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In this study, we aimed to investigate the influence of resilience or public service motivation (PSM) on firefighters' work engagement during the coronavirus disease (COVID-19) pandemic. We conducted an online survey with 304 firefighters assigned to Gyeonggi-do between October 27 and 28, 2022, and collected their demographic information; work-related data; mood, anxiety and insomnia symptoms; and work-related attitudes. The leading causes of firefighters' stress were physical and mental health decline due to heavy workloads (46.4%), verbal abuse and assault from civilians (33.9%), conflict with coworkers (18.4%), and death of colleagues (13.2%). The results of the logistic regression analysis revealed that high levels of resilience (OR = 1.28, p < 0.001), service motivation (OR = 1.17, p < 0.001), and non-exposure to death (OR = 0.33, p = 0.005) led to high work engagement. Mediation analysis showed that resilience and PSM mediated the influence of depression on work engagement. The work engagement of firefighters is influenced by resilience, PSM, and exposure to death. [ABSTRACT FROM AUTHOR]

Alternative refrigerants for R410A, which is most commonly used in building cooling and heating, are being requested with a global warming potential of 750 or lower and these regulations will continue to be implemented. At the current stage, several candidates are being discussed, but these will not be the final solution. What is certain is the R410A replacement refrigerant will be proposed in the form of mixed refrigerants. To figure out the thermodynamic properties of the mixed refrigerant, VLE data must be obtained first. In this study, we performed VLE experiments on a representative mixed refrigerant (R32-R125) to verify our newly constructed VLE experiment facility, and compared the results with the REFPROP 10 and the results of other researchers. The experiment was conducted at a temperature of 273.15 K to 313.15 K, and the maximum MAPE for pressure was found to be 0.0178 % and the maximum MAE for composition was found to be 0.0029. In the future, the facility will be used to present VLE test data with new mixed refrigerants as candidate replacement refrigerants for R410A. [ABSTRACT FROM AUTHOR]

Contact angle is a physical quantity used to evaluate the interaction between a solid surface and a liquid. However, many research laboratories or educational institutions with budget constraints have limited access to a commercial contact-angle goniometer with a high-resolution imaging system. In this study, we fabricated a custom-made contact angle goniometer with a smartphone and quantified the contact angles of water on various surfaces. We found that the receding contact angles on the surfaces were sensitive to the change in flow rates. The receding angle sharply decreases when the flow rate exceeds 50 µl/min, indicating that accurate flow control is required in contact angle measurements. The dynamic contact angles could also be quantified by the developed goniometer in an extremely low-capillary number regime. The dynamic advancing and receding contact angles on tested surfaces followed the molecular-kinetic theory. [ABSTRACT FROM AUTHOR]

Gliomas are the most common primary tumors in the brain and spinal cord. In previous GWASs, SNPs in epidermal growth factor receptor (EGFR) have been reported as risk loci for gliomas. However, EGFR variants associated with gliomas in the Korean population remain unstudied. This study explored the association of EGFR SNPs with the risk of glioma. We genotyped 13 EGFR exon SNPs in a case–control study that included 324 Korean patients diagnosed with glioma and 480 population-based controls. Statistical analyses of the association between EGFR SNPs and glioma risk were conducted using logistic regression. Both stepwise analysis and conditional logistic analysis were performed to identify independent associations among genotyped variants. We confirmed that two SNPs (rs2227983, rs1050171) were significantly associated with glioma (rs2227983: odds ratio = 1.42, Pcorr = 0.009; rs1050171: odds ratio = 1.68, Pcorr = 0.005). Additionally, the stepwise analysis and conditional logistic analysis indicated that both SNPs created variants with independent genetic effects. This study is the first to show evidence that functional variants of EGFR, namely, rs2227983 (K521R) and rs1050171 (Q787Q), are associated with an increased risk of glioma in the Korean population. Future work should confirm the functional association between EGFR variants and glioma. [ABSTRACT FROM AUTHOR]

Background: Previous genomewide association studies (GWASs), single nucleotide polymorphisms (SNPs) on cyclin-dependent kinase inhibitor 2 A (CDKN2A), cyclin-dependent kinase inhibitor 2B (CDKN2B), and cyclin-dependent kinase inhibitor 2B antisense RNA1 (CDKN2B-AS1) were reported as risk loci for glioma, a subgroup of the brain tumor. To further characterize this association with the risk of brain tumors in a Korean population, we performed a fine-mapping association study of CDKN2A, CDKN2B, and CDKN2B-AS1. Methods and Results: A total of 17 SNPs were selected and genotyped in 1,439 subjects which were comprised of 959 patients (pituitary adenoma 335; glioma 324; meningioma 300) and 480 population controls (PCs). We discovered that a 3'untranslated region (3'UTR) variant, rs181031884 of CDKN2B (Asian-specific variant), had significant association with the risk of pituitary adenoma (PA) (Odds ratio = 0.58, P = 0.00003). Also, rs181031884 appeared as an independent causal variant among the significant variants in CDKN2A and CDKN2B, and showed dose-dependent effects on PA. Conclusions: Although further studies are needed to verify the impact of this variant on PA susceptibility, our results may help to understand CDKN2B polymorphism and the risk of PA. [ABSTRACT FROM AUTHOR]

In this study, the macroscopic dynamic advancing and receding contact angles of an aqueous glycerin solution on lubricant-infused surfaces (LISs) were measured using the Wilhelmy plate technique. To construct LISs, polytetrafluoroethylene (PTFE) was roughened using 240-grit sandpaper to introduce micro-/nanostructures on the surface. Then, fluorinated synthetic oils were infused into the structures of the sanded PTFE surface to form the LISs. We found that the dynamic advancing contact angles increased with increasing capillary number, whereas the dynamic receding contact angles decreased with increasing capillary number. The viscosity ratio between the working fluid and lubricant oil was found to change the increasing/decreasing trends in the dynamic contact angles. As the viscosity ratio increased, the reduction in shear stress on the LISs shifted the change in the dynamic contact angles to higher capillary numbers. Unlike the contact angles measured by an optical method, the force-based contact angles are affected by the viscous force acting on the LISs. A sharp transition in the dynamic contact angle data at the critical capillary number was observed, and this was shifted toward higher capillary numbers as the viscosity ratio increased. The scaling behavior of the dynamic contact angles was found to follow the Cox-Voinov-Tanner scaling law. This study describes how LISs can be characterized based on dynamic contact angles. [ABSTRACT FROM AUTHOR]

