Tidal torques. A critical review of some techniques

We point out that the MacDonald formula for body-tide torques is valid only in the zeroth order of e/Q, while its time-average is valid in the first order. So the formula cannot be used for analysis in higher orders of e/Q. This necessitates corrections in the theory of tidal despinning and libration damping. We prove that when the inclination is low and phase lags are linear in frequency, the Kaula series is equivalent to a corrected version of the MacDonald method. The correction to MacDonald's approach would be to set the phase lag of the integral bulge proportional to the instantaneous frequency. The equivalence of descriptions gets violated by a nonlinear frequency-dependence of the lag. We explain that both the MacDonald- and Darwin-torque-based derivations of the popular formula for the tidal despinning rate are limited to low inclinations and to the phase lags being linear in frequency. The Darwin-torque-based derivation, though, is general enough to accommodate both a finite inclination and the actual rheology. Although rheologies with Q scaling as the frequency to a positive power make the torque diverge at a zero frequency, this reveals not the impossible nature of the rheology, but a flaw in mathematics, i.e., a common misassumption that damping merely provides lags to the terms of the Fourier series for the tidal potential. A hydrodynamical treatment (Darwin 1879) had demonstrated that the magnitudes of the terms, too, get changed. Reinstating of this detail tames the infinities and rehabilitates the "impossible" scaling law (which happens to be the actual law the terrestrial planets obey at low frequencies).Comment: arXiv admin note: sections 4 and 9 of this paper contain substantial text overlap with arXiv:0712.105

Deep Brain Stimulation for Parkinson's Disease with Early Motor Complications:A UK Cost-Effectiveness Analysis

International audienceBackground: Parkinson’s disease (PD) is a debilitating illness associated with considerable impairment of quality of life and substantial costs to health care systems. Deep brain stimulation (DBS) is an established surgical treatment option for some patients with advanced PD. The EARLYSTIM trial has recently demonstrated its clinical benefit also in patients with early motor complications. We sought to evaluate the cost-effectiveness of DBS, compared to best medical therapy (BMT), among PD patients with early onset of motor complications, from a United Kingdom (UK) payer perspective.Methods: We developed a Markov model to represent the progression of PD as rated using the Unified Parkinson's Disease Rating Scale (UPDRS) over time in patients with early PD. Evidence sources were a systematic review of clinical evidence; data from the EARLYSTIM study; and a UK Clinical Practice Research Datalink (CPRD) dataset including DBS patients. A mapping algorithm was developed to generate utility values based on UPDRS data for each intervention. The cost-effectiveness was expressed as the incremental cost per quality-adjusted life-year (QALY). One-way and probabilistic sensitivity analyses were undertaken to explore the effect of parameter uncertainty.Results: Over a 15-year time horizon, DBS was predicted to lead to additional mean cost per patient of £26,799 compared with BMT (£73,077/patient versus £46,278/patient) and an additional mean 1.35 QALYs (6.69 QALYs versus 5.35 QALYs), resulting in an incremental cost-effectiveness ratio of £19,887 per QALY gained with a 99% probability of DBS being cost-effective at a threshold of £30,000/QALY. One-way sensitivity analyses suggested that the results were not significantly impacted by plausible changes in the input parameter values.Conclusion: These results indicate that DBS is a cost-effective intervention in PD patients with early motor complications when compared with existing interventions, offering additional health benefits at acceptable incremental cost. This supports the extended use of DBS among patients with early onset of motor complications

Immune sensing of Candida albicans requires cooperative recognition of mannans and glucans by lectin and Toll-like receptors

Peer reviewedPublisher PD

Formation of hot tear under controlled solidification conditions

Aluminum alloy 7050 is known for its superior mechanical properties, and thus finds its application in aerospace industry. Vertical direct-chill (DC) casting process is typically employed for producing such an alloy. Despite its advantages, AA7050 is considered as a "hard-to-cast" alloy because of its propensity to cold cracking. This type of cracks occurs catastrophically and is difficult to predict. Previous research suggested that such a crack could be initiated by undeveloped hot tears (microscopic hot tear) formed during the DC casting process if they reach a certain critical size. However, validation of such a hypothesis has not been done yet. Therefore, a method to produce a hot tear with a controlled size is needed as part of the verification studies. In the current study, we demonstrate a method that has a potential to control the size of the created hot tear in a small-scale solidification process. We found that by changing two variables, cooling rate and displacement compensation rate, the size of the hot tear during solidification can be modified in a controlled way. An X-ray microtomography characterization technique is utilized to quantify the created hot tear. We suggest that feeding and strain rate during DC casting are more important compared with the exerted force on the sample for the formation of a hot tear. In addition, we show that there are four different domains of hot-tear development in the explored experimental window-compression, microscopic hot tear, macroscopic hot tear, and failure. The samples produced in the current study will be used for subsequent experiments that simulate cold-cracking conditions to confirm the earlier proposed model.This research was carried out within the Materials innovation institute (www.m2i.nl) research framework, project no. M42.5.09340

Defects in Stratum Corneum Desquamation Are the Predominant Effect of Impaired ABCA12 Function in a Novel Mouse Model of Harlequin Ichthyosis.

