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Selected AbstractsDeterminants of hospital costs associated with traumatic brain injury in England and Wales,ANAESTHESIA, Issue 5 2008S. Morris Summary Using data from the Trauma Audit Research Network, we investigated the costs of acute care in patients , 18 years of age hospitalised for traumatic brain injury between January 2000 and December 2005 in England and Wales. Traumatic brain injury patients were defined and stratified using the Abbreviated Injury Scale. A total of 6484 traumatic brain injury patients were identified; 22.3% had an Abbreviated Injury Scale score of three, 38.0% of four and 39.7% of five. Median age (IQR) was 42 years (28,59) and 76.7% were men. Primary cause of injury was motor vehicle collisions (42.4%) followed by falls (38.0%). In total 23.7% of the patients died before discharge. Hospitalisation costs averaged £15 462 (SD £16 844). Costs varied significantly by age, Glasgow Coma Score, Injury Severity Score, coexisting injuries of the thorax, spine and lower limb, hospital mortality, availability of neurosurgical services, and specialty of attendants seen in the Accident and Emergency department. [source] Inappropriate stents: Primary cause of failure of stent redilation in coarctation of the aorta,CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, Issue 4 2008Charles E. Mullins MD No abstract is available for this article. [source] Differential Long-Term Stimulation of Type I versus Type III Collagen After Infrared IrradiationDERMATOLOGIC SURGERY, Issue 7 2009YOHEI TANAKA MD BACKGROUND The dermis is composed primarily of type I (soft) and type III (rigid scar-like) collagen. Collagen degradation is considered the primary cause of skin aging. Studies have proved the efficacy of infrared irradiation on collagen stimulation but have not investigated the differential long-term effects of infrared irradiation on type I and type III collagen. OBJECTIVE To determine differential long-term stimulation of type I and type III collagen after infrared (1,100,1,800 nm) irradiation. METHODS AND MATERIALS In vivo rat tissue was irradiated using the infrared device. Histology samples were analyzed for type I and III collagen stimulation, visual changes from baseline, and treatment safety up to 90 days post-treatment. RESULTS Infrared irradiation provided long-term stimulation of type I collagen and temporary stimulation of type III collagen. Treatment also created long-term smoothing of the epidermis, with no observed complications. CONCLUSIONS Infrared irradiation provides safe, consistent, long-term stimulation of type I collagen but only short-term stimulation in the more rigid type III collagen. This is preferential for cosmetic patients looking for improvement in laxity and wrinkles while seeking smoother, more youthful skin. [source] Changes within maturing neurons limit axonal regeneration in the developing spinal cordDEVELOPMENTAL NEUROBIOLOGY, Issue 4 2006Murray Blackmore Abstract Embryonic birds and mammals display a remarkable ability to regenerate axons after spinal injury, but then lose this ability during a discrete developmental transition. To explain this transition, previous research has emphasized the emergence of myelin and other inhibitory factors in the environment of the spinal cord. However, research in other CNS tracts suggests an important role for neuron-intrinsic limitations to axon regeneration. Here we re-examine this issue quantitatively in the hindbrain-spinal projection of the embryonic chick. Using heterochronic cocultures we show that maturation of the spinal cord environment causes a 55% reduction in axon regeneration, while maturation of hindbrain neurons causes a 90% reduction. We further show that young neurons transplanted in vivo into older spinal cord can regenerate axons into myelinated white matter, while older axons regenerate poorly and have reduced growth cone motility on a variety of growth-permissive ligands in vitro, including laminin, L1, and N-cadherin. Finally, we use video analysis of living growth cones to directly document an age-dependent decline in the motility of brainstem axons. These data show that developmental changes in both the spinal cord environment and in brainstem neurons can reduce regeneration, but that the effect of the environment is only partial, while changes in neurons by themselves cause a nearly complete reduction in regeneration. We conclude that maturational events within neurons are a primary cause for the failure of axon regeneration in the spinal cord. © 2006 Wiley Periodicals, Inc. J Neurobiol, 2006 [source] Strategies to prevent type 1 diabetesDIABETES OBESITY & METABOLISM, Issue 10 2009S. L. Thrower Type 1 diabetes is a chronic autoimmune condition resulting from T cell,mediated destruction of the insulin-producing cells in the islets of Langerhans. Its primary cause remains unknown, but it has been established that the clinical presentation is preceded by a long prodrome. This enables individuals at high risk of disease to be identified and offers the possibility of intervention to prevent clinical disease. Many groups are working in this field, concentrating on manipulation of environmental exposures that are potential triggers of autoimmunity and on immunomodulation strategies that aim to prevent destruction of ,-cells. Some interventions have shown promising results in early trials, but effective disease prevention remains elusive. This article reviews current progress in the field. [source] HOW TO CLEAR UP THE PENSIONS MESSECONOMIC AFFAIRS, Issue 3 2003David Simpson All three pillars of the British pensions system are crumbling. The basic state pension is unsustainable