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BACKGROUND@#Sweat secreted by eccrine sweat glands is transported to the skin surface through the lumen. The eccrine sweat gland develops from the initial solid bud to the final gland structure with a lumen, but how the lumen is formed and the mechanism of lumen formation have not yet been fully elucidated. This study aimed to investigate the mechanism of lumen formation of eccrine gland organoids (EGOs).@*METHODS@#Human eccrine sweat glands were isolated from the skin for tissue culture, and the primary cultured cells were collected and cultured in Matrigel for 14 days in vitro. EGOs at different development days were collected for hematoxylin and eosin (H&E) staining to observe morphological changes and for immunofluorescence staining of proliferation marker Ki67, cellular motility marker filamentous actin (F-actin), and autophagy marker LC3B. Western blotting was used to detect the expression of Ki67, F-actin, and LC3B. Moreover, apoptosis was detected using a terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) apoptosis assay kit, and the expression of poly (ADP-ribose) polymerase and Caspase-3 was detected by Western blot. In addition, 3-methyladenine (3MA) was used as an autophagy inhibitor to detect whether the formation of sweat glands can be effectively inhibited.@*RESULTS@#The results showed that a single gland cell proliferated rapidly and formed EGOs on day 4. The earliest lumen formation was observed on day 6. From day 8 to day 14, the rate of lumen formation in EGOs increased significantly. The immunofluorescence and Western blot analyses showed that the expression of Ki67 gradually decreased with the increase in days, while the F-actin expression level did not change. Notably, the expression of autophagy marker LC3B was detected in the interior cells of EGOs as the apoptosis signal of EGOs was negative. Compared with the control group, the autophagy inhibitor 3MA can effectively limit the formation rate of the lumen and reduce the inner diameter of EGOs.@*CONCLUSION@#Using our model of eccrine gland 3D-reconstruction in Matrigel, we determined that autophagy rather than apoptosis plays a role in the lumen formation of EGOs.
Subject(s)
Humans , Apoptosis , Autophagy , Eccrine Glands , Epithelial Cells , OrganoidsABSTRACT
To unravel the role of hematopoietic pre-B-cell leukemia transcription factor interacting protein(HPIP)in the proliferation,cell cycle,and apoptosis of pancreatic ductal adenocarcinoma(PDAC)cells. The HPIP expression in PDAC tissue was determined by immunohistochemical staining.Knockdown of HPIP was accomplished in MIA PaCa-2 and BxPC-3 cell lines by transient transfection of HPIP siRNA and validated by Western blotting.Cell proliferation was assessed using the cell counting kit-8 assay and colony formation assay.Cell cycle and apoptosis were detected by flow cytometry.Western blotting was performed to detect the expression levels of cyclin D1,caspase 7,and cleaved caspase 7. HPIP was overexpressed in PDAC tissue compared with matched adjacent pancreatic tissue(=-2.060,=0.039).Knockdown of HPIP inhibited the proliferation of MIA PaCa-2 and BxPC-3 cells(all <0.05).Knockdown of HPIP significantly reduced the positive colonies formed by MIA PaCa-2 and BxPC-3 cells(=4.706,=0.009;=9.514,=0.000).Knockdown of HPIP decreased the proportion of S phase cells(=7.642,=0.001;=2.714,=0.051)and increased the proportion of G/G phase cells(=3.244,=0.031;=6.095,=0.003)in MIA PaCa-2 and BxPC-3 cells.Meanwhile,knockdown of HPIP increased the proportions of late-phase MIA PaCa-2 and BxPC-3 cells(=24.58,=0.000;=36.45,=0.000)and the overall apoptosis rate(=29.43,=0.000;=43.52,=0.000).In MIA PaCa-2 and BxPC-3 cells,knockdown of HPIP decreased the expression level of cyclin D1(=6.705,=0.002;=6.238,=0.003)and increased the expression level of cleaved caspase 7(=3.991,=0.016;=6.536,=0.002). HPIP is overexpressed in PDAC tissue.Knockdown of HPIP inhibits the proliferation and G/G to S transition of PDAC cells.Meanwhile,knockdown of HPIP promotes the apoptosis of PDAC cells.Thus,HPIP may act as an oncogene in PDAC.
