精囊镜术后双J管留置技术减少射精管瘢痕性梗阻复发

目的:介绍一种尿道精囊镜检查(TSV)术后精囊内留置双J(D-J)管的方法,以期减少瘢痕相关性射精管阻塞(EDO)复发。方法:采用一项随机对照试验,比较TSV术后是否留置D-J管的手术治疗效果和并发症情况,以及复发率和复发时间。对患者的基线资料和TSV相关手术参数进行统计分析比较。其中,基线资料包括年龄、体质量指数(BMI)、术前抗生素使用情况、尿路相关病史、TSV相关手术参数包括手术时间以及术中和术后的并发症等。比较两组患者的术后并发症和术后住院天数,并重点对EDO的复发率及复发时间进行进一步分析。结果:本研究共纳入56例患者。其中,27例患者予留置D-J管(试验组)治疗,29例患者非留置D-J管(对照组)的常规TSV手术治疗。试验组和对照组的术后随访时间分别为(40.5±10.6)、(32.5±14.8)个月。两组患者在基线资料、术中和术后并发症以及术后住院天数方面无显著统计学差异(P>0.05),但手术时间和复发率有显著统计学差异(P均<0.05),试验组的复发率(18.5%)显著低于对照组(44.8%),两组中位复发时间接近(对照组21.0个月,试验组22.0个月)。结论:TSV术后留置D-J管的新方法,可以减少EDO术后复发。

Effect of ALA-PDT on the expressions of MMP-9, MMP-13 and TIMP-1 of hypertrophic scar model in rabbit ears

Objective: To investigate the effect of 5-aminolevulinic(ALA)-photodynamic therapy(PDT) on the expressions of MMP-9, MMP-13 and TIMP-1 of hypertrophic scar model in rabbit ears, and analyze the possible therapeutic mechanisms of ALA-PDT treatment to hypertrophic scars of rabbit ears. Methods: The experimental animals were randomly divided into normal control, negative control, high concentration of ALA-PDT, low concentration of ALA-PDT and PDT groups. The latter three groups received ALA-PDT treatment or PDT treatment once a week for 3 weeks. The specimens of the rabbits were collected respectively 1, 2 and 3 months after treatment to be used for RT-PCR and Western-blot test. Results: 1, 2 and 3 months after PDT treatment, the expressions of MMP-9 and MMP-13(including mRNA and protein) in hypertrophic scar tissues of three treatment groups were significantly higher than those of the negative control group(P<0.01), and the expression of TIMP-1 mRNA and protein of three treatment groups were significantly lower than that of the negative control group(P<0.01). There were also significant differences between high-concentration ALA-PDT treatment group and the low one(P<0.05). Conclusion: ALA-PDT is effective in treating hypertrophic scars of rabbit ears, and its possible therapeutic mechanisms are that ALA-PDT treatment generates oxidation activation effect to activate the activity of MMPs and induces the photoaging of fibroblasts of hypertrophic scar tissues of rabbit ears to inhibit the activity of TIMPs, which causes the up-regulation of MMPs and the down-regulation of TIMPs. Because of this, the degradation of collagen and ECM is accelerated and the formation of scars is suppressed.

Surgery and follow-up care for auricular keloid:a report of 156 cases

Objective:To treat and prevent auricular keloid so as to imporve the cure rate and lower the rate of recurrence. Methods:Taking 156 sufferers of auriclar keloid at the orthopaedics department of the Southwest Hospital under the Third Military Medical University from June, 2008 to June, 2011 as the research subject, this research carried out retrospective analysis and summary of different surgical methods with the clinical data of subseque nt treatments, including medicament, radiotheropy, pressure, etc. Results:There was no auricular cartilage necrosis and deformation in the total of 156 cases. It was found that 134 cases were cured in a year of postoperative follow-up, getting the care rate to 85.9%. The treatment was effective on 20 cases, with the effective rate of 12.8%, while it was ineffective on 2 cases, with the ineffective rate being 1.3%. However, two cases showed tendency towards recurrence, which were treated effectively by non-surgical methods like local hormone injection. There was neither recurrence nor apparent hyperplasia of hypertrophic scars on the rest cases, with the auricle and the earlobe in good shape. Conclusion:By auricular keloid excision and stripping surgery, surgical suture tension was reduced. Glucocorticoid and radiotherapy were instantly applied to inhibit pyperplasia of cicatrical tissue. Subsequently, pressure, anti-scarring drugs and silicone membrane were adopted to ensure fine postoperative apperance and reduce recurrence. These methods were proved to be effectiveand they provided systematic and effective treatment for auricular keloid.

