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Efficient electrochemical reduction of CO2 to formate is demonstrated by fabricating Bi nanoflake with pulse electrodeposition. The effect of pulse voltage on morphology of the Bi nanoflake and electrochemical property was investigated. The pulse voltage of 80 mVAg/AgCl with six pulse cycles successfully produces ultrathin Bi nanoflakes. The finite-element-based simulation shows that the two-dimensional geometry with large lateral dimensions and ultrathin thickness can localize a strong electric field at the corner site of the flakes, resulting in facilitating efficient reduction of CO2 to formate. As a result, formate Faradaic efficiency of the Bi nanoflakes showed over 90% at − 0.8 VRHE. Also, the formate production rate reached 69 µmol/cm2/h at − 0.8 VRHE. The pulse electrodeposition provides highly dense and uniform and tailored nanostructures in the large area without the requirements of high vacuum or high temperatures process.

T-cadherin is frequently down regulated in various cancers, however, the underlying mechanisms responsible have yet to be elucidated. A genome wide association study of a cohort of Korean adults revealed that the T-cadherin rs3865188 single nucleotide polymorphism (SNP) was associated with serum Adiponectin levels and that its genotypic variants were correlated with risk for colorectal cancer (CRC). To test the function of rs12444338, a SNP tightly linked to the rs3865188 SNP, in T-cadherin transcriptional regulation in colorectal cancer, its effect on transcriptional activity and the capacity of binding activity attributable to allelic variation of the rs12444338 SNP was investigated. An electrophoretic-mobility-shift assay (EMSA) revealed a specific nucleoprotein complex unique to the T allele probe, which displayed lower promoter activity when compared to the G allele. Based on the results of the EMSA using mutant probes, the consensus sequence of the putative transcription factor binding site was determined. Additionally, candidates for putative binding factors to the T allele were also identified. Collectively, the study data suggested that the rs12444338 SNP was involved in transcriptional regulation of T-cadherin gene (CDH13) and that the differential binding of transcription factors at the rs12444338 SNP resulted in altered gene expression. These results elucidate, at least in part, the regulation of T-cadherin expression in CRC and provide further information regarding the effect of nucleotide variation in its promoter region.

During the hair follicle (HF) cycle, HR protein expression is not concordant with the presence of the Hr mRNA transcript, suggesting an elaborate regulation of Hr gene expression. Here we present evidence that the 5' untranslated region (UTR) of the Hr gene has internal ribosome entry site (IRES) activity and this activity is regulated by the binding of poly (rC) binding protein 2 (PCBP2) to Hr mRNA. Overexpression and knockdown of PCBP2 resulted in a decrease in Hr 5' UTR IRES activity and an increase in HR protein expression without changing mRNA levels. We also found that this regulation was disrupted in a mutant Hr 5' UTR that has a mutation responsible for Marie Unna hereditary hypotrichosis (MUHH) in both mice and humans. These findings suggest that Hr mRNA expression is regulated at the post-transcriptional level via IRES-mediated translation control through interaction with PCPB2, but not in MUHH.

Background Adiponectin levels have been shown to be associated with colorectal cancer (CRC). Furthermore, a newly identified adiponectin receptor, T-cadherin, has been associated with plasma adiponectin levels. Therefore, we investigated the potential for a genetic association between T-cadherin and CRC risk. Result We conducted a case–control study using the Korean Cancer Prevention study-II cohort, which is composed of 325 CRC patients and 977 normal individuals. Study results revealed that rs3865188 in the 5’ flanking region of the T-cadherin gene (CDH13) was significantly associated with CRC (p = 0.0474). The odds ratio (OR) for the TT genotype as compared to the TA + AA genotype was 1.577 (p = 0.0144). In addition, the interaction between CDH13 and the adiponectin gene (APN) for CRC risk was investigated using a logistic regression analysis. Among six APN single nucleotide polymorphisms (rs182052, rs17366568, rs2241767, rs3821799, rs3774261, and rs6773957), an interaction with the rs3865188 was found for four (rs2241767, rs3821799, rs3774261, and rs6773957). The group with combined genotypes of TT for rs3865188 and GG for rs377426 displayed the highest risk for CRC development as compared to those with the other genotype combinations. The OR for the TT/GG genotype as compared to the AA/AA genotype was 4.108 (p = 0.004). Furthermore, the plasma adiponectin level showed a correlation with the gene-gene interaction, and the group with the highest risk for CRC had the lowest adiponectin level (median, 4.8 μg/mL for the TT/GG genotype vs.7.835 μg/mL for the AA/AA genotype, p = 0.0017). Conclusions The present study identified a new genetic factor for CRC risk and an interaction between CDH13 and APN in CRC risk. These genetic factors may be useful for predicting CRC risk. Electronic supplementary material The online version of this article (doi:10.1186/s12929-015-0180-9) contains supplementary material, which is available to authorized users.

