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Over the past 20 years, there have been substantial divergences in academia around the world on the issue of whether bacteria have transcription factors (TFs). The traditional view is that bacteria do not have TFs, and their transcriptional activators and/or repressors regulate the transcription initiation, and TFs only bind to eukaryotic promoters. The typical representative of the traditional view is the mainstream international textbooks of Biochemistry and Molecular biology edited by some academic authorities. However, the new idea is that DNA binding transcriptional activators and repressors in bacteria are TFs, and the content and importance of which are no less than those of eukaryotes. Although the new idea has long been common in academic papers published in international academic journals, many scholars still have doubts. The concept of " transcription factor", like many terms of molecular biology, is constantly updated with the development of sciences, from narrowly-defined sense to broadly-defined sense. In the beginning, people thought that TFs were only necessary for the transcription initiation of eukaryotic genes, and bacteria did not need TFs. It was understandable that bacteria were excluded from the TFs’ scope of application at that time. The rich scientific research achievements in the past 40 years have proved that a large number of transcriptional activators and repressors bind to cis-regulatory elements other than promoters, including enhancers, silencers, and insulators in eukaryotes, as well as a variety of positive and negative regulatory elements in bacteria. These transcriptional regulatory proteins conform to all the basic characteristics of TFs, which make them worthy of the name " transcription factors". Therefore, the new idea is scientific, reasonable, and should be widely accepted and adopted by the academic community. In the future, whether the concept of " transcription factor " will be further expanded to chromatin-modifying proteins such as histone acetyltransferase (HAT) and ncRNAs, and even to " elongation factors" and " termination factors" of transcription, we should be open to this issue.
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PURPOSE: Studies suggest that regular use of metformin may decrease cancer mortality. We investigated the association between diabetes medication use and cancer survival. MATERIALS AND METHODS: The current study includes 633 breast, 890 colorectal, 824 lung, and 543 gastric cancer cases identified from participants of two population-based cohort studies in Shanghai. Information on diabetes medication use was obtained by linking to electronic medical records. The associations between diabetes medication use (metformin, sulfonylureas, and insulin) and overall and cancer-specific survival were evaluated using time-dependent Cox proportional hazards models. RESULTS: After adjustment for clinical characteristics and treatment factors, use of metformin was associated with better overall survival among colorectal cancer patients (hazards ratio [HR], 0.55; 95% confidence interval [CI], 0.34 to 0.88) and for all four types of cancer combined (HR, 0.75; 95% CI, 0.57 to 0.98). Ever use of insulin was associated with worse survival for all cancer types combined (HR, 1.89; 95% CI, 1.57 to 2.29) and for the four cancer types individually. Similar associations were seen for diabetic patients. Sulfonylureas use was associated with worse overall survival for breast or gastric cancer (HR, 2.87; 95% CI, 1.22 to 6.80 and HR, 2.05; 95% CI, 1.09 to 3.84, respectively) among diabetic patients. Similar association patterns were observed between diabetes medication use and cancer-specific survival. CONCLUSION: Metformin was associated with improved survival among colorectal cancer cases, while insulin use was associated with worse survival among patients of four major cancers. Further investigation on the topic is needed given the potential translational impact of these findings.
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Humans , Breast , Cohort Studies , Colorectal Neoplasms , Electronic Health Records , Insulin , Lung , Metformin , Mortality , Proportional Hazards Models , Stomach NeoplasmsABSTRACT
Objective To explore the application of event-related potentials (ERP) by positive, negative, and neutral face expression images in the evaluation of mood disorders in brain traumatic patients.Methods ERP was tested by face expression images in 24 patients mainly with anxiety and depression symptoms (depression group) and 19 patients mainly with hostile and suspicion symptoms (hostile group), respectively.The findings were compared with those of the control group.Results There were no significant differences, between the depression group and the hostile group, on latencies and amplitudes of late positive potential (LPP) induced by the three types of face expression images, except the amplitude induced by negative face expression image.Compared with the control group, the latencies were extended and the amplitudes were lower in both depression and hostile groups.Within each group, the difference of latencies induced by the three images was not significant.The amplitudes induced by negative face expression image was higher than those induced by positive and neutral face expression images, with significant differences in the hostile group and the control group (P＜0.05) but not in the depression group.Conclusion Changes in latencies and amplitudes of LPP could be an objective indicator in the evaluation of mood disorders of brain traumatic patients.The LPP induced by negative face expression images could be more meaningful for patients mainly with anxiety and depression symptoms.