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Pancreatic ductal adenocarcinoma (PDAC) is an extremely malignant disease, which has an extremely low survival rate of <9% in the United States. As a new hallmark of cancer, metabolism reprogramming exerts crucial impacts on PDAC development and progression. Notably, arginine metabolism is altered in PDAC cells and participates in vital signaling pathways. In addition, arginine and its metabolites including polyamine, creatine, agmatine, and nitric oxide regulate the proliferation, growth, autophagy, apoptosis, and metastasis of cancer cells. Due to the loss of argininosuccinate synthetase 1 (ASS1) expression, the key enzyme in arginine biosynthesis, arginine deprivation is regarded as a potential strategy for PDAC therapy. However, drug resistance develops during arginine depletion treatment, along with the re-expression of ASS1, metabolic dysfunction, and the appearance of anti-drug antibody. Additionally, arginase 1 exerts crucial roles in myeloid-derived suppressor cells, indicating its potential targeting by cancer immunotherapy. In this review, we introduce arginine metabolism and its impacts on PDAC cells. Also, we discuss the role of arginine metabolism in arginine deprivation therapy and immunotherapy for cancer.
Subject(s)
Humans , Arginine/metabolism , Argininosuccinate Synthase , Carcinoma, Pancreatic Ductal/drug therapy , Cell Line, Tumor , Pancreatic Neoplasms/drug therapyABSTRACT
Background@#Plasminogen activator inhibitor 1 (PAI-1) was previously established to impact several phenotypes in many kinds of cancer, including pancreatic cancer. However, its prognostic significance in pancreatic ductal adenocarcinoma (PDAC) needs support of further evidence. This study was designed to address the issue.@*Methods@#PAI-1 expression was detected by tissue microarray-based immunohistochemical staining in formalin-fixed paraffin-embedded specimens from 93 PDAC patients with surgical resection from September 2004 to December 2008. Its relationships with clinicopathologic variables and tumor-specific survival (TSS) were further evaluated using Chi-square, Kaplan-Meier, log-rank, as well as Cox regression analyses.@*Results@#Expression of PAI-1 was much higher in tumor than that in nontumor tissues, based on comparison of all samples and 74 matched ones (95 [47.5, 180] vs. 80 [45, 95], Z = -2.439, P = 0.015 and 100 [46.9, 182.5] vs. 80 [45, 95], Z = -2.594, P = 0.009, respectively). In addition, tumoral PAI-1 expression was positively associated with N stage (22/35 for N1 vs. 21/51 for N0, χ = 3.903, P = 0.048). Univariate analyses showed that TSS of patients with high PAI-1 tumors was significantly poorer than that of those with low PAI-1 tumors (log rank value = 19.00, P < 0.0001). In multivariate Cox regression test, PAI-1 expression was identified as an independent predictor for long-term prognosis of resectable PDAC (hazard ratio = 2.559, 95% confidence interval = 1.499-4.367, P = 0.001).@*Conclusion@#These results suggest that expression of PAI-1 is upregulated in PDAC and might serve as a poor prognostic indicator.
Subject(s)
Adult , Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Carcinoma, Pancreatic Ductal , Chemistry , Mortality , Pathology , Immunohistochemistry , Pancreatic Neoplasms , Chemistry , Mortality , Pathology , Plasminogen Activator Inhibitor 1 , Prognosis , Proportional Hazards ModelsABSTRACT
Objective To investigate the impact of 5-fluorouracil (5-FU) on miR-22 expression in human hepato-cellular carcinoma (HCC) cell lines and to elucidate the molecular mechanism of 5-fluorouracil for HCC chemo-therapy. Methods Real-time PCR analysis was conducted to determine the expression levels of miR-22 in HCC tissue specimens and HCC cell lines. The expression of miR-22 and pri-miR-22 (primary miR-22) was evaluated in HepG2 and Huh7 cells with 5-FU treatment by using real-time PCR and we also performed Western blot analysis to detect the protein level of HDAC4 in HCC cells with the same treatment. A rescue assay was employed by using 5-FU treatment in combination with miR-22 inhibitor(Anti-22) to further investigate the correlation among 5-FU, miR-22,and HCC cell growth. Results miR-22 expression depicted a significant downregulation in HCC tissues and cell lines (P<0.01). 5-FU treatment led to an augment of miR-22 expression in HepG2 and Huh7 cells(P<0.001) and resulted in a decrease of HDAC4 protein levels, which was verified as a direct target of miR-22 in HCC cells (P<0.01). Conclusions 5-FU has suppressive effect on HCC growth which could be potentially ex-plained by miR-22-mediated HDAC4 axis.
