No abstract available.
Animals ; Apoptosis* ; Collagen* ; Insulin* ; Rats* ; Streptozocin*

PURPOSE:Ghrelin is an endogenous ligand of the growth hormone secretagogue receptor, and stomach is the major site of ghrelin secretion. The purpose of this study is to compare the serum ghrelin concentrations between patients with type 2 diabetes mellitus (DM) and normal adults. We studied also whether serum ghrelin levels in the patients with type 2 DM are correlated with body mass index (BMI), serum insulin, lipid profiles, and creatinine levels. METHODS:Forty patients with type 2 DM and forty normal adults were included in this study. We measured heights and weights of the subjects and calculated their BMIs. Blood samples were obtained to measure the ghrelin concentration and their sera were stored at -20degreeC until used. In all subjects, serum ghrelin levels were measured using the commercially available Ghrelin(human) EIA kit. RESULTS:No differences of mean values were detected between the control group and the type 2 diabetic group for age, body weight, BMI, and the levels of serum total cholesterol, triglyceride, HDL cholesterol, and creatinine. But ghrelin level of the type 2 diabetic group (71.1+/-30.5 ng/L) was significantly lower than the control group (139.7+/-36.9 ng/L). In the control group, the ghrelin level showed positive correlation with HDL cholesterol (Pearson's correlation coefficient=0.37, P<0.05). In the diabetic group, the ghrelin level showed weakly positive correlation with insulin concentration. However, there was no significant relationship between serum ghrelin and various parameters in the diabetic patients group. CONCLUSION: In this study, ghrelin concentration in type 2 diabetic patients was lower than that in the control group. In the control group, serum ghrelin concentrations were positively correlated with HDL cholesterol. In the type 2 diabetic group, there was no significant correlation between insulin and ghrelin concentrations.
Adult ; Body Mass Index ; Body Weight ; Cholesterol ; Cholesterol, HDL ; Creatinine ; Diabetes Mellitus ; Diabetes Mellitus, Type 2* ; Ghrelin* ; Humans ; Insulin ; Receptors, Ghrelin ; Stomach ; Triglycerides ; Weights and Measures

BACKGROUND: The central physiological derangement of hemorrhagic fever with renal syndrome (HFRS) caused by hantaan virus (HTNV) is a vascular dysfunction, manifested by hemorrhage, impaired vascular tone and increased vascular permeability. Platelet activating factor (PAF), whose actions are mediated through a specific receptor, is a potent bioactive lipid. PAF has diverse biological functions in the vascular system, such as increasing vascular permeability, adhesion of leukocytes to the endothelium and reduction of cardiac output, which result in hypotension and shock. The goal of the present study was to investigate whether PAF is involved in the pathogenesis of HFRS. For this purpose, we evaluated the effect of HTNV on the expression of PAF receptor (PAF-R) and on the activity of PAF-acetylhydrolase (PAF-AH) instead of PAF because PAF is rapidly degraded by PAF-AH in vivo. MATERIALS AND METHODS: To evaluate the expression of PAF-R, we performed reverse-transcription PCR, western blot and FACS analyses using HTNV-infected human umbilical vein endothelial cells (HUVECs) and non-infected (control) HUVECs. In addition, we measured the activity of plasma PAF-AH in HFRS patients and normal healthy persons. RESULTS: The mRNA and protein expression of PAF-R was increased in HTNV-infected HUVECs compared with control HUVECs at 2 and 3 days post-infection (d.p.i.). FACS analysis showed that HTNV induced the surface expression of PAF-R in HUVECs from 2 d.p.i. The activity of plasma PAF-AH was 2.5-fold lower in HFRS patients than in normal healthy persons. CONCLUSION: Increased PAF-R expression by HTNV might increase the responsiveness to PAF in endothelial cells. Reduced PAF-AH activity in the blood of HFRS patients might delay PAF degradation. These results suggest that changes in PAF-R and PAF-AH by HTNV might influence to PAF activity and might be involved in the vascular dysfunction of HFRS.
Blood Platelets ; Blotting, Western ; Capillary Permeability ; Cardiac Output ; Endothelial Cells ; Endothelium ; Hantaan virus ; Hemorrhage ; Hemorrhagic Fever with Renal Syndrome ; Human Umbilical Vein Endothelial Cells ; Humans ; Hypotension ; Leukocytes ; Plasma ; Platelet Activating Factor ; Platelet Membrane Glycoproteins ; Polymerase Chain Reaction ; Receptors, G-Protein-Coupled ; RNA, Messenger ; Shock

