No abstract available.
Cervix Uteri* ; Female ; Rhabdomyosarcoma*

No abstract available.
Diagnosis* ; Hemoglobinuria*

Objective: We evaluated the protective effect of dexamethasone (DX) administration on brain damage produced in a perinatal model of cerebral hypoxia-ischemia in the rat. Since hyperglycemia has been shown to reduce hypoxic-ischemic brain injury (HI) in immature tar, we investigated the role of glucocorticoid-induced hyperglycemia in the neuroprotective mechanism of DX. Methods: Hypoxic-ischemic brain injury in 7-day-old rats was induced by right common carotid artery occlusion and 2 hours of 8% oxygen. Pups received 3 doses of DX (0.5mg/kg/d intraperitoneally) 48 hours, 24 hours and immediately before HI (Dx1)(n=12), a single dose of DX 24 hours(DX2)(n=16), 3 hours (DX3)(N=10)or immediately before HI (DX4)(n=14), a single dose of DX immediately after HI (DX5) (n=9), 3 doses of DX immediately, 24 hours and 48 hours after HI (DX6) (n=14) and a single dose of DX 24 hours before HI with insulin (0.5U/kg, subcutaneously, 1.5 hours before HI)(IN)(n=8). Control pups (n=15) received a single dose of normal saline 24 hours before HI. Blood glucose was estimated before hypoxia, 1 hour and 2 hours after hypoxia using glucometer in DX 1~4. IN and control rats. Pups were killed at 14 days of age for determination of mortality during HI, gross cerebral infarction and right cerebral hemisphere atrophy. We measured the diameter of each cerebral hemisphere and cortical thickness from a coronal section at the dorsal hippocampus level, and expressed the % atrophy from the change in the right vs left hemisphere diameter. Results: The mortality that occurred during and after HI was similar in all groups. The incidence of gross cerebral infarction was 0.0%, 0.0%, 75.0%, 83.3%, 87.5%, and 90.0% in DX 1~6, respectively, 0.0%in IN, and 100.0% in control group. There was a significant difference (p<0.001)in the incidence of gross cerebral infarction of DX1, DX2, IN vs control group. The mean % atrophy was 5.4 +/- 2.2, 4.9 +/- 1.8, 21.7 +/- 8.1, 29.7 +/- 5.0, 37.4 +/- 5.5, 33.4 +/- 9.3 in DX 1~6, respectively, 1.5 +/- 1.1 in IN, and 29.1 +/- 3.4 (mean+/-SEM) in control group. There was a significant difference in % atrophy of DX1, DX2, IN vs control group. Before hypoxia, there was no significant difference in blood glucose between saline, all DX, and DX with insulin treated groups. But after hypoxia, pups in DX1 and Dx2 were more hyperglycemic compared to DX 3~4, IN, or saline treated groups. Conclusions: Dexamethasone administration in the neonatal period protects the brain during the subsequent periods of hypoxia-ischemia in rats and glucocorticoid-induced hyperglycemia does not explain the neuroprotective effects dexamethasone.
Animals ; Anoxia ; Atrophy ; Blood Glucose ; Brain Injuries ; Brain* ; Carotid Artery, Common ; Cerebral Infarction ; Cerebrum ; Dexamethasone* ; Hippocampus ; Hyperglycemia* ; Hypoxia-Ischemia, Brain ; Incidence ; Insulin ; Mortality ; Neuroprotective Agents ; Oxygen ; Rats*

