What's Interesting About Strangeness Production? - An Overview of Recent Results

In this paper I highlight a few selected topics on strange particle production in heavy-ion collisions. By studying the yield and spectra of strange particles we hope to gain understanding of the conditions reached in, and the ensuing dynamics of, the systems produced when ultra-relativistic heavy-ions are collided.Comment: 17 Pages, 18 figures, Hot Quarks 2004 Proceeding

Local structure of a switchable dielectric Prussian blue analogue

The Prussian blue (cyanide-bridged, ordered double perovskite) analogue potassium imidazolium hexacyanoferrate, (C3N2H5)2KijFeIJCN)6], contains imidazolium cations encapsulated within a metal-cyanide framework. These are free to rotate in the intermediate- and high-temperature phases, but freeze into fixed orientations in the low-temperature phase. The phase transition between intermediate- and low temperature phases thus causes a substantial change in this material's dielectric constant. However, the detailed cation dynamics, and in particular how they differ between intermediate- and high-temperature phases, remain unclear. We report here total neutron scattering measurements on a perdeuterated sample of this material. Reverse Monte Carlo modelling reveals that the intermediate-temperature phase is associated with a stiffening of the metal-cyanide framework compared to either of the other phases. This shows that the dynamics responsible for the phase transitions involve competition between the energetic penalty for bending the metal-cyanide links and the benefit of host–guest hydrogen bonding. Our results demonstrate both that disordered framework materials have important local structure that is not visible to Bragg scattering, and that there is a crucial link between this structure and the dynamics that give rise to exploitable electric properties

Dental and craniofacial defects in the Crtap−/− mouse model of osteogenesis imperfecta type VII

BackgroundInactivating mutations in the gene for cartilage‐associated protein (CRTAP) cause osteogenesis imperfecta type VII in humans, with a phenotype that can include craniofacial defects. Dental and craniofacial manifestations have not been a focus of case reports to date. We analyzed the craniofacial and dental phenotype of Crtap−/− mice by skull measurements, micro‐computed tomography (micro‐CT), histology, and immunohistochemistry.ResultsCrtap−/− mice exhibited a brachycephalic skull shape with fusion of the nasofrontal suture and facial bones, resulting in mid‐face retrusion and a class III dental malocclusion. Loss of CRTAP also resulted in decreased dentin volume and decreased cellular cementum volume, though acellular cementum thickness was increased. Periodontal dysfunction was revealed by decreased alveolar bone volume and mineral density, increased periodontal ligament (PDL) space, ectopic calcification within the PDL, bone‐tooth ankylosis, altered immunostaining of extracellular matrix proteins in bone and PDL, increased pSMAD5, and more numerous osteoclasts on alveolar bone surfaces.ConclusionsCrtap−/− mice serve as a useful model of the dental and craniofacial abnormalities seen in individuals with osteogenesis imperfecta type VII.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/155878/1/dvdy166.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/155878/2/dvdy166_am.pd

VEGF Induces More Severe Cerebrovascular Dysplasia in Eng+/− than in Alk1+/− Mice

Brain arteriovenous malformations (BAVMs) are an important cause of intracranial hemorrhage (ICH) in young adults. A small percent of BAVMs is due to hereditary hemorrhagic telangiectasia 1 and 2 (HHT1 and 2), which are caused by mutations in two genes involved in transforming growth factor-β signaling: endoglin (Eng), and activin-like kinase 1 (Alk1). The BAVM phenotype has incomplete penetrance in HHT patients, and the mechanism is unknown. We tested the hypothesis that a “response-to-injury” triggers abnormal vascular (dysplasia) development, using Eng and Alk1 haploinsufficient mice. Adeno-associated virus (AAV) expressing vascular endothelial growth factor (VEGF) was used to mimic the injury conditions. VEGF overexpression caused a similar degree of angiogenesis in the brain of all groups, except that the cortex of Alk1+/− mice had a 33% higher capillary density than other groups. There were different levels of cerebrovascular dysplasia observed in haploinsufficient mice (Eng+/− > Alk1+/−), which simulates the relative penetrance of BAVM in HHT patients (HHT1 > HHT2). Few dysplastic capillaries were observed in AAV-LacZ-injected mice. Our data indicate that both angiogenic stimulation and genetic alteration are necessary for the development of vascular dysplasia, suggesting that anti-angiogenic therapies might be adapted to slow the progression of the disease and decrease the risk of spontaneous ICH

Clinical Perspective on Passive Audio Vocal Measurement in the Evaluation of Selective Mutism

Selective Mutism (SM) is an anxiety disorder often diagnosed in early childhood and characterized by persistent failure to speak in certain social situations but not others. Diagnosing SM and monitoring treatment response can be quite complex, due in part to changing definitions of and scarcity of research about the disorder. Subjective self-reports and parent/teacher interviews can complicate SM diagnosis and therapy, given that similar speech problems of etiologically heterogeneous origin can be attributed to SM. The present perspective discusses the potential for passive audio capture to help overcome psychiatry's current lack of objective and quantifiable assessments in the context of SM. We present supportive evidence from two pilot studies indicating the feasibility of using a digital wearable device to quantify child vocalization features affected by SM. We also highlight comparative analyses of passive audio capture and its potential to enhance diagnostic characterizations for SM, as well as possible limitations of such technologies

