No abstract available.
Chlamydia* ; Fluorescent Antibody Technique, Indirect*

OBJECTIVES: Chronic pain is one of the most common experiences of humans and a typical psychophysiological disorder. The aim of this study was to measure the psychophysiological responses in chronic pain patients using a biofeedback system, and to compare them with the results from normal healthy subjects. METHODS: Forty two patients with chronic pain (17 males and 25 females, average age 44.67+/-11.10 years) and 42 normal healthy controls (17 males and 25 females, average age 45.17+/-10.46 years) participated in this study. Electromyography (EMG), skin conductance (SC), and skin temperature (ST) were recorded using biofeedback system during the 3 phases (baseline, stress, and recovery) of stress reactivity test, and average values of them were calculated. Difference of values between two groups in each corresponding phase was analyzed with independent t-test, and change of values across phases of stress reactivity test was analyzed with paired t-test (all two-tailed, p<0.05). RESULTS: Compared to normal controls, chronic pain patients had higher value of EMG (baseline : 8.10+/-5.97 micronV vs 4.72+/-1.52 micronV, t=-3.56, p<0.01 ; stress : 11.25+/-6.89 micronV vs 8.49+/-4.78 micronV, t=-2.13, p<0.05 ; recovery : 7.12+/-3.77 micronV vs 4.78+/-1.59 micronV, t= -3.70, p<0.01) and SC (baseline : 1.06+/-1.0 micronS vs 0.42+/-0.29 micronS, t=-4.0. p<0.01 ; stress : 1.87+/-2.05 micronS vs 1.03+/-0.86 micronS, t=-2.47, p<0.05 ; recovery : 1.74+/-1.77 micronS vs 0.64+/-0.59 micronS, t=-3.8, p<0.01) in all the 3 phases. But, skin temperature comparison did not reveal significant differences in all the 3 phases between two groups. CONCLUSION: Psychophysiological responses of chronic pain patients in stress reactivity test were different from those of normal healthy controls. These results suggest that sympathetic nervous system is more activated in chronic pain patients.
Biofeedback, Psychology ; Chronic Pain ; Electromyography ; Female ; Humans ; Male ; Psychophysiologic Disorders ; Psychophysiology ; Skin ; Skin Temperature ; Sympathetic Nervous System

OBJECTIVE: The purpose of this paper is to study the possible differences in clinical and polysomnographic findings, depending on the presence or absence of subjective complaints of abnormal sleep behavior, in patients with RWA on polysomnography. METHOD: We reviewed patient records and polysomnographic data of patients referred to the Sleep Laboratory at Seoul National University Hospital from June 1996 through October 2002. We defined the manifest RBD group (n=32) as patients having both complaints of abnormal sleep behavior and RWA on polysomnography. The latent RBD group (n=20) consisted of patients who exhibited RWA on polysomnography but did not complain of abnormal sleep behavior. The clinical characteristics and polysomnographic findings between the two groups were compared and analyzed. RESULTS: Fifty-two subjects had RWA, as detected by polysomnography (42 males and 10 females, mean age of 55.1+/-19.1 years). Subjects in the manifest RBD group were significantly older than those in the latent RBD group (61.59+/-13.5 vs. 44.70+/-2.76 years, independent t-test, p<0.01). More subjects in the manifest RBD group exhibited abnormal REM behavior on polysomnography than did subjects in the latent RBD group (81.3 vs. 50.0%, Fisher's exact test, p<0.05). No significant differences between the groups were found in the prevalence of brain disorders and primary sleep disorders, gender proportion, and sleep architecture. CONCLUSION: No difference in sleep architecture was found between the manifest and the latent RBD groups. Only age and the presence of abnormal sleep behavior on polysomnography differentiated the two groups. We suggest that RWA on polysomnography without complaints of abnormal sleep behavior may be early manifestation of manifest RBD. Attention to RWA on polysomnography is necessary to help prevent full-blown RBD from developing.
Brain Diseases ; Female ; Humans ; Male ; Mental Disorders* ; Polysomnography ; Prevalence ; REM Sleep Behavior Disorder ; Seoul ; Sleep Wake Disorders ; Sleep, REM*

