Association of Interleukin-10 A-592C Polymorphism in Taiwanese Children with Kawasaki Disease

[[abstract]]Abstract: Elevated serum levels of interleukin-10 (IL-10) have been reported in patients with Kawasaki disease (KD). IL-10 reduces the inflammatory actions of macrophages and T cells and it may play a significant role in the regulation of inflammatory vascular damage associated with systemic vasculitis. The aim of this study was to examine whether -592 IL-10 promoter polymorphism is a susceptibility or severity marker of KID in Chinese patients in Taiwan. The study included 105 KD patients and 100 normal controls. Genotype and allelic frequencies for the IL-10 gene polymorphism in both groups were compared. There were no significant between-group differences in the genotype distribution of IL-10 A-592C gene polymorphism (P=0.08). However, the frequency of the -592*A allele was significantly increased in the patients with KD compared with controls (71.9% vs. 61.0%, P=0.019). The odds ratio for developing KD in individuals with IL-10 -592*A allele was 1.64 (95% confidence interval, 1.06-2.52) compared to individuals with the IL-10-592*C allele. No significant difference was observed in the genotype and allelic frequencies for the IL-10 A-592C polymorphism between patients with and without coronary artery lesions. The IL-10-592*A allele may be involved in the development of KD in Taiwanese children

Improved Algorithms for Recognizing Perfect Graphs and Finding Shortest Odd and Even Holes

Various classes of induced subgraphs are involved in the deepest results of graph theory and graph algorithms. A prominent example concerns the {\em perfection} of $G$ that the chromatic number of each induced subgraph $H$ of $G$ equals the clique number of $H$. The seminal Strong Perfect Graph Theorem confirms that the perfection of $G$ can be determined by detecting odd holes in $G$ and its complement. Chudnovsky et al. show in 2005 an $O(n^9)$ algorithm for recognizing perfect graphs, which can be implemented to run in $O(n^{6+\omega})$ time for the exponent $\omega<2.373$ of square-matrix multiplication. We show the following improved algorithms. 1. The tractability of detecting odd holes was open for decades until the major breakthrough of Chudnovsky et al. in 2020. Their $O(n^9)$ algorithm is later implemented by Lai et al. to run in $O(n^8)$ time, leading to the best formerly known algorithm for recognizing perfect graphs. Our first result is an $O(n^7)$ algorithm for detecting odd holes, implying an $O(n^7)$ algorithm for recognizing perfect graphs. 2. Chudnovsky et al. extend in 2021 the $O(n^9)$ algorithms for detecting odd holes (2020) and recognizing perfect graphs (2005) into the first polynomial algorithm for obtaining a shortest odd hole, which runs in $O(n^{14})$ time. We reduce the time for finding a shortest odd hole to $O(n^{13})$. 3. Conforti et al. show in 1997 the first polynomial algorithm for detecting even holes, running in about $O(n^{40})$ time. It then takes a line of intensive efforts in the literature to bring down the complexity to $O(n^{31})$, $O(n^{19})$, $O(n^{11})$, and finally $O(n^9)$. On the other hand, the tractability of finding a shortest even hole has been open for 16 years until the very recent $O(n^{31})$ algorithm of Cheong and Lu in 2022. We improve the time of finding a shortest even hole to $O(n^{23})$.Comment: 29 pages, 5 figure

An Optimal Algorithm for the Maximum-Density Segment Problem

We address a fundamental problem arising from analysis of biomolecular sequences. The input consists of two numbers $w_{\min}$ and $w_{\max}$ and a sequence $S$ of $n$ number pairs $(a_i,w_i)$ with $w_i>0$. Let {\em segment} $S(i,j)$ of $S$ be the consecutive subsequence of $S$ between indices $i$ and $j$. The {\em density} of $S(i,j)$ is $d(i,j)=(a_i+a_{i+1}+...+a_j)/(w_i+w_{i+1}+...+w_j)$. The {\em maximum-density segment problem} is to find a maximum-density segment over all segments $S(i,j)$ with $w_{\min}\leq w_i+w_{i+1}+...+w_j \leq w_{\max}$. The best previously known algorithm for the problem, due to Goldwasser, Kao, and Lu, runs in $O(n\log(w_{\max}-w_{\min}+1))$ time. In the present paper, we solve the problem in O(n) time. Our approach bypasses the complicated {\em right-skew decomposition}, introduced by Lin, Jiang, and Chao. As a result, our algorithm has the capability to process the input sequence in an online manner, which is an important feature for dealing with genome-scale sequences. Moreover, for a type of input sequences $S$ representable in $O(m)$ space, we show how to exploit the sparsity of $S$ and solve the maximum-density segment problem for $S$ in $O(m)$ time.Comment: 15 pages, 12 figures, an early version of this paper was presented at 11th Annual European Symposium on Algorithms (ESA 2003), Budapest, Hungary, September 15-20, 200

Association of Interleukin-10 A-592C Polymorphism in Taiwanese Children with Kawasaki Disease

