No abstract available.
Spine*

OBJECTIVE: To report three cases of monozygotic twinning after IVF-ET transfer. METHODS: Private practice in two different assisted reproductive technology clinics. RESULTS: Three intrauterine monozygotic twin pregnancies occurred after IVF-ET. One of them was complicated by cord entanglement, another is progressing normal pregnancy without complication and the other was had a normal pregnancy without complication and delivered twin by cesarean section. CONCLUSION: The reported prevalence of multiple gestations in IVF-ET is a approximately 30%, and it is only 2.7% to be monozygotic twinning in IVF-ET. We report three cases of monozygotic twining after IVF-ET.
Cesarean Section ; Female ; Humans ; Pregnancy* ; Prevalence ; Private Practice ; Reproductive Techniques, Assisted ; Twinning, Monozygotic ; Twins, Monozygotic*

OBJETIVE: To assess the effects of progesterone and acetyl-L-carnitine used after treated with IsolateR gradient before semen cryopreservation-thawing on sperm parameters and membrane integrity. MATERIALS AND METHODS: From April 2001 to July 2001, ten normal male partner of couples who were visited in vitro fertilization (IVF) clinics. the semens were treated with IsolateR gradient before cryopreservation, spermatozoa was incubated with progesterone (1, 5 and 10 micrometer), acetyl-L-carnitine (2.5, 5 and 10 micrometer), or both (progesterone, 1 micrometer; and acetyl-L-carnitine, 5 micrometer) for 30 min. RESULTS: There were no differences in sperm parameters and vital stain among isolate only treated group, progesterone (1, 5 and 10 micrometer), acetyl-L-carnitine (2.5, 5 and 10 micrometer) and both (progesterone, 1 micrometer; and acetyl-L-carnitine, 5 micrometer). But, in high concentration of acetyl-L-carnitine (10 micrometer) treated group, sperm parameters and vital stain were decreased. The statistical method was used ANOVA (Kruskal-Wallis test) and p value was <0.01. CONCLUSIONS: Neither progesterone nor acetyl-L-carnitine show to be protective effect on the cryodamage assessed by sperm parameters and vital stain (eosin-Y stain) in normal sperm. High concentration of acetyl-L-carnitine (10 micrometer), however, was harmful effect on cryoprevention.
Acetylcarnitine* ; Cryopreservation ; Family Characteristics ; Fertilization in Vitro ; Humans ; Male ; Membranes* ; Progesterone ; Semen ; Spermatozoa*

BACKGROUND: Reperfusion of ischemic myocardium is clinically encountered during thrombolytic therapy of acute myocardial infarction, percutaneous transluminal coronary angioplasty(PTCA), and coronary artery bypass graft(CABG). Reperfusion results in endothelial dysfunction characterized by a reduced release of endothelium-derived relaxing factor(EDRF) in animal studies. Studies with experimental animals have emphasized the role of oxygen free radicals and lipid peroxidation in pathophysiology of reperfusion injury and myocardial stunning. The object of this study is to determine whether endothelial dysfunction was developed after open heart surgery and to evaluated the role of oxygen free radical and lipid peroxidation in reperfusion injury. METHODS: The study group was comprised 13 patients who underwent open heart surgery(male/female : 2/11, mean age : 43+/-4 year, Atrial septal defect in 4, Ventricular septal defect in 1, Mitral regurgitation in 2, Tetralogy of Fallot in 1, and Aortic stenosis and Regurgitation with Mitral stenosis in 5 patients). The endothelial function was evaluated with the vasomotor response to acetylcholine and nitroglycerin by change of arterial diameter during the continous infusion of acetylcholin, from 10(-9) to 10(-6) molar concentration to the coronary artery and intracoronary injection of 200microg nitroglycerin after acetylcholine infusion. The infusion study was performed before and 10 days after surgery. For analysis of the role of oxygen free radical and lipid peroxidation in reperfusion injury, blood samples for malondialdehyde and neutrophil respiratory burst test(hydrogen peroxide amount of neutrophils) were obtained in pre-declamping of aorta and 5 min, 10 min, and 20 min after declamping of aorta from coronary sinus. RESULTS: 1) The vasoconstrictor response to acetylcholine, 10(-9) to 10(-6)M concentration, at proximal and distal left anterior descending coronary artery, were increased significantly in post-operation infusion study but there was no singnificant difference in vasodilator response to nitroglycerin. 2) The mean absorbance value of malondialdehyde(MDA) in pre-declamping and 5min, 10min, and 20min after reperfusion were 96+/-12, 73+/-12, 89+/-11 and 77+/-12, respectively. There was no significant difference in plasma MDA level and hydrogen peroxide amount of neutrophils after reperfusion(aortic declamping). CONCLUSION: These data suggest that endothelium dependent vascular relaxation is impaired in patients with open heart surgery and post-ischemic reperfusion injury may be responsible for the abnormal response. But we did not determine the role of lipid peroxidation and oxygen free radical in reperfusion injury.
Acetylcholine ; Animals ; Aorta ; Aortic Valve Stenosis ; Coronary Artery Bypass ; Coronary Sinus ; Coronary Vessels ; Endothelium ; Free Radicals ; Heart Septal Defects, Atrial ; Heart Septal Defects, Ventricular ; Heart* ; Humans ; Hydrogen Peroxide ; Lipid Peroxidation* ; Malondialdehyde ; Mitral Valve Insufficiency ; Mitral Valve Stenosis ; Molar ; Myocardial Infarction ; Myocardial Stunning ; Myocardium ; Neutrophils ; Nitroglycerin ; Oxygen* ; Plasma ; Relaxation ; Reperfusion Injury* ; Reperfusion* ; Respiratory Burst ; Tetralogy of Fallot ; Thoracic Surgery* ; Thrombolytic Therapy

