No abstract available.

No abstract available.
Leukemia, Plasma Cell* ; Plasma Cells* ; Plasma*

OBJECTIVE: The purpose of this study was to investigate the prenatal hypoxic effect on the fetal brain development. METHODS: We used the guinea pig chronic placental insufficiency model to investigate the effect of hypoxia on fetal brain development. We ligated unilateral uterine artery at 30-32 days of gestation (dg : with term defined as -67 dg). At 50 dg, 60 dg, fetuses were sacrificed and assigned to either the growth-restricted (GR) or control (no ligation) group. After fixation, dissection, and sectioning of cerebral tissue from these animals, immunohistochemistry was performed with NeuN antibody, which is a mature neuronal marker in the cerebral cortex. RESULTS: The number of NeuN-immunoreactive (IR) cells in the cerebral cortex did not differ between the GR and control groups at 50 dg. However, the number of NeuN-IR cells was lesser in GR fetuses than in controls at 60 dg (p<0.05). CONCLUSION: These findings show that chronic prenatal hypoxia affect the number of neuron in the cerebral cortex of guinea pig fetus at 60 dg. The approach used in this study is helpful for extending our understanding of neurogenesis in the cerebral cortex, and the findings may be useful for elucidating the brain injury caused by prenatal hypoxia.
Animals ; Anoxia* ; Brain ; Brain Injuries ; Cerebral Cortex ; Fetus ; Guinea Pigs ; Immunohistochemistry ; Neurogenesis ; Neurons* ; Placental Insufficiency ; Pregnancy ; Uterine Artery

BACKGROUND: Stellate ganglion block (SGB) has been used to treat over 150 diseases which include diabetes mellitus and gout. This study was planned to investigate whether stellate ganglion block (SGB) could lower the levels of blood glucose, uric acid, epinephrine, and norepinephrine. METHODS: Sixty Sprague-Dawley rats within the weight of 250-350 gm were randomly devided into four groups. CS group was normal group with sham SGB with normal saline, CL group was normal group with SGB with lidocaine, DS group was diabetic group with SGB with normal saline, DL group was diabetic group with SGB with lidocaine. The diabetes was induced by intraperitoneal injection of 40 mg/kg of streptozotocin in citrate buffer (0.01 M, pH 4.5). Nondiabetic groups were given same amount of the citrate buffer. Seven days after the last injection of the streptozotocin blood glucose level was checked and more than 300 mg/dl was considered diabetic. The SGB was performed three times at right superior cervical ganglion two days apart from two days after the conformation of diabetes. Successful SGB was conformed by the ipsilateral ptosis or conjunctival congestion. Blood samplings from tail vein for the check of glucose, uric acid, and catecholamines were done before the injection of streptozotocin, seven days after the last injection of streptozotocin, and two days after the last SGB. RESULTS: The SGB with lidocaine reduced the blood glucose level only in the diabetic rats while SGB with the saline did not. The epinephrine levels were increased in the diabetics and decreased by the SGB with lidocaine without any statistical significance. Norepinephrine and uric acid levels had not been effected by the SGB and both of them had no correlationship with the glucose level. CONCLUSIONS: SGB in the diabetic rats decreases the blood glucose level. But for the effects of the SGB on the level of epinephrine further study would be needed.
Animals ; Blood Glucose* ; Catecholamines* ; Citric Acid ; Diabetes Mellitus ; Epinephrine ; Estrogens, Conjugated (USP) ; Glucose ; Gout ; Hydrogen-Ion Concentration ; Injections, Intraperitoneal ; Lidocaine ; Norepinephrine ; Rats* ; Rats, Sprague-Dawley ; Stellate Ganglion* ; Streptozocin ; Superior Cervical Ganglion ; Uric Acid* ; Veins

BACKGROUND: Propofol, 2,6-diisopropyl phenol, is a short-acting, potent intravenous anesthetics agent. In both general anesthetic care and the anesthetic care of patients undergoing cardiovascular surgery, the unique characteristics of propofol might make it a logical part of the anesthetic plan for patients such as pulmonary hypertension. But there are limited experimental and clinical data on the effects of propofol on pulmonary vascular resistance, and they are somewhat contradictory. the purpose of this study was to investigated.the effect and mechanism of vasodilation induced by propofol using isolated rat pulmonary artery rings. METHODS: Cumulative dose-response curves for propofol(10(-6)~10(-3)M) were obtained from tension measurements of rings that contracted with phenylephrine(10(-6)M) and KCI(40 mM) in the presence and absence of endothelium, and in the pretreatment of L-NAME(3x10(-4)M) and substance P(3x10(-4)M). Thereafter the effect of propofol(10(-4)M) on vascular smooth muscle contration in response to Ca++ mobilization in vscular rings were investigated. RESULTS: Propofol(10(-6)~10(-3)M) produced dose-dependent relaxation and had no signficant effect from endothelium. Pretreatment of L-NAME and substance P failed to have influence on cumulative dose-respose curves. Therefore vasodilator effect of propofol was not endothelium-dependent. And 10(-4)M propofol attenuated a contraction in response to CaCl2 in vascular rings depolarized by KCI, and vasoconstraction in response to calcium entry in the presence of phenylephine was attenuated by 10(-4)M propofol. Ryanodine preteament had not influence on contractile response. CONCLUSIONS: These results suggest that vasodilation produced by propofol is not endothelium-dependent but is probably due to nonspecific intracellular Ca++ influx blockade through voltage-operated calcium channels and receptor-operated channels.
Anesthetics ; Anesthetics, Intravenous ; Animals ; Calcium ; Calcium Channels ; Endothelium ; Humans ; Hypertension, Pulmonary ; Logic ; Muscle, Smooth, Vascular ; NG-Nitroarginine Methyl Ester ; Phenol ; Propofol* ; Pulmonary Artery* ; Rats* ; Relaxation ; Ryanodine ; Substance P ; Vascular Resistance ; Vasodilation

