BACKGROUND: Obstructive sleep apnea syndrome(OSAS) in patients with serious micrognathia affects the respiratory function and can be life-threatening. Conventional surgical therapies are often highly risky and unsuitable in patients with the craniomaxillofacial skeleton still in development.OBJECTIVE: To assess the value of mandibular distraction osteogenesis in treatment of OSAS in patients with congenital micrognathia and the effect of the surgery on the patients' respiratory functions.DESIGN: A self-controlled study.SETTING: Plastic Surgery Hospital of Peking Union Medical College and Plastic and Maxillofacial Surgery Unit of Royal Children's Hospital of Melbourne, Australia.PARTICIPANTS: Eight consecutive patients with congenital micrognathia who developed OSAS were hospitalized from October 2001 to July 2004 at the Center of Craniomaxillofacial Surgery, Plastic Surgery Hospital of Peking Union Medical College and Plastic and Maxillofacial Surgery Unit of Royal Children's Hospital of Melbourne, Australia. This group included 5 male and 3 female patients aged 4 months to 17 years.METHODS: The 8 patients underwent mandibular distraction osteogenesis,and altogether 16 distractors were placed through extraoral or intraoral incisions for bilateral distraction. The distraction device proceeded at the rate of 1 to 1.5 mm per day and consolidated for 4 to 12 weeks. The follow-up lasted for 2 to 18 months. Each patient was evaluated pre-and postoperatively with cephalometry or polysomnography (PSG).MAIN OUTCOME MEASURES: The distraction distance, posterior airway space, and improvement of the respiratory function of the patients were recorded.RESULTS: Osteotomy and distraction procedures were smooth in all the patients who had good ontogenesis. The average distraction distance was 19.12 mm(ranging from 15 to 25 mm) . The posterior airway space was increased from a mean of 4.5 mm preoperatively to 11 mm after the surgery. Seven patients had normal respiration and sleep after removal of the nasopharyngeal intubation or tracheal decannulation. One patient required a second-stage distraction with a horizontal vector. The therapeutic effect was stable without relapse in the follow-up.CONCLUSION: Mandibular distraction osteogenesis is an important and effective means for treating OSAS. It effectively corrects airway stricture and improve the patients' respiratory function, allowing mandibular development in young patients. When more cases are studied, the role of distraction osteogenesis can be better defined.

Objective To explore the therapeutic methods and effects of orbital blow-out fractures.Methods Thirty-three cases (36 eyes) of orbital pure blow-out fracture were treated by surgery from January 2007 to July 2013.The features of orbital fractures were determined with three-dimensional computed tomography scans.The area of fractures was exposed through sub-ciliary incision,the herniated orbital contents were released and reduced to the orbital cavity.The fractured orbital walls were repaired precisely with autologous bone or Medpor.Results After 6 to 12 months followup,there were no serious complications such as infection of bone graft,exposure of implants in all 33 cases,and all the cases got satisfactory appearance of eyelids and orbit,of which the diplopia disappeared and eyeball movement function recovered normally.The protrution of eyeball in 29 cases were symmetrical,but 4 cases presented mild enophthalmos at affected side.Conclusions The orbital volume enlarges and orbital content herniating into paranasal sinuses is caused by orbital blow-out fracture.Implanting autogenous grafts and Medpor to restore orbital volume are proved to be effective.Early CT examination is an effective method for the diagnosis.In order to avoid complications,the orbital blow-out fracture should be subjected to surgical treatment as soon as possible.

Histopathological and ultrastructural changes of the lungs were observed in various intervals after high-velocity bullet wounds of the two thighs of dogs. It was found that histologically there were microvascular dilatation, congestion, capillary rupture, interstitial and alveolar bleeding, focal atelecta-sis and pulmonary emphysema in the first half hour and the 6th hour after injury. In addition, microvascular embolism and hyaline membrane formation were seen in the 24th and 72nd hour after injury. Under electron microscopy, there were swelling of capillary endothelium, swelling, degeneration and necrosis of type I pneumocytes, shortening and decreasing of the microvilli of type II pneu-mocytes, significant vacuolation of the lamonar bodies, accumulation of leucocytes and platelets in the capillary lumen,and obvious decrease of the granules in the leucocytes. The mechanism of the pulmonary injury accompanying bullet wound of the thighs was discussed.

