Percutaneous Sclerotherapy of Renal Cysts with a Beta-Emitting Radionuclide, Holmium-166-chitosan Complex

OBJECTIVE: To evaluate the usefulness of a beta-emitting radionuclide (holmium-166-chitosan complex) as a sclerosing agent for the treatment of renal cysts. MATERIALS AND METHODS: Using 10-30 mCi of holmium-166-chitosan complex, 20 renal cysts in 17 patients (14 male and 3 female patients, ranging in age from 47 to 82 years) were treated by percutaneous sclerotherapy under ultrasonographic guidance. The volume of the cysts before and after the sclerotherapy and the percentage change in volume were calculated in order to evaluate the response to therapy, which was classified as either complete regression (invisible), nearly complete regression ( 50 volume%). RESULTS: The follow-up period ranged from 6 to 36 months (mean 28 months). Eighteen cysts (90%) regressed completely (n=11, 55%) or near-completely (n=7, 35%). Partial regression was obtained in one patient (5%) and there was no regression in one patient (5%). No significant complications were encountered. CONCLUSION: The holmium-166-chitosan complex seems to be useful as a new painless sclerosing agent for the treatment of renal cysts with no significant complications.ope

Profiling age-related epigenetic markers of stomach adenocarcinoma in young and old subjects

The purpose of our study is to identify epigenetic markers that are differently expressed in the stomach adenocarcinoma (STAD) condition. Based on data from The Cancer Genome Atlas (TCGA), we were able to detect an age-related difference in methylation patterns and changes in gene and miRNA expression levels in young (n = 14) and old (n = 70) STAD subjects. Our analysis identified 323 upregulated and 653 downregulated genes in old STAD subjects. We also found 76 miRNAs with age-related expression patterns and 113 differentially methylated genes (DMGs), respectively. Our further analysis revealed that significant upregulated genes (n = 35) were assigned to the cell cycle, while the muscle system process (n = 27) and cell adhesion-related genes (n = 57) were downregulated. In addition, by comparing gene and miRNA expression with methylation change, we identified that three upregulated genes (ELF3, IL1??, and MMP13) known to be involved in inflammatory responses and cell growth were significantly hypomethylated in the promoter region. We further detected target candidates for age-related, downregulated miRNAs (hsa-mir-124-3, hsa-mir-204, and hsa-mir-125b-2) in old STAD subjects. This is the first report of the results from a study exploring age-related epigenetic biomarkers of STAD using high-throughput data and provides evidence for a complex clinicopathological condition expressed by the age-related STAD progression. © the authors, publisher and licensee Libertas Academica Limitedopen

Short-term calorie restriction ameliorates genomewide, age-related alterations in DNA methylation

DNA methylation plays major roles in many biological processes, including aging, carcinogenesis, and development. Analyses of DNA methylation using next-generation sequencing offer a new way to profile and compare methylomes across the genome in the context of aging. We explored genomewide DNA methylation and the effects of short-term calorie restriction (CR) on the methylome of aged rat kidney. Whole-genome methylation of kidney in young (6 months old), old (25 months old), and OCR (old with 4-week, short-term CR) rats was analyzed by methylated DNA immunoprecipitation and next-generation sequencing (MeDIP-Seq). CpG islands and repetitive regions were hypomethylated, but 5'-UTR, exon, and 3'-UTR hypermethylated in old and OCR rats. The methylation in the promoter and intron regions was decreased in old rats, but increased in OCR rats. Pathway enrichment analysis showed that the hypermethylated promoters in old rats were associated with degenerative phenotypes such as cancer and diabetes. The hypomethylated promoters in old rats related significantly to the chemokine signaling pathway. However, the pathways significantly enriched in old rats were not observed from the differentially methylated promoters in OCR rats. Thus, these findings suggest that short-term CR could partially ameliorate age-related methylation changes in promoters in old rats. From the epigenomic data, we propose that the hypermethylation found in the promoter regions of disease-related genes during aging may indicate increases in susceptibility to age-related diseases. Therefore, the CR-induced epigenetic changes that ameliorate age-dependent aberrant methylation may be important to CR's health-and life-prolonging effects.ope

A Dispermic Chimera with Mixed Field Blood Group B and Mosaic 46,XY/47,XYY Karyotype

