Objective To investigate the effects of 5-Aza-CdR( methylation transferase inhibitor) on the expression levels of leptin gene in chondrocytes and methylation states of leptin promoter region between osteoarthritis (OA) group and control. Methods The chondrocytes in osteoarthritis group were treated with 5-Aza-CdR with different doses and time-points, and the expression level of leptin was detected by real-time polymerase chain reaction for picking up the optimum dose and time-point. Next, the chondrocytes in 5 osteoarthritis patients and 5 control patients (amputation due to severe trauma) were treated with 5-Aza-CdR. Lastly, leptin mRNA expression levels in the four groups osteoarthritis and control chondrocytes treated with/without 5-Aza-CdR were measured by real-time PCR and the methylation state of promoter region ( - 280- + 79) was detected by epityper quantitative DNA methylation analysis. Results ( 1 ) After treating the chondrocytes in OA groups with 10 μmol/L 5-Aza-CdR for 72 h, the mRNA expression levels of leptin were increased significantly. ( 2 ) The mRNA expression levels of leptin were significantly different among the four groups ( P ＜ 0. 05 ), and the chondrocytes in osteoarthritis groups treated with 5-Aza-CdR showed a marked induction of leptin mRNA expression. (3) Analysis of quantitative methylation data using an unsupervised hierarchical clustering algorithm, showed that methylation patterns of leptin promoter was different between control and osteoarthritis chondrocyte treated with/without 5-Aza-CdR. Conclusion Demethylation of leptin promoter might up-regulate leptin gene expression level and it might contribute to osteoarthritis.

Objective To discuss clinical curative effects of using Forehead skin expansion combine with auricular cartilage for repairing nose alar full-thickness defects.Methods From August 2010 to August 2010,36 patients with nose alar full-thickness defects in the second affiliated hospital of kunmin medical university,The defect range exceed 1.5 cm× 1.2 cm.50-80 ml expander was implanted in forehead and injected saline water to expand in order to acquire extra skin.We Turn around the skin of defect as the lining of nose,harvest ipsilateral auricular cartilage for nose ala framework,Expanded forehead pedicle flap was transferred to cover framework.The donor area was sutured directly.The pedicle of flap was cut and trimmed after 2 months.Results Follow-up time of 3-18 months after the operation,All flaps are survive,nose alar defects are repaired successfully.Some cases were performed second surgery,postoperative,nose alar color,thickness,nostril size and shape the same with the contralateral side.Donor site healed with linear scar.Conclusions This method could be easy to obtain excess skin,for repairing large sides nose alar full-thickness defect.Frontal scar is not obvious,It is a practical.

Objective To investigate the effects of CD147/MMP-9 pathway on early left ventricular remodeling Methods 30 healthy eight-week male SHR were divided into 3 groups (n = 10 for each group). SHR group received tail vein injections of normal saline weekly; CD147 group received CD147 of 600 ng·kg-1 weekly; and CD147+DOX group received CD147 of 600 ng/kg weekly and intragastric administration of DOX ( doxycycline ) of 30 mg/kg daily . 10 healthy eight-week male Wistar-Kyoto rats (WKY group) were treated as SHR group. Echocardiography, myocardial sections microscopy examination (HE and VG stain), and Western blot (for assessing levels of MMP-9, TIMP-1, CD147, and collagen I and Ⅲin myocardial tissues) were performed on day 56. Left ventricular weight index (LVWI)was measured and calculated. Collagen volume fractions (CVF) were obtained by image analysis. Results As compared with WKY group , levels of CD147 , MMP-9 , and MMP-9/TIMP-1 were lower but TIMP-1 and collagenⅠand Ⅲ were significantly higher in SHR group. The abundance of CD147 and MMP-9 protein and the ratio of MMP-9/TIMP-1 were obviously increased in CD147 group than in SHR group (P < 0.05). Levels of CD147, MMP-9, and MMP-9/TIMP-1 did no differ between CD147+DOX group and CD147 group. LVWI and contents of collagenⅠand Ⅲ were obviously declined in CD147 group as compare with SHR group. Cardiomyocyte hypertrophy , partial myocardial fibre rupture , myocyte dissolution and fuzzy myocardial fibre boundaries , more abundant of collagen fibers, and higher CVF were found in SHR group. Cardiac fibrosis was significantly improved after CD147 intervention, but the action was suppressed as DOX was administrated simultaneously. Conclusions Early ventricular remodeling may be involved in the inhibition of CD147/MMP-9 pathway in SHR. Input of CD147 to upregulate the pathway can improve the remodeling.

