BACKGROUND : DHEAS, the major circulating adrenal hormone, has been suggested to have a role in many aging related diseases and perhaps in aging itself. But, there is no epidemiologic data of DHEAS in normal adults in Korea. We studied age changes and sex differences in serum DHEAS & its related factors throughout adulthood. METHODS : We administ structured questionnaires to the study subjects. We measured serum DHEAS levels and several biochemical markers (total cholesterol, triglyceride, HDL-cholesterol, glucose etc) in 1.710 healthy men(857) and women (853), aged 17-76 years. We also measured their height, weight, waist & hip circumference and body fat contents with bioimpedance method. We analyzed various variables relating to serum DHEAS levels by using SPSS. Reference data of serum DHEAS level in normal adults were also suggested. RESULTS : The DHEAS concentration peaked at age group blow age of 30 years in man(260.9 microgram/dL). Then mean values declined steadily in both sexes (r=-0.38, p<0.001 in men and r=-0.46, p<0.001 in women). At age group above 70 years, only 30.9% in men & 30.4% in women, when compared with age group below 30 years, was remained. DHEAS concentration were significantly higher in men than women at all age group except age group above 70 years. Average 1.5 times higher concentration in men than in women (at least 1.28 times at age<30 and max 2.00 times at age 60-64). In men, DHEAS had higher mean value in smokers (218.1 vs 199.1 microgram/dL, p<0.05), drinkers (>or=2 times/week, 219.1 vs 185.3 microgram/dL, p<0.01), android type fat distribution group (waist/hip>0.85, 227.1 vs 197.4 microgram/dL) after adjusting age. DHEAS was positively correlated with body mass index (r=0.12, p<0.01). But in women, drinkers (154.3 vs 131.7 microgram/dL, p<0.05) and regular exercise group (146.1 vs 131.6 microgram/dL, p=0.05) had higher mean DHEAS value. There were no significant association between DHEAS and lipid profile (total cholesterol, triglyceride, HDL-cholesterol, LDL-cholesterol) & fasting glucose level in both sex. CONCLUSION : Our data suggest that DHEAS levels may influenced by several sociodemographic factors (e.g. smoking, alcohol, exercise etc) and body mass index. DHEAS level was inversely correlated by age in both sex and men had 1.5 times higher DHEAS values than women. We could not find any association between DHEAS level and lipid profile & fasting blood sugar.
Adipose Tissue ; Adult ; Aging ; Biomarkers ; Blood Glucose ; Body Mass Index ; Cholesterol ; Dehydroepiandrosterone Sulfate* ; Dehydroepiandrosterone* ; Fasting ; Female ; Glucose ; Hip ; Humans ; Korea ; Male ; Surveys and Questionnaires ; Sex Characteristics* ; Smoke ; Smoking ; Triglycerides ; Waist-Hip Ratio

No Abstract Available.

BACKGROUND: Immediate early gene (IEG) is supposed to be linked in the continuous seizure induced long-term changes of specific neurons. We tried to investigate the effects of focal interictal epileptiform discharges on the c-JUN expression in the rat brain which is not clearly understood. METHODS:Epidural electrodes were placed on a male Sprague-Dawley weighing 150~230 g and benzathine penicillin (Pc) was applied cortically. After focal interictal epileptiform discharges were successfully identified, EEG was recorded regularly. Cardiac perfusion and extraction of the brain was done at 2, 4, 24 hours and 1 week after the Pc application. Sixteen rats were evenly distributed into 4 groups. Immunocytochemical staining with specific antisera (Santa Cruz) was performed. RESULTS: The epileptiform discharges were induced within an hour after topical Pc applications. At 2 hours after Pc application, c-JUN was moderately expressed in the dentate gyrus (DG) and weakly expressed in the CA3 pyramidal cell, amygdala, pyriform cortex, thalamus, and neocortex. At 4 hours, c-JUN was minimally expressed in DG and other regions. Whereas, at 24 hours, c-JUN was maximally expressed in the DG and also in the CA3 pyramidal cell, amygdala, pyriform cortex, thalamus, and neocortex. One week after Pc application, c-JUN was moderately expressed in the DG and weakly expressed in the CA3 pyramidal cell, amygdala, pyriform cortex, and neocortex. CONCLUSIONS: This data showed that even focal interictal epileptic activity can induce IEG encoded c-JUN protein in the specific distant brain regions of a rat until a late period and the expression pattern showed a synchronous and bimodal pattern.
Amygdala ; Animals ; Brain* ; Dentate Gyrus ; Electrodes ; Electroencephalography ; Humans ; Immune Sera ; Male ; Neocortex ; Neurons ; Penicillin G ; Penicillin G Benzathine ; Perfusion ; Pyramidal Cells ; Rats* ; Rats, Sprague-Dawley ; Seizures ; Thalamus

