No abstract available.
Dermatitis, Atopic* ; Humans ; Immunoglobulin E*

No abstract available.
Keloid* ; Recurrence*

No abstract available.
Transplants*

Prader-Willi(PW)syndrome is characterized by obesity, hypotonia, mental retardation, hypogonadism, short stature, excessive eating and characteristic facial appearance. Diabetes mellitus has been considered a component of PW syndrome. Recently this syndrome is caused by the absence of paternally derived genes normally located on chromosome segment 15 q11-q13 or may be the result of maternal uniparental disomy with the absence of paternally derived 15 q11-q13 region. The developement of probes containing segments of DNA from chromosome region 15 q11-q13 provides the oppotunity to confirm the diagnosis of PW syndrome by fluorescence in situ hybridization(FISH). We experienced a 15-year-old boy of PW syndrome with diabetes mellitus, who revealed mental retardation, hypogonadism, obesity and microdeletion of chromosome 15 q11-q13 comfirmed by FISH.
Adolescent ; Chromosomes, Human, Pair 15* ; Diabetes Mellitus ; Diagnosis ; DNA ; Eating ; Fluorescence ; Humans ; Hypogonadism ; Intellectual Disability ; Male ; Muscle Hypotonia ; Obesity ; Prader-Willi Syndrome* ; Uniparental Disomy

In the therapeutic or the nutritional aspects, Zn2+ has been used as a supplement in a variety of drugs. Most of divalent or trivalent cations affect ion channels in the cell membranes of various organs. In particular, Zn2+ has been regarded as a potassium (K+) channel blocker in the field of electrophysiology. ATP-sensitive K+ (KATP) channel, which is a kind of inward rectifier K+ channel, resides in the cell membrane of pancreatic beta cells and plays an important role in glucose-induced insulin secretion. The glucose increases intracellular ATP concentration, and this inhibits KATP channels. The inhibition of KATP channels activity depolarizes the cell, and subsequently, insulin is released by Ca2+ influx through the voltage- gated Ca2+ channels. Here, we demonstrate that KATP channels in the pancreatic beta cells are also the targets of extracellular Zn2+ blockade and its blockade is dependent on intracellular ATP concentration. This may be a compensatory mechanism preventing the oversecretion of insulin from the Pancreatic beta cells triggered by Zn2+ intake in a physiologically fasting condition.
Adenosine Triphosphate* ; Cations ; Cell Membrane ; Electrophysiology ; Fasting ; Glucose ; Insulin ; Insulin-Secreting Cells* ; Ion Channels ; KATP Channels* ; Potassium ; Potassium Channels, Inwardly Rectifying

No abstract available.
Fetal Blood* ; Growth Hormone* ; Humans ; Infant, Newborn* ; Insulin-Like Growth Factor I* ; Somatomedins* ; Umbilical Cord*

No abstract available.
Diskectomy*

No abstract available.
alpha-Fetoproteins* ; Female ; Humans ; Pregnancy ; Pregnancy Trimester, Second*

