滑膜间充质干细胞修复膝关节软骨损伤的应用与进展

背景:膝关节软骨损伤后很难愈合,是临床上亟需解决的重要课题。目的:总结滑膜间充质干细胞在膝关节软骨损伤治疗上的优越性。方法:用英文主题词"Knee Joint,Cartilage,Synovial Membrane,Tissues,Injuries,Repair"在Pub Med数据库中检索2005年8月至2015年8月文献总共625篇。采纳并分析滑膜间充质干细胞治疗膝关节软骨损伤文献48篇。排除其他非滑膜间充质干细胞及非膝关节软骨损伤治疗的相关文章,保留35篇文章进行综述。结果与结论:应用滑膜间充质干细胞治疗膝关节软骨损伤,能够获得更加理想的治疗效果,损伤组织本身固有的间充质干细胞是修复损伤组织的最佳种子细胞。

Fanconi Anemia and Ubiquitination

Fanconi anemia （FA） is a rare recessive hereditary disease characterized clinically by congenital defects, progressive bone-marrow failure, and cancer predisposition. Cells from FA patients exhibit hypersensitivity to DNA cross-linking agents, such as mitomycin C （MMC）. To date, at least 12 FA genes have been found deleted or mutated in FA cells, and 10 FA gene products form a core complex involved in FA/BRCA2 DNA repair pathway-FA pathway. The ubiquitin E3 ligase FANCL, an important factor of FA core complex, co-functions with a new ubiquitin conjugating enzyme UBE2T to catalyze the monoubiquitination of FANCD2. FANCD2-Ub binds BRCA2 to form a new complex located in chromatin foci and then take part in DNA repair process. The deubiquitylating enzyme USP1 removes the mono-ubiquitin from FANCD2-Ub following completion of the repair process, then restores the blocked cell cycle to normal order by shutting off the FA pathway. In a word, the FANCD2 activity adjusted exquisitely by ubiquitination and/or deubiquitination in vivo may co-regulate the FA pathway involving in variant DNA repair pathway.

Roles of NF-κB in central nervous system damage and repair

NF-κB family is a kind of nuclear factors in B lymphocyte that can bind to the immunoglobulin κ-chain enhancer and enhance transcriptional activity. NF-κB/Rel proteins, as a dimeric transcription factor, control the expression of genes that regulate a broad range of biological processes through canonical and non-canonical pathways. In the central nervous system, NF-κB controls inflammatory reactions and the apoptotic cell death following nerve injury. It also contributes to the infarction and cell death in stroke models and patients. However, NF-κB is essential for neurosurvival as well. NF-κB activation is a part of recovery process that may protect neurons against oxidative-stresses or brain ischemia-induced apoptosis and neurodegeneration. Inhibition of NF-κB may reduce its neuroprotection activity. Hence the dual opposite effects of NF-κB on cells. The ultimate survival or death of neurons depends on which, where and when the NF-κB factors are activated.

DNA Damage and Repair of Two Ecotypes of Phragmites communis Subjected to Water Stress

In order to thoroughly understand the mechanism Of drought resistance in plants at DNA level, the DNA damage of two ecotypes of reeds (Phragmites communis T.) stressed by PEG 6000 was analyzed by means of fluorescence analysis of DNA unwinding (FADU). The results showed that the residual double strand DNA percentages (dsDNA%) in dune reed (DR) were significantly higher than those in swamp reed (SR) treated with either 20% or 30% PEG 6000. This meant that the DNA of DR was less damaged in comparison with SR. Similarly, DR resisted DNA damage more strongly than SR as reactive oxygen species (ROS) increased by adding ROS producers diethyldithio carbamate (DDC), H2O2 and Fe2+ of different concentrations. Meanwhile, treating PEG stressed SR with ROS scavengers such as dimethyl sulphoxide (DMSO) and ascorbic acid (Vc) resulted in the reduction of DNA damage, suggesting that ROS could cause DNA damage. In addition, the DNA repair for water-stressed reeds indicated that DR repaired DNA damage much faster and more completely. This might be the first indication that drought stress led to DNA damage in plants and that drought resistance of plants was closely related to DNA damage and repair.