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Objective To investigate the impact of 5-fluorouracil (5-FU) on miR-22 expression in human hepato-cellular carcinoma (HCC) cell lines and to elucidate the molecular mechanism of 5-fluorouracil for HCC chemo-therapy. Methods Real-time PCR analysis was conducted to determine the expression levels of miR-22 in HCC tissue specimens and HCC cell lines. The expression of miR-22 and pri-miR-22 (primary miR-22) was evaluated in HepG2 and Huh7 cells with 5-FU treatment by using real-time PCR and we also performed Western blot analysis to detect the protein level of HDAC4 in HCC cells with the same treatment. A rescue assay was employed by using 5-FU treatment in combination with miR-22 inhibitor(Anti-22) to further investigate the correlation among 5-FU, miR-22,and HCC cell growth. Results miR-22 expression depicted a significant downregulation in HCC tissues and cell lines (P<0.01). 5-FU treatment led to an augment of miR-22 expression in HepG2 and Huh7 cells(P<0.001) and resulted in a decrease of HDAC4 protein levels, which was verified as a direct target of miR-22 in HCC cells (P<0.01). Conclusions 5-FU has suppressive effect on HCC growth which could be potentially ex-plained by miR-22-mediated HDAC4 axis.
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<p><b>BACKGROUND</b>Pancreatic cancer is a lethal disease that is often diagnosed at an advanced stage. There is a lack of information to predict the prognosis of pancreatic cancer. Krüppel-like factor (KLF) 8 has been found to be deregulated in multiple cancers, and its high expression was correlated with poor prognosis. However, so far, no information was reported about the expression of KLF8 in pancreatic cancer. In the present study, we investigated, possibly for the first time, the expression of KLF8 in pancreatic cancer samples and analyzed its correlation with clinical parameters and overall survival (OS) rate.</p><p><b>METHODS</b>We used immunohistochemical staining to detect KLF8 in 68 samples from patients who underwent surgery and its correlation with the clinicopathological characteristics. We used Kaplan-Meier curve to analyze the relationship between KLF8 expression and the OS time. Univariate analysis was performed in addition to multivariate hazard models with clinicopathological features to assess KLF8 as an independent prognostic factor.</p><p><b>RESULTS</b>KLF8 was present in the cytoplasm of pancreatic cancer cells and 52.9% of the 68 cases had positive expression. KLF8 expression was not associated with sex, age, tumor location, lymph node stage, and metastasis stage, but was associated with tumor stage (P = 0.04). Kaplan-Meier method demonstrated that patients with negative expression of KLF8 had a better prognosis. In univariate and multivariate models, KLF8 was a significant predictor of OS in pancreatic cancer.</p><p><b>CONCLUSION</b>Our results revealed that KLF8 may be a potential prognostic factor for pancreatic cancer.</p>
Subject(s)
Aged , Female , Humans , Male , Middle Aged , Immunohistochemistry , Kaplan-Meier Estimate , Pancreatic Neoplasms , Metabolism , Pathology , Prognosis , Repressor Proteins , MetabolismABSTRACT
Objective To investigate the inhibitory effect of 5-fluorouracil (5-FU) on hepatocellular carcinoma (HCC) cell growth and to elucidate its potential molecular mechanism.Methods Real-time PCR analysis was conducted to determine the expression of miR-373 in HCC tissue specimens and HCC cell lines.The expression of miR-373 was also evaluated in HepG2 cells after 5-FU treatment.Western blot analysis was performed to detect the protein levels of PPP6C,a verified target of miR-373,with transfection of miR-373 mimics or 5-FU treatment.A rescue assay was conducted to investigate the cell growth in HepG2 cells by using CCK-8.Results miR-373 expression was up-regulated in both HCC tissues and cell lines.miR-373 expression depicted about 2.94-fold augment in HepG2 cells as compared to normal liver cells control (P ＜0.01).5-FU treatment led to a significant decrease of miR-373 levels (approximately 50％,P ＜0.01,48 h) and resulted in a marked increase of PPP6C protein (approximately 2.1-fold,48 h) in HepG2 cells.The overexpression of miR-373 could prevent the impact of 5-FU treatment on cell growth in HepG2 cells and CCK-8 assay showed that HepG2 cell growth was rescued approximately 81％ and 84％ at 24 h (P ＜ 0.05) and 48 h (P ＜ 0.01),respectively.Conclusion 5-FU can repress endogenous miR-373 level,which activates the expression of downstream targeted gene PPP6C,thereby exerting an inhibitory effect on HepG2 cells.
