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In this paper, a new optimization framework is presented for the joint design of user selection, power allocation, and precoding in multi-cell multi-user multiple-input multiple-output (MU-MIMO) systems when imperfect channel state information at transmitter (CSIT) is available. By representing the joint optimization variables in a higher-dimensional space, the weighted sum-spectral efficiency maximization is formulated as the maximization of the product of Rayleigh quotients. Although this is still a non-convex problem, a computationally efficient algorithm, referred to as generalized power iteration precoding (GPIP), is proposed. The algorithm converges to a stationary point (local maximum) of the objective function and therefore it guarantees the first-order optimality of the solution. By adjusting the weights in the weighted sum-spectral efficiency, the GPIP yields a joint solution for user selection, power allocation, and downlink precoding. The GPIP is also extended to a multi-cell scenario, where cooperative base stations perform joint user selection and design their precoding vectors by sharing global yet imperfect CSIT within the cooperative BSs. System-level simulations show the gains of the proposed approach with respect to conventional user selection and linear downlink precoding.

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Due to the rapid development of mobile phone technology, we are continuously exposed to 1.7 GHz LTE radio frequency electromagnetic fields (RF-EMFs), but their biological effects have not been clarified. Here, we investigated the non-thermal cellular effects of these RF-EMFs on human cells, including human adipose tissue-derived stem cells (ASCs), Huh7 and Hep3B liver cancer stem cells (CSCs), HeLa and SH-SY5Y cancer cells, and normal fibroblast IMR-90 cells. When continuously exposed to 1.7 GHz LTE RF-EMF for 72 h at 1 and 2 SAR, cell proliferation was consistently decreased in all the human cells. The anti-proliferative effect was higher at 2 SAR than 1 SAR and was less severe in ASCs. The exposure to RF-EMF for 72 h at 1 and 2 SAR did not induce DNA double strand breaks or apoptotic cell death, but did trigger a slight delay in the G1 to S cell cycle transition. Cell senescence was also clearly observed in ASC and Huh7 cells exposed to RF-EMF at 2 SAR for 72 h. Intracellular ROS increased in these cells and the treatment with an ROS scavenger recapitulated the anti-proliferative effect of RF-EMF. These observations strongly suggest that 1.7 GHz LTE RF-EMF decrease proliferation and increase senescence by increasing intracellular ROS in human cells. The development of wireless communication technology has made our life efficient and convenient. In return, we are continuously exposed to radio frequency electromagnetic fields (RF-EMFs) and environmental exposure to RF-EMFs has steadily increased. The International Agency for Research on Cancer (IARC) classified radiofrequency electromagnetic fields as Group 2B carcinogens in 2011 1,2. However, biological studies have not consistently supported or clarified the carcinogenic effect of RF-EMF. A review of 2012 suggested that the currently available data did not show genotoxic effect from RF-EMF 3. Two recent animal studies by the US National Toxicology Program 4,5 and the Ramazzini Institute 6 investigated the carcinogenic potential of long-term exposure to RF-EMFs associated with mobile phones. The International Commission on Non-ionizing Radiation Protection (ICNRP) evaluated these two reports and recently announced that the conclusions concerning the carcinogenic potential of RF-EMFs could not be drawn due to the technical limitations of the studies 7. On the other hand, a recent report showed that rats exposed from prenatal life until natural death to 1.8 GHz global system for mobile (GSM) communication increased the incidence of heart malignant schwannoma among males exposed at the highest dose 8. Thus, the carcinogenic effects of RF-EMF are still unclear.