No abstract available.
Travel Medicine

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

No abstract available.

No abstract available.

No abstract available.
Fixatives* ; Mast Cells*

BACKGROUND: During the last three decades, the resistance of S. pneumoniae to penicillin has been rapidly increasing in many parts of the world, especially in Korea. To characterize the clinical features and epidemiology of penicillin-resistant S. pneumoniae (PRSP) infections in the community and hospital, as well as to investigate the possible spread of resistant clone, we performed the antimicrobial susceptibility tests, pulsed filed gel electrophoresis (PFGE) and penicillin-binding protein (PBP) profile analysis of PRSP isolates. METHODS: A total 48 PRSP isolates from patients who visited or were admitted to Korea University Guro hospital during the period form July 1998 to June 1999 were studied. Anitimicrobial susceptibility tests for 48 isolates were performed with microbroth dilution method to determine the minimal inhibitory concentration of 11 antibiotics. 39 isolates and 35 isolates were subjected to PFGE and PBP profile analysis, respectively to investigate the genetic relatedness between PRSP isolates. RESULTS: Pneumonia was most common site of infection in the community and the hospital as 50%. There were no significant differences of clinical features and prognosis between community and hospital isolates. But, patients with serious underlying diseases had poor prognosis despite of acquisition site. High level penicillin resistance were observed in 69%, multi-drug resistance were 64.6% of isolates. PFGE showed that 13 of 29 community acquired infection were identical PFGE pattern but not that of 23F Spanish clone. There were various PFGE patterns were observed from community and hospital acquired infection isolates. Some of them were existed in both. PBP profiles showed more diverse, even if in isoaltes of the same PFGE pattern. CONCLUSOIN: In our study, high level penicillin resistance and multi-drug resistance were observed in PRSP clinical isolates. No clinical and prognostic differeces were observed between community and hospital acquired infections. Molecular epidemiology study were suggest the there were various genotypes of PRSP within our society. Some of them were observed in the hospital and community. Therefore, there was an evidence of communication of PRSP clones between the community and hospital.
Anti-Bacterial Agents ; Clone Cells ; Drug Resistance, Multiple ; Electrophoresis ; Epidemiology ; Genotype ; Humans ; Korea ; Molecular Epidemiology ; Penicillin Resistance ; Penicillin-Binding Proteins ; Penicillins ; Pneumonia ; Prognosis ; Streptococcus pneumoniae* ; Streptococcus*

We Reviewed 10 hypertensive children with pheochromocytoma retrospectively and the following results were obtained. 1) Out of 10 patients, 7 were male and 3 female. Age ranged from 5.5 years to 13.8 years and their median age was 9.9 years. 2) They complained of sweating, lethargy, headache. or chest pain and so on. Hypertension were noticed in all patients. Heart murmurs were detected in 7 patients and hypertensive retinopathy in 70%. 3) The three cases arised at extraadrenal gland and bilaterality was seen in 3 patients. In the view of diagnosis, abdominal sonography, computerized tomography and urine VMA test revealed the sensitivity of 100%. But MIBG scan showed 60% in sensitivity. 4) Waiting for operation, their hypertension were controlled by adrenergic blockers or calcium channel blockers. They received tumorectomy successfully except one who was in hypertensive state after operation and followed up through OPD. In conclusion high suspicion for the existence of pheochromocytoma from the clinical manifestations should be entertained in any pediatric patients and biochemical and imaging studies were mandatory. Furthermore, for the accurate localization of tumors, several imaging studies should be collaborated.
3-Iodobenzylguanidine ; Adrenergic Antagonists ; Calcium Channel Blockers ; Chest Pain ; Child* ; Diagnosis ; Female ; Headache ; Heart Murmurs ; Humans ; Hypertension ; Hypertensive Retinopathy ; Lethargy ; Male ; Pheochromocytoma* ; Retrospective Studies ; Sweat ; Sweating

