No abstract available.
6-Cyano-7-nitroquinoxaline-2,3-dione* ; Cycloheximide* ; Dizocilpine Maleate*

PURPOSE: Retinopathy of prematurity (ROP) is one of the leading causes of blindness, with retinal detachment occurring due to oxygen toxicity in preterm infants. Recently, advances in neonatal care have led to improved survival rates for preterm infants, and ROP has increased in incidence. In the present study, we aimed to determine whether or not resveratrol exhibits protective effects in an animal model of ROP and in primary retinal cell cultures of neonatal rat via nitric oxide (NO)-modulating actions using western blotting and real-time PCR with inducible nitric oxide synthase (iNOS), endothelial NOS (eNOS) and neuronal NOS (nNOS) antibodies and mRNAs. METHODS: In an in vivo oxygen-induced retinopathy (OIR) model, cyclic hyperoxia was induced with 80% O2 for one day and 21% O2 for one day from P1 to P14 in newborn Sprague-Dawley (SD) rats. Resveratrol was injected intravitreally for seven days and rats were sacrificed at P21. In vitro OIR primary retinal cell culture was performed using P0-2 SD rats. Hyperoxia injuries were induced through 100% O2 exposure for six hours. Western blotting and real-time PCR using iNOS, eNOS, nNOS antibodies and primers were performed in the rat model of ROP and the dispersed retinal cell culture. RESULTS: In both in vivo and in vitro OIR, the expression of iNOS antibody and mRNA was increased and of eNOS and nNOS were reduced in the resveratrol-treated group. CONCLUSIONS: In conclusion, resveratrol appeared to exert retinal protective effects via modulation of NO-mediated mechanism in in vivo and in vitro OIR models.
Analysis of Variance ; Animals ; Animals, Newborn ; Blotting, Western ; Disease Models, Animal ; Electrophoresis, Polyacrylamide Gel ; Humans ; Infant, Newborn ; Nitric Oxide Synthase/*metabolism ; Oxygen/toxicity ; RNA/metabolism ; RNA, Messenger/metabolism ; Rats ; Rats, Sprague-Dawley ; Retina/drug effects/pathology ; Retinopathy of Prematurity/*metabolism/pathology/*prevention & control ; Reverse Transcriptase Polymerase Chain Reaction ; Stilbenes/*pharmacology

Since the nose is the most prominent part in the face, the plastic surgeons are interested in the continued effort for rhinoplasty. Nasal tip projection is essential to optimal nasal for the patient's face. But, the nasal tips of Orientals are characterized by bulbous appearance due to thick and tense skin, flaring of nostril. and restriction of nasal tip projection due to underdevelopment of medial crus of alar cartilage and short columella. Most orientals want to correct their nasal tip as well as shape of nose. We present clinical cases of various nasal tip deformities which were corrected with various operative methods through either alar rim incision of open rhinoplasty incision depending upon the severity of tip deformity in order to achieve more natural tips and good nasal tip projection. And the clinical cases were categorized into causes of nasal tip deformity and methods of nasal tip augmentation. We are reporting these reporting these cases with review of literatures.
Cartilage ; Congenital Abnormalities ; Nose ; Rhinoplasty ; Skin ; Transcutaneous Electric Nerve Stimulation

Partial monosomy of chromosome 10q is a rare chromosomal anomaly. Most cases of partial deletion 10q have chromosome breakpoints in the 10q25 or 10q26 region. Recently about 30 cases with breakpoint in the 10q26 region have been reported. Partial trisomy of chromosome 22q is also a rare chromosomal anomaly. Most cases of partial duplication 22q are 22q proximal segment duplications known as Cat-eye syndrome. The other cases, 22q11.2 microduplications and 22q distal long arm (22qter) duplications, are also reported but exceedingly rare. We experienced a male neonate who had facial dysmorphisms, congenital heart defect and cryptorchidism. His chromosomal analysis revealed an deletion of chromosome 10q26.1-->qter and duplication of chromosome 22q11.2-->qter caused by maternal balanced translocation e.g. partial monosomy 10q and partial trisomy 22q. Although some cases of partial monosomy 10q were accompanied by other chromosomal abnormalities, this combination of chromosomal abnormalities has not been reported in the literature.
Arm ; Chromosome Aberrations ; Chromosome Breakpoints ; Chromosome Deletion* ; Cryptorchidism ; Heart Defects, Congenital ; Humans ; Infant, Newborn ; Male ; Trisomy*

No abstract available.
Emergencies* ; Hematoma, Subdural, Acute* ; Trephining*

PURPOSE: To evaluate the surgical procedure and results of arthroscopically assisted minimal invasive surgery of calcaneus intraarticular fractures. MATERIALS AND METHODS: Between June 2001 and March 2004, 10 patients were treated with that method. 9 cases were Sanders type 2 fracture and only one case was Sanders 3 fracture. During calcaneal traction using percutaneus K-wire and tension device into the tuberosity fragment, anatomical reduction was performed under direct arthroscopic and fluoroscopic control. After anatomical reduction was achieved, the fragment was fixed with cannulated screws via incisions. RESULTS: The functional results were good to excellent, with an average AOFAS ankle-hindfoot score of 90.4 (range 85-95) and there were no wound problems. CONCLUSION: Arthroscopically assisted minimal invasive surgery allowed exact assessment of the articular surface and allowed anatomical reduction while adhering to the principles of minimally invasive surgery.
Arthroscopy ; Calcaneus ; Humans ; Intra-Articular Fractures* ; Surgical Procedures, Minimally Invasive ; Traction ; Wounds and Injuries