PURPOSE: To compare the results of IM nailing of femur shaft fractures using trochanteric and piriformis fossa entry portal. MATERIALS AND METHODS: 37 patients were treated with IM nail using Trochanteric (Trochanter group: TG, n=17) and piriformis fossa entry portal (piriformis group: PG, n=20) and were followed from February 2004 to 2007. The outcomes were assessed based on the clinical and radiographic findings. RESULTS: The functional result, ROM and union time were similar in both groups. The alignment was similar in both groups but PG showed variable alignment in proximal 1/3. Incision was larger in PG (PG=8.7 cm, TG=5.8 cm, p<0.05) and there was a difference between overweight and normal weight group. Operative time was 95 minutes in PG, 87 minutes in TG (p>0.05), there was statistically significant difference in overweight groups (PG=125 minutes, TG=90 minutes, p<0.05). Blood loss was 313 cc in PG, 268 cc in TG and less in TG in overweight patients (p<0.05). There was 5.7degrees of varus angulation in PG, 2 nonunion cases in both groups. CONCLUSION: The femoral nail specially designed for trochanteric insertion resulted in high union rates, low complication rates similar to conventional nail and the trochanteric nail can be the alternative choice especially in proximal femur fracture and overweight patients.
Femur ; Humans ; Nails ; Operative Time ; Overweight

PURPOSE: To investigate the effect of 21-aminosteroid U74389G (U) on the extent of brain damage and edema formation in the newborn rats with hypoxic ischemic (HI) brain injury. METHODS: This is a randomized, placebo-controlled, experimental study. The subjects were 113 seven-days-old rats with HI injury. Pups were treated with 3, 10, or 20 mg/ kg of U intraperitoneally 30 minutes before hypoxia (Group 1, 2, 3: n=10, 13, 11), 10 mg/kg of U immediately after hypoxia (n=11) (Group 4), 10 mg/kg of U 30 minutes before and after hypoxia (n=n=13) (Group 5), or vehicle (n=12) (Group C). We expressed the degree of brain infarction and brain edema in % atrophy (Left hemisphere-Right hemisphere/Left hemispherex100) and water content % (wet weight-dry weight/wet weightx100) RESULTS: There were significant reductions in the diameters of right hemisphere compared with those of left hemisphere in vehicle and U treated animals (P<0.05). As to the cortical thickness, group 2, 3 and 5 pups showed no significant reductions in the right side compared with the left side implicating that U treatment in these groups was of benefit in attenuating HI cortical injury, while there was significant difference between the right and left side in group 1, 4 and C animals (P<0.001). There was a significant difference (P< 0.01) in % atrophy of group 2, 3, 5 versus group C, but the mean % atrophy was similar in groups 1, 4 and C. There was a significant (P<0.05) increase of water content in right hemisphere compared with left hemisphere both in U and vehicle treated groups. CONCLUSION: Pre-treatment and prepost-treatment at moderate doses (10 or more mg/kg) of 21-aminosteroid U74389G reduced the extent of perinatal hypoxic-ischemic brain damages, especially in the cortex, but do not affect the extent of brain edema.
Animals ; Anoxia ; Atrophy ; Brain Edema ; Brain Infarction ; Brain Injuries ; Brain* ; Edema* ; Humans ; Infant, Newborn* ; Lipid Peroxidation ; Rats*

No abstract available.
Dexamethasone* ; Humans ; Infant, Newborn* ; Meningitis, Bacterial*

BACKGROUND: Spinally administered neostigmine, but not morphine, has been well known to reverse the mechanical allodynia in human and animal studies. The efficacy of morphine in neuropathic pain state is somewhat controversial. Using an isobolographic analysis, we examine the spinal interaction between neostigmine and morphine in a rat model of neuropathic pain. METHODS: Male Sprague Dawley rats were prepared with tight ligation of left lumbar 5th and 6th spinal nerves and chronic lumbar intrathecal catheter. Intrathecal dose response curves were established for the antiallodynic effect of neostigmine (0.3, 1.0, 3.0, and 10 microgram) and morphine (0.3, 1.0, 3.0, and 10 microgram) alone to obtain the ED50 for each agent. ED50 fractions (1/2, 1/4, 1/8, and 1/16) of drug combination of neostigmine-morphine were administered. Allodynic thresholds for left hindpaw withdrawal to von Frey hairs application were assessed and converted to %MPE. The ED50 of neostigmine-morphine combinations was established and isobolographic analysis of the drug interaction was carried out. RESULTS: Intrathecal neostigmine and morphine alone produced dose-dependent reductions of tactile allodynia. ED50 values are 0.43 microgram (0.21~0.86 microgram) for neostigmine and 0.39 microgram (0.07~2.01 microgram) for morphine. The log dose responses were plotted from the peak effect of %MPE in each group of neostigmine and morphine. The experimental ED50 1.34E-2 microgram (2.1E-4-0.85 microgram) for neostigmine and morphine combination was found to be significantly below the theoretical additive ED50 value 0.41 microgram (P<0.05). CONCLUSION: The results suggest that intrathecal neostigmine and morphine alone produce a dose dependent antagonism on touch evoked allodynia and intrathecal neostigmine is synergistic at the spinal level when combined with intrathecal morphine in a rat model of neuropathy.
Animals ; Catheters ; Drug Interactions ; Hair ; Humans ; Hyperalgesia ; Ligation ; Male ; Models, Animal ; Morphine* ; Neostigmine* ; Neuralgia* ; Rats, Sprague-Dawley ; Spinal Nerves