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Pancreatic cancer is one of the most malignant tumors with a high mortality rate attributed to its widespread metastasis.A number of cellular signal transduction pathways involved in multiple genes play an important role in regulating this complex metastatic cascade of pancreatic cancer.NF-kappa B is one of the crucial signaling pathways.Studies has indicated that NF-kappa B could modulate a series of biological events relevant to tumor progress by controlling multiple targeted genes expression,such as cell proliferation,anti-apoptosis,angiogenesis,epithelial-mesenchymal transition,inflammation,stress response,etc.Furthermore,it can also up-regulate Hedgehog and MMPs signaling pathways.To help us better understand the potential mechanism and identify more sensitive tumor markers and selective targets,this review will underline the significant roles of NF-kappa B signaling pathway in regulatory network of pancreatic cancer metastasis.
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<p><b>BACKGROUND</b>Vitamin D status in relation to pancreatic cancer risks is still inconsistent. This study was performed to evaluate the association between vitamin D status and risk of pancreatic cancer using a meta-analysis approach.</p><p><b>METHODS</b>A systemic review of all relevant literature in English was performed by searching Pubmed, Web of Science and Embase to identify eligible studies from the earliest available date to April 1, 2012. The search terms "vitamin D", "25-hydroxyvitamin D", "pancreatic cancer" or "pancreatic neoplasms" were used to retrieve relevant papers. Inclusion criteria were: (1) the exposure of interest was intake of vitamin D or blood levels of vitamin D; (2) the outcome of interest was pancreatic cancer; (3) data on high and low intake or blood vitamin D in cases and controls were available; (4) odds ratio (OR) estimates with 95% confidence interval (CI) were provided; (5) primary epidemiological data were provided reporting pancreatic cancer incidence. The combined OR values and their 95% CIs were calculated via a meta-analysis. The potential presence of publication bias was estimated using Egger's regression asymmetry test.</p><p><b>RESULTS</b>Nine studies with a total of 1 206 011 participants met the inclusion criteria. The test for heterogeneity showed there were significant differences among the included studies (I(2)=70.9%, P=0.001), so a randomized-effects model was used in the meta-analysis. The pooled OR of pancreatic cancer for the highest versus the lowest categories of vitamin D level was 1.14 (95% CI 0.896-1.451), and the Z-score for the overall effect was 1.06 (P=0.288), showing that there was no significant association between vitamin D levels and the risk of pancreatic cancer. Egger's test indicated there was a low possibility of publication bias in this study (P=0.348).</p><p><b>CONCLUSION</b>Dietary vitamin D or circulating concentrations of 25-hydroxyvitamin D are not associated with the risk of pancreatic cancer based on evidence from currently published studies.</p>
Subject(s)
Humans , Pancreatic Neoplasms , Blood , Epidemiology , Risk Factors , Vitamin D , BloodABSTRACT
<p><b>OBJECTIVE</b>To detect the expression of eukaryotic translation initiation factor 5A2(EIF5A2) in pancreatic adenocarcinoma and its correlation with the clinicopathological characteristics and prognosis.</p><p><b>METHODS</b>A total of 73 patients who were treated in our hospital from March 2007 to December 2008 were enrolled in this study. The expression of EIF5A2 in the surgical samples was detected using immunohistochemical staining. Complete clinicopathological data were obtained from all the patients. The potential correlation between EIF5A2 expression and the clinicopathological features, particularly its role in prognosis, were analyzed.</p><p><b>RESULTS</b>Of these 73 patients, 43 had a high EIF5A2 expression. EIF5A2 expression was significantly correlated with the pathological T stage(P<0.001), N stage(P=0.004), M stage(P=0.039), and TNM stage(P=0.005). Kaplan-Meier method demonstrated that the survival was significantly longer in the low EIF5A2 expression group than in the high EIF5A2 expression group(P=0.003). Cox's hazard model showed EIF5A2 was a significant predictor of overall survival in patients with pancreatic adenocarcinoma.</p><p><b>CONCLUSION</b>EIF5A2 may be a potential predictor of the poor prognosis in patients with pancreatic adenocarcinoma.</p>
Subject(s)
Humans , Adenocarcinoma , Diagnosis , Metabolism , Neoplasm Staging , Pancreatic Neoplasms , Diagnosis , Metabolism , Peptide Initiation Factors , Metabolism , Prognosis , RNA-Binding Proteins , MetabolismABSTRACT
