Mats Bengtsson

Bio: Mats Bengtsson is an academic researcher from Royal Institute of Technology. The author has contributed to research in topics: MIMO & Precoding. The author has an hindex of 42, co-authored 259 publications receiving 7096 citations. Previous affiliations of Mats Bengtsson include Linköping University & University of Oulu.

Convex Optimization-Based Beamforming

Abstract: In this article, an overview of advanced convex optimization approaches to multisensor beamforming is presented, and connections are drawn between different types of optimization-based beamformers that apply to a broad class of receive, transmit, and network beamformer design problems. It is demonstrated that convex optimization provides an indispensable set of tools for beamforming, enabling rigorous formulation and effective solution of both long-standing and emerging design problems.

Optimal Multiuser Transmit Beamforming: A Difficult Problem with a Simple Solution Structure [Lecture Notes