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Background and purpose: Abnormal expression and amplification of transforming growth factor beta 1 (TGF-β1) and Notch3 in ovarian carcinoma tissues are associated with metastasis and low survival rate, respectively. The crosstalk between TGF-β1 and Notch3 signaling pathway promotes invasion and metastasis in various cancers. However, the mechanism is still under debate. Therefore, this study was designed, using in vitro cytological assays, to investigate the effects of TGF-β1 and Notch3 signaling pathway on ovarian cancer cell biological behavior and the potential mechanisms in terms of the crosstalk between TGF-β1 and Notch3 signaling pathway. Methods: Hey A8 and Hey cell lines were used as models in the study. The levels of TGF-β1 in supernatants from culture media were measured by ELISA. Both cell lines were treated with 500 ng/mL TGF-β1 neutralizing antibody (control group), 10 ng/mL TGF-β1, 50 μmol/L DAPT, 10 ng/mL TGF-β1 and 50 μmol/L DAPT, 50 μmol/L tumor necrosis factor receptor-associated factor 6 (TRAF6) peptide inhibitor, 10 ng/mL TGF-β1 and 50 μmol/L TRAF6 peptide inhibitor, respectively. The protein expression levels of TGF-β1 and Notch3 signaling pathway molecules as well as TRAF6 from cell lines with different treatments were detected by Western blot. Cell proliferation, migration and invasion were tested by cell counting kit-8 (CCK-8), scratch and Transwell assays, respectively. Results: The levels of TGF-β1 were timedependently increased in supernatants of culture media from Hey A8 and Hey cell lines. Compared with control group, TGF-β1 treatment increased the expression levels of Notch3-ICD and Hes1, while no obvious change was observed in the group treated with DAPT and TGF-β1. Moreover, TGF-β1 promoted cell proliferation, migration and invasion while DAPT decreased the proliferation, migration and invasion in cell lines treated with TGF-β1. These results indicated that TGF-β1 might promote proliferation, invasion and migration of ovarian epithelial cancer cells through activating the Notch3 signaling pathway. Further study showed that TGF-β1 up-regulated TRAF6 and activated the Notch3 signaling pathway. The activation of the Notch3 signaling pathway by TGF-β1 was inhibited in cells treated with the TRAF6 specific inhibitor. Conclusions: TGF-β1 may promote the proliferation, invasion and migration of ovarian epithelial carcinoma cells through TRAF6-mediated activation of the Notch3 signaling pathway.
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Ovarian cancer bears the highest mortality in gynecologic cancer, and its 5-year survival rate is about 30%. Although 70% to 80% ovarian cancer is epithelial origin, increasing evidence indicates that reciprocal interactions between tumor cells and various types of stromal cells also play important roles in driving ovarian tumor progression and that these stromal cells represent attractive therapeutic targets. This review discusses the biological signiifcance of the cross-talk between ovarian cancer cells and three major types of stromal cells (endothelial cells, ifbroblasts and macrophages) and the development of new-generation therapies that target the ovarian tumor micro-environment.