in its present form. Defined benefit occupational pension schemes are fast disappearing, and with them the retirement hopes of millions of workers. A further 3 million low-income earners are not saving enough for their retirement. And uncertainty about pensions choices is widespread. In each case the primary cause of the problem is governmental or regulatory failure. The paper makes eight general and four specific proposals for restoring the system. [source] The association between non-biting midges and Vibrio choleraeENVIRONMENTAL MICROBIOLOGY, Issue 12 2008Meir Broza Summary Vibrio cholerae is a natural inhabitant of aquatic ecosystems, yet its interactions within this habitat are poorly understood. Here we describe the current knowledge on the interaction of V. cholerae with one group of co-inhabitants, the chironomids. Chironomids, non-biting midges (Chironomidae, Diptera), are an abundant macroinvertebrate group encountered in freshwater aquatic habitats. As holometabolous insects, chironomids start life when their larvae hatch from eggs laid at the water/air interface; through various feeding strategies, the larvae grow and pupate to become short-lived, non-feeding, adult flying insects. The discovery of the connection between V. cholerae and chironomids was accidental. While working with Chironomus transavaalensis, we observed the disintegration of its egg masses and searched for a possible microbial agent. We identified V. cholerae as the primary cause of this phenomenon. Haemagglutinin/protease, a secreted extracellular enzyme, degraded the gelatinous matrix surrounding the eggs, enabling bacterial growth. Observation of chironomids in relation to V. cholerae continuously for 7 years in various types of water bodies in Israel, India, and Africa revealed that environmental V. cholerae adhere to egg-mass surfaces of various Chironomini (,bloodworms'). The flying adults' potential to serve as mechanical vectors of V. cholerae from one water body to another was established. This, in turn, suggested that these insects play a role in the ecology of V. cholerae and possibly take part in the dissemination of the pathogenic serogroups during, and especially between, epidemics. [source] Bioassays with caged Hyalella azteca to determine in situ toxicity downstream of two Saskatchewan, Canada, uranium operations,ENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 11 2007Erin L. Robertson Abstract The main objectives of this in situ study were to evaluate the usefulness of an in situ bioassay to determine if downstream water bodies at the Key Lake and Rabbit Lake uranium operations (Saskatchewan, Canada) were toxic to Hyalella azteca and, if toxicity was observed, to differentiate between the contribution of surface water and sediment contamination to in situ toxicity. These objectives were achieved by performing 4-d in situ bioassays with laboratory-reared H. azteca confined in specially designed, paired, surface water and sediment exposure chambers. Results from the in situ bioassays revealed significant mortality, relative to the respective reference site, at the exposure sites at both Key Lake (p , 0.001) and Rabbit Lake (p = 0.001). No statistical differences were found between survival in surface water and sediment exposure chambers at either Key Lake (p = 0.232) or Rabbit Lake (p = 0.072). This suggests that surface water (the common feature of both types of exposure chambers) was the primary cause of in situ mortality of H. azteca at both operations, although this relationship was stronger at Key Lake. At Key Lake, the primary cause of aquatic toxicity to H. azteca did not appear to be correlated with the variables measured in this study, but most likely with a pulse of organic mill-process chemicals released during the time of the in situ study , a transient event that was caused by a problem with the mill's solvent extraction process. The suspected cause of in situ toxicity to H. azteca at Rabbit Lake was high levels of uranium in surface water, sediment, and pore water. [source] H63D homozygotes with hyperferritinaemia: is this genotype, the primary cause of iron overload?EUROPEAN JOURNAL OF HAEMATOLOGY, Issue 1 2007Carles De Diego Abstract Objectives:,Hereditary haemochromatosis is a disease that affects iron metabolism and leads to iron overload. Homozygosity for the H63D mutation is associated with increased transferrin saturation (TS) and ferritin levels. Our objective was to find out if the homozygosity of H63D mutation was the primary cause of iron overload. Patients and methods:,We studied 45 H63D homozygotes (31 males and 14 females) with biochemical iron overload and/or clinical features of haemochromatosis. The simultaneous detection of 18 known HFE, TFR2 and FPN1 mutations and sequencing of the HAMP gene were performed to rule out the possible existence of genetic modifier factors related with iron overload. Results:,Values of biochemical iron overload, measured as percentage TS and serum ferritin concentration (SF), in our H63D homozygotes were significantly higher in patients than in controls: TS 55 ± 15% vs. 35 ± 15% and SF 764 (645,883) ,g/L vs. 115 (108,123) ,g/L for patients and controls, respectively. These H63D homozygotes presented extreme hyperferritinaemia and no additional mutations in HFE, TFR2, FPN1 and HAMP genes were detected. Conclusions:,The lack of additional mutations in our H63D homozygotes suggests that this genotype could be the primary cause of iron overload in these patients. Despite our results, we cannot entirely discount the possibility that one or more genetic modifier factor exists, simply because we were unable to find it, although there was a precedent in the HFE