BACKGROUND: Beta-adrenergic receptor Kinase 1(betaARK1) is a serine/threonine kinase attached, which inhibits the coupling of beta-adrenergic receptor with G-protein. Myocardial betaARK1 level is usually elevated in heart failure and hypertrophy, but it is not known whether the circulating betaARK1 level is related with the degree of cardiac hypertrophy. This study was performed to evaluate the association of the betaARK1 level in circulating mononuclear leukocytes(MNL) in untreated hypertension with left ventricular mass in hypertensive patients. Method: Nineteen non-treated hypertensive patients were included for this study. High blood pressure was confirmed when systolic BP is over 150 mmHg or diastoli BP is over 95 mmHg. Echocardiography was performed to evaluate the degree of hypertrophy by measuring the left ventricular mass index(LVMI) and relative wall thickness(RWT), and test the LV function by measuring the ejection fraction(EF) according to ASE guideline. At the same time, blood was collected from each patient and MNL were isolated by gradient centrifuge with Ficoll-400. Total RNA was purified from MNL and semi-quantitative RT-PCR was performed. After reverse transcription, PCR was done with primers for human betaARK1 and GAPDH as external control. betaARK1 levels were expressed by ratio to GAPDH level and estimated the relations with clinical and Echocardiographic parameters. Result: We studied confirmed 19 hypertensive patients(10 men and 9 women, mean age of 50.6 years). Echocardiographically measured indices(mean+/-SD) were as follows; LVMI(137.3+/-30.6g/m2), PWT(0.53+/-0.09) and EF(54.6+/-8.5%). Ratio of betaARK1 levels to GAPDH was from 0.10 to 0.96 (0.62+/-0.25). betaARK1 levels were correlated with LVMI(correlation coefficient: r=.502, p=.029) and RWT(r=.627, p=.004). But Systolic BP(r=0.009, p=.93), diastolic BP(r=.07, p=.85) or EF(r=.045, p=.84) were not related to level of betaARK1. CONCLUSIONS: The betaARK1 level of circulating MNL was correlated well with the degree of the cardiac hypertrophy estimated by LVMI and RWT. This data suggests that activation of sympatho-adrenal system would exert a major role in developing cardiac hypertrophy and we can expect the decreased responsiveness to catecholamine in the heart of hypertensive patients. betaARK1 in circulating MNL might be used as a predictor or marker for LV hypertrophy in hypertensive patients.
beta-Adrenergic Receptor Kinases ; Cardiomegaly ; Echocardiography ; Female ; GTP-Binding Proteins ; Heart ; Heart Failure ; Humans ; Hypertension ; Hypertrophy ; Leukocytes, Mononuclear* ; Male ; Phosphotransferases ; Polymerase Chain Reaction ; Reverse Transcription ; RNA

We report on a 28 years old female with recurred cardiac myxomas who presented with dizziness, headache, and blurred vision. She had an excision of biatrial atrial myxomas 10 years age. Varying sized multiple cerebral aneuysms and myxomas in left atrium and left ventricle were found on a cerebral angiogram and echocardiogram, respectively. After wide excision including interatrial septum and part of left ventricular septum, her symptoms were much improved.
Adult ; Dizziness ; Female ; Headache ; Heart Atria ; Heart Ventricles ; Humans ; Intracranial Aneurysm ; Myxoma* ; Ventricular Septum