Atopic dermatitis (AD) is a common skin disease in childhood whose diagnosis requires expertise in dermatology. Recent studies have indicated that host genes–microbial interactions in the gut contribute to human diseases including AD. We sought to develop an accurate and automated pipeline for AD diagnosis based on transcriptome and microbiota data. Using these data of 161 subjects including AD patients and healthy controls, we trained a machine learning classifier to predict the risk of AD. We found that the classifier could accurately differentiate subjects with AD and healthy individuals based on the omics data with an average F1-score of 0.84. With this classifier, we also identified a set of 35 genes and 50 microbiota features that are predictive for AD. Among the selected features, we discovered at least three genes and three microorganisms directly or indirectly associated with AD. Although further replications in other cohorts are needed, our findings suggest that these genes and microbiota features may provide novel biological insights and may be developed into useful biomarkers of AD prediction. [ABSTRACT FROM AUTHOR]

All aerial tissues and organs of higher plants are generated from the shoot apical meristem (SAM) containing a pluripotent stem cell population. The maintenance of shoot meristem activity, such as cell proliferation and differentiation, is important for appropriate normal growth as well as adaptive plastic development under abiotic stress conditions. Here we report that the effects of salt tolerance on Arabidopsis shoot growth may occur via shoot meristem activity. Interestingly, the clv3-2 and clv1 bam1 mutants showed the salt tolerant phenotype on shoot growth and development through the increased number of actively dividing cells in the SAM but not the promoted expression levels of the typical stress-responsive genes. The reduction of 5-ethynyl-2′-deoxyuridine (EdU)-labeled dividing cells in the SAM by the treatment of abiotic stresses occurred most likely through abscisic acid (ABA) and reactive oxygen species (ROS). In addition, shoot meristem activity via cell proliferation was regulated dynamically depending on the presence or absence of abiotic stimuli. Therefore, these results suggest that stem cell maintenance and differentiation in the SAM may play an important role in stress tolerance for developmental plasticity on plant growth against unfavorable environmental conditions. [ABSTRACT FROM AUTHOR]

The number of cancer patients has been rapidly increasing, and while there have been wide variations, cancer survival rates also improved globally. Despite the improved survival rates, supportive care needs of cancer patients have been unmet in various domains. The current study aimed to investigate unmet needs that had potential to be managed by peer supports according to cancer trajectories. We used the comprehensive needs assessment tool in cancer (CNAT) and a modified CNAT to evaluate the unmet needs and peer support needs of cancer patients at the tertiary hospital of South Korea. Of the 402 participants, 335 (83.3%) needed peer support. For patients who had been diagnosed with cancer for more than 5 years, the highest proportion of peer support needs to unmet supportive care was reported in information domain (92.9%). Patients with advanced cancer reported peer support needs in the social/religious/spiritual (84.4%) and practical domains (81.1%). Most of stomach cancer patients needed peer supports to receive information (96.6%). The need for peer supports in the information domain was reported highest according to longer survival period and also according to advanced cancer stages. The proportion of peer support needs in unmet supportive care varied by cancer type. Further interventional studies are needed to investigate satisfaction with peer support in specific domains. [ABSTRACT FROM AUTHOR]

Purpose: Previous studies have revealed that PHLDB1 single-nucleotide polymorphisms (SNPs) are associated with glioma risk. Nonetheless, the association between PHLDB1 SNPs and the risk of pituitary adenoma has not been studied. The present study evaluated the association of PHLDB1 SNPs with the risk of pituitary adenomas. Methods: We genotyped 27 PHLDB1 tagging and exon SNPs in a case–control study that included 148 patients who got a diagnosis of nonfunctional pituitary adenoma (NFPA) and 375 normal controls within the Korean population. Statistical analyses of the association between PHLDB1 SNPs and the NFPA risk were conducted using logistic regression. Results: We detected an association between a PHLDB1 SNP and the risk of NFPA in the Korean population. Rs67307131 in intron 2 was significantly associated with NFPA (odds ratio [OR] = 2.15, 95% confidence interval [CI] 1.44–3.20; P = 0.0002 in the dominant model). In the referent analysis, a higher OR and stronger association (lower P value) were observed among patients with the "C/T" genotype (OR = 2.39, 95% CI 1.60–3.58; P = 0.00002). In a functional analysis with a SNP annotation tool, this SNP was predicted to be a CpG site and copy number variant; these properties are associated with susceptibility to diseases. Conclusions: Our findings suggest that genetic variation of PHLDB1 may be associated with the risk of NFPA. This is the first report of an association between PHLDB1 variants and NFPA. Further research is needed to confirm the impact of this SNP on NFPA susceptibility. [ABSTRACT FROM AUTHOR]

Hirschsprung disease (HSCR) is a congenital and complex disorder characterized by intestinal obstruction due to the absence of enteric neurons along variable lengths of the hindgut. Our recent genome-wide association study (GWAS) has revealed regional associations with HSCR at several loci of inositol-trisphosphate 3-kinase C ( ITPKC). For fine mapping, we additionally selected and genotyped a total of 12 single nucleotide polymorphisms (SNPs) of ITPKC in 187 HSCR patients and 283 unaffected controls, and performed a further combined imputation analysis based on genotype data from this second stage of fine mapping and our previous GWAS stage, totaling 902 subjects (187 HSCR cases and 715 controls). As a result, several SNPs (minimum P = 0.004) and a haplotype ( P = 0.02) were found to be significantly associated with HSCR. In further in silico analyses to ascertain the potential functions of the significant variants, the change from the common allele to the rare allele of the highly conserved nonsynonymous rs76785336 showed a difference in mRNA folding structure. In the case of intronic SNPs, rs2607420 with a high consensus value was predicted to be a new splice site. Although this study has limitations (such as lack of functional evaluations, small number of cases, and further need of replication in other cohorts), our findings suggest that genetic variants of ITPKC may have a potential association with HSCR susceptibility and/or developmental diseases related to enteric nervous system development. [ABSTRACT FROM AUTHOR]