BACKGROUND: Reperfusion of ischemic myocardium is clinically encountered during thrombolytic therapy of acute myocardial infarction, percutaneous transluminal coronary angioplasty(PTCA), and coronary artery bypass graft(CABG). Reperfusion results in endothelial dysfunction characterized by a reduced release of endothelium-derived relaxing factor(EDRF) in animal studies. Studies with experimental animals have emphasized the role of oxygen free radicals and lipid peroxidation in pathophysiology of reperfusion injury and myocardial stunning. The object of this study is to determine whether endothelial dysfunction was developed after open heart surgery and to evaluated the role of oxygen free radical and lipid peroxidation in reperfusion injury. METHODS: The study group was comprised 13 patients who underwent open heart surgery(male/female : 2/11, mean age : 43+/-4 year, Atrial septal defect in 4, Ventricular septal defect in 1, Mitral regurgitation in 2, Tetralogy of Fallot in 1, and Aortic stenosis and Regurgitation with Mitral stenosis in 5 patients). The endothelial function was evaluated with the vasomotor response to acetylcholine and nitroglycerin by change of arterial diameter during the continous infusion of acetylcholin, from 10(-9) to 10(-6) molar concentration to the coronary artery and intracoronary injection of 200microg nitroglycerin after acetylcholine infusion. The infusion study was performed before and 10 days after surgery. For analysis of the role of oxygen free radical and lipid peroxidation in reperfusion injury, blood samples for malondialdehyde and neutrophil respiratory burst test(hydrogen peroxide amount of neutrophils) were obtained in pre-declamping of aorta and 5 min, 10 min, and 20 min after declamping of aorta from coronary sinus. RESULTS: 1) The vasoconstrictor response to acetylcholine, 10(-9) to 10(-6)M concentration, at proximal and distal left anterior descending coronary artery, were increased significantly in post-operation infusion study but there was no singnificant difference in vasodilator response to nitroglycerin. 2) The mean absorbance value of malondialdehyde(MDA) in pre-declamping and 5min, 10min, and 20min after reperfusion were 96+/-12, 73+/-12, 89+/-11 and 77+/-12, respectively. There was no significant difference in plasma MDA level and hydrogen peroxide amount of neutrophils after reperfusion(aortic declamping). CONCLUSION: These data suggest that endothelium dependent vascular relaxation is impaired in patients with open heart surgery and post-ischemic reperfusion injury may be responsible for the abnormal response. But we did not determine the role of lipid peroxidation and oxygen free radical in reperfusion injury.
Acetylcholine ; Animals ; Aorta ; Aortic Valve Stenosis ; Coronary Artery Bypass ; Coronary Sinus ; Coronary Vessels ; Endothelium ; Free Radicals ; Heart Septal Defects, Atrial ; Heart Septal Defects, Ventricular ; Heart* ; Humans ; Hydrogen Peroxide ; Lipid Peroxidation* ; Malondialdehyde ; Mitral Valve Insufficiency ; Mitral Valve Stenosis ; Molar ; Myocardial Infarction ; Myocardial Stunning ; Myocardium ; Neutrophils ; Nitroglycerin ; Oxygen* ; Plasma ; Relaxation ; Reperfusion Injury* ; Reperfusion* ; Respiratory Burst ; Tetralogy of Fallot ; Thoracic Surgery* ; Thrombolytic Therapy