A 41-year-old female patient developed round,bright yellow patches on the left calvarial region without obvious precipitating factors 40 years prior to the presentation,which gradually grew to form plaques with age.Two years prior to the presentation,nipple-like lesions appeared in the calvarial and temporal region with an erythematous and wet surface; concurrently,black masses developed in the left temporal region and gradually enlarged with central ulceration but no subjective symptoms.At about 1 year of age,pitchy macules developed on the light tan patches located on the left jaw,posterior and anterior neck,trunk and upper limbs,and gradually increased in quantity and size with the involvement of the homolateral dorsal hand and gradual appearance of papules.Skin examination revealed two well-marginated,indurated,bright red neoplasms sized 3 cm × 2 cm and 2 cm × 1 cm respectively,with erosive and cauliflower-like surface; black or pink papules were scattered between these neoplasms.There was a ring-shaped black mass sized 1.5 cm × 1.5 cm in the left temporal region with central ulceration.Pitchy tough macules and papules were observed on the light tan patches located in the left cheek,lower mandible,posterior and anterior neck,protothorax,shoulder and back,upper limbs and dorsal hand.Based on the histopathology of multiple lesions,the cauliflower-like lesions on the head were diagnosed as syringocystadenoma papilliferum,the yellow plaques as syringocystadenoma papilliferum complicated by sebaceous adenoma,the black proliferative lesions in the temporal region as trichoblastoma accompanied by basal cell epithelioma,the black papuloid lesions and brown maculopapuloid lesions on the lower mandible as nevus spilus.The patient was diagnosed with skin adnexal tumor with multipotential differentiation (syringocystadenoma papilliferum,sebaceous adenoma,trichoblastoma and basal cell epithelioma)accompanied by nevus spilus.
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<p><b>OBJECTIVE</b>Pancreatic cancer is a highly aggressive malignancy that has been resistant to treatment. Advances in cancer genetics have improved our understanding of this disease, but the genetics of pancreatic cancer remain poorly understood. A better understanding of the pathogenic role of specific gene mutations and core signaling pathways would propel the development of more effective treatments. The objective in this review was to highlight recent research that shows promise for new treatments for pancreatic cancer.</p><p><b>DATA SOURCES</b>All articles cited in this review were mainly searched from PubMed, which were published in English from 1993 to 2009.</p><p><b>STUDY SELECTION</b>Original articles and critical reviews selected were relevant to the molecular mechanisms of pancreatic cancer.</p><p><b>RESULTS</b>Dysregulation of core signaling pathways and processes through frequently genetic alterations can explain the major features of pancreatic tumorigenesis. New therapeutic targets based on recent research are emerging that hold promise for the future management of pancreatic cancer.</p><p><b>CONCLUSION</b>New agents used in conjunction with standard radiotherapy and chemotherapy might help to overcome drug resistance by targeting multiple signaling pathways to induce responsiveness of pancreatic cancer cells to death signals.</p>
Subject(s)
Humans , Pancreatic Neoplasms , Drug Therapy , Metabolism , Radiotherapy , Signal Transduction , Radiation EffectsABSTRACT
<p><b>OBJECTIVE</b>To assess the safety and efficacy of hyaluronic acid-based gel of non-animal origin (NASHA gel [Restylane]; Q-Med AB, Uppsala, Sweden)for correcting nasolabial folds in Chinese.</p><p><b>METHODS</b>Patients with moderate or severe nasolabial fold (Wrinkle Severity Rating Scale, WSRS) were recruited to receive NASHA gel injection ( < 1.5 ml). The patients were followed up for 6 months. The efficacy was assessed by physicians and patients, respectively. Adverse events (AEs) were recorded and laboratory tests were performed before and after operation.</p><p><b>RESULTS</b>86 patients were treated. 6 months after injection, improved esthetic results was assessed by patients and physicians independently. 52 AEs happened in 32 cases (37.2%). Most of them were local injection reaction and minor, which were recovered spontaneously. No systemic reaction was found.</p><p><b>CONCLUSIONS</b>NASHA gel can improve the nasolabial folds. It is very safe and tolerated.</p>
Subject(s)
Adult , Female , Humans , Male , Middle Aged , Young Adult , Asian People , Hyaluronic Acid , Therapeutic Uses , Rhytidoplasty , Methods , Skin AgingABSTRACT
