Conservation and diversification of the transcriptomes of adult Paragonimus westermani and P. skrjabini.

BACKGROUND: Paragonimiasis is an important and widespread neglected tropical disease. Fifteen Paragonimus species are human pathogens, but two of these, Paragonimus westermani and P. skrjabini, are responsible for the bulk of human disease. Despite their medical and economic significance, there is limited information on the gene content and expression of Paragonimus lung flukes. RESULTS: The transcriptomes of adult P. westermani and P. skrjabini were studied with deep sequencing technology. Approximately 30 million reads per species were assembled into 21,586 and 25,825 unigenes for P. westermani and P. skrjabini, respectively. Many unigenes showed homology with sequences from other food-borne trematodes, but 1,217 high-confidence Paragonimus-specific unigenes were identified. Analyses indicated that both species have the potential for aerobic and anaerobic metabolism but not de novo fatty acid biosynthesis and that they may interact with host signaling pathways. Some 12,432 P. westermani and P. skrjabini unigenes showed a clear correspondence in bi-directional sequence similarity matches. The expression of shared unigenes was mostly well correlated, but differentially expressed unigenes were identified and shown to be enriched for functions related to proteolysis for P. westermani and microtubule based motility for P. skrjabini. CONCLUSIONS: The assembled transcriptomes of P. westermani and P. skrjabini, inferred proteins, and extensive functional annotations generated for this project (including identified primary sequence similarities to various species, protein domains, biological pathways, predicted proteases, molecular mimics and secreted proteins, etc.) represent a valuable resource for hypothesis driven research on these medically and economically important species.

[Screening and analysis of peptides specifically binding to the schistosomulum tegument of Schistosoma japonicum].

OBJECTIVE: To screen and analyze the peptides in 12 phage-display peptide library specifically binding to the schistosomulum, not cercaria, tegument of Schistosoma japonicum. METHODS: A 12 phage-display peptide library was screened with the S. japonicum schistosomula and cercariae as the target cells for biopanning by degrees, 15 positive clones were picked randomly and deduced by DNA sequencing. According the sequencing result, ELISA test, elution recovery test and immunohistochemical staining were performed to determine the specificity of the phages to the tegument. To further examine its binding properties, the positive peptide conjugated to RhB and recombinant pEGFP-C2 plasmid were similarly synthesized. RESULTS: After 3 rounds of biopanning, the phage recovery rate increased from 3.50 x 10(-5)% to 3.20 x 10(-2)%, indicating that the phage library was successfully enriched in the tegument of schistosomula. The analyzed sequences were identical with 3 peptide sequence of ZL6, ZL4 and ZL1. ELISA showed that the P/N value of MppZL4, MppZL6 and MppZL binding the schistosomulum membrane protein was 6.72, 3.65 and 2.22, while 1.58, 5.15 and 1.20 of binding the membrane protein of cercariae, respectively. Elution recovery test showed that the elution recovery rate of MppZL4 [(4.60 +/- 0.27) x 10(-2)%] was much higher than that of MppZL6 [(2.10 +/- 0.23) x 10(-3)%], MppZL1 [(1.20 +/- 0.28) x 10(-3)%] and M13KE [(1.30 +/- 0.60) x 10(-7)%] (P<0.01). Immunohistochemical staining showed that MppZL4 specifically bound to the tegument of schistosomula with a positive rate of 83.0% (83/100). Fluorescent microscopy revealed that the synthesized RhB-ZL4 bound to the tegument of schistosomula. The ZL4/pEGFP-C2 plasmid was introduced into juvenile S. japonicum and expressed in the parasite. CONCLUSION: The peptide of ZL4 specifically binds to the schistosomulum tegument but not to that of cercaria.