gene. Genetic modifier factors have been described for C282Y mutations in the HFE gene, but at the present time they have never been reported in H63D homozygotes. [source] Rupture of chordae tendineae in patients with ,-thalassemiaEUROPEAN JOURNAL OF HAEMATOLOGY, Issue 4 2004Dimitrios Farmakis Abstract: Cardiac disease is the primary cause of mortality in , -thalassemia patients. Except for ventricular dysfunction and pulmonary hypertension that represent the main forms of heart disease in these patients, valvular abnormalities including valvular regurgitation, endocardial thickening and calcification and mitral valve prolapse have also been described. Here we present two patients with thalassemia major and mitral chordal rupture, a previously undescribed abnormality in this population. Pathogenesis of this finding may involve thalassemia-related pseudoxanthoma elasticum-like syndrome, a diffuse elastic tissue defect, which is observed with a notable frequency in these patients and has been associated with numerous cardiovascular complications, including valvular ones. [source] IL-6: Regulator of Treg/Th17 balanceEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 7 2010Akihiro Kimura Abstract IL-6 is a pleiotropic cytokine involved in the physiology of virtually every organ system. Recent studies have demonstrated that IL-6 has a very important role in regulating the balance between IL-17-producing Th17 cells and regulatory T cells (Treg). The two T-cell subsets play prominent roles in immune functions: Th17 cell is a key player in the pathogenesis of autoimmune diseases and protection against bacterial infections, while Treg functions to restrain excessive effector T-cell responses. IL-6 induces the development of Th17 cells from naïve T cells together with TGF-,; in contrast, IL-6 inhibits TGF-,-induced Treg differentiation. Dysregulation or overproduction of IL-6 leads to autoimmune diseases such as multiple sclerosis (MS) and rheumatoid arthritis (RA), in which Th17 cells are considered to be the primary cause of pathology. Given the critical role of IL-6 in altering the balance between Treg and Th17 cells, controlling IL-6 activities is potentially an effective approach in the treatment of various autoimmune and inflammatory diseases. Here, we review the role of IL-6 in regulating Th17/Treg balance and describe the critical functions of IL-6 and Th17 in immunity and immune-pathology. [source] Cognitive performance following endarterectomy in asymptomatic severe carotid stenosisEUROPEAN JOURNAL OF NEUROLOGY, Issue 5 2003J. Aharon-Peretz Cognition and the effects of carotid endarterectomy (CEA) were evaluated in 22 non-demented subjects with vascular risk factors (VRF) and asymptomatic severe carotid artery stenosis (ASCAS), 14 volunteers with VRF but without stenosis, and 24 healthy controls (HC) without VRF. Non-demented subjects with VRF, with or without carotid stenosis scored inferior to HC. It is concluded that carotid stenosis is not a primary cause of cognitive deterioration and CEA does not improve cognition in patients with ASCAS. [source] The neuroanatomy of grapheme,color synesthesiaEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 6 2009Lutz Jäncke Abstract Grapheme,color synesthetes perceive particular colors when seeing a letter, word or number (grapheme). Functional neuroimaging studies have provided some evidence in favor of a neural basis for this type of synesthesia. Most of these studies have reported extra activations in the fusiform gyrus, which is known to be involved in color, letter and word processing. The present study examined different neuroanatomical features (i.e. cortical thickness, cortical volume and cortical surface area) in a sample of 48 subjects (24 grapheme,color synesthetes and 24 control subjects), and revealed increased cortical thickness, volume and surface area in the right and left fusiform gyrus and in adjacent regions, such as the lingual gyrus and the calcarine cortex, in grapheme,color synesthetes. In addition, we set out to analyze structural connectivity based on fractional anisotropy (FA) measurements in a subsample of 28 subjects (14 synesthetes and 14 control subjects). In contrast to the findings of a recent neuroanatomical study using modern diffusion tensor imaging measurement techniques, we did not detect any statistically significant difference in FA between synesthetes and non-synesthetes in the fusiform gyri. Our study thus supports the hypothesis of local anatomical differences in cortical characteristics in the vicinity of the V4 complex. The observed altered brain anatomy in grapheme,color synesthetes might be the anatomical basis for this particular form of synesthesia but it is also possible that the detected effects are a consequence (rather than the primary cause) of the life-long experience of grapheme,color synesthesia. [source] EPISTASIS AND THE TEMPORAL CHANGE IN THE ADDITIVE VARIANCE-COVARIANCE MATRIX INDUCED BY DRIFTEVOLUTION, Issue 8 2004Carlos López-Fanjul Abstract The effect of population bottlenecks on the components of the genetic covariance generated by two neutral independent epistatic loci has been studied theoretically (additive, covA; dominance, covD; additive-by-additive, covAA; additive-by-dominance, covAD; and dominance-by-dominance, covDD). The additive-by-additive model and a more general model covering all possible types of marginal gene action at the single-locus level (additive/dominance epistatic model) were considered. The covariance components in an infinitely large panmictic population (ancestral components) were compared with their expected values at equilibrium over replicates randomly derived from the base