Air Pollutants, Occupational ; analysis ; Benzenesulfonates ; analysis ; Chromatography, High Pressure Liquid ; methods ; Workplace

Adolescent ; Heart Valve Diseases ; etiology ; Heart Valves ; pathology ; Humans ; Lupus Erythematosus, Systemic ; complications ; pathology ; Male

Aspergillosis, Allergic Bronchopulmonary ; diagnosis ; drug therapy ; Child ; Humans ; Male

Coronary Restenosis ; pathology ; Fibroblasts ; metabolism ; pathology ; Fibrosis

Thirteen Polio patients with leg length inequality were undergone Ilizarov lengthening procedures and have been followed along for an average two years(range, 1-3.8 years) after removal of the fixator. The age of patients(M:F=7:6) ranged from 18.0 to 32.2 years(average 26.4 years). The difference of true leg length averaged 2.1cm with the tibia being 3.3cm the femur, 1.2cm. The corticotomy was done at the proximal tibia and distal fibula in all case. The fixation period of the Ilizarov apparatus averaged 9.3 months. The length gain averaged 3.0cm for an average 3.8cm inequality. The healing index averaged 3.1mon/cm. Two out of thirteen patients complained of pain in the operated leg. The limping gait was improved in all patients except one. According to Paley's classification, there were ten cases of problems, one obstacle and four true complications. The problems were pin site infection controled with local antibiotics injection. There was one case of obstacle; tibial valgus deformity developed during lengthening. True complications included peroneal nerve injury, aggravation of preexsiting equinovalgus and claw toe deformities, aggravation of preexsiting valgus deformity of ankle and tibial valgus deformity. The complications execpt in one case of peroneal nerve palsy were solved out by the secondary procedures. In summery, the bone healing by distraction osteogenesis with the Ilizarov technique was relatively delayed in polio patients and it seems necessary to modify the technique to shorten the prolonged external fixation period.
Ankle ; Anti-Bacterial Agents ; Classification ; Congenital Abnormalities ; Femur ; Fibula ; Gait ; Hammer Toe Syndrome ; Humans ; Ilizarov Technique ; Infection Control ; Leg Length Inequality ; Leg ; Osteogenesis, Distraction ; Paralysis ; Peroneal Nerve ; Poliomyelitis ; Socioeconomic Factors ; Tibia

AIM: To screen the binding proteins to HMGB1 promoter by phage display technique. METHODS: HMGB1 promoter was incubated with phage display library. Unbound phages were eluted and phages bound to HMGB1 promoter were amplified. Twenty individual clones were randomly selected and identified by enzyme-linked immunosorbent assay (ELISA). Positive clones were characterized by DNA sequencing and the sequences were subjected for computer analysis. RESULTS: Positive phages binding to HMGB1 promoter were enriched after 4 rounds of biopanning. Twenty phage clones were selected and eleven clones of which were identified to bind specifically to HMGB1 promoter. The sequences in full length were obtained and searched for homologous sequences from GenBank. Altogether eight coding sequences were obtained, six of which were known proteins including activator protein-1(AP-1) and two of which were uncharacterized ones. CONCLUSION: Several proteins were obtained that bind specifically with HMGB1 promoter. The results will be useful for further studying the expression and regulation mechanism of HMGB1.

Objective To investigate the role of extracellular regulated protein kinase (ERK) signal pathway in mechanical stretch induced high mobility group box 1 protein (HMGB1) expression on alveolar epithelial cells (A549). MethodsA549 cells were cultured and seeded at 1×10~5 cells/ml in 6-well Bioflex cell culture plates. Subsequently, the cells were exposed to cyclic mechanical stretch at 14% (group B) elongation for 4 hours using Flexercell 4000T cell stretching unit. In group C, cells were pretreated with PD98059 for 2 hours before mechanical stretch. Cells in group A without stretch were served as control. The expression of HMGB1 protein and mRNA in A549 cells were detected by immunocytochemisty staining and RT-PCR, respectively. ERK activity was measured by Western blotting method. Results Immunocytochemisty staining indicated that the expression of HMGB1 protein in A549 cells was increased obviously in group B (P<0.05) and decreased in group C (P<0.05). Polymerase chain reaction (RT-PCR) showed that the expression of HMGB1 mRNA was also significantly increased in group B (P<0.05) and decreased in group C (P<0.05). Western blotting analysis confirmed the activation of ERK in A549 cells by mechanical stretch (P<0.05). PD98059, an inhibitor of ERK, might significantly inhibit mechanical stretch induced HMGB1 protein and mRNA expression in A549 cells (P<0.05). Conclusion Mechanical stretch could regulate the expression of HMGB1 gene and protein in A549 cells through ERK signal pathway.