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Background and purpose:Senescent cancer-associated ifbroblasts (CAFs) in tumor microenvi-ronment are known to mediate the invasion and radio- or chemo-resistance of epithelial cancers. The inflammatory cytokine IL-6 derived from CAFs may promote the invasion and radio-resistance of epithelial cervical cancer. However, the detailed mechanism is not clear. This study aimed to investigate the effects of IL-6 on CAFs senescence, cervical cancer cell invasiveness and radio-resistance.Methods:CAFs from cervical cancer, normal ifbroblasts (NFs) from nor-mal cervical tissues, and cervical cancer cell lines including HeLa, Siha and ME180 were used in this study. Different treatments of cells with IL-6 and inhibitors of STAT3 and Notch were conducted to investigate the alterations of cellular senescence, STAT3/Notch signaling, cell invasiveness, and radiotherapy-induced apoptosis by using cell staining, immunolfuorescence, Western blot, and lfow cytometery.Results:This study found that the conditioned medium (CM) of CAFs or IL-6 could activate the STAT3 and Notch signaling to promote cellular senescence and cervical cancer cell invasiveness. Co-culture of cervical cancer cells HeLa or Siha along with CAFs also increased the invasiveness of can-cer cells, but further treatments of cells by addition of an IL-6 antibody or the inhibitors of STAT3 (S31-201) or Notch (DAPT) blocked the cancer cell invasion. Meanwhile, this study also found that STAT3 functions at the upstream of the Notch signaling to up-regulate Jagged-1, one of the key ligands of Notch in ifbroblasts or epithelial cancer cells through IL-6-mediated autocrine or paracrine pathways, which eventually confers the radio-resistance of cervical cancer cells/tissues.Conclusion:CAFs in tumor microenvironment could induce cervical cancer cell invasiveness and radio-re-sistance through IL-6/STAT3-mediated Notch activation, and that targeting of the STAT3/Notch signaling-associated molecules may improve the effcacy of radiotherapy for cervical cancer.
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Background and purpose:About 80%patients with oral and maxillofacial malignant tumor are oral squamous cell carcinoma (OSCC). OSCC is one of the most common cancers in the world with less than 50%survival rate over 5 years. This experiment aimed to explore the effect of stanniocalcin 2 (STC2) on apoptosis, proliferation, migration and invasion of OSCC cell. Methods:RNA interference (RNAi) vector pLKO.1-shSTC2 was constructed and transfected into KB cells. Cell proliferation and cell apoptosis were then assessed by CCK8, APC Annexin V/7-AAD and lfow cytometry. Differences of migration and invasion between KB scr and KB STC2i were examined by cell scratch and transwell tests. Finally, this study detected the apoptosis-associated proteins and metastasis-associated proteins by Western blot. Results:STC2 down-regulation plasmid was constructed and transfected into KB cells. CCK8 prolifera-tion assay revealed that the STC2 down-regulation inhibited KB cells proliferation. By treating with cisplatin, this study found that STC2 silence could facilitate cell apoptosis signiifcantly. With the knock down of STC2 gene, the expressions of Bcl-2, Caveolin-1 andβ-catenin were decreased but the expression of bax was obviously increased. Conclusion:These data suggest that STC2 may be involved in the apoptosis, proliferation, migration and invasion of OSCC KB cells. Simultaneously, it can signiifcantly weaken the sensitivity of KB cells to chemotherapeutic drug cisplatin.
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<p><b>BACKGROUND</b>The N400 component of event-related potentials (ERP) has recently drawn widespread attention at home and abroad. This study was to explore the relationship between N400 changes and risperidone treatment and rehabilitation infirst-episode schizophrenia (FES).</p><p><b>METHODS</b>ERP component N400 was recorded by Guangzhou Runjie WJ-1 ERP instruments, in 58 FES before and 6 months, 15 months after risperidone treatment, and in 62 normal controls. The patients' syndromes were assessed by Positive and Negative Syndrome Scale (PANSS). And the stimuli are Chinese sentences with matching (congruent) or mismatching (incongruent) ending words.</p><p><b>RESULTS</b>N400 latencies were prolonged, and amplitudes were decreased in Cz, Pz, Fz, C3, C4, in FES compared with in NC, before treatment. The prolonged N400 latencies and decreased amplitudes were negatively correlated with the patients' positive scale and total scale of PANSS. There are significant differences of N400 amplitudes and latencies in 6 months and 15 months follow-up after treatment. Before treatment, 6 months and 15 months after treatment, N400 latencies are 446 ± 35 ms, 440 ± 37 ms, 414 ± 31 ms (F = 9.72, P < 0.01) in incongruent situation; N400 amplitudes are 5.2 ± 4.6 μV, 5.7 ± 4.8 μV, 7.3 ± 5.0 μV (F = 2.06, P > 0.05) in congruent situation, and 8.5 ± 5.9 μV, 10.1 ± 5.0 μV, 11.9 ± 7.0 μV (F = 3.697, P < 0.05) in incongruent situation.</p><p><b>CONCLUSIONS</b>N400 could be used to predict the effects of treatment of schizophrenia to some degree. The linguistic and cognitive impairment in schizophrenia can be improved by antipsychotic drugs.</p>