OBJECTIVE: The purpose of this study is to investigate the prevalence rate of OSA in subjects whose main sleep complaint is insomnia and to find differential factors of OSA in these insomniac subjects. METHOD: We reviewed the medical records and polysomnographic findings of patients referred to the Sleep Laboratory at Seoul National University Hospital from January 1996 to December 2002. Four-hundred and seventy subjects complained of insomnia as their main sleep problem (235 males and 235 females, mean age 53.6+/-12.4 years). First, we investigated the prevalence rate of OSA in these insomniac patients. Second, we compared the clinical and demographic characteristics of the OSA-associated group with those of the non-associated group. Third, we examined whether the degree or presence of differential factors within the OSA group correlate with severity of OSA, as determined by the respiratory disturbance index (RDI). RESULTS: Among 470 insomniac subjects, 125 subjects (26.6%) were diagnosed as OSA by nocturnal polysomnography. OSA-associated subjects were significantly older (58.4+/-12.3 years vs. 51.8+/-11.2 years, p<0.01), and had significantly higher body mass index (BMI) (23.4+/-3.3 kg/m2 vs. 22.5+/-3.1 kg/m2, p=0.44) than non-associated subjects. The OSA-associated group had more subjects with male gender (64.0 % vs. 44.9 %, p<0.01), hypertension (20.0 % vs. 9.3 %, p<0.01) or snoring (96.0 % vs. 63.5 %, p<0.01). Within the OSA-associated group, age had a significant positive correlation with RDI (p=0.01). CONCLUSION: We found that a considerable portion of patients complaining of insomnia as their main sleep problem were diagnosed as OSA. Snoring, old age, male gender, obesity, and comorbid hypertension were found to be differential factors of OSA in insomniac patients. We suggest that diagnostic efforts including nocturnal polysomnography are needed for insomniac patients with any of the above risk factors of OSA.
Body Mass Index ; Female ; Humans ; Hypertension ; Male ; Medical Records ; Obesity ; Polysomnography ; Prevalence ; Risk Factors ; Seoul ; Sleep Apnea, Obstructive* ; Sleep Initiation and Maintenance Disorders* ; Snoring

BACKGROUND/OBJECTIVES: p-Coumaric acid (CA), a 4-hydroxycinnamic acid derivative, is widely distributed in nature and exerts various beneficial biological effects. However, the effects of CA on metabolic abnormalities triggered by excessive fructose intake, such as dyslipidemia, hyperglycemia, non-alcoholic fatty liver disease (NAFLD), and insulin resistance, have not been sufficiently investigated. Our objective was to investigate whether CA ameliorates high-fructose diet (HFrD)-induced metabolic dysregulation.MATERIALS/METHODS: Golden Syrian hamsters were randomly assigned to 3 groups and were fed diets containing 60% cornstarch (CON group), 60% fructose (HFrD group), or 60% fructose with CA (0.02%) (HFrD+CA group) for 5 weeks. RESULTS: HFrD feeding significantly increased the levels of plasma triglyceride, apolipoprotein (apo)-CIII, fasting blood glucose, and homeostatic model assessment insulin resistance, and tended to increase plasma total cholesterol (TC) and low-density lipoprotein/very low-density lipoprotein cholesterol (LDL/VLDL-C) compared with the CON group. In HFrD-fed hamsters, CA supplementation significantly decreased plasma TC, LDL/VLDL-C, apo-CIII, and fasting blood glucose levels. Moreover, CA significantly decreased the hepatic lipid levels and fibrosis induced by HFrD. The plasma and hepatic lipid-lowering effects of CA were associated with decreased enzyme activity and mRNA expression of genes involved in fatty acid, triglyceride, and cholesterol synthesis as well as increased activity of carnitine palmitoyltransferase, a rate-limiting enzyme in fatty acid oxidation, in the liver. CA-treated hamsters also exhibited decreased hepatic gluconeogenic enzyme activity and increased hepatic glycolytic enzyme activity, with mRNA expression changes similar to these activity patterns. CONCLUSION Our findings indicate that CA potentially improves metabolic abnormalities associated with excessive fructose intake, such as hyperglycemia, dyslipidemia, and NAFLD.

BACKGROUND/OBJECTIVES: p-Coumaric acid (CA), a 4-hydroxycinnamic acid derivative, is widely distributed in nature and exerts various beneficial biological effects. However, the effects of CA on metabolic abnormalities triggered by excessive fructose intake, such as dyslipidemia, hyperglycemia, non-alcoholic fatty liver disease (NAFLD), and insulin resistance, have not been sufficiently investigated. Our objective was to investigate whether CA ameliorates high-fructose diet (HFrD)-induced metabolic dysregulation.MATERIALS/METHODS: Golden Syrian hamsters were randomly assigned to 3 groups and were fed diets containing 60% cornstarch (CON group), 60% fructose (HFrD group), or 60% fructose with CA (0.02%) (HFrD+CA group) for 5 weeks. RESULTS: HFrD feeding significantly increased the levels of plasma triglyceride, apolipoprotein (apo)-CIII, fasting blood glucose, and homeostatic model assessment insulin resistance, and tended to increase plasma total cholesterol (TC) and low-density lipoprotein/very low-density lipoprotein cholesterol (LDL/VLDL-C) compared with the CON group. In HFrD-fed hamsters, CA supplementation significantly decreased plasma TC, LDL/VLDL-C, apo-CIII, and fasting blood glucose levels. Moreover, CA significantly decreased the hepatic lipid levels and fibrosis induced by HFrD. The plasma and hepatic lipid-lowering effects of CA were associated with decreased enzyme activity and mRNA expression of genes involved in fatty acid, triglyceride, and cholesterol synthesis as well as increased activity of carnitine palmitoyltransferase, a rate-limiting enzyme in fatty acid oxidation, in the liver. CA-treated hamsters also exhibited decreased hepatic gluconeogenic enzyme activity and increased hepatic glycolytic enzyme activity, with mRNA expression changes similar to these activity patterns. CONCLUSION Our findings indicate that CA potentially improves metabolic abnormalities associated with excessive fructose intake, such as hyperglycemia, dyslipidemia, and NAFLD.