OBJECTIVES: The Korean government in January 2006 instigated an exemption policy for hospitalized children under the age of six years old. This study examines how this policy affected the utilization of medical care in Korea. METHODS: A total of 1,513,797 claim records from the Health Insurance Review Agency were analyzed by complete enumeration methods. The changes of medical utilization were compared from 2005 to 2006. In addition, the changes of medical utilization between 2004 and 2005 were compared as a pseudocontrol group. RESULTS: The admission rate increased 1.14-fold from 15.20% in 2004 to 17.32% in 2005, and this further increased 1.08-fold to 18.65% in 2006. The increase of patients with a common cold (1.2-fold) was higher than that of both the general patients (1.08-fold) and the patients with the top 10 fatal diseases (0.91-fold). The average length of stay per case for clinics showed the highest increase rates (1.06-fold). The rates of patients with the common cold showed a higher increase (1.05-fold) than that of the general patients. The average medical expense per case was increased by 1.10-fold from 2005 to 2006, which was higher than that from 2004 to 2005 (1.04-fold). The increase rate for patients with the common cold was higher at 1.18-fold than that of the general patients. CONCLUSIONS: The cost exemption policy has especially led to an increase in the utilization of clinics and the utilization by patients with a common cold.
Child, Preschool ; Cost Sharing/*legislation & jurisprudence ; *Health Policy ; Health Services/*utilization ; Hospitalization ; Humans ; Insurance Claim Review ; Korea ; Length of Stay

BACKGROUND: During coronary angiography, some electrocardiographic changes occured due to contrast media, which do life threatening influences. METHODS: We compared the electrocardiographic changes which were induced by injection of three radiopaque contrast media during selective coronary angiography in 49 patients with chest pain. One of the contrast media was high osmolar ionic(Urografin_76) and the another was low osmolar ionic(Hexabrix) and the last was non-ionic(Ioversol). Electrocardiograms were obtained before, during and after selective coronary angiography. RESULTS: The changes of S-T segment or T were decreased in non-ionic group rather than high osmolar or ionic group. And there was significant Q-Tc interval prolongation among all three groups except comparision of low osmolar ionic contrast dye and non-ionic contrast dye in left coronary angiography. CONCLUSION: Non-ionic low osmolar contrast media was safer than high osmolar or ionic contrast medial because of lesser change of Q-Tc interval during selective coronary angiography.
Chest Pain ; Contrast Media* ; Coronary Angiography* ; Diatrizoate Meglumine ; Electrocardiography* ; Humans ; Ioxaglic Acid ; Osmolar Concentration

Cytochrome P450 3A4 (CYP3A4), is the dominant human liver hemoprotein enzyme localized in the endoplasmic reticulum (ER), and is responsible for the metabolism of more than 50% of clinically relevant drugs. While we were studying CYP3A4 expression and activity in human liver, we found that anti-CYP3A4 antibody cross-reacted with a lower band in liver cytoplasmic fraction. We assessed the activities of CYP3A4 and its truncated form in the microsomal and cytoplasmic fraction, respectively. In the cytoplasmic fraction, truncated CYP3A4 showed catalytic activity when reconstituted with NADPH-cytochrome P-450 reductase and cytochrome b5. In order to determine which site was deleted in the truncated form in vitro, we transfected cells with N-terminal tagged or C-terminal tagged human CYP3A4 cDNA. The truncated CYP3A4 is the N-terminal deleted form and was present in the soluble cytoplasmic fraction. Our result shows, for the first time, that N-terminal truncated, catalytically active CYP3A4 is present principally in the cytoplasm of human liver cells.
Blotting, Western ; Catalysis ; Cell Line ; Cytochrome P-450 CYP3A/chemistry/*metabolism ; Cytoplasm/*enzymology ; Humans ; Microsomes, Liver/*enzymology