In this paper, we present a simple and cost-effective replication method of high-aspect-ratio polymer nanopillar array as a biomimetic gecko’s foot hair prototype. A UV nano embossing process was applied for the replication of polymer nanopillar arrays. Highly ordered straight nanoporous AAO (anodic aluminum oxide) templates were utilized as reusable master molds. Densely arranged high-aspect-ratio nanopillar arrays have been successfully fabricated by means of the UV nano embossing process with the AAO mold. Pull-off force measurements were carried out to characterize the adhesive force of the replicated nanopillar arrays on the polymer substrates based on the force–distance curves obtained from the atomic force microscope (AFM) with a modified AFM cantilever. The force measurement results showed that the larger diameter and the taller height of the nanopillars result in the larger adhesive force.

The SCN5A gene encodes the alpha subunit of the human cardiac voltage-gated sodium channel. Mutations in SCN5A are responsible for Brugada syndrome, an inherited cardiac disease that leads to idiopathic ventricular fibrillation (IVF) and sudden death. In this study, we screened nine individuals from a single family and 12 sporadic patients who were clinically diagnosed with Brugada syndrome. Using PCR-SSCP, DHPLC, and DNA sequencing analysis, we identified a novel single missense mutation associated with Brugada syndrome in the family and detected a C5607T polymorphism in Korean subjects. A single nucleotide substitution of G to A at nucleotide position 3934 changed the coding sense of exon 21 of the SCN5A from glycine to serine (G1262S) in segment 2 of domain III (DIII-S2). Four individuals in the family carried the identical mutation in the SCN5A gene, but none of the 12 sporadic patients did. This mutation was not found in 150 unrelated normal individuals. This finding is the first report of a novel mutation in SCN5A associated with Brugada syndrome in Koreans.

Acquisition of resistance to anti-cancer drugs is a significant obstacle to effective cancer treatment. Although several efforts have been made to overcome drug resistance in cancer cells, the detailed mechanisms have not been fully elucidated. Here, we investigated whether microRNAs (miRNAs) function as pivotal regulators in the acquisition of anti-cancer drug resistance to 5-fluorouracil (5-FU). A survey using a lentivirus library containing 572 precursor miRNAs revealed that five miRNAs promoted cell survival after 5-FU treatment in human hepatocellular carcinoma Hep3B cells. Among the five different clones, the clone expressing miR-200a-3p (Hep3B-miR-200a-3p) was further characterized as a 5-FU-resistant cell line. The cell viability and growth rate of Hep3B-miR-200a-3p cells were higher than those of control cells after 5-FU treatment. Ectopic expression of a miR-200a-3p mimic increased, while inhibition of miR-200a-3p downregulated, cell viability in response to 5-FU, doxorubicin, and CDDP (cisplatin). We also showed that dual-specificity phosphatase 6 (DUSP6) is a novel target of miR-200a-3p and regulates resistance to 5-FU. Ectopic expression of DUSP6 mitigated the pro-survival effects of miR-200a-3p. Taken together, these results lead us to propose that miR-200a-3p enhances anti-cancer drug resistance by decreasing DUSP6 expression.

Triple A syndrome is a rare genetic disorder caused by mutations in the achalasia-addisonianism-alacrima syndrome (AAAS) gene which encodes a tryptophan aspartic acid (WD) repeat-containing protein named alacrima-achalasia-adrenal insufficiency neurologic disorder (ALADIN). Northern blot analysis shows that the 2.1 kb AAAS mRNA is expressed in various tissues with stronger expression in testis and pancreas. We show that human ALADIN is a protein with an apparent molecular weight of 60 kDa, and expressed in the adrenal gland, pituitary gland and pancreas. Furthermore, biochemical analysis using anti-ALADIN antibody supports the previous finding of the localization of ALADIN in the nuclear membrane. The mutations S544G and S544X show that alteration of S544 residue affects correct targeting of ALADIN to the nuclear membrane.