population, after t consecutive bottlenecks of equal size N (derived components). Formulae were obtained in terms of the allele frequencies and effects at each locus, the corresponding epistatic effects and the inbreeding coefficient Ft. These expressions show that the contribution of nonadditive loci to the derived additive covariance (covAt) does not linearly decrease with inbreeding, as in the pure additive case, and may initially increase or even change sign in specific situations. Numerical examples were also analyzed, restricted for simplicity to the case of all covariance components being positive. For additive-by-additive epistasis, the condition covAt > covA only holds for high frequencies of the allele decreasing the metric traits at each locus (negative allele) if epistasis is weak, or for intermediate allele frequencies if it is strong. For the additive/dominance epistatic model, however, covAt > covA applies for low frequencies of the negative alleles at one or both loci and mild epistasis, but this result can be progressively extended to intermediate frequencies as epistasis becomes stronger. Without epistasis the same qualitative results were found, indicating that marginal dominance induced by epistasis can be considered as the primary cause of an increase of the additive covariance after bottlenecks. For all models, the magnitude of the ratio covAt/covA was inversely related to N and t. [source] THE EFFECT OF EPISTASIS ON THE EXCESS OF THE ADDITIVE AND NONADDITIVE VARIANCES AFTER POPULATION BOTTLENECKSEVOLUTION, Issue 5 2002Carlos López-Fanjul Abstract The effect of population bottlenecks on the components of the genetic variance generated by two neutral independent epistatic loci has been studied theoretically (VA, additive; VD, dominant; VAA, additive × additive; VAD, additive × dominant; VDD; dominant × dominant components of variance). Nonoverdominance and overdominance models were considered, covering all possible types of marginal gene action at the single locus level. The variance components in an infinitely large panmictic population (ancestral components) were compared with their expected values at equilibrium, after t consecutive bottlenecks of equal size N (derived components). Formulae were obtained in terms of allele frequencies and effects at each locus and the corresponding epistatic value. An excess of VA after bottlenecks can be assigned to two sources: (1) the spatiotemporal changes in the marginal average effects of gene substitution ai, which are equal to zero only for additive gene action within and between loci; and (2) the covariance between a2i and the heterozygosity at the loci involved, which is generated by dominance, with or without epistasis. Numerical examples were analyzed, indicating that an increase in VA after bottlenecks will only occur if its ancestral value is minimal or very small. For the nonoverdominance model with weak reinforcing epistasis, that increase has been detected only for extreme frequencies of the negative allele at one or both loci. With strong epistasis, however, this result can be extended to a broad range of intermediate frequencies. With no epistasis, the same qualitative results were found, indicating that dominance can be considered as the primary cause of an increase in VA following bottlenecks. In parallel, the derived total nonadditive variance exceeded its ancestral value (VNA= VD+ VAA+VAD+ VDD) for a range of combinations of allele frequencies covering those for an excess of VA and for very large frequencies of the negative allele at both loci. For the overdominance model, an increase in VA and VNA was respectively observed for equilibrium (intermediate) frequencies at one or both loci or for extreme frequencies at both loci. For all models, the magnitude of the change of VA and VNA was inversely related to N and t. At low levels of inbreeding, the between-line variance was not affected by the type of gene action. For the models considered, the results indicate that it is unlikely that the rate of evolution may be accelerated after population bottlenecks, in spite of occasional increments of the derived VA over its ancestral value. [source] REJOINDER TO GARDNER'S "COMMENTARY ON KELLY AND JOHNSTON'S ,THE ALIENATED CHILD: A REFORMULATION OF PARENTAL ALIENATION SYNDROME'"FAMILY COURT REVIEW, Issue 4 2004Janet R. Johnston In this reply to Richard Gardner, we outline our points of disagreement with his formulation of parental alienation syndrome (PAS), showing that his focus on the alienating parent as the primary cause of children's negative attitudes and rejecting behavior toward the other parent is overly simplistic and not supported by findings from recent empirical research. It follows that we strongly object to Gardner's recommendations for legal and mental health interventions with alienated children as well as the use of the term PAS when referring to this problem. [source] On the kinetics of voltage formation in purple membranes of Halobacterium salinariumFEBS JOURNAL, Issue 19 2000Richard W. Hendler The kinetics of the bacteriorhodopsin photocycle, measured by voltage changes in a closed membrane system using the direct electrometrical method (DEM) of Drachev, L.A., Jasaitus, A.A., Kaulen, A.D., Kondrashin, A.A., Liberman, E.A., Nemecek, I.B., Ostroumov, S.A., Semenov, Yu, A. & Skulachev, V.P. (1974) Nature249, 321,324 are sixfold slower than the kinetics obtained in optical studies with suspensions of purple membrane patches. In this study, we have investigated the reasons for this discrepancy. In the presence of the uncouplers carbonyl cyanide m -chlorophenylhydrazone or valinomycin, the rates in the DEM system are similar to the rates in suspensions