No abstract available.
Paragonimiasis*

Chlamydia trachomatis is known as a major causative microorganism in non-gonococcal urethritis(NGU) in men. We examined two kinds of specimens simultaneously, endourethral swab and urine, in each patient to determine the reliability of these two different specimens for the detection of the Chlamydia trachomatis antigen in male NGU patients using ELISA method. Tota1 273 patients entered this study were divided into two groups according to sampling order of urine and endourethral swab. In group A(141 patients), we took endourethral swab first, then first portion of voided urine was caught. In group B(132 patients), endourethral swab was performed after urine sampling. Twenty five out of 273 patients(9.2%) showed Chlamydia trachomatis antigen positive in endourethral swab sample and 1 out of 273 patients(0.4%) was positive in urine sample. There was no significant difference of antigen positive rate of endourethral swab examination between group A and group B. Our data suggest that examination of endourethral swab is more reliable method for the detection of the Chlamydia trachomatis antigen than urine examination in male NGU patient.
Chlamydia trachomatis* ; Chlamydia* ; Enzyme-Linked Immunosorbent Assay ; Humans ; Male

No abstract available.
Erythropoietin* ; Humans* ; Kidney Failure, Chronic*

BACKGROUND: Left ventricular hypertrophy(LVH) is one of the complications of hypertension and has been known as an independent risk factor of cardiovascular complications. Recently, it has been reported that hypertensive patients with LVH had the most advanced extracardiac target-organ damage compared with other groups. Previous reports have shown that mean plasma atrial natriuretic peptide(ANP) and brain natriuretic peptide(BNP) levels in hypertensive patients are higher than in normotensive subjects. Therefore, in this study, we investigated the relationships between the plasma ANP and BNP levels and the degree of LVH in hypertensive patients and in normotensive subjects and also investigated the clinical significance of measurement of plasma ANP and BNP levels. METHODS: In all study subjects, left ventricle mass index(LVMI) and left ventricle geometry were measured by M-mode echocardiography. Measurements were made by the recommendations of the American Society of Echocardiography. Plasma ANP and BNP levels were measured by radioimmunoassay method. RESULTS: 1) 57% of the hypertensive patients had eccentric hypertrophy and 6% had concentric hypertrophy. 2) LV mass and LVMI of normotensive subjects and hypertensive patients were 169+/-53 g, 229+/-64 g and 99+/-27.3 g/m2, 142+/-37.7 g/m2, respectively(P<0.05). 3) There were statistically significant correlations between blood pressure and LVMI in all subjects(r=.43, P<0.05). 4) Plasma ANP levels were significantly increased in hypertensive patients than normotensive subjects (28.2+/-14.3 pg/mL and 42.8+/-26 pg/mL, respectively; P<0.05). 5) Plasma BNP levels were significantly increased in hypertensive patients than normotensive subjects (18.4+/-5.4 pg/mL and 36.5+/-26 pg/mL; respectively, P<0.05). 6) Plasma BNP levels were significantly increased in 63% of the hypertensive patients with LVH(P<0.05). 7) There were statistically significant correlations between blood pressure and plasma ANP and BNP levels(ANP:r=.39, p<0.05, BNP:r=.31, P<0.05). CONCLUSIONS: Plasma ANP and BNP levels were increased in the hypertensive patients but only plasma BNP levels were significantly increased in the hypertensive patients with LVH. Measurement of plasma BNP levels may be useful for early detection of LVH, an independent risk factor of cardiovascular complications. Therefore intensive blood pressure control in these patients may reduce cardiovascular morbidity and mortality.
Atrial Natriuretic Factor ; Blood Pressure ; Brain* ; Echocardiography ; Heart Ventricles ; Humans ; Hypertension* ; Hypertrophy ; Hypertrophy, Left Ventricular ; Mortality ; Natriuretic Peptides* ; Plasma* ; Radioimmunoassay ; Risk Factors

