This study evaluated the consistency between two quantitative fit test devices with different methods of ambient aerosol counting. Three types of respirators (N95, half mask, and full facepiece) were worn by 50 participants (male, n = 25; female, n = 25), PortaCount (Pro+ 8038) and MT (05U) were connected to one probe to one mask, and fit factors (FFs) were measured simultaneously with the original and modified protocols. As a result of comparing MT FFs with PortaCount FFs as references and by applying for the pass/fail criteria (FF = 100), the consistency between the two devices for half masks and full facepieces was very high. N95 was somewhat weaker than the two type of respirators in the consistency; however, the correlation between the two devices was very strong (p < 0.0001). The results showed that an FF of 100 as measured by PortaCount was likely to be measured as 75 by the MT. Therefore, when performing the fit test for N95 using the MT and pass level of FF 100, a certain level of adjustment is necessary, whether end-user or putting a scaling factor by manufacturer.

PURPOSE: Angiogenesis is involved in the pathogenesis of chronic rhinosinusitis with nasal polyps. We aimed to investigate the effects of prostaglandin E2 (PGE2) on vascular endothelial growth factor (VEGF) production, the role of E-prostanoid (EP) 4 receptors, and the signal transduction pathway mediating VEGF production in nasal polyp-derived fibroblasts (NPDFs). METHODS: Eight primary NPDF cultures were established from nasal polyps, which were incubated with or without PGE2. Reverse transcription-polymerase chain reaction amplification of EP receptors (EP1, EP2, EP3, and EP4) and immunofluorescence staining for VEGF production were performed. VEGF production via the cyclic adenosine monophosphate (cAMP)-dependent protein kinase A (PKA) and phosphatidylinositol 3-kinase (PI3K) pathways was evaluated by enzyme-linked immunosorbent assay. RESULTS: All EP receptors were expressed in NPDFs. PGE2 significantly increased VEGF production concentration- and time dependently, and VEGF production was regulated by an EP4 receptor. Activation of intracellular cAMP regulated VEGF production. VEGF production was decreased by PKA and PI3K inhibitors via intracellular cAMP. CONCLUSIONS: PGE2 stimulates VEGF production via the EP4 receptor in NPDFs. These results indicate that PGE2-induced VEGF production is mediated, at least partially, through cAMP-dependent signaling pathways. Therapies targeting the EP4 receptor may be effective in inhibiting the development of nasal polyps.
Adenosine Monophosphate ; Cyclic AMP-Dependent Protein Kinases ; Dinoprostone ; Fibroblasts ; Fluorescent Antibody Technique ; Nasal Polyps ; Negotiating ; Phosphatidylinositol 3-Kinase ; Signal Transduction ; Vascular Endothelial Growth Factor A

BACKGROUND: Leukocyte reduction filters are widely used to prevent transfusion reactions caused by leukocytes in blood components. Commercial filters are not sufficient for removal of leukocytes for prevention of transfusion associated graft-versus-host disease; therefore, irradiation of blood components was performed using expensive equipment. Techniques using an aptamer substituted for antibody have been developed and are available in clinical areas. The purpose of this study is to develop the aptamer filter system and to evaluate its efficiency and the possibility of its clinical application. METHODS: Aptamers targeted to CD45 were selected by the Postech Aptamer Initiative. The aptamer filter in which aptamers attached to beads were bound to leukocytes and removed by magnetic field was developed. Filtration of 14 units of leukoreduction-red blood provided by Korean Red Cross Blood Services was performed using aptamer filters. Leukocyte removal rate and red cell recovery rate were evaluated and bacterial culture was performed. RESULTS: After filtration using the aptamer filters, 45.6% of leukocytes were additionally removed and the red cell recovery rate was 92.8%. No growth in the bacterial culture was observed. CONCLUSION: In order to apply the cell depletion technique utilizing an aptamer to blood filter system, we developed and evaluated the aptamer filter system. Through improvement of the binding efficiency of the aptamer and the filtering process, and application of the various aptamers for other different cells, we suggest that this technique can be applied in the clinical area, such as a substitution for the irradiation process for TAGVHD prevention.
Blood Group Incompatibility ; Filtration ; Leukocytes ; Magnetic Fields ; Red Cross