XPERNATO-TOX: an Integrated Toxicogenomics Knowledgebase

Toxicogenomics combines transcriptome, proteome and metabolome profiling with conventional toxicology to investigate the interaction between biological molecules and toxicant or environmental stress in disease caution. Toxicogenomics faces the problems of comparison and integration across different sources of data. Cause of unusual characteristics of toxicogenomic data, researcher should be assisted by data analysis and annotation for getting meaningful information. There are already existing repositories which claim to stand for toxicogenomics database. However, those just contain limited abilities for toxicogenomic research. For supporting toxicologist who comes up against toxicogenomic data flood, now we propose novel toxicogenomics knowledgebase system, XPERANTO-TOX. XPERANTO-TOX is an integrated system for toxicogenomic data management and analysis. It is composed of three distinct but closely connected parts. Firstly, Data Storage System is for reposit many kinds of '-omics' data and conventional toxicology data. Secondly, Data Analysis System consists of analytical modules for integrated toxicogenomics data. At last, Data Annotation System is for giving extensive insight of data to researcher.

[Study on the theory of "selection of distal acupoints"].

The meridians belong to zang-fu organs inside and connect with the extremities outside. They keep information exchange among different tissues and make various organs of the human body as an organic whole. If the meridians are blocked and the information exchange makes mistake, the body will produce pathologic changes. Because the location of the blocked part is difficult to identify, in this paper it is explained that selection of distal acupoints is the best way to dredge the nodes of disease, and the theoretical basis is closely related with the theories of "the root cause and symptoms of a disease", "Genjie", and "Jing, Xing, Shu, Jing, He", and also implies the thought of "to cure a disease must treat the root of the disease".

Genetic Polymorphism of Xenobiotics Metabolizing Enzymes and Individual Susceptible Genes to Colorectal Cancer Patients in Korea

Individual susceptibility to cancers may result from several factors including differences in xenobiotics metabolism, DNA repair, altered oncogenes and suppressor genes, and environmental carcinogen exposures. To determine the frequencies of the genotypes of phase I (CYP1A1 and CYP2E1) and phase II (GSTM1 and NAT2) metabolizing enzymes and to identify the high-risk genotypes of these metabolic enzymes to colon cancer in Korean, we have analyzed 113 colorectal cancer patients and corresponding age and sex matched healthy controls using polymerase chain reaction-restriction fragment length polymorphi(PCR-RFLP). In analysis of phase I enzymes, m1/m2, m2/m2 and Val/Val genotypes in CYP1A1 enzyme polymorphisms and C1/C2 genotype in CYP2E1 polymorphism were associated with high relative risks to colorectal cancers (Odds ratio; 1.51, 1.59, 1.76 and 1.38, respectively). Among the phase II enzymes polymorphisms, GSTM (-) genotype of GSTM1 enzyme and slow acetylator (S/S) of NAT2 enzyme had 1.48 and 1.34 times of relative risks to colorectal cancers, respectively. In combined genotyping of phase I enzymes and GSTM1 polymorphisms, the patients with m1/m2 and GSTM (-), Val/Val and GSTM (-), and C1/C2 and GSTM (-) combined genotypes had higher relative risk than the patients with each baseline of combined genotypes (Odds ratio; 2.15, 5.81 and 2.20, respectively). In combined genotyping of phase I enzyme and NAT2 polymorphisms, the combined genotypes of m1/m2 with slow acetylator and C1/C2 with slow acetylator were more susceptible to colorectal cancer (Odds ratio; 3.5 and 4.5, respectively). These results suggest that the combined genotypes of Val/Val and GSTM (-), m1/m2 and slow acetylator, and C1/C2 and slow acetylator were more susceptible to colorectal cancer in Korean. And genotyping of xenobiotics metabolizing enzymes could be useful for predicting an individual susceptibility to colorectal cancer.

Role of Immune-Inflammatory Mechanisms in Alzheimer's Disease and Other Degenerative Diseases

Recent studies suggest that alterations of the immune-inflammatory system contribute to the pathogenesis of Alzheimer's disease (AD), Parkinson's disease (PD) and Amyotrophic Lateral Sclerosis (ALS). Neuroinflammatory response initiated by innate immune mechanism that self-attack on neurons, known as "autotoxicity" could be an initial key mechanism of chronic neurodegenerative diseases. Numerous experimental and pathological evidences showing upregulated inflammatory cytokines and chemokines, and the activation of complement cascade and accumulation of activated microglia in damaged regions support the important role of immune-inflammatory mechanism in the pathogenesis of neurodegenerative diseases. Epidemiological studies on the non-steroidal anti-inflammatory drugs (NSAIDs), coupled with results from animal model of AD, PD and ALS, have prompted the studies to determine if immune-inflammatory modifying agents or molecules could be a new therapeutic paradigm of neurodegenerative diseases. Molecules inhibiting proinflammatory cytokines and chemokines released from microglia, agents that inhibit activation of microglia, COX2 and complement system are now considered as a good candidate of immune-inflammatory modulating treatment. By better understanding inflammatory and immunoregulatory processes, it should be possible to develop anti-inflammatory approach that may not completely cure AD, PD, and ALS but will likely help slow the progression or delay the onset of these devastating diseases.

