Objective To analyze MRI features of real tears and pseudotears of posterior horn of the lateral meniscus (PHLM) at the insertion site of meniscofemoral ligament(MFL), and to discuss main points of differential diagnosis. Methods MR images of 32 patients with PHLM tears and 30 patients with anterior cruciate ligament tears but without PHLM tears confirmed by arthroscopy were analyzed retrospectively. Another 20 asymptomatic volunteers as controls underwent MR examination and analyzed. The number of consecutive slices displaying longitudinal increased signal in sagittal images and the length in axial images were evaluated. The one?way analysis of variance, χ2 test and ROC curve were used to analyze diagnostic value of different MRI findings. Results Longitudinal line with abnormal increased signal (pseudotear) was found in 82.0% (41/50) normal insertion site of MFLs. The typical MRI finding of real tears was peripheral longitudinal linear high signal in PHLM which reached the margin of articular surface. In sagittal images, longitudinal linear high signal was shown in (5.8 ± 1.2) slices in knees of real tears, which was more than (2.6±1.1) slices and (2.7±1.4) slices in pseudo?tear groups (F=60.9, P<0.01). The area under ROC curve was 0.96 for differentiating real tear from pseudo-tear using the number of consecutive slices displaying longitudinal increased signal in sagittal images. With a threshold of five or more consecutive images with abnormal longitudinal increased signal as the positive standard of continuous?line sign, the overall sensitivity, specificity and accuracy for diagnosing real tear were 90.6%(29/32), 90.2%(37/41) and 90.4%(66/73), respectively. The axial images showed that the length of increased signal line in the outer of PHLM was (16.4±4.9) mm in patients with real tears, which was longer than pseudo?tear groups with length of (8.1 ± 3.2) mm and (6.0 ± 3.1) mm (F=17.0, P<0.01). The area under ROC curve was 0.92 for differentiating real tear from pseudo?tear using the length in axial images. The zip sign was defined when its length was not less than 10 mm. The sensitivity, specificity and accuracy of the zip sign was 84.4%(27/32), 90.2%(37/41) and 87.7%(64/73) respectively. In coronal images, high signal of MFL attachment insertion was shown in 71.9%(23/32), 60.0%(15/25) and 10/16 cases, there was no significant difference (χ2=0.98, P=0.61). Conclusion The continuous?line sign and zip sign are characteristic findings of PHLM tears at the insertion site of MFL attachment, which are valuable for differential diagnosis with pseudotears at the insertion site of MFL.

AIM: To observe the level of vascular endothelial growth factor (VEGF) secreted by monocytes cultured with electrical burn serum, and to explore the effect of VEGF on monocyte-endothelial cell adhesion.METH-ODS:The electrical burn serum of the rat was prepared.The normal serum from the rats without treating electric current was also collected for control.The contents of VEGF and its soluble receptor sFlt-1 in electrical burn group were determined by double-antibody sandwich ELISA.THP-1 cells were randomly divided into normal serum group and electrical burn serum group.The contents of VEGF and sFlt-1 in the culture supernatants were measured by double-antibody sandwich ELISA. THP-1 cells were also randomly divided into another 4 groups:normal serum group, electrical burn serum group, normal serum +inhibitor group and electrical burn serum +inhibitor group.THP-1 cells, which were incubated with the serum for 3 h and 6 h, were labeled with calcein-AM and then were added into the well with monolayer of endothelial cell line EA.hy926 to detect monocyte-endothelial cell adhesion.RESULTS:The levels of serum VEGF of the rats with electrical burns were significantly increased, the levels of serum sFlt-1 were significantly decreased as compared with the controls. The levels of VEGF secreted by THP-1 cells cultured with electrical burn serum were significantly increased, the levels of sFlt-1 were decreased correspondingly.Electrical burn serum enhanced monocyte-endothelial cell adhesion, sFlt-1 inhibi-ted the adhesion between monocytes and endothelial cells.CONCLUSION:The monocytes exposed to the electrical burn serum secrete VEGF, which enhance the adhesion between monocytes and endothelial cells.Blockage of VEGF activity may effectively inhibit monocyte-endothelial cell adhesion.