PURPOSE: A hypomotor seizure is a useful descriptive terminology, but its clinical and ictal characteristics are not fully understood. We investigated the clinical and electrophysiological characteristics of hypomotor seizures in children. METHODS: We reviewed 394 video-taped recordings, performed between Dec. 1994 and Feb. 2003., to select patients of hypomotor seizures. Exclusion criteria were as follows; i) hypomotor seizures accompanied with other types of seizures in a single event, ii) patients without neurocognitive dysfunctions who were older than 3 years old, iii) non-convulsive status epilepticus, iv) poor video quality. A total of 329 hypomotor seizures from 42 patients (M:F=27:15) were included. The mean age of onset was 1.9 years old, the mean age at the monitoring 4.5 years old, and the mean duration of follow-ups 3.9 years. RESULTS: Thirteen patients (31%) showed generalized onset, hypomotor seizures while 29 patients (69%) showed partial onset hypomotor seizures. 35 patients (83.3%) had neurocognitive deficits. Significant abnormalities in the on brain MRIs were revealed in 23 patients (54.8 %). The concordance rates of interictal epileptiform discharges were 29.0%. In 8 patients, (hypomotor seizures were separately accompanied by other types of seizures (19.0%)). Comparing generalized seizures (group 1) with partial seizures (group 2), there were no significant differences in the clinical parameters between the two groups. In brain MRIs, group 2 tended to have focal lesions. On the analysis of ictal rhythms in group 1, diffuse spike and wave discharges were noted in 8 patients, rhythmic beta in 2 patients, semirhythmic theta in 1 patient, diffuse attenuation of the background in 1 patient, and bilateral beta in 1 patient. Among 5 patients with ictal rhythms other than diffuse spike and wave discharges, 4 patients were younger than 3 years old. On the analysis in group 2, rhythmic ictal patterns were noted in 24 patients (82.8%), seimirhythmic in 2 patients (6.9%), and irregular in 3 patients (10.3%). The distribution of ictal frequencies was as follows:alpha in 3 (10.3%), beta in 4 (13.8%), theta in 10 (34.5%), delta in 4 (13.8%), repetitive spikes or sharp waves in 5 (17.3%), and spikes and waves in 3 (10.3%). Rhythmic beta patterns tended to be localized into the posterior quadrant. CONCLUSION: Hypomotor seizures consist of generalized-onset (31%) and partial-onset (69 %). No clinical parameters can predict the ictal patterns. Various patterns in patients with generalized onset hypomotor seizures under 3 years old may suggest different mechanisms of generalized hypomotor seizures from absence seizures. Rhythmic beta patterns from the posterior quadrant may suggest the localization-specific ictal patterns.
Age of Onset ; Brain ; Child* ; Child, Preschool ; Electroencephalography ; Epilepsy, Absence ; Follow-Up Studies ; Humans ; Magnetic Resonance Imaging ; Seizures* ; Status Epilepticus

PURPOSE: The channelopathies has been implicated in the pathogenesis of idiopathic generalized epilepsy(IGE). Recently, nonsense and missense mutations in a voltage-gated chloride channel gene(CLCN2) have been shown to be associated with IGE. Loss of CLCN2 function results in loss of sustained GABA inhibition, increasing the risk of uncontrolled firing leading to seizure activity. This study assessed the relevance of mutations in the CLCN2 gene in the Korean patients with IGE. METHODS: Twenty seven patients with IGE were recruited in the Seoul National University Boramae Hospital. PCR and direct sequencing of genomic DNA were done to analyze the complete coding region of CLCN2. 99 controls were tested for two identified polymorphisms. Genotypes and allelic frequencies were compared to controls with epilepsy patients and subgroup of IGE: 10 generalized epilepsy with febrile seizure plus(GEFSP), 9 childhood absence epilepsy(CAE) and 8 other IGE patients. RESULTS: Twelve CLCN2 polymorphisms: 3 exonic, 2 promotor and 7 intronic, were found in 22 patients(81%) and 2 polymorphisms were noble. Two polymorphisms in the exonic region with changes of amino acid, p.L15P and p.T668S and 2 polymorphisms in the promoter regions(c.1-1990T>C, c.1-693G>A) may affect on the CLCN channel function. The odds ratio for developing other IGE in patients with RS9820367-CG type was 4.2 compared to individuals with CC type. In addition, the odds ratio for developing other GEFSP in patients with RS9820367-CC type was 4.0 compared with individuals with CG type. CONCLUSION: Our findings suggest that genomic variations of CLCN2 may be implicated in the pathogenesis of IGE.
Channelopathies ; Chloride Channels ; Clinical Coding ; DNA ; Epilepsy ; Epilepsy, Generalized ; Exons ; Fires ; gamma-Aminobutyric Acid ; Genotype ; Humans ; Immunoglobulin E ; Introns ; Mutation, Missense ; Odds Ratio ; Polymerase Chain Reaction ; Seizures ; Seizures, Febrile

