased in EGF-stimulated cells. These results demonstrate that EGF induces PPARbeta/delta expression in a c-Jun-dependent manner and PPARbeta/delta plays a vital role in EGF-stimulated proliferation of HaCaT cells.

[Repair of high-voltage electrical burn in the neck].

OBJECTIVE: To explore methods of repair of high-voltage electrical burn in the neck. METHODS: Thirty-seven patients with high-voltage electrical burn in neck hospitalized since 1985 were enrolled in this study. After debridement, the wounds were repaired with latissimus dorsi myocutaneous flap, trapezius myocutaneous flap, platysma myocutaneous flaps, pectoralis major myocutaneous flap, or latissimus dorsi myocutaneous flap combined with pectoralis major myocutaneous flap. RESULTS: Necrosis occurred at edge of flap (about 1 - 2 cm in breadth) in 3 patients, and the other flaps survived well with perfect appearance and local function. CONCLUSION: To repair with pedicled myocutaneous flaps and combined flaps after early debridement can be safe, effective and reliable in the management of patients with high-voltage electrical burn in the neck.

[Expression of myeloid cell triggering receptor-1 in monocytes at early post-burn stage].

OBJECTIVE: To investigate the expression of triggering receptor expressed on myeloid cells (TREM-1) in monocytes of burn patients at early post-burn stage, and its significance. METHODS: The monocytes of 8 healthy volunteers (A group), 29 patients with mild and moderate burn (B group), and 9 patients with severe and very serious burns (C group) were isolated from the blood, and the THEM-1 mRNA and protein expression were determined by semi-quantitative RT-PCR and flow cytometry, respectively. The plasma levels of TNF-alpha, IL-1beta were determined by ELISA method. RESULTS: The value of TREM-1 mRNA expression in A, B and C groups were 0.74 +/- 0.13, 1.24 +/- 0.09, and 1.46 +/-0.07, respectively, and the expression rates on cell surface in the 3 groups were (9 +/- 4)%, (51 +/- 6)%, and (71 +/- 7)%, respectively, and there were significant differences among the three groups (P = 0.000). the plasma levels of TNF-alpha and IL-1beta in B and C groups were obviously higher than that in A group (P = 0.000), and they were positively correlated to TREM-1 expression (rs = 0.68, 0.72, P = 0.000). CONCLUSION: Increased expression of TREM-1 in monocytes of burn patients at early post-burn stage is correlated with the release of inflammatory factors, indicating that TREM-1 might contribute to the onset and development of acute inflammatory response after burns.

[Repair of skin and soft tissue defect around the malleolus by superior regressive island fasciocutaneous skin flap graft].

OBJECTIVE: To discuss the repairing procedure of skin and soft tissue defect around the malleolus, achilles tendon exposure, or calcaneus tendon exposure by superior regressive island fasciocutaneous skin flap graft. METHODS: We used the superior regressive island fasciocutaneous skin flaps to repair 13 cases of skin and soft tissue defect or achilles tendon exposure around malleolus after trauma, scar ulcer, tumor, or other occasions. The maximal size of skin and soft tissue defect was 6 cm x 14 cm. The maximal size of calcaneus exposure was 5 cm x 10 cm. RESULTS: Twelve cases obtained complete success with satisfactory results, and 1 case of necrosis delayed wound healing by latissimus dorsal myocutaneous flap graft. The follow-up lasted from 6 months to 4 years with satisfactory results. CONCLUSION: The superior regressive island fasciocutaneous skin flap graft is an effective and convenient method to repair skin and soft tissue defect around the malleolus, achilles tendon exposure, or calcaneus tendon exposure.

[Effect of antisense oligonucleotide against Smac/DIABLO on inhibition of hydrogen peroxide induced myocardial apoptosis of neonatal rats].

OBJECTIVE: To investigate the effects of antisense phosphorothioate oligonucleotides against Smac/DIABLO (asODN) on hydrogen peroxide (H2O2) induced myocardial apoptosis in neonatal rats. METHODS: Primary myocardial cells from neonatal rats were cultured in vitro, and randomly divided into A (normal control, without transfection), B (with treatment of single liposome), C (with transfection of scrODN), D (with transfection of asODN), E (with H2O2, stimulation), F (with H2O2 stimulation after scrODN transfection), and G (with H2O2 stimulation after asODN transfection) groups. The expression of asODN mRNA and protein were determined with RT-PCR and Western blotting, respectively. The changes in cellular nuclear morphology were observed with 33258 fluorescent staining, and the percentage of nuclear apoptosis was calculated. DNA fragmentation was observed by agarose gel electrophoresis. Activation of caspase-3 and caspase-9 were evaluated by caspase colorimetric analysis kit. RESULTS: The expression of Smac/DIABLO mRNA and protein was obviously inhibited by asODN, which was about 80% percent lower than the protein level in A,B and C groups, but there was no difference noted among A,B and C groups( P > 0.05). Not only the nuclear apoptotic percentage, but also the activity of caspase-3 and caspase-9 in A, C and D groups were in very low levels. But these indices in G group 24 hours after H2O2 stimulation were obviously lower than that in E and F groups [the nuclear apoptotic percentage were (19 +/- 5) %, (52 +/- 3) %, (55 +/- 5) %, respectively, P < 0.01)]. The DNA ladders in G group were also decreased markedly. CONCLUSION: Myocardial apoptosis induced by H2O2 can be inhibited by asODN in rat.