Periodicities in Solar Coronal Mass Ejections

Mid-term quasi-periodicities in solar coronal mass ejections (CMEs) during the most recent solar maximum cycle 23 are reported here for the first time using the four-year data (February 5, 1999 to February 10, 2003) of the Large Angle Spectrometric Coronagraph (LASCO) onboard the Solar and Heliospheric Observatory (SOHO). In parallel, mid-term quasi-periodicities in solar X-ray flares (class >M5.0) from the Geosynchronous Operational Environment Satellites (GOES) and in daily averages of Ap index for geomagnetic disturbances from the World Data Center (WDC) at the International Association for Geomagnetism and Aeronomy (IAGA) are also examined for the same four-year time span. Several conceptual aspects of possible equatorially trapped Rossby-type waves at and beneath the solar photosphere are discussed.Comment: Accepted by MNRAS, 6 figure

Symbol error rate analysis for M-QAM modulated physical-layer network coding with phase errors

Recent theoretical studies of physical-layer network coding (PNC) show much interest on high-level modulation, such as M-ary quadrature amplitude modulation (M-QAM), and most related works are based on the assumption of phase synchrony. The possible presence of synchronization error and channel estimation error highlight the demand of analyzing the symbol error rate (SER) performance of PNC under different phase errors. Assuming synchronization and a general constellation mapping method, which maps the superposed signal into a set of M coded symbols, in this paper, we analytically derive the SER for M-QAM modulated PNC under different phase errors. We obtain an approximation of SER for general M-QAM modulations, as well as exact SER for quadrature phase-shift keying (QPSK), i.e. 4-QAM. Afterwards, theoretical results are verified by Monte Carlo simulations. The results in this paper can be used as benchmarks for designing practical systems supporting PNC. © 2012 IEEE

Emerging targets in human lymphoma: targeting the MYD88 mutation

B cell neoplasms co-opt the molecular machinery of normal B cells for their survival. Technological advances in cancer genomics has significantly contributed to uncovering the root cause of aggressive lymphomas, revealing a previously unknown link between TLR signaling and B cell neoplasm. Recurrent oncogenic mutations in MYD88 have been found in 39% of the activated B cell-like subtype of diffuse large B cell lymphoma (ABC DLBCL). Interestingly, 29% of ABC DLBCL have a single amino acid substitution of proline for the leucine at position 265 (L265P), and the exact same variant has also been identified in a number of lymphoid malignancies. The MYD88 L265P variant was recently identified in 90% of Wadenstrom's macroglobulinemia patients. These recent developments warrant the need for novel diagnostic tools as well as targeted therapeutics. In this review, we discuss the physiological functions of MYD88 and focus on its role in B cell lymphomas, evaluating the potential for targeting oncogenic MYD88 in lymphoma