No abstract available.
Mandibular Reconstruction*

No abstract available.

No Abstract Available.
Blepharoptosis* ; Silicones*

No abstract available.
Apgar Score* ; Humans

PURPOSE: Pulmonary interstitial emphysema (PIE) primarily occurs in preterm infants suffering from respiratory distress syndrome (RDS) and kept under mechanical ventilator care. Therefore, this study aimed to examine various risk factors for PIE, to identify conditions that can decrease the possibility of PIE development. METHODS: PIE classification was conducted for 183 patients diagnosed to have RDS and receiving mechanical ventilator care with pulmonary surfactant between March 2000 and February 2007. The characteristics of each patient were analyzed through retrospective examination of their medical histories. RESULTS: Among 183 patients, 17 had PIE; all factors, including birth weight, gestational age, RDS grade III or above, chorioamnionitis, and premature rupture of membranes, were statistically significant (P<0.05). The period of mechanical ventilator use was statistically significant, but the peak mean airway pressure and peak partial pressure of inspired oxygen were not. PIE mainly occurred on the right side or both sides rather than the left side and mostly developed within 72 h. The PIE group showed higher mortality rate than the control group, and the major cause of mortality was pneumothorax. CONCLUSION: Risk factors for PIE in infants suffering from RDS and kept under mechanical ventilator care include low gestational age, low birth weight, chorioamnionitis, and premature rupture of membranes. If any risk factors are noted, the infant must be observed closely for at least 72 h after birth.
Birth Weight ; Chorioamnionitis ; Emphysema ; Female ; Gestational Age ; Humans ; Infant ; Infant, Low Birth Weight ; Infant, Newborn ; Infant, Premature ; Membranes ; Oxygen ; Partial Pressure ; Parturition ; Pneumothorax ; Pregnancy ; Pulmonary Surfactants ; Retrospective Studies ; Risk Factors ; Rupture ; Stress, Psychological ; Ventilators, Mechanical

Treatment with cisplatin for cancer therapy has a major side effect such as nephrotoxicity; however, the role of poly (ADP-ribose) polymerase 1 (PARP1) in necrosis in response to cisplatin nephrotoxicity remains to be defined. Here we report that cisplatin induces primary necrosis through PARP1 activation in kidney proximal tubular cells derived from human, pig and mouse. Treatment with high dose of cisplatin for 4 and 8 hours induced primary necrosis, as represented by the percentage of propidium iodide-positive cells and lactate dehydrogenase release. The primary necrosis was correlated with PARP1 activation during cisplatin injury. Treatment with PJ34, a potent PARP1 inhibitor, at 2 hours after injury attenuated primary necrosis after 8 hours of cisplatin injury as well as PARP1 activation. PARP1 inhibition also reduced the release of lactate dehydrogenase and high mobility group box protein 1 from kidney proximal tubular cells at 8 hours after cisplatin injury. Oxidative stress was increased by treatment with cisplatin for 8 hours as shown by 8-hydroxy-2'-deoxyguanosine and lipid hydroperoxide assays, but PARP1 inhibition at 2 hours after injury reduced the oxidative damage. These data demonstrate that cisplatin-induced PARP1 activation contributes to primary necrosis through oxidative stress in kidney proximal tubular cells, resulting in the induction of cisplatin nephrotoxicity and inflammation.
Animals ; Cisplatin* ; Humans ; Inflammation ; Kidney* ; L-Lactate Dehydrogenase ; Lipid Peroxides ; Mice ; Necrosis* ; Oxidative Stress ; Poly(ADP-ribose) Polymerases* ; Propidium

Enhanced oxidative stress is a hallmark of cisplatin nephrotoxicity, and inhibition of poly(ADP-ribose) polymerase 1 (PARP1) attenuates oxidative stress during cisplatin nephrotoxicity; however, the precise mechanisms behind its action remain elusive. Here, using an in vitro model of cisplatin-induced injury to human kidney proximal tubular cells, we demonstrated that the protective effect of PARP1 inhibition on oxidative stress is associated with sirtuin 3 (SIRT3) activation. Exposure to 400 µM cisplatin for 8 hours in cells decreased activity and expression of manganese superoxide dismutase (MnSOD), catalase, glutathione peroxidase (GPX), and SIRT3, while it increased their lysine acetylation. However, treatment with 1 µM PJ34 hydrochloride, a potent PARP1 inhibitor, restored activity and/or expression in those antioxidant enzymes, decreased lysine acetylation of those enzymes, and improved SIRT3 expression and activity in the cisplatin-injured cells. Using transfection with SIRT3 double nickase plasmids, SIRT3-deficient cells given cisplatin did not show the ameliorable effect of PARP1 inhibition on lysine acetylation and activity of antioxidant enzymes, including MnSOD, catalase and GPX. Furthermore, SIRT3 deficiency in cisplatin-injured cells prevented PARP1 inhibition-induced increase in forkhead box O3a transcriptional activity, and upregulation of MnSOD and catalase. Finally, loss of SIRT3 in cisplatin-exposed cells removed the protective effect of PARP1 inhibition against oxidative stress, represented by the concentration of lipid hydroperoxide and 8-hydroxy-2'-deoxyguanosine; and necrotic cell death represented by a percentage of propidium iodide–positively stained cells. Taken together, these results indicate that PARP1 inhibition protects kidney proximal tubular cells against oxidative stress through SIRT3 activation during cisplatin nephrotoxicity.
Acetylation ; Catalase ; Cell Death ; Cisplatin* ; Deoxyribonuclease I ; Down-Regulation* ; Glutathione Peroxidase ; Humans ; In Vitro Techniques ; Kidney ; Lipid Peroxides ; Lysine ; Oxidative Stress* ; Plasmids ; Poly Adenosine Diphosphate Ribose* ; Poly(ADP-ribose) Polymerases* ; Propidium ; Sirtuin 3* ; Superoxide Dismutase ; Transfection ; Up-Regulation

