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

Biodiversity conservation and the earth system – mind the gap

One of the most striking human impacts on global biodiversity is the ongoing depletion of large vertebrates from terrestrial and aquatic ecosystems. Recent work suggests this loss of megafauna can affect processes at biome or Earth system scales with potentially serious impacts on ecosystem structure and function, ecosystem services, and biogeochemical cycles. We argue that our contemporary approach to biodiversity conservation focuses on spatial scales that are too small to adequately address these impacts. We advocate a new global approach to address this conservation gap, which must enable megafaunal populations to recover to functionally relevant densities. We conclude that re-establishing biome and Earth system functions needs to become an urgent global priority for conservation science and policy

Effects of estradiol and FSH on maturation of the testis in the hypogonadal (hpg) mouse

<p>Abstract</p> <p>Background</p> <p>The hypogonadal (hpg) mouse is widely used as an animal model with which to investigate the endocrine regulation of spermatogenesis. Chronic treatment of these GnRH-deficient mice with estradiol is known to induce testicular maturation and restore qualitatively normal spermatogenesis. The aim of the current studies was to investigate whether these effects of estradiol are direct effects in the testis, or indirect actions via paradoxical stimulation of FSH secretion from the pituitary gland.</p> <p>Methods</p> <p>Initially, Western blot and immunohistochemistry were used to analyse tissues from hpg mice to identify potential sites of action of estradiol. In the main study, hpg mice were treated for 50 days with either an estradiol implant or daily injections of recombinant human FSH, or a combination of both, to determine whether estradiol would have an additive or synergistic effect with FSH on testis development, as assessed by histological analysis and stereological quantification of Leydig, Sertoli and germ cell proliferation.</p> <p>Results</p> <p>Western blot analysis revealed ERα immunoreactive bands of appropriate molecular weight in extracts of testis and pituitary glands from hpg mice, and immunohistochemical studies confirmed ERα in nuclei of anterior pituitary cells and Leydig and peritubular cells in hpg mice. Histological and morphometric analyses revealed that estradiol treatment alone was as effective as FSH in promoting Sertoli cell production and proliferation of the seminiferous epithelium, resulting in the production of elongating spermatids. Combined estradiol and FSH treatment did not produce a greater effect than either treatment alone, though an increased dose of FSH significantly increased seminiferous tubule volume and testis weight and increase Sertoli cell numbers further within the same time frame. In contrast, estradiol caused substantial increases in the wet weight of the seminal vesicles, whereas FSH was without effect on this tissue, and did not augment the actions of estradiol.</p> <p>Conclusion</p> <p>As ERalpha receptor is abundantly expressed in the pituitary gland of hpg mice, and estradiol did not exert effects on testis development over and above those of FSH, we conclude that the action of estradiol on testis development in <it>hpg </it>mice is predominantly via the stimulation of pituitary FSH release.</p

Cirsium species show disparity in patterns of genetic variation at their range-edge, despite similar patterns of reproduction and isolation

Genetic variation was assessed across the UK geographical range of Cirsium acaule and Cirsium heterophyllum. A decline in genetic diversity and increase in population divergence approaching the range edge of these species was predicted based on parallel declines in population density and seed production reported seperately. Patterns were compared with UK populations of the widespread Cirsium arvense.Populations were sampled along a latitudinal transect in the UK and genetic variation assessed using microsatellite markers. Cirsium acaule shows strong isolation by distance, a significant decline in diversity and an increase in divergence among range-edge populations. Geographical structure is also evident in C. arvense, whereas no such patterns are seen in C.heterophyllum. There is a major disparity between patterns of genetic variation in C. acaule and C. heterophyllum despite very similar patterns in seed production and population isolation in these species. This suggests it may be misleading to make assumptions about the geographical structure of genetic variation within species based solely on the present-day reproduction and distribution of populations

The frequency of missed test results and associated treatment delays in a highly computerized health system

<p>Abstract</p> <p>Background:</p> <p>Diagnostic errors associated with the failure to follow up on abnormal diagnostic studies ("missed results") are a potential cause of treatment delay and a threat to patient safety. Few data exist concerning the frequency of missed results and associated treatment delays within the Veterans Health Administration (VA).</p> <p>Objective:</p> <p>The primary objective of the current study was to assess the frequency of missed results and resulting treatment delays encountered by primary care providers in VA clinics.</p> <p>Methods:</p> <p>An anonymous on-line survey of primary care providers was conducted as part of the health systems ongoing quality improvement programs. We collected information from providers concerning their clinical effort (e.g., number of clinic sessions, number of patient visits per session), number of patients with missed abnormal test results, and the number and types of treatment delays providers encountered during the two week period prior to administration of our survey.</p> <p>Results:</p> <p>The survey was completed by 106 out of 198 providers (54 percent response rate). Respondents saw and average of 86 patients per 2 week period. Providers encountered 64 patients with missed results during the two week period leading up to the study and 52 patients with treatment delays. The most common missed results included imaging studies (29 percent), clinical laboratory (22 percent), anatomic pathology (9 percent), and other (40 percent). The most common diagnostic delays were cancer (34 percent), endocrine problems (26 percent), cardiac problems (16 percent), and others (24 percent).</p> <p>Conclusion:</p> <p>Missed results leading to clinically important treatment delays are an important and likely underappreciated source of diagnostic error.</p

Abnormal cognition, sleep, EEG and brain metabolism in a novel knock-in Alzheimer mouse, PLB1