Pharyngeal dysphagia can be caused by structural abnormalities or neurological disorders such as stroke, meningitis, and other conditions. Herpes zoster (HZ), caused by the varicella-zoster virus (VZV), is a rare cause of pharyngeal dysphagia. The symptoms of HZ usually involve a painful rash with vesicles along the dermatome area, but it can also affect the cranial nerves (CN), such as CN VII (Ramsay-Hunt syndrome), and less commonly, other CN. A 69-year-old man presented with a sore throat and dysphagia symptoms. A laryngoscopy revealed multiple ulcerative mucosal lesions on the right soft palate and lateral pharynx. The patient was treated with oral valacyclovir, and although the lesions disappeared, the dysphagia symptoms remained. While dysphagia associated with a VZV infection is rare, it can occur with the additional symptoms of vocal cord paralysis. This paper reports a rare case of pharyngeal dysphagia caused by a VZV infection, and the patient presented only with the initial symptoms of sore throat and dysphagia without skin lesions or signs of vocal cord paralysis.

Pharyngeal dysphagia can be caused by structural abnormalities or neurological disorders such as stroke, meningitis, and other conditions. Herpes zoster (HZ), caused by the varicella-zoster virus (VZV), is a rare cause of pharyngeal dysphagia. The symptoms of HZ usually involve a painful rash with vesicles along the dermatome area, but it can also affect the cranial nerves (CN), such as CN VII (Ramsay-Hunt syndrome), and less commonly, other CN. A 69-year-old man presented with a sore throat and dysphagia symptoms. A laryngoscopy revealed multiple ulcerative mucosal lesions on the right soft palate and lateral pharynx. The patient was treated with oral valacyclovir, and although the lesions disappeared, the dysphagia symptoms remained. While dysphagia associated with a VZV infection is rare, it can occur with the additional symptoms of vocal cord paralysis. This paper reports a rare case of pharyngeal dysphagia caused by a VZV infection, and the patient presented only with the initial symptoms of sore throat and dysphagia without skin lesions or signs of vocal cord paralysis.

Pharyngeal dysphagia can be caused by structural abnormalities or neurological disorders such as stroke, meningitis, and other conditions. Herpes zoster (HZ), caused by the varicella-zoster virus (VZV), is a rare cause of pharyngeal dysphagia. The symptoms of HZ usually involve a painful rash with vesicles along the dermatome area, but it can also affect the cranial nerves (CN), such as CN VII (Ramsay-Hunt syndrome), and less commonly, other CN. A 69-year-old man presented with a sore throat and dysphagia symptoms. A laryngoscopy revealed multiple ulcerative mucosal lesions on the right soft palate and lateral pharynx. The patient was treated with oral valacyclovir, and although the lesions disappeared, the dysphagia symptoms remained. While dysphagia associated with a VZV infection is rare, it can occur with the additional symptoms of vocal cord paralysis. This paper reports a rare case of pharyngeal dysphagia caused by a VZV infection, and the patient presented only with the initial symptoms of sore throat and dysphagia without skin lesions or signs of vocal cord paralysis.