Hypoxic placentation has been considered as a key step for the development of preeclampsia (PE); however, the underlying epigenetic mechanisms are still not fully understood. The purpose of this study is to investigate the whole genome DNA methylation status of PE. A microarray analysis using the Infinium HumanMethylation450 BeadChip assay in the placentas and maternal peripheral blood (PB) from PE patients and normal controls was performed. For validation, a quantitative RT-PCR analysis was used. Maternal PB showed 71 differentially methylated CpG loci (44 hypermethylated and 27 hypomethylated), while placenta revealed 365 loci (37 hypermethylated and 328 hypomethylated) at the statistical significance level of |Δβ| ≥ 0.17 and P ≤ 0.01. Notably, among the candidates showing significant signals, GRK5 (a member of G protein-coupled receptor kinase family that has previously been known to be associated with PE) showed a significantly hypomethylated level in the placentas of PE patients (Δβ = −0.176, P = 2.8 × 10). In the validation for the potential effect of GRK5 methylation on the gene regulation, GRK5 expression was significantly increased in the placentas from PE patients compared to those from controls ( P = 0.027). In further GO analysis, genes of MHC class II protein complex showed the most significant differential methylation in the maternal PB of PE patients, while genes of palate development were differentially methylated in the placenta. Although further replication and functional studies are required, our preliminary results suggest that PE has distinct DNA methylation profiles in the maternal PB and placentas, which may provide insight into future research. [ABSTRACT FROM AUTHOR]

Purpose: The solute carrier family 29 (equilibrative nucleoside transporter), member 1 (SLC29A1) is known to be involved in the transportation and resistance of the nucleoside analog cytosine arabinoside (AraC), one of the most effective drugs in the treatment of acute myeloid leukemia (AML).Methods: In vitro functional analysis in AML cells and genetic association study were performed.Results: Our functional analysis of SLC29A1 on anticancer effects of AraC showed that cytotoxic effects of AraC in AML cell lines were decreased by the reduction of SLC29A1 expression (P < 0.05). To investigate whether SLC29A1 polymorphisms could affect the achievement of complete remission (CR) in AML, we genotyped a total of six common single nucleotide polymorphisms on SLC29A1 in 103 AML patients, including 17 successes and 86 failures in CR. As a result, rs3734703 in 3'-untranslated region was significantly associated with CR even after correction for multiple testing (Fisher's exact test, P = 0.008; P corr = 0.04). A haplotype, ht3 (A-G-G-T-C-A; frequency = 0.294 in success group; frequency = 0.120 in failure group), also revealed a significant association with CR (P = 0.01; simulated P sim = 0.02).Conclusions: Although further replication in larger subjects and further functional evaluations are required, our results suggest the contribution of SLC29A1 to cytotoxic effects of AraC. In addition, genetic variations of SLC29A1 could be a potential marker for the achievement of CR of cancers of white blood cells including AML. [ABSTRACT FROM AUTHOR]

In this study, pressure drops on liquid-infused superhydrophobic surfaces were measured through a microchannel. A number of different superhydrophobic surfaces were prepared and tested. These surfaces included several PDMS surfaces containing precisely patterned microposts and microridges as well as a number of PTFE surfaces with random surface roughness created by sanding the PTFE with different sandpapers. Silicone oil was selected as the lubricant fluid and infused into the microstructures of the superhydrophobic surfaces. Several aqueous glycerin solutions with different viscosities were used as working fluids so that the viscosity ratio between the lubricant and the working fluid could be varied. The lubricant layer trapped within the precisely patterned superhydrophobic PDMS surfaces was found to be easily depleted over a short period of time even in limit of low flow rates and capillary numbers. On the other hand, the randomly rough superhydrophobic PTFE surfaces tested were found to maintain the layer of lubricant oil even at moderately high capillary numbers resulting in drag reduction that was found to increase with increasing viscosity ratio. The pressure drops on the liquid-infused PTFE surfaces were measured over time to determine the longevity of the lubricant layer. The pressure drops for the randomly rough PTFE surfaces were found to initially diminish with time before reaching a short-time plateau which is equivalent to maximum drag reduction. This minimum pressure drop was maintained for at least three hours in all cases regardless of feature size. However, as the depletion of the oil from the lubricant layer was initiated, the pressure drop was observed to grow slowly before reaching a second long-time asymptote which was equivalent to a Wenzel state. [ABSTRACT FROM AUTHOR]

Low density lipoprotein receptor (LDLR) plays an important role in plasma lipoprotein metabolism and pharmacological responses. Although mutations of LDLR and their functional associations with plasma LDL cholesterol concentrations have been described, no comprehensive comparisons of LDLR variants among populations are established. The aim of this study is to define the distribution of single nucleotide polymorphisms (SNPs) of LDLR and to discover novel variants across population groups. A total of 288 DNAs from 96 Korean, 48 Chinese, 48 Japanese, 48 African-American, and 48 European-American subjects were resequenced. A total of 59 SNPs (18 in the coding regions, 37 in the introns, and 4 in the 3′-untranslated region) were identified, including eight novel variants. Polymorphisms of LDLR showed significantly different distributions in comparisons among ethnic population groups ( P < 0.05, Fisher's exact test). Moreover, almost all of these differently distributed SNPs were common variants. Notably, prevalent variations-rs1003723, rs1799898, rs688, rs5925, rs6413504 in Europeans, nonsynonymous rs11669576 (Ala391Thr) in Africans, and rs14158 in Asians-were observed. In further in silico analyses for the novel SNPs, 2 intronic variants (+17716G>A in the intron 5 and +38569A>C in the intron 16) were predicted as potential branch point sites for alternative splicing. Although this study is not free from limitations such as insufficient sample size and no functional studies on the novel SNPs, our findings provides supporting information about LDLR genetic variability among ethnic groups and pharmacogenetics studies for plasma lipoprotein metabolism. [ABSTRACT FROM AUTHOR]