Pneumocephalus is the presence of intracranial air, the most common cause of which is head trauma that allows contact between the intracranial cavity and the atmosphere. Pneumocephalus, commonly associated with increased intracranial pressure, causes rapid neurologic deterioration requiring emergent intervention. Recently, endoscopic sinus surgery techniques have been used in the diagnosis and repair of cerebrospinal fluid leaks. We present a case in which endoscopic techniques were used to treat pneumocephalus that occurred three years after head trauma. The procedure for and advantages of the endoscopic endonasal approach over the external approach are presented in this paper.
Atmosphere ; Craniocerebral Trauma ; Intracranial Pressure ; Pneumocephalus

The aim of the present study was to investigate the physiological role of nicotinamide phosphoribosyltransferase (NAMPT) associated with odontogenic differentiation during tooth development in mice. Mouse dental papilla cell-23 (MDPC-23) cells cultured in differentiation media were stimulated with the specific NAMPT inhibitor, FK866, and Visfatin (NAMPT) for up to 10 days. The cells were evaluated after 0, 4, 7, and 10 days. Cell viability was measured using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. The mineralization assay was performed by staining MDPC-23 cells with Alizarin Red S solution. After cultivation, MDPC-23 cells were harvested for quantitative PCR or Western blotting. Analysis of variance was performed using StatView 5.0 software (SAS Institute Inc., Cary, NC, USA). Statistical significance was set at p < 0.05. The expression of NAMPT increased during the differentiation of murine odontoblast-like MDPC-23 cells. Furthermore, the up-regulation of NAMPT promoted odontogenic differentiation and accelerated mineralization through an increase in representative odontoblastic biomarkers, such as dentin sialophosphoprotein, dentin matrix protein-1, and alkaline phosphatase in MDPC-23 cells. However, treatment of the cells with the NAMPT inhibitor, FK866, attenuated odontogenic differentiation, as evidenced by the suppression of odontoblastic biomarkers. These data indicate that NAMPT regulated odontoblastic differentiation through the regulation of odontoblastic biomarkers. The increase in NAMPT expression in odontoblasts was closely related to the formation of the extracellular matrix and dentin via the Runx signaling pathway. Therefore, these data suggest that NAMPT is a critical regulator of odontoblast differentiation during tooth development.

Demethoxycurcumin (DMC), which is a curcuminoid found in turmeric, has anti-proliferative effects on cancer cells. However, the effect of DMC on osteosarcoma has not been established. The aim of this study was to examine the effects of DMC on cell growth and apoptosis induction in MG-63 human osteosarcoma cells. This study was investigated using 3-[4, 5-dimethylthiazol-2-yl]-2, 5 diphenyl tetrazolium bromid assay, Live/Dead cell assay, 4’, 6-diamidino-2-phenylindole staining, and immunoblotting in MG-63 cells. DMC induced MG-63 cell death in a dosedependent manner, with an estimated IC50 value of 54.4 μM. DMC treatment resulted in nuclear condensation in MG-63 cells. DMC-induced apoptosis in MG-63 cells was mediated by the expression of Fas and activation of caspase-8, caspase-3, and poly (ADP-ribose) polymerase. Immunoblotting results showed that Bcl-2 and Bcl-xL were downregulated, while Bax and Bad were upregulated by DMC in MG-63 cells. These results indicated that DMC inhibits cell proliferation and induces apoptotic cell death in MG-63 human osteosarcoma cells via the death receptormediated extrinsic apoptotic pathway and mitochondria-mediated intrinsic apoptotic pathway.

Demethoxycurcumin (DMC), which is a curcuminoid found in turmeric, has anti-proliferative effects on cancer cells. However, the effect of DMC on osteosarcoma has not been established. The aim of this study was to examine the effects of DMC on cell growth and apoptosis induction in MG-63 human osteosarcoma cells. This study was investigated using 3-[4, 5-dimethylthiazol-2-yl]-2, 5 diphenyl tetrazolium bromid assay, Live/Dead cell assay, 4’, 6-diamidino-2-phenylindole staining, and immunoblotting in MG-63 cells. DMC induced MG-63 cell death in a dosedependent manner, with an estimated IC50 value of 54.4 μM. DMC treatment resulted in nuclear condensation in MG-63 cells. DMC-induced apoptosis in MG-63 cells was mediated by the expression of Fas and activation of caspase-8, caspase-3, and poly (ADP-ribose) polymerase. Immunoblotting results showed that Bcl-2 and Bcl-xL were downregulated, while Bax and Bad were upregulated by DMC in MG-63 cells. These results indicated that DMC inhibits cell proliferation and induces apoptotic cell death in MG-63 human osteosarcoma cells via the death receptormediated extrinsic apoptotic pathway and mitochondria-mediated intrinsic apoptotic pathway.

