23 resultados para virus causing behavioral changes


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Accurate pain assessment in preterm infants in the neonatal intensive care unit (NICU) is complex. Infants who are born at early gestational ages (GA), and who have had greater early pain exposure, have dampened facial responses which may lead to under-treatment. Since behavioral and physiological responses to pain in infants are often dissociated, using multidimensional scales which combine these indicators into a single score may limit our ability to determine the effects of interventions on each system. Our aim was to design a unidimensional scale which would combine the relatively most specific, individual, behavioral indicators for assessing acute pain in this population. The Behavioral Indicators of Infant Pain (BIIP) combines sleep/wake states, 5 facial actions and 2 hand actions. Ninety-two infants born between 23 and 32 weeks GA were assessed during 3, 1 min Phases of blood collection. Outcome measures included changes in BIIP and in Neonatal Infant Pain Scale (NIPS) scores coded in real time from continuous bedside video recordings; changes in heart rate (HR) were obtained using custom physiological processing software. Scores on the BIIP changed significantly across Phases of blood collection (p

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The SH gene and its flanking sequences have been analysed for 10 strains of mumps virus (MuV) and compared to 5 others. A new lineage has been identified among UK isolates. Changes in the transcription pattern could not be correlated with differences in the sequences of the F-SH and SH-HN intergenic regions of the genome.

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Phylogenetic analysis of the sequence of the H gene of 75 measles virus (MV) strains (32 published and 43 new sequences) was carried out. The lineage groups described from comparison of the nucleotide sequences encoding the C-terminal regions of the N protein of MV were the same as those derived from the H gene sequences in almost all cases. The databases document a number of distinct genotype switches that have occurred in Madrid (Spain). Well-documented is the complete replacement of lineage group C2, the common European genotype at that time, with that of group D3 around the autumn of 1993. No further isolations of group C2 took place in Madrid after this time. The rate of mutation of the H gene sequences of MV genotype D3 circulating in Madrid from 1993 to 1996 was very low (5 x 10(-4) per annum for a given nucleotide position). This is an order of magnitude lower than the rates of mutation observed in the HN genes of human influenza A viruses. The ratio of expressed over silent mutations indicated that the divergence was not driven by immune selection in this gene. Variations in amino acid 117 of the H protein (F or L) may be related to the ability of some strains to haemagglutinate only in the presence of salt. Adaptation of MV to different primate cell types was associated with very small numbers of mutations in the H gene. The changes could not be predicted when virus previously grown in human B cell lines was adapted to monkey Vero cells. In contrast, rodent brain-adapted viruses displayed a lot of amino acid sequence variation from normal MV strains. There was no convincing evidence for recombination between MV genotypes.

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This study investigated how damage changes the modal parameters of a real bridge by means of a field experiment which was conducted on a real steel truss bridge consecutively subjected to four artificial damage scenarios. In the experiment, both the forced and free vibrations of the bridge were recorded, the former for identifying higher modes available exclusively and the latter for lower modes with higher resolution. Results show that modal parameters are little affected by damage causing low stress redistribution. Modal frequencies decrease as damage causing high stress redistribution is applied; such a change can be observed if the damage is at the non-nodal point of the corresponding mode shape. Mode shapes are distorted due to asymmetric damage; they show an amplification in the damaged side as damage is applied at the non-nodal point. Torsion modes become more dominant as damage is applied either asymmetrically or on an element against large design loads. © 2013 Taylor & Francis Group, London.

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We present a new, diatom-based sea-level reconstruction for Iceland spanning the last -500 years, and investigate the possible mechanisms driving the sea-level changes. A sea-level reconstruction from near the Icelandic low pressure system is important as it can improve understanding of ocean-atmosphere forcing on North Atlantic sea-level variability over multi-decadal to centennial timescales. Our reconstruction is from Viarhólmi salt marsh in Snæfellsnes in western Iceland, a site from where we previously obtained a 2000-yr record based upon less precise sea-level indicators (salt-marsh foraminifera). The 20th century part of our record is corroborated by tide-gauge data from Reykjavik. Overall, the new reconstruction shows ca0.6m rise of relative sea level during the last four centuries, of which ca0.2m occurred during the 20th century. Low-amplitude and high-frequency sea-level variability is super-imposed on the pre-industrial long-term rising trend of 0.65m per 1000 years. Most of the relative sea-level rise occurred in three distinct periods: AD 1620-1650, AD 1780-1850 and AD 1950-2000, with maximum rates of ~3±2mm/yr during the latter two of these periods. Maximum rates were achieved at the end of large shifts (from negative to positive) of the winter North Atlantic Oscillation (NAO) Index as reconstructed from proxy data. Instrumental data demonstrate that a strong and sustained positive NAO (a deep Icelandic Low) generates setup on the west coast of Iceland resulting in rising sea levels. There is no strong evidence that the periods of rapid sea-level rise were caused by ocean mass changes, glacial isostatic adjustment or regional steric change. We suggest that wind forcing plays an important role in causing regional-scale coastal sea-level variability in the North Atlantic, not only on (multi-)annual timescales, but also on multi-decadal to centennial timescales.