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Adult , Humans , Middle Aged , Evoked Potentials , Follow-Up Studies , Risperidone , Therapeutic Uses , Schizophrenia , Drug Therapy , RehabilitationABSTRACT
Background and purpose: Cancer-associated fibroblasts (CAFs) are known to promote the invasion and metastasis of epithelial cancers. The cytokine IL-6 may mediate the interaction between stromal cells and epithelia in tumor microenvironment to facilitate the invasiveness and metastasis of cancer, however, such mechanism has not been fully covered yet.Methods:We used cervical cancer cell line HeLa as a model for this study. ELISA was used to measure the levels of IL-6 in CAFs and normal ifbroblasts (NFs) isolated from squamous cervical cancer or normal cervical tissues. CAFs conditioned medium or IL-6 was used to treat cervical cancer HeLa cell line. The epithelial-mesenchymal transition (EMT) markers such as N-Cadherin and Vimentin were detected by Western blot in cells before and after treatment. Scratches and transwell chambers were used to test the abilities of cell migration and invasion. Results:The levels of IL-6 were 4-5 folds higher in CAFs than in NFs. Treatment of HeLa cells with CAF conditioned medium or IL-6 upregulated N-Cadherin and Vimentin, but down-regulated E-Cadherin and cytokeratin, compared with control cells, indicating that IL-6 may stimulate HeLa cells to EMT. Further study found that Snail 1, the featured transcription factor for stem cells, was increased along with the enhanced phosphorylation of STAT3. Meanwhile, the migration and invasion of HeLa cells treated with IL-6 or CAF conditioned medium were markedly increased. Conclusion:CAF induces the EMT of cervical epithelial cancer cells through IL-6/STAT3/Snail pathway, which thereby promotes the invasiveness and metastasis cervical epithelial cancer.
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Background and purpose:Ovarian cancer-associated ifbroblasts (CAF) are known to promote epithelial malignancy. The chemoattractant cytokine growth-regulated oncogene alpha (Gro-α) secreted from CAF has been reported to mediate the stroma-epithelia interaction in tumor microenvironment, leading to the development of epithelial ovarian cancer, however, the detailed mechanism is unknown.This study was to determine whether Gro-αcould promote ovarian tumorigenesis through activating NF-кB nuclear translocation and VEGF expression in stromal ifbroblasts. Methods:ELISA was used to measure the levels of Gro-αin two cancer-associated ifbroblasts (CAF) and normal ifbroblasts (NF) isolated from high-grade serous ovarian cancer or normal ovarian tissues. CAF conditioned medium (CM) or Gro-αwas used to treat NF, while PS1145, the inhibitor of NF-кB, was used as control. NF-кB subunit p65 and vascular endothelial growth factor (VEGF) were detected by Western blot in cells after treatment. Xenograft tumors from nude mice were generated by injection of CAF, NF, or OVCA429 alone or OVCA429 mixed with CAF or NF, and by injection of OVCA429 mixed with NF cells that were treated with or without CAF-CM or Gro-α, or with NF cells that were treated with CAF-CM or Gro-αplus PS1145. The tumor growth curve was measured and the blood vessel density in xenograft tumor tissues was examined by histopathological analysis. Results:The levels of Gro-αwere 5-6 folds higher in CAF than in NF. Treatment of NF with CAF-CM or Gro-αstimulated the nuclear translocation of NF-кB subunit p65, and the expression of VEGF, but suppressed the expression of thrombospondin 1, the anti-angiogenesis factor, compared with control cells. However, treatment of NF with the NF-кB inhibitor PS1145 reversed these results. The animal assay revealed that CAF stimulated tumor growth stronger than NF, and NF treated with CAF-CM or Gro-α, but not along with PS1145, enhanced xenograft tumor growth through promoting angiogenesis. Conclusion:Ovarian CAF promotes the nuclear translocation of NF-кB and the expression of VEGF through Gro-αautocrine in tumor microenvironment to facilitate angiogenesis and ovarian cancer development.