Poly (ADP-Ribose) Polymerase immunoreactivity in Motor Neurons and Astrocytes in the Spinal Cord of Sporadic Amyotrophic Lateral Sclerosis Patients

BACKGROUND: The evidence for increased oxidative stress and DNA damage in amyotrophic lateral sclerosis (ALS) prompted studies to determine if the expression of poly (ADP-ribose) polymerase (PARP) is increased in ALS. METHOD: Twenty Spinal cord specimens were obtained at the autopsy of sALS patients (n=11) and age-matched controls with non-neurological diseases (n=9). RESULTS: Using western analyses of postmortem tissue, we demonstrated that PARP-immunoreactivity (PARP-IR) was increased three-fold in spinal cord tissues of sporadic ALS (sALS) patients compared with non-neurological disease controls. Despite the increased PARP-IR, PARP mRNA expression was not increased significantly. Immunohistochemical analyses revealed PARP-IR was increased in both white and gray matter of sALS spinal cord. While PARP-IR was predominantly seen in astrocytes, large motor neurons displayed reduced staining compared with the controls. PARP-IR was increased in the pellet fraction of sALS homogenates compared with the control homogenates, representing potential PARP binding to chromatin or membranes and suggesting a possible mechanism of PARP stabilization. CONCLUSIONS: The present results demonstrate glial alterations in sALS tissue and support the role of glial alterations in sALS pathogenesis.

Increased Neuronal and Glial Poly (ADP-Ribose) Polymerase Immunoreactivity in the Brain of Sporadic Amyotrophic Lateral Sclerosis

BACKGROUND: Over activation of the DNA repairing enzyme, poly (ADP-ribose) polymerase (PARP) in response to oxidative damage of DNA appears to play a role in cellular death in neurodegenerative diseases. Previous data suggested that PARP immunoreactivity (IR) was increased in the white and gray matter in spinal cord of the sporadic amyotrophic lateral sclerosis (sALS), predominantly in cells with astroglial morphology. METHODS: In the present study, we evaluated whether the PARP expression was present widespread in various regions of brain tissue including the motor cortex, parietal cortex and cerebellum. RESULTS: By western blot, PARP-IR in motor cortex from sALS patients, compared to the same region from age-matched normal controls, was also significantly increased (p=0.006). Importantly, PARP-IR was also increased in the parietal cortex, and cerebellum of sALS patients compared to the controls, in regions that are usually clinically unaffected in ALS (p=0.043, p=0.035, respectively). In addition, increased PARP expression in ALS was more prominent compared to Alzheimer's brain. Immunohistochemistry revealed that PARP staining was more significant in the cortical neurons and in the subcortical white matter glial cells from sALS patients compared to normal controls and Alzheimer's disease. CONCLUSIONS: The data demonstrate that increase in PARP-IR is not limited only to the vulnerable motor cortex. Furthermore, PARP-IR is present in both cortical neuronal and subcortical glial cells. The data suggest that widespread cellular stress on neuronal and glial cells is present in the brain of sporadic ALS patients.

