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

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

There is an error in a grant number in Acknowledgements.

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.

The p53 tumor suppressor has long been envisaged to preserve genetic stability by the induction of cell cycle checkpoints and apoptosis. More recently, p53 has been implicated to play roles in DNA repair responses to genotoxic stresses. UV-damage and the damage caused by certain chemotherapeutics including cisplatin and nitrogen mustards are known to be repaired by the nucleotide excision repair (NER) pathway which is reportedly regulated by p53 and its downstream genes. There are evidences to suggest that the base excision repair (BER) induced by the base-damaging agent methyl methanesulfonate (MMS) is partially deficient in cells lacking functional p53. This result suggests that the activity of BER might be also dependent on the p53 status. In this review, we discuss the possibilities that p53 regulates BER as well as NER; these are one of the most significant potentials of p53 tumor suppressor for repairing the vast majority of DNA damages that is incurred from various environmental stresses.
Animals ; Antineoplastic Agents/pharmacology ; DNA/drug effects ; *DNA Damage ; DNA Repair/*physiology ; Humans ; Mice ; Protein p53/*physiology ; Research Support, Non-U.S. Gov't

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

Periventricular leukomalacia is a major cause of neuro-developmental delay in premature infant. Although it develops in only a small percentage of preterm infants, the condition poses a major problem. The pathogenesis of periventricular leukomalacia is not well established. Because of the topography of the lesion, a decreased cerebral perfusion occurred before delivery is thought to be a critical pathogenetic factor. Therefore, hypoxic brain damage is thought to be a major cause of periventricular leukomalacia. The importance of neurochemically mediated injury to the white matter has been stressed. Recently, high incidence of placental chorioamnionitis with periventricular leukomalacia. We experienced a case of periventricular leukomalacia related to chorioamnionitis. The pathology of placenta was chorioamniontis, and it was thought to be a cause of periventricular leukomalacia. So, we report our case with a short literature review to ensuring that chorioamionitis without perinatal asphyxia cause a periventricular leukomalacia.
Asphyxia ; Chorioamnionitis* ; Female ; Humans ; Hypoxia, Brain ; Incidence ; Infant, Newborn ; Infant, Premature ; Leukomalacia, Periventricular* ; Pathology ; Perfusion ; Placenta ; Pregnancy