of purple membrane. Two alternative explanations for the effects of uncouplers were evaluated: (a) the ,back-pressure' of the ,µ,H+ slows the kinetic steps leading to its formation, and (b) the apparent difference between the two systems is due to slow major electrogenic events that produce little or no change in optical absorbance. In the latter case, the uncouplers would decrease the RC time constant for membrane capacitance leading to a quicker discharge of voltage and concomitant decrease in photocycle turnover time. The experimental results show that the primary cause for the slower kinetics of voltage changes in the DEM system is thermodynamic back-pressure as described by Westerhoff, H.V. & Dancshazy, Z. (1984) Trends Biochem. Sci.9, 112,117. [source] Morphology and environment: geographic distribution, ecological disjunction, and morphological variation in Actinocephalus polyanthus (Bong.) Sano (Eriocaulaceae)FEDDES REPERTORIUM, Issue 7-8 2008M. Trovó Most Brazilian Eriocaulaceae have highly restricted geographic distributions. Actinocephalus polyanthus (Bong.) Sano is one of the few widely distributed species; furthermore this distribution includes an interesting ecological disjunction. Actinocephalus polyanthus occurs in montane areas from northern Minas Gerais to Paraná, as well as coastal sand dune habitats in Santa Catarina and Rio Grande do Sul. In attempt to investigate whether there is any correlation between the ecological disjunction and the patterns of morphology exhibited by this species, eight populations were sampled covering the geographic distribution and the ecological disjunction. We used multivariate statistical methods (UPGMA, PCA and DF) to describe the morphology, and to verify its correlation with its distribution and habitat. We conclude that sand dune populations are morphologically different from the montane populations. The main difference in these plants is the robustness. The sand dune plants are significantly smaller than the plants from montane areas. We also verified that these populations have a morphological identity. The occurrence of this species in such diverse environments may reflect the morphological diversity of the various populations of the species, and may be the primary cause of the difference in these populations. (© 2008 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim) Morphologie und Umgebung: geographische Verbreitung, ökologische Disjunktion und morphologische Variabilität bei Actinocephalus polyanthus (Bong.) Sano (Eriocaulaceae) Die meisten brasilianischen Eriocaulaceae haben nur eine eng begrenzte geographische Verbreitung. Actinocephalus polyanthus (Bong.) Sano ist eine der wenigen weit verbreiteten Arten. Diese Verbreitung zeigt eine interessante ökologische Disjunktion: Actinocephalus polyanthus tritt auf in den Gebirgsregionen vom nördlichen Minas Gerais bis Paraná und in den Küsten-Sanddünen in Santa Catarina und Rio Grande do Sul. Im Versuch, ob sich irgendeine Korrelation zwischen der ökologischen Disjunktion und der morphologischen Ausprägung bei dieser Art finden lässt, sammelten wir acht Populationen aus dem geographischen Verbreitungsgebiet und der ökologischen Disjunktion. Es wurden multivariate statistische Methoden (UPGMA, PCA und DF) eingesetzt um die Morphologie zu beschreiben und diese Korrelation zwischen Verbreitung und Habitat zu vergleichen. Wir konnten daraus schließen, dass die Populationen der Sanddünen sich von den montanen Populationen unterscheiden. Der Hauptunterschied liegt in der Robustheit der Pflanzen: die der Sanddünen sind deutlich kleiner als die aus den Bergregionen. Wir beobachteten auch, dass diese Populationen morphologisch identisch sind. Das Vorkommen dieser Art in so unterschiedlicher Umgebung widerspiegelt die morphologischen Unterschiede der verschiedenen Populationen der Art, und stellt vermutlich die Hauptursache für die Unterschiede zwischen den Populationen dar. [source] Laser-Induced Rapid Carbon Nanotube Micro-ActuatorsADVANCED FUNCTIONAL MATERIALS, Issue 5 2010Zhi Han Lim Abstract Laser-induced rapid actuating microstructures made of aligned carbon nanotube (CNT) arrays are achieved. Desirable operational features of the CNT micro-actuators include low laser power activation, rapid response, elastic and reversible motion, and robust durability. Experimental evidence suggests a laser-induced electrostatic interaction mechanism as the primary cause of the optomechanical phenomenon. Oscillating CNT micro-actuators up to 40,kHz are achieved by driving them with a modulated laser beam. The micro-actuators are utilized in exerting a sub-micro-Newton force to bend nanowires. Electrical coupling of the micro-actuator and feasibilities of multi-actuator systems made entirely out of CNTs are also demonstrated. [source] Regional earthquake location using empirical traveltimes in a region of strong lateral velocity heterogeneityGEOPHYSICAL JOURNAL INTERNATIONAL, Issue 2 2008T. Nicholson SUMMARY The unmodelled effects of lateral heterogeneity are a primary cause of earthquake mislocation using routine methods. Approaches that account for the traveltime effects of lateral heterogeneity are a common feature of specialized studies, but some earthquake location methods have been developed that are also suitable for routine location. Here we investigate the use of one such method (3-D empirical traveltimes, ETTs) for local and regional earthquake location in an area of pronounced lateral velocity heterogeneity. We focus on New Zealand and the surrounding region due to the presence of strongly heterogeneous subduction zone environments. The New Zealand example poses significant challenges since most of the seismicity