Field-Selective Anomaly and Chiral Mode Reversal in Type-II Weyl Materials

Three-dimensional condensed matter incarnations of Weyl fermions generically have a tilted dispersion—in sharp contrast to their elusive high-energy relatives where a tilt is forbidden by Lorentz invariance, and with the low- energy excitations of two-dimensional graphene sheets where a tilt is forbidden by either crystalline or particle-hole symmetry. Very recently, a number of materials (MoTe2, LaAlGe, and WTe2) have been identified as hosts of so-called type-II Weyl fermions whose dispersion is so strongly tilted that a Fermi surface is formed, whereby the Weyl node becomes a singular point connecting electron and hole pockets. We here predict that these systems have remarkable properties in the presence of magnetic fields. Most saliently, we show that the nature of the chiral anomaly depends crucially on the relative angle between the applied field and the tilt, and that an inversion-asymmetric overtilting creates an imbalance in the number of chiral modes with positive and negative slopes. The field-selective anomaly gives a novel magneto-optical resonance, providing an experimental way to detect concealed Weyl nodes

Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease

Background: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P = 0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P = 0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P = 0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P = 0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P = 0.31). Conclusions: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846.

One-dimensional theory of the quantum Hall system

The quantum Hall (QH) system---cold electrons in two dimensions in a perpendicular magnetic field---is a striking example of a system where unexpected phenomena emerge at low energies. The low-energy physics of this system is effectively one-dimensional due to the magnetic field. We identify an exactly solvable limit of this interacting many-body problem, and provide strong evidence that its solutions are adiabatically connected to the observed QH states in a similar manner as the free electron gas is related to real interacting fermions in a metal according to Landau's Fermi liquid theory. The solvable limit corresponds to the electron gas on a thin torus. Here the ground states are gapped periodic crystals and the fractionally charged excitations appear as domain walls between degenerate ground states. The fractal structure of the abelian Haldane-Halperin hierarchy is manifest for generic two-body interactions. By minimizing a local k+1-body interaction we obtain a representation of the non-abelian Read-Rezayi states, where the domain wall patterns encode the fusion rules of the underlying conformal field theory. We provide extensive analytical and numerical evidence that the Laughlin/Jain states are continuously connected to the exact solutions. For more general hierarchical states we exploit the intriguing connection to conformal field theory and construct wave functions that coincide with the exact ones in the solvable limit. If correct, this construction implies the adiabatic continuation of the pertinent states. We provide some numerical support for this scenario at the recently observed fraction 4/11. Non-QH phases are separated from the thin torus by a phase transition. At half-filling, this leads to a Luttinger liquid of neutral dipoles which provides an explicit microscopic example of how weakly interacting quasiparticles in a reduced (zero) magnetic field emerge at low energies. We argue that this is also smoothly connected to the bulk state

Antiinflammatory therapy with canakinumab for atherosclerotic disease

BACKGROUND: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. METHODS: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P=0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P=0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P=0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P=0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P=0.31). CONCLUSIONS: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. Copyright © 2017 Massachusetts Medical Society