Response of bubbles to diagnotic ultrasound:a unifying theoretical approach

The scattering of ultrasound from bubbles of $\sim 1~\mu$m radius, such as used in contrast enhancers for ultrasound diagnostics, is studied. We show that sound scattering and ``active'' emission of sound from oscillating bubbles are not contradictory, but are just two different aspects derived from the same physics. Treating the bubble as a nonlinear oscillator, we arrive at general formulas for scattering and absorption cross-sections. We show that several well-known formulas are recovered in the linear limit of this ansatz. In the case of strongly nonlinear oscillations, however, the cross-sections can be larger than those for linear response by several orders of magnitude. The major part of the incident sound energy is then converted into emitted sound, unlike what happens in the linear case, where the absorption cross-sections exceed the scattering cross-sections

Resolving Structure in Human Brain Organization: Identifying Mesoscale Organization in Weighted Network Representations

Human brain anatomy and function display a combination of modular and hierarchical organization, suggesting the importance of both cohesive structures and variable resolutions in the facilitation of healthy cognitive processes. However, tools to simultaneously probe these features of brain architecture require further development. We propose and apply a set of methods to extract cohesive structures in network representations of brain connectivity using multi-resolution techniques. We employ a combination of soft thresholding, windowed thresholding, and resolution in community detection, that enable us to identify and isolate structures associated with different weights. One such mesoscale structure is bipartivity, which quantifies the extent to which the brain is divided into two partitions with high connectivity between partitions and low connectivity within partitions. A second, complementary mesoscale structure is modularity, which quantifies the extent to which the brain is divided into multiple communities with strong connectivity within each community and weak connectivity between communities. Our methods lead to multi-resolution curves of these network diagnostics over a range of spatial, geometric, and structural scales. For statistical comparison, we contrast our results with those obtained for several benchmark null models. Our work demonstrates that multi-resolution diagnostic curves capture complex organizational profiles in weighted graphs. We apply these methods to the identification of resolution-specific characteristics of healthy weighted graph architecture and altered connectivity profiles in psychiatric disease.Comment: Comments welcom

R116C mutation of cationic trypsinogen in a Turkish family with recurrent pancreatitis illustrates genetic microheterogeneity of hereditary pancreatitis

Hereditary pancreatitis is due to heterozygosity for gain-of-function mutations in the cationic trypsinogen gene which result in increased levels of active trypsin within pancreatic acinar cells and autodigestion of the pancreas. The number of disease-causing defects is generally considered to be low. To gain further insight into the molecular basis of this disorder, DNA sequence analysis of all five exons was performed in 109 unrelated patients with idiopathic chronic pancreatitis in order to determine the variability of the underlying mutations. Two German females and one German male were carriers of the most common N291 and R122H mutations (trypsinogen numbering system). In a Turkish proband, an arginine (CGT) to cysteine (TGT) substitution at amino acid position 116 was identified. Family screening demonstrated that the patient had inherited the mutation from his asymptomatic father and that he had transmitted it to both of his children, his daughter being symptomatic since the age of 3 years. In addition, a German male was found to be a heterozygote for a D100H (GAC-->CAC) amino acid replacement. Our data provide evidence for genetic heterogeneity of hereditary pancreatitis. The growing number of cationic trypsinogen mutations is expected to change current mutation screening practices for this disease

Gas Enrichment at Liquid-Wall Interfaces

Molecular dynamics simulations of Lennard-Jones systems are performed to study the effects of dissolved gas on liquid-wall and liquid-gas interfaces. Gas enrichment at walls is observed which for hydrophobic walls can exceed more than two orders of magnitude when compared to the gas density in the bulk liquid. As a consequence, the liquid structure close to the wall is considerably modified, leading to an enhanced wall slip. At liquid-gas interfaces gas enrichment is found which reduces the surface tension.Comment: main changes compared to version 1: flow simulations are included as well as different types of gase

Fractal dimension crossovers in turbulent passive scalar signals

The fractal dimension $\delta_g^{(1)}$ of turbulent passive scalar signals is calculated from the fluid dynamical equation. $\delta_g^{(1)}$ depends on the scale. For small Prandtl (or Schmidt) number $Pr<10^{-2}$ one gets two ranges, $\delta_g^{(1)}=1$ for small scale r and $\delta_g^{(1)}$=5/3 for large r, both as expected. But for large $Pr> 1$ one gets a third, intermediate range in which the signal is extremely wrinkled and has $\delta_g^{(1)}=2$. In that range the passive scalar structure function $D_\theta(r)$ has a plateau. We calculate the $Pr$-dependence of the crossovers. Comparison with a numerical reduced wave vector set calculation gives good agreement with our predictions.Comment: 7 pages, Revtex, 3 figures (postscript file on request

Clinical and functional characterisation of a novel TNFRSF1A c.605T > A/V173D cleavage site mutation associated with tumour necrosis factor receptor-associated periodic fever syndrome (TRAPS), cardiovascular complications and excellent response to etanercept treatment.

Objectives: To study the clinical outcome, treatment response, T-cell subsets and functional consequences of a novel tumour necrosis factor (TNF) receptor type 1 (TNFRSF1A) mutation affecting the receptor cleavage site. Methods: Patients with symptoms suggestive of tumour necrosis factor receptor-associated periodic syndrome (TRAPS) and 22 healthy controls (HC) were screened for mutations in the TNFRSF1A gene. Soluble TNFRSF1A and inflammatory cytokines were measured by ELISAs. TNFRSF1A shedding was examined by stimulation of peripheral blood mononuclear cells (PBMCs) with phorbol 12-myristate 13-acetate followed by flow cytometric analysis (FACS). Apoptosis of PBMCs was studied by stimulation with TNFa in the presence of cycloheximide and annexin V staining. T cell phenotypes were monitored by FACS. Results: TNFRSF1A sequencing disclosed a novel V173D/ p.Val202Asp substitution encoded by exon 6 in one family, the c.194–14G.A splice variant in another and the R92Q/p.Arg121Gln substitution in two families. Cardiovascular complications (lethal heart attack and peripheral arterial thrombosis) developed in two V173D patients. Subsequent etanercept treatment of the V173D carriers was highly effective over an 18-month follow-up period. Serum TNFRSF1A levels did not differ between TRAPS patients and HC, while TNFRSF1A cleavage from monocytes was significantly reduced in V173D and R92Q patients. TNFa-induced apoptosis of PBMCs and T-cell senescence were comparable between V173D patients and HC. Conclusions: The TNFRSF1A V173D cleavage site mutation may be associated with an increased risk for cardiovascular complications and shows a strong response to etanercept. T-cell senescence does not seem to have a pathogenetic role in affected patients

Observation of coasting beam at the HERA Proton--Ring

We present data collected with the HERA-B wire target which prove the existence of coasting beam at the HERA proton storage ring. The coasting beam is inherently produced by the proton machine operation and is not dominated by target effects.Comment: 17 pages (Latex), 12 figures (Enc. Postscript

Periodically kicked turbulence

Periodically kicked turbulence is theoretically analyzed within a mean field theory. For large enough kicking strength A and kicking frequency f the Reynolds number grows exponentially and then runs into some saturation. The saturation level can be calculated analytically; different regimes can be observed. For large enough Re we find the saturation level to be proportional to A*f, but intermittency can modify this scaling law. We suggest an experimental realization of periodically kicked turbulence to study the different regimes we theoretically predict and thus to better understand the effect of forcing on fully developed turbulence.Comment: 4 pages, 3 figures. Phys. Rev. E., in pres