RAD51和BRCA1联合检测在肿瘤发生及对放化疗影响的研究进展

大量体内外因素如紫外线、放射线、烷化剂、化学致突变剂、DNA交联剂、DNA修复抑制剂、DNA复制过程中复制叉的破坏及淋巴细胞生成过程中的抗原受体重组等都可致细胞DNA的损伤,其中DNA双链断裂（DNA double-stand break,DSB）被认为是细胞凋亡的直接诱因。而对各种因素不敏感的细胞通过各种基因表达,对受损细胞DNA进行修复,来维持细胞的正常存活。

Relationship between acute kidney injury before thoracic endovascular aneurysm repair and in-hospital outcomes in patients with type B acute aortic dissection

Objective Acute kidney injury （AKI） frequently occurs after catheter-based interventional procedures and increases mortality. However, the implications of AKI before thoracic endovascular aneurysm repair （TEVAR） of type B acute aortic dissection （AAD） remain unclear. This study evaluated the incidence, predictors, and in-hospital outcomes of AKI before TEVAR in patients with type B AAD. Methods Between 2009 and 2013, 76 patients were retrospectively evaluated who received TEVAR for type B AAD within 36 h from symptom onset. The patients were classified into no-AKI vs. AKI groups, and the severity of AKI was further staged according to kidney disease： im- proving global outcomes criteria before TEVAR. Results The incidence of preoperative AKI was 36.8%. In-hospital complications was significantly higher in patients with preoperative AKI compared with no-AKI （50.0% vs. 4.2%, respectively; P 〈 0.001）, including acute renal failure （21.4% vs. O, respectively; P 〈 0.001）, and they increased with severity of AKI （P 〈 0.001）. The maximum levels of body tem- perature and white blood cell count were significantly related to maximum serum creatinine level before TEVAR. Multivariate analysis showed that systolic blood pressure on admission （OR： 1.023; 95% CI： 1.003-1.044; P ： 0.0238） and bilateral renal artery involvement （OR： 19.076; 95% CI： 1.914 190.164; P = 0.0120） were strong predictors of preoperative AKI. Conclusions Preoperative AKI frequently occurred in patients with type B AAD, and correlated with higher in-hospital complications and enhanced inflammatory reaction. Systolic blood pressure on admission and bilateral renal artery involvement were major risk factors for AKI before TEVAR.

Cell and gene therapy for arrhythmias： Repair of cardiac conduction damage

Action potentials generated in the sinoatrial node （SAN） dominate the rhythm and rate of a healthy human heart. Subsequently, these action potentials propagate to the whole heart via its conduction system. Abnormalities of impulse generation and/or propagation in a heart can cause arrhythmias. For example, SAN dysfunction or conduction block of the atrioventricular node can lead to serious bradycardia which is currently treated with an implanted electronic pacemaker. On the other hand, conduction damage may cause reentrant tachyarrhythmias which are primarily treated pharmacologically or by medical device-based therapies, including defibrillation and tissue ablation. However, drug therapies sometimes may not be effective or are associated with serious side effects. Device-based therapies for cardiac arrhythmias, even with well developed technology, still face inadequacies, limitations, hardware complications, and other challenges. Therefore, scientists are actively seeking other alternatives for antiarrhythmic therapy. In particular, cells and genes used for repairing cardiac conduction damage/defect have been investigated in various studies both in vitro and in vivo. Despite the complexities of the excitation and conduction systems of the heart, cell and gene-based strategies provide novel alternatives for treatment or cure of cardiac arrhythmias. This review summarizes some highlights of recent research progress in this field.

Protective effects of Rad23 protein on ultraviolet damage to HeLa cells

Protein Rad23, a nucleotide excision repair factor, mainly involves in repairing the DNA damage from environment, such as UV light. The function of Rad23 protein involved in DNA damage repair from many environmental factors has been studied extensively, but it is not clear from ultraviolet irradiation. To further investigate the photo-protective function of Rad23 protein on HeLa cells damaged from UV light irradiation, firstly, HeLa cells were irradiated by UV light and incubated with the fusion protein of pCold-Rad23, then the cell viability and apoptosis rate were detected by MTT and Hoechst33342/Pl fluorescent staining, respectively. The results show that the recombinant Rad23 protein can protect the HeLa cells from UV irradiation, and inhibit the apoptosis of HeLa cell by UV irradiation.