Solid pseudopapillary tumors are rare primary neoplasms of the pancreas that have a relatively favorable prognosis, with a low malignant potential. Most patients present with non-specific clinical features, such as vague abdominal discomfort and a palpable abdominal mass. A 50-year-old woman who presented with hematemesis had an incidental pancreatic cystic mass on abdominal computed tomography (CT). We performed several tests, including upper endoscopy and angiography, but we could not find the bleeding focus. Therefore, we performed a pancreaticoduodenectomy. At laparotomy, there was a 10-cm encapsulated pancreatic mass with duodenal invasion, which showed a bleeding ulcer. A solid pseudopapillary tumor was diagnosed pathologically. We report a solid pseudopapillary tumor that presented with gastrointestinal bleeding.
Angiography ; Endoscopy ; Female ; Hematemesis ; Hemorrhage ; Humans ; Laparotomy ; Middle Aged ; Pancreas ; Pancreatic Cyst ; Pancreaticoduodenectomy ; Prognosis ; Ulcer

PURPOSE: The tumor suppressor gene, p53, has been established as an essential component for the suppression of tumor cell growth. In this study, we investigated the time-course anticancer effects of adenoviral p53 (Adp53) infection on human ovarian cancer cells to provide insight into the molecular-level understanding of the growth suppression mechanisms involved in Adp53-mediated apoptosis and cell cycle arrest. MATERIALS AND METHODS: Three human cervical cancer cell lines (SiHa, CaSki, HeLa and HT3) were used. The effect of Adp53 infection was studied via cell count assay, cell cycle analysis, FACS, Western blot and macroarray assay. RESULTS: Adp53 exerts a significant role in suppressing cervical cancer cell growth. Adp53 also showed growth inhibitory effects in each cell line, and it induced apoptosis and cell cycle arrest. Adp53 differentially regulated the expression of genes and proteins, and the gene expression profiles in the SiHa cells revealed that the p21, p53 and mdm2 expressions were significantly up-regulated at 24 and 48 hr. Western blot shows that the p21 and p53 expressionlevels were significantly increased after Adp53 infection. In addition, in all cell lines, both the CDK4 and PCNA protein expression levels were decreased 48 h after Adp53 infection. Cell cycle arrest at the G1 phase was induced only in the SiHa and HeLa cells, suggesting that exogenous infection of Adp53 in cancer cells was significantly different from the other HPV-associated cervical cancer cells. CONCLUSION: Adp53 can inhibit cervical cancer cell growth through induction of apoptosis and cell cycle arrest, as well as through the regulation of the cell cycle-related proteins. The Adp53-mediated apoptosis can be employed as an advanced strategy for developing preferential tumor cell-specific delivery.
Adenoviridae* ; Apoptosis ; Blotting, Western ; Cell Count ; Cell Cycle Checkpoints ; Cell Cycle* ; Cell Line ; G1 Phase ; Genes, Tumor Suppressor ; Genetic Therapy ; HeLa Cells ; Humans* ; Ovarian Neoplasms ; Papilloma* ; Proliferating Cell Nuclear Antigen ; Transcriptome ; Uterine Cervical Neoplasms*

PURPOSE: Screening in cervical cancer is now progressing to discover candidate genes and proteins that may serve as biological markers and that play a role in tumor progression. We examined the protein expression patterns of the squamous cell carcinoma (SCC) tissues from Korean women with using two-dimensional polyacrylamide gel electrophoresis (2-DE) and matrix assisted laser desorption/ionization-time of flight (MALDI-TOF) mass spectrometer. MATERIALS AND METHODS: Normal cervix and SCC tissues were solubilized and 2-DE was performed using pH 3~10 linear IPG strips of 17 cm length. The protein expression was evaluated using PDQuest 2-D software(TM). The differentially expressed protein spots were identified with a MALDI-TOF mass spectrometer, and the peptide mass spectra identifications were performed using the Mascot program and by searching the Swiss-prot or NCBInr databases. RESULTS: A total of 35 proteins were detected in SCC. 17 proteins were up-regulated and 18 proteins weredown-regulated. Among the proteins that were identified, 12 proteins (pigment epithelium derived factor, annexin A2 and A5, keratin 19 and 20, heat shock protein 27, smooth muscle protein 22 alpha, alpha-enolase, squamous cell carcinoma antigen 1 and 2, glutathione S-transferase and apolipoprotein a1) were protein previously known to be involved in tumor, and 21 proteins were newly identified in this study. CONCLUSION: 2-DE offers the total protein expression profiles of SCC tissues; further characterization of these differentially expressed proteins will give a chance to identify the badly needed tumor-specific diagnostic markers for SCC.
Annexin A2 ; Apolipoproteins ; Biomarkers ; Carcinoma, Squamous Cell ; Cervix Uteri ; Databases, Protein ; Electrophoresis, Polyacrylamide Gel ; Epithelium ; Female ; Glutathione Transferase ; HSP27 Heat-Shock Proteins ; Humans ; Hydrogen-Ion Concentration ; Keratin-19 ; Mass Screening ; Muscle, Smooth ; Phosphopyruvate Hydratase ; Uterine Cervical Neoplasms*