No abstract available.
Conus Snail* ; Hemangioblastoma*

No abstract available.
Conus Snail* ; Hemangioblastoma*

PURPOSE: Retinopathy of prematurity (ROP) is a leading cause of blindness with retinal detachment due to oxygen toxicity in preterm infants. Recently advances in neonatal care had to led improved survival rates in premature infants and ROP re-emerged as a significant clinical problem. In the present study, we aimed to determine the protective abilities of minocycline in a animal model of ROP and a primary retinal cell cultures of neonatal rat via anti-apoptotic actions using Western blotting and real-time PCR with Bcl-2, Bax and caspase-3 antibodies and mRNAs. METHODS: In the in vivo oxygen-induced retinopathy (OIR), the cyclic hyperoxia was performed that 80% O2 for 1 day and 21% O2 for 1 day from P1-14 of newborn rats. Minocycline was injected intravitreously for 7 days and sacrificed at P21. In the in vitro OIR, primary retinal cell culture was done using P0-P2 SD rats. Hyperoxia injury was done for 100% O2 exposure for 6 hours. Western blotting and real-time PCR using Bcl-2, Bax and caspase-3 antibody and primer were done in the rat model of ROP and the dispersed retinal cell culture. To identify photoreceptors of retinal cells the immunofluorescence assay photoreceptor marker, IRBP, was used. RESULTS: In the in vivo OIR, the expression of Bcl-2 antibody and mRNA was increased and those of Bax and caspase-3 were reduced in the minocycline-treated group. In the in vitro OIR, the result was the same as above. CONCLUSION: In conclusion, minocycline was suggested to have retinal protective effects for hyperoxic injury via anti-apoptotic mechanism.
Animals ; Antibodies ; Apoptosis ; Blindness ; Blotting, Western ; Caspase 3 ; Cell Culture Techniques ; Diterpenes ; Fluorescent Antibody Technique ; Humans ; Hyperoxia ; Infant, Newborn ; Infant, Premature ; Minocycline ; Models, Animal ; Oxygen ; Rats ; Real-Time Polymerase Chain Reaction ; Retinal Detachment ; Retinaldehyde ; Retinopathy of Prematurity ; RNA, Messenger ; Survival Rate

A brief period of cerebral ischemia produces neuronal damage in the vulnerable regions of the brain, such as the CA1 area of the hippocampus. However, mild ischemic episodes may limit damage from subsequent ischemic insults, the phenomenon known as ischemic tolerance or preconditioning. We used hippocampal slices as an experimental model to investigate the possible utilization of ischemic tolerance, and to determine the effects of various drugs acting on glutamate and adenosine receptors following a conditioned ischemic insult. Preconditioning ischemic insult was induced in hippocampal slices of 450nm thickness for 60-70 seconds. Glutamate and adenosine receptors were pretreated 1 hour later with D,L-2-amino-5-phosphonovaleric acid(AP-5, 50nM), propentofylline(PPF, 200nM), 6-cyano-7-nitroquinoxaline-2,3-dione(CNQX, 10nM), 8-cyclopentyl-3,7-dihydro-1,3-dipropyl-1H-purine-2,6-dione(DPCPX, 1, 10nM) and 2-chloro-N6-cyclopentyl-adenosine (CCPA, 1, 10, 50nM). The slices were reoxygenated for 3 hours, after then a second ischemic insult was induced by substituting 95% O2, 5% CO2 and glucose for 95% N2, 5% CO2 and sucrose for 10 minutes. Population spikes(PS) were estimated from extracellular electrophysiological recordings of the hippocampal CA3-CA1 synaptic conduction 1 hour following the second ischemic insult. The PS(mV) was 2.69+/-0.06 in the normal hippocampal slice, while it was reduced to 1.21+/-0.05 in the hippocampal slice induced with 10 minutes of ischemia. The effects of the A1 selective agonist CPPA revealed a reduction of PS to 0.98+/-0.06 with low concentration(1nM), similar PS as the control group with a concentration of 10nM, and an increase in ischemic tolerance of 1.78+/-0.05 at a higher concentration(50nM). The selective A1 antagonist DPCPX(1nM) showed minimal reduction in PS of 1.10+/-0.04, while the NMDA antagonist AP-5(5nM) had a more profound weakening effect(1.05+/-0.04). The adenosine uptake inhibitor profentophylline(200nM) augmented the PS to 1.56+/-0.06; this effect was not influenced by 1nM DPCPX(1.60+/-0.07), but was abolished by a higher concentration of 10nM(1.36+/-0.05). These results confirmed ischemic tolerance in the hippocampal experimental model. We conclude that adenosine plays an important role in ischemic tolerance as activation of adenosine receptors or adenosine uptake inhibition enhances ischemic tolerance.
Adenosine ; Brain ; Brain Ischemia ; Glucose ; Glutamic Acid ; Hippocampus ; Ischemia* ; Models, Theoretical ; N-Methylaspartate ; Neurons ; Receptors, Purinergic P1 ; Sucrose