Peripheral nerve repair by conduits made of human hair keratin: An experimental study

Objective: To explore the method to repair injured peripheral nerve using conduits made of human hair keratin (HHK). Methods: The tibial nerves of rabbits were transected leaving a gap 10 mm in length between the 2 severed ends, which were either routinely sutured or bridged using HHK nerve conduits. Electro-physiological , anatomical and histological examinations were performed at different time postoperatively. Results: Electrophysiological study showed more obvious improvement in the neural function recovery in rabbits with HHK conduits bridging as compared with that in rabbits with routine suture. In the former group, HHK conduits were gradually degraded and absorbed with large amount of myelinated nerve fibers and Schwann cells regenerated around HHK conduits. In the latter group, however, the nerve tissues around the suture were degenerated and replaced by connective tissues. Conclusion: HHK may induce the regeneration of the nerve fibers and provides an ideal approach to repair nerve damages.

The DNA injury-repair of esophageal cancer EC109 cells to diallyl trisulfide (DATS) combining radiation

Objective: The aim of our study was to investigate the effect of diallyl trisulfide (DATS) combining radiation on DNA injury-repair of Esophageal cancer EC109 cells. Methods: Using 10 and 20 μg/mL DATS on EC109 cells, and taking X-ray radiation 24 h later. Investigate the radiosensitization effect of DATS on EC109 cells by clone formation, and the mechanism of DNA injury-repair by Comet Assay. Results: The clone formation resulted that DATS had radiosensitization effect on EC109 cells. Radiosensitization enhancement ratios of 10 and 20 μg/mL DATS in combination with radiation were 1.55, 1.64 (Do) and 1.43, 1.75 (Dq) respectively. In the comet assay, the TM (tail moments) of 20 μg/mL DATS combining radiation group lines at 0 h, 2 h, 6 h and 24 h were 7.16 ± 2.61, 3.65 ± 2.06, 2.09 ± 0.83, 1.45 ± 1.37 respectively. They were slightly increased than radiation group (0.95 ± 0.65, 0.11 ± 0.07, 0.1 ± 0.05, 0.11 ± 0.08) and DATS group (1.81 ± 1.23, 1.58 ± 1.40, 0.45 ± 0.25, 0.60 ± 0.40) (P < 0.01). The result showed that DATS combining radiation had the effect of increasing DNA damage and inhibiting DNA repair on EC109 cells. Conclusion: DATS has radiosensitization effect on Esophageal cancer EC109 cells. And the effect is probably related with DNA injury-repair.

Effects of UV-B radiation on tetraspores of Chondrus ocellatus Holm(Rhodophyta),and effects of red and blue light on repair of UV-B-induced damage

We evaluated the effects of red and blue light on the repair of UV-B radiation-induced damage in tetraspores of Chondrus ocellatus Holm. Tetraspores of C. ocellatus were treated with different UV-B radiation levels(0,36,72,108,144 and 180 J/m2),and thereafter subjected to PAR,darkness,or red or blue light during a 2-h repair stage,each day for 48 days. The diameters and cellular contents of cyclobutane pyrimidine dimmers(CPDs),chlorophyll a(Chl a),phycoerythrin,and UV-B-absorbing mycosporinelike amino acids(MAAs) contents of the tetraspores were determined. Our results show that low doses of UV-B radiation(36 and 72 J/m 2) promoted the growth of C. ocellatus; however,increased UV-B radiation gradually reduced the C. ocellatus growth(greater than 72 J/m2). The MAAs(palythine and asterina-330) in C. ocellatus were detected and analyzed by LC/MS. Our results suggest that moderate red light could induce the growth of this alga in aquaculture. In addition,photorepair was inhibited by red light,so there may be some other DNA repair mechanism activated by red light. Blue light promoted the activity of DNA photolyase,greatly improving remediation efficiency. Red and blue lights were found to reduce the capacity of C. ocellatus to form MAAs. Therefore,PAR,red light,and blue light play different roles during the repair processes for damage induced by UV-B radiation.

Transferring superior gluteal nerve to pudendal nerve in reconstructing functional impairment in simple conus medullaris or pudendal nerve injury

