Impacts of climate change: challenges of flooding in coastal East Asia

Over recent years a body of evidence has grown to suggest that East Asia is experiencing the effects of climate change. Allied to this is that coastal populations and economic assets are becoming more vulnerable to flood hazards. Flood vulnerability has increased owing to the combination of a number of human and physical variables: a) rapid coastal urban growth, b) anthropogenic changes to the environment, such as land subsidence through natural resource extraction or the removal of natural protective barriers, and c) increase in frequency and magnitude of coastal hazards associated with typhoons, storm surges, and sea-level rise. East Asia’s population is highly concentrated on low-lying coastal regions and deltaic cities are especially at risk. However, effective adaptation to climate impacts on many coasts is yet to develop. In this chapter, the drivers of coastal vulnerability are reviewed and examined in East Asia, exemplified by the Pearl River Delta (PRD), and its megacities of Guangzhou, Hong Kong and Shenzhen. The population of the PRD is expected to reach 120 million by 2050 and the delta is one of the most important economic centres in East Asia. Flood risk is substantial in the PRD, but flood-risk management appears to suffer from a lack of sufficient strategic planning to prepare for future climate extremes. Drawing on international experience of climate change adaptation and flood risk management, we suggest a path forward to develop adaptation strategies for deltaic and coastal cities in East Asia

A Time-Space Tradeoff for Triangulations of Points in the Plane

In this paper, we consider time-space trade-offs for reporting a triangulation of points in the plane. The goal is to minimize the amount of working space while keeping the total running time small. We present the first multi-pass algorithm on the problem that returns the edges of a triangulation with their adjacency information. This even improves the previously best known random-access algorithm

Association of two apolipoprotein A-I gene MspI polymorphisms with high density lipoprotein (HDL)-cholesterol levels and indices of obesity in selected healthy Chinese subjects and in patients with early-onset type 2 diabetes

OBJECTIVE: Previous studies have reported associations between two apolipoprotein A-I (apoA-I) gene MspI polymorphisms (G-75A and C83T) and high density lipoprotein (HDL)-cholesterol and/or apoA-I levels, but have not investigated the relationship with obesity. METHODS: We determined the distribution of these polymorphisms in 482 early-onset (< or = 40 years) Type 2 Chinese diabetics and 167 Chinese selected healthy controls. RESULTS: The -75A and 83T allele frequencies were similar in the diabetic and healthy subjects. In the healthy control subjects, HDL-cholesterol levels were significantly higher in the AA homozygotes than in the GG/GA carriers (1.74 +/- 0.58 vs. 1.45 +/- 0.58 mmol/l, P<0.001). Furthermore, analyses showed a significant relationship between increasing HDL-cholesterol tertiles and the AA genotype frequency in the selected healthy subjects (3.6, 8.9 and 16.1%, P=0.026). For the C83T polymorphism, healthy male CT carriers had higher HDL-cholesterol levels than CC homozygotes (1.71 +/- 0.57 vs. 1.25 +/- 0.30 mmol/l, P=0.001), but this was not found in females. No relationship between these polymorphisms and lipid levels was found in the diabetics, who had a more adverse lipid profile than the selected controls. In the diabetics, but not the controls, in CT carriers compared to CC homozygotes there were lower levels of body mass index (BMI; 23.8 +/- 3.9 vs. 25.4 +/- 4.7 kg/m2, P=0.048) and waist-to-height ratio (0.49 +/- 0.06 vs. 0.52 +/- 0.07, P=0.023), and this relationship was supported by tertile analysis. CONCLUSIONS: The -75AA genotype was associated with higher HDL-cholesterol levels in the selected healthy, but not diabetic, subjects. The 83T allele was associated with greater indices of obesity in the diabetic patients, and with higher HDL-cholesterol in heterozygous healthy male subjects.postprin

Albuminuria is a marker of increasing intracranial and extracranial vascular involvement in Type 2 diabetic Chinese patients