The roles of inducible nitric oxide synthase expression in pancreatic cancer / 대한내과학회지

BACKGROUND: The finding of frequent inducible nitric oxide synthase (iNOS) expression in human cancer indicates that nitric oxide has a pathological role in tumor progression. Increased expression of iNOS in human pancreatic cancer cells was also recently reported, but the clinicopathological and biological significance of the iNOS expression remains unclear. The aim of our study was to look for possible roles and clinical significance of iNOS expression in pancreatic cancer. METHODS: 72 pancreatic adenocarcinoma tissue specimens were obtained from surgical resection. We investigated the immunohistochemical expression of iNOS in respect to variable clinicopathological characteristics, proliferation activity (assayed by Ki-67 expression), apoptosis (by TUNEL stain), and microvessel density (by CD34 expression; angiogenesis). RESULTS: Immunohistochemical positivity for iNOS in pancreatic epithelial cells was observed in 48/72 (66.7%). Apoptotic index (AI) of positive iNOS expressions were significantly higher than for negative expression (p <0.001) and increasing intensity of COX-2 expression showed a trend with increasing AI (p<0.001). No significant association was found between iNOS expression and proliferation index or microvessel density in pancreatic cancer. The expression of iNOS protein did not correlated with age, bilirubin, CA 19-9, location, size, AJCC stage, differentiation, distant metastasis or patient survival. CONCLUSION: The expression of iNOS enzyme in pancreatic cancer contributes to apoptosis of tumor cells. However, we could not find any correlation between iNOS expression and cell proliferation, angiognesis or clinical characteristics. Further in vivo investigations are necessary to determine the putative role of the iNOS expression for tumor progression in human pancreatic cancer.

Inhibition of rac1 Reduces PDGF-induced Reactive Oxygen Species and Proliferation in Vascular Smooth Muscle Cells

In vascular smooth muscle cells, reactive oxygen species (ROS) were known to mediate platelet-derived growth factor (PDGF)-induced cell proliferation and NADH/NADPH oxidase is the major source of ROS. NADH/NADPH oxidase is controlled by rac1 in non-phagocytic cells. In this study, we examined whether the inhibition of rac1 by adenoviral-mediated gene transfer of a dominant negative rac1 gene product (Ad.N17rac1) could reduce the proliferation of rat aortic vascular smooth muscle cells (RASMC) stimulated by PDGF via decreasing intracellular ROS. RASMC were stimulated by PDGF (80 ng/mL) with or without N-acetylcysteine 1 mM or infected with 100 mutiplicity of infection of Ad.N17rac1. Intracellular ROS levels were measured at 12 hr using carboxyl-2', 7'-dichlorodi-hydrofluorescein diacetate confocal microscopy. At 72 hr, cellular proliferation was evaluated by cell number counting and XTT assay. Compared with control, ROS levels were increased by 2-folds by PDGF. NAC and Ad.N17rac1 inhibited PDGF-induced increase of ROS by 77% and 65%, respectively. Cell number was increased by PDGF by 1.6-folds compared with control. NAC and Ad.N17rac1 inhibited PDGF-induced cellular growth by 45% and 87%, respectively. XTT assay also showed similar results. We concluded that inhibition of rac1 in RASMCs could reduce intracellular ROS levels and cellular proliferation induced by PDGF.

The Differences Between Cyclosporine and Tacrolimus in the Generation of ROS and Extracellular Matrix Accumulation in Primary Cultured Human Mesangial Cells / 대한신장학회잡지