occurs outside the national seismograph network, and many of the observed ray paths traverse the high-velocity subducting slab. We show that in this environment, >60 per cent of the P and S residuals observed when a 1-D model velocity model is used stem from the resolvable lateral heterogeneity signal. For stations that have been in operation for more than five years, 85 per cent of observed residuals can be ascribed to this resolvable signal. We produce consistent 3-D traveltime corrections for all of New Zealand and the surrounding region and demonstrate their application to clusters of earthquakes occurring off the east coast of the North Island. [source] Loss of forb diversity in relation to nitrogen deposition in the UK: regional trends and potential controlsGLOBAL CHANGE BIOLOGY, Issue 10 2006CARLY J. STEVENS Abstract In this study we investigate the impact of nitrogen (N) deposition on the diversity of three different vegetation functional groups , forbs, grasses and mosses , using a field survey of acid grasslands across Great Britain. Our aim is to identify the vegetation types that are most vulnerable to enhanced N deposition, and to shed light on the mechanisms that may be driving N-initiated species changes in the UK. Sixty-eight randomly selected grasslands belonging to the UK National Vegetation Classification group U4 (Festuca ovina,Agrostis capillaris,Galium saxatile grassland) were studied along a gradient of atmospheric N deposition ranging from 6 to 36 kg N ha,1 yr,1. At each site, vegetation was surveyed and samples were taken from the topsoil and subsoil. Aboveground plant material was collected from three species: a forb, grass and moss. Both the species richness and cover of forbs declined strongly with increasing N deposition, from greater than eight species/20% cover per m2 quadrat at low levels of N to fewer than two species/5% cover at the highest N deposition levels. Grasses showed a weak but significant decline in species richness, and a trend toward increasing cover with increasing N input. Mosses showed no trends in either species richness or cover. Most of the decline in plant species richness could be accounted for by the level of ammonium deposition. Soil KCl-extractable ammonium concentration showed a significant positive correlation with N input, but there was no relationship between N deposition and extractable nitrate. In the soil O/A horizon, there was no relationship between N deposition and %N, and only a very weak positive relationship between the level of N deposition and the C : N ratio. Finally, in the vegetation, there was no relationship between N deposition and either shoot tissue N concentration or N : P ratio for any of the three reference species. Combining our regional survey with the results of published N-addition experiments provides compelling evidence that there has been a significant decline in the species richness and cover of forbs across Great Britain, and that the primary cause is competition due to an increase in the cover of grasses in response to enhanced deposition of reactive N, primarily NH4+. [source] Winter rain on snow and its association with air temperature in northern EurasiaHYDROLOGICAL PROCESSES, Issue 15 2008Hengchun Ye Abstract This study examines the characteristics of winter (Dec,Feb) rain-on-snow events and their relationship to surface air temperatures to reveal potential changes in rain-on-snow days under a warming climate over northern Eurasia. We found that rain-on-snow events mostly occur over European Russia during winter. Rain-on-snow days increase as air temperature increases and are primarily attributable to the increase in rainfall days. Air temperature is the primary cause for these changes, while the North Atlantic Oscillation has some influence on the rain on snow and rainfall over the northern part of European Russia. The magnitude of rain-on-snow increase ranges from 0·5 day to 2·5 days per degree Celsius increase in air temperature. Higher rates of increase in rain-on-snow days occur in the northern and eastern parts of European Russia where the air temperature is lower, in contrast to rainfall days which have higher rates at locations with higher air temperatures. This suggests that a decrease in snowfall days might be limiting the rate of increase in rain-on-snow events over warmer regions where the temperature is about , 8 °C or higher. This study also implies that rain-on-snow days will become more common over regions in which it is currently a rare event as air temperatures increase. Copyright © 2008 John Wiley & Sons, Ltd. [source] Carbon isotope fractionation of dissolved inorganic carbon (DIC) due to outgassing of carbon dioxide from a headwater streamHYDROLOGICAL PROCESSES, Issue 14 2008Daniel H. Doctor Abstract The stable isotopic composition of dissolved inorganic carbon (,13C-DIC) was investigated as a potential tracer of streamflow generation processes at the Sleepers River Research Watershed, Vermont, USA. Downstream sampling showed ,13C-DIC increased between 3,5, from the stream source to the outlet weir approximately 0·5 km downstream, concomitant with increasing pH and decreasing PCO2. An increase in ,13C-DIC of 2·4 ± 0·1, per log unit decrease of excess PCO2 (stream PCO2 normalized to atmospheric PCO2) was observed from downstream transect data collected during snowmelt. Isotopic fractionation of DIC due to CO2 outgassing rather than exchange with atmospheric CO2 may be the primary cause of increased ,13C-DIC values downstream when PCO2 of surface freshwater exceeds twice the atmospheric CO2 concentration. Although CO2 outgassing caused a general increase in stream ,13C-DIC values, points of localized groundwater