Investigation of superstorm Sandy 2012 in a multi-disciplinary approach

At the end of October 2012, Hurricane Sandy moved from the Caribbean Sea into the Atlantic Ocean and entered the United States not far from New York. Along its track, Sandy caused more than 200 fatalities and severe losses in Jamaica, The Bahamas, Haiti, Cuba, and the US. This paper demonstrates the capability and potential for near-real-time analysis of catastrophes. It is shown that the impact of Sandy was driven by the superposition of different extremes (high wind speeds, storm surge, heavy precipitation) and by cascading effects. In particular the interaction between Sandy and an extra-tropical weather system created a huge storm that affected large areas in the US. It is examined how Sandy compares to historic hurricane events, both from a hydro-meteorological and impact perspective. The distribution of losses to different sectors of the economy is calculated with simple input-output models as well as government estimates. Direct economic losses are estimated about USD 4.2 billion in the Caribbean and between USD 78 and 97 billion in the US. Indirect economic losses from power outages is estimated in the order of USD 16.3 billion. Modelling sector-specific dependencies quantifies total business interruption losses between USD 10.8 and 15.5 billion. Thus, seven years after the record impact of Hurricane Katrina in 2005, Hurricane Sandy is the second costliest hurricane in the history of the United States

Investigation of superstorm Sandy 2012 in a multi-disciplinary approach

At the end of October 2012, Hurricane Sandy moved from the Caribbean Sea into the Atlantic Ocean and entered the United States not far from New York. Along its track, Sandy caused more than 200 fatalities and severe losses in Jamaica, The Bahamas, Haiti, Cuba, and the US. This paper demonstrates the capability and potential for near-real-time analysis of catastrophes. It is shown that the impact of Sandy was driven by the superposition of different extremes (high wind speeds, storm surge, heavy precipitation) and by cascading effects. In particular the interaction between Sandy and an extra-tropical weather system created a huge storm that affected large areas in the US. It is examined how Sandy compares to historic hurricane events, both from a hydro-meteorological and impact perspective. The distribution of losses to different sectors of the economy is calculated with simple input-output models as well as government estimates. Direct economic losses are estimated about USD 4.2 billion in the Caribbean and between USD 78 and 97 billion in the US. Indirect economic losses from power outages is estimated in the order of USD 16.3 billion. Modelling sector-specific dependencies quantifies total business interruption losses between USD 10.8 and 15.5 billion. Thus, seven years after the record impact of Hurricane Katrina in 2005, Hurricane Sandy is the second costliest hurricane in the history of the United States

A spatial-temporal vulnerability assessment to support the building of community resilience against power outage impacts

Power outages are among the most serious Critical Infrastructure (CI) disruptions and require effective disaster management with collaboration of affected CI providers and disaster management authorities. To support building community resilience, we introduce a vulnerability assessment which allows an enhanced spatial-temporal understanding of initial power outage impacts. Using the assessment enables planers to better identify which and when CIs become vulnerable and how important they are in comparison to other CIs before the overall crisis situation escalates and unmanageable cascading effects occur. The assessment addresses the initial phase of a power outage and corresponding early measures of local risk and crisis management organizations according to the German disaster management system. The assessment is an indicator-based approach which is extended to consider time-depending effects through time-referenced demand and the depletion of Coping Capacity Resources (CCR). The estimation of the relevance of CIs regarding the provision of vital services and products is addressed by a modified Delphi method. In addition, an expert survey was conducted to shed light on the evaluation of coping resources. In this paper, we describe the components of the assessment and propose different aggregation approaches which each enhances the understanding of spatial-temporal impacts of a power outage, and, hence, increases the forecasting capability for disaster management authorities. For demonstration purposes, the assessment is implemented for the case of the city of Mannheim, Germany.Thomas Münzberg, Marcus Wiens, Frank Schultman

Sequence Variations and Protein Expression Levels of the Two Immune Evasion Proteins Gpm1 and Pra1 Influence Virulence of Clinical <i>Candida albicans</i> Isolates

<div><p><i>Candida albicans</i>, the important human fungal pathogen uses multiple evasion strategies to control, modulate and inhibit host complement and innate immune attack. Clinical <i>C. albicans</i> strains vary in pathogenicity and in serum resistance, in this work we analyzed sequence polymorphisms and variations in the expression levels of two central fungal complement evasion proteins, Gpm1 (phosphoglycerate mutase 1) and Pra1 (pH-regulated antigen 1) in thirteen clinical <i>C. albicans</i> isolates. Four nucleotide (nt) exchanges, all representing synonymous exchanges, were identified within the 747-nt long <i>GPM1</i> gene. For the 900-nt long <i>PRA1</i> gene, sixteen nucleotide exchanges were identified, which represented synonymous, as well as non-synonymous exchanges. All thirteen clinical isolates had a homozygous exchange (A to G) at position 73 of the <i>PRA1</i> gene. Surface levels of Gpm1 varied by 8.2, and Pra1 levels by 3.3 fold in thirteen tested isolates and these differences influenced fungal immune fitness. The high Gpm1/Pra1 expressing candida strains bound the three human immune regulators more efficiently, than the low expression strains. The difference was 44% for Factor H binding, 51% for C4BP binding and 23% for plasminogen binding. This higher Gpm1/Pra1 expressing strains result in enhanced survival upon challenge with complement active, Factor H depleted human serum (difference 40%). In addition adhesion to and infection of human endothelial cells was increased (difference 60%), and C3b surface deposition was less effective (difference 27%). Thus, variable expression levels of central immune evasion protein influences immune fitness of the human fungal pathogen <i>C. albicans</i> and thus contribute to fungal virulence.</p></div

Pra1 secretion and effect of secreted Pra1 on C3b/iC3b surface deposition.