Recently, CYP2A6, CYP2B6, CYP2C8, and CYP2E1 have been reported to play a role in the metabolic effect of pharmacological and carcinogenic compounds. Moreover, genetic variations of drug metabolism genes have been implicated in the interindividual variation in drug disposition and pharmacological response. To define the distribution of single nucleotide polymorphisms (SNPs) in these four CYP2 family genes and to discover novel SNPs across ethnic groups, 288 DNAs composed of 48 African-Americans, 48 European-Americans, 48 Japanese, 48 Han Chinese, and 96 Koreans were resequenced. A total of 143 SNPs, 26 in CYP2A6, 45 in CYP2B6, 29 in CYP2C8, and 43 in CYP2E1, were identified, including 13 novel variants. Notably, two SNPs in the regulatory regions, a promoter SNP rs2054675 and a nonsynonymous rs3745274 (p.172Q>H) in CYP2B6, showed significantly different minor allele frequencies (MAFs) among ethnic groups (minimum P = 4.30 × 10). In addition, rs2031920 in the promoter region of CYP2E1 showed a wide range of MAF between different ethnic groups, and even among other various ethnic groups based on public reports. Among 13 newly discovered SNPs in this study, 5 SNPs were estimated to have potential functions in further in silico analyses. Some differences in genetic variations and haplotypes of CYP2A6, CYP2B6, CYP2C8, and CYP2E1 were observed among populations. Our findings could be useful in further researches, such as genetic associations with drug responses. [ABSTRACT FROM AUTHOR]

In the present study, we explored the possible association between KIF1B polymorphisms and inflammatory demyelinating disease (IDD) susceptibility. Eleven single nucleotide polymorphisms (SNPs) were selected for the present study based on the literature, as well as linkage disequilibrium, minor allele frequency, and location. The SNPs were genotyped in 178 IDD subjects consisting of 99 neuromyelitis optica subjects, 79 multiple sclerosis subjects, and 237 healthy controls (Total N = 415). We next preformed logistic analysis to validate associations between the KIF1B polymorphisms and the risk of IDD. Statistical analyses revealed that rs17396382 and ht4 were significantly associated with IDD susceptibility with odds ratios of 2.22 and 2.17 ( P = 0.001 and 0.004; P = 0.01 and 0.03, respectively). In addition, although P values for six variants (rs3748576, rs7520935, rs2275424, rs11576866, rs17411502, and rs11121552) and one haplotype (ht1) did not reach the threshold of significance after correction for multiple testing, the SNPs showed a nominal association in primary analysis ( P = 0.02 ~ 0.04). Our results suggest that rs17396382 and ht4 might be involved in IDD pathogenesis. [ABSTRACT FROM AUTHOR]

Asthma is a global health problem which threatens approximately 300 million patients worldwide. Among them, up to 20 % of the asthma patients are classified as aspirin exacerbated respiratory disease (AERD). Interleukin- 1 receptor associated kinase ( IRAK2) is associated with necrosis factor kappa B (NF-кB) pathway via interleukin-1 (IL-1) signaling. NF-кB pathway is known to be involved in asthma development, and several interleukin and IRAK family members have also been reported to be associated with asthma or AERD. Since IRAK2 plays an important role in the asthma etiology, we hypothesized that the genetic variants of IRAK2 may be associated with AERD. This study genotyped a total of 25 common single nucleotide polymorphisms (SNPs) in 163 AERD cases and 429 aspirin-tolerant asthma (ATA) controls. As a result, no significant association was found between the genetic variants of IRAK2 and AERD ( P > 0.05). In further regression analysis for the forced expiratory volume in 1 s (FEV) decline, an important phenotype for diagnosing AERD, although one haplotype ( BL1_ht3) showed a nominal association with FEV decline ( P = 0.04), the significance disappeared after correction for multiple testing ( P > 0.05). Despite limitations in our study and need for replications, our results suggest that the genetic variants of IRAK2 might not be associated with AERD and the obstructive symptoms in asthma. [ABSTRACT FROM AUTHOR]

The purpose of this study was to evaluate the microscopic changes and surface roughness on hydroxyapatite (HA)-coated implants following exposure to different powers and durations of Er:YAG laser irradiation in order to determine the proper pulse energy level and irradiation time. Ten HA-coated implants and ten fluoride-modified TiO2 implants were used. The implants were divided into a control (one implant) and test group (nine implants) for each implant type. Implants in the test groups were sub-divided into three groups (three implants per group) based on the applied laser pulse energy and irradiation time. The measurement of surface roughness was performed on all implants in the test groups using a white light interferometer before and after laser irradiation. R a values were recorded and compared in order to evaluate changes in surface roughness. For HA-coated implants, the R a values increased in all test groups after laser irradiation. However, mean R a values in the fluoride-modified TiO2-blasted implant test group were decreased after irradiation. There was no statistical difference. Scanning electron microscope analysis revealed surface alterations in both the HA-coated and fluoridated TiO2-blasted implants irradiated for 1.5 min at 100 mJ/pulse, 10 Hz. When the pulse energy and irradiation time increased, greater surface alterations, including surface flattening and microfractures, were observed. In conclusion, the results of the current study suggest that no changes could be observed in both HA-coated implants and fluoride-modified TiO2-blasted implants after irradiation at an intensity of 100 mJ/pulse, 10 Hz for 1 min performed to achieve surface detoxification. [ABSTRACT FROM AUTHOR]

Three-photon excitation is a process that occurs when three photons are simultaneously absorbed within a luminophore for photo-excitation through virtual states. Although the imaging application of this process was proposed decades ago, three-photon biomedical imaging has not been realized yet owing to its intrinsic low quantum efficiency. We herein report on high-resolution in vitro and in vivo imaging by combining three-photon excitation of ZnS nanocrystals and visible emission from Mn2+ dopants. The large three-photon cross-section of the nanocrystals enabled targeted cellular imaging under high spatial resolution, approaching the theoretical limit of three-photon excitation. Owing to the enhanced Stokes shift achieved through nanocrystal doping, the three-photon process was successfully applied to high-resolution in vivo tumour-targeted imaging. Furthermore, the biocompatibility of ZnS nanocrystals offers great potential for clinical applications of three-photon imaging. [ABSTRACT FROM AUTHOR]

