Mixed debris interaction with obstacle array under extreme flood conditions

This investigation explores the interactions of different shaped debris with an array of obstacles under subcritical flow conditions, representative of a flood associated with a storm surge or tsunami. Panels, blocks and cylinders were used in a flow channel, as analogues for house panels, cars/containers and trees respectively, whilst some tests used a mix of debris. The backwater effect due to the blockage caused by the obstacles was most (least) significant for panels (cylinders). There was some evidence that smaller key log types and higher flow rates led to smaller dams. It was also evident that key logs formed at different depths depending on debris shape; debris shape also determined the vertical shape of the dam. Capture efficiency had a broadly negative (positive) correlation with the Froude number (permeability). Also, from video footage there were examples of the debris moving more quickly through partial dams. Finally, the drag force, deduced from only the water depths and the flow discharge, showed a clear relationship between drag force and Froude number, and a dependency of drag force on debris shape. There are some implications for the layout of building footprints in the inundation zones and the use of large, break-away panels

Zooplankton Assemblage in Hambanota Port and Adjacent Coastal Waters of Sri Lanka

Present study was to investigate zooplankton assemblage in Hambantota port andadjacent coastal waters in Sri Lanka. Samples were collected from the port before thecommencement of commercial operations in order to have baseline information onzooplankton assemblage that can be used in the future to study any community change.Species composition, abundance, spatial distribution and diversity of zooplankton wereinvestigated over a period of six months from January 2011 to June 2011. Monthlysamples were collected from both inner-harbor and outer-harbor. Physico-chemicalparameters such as temperature, pH, salinity, density, conductivity, nitrate,orthophosphate, DO, BOD5 and Ch a were also measured. Zooplankton diversity, speciesrichness and evenness were calculated using Shannon-Weiner diversity index (Hˊ ),Simpson‟s index (D) and Pielou‟s evenness (E). A total of 72 zooplankton types wereidentified throughout the research project mainly Calanus sp., Paracalanus sp.,Sapphirina sp., Acartia tranteri, Barnacle nauplii, Crustacean cypris larvae, Oikopleurasp., Tunicate larvae, Brachionus calyciflorus calyciflorus, Brachionus forficula, Fishlarvae, Discorbis sp., Actinula larvae and Sagitta sp.. Copepod nauplii dominated thezooplankton. According to percentage occurrences arthropods (71%), protozoans (10%)and ichthyoplankton (9%) were abundant in the inner harbor. In the outer harbor alsoarthropods (66%), ichthyoplankton (11%) and protozoans (7%) were recorded in highernumbers. Highest species diversity (Hˊ =2.685), highest species richness (S=39) andhighest evenness (E=0.856) were recorded from outer harbor locations (HFHB1 andHPM). Several species such as Ceratium furca, Chaetoceros sp., Thalassiosira sp.,Rhizosolenia sp. and Protoperidinium sp. known to form harmful algal blooms were alsoobserved in this study.Key words: Zooplankton assemblage, Hambantota port, Ballast water, Invasive AlienSpecies (IAS

mGluR5 Regulates Glutamate-Dependent Development of the Mouse Somatosensory Cortex

We have previously reported that mGluR5 signaling via PLC-β1 regulates the development of whisker patterns within S1 (barrel) cortex of mice (Hannan et al., 2001). However, whether these defects arise from the loss of postsynaptic mGluR5 signaling, and whether the level of mGluR5 is important for barrel formation, was not examined. Furthermore, whether mGluR5 regulates other developmental processes that occur before or after barrel development is not known. We now show that mGluR5 is present postsynaptically at thalamocortical synapses during barrel formation. In addition, Mglur5(+/−) mice exhibit normal TCA patch formation but reduced cellular segregation in layer 4, indicating a dose-dependent role for mGluR5 in the regulation of pattern formation. Furthermore Mglur5(−/−) and Mglur5(+/−) mice display normal cortical arealization, layer formation, and size of PMBSF indicating the defects within S1 do not result from general abnormalities of cortical mapping during earlier stages of development. At P21 layer 4 neurons from Mglur5(−/−) and Mglur5(+/−) mice show a significant reduction in spine density but normal dendritic complexity compared with Mglur5(+/+) mice indicating a role in synaptogenesis during cortical development. Finally, mGluR5 regulates pattern formation throughout the trigeminal system of mice as the representation of the AS whiskers in the PrV, VpM, and S1 cortex was disrupted in Mglur5(−/−) mice. Together these data indicate a key role for mGluR5 at both early and late stages of neuronal development in the trigeminal system of mice

The molecular characterisation of Escherichia coli K1 isolated from neonatal nasogastric feeding tubes

Background: The most common cause of Gram-negative bacterial neonatal meningitis is E. coli K1. It has a mortality rate of 10–15%, and neurological sequelae in 30– 50% of cases. Infections can be attributable to nosocomial sources, however the pre-colonisation of enteral feeding tubes has not been considered as a specific risk factor. Methods: Thirty E. coli strains, which had been isolated in an earlier study, from the residual lumen liquid and biofilms of neonatal nasogastric feeding tubes were genotyped using pulsed-field gel electrophoresis, and 7-loci multilocus sequence typing. Potential pathogenicity and biofilm associated traits were determined using specific PCR probes, genome analysis, and in vitro tissue culture assays. Results: The E. coli strains clustered into five pulsotypes, which were genotyped as sequence types (ST) 95, 73, 127, 394 and 2076 (Achman scheme). The extra-intestinal pathogenic E. coli (ExPEC) phylogenetic group B2 ST95 serotype O1:K1:NM strains had been isolated over a 2 week period from 11 neonates who were on different feeding regimes. The E. coli K1 ST95 strains encoded for various virulence traits associated with neonatal meningitis and extracellular matrix formation. These strains attached and invaded intestinal, and both human and rat brain cell lines, and persisted for 48 h in U937 macrophages. E. coli STs 73, 394 and 2076 also persisted in macrophages and invaded Caco-2 and human brain cells, but only ST394 invaded rat brain cells. E. coli ST127 was notable as it did not invade any cell lines. Conclusions: Routes by which E. coli K1 can be disseminated within a neonatal intensive care unit are uncertain, however the colonisation of neonatal enteral feeding tubes may be one reservoir source which could constitute a serious health risk to neonates following ingestion