No abstract available.
Hemorrhage* ; Kidney Transplantation*

Internal capsular genu infarcts infrequently cause cognitive impairment and behavioral changes, and little is known about the underlying mechanism. Using diffusion-tensor imaging (DTI) and the fractional anisotropy (FA) index in the region of interest (ROI) and ipsilesional frontal cortex, we evaluated two patients with internal capsular genu infarction who presented with frontal dysfunction and cognitive impairment. The reported findings help to elucidate the mechanism underlying cognitive deterioration in internal capsular genu infarction.
Anisotropy ; Diffusion ; Diffusion Tensor Imaging ; Humans ; Infarction

BACKGROUND: Defects in mitochondrial function have been shown to participate in the induction of neuronal cell injury. The extracellular-signal-regulated kinase (ERK) signaling pathway plays a crucial role in almost all cell functions, including proliferation, differentiation, survival, and death. However, the effect of ERK inhibition on oxysterol-induced apoptosis remains uncertain. METHODS: This study assessed the effect of ERK inhibition on the apoptotic effect of 7-ketocholesterol. RESULTS: Treatment with 7-ketocholesterol increased phosphorylated-ERK1/2 levels in differentiated PC12 cells, while the total amount of ERK was not altered. 7-Ketocholesterol decreased Bid and Bcl-2 levels, increased Bax and p53 levels, and promoted cytochrome c release, which elicits the activation of caspases (-8, -9, and -3), nuclear damage, and cell death. ERK and farnesyltransferase inhibitors inhibited the 7-ketocholesterol-induced phosphorylation of ERK1/2, activation of apoptosis-related proteins, and cell death in PC12 cells. CONCLUSIONS: The ERK and farnesyltransferase inhibitors, which did not exhibit toxicity, may inhibit the 7-ketocholesterol toxicity on differentiated PC12 cells by suppressing the activation of the caspase-8-dependent pathway as well as activation of the mitochondria-mediated cell-death pathway, leading to the activation of caspases. The inhibition of ERK may confer a beneficial protective effect against the neuronal cell injury induced by cholesterol oxidation products.
Animals ; Apoptosis ; Caspases ; Cell Death ; Cholesterol ; Cytochromes c ; Farnesyltranstransferase ; Ketocholesterols ; Neurons ; PC12 Cells ; Phosphorylation ; Phosphotransferases ; Proteins

BACKGROUND: Protein casein kinase 2 is involved in signal transduction, cell growth, and apoptosis. However, it has not been elucidated whether parkinsonian toxin 1-methyl-4-phenylpyridinium (MPP+)-induced neuronal cell death is mediated by a casein-kinase-2-mediated pathway. METHODS: We monitored apoptosis-related protein activation, changes in the level of casein kinase 2, nuclear damage, and apoptosis in differentiated PC12 cells exposed to MPP+ in combination with casein kinase 2 inhibitor. RESULTS: Casein kinase 2 inhibitors [4,5,6,7-tetrabromobenzotriazole (TBB), 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole, and apigenin] reduced MPP+- and rotenone-induced cell death in differentiated PC12 cells. TBB inhibited the MPP+-induced activation of apoptosis-related proteins (decreases in Bid and Bcl-2 levels, increase in Bax levels, cytochrome c release, and caspase-3 activation), increase in casein kinase 2 levels, and nuclear damage. CONCLUSIONS: Administering casein kinase 2 inhibitor TBB at concentrations that do not induce toxic effects may reduce MPP+-induced cell death in differentiated PC12 cells by suppressing the apoptosis-related protein activation that leads to cytochrome c release and subsequent activation of caspase-3. The results suggest that MPP+-induced cell death process is mediated by a casein kinase 2 pathway.
1-Methyl-4-phenylpyridinium ; Animals ; Apoptosis ; Casein Kinase II ; Casein Kinases ; Caseins ; Caspase 3 ; Cell Death ; Cytochromes c ; Neurons ; PC12 Cells ; Proteins ; Signal Transduction ; Triazoles

No abstract available.
Female ; Fertilization* ; Humans ; Pregnancy ; Pregnancy Outcome* ; Pregnancy* ; Pregnancy, Twin*