No abstract available.
Adamantane ; Humans ; Nitriles ; Pyrrolidines

No abstract available.
Adolescent ; Cotinine ; Humans ; Tobacco

No abstract available.
Apnea* ; Doxapram*

Objectives: The reliability of surveys on smoking habits based on questionnaires was investigated, using the urinary cotinine content as an objective index. Methods: The subjects tested were 2,849 office workers of middle age, who responded to questions concerning their smoking status, and also their urinary cotinine was measured by the HPLC method. Results: The boundary value between smokers and non-smokers, determined by the histogram independent of the questionnaire, was 63.1 and 79.4 ng/mg of creatinine for males and females, respectively. The rate of misclassification of the non-smokers and former smokers as smokers was 1.3% for males and 1.8% for females, whereas that of current smokers as non-smokers was 6.3% and 2.1%. We also assessed the effect of smoke inhalation on the urinary cotinine value, and found a significant difference for males in the cotinine value by the presence of inhalation and also its depth. Conclusions: The rate of misclassification in this study was considered to be comparatively low. Several studies have also assessed the reliability of the questionnaire on smoking habits, and found different misclassification rates, indicating the dependence on the race and number of subjects tested. To our knowledge, there were only a few surveys on smoking among large groups, particularly in Japan, such as this one, therefore the results obtained in this study are meaningful.
Smoking ; Cotinine ; Indexes ; seconds ; Urine

It was attempted to clarify the participation of K+ channels in the post-receptor mechanisms of the muscarinic and A1-adenosine receptor-mediated control of acetylcholine (ACh) release in the present study. Slices from the rat hippocampus were equilibrated with (3H)choline and the release of the labelled products was evoked by electrical stimulation (3 Hz, 5 V/cm, 2 ms, rectangular pulses), and the influence of various agents on the evoked tritium-outflow was investigated. Oxotremorine (Oxo, 0.1~10 micrometer), a muscarinic agonist, and N6-cyclopentyladenosine (CPA, 1~30 micrometer), a specific A1-adenosine agonist, decreased the ACh release in a dose-dependent manner, without affecting the basal rate of release. 4-aminopyridine (4AP), a specific A-type K+-channel blocker (1~100 micrometer), increased the evoked ACh release in a dose-related fashion, and the basal rate of release is increased by 3 and 100 micrometer. Tetraethylammonium (TEA), a non-specific K+-channel blocker (0.1~10 mM), increased the evoked ACh release in a dose-dependent manner without affecting the basal release. The effects of Oxo and CPA were not affected by 3 micrometer 4AP co-treatment, but 10 mM TEA significantly inhibited the effects of Oxo and CPA. 4AP (10 micrometer- and TEA (10 mM)-induced increments of evoked ACh release were completely abolished in Ca2+-free medium, but these were recovered in low Ca2+ medium. And the effects of K+-channel blockers in low Ca2+ medium were inhibited by Mg2+ (4 mM) and abolished by 0.3 micrometer tetrodotoxin (TTX). These results suggest that the changes in TEA-sensitive potassium channel permeability and the consequent limitation of Ca2+ influx are partly involved in the presynaptic modulation of the evoked ACh-release by muscarinic and A1-adenosine receptors of the rat hippocampus.
4-Aminopyridine ; Acetylcholine* ; Animals ; Electric Stimulation ; Hippocampus* ; Muscarinic Agonists ; Oxotremorine ; Permeability ; Potassium Channels ; Rats* ; Receptors, Muscarinic ; Tea ; Tetraethylammonium ; Tetrodotoxin

OBJECTIVES: To examine emotional and psychological characteristics associated with suicide attempts in depressed patients. METHODS: A sample of 37 inpatients diagnosed with major depressive disorder or depressive disorder NOS was divided into two groups : lifetime suicide attempters(N=15 ; 40.54%), non-attempters(N=22 ; 59.46%). Beck Depression Scale(BDI), Beck Anxiety Scale(BAI), Hamilton Depression Rating Scale(HDRS), Hamilton Anxiety Rating Scale(HARS), and MMPI-2 were used to evaluate symptoms severity and psychological characteristics. RESULTS: Suicide attempters scored higher on the BDI though there were no group differences on the HDRS and on the both anxiety scales. Also they showed higher scores on the F, Fb, Pa, RC1, DEP, HEA, PK, AAS among MMPI-2 subscales. Our findings suggest that suicide attempters among depressed patients undergo more severe subjective distress and difficulties in adjustment than non-attempters. Also they were more hostile to others and showed lower trust. Lastly, they showed more somatic complaints and substance related problems. CONCLUSION: The present study showed that suicide attempters among depressed patients have distinct emotional and psychological characteristics. MMPI-2 would be helpful to assess suicidal risk of depressed patients.
Anxiety ; Depression ; Depressive Disorder ; Depressive Disorder, Major ; Humans ; Inpatients ; Pyrrolidines ; Suicide ; Weights and Measures

