No abstract available.
Epidermis* ; Urocanic Acid*

No abstract available.
Necrosis* ; Typhoid Fever*

OBJECTIVE: This study was aimed to compare the efficacy and tolerability of milnacipran and sertraline treatment in patients with major depressive disorder and to evaluate the relationships between beta-adrenergic receptor responsiveness and depressive mood states. METHODS: Fifty three patients who had a diagnosis of major depressive disorder according to the DSM-IV and showed scores of 17 or more on the 17-item Hamilton Rating Scale for Depression (HAM-D) were randomly assigned to either milnacipran or sertraline treatment group. Each patient received 8 weeks of antidepressant treatment with one of the two drugs. Efficacy was assessed using the HAM-D, Beck Depression Inventory (BDI), Montgomery and Asberg Depression Rating Scale (MADRS) and Clinical Global Impression (CGI). Twenty normal control subjects who had no history of psychiatric and major medical illness and were matched with the depressed patients considering age, sex and body mass index were recruited for the comparison of beta-adrenergic receptor responsiveness between depressed patients and normal control subjects. We measured beta-adrenergic receptor density, lymphocyte cAMP ratio (ratio of isoproterenol-stimulated cAMP/basal cAMP), and receptor affinity (Kd) in all subjects. We also investigated beta-adrenergic receptor responsiveness before and after treatment in depressed patients. RESULTS: Twelve patients in milnacipran group and 15 patients in sertraline group were completed this study. In all assessment scales for depression, we found significant decrease in depression severity in both milnacipran and sertraline groups. Both of the two drugs proved equally effective for reduction of the overall symptoms of depression throughout the treatment period. And there were significant differences in the means of Kd values between control subjects and depressed patients before treatment. We found a significant negative correlation between Kd values and BDI scores. After treatment with either milnacipran or sertraline, cAMP ratio (4.8+/-1.6 vs 5.7+/-2.5, p=0.095) and Kd value (65.6+/-11.9 vs 74.6+/-7.8, p=0.066) tended to increase, but there was no significant difference in beta-adrenergic receptor responsiveness between milnacipran and sertraline group. CONCLUSION: Both milnacipran and sertraline were not different in the clinical efficacy in major depressive disorder. In depressed patients, beta-adrenergic receptor responsiveness is reduced and both milnacipran and sertraline antidepressants tended to increase beta-adrenergic receptor responsiveness.
Antidepressive Agents ; Body Mass Index ; Depression ; Depressive Disorder, Major* ; Diagnosis ; Diagnostic and Statistical Manual of Mental Disorders ; Humans ; Lymphocytes ; Sertraline* ; Weights and Measures

PURPOSE: This study was done to examine actor and partner effect of self-esteem and family stress on depression of middle-aged married couples. METHODS: Participants were 133 couples aged 40-60 years, who lived in Seoul, Incheon, or Gyeonggi provinces. All measures were self-administered. Data were analyzed using SPSS 18.0 and AMOS 18.0 program. RESULTS: Husband and wife's self-esteem had an actor effect (wife beta=-.45, p<.001; husband beta=-.35, p<.001 respectively) on their depression. Wife's family stress had an actor effect (beta=.27, p=.006) on her depression and a partner effect (beta=.31, p=.002) on her husband's depression. Meanwhile, it also had an indirect effect on her depression through self-esteem (beta=-.28, p<.001). Husband's family stress did not have an actor effect or a partner effect on his depression, but it had an indirect effect on his depression through self-esteem (beta=-.35, p<.001). CONCLUSION: Results indicate that to prevent the constantly increasing depression of middle-aged married couples, programs should be conducted for both of the couple, but focused differently for wife and husband.
Depression* ; Family Characteristics* ; Gyeonggi-do ; Humans ; Incheon ; Seoul ; Spouses

OBJECTIVE: High-molecular-weight hydroxyethyl starch (HES) compromises blood coagulation more than does low-molecular-weight HES. We compared the effects of low- and high-molecular-weight HES for the treatment of vasospasm and investigated the dose relationship with each other. METHODS: Retrospectively, in a series of consecutive 102 patients with subarachnoid hemorrhage (SAH), 35 patients developed clinical symptoms of vasospasm of these fourteen patients were treated with low-molecularweight HES for volume expansion while the other 21 received high-molecular-weight HES as continuous intravenous infusion. Prothrombin time (PT), partial thromboplastin time (PTT), fibrinogen level, and platelet count were all measured prior to initiation, during treatment and after termination of therapy for symptomatic vasospasm. The total dose of HES ranged from 5 L to 14 L and median infusion duration was 10 days. RESULTS: A more pronounced PTT prolongation was observed in high-molecular-weight HES group compared with low-molecular-weight HES group. No other coagulation parameters were altered. Dosage (=duration) shows a positive correlation with PTT. Clinically, significant bleeding episodes were noted in four patients who received high-molecular-weight HES. CONCLUSION: Coagulopathy was developed in direct proportion to molecular weight of starch and dosages. We propose the extreme caution in the administration of HES solution for the vasospasm treatment.
Blood Coagulation ; Fibrinogen ; Hemorrhage ; Humans ; Infusions, Intravenous ; Molecular Weight ; Partial Thromboplastin Time ; Platelet Count ; Prothrombin Time ; Retrospective Studies ; Starch* ; Subarachnoid Hemorrhage