OBJECTIVETo explore the molecular mechanism of microRNA-21 in myocardial damage of rats in the early stage of severe scald injury by observing the expression of microRNA-21 and programmed cell death 4 (PDCD4) in myocardial tissue of rat and to validate the relationship between them in cell model.

METHODS(1) Forty SD rats were divided into sham injury group (n =8, sham injured) and scald injury group (n =32, inflicted with 30% TBSA full-thickness scald on the back) according to the random number table. The left ventricular tissue was collected from rats in sham injury group at post injury hour 1 without any fluid infusion. Rats in scald injury group were given an intraperitoneal injection of lactic acid Ringer's solution and 8 rats were respectively sacrificed at post injury hour 3, 6, 12, 24 to harvest left ventricular tissue. The expression of microRNA-21 in myocardial tissue was assessed by real-time fluorescent quantitative RT-PCR. The protein expression of PDCD4 in myocardial tissue was assessed by Western blotting. (2) Rat myocardial cell line H9C2 was divided into microRNA-21 inhibitor group (cells were transfected with microRNA-21 inhibitor) and negative transfection control group (cells were transfected with negative control of microRNA inhibitor) according to the random number table. At post transfection hour 48, real-time fluorescent quantitative RT-PCR and Western blotting were performed respectively to determine the mRNA and protein expression levels of PDCD4 in cells. Data were processed with one-way analysis of variance, LSD-t and two independent samples t test. The relationship between microRNA-21 expression and PDCD4 protein level in myocardial tissue of rats was assessed by linear correlation analysis.

RESULTS(1) The expression levels of microRNA-21 in myocardial tissue of rats in sham injury group at post injury hour 1 and in scald injury group at post injury hour 3, 6, 12, 24 were respectively 0. 96 ± 0. 13, 0. 44 ± 0. 08, 0. 42 ± 0. 10, 0.33 +0.07, and 0.61 0.10 (F = 27.331, P <0.001). Compared with that in myocardial tissue of rats in sham injury group at post injury hour 1, expression level of microRNA-21 was significantly decreased in scald injury group at post injury hour 3, 6, 12, 24 (with t values from 4. 558 to 9.410, P values below 0.01). The protein expression levels of PDCD4 in myocardial tissue of rats in sham injury group at post injury hour 1 and in scald injury group at post injury hour 3, 6, 12, 24 were respectively 0.44 ± 0.05, 0.60 ± 0.09, 0.92 ± 0. 15, 0. 86 ± 0.11, and 0.57 ± 0. 10 (F =8.622, P =0.003). Compared with that in sham injury group at post injury hour 1, protein expression level of PDCD4 was significantly increased in scald injury group at post injury hour 6 and 12 (with t values respectively 4. 968 and 4. 122, P values below 0.01). A significant negative correlation between the expression of microRNA-21 and PDCD4 protein in myocardial tissue of rats of scald injury group was observed at each time point (r = -0. 572, P = 0. 026). (2) The mRNA and protein expression levels of PDCD4 of myocardial cells in microRNA-21 inhibitor group were respectively 1.73 ± 0. 29 and 0. 38 ± 0. 08, which were significantly higher than those in negative transfection control group (0.95 ± 0.14 and 0.23 ± 0.03, with t values respectively 4. 857 and 3.356, P <0.05 or P <0.01).

CONCLUSIONSExpression of microRNA-21 was decreased, while expression of PDCD4 was increased, in myocardial tissue of rats in the early stage of severe scald injury. MicroRNA-21 might participate in myocardial damage in the early stage of scald injury by negatively regulating expression of PDCD4.

Animals ; Apoptosis Regulatory Proteins ; metabolism ; Blotting, Western ; Burns ; metabolism ; pathology ; MicroRNAs ; genetics ; metabolism ; Myocardium ; metabolism ; pathology ; Myocytes, Cardiac ; metabolism ; pathology ; Rats ; Reverse Transcriptase Polymerase Chain Reaction ; Soft Tissue Injuries

OBJECTIVETo compare the DNA methylation-related alteration induced by trichloroethylene (TCE) in human hepatic L-02 cells (L-02 cells) and SET deficient cells, and reveal the role of SET on the mechanisms in TCE-induced epigenetic pathway.