BACKGROUND: The pediatric CPR is rather uncommon practice than adult CPR in emergency room. Therefore, few interest and studies were focused in pediatric CPR. The object of this study is to make an analysis about pediatric CPR performed within hospital setting. METHOD: From January 1. 1990 to December 31. 1996, a total of 59 patients, less than 15-year-old, who received cardiopulmonary resuscitation were subject of this study. The study was done retrospective chart analysis for sex, age, weight, the place of cardiac arrest, initial EKG rhythms, endotracheal tube size, the causes of arrest, CPR time, ROSC, the amount and types of CPR drugs used during resuscitation. Wilcoxon rank sum test and chi2 test were used to compare the dose of drugs during CPR in each group. RESULTS: There were no statistical difference between ROSC and non-ROSC group in place of arrest, initial EKG rhythms, CPR time, dosage of CPR drugs. CONCLUSION: The uniform reporting guideline of pediatric advanced life support should be used for future pediatric CPR study, such as Utstein style guideline in pediatric CPR.
Adolescent ; Adult ; Cardiopulmonary Resuscitation* ; Electrocardiography ; Emergency Service, Hospital ; Heart Arrest ; Humans ; Resuscitation ; Retrospective Studies

BACKGROUND: The end-tidal carbon dioxide (ETCO2) is defined as a partial pressure of carbon dioxide at the end of an exhaled breath. And it has been found to correlate with cardiac output during cardiopulmonary resuscitation (CPR) in animal model. The purpose of this study is to determine that the assessment of ETCO2 could provide a highly sensitive predictor of return of spontaneous circulation (ROSC) during CPR. METHODS: Prospective, observational study was performed from Oct 1996 to Mar 1997 at the Severance hospital. All patients were endotracheally intubated and connected immediately to mainstream capnography sensor. We measured ETCO2 with Escort II model 20100 monitor(Medical Data Electronics, Inc, USA). It works on the principle of nondispersed infrared absorption with radiometric single beam optics. RESULTS: This study included 70 patients (52 were men) with a mean age of 54+/-15 years. ROSC was obtained in 43 patients. The initial ETCO2 averaged 15.5 +/-8.2 mmHg in survivors and 6.5+/-5.3 mmHg in nonsurvivors (p<0.01), and during the first 20 minutes of CPR, the maximal ETCO2 averaged 29.7+/-10.3 mmHg in survivors and 10.2+/-8.9 mmHg in nonsurvivors (p<0.01). ETCO2 was not significantly different in relation to initial rhythm, survival time after ROSC and possible cause of arrest. There is no cutoff value of ETCO2 satisfying greater than 90% of both sensitivity and specificity in predict ROSC. When maximal ETCO2 was less than 12 mmHg, we observed sensivity of 100% in predicting ROSC. CONCLUSION: Our results demonstrate that ETCO2 measurement represents a valuable, noninvasive, and clinical tool for monitoring patients during CPR.
Absorption ; Capnography ; Carbon Dioxide* ; Carbon* ; Cardiac Output ; Cardiopulmonary Resuscitation* ; Humans ; Models, Animal ; Observational Study ; Partial Pressure ; Prospective Studies ; Sensitivity and Specificity ; Survivors

Ten pigmented raqbits were dark adapted for 30 minutes previously and then exposed to room illumination of 200 lux for 10 seconds. In mesopic adaptation, the oscillatory potentials(OPs) were recorded. The coefficient of variation in the peak latency, time interval, summed amplitude, and amplitude of each individual OP wavelet were obtained. The peak latency showed the smallest coefficient of variation. The summed amplitude of the OPa and the time interval showed smaller coefficient of variation than amplitude of each individual OP component. Therefore the peak latency, summed amplitude, and time interval may be reliable factors to evaluate the OPs. The increase of the light stimulus did not affect the amplitude of O3. However, O1 and O2 tended to increase in amplitude and O4 to decrease as the intensity of light stimulus increased. These facts may suggest that each individual component of OP has different orign. As the intensity of light stimulus increased, the summed amplitude of OPs was increased and peak latency of O1, O2, O3, and O4 were decreased. Time intervals showed no significant changes.
Lighting ; Rabbits*