Renormalization of Coulomb interactions in s-wave superconductor Nax_xCoO2_2

We study the renormalized Coulomb interactions due to retardation effect in Na$_x$CoO$_2$. Although the Morel-Anderson's pseudo potential for $a_{1g}$ orbital $\mu^*_{a1g}$ is relatively large because the direct Coulomb repulsion $U$ is large, that for interband transition between $a_{1g}$ and $e_g'$ orbitals $\mu^*_{a1g,eg'}$ is very small since the renormalization factor for pair hopping $J$ is square of that for $U$. Therefore, the s-wave superconductivity due to valence-band Suhl-Kondo mechanism will survive against strong Coulomb interactions. The interband hopping of Cooper pairs due to shear phonons is essential to understand the superconductivity in Na$_x$CoO$_2$.Comment: 2pages, 2figures, Proceedings of ICM in Kyoto, 200

36-month clinical outcomes of patients with venous thromboembolism:GARFIELD-VTE

Background: Venous thromboembolism (VTE), encompassing both deep vein thrombosis (DVT) and pulmonary embolism (PE), is a leading cause of morbidity and mortality worldwide. Methods: GARFIELD-VTE is a prospective, non-interventional observational study of real-world treatment practices. We aimed to capture the 36-month clinical outcomes of 10,679 patients with objectively confirmed VTE enrolled between May 2014 and January 2017 from 415 sites in 28 countries. Findings: A total of 6582 (61.6 %) patients had DVT alone, 4097 (38.4 %) had PE ± DVT. At baseline, 98.1 % of patients received anticoagulation (AC) with or without other modalities of therapy. The proportion of patients on AC therapy decreased over time: 87.6 % at 3 months, 73.0 % at 6 months, 54.2 % at 12 months and 42.0 % at 36 months. At 12-months follow-up, the incidences (95 % confidence interval [CI]) of all-cause mortality, recurrent VTE and major bleeding were 6.5 (7.0–8.1), 5.4 (4.9–5.9) and 2.7 (2.4–3.0) per 100 person-years, respectively. At 36-months, these decreased to 4.4 (4.2–4.7), 3.5 (3.2–2.7) and 1.4 (1.3–1.6) per 100 person-years, respectively. Over 36-months, the rate of all-cause mortality and major bleeds were highest in patients treated with parenteral therapy (PAR) versus oral anti-coagulants (OAC) and no OAC, and the rate of recurrent VTE was highest in patients on no OAC versus those on PAR and OAC. The most frequent cause of death after 36-month follow-up was cancer (n = 565, 48.6 %), followed by cardiac (n = 94, 8.1 %), and VTE (n = 38, 3.2 %). Most recurrent VTE events were DVT alone (n = 564, 63.3 %), with the remainder PE, (n = 236, 27.3 %), or PE in combination with DVT (n = 63, 7.3 %). Interpretation: GARFIELD-VTE provides a global perspective of anticoagulation patterns and highlights the accumulation of events within the first 12 months after diagnosis. These findings may help identify treatment gaps for subsequent interventions to improve patient outcomes in this patient population.</p

Fiskalische Kosten einer steuerlichen Förderung von Forschung und Entwicklung in Deutschland - Eine empirische Analyse verschiedener Gestaltungsoptionen

Der Beitrag berechnet die Aufkommensausfälle verschiedener Gestaltungsmodelle für eine steuerliche Forschungsförderung in Deutschland auf Basis eines Mikrosimulationsmodells. Die fiskalischen Kosten betragen zwischen 464 Mio. € und 5.701 Mio. €. Eine Erstattungsoption der Steuergutschrift über die Gewerbe- und Körperschaftsteuerschuld hinaus ist unerlässlich, da sonst etwa ein Drittel der Unternehmen nicht oder nur teilweise in den Genuss der Förderung kommen würde und sich dadurch starke Verzerrungen zwischen ertragsstarken und ertragsschwachen Unternehmen ergeben. Eine Differenzierung der Fördersätze für KMU und große Unternehmen kann die Aufkommensausfälle wirksam begrenzen. Eine Kappungsgrenze in Höhe eines absoluten Betrages ist wegen der Verzerrungen innerhalb der Gruppe großer Unternehmen ungünstig. Als besonders pragmatisch erscheint eine Verrechnung der Steuergutschrift mit der abzuführenden Lohnsteuer

Advances in modeling transport phenomena in material-extrusion additivemanufacturing: Coupling momentum, heat, and mass transfer