METHODSThe L-02 cells and pre-established SET deficient cells were treated with different TCE concentrations, and the changes of total cell viability, DNA methylation level and DNA methyltransferases (DNMTs) activity were measured, respectively. In addition, the TCE-induced alteration in the protein expression of DNMT1, DNMT3a and DNMT3b were analyzed by Western blotting.

RESULTSAfter treatment with TCE for 24 h, the cell proliferation level was significantly decreased in both cell lines. When concentrations of TCE were 0, 1.0, 2.0, 4.0 and 8.0 mmol/L, the proliferation levels of L-02 cells were 100.00±2.70, 83.34±2.38, 75.56±4.51, 71.67±2.77 and 66.67±1.63, respectively (F = 58.29, P < 0.001); the cell proliferation levels of SET deficient cells were 101.12±1.67, 85.01±2.33, 79.44±1.67, 78.337±3.89 and 76.11±3.33, respectively (F = 42.41, P < 0.001). When concentration of TCE reached 4.0 mmol/L, the difference of cell proliferation level between two groups was statistically significant (t = -3.51; P = 0.013). After treated by TCE for 24 h, the global DNA methylation significantly decreased in both cell lines (F value was 212.87 and 79.32, respectively, P < 0.001). The difference between two groups was not statistically significant. After treated by TCE for 24 h, the methyltransferases activities were significantly decreased in both cell cells (F values were 77.92 and 113.80, respectively, P-0.001). The SET deficiency could inhibit the decrease of methyltransferases activity under TCE treatment. When the concentration of TCE reached 8.0 mmol/L, the enzymatic activity of L-02 cells and SET deficient cells decreased to 67.61%±2.85% and 72.97%± 1.94%, respectively. The difference between two groups was statistically significant (t = -3.94, P = 0.008). After treated with TCE for 24 h, concentrations of TCE were 0, 1.0, 2.0, 4.0 and 8.0 mmol/L, and the relative protein levels of DNMT1 in normal L-02 cells increased significantly to 1.00±0.03, 1.28±0.04, 1.20±0.04, 1.62±0.05, 1.43±0.04 (F = 103.00, P < 0.001); In SET deficient cells, the expressions of DNMT1 were 1.00±0.04, 0.96±0.02, 1.19±0.05, 0.85±0.03, 0.83±0.03, which was significantly down-regulated under TCE treatment (F = 44.18, P < 0.001).

CONCLUSIONSET deficiency can significantly attenuate the TCE-induced decreases of cell viability and DNMTs activity, as well as alteration of protein expression of DNMT1 in L-02 cells, which indicated that SET was involved in the mechanism of TCE-induced cytotoxicity and epigenetic pathway in L-02 cells.

Cell Line ; Cell Survival ; DNA (Cytosine-5-)-Methyltransferase 1 ; DNA (Cytosine-5-)-Methyltransferases ; DNA Methylation ; Humans ; Liver ; Trichloroethylene

Objective To explore the correlation of MTHFD1 gene polymorphism with genetic susceptibility to colorec-tal cancer. Methods Ninety-six cases of colorectal cancer patients and 96 cases of healthy controls were investigated by questionnaire, the polymerase chain reaction - restriction fragment length polymorphism (PCR-RFLP) detection method was applied. Results Compared with normal control group, MTHFD1 G1958A polymorphism rs2236225 locus allele frequencies of patients with colorectal cancer had significant difference(P<0.05);rs2236225 genotype risk of col-orectal cancer increased 1.6 times(OR=1.603, 95%CI=0.331~2.534, P<0.05). Conclusion MTHFD1 gene polymorphism is closely related to the susceptibility of colorectal cancer, the main course of colorectal cancer is the rs2236225 gen changes in G1958A site of MTHFD1.