OBJECTIVE: To make a guideline for cytogenetic study and diagnosis through systematic analysis of types and the incidences of chromosomal abnormalities obtained from various types of congenital disorder in Korea. METHODS: The cytogenetic study was performed on 14,402 patients with suspected chromosomal abnormalities at our genetic laboratory of the medical research center between January 1, 1974 to December 31, 2004 and additionally the FISH (Fluorescence in situ hybridization) study was done on 272 patients between January 1, 1998 to December 31, 2004. RESULTS: Total number of case requiring cytogenetic study were 33 in starting year (1974) and by 1983, the number increased rapidly to 481 cases. The number of case was maximum of 894 cases in 1993 and it started to decline from 1996 to 714. Overall chromosomal aberrations were 2,100 cases (14.58%). Autosomal chromosomal abnormalities were 1,257 cases (8.73%). Among those cases, Down syndrome was 848 cases (5.89%), Edward syndrome was 38 cases (0.26%), and Patau syndrome was 6 cases (0.04%) in order of frequency. Sex chromosomal abnormalities were 843 cases (5.85%) in total. Among those cases, Turner syndrome was 527 cases (3.66%), Kleinfelter syndrome was 267 cases (1.85%). Chromosomal abnormality rate in 535 couples with recurrent spontaneous abortions was 5.98% (32 couples). And chromosomal aberration in 1068 cases with primary amenorrhea was 63.95% (683 cases). The diagnostic rate of microdeletion syndrome by FISH method was 22.71%, and marker chromosome was 20.56%. CONCLUSION: From cytogenetic analysis of 14,402 cases performed in single institute during 31 years, we performed a study on the types and the incidences of chromosomal abnormalities. We hope we could suggest a guideline for studies and treatments of congenital disorders in Korea. Along with the cytogenetic study, FISH study was also required.
Abortion, Spontaneous ; Amenorrhea ; Chromosome Aberrations ; Congenital, Hereditary, and Neonatal Diseases and Abnormalities* ; Cytogenetic Analysis ; Cytogenetics* ; Diagnosis ; Down Syndrome ; Family Characteristics ; Female ; Hope ; Humans ; Incidence ; Korea* ; Pregnancy ; Turner Syndrome

Objective: Whether elevation in plasma levels of amyloid and tau protein biomarkers are better indicators of cognitive decline than higher baseline levels in patients with amnestic mild cognitive impairment (aMCI) and Alzheimer’s disease (AD) remains understudied. Methods: We included 67 participants with twice testing for AD-related plasma biomarkers via immunomagnetic reduction (IMR) assays (amyloid beta [Aβ]1-40, Aβ1-42, total tau [t-Tau], phosphorylated tau [p-Tau] 181, and alpha-synuclein [α-Syn]) and the Mini-Mental State Examination (MMSE) over a 1-year interval. We examined the correlation between biomarker levels (baseline vs. longitudinal change) and annual changes in the MMSE scores. Receiver operating characteristic curve analysis was conducted to compare the biomarkers. Results: After adjustment, faster cognitive decline was correlated with lower baseline levels of t-Tau (β=0.332, p=0.030) and p-Tau 181 (β=0.369, p=0.015) and rapid elevation of t-Tau (β=-0.330, p=0.030) and p-Tau 181 levels (β=-0.431, p=0.004). However, the levels (baseline and longitudinal changes) of Aβ1-40, Aβ1-42, and α-Syn were not correlated with cognitive decline. aMCI converters had lower baseline levels of p-Tau 181 (p=0.002) but larger annual changes (p=0.001) than aMCI non-converters. The change in p-Tau 181 levels showed better discriminatory capacity than the change in t-Tau levels in terms of identifying AD conversion in patients with aMCI, with an area under curve of 86.7% versus 72.2%. Conclusion We found changes in p-Tau 181 levels may be a suitable biomarker for identifying AD conversion.

