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POSTER PRESENTATION, Proceedings of 20th Pediatric Rheumatology European Society (PReS) Congress / 25-29 September 2013 / Ljubljana, Slovenia

The stability of the magnetic field in the solar corona is important for understanding the causes of solar eruptions. Although various scenarios have been suggested to date, the tether-cutting reconnection scenario proposed by Moore et al.(2001) is one of the widely accepted models to explain the onset process of solar eruptions. Although the tether-cutting reconnection scenario proposed that sigmoidal field formed by the internal reconnection is the magnetic field in pre-eruptive state, the stability of the sigmoidal field has not yet been investigated quantitatively. In this paper, in order to elucidate the stability problem of pre-eruptive state, we developed a simple numerical analysis, in which the sigmoidal field is modeled by a double arc electric current loop and its stability is analyzed. As a result, we found that the double arc loop is more easily destabilized than the axisymmetric torus, and it becomes unstable even if the external field does not decay with altitude, which is in contrast to the axisymmetric torus instability. This suggests that the tether-cutting reconnection may well work as the onset mechanism of solar eruptions, and if so the critical condition for eruption under certain geometry may be determined by a new type of instability rather than the torus instability. Based on them, we propose a new type of instability called double arc instability (DAI). We discuss the critical conditions for DAI and derive a new parameter $\kappa$ defined as the product of the magnetic twist and the normalized flux of tether-cutting reconnection., Comment: 8 pages, 7 figures, accepted for publication in ApJ

The stability of the magnetic field in the solar corona is important for understanding the causes of solar eruptions. Although various scenarios have been suggested to date, the tether-cutting reconnection scenario proposed by Moore et al.(2001) is one of the widely accepted models to explain the onset process of solar eruptions. Although the tether-cutting reconnection scenario proposed that sigmoidal field formed by the internal reconnection is the magnetic field in pre-eruptive state, the stability of the sigmoidal field has not yet been investigated quantitatively. In this paper, in order to elucidate the stability problem of pre-eruptive state, we developed a simple numerical analysis, in which the sigmoidal field is modeled by a double arc electric current loop and its stability is analyzed. As a result, we found that the double arc loop is more easily destabilized than the axisymmetric torus, and it becomes unstable even if the external field does not decay with altitude, which is in contrast to the axisymmetric torus instability. This suggests that the tether-cutting reconnection may well work as the onset mechanism of solar eruptions, and if so the critical condition for eruption under certain geometry may be determined by a new type of instability rather than the torus instability. Based on them, we propose a new type of instability called double arc instability (DAI). We discuss the critical conditions for DAI and derive a new parameter $\kappa$ defined as the product of the magnetic twist and the normalized flux of tether-cutting reconnection., Comment: 8 pages, 7 figures, accepted for publication in ApJ

Inpatients who had been in close contact with patients with influenza were given oseltamivir [75 mg capsules once daily for adults or 2 mg/kg (maximum of 75 mg) once daily for children] for three days as postexposure prophylaxis (PEP). The index patients with influenza were prescribed a neuraminidase inhibitor and were discharged immediately or transferred to isolation rooms. The protective efficacy of oseltamivir for three days was 93% overall [95% confidence interval (CI) 53-99%; P = 0.023] and 94% for influenza A (95% CI 61-99%; P = 0.017), which is comparable to that of seven- to 10-day regimens of oseltamivir as PEP.

Inpatients who had been in close contact with patients with influenza were given oseltamivir [75 mg capsules once daily for adults or 2 mg/kg (maximum of 75 mg) once daily for children] for three days as postexposure prophylaxis (PEP). The index patients with influenza were prescribed a neuraminidase inhibitor and were discharged immediately or transferred to isolation rooms. The protective efficacy of oseltamivir for three days was 93% overall [95% confidence interval (CI) 53-99%; P = 0.023] and 94% for influenza A (95% CI 61-99%; P = 0.017), which is comparable to that of seven- to 10-day regimens of oseltamivir as PEP.

Inpatients who had been in close contact with patients with influenza were given oseltamivir [75 mg capsules once daily for adults or 2 mg/kg (maximum of 75 mg) once daily for children] for three days as postexposure prophylaxis (PEP). The index patients with influenza were prescribed a neuraminidase inhibitor and were discharged immediately or transferred to isolation rooms. The protective efficacy of oseltamivir for three days was 93% overall [95% confidence interval (CI) 53-99%; P = 0.023] and 94% for influenza A (95% CI 61-99%; P = 0.017), which is comparable to that of seven- to 10-day regimens of oseltamivir as PEP.

Inpatients who had been in close contact with patients with influenza were given oseltamivir [75 mg capsules once daily for adults or 2 mg/kg (maximum of 75 mg) once daily for children] for three days as postexposure prophylaxis (PEP). The index patients with influenza were prescribed a neuraminidase inhibitor and were discharged immediately or transferred to isolation rooms. The protective efficacy of oseltamivir for three days was 93% overall [95% confidence interval (CI) 53-99%; P = 0.023] and 94% for influenza A (95% CI 61-99%; P = 0.017), which is comparable to that of seven- to 10-day regimens of oseltamivir as PEP.

Amyloidoses are a group of protein-misfolding disorders that are characterized by the deposition of amyloid fibrils in organs and/or tissues. In reactive amyloid A (AA) amyloidosis, serum AA (SAA) protein forms deposits in mice, domestic and wild animals, and humans that experience chronic inflammation. AA amyloid fibrils are abnormal beta-sheet-rich forms of the serum precursor SAA, with conformational changes that promote fibril formation. Extracellular deposition of amyloid fibrils causes disease in affected animals. Recent findings suggest that AA amyloidosis could be transmissible. Similar to the pathogenesis of transmissible prion diseases, amyloid fibrils induce a seeding-nucleation process that may lead to development of AA amyloidosis. We review studies of possible transmission in bovine, avian, mouse, and cheetah AA amyloidosis.