OBJECTIVETo observe the changes in the expressions of microRNA-126 in myocardial tissue and cardiac troponin I (cTnI) in serum of rats in the early stage of severe burn injury with analysis of their relationship, and to validate the relationship between microRNA-126 and myocardial damage in cellular level.

METHODS(1) Forty-eight SD rats were divided into sham injury group (n=8, without fluid therapy after sham injury) and burn injury group (n=40, inflicted with 30% TBSA full-thickness scald on the back, hereinafter referred to as burn, and received intraperitoneally injection of lactic acid Ringer's solution) according to the random number table. Blood was collected from abdominal aorta of rats in sham injury group at post injury hour (PIH) 1, and then these 8 rats were sacrificed for obtaining left ventricular tissue. Blood was respectively collected from abdominal aorta of 8 rats in burn injury group at PIH 3, 6, 12, 24, and 48, and then they were sacrificed and the left ventricular tissue was obtained at each time point. The expression of microRNA-126 in myocardial tissue was assessed by real-time fluorescent quantitative RT-PCR. Serum level of cTnI was assessed by ELISA. (2) Rat myocardial cell line H9C2 was divided into normal control group (NC, routinely cultured), stimulation group (S), negative transfection+stimulation group (NT+S), and transfection+stimulation group (T+S) according to the random number table. Cells in S group were treated with hypoxia for 24 h after being cultured with DMEM containing 10% burn serum obtained from rats in burn injury group at PIH 6 in experiment (1). Cells in NT+S group and T+S group were respectively transfected with the negative control of microRNA mimics and microRNA-126 mimics for 24 h, and then were given the same treatment as that of S group. The expression of microRNA-126 in myocardial cells was determined by real-time fluorescent quantitative RT-PCR (with the sample number of 3). Cell counting kit 8 was used to examine the vitality of myocardial cell (with the sample number of 4, denoted as absorbance value). Apoptotic rate of myocardial cells was determined by flow cytometer (with the sample number of 3). Data were processed with one-way analysis of variance and LSD-t test. The relationship between microRNA-126 expression in myocardial tissue and serum level of cTnI of rats was assessed by linear correlation analysis.

RESULTS(1) Compared with that of sham injury group at PIH 1, the expression levels of microRNA-126 in myocardial tissue of rats in burn injury group at PIH 3, 6, 12, 24, and 48 were significantly decreased (with t values from 5.68 to 9.79, P values below 0.01), reaching its nadir at PIH 24 (0.40 ± 0.08). Compared with that of sham injury group at PIH 1, the serum levels of cTnI of rats in burn injury group at PIH 3, 6, 12, 24, and 48 were significantly increased (with t values from 6.68 to 12.79, P values below 0.01), peaking at PIH 12 [(1 035 ± 177) pg/mL]. A significant negative correlation between the expression level of microRNA-126 in myocardial tissue and serum level of cTnI was observed in rats of burn injury group at each time point (r=-0.797, P<0.001). (2) Compared with those of NC group, the microRNA-126 expression levels in myocardial cells of S group and T+S group were respectively decreased and increased (with t values respectively 4.57 and 5.73, P<0.05 or P<0.01), the cell vitality levels were obviously decreased (with t values respectively 14.88 and 6.48, P values below 0.01), and the apoptotic rates were significantly increased (with t values respectively 13.82 and 6.96, P values below 0.01). Compared with that in NT+S group, the microRNA-126 expression level in myocardial cells of T+S group was significantly increased (t=6.77, P<0.01), the cell vitality level was obviously increased (t=8.23, P<0.001), and the apoptotic rate was significantly decreased (t=6.14, P<0.001).

CONCLUSIONSExpression level of microRNA-126 in myocardial tissue of rat was decreased in the early stage of severe burn injury. It may participate in regulating myocardial damage and play a protective role.