Objective: Whether elevation in plasma levels of amyloid and tau protein biomarkers are better indicators of cognitive decline than higher baseline levels in patients with amnestic mild cognitive impairment (aMCI) and Alzheimer’s disease (AD) remains understudied. Methods: We included 67 participants with twice testing for AD-related plasma biomarkers via immunomagnetic reduction (IMR) assays (amyloid beta [Aβ]1-40, Aβ1-42, total tau [t-Tau], phosphorylated tau [p-Tau] 181, and alpha-synuclein [α-Syn]) and the Mini-Mental State Examination (MMSE) over a 1-year interval. We examined the correlation between biomarker levels (baseline vs. longitudinal change) and annual changes in the MMSE scores. Receiver operating characteristic curve analysis was conducted to compare the biomarkers. Results: After adjustment, faster cognitive decline was correlated with lower baseline levels of t-Tau (β=0.332, p=0.030) and p-Tau 181 (β=0.369, p=0.015) and rapid elevation of t-Tau (β=-0.330, p=0.030) and p-Tau 181 levels (β=-0.431, p=0.004). However, the levels (baseline and longitudinal changes) of Aβ1-40, Aβ1-42, and α-Syn were not correlated with cognitive decline. aMCI converters had lower baseline levels of p-Tau 181 (p=0.002) but larger annual changes (p=0.001) than aMCI non-converters. The change in p-Tau 181 levels showed better discriminatory capacity than the change in t-Tau levels in terms of identifying AD conversion in patients with aMCI, with an area under curve of 86.7% versus 72.2%. Conclusion We found changes in p-Tau 181 levels may be a suitable biomarker for identifying AD conversion.

Objective: Whether elevation in plasma levels of amyloid and tau protein biomarkers are better indicators of cognitive decline than higher baseline levels in patients with amnestic mild cognitive impairment (aMCI) and Alzheimer’s disease (AD) remains understudied. Methods: We included 67 participants with twice testing for AD-related plasma biomarkers via immunomagnetic reduction (IMR) assays (amyloid beta [Aβ]1-40, Aβ1-42, total tau [t-Tau], phosphorylated tau [p-Tau] 181, and alpha-synuclein [α-Syn]) and the Mini-Mental State Examination (MMSE) over a 1-year interval. We examined the correlation between biomarker levels (baseline vs. longitudinal change) and annual changes in the MMSE scores. Receiver operating characteristic curve analysis was conducted to compare the biomarkers. Results: After adjustment, faster cognitive decline was correlated with lower baseline levels of t-Tau (β=0.332, p=0.030) and p-Tau 181 (β=0.369, p=0.015) and rapid elevation of t-Tau (β=-0.330, p=0.030) and p-Tau 181 levels (β=-0.431, p=0.004). However, the levels (baseline and longitudinal changes) of Aβ1-40, Aβ1-42, and α-Syn were not correlated with cognitive decline. aMCI converters had lower baseline levels of p-Tau 181 (p=0.002) but larger annual changes (p=0.001) than aMCI non-converters. The change in p-Tau 181 levels showed better discriminatory capacity than the change in t-Tau levels in terms of identifying AD conversion in patients with aMCI, with an area under curve of 86.7% versus 72.2%. Conclusion We found changes in p-Tau 181 levels may be a suitable biomarker for identifying AD conversion.

Objective: Whether elevation in plasma levels of amyloid and tau protein biomarkers are better indicators of cognitive decline than higher baseline levels in patients with amnestic mild cognitive impairment (aMCI) and Alzheimer’s disease (AD) remains understudied. Methods: We included 67 participants with twice testing for AD-related plasma biomarkers via immunomagnetic reduction (IMR) assays (amyloid beta [Aβ]1-40, Aβ1-42, total tau [t-Tau], phosphorylated tau [p-Tau] 181, and alpha-synuclein [α-Syn]) and the Mini-Mental State Examination (MMSE) over a 1-year interval. We examined the correlation between biomarker levels (baseline vs. longitudinal change) and annual changes in the MMSE scores. Receiver operating characteristic curve analysis was conducted to compare the biomarkers. Results: After adjustment, faster cognitive decline was correlated with lower baseline levels of t-Tau (β=0.332, p=0.030) and p-Tau 181 (β=0.369, p=0.015) and rapid elevation of t-Tau (β=-0.330, p=0.030) and p-Tau 181 levels (β=-0.431, p=0.004). However, the levels (baseline and longitudinal changes) of Aβ1-40, Aβ1-42, and α-Syn were not correlated with cognitive decline. aMCI converters had lower baseline levels of p-Tau 181 (p=0.002) but larger annual changes (p=0.001) than aMCI non-converters. The change in p-Tau 181 levels showed better discriminatory capacity than the change in t-Tau levels in terms of identifying AD conversion in patients with aMCI, with an area under curve of 86.7% versus 72.2%. Conclusion We found changes in p-Tau 181 levels may be a suitable biomarker for identifying AD conversion.