Aspirin-exacerbated respiratory disease (AERD) is a nonallergic clinical syndrome characterized by a severe decline in forced expiratory volume in one second (FEV1) following the ingestion of non-steroidal anti-inflammatory drugs (NSAIDs) such as aspirin. The effects of genetic variants have not fully explained all of the observed individual differences to an aspirin challenge despite previous attempts to identify AERD-related genes. In the present study, we performed genome-wide association study (GWAS) and targeted association study in Korean asthmatics to identify new genetic factors associated with AERD. A total of 685 asthmatic patients without AERD and 117 subjects with AERD were used for the GWAS of the first stage, and 996 asthmatics without AERD and 142 subjects with AERD were used for a follow-up study. A total of 702 SNPs were genotyped using the GoldenGate assay with the VeraCode microbead. GWAS revealed the top-ranked variants in 3′ regions of the HLA-DPB1 gene. To investigate the detailed genetic effects of an associated region with the risk of AERD, a follow-up targeted association study with the 702 single nucleotide polymorphisms (SNPs) of 14 genes was performed on 802 Korean subjects. In a case-control analysis, HLA-DPB1 rs1042151 (Met105Val) shows the most significant association with the susceptibility of AERD ( p = 5.11 × 10; OR = 2.40). Moreover, rs1042151 also shows a gene dose for the percent decline of FEV1 after an aspirin challenge ( p = 2.82 × 10). Our findings show that the HLA-DPB1 gene polymorphism may be the most susceptible genetic factor for the risk of AERD in Korean asthmatics and confirm the importance of HLA-DPB1 in the genetic etiology of AERD. [ABSTRACT FROM AUTHOR]

This paper proposes a method for mapping the height information on an area around a vehicle and of identifying a drivable area by fusing a stereo camera and a laser sensor. A SOM (Self Organizing Map) clustering algorithm obtained from the depth information of the stereo camera is used to analyze the front part area of a vehicle in forms of several candidate planes. In addition, an IMU indicating the current pose of a vehicle is applied to detect a drivable plane. A laser sensor installed on a vehicle's roof scans the front part with a single line and informs a distance value. A drivable plane detected is utilized to calculate height value in the normal direction detected by the laser scan data. Additionally, when the height already mapped has a value higher than that of the threshold, it is regarded as an obstacle and the vehicle is prevented from coming into contact with it. Regarding the vehicle position estimation, a Kalman filter method is used for real-time mapping during driving. The moving location of the vehicle is dead reckoned based on steering angle and velocity, and this value is compensated using the position value received from the GPS. The vehicle's position and mapping coordinates are converted into latitude and longitude values. This study demonstrates that it is possible to generate a precise 2D height map by conducting a test in a real road environment with various slope angles and obstacles. [ABSTRACT FROM AUTHOR]

Modest effects of genes in various pathways are significant in the etiology of complex human diseases, including aspirin exacerbated respiratory disease (AERD). By functioning as a relevant component of respiratory processes, the human kinesin family member C1 ( KIFC1) is hypothesized to play a role in AERD pathogenesis. A case-control analysis was carried out by comparing the genotype distribution of six KIFC1 single-nucleotide polymorphisms between 93 AERD cases and 96 aspirin-tolerant asthma controls in a Korean population. After controlling for confounds, logistic and regression models via various modes of genetic inheritance facilitated the association analysis. Initial results revealed significant association at 0.05 level of significance between several KIFC1 variations and AERD ( P = 0.01-0.05, OR = 1.81-1.90) as well as fall rate of forced expiratory volume in the 1st second, an important diagnostic marker of airways constriction ( P = 0.04-0.05). However, the signals were not deemed significant after multiple testing corrections ( P > 0.05). Although the results do not support a major role of KIFC1 in AERD pathogenesis in a Korean asthma cohort, further replication and validation studies are required to clarify the current findings. [ABSTRACT FROM AUTHOR]

A Pt-loaded carbon black electrode was prepared by pulsed electrophoresis deposition in a Pt colloid solution as a plating bath to overcome the growth problem of a Pt catalyst during deposition in an electrochemical process. This method is a promising technique for preparing Pt catalyst layers at the polymer electrolyte/electrode interface. The particle size of the Pt catalyst loaded by electrophoresis deposition was the same as that of Pt nanoparticles (3-4 nm) in a colloid and the particle size was maintained even during deposition. The loading of the Pt catalyst was controlled by the pH of the Pt colloid and deposition time. The Pt nanoparticles were deposited on a carbon black electrode to a depth of 2.5 μm. [ABSTRACT FROM AUTHOR]

Background: Nasal polyps are abnormal lesions that cause airway obstruction and can occur along with other respiratory diseases. On account of its association with aspirin exacerbated respiratory disease (AERD), the human discoidin, CUB and LCCL domain containing 2 ( DCBLD2) is hypothesized to be a candidate gene for the development of nasal polyps in asthma patients. Methods: A total of 12 single-nucleotide polymorphisms (SNPs) were genotyped in 467 Korean asthma patients who were stratified further into 108 AERD and 353 aspirin-tolerant asthma (ATA) subgroups. Five major haplotypes were inferred from pairwise comparison of the polymorphisms. The patients were matched to control for confounds, and differences in the frequency distribution of DCBLD2 SNPs and haplotypes were analyzed using logistic models via various modes of genetic inheritance. Results: Results reveal significant association of rs828618 and DCBLD2_ht1 with nasal polyposis in the overall asthma patients group ( P = 0.006, P = 0.05). Interestingly, the strength of association were maintained in the ATA subgroup ( P = 0.007, P = 0.06), and moderate correlation was detected in the AERD subgroup ( P = 0.04-0.05, P > 0.05). Conclusions: Although further replication and validation are needed, these findings suggest that DCBLD2 could be a potential marker and drug target for treatment of nasal polyposis in Korean asthma patients. [ABSTRACT FROM AUTHOR]

Aspirin exacerbated respiratory disease (AERD) is a clinical condition characterized by severe decline in forced expiratory volume in one second (FEV1) following the ingestion of non-steroidal anti-inflammatory drugs (NSAIDs), including aspirin. The exacerbated inflammatory response in Fancc-deficient mice has been reported to be associated with hemopoietic responses that are also related to AERD pathogenesis. To investigate associations of FANCC polymorphisms with AERD and related phenotypes, this study genotyped 25 common single nucleotide polymorphisms (SNPs) in a total of 592 Korean asthmatics including 163 AERD and 429 aspirin-tolerant asthma (ATA) subjects. Logistic analysis revealed that genetic polymorphisms of the FANCC gene might not be directly related to AERD development and nasal polyposis ( P > 0.05). However, the FEV1 decline by aspirin provocation showed significant associations with FANCC polymorphisms ( P = 0.006-0.04) and a haplotype (unique to rs4647416G > A, P = 0.01 under co-dominant, P = 0.006 under recessive model). In silico analysis showed that the 'A' allele of rs4647376C > A, which was more prevalent in AERD than in ATA, could act as a potential branch point (BP) site for alternative splicing (BP score = 4.16). Although replications in independent cohorts and further functional evaluations are still needed, our preliminary findings suggest that FANCC polymorphisms might be associated with the obstructive symptoms in allergic diseases. [ABSTRACT FROM AUTHOR]