Material-extrusion (MatEx) additive manufacturing involves layer-by-layer assembly ofextruded material onto a printer bed and has found applications in rapid prototyping.Both material and machining limitations lead to poor mechanical properties of printedparts. Such problems may be addressed via an improved understanding of thecomplex transport processes and multiphysics associated with the MatEx process.Thereby, this review paper describes the current (last 5 years) state of the art modelingapproaches based on momentum, heat and mass transfer that are employed in aneffort to achieve this understanding. We describe how specific details regardingpolymer chain orientation, viscoelastic behavior and crystallization are often neglectedand demonstrate that there is a key need to couple the transport phenomena. Such acombined modeling approach can expand MatEx applicability to broader applicationspace, thus we present prospective avenues to provide more comprehensive modelingand therefore new insights into enhancing MatEx performanc

B cell homeostasis and activation following spinal cord injury or stimulation by TLR9 linked antigens

The immune system is subject to homeostatic and regulatory mechanisms that afford robust responses against pathogens, while simultaneously avoiding reactivity to self. The studies herein examine aspects of these mechanisms under two different conditions. The first examines how chronic spinal cord injury influences B cell development, homeostasis, and responses. Mice received complete crush injury or control laminectomy at either thoracic level 3, which disrupts autonomic control of the spleen, or at thoracic level 9, which conserves most splenic sympathetic activity. Bone marrow B cell production was transiently but profoundly depressed after injury. Further, mice receiving thoracic level 3 injury showed a significant reduction in their ability to mount primary immune responses. Importantly, injury did not affect affinity maturation per se, pre-existing B cell memory, or secondary humoral immune responses. Taken together, these findings show that chronic high thoracic SCI impairs the ability to mount optimal antibody responses to new antigenic challenges, but spares previously established humoral immunity. Further, they suggest that dysregulated sympathetic nervous system signaling to the spleen underlies the immune depression syndrome that accompanies spinal cord injury. The second set of studies describes a novel post-proliferative death response in B cells activated by BCR-delivered TLR9 ligands. Death involves the intrinsic mitochondrial apoptotic pathway, is mediated by p38, occurs following G1 cell cycle arrest, and is common to all pre-immune murine B cell subsets and naïve human B cells. BLyS binding to BR3 rescues cells from death and affords survival and differentiation to antibody secretion. Importantly, this pathway is not operative in B cells from SLE susceptible Lyn-/- mice. Together, these findings reveal an unappreciated system of crosstalk between BCR and TLR9 signaling pathways that limits responses to antigens containing TLR9 ligands, and may help explain why circumventing this response-limiting system can lead to sustained autoantibody production

B cell homeostasis and activation following spinal cord injury or stimulation by TLR9 linked antigens

The immune system is subject to homeostatic and regulatory mechanisms that afford robust responses against pathogens, while simultaneously avoiding reactivity to self. The studies herein examine aspects of these mechanisms under two different conditions. The first examines how chronic spinal cord injury influences B cell development, homeostasis, and responses. Mice received complete crush injury or control laminectomy at either thoracic level 3, which disrupts autonomic control of the spleen, or at thoracic level 9, which conserves most splenic sympathetic activity. Bone marrow B cell production was transiently but profoundly depressed after injury. Further, mice receiving thoracic level 3 injury showed a significant reduction in their ability to mount primary immune responses. Importantly, injury did not affect affinity maturation per se, pre-existing B cell memory, or secondary humoral immune responses. Taken together, these findings show that chronic high thoracic SCI impairs the ability to mount optimal antibody responses to new antigenic challenges, but spares previously established humoral immunity. Further, they suggest that dysregulated sympathetic nervous system signaling to the spleen underlies the immune depression syndrome that accompanies spinal cord injury. The second set of studies describes a novel post-proliferative death response in B cells activated by BCR-delivered TLR9 ligands. Death involves the intrinsic mitochondrial apoptotic pathway, is mediated by p38, occurs following G1 cell cycle arrest, and is common to all pre-immune murine B cell subsets and naïve human B cells. BLyS binding to BR3 rescues cells from death and affords survival and differentiation to antibody secretion. Importantly, this pathway is not operative in B cells from SLE susceptible Lyn-/- mice. Together, these findings reveal an unappreciated system of crosstalk between BCR and TLR9 signaling pathways that limits responses to antigens containing TLR9 ligands, and may help explain why circumventing this response-limiting system can lead to sustained autoantibody production