Anisotropic magnetic excitations from single-chirality antiferromagnetic state in Ca-kapellasite

We present a $^{35}$Cl NMR study for spin $S=1/2$ perfect kagome antiferromagnet Ca-kapellasite (CaCu$_{3}$(OH)$_{6}$Cl$_{2}\cdot$0.6H$_{2}$O) with a magnetic transition at $T^{\ast}=7.2$ K. The static magnetic structure in the ground state has been determined to be a chirality-ordered $Q=0$ state, which is selected by a finite Dzyaloshinskii-Moriya interaction. The low-energy magnetic excitations in the ordered state are investigated by the nuclear spin-lattice relaxation rate measurement. We detect a weakly temperature dependent contribution in the magnetic fluctuations perpendicular to the kagome plane in addition to the dispersive spin-wave contribution in the kagome plane. The low-energy magnetic excitations from the coplanar spin structure are attributed to the zero mode originating from the flat band in this kagome antiferromagnet.Comment: 5 pages, 5 figure

トブ コト ノ ユカイ ヤンコ ポリチ カモフ ノ キカ ニテ

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Chronic fatigue syndrome: Harvey and Wessely's (bio)psychosocial model versus a bio(psychosocial) model based on inflammatory and oxidative and nitrosative stress pathways

<p>Abstract</p> <p>Background</p> <p>In a recently published paper, Harvey and Wessely put forward a 'biopsychosocial' explanatory model for myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), which is proposed to be applicable to (chronic) fatigue even when apparent medical causes are present.</p> <p>Methods</p> <p>Here, we review the model proposed by Harvey and Wessely, which is the rationale for behaviourally oriented interventions, such as cognitive behaviour therapy (CBT) and graded exercise therapy (GET), and compare this model with a biological model, in which inflammatory, immune, oxidative and nitrosative (IO&NS) pathways are key elements.</p> <p>Discussion</p> <p>Although human and animal studies have established that the pathophysiology of ME/CFS includes IO&NS pathways, these abnormalities are not included in the model proposed by Harvey and Wessely. Activation of IO&NS pathways is known to induce fatigue and somatic (F&S) symptoms and can be induced or maintained by viral and bacterial infections, physical and psychosocial stressors, or organic disorders such as (auto)immune disorders. Studies have shown that ME/CFS and major depression are both clinical manifestations of shared IO&NS pathways, and that both disorders can be discriminated by specific symptoms and unshared or differentiating pathways. Interventions with CBT/GET are potentially harmful for many patients with ME/CFS, since the underlying pathophysiological abnormalities may be intensified by physical stressors.</p> <p>Conclusions</p> <p>In contrast to Harvey and Wessely's (bio)psychosocial model for ME/CFS a bio(psychosocial) model based upon IO&NS abnormalities is likely more appropriate to this complex disorder. In clinical practice, we suggest physicians should also explore the IO&NS pathophysiology by applying laboratory tests that examine the pathways involved.</p

Prevalence of Pasteurella in Japan

Tadao Ikeda, Yasutomo Arashima. Prevalence of Pasteurella in Japan. In: Bulletin de l'Académie Vétérinaire de France tome 159 n°5, 2006. Séances thématiques exceptionnelles : Les maladies infectieuses. p. 407