Fabrication of CuO nanoparticle interlinked microsphere cages by solution method

Here we report a very simple method to convert conventional CuO powders to nanoparticle interlinked microsphere cages by solution method. CuO is dissolved into aqueous ammonia, and the solution is diluted by alcohol and dip coating onto a glass substrate. Drying at 80 °C, the nanostructures with bunchy nanoparticles of Cu(OH)2can be formed. After the substrate immerges into the solution and we vaporize the solution, hollow microspheres can be formed onto the substrate. There are three phases in the as-prepared samples, monoclinic tenorite CuO, orthorhombic Cu(OH)2, and monoclinic carbonatodiamminecopper(II) (Cu(NH3)2CO3). After annealing at 150 °C, the products convert to CuO completely. At annealing temperature above 350 °C, the hollow microspheres became nanoparticle interlinked cages

Objective comparison of particle tracking methods

Particle tracking is of key importance for quantitative analysis of intracellular dynamic processes from time-lapse microscopy image data. Because manually detecting and following large numbers of individual particles is not feasible, automated computational methods have been developed for these tasks by many groups. Aiming to perform an objective comparison of methods, we gathered the community and organized an open competition in which participating teams applied their own methods independently to a commonly defined data set including diverse scenarios. Performance was assessed using commonly defined measures. Although no single method performed best across all scenarios, the results revealed clear differences between the various approaches, leading to notable practical conclusions for users and developers

Molecular and Antigenic Characterization of Reassortant H3N2 Viruses from Turkeys with a Unique Constellation of Pandemic H1N1 Internal Genes

Triple reassortant (TR) H3N2 influenza viruses cause varying degrees of loss in egg production in breeder turkeys. In this study we characterized TR H3N2 viruses isolated from three breeder turkey farms diagnosed with a drop in egg production. The eight gene segments of the virus isolated from the first case submission (FAV-003) were all of TR H3N2 lineage. However, viruses from the two subsequent case submissions (FAV-009 and FAV-010) were unique reassortants with PB2, PA, nucleoprotein (NP) and matrix (M) gene segments from 2009 pandemic H1N1 and the remaining gene segments from TR H3N2. Phylogenetic analysis of the HA and NA genes placed the 3 virus isolates in 2 separate clades within cluster IV of TR H3N2 viruses. Birds from the latter two affected farms had been vaccinated with a H3N4 oil emulsion vaccine prior to the outbreak. The HAl subunit of the H3N4 vaccine strain had only a predicted amino acid identity of 79% with the isolate from FAV-003 and 80% for the isolates from FAV-009 and FAV-0010. By comparison, the predicted amino acid sequence identity between a prototype TR H3N2 cluster IV virus A/Sw/ON/33853/2005 and the three turkey isolates from this study was 95% while the identity between FAV-003 and FAV-009/10 isolates was 91%. When the previously identified antigenic sites A, B, C, D and E of HA1 were examined, isolates from FAV-003 and FAV-009/10 had a total of 19 and 16 amino acid substitutions respectively when compared with the H3N4 vaccine strain. These changes corresponded with the failure of the sera collected from turkeys that received this vaccine to neutralize any of the above three isolates in vitro

The 10th Biennial Hatter Cardiovascular Institute workshop: cellular protection—evaluating new directions in the setting of myocardial infarction, ischaemic stroke, and cardio-oncology

Due to its poor capacity for regeneration, the heart is particularly sensitive to the loss of contractile cardiomyocytes. The onslaught of damage caused by ischaemia and reperfusion, occurring during an acute myocardial infarction and the subsequent reperfusion therapy, can wipe out upwards of a billion cardiomyocytes. A similar program of cell death can cause the irreversible loss of neurons in ischaemic stroke. Similar pathways of lethal cell injury can contribute to other pathologies such as left ventricular dysfunction and heart failure caused by cancer therapy. Consequently, strategies designed to protect the heart from lethal cell injury have the potential to be applicable across all three pathologies. The investigators meeting at the 10th Hatter Cardiovascular Institute workshop examined the parallels between ST-segment elevation myocardial infarction (STEMI), ischaemic stroke, and other pathologies that cause the loss of cardiomyocytes including cancer therapeutic cardiotoxicity. They examined the prospects for protection by remote ischaemic conditioning (RIC) in each scenario, and evaluated impasses and novel opportunities for cellular protection, with the future landscape for RIC in the clinical setting to be determined by the outcome of the large ERIC-PPCI/CONDI2 study. It was agreed that the way forward must include measures to improve experimental methodologies, such that they better reflect the clinical scenario and to judiciously select combinations of therapies targeting specific pathways of cellular death and injury