seepage into the stream were identified by decreases in ,13C-DIC and increases in DIC concentration of the stream water superimposed upon the general downstream trend. In addition, comparison between snowmelt, early spring and summer seasons showed that DIC is flushed from shallow groundwater flowpaths during snowmelt and is replaced by a greater proportion of DIC derived from soil CO2 during the early spring growing season. Thus, in spite of effects from CO2 outgassing, ,13C of DIC can be a useful indicator of groundwater additions to headwater streams and a tracer of carbon dynamics in catchments. Copyright © 2007 John Wiley & Sons, Ltd. [source] Immunization with a P53 synthetic long peptide vaccine induces P53-specific immune responses in ovarian cancer patients, a phase II trial,INTERNATIONAL JOURNAL OF CANCER, Issue 9 2009Ninke Leffers Abstract The prognosis of ovarian cancer, the primary cause of death from gynecological malignancies, has only modestly improved over the last decades. Immunotherapy is one of the new treatment modalities explored for this disease. To investigate safety, tolerability, immunogenicity and obtain an impression of clinical activity of a p53 synthetic long peptide (p53-SLP) vaccine, twenty patients with recurrent elevation of CA-125 were included, eighteen of whom were immunized 4 times with 10 overlapping p53-SLP in Montanide ISA51. The first 5 patients were extensively monitored for toxicity, but showed no , grade 3 toxicity, thus accrual was continued. Overall, toxicity was limited to grade 1 and 2, mostly locoregional, inflammatory reactions. IFN-, producing p53-specific T-cell responses were induced in all patients who received all 4 immunizations as measured by IFN-, ELISPOT. An IFN-, secretion assay showed that vaccine-induced p53-specific T-cells were CD4+, produced both Th1 and Th2 cytokines as analyzed by cytokine bead array. Notably, Th2 cytokines dominated the p53-specific response. P53-specific T-cells were present in a biopsy of the last immunization site of at least 9/17 (53%) patients, reflecting the migratory capacity of p53-specific T-cells. As best clinical response, stable disease evaluated by CA-125 levels and CT-scans, was observed in 2/20 (10%) patients, but no relationship was found with vaccine-induced immunity. This study shows that the p53-SLP vaccine is safe, well tolerated and induces p53-specific T-cell responses in ovarian cancer patients. Upcoming trials will focus on improving T helper-1 polarization and clinical efficacy. © 2009 UICC [source] TP53 mutation signature supports involvement of aristolochic acid in the aetiology of endemic nephropathy-associated tumoursINTERNATIONAL JOURNAL OF CANCER, Issue 4 2009Tatiana Nedelko Abstract The proposal has been put forward that the primary cause of Balkan endemic nephropathy (BEN) is exposure to food crops contaminated with seeds of Aristolochia spp, which contain high levels of aristolochic acids (AA). Recently, tumour DNA samples from patients with BEN were found to harbour principally A to T mutations in the TP53 tumour suppressor gene (Grollman et al., Proc Natl Acad Sci USA 2007;104:12129,34). Using a novel mutation assay in which we can induce and select mutations in human TP53 sequences in vitro by exposure of cultured cells to a mutagen, we found that A to T mutations were elicited by aristolochic acid at sites in TP53 rarely mutated in human cancers in general, but which were observed in the BEN patients. This concordance of specific mutations in patient tumours and aristolochic acid I-exposed cultures supports the argument that AA has a direct role in the aetiology of BEN-associated cancer. © 2008 Wiley-Liss, Inc. [source] Residual rickets or osteomalacia: a case dating from the 16,18th centuries from Krosno Odrza,skie, PolandINTERNATIONAL JOURNAL OF OSTEOARCHAEOLOGY, Issue 5 2009E. Haduch Abstract A skeleton from a 16,18th century burial site in Krosno Odrza,skie, Poland, was examined using classical morphological, metric and macroscopic palaeopathological observations, as well as radiography and tomography of the skull and long bones. A wide variety of the observed bone deformations probably occurred as a consequence of past rickets and/or osteomalacia, whose primary cause may also have been chronic renal failure. Preservation of the bones enables a discussion of the cause of such pathological changes. The subject under study appears to be a very interesting example of an individual whose skeleton shows advanced pathological alterations associated with the subject's vitamin D deficiency, overall health conditions and relatively long lifespan. Copyright © 2008 John Wiley & Sons, Ltd. [source] Does low-intensity pulsed ultrasound stimulate maturation of tissue-engineered cartilage?JOURNAL OF BIOMEDICAL MATERIALS RESEARCH, Issue 1 2004Georg N. Duda Abstract Traumatic events are a primary cause of local lesions of articular cartilage. Tissue engineered, cartilage-like structures represent an alternative to current treatment methods. The time necessary for tissue maturation and the mechanical quality of the regenerate at implantation are both critical factors for clinical success. Low-intensity pulsed ultrasound has proven to accelerate chondrogenesis in vitro. The goal of this study was to evaluate whether low-intensity pulsed ultrasound is capable of accelerating the process of cartilage maturation and increasing regenerate stability. Hyaline-like cartilage specimens were generated in vitro and subcutaneously implanted in the backs of nude mice. Twenty-eight animals received 20 min of low-intensity pulsed ultrasound treatment daily, and 28 animals received a sham treatment. Specimens were explanted after 