Excitation of Whispering Gallery Magnons in a Magnetic Vortex.

We present the generation of whispering gallery magnons with unprecedented high wave vectors via nonlinear 3-magnon scattering in a µm-sized magnetic Ni_{81}Fe_{19} disc which is in the vortex state. These modes exhibit a strong localization at the perimeter of the disc and practically zero amplitude in an extended area around the vortex core. They originate from the splitting of the fundamental radial magnon modes, which can be resonantly excited in a vortex texture by an out-of-plane microwave field. We shed light on the basics of this nonlinear scattering mechanism from an experimental and theoretical point of view. Using Brillouin light scattering microscopy, we investigated the frequency and power dependence of the 3-magnon splitting. The spatially resolved mode profiles give evidence for the localization at the boundaries of the disc and allow for a direct determination of the modes wave number.

Carbon dioxide, hypoxia and low pH lead to overexpression of c-myc and HMGB-1 oncogenes in neuroblastoma cells.

PURPOSE: It has been reported that CO (2) gas, used to establish a pneumoperitoneum during laparoscopy, affects the behavior of tumor cells. The proto-oncogenes C-MYC and HMGB-1 mediate aggressive behavior of neuroblastomas. We studied whether exposure to CO (2), hypoxia or acidosis affects the expression of C-MYC and HMGB-1 in neuroblastoma cells. METHODS: SH-SY5Y cells were incubated with 100% CO (2), 95% helium/5% CO (2) or pH 6.2 for 2 h. The expression of C-MYC and HMGB-1 was measured by Western blot test immediately, 3 h and 6 h after incubation. Additionally, we measured apoptosis after incubation using fluorometric measurements of caspase 3 and 7 activity. RESULTS: C-myc (160+/-26%, p=0.007 and 138+/-16% vs. control, p=0.04) and HMGB-1 proteins (140+/-13% and 136+/-11%, both p=0.037) were found to be significantly upregulated 6 h after incubation with CO (2) and helium. There was early upregulation of both oncogenes 3 h after CO (2) incubation (251+/-79%, p=0.04 and 292+/-136, p=0.037). Correspondingly, pH 6.2 led to significant overexpression. Levels of apoptosis were reduced. CONCLUSIONS: Exposures mimicking conditions of CO (2) pneumoperitoneum lead to significant overexpression of C-MYC and HMGB-1 in neuroblastoma cells with decreased apoptosis. These results point to a negative influence and potentially increased malignancy of tumor cells.

Functional Mx protein does not prevent experimental biliary atresia in Balb/c mice.

Biliary atresia (BA) is a rare cholestatic disease, which manifests itself in the form of inflammation of the liver and bile ducts in newborns, with an unknown etiology and a poor outcome. Mx proteins, which are mediators of innate, antiviral resistance induced by type I interferon, were recently detected in the livers of children with BA. Therefore, the aim of this study was to examine whether the expression of Mx protein could affect the course of experimental BA in mice. A total of 185 newborn Balb/c mice (expressing dysfunctional Mx protein) and Balb/c-Mx+-A2G mice (with functional Mx protein) were intraperitoneally infected with rhesus rotavirus (RRV) or injected with saline solution as controls. They were sacrificed if they showed signs of cholestasis or at three weeks after infection. The expression of hepatic Mx protein was detected by immunostaining (POX) and the hepatic virus load was determined. There was no significant difference in the incidence of cholestasis between wild-type Balb/c mice and Balb/c-Mx+-A2G mice (67 % vs. 65 %). However, Mx protein was highly expressed in Balb/c-Mx+-A2G mice with BA phenotype, but not in wild type Balb/c mice or disease-free Balb/c-Mx+-A2G mice despite RRV infection. The difference in the hepatic virus load was not statistically significant in mice with BA. In conclusion, Mx protein does not prevent newborn Balb/c mice from developing biliary atresia after RRV infection. However, the expression of Mx protein is independent of the hepatic virus load and could be used as a marker of BA in humans, as well as in the RRV model.