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Breast cancer stem cells comprise a sub-population, which enables the capacity for self-renewal and the potentiality for differentiation and high tumorigenicity. Growing evidence suggests that breast cancer stem cells most likely contribute to tumor generation, progression, relapse, metastasis and therapeutic resistance. Herein, the recent advances in breast cancer stem cells were highlighted in this review.
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10.3969/j.issn.1007-3969.2013.04.00X
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Background and purpose:Aurora-A is a member of serine/threonine kinase family. The abnormal expression of Aurora-A induces tumorigenesis and radioresistance. This study was aimed to investigate the association of Aurora-A with radioresistance. Methods: Capan-1 cells were treated with Aurora-A kinase inhibitor, and then used to test cell proliferation, anchorage independent assay, cell cycle, and cell cycle regulatory proteins. Treated cells were also used to detect cell apoptosis afterγ-irradiation. Results:Cell growth and colony number in soft agar were decreased after treatment with Aurora-A inhibitor. Treatment of cells with Aurora-A inhibitor also down-regulated the expression of Cyclin D1, CDK2 and CDK6 to induce cell cycle arrest at G1/S and G2/M phases, but promoted cell apoptosis afterγ-irradiation. Conclusion:Treatment of pancreatic cancer cells with Aurora-A kinase inhibitor blocks cell proliferation and cell cycle progression, and promotes sensitivity of cells to radiation. Thus, Aurora-A may be used as one of therapeutic targets to increase the sensitivity of pancreatic cancer radiotherapy.
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Background and purpose:Triple-negative breast cancer (TNBC) possesses high risk of relapse and metastasis. Clinically, there are no speciifc targeted-therapies to TNBC except chemotherapy. Therefore, studying the mechanism of relapse and metastasis has signiifcance to improve the patients’ survival rate. This experiment aimed to study the effect of MAPK activation on migration and invasion of triple-negative breast cancer cells. Methods:Difference of migration and invasion between lung-high metastasis breast cancer cell line 231-HM and its parental cell line 231-p were first examined by cell scratch and transwell;Then, metastasis-associated proteins and MAPK-associated molecules were detected by Western blot; Last, 231-p cells were treated with P38/MAPK inhibitor and used to determine cell migration, invasion, and metastasis-associated proteins thereafter. Results:Compared with the parental cell line 231-p, 231-HM cells displayed obviously higher ability of migration and invasion. With the increased expression of Caveolin-1and β-catenin, the phosphorylation of MAPK-associated molecules including P38, Erk1/2, and MEK was highly decreased. Treatment of 231-p cells with low concentration (10 μmol/L) of the P38/MAPK inhibitor SB202190 increased the migration and invasion of 231-p cells, and the expression of Caveolin-1 andβ-catenin. Conclusion:Activation of MAPK signaling inhibits the migration and invasion of triple-negative breast cancer.
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Notch signal pathway is one of crucial pathways related to cell fate determination, regulating cell differentiation, proliferation and apoptosis, with an effect of organ formation and morphogenesis. Abnormal activation of Notch gene occurs in many tumor cells, such as brain tumors, breast cancer and hepatoma. Recent studies have been found that the notch pathway out of control was related with growth of ovarian cancer. And Notch3 involving in the development and progression of ovarian cancer has been attracted extensive attention by experts and scholars. This review focuses on the literatures of Notch3 and related molecules regulating the development and progression of epithelial ovarian cancer.