Elevated serum levels of interleukin-10 (IL-10) have been reported in patients with Kawasaki disease (KD). IL-10 reduces the inflammatory actions of macrophages and T cells and it may play a significant role in the regulation of inflammatory vascular damage associated with systemic vasculitis. The aim of this study was to examine whether -592 IL-10 promoter polymorphism is a susceptibility or severity marker of KD in Chinese patients in Taiwan. The study included 105 KD patients and 100 normal controls. Genotype and allelic frequencies for the IL-10 gene polymorphism in both groups were compared. There were no significant between-group differences in the genotype distribution of IL-10 A-592C gene polymorphism (P=0.08). However, the frequency of the -592*A allele was significantly increased in the patients with KD compared with controls (71.9% vs. 61.0%, P=0.019). The odds ratio for developing KD in individuals with IL-10-592*A allele was 1.64 (95% confidence interval, 1.06-2.52) compared to individuals with the IL-10-592*C allele. No significant difference was observed in the genotype and allelic frequencies for the IL-10 A-592C polymorphism between patients with and without coronary artery lesions. The IL-10-592*A allele may be involved in the development of KD in Taiwanese children

Reduced Health-Related Quality of Life in Elders with Frailty: A Cross-Sectional Study of Community-Dwelling Elders in Taiwan

PURPOSE: Exploring the domains and degrees of health-related quality of life (HRQOL) that are affected by the frailty of elders will help clinicians understand the impact of frailty. This association has not been investigated in community-dwelling elders. Therefore, we examined the domains and degree of HRQOL of elders with frailty in the community in Taiwan. METHODS: A total of 933 subjects aged 65 years and over were recruited in 2009 from a metropolitan city in Taiwan. Using an adoption of the Fried criteria, frailty was defined by five components: shrinking, weakness, poor endurance and energy, slowness, and low physical activity level. HRQOL was assessed by the short form 36 (SF-36). The multiple linear regression model was used to test the independent effects of frailty on HRQOL. RESULTS: After multivariate adjustment, elders without frailty reported significantly better health than did the pre-frail and frail elders on all scales, and the pre-frail elders reported better health than did the frail elders for all scales except the scales of role limitation due to physical and emotional problems and the Mental Component Summary (MCS). The significantly negative differences between frail and robust elders ranged from 3.58 points for the MCS to 22.92 points for the physical functioning scale. The magnitude of the effects of frail components was largest for poor endurance and energy, and next was for slowness. The percentages of the variations of these 10 scales explained by all factors in the models ranged from 11.1% (scale of role limitation due to emotional problems) to 49.1% (scale of bodily pain). CONCLUSIONS: Our study demonstrates that the disabilities in physical health inherent in frailty are linked to a reduction in HRQOL. Such an association between clinical measures and a generic measure of the HRQOL may offer clinicians new information to understand frailty and to conceptualize it within the broader context of disability

Genome-Wide Association Study and Functional Characterization Identifies Candidate Genes for Insulin-Stimulated Glucose Uptake

Distinct tissue-specific mechanisms mediate insulin action in fasting and postprandial states. Previous genetic studies have largely focused on insulin resistance in the fasting state, where hepatic insulin action dominates. Here we studied genetic variants influencing insulin levels measured 2 h after a glucose challenge in \u3e55,000 participants from three ancestry groups. We identified ten new loci (P \u3c 5 × 10-8) not previously associated with postchallenge insulin resistance, eight of which were shown to share their genetic architecture with type 2 diabetes in colocalization analyses. We investigated candidate genes at a subset of associated loci in cultured cells and identified nine candidate genes newly implicated in the expression or trafficking of GLUT4, the key glucose transporter in postprandial glucose uptake in muscle and fat. By focusing on postprandial insulin resistance, we highlighted the mechanisms of action at type 2 diabetes loci that are not adequately captured by studies of fasting glycemic traits

Association of Vascular Endothelial Growth Factor C-634 G Polymorphism in Taiwanese Children With Kawasaki Disease

[[abstract]]High expression of circulating vascular endothelial growth factor (VEGF) has been reported in patients with Kawasaki disease (KD). In the pathophysiology of KD, VEGF is considered to be involved, especially in the development of coronary artery lesions. This study aimed to examine whether the VEGF-634 promoter polymorphism is a marker of KD susceptibility or severity in Chinese patients in Taiwan. The study included 93 KD patients and 96 normal control subjects. Genotype and allelic frequencies for the VEGF gene polymorphism in the two groups were compared. The number of individuals with the VEGF-634 G/G genotype was significantly greater among the patients with KD than among the healthy control subjects (p = 0.011). The odds ratio for the development of KD in individuals with the VEGF-634 G/G genotype was found to be 2.03 (95% confidence interval [CI], 1.14–3.63) compared with the VEGF-634 G/C and VEGF-634 C/C genotypes. No significant difference was observed in the genotype or allelic frequencies of VEGF C-634 G polymorphism between the patients with and those without coronary artery lesions. In conclusion, the results suggest that VEGF-634 G/G genotype may be involved in the development of KD in Taiwanese children

Miller Fisher syndrome possibly related to mycoplasma pneumoniae infection: report of one case

[[abstract]]Ophthalmoplegia, ataxia, and areflexia were first described in 1956 by Miller Fisher and later were referred to as symptoms of Miller Fisher syndrome (MFS). This syndrome shares certain features with the Guillain-Barr? syndrome (GBS), including areflexia, cerebrospinal fluid findings and often a postinfectious presentation. It was believed to be a variant of GBS, but Miller Fisher syndrome has several key clinical features which differ from GBS. The anatomic location and pathogenesis of MFS continue to be a matter of debate. Our report focuses on a 6-year-old female patient who developed MFS following a respiratory tract infection with a serologically proven Mycoplasma pneumoniae infection. Although several neurological complications after Mycoplasma pneumoniae infection have been reported, subsequent MFS development has rarely been reported previously