BACKGROUND/OBJECTIVES: p-Coumaric acid (CA), a 4-hydroxycinnamic acid derivative, is widely distributed in nature and exerts various beneficial biological effects. However, the effects of CA on metabolic abnormalities triggered by excessive fructose intake, such as dyslipidemia, hyperglycemia, non-alcoholic fatty liver disease (NAFLD), and insulin resistance, have not been sufficiently investigated. Our objective was to investigate whether CA ameliorates high-fructose diet (HFrD)-induced metabolic dysregulation.MATERIALS/METHODS: Golden Syrian hamsters were randomly assigned to 3 groups and were fed diets containing 60% cornstarch (CON group), 60% fructose (HFrD group), or 60% fructose with CA (0.02%) (HFrD+CA group) for 5 weeks. RESULTS: HFrD feeding significantly increased the levels of plasma triglyceride, apolipoprotein (apo)-CIII, fasting blood glucose, and homeostatic model assessment insulin resistance, and tended to increase plasma total cholesterol (TC) and low-density lipoprotein/very low-density lipoprotein cholesterol (LDL/VLDL-C) compared with the CON group. In HFrD-fed hamsters, CA supplementation significantly decreased plasma TC, LDL/VLDL-C, apo-CIII, and fasting blood glucose levels. Moreover, CA significantly decreased the hepatic lipid levels and fibrosis induced by HFrD. The plasma and hepatic lipid-lowering effects of CA were associated with decreased enzyme activity and mRNA expression of genes involved in fatty acid, triglyceride, and cholesterol synthesis as well as increased activity of carnitine palmitoyltransferase, a rate-limiting enzyme in fatty acid oxidation, in the liver. CA-treated hamsters also exhibited decreased hepatic gluconeogenic enzyme activity and increased hepatic glycolytic enzyme activity, with mRNA expression changes similar to these activity patterns. CONCLUSION Our findings indicate that CA potentially improves metabolic abnormalities associated with excessive fructose intake, such as hyperglycemia, dyslipidemia, and NAFLD.

BACKGROUND/OBJECTIVES: p-Coumaric acid (CA), a 4-hydroxycinnamic acid derivative, is widely distributed in nature and exerts various beneficial biological effects. However, the effects of CA on metabolic abnormalities triggered by excessive fructose intake, such as dyslipidemia, hyperglycemia, non-alcoholic fatty liver disease (NAFLD), and insulin resistance, have not been sufficiently investigated. Our objective was to investigate whether CA ameliorates high-fructose diet (HFrD)-induced metabolic dysregulation.MATERIALS/METHODS: Golden Syrian hamsters were randomly assigned to 3 groups and were fed diets containing 60% cornstarch (CON group), 60% fructose (HFrD group), or 60% fructose with CA (0.02%) (HFrD+CA group) for 5 weeks. RESULTS: HFrD feeding significantly increased the levels of plasma triglyceride, apolipoprotein (apo)-CIII, fasting blood glucose, and homeostatic model assessment insulin resistance, and tended to increase plasma total cholesterol (TC) and low-density lipoprotein/very low-density lipoprotein cholesterol (LDL/VLDL-C) compared with the CON group. In HFrD-fed hamsters, CA supplementation significantly decreased plasma TC, LDL/VLDL-C, apo-CIII, and fasting blood glucose levels. Moreover, CA significantly decreased the hepatic lipid levels and fibrosis induced by HFrD. The plasma and hepatic lipid-lowering effects of CA were associated with decreased enzyme activity and mRNA expression of genes involved in fatty acid, triglyceride, and cholesterol synthesis as well as increased activity of carnitine palmitoyltransferase, a rate-limiting enzyme in fatty acid oxidation, in the liver. CA-treated hamsters also exhibited decreased hepatic gluconeogenic enzyme activity and increased hepatic glycolytic enzyme activity, with mRNA expression changes similar to these activity patterns. CONCLUSION Our findings indicate that CA potentially improves metabolic abnormalities associated with excessive fructose intake, such as hyperglycemia, dyslipidemia, and NAFLD.