The present study was carried out to investigate the effect of Arctigenin on cell growth and the mechanism of cell death elicited by Arctigenin were examined in FaDu human pharyngeal carcinoma cells. To determine the apoptotic activity of Arctigenin in FaDu human pharyngeal carcinoma cells, cell viability assay, DAPI staining, caspase activation analysis, and immunoblotting were performed. Arctigenin inhibited the growth of cells in a dose-dependent manner and induced nuclear condensation and fragmentation. Arctigenin-treated cells showed caspase-3/7 activation and increased apoptosis versus control cells. FasL, a death ligand associated with extrinsic apoptotic signaling pathways, was up-regulated by Arctigenin treatment. Moreover, caspase-8, a part of the extrinsic apoptotic pathway, was activated by Arctigenin treatments. Expressions of anti-apoptotic factors such as Bcl-2 and Bcl-xL, components of the mitochondria-dependent intrinsic apoptosis pathway, significantly decreased following Arctigenin treatment. The expressions of pro-apoptotic factors such as BAX, BAD and caspase-9, and tumor suppressor -53 increased by Arctigenin treatments. In addition, Arctigenin activated caspase-3 and poly (ADP-ribose) polymerase (PARP) induced cell death. Arctigenin also inhibited the proliferation of FaDu cells by the suppression of p38, NF-κB, and Akt signaling pathways. These results suggest that Arctigenin may inhibit cell proliferation and induce apoptotic cell death in FaDu human pharyngeal carcinoma cells through both the mitochondria-mediated intrinsic pathway and the death receptormediated extrinsic pathway.

PURPOSE: To maintain the homeostasis of stem cells and prevent their ability to initiate tumorigenesis, it is important to identify and modify factors that prevent or accelerate stem cell senescence. We used microarrays to attempt to identify such factors in human amniotic fluid (HAF)-derived stem cells. MATERIALS AND METHODS: To identify gene expression changes over a time course, we compared gene expression profiles of HAF-derived stem cells in different passages (1st, 2nd, 4th, 6th, 8th, and 10th) using a Sentrix Human illumina microarray. RESULTS: Of the 25,804 genes in the microarray chip, 1,970 showed an over 2-fold change relative to the control (the 1st passage)-either upregulated or downregulated. Quantitative real-time PCR validated the microarray data for selected genes: markedly increased genes were CXCL12, cadherin 6 (CDH6), and folate receptor 3 (FOLR3). Downregulated genes included cyclin D2, keratin 8, insulin-like growth factor 2 (IGF2), natriuretic peptide precursor B (NPPB) and cellular retinoic acid binding protein 2 (CRABP2). The expression pattern of the selected genes was consistent with the microarray data except for CXCL12 and IGF2. Interestingly, the expression of NPPB was dramatically downregulated along the time course; it was almost completely shut-down by the 10th passage. In contrast, FOLR3 mRNA expression was dramatically increased. CONCLUSION: Taken together, although a function for NPPB and FOLR3 in stem cell senescence has not been reported, our results strongly suggest that NPPB and/or FOLR3 play a significant role in the regulation of stem cell senescence.
Aging ; Amniotic Fluid ; Carrier Proteins ; Cell Transformation, Neoplastic ; Cyclin D2 ; Female ; Folic Acid ; Gene Expression ; Homeostasis ; Humans ; Keratin-8 ; Nitrobenzoates ; Real-Time Polymerase Chain Reaction ; RNA, Messenger ; Stem Cells ; Transcriptome ; Tretinoin