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Human respiratory syncytial virus (HRSV) is the most important viral cause of severe respiratory tract disease in infants. Two subgroups (A and B) have been identified, which cocirculate during, or alternate between, yearly epidemics and cause indistinguishable disease. Existing in vitro and in vivo models of HRSV focus almost exclusively on subgroup A viruses. Here, a recombinant (r) subgroup B virus (rHRSV(B05)) was generated based on a consensus genome sequence obtained directly from an unpassaged clinical specimen from a hospitalized infant. An additional transcription unit containing the gene encoding enhanced green fluorescent protein (EGFP) was introduced between the phosphoprotein and matrix genes (position 5) of the genome to generate rHRSV(B05)EGFP(5). The recombinant viruses replicated efficiently in both HEp-2 cells and in well-differentiated normal human bronchial cells grown at air-liquid interface. Intranasal infection of cotton rats (Sigmodon hispidus) resulted in high numbers of EGFP(+) cells in epithelia of the nasal septum and conchae. When administered in a relatively large inoculum volume, the virus also replicated efficiently in bronchiolar epithelial cells and spread extensively in both the upper and lower respiratory tracts. Virus replication was not observed in ciliated epithelial cells of the trachea. This is the first virulent rHRSV strain with the genetic composition of a currently circulating wild-type virus. In vivo tracking of infected cells by means of EGFP fluorescence in the absence of cytopathic changes increases the sensitivity of virus detection in HRSV pathogenesis studies.

IMPORTANCE

Virology as a discipline has depended on monitoring cytopathic effects following virus culture in vitro. However, wild-type viruses isolated from patients often do not cause significant changes to infected cells, necessitating blind passage. This can lead to genetic and phenotypic changes and the generation of high-titer, laboratory-adapted viruses with diminished virulence in animal models of disease. To address this, we determined the genome sequence of an unpassaged human respiratory syncytial virus from a sample obtained directly from an infected infant, assembled a molecular clone, and recovered a wild-type recombinant virus. Addition of a gene encoding enhanced green fluorescent protein allowed this wild-type virus to be tracked in primary human cells and living animals in the absence of significant cytopathic effects. Imaging of fluorescent cells proved to be a highly valuable tool for monitoring the spread of virus and may help improve assays for evaluating novel intervention strategies.

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Anthropogenic noise can affect behaviour across a wide range of species in both terrestrial and aquatic environments. However, behaviours might not be affected in isolation. Therefore, a more holistic approach investigating how environmental stressors, such as noise pollution, affect different behaviours in concert is necessary. Using tank-based noise exposure experiments, we tested how changes in the acoustic environment affect the behaviour of the cichlid Amatitlania nigrofasciata. We found that exposure to anthropogenic noise affected a couple of behaviours: an increase in sheltering was accompanied by a decrease in foraging. Our results highlight the multiple negative effects of an environmental stressor on an individual's behaviour.

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Triclabendazole (TCBZ), the anthelmintic drug active against both mature and immature liver flukes, was used to investigate the effect of in vivo treatment on the tegumental surface of juvenile Fasciola gigantica. Five goats were infected with 150 F. gigantica metacercariae each by oral gavage. Four of them were treated with single dose of TCBZ at 10mg/kg at four weeks post-infection. They were euthanized at 0 (untreated), 24, 48, 72 and 96h post treatment. Juvenile flukes were manually retrieved from the goat livers and processed for scanning electron microscopy. In control flukes, the anterior region was adorned with sharply pointed spines projecting away from the surface, while in the posterior region, spines become shorter and narrower, loosing serration and with the appearance of distinct furrows and papillae. The dorsal surface retained the same pattern of surface architecture similar to that of ventral surface. Flukes obtained from 24h post-treatment did not show any apparent change and were still very active. However, there were limited movements and some blebbing, swelling, deposition of tegumental secretions and some flattening displayed by the flukes of 48h post-treatment. All the worms were found dead 72h post-treatment and showed advanced level of tegumental disruptions, consisting of severe distortion of spines, sloughing off the tegument to expose the basal lamina, formation of pores and isolated patches of lesions. By 96h post-treatment, the disruption was extremely severe and the tegument was completely sheared off causing deeper lesions that exposed the underlying musculature. The disruption was more severe at posterior than anterior region and on ventral than dorsal surface. The present study further establishes the time-course of TCBZ action in vivo with 100% efficacy against the juvenile tropical liver fluke.