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Abstract-In this paper, we first verify a previously proposed Kronecker-structure-based narrow-band model for nonline-ofsight (NLoS) indoor multiple-input-multiple-output (MIMO) radio channels based on 5.2-GHz indoor MIMO channel measurements. It is observed that, for the narrow-band case, the measured channel coefficients are complex Gaussian distributed and, consequently, we focus on a statistical description using the first-and second-order moments of MIMO radio channels. It is shown that the MIMO channel covariance matrix can be well approximated by the Kronecker product of the covariance matrices, seen from the transmitter and receiver, respectively. A narrow-band model for NLoS indoor MIMO channels is thus verified by these results. As for the wide-band case, it is observed that the average power-delay profile of each element of the channel impulse response matrix fits the exponential decay curve and that the Kronecker structure of the second-order moments can be extended to each channel tap. A wide-band MIMO channel model is then proposed, combining a simple COST 259 single-inputsingle-output channel model and the Kronecker structure. Monte Carlo simulations are used to generate indoor MIMO channel realizations according to the models discussed. The results are compared with the measured data using the channel capacity and good agreement is found.

23 VOCs, whose areas under curve (AUC) of receiver operating characteristic (ROC) > 0.60 and p < 0.01, were confirmed as the VOCs biomarkers for lung cancer. Three diagnostic models based on 23 VOCs could easily discriminate lung cancer patients from controls with 96.47% sensitivity and 97.47% specificity. However, the discrimination between early stage and later stage lung cancer was not very obvious.

This paper reviews recently published results on multiple input multiple output (MIMO) channel modeling. Both narrowband and wideband models are considered. We distinguish between two main approaches to MIMO channel modeling, that is, physically based and nonphysically based modeling. The nonphysical models primarily rely on the statistical characteristics of the MIMO channels obtained from the measured data, while the physical models describe the MIMO channel (or its distribution) via some physical parameters. We briefly review different MIMO channel models and discuss their relationships. Some interesting aspects will be described in more detail and we note areas in which few results are available. Copyright © 2002 John Wiley & Sons, Ltd.

The molecular mechanisms underlying acute leptin and serotonin 2C receptor induced hypophagia remain unclear. Here we show that neuronal and pro-opiomelanocortin (Pomc)-specific loss of transient receptor potential cation 5 (TrpC5) subunits is sufficient to decrease energy expenditure and increase food intake resulting in elevated body weight. Deficiency of Trpc5 subunits in Pomc neurons was also sufficient to block the anorexigenic effects of leptin and serotonin 2C receptor (Ht2Cr) agonists. The loss of acute anorexigenic effects of these receptors was concomitant with a blunted electrophysiological response to both leptin and Ht2Cr agonists in arcuate Pomc neurons. We also demonstrate that the Ht2Cr agonist lorcaserin-induced improvements in glucose and insulin tolerance were blocked by TrpC5 deficiency in Pomc neurons. Together, our results link TrpC5 subunits in the brain with leptin- and serotonin 2C receptor-dependent changes in neuronal activity as well as energy balance, feeding behavior, and glucose metabolism.