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<p><b>OBJECTIVE</b>To discuss the clinical safety about repairing the peripheral nerve defects with the acellular allogeneic nerve.</p><p><b>METHODS</b>The 41 patients (male 38, female 3, age 10 - 55 years old, average 28.9 years old) who were performed chemically extracted acellular nerve allograft transplanting to repair nerve defects from 2002 to 2011. The average interval from injury to nerve repairing was 4.1 months (range, 10 hours to 9 months). There were 41 cases nerve defects including 10 brachial plexus nerves, 3 radial nerves of upper arm, 4 ulnar nerves of forearm, 12 digital and toe nerves, 2 sciatic nerves, 2 femoral nerves, 3 tibial nerves and 5 common peroneal nerves. There were 12 cases combined fractures and 20 soft tissue injury or defects. The average length of the nerve allograft to bridge the nerve defects was 6.1 cm (range, 2 - 10 cm). No immunosuppressive drugs were used in all cases. The clinical safety was evaluated through physical examination, blood biochemistry and immunity detection.</p><p><b>RESULTS</b>All cases were followed up post-operation. They got primary wound healing except 2 superficial infection who got delay healing through dressings changing. No any adverse effects happened including immunological rejection, hypersensitivity reaction, deep infection, hepatotoxicity and nephrotoxicity.</p><p><b>CONCLUSIONS</b>It is safe and feasible to repairing human peripheral nerve defects with chemically extracted acellular nerve allograft.</p>
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Adolescent , Adult , Child , Female , Humans , Male , Middle Aged , Young Adult , Follow-Up Studies , Peripheral Nerve Injuries , General Surgery , Peripheral Nerves , Transplantation , Transplantation, Homologous , Treatment OutcomeABSTRACT
<p><b>BACKGROUND</b>Intensive blood glucose control is proven to be associated with the diabetic microvascular and macrovascular complications, which could affect quality of life (QOL). This study was performed to determine the effects of intensive glucose control therapy on QOL of elderly patients with type 2 diabetes in Anhui Province.</p><p><b>METHODS</b>Ninety-seven elderly patients with type 2 diabetes in Anhui were randomly assigned to standard treatment group and intensive therapy group. All patients were followed up for five years on average. Correlated information has been collected during the regular follow-up.</p><p><b>RESULTS</b>Patients with microvascular complications reported significantly lower European Quality of Life-5 Dimensions (EQ-5D) scores and had more problems with usual activities, pain and anxiety than those without complications (P < 0.05). Patients having experienced hypoglycemic episodes had significantly more problems with anxiety than those without hypoglycemic episodes (P < 0.05). No significant difference was detected in all dimensions in quality of life, as well as in Visual Analog Scale score between two groups (P > 0.05). There was no significant difference in quality of life at the fifth year compared with that of the first year in both groups. Women had more feelings of pain and anxiety than men (P < 0.05) and longer disease course was associated with increased levels of pain and anxiety (P < 0.05), as well as with lower QOL. In addition, patients with higher body mass index (BMI) had more problems with daily activities than patients with lower BMI (P < 0.05).</p><p><b>CONCLUSIONS</b>Anxiety is common in elderly diabetic patients and they experienced frequent hypoglycemic episodes. Diabetic vascular complications significantly affect QOL of the patients. Intensive glucose control has no significant effect on QOL of the diabetic patients. Female, older age, long disease course, less education and high BMI are all factors caused reduced QOL and patients with these factors should be given more psychological support. Frequent mild hypoglycemic episodes do not cause impaired function of the central nervous system.</p>
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Aged , Female , Humans , Male , Middle Aged , Blood Glucose , Metabolism , Diabetes Mellitus, Type 2 , Blood , Fasting , Blood , Glycated Hemoglobin , Metabolism , Quality of LifeABSTRACT