OBJECTIVE: Cyclosporine(CsA) and tacrolimus, albeit different in structure, exert immunosuppressive effect by similar mechanism. Although most of clinical manifestations, including nephrotoxicity, are similar in the patients using these drugs, there are some differences including gum hyperplasia, neurotoxicity, and hepatic fibrosis between two drugs. There are several reports about association between reactive oxygen species(ROS) and CsA. In contrast, tacrolimus is known to decrease ROS in central nervous system. Thus, we investigated the possibility of different effects of tacrolimus and CsA on the generation of ROS, on the synthesis and degradation of collagen. METHODS: Experiments were done in primary cultured mesangial cells between 4th and 8th passages. CsA was added to the culture dishes in different concentration(making final CsA concentration of 0, 2, 4, 8 microgram/milliliter) and N-acetylcysteine(NAC) was also added in another mesangial cell culture at 4 microgram/milliliter of CsA concentration; tacrolimus was added in similar pattern(making final tacrolimus concentration of 0, 0.1, 0.2, 0.4 microgram/milliliter, NAC in 0.2 microgram/milliliter of tacrolimus concentration). RESULTS: No significant decrease in viability was noted in both cell groups, but growth retardation was weak in tacrolimus treated cells comparing with CsA treated cells. By flow cytometry, we could find the generation of ROS in CsA treated cells, but not in tacrolimus treated cells. In RT-PCR, there is no significant difference in m-RNA expression for a number of molecules including collagen III, MMP-2, TIMP-2, MT1-MMP in either CsA treated cells or tacrolimus cells. But in zymogram, MMP-2 activities were decreased at higher CsA concentration, then increased with addition of NAC. In tacrolimus cells, MMP2 activity was not changed at 0.1 and 0.2 microgram/milliliter; but, at the concentration of 0.4 microgram/milliliter, changed and not reversed by NAC. MMP-9 activity was similar in both cells. CONCLUSION: We could find ROS generation in CsA treated human mesangial cells, but not in tacrolimus treated cells. We think this difference resulted in the decrease of post-transcriptional MMP-2 activity in CsA treated cells and we also think tacrolimus cells in our experiments were not influenced by ROS. From these results, tacrolimus and CsA are different in the generation of ROS that have some effects in the matrix accumulation in mesangial cells. These result does not mean that tacrolimus is superior to CsA in nephrotoxicity, because nephrotoxicity is similar between two drugs. In conclusion, the mechanisms of nephrotoxicity are different between CsA and tacrolimus.

Effect of Transforming Growth Factor-beta1 on Expressions of Epidermal Growth Factor and Transforming Growth Factor-alpha in DU145 Androgen-Independent Prostate Cancer Cells / 대한비뇨기과학회지

PURPOSE: This study was designed to identify the possible mechanism of insensitivity of DU145 prostate cancer cells to the transforming growth factor (TGF)-beta1-mediated growth inhibition. MATERIALS AND METHODS: DU145 cells were treated with 4, 40, 100 pM TGF-beta1 for 3, 6, 9 days. Initially we performed the growth assay. After that, we analysed the change of cell cycle using fluorescence flow cytometry. At each time point, Western blot analysis with cell pellets was performed to investigate the change of expressions of epidermal growth factor(EGF), TGF-alpha, EGF receptor(EGFR) and TGF receptorII(TbetaR-II) proteins. RESULTS: The growth rate of TGF-beta1-treated cells was initially suppressed, but over time returned to control level. Flow cytometric analysis revealed that TGF-beta1-treated cells showed an increase in apoptotic/G1 phases, and concurrent decrease in S, G2/M phases until 6days. On day 9, however, TGF-beta1-treated cells showed a persistent increase of apoptotic unclei in spite of recovery of apoptotic/G1, S and G2/M phases. Western blot analysis showed that the intensity of EGF or TGF-alpha band decreased in dose-sependent manner on day 6. However, the intensity of each band increased up to the control level on day 9. the expression of EGFR or TbetaR-II protein did not change after treatment of TGF-beta1. CONCLUSIONS: these results suggest that EGF and TGF-alpha sould mediate in part the escape fron the inhibitory effect of TGF-beta1 in DU145 cells.

Genetic susceptibilities of cytochrome P450 1A1, 2E1, and N-acetyltransferase 2 to the risks for Korean head and neck cancer patients

The Effects of Cyclosporine on the Generation of ROS and Extracellular Matrix Accumulation in Cultured Human Mesangial Cells / 대한신장학회잡지

OBJECTIVE: Treatment with cyclosporine(CsA) for a long-term period may induce renal glomerulosclersosis and interstitial fibrosis. Reactive oxygen species(ROS) seems to be involved in the process of glomerulosclersosis and interstitial fibrosis. We investigated the effect of CsA on the generation of ROS and extracellular matrix accumulation in cultured human mesangial cells. We also studied the relationship between ROS formation and extracellular matrix and the effect of antioxidant on ROS formation and/or extracellular matrix degradation. METHODS: Mesangial cells were treated with varying dose of Cyclosporine(0, 2.5, 5, 7.5 and 10microgram/ mL) and also with cyclosporine(5microgram/mL) plus N- acetylcysteine(1mM). ROS was measured by flow cytometric analysis. mRNA expression of MMP-2, TIMP-2, MT1-MMP and collagen III was assessed by RT-PCR method. MMP-2 activity was measured by gelatin zymography. RESULTS: No significant difference was noted in cell viability with each CsA concentration. CsA inhibited the cell proliferation in a dose dependent manner and induced the expression of ROS. Antioxidant NAC reversed the effect of cyclosporine. CsA had no effect on the mRNA expression of collagen III, MMP-2, TIMP-2, MT1-MMP. However CsA decreased the MMP-2 activity in a dose dependent manner, which was also reversed by NAC. CONCLUSION: Cyclosporine-induced ROS may be associated with the extracellular matrix accumulation, that is glomerulosclersosis and interstitial fibrosis by inhibiting the cell proliferation and by decreasing the degradation of extracellular matrix. Antioxidant, at least in vitro, may prevent some of the adverse effects of CsA on renal function.