Animals ; Burns ; metabolism ; pathology ; Cell Line ; Enzyme-Linked Immunosorbent Assay ; Hypoxia ; MicroRNAs ; genetics ; metabolism ; Myocardium ; metabolism ; pathology ; Myocytes, Cardiac ; metabolism ; pathology ; Rats ; Rats, Sprague-Dawley ; Real-Time Polymerase Chain Reaction ; Reverse Transcriptase Polymerase Chain Reaction ; Serum ; Soft Tissue Injuries ; Transfection ; Troponin I ; metabolism

OBJECTIVETo observe the change in phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) signal pathway in monocytes as induced by serum of rats with electrical burn, and to explore the effects of PI3K/Akt pathway on monocyte-endothelial cell adhesion.

METHODSSixty-four SD rats of clean grade were inflicted with electrical burn for the collection of serum of rats with electrical burn; another group of twenty-four SD rats were used to obtain normal serum without treatment. (1) Human monocyte line THP-1 was routinely cultured. The THP-1 cells in logarithmic phase were divided into normal serum group (resuspended in RPMI 1640 medium with 20% normal rat serum) and burn serum group (resuspended with RPMI 1640 medium with 20% serum of rats with electrical burn) according to the random number table, with 6 wells in each group. Morphology of THP-1 cells in normal serum group was observed at post culture hour (PCH) 24, and that in burn serum group at PCH 3, 6, 24. The contents of TNF-α in culture supernatant were determined by double-antibody sandwich ELISA at the corresponding time point in each group. The state of Akt activation was determined by Western blotting at PCH 3, 6, 24. (2) Another portion of THP-1 cells were divided into 4 groups according to the random number table, with 6 wells in each group. Cells in normal serum group and burn serum group were given with the same culture condition as above; cells in normal serum+inhibitor group and burn serum+inhibitor group were cultured with the same culture conditions as in the former two groups correspondingly with addition of 100 nmol/L wortmannin in the nutrient solution. At PCH 3 and 6, THP-1 cells were added into the well with a monolayer of endothelial cell line EA.hy926 to observe the monocyte-endothelial cell adhesion. Data were processed with one-way analysis of variance and LSD- t test.

RESULTS(1) In normal serum group, THP-1 cells showed growth in suspension, with uniform shape at PCH 24. In burn serum group, the cell shape became irregular though the membrane was complete at PCH 3; cellular size became irregular and cell membrane and cytoplasm were swollen at PCH 6; cell membrane was disrupted with death of cells at PCH 24. The contents of TNF-α in culture supernatant in normal serum group at PCH 24 and in burn serum group at PCH 3, 6, 24 were respectively (38.5 ± 1.4), (75.1 ± 1.5), (91.5 ± 1.8), (117.0 ± 1.4) pg/mL (F = 1 415.306, P < 0.01). The contents of TNF-α in culture supernatant in burn serum group at PCH 3, 6, 24 were all significantly higher than the content of TNF-α in normal serum group at PCH 24 (with t values respectively 29.614, 42.852, 63.485, P values below 0.01). The ratio values of phosphorylated Akt to Akt in burn serum group at PCH 3, 6, 24 were respectively 2.66, 3.69, 1.17 times of those in normal serum group at the corresponding time point. (2) In normal serum group, normal serum+inhibitor group, burn serum group, and burn serum+inhibitor group at PCH 3 and 6, the numbers of THP-1 cells adherent to endothelial cells were respectively (231 ± 45), (280 ± 47), (703 ± 169), (335 ± 85) per 100-time field; (219 ± 49), (235 ± 21), (562 ± 123), (226 ± 29) per 100-time field (with F values respectively 25.630 and 18.975, P values below 0.01). The number of THP-1 cells adhered to EA.hy926 cells was significantly more in burn serum group than in normal serum group at PCH 3 and 6 (with t values respectively 6.189 and 6.601, P values below 0.01). The number of THP-1 cells adherent to EA.hy926 cells was significantly fewer in burn serum+inhibitor group than in burn serum group at PCH 3 and 6 (with t values respectively 6.821 and 6.465, P values below 0.01).

CONCLUSIONSThe serum of rats suffering from electrical burn can induce the monocytes to secrete TNF-α, thus enhancing monocyte-endothelial cell adhesion, but it can be inhibited by blocking PI3K/Akt signal pathway.

