No abstract available.
Gestational Age* ; Humans ; Infant*

PURPOSE: We investigated whether psychological factors could influence on the symptoms of chronic prostatitis based on general population that have not previously been examined or treated. MATERIALS AND METHODS: Between August and November 2000, we randomly selected 100 male residents in the area of Chung-nam including Daejoen city. The participants completed self- administered questionnaires. Based on our inclusion criteria, 87 participants were included in this study. RESULTS: Scores of Beck Depression Inventory of participants with higher pain and urinary symptoms domain scores were significantly higher than those with lower pain and urinary symptoms domain scores of the National Institutes of Health-chronic prostatitis symptom index (p=0.001 and p=0.028, respectively). However, anxiety did not influence on the symptoms of chronic prostatitis based on the results of State-Trait Anxiety Inventory. Based on the results of Bem Sex Role Inventory, masculinity score of participants with higher urinary symptoms domain scores were significantly lower than those with lower urinary symptoms domain scores (p=0.042). CONCLUSIONS: Our results suggest that psychological problems may involve in an early stage of chronic prostatitis and have a causative role in chronic prostatitis.
Academies and Institutes ; Anxiety ; Depression ; Gender Identity ; Humans ; Male ; Masculinity ; Prostatitis* ; Psychology ; Surveys and Questionnaires

BACKGROUND: During and immediately after percutaneous transluminal coronary angioplasty(PTCA), reversible ischemic electrocardiographic change and/of left ventricular dysfunction are developed. But it is not investigated whether there are potential myocardial cell damages following PTCA or not, and the clinical Significance of myocardial cell damage following PTCA. Recently cardiac Troponin-T has been developed as a new myocardial specific marker, especially myocardial damage. The object of this study is to investigate whether potential Myocardial damage following PTCA was occurred and the utility of cardiac Tropoin-T for predicting the complications during and immediately after PTCA. METHODS: The study group comprised 12 patients(M/F;8/4mean age;60 +/- 4year,AMI in 6) undergoing PTCA, Samples for Troponin-T were obtained before, directly after, after 2 hours, 6 hours, and after 12 hours and was determined by enzyme immunoassay on an ES 300 analyzer(Boehringer Mannheim). Discrimination limit for myocardial cell damage is 0.1 ng/ml in normal baseline level but if the baseline level is elevated such as acute myocardial infarction or unstable angina, myocardial cell damage is defined with further increase of cardiac Troponin-T(>0.1 ng/ml) compare to baseline level. RESULTS: 1) The mean duration of total balloon inflation is 10.7 +/- 2(3-22) minutes and the mean duration of single maximal inflation is 3.9 +/- 0.6(1-8) minutes. There are no significant change in concentration of Troponin-T by inflation time. None of the patients showed electroca rdiographic evidence for myocardial infarction. 2) Troponin-T were increased in 2 patients with unstable angina(0.01 vs 0.11 ng/ml) which were developed major dissection including acute closure during PTCA, and 2 patients with acute myocardial infarction(2.37 vs 3.73 ng/ml) which didn't developed dcomplication. The increase of cardiac Troponin-T were observed in 2 of 10 patients with uncomplicated PTCA(20%). 3)The subacute complications were not developed. CONCLUSION: The cardiac Troponin-T were increased significantly in two AMI patients with uncomplicated PTCA(2/10,20%). The increase of cardiac Troponin-T following PTCA is associated with periprocedural complications but the prognostic significance to detect postprocedural complication did not define in this study because there were no subacute complications after PTCA and may be limited value due to time course of complication(usaully within 1 hour after PTCA) and relatively long analytic time.
Angina, Unstable ; Discrimination (Psychology) ; Electrocardiography ; Humans ; Immunoenzyme Techniques ; Inflation, Economic ; Myocardial Infarction ; Troponin T* ; Ventricular Dysfunction, Left

There is an error in a grant number in Acknowledgements.

BACKGROUND: Excess energy supply induces chronic low-grade inflammation in association with oxidative stress in various tissues including intestinal epithelium. The objective of this study was to investigate the effect of high-fat diet (HFD) on intestinal cell membrane integrity and intestinal tumorigenesis in ApcMin/+ mice. METHODS: Mice were fed with either normal diet (ND) or HFD for 12 weeks. The number of intestinal tumors were counted and biomarkers of endotoxemia, oxidative stress, and inflammation were determined. Changes in intestinal integrity was measured by fluorescein isothiocyanate (FITC)-dextran penetration and membrane gap junction protein expression. RESULTS: HFD group had significantly higher number of tumors compared to ND group (P < 0.05). Blood total antioxidant capacity was lower in HFD group, while colonic 8-hydroxy-2'-deoxyguanosine level, a marker of oxidative damage, was higher in HFD group compared to that of ND group (P < 0.05). The penetration of FITC-dextran was substantially increased in HFD group (P < 0.05) while the expressions of membrane gap junction proteins including zonula occludens-1, claudin-1, and occludin were lower in HFD group (P < 0.05) compared to those in ND group. Serum concentration of lipopolysaccharide (LPS) receptor (CD14) and colonic toll-like receptor 4 (a LPS receptor) mRNA expression were significantly higher in HFD group than in ND group (P < 0.05), suggesting that significant endotoxemia may occur in HFD group due to the increased membrane permeability. Serum interleukin-6 concentration and myeloperoxidase activity were also higher in HFD group compared to those of ND group (P < 0.05). CONCLUSIONS: HFD increases oxidative stress disrupting intestinal gap junction proteins, thereby accelerating membrane permeability endotoxemia, inflammation, and intestinal tumorigenesis.
Animals ; Biomarkers ; Carcinogenesis* ; Cell Membrane* ; Claudin-1 ; Colon ; Colonic Neoplasms ; Connexins ; Diet ; Diet, High-Fat* ; Endotoxemia ; Fluorescein ; Inflammation ; Interleukin-6 ; Intestinal Mucosa ; Membranes ; Mice ; Occludin ; Oxidative Stress ; Permeability ; Peroxidase ; RNA, Messenger ; Toll-Like Receptor 4