No abstract available.
Apoptosis* ; Carcinoma, Renal Cell* ; Cell Line* ; Interferon-gamma*

Herpes zoster infections are frequently complicated by a postherpetic neuropathy. Postherpetic neuralgia is one of the most troublesome disease in pain clinic. Current therapy includes tricyclic antidepressant, anticonvulsants, sympathetic and somatic nerve blocks, and transcutaneous electrical nerve stimulation(TENS). However, in a number of case, the illness dose not respond to treatment very well. The N-methyl-D-aspartate(NMDA) receptor is one of the receptor subtypes of the excitatory amino acids(EAA) glutamate, and seems to play a significant role in the pathogenesis of nerve injury pain and neuropathic pain. The non-competitive NMDA receptor blocker ketamine reduced continuous and evoked pain in patients with injury of the peripheral or central nervous system. We present three cases in which patients suffering from postherpetic neuralgia did not respond to conventional therapy and in whom continuous intravenous infusion of ketamine reduced severe pain.
Anesthetics ; Anticonvulsants ; Central Nervous System ; Glutamic Acid ; Herpes Zoster ; Humans ; Infusions, Intravenous* ; Ketamine* ; N-Methylaspartate ; Nerve Block ; Neuralgia* ; Neuralgia, Postherpetic ; Pain Clinics

Many fungi including Penicillium, Aspergillus, Gliocladium, and Thermoascus produce an epipolythiodioxopiperazine class of fungal metabolite, gliotoxin, which contirbutes the pathogenesis of fungal infection as an immunomodulator and cytotoxic agent. This study is designed to define the mechanism by which gliotoxin exerts the cytotoxic effect of gliotoxin on human promyelocytic leukemic cells, HL-60. Gliotoxin induces the apoptosis of HL-60 cells which is characterized by the ladder pattern fragmentation of DNA. Gliotoxin induces the activation of DEVD-specific cysteine protease in a time- and dose-dependent rnanner. It also increases the phosphotransferase activities of c-Jun N-terminal kinase1 (JNK1) and p38 in gliotoxin-treated HL-60 cells. Furthermore, gliotoxin decreases the activation of transcriptional activator, actiating protein (AP-1) and NF-kB. These results suggest that gliotoxin induces the apoptotic death of HL-60 cells via activation of DEVD- specific caspase as well as mitogen activated protein kinases (MAP kinases) including JNK1 and p38, and inhibition of transcriptional activators, AP-1 and NF-kB.
Apoptosis* ; Aspergillus ; Caspase 3 ; Cysteine Proteases ; DNA ; Fungi ; Gliocladium ; Gliotoxin* ; HL-60 Cells* ; Humans ; Mitogen-Activated Protein Kinases ; NF-kappa B ; Penicillium ; Thermoascus ; Transcription Factor AP-1 ; Transcription Factors

Pulmonary alveolar proteinosis (PAP) is a noninflammatory diffuse lung disease, characterized by a dense accumulation of lipoproteinaceous material within the alveoli, causing hypoxemia, restrictive lung disease, and abnormalities on chest radiograph. The etiology of PAP is uncertain and various forms, including idiopathic and disease secondary to dust or fume exposure. Bronchopulmonary lavage (BPL) is a safe and effective treatment in PAP, and a unique procedure which requires general anesthesia and separation of the lung with a double lumen endobronchial tube. We experienced anesthetic management of BPL for the successful treatment of a 33 years old female patient with PAP.
Adult ; Anesthesia, General ; Anoxia ; Bronchoalveolar Lavage* ; Dust ; Female ; Humans ; Lung ; Lung Diseases ; Pulmonary Alveolar Proteinosis* ; Radiography, Thoracic

To further define the prognostic factors associated with long term survival of hepatocellular carcinoma, we retrospectively studied 371 patients with pathologically diagnosed hepatocellular carcinoma who underwent curative hepatic resection between 1991 and 1995. We included the 16 patients who underwent noncurative hepatic resection in calculating overall survival. The male to female ratio was 5.1 to 1 and their average age was 52.5 years. About 20 variables were subject to univariate and multivariate analysis and their survivals were calculated using the Kaplan-Meier method. 55.6% of (220 of 396) patients had liver cirrhosis and 73.2% of (290 of 396) patients were positive in HBsAg. Operative mortality and inhospital death rate were 1.5% and 0.8%, each and postoperative morbidity rate was 22.5%. The cumulative 1, 3 and 5 year survival rates including noncurative resected cases were 85.9%, 67.2% and 54.8%, respectively. The cumulative 1, 3 and 5 year survival rates of 371 curative resected cases were 87.3%, 68.7% and 56.4%, respectively. Disease free 1, 3, 5 year survival rates of 371 curative resected cases were 74.8%, 48.2% and 40.8%, respectively. The factors such as alpha- fetoprotein, Child's classification, prothrombin time, extent of liver resection, and number of tumor were statistically significant factors associated with cumulative survival.(p<0.05) And alpha-fetoprotein, total necrosis after TACE, viral hepatitis, and invasion of portal vein were significant factors associated with cumulative disease free survival. Only alpha-fetoprotein was associated significantly with cumulative survival and cumulative disease free survival. Length to the resection margin was not significantly associated with survival.
alpha-Fetoproteins ; Carcinoma, Hepatocellular* ; Classification ; Disease-Free Survival ; Female ; Fetal Proteins ; Hepatectomy ; Hepatitis ; Hepatitis B Surface Antigens ; Humans ; Liver ; Liver Cirrhosis ; Male ; Mortality ; Multivariate Analysis ; Necrosis ; Portal Vein ; Prothrombin Time ; Retrospective Studies ; Survival Rate