Objective: 1Department of Anatomy, College of Basic Medical Sciences, Second Military Medical University, Shanghai 200433, China 2Department of Orthopedic Surgery, Changhai Hospital, Second Military Medical University, Shanghai 200433, China Abstract Objective: To study the anatomical basis of transferring the superior gluteal nerve to the pudendal nerve in reconstructing the functional impairment in simple conus medullaris or pudendal nerve injury. Methods: Superior gluteal nerve and pudendal nerve were observed and measured by the gross and microsurgical anatomical methods in 62 sides of 31 adult cadavers. Results: Superior gluteal nerve came out of the superior foreman of piriformis as 1 to 4 branches(29.03%,56.45%,12.90% and 1.61% respectively) and the pelvic-leaving points were mainly in the middle 1/3(85.48%) of the line from the posterior superior iliac spine to the ischial tuberosity. The length of the inferior branch of the superior gluteal nerve was more than 5 cm, and the distance between the pelvic-leaving points of the superior gluteal nerve and pudandal nerve was about 4 cm only. The pudendal nerve left the pelvis mainly in the middle 1/3(48.39%) of the line from the posterior superior iliac spine to the ischial tuberosity,or at the junction of its inferior-middle 1/3(46.77%). In clinic, we have successfully made the operation transferring the superior gluteal nerve to the pudendal nerve in 3 patients suffered from the injury of conus medullaris. Conclusion: Distance between the pelvic-leaving points of the superior gluteal nerve and the pudendal nerve is close, so the inferior branch of the gluteal nerve can be anastomosed with the pudendal nerve directly. Transferring the superior gluteal nerve with higher spinal segemental origin to the pudendal nerve of a lower spinal segemental origin is practical and easy.

Investigation of the active components and mechanism of Sanao Decoction in treating chronic cough by network pharmacology and molecular docking

Objective To investigate the active components and mechanism of Sanao Decoction(三拗汤,SAD)in treating chronic cough based on network pharmacology and molecular docking.Methods Active components and their targets were obtained from the Traditional Chinese Medicine Systems and Pharmacology Database and Analysis Platform(TCMSP),Bioinformatics Analysis Tool for Molecular mech ANism of Traditional Chinese Medicine(BATMAN-TCM)database,and the literature.The component-target regulatory network and protein-protein interaction(PPI)network were constructed by Cytoscape 3.7.2,and a bioinformatics analysis was performed to identify the significant pathways and their relevant targets.Molecular docking of the core active components and relevant targets was performed.Results A total of 98 active components of SAD and the corresponding 113 drug targets were identified.The component-target regulatory network and PPI network were successfully established.Results of the bioinformatics analysis indicated that 2281 Gene Ontology(GO)terms were enriched in chronic cough,including 2062 terms were in biological processes,77 in cellular components,and 142 in molecular functions,and top 20 significant pathways in Kyoto Encyclopedia of Genes and Genomes(KEGG)analysis.Molecular docking study demonstrated that quercetin,luteolin,kaempferol,and naringenin were in good agreement with the corresponding targets.Conclusion The active compounds of SAD,such as quercetin,luteolin,kaempferol,and naringenin,may act on AKT1,MAPK1,RELA,EGFR,and Bcl-2 and regulate the PI3 K-Akt signaling pathway,AGE-RAGE signaling pathway,and fluid shear stress and atherosclerosis pathway to exert the effects of anti-inflammatory,anti-airway remodeling,anti-oxidant stress effects,and repair airway damage,thus treating chronic cough.

Modeling of DSBs Generation and Repair Process under Ion Radiation

Under acute perturbations from outside, cell can trigger the self-defense mechanisms in fighting against these genome stresses. To simulate the investigation of the complicated mechanisms of cellular responding DNA damage at single cell level, a model of the double strand breaks (DSBs) generation and repair process is proposed under continuous effect of acute IR. Under different IR dose domains, this model can be used to simulate the complicated interactions among vital components within the cell, and the plausible outcomes of cellular response in fighting against DNA damage.

Implications of oxidative damage to proteins and DNA in aging and its intervention by caloric restriction and exercise

In this short review we describe implications of age-related changes of protein and DNA oxidation as a public mechanism of biological aging. Oxidatively modified protein and DNA have been demonstrated to increase with advancing age in rodents. Half-life of proteins is extended and DNA repair activity declines in old animals. Dietary restriction initiated late in life can shorten the half-life of proteins to levels of young animals, thus contributing to reduce level of altered proteins in old animals by the regimen. Regular exercise reduced oxidatively modified proteins in the brain with improved cognitive functions. It attenuated oxidative stress in the liver, i.e., ameliorating activation of nuclear factor κB, increasing reduced glutathione, and decreasing oxidized guanine base in nuclear and mitochondrial DNA. These findings suggest that regular exercise has systemic effects in reducing oxidative stress. Thus, life-styles such as diet and exercise may extend health span, by up-regulating overall anti-oxidant capacities that include proteins involved in protein turnover and DNA repair, resulting in reduction of damaged proteins and DNA that potentially promote physiological and pathological aging.