Harlequin Ichthyosis is a severe skin disease caused by mutations in the human gene encoding ABCA12. Here, we characterize a novel mutation in intron 29 of the mouse Abca12 gene that leads to the loss of a 5' splice donor site and truncation of the Abca12 RNA transcript. Homozygous mutants of this smooth skin or smsk allele die perinatally with shiny translucent skin, typical of animal models of Harlequin Ichthyosis. Characterization of smsk mutant skin showed that the delivery of glucosylceramides and CORNEODESMOSIN was defective, while ultrastructural analysis revealed abnormal lamellar bodies and the absence of lipid lamellae in smsk epidermis. Unexpectedly, mutant stratum corneum remained intact when subjected to harsh chemical dissociation procedures. Moreover, both KALLIKREIN 5 and -7 were drastically decreased, with retention of desmoplakin in mutant SC. In cultured wild type keratinocytes, both KALLIKREIN 5 and -7 colocalized with ceramide metabolites following calcium-induced differentiation. Reducing the intracellular levels of glucosylceramide with a glucosylceramide synthase inhibitor resulted in decreased secretion of KALLIKREIN proteases by wild type keratinocytes, but not by smsk mutant keratinocytes. Together, these findings suggest an essential role for ABCA12 in transferring not only lipids, which are required for the formation of multilamellar structures in the stratum corneum, but also proteolytic enzymes that are required for normal desquamation. Smsk mutant mice recapitulate many of the pathological features of HI and can be used to explore novel topical therapies against a potentially lethal and debilitating neonatal disease

Tidal friction in close-in satellites and exoplanets. The Darwin theory re-visited

This report is a review of Darwin's classical theory of bodily tides in which we present the analytical expressions for the orbital and rotational evolution of the bodies and for the energy dissipation rates due to their tidal interaction. General formulas are given which do not depend on any assumption linking the tidal lags to the frequencies of the corresponding tidal waves (except that equal frequency harmonics are assumed to span equal lags). Emphasis is given to the cases of companions having reached one of the two possible final states: (1) the super-synchronous stationary rotation resulting from the vanishing of the average tidal torque; (2) the capture into a 1:1 spin-orbit resonance (true synchronization). In these cases, the energy dissipation is controlled by the tidal harmonic with period equal to the orbital period (instead of the semi-diurnal tide) and the singularity due to the vanishing of the geometric phase lag does not exist. It is also shown that the true synchronization with non-zero eccentricity is only possible if an extra torque exists opposite to the tidal torque. The theory is developed assuming that this additional torque is produced by an equatorial permanent asymmetry in the companion. The results are model-dependent and the theory is developed only to the second degree in eccentricity and inclination (obliquity). It can easily be extended to higher orders, but formal accuracy will not be a real improvement as long as the physics of the processes leading to tidal lags is not better known.Comment: 30 pages, 7 figures, corrected typo

Trained Immunity or Tolerance: Opposing Functional Programs Induced in Human Monocytes After Engagement of Various Pattern Recognition Receptors

Upon priming with Candida albicans or with the fungal cell wall component β-glucan, monocytes respond with an increased cytokine production upon restimulation, a phenomenon termed trained immunity. In contrast, the prestimulation of monocytes with lipopolysaccharide has long been known to induce tolerance. Because the vast majority of commensal microorganisms belong to bacterial or viral phyla, we sought to systematically investigate the functional reprogramming of monocytes induced by the stimulation of pattern recognition receptors (PRRs) with various bacterial or viral ligands. Monocytes were functionally programmed for either enhanced (training) or decreased (tolerance) cytokine production, depending on the type and concentration of ligand they encountered. The functional reprogramming of monocytes was also associated with cell shape, granulocity, and cell surface marker modifications. The training effect required p38- and Jun N-terminal protein kinase (JNK)-mediated mitogen-activated protein kinase (MAPK) signaling, with specific signaling patterns directing the functional fate of the cell. The long-term effects on the function of monocytes were mediated by epigenetic events, with both histone methylation and acetylation inhibitors blocking the training effects. In conclusion, our experiments identify the ability of monocytes to acquire adaptive characteristics after prior activation with a wide variety of ligands. Trained immunity and tolerance are two distinct and opposing functional programs induced by the specific microbial ligands engaging the monocytes

Efficient Selfconsistent Calculations of Multiband Superconductivity in UPd2_2Al3_3

An efficient physically motivated computational approach to multiband superconductivity is introduced and applied to the study of the gap symmetry in a heavy-fermion, UPd$_2$Al$_3$. Using realistic pairing potentials and accurate energy bands that are computed within density functional theory, self-consistent calculations demonstrate that the only accessible superconducting gap with nodes exhibits d-wave symmetry in the $A_{1g}$ representation of the $D_{6h}$ point group. Our results suggest that in a superconductor with gap nodes the prevailing gap symmetry is dictated by the constraint that nodes must be as far as possible from high-density areas

Looking for magnetic monopoles at LHC with diphoton events

Magnetic monopoles have been a subject of interest since Dirac established the relation between the existence of monopoles and charge quantization. The intense experimental search carried thus far has not met with success. The Large Hadron Collider is reaching energies never achieved before allowing the search for exotic particles in the TeV mass range. In a continuing effort to discover these rare particles we propose here other ways to detect them. We study the observability of monopoles and monopolium, a monopole-antimonopole bound state, at the Large Hadron Collider in the $\gamma \gamma$ channel for monopole masses in the range 500-1000 GeV. We conclude that LHC is an ideal machine to discover monopoles with masses below 1 TeV at present running energies and with 5 fb$^{-1}$ of integrated luminosity.Comment: This manuscript contains information appeared in Looking for magnetic monopoles at LHC, arXiv:1104.0218 [hep-ph] and Monopolium detection at the LHC.,arXiv:1107.3684 [hep-ph] by the same authors, rewritten for joint publication in The European Physica Journal Plus. 26 pages, 22 figure