BACKGROUND: Through a genome-wide search using the genetic markers(RFLP genetic markers), the familial hypertrophic cardiomyopathy(FHCM) with an autosomal dominant mode of inheritance has been firstly detected to be genetically linked to chromosome 14q1. The subsequent studies have shown that the point mutations at the exons encoding for the head and head /rod junction of the cardiac beta myosin heavy chain(beta-MHC) are the most frequent type of mutation in the FHCM families genetically implicated with a linkage to beta-MHC, whereas the alpha/beta-MHC hybrid gene and a large deletion at the 3' region of beta-MHC gene were also rarely detected. With the other families genetically implicated with the chromosomes 1,11,15,16 and 18, FHCM also manifests locus heterogeneity, a phenomenon in which abnormalities at different genes are involved in different families. In addition, a korean FHCM family with 403Arg-->Gln mutation of beta-MHC gene has been previously found by an american research group. METHODS: For clinical diagnosis, echocardiography and electrocardiography were performed on the individual members of a korean FHCM family. The microsatellite markers(MYO-I,MYO-II) located in the beta-MHC gene region were amplified by PCR(polymerase chain reaction) and the polymorphism was analyzed for the possible linkage to the phenotypic expression of FHCM. Independently, the same PCR products of the exons 13 and 23 were digested with the specific restriction enzymes for the presence of the most frequently reported point mutations of beta-MHC gene (403 and 908 amino acid mutations). Single strand conformation polymorphism(SSCP) of the exon 13 and 23 of the beta-MHC gene was also analyzed of the mobility shift expected if any point mutation is present at these two exons. RESULTS: The inheritance pattern of HCM(hypertrophic cardiomyopathy) in the family is considered as autosomal dominant. In this family(KU 101), one of the microsatellite markers(MYO-II) indicated the possible cosegregation between the allele was also present in the 32-year-old brother of the proband, who reveals no clinical signs of the disease. The other microsatellite genetic marker(MYO-I) was uninformative, without giving the discriminating power to verify the linkage to beta-MHC gene. In the analysis for two common mutations of beta-MHC gene by PCR-RFLP and PCR-SSCP, no evidence was found for 403 and 908 amino acid mutations and any point mutation in the exons 13 and 23. CONCLUSIONS: Based on the linkage analysis using microsatellite genetic markers, there was a possibility that the disease could be linked to an abnormality in the beta-MHC gene of the chromosome 14q1.
Adult ; Alleles ; Cardiomyopathy, Hypertrophic, Familial* ; Diagnosis ; Echocardiography ; Electrocardiography ; Exons ; Genetic Markers ; Head ; Humans ; Inheritance Patterns ; Mass Screening* ; Microsatellite Repeats ; Point Mutation ; Polymerase Chain Reaction ; Population Characteristics ; Siblings ; Ventricular Myosins* ; Wills

