No abstract available.
Animals ; Female ; Hysterectomy* ; Ovariectomy* ; Rats* ; Spine* ; Tibia*

No abstract available.
Ectopia Cordis* ; Ultrasonography*

No abstract available.
Anemia, Hypoplastic, Congenital*

No abstract available.
Free Tissue Flaps* ; Lower Extremity*

No abstract available.
Carcinoma, Squamous Cell* ; Cervix Uteri* ; Female ; Biomarkers, Tumor*

Recent studies suggest that apolipoproteins may be better predictor of ischemic heart disease than are plasma lipids, such as total cholesterol and high density lipoprotein cholesterol(HDL-C). To examine this hypothesis, plasma levels of major lipids and major apolipo-proteins were measured and their derivatives were calculated in 30 male patients with ischemic heart disease(16 angina pectoris and 14 old myocardial infarction) and 30 age-matched male healthy controls. Plasma levels of lipids were obtained by conventional methods and apolipoproteins by Rocket immunoelectrophoresis. Levels of HDL-C, HDL2-cholesterol(HDL2-C), and apolipoprotein-AII, and ratios of HDL-C/total cholesterol, HDL2-C/total cholesterol, and apolipoprotein-AI/apolipoprotein-B were lower in the group of patients than in controls. Levels of low density lipoprotein cholesterol(LDL-C) and apolipoprotein-B, and ratios of lDL-C/HDL-C and apolipoprotein-AI/apolipoprotein-AII were higher in the group of patients. There were no statistically significant differences in the levels of total cholesterol and apolipoprotein-AI between the two groups. Stepwise discriminators analysis showed that apolipoprotein-B and apolipoprotein-AII were better discriminators than plasma lipids for identifying those with ischemic heart disease. One could correctly classify 78% of the cases by using the levels of the two apolipoproteins. By using the level of apolipoprotein-B, one could correctly classify 73% of the cases. There were no correlations between the levels of total cholesterol and HDL-C in the controls whereas there were positive correlations between the levels in the group of patients. In conclusion, this study showed that apolipoprotein-B was the best single discriminator for identifying the patients with ischemic heart disease, followed by apolipoprotein-AII.
Angina Pectoris ; Apolipoproteins A* ; Apolipoproteins* ; Cholesterol ; Heart ; Humans ; Immunoelectrophoresis ; Lipoproteins ; Male ; Myocardial Ischemia* ; Plasma* ; Risk Factors*

No abstract available.
Uterus*

Since 1970, the group B streptococcus(GBS) has been a significant cause of neonatal sepsis in the West. Two distinct forms of disease occur in neonates. Early-onset disease which occurs within 7 days after birth is characterized by respiratory distress, apnea, shock, pneumonia, and occasionally meningitis. Late onset disease usually occurs at 3-4 weeks of age(ranging from 7 days to 3 months) and presents occult bacteremia or meningitis. The GBS is thought to be a rare causative agent for neonatal sepsis in Korea. Lately, we experience a case of early-onset GBS sepsis who died at 3rd day of life. We present this case with brief review of literatures.
Apnea ; Bacteremia ; Humans ; Infant, Newborn ; Korea ; Meningitis ; Parturition ; Pneumonia ; Sepsis* ; Shock

No abstract available.
Diagnosis* ; Gynecology* ; Laparoscopy*

BACKGROUND AND PURPOSE: While the etiology and clinical features of "EMG disease" - which is characterized by diffusely increased insertional activity on needle electromyography (EMG) in the absence of neuromuscular disease - are not well known, some authorities believe it may be a form of myotonia congenita (MC). The aims of this study were to determine the clinical features of EMG disease and its relationship with CLCN1 mutations in patients. METHODS: The detailed clinical and electrophysiological features of EMG disease were evaluated in six patients. All 23 coding exons and exon-intron boundaries in CLCN1 gene were analyzed by direct sequencing to detect nucleotide changes. RESULTS: The common clinical symptoms of EMG disease were chronic muscle stiffness or generalized myalgia, which were aggravated in a cold environment. Four patients complained of action myotonia several times a year. Short trains of provoked positive sharp waves were documented on needle EMG, but myotonic discharges, fibrillation potentials, and fasciculations were not. Increased insertional activity was identified at the asymptomatic muscles studied. One novel heterozygous mutation was identified in one patient following genetic testing for CLCN1 mutations (c.1679T>C, p.Met560Thr). CONCLUSIONS: The clinical features of EMG disease might be quite similar to those of MC, but CLCN1 mutation was found in only one subject. It is thus difficult to accept that EMG disease lies within the phenotypic spectrum of MC. Additional testing is needed to verify the pathogenetic cause of the diffusely increased insertional activity associated with this condition.
Chloride Channels ; Clinical Coding ; Cold Temperature ; Electromyography ; Exons ; Fasciculation ; Genetic Testing ; Humans ; Muscles ; Myotonia ; Myotonia Congenita ; Needles ; Neuromuscular Diseases