Objective Interferon regulatory factors 3 (IRF-3) is a key transcription factor to regulate gene expression of interferon after virus infection. This study aims to look for new spliced isoforms of IRF-3 and to investigate their structures and functions. Methods RNA extracts from human embryonic kidney 293 cells were amplified by RACE and RT-PCR. New sequences were compared with published sequences of IRF-3 and murine EST database using bioinformatics method. A new sequence, IRF-3c, was subcloned into pcDNA3.1-flag. The IRF-3c/pcDNA3.1-flag plasmid was transfected in HEK 293 cells. Whole cell extract was analysed by Western blot and then probed with monoclonal Flag antibody. Luciferase assay was carried out by co-transfection with reporter plasmid, pGL2B with interferon ? promoter, and IRF-3c cDNA expression plasmid. At 16 hours posttransfection, cells were infected with Sendai virus for 8 hours. Cells were collected and assayed for luciferase activity. Results A novel spliced isoform of IRF-3, named IRF-3c was discovered. The new isoform is almost the same as IRF-3, except for the utilization of the 180 bp bases in intron 6 adjacent to exon 6. The first 2,3 and 4 bases are a stop codon, which may produce a protein with a truncated C-terminal stoped at amino acids 327. Western blot analysis confirmed an expected 44 kDa strong band. The new inserted bases can be found in murine EST database, suggesting a conservative function in evolution. The functional luciferase assay showed that IRF-3c inhibited the IFN? promoter activity to (around) 40%～50% as that of control after Sendai virus infection. Conclusions The discovery of a new isoform of IRF-3 provides a new insight into the functional regulation of IRF-3 family. It is a dominant-negative inhibitor for interferon ? promoter activity in the virus infection pathway, provides a mechanism for the fine-tuning of the virus-induced activation of the interferon response, and prevents interferon ? from its overexpression and its toxic effects. It is worthwhile to explore the role of IRF-3c in the pathogenesis of human diseases using IRF-3c’s specific sequence.

Objective To explore the inhibitory effect of mutant influenza A viruses to the activation of interferon regulatory factor 3 (IRF-3). Methods HEK293 cells were infected with A/FM/1/47,A/HK/1/68, A/HK/1/68-MA20, A/HK/1/68-MA20C and positive control Sendai virus (SV). Whether the slowly moved phosphorylation form Ⅲ and Ⅳ of IRF-3 appeared or not was compared by Western blot in cells infected with these viruses. Wild type of NS1 from A/HK/1/68 and mutant NS1 from A/HK/1/68-MA20 were subcloned into pcDNA3.1-flag respectively. They were transfected in HEK 293 cells respectively. At 16 hours posttransfection, cells were infected with Sendai virus for 8 hours. Whole cell extracts were analyzed by Western blot and then probed with monoclonal flag antibody to check the expression of NS1, or with anti-IRF-3 to observe the inhibitory effects of the wild and mutant NS1 to the activated IRF-3. Luciferase assay was carried out by co-transfection with reporter plasmid, pGL2B with interferon ? promoter, and wild or mutant NS1 cDNA expression plasmid. SV was used to infect these cells after the co-transfection. Results Only less virulent A/HK/1/68-MA20 and positive control SV can activate IRF-3. Activated form Ⅲ and Ⅳ of IRF-3 began to appear 9 hours post infection (h.p.i), and most significant activated IRF-3 appeared 23 and 26 h.p.i. Sequence analysis of NS1 of MA20 revealed that nucleotide position number 94 is mutated from T to C, and amino acid at position number 23 is changed from valine to alanine. Co-transfected with wild type NS1 made form Ⅲ and Ⅳ of IRF-3 almost disappear, but not mutant NS1. In the luciferase functional analysis, wild type NS1 can inhibit the luciferase activity of IFN-? promoter, which was induced by SV, to around 1/10. Again no inhibitory effects was observed of mutant NS1 in the luciferase assay. Conclusion The mechanism that A/HK/1/68-MA20 can activate IRF-3 is that point mutant NS1 abolished the inhibitory function of NS1.

Ashi points, movable cupping and traction were employed to treat 120 cases of prolapase of lumber intervertebral disk, and the total effective rate was 95.6%.

Objective To explore the effect of subcutaneous composite flaps by crossed filling and supporting within areola combined with continuous distraction on moderate and severe inverted nipple.Methods 33 patients with 59 moderate and severe inverted nipples were involved in this study.The bilateral subcutaneous triangular composite tissue flaps pedicled with the base of the nipple were harvested within areola,the two triangular composite tissue flaps were revolved and advanced either horizontally to the opposite pedicle through the tunnel beneath the nipple and fixed as supporting.After the operation,the continuous distraction of the nipple lasted for two to four weeks,clinical effect and complications were analyzed.Results None of these 59 nipples appeared blood circulation disorder after operation.Postoperative follow-up for 6 months to 3 years showed that 54 inverted nipples were corrected completely without complications,such as nipple and areola necrosis,and there were no recurrence.The patients and doctors were satisfied with the appearance of the nipples.Conclusions Correcting the moderate and severe inverted nipple with subcutaneous composite flaps by crossed filling and supporting within areola combined with continuous distraction is simple,microinvasive,effective,and the incision scar is invisible,and it therefore is an ideal method for correcting the inverted nipple.