Schizophrenia is a serious and disabling mental disorder with a high heritability rate. The human neuregulin 1 ( NRG1) on 8p12 has been implicated as a candidate gene for schizophrenia. However, controversial results of the associations of NRG1 polymorphisms with schizophrenia and related phenotypes have been reported. In this study, four NRG1 single nucleotide polymorphisms, three in the promoter region, and one nonsynonymous in coding region, were genotyped in a total of 825 subject including 435 schizophrenia cases and 390 normal controls of Korean ethnicity. Although logistic association analysis of NRG1 polymorphisms and haplotypes with schizophrenia showed a nominal association in rs4623364G > C ( P = 0.04), the significance disappeared after corrections for multiple testing (corrected P > 0.05). Additional case/control and multiple regression analyses in schizophrenia patients using a method that measures the smooth pursuit eye movement (SPEM) function globally based on natural logarithmic values of the signal/noise ratio also showed no association between NRG1 variants and SPEM abnormality among patients with schizophrenia ( P > 0.05). Despite the need for further replications in other cohorts, our findings provide additional supporting information that four variants in NRG1 investigated in this study may not be associated with schizophrenia and its related SPEM function in a Korean population. [ABSTRACT FROM AUTHOR]

Several studies have investigated the roles of genetic polymorphisms in rheumatoid arthritis (RA). Some of these studies reported that polymorphisms of poly(ADP-ribose) polymerase 1 gene ( PARP- 1) are linked to rheumatoid arthritis. Poly(ADP-ribose) polymerase is an enzyme involved in DNA repair, genomic stability, apoptosis, gene transcription, proliferation, and autoimmunity. To determine whether genetic polymorphisms of PARP- 1 are related to rheumatoid arthritis in a Korean population, six single nucleotide polymorphisms (SNPs), which were selected based on LDs and minor allele frequency (MAF > 0.05) in our previous study, were genotyped in 1,202 patients with rheumatoid arthritis and 979 unrelated healthy controls. As a result, no significant association between the susceptibility to rheumatoid arthritis and PAPR- 1 polymorphisms was found. However, in further analysis depending on the radiological severity of rheumatoid arthritis, one PARP- 1 polymorphism, rs1805413 (OR = 0.11; 95% CI = 0.02-0.55; P = 0.007; P = 0.04), and one haplotype ( ht6, OR = 0.11; 95% CI = 0.02-0.55; P = 0.007; P = 0.04) were significantly associated with the radiological severity risk of RA in a recessive model. In addition, a recessive model revealed a correlation between one RA haplotype ( ht4) and anti-CCP antibody negativity (OR 0.24, 95% CI 0.10-0.63, P = 0.003; P = 0.02). Despite a possible association between PARP- 1 and the radiological severity of RA, this study found no statistical association between PARP- 1 polymorphisms and the susceptibility to rheumatoid arthritis in a Korean population. [ABSTRACT FROM AUTHOR]

The human HLA class II histocompatibility antigen, DR alpha chain ( HLA-DRA) is a member of the MHC class II gene family that activates T cells allowing secretion in various cytokines to immune responses. Thus, we explored whether the genetic variations in HLA-DRA gene can influence susceptibility for aspirin exacerbated respiratory disease (AERD). To carry out the investigation, 22 single nucleotide polymorphisms (SNPs) in HLA-DRA were genotyped in 592 Korean asthma patients. Logistic and regression analyseis wereas used to evaluate the P-values for associations of HLA-DRA polymorphisms with AERD and a relevant phenotype, the fall rate of forced expiratory volume in the 1 second (FEV). Logistic analyses revealed that two variants, rs6911777 and HLA_DRA_BL1_ht3 were initially associated with AERD via dominant and recessive models ( P = 0.05 and 0.01, respectively), however, the signals did not reach the threshold of significance after multiple corrections. Furthermore, we observed that fall rate of FEV1 by aspirin provocation was marginally different between AERD cases and aspirin-tolerant asthma (ATA) controls (mean = 24.63 vs 3.54, respectively). This study provides result of first association analysis between the variants of HLA-DRA and the risk of AERD, and conclusions derived from the study do not support significant roles of polymorphisms in HLA-DRA with AERD. [ABSTRACT FROM AUTHOR]

The human ubiquitin protein ligase E3C (UBE3C) regulates airway inflammatory responses and is hypothesized to be associated with the presence of nasal polyps in asthma-related diseases. A total of 24 UBE3C single-nucleotide polymorphisms (SNPs) were genotyped in a 467 Korean asthma cohort that was stratified into more homogenous phenotypes of 114 aspirin-exacerbated respiratory disease subgroup and 353 aspirin-tolerant asthma (ATA) subjects. Association analysis revealed that 16 UBE3C SNPs were significantly associated with presence of nasal polyps in the overall asthma group (P=0.0008 and Pcorr=0.01; odds ratio (OR)=0.60). The strength of association from 10 polymorphisms was increased in the ATA subgroup (P=0.0002 and Pcorr=0.003; OR=0.49). In addition, UBE3C_ht1 was found to be consistently associated with nasal polyps in the overall asthmatics group (P=0.006) and the ATA phenotype (P=0.002; Pcorr=0.02) via a codominant mechanism. Our findings provide evidence that variations in UBE3C are potent genetic markers of nasal polyps development in Korean asthmatics and may contribute novel insights into the clinical relevance and potential involvement of UBE3C in respiratory deficiencies. [ABSTRACT FROM AUTHOR]

Aspirin exacerbated respiratory disease (AERD) induces bronchoconstriction in asthmatic patients characterized with a clinical condition of severe decline in forced expiratory volume in one second (FEV1) after ingestion of aspirin. Two genes consisting a heterodimer, transporter 1 and 2, ATP-binding cassette, sub-family B (MDR/TAP) (TAP1 and TAP2) within the major histocompatibility complex (MHC) region, have been implicated in immunodeficiency and bronchiectasis development. To investigate the associations of TAP1 and TAP2 genetic polymorphisms with AERD and phenotypic FEV1 decline, a total of 43 common single-nucleotide polymorphisms (SNPs) including 12 SNPs of TAP1 and 31 SNPs of TAP2 were genotyped in 93 AERD patients and 96 aspirin-tolerant asthma controls. Interestingly, regression analysis revealed that polymorphisms and haplotypes of TAP2 were associated with FEV1 decline by aspirin provocation (P=0.002-0.04), with about twofold decline rate of FEV1 in most of minor homozygotes compared with major homozygotes. In addition, nominal evidences of association between TAP2 and AERD development were observed (P=0.02-0.04). However, TAP1 polymorphisms showed no relations to both AERD and FEV1 decline after aspirin challenge (P>0.05). Although further functional evaluations and replications are required, our preliminary findings provide supporting information that variants of TAP2 might be predisposing factors for FEV1 decline-related symptoms. [ABSTRACT FROM AUTHOR]