AIMS/HYPOTHESIS: Albuminuria has been reported to be a marker of cardiovascular risk factors and disease morbidity and mortality, but its relationship with intracerebral atherosclerotic disease is less clear. The aim of this study was to investigate the association between albuminuria and intracranial and extracranial vascular involvement in Chinese Type 2 diabetic patients. METHODS: The anthropometric and fasting biochemical measurements of 966 Type 2 diabetic patients with normoalbuminuria (55.6%), microalbuminuria (27.7%) or macroalbuminuria (16.7%) were compared. The prevalence of microvascular and macrovascular disease and middle cerebral artery (MCA) stenosis, measured by transcranial Doppler ultrasound, were also compared between the groups. RESULTS: Albuminuria was closely associated with a range of adverse parameters, including high BP, dyslipidaemia, smoking and adiposity (all p<0.01). The prevalence of microvascular disease (retinopathy p<0.001) and macrovascular disease (peripheral vascular disease p=0.012, myocardial infarction, p=0.004, MCA stenosis p<0.001) increased significantly with increasing levels of albuminuria. Albuminuria was also found to be an independent predictor of microvascular and macrovascular disease. CONCLUSIONS/INTERPRETATION: Albuminuria was an independent predictor of increasing levels of vascular risk factors and microvascular and macrovascular disease in this group of Type 2 diabetic patients, and a possible role for albuminuria as a marker of intracranial cerebrovascular disease should be further investigated.postprin

Influenza vaccination and hospitalisation in Elderly Health Centres.

1. A cohort of Elderly Health Centres was examined to determine whether influenza vaccination decreased hospitalisation and mortality. 2. In the influenza season, influenza vaccination reduced all-cause mortality by half and cardiorespiratory hospitalisation by a quarter. The extent to which influenza vaccination protects older people from serious morbidity and mortality needs to be confirmed in appropriately designed studies, so that scarce health care resources can be used effectivelypublished_or_final_versio

Finding the Median (Obliviously) with Bounded Space

We prove that any oblivious algorithm using space $S$ to find the median of a list of $n$ integers from $\{1,...,2n\}$ requires time $\Omega(n \log\log_S n)$. This bound also applies to the problem of determining whether the median is odd or even. It is nearly optimal since Chan, following Munro and Raman, has shown that there is a (randomized) selection algorithm using only $s$ registers, each of which can store an input value or $O(\log n)$-bit counter, that makes only $O(\log\log_s n)$ passes over the input. The bound also implies a size lower bound for read-once branching programs computing the low order bit of the median and implies the analog of $P \ne NP \cap coNP$ for length $o(n \log\log n)$ oblivious branching programs

Interpolated sequences and critical LL-values of modular forms

Recently, Zagier expressed an interpolated version of the Ap\'ery numbers for $\zeta(3)$ in terms of a critical $L$-value of a modular form of weight 4. We extend this evaluation in two directions. We first prove that interpolations of Zagier's six sporadic sequences are essentially critical $L$-values of modular forms of weight 3. We then establish an infinite family of evaluations between interpolations of leading coefficients of Brown's cellular integrals and critical $L$-values of modular forms of odd weight.Comment: 23 pages, to appear in Proceedings for the KMPB conference: Elliptic Integrals, Elliptic Functions and Modular Forms in Quantum Field Theor

Associations of apolipoprotein E exon 4 and lipoprotein lipase S447X polymorphisms with acute ischemic stroke and myocardial infarction

Background: Because apolipoprotein E (apoE) and lipopoprotein lipase (LPL) polymorphisms interact with each other and with other factors to affect lipid metabolism, we sought to determine their separate and combined effects in association with ischemic vascular disease. Methods: We performed a case-control study of 816 subjects: 246 acute ischemic stroke patients, 234 acute myocardial infarction patients, and 336 controls. APOE exon 4 and LPL S447X genotypes were determined. Results: APOE ε2 and ε4 homozygotes were increased in stroke (4.5% vs. 1.0%, p = 0.008), while in myocardial infarction the ε4 allele was increased (12.6% vs. 9.5%, p = 0.006) but ε2 was decreased (3.7% vs. 12.1%, p = 0.000006). For subjects with either APOE ε2 or ε4 alleles, LPL X alleles were increased in vascular disease (OR = 2.2, p = 0.01). LPL X alleles displayed opposite tendencies toward association with disease when subjects were divided by sex, smoking, or APOE genotype. Meta-analysis and regression analysis of previous studies supported the sex and smoking dichotomies. Conclusion: This is the first report of an association of vascular disease with an interaction of APOE exon 4 and LPL S447X genotypes. Therefore, APOE genotypes and LPL S447X interactions with apoE, sex, and smoking may affect the risk of myocardial infarction and ischemic stroke. © 2006 by Walter de Gruyter.published_or_final_versio