BACKGROUND: The relationship between infection of microorganism and atherosclerosis has been studied because the pathophysiology after infection is similar to those of cell injury and/or lipid theory. Although there are many reports which described the relationships between the infection of chalamydia pneumoniae and the atherosclerosis. In Korea, even the prevalence of chlamydia infection has not been studied yet. This study was purposed on the prevalence of chlamydia infection and it's correlation to atherosclerosis. METHODS: 235 subjects were enrolled and age and sex adjusted subjects were divided into two groups, normal controls (n=43), atherosclerosis (AS, n=90) group:coronary artery disease (CAD, n=61) and cerebrovascular disease (CVD, n=29). Serum total cholesterol (TC), triglyceride (TG), HDL-cholesterol (HDL-C) were measured, LDL-cholesterol (LDL-C) was calculated. Serum IgG chlamydia antibody were measured by ELISA method. RESULTS: TG was significantly higher in AS (162.51+/-100.04 mg/dL vs 122.91+/-63.31 mg/dL, mean+/-SD, p=0.019), and HDL-C was significantly higher in controls (47.30+/-9.88 mg/dL vs 39.38+/-8.29 mg/dL, p<0A65A>0.01). Levels of LDL-C and TC were not statistical significant. Serum IgG chlamydia antibody was positive in 29.8% (70/235), 30% (27/90) in AS group and 28% in controls and there was no statistical significance between groups (p=0.804). CONCLUSION: In conclusion, there was no significant differences in positivity of IgG chlamydia antibody in AS compared with that of controls. Overall positivity of chlamydia antibody was lower in Korea than in other country. It is still controversial whether Chlamydia pneumoniae is a primary etiologic agent of atherosclerosis or not. This study could not demonstrate the relationship between chlamydia infection and atherosclerosis in Korea. The effectiveness and indications of antichlamydial antibiotics for prevention of cardiovascular complications in atherosclerosis and overall chlamydia infection in general population will be needed in large scale trials.
Anti-Bacterial Agents ; Arteries ; Atherosclerosis* ; Chlamydia Infections ; Chlamydia* ; Chlamydophila pneumoniae* ; Cholesterol ; Coronary Artery Disease ; Enzyme-Linked Immunosorbent Assay ; Immunoglobulin G ; Korea ; Pneumonia ; Prevalence ; Triglycerides

OBJECTIVES: Delphinidin is one of the anthocyanidins. It is believed to have anti-inflammatory property including antioxidant, antiangiogenic, and anti-cancer properties. However, the anti-inflammatory effect of delphinidin in mucin-producing human airway epithelial cells has not been determined. Therefore, this study was conducted in order to investigate the effect and the brief signaling pathway of delphinidin in lipopolysaccharide (LPS)-induced MUC8 and MUC5B expression in human airway epithelial cells. METHODS: In mucin-producing human NCI-H292 airway epithelial cells and primary cultures of normal nasal epithelial cells, the reverse transcriptase-polymerase chain reaction (RT-PCR), real-time PCR, enzyme immunoassay were used for investigating the expressions of MUC8, MUC5, and Toll-like receptor 4 (TLR4), after LPS treatment and delphinidin treatment. And the signaling pathway of delphinidin on LPS-induced MUC8 and MUC5B expression was investigated using the RT-PCR, and immunoblot analysis. To confirm the involvement of TLR4 in LPS-induced MUC8 and MU5B expression, the cells were transfected with TLR4 siRNA. RESULTS: In NCI-H292 airway epithelial cells, LPS (100 ng/mL) significantly induced TLR4, MUC8, and MUC5B expression. TLR4 siRNA significantly blocked LPS-induced MUC8 and MUC5B mRNA expression. LPS (100 ng/mL) significantly activated the phosphorylation of extracellular signal related kinase (ERK) 1/2 and p38 mitogen-activated protein kinase (MAPK). Delphinidin (50 and 100 microM) inhibited LPS-induced TLR4, MUC8, and MUC5B expression and LPS-induced phosphorylation of ERK1/2 and p38 MAPK. In the primary cultures of normal nasal epithelial cells, delphinidin (50 and 100 microM) significantly inhibited LPS-induced TLR4, MUC8, and MUC5B gene expression. CONCLUSION: These results suggest that delphinidin attenuates LPS-induced MUC8 and MUC5B expression through the TLR4-mediated ERK1/2 and p38 MAPK signaling pathway in human airway epithelial cells. These findings indicated that delphinidin may be a therapeutic agent for control of inflammatory airway diseases.
Anthocyanins ; Epithelial Cells* ; Gene Expression ; Humans ; Immunoenzyme Techniques ; Lipopolysaccharides ; p38 Mitogen-Activated Protein Kinases* ; Phosphorylation ; Phosphotransferases ; Protein Kinases ; Real-Time Polymerase Chain Reaction ; RNA, Messenger ; RNA, Small Interfering ; Toll-Like Receptor 4 ; Toll-Like Receptors*