BACKGROUND: The long-term prognosis of patients with hepatocellular carcinomas is still disappointing primarily because of intrahepatic recurrence. Among many factors, portal vein invasion is considered to be the most important risk factor leading to recurrence, and it is thought to be the direct evidence of tumor invasiveness. In clinical aspects, it seems to be more practical to determine the factors associated with portal vein invasion. METHODS: Three hundred and seventy-one patients who underwent a curative hepatic resection for hepatocellular carcinomas between 1991 and 1995 at Seoul National University Hospital were included in this study. Portal vein invasion was identified histopathologically. The prognostic factors of hepatocellular carcinoma and the risk factors linked to portal vein invasion were analyzed by both univariate and multivariate analyses. RESULTS: Portal vein invasion was detected in thirty seven patients (10%), and the 5-year overall and disease-free survival rates in this group were 39.9% and 6.5%, respectively. The 5-year overall and disease-free survival rates of patients without portal vein invasion were 60.1% and 36.8%, respectively. In multivariate analysis using Cox's proportional hazards model, portal vein invasion was proven to be the most important risk factor in both overall and disease-free survival. In a multiple stepwise logistic regression analysis, the size and the number of the tumors were strong independent predictors of portal vein invasion by a hepatocellular carcinoma. CONCLUSIONS: Intrahepatic recurrence and patient survival in cases of hepatocellular carcinomas were closely related to portal vein invasion. Patients with tumor sizes larger than 4 cm or with multiple tumors should be monitored closely for early recurrence.
Carcinoma, Hepatocellular* ; Disease-Free Survival ; Humans ; Logistic Models ; Multivariate Analysis ; Portal Vein* ; Prognosis ; Proportional Hazards Models ; Recurrence ; Risk Factors* ; Seoul

OBJECTIVE: Triptolide (TP) has been reported to suppress the expression of mitogen-activated protein kinase (MAPK) phosphatase-1 (MKP-1), of which main function is to inactivate the extracellular signal-regulated kinase-1/2 (ERK-1/2), the p38 MAPK and the c-Jun N-terminal kinase-1/2 (JNK-1/2), and to exert antiproliferative and pro-apoptotic activities. However, the mechanisms underlying antiproliferative and pro-apoptotic activities of TP are not fully understood. The purpose of this study was to examine whether the down-regulation of MKP-1 expression by TP would account for antiproliferative activity of TP in immortalized HT22 hippocampal cells. METHODS: MKP-1 expression and MAPK phosphorylation were analyzed by Western blot. Cell proliferation was assessed by 3H-thymidine incorporation. Small interfering RNA (siRNA) against MKP-1, vanadate (a phosphatase inhibitor), U0126 (a specific inhibitor for ERK-1/2), SB203580 (a specific inhibitor for p38 MAPK), and SP600125 (a specific inhibitor for JNK-1/2) were employed to evaluate a possible mechanism of antiproliferative action of TP. RESULTS: At its non-cytotoxic dose, TP suppressed MKP-1 expression, reduced cell growth, and induced persistent ERK-1/2 activation. Similar growth inhibition and ERK-1/2 activation were observed when MKP-1 expression was blocked by MKP-1 siRNA and its activity was inhibited by vanadate. The antiproliferative effects of TP, MKP-1 siRNA, and vanadate were significantly abolished by U0126, but not by SB203580 or SP600125. CONCLUSION: Our findings suggest that TP inhibits the growth of immortalized HT22 hippocampal cells via persistent ERK-1/2 activation by suppressing MKP-1 expression. Additionally, this study provides evidence supporting that MKP-1 may play an important role in regulation of neuronal cell growth.
Anthracenes ; Blotting, Western ; Butadienes ; Cell Proliferation ; Diterpenes ; Down-Regulation ; Epoxy Compounds ; Imidazoles ; Neurons ; Nitriles ; p38 Mitogen-Activated Protein Kinases ; Phenanthrenes ; Phosphorylation ; Protein Kinases ; Pyridines ; RNA, Small Interfering ; Vanadates