Characterizing the pathotype of neonatal meningitis causing <i>Escherichia coli</i> (NMEC)

Background Neonatal meningitis-causing Escherichia coli (NMEC) is the predominant Gram-negative bacterial pathogen associated with meningitis in newborn infants. High levels of heterogeneity and diversity have been observed in the repertoire of virulence traits and other characteristics among strains of NMEC making it difficult to define the NMEC pathotype. The objective of the present study was to identify genotypic and phenotypic characteristics of NMEC that can be used to distinguish them from commensal E. coli. Methods A total of 53 isolates of NMEC obtained from neonates with meningitis and 48 isolates of fecal E. coli obtained from healthy individuals (HFEC) were comparatively evaluated using five phenotypic (serotyping, serum bactericidal assay, biofilm assay, antimicorbial susceptibility testing, and in vitro cell invasion assay) and three genotypic (phylogrouping, virulence genotyping, and pulsed-field gel electrophoresis) methods. Results A majority (67.92 %) of NMEC belonged to B2 phylogenetic group whereas 59 % of HFEC belonged to groups A and D. Serotyping revealed that the most common O and H types present in NMEC tested were O1 (15 %), O8 (11.3 %), O18 (13.2 %), and H7 (25.3 %). In contrast, none of the HFEC tested belonged to O1 or O18 serogroups. The most common serogroup identified in HFEC was O8 (6.25 %). The virulence genotyping reflected that more than 70 % of NMEC carried kpsII, K1, neuC, iucC, sitA, and vat genes with only less than 27 % of HFEC possessing these genes. All NMEC and 79 % of HFEC tested were able to invade human cerebral microvascular endothelial cells. No statistically significant difference was observed in the serum resistance phenotype between NMEC and HFEC. The NMEC strains demonstrated a greater ability to form biofilms in Luria Bertani broth medium than did HFEC (79.2 % vs 39.9 %). Conclusion The results of our study demonstrated that virulence genotyping and phylogrouping may assist in defining the potential NMEC pathotype

Developing a utility index for the Aberrant Behavior Checklist (ABC-C) for fragile X syndrome

Purpose This study aimed to develop a utility index (the ABC-UI) from the Aberrant Behavior Checklist-Community (ABC-C), for use in quantifying the benefit of emerging treatments for fragile X syndrome (FXS). Methods The ABC-C is a proxy-completed assessment of behaviour and is a widely used measure in FXS. A subset of ABC-C items across seven dimensions was identified to include in health state descriptions. This item reduction process was based on item performance, factor analysis and Rasch analysis performed on an observational study dataset, and consultation with five clinical experts and a methodological expert. Dimensions were combined into health states using an orthogonal design and valued using time trade-off (TTO), with lead-time TTO methods used where TTO indicated a state valued as worse than dead. Preference weights were estimated using mean, individual level, ordinary least squares and random-effects maximum likelihood estimation [RE (MLE)] regression models. Results A representative sample of the UK general public (n = 349; mean age 35.8 years, 58.2 % female) each valued 12 health states. Mean observed values ranged from 0.92 to 0.16 for best to worst health states. The RE (MLE) model performed best based on number of significant coefficients and mean absolute error of 0.018. Mean utilities predicted by the model covered a similar range to that observed. Conclusions The ABC-UI estimates a wide range of utilities from patient-level FXS ABC-C data, allowing estimation of FXS health-related quality of life impact for economic evaluation from an established FXS clinical trial instrument

Recessive mutations in SPTBN2 implicate β-III spectrin in both cognitive and motor development

β-III spectrin is present in the brain and is known to be important in the function of the cerebellum. Heterozygous mutations in SPTBN2, the gene encoding β-III spectrin, cause Spinocerebellar Ataxia Type 5 (SCA5), an adult-onset, slowly progressive, autosomal-dominant pure cerebellar ataxia. SCA5 is sometimes known as "Lincoln ataxia," because the largest known family is descended from relatives of the United States President Abraham Lincoln. Using targeted capture and next-generation sequencing, we identified a homozygous stop codon in SPTBN2 in a consanguineous family in which childhood developmental ataxia co-segregates with cognitive impairment. The cognitive impairment could result from mutations in a second gene, but further analysis using whole-genome sequencing combined with SNP array analysis did not reveal any evidence of other mutations. We also examined a mouse knockout of β-III spectrin in which ataxia and progressive degeneration of cerebellar Purkinje cells has been previously reported and found morphological abnormalities in neurons from prefrontal cortex and deficits in object recognition tasks, consistent with the human cognitive phenotype. These data provide the first evidence that β-III spectrin plays an important role in cortical brain development and cognition, in addition to its function in the cerebellum; and we conclude that cognitive impairment is an integral part of this novel recessive ataxic syndrome, Spectrin-associated Autosomal Recessive Cerebellar Ataxia type 1 (SPARCA1). In addition, the identification of SPARCA1 and normal heterozygous carriers of the stop codon in SPTBN2 provides insights into the mechanism of molecular dominance in SCA5 and demonstrates that the cell-specific repertoire of spectrin subunits underlies a novel group of disorders, the neuronal spectrinopathies, which includes SCA5, SPARCA1, and a form of West syndrome