Objective To evaluate the efficacy of accelerated partial breast irradiation ( APBI ) and whole breast irradiation ( WBI ) with simultaneous integrated boost ( SIB ) from the perspective of economics, and provide a reference for postoperative adjuvant therapy mode selection for early-stage breast cancer after breast-conserving surgery. Methods A total of 355 early-stage breast cancer patients who underwent APBI or WBI-SIB after breast-conserving surgery were evaluated on efficacy and cost-effectiveness, of which 177 patients received APBI, and 178 patients received WBI-SIB. Survival analysis was done according to treatment received. NCI-CTC 3.0 was used to score the toxicities. Breast aesthetic outcome were evaluated with Harris standards. Results Median follow-up was 42 months ( 5.8 -92.7 months) . The 3-year locoregional recurrence free survival( LRFS) rates in APBI group and WBI-SIB group were 98.2％ and 97.6％, distant metastasis free survival( DMFS) were 94.3％ and 93.7％, disease-free survival ( DFS) were 93.1％ and 91.6％, and overall survival 95.5％ and 94.3％, respectively, without statistically significant differences(P>0.05). Compared with WBI-SIB group, the acute reaction rates in APBI group decreased from 5. 6％ to 3.4％(χ2 =6.044, P <0. 05), and late reactions from 5.6％ to 2.3％ (χ2 =6.149, P<0. 05), while the cosmetic outcome improved from 88.8％ to 93.8％(χ2 =5.22, P<0. 05). Moreover, the processing average time was shortened by 26.5 d (χ2 =40.76, P<0. 05). Conclusions After breast-conserving surgery, the efficacy of APBI showed no difference from WBI-SIB with respect to 3-year local control, disease-free survival, and overall survival, but displayed a significantly better toxicity profile and cost-effectiveness ratio for early breast cancer patients. It can be used as a good radiotherapy model after breast-conserving surgery in early-stage breast cancer.

Objective:To clarify the mechanism of Fat1 on the proliferation of esophageal squamous cell carcinoma (ESCC).Methods:KYSE450 cells were transfected with Plko.1-puro-GFP-shRNA-Fat1 plasmid and real time polymerase chain reaction (PCR) was used to verify the efficiency of Fat1 knockdown. The effects of Fat1 and extracellular regulated protein kinase (ERK) pathway inhibitor U0126 on the proliferation of ESCC cells were detected by methyl thiazolyl tetrazolium (MTT). Colony formation assay was used to detect the colony formation ability. Cell cycle was detected by live cell imaging. Western blot was used to observe the level of target protein. Mouse xenograft assay was applied to detect the effect of Fat1 knockdown on KYSE450 cell tumor growth. Immunohistochemistry was used to detect the expressions of related proteins in tumor sections.Results:The efficiency of Fat1 knockdown was (77.1±6.9)% in Fat1 sh1 group and (77.7±7.1)% in Fat1sh2 group. Compared with the control group, the cell proliferation and the expression of p-ERK1/2 were significantly increased in Fat1 sh1 and Fat1sh2 group ( P<0.05). After U0126 treatment, the effect of Fat1 knockdown on the proliferation of KYSE450 cells disappeared, and the expression of p-ERK1/2 in KYSE450 cells decreased to a level similar to that in the control group. The number of cell clones in the control group was (72±8), lower than (155±28) and (193±9) in the Fat1sh1 and Fat1sh2 groups, respectively ( P<0.05). In KYSE450 cell, division time was shortened from 1 622±32 min in control group to 1 408±29 min in Fat1 sh1 group, the difference was statistically significant ( P<0.05). Compared with the control group, the tumor volume of Fat1 knockdown group increased significantly. The tumor weight of control group and Fat1 knockdown group were (0.224±0.028) g and (1.532±0.196) g, respectively, at 4 weeks after inoculation, and the difference was statistically significant ( P<0.05). Conclusion:Fat1 inhibits cell proliferation via ERK signaling in ESCC.