Animals ; Burns, Electric ; blood ; Cell Line ; Humans ; Monocytes ; Phosphatidylinositol 3-Kinases ; metabolism ; Proto-Oncogene Proteins c-akt ; metabolism ; Rats ; Serum ; Signal Transduction ; Tissue Adhesions ; metabolism ; pathology ; Tumor Necrosis Factor-alpha ; metabolism

OBJECTIVETo explore the effects of microRNA-21 on apoptosis of myocardial cell of rats as induced by ischemia and hypoxia, and to analyze the underlying mechanisms.

METHODS(1) Rat myocardial cell line H9C2 was cultured in a serum-free and low glucose DMEM medium using a hypoxic incubator which was filled with 1% oxygen, 5% carbon dioxide, and 94% nitrogen to simulate ischemic environment. The expression of microRNA-21 in normal myocardial cells and cells treated with low oxygen exposure for 6 and 24 h were assessed by real-time fluorescent quantitative RT-PCR. (2) Another portion of myocardial cells were divided into 4 groups according to the random number table: normal control group (NC, ordinary culture without any treatment), ischemia/hypoxia group (IH, treated with ischemia and hypoxia for 24 h), negative transfection control+ischemia/hypoxia group (NC+IH, treated with ischemia and hypoxia for 24 h after the transfection of microRNA mimics control for 24 h), microRNA-21+ischemia/hypoxia group (M+IH, treated with ischemia and hypoxia for 24 h after the transfection of microRNA-21 mimics for 24 h). The cells in the latter three groups were examined immediately after treatment, and cells in group NC were collected and examined at the same time point. Apoptosis rate of myocardial cells was determined by flow cytometer. The mRNA and protein expression levels of programmed cell death 4 (PDCD4) in myocardial cells were determined by real-time fluorescent quantitative RT-PCR and Western blotting respectively. The sample numbers in this experiment were 6 or 3. Data were processed with one-way analysis of variance and LSD- t test.

RESULTS(1) The expression level of microRNA-21 in normal myocardial cells and cells treated with ischemia and hypoxia for 6 and 24 h were respectively 1.09 ± 0.17, 0.75 ± 0.08, and 0.67 ± 0.08 (F = 11.280, P = 0.009). Compared with expression level of microRNA-21 in normal myocardial cells, those of cells treated for 24 h (t = 4.461, P = 0.004) and 6 h (t = 3.642, P = 0.011) were both lower, and the former was more obvious. Therefore all the ischemia and hypoxia treatment time of cells in the following experiment was 24 h. (2) The apoptosis rate of myocardial cells in group NC was (3.5 ± 0.7)%. After being treated with ischemia and hypoxia for 24 h, the apoptosis rates of myocardial cells in groups IH, NC+IH, and M+IH were respectively (17.3 ± 3.2)%, (16.4 ± 3.0)%, and (7.6 ± 2.0)% (F = 15.176, P = 0.001). Compared with that of group NC, the apoptosis rate of myocardial cells of group IH was significantly increased (t = 5.641, P < 0.001), while it was significantly decreased in group M+IH as compared with group NC+IH (t = 3.588, P = 0.007). The mRNA expression level of PDCD4 in group NC was 1.06 ± 0.21. After being treated with ischemia and hypoxia for 24 h, the mRNA expression levels of PDCD4 in groups IH, NC+IH, and M+IH were respectively 3.01 ± 0.34, 3.05 ± 0.25, and 1.48 ± 0.24 (F = 44.952, P < 0.001). Compared with that of group NC, the mRNA expression level of PDCD4 in group IH was higher (t = 8.945, P < 0.001), while it was significantly lower in group M+IH as compared with group NC+IH (t = 7.253, P < 0.001). The protein expression level of PDCD4 in group NC was 0.44 ± 0.08. After being treated with ischemia and hypoxia for 24 h, the protein expression levels of PDCD4 in groups IH, NC+IH, and M+IH were respectively 0.96 ± 0.13, 1.05 ± 0.12, and 0.58 ± 0.12 (F = 18.804, P = 0.008). Compared with that of group NC, the protein expression level of PDCD4 in group IH was higher (t = 5.429, P = 0.006), while it was significantly reduced in group M+IH as compared with group NC+IH (t = 4.903, P = 0.008).