<p><b>OBJECTIVE</b>To screen human stem cell factor (hSCF) mimetic peptides in vitro with a phage-display random peptide library.</p><p><b>METHODS</b>Phage clones with high hSCF receptor (rc-kit/Ig 1-3)-binding activity was screened from phage-displayed random hepta/dodecapeptide library by phage enzyme-linked immunosorbent assay (ELISA). Phage single DNA was extracted and sequenced. Four kinds of peptide with higher c-Kit/Ig 1-3 binding activity were chosen for synthesis and characterized by using cell proliferation assay with 3-(4,5-dimethylthiazol-2-yl)2,5-diphenyltetrazolium bromide (MTT) method in UT-7 cells.</p><p><b>RESULTS</b>Eleven Ph.D.-C7C clones and eight Ph.D-12 phage clones with high hSCF receptor-binding activity were selected from phage-displayed random hepta/dodecapeptide library, respectively. Sequence analysis showed there were no homologous sequence between hSCF and these screened mimetic peptides except one homologous sequence DPSPHTH found in heptapeptide library. All these four synthesized peptides (CE3, CE16, LE4, and LE20), particularly CE16 and LE20, stimulated UT-7 cell proliferation.</p><p><b>CONCLUSION</b>Four hSCF mimetic peptides were successfully isolated from phage-displayed random peptide library..</p>
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Humans , Peptide Library , Peptides , Genetics , Stem Cell Factor , GeneticsABSTRACT
<p><b>OBJECTIVE</b>To study the value and surgical techniques of transplantation of large anterior latissimus dorsi muscular flap combination with musculus rectus abdominis flap.</p><p><b>METHODS</b>Three cases (2 male and 1 female) with skin defect and bone exposed were reviewed from May 2005 to January 2007. Two patients suffered from trauma, and 1 suffered from tumor resection. Flaps size were: 60 cm x 32 cm, 55 cm x 30 cm and 50 cm x 25 cm, flaps pattern including: 1 free flap with 2 ends of vascular, 1 flap with pedicle and free vascular end, 1 flap with 2 ends of pedicle.</p><p><b>RESULTS</b>Two flaps survived completely, 1 flap with necrosis edge eventually healed after change of dressing. The infection had been effectively controlled and ready for function recovered. One case caused by trauma recovered with fracture healing, full weight-bearing and restore the original work.</p><p><b>CONCLUSIONS</b>Large anterior latissimus dorsi muscular flap combination with musculus rectus abdominis flap can be used for repair of large skin defect. For the difficulty and technical requirements, surgical indications should be strictly controlled.</p>
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Adult , Female , Humans , Male , Middle Aged , Follow-Up Studies , Microsurgery , Muscle, Skeletal , General Surgery , Rectus Abdominis , General Surgery , Skin , Wounds and Injuries , Skin Transplantation , Methods , Surgical FlapsABSTRACT
<p><b>OBJECTIVE</b>To discuss the curative effect of the external fixator for complex tissue defect in the forearm.</p><p><b>METHODS</b>From May, 2005 through December, 2008, the external fixators were used in 17 patients to treat the complex tissue defect in the forearm caused by trauma. There were 11 male and 6 female, with a mean age of 25.6. All patients were accompanied with the exposure of tendon, muscle or screw. The skin defect ranged from 7 cm x4 cm to 19 cm x9 cm. All patients underwent pedicle flap repair. The flap ranged from 10 cm x 6 cm to 20 cm x 15 cm. The proximal pedicle of the flap was sutured into a tubular. The position of the pedicle was fixed by the external fixator. The pin was at the ulnar and the iliac (n=5), and the radius and the iliac (n=12). The immobilization lasted 3 to 8 weeks, 5.1 weeks in average.</p><p><b>RESULTS</b>All patients were followed up for 3 to 20 months, 11.3 in average. All pedicle flaps survived with no pressure ulcer, or no erosion in the axilla. No compartment syndrome or osteomyelitis occurred. Four to six week after surgery, the pedicle was cut. Infection occurred at the cutting end in 1 patient. The wound healed after addressing. The wound in the other 16 patients healed successfully. The fracture of the ulnar and the radius healed 8.5 or 15 weeks after surgery, 13.5 weeks in average. Eleven patients underwent second stage reshape and function restoration. The function of the hands and forearms recovered satisfactorily. Eleven patients returned to their work. Six patients can live with basic function for living.</p><p><b>CONCLUSIONS</b>The external fixator used for complex tissue defect in the forearm can keep the position of the pedicle, replacing plaster fixation. It can reduce the incidence of flap and vessel spasm, and get good outcomes.</p>