Objective:To investigate the regulatory effect of deoxycytidine kinase (dCK) on ionizing radiation (IR) induced ferroptosis in triple-negative breast cancer (TNBC).Methods:TNBC cell line MDA-MB-231 was used to establish dCK knockdown and different phosphorylation phenotypes cell models, and were treated with ferroptosis activator Erastin and / or ferroptosis inhibitor ferrostatin-1 (Fer-1) combined with / without X-ray irradiation. Cell viability was detected by MTT assay. The level of reactive oxygen species (ROS) was measured by 2′,7′-dichlorofluorescin diacetate (DCFH-DA) staining. The expression levels of dCK, transferrin, transferrin receptor (TfR1), ferroportin (FPN) and ferritin heavy chain 1 (FTH1) were detected by Western blot. Statistical analysis was performed by SPSS 17.0 and Origin 2021 software. Measurement data with normal distribution were expressed by Mean ±SD. The comparison between two groups was conducted by Student t-test. The comparison among three or more groups was performed by one-way analysis of variance. Results:In MDA-MB-231 cells, IR induced cell death was observed and Erastin significantly promoted radiation induced cell death, while Fer-1 was able to reverse radiation induced cell death. Compared with the control group, IR induced cell death was increased, the level of ROS was suppressed in the dCK knockdown group. Erastin combined with IR induced reduced cell death and weakened ROS level. Fer-1 reduced the degree of IR induced cell death, and it could not inhibit the induction of ROS by IR.Compared with the control cells, the rate of cell death was decreased induced by IR, the level of ROS was decreased, the expression of FTH1 was down-regulated after IR in the dCK wild-type (dCK-WT ) or dCK hyperphosphorylated (dCK-S74E) MDA-MB-231 cells. In addition, Erastin promotes IR induced cell death and increased ROS levels, while Fer-1 significantly enhances the degree of reversal of IR induced ROS and cell death in these cells. Conclusions:dCK phosphorylation increases ferroptosis induced by IR in TNBC cells. Targeting dCK may be a novel therapeutic approach to overcome radioresistance in TNBC treatment.

Objective:To clarify the mechanism of Fat1 on the proliferation of esophageal squamous cell carcinoma (ESCC).Methods:KYSE450 cells were transfected with Plko.1-puro-GFP-shRNA-Fat1 plasmid and real time polymerase chain reaction (PCR) was used to verify the efficiency of Fat1 knockdown. The effects of Fat1 and extracellular regulated protein kinase (ERK) pathway inhibitor U0126 on the proliferation of ESCC cells were detected by methyl thiazolyl tetrazolium (MTT). Colony formation assay was used to detect the colony formation ability. Cell cycle was detected by live cell imaging. Western blot was used to observe the level of target protein. Mouse xenograft assay was applied to detect the effect of Fat1 knockdown on KYSE450 cell tumor growth. Immunohistochemistry was used to detect the expressions of related proteins in tumor sections.Results:The efficiency of Fat1 knockdown was (77.1±6.9)% in Fat1 sh1 group and (77.7±7.1)% in Fat1sh2 group. Compared with the control group, the cell proliferation and the expression of p-ERK1/2 were significantly increased in Fat1 sh1 and Fat1sh2 group ( P<0.05). After U0126 treatment, the effect of Fat1 knockdown on the proliferation of KYSE450 cells disappeared, and the expression of p-ERK1/2 in KYSE450 cells decreased to a level similar to that in the control group. The number of cell clones in the control group was (72±8), lower than (155±28) and (193±9) in the Fat1sh1 and Fat1sh2 groups, respectively ( P<0.05). In KYSE450 cell, division time was shortened from 1 622±32 min in control group to 1 408±29 min in Fat1 sh1 group, the difference was statistically significant ( P<0.05). Compared with the control group, the tumor volume of Fat1 knockdown group increased significantly. The tumor weight of control group and Fat1 knockdown group were (0.224±0.028) g and (1.532±0.196) g, respectively, at 4 weeks after inoculation, and the difference was statistically significant ( P<0.05). Conclusion:Fat1 inhibits cell proliferation via ERK signaling in ESCC.