The human FYVE, RhoGEF and PH domain containing 6 ( FGD6) gene regulates mechanisms that are implicated in airway bronchospasm, and therefore, may be a risk factor for aspirin exacerbated respiratory disease (AERD). This study aims to investigate the association between FGD6 variations and AERD in a Korean asthma cohort. A total of 34 single nucleotide polymorphisms (SNPs) were selected for genotyping based on previously reported polymorphisms in the HapMap database. Genotyping was carried out using TaqMan assay and nine major haplotypes from two haplotype blocks were obtained in 163 AERD cases and 429 aspirin-tolerant asthma (ATA) controls. Genotype frequency distributions of FGD6 polymorphisms and haplotypes were analyzed using logistic and regression models. Findings from logistic and regression analyses revealed a lack of association of FGD6 genetic variations with AERD and fall rate of FEV ( P > 0.05 in co-dominant, dominant and recessive models). This preliminary report provides evidences that variations in the FGD6 gene do not influence the risk of AERD and its relevant phenotype in a Korean population. This report may contribute to the etiology of aspirin hypersensitivity in Korean asthma patients. [ABSTRACT FROM AUTHOR]

Background: The complement component 9 (C9), a major cytolytic protein in the complement system, plays an important role in the immunological process. However, associations between genetic variations of the complement factor and chronic hepatitis B virus infection still need to be investigated.Aims: We hypothesized that genetic variations in the complement component 9 gene can influence the clearance of chronic hepatitis B virus infection, hepatocellular carcinoma occurrence, and onset age of hepatocellular carcinoma. To investigate the relationship between complement component 9 variations and these disease phenotypes, we performed a case-control association analysis in a Korean population.Methods: Genetic variations were identified through direct DNA sequencing and genotyped using TaqMan assay (n = 1,103). In order to investigate the relationship of complement component 9 with chronic hepatitis B virus clearance and hepatocellular carcinoma occurrence, differences in SNP and haplotype frequency distributions were analyzed using logistic and multiple regression analyses with adjusted age and gender as covariates.Results: Although +23189C>T polymorphism in exon 4 and C9_ht2 [T-G-C-A-C] were significantly associated with clearance of chronic hepatitis B virus infection and hepatocellular carcinoma occurrence, the association signals were not retained after multiple testing corrections.Conclusions: We conclude that variations in the complement component 9 gene are unlikely to influence clearance of chronic hepatitis B virus infection and hepatocellular carcinoma occurrence. Although this preliminary result provides meaningful information, further functional investigations in other genetic factors for pathway analyses are required. [ABSTRACT FROM AUTHOR]

Human v-Fos Finuel-Biskis-Jinkins (FBJ) murine osteosarcoma viral oncogene homolog ( FOS) is located in 14q24.3. The FOS protein is a constituent of the activating protein-1 (AP-1) and its increased expression in the hepatocellular carcinoma (HCC) have been reported. In this study, the association of FOS polymorphisms with the HBV infection and HCC occurrence were evaluated in Korean patients. After re-sequencing in 24 unrelated healthy individuals, two common single nucleotide polymorphisms (SNPs) in regulatory regions that were selected based on linkage disequilibrium were genotyped in a total of 1,093 Korean subjects including 656 HBV chronic carriers, who were further stratified into chronic hepatitis/liver cirrhosis (CH/LC, n = 339) and HCC ( n = 317) groups, and 437 spontaneously recovered (SR) controls. Logistic regression and Cox relative hazard analysis showed no significant association of regulatory polymorphisms and haplotypes in FOS with HBV clearance and HCC development ( P > 0.05, respectively). [ABSTRACT FROM AUTHOR]

Development of liver cirrhosis (LC) and hepatocellular carcinoma (HCC). The transferrin ( TF) gene encodes a blood plasma protein that delivers iron ion in the body. The iron uptake level has been shown to be different in HCC tumor regions, indicating a possible association between iron uptake level and HCC. To investigate whether genetic polymorphisms of TF are related with HBV clearance and/or HCC occurrence, we sequenced genomes of 24 individuals and detected 37 variants. Subsequently, eight single nucleotide polymorphisms (SNPs) in TF including 4 in the promoter region, 1 in 5′UTR and 3 in coding regions were selected and genotyped in 1,101 Korean subjects including 428 spontaneously recovered (SR) patients as controls and 673 chronic carriers (CC) as cases. Results of logistic analyses adjusted for age and gender, however, revealed no significant associations of polymorphisms and haplotypes in the TF gene with HBV clearance and HCC occurrence ( P > 0.05). Since age of HBV infection is a risk factor in progression to HCC, further Cox proportional regression analysis for age of HCC as a relative hazard was performed; but no association between TF polymorphisms and onset age of HCC was found ( P > 0.05). Although TF gene polymorphisms have been previously reported to be associated with various diseases, our findings indicate that genetic variations of the TF gene do not influence HBV clearance and HCC occurrence in a Korean population. [ABSTRACT FROM AUTHOR]

pirin-intolerant asthma (AIA) is an asthma phenotype characterized by the development of bronchoconstriction following ingestion of aspirin. Despite the well-defined pathological trigger, the underlying mechanisms of AIA are still unclear. With the biophysical characteristics of the human EMI domain-containing protein 2 ( EMID2) gene in relation to the extracellular matrix deposition and epithelial-mesenchymal transition as pivotal characteristics of airway remodeling in asthma, we hypothesized that genetic polymorphisms of EMID2 might affect the development of AIA. In this study, the allelic associations of 49 single-nucleotide polymorphisms (SNPs) of the human EMID2 gene were evaluated from 163 AIA patients and 429 aspirin-tolerant asthma (ATA) subjects as controls in a Korean population. Logistic analysis showed that five SNPs ( P = 0.01-0.04, but P > 0.05) and EMID2_BL2_ht2 haplotype (unique to the minor alleles of rs4727494 and rs13233066; P = 0.02; P = 0.02) were significantly associated with AIA. More interestingly, regression analysis of the decline of forced expiratory volume in one second (FEV) by aspirin provocation revealed that 10 SNPs ( P = 0.003-0.04) and four relevant haplotypes ( P = 0.002-0.02) were significantly associated with the fall rate of FEV by aspirin provocation, indicating that genetic polymorphisms of EMID2 could cause meaningful deficits in the upper and lower airways among AIA patients. These findings provide evidence that EMID2 may be a susceptible genetic factor for aspirin hypersensitivity among asthmatics in Korean population. [ABSTRACT FROM AUTHOR]

