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BackgroundIdiopathic membranous nephropathy (IMN) is one of the most common forms of autoimmune nephritic syndrome in adults. The purpose of this study is to evaluate whether polymorphisms of PLA2R1 affect the development of IMN.MethodsTaiwanese-Chinese individuals (129 patients with IMN and 106 healthy controls) were enrolled in this study. The selected single nucleotide polymorphisms (SNPs) in PLA2R1 were genotyped by real-time polymerase chain reaction using TaqMan fluorescent probes, and were further confirmed by polymerase chain reaction-restriction fragment length polymorphism. The roles of the SNPs in disease progression were analyzed.ResultsGenotype distribution was significantly different between patients with IMN and controls for PLA2R1 SNP rs35771982 (p = 0.015). The frequency of G allele at rs35771982 was significantly higher in patients with IMN as compared with controls (p = 0.005). In addition, haplotypes of PLA2R1 may be used to predict the risk of IMN (p = 0.004). Haplotype H1 plays a role in an increased risk of IMN while haplotype H3 plays a protective role against this disease. None of these polymorphisms showed a significant and independent influence on the progression of IMN and the risk of end-stage renal failure and death (ESRF/death). High disease progression in patients having C/T genotype at rs6757188 and C/G genotype at rs35771982 were associated with a low rate of remission.ConclusionsOur results provide new evidence that genetic polymorphisms of PLA2R1 may be the underlying cause of IMN, and the polymorphisms revealed by this study warrant further investigation.

Objective. Kawasaki disease (KD) is a pediatric systemic vasculitis of unknown cause for which a genetic influence is supposed. The purpose of this study was to identify possible genetic variants in the major histocompatibility complex (MHC) region that are associated with KD and the development of coronary artery aneurysms (CAAs) in a Taiwanese population.Methods. The 168 genetic variants covering the MHC locus were analyzed in an association study of a Taiwanese cohort of 93 KD patients and 680 unrelated healthy children matched for sex and age with the study patients.Results. Eleven single-nucleotide polymorphisms (SNPs) were associated with the occurrence of KD. The SNP located at the 3 -untranslated region of HLA-E (rs2844724) was highly associated (P < 1 ؋ 10 ؊7 ). In addition, the frequency of the C allele was higher in KD patients without CAAs than in controls (P < 0.001) due to a significantly increased frequency of the CC and CT genotypes. Plasma levels of soluble HLA-E were significantly higher in KD patients than in controls regardless of the presence of CAAs. Furthermore, there was a trend toward higher plasma levels of soluble HLA-E in KD patients with the CT and TT genotypes of the HLA-E gene polymorphism.Conclusion. Our results suggest that the HLA-E gene polymorphism may play a role in the pathogenesis of KD.

Cytolethal distending toxin (CDT) produced by Campylobacter jejuni comprises a heterotrimeric complex formed by CdtA, CdtB, and CdtC. Among these toxin subunits, CdtA and CdtC function as essential proteins that mediate toxin binding to cytoplasmic membranes followed by delivery of CdtB into the nucleus. The binding of CdtA/CdtC to the cell surface is mediated by cholesterol, a major component in lipid rafts. Although the putative cholesterol recognition/interaction amino acid consensus (CRAC) domain of CDT has been reported from several bacterial pathogens, the protein regions contributing to CDT binding to cholesterol in C. jejuni remain unclear. Here, we selected a potential CRAC-like region present in the CdtC from C. jejuni for analysis. Molecular modeling showed that the predicted functional domain had the shape of a hydrophobic groove, facilitating cholesterol localization to this domain. Mutation of a tyrosine residue in the CRAC-like region decreased direct binding of CdtC to cholesterol rather than toxin intermolecular interactions and led to impaired CDT intoxication. These results provide a molecular link between C. jejuni CdtC and membrane-lipid rafts through the CRAC-like region, which contributes to toxin recognition and interaction with cholesterol.

Hsueh K‐C, Lin Y‐J, Lin HC, Lin C‐Y. Serum leptin and adiponectin levels correlate with severity of allergic rhinitis.
Pediatr Allergy Immunol 2010: 21: e155–e159.
© 2009 John Wiley & Sons A/S The aim of this study was to evaluate the roles of leptin and adiponectin, which are adipokines produced by adipose tissue, in childhood allergic rhinitis (AR), and their association with severity of AR, parameters of atopy and pro‐/anti‐inflammatory cytokines. Serum levels of leptin, adiponectin, mite allergen‐specific and total immunoglobulin E, eosinophil cationic protein (ECP), and pro‐ and anti‐inflammatory cytokines were analysed in 97 non‐asthmatic children presenting with persistent AR and in 64 controls. The nasal symptom scores and body mass index were evaluated at the time of blood collection. We found that patients had significantly higher serum levels of leptin and significantly lower serum levels of adiponectin than controls. Furthermore, multivariate logistic regression analysis revealed that leptin and adiponectin were significant predictive factors for AR. Serum levels of leptin and adiponectin were significantly correlated with nasal symptom scores. There was no correlation between levels of pro‐ and anti‐inflammatory cytokines and level of leptin or adiponectin. A significant negative correlation was observed between serum levels of adiponectin and ECP levels in AR children. Our findings suggest that serum leptin and adiponectin levels may serve as predictors of disease severity in childhood AR and both of them appear to be attractive candidates for unmasking or modulating AR.

Food 3D printing enables the creation of customized food structures based on a person's individual needs. In this paper, we explore the use of food 3D printing to create perceptual illusions for controlling the level of perceived satiety given a defined amount of calories. We present FoodFab, a system that allows users to control their food intake through modifying a food's internal structure via two 3D printing parameters: infill pattern and infill density. In two experiments with a total of 30 participants, we studied the effect of these parameters on users' chewing time that is known to affect people's feeling of satiety. Our results show that we can indeed modify the chewing time by varying infill pattern and density, and thus control perceived satiety. Based on the results, we propose two computational models and integrate them into a user interface that simplifies the creation of personalized food structures.

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Interleukin-18 (IL-18) is associated with chronic inflammation, autoimmune diseases and various cancers and infectious diseases. An IL-18 genetic A/C polymorphism at coding position 105 (rs549908) has been linked with asthma and rheumatoid arthritis. We tested a hypothesis that the IL-18 genetic polymorphism confers systemic lupus erythematosus (SLE) susceptibility. Study participants were Taiwanese SLE patients and a healthy control group. Our results indicate (1) a significantly higher A allele frequency in SLE patients (P = 0.003; OR = 1.97; 95% CI = 1.26-3.08) and (2) a significantly higher A allele frequency in SLE patients with a central nervous system disorder (P = 0.027; OR = 7.18; 95% CI = 0.95-54.28). Our results suggest that the A/C polymorphism contributes to SLE pathogenesis.