Objective To investigate the clinical effect of free pre-expanded scapular skin flap for repairing of large size facial and cervical scar .Methods 15 patients suffering from post-burn facial and cervical scar contractures were treated in the Department of Plastic Surgery of Second Affiliated Hospital of Kunming Medical University.The reconstruction was performed in two operative stages .First, the skin incision were made paralleling with the descending branches of the circumflex scapular artery near posterior axillary line and the scapular skin flap was elevated .A 300 to 400 ml kidney -shaped expander was implanted under scapular region skin .The expansion began 1 week post-operatively.After the expander was fully expanded and could supply sufficient flap , the facial and cervical scar was resected and the contracture was released .The pre-expanded scapular flap was harvested and transferred to repair the defects.Then the facial vascular anastomosis with circumflex scapular vascular was performed .The expander was removed and the wound was closed directly .Results The expansion time ranged from 2 to 4 months with the average time of 2.8 months.The flap size ranged from 14 cm ×7 cm to 25 cm ×14 cm. All flaps survived post-operatively and wounds at donor sites healed primarily .The face and neck have good appearance .Conclusions Pre-expanded scapular skin flap is suitable for repairing of larger face and neck scar with good color and thickness match .Expanded skin flap can provide large size flap , leaving less morbidity at the donor sites .

Objective To investigate the clinical effect of free pre-expanded scapular skin flap for repairing of large size facial and cervical scar .Methods 15 patients suffering from post-burn facial and cervical scar contractures were treated in the Department of Plastic Surgery of Second Affiliated Hospital of Kunming Medical University.The reconstruction was performed in two operative stages .First, the skin incision were made paralleling with the descending branches of the circumflex scapular artery near posterior axillary line and the scapular skin flap was elevated .A 300 to 400 ml kidney -shaped expander was implanted under scapular region skin .The expansion began 1 week post-operatively.After the expander was fully expanded and could supply sufficient flap , the facial and cervical scar was resected and the contracture was released .The pre-expanded scapular flap was harvested and transferred to repair the defects.Then the facial vascular anastomosis with circumflex scapular vascular was performed .The expander was removed and the wound was closed directly .Results The expansion time ranged from 2 to 4 months with the average time of 2.8 months.The flap size ranged from 14 cm ×7 cm to 25 cm ×14 cm. All flaps survived post-operatively and wounds at donor sites healed primarily .The face and neck have good appearance .Conclusions Pre-expanded scapular skin flap is suitable for repairing of larger face and neck scar with good color and thickness match .Expanded skin flap can provide large size flap , leaving less morbidity at the donor sites .

In October 2016, a male patient attacked by a black bear was treated in the Department of Plastic Surgery, the Second Affiliated Hospital of Kunming Medical University.The patient had facial skin and soft tissue defects, and zygomatic arch and buccal damage. The patient received three operations, including debridement, scapular free skin flap transplantation, and reconstruction of zygomatic arch. The facial appearance recovered well after 6-months follow-up.