Exploring quantum quasicrystal patterns: a variational study

We study the emergence of quasicrystal configurations produced purely by quantum fluctuations in the ground-state phase diagram of interacting bosonic systems. By using a variational mean-field approach, we determine the relevant features of the pair interaction potential that stabilize such quasicrystalline states in two dimensions. Unlike their classical counterpart, in which the interplay between only two wave vectors determines the resulting symmetries of the solutions, the quantum picture relates in a more complex way to the instabilities of the excitation spectrum. Moreover, the quantum quasicrystal patterns are found to emerge as the ground state with no need of moderate thermal fluctuations. The study extends to the exploration of the excitation properties and the possible existence of super-quasicrystals, i.e. supersolid-like quasicrystalline states in which the long-range non-periodic density profile coexist with a non-zero superfluid fraction. Our calculations show that, in an intermediate region between the homogeneous superfluid and the normal quasicrystal phases, these exotic states indeed exist at zero temperature. Comparison with full numerical simulations provides a solid verification of the variational approach adopted in this work.Comment: 10 pages, 6 Figure

Antinociceptive Activity of the Ethanolic Extract, Fractions, and Aggregatin D Isolated from <i>Sinningia aggregata</i> Tubers

<div><p>The present study investigated the effects of the ethanolic extract (ESa), fractions, and compounds isolated from <i>Sinningia aggregata</i> in male Swiss mice on carrageenan-induced paw edema, neutrophil migration, mechanical hyperalgesia, formalin-induced nociception, and lipopolysaccharide-induced fever. The ESa did not alter edema, neutrophil migration, or fever at any of the doses tested. However, the ESa reduced phase II of formalin-induced nociception and carrageenan-induced mechanical hyperalgesia. The petroleum ether (PE) and ethyl acetate (EA) fractions and aggregatin D (AgD; isolated from the EA fraction) reduced formalin-induced nociception. Anthraquinones from the PE fraction were ineffective. AgD also inhibited carrageenan-induced mechanical hyperalgesia. Neither the ESa nor AgD altered thermal nociception or motor performance. Local administration of AgD also reduced hyperalgesia induced by carrageenan, bradykinin, tumor necrosis factor-α, interleukin-1β, cytokine-induced neutrophil chemoattractant, prostaglandin E₂, and dopamine but not hyperalgesia induced by forskolin or dibutyryl cyclic adenosine monophosphate. The positive control dipyrone reduced the response induced by all of the stimuli. Additionally, glibenclamide abolished the analgesic effect of dipyrone but not the one induced by AgD. AgD did not change lipopolysaccharide-induced nitric oxide production by macrophages or the nociception induced by capsaicin, cinnamaldehyde, acidified saline, or menthol. These results suggest that the ESa has important antinociceptive activity, and this activity results at least partially from the presence of AgD. AgD reduced mechanical hyperalgesia induced by several inflammatory mediators through mechanisms that are different from classic analgesic drugs.</p></div

Effect of AgD on nociceptive behavior induced by formalin and on mechanical hyperalgesia induced by carrageenan.

<p>Animals were treated with Aggregatin D (AgD) 0.21 mg/kg or vehicle (Veh), by oral route 1 h before the administration of formalin (2.5%, panel A) or carrageenan (Cg, 300 μg, panel B) into the right paw or AgD (0.07, 0.7, 7 ng/paw), Dipyrone (Dip, 320 μg/paw) or vehicle (Veh) 15 min before the injection of Cg (panel C) into the right paw. On panel D, AgD (7ng/paw) was injected in right or left paw as indicated and Cg (300 μg) was injected in the right paw. Basal (B) threshold was evaluated before any injection in panels B, C and D. Formalin-induced nociceptive behavior was evaluated in phase I (0–5 min) or in phase II (15 to 30 min) and the mechanical threshold was evaluated again 3 h after the injection of Cg. Bars represent the mean±s.e.mean of the nociceptive behavior (s) induced by formalin in each phase or the mechanical threshold (n = 10–20). Symbols denote statistical difference in relation to basal threshold (*<i>P</i><0.05, ***<i>P</i><0.001) or to veh-treated group (^##<i>P</i><0.01, ^###<i>P</i><0.001).</p

Effect of ESa on nociception.

<p>Animals were treated with ethanolic extract form <i>S</i>. <i>aggregata</i> (ESa, 10 to 100 mg/kg, as indicated), Indomethacin (Ind, 5 mg/kg) or Diazepam (Dzp, 5 mg/kg) by oral route or with Fentanil (Fent, 0.5 mg/kg, s.c.) or the appropriate vehicles (Veh) as described in Methods. One hour after the oral treatment or 15 min after s.c. tretatment, animals were injected with formalin 2.5% in the paw (panel A) or carrageenan (300 μg) in the paw (panels B) or submitted to the hot plate (panel C) or rota-rod task (panel D). On panel B, basal (B) mechanical threshold means the threshold before any injection. Data show the mean ± s.e.mean of the change in the nociceptive behavior (s, panel A), mechanical threshold (mg, panel B), MEP (%, panel C) and motor performance (s, panel D) (n = 7–14). Symbols denote statistical difference in relation to the basal (B) group (***<i>P</i><0.001) or to Veh-treated animals (^#<i>P</i><0.05, ^##<i>P</i><0.01 and ^###<i>P</i><0.001).</p

Effect of AgD on mechanical hyperalgesia induced by BK and cytokines.

<p>Animals were treated with Aggregatin D (AgD, 7 ng/paw), Dipyrone (Dip, 320 μg/paw) or vehicle (Veh) 15 min before the injection of bradykinin (BK, 500 ng/paw, panel A), tumor necrosis factor-α (TNF-α, 1 pg/paw, panel B), interleukin-1β (IL-1β, 0.5 pg/paw, panel C) or cytokine-induced neutrophil chemoattractant (CINC-1, 10 pg/paw, panel D) in the right paw. Basal (B) threshold was evaluated before any injection. The mechanical threshold was evaluated again 3 h after the injection of the nociceptive stimuli. Bars represent the mean±s.e.mean of the mechanical threshold (mg, n = 8–10). Symbols denote statistical difference in relation to basal threshold (***<i>P</i><0.001) or to veh-treated group (^#<i>P</i><0.05, ^##<i>P</i><0.01).</p

Effect of AgD on mechanical hyperalgesia induced by PGE_2, dopamine, forskolin and dbAMPc.

<p>Animals were treated with Aggregatin D (AgD, 7 ng/paw), Dipyrone (Dip, 320 μg/paw) or vehicle (Veh) 15 min before the injection of prostaglandin E₂ (PGE₂, 100 ng/paw, panel A), Dopamine (Dopa, 3 μg/paw, panel B), forskolin (Forsk, 1 μg/paw, panel C) or dybutiryl cAMP (dbcAMP, 5 μg/paw, panel D) in the right paw. Basal (B) threshold was evaluated before any injection. The mechanical threshold was evaluated again 3 h after the injection of the nociceptive stimuli. Bars represent the mean±s.e.mean of the mechanical threshold (n = 6–16). Symbols denote statistical difference in relation to basal threshold (**<i>P</i><0.01, ***p<0.001) or to Veh-treated group (^##<i>P</i><0.01, ^###<i>P</i><0.001).</p