Introduction: The kinesin family number 3A ( KIF3A) gene on the human chromosomal 5q31-33 region, which is known as a susceptibility locus for immune diseases including asthma, plays a crucial role in generation of cilia. Results: A treatment with aspirin in the human bronchial epithelial cells increased the mRNA expression level of KIF3A compared to that of the untreated control ( P ≤ 0.01), and nasal polyp epithelia from aspirin-intolerant asthma (AIA) patients also showed a higher expression of KIF3A protein than aspirin-tolerant asthma controls. Further logistic analyses revealed that most polymorphisms of KIF3A were significantly associated with AIA ( P = 0.0004-0.02; P = 0.004-0.04) and the decline of forced expiratory volume at 1 s (FEV)% by aspirin provocation ( P = 0.004-0.04; P = 0.03). Discussion: Our findings suggest that the KIF3A gene and/or its polymorphisms might have a susceptibility effect on AIA, providing a new step toward controlling aspirin intolerance in asthmatics. [ABSTRACT FROM AUTHOR]

In this paper, a novel method of real-time fire detection based on HMMs is presented. First, we present an analysis of fire characteristics that provides evidence supporting the use of HMMs to detect fire; second, we propose an algorithm for detecting candidate fire pixels that entails the detection of moving pixels, fire-color inspection, and pixels clustering. The main contribution of this paper is the establishment and application of a hidden Markov fire model by combining the state transition between fire and non-fire with fire motion information to reduce data redundancy. The final decision is based on this model which includes training and application; the training provides parameters for the HMM application. The experimental results show that the method provides both a high detection rate and a low false alarm rate. Furthermore, real-time detection has been effectively realized via the learned parameters of the HMM, since the most time-consuming components such as HMM training are performed off-line. [ABSTRACT FROM AUTHOR]

The rhizome of Atractylodes japonica Koidzumi (AJK) has been used in traditional medicine for treatment of arthritis, bronchitis and respiratory infectious disease, whereas its effects on inflammatory reactions have not been unknown recently. In this study, the effects of AJK on allergic inflammation and its signaling were investigated in the induced human mast cells and animal model. This study showed that ethanol extract of AJK interestingly suppressed the production and mRNA expression of TNF-α, IL-6 and IL-8, as important inflammatory cytokines. Furthermore, AJK inhibited the nuclear translocation of nuclear factor (NF)-κB through inhibition of the phosphorylation of IB-κ, which was additionally elucidated by NF-κB promoter-mediated luciferase activity. In addition, the phosphorylation of ERK was increased in pretreatment with AJK, whereas there was no change in JNK and p38 MAPK. However, AJK showed no effects on anti-DNP IgE-mediated in vivo PCA reaction and histamine release, as key events of mast cell-mediated immediate allergic reactions. These results suggest that AJK might be involved in not early-phase but transition to late-phase reactions of allergic inflammation and could modulate through other signal pathways. Taken together, AJK could be used as a treatment for mast cell mediated late-phase/chronic allergic inflammatory reactions. [ABSTRACT FROM AUTHOR]

An amendment to this paper has been published and can be accessed via a link at the top of the paper. [ABSTRACT FROM AUTHOR]

Chronic hepatitis B virus (HBV) infection can cause cirrhosis and hepatocellular carcinoma and is therefore a serious public health problem. Infected patients are currently treated with nucleoside/nucleotide analogs and interferon α, but this approach is not curative. Here, we screen 978 FDA-approved compounds for their ability to inhibit HBV replication in HBV-expressing HepG2.2.15 cells. We find that ciclopirox, a synthetic antifungal agent, strongly inhibits HBV replication in cells and in mice by blocking HBV capsid assembly. The crystal structure of the HBV core protein and ciclopirox complex reveals a unique binding mode at dimer-dimer interfaces. Ciclopirox synergizes with nucleoside/nucleotide analogs to prevent HBV replication in cells and in a humanized liver mouse model. Therefore, orally-administered ciclopirox may provide a novel opportunity to combat chronic HBV infection by blocking HBV capsid assembly. Current treatments for chronic hepatitis B virus (HBV) infection are not curative. Here, the authors show that an antifungal drug, ciclopirox, inhibits HBV capsid assembly and synergizes with nucleoside/nucleotide analogs to prevent HBV replication in cells and in a humanized liver mouse model. [ABSTRACT FROM AUTHOR]

Fatigue is a major symptom among patients with Hepatitis B virus (HBV). However, the physiological mechanisms regarding mediate fatigue and the relationships between fatigue, cortisol and cytokines are unclear in patients with HBV. The purpose of this study was to examine the relationships between perceived fatigue, cortisol, and cytokines in Korean patients with HBV. The mean score for overall fatigue was moderate. In linear regression analyses, TNF-α was only significant as a predictor of fatigue. In quantile regression analyses, the cortisol level was significant in the 70th, 80th, 90th quantiles in the cognitive/mood fatigue subdimension, which correspond to severe levels of fatigue. IL-6 levels were significant in 90th quantile in overall fatigue and in the cognitive/mood fatigue subdimension. Cortisol, IL-6, and TNF- α were related to perceived fatigue in patients with HBV, particularly in the cognitive/mood dimension. This suggests that the fatigue patterns of patients with HBV are related to their mental and mood states and physical responses, such as cortisol and cytokine levels, are correlated with the nature of the fatigue. In the clinic, interventions to manage fatigue in patients with HBV should be developed based on the characteristics of the fatigue. [ABSTRACT FROM AUTHOR]