Chimerism in humans is a rare phenomenon often initially identified in the resolution of an ABO blood type discrepancy. We report a dispermic chimera who presented with mixed field in his B antigen typing that might have been mistaken for the B3 subtype. The propositus is a healthy Korean male blood donor. Neither his clinical history nor initial molecular investigation of his ABO gene explained his mixed field agglutination with murine anti-B. Chimerism was suspected, and 9 short tandem repeat (STR) loci were analyzed on DNA extracted from blood, buccal swabs, and hair from this donor and on DNA isolated from peripheral blood lymphocytes from his parents. The propositus' red blood cells demonstrated mixed field agglutination with anti-B. Exon 6 and 7 and flanking intronic regions of his ABO gene were sequenced and revealed an O01/O02 genotype. B allele haplotype-specific PCR, along with exon 6 and 7 cloning and sequencing demonstrated a third ABO allele, B101. Four STR loci demonstrated a pattern consistent with a double paternal chromosome contribution in the propositus, thus confirming chimerism. His karyotype revealed a mosaic pattern: 32/50 metaphases were 46,XY and 18/50 metaphases demonstrated 47,XYY

Design of Highly Sensitive C2H5OH Sensors Using Self-Assembled ZnO Nanostructures

Various ZnO nanostructures such as porous nanorods and two hierarchical structures consisting of porous nanosheets or crystalline nanorods were prepared by the reaction of mixtures of oleic-acid-dissolved ethanol solutions and aqueous dissolved Zn-precursor solutions in the presence of NaOH. All three ZnO nanostructures showed sensitive and selective detection of C2H5OH. In particular, ultra-high responses (Ra/Rg = ∼1,200, Ra: resistance in air, Rg: resistance in gas) to 100 ppm C2H5OH was attained using porous nanorods and hierarchical structures assembled from porous nanosheets, which is one of the highest values reported in the literature. The gas response and linearity of gas sensors were discussed in relation to the size, surface area, and porosity of the nanostructures

Frequent Occurrence of Mitochondrial DNA Mutations in Barrett’s Metaplasia without the Presence of Dysplasia

BACKGROUND: Barrett's esophagus (BE) is one of the most common premalignant lesions and can progress to esophageal adenocarcinoma (EA). The numerous molecular events may play a role in the neoplastic transformation of Barrett's mucosa such as the change of DNA ploidy, p53 mutation and alteration of adhesion molecules. However, the molecular mechanism of the progression of BE to EA remains unclear and most studies of mitochondrial DNA (mtDNA) mutations in BE have performed on BE with the presence of dysplasia. METHODS/FINDINGS: Thus, the current study is to investigate new molecular events (Barrett's esophageal tissue-specific-mtDNA alterations/instabilities) in mitochondrial genome and causative factors for their alterations using the corresponding adjacent normal mucosal tissue (NT) and tissue (BT) from 34 patients having Barrett's metaplasia without the presence of dysplasia. Eighteen patients (53%) exhibited mtDNA mutations which were not found in adjacent NT. mtDNA copy number was about 3 times higher in BT than in adjacent NT. The activity of the mitochondrial respiratory chain enzyme complexes in tissues from Barrett's metaplasia without the presence of dysplasia was impaired. Reactive oxygen species (ROS) level in BT was significantly higher than those in corresponding samples. CONCLUSION/SIGNIFICANCE: High ROS level in BT may contribute to the development of mtDNA mutations, which may play a crucial role in disease progression and tumorigenesis in BE

Species Distribution and Susceptibility to Azole Antifungals of Candida Bloodstream Isolates from Eight University Hospitals in Korea