Repair of a mal-repaired biliary injury:A case report

Iatrogenic bile-duct injury post-laparoscopic cholecystectomy remains a major serious complication with unpredictable long-term results. We present a patient who underwent laparoscopic cholecystectomy for gallstones, in which the biliary injury was recognized intraoperatively. The surgical procedure was converted to an open one. The first surgeon repaired the injury over a T-tube without recognizing the anatomy and type of the biliary lesion, which led to an unusual biliary mal-repair. Immediately postoperatively, the abdominal drain brought a large amount of bile. A T-tube cholangiogram was performed. Despite the contrast medium leaking through the abdominal drain, the mal-repair was recognized intraoperatively. The surgical procedure was converted to an open one. The first surgeon repaired the injury over a T-tube without recognizing the anatomy and type of the biliary lesion, which led to an unusual biliary mal-repair. Immediately postoperatively, the abdominal drain brought a large amount of bile. A T-tube cholangiogram was performed. Despite the contrast medium leaking through the abdominal drain, the mal-repair was unrecognized. The patient was referred to our hospital for biliary leak. Ultrasound and cholangiography was repeated, which showed an unanatomical repair （right to left hepatic duct anastomosis over the T-tube）,with evidence of contrast medium coming out through the abdominal drain. Eventually the patient was subjected to a definitive surgical treatment. The biliary continuity was re-established by a Roux-en-Y hepaticojejunostomy, over transanastomotic external biliary stents. The patient is now doing well 4 years after the second surgical procedure. In reviewing the literature, we found a similar type of injury but we did not find a similar surgical real-repair. We propose an algorithm for the treatment of early and late biliary injuries.

Relationship between transmembrane signal transduction pathway and DNA repair and the mechanism after global cerebral ischemia-reperfusion in rats

Objective To !nvestigate the protein levels of phospho-ERK and phospho-APE/Ref-1 in hippocampal neurons after global cerebral ischemia reperfusion in rats, and observe the relationship between transmembrane signal transduction and repair of DNA damage. The role of ERK signal transduction pathway following global cerebral ischemia reperfusion in rats is further discussed. Methods Ninety healthy male SD rats were divided into 3 groups randomly： Sham group （S group）, Ischemia reperfusion group （IR group） and Pd98059 pretreatment/ischemia reperfusion group （PD group）. Global cerebral ischemia reperfusion model was established by four-vessel occlusion （4-VO） method, and reperfusion was performed 5 minutes following ischemia. Protein levels of phospho-ERK and phospho-APE/Ref-1 were detected using immunohistochemical method at 2 h, 6 h, 12 h, 24 h, 48 h and 72 h after reperfusion, and neuron apoptosis was observed by HE and TUNEL staining. Results In CA1 region of IR group, TUNEL positive cells began to appear at 6 h after IR, and reached the apex during 24 h to 48 h. However, TUNEL positive was most strongly exhibited in PD group. In IR group, phospho-ERK was obviously detected in CA3 region at 2 h after IR, and its level was phospho-ERK expression in PD group was weaker than gradually decreased from 6 h until totally absent at 48 h. Besides, that in IR group. For phospho-APE/Ref-1, its expression began to appear in CA1 region in IR group at 2 h after IR, with no obvious changes during 2 h to 12 h. Phospho-APE/Ref-1 expression began to decrease at 24 h and this decrease continued thereafter. Expression level of phospho-APE/Ref-1 in PD group was lower than that in IR group. Results showed the concurrence of decreased phospho-ERK expression level and increased neuron apoptosis after cerebral ischemia reperfusion, the former of which was consistent with the decrease of phospho-APE/ Ref- 1 expression. Also, the greater the inhibition of ERK phosphorylation was, the greater decrease of APE/Ref- 1 expression occurred. Conclusion Activation of ERK signal transduction pathway increased the expression of phospho-APE/Ref-1, and thus faciliated the repair of DNA damage. So, activation of ERK signal transduction pathway may protect neurons from apoptosis after cerebral ischemia reperfusion.