1, 3, 6, and 12 weeks, mechanically tested with the use of an indentation test, histologically examined, and processed for RT-PCR. The Young's moduli significantly increased from 3 to 12 weeks, and at 6 weeks were comparable to those of native articular cartilage. In histological examination, specimens showed neocartilage formation. There was no significant difference between ultrasound-treated and sham-treated groups. The mechanical stability of the neocartilage specimens increased with treatment time and reached values of native cartilage after 6 weeks in vivo. Low-intensity pulsed-ultrasound stimulation showed no stimulatory effect on tissue maturation. In contrast, ultrasound-treated specimens showed a reduced Col 2 expression at 1 week and were significantly less stiff compared to native cartilage at 6 and 12 weeks. An acceleration of the maturation of tissue-engineered neocartilage in a clinical setting by means of low-intensity pulsed ultrasound therefore appears rather unrealistic. © 2003 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater 68B: 21,28, 2004 [source] Estrogen and Bone,a Reproductive and Locomotive Perspective,JOURNAL OF BONE AND MINERAL RESEARCH, Issue 11 2003Teppo Ln Järvinen MD Abstract The primary function of the skeleton is locomotion, and the primary function of estrogen is reproduction. When the skeleton is considered within this locomotive context, the onset of estrogen secretion at puberty leads to packing of mechanically excess mineral into female bones for reproductive needs. Accordingly, the unpacking of this reproductive safety deposit at menopause denotes the origin of type I osteoporosis. Introduction: According to the prevailing unitary model of involutional osteoporosis, female postmenopausal bone loss can be described as having an initial accelerated, transient phase (type I), followed by a gradual continuous phase (type II). Estrogen withdrawal is generally accepted as the primary cause of the type I osteoporosis. Thus, the quest to uncover the origin of type I osteoporosis has focused on the estrogen withdrawal-related skeletal changes at and around the menopause. However, considering that the cyclical secretion of estrogen normally begins in early adolescence and continues over the entire fertile period, one could argue that focusing on perimenopause alone may be too narrow. Materials and Methods: This is not a systematic review of the literature on the skeletal function of estrogen(s), but rather, an introduction of a novel structure- and locomotion-oriented perspective to this particular issue through pertinent experimental and clinical studies. Results and Conclusions: When considering locomotion as the primary function of the skeleton and integrating the classic findings of the pubertal effects of estrogen on female bones and the more recent hypothesis-driven experimental and clinical studies on estrogen and mechanical loading on bone within this context, a novel evolution-based explanation for the role of estrogen in controlling female bone mass can be outlined: the onset of estrogen secretion at puberty induces packing of mechanically excess bone into female skeleton for needs of reproduction (pregnancy and lactation). Accordingly, the unpacking of this reproductive safety deposit of calcium at menopause denotes the accelerated phase of bone loss and thus the origin of type I osteoporosis. [source] Atrioventricular Nodal Tachycardia Occurring During Atrial FibrillationJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 7 2000JANE CHEN M.D. AVNRT During Atrial Fibrillation. We describe the case of a 32-year-old woman with palpitations and atrial fibrillation (AF) as the only documented arrhythmia. The patient underwent electrophysiologic study and was found to have inducible AV nodal reentrant tachycardia (AVNRT). During a prolonged episode of AVNRT, AF developed in both atria, hut AVNRT persisted. Dissociation of the atria during AVNRT is evidence that the atrium is not necessary in AVNRT. This case also illustrates the utility of an electrophysiologic study in locating a potentially curable arrhythmia as the primary cause of AF in young patients. [source] The renin,angiotensin system as a primary cause of polyarteritis nodosa in ratsJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 6a 2010Barbara S. Peters Abstract Polyarteritis nodosa is a necrotizing vasculitis of medium-sized arteries of unknown origin. Hypertension is present in 30% of patients with polyarteritis nodosa. In those cases, high renin levels are thought to be secondary to renal involvement. The present study was performed to identify causal factors of polyarteritis nodosa. In cyp1a1ren-2 transgenic rats, vasculitis of medium-sized arteries resembling classical polyarteritis nodosa can be induced. In this model, oral administration of indole-3-carbinol (I3C) activates the liver-specific cyp1a1 promoter, leading to prorenin expression in a dose-dependent manner. After the first 6 weeks of chronic induction with 0.125% I3C, the mean arterial pressure reached a plateau of about 170 mmHg. Ten out of 11 I3C-treated rats, which were chronically instrumented with a telemetric device to measure blood pressure, developed polyarteritis nodosa within 10 weeks of I3C treatment. I3C alone or instrumentation alone did not cause polyarteritis nodosa. The angiotensin-converting enzyme inhibitor captopril completely prevented the development of polyarteritis nodosa, indicating that local angiotensin II generation is a pathogenetic factor in this model. The renin,angiotensin system can play a primary role in the development of polyarteritis nodosa in rats. [source] | ||||||||||||||||||||||||||||||||||||||||||||||