PURPOSE: The incidence of Candida bloodstream infections (BSI) has increased over the past two decades. The rank order of occurrence and the susceptibility to antifungals of the various Candida species causing BSI are important factors driving the establishment of empirical treatment protocols; however, very limited multi-institutional data are available on Candida bloodstream isolates in Korea. MATERIALS AND METHODS: We investigated the susceptibility to azole antifungals and species distribution of 143 Candida bloodstream isolates recovered from eight university hospitals over a six-month period. Minimal inhibitory concentrations (MICs) of fluconazole, itraconazole, and voriconazole for each isolate were determined by the broth microdilution method of the Clinical and Laboratory Standards Institute (CLSI). RESULTS: The Candida species recovered most frequently from the blood cultures was C. albicans (49%), followed by C. parapsilosis (22%), C. tropicalis (14%), and C. glabrata (11%). The MIC ranges for the Candida isolates were 0.125 to 64 microg/mL for fluconazole, 0.03 to 2 microg/mL for itraconazole, and 0.03 to 1 microg/mL for voriconazole. Overall, resistance to fluconazole was found in only 2% of the Candida isolates (3/143), while the dose-dependent susceptibility was found in 6% (8/143). The resistance and dose-dependent susceptibility of itraconazole were found in 4% (6/143) and 14% (20/143) of the isolates, respectively. All bloodstream isolates were susceptible to voriconazole (MIC, < or = 1 microg/mL). CONCLUSION: Our findings show that C. albicans is the most common cause of Candida-related BSI, followed by C. parapsilosis, and that the rates of resistance to azole antifungals are still low among bloodstream isolates in Korea.ope

Candida haemulonii and Closely Related Species at 5 University Hospitals in Korea: Identification, Antifungal Susceptibility, and Clinical Features

Background. Candida haemulonii, a yeast species that often exhibits antifungal resistance, rarely causes human infection. During 2004-2006, unusual yeast isolates with phenotypic similarity to C. haemulonii were recovered from 23 patients (8 patients with fungemia and 15 patients with chronic otitis media) in 5 hospitals in Korea. Methods. Isolates were characterized using D1/D2 domain and ITS gene sequencing, and the susceptibility of the isolates to 6 antifungal agents was tested in vitro. Results. Gene sequencing of the blood isolates confirmed C. haemulonii group I (in 1 patient) and Candida pseudohaemulonii (in 7 patients), whereas all isolates recovered from the ear were a novel species of which C. haemulonii is its closest relative. The minimum inhibitory concentration (MIC) ranges of amphotericin B, fluconazole, itraconazole, and voriconazole for all isolates were 0.5-32 mu g/mL (MIC(50), 1 mu g/mL), 2-128 mu g/mL (MIC(50), 4 mu g/mL), 0.125-4 mu g/mL (MIC(50), 0.25 mu g/mL), and 0.03-2 mu g/mL (MIC(50), 0.06 mu g/mL), respectively. All isolates were susceptible to caspofungin (MIC, 0.125-0.25 mu g/mL) and micafungin (MIC, 0.03-0.06 mu g/mL). All cases of fungemia occurred in patients with severe underlying diseases who had central venous catheters. Three patients developed breakthrough fungemia while receiving antifungal therapy, and amphotericin B therapeutic failure, which was associated with a high MIC of amphotericin B (32 mu g/mL), was observed in 2 patients. Conclusions. Candida species that are closely related to C. haemulonii are emerging sources of infection in Korea. These species show variable patterns of susceptibility to amphotericin B and azole antifungal agents.Shin JH, 2007, J CLIN MICROBIOL, V45, P2385, DOI 10.1128/JCM.00381-07Khan ZU, 2007, J CLIN MICROBIOL, V45, P2025, DOI 10.1128/JCM.00222-07Lee JS, 2007, J CLIN MICROBIOL, V45, P1005, DOI 10.1128/JCM.02264-06Pfaller MA, 2006, J CLIN MICROBIOL, V44, P819, DOI 10.1128/JCM.44.3.819-826.2006Sugita T, 2006, MICROBIOL IMMUNOL, V50, P469Clancy CJ, 2005, ANTIMICROB AGENTS CH, V49, P3171, DOI 10.1128/AAC.49.8.3171-3177.2005Odds FC, 2004, J CLIN MICROBIOL, V42, P3475, DOI 10.1128/JCM.42.8.3475-3482.2004Rodero L, 2002, J CLIN MICROBIOL, V40, P2266, DOI 10.1128/JCM.40.6.2266-2269.2002*CLSI, 2002, M27A2 CLSISugita T, 1999, J CLIN MICROBIOL, V37, P1985Pfaller MA, 1998, DIAGN MICR INFEC DIS, V32, P223Nguyen MH, 1998, J INFECT DIS, V177, P425Kurtzman CP, 1997, J CLIN MICROBIOL, V35, P1216LEHMANN PF, 1993, J CLIN MICROBIOL, V31, P1683GARGEYA IB, 1991, J MED VET MYCOL, V29, P335