Repair of acutely injured spinal cord through constructing tissue-engineered neural complex in adult rats

Objective： To construct tissue-engineered neural complex in vitro and study its effect in repairing acutely injured spinal cord in adult rats. Methods： Neural stem cells were harvested from the spinal cord of embryo rats and propagated in vitro. Then the neural stem cells were seeded into polygiycolic acid scaffolds and co-cultured with extract of embryonic spinal cord in vitro. ce histochemistry and scanning electron microscope were used to observe the microstructure of this complex. Animal model of spine semi-transection was made and tissue-engineered neural complex was implanted by surgical intervention. Six weeks after transplantation, functional evaluation and histochemistry were applied to evaluate the functional recovery and anatomic reconstruction. Results： The tissue-engineered neural complex had a distinct structure, which contained neonatal neurons, oligodendrocytes and astrocytes. After tissue-engineered neural complex was implanted into the injured spinal cord, the cell components such as neurons, astrocytes and oligodendrocytes, could survive and keep on developing. The adult rats suffering from spinal cord injury got an obvious neurological recovery in motor skills. Conclusions： The tissue-engineered neural complex appears to have therapeutic effects on the functional recovery and anatomic reconstruction of the adult rats with spinal cord injury.

Experimental Study on Mechanical Vibration Massage for Treatment of Brachial Plexus Injury in Rats

Objective: To investigate the curative effect of the self-made mechanical vibration massage instrument for treatment of brachial plexus injury in rats and to explore its mechanism. Methods: Brachial plexus injury models were made in 144 Wistar rats and one week after natural healing of the wound, they were randomly divided into 3 groups, mechanical vibration treatment group (MV group), nerve growth factor treatment group (NGF group) and model group, 48 rats in each group. Then again, the each group was randomly divided into 4 subgroups, 7-day group, 14-day group, 21-day group and 28-day group, 12 rats in each subgroup. The MV group were treated by mechanical vibration at acupoints on three-yang and three-yin channels of the hand with the mechanical vibration massage instrument; The NGF group were treated with injection of NGF into musculus pectoralis major on the affected side; And the model group were normally fed with no treatment. After treatment for 7, 14, 21 and 28 days, the diameter of both forelimbs were measured, the electrophysiological examination on the brachial plexus in vitro and the ultrastructure observation with electron microscope on the affected side were carried out, the motor nerve conduction velocity (MNCV) and motor nerve action potential (MNAP) of the brachial plexus on the affected side, NGF content of submaxillary gland as well as muscular Na+, K+-ATPase activity were determined respectively. Results: The different rates of the forelimb diameter in the MV group and the NGV group on the 14th d, 21st d and 28th d were better than those in the model group (P<0.05 or P<0.001), and in the MV group were better than those in the NGF group on the 21st d and the 28th d (P<0.05). MNCV in the MV group and the NGV group on the 21st d and 28th d was better than that in the model group (P<0.05 or P<0.001), and in the MV group was better than that in the NGF group on the 28th d (P<0.05). MNAP in the MV group and the NGV group on the 14th d, 21st d and 28th d was better than that in the model group (P<0.05 or P<0.001), and in the MV group was better than that in the NGF group on the 21st d and 28th d (P<0.05). The NGF mean gray index of submaxillary gland in the model group was higher than that in the MV group and the NGF group on the 7th d (P<0.05); in the NGF group and the model group was higher than that in the MV group on the 14th d (P<0.05); and in the NGF group and the MV group was higher than that in the model group on the 21st d and 28th d (P<0.05). Na+, K+-ATPase activity in the model group and the MV group was higher than that in the NGF group (P<0.05) on the 14th d, and in the MV group was higher than that in the model group on the 28th d (P<0.05). Conclusion: As compared with the NGF group and the model group, mechanical vibration treatment can effectively accelerate repair of injured brachial plexus, slow down atrophy of skeletal muscle, and promote secretion of NGF in submaxillary gland.

Treatment for 332 cases of lower leg fracture in ＂5.12＂ Wenchuan earthquake

Objective： To retrospectively analyze the medical treatment of 332 patients with lower leg fracture in Wenchuan earthquake admitted in West China Hospital. Methods： From May 12, 2008 to June 15, 2008, 332 patients with lower leg fracture injured in Wenchuan earthquake were treated in our hospital. The data on trauma condition and clinical treatment were collected and analyzed. Results： Among the 332 cases of lower leg fracture, there were 179 eases of open fracture, accounting for 53.9%, in which 91% belonged to Gustilo Ⅱ or Ⅲ injury with serious pollution. Many patients had posttraumatic complications, vascular and nerve injury, wound infection or osteofascial compartment syndrome. After medical treatment, blood vessels were reconnected, wound surface was repaired and wound infection was under control. Conclusion： For the patients with lower leg fracture in earthquake, we followed the principle of ＂complete debridement - restoring the continuity of bone bracket - timely recovering blood supply of limbs and repairing nerve damage - repair the wound surface at stage Ⅰ or Ⅱ ＂ so as to reduce the incidence of amputation and infection.