BACKGROUND/OBJECTIVES: p-Coumaric acid (CA), a 4-hydroxycinnamic acid derivative, is widely distributed in nature and exerts various beneficial biological effects. However, the effects of CA on metabolic abnormalities triggered by excessive fructose intake, such as dyslipidemia, hyperglycemia, non-alcoholic fatty liver disease (NAFLD), and insulin resistance, have not been sufficiently investigated. Our objective was to investigate whether CA ameliorates high-fructose diet (HFrD)-induced metabolic dysregulation.MATERIALS/METHODS: Golden Syrian hamsters were randomly assigned to 3 groups and were fed diets containing 60% cornstarch (CON group), 60% fructose (HFrD group), or 60% fructose with CA (0.02%) (HFrD+CA group) for 5 weeks. RESULTS: HFrD feeding significantly increased the levels of plasma triglyceride, apolipoprotein (apo)-CIII, fasting blood glucose, and homeostatic model assessment insulin resistance, and tended to increase plasma total cholesterol (TC) and low-density lipoprotein/very low-density lipoprotein cholesterol (LDL/VLDL-C) compared with the CON group. In HFrD-fed hamsters, CA supplementation significantly decreased plasma TC, LDL/VLDL-C, apo-CIII, and fasting blood glucose levels. Moreover, CA significantly decreased the hepatic lipid levels and fibrosis induced by HFrD. The plasma and hepatic lipid-lowering effects of CA were associated with decreased enzyme activity and mRNA expression of genes involved in fatty acid, triglyceride, and cholesterol synthesis as well as increased activity of carnitine palmitoyltransferase, a rate-limiting enzyme in fatty acid oxidation, in the liver. CA-treated hamsters also exhibited decreased hepatic gluconeogenic enzyme activity and increased hepatic glycolytic enzyme activity, with mRNA expression changes similar to these activity patterns. CONCLUSION Our findings indicate that CA potentially improves metabolic abnormalities associated with excessive fructose intake, such as hyperglycemia, dyslipidemia, and NAFLD.

The effect of NDMA after oral administration (17 mg/ml) on the glycoconjugates of lingual von Ebner's gland and mucous gland were investigated with lectin histochemical methods. For lectin histochemical studies, the biotinylated lectins (DBA, PNA, SBA, BSL -1, sWGA, RCA -1, LCA, UEA -1, and ConA) were applied. Lectin binding patterns of glycoconjugates of lingual von Ebner's gland showed the decreased affinity for DBA, PNA, BSL -1 and sWGA in NDMA -treated group compared with control group. The remarkable decrease of binding affinity of NDMA -treated group was observed in PNA for 12 and 24 hours, DBA for 96 hours, BSL -1 for 72 hours, and sWGA for 3 hours, while the striking decrease of BSL -1 and sWGA binding was observed in NDMA -treated group for 12 hours. But these decreases of binding were tended to recover in PNA and sWGA after 72 hours of NDMA treatment, and in DBA after 120 hours. The binding affinity of SBA and RCA -1 was decreased in NDMA -treated group for 3 hours, while the other NDMA -treated group showed an increased affinity. Especially, the increase of SBA binding was remarkable. There was a little change in binding affinity of UEA -1, LCA and Con A in NDMA -treated group. Lectin binding patterns of glycoconjugates of lingual mucous gland showed decreased affinities for SBA, sWGA and UEA -1 in NDMA -treated group. The striking decreases of binding affinity for NDMA -treated group was observed in SBA and sWGA for 3 hours, and UEA -1 for 3 and 24 hours. And the remarkable decreases of binding affinity for NDMA -treated group was found in SBA for 24 and 48 hours, sWGA for 48, 72 and 96 hours, and UEA -1 for 48 hours. These decreases of binding affinity of NDMA -treated group were tended to recover in SBA and UEA -1 after 96 hours and in sWGA after 120 hours. The binding affinity for PNA and ConA showed a little but not remarkable increase in NDMA - treated group, and LCA binding showed a little decrease following a little increase in NDMA - treated group. The affinity of DBA binding was decreased in NDMA -treated group for 12 hours and 24 hours, while the other NDMA -treated group showed an increased affinity. Especially, there was a remarkable increase in NDMA -treated group for 96 hours. From these results, it is suggested that the toxicity of NDMA may be related with the carcinogen of the rat tongue, and glycoconjugates are concerned with the repaire of the destruction of the lingual mucous acini.
Administration, Oral ; Animals ; Dimethylnitrosamine* ; Glycoconjugates* ; Lectins ; Rats* ; Salivary Glands* ; Strikes, Employee ; Tongue ; von Ebner Glands