Peer reviewedPublisher PD

Routes for breaching and protecting genetic privacy

We are entering the era of ubiquitous genetic information for research, clinical care, and personal curiosity. Sharing these datasets is vital for rapid progress in understanding the genetic basis of human diseases. However, one growing concern is the ability to protect the genetic privacy of the data originators. Here, we technically map threats to genetic privacy and discuss potential mitigation strategies for privacy-preserving dissemination of genetic data.Comment: Draft for comment

Interleukin-6 gene (IL-6): a possible role in brain morphology in the healthy adult brain

Background: Cytokines such as interleukin 6 (IL-6) have been implicated in dual functions in neuropsychiatric disorders. Little is known about the genetic predisposition to neurodegenerative and neuroproliferative properties of cytokine genes. In this study the potential dual role of several IL-6 polymorphisms in brain morphology is investigated. Methodology: In a large sample of healthy individuals (N = 303), associations between genetic variants of IL-6 (rs1800795; rs1800796, rs2069833, rs2069840) and brain volume (gray matter volume) were analyzed using voxel-based morphometry (VBM). Selection of single nucleotide polymorphisms (SNPs) followed a tagging SNP approach (e.g., Stampa algorigthm), yielding a capture 97.08% of the variation in the IL-6 gene using four tagging SNPs. Principal findings/results: In a whole-brain analysis, the polymorphism rs1800795 (−174 C/G) showed a strong main effect of genotype (43 CC vs. 150 CG vs. 100 GG; x = 24, y = −10, z = −15; F(2,286) = 8.54, puncorrected = 0.0002; pAlphaSim-corrected = 0.002; cluster size k = 577) within the right hippocampus head. Homozygous carriers of the G-allele had significantly larger hippocampus gray matter volumes compared to heterozygous subjects. None of the other investigated SNPs showed a significant association with grey matter volume in whole-brain analyses. Conclusions/significance: These findings suggest a possible neuroprotective role of the G-allele of the SNP rs1800795 on hippocampal volumes. Studies on the role of this SNP in psychiatric populations and especially in those with an affected hippocampus (e.g., by maltreatment, stress) are warranted.Bernhard T Baune, Carsten Konrad, Dominik Grotegerd, Thomas Suslow, Eva Birosova, Patricia Ohrmann, Jochen Bauer, Volker Arolt, Walter Heindel, Katharina Domschke, Sonja Schöning, Astrid V Rauch, Christina Uhlmann, Harald Kugel and Udo Dannlowsk

Sequentially based analysis versus image based analysis of Intima Media Thickness in common carotid arteries studies - Do major IMT studies underestimate the true relations for cardio- and cerebrovascular risk?

<p>Abstract</p> <p>Background</p> <p>Image-based B-mode ultrasound has gained popularity in major studies as a non-invasive method of measuring cardio- and cerebrovascular risk factors. However, none of the major studies appears to have paid sufficient attention to the variation in end diastolic wall process. By using sequentially based analyses (SBA) of Intima-Media Thickness (IMT), the general purpose of this study was to show that the current image based (ECG tracked) analysis (IBA) has some major variations and might underestimate the true relations for cardiovascular events and stroke for IMT measurement.</p> <p>Method</p> <p>The study group consisted of 2500 healthy male subjects aged between 35 to 55 years. 4 sequences (300 images) were analyzed per subject. 750,000 images were analysed throughout the course of this study.</p> <p>Results</p> <p>IBA showed significantly lower mean, maximal, and minimal values for IMT in CCA than for SBA. The correlation analysis between IBA and SBA with the cardio- and cerebrovascular risk factors showed a higher correlation of SBA for all risk factors. The Pearson coefficient was 0.81, p < 0.01, for SBA versus Framingham CHD risk level (FCRL) and 0.49, p = 0.01, for IBA versus FCRL.</p> <p>Conclusion</p> <p>IBA did not measure the true maximal values of the IMT in this study. Together with the correlation analysis, this indicates that IBA might underestimate the true relations for IMT and risk factors.</p

Associations between Polycyclic Aromatic Hydrocarbon–Related Exposures and p53 Mutations in Breast Tumors

Background: Previous studies have suggested that polycyclic aromatic hydrocarbons (PAHs) may be associated with breast cancer. However, the carcinogenicity of PAHs on the human breast remains unclear. Certain carcinogens may be associated with specific mutation patterns in the p53 tumor suppressor gene, thereby contributing information about disease etiology. Objectives: We hypothesized that associations of PAH-related exposures with breast cancer would differ according to tumor p53 mutation status, effect, type, and number. Methods: We examined this possibility in a population-based case–control study using polytomous logistic regression. As previously reported, 151 p53 mutations among 859 tumors were identified using Surveyor nuclease and confirmed by sequencing. Results: We found that participants with p53 mutations were less likely to be exposed to PAHs (assessed by smoking status in 859 cases and 1,556 controls, grilled/smoked meat intake in 822 cases and 1,475 controls, and PAH–DNA adducts in peripheral mononuclear cells in 487 cases and 941 controls) than participants without p53 mutations. For example, active and passive smoking was associated with p53 mutation–negative [odds ratio (OR) = 1.55; 95% confidence interval (CI), 1.11–2.15] but not p53 mutation–positive (OR = 0.77; 95% CI, 0.43–1.38) cancer (ratio of the ORs = 0.50, p < 0.05). However, frameshift mutations, mutation number, G:C→A:T transitions at CpG sites, and insertions/deletions were consistently elevated among exposed subjects. Conclusions: These findings suggest that PAHs may be associated with specific breast tumor p53 mutation subgroups rather than with overall p53 mutations and may also be related to breast cancer through mechanisms other than p53 mutation