BACKGROUND: The aims of this study are to investigate the glycemic efficacy and predictive parameters of vildagliptin therapy in Korean subjects with type 2 diabetes. METHODS: In this retrospective study, we retrieved data for subjects who were on twice-daily 50 mg vildagliptin for at least 6 months, and classified the subjects into five treatment groups. In three of the groups, we added vildagliptin to their existing medication regimen; in the other two groups, we replaced one of their existing medications with vildagliptin. We then analyzed the changes in glucose parameters and clinical characteristics. RESULTS: Ultimately, 327 subjects were analyzed in this study. Vildagliptin significantly improved hemoglobin A1c (HbA1c) levels over 6 months. The changes in HbA1c levels (DeltaHbA1c) at month 6 were -2.24% (P=0.000), -0.77% (P=0.000), -0.80% (P=0.001), -0.61% (P=0.000), and -0.34% (P=0.025) for groups 1, 2, 3, 4, and 5, respectively, with significance. We also found significant decrements in fasting plasma glucose levels in groups 1, 2, 3, and 4 (P<0.05). Of the variables, initial HbA1c levels (P=0.032) and history of sulfonylurea use (P=0.026) were independently associated with responsiveness to vildagliptin treatment. CONCLUSION: Vildagliptin was effective when it was used in subjects with poor glycemic control. It controlled fasting plasma glucose levels as well as sulfonylurea treatment in Korean type 2 diabetic subjects.
Adamantane ; Diabetes Mellitus ; Dipeptidyl Peptidase 4 ; Fasting ; Glucose ; Hemoglobins ; Nitriles ; Plasma ; Pyrrolidines ; Retrospective Studies

Zinc released from excited glutamatergic neurons accelerates amyloid beta (A beta) aggregation, underscoring the therapeutic potential of zinc chelation for the treatment of Alzheimer's disease (AD). Zinc can also alter A beta concentration by affecting its degradation. In order to elucidate the possible role of zinc influx in secretase-processed A beta production, SH-SY5Y cells stably expressing amyloid precursor protein (APP) were treated with pyrrolidine dithiocarbamate (PDTC), a zinc ionophore, and the resultant changes in APP processing were examined. PDTC decreased A beta40 and A beta42 concentrations in culture media bathing APP-expressing SH-SY5Y cells. Measuring the levels of a series of C-terminal APP fragments generated by enzymatic cutting at different APP-cleavage sites showed that both beta- and alpha-cleavage of APP were inhibited by zinc influx. PDTC also interfered with the maturation of APP. PDTC, however, paradoxically increased the intracellular levels of A beta40. These results indicate that inhibition of secretase-mediated APP cleavage accounts -at least in part- for zinc inhibition of A beta secretion.
Alzheimer Disease ; Amyloid ; Baths ; Culture Media ; Neurons ; Proline ; Pyrrolidines ; Thiocarbamates ; Zinc

BACKGROUND: Cotinine, a nicotine metabolite detected in urine, has been recommended as the best quantitative marker of smoking and environmental tobacco smoke (ETS) exposure. The aim of this study was to analyze the relationship between indoor ETS and urinary cotinine level of the passive smokers. METHODS: We selected 42 nonsmokers who lived in Seoul and were not exposed to passive smoking at least 5 days before test. Urinary cotinine levels were measured by Smokescreen Colorimeter (Surescreen Diagnostics LTD, U.K.). We measured urinary cotinine levels twice (before and after smoking exposure). RESULTS: The mean urinary cotinine level was 0.33microgram/mL before smoking exposure, and 0.46microgram/mL after smoking exposure. There was statistically significant difference (P-value=0.003). There was no significant difference between exposure time and increase of urinary cotinine level(P=0.138, r=-0.233). There was also no significant difference between measuring time taking after exposure and increase of urinary cotinine level (P=0.671, r=0.067). CONCLUSION: One experience of indoor exposure to ETS caused significant elevation of urinary cotinine level.
Cotinine* ; Nicotine ; Seoul ; Smoke* ; Smoking ; Tobacco ; Tobacco Smoke Pollution

BACKGROUND: Cotinine, a nicotine metabolite detected in urine, has been recommended as the best quantitative marker of smoking and environmental tobacco smoke (ETS) exposure. The aim of this study was to analyze the relationship between indoor ETS and urinary cotinine level of the passive smokers. METHODS: We selected 42 nonsmokers who lived in Seoul and were not exposed to passive smoking at least 5 days before test. Urinary cotinine levels were measured by Smokescreen Colorimeter (Surescreen Diagnostics LTD, U.K.). We measured urinary cotinine levels twice (before and after smoking exposure). RESULTS: The mean urinary cotinine level was 0.33microgram/mL before smoking exposure, and 0.46microgram/mL after smoking exposure. There was statistically significant difference (P-value=0.003). There was no significant difference between exposure time and increase of urinary cotinine level(P=0.138, r=-0.233). There was also no significant difference between measuring time taking after exposure and increase of urinary cotinine level (P=0.671, r=0.067). CONCLUSION: One experience of indoor exposure to ETS caused significant elevation of urinary cotinine level.
Cotinine* ; Nicotine ; Seoul ; Smoke* ; Smoking ; Tobacco ; Tobacco Smoke Pollution