BACKGROUND: Through a genome-wide search using the genetic markers(RFLP genetic markers), the familial hypertrophic cardiomyopathy(FHCM) with an autosomal dominant mode of inheritance has been firstly detected to be genetically linked to chromosome 14q1. The subsequent studies have shown that the point mutations at the exons encoding for the head and head /rod junction of the cardiac beta myosin heavy chain(beta-MHC) are the most frequent type of mutation in the FHCM families genetically implicated with a linkage to beta-MHC, whereas the alpha/beta-MHC hybrid gene and a large deletion at the 3' region of beta-MHC gene were also rarely detected. With the other families genetically implicated with the chromosomes 1,11,15,16 and 18, FHCM also manifests locus heterogeneity, a phenomenon in which abnormalities at different genes are involved in different families. In addition, a korean FHCM family with 403Arg-->Gln mutation of beta-MHC gene has been previously found by an american research group. METHODS: For clinical diagnosis, echocardiography and electrocardiography were performed on the individual members of a korean FHCM family. The microsatellite markers(MYO-I,MYO-II) located in the beta-MHC gene region were amplified by PCR(polymerase chain reaction) and the polymorphism was analyzed for the possible linkage to the phenotypic expression of FHCM. Independently, the same PCR products of the exons 13 and 23 were digested with the specific restriction enzymes for the presence of the most frequently reported point mutations of beta-MHC gene (403 and 908 amino acid mutations). Single strand conformation polymorphism(SSCP) of the exon 13 and 23 of the beta-MHC gene was also analyzed of the mobility shift expected if any point mutation is present at these two exons. RESULTS: The inheritance pattern of HCM(hypertrophic cardiomyopathy) in the family is considered as autosomal dominant. In this family(KU 101), one of the microsatellite markers(MYO-II) indicated the possible cosegregation between the allele was also present in the 32-year-old brother of the proband, who reveals no clinical signs of the disease. The other microsatellite genetic marker(MYO-I) was uninformative, without giving the discriminating power to verify the linkage to beta-MHC gene. In the analysis for two common mutations of beta-MHC gene by PCR-RFLP and PCR-SSCP, no evidence was found for 403 and 908 amino acid mutations and any point mutation in the exons 13 and 23. CONCLUSIONS: Based on the linkage analysis using microsatellite genetic markers, there was a possibility that the disease could be linked to an abnormality in the beta-MHC gene of the chromosome 14q1.
Adult ; Alleles ; Cardiomyopathy, Hypertrophic, Familial* ; Diagnosis ; Echocardiography ; Electrocardiography ; Exons ; Genetic Markers ; Head ; Humans ; Inheritance Patterns ; Mass Screening* ; Microsatellite Repeats ; Point Mutation ; Polymerase Chain Reaction ; Population Characteristics ; Siblings ; Ventricular Myosins* ; Wills

BACKGROUND: Target point mutation of DNA topoisomerase, which is the typical mode of quinolone resistance, cannot explain high level resistance to quinolones. Therefore, many authors looked into over expression of efflux pump as the possibility. After quantificating the arcA mRNA, which controls AcrAB- TolC, the authors tried to find out the difference in the expression of arcA mRNA according to MIC of ciprofloxacin. The authors also tried to determine the usefulness of real time PCR, which is more reproducible and takes less time than preexisting immunoblot assay, through quantification of acrA. MATERIAL AND METHODS: Mutations in topoisomerase (GyrA, ParC) of 20 quinolone resistant E. coli isolates were identified by PCR and direct DNA sequencing. AcrA level was measured by real time PCR. GAPDH of E.coli was used as endogenous control. The expression of acrA was confirmed through northern hybridization method, the results obtained by real time PCR were compared. RESULTS: 1) Topoisomerase mutations were found in all quinolone resistant E. coli strains. 2) AcrA expression in fluoroquinolone-resistant E. coli was quantified by using real time PCR. There was no relationship between the ratio of acrA expression to GAPDH and MIC of ciprofloxacin. 3) With Northern hybridization, we compared the band of acrA to that of GAPDH in compactness and area. No difference in the expression according to MIC could be found. 4) The results of AcrA/GAPDH were significantly correlated between the real-time PCR and northern blot (P<0.05, correlation coefficiency 0.98). CONCLUSION: In this study, no relationship between overexpression of AcrA gene and high level fluoroquinolone resistance. Therefore, we assume that mechanism other than AcrAB efflux pump is involved in and contribute to high-level fluoroquinolone resistance. However, the degree of efflux pump expression could be confirmed with real time PCR using acrA mRNA. Therefore, real time PCR could be used in the molecular biologic study on the mechanism of resistance to antibiotics.
Anti-Bacterial Agents ; Blotting, Northern ; Ciprofloxacin ; DNA Topoisomerases, Type I ; Escherichia* ; Fluoroquinolones* ; Point Mutation ; Polymerase Chain Reaction ; Quinolones ; Real-Time Polymerase Chain Reaction* ; RNA, Messenger ; Sequence Analysis, DNA