CONCLUSIONSIschemia and hypoxia reduce the expression of microRNA-21 in myocardial cells, while increasing the expression of microRNA-21 can alleviate the ischemia/hypoxia-induced apoptosis by lowering the expression of PDCD4.

Animals ; Apoptosis ; genetics ; physiology ; Apoptosis Regulatory Proteins ; genetics ; metabolism ; Blotting, Western ; Cell Line ; Flow Cytometry ; Hypoxia ; Ischemia ; MicroRNAs ; genetics ; Myocardium ; Myocytes, Cardiac ; RNA, Messenger ; genetics ; Rats ; Reverse Transcriptase Polymerase Chain Reaction ; Transfection

OBJECTIVETo investigate the clinical manifestation, diagnosis, and treatment of patients with Marjolin's ulcers.

METHODSThe clinical materials of 21 patients with Marjolin's ulcers hospitalized from January 2007 to January 2013 were retrospectively analyzed, including age, gender, injury causes, duration time of primary disease in developing Marjolin's ulcer, duration of ulcer, lesion site, ulcer area, symptoms and signs of ulcer region, bacterial culture results before operation, histopathological type, grade of carcinoma cell differentiation, depth of invasion, treatment, and outcome.

RESULTS(1) The age of 21 patients at the time of diagnosis of Marjolin's ulcers was 19-74 (47 ± 13) years, and the ratio of male to female was nearly 0.9:1.0. (2) The main primary lesions were flame burns and high temperature liquid scald, respectively occurred in 12 cases (57.1%) and 7 cases (33.3%). The time for development of Marjolin's ulcers from primary injury was 10-56 (40 ± 14) years. (3) Ulceration on top of scar lasted for longer than one year in 12 patients (57.1%). (4) Lesion site was mainly located in the limbs in 13 patients (61.9%), and on head and face in 6 patients (28.6%), respectively. (5) Ulcer area ranged 0.25-74.25 (39 ± 25) cm(2). Foul excretion, bleeding, intensified pain, and gradual enlargement of ulceration were observed in the lesion of most patients. (6) Bacterial culture of wound excretion before operation showed positive results in 16 patients (76.2%).

RESULTSof bacterial culture of blood were negative in all patients. (7) Pathological examination revealed squamous cell carcinoma in 20 cases and basal cell carcinoma in 1 case, and mostly of high or medium differentiation. Cancer cells in nearly 40% patients had invaded the subcutaneous tissue or deeper area. (8) All patients were treated by surgery, among them autologous skin grafting was done after excision of lesion in 11 patients, and in 5 patients the defects were closed with skin flaps after excision of lesion, and in 5 patients limbs harboring the lesion were amputated. Twelve patients (57.1%) received postoperative rehabilitation treatment. Two patients with pulmonary metastasis received chemotherapy. (9) Most of the flaps and skin grafts survived well after surgery, and a few cases with failure of skin grafting or transplantation of flaps underwent skin grafts again. Patients were followed up for 6 months to 5 years, in 4 patients recurrence occurred after surgery, and 2 of them died. The other patients survived without recurrence.

CONCLUSIONSSquamous cell carcinoma was the most common pathological type of Marjolin's ulcer admitted to our unit. A recurrent ulcer with long course should be considered as Marjolin's ulcer, and it should be scrutinized pathologically. Currently, surgery remains the optimal treatment for Marjolin's ulcer. Regular follow-up should be carried out after resection of the lesion to detect carcinoma recurrence and metastasis.

Burns ; complications ; Carcinoma, Squamous Cell ; etiology ; pathology ; surgery ; Cicatrix ; Female ; Humans ; Male ; Retrospective Studies ; Skin Neoplasms ; etiology ; pathology ; surgery ; Skin Transplantation ; Skin Ulcer ; etiology ; pathology ; surgery ; Surgical Flaps ; Treatment Outcome