Effects of Human Recombinant Interferon-Gamma and Tumor Necrosis Factor-Alpha on Expressions of Matrix Metalloproteinases and Their Activity Human Bladder Cancer Cell Lines / 대한비뇨기과학회지

No abstract available.

Effects of Human Recombinant Interferon-Gamma and Tumor Necrosis Factor-Alpha on Expressions of Matrix Metalloproteinases and Their Activity Human Bladder Cancer Cell Lines / 대한비뇨기과학회지

No abstract available.

Genetic Alterations of Human Oral Cancers Using Comparative Genomic Hybridization

The development and progression of oral cancer is associated with an accumulation of multiple genetic alterations through the multistep processes. Comparative genomic hybridization(CGH), newly developed cytogenetic and molecular biologic technique, has been widely accepted as a useful method to allow the detection of genetic imbalance in solid tumors and the screening for chromosome sites frequently affected by gains or losses in DNA copy number. The authors examined 19 primary oral squamous cell carcinomas using CGH to identify altered chromosome regions that might contain novel oncogenes and tumor suppressor genes. Interrelationship between these genetic aberrations detected and major oncogenes and tumor suppressor genes previously recognized in carcinogenesis of oral cancers was studied. 1. Changes in DNA copy number were detected in 14 of 19 oral cancers (78.9%, mean: 5.58, range: 3~13). High level amplification was present in 4 cases at 9p23, 12p21.1~q13.1, 3q and 8q24~24.3. Fourteen cases(78.9%, mean: 3.00, range: 1~8) showed gains of DNA copy number and 12 cases(70.5%, mean: 2.58, range: 1~9) revealed losses of DNA copy number. 2. The most common gains were detected on 3q(52.6%), 5p(21.0%), 8q(21.0%), 9p(21.0%), and 11q(21.0%). The losses of DNA copy number were frequently occurred at 9p(36.8%), 17q(36.8%), 13q(26.3%), 4p(21.0%) and 9p(21.0%). 3. The minimal common regions of gains were repeatedly observed at 3q24~26.7, 3q27~29, 1q22~31, 5p12~13.3, 8q23~24, and 11q13.1-13.3. The minimal common regions of losses were detected at 9q11~21.3, 17p31, 13q22~34, and 14p16. 4. In comparison of CGH results with tumor stages, the lower stage group showed more frequent gain at 3q, 5q, 9p, and 14q, whereas gains at 1q(1q22~31) and 11q(11q13.1~13.3) were mainly detected in higher stage group. The loss at 13q22~34 was exclusively detected in higher stage. The results indicate that the most frequent genetic alterations in the development of oral cancers were gains at 3q24~26.3, 1q22~31, and 5p12~13.3 and losses at 9q11~21.3, 17p31, and 13q. It is suggested that genetic alterations manifested as gains at 3q24~26.3, 3q27~29, 5p12~13.3 and 5p are associated with the early progression of oral cancer. Gains at 1q22~31 and 11q13.1~13.3 and loss at 13q22-34 could be involved in the late progression of oral cancers.