Endostatin inhibits hypertrophic scarring in a rabbit ear model

Objective： The present study was designed to use an in vivo rabbit ear scar model to investigate the efficacy of systemic administration of endostatin in inhibiting scar formation. Methods： Eight male New Zealand white rabbits were randomly assigned to two groups. Scar model was established by making six full skin defect wounds in each ear. For the intervention group, intraperitoneal injection of endostatin was performed each day after the wound healed （about 15 d post wounding）. For the control group, equal volume of saline was injected. Thickness of scars in each group was measured by sliding caliper and the scar microcirculatory perfusion was assessed by laser Doppler flowmetry on Days 15, 21, 28, and 35 post wounding. Rabbits were euthanatized and their scars were harvested for histological and proteomic analyses on Day 35 post wounding. Results： Macroscopically, scars of the control group were thicker than those of the intervention group. Significant differences between the two groups were observed on Days 21 and 35 （p〈0.05）. Scar thickness, measured by scar elevation index （SEI） at Day 35 post wounding, was significantly reduced in the intervention group （1.09±0.19） compared with the controls （1.36±0.28）. Microvessel density （MVD） observed in the intervention group （1.73±0.94） was significantly lower than that of the control group （5.63±1.78） on Day 35. The distribution of collagen fibers in scars treated with endostatin was relatively regular, while collagen fibers in untreated controls were thicker and showed disordered alignment. Western blot analysis showed that the expressions of type I collagen and Bcl-2 were depressed by injection of endostatin. Conclusions： Our results from the rabbit ear hypertrophic scar model indicate that systemic application of endostatin could inhibit local hypertrophic scar formation, possibly through reducing scar vascularization and angiogenesis. Our results indicated that endostatin may promote the apoptosis of endothelial cells and block their release of platelet-dedved growth factor （PDGF） and fibroblast growth factor （FGF）, thereby controlling collagen production by fibroblasts. Blood vessel-targeted treatment may be a promising strategy for scar therapy.

Endostatin inhibits fibrosis by modulating the PDGFR/ERK signal pathway:an in vitro study

Accumulating evidence indicates that endostatin inhibits fibrosis. However, the mechanism is yet to be clarified. The aim of this study is to evaluate the effect of endostatin on platelet-derived growth factor-BB （PDGF-BB）- or transforming growth factor β1 （TGF-β1）-induced fibrosis in cultured human skin fibroblasts, and to further examine the molecular mechanisms involved. Human dermal flbroblasts were cultured in Dulbecco＇s modified Eagle＇s medium （DMEM） and serum-starved for 48 h before treatment. Cells were grouped as follows： ＂PDGF-BB＂, ＂PDGF-BB＋ endostatin＂, ＂TGF-β1＂, ＂TGF-β1＋endostatin＂, ＂endostatin＂, and ＂blank control＂. The fibroblasts were stimulated with either TGF-β1 or PDGF-BB for 72 h in order to set up the fibrosis model in vitro. The cells were co-cultured with either TGF-β1 or PDGF-BB and endostatin and were used to check the inhibiting effect of endostatin. A blank control group and an endostatin group were used as negative control groups. The biomarkers of fibrosis, including the expression of collagen I, hydrroxyproline, and α-smooth muscle actin （a-SMA）, were evaluated using an enzyme-linked immune- sorbent assay （ELISA） and Western blot. The expression of phosphorylated PDGF receptor β （p-PDGFRβ）, PDGFRβ, phosphorylated extracellular signal-regulated kinase （p-ERK）, and ERK was detected using Western blot and im- munofiuorescent staining was used to explore the mechanisms. Both PDGF-BB and TGF-β1 significantly up-regulated the expression of collagen I, hydroxyproline, and a-SMA. Endostatin significantly attenuated both the PDGF-BB- and TGF-β1-induced over-expression of collagen I, hydroxyproline, and a-SMA. PDGF-BB and TGF-β1 both promoted the expression of PDGFR, ERK, and p-ERK. Endostatin inhibited the expression of PDGFR and p-ERK but did not affect the expression of total ERK. Endostatin inhibited hypertrophic scar by modulating the PDGFRI3/ERK pathway. En- dostatin could be a promising multi-target drug in future fibrosis therapy.