Development of an in vitro periodontal biofilm model for assessing antimicrobial and host modulatory effects of bioactive molecules

Background: Inflammation within the oral cavity occurs due to dysregulation between microbial biofilms and the host response. Understanding how different oral hygiene products influence inflammatory properties is important for the development of new products. Therefore, creation of a robust host-pathogen biofilm platform capable of evaluating novel oral healthcare compounds is an attractive option. We therefore devised a multi-species biofilm co-culture model to evaluate the naturally derived polyphenol resveratrol (RSV) and gold standard chlorhexidine (CHX) with respect to anti-biofilm and anti-inflammatory properties.&lt;p&gt;&lt;/p&gt; Methods: An in vitro multi-species biofilm containing &lt;i&gt;S. mitis, F. nucleatum, P. Gingivalis&lt;/i&gt; and &lt;i&gt;A. Actinomycetemcomitans&lt;/i&gt; was created to represent a disease-associated biofilm and the oral epithelial cell in OKF6-TERT2. Cytotoxicity studies were performed using RSV and CHX. Multi-species biofilms were either treated with either molecule, or alternatively epithelial cells were treated with these prior to biofilm co-culture. Biofilm composition was evaluated and inflammatory responses quantified at a transcriptional and protein level.&lt;p&gt;&lt;/p&gt; Results: CHX was toxic to epithelial cells and multi-species biofilms at concentrations ranging from 0.01-0.2%. RSV did not effect multi-species biofilm composition, but was toxic to epithelial cells at concentrations greater than 0.01%. In co-culture, CHX-treated biofilms resulted in down regulation of the inflammatory chemokine IL-8 at both mRNA and protein level. RSV-treated epithelial cells in co-culture were down-regulated in the release of IL-8 protein, but not mRNA.&lt;p&gt;&lt;/p&gt; Conclusions: CHX possesses potent bactericidal properties, which may impact downstream inflammatory mediators. RSV does not appear to have bactericidal properties against multi-species biofilms, however it did appear to supress epithelial cells from releasing inflammatory mediators. This study demonstrates the potential to understand the mechanisms by which different oral hygiene products may influence gingival inflammation, thereby validating the use of a biofilm co-culture model.&lt;p&gt;&lt;/p&gt

Friedreich ataxia patient tissues exhibit increased 5-hydroxymethylcytosine modification and decreased CTCF binding at the FXN locus

© 2013 Al-Mahdawi et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use,distribution, and reproduction in any medium, provided the original author and source are credited.This article has been made available through the Brunel Open Access Publishing Fund.Friedreich ataxia (FRDA) is caused by a homozygous GAA repeat expansion mutation within intron 1 of the FXN gene, which induces epigenetic changes and FXN gene silencing. Bisulfite sequencing studies have identified 5-methylcytosine (5 mC) DNA methylation as one of the epigenetic changes that may be involved in this process. However, analysis of samples by bisulfite sequencing is a time-consuming procedure. In addition, it has recently been shown that 5-hydroxymethylcytosine (5 hmC) is also present in mammalian DNA, and bisulfite sequencing cannot distinguish between 5 hmC and 5 mC.The research leading to these results has received funding from the European Union Seventh Framework Programme (FP7/2007-2013) under grant agreement number 242193/EFACTS (CS), the Wellcome Trust [089757] (SA) and Ataxia UK (RMP) to MAP