OBJECTIVE: Cervical cancer has long been linked to the sexually transmitted human papillomavirus (HPV), and the oncoproteins E6 and E7 disrupt the functions of tumour suppressor genes, resulting in genetic alteration. It was shown that loss of heterozygosity at 6p is a common genetic alteration in cervical cancer. However, the molecular genetics of cancer have only recently been understood, and for the development of cervical cancer additional genetic alterations in host cell genes are required. The present study has identified the differential changes of the cervical cancer-associated genetic alterations by a genome-wide array based comparative genomic hybridization (array-CGH). METHODS: We analyzed 15 cases of cervical cancer from St. Mary's hospital of The paraffin-fixed tissue samples were microdissected under microscope and DNA was extracted by the procedures of proteinase K digestion and chloroform extraction. Array-based CGH and genomic PCR were carried out with statistical analyses such as hierarchical clustering and Gene Ontology. The BAC array used in this study consisted of 1,440 human BACs, the space among the clones were approximately 2.08 megabase (Macrogen, Seoul, Korea). RESULTS: All of 15 cases of cervical cancer showed specific gains and losses. The analysis limit of average gains and losses was 53%. A significant positive correlation was found between 1p36.32, 3p14.2, 3q27.1, 7p21.1, 8q24.3 and 11q13.1 changes through the cervical carcinogenesis. The high-level of gain regions, BAC clones encoded GSDMDC1, RECQL4, TP73, ABCF3, ALG3, HDAC9, ESRRA and RPS6KA4 genes. Frequently gained BAC clones encoded genes were PRSS8, FUS, COL18A1, PCOLN3, MAFG and ASPSCR1. The genes encoded by frequently lost BAC clones were PTPRG, GRM7, ZDHHC3, EXOSC7, LRP1B and NR3C2. Also, hierarchical clustering of the expression data readily distinguished genomic alterations in cervical cancer. A subset of cellular processes from each gene was clustered by Gene Ontology database. CONCLUSION: Using Array-CGH, genomic alterations related to cervical cancer were identified to determine whether induction of chromosomal imbalances occurs prior to carcinogenesis. The high resolution of array-CGH combined with human genome database would give a chance to find out possible target genes present in the gained or lost clones.
Carcinogenesis ; Chloroform ; Clone Cells ; Comparative Genomic Hybridization ; Digestion ; DNA ; Endopeptidase K ; Gene Ontology ; Genes, Suppressor ; Genome, Human ; Humans ; Loss of Heterozygosity ; Molecular Biology ; Oncogene Proteins ; Polymerase Chain Reaction ; Seoul ; Uterine Cervical Neoplasms*

OBJECTIVE: Previous studies were showed that adenoassocited virus (AAV) infection was had negative effects on human papillomavirus (HPV) infection and that the cervical cancer cell growth is inhibited by AAV infection. We detected of AAV 2 and high-risk HPV infection and researched correlation with AAV 2 and HPV in cervical cell. METHODS: Cell of normal cervix (49 persons), infected HPV cervix (45 persons), cervical intraepithelial neoplasm (CIN) I (31 persons), II (20 persons), III (35 persons), and invasive cancer (30 persons) were investigated by PCR using AAV-2 and HPV type 16 and 18 specific primers. RESULTS: AAV 2 was detected in 8 out of 49 normal cervix (16.3%), 2 out of 45 infected HPV cervix (4.4%), 3 out of 31 CIN I (9.7%), 4 out of 20 CIN II (20%), 8 out of 35 CIN III (22.8%), and 3 out of 30 invasive cervical cancer cases (30%). However, HPV 16 was detected in 5 out of 49 normal cervix (10.2%), 20 out of 45 infected HPV cervix (44.4%), 13 out of 31 CIN I (42%), 11 out of 20 CIN II (55%), 19 out of 35 CIN III (54.3%), and 21 out of 30 invasive cervical cancer cases (70%). HPV 18 was detected in 6 out of 49 normal cervix (12.2%), 18 out of 45 infected HPV cervix (40%), 16 out of 31 CIN I (51.6%), 10 out of 20 CIN II (50%), 22 out of 35 CIN III (62.8%), and 13 out of 30 invasive cervical cancer cases (43.3%). CONCLUSION: AAV 2 was detected in normal and infected HPV cervix, CIN (I, II, III) and invasive cervical cancer. As compared to normal, CIN I and CIN II, suggesting significant correlation between AAV 2 and HPV type 16. Further, researches continue to be done relationship to AAV 2 and HPV infection in cervix.
Cervical Intraepithelial Neoplasia ; Cervix Uteri* ; Female ; Human papillomavirus 16 ; Human papillomavirus 18 ; Humans* ; Polymerase Chain Reaction ; Uterine Cervical Neoplasms