A Demonhstration of a Tracheal Bronchus by Bronchoscopy and Computed Tompgraphy

Tracheal bronchus is an aberrant bronchus that arises most often from the right tracheal wall above the carina and is the result of an additional tracheal outgrowth early in embryonic life. It; incidence ranges between 0.1 and 5%. This anomaly is usually diagnosed incidentally during bronchoscopy, bronchography or computed tomography. Occasionally, it represents the underlying etiology for chronic pulmonary disease, especially if it involves the right upper lobe and reflects an abnorrnal pulmonary clearing mechanism. The tracheal bronchus may be associated with other bronchopulmonary anomalies, tracheal stenosis, or Down's syndrome. Asymptornatic tracheal bronchus does not require any treatment. In case of tracheal bronchus associated recurrent right upper lobe diseases, tracheal bronchus therapy should include resection of the aberrant bronchus as well as the lob it supplies. (J Korgan Pediatr Soc 2000;43:1501-1504)

The Frequency of CD34 and CD34 CD38 Hematopoietic Stem/Progenitor Cells in the Cord Blood and Adult Peripheral Blood / 대한소아혈액종양학회지

PURPOSE: The umbilical cord blood has been considered as an alternative source of hematopoietic stem cells for transplantation. The CD34+ is known as a common stem cell antigen and the CD34+ CD38- immunophenotype reportedly defines a primitive subpopulation of progenitor cells. In this study the frequency of CD34+ and CD34+ CD38- hematopoietic stem/progenitor cells in placental/cord blood (UCB), and adult peripheral blood (PB) were determined. METHODS: Between July and September 1998, 27 collections of UCB were performed at the obstetric units of Hanyang University Hospital. Fifteen adult PB samples were also obtained for control. RESULTS: The frequency of total CD34+ cells in UCB was higher (1.13+/-0.58% vs 0.46+/-0.30%, P=0.0002) than PB and the frequency of CD34+ CD38- cells in UCB was also greater (0.02+/-0.02 vs 0.01+/-0.01, P=0.035) than PB. The majority of UCB- and PB-derived CD34+ cells expressed CD38- antigen (98.22+/-2.11% in UCB and 97.85+/-2.56% in PB). The frequency of CD38- expression by UCB derived CD34+ cells was slightly higher (not statistically significant) than that by PB derived CD34+ cells. The frequency of CD34+ cells was increased linearly with birth weight (r=0.413). CONCLUSION: These results suggest that UCB could be a useful source of highly primitive hematopoietic stem cells for marrow reconstitution after bone marrow ablation.

Genetic Susceptibilities of Cytochrome P4501A1 and Glutathione S-transferase M1 to the Risk for Korean Head and Neck Squamous Cell Carcinoma Patients / 대한이비인후과학회지

BACKGROUND AND OBJECTIVES: Individual genetic susceptibilities to chemical carcinogens have been recognized as a major important host factors in human cancers. The cytochrome P450 family (CYPs) and glutathione-S-transferase (GST) have been reported to be associated with risks to the smoking-related human cancers. The purpose of this study is to determine the frequencies of the genotypes of CYP1A1 and GSTM1 genes in healthy control of Koreans and to identify the high-risk genotypes of these metabolic genes in head and neck cancer patients. MAERIALS AND METHODS: Ninety-six healthy controls and 93 head and neck squamous cell carcinoma patients are analysed using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). RESULTS: The distributions of CYP1A1 and GSTM1 in healthy controls according to the MspI site and absence or presence of PCR products were as following: m1/m1:m1/m2:m2/m2=39.6%:47.9%:12.5%, GSTM1 (-):GSTM1 (+)=45%:55%. GSTM1 (-) type and CYP1A1 m2/m2 types were more frequent in cancer patients than healthy controls. Among the combined genotypes of CYP1A1 and GSTM1 genes, the relative risk of CYP1A1 m1/m2, GSTM1 (-) genotypes was 2.13 times of relative odds' ratio in head and neck cancer patients. According to the tumor location, CYP1A1 m2/m2, GSTM1 (-) genotypes of larynx and CYP1A1 m1/m2, GSTM1 (-) genotypes of oral and pharynx were the highest risk groups to cancers in their locations. CONCLUSION: These results suggest that the genetic polymorphisms of CYP1A1 and GSTM1 were an important major factor to determine the individual susceptibility to head and neck cancers in Korean. And these polymorphisms and cancers susceptibile genotypes of CYP1A1 and GSTM1 in Korean population are very unique in comparison with the other ethinics.