BACKGROUND: The Histidine-Tryptophan-Ketoglutarate (HTK) solution has been shown to provide the excellent myocardial protection as a cardioplegia. The HTK solution has relatively low potassium as an arresting agent of myocardium, and low sodium content, and high concentration of histidine biological buffer which confer a buffering capacity superior to that of blood. Since HTK solution has an excellent myocardial protective ability, it is reported to protect myocardium from ischemia for a considerable time (120 minutes) with the single infusion of HTK solution as a cardioplegia. The purpose of this study is to evaluate the cardioprotective effect of HTK solution on myocardium when the ischemia is exceeding 120 minutes at two different temperature (10 to 12degrees C, 22 to 24degrees C) using the Langendorff apparatus. MATERIAL AND METHOD: Hearts from Sprague-Dawley rat, weighing 300 to 340 g, were perfused with Krebs-Henseleit solution at a perfusion pressure of 100 cm H2O. After the stabilization, the heart rate, left ventricular developed pressure (LVDP), and coronary flow were measured. Single dose of HTK solution was infused into the ascending aorta of isolated rat heart and hearts were preserved at four different conditions. In group 1 (n=10), hearts were preserved at deep hypothermia (10~12degrees C) for 2 hours, in group 2 (n=10), hearts were preserved at moderate hypothermia (22~24degrees C) for 2 hours, in group 3 (n=10), hearts were preserved at deep hypothermia for 3 hours, and in group 4 (n=10), hearts were preserved at moderate hypothermia for 3 hours. After the completion of the preservation, the heart rate, left ventricular developed pressure, and coronary flow were measured at 15 minutes, 30 minutes, and 45 minutes after the initiation of reperfusion to assess the cardiac function. Biopsies were also done and mitochondrial scores were counted in two cases of each group for ultrastructural assessment. RESULT: The present study showed that the change of heart rate was not different between group 1 and group 2, and group 1 and group 3. The heart rate was significantly decreased at 15 minutes in group 4 compared to that of group 1 (p<0.05 by ANCOVA). The heart rate was recovered at 30 minutes and 45 minutes in group 4 with no significant difference compared to that of group 1. The decrease of LVDP was significant at 15 minutes, 30 minutes and 45 minutes in group 4 compared to that of group 1 (p<0.001 by ANCOVA). Coronary flow was significantly decreased at 15 minutes, 30 minutes, and 45 minutes in group 4 compared to that of group 1 (p<0.001 by ANCOVA). In ultrastructural assessment, the mean myocardial mitochondrial scores in group 1, group 2, group 3, and group 4 were 1.02+/-0.29, 1.52+/-0.26, 1.56+/-0.45, 2.22+/-0.44 respectively. CONCLUSION: The HTK solution provided excellent myocardial protection regardless of myocardial temperature for 2 hours. But, when ischemic time exceeded 2 hours, the myocardial hemodynamic function and ultrastructural changes were significantly deteriorated at moderate hypotherma (22~24degrees C). This indicates that it is recommended to decrease myocardial temperature when myocardial ischemic time exceeds 2 hours with single infusion of HTK solution as a cardioplegia.
Animals ; Aorta ; Biopsy ; Cardioplegic Solutions ; Heart Arrest, Induced ; Heart Rate ; Heart* ; Hemodynamics ; Histidine ; Hypothermia ; Ischemia ; Myocardium ; Organ Preservation ; Perfusion ; Potassium ; Rats* ; Rats, Sprague-Dawley ; Reperfusion ; Sodium

PURPOSE: To evaluate value of superparamagnetic iron oxide (SPIO) as a negative oral contrast agent in MR cholangiopancreatography (MRCP). MATERIALS AND METHODS: Forty-eight patients with suspected biliary tract or pancreatic diseases and six healthy volunteers were enrolled in this study. All MR images were obtained using a 1.5 T MR unit. MRCP using fat-suppressed half-Fourier acquisition single-shot turbo spin echo (HASTE) and turbo spin echo (TSE) techniques were performed and reconstructed with maximal intensity projection (MIP). To determine the most optimal concentration of SPIO to obliterate the high signal intensity of water, a phantom experiment was conducted with various concentrations of SPIO-water mixture. Two radiologists evaluated pre- and postcontrast MRCPs. The contrast enhancement was assessed on the basis of loss of signal intensity in the stomach and duodenum. RESULTS: In the phantom experiment, a significant increase of percentage of signal intensity loss (PSIL) occurred in concentration of 22.4 ugFe/ml (Feridex 1 ml diluted with water 500 ml). Postcontrast MRCP showed an improved image quality compared with precontrast images. The rate of improvement in the diagnosis of diseases of the common bile duct and pancreatic duct was 25% (12/48). CONCLUSION: In patients with suspected biliary tract and pancreatic diseases, the SPIO is useful as a negative oral contrast agent for MRCP and provides an improvement of image quality.
Biliary Tract ; Common Bile Duct ; Diagnosis ; Duodenum ; Healthy Volunteers ; Humans ; Iron* ; Pancreatic Diseases ; Pancreatic Ducts ; Stomach ; Water