<p><b>BACKGROUND</b>In the past decade, there has been increasing breast reconstructions after mastectomy. The ideal material for reconstruction of a breast is fat and skin. The transverse rectus abdominis myocutaneous (TRAM) flap has been the gold standard for breast reconstruction until recently. Abdominal wall function is a major concern for plastic surgeons in breast reconstruction with TRAM flaps. The deep inferior epigastric perforator (DIEP) free flap spares the whole rectus abdominis muscle, includes skin and fat only, and therefore preserves adequate abdominal wall competence. The aim of this study was to summarize our experience in breast reconstruction with DIEP flap.</p><p><b>METHODS</b>Between March 2000 and August 2005, a total of 43 breast reconstructions were performed on 40 patients by our surgeons using DIEP flap (3 patients had bilateral procedures), 14 of them were immediate surgeries and 26 were delayed. Abdominal function, satisfaction with the donor site and reconstructed breast, and the sensation recovery was assessed respectively during follow-up.</p><p><b>RESULTS</b>The mean age of the patients was 38.6 years (range, 28 - 50). The size of the flaps was 11 cm x 26 cm in average (height 10 - 12 cm, width 15 - 33 cm). The mean length of the vascular pedicles was 9.3 cm (range, 7 - 12). The patients were followed up for a mean of 16 months (range, 6 - 30 months). During the follow-up, 2 (5%) patients had total flap loss, 2 (5%) had partial necrosis, 4 (9%) had wound edge necrosis in the abdomen, and 1 had axillary seroma. None of the patients had hernia, and all of them were able to resume their daily activities after the operation. Patient satisfaction with the reconstructed breast rated high, 95% of the patients achieved spontaneous return of sensation in the reconstructed breast, but none of them had a sensation equivalent or approximate to the normal.</p><p><b>CONCLUSIONS</b>The DIEP flap has the same benefits as the TRAM flap without destroying the continuity of the rectus muscle. It can reduce donor-site morbidity and provide an aesthetic refinement in breast reconstruction.</p>
Subject(s)
Adult , Female , Humans , Middle Aged , Abdominal Wall , Mammaplasty , Methods , Patient Satisfaction , Sensation , Surgical FlapsABSTRACT
<p><b>OBJECTIVE</b>To present a method for bilateral breast reconstruction with deep inferior epigastric perforator (DIEP) flap following modified radical mastectomy.</p><p><b>METHODS</b>From 2004 to 2005, three patients with bilateral modified radical mastectomy have undergone delayed bilateral breast reconstruction with deep inferior epigastric perforator flap.</p><p><b>RESULT</b>The flaps in all the cases survived. Follow-up more than 3 months, postoperative abdominal wall examination didn't reveal hernia and bulging. The bilateral reconstructed breast achieved good results in shape and symmetry. Bilateral reconstructed breasts are symmetry.</p><p><b>CONCLUSION</b>The procedure introduced is a reliable method for bilateral breast reconstruction.</p>
Subject(s)
Adult , Female , Humans , Breast Neoplasms , General Surgery , Follow-Up Studies , Graft Survival , Mammaplasty , Methods , Mastectomy, Modified Radical , Surgical FlapsABSTRACT
Only a specifc subset of cancer cells in each tumor with characteristics of self-renewal and multilineage differentiation is responsible for tumor initiation,propagation and chemoresistance,they are termed as cancer initiating cells or cancer stem cells (CSCs). This review summarizes the latest advances about the isolation and identification of pancreatic cancer stem cells and and its relationship with invasion and metastasis,chemotherapy resistance.
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Objective To establish the acute hind limb ischemia on Wistar rat with diabetes mellitus.MethodsThirty diabetes rats were induced by intraperitoneal STZ (50 mg/kg) injection, as well as the blood glucose level tested over 16.8 mmol/L. The rats were ligated on the left femoral artery, then the blood perfusion on the hind limbs ischemia was measured by LDPI after the operation. Results The fasting plasma glucose level on 22 Wistar rats(81.5%) was kept above 16.8 mmol/L, and the hind limb blood perfusion would recover slowly to the level of the right side from 1 to 14 day (P
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<p><b>OBJECTIVE</b>To find a satisfied and applicable repairing method for big auricle defect.</p><p><b>METHODS</b>an auricular posterior flap with has two subcutaneous pedicles on mastoidea, was applied for repairing of big auricle defect. A framework of rib cartilage was embedding into the flap to shape auricle.</p><p><b>RESULT</b>Satisfied result was abtained in all 12 cs-es.</p><p><b>CONCLUSION</b>Using auricular posterior flap with two subcutaneous pedicles to repair big auricular defect is a satisfied and applicable method.</p>