No abstract available.
Classification* ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive*

To evaluate the effect of superior oblique tenotomy on horizontal deviation at primary position in A-pattern exotropia with bilateral superior oblique overaction.We performed adjustable strabismus surgeries under topical anesthesia in 6 patients with A-pattern exotropia. After adjusting horizontal deviation to orthotropia in primary position by horizontal muscle surgery, we measured angle deviation in up, primary, downgaze position and added bilateral superior oblique tenotomy, and remeasured the angle deviation at same positions. We analyzed the angle deviation at postoperative one day, one month, and three month in comparison with the preoperative value. There were no change of horizontal deviation in primary position in 2 patients, qhile 3 to 8 prism diopter(PD) esotropic shift occurred in 4 patients(average 3.3PD) after bilateral superior oblique tenotomy at last follow-up of 3 month. At 3 month postoperatively, there was a tendency of exotropic shift from esotropia noted at immediate postoperative period. When combined surgeries of superior oblique and horizontal muscle are considered and intraoperative adjustable surgery is not permitted, horizontal muscle surgery can be performed with disregarding the effect of bilateral superior oblique tenotomy on primary position horizontal alignment.
Anesthesia ; Esotropia ; Exotropia ; Follow-Up Studies ; Humans ; Postoperative Period ; Strabismus ; Tenotomy*

In addition to many of the widely accepted risk factors of bronchopulmonary dysplasia (BPD), such as prematurity, oxygen toxicity, barotrauma, and infection, the amount of fluid intake during the early phase of life has recently been reported to be an important factor, especially the amount of colloid. Forty-one premature infants who were admitted to the NICU of Severance Hospital, Yonsei University College of Medicine between Jan. 1990 and Jun. 1992 and treated for respiratory difficulty with mechanical ventilation and restrictive fluid therapy were included in the study. fourteen were diagnosed as BPD and the rest were grouped as Non-BPD. We confirmed prematurity, low birth weight, high oxygen concentration, high ventilator pressures and rates, perinatal asphyxia, acidosis, and low blood pressures as risk factors. However, with restrictive fluid therapy that we have used, there was no difference in the amount of total fluid, of crystalloid, or of colloid between BPD and Non-BPD groups, as were the urine output, serum electrolyte concentrations, and percent body weight change. The amount of colloid when used for the maintenance of adequate blood pressures and for the prevention and treatment of hypovolemia, oliguria, anemia of sepsis under the scheme of restrictive fluid therapy would not influence adversely in the development of BPD. Instead, the amount of colloid used may imply the severity of illness of the patient; that is, the more severe the condition of the patient the more the amount of colloid used.
Acidosis ; Anemia ; Asphyxia ; Barotrauma ; Body Weight Changes ; Bronchopulmonary Dysplasia* ; Colloids ; Fluid Therapy* ; Humans ; Hypovolemia ; Infant, Low Birth Weight ; Infant, Newborn ; Infant, Premature* ; Oliguria ; Oxygen ; Respiration, Artificial* ; Risk Factors* ; Sepsis ; Ventilators, Mechanical