Endocarditis due to anaerobes is not a rare ocurrence. However, Clostridial endocarditis, most cases are caused by Clostridium perfringens, is an uncommon disease. Clostridium are gram positive spore forming obligate anaerobes that are found widely in soil, water, and foods. They naturally inhabit the respiratory, gastrointestinal, and female genital tract. We observed a case of Clostridium perfringens endocarditis in a 67 years old woman. Who experienced fever, chronic diarrhea and vegetation in the aortic valve.
Aged ; Aortic Valve ; Clostridium perfringens* ; Clostridium* ; Diarrhea ; Endocarditis* ; Female ; Fever ; Humans ; Soil ; Spores

Methods: Patients with and without TCLH were assigned to groups A and B, respectively. POSEH between the two groups was compared morphometrically and symptomatically. The risk factors for symptomatic and morphometric POSEH in BESS were identified. Results: The morphometric POSEH was greater in group B, and the difference was significant (p =0.019). The incidence of symptomatic POSEH was lower in group A with 4.6% (5/109) than in group B with 9.5% (9/95); however, the rate was not significantly different (p =0.136). The morphometric POSEH was classified into two small (hG1 and hG2) and large (hG3 and hG4) and were compared between groups A and B, and the difference was significant (p =0.02). In the multivariable logistic regression, nonuse of TCLH (p =0.004) and preoperative diagnosis of stenosis (p =0.016) were variables found to be significant risk factors of morphometric POSEH. Conclusions Severe compression of the thecal sac by POSEH is more common in patients without TCLH. The risk of hematoma formation was higher when bilateral decompression was needed and the cut bone surface was more exposed.

Almost all heavy metals are serious toxicants as carcinogens. However, due to their chemical and physiological properties, heavy metals are useful in industrial areas including alloy, smelting and production of commercial products. Such applications increase the opportunity for heavy metal exposure. Waste from industrial processes is also a major source of environmental contamination and accumulation in the human body. Arsenic, cadmium, chromium, and nickel are classified as group 1 carcinogens by the International Agency for Research on Cancer, and are utilized commercially. In this review, we used molecular pathway analysis to understand the toxicity and carcinogenic mechanisms of these metals. Our analyzed data showed that above-mentioned metallic substances induce oxidative stress, DNA damage, and cell death processes, resulting in increase the risk of cancer and cancer-related diseases. Thus, we might think phytochelatin molecules and antioxidative phytochemical substances are helpful for prevention of heavy metal-induced cancer.
Alloys ; Arsenic ; Cadmium ; Carcinogens ; Cell Death ; Chromium ; DNA Damage ; Human Body ; International Agencies ; Metals ; Metals, Heavy ; Nickel ; Osmeriformes ; Oxidative Stress ; Phytochelatins

Treatment with certain DNA-damaging agents induce a complex cellular response comprising pertubation of cell cycle progression and/or apoptosis on proliferating mammalian cells. Our studies were focused on the cellular effects of nickel (II) acetate, DNA-damaging agent, on Chinese hamster ovary (CHO) cells. Fragmented DNAs were examined by agarose gel electrophoresis and cell cycle was determined by DNA flow cytometry using propidium iodide fluorescence. Apparent DNA laddering was observed in cells treated with 240 microM nickel (II) and increased with a concentration-dependent manner. Treatment of nickel (II) acetate resulted in apoptosis which was accompanied by G2/M cell accumulation. Proportion of CHO cells in G2/M phase was also significantly increased in cells exposed to at least 480 microM nickel (II) from 57.7% of cells in the G0/G1 phase, 34.7% in the S phase, and 7.6% in the G2/M1 phase for 0 microM nickel (II), to 58.6%, 14.5%, and 26.9% for 640 microM nickel (II). These findings suggest that nickel (II) can modulate cellular response through some common effectors involving in both apoptotic and cell cycle regulatory pathways.
Animal ; Apoptosis/drug effects* ; CHO Cells/drug effects* ; CHO Cells/cytology ; Cell Cycle/drug effects* ; DNA Fragmentation/drug effects ; Flow Cytometry ; G2 Phase/drug effects ; Hamsters ; Mitosis/drug effects ; Nickel/pharmacology*

Endocrine disruptors are known to cause harmful effects to human through various exposure routes. These chemicals mainly appear to interfere with the endocrine or hormone systems. As importantly, numerous studies have demonstrated that the accumulation of endocrine disruptors can induce fatal disorders including obesity and cancer. Using diverse biological tools, the potential molecular mechanisms related with these diseases by exposure of endocrine disruptors. Recently, pathway analysis, a bioinformatics tool, is being widely used to predict the potential mechanism or biological network of certain chemicals. In this review, we initially summarize the major molecular mechanisms involved in the induction of the above mentioned diseases by endocrine disruptors. Additionally, we provide the potential markers and signaling mechanisms discovered via pathway analysis under exposure to representative endocrine disruptors, bisphenol, diethylhexylphthalate, and nonylphenol. The review emphasizes the importance of pathway analysis using bioinformatics to finding the specific mechanisms of toxic chemicals, including endocrine disruptors.
Computational Biology ; Endocrine Disruptors ; Humans ; Obesity