<p>(<b>A</b>) Presence of Pra1 in the culture supernatant. Culture supernatant (YPD medium following overnight culture) of the selected clinical <i>C</i>. <i>albicans</i> strains (1x10⁶ cells) was separated by SDS-PAGE, transferred to a membrane and Pra1 levels were detected by rabbit Pra1 antiserum, followed by a HPR swine anti-rabbit serum as a secondary antibody. Pra1 was detected as a 60 kDa protein in culture supernatant derived from medium (lanes 3 and 4) and of high expression Gpm1/Pra1 strains (lanes 6 and 7). The additional bands of higher molecular mass and of slower mobility (arrow heads), represent Pra1 in complex with additional soluble proteins. Pra1 was not detectable in the culture supernatant derived from the two low Gpm1/Pra1 expressing strains (lanes 2 and 3). The arrow shows the 60 kDa Pra1 monomer and the position of the additional dimmer or multimeric forms and Pra1 containing complexes are likely indicated by the arrow heads. (<b>B</b>) Supernatant derived from the clinical <i>C</i>. <i>albicans</i> isolates blocked C3b/iC3b deposition on the yeast surface. The selected <i>C</i>. <i>albicans</i> clinical isolates were cultivated in YPD medium overnight, and culture supernatant derived from 5x10⁶ cells of each isolate was added to NHS (7.5%) diluted in Mg-EGTA, then heat treated C. <i>albicans</i> were challenged with this serum-supernatant mixture for 30 min at 37°C. Following washing C3b/iC3b surface deposition was analyzed by flow cytometry using goat anti C3 serum. Candida cells treated in the absence of NHS are shown as control. The histogram shown here is one representative experiment out of three performed. (<b>C</b>) The mean values of median fluorescence intensity of C3b/iC3b from three independent experiments. C3B/iC3b levels on the surface of cells incubated in NHS were set 100%. The mean values of each group, i.e. the low, medium or high Gpm1/Pra1 expressing isolates are indicated by the crossed circle in the middle of each group. The mean values of median fluorescence intensity from three independent experiments ± SD are shown.</p

Phenotyping of nNOS neurons in the postnatal and adult female mouse hypothalamus

Neurons expressing nitric oxide (NO) synthase (nNOS) and thus capable of synthesizing NO play major roles in many aspects of brain function. While the heterogeneity of nNOS-expressing neurons has been studied in various brain regions, their phenotype in the hypothalamus remains largely unknown. Here we examined the distribution of cells expressing nNOS in the postnatal and adult female mouse hypothalamus using immunohistochemistry. In both adults and neonates, nNOS was largely restricted to regions of the hypothalamus involved in the control of bodily functions, such as energy balance and reproduction. Labeled cells were found in the paraventricular, ventromedial, and dorsomedial nuclei as well as in the lateral area of the hypothalamus. Intriguingly, nNOS was seen only after the second week of life in the arcuate nucleus of the hypothalamus (ARH). The most dense and heavily labeled population of cells was found in the organum vasculosum laminae terminalis (OV) and the median preoptic nucleus (MEPO), where most of the somata of the neuroendocrine neurons releasing GnRH and controlling reproduction are located. A great proportion of nNOS-immunoreactive neurons in the OV/MEPO and ARH were seen to express estrogen receptor (ER) &#x3B1;. Notably, almost all ER&#x3B1;-immunoreactive cells of the OV/MEPO also expressed nNOS. Moreover, the use of EYFPVglut2 , EYFPVgat , and GFPGad67 transgenic mouse lines revealed that, like GnRH neurons, most hypothalamic nNOS neurons have a glutamatergic phenotype, except for nNOS neurons of the ARH, which are GABAergic. Altogether, these observations are consistent with the proposed role of nNOS neurons in physiological processes

Sequence variations of <i>GPM1</i> and <i>PRA1</i> in clinical <i>C</i>. <i>albicans</i> isolates.

<p>(<b>A</b>) The sequence variations identified in the thirteen clinical <i>C</i>. <i>albicans</i> isolates are indicated in the structure of the candida <i>GPM1</i> cDNA (top) and of the 747-nt Gpm1 protein (bottom). The <i>GPM1</i> gene of each clinical <i>C</i>. <i>albicans</i> isolate was amplified by PCR and the nucleotide sequences were determined. Four synonymous nucleotide exchanges were identified which appeared as homozygous or heterozygous variations and which did not affect the sequence of the Gpm1 protein (lower panel) (see also <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0113192#pone.0113192.t001" target="_blank">Table 1</a>). (<b>B</b>) Sequence variations identified in the thirteen clinical <i>C</i>. <i>albicans</i> isolates in the <i>PRA1</i> gene and protein. Nucleotide exchanges are indicated for the <i>PRA1</i> cDNA (top) and for the 299 amino acid long Pra1 protein (bottom). A total of sixteen nucleotide exchanges occurred as homozygous or heterozygous variation (upper panel). Seven non synonymous nucleotide changes which affect the protein sequence are shown in <i>red characters</i>. The structure of the Pra1 protein includes the signal peptide (sp), the serine rich motive (ser), as well as the putative zinc binding region (Zn). Three amino acid exchanges, result in substitution of uncharged residues (i.e. Asn25, Gly105 or Ile111 to negatively charged residues, Asp25, Asp 105 or to a polar uncharged Ser 111 (shown with blue characters). All analyzed clinical isolates had the negatively charged Asp25, in homozygocity. In addition exchange of the non polar Gly₁₀₅ residue to negatively charged Asp residue occurs in some clinical isolates and exchange of the non polar Ile₁₁₁ to the polar, uncharged Ser residue is identified in one single isolate (<i>marked in blue</i>).</p