Objective To investigate the effects of sulforaphane (SFN) on the proliferation of prostate cancer DU145 cells and hypoxia-inducible factor-1α(HIF-lα) expression,and to explore the possibility of SFN in the prevention of prostate cancers.Methods The DU145 cells were treated with different doses and different time of SFN.The cell proliferation viability were measured by 3-(4,5)-dimethylthiahiazo (-zy1)-3,3,5-di-phenytetrazo`liumromide (MTT) proliferation and cytotoxicity assay kit.The hypoxia tumor microenvironment was stimulated by pretreating cells with 1％ O2,HIF-lα expression and vascular endothelial growth factor (VEGF) activitity were detected by Western-blot and ELISA,respectively.Results SFN had an inhibitory effect on the proliferation of human prostate cancer DU145 cells in a dose-and time-dependent manner.The cell proliferation inhibition rate exceeded 50％ in more than 20 μ mol/L SFN-treated groups after 48 hours.SFN could inhibit the expression of HIF-1α induced by 1％ O2 and VEGF activity.10 μmol/L SFN showed inhibitory effect on the expression of HIF-1α after 24 hours.20 μ mol/L SFN showed a significant inhibitory effect on the expression of HIF-1α after 12 hours.And peroxidase had synergistic inhibition on HIF-1α.Conclusions SFN can inhibit the proliferation of DU145 prostate cancer cells and HIF-lα expression.SFN can be used as a potential chemotherapeutic agent against human prostate cancer.

Objective To investigate the oxidative mechanism of homocysteine ( Hey) -induced apoptosis in endothelial progenitor cells( EPCs). Methods Total mononuclear cells were isolated from mouse bone marrow by Ficoll density gradient centrifugation and were cultured in vitro for 7 d. Adherent cells were harvested and identified by fluorescence microscopy. EPCs were cultured with Hey (0, 50, 100 and 500 μmol/L) for 12, 24 and 48 h, or pretreated with NAC (1 mmol/L), DPI( 10 μmol/L) or SB203580 (10 μmol/L) for 30 min, then cultured with 500 μmol/L Hey for 24 h. Apoptosis was detected by Annexin-V/PI flow cytometry, levels of reactive oxygen species (ROS) in cells were measured using H2DCF-DA as a fluorescence probe, NADPH oxidases were evaluated with lucigenin-enhanced chemilumine9cence, and NO in the supernatant was determined by nitrate reductase assay. Results Hey induced EPCs apoptosis, ROS accumulation, NADPH oxidase activation and decrease of NO in a time-dose dependent manner( P <0.05 or P < 0.01). Pretreatment with NAC, DPI and SB203580 could inhibit these effects (P < 0.05 or P < 0.01). Conclusion Hey could activate NADPH oxidase, induce ROS increase and NO decrease, and activate p38MAPK to enhance EPCs apoptosis.

AIM: Direct exposure of cells to reactive oxygen species can induce apoptosis. In this study we investigate how oxidative stress induces cell death in HepG2 cells and characterize the molecular events involved. METHODS: Oxidative stress was created by exposing HepG2 cells to 2 mmol/L H2O2. Apoptosis was determined by analysis of DNA fragmentation by agarose gel electorphoresis. The mitochondrial membrane potential was analyzed using DePsipher fluorescent staining and the expression of cytochrome c in the cytosolic fraction was measured by Western blotting analysis.The caspase activity was detected using fluorometric assay kit by a fluorescence microplate reader. RESULTS: When HepG2 cells were treated with 2 mmol/L H2O2, the cells displayed DNA fragmentation, a typical feature of apoptosis, after 12 h. The mitochondrial membrane potential appeared different in two group of cells. H2O2 -treated cells appeared green fluorescence as early as 4 h, which represents de - energized mitochondria, the untreated cells appeared red fluorescence,a feature of mitochondria with intact membrane potential. In treated cells, the expression of cytochrome c increased and accumulated in cytosolic fraction with treatment time, caspase - 3 activity increased by 6.7 - fold ( P ＜ 0.01 ) at 8 h and caspase -9 activity increased by 3.6 - fold (P ＜ 0.01 ) at 12 h, respectively, however, the activity of caspase - 8 remained unchanged. CONCLUSION: These findings suggest that oxidative stress can induce apoptotic cell death in HepG2 cells, and the mechanism is related to mitochondrial pathway, which activates caspase -9 and- 3, but not caspase -8.