OBJECTIVE: The aim of this study was to investigate the gene expression profiles using GeneFishing(TM) DEG kit in Korean women with cervical squamous cell carcinoma. METHODS: Cervical cancer biopsies were obtained from patients at the Department of Obstetrics and Gynecology, St. Mary's hodpital. In this study, we used a common reference that was mixed with an equal amount of RNA extracted from non-cervical cancer patients. The profiles of expression genes between cervical normal and squamous cell carcinoma tissue were identified using GeneFishing(TM) DEG Kit and screened by BLAST search. RESULTS: Almost 100 differential expressed genes were identified in universal control and cervical squamous cell carcinoma, 53 of differential expressed genes, up-regulated expression of 32 and 21 down-regulated expression was sequenced. Up-regulated genes were calcylin, calgranulin A, TRK oncogene, HLC5, fibrillarin, collagene type I alpha1 etc. and down-regulated genes were galectin 1, PRP8 pre-mRNA precessing factor 8 homology, clusterin etc. CONCLUSION: We identified gene expression profile in cervical squamous cell carcinoma using GeneFishing(TM) Kit in Korean women. The functional genomics of these genes should be further studied.
Biopsy ; Calgranulin A ; Carcinoma, Squamous Cell* ; Clusterin ; Collagen ; Female ; Galectin 1 ; Gene Expression* ; Genomics ; Gynecology ; Humans ; Obstetrics ; Oncogenes ; Polymerase Chain Reaction* ; RNA ; RNA Precursors ; Transcriptome ; Uterine Cervical Neoplasms

PURPOSE: Human papillomavirus (HPV) infection has a significant role in cervical carcinogenesis, and HPV oncoprotein E7 plays an important part in the formation and maintenance of cervical cancer. Interleukin-12 (IL-12) has been reported to induce a cellular immune response, and to suppress the tumor growth and the E7 production. Here we describe the use of adenoviral delivery of the HPV 16 E7 subunit (AdE7) along with adenoviral delivery of IL-12 (AdIL-12) in mice with HPV-associated tumors. MATERIALS AND METHODS: Mice were injected with TC-1 cells to establish TC-1 tumor, and then they were immunized with AdIL-12 and/or AdE7 intratumorally. The anti tumor effects induced by AdIL-12 and/or E7 were evaluated by measuring the size of the tumor. E7-specific antibody and INF-gamma production in sera, and the T-helper cell proliferative responses were then measured. Cytotoxic T-lymphocyte (CTL) and T cell subset depletion studies were also performed. RESULTS: Combined AdIL-12 and AdE7 infection at the tumor sites significantly enhanced the antitumor effects more than that of AdIL-12 or AdE7 single infection. This combined infection resulted in regression of the 9 mm sized tumors in 80% of animals as compare to the PBS group. E7-specific antibody and INF-gamma production in the sera, and the T-helper cell proliferative responses were significantly higher with coinfection of AdIL-12 and AdE7 than with AdIL-12 or AdE7 alone. CTL response induced by AdIL-12 and AdE7 in the coinjected group suggested that tumor suppression was mediated by mostly CD8+ and only a little by the CD4+ T cells. CONCLUSION: IL-12 and E7 application using adenovirus vector showed antitumor immunity effects against TC-1 tumor, and this system could be use in clinical applications for HPV-associated cancer.
Adenoviridae ; Animals ; Carcinogenesis ; Coinfection ; Human papillomavirus 16 ; Humans* ; Immunity, Cellular ; Immunization* ; Interleukin-12* ; Mice ; T-Lymphocytes ; T-Lymphocytes, Cytotoxic ; Uterine Cervical Neoplasms