Joint compensation of IQ-imbalance and carrier phase sychronization errors in communication receivers

This work addresses the joint compensation of IQimbalances and carrier phase synchronization errors of zero- IF receivers. The compensation scheme based on blind-source separation which provides simple yet potent means to jointly compensate for these errors independent of modulation format and constellation size used. The low-complexity of the algorithm makes it a suitable option for real-time deployment as well as practical for integration into monolithic receiver designs.

Performance of an adaptive homodyne receiver in the presence of multipath, Rayleigh-fading and time-varying quadrature errors

In this paper, we carry out a detailed performance analysis of the blind source separation based I/Q corrector operating at the baseband. Performance of the digital I/Q corrector is evaluated not only under time-varying phase and gain errors but also in the presence of multipath and Rayleigh fading channels. Performance under low-SNR and different modulation formats and constellation sizes is also evaluated. What is more, BER improvement after correction is illustrated. The results indicate that the adaptive algorithm offers adequate performance for most communication applications hence, reducing the matching requirements of the analog front-end enabling higher levels of integration.

Correction of transmitter gain and phase errors at the receiver

This paper explores the benefits of compensating transmitter gain and phase inbalances in the receiver for quadrature communication systems. It is assumed that the gain and phase imbalances are introduced at the transmitter only. A simple non-data aided DSP algorithm is used at the reciever to compensate for the imbalances. Computer simulation has been formed to study a coherent QPSK communication system.

Distinct H3F3A and H3F3B driver mutations define chondroblastoma and giant cell tumor of bone

It is recognized that some mutated cancer genes contribute to the development of many cancer types, whereas others are cancer type specific. For genes that are mutated in multiple cancer classes, mutations are usually similar in the different affected cancer types. Here, however, we report exquisite tumor type specificity for different histone H3.3 driver alterations. In 73 of 77 cases of chondroblastoma (95%), we found p.Lys36Met alterations predominantly encoded in H3F3B, which is one of two genes for histone H3.3. In contrast, in 92% (49/53) of giant cell tumors of bone, we found histone H3.3 alterations exclusively in H3F3A, leading to p.Gly34Trp or, in one case, p.Gly34Leu alterations. The mutations were restricted to the stromal cell population and were not detected in osteoclasts or their precursors. In the context of previously reported H3F3A mutations encoding p.Lys27Met and p.Gly34Arg or p.Gly34Val alterations in childhood brain tumors, a remarkable picture of tumor type specificity for histone H3.3 driver alterations emerges, indicating that histone H3.3 residues, mutations and genes have distinct functions.