No abstract available.
Mandibular Reconstruction*

No abstract available.

No abstract available.
Apgar Score* ; Humans

No Abstract Available.
Blepharoptosis* ; Silicones*

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

Although the sternalis muscle has been well known to anatomists, it is quite unfamiliar to clinicians. During routine educational dissection, we came across a well-defined bilateral double sternalis muscle innervated by the intercostal nerve, respectively. The right sternalis muscle 1) became tendinous to insert into the sternum and 2) crossed midline and then intermingled with the left pectoralis major muscle, which could be classified into a double with single cross based on Snosek et al.'s criteria. The left sternalis muscle was composed of two bellies, which were combined at the midway, and became tendinous to insert into the contralateral manubrium, which could be classified into a bicipital diverging with double cross based on Snosek et al.'s criteria. The detailed knowledge on the sternalisis is important for clinicians as well as for anatomists, since the clinical importance of the sternalis muscle has been highlighted in recent years.
Anatomists ; Cadaver* ; Humans ; Intercostal Nerves ; Manubrium ; Sternum

The reconstruction of soft tissue defects with open fracture around the knee joint is limited by its unique location. Free tissue transfer is hindered by the selection of the recipient vessel and problems of microsurgery. The arc of rotation, defect size, and location must be taken into consideration in the use of regional muscle transfer such as gastrocnemius. According to Mathes et al, the flap survival can be enhanced by selective division of the dominant segmental pedicles, only a part of which can normally be transposed safely on its minor segmental pedicle. Neovascularization, vascular proliferation, and dilatation have also been produced by the delay procedure using silicone sheets. The authors have used the delay procedures with wrapping of the gracilis or sartorius muscle which enabled distally-based transposition of these muscles. The method showed satisfactory outcome in resurfacing the wound around the knee joint. The indictions for this procedure were defects of moderate size and those difficult to reach with conventional muscle flaps. The flap could reach the upper one-third of the lower leg. Other merits are relative simplicity and reliability without significant extension of hospital stay. The drawbacks are the two operative procedures necessary and the risk of infection due to silicone sheets.
Dilatation ; Fractures, Open ; Knee Joint* ; Knee* ; Leg ; Length of Stay ; Microsurgery ; Muscles ; Silicones ; Surgical Procedures, Operative ; Wounds and Injuries*

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

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*

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