BACKGROUND:Taurine is an important non-enzymatic system antioxidant in the lens.The mechanism of its anti-oxidative effect is mainly to protect lens from oxidative injury by anti-lipid peroxidation.OBJECTIVE:This study was to observe the effect of exogenous taurine on lens epithefial cell apoptosis-induced by H2O2 in vitro.DESIGN:A randomized controlled animal experiment.SETTING:Department of Ophthalmology,Affiliated Hospital of Qingdao University Medical College.MATERIALS:Seventy-five adult New Zealand standard tabbits,of either gender,weighing 1.5-2.5 kg,were provided by Qingdao Laboratory Animal Center.Reagent kit for in situ detecting cell apoptosis(Sigma Company,USA),taurine and H2O2(Shanghai Guangda Chemical Reagent Factory,China)were included in this study.METHODS:This study was performed in the Department of Ophthalmology and Central Laboratory.Affiliated Hospital of Qingdao University Medical College from Mav 2005 to June 2007.Rabbit lenses were harvested and randomly divided into 3 groups:control group,in which,clear lenses were incubated in non-serum and non-phenolsulfonphthalein MEM medium which was renewed every 24 hours,H2O2 group,in which,clear lenses were incubated in non-serum and non-phenolsulfonphthalein MEM medium containing 1 mmol/L H2O2 with addition of 62 μL H202(30 g/L)every 6 hours,and H2O2+taurine group,in which,clear lenses were incubated in non-serum and non-phenolsulfonphthalein MEM medium containing 1 mmol/L H2O2 and 10 g/L taurine.which was renewed every 6 hours.The protocol was conducted in accordance with ethical guidelines for the use and care of animals.MAIN OUTCOME MEASURES:Observation of lens opacity 6.12,24.48 and 72 hours after culture;Lens epithelial cell apoptosis determined by DNA in situ end labeling and DNA fragment analysis.RESULTS:Lens opacity:The lens opacity in the H2O2 group was aggregrated gradually along with the time of oxidative injury.The lens opacity in the H2O2 group was severer than that in the H2O2+taurine group.Lens epithelial cell apoptosis:There were no apoptotic cells in the control group within 72 hours.The number of apoptotic cells in the H2O2 group was increased gradually with the prolonged time of oxidative injury.Till the 72nd hour,the cells were all tamed into apoptotic cells.A few aopototic celIs were found in the H2O2+taurine group since hour 24,and then were more and more,and the number of apoptotic cells accounted for about 30%at hour 72.The apoptotic rate in the H202+taurine group was significantly lower than that in the H2O group at each time point(q=8.6845,P＜0.01).There was no significant difference in apoptotic rate between the H202+taurine group and the control group (P＞0.05). Findings of DNA fragmentation assay:The DNA"ladder"was found in the H2O2 group at hours 24,36,48 and 72,while no DNA"ladder"but only normal electrophoresis straps were present in the other two groups 24 hours after culture.CONCLUSION:Taurine can inhibit the oxidative injury-induced apoptosis of rabbit lens epithelial cells,and alleviate lens opacity.

Objective To investigate the role of p38 MAPK pathway in the expression of high mobility group box 1 (HMGB1) in lung tissue in a rat model of ventilator-induced lung injury. Method Twenty-fonr healthy Sprague Dawley (SD) rats were randomly divided into 3 groups (n = 8 each) : group A, spontaneous breathing; group B, small tidal volume ventilation (Vt = 8 mL/kg) and group C, high tidal volume ventilation (Vt = 40 mL/kg). 1he animals in group B and C were mechanically ventilated for 4 hours and all animals were sacri-riced. The lungs were removed for: (1) lung lavage and determination of total protein contnt and WBC and neu-trophil counts in broncho-alveolar lavage fluid (BALF) ; (2) determination of W/D lung weight ratio and myelop-erexidnse (MPO) activity; (3) detennination of HMGB1 protein and mRNA expression and p38 MAPK activity in lung tissue. Differences within the groups were analyzed using One way ANOVA. Results The inflammatory re-sponse as evidenced by total protein (1.77 ± 0.68) g/L and WBC (106.55 ± 28.17) × 10~7/L in BALF, W/D lung weight ratio (7.16±1.02) and MPO activity (3.94±1.21) U/g were significantly higher in group C com-pared with group A (P <0.05); HMGB1 protein (0.64±0.17) and mRNA (1.17±0.45) expression and p38 activity (0.51±0.12) also significantly increased in group C (P <0.05). Of the above indexes, there were no statistical differences between group B and group A (P > 0.05). Conclusions High tidal volume ventilation in-daces acute lung injury, which may be related with upregulation of HMGB1 expression through p38 MAPK signal pathway.

Objective To determine whether pyloric measurements with ultrasound, that muscle thickness and channel of pyloric, correlated with weight and age in patients with hypertrophic pyloric stenosis (HPS). Methods A retrospective analysis was conducted on 111 cases diagnosed with HPS by operation from 2008 to 2012. Pearson correlation and linear regression analyses were used to determine if there were sta?tistically signiifcant associations between these combinations of factors:age and pyloric muscle thickness, weight and pyloric muscle thickness, age and pyloric length, and weight and pyloric length. Results Patients’mean age was 39.1 d (8-92 days). Their mean weight was 4.3 kg (2.2-7.9 kg). Mean pyloric muscle thickness was 4.8 mm (2-4.6 mm), and mean pyloric length was 17.5 mm (12-23.5 mm). Pearson correlation coefifcient analysis showed a signiifcant correlation between age and muscle thickness (r=0.6, P<0.001) as well as weight and muscle thickness (r=0.486, P<0.001). No signiifcant correlation was found be?tween pyloric length and age or weight. Linear regression analysis demonstrated similar results. Conclusions In patients with HPS, pyloric muscle thickness was directly related to age and weight. Smaller and younger infants with suspected diagnosis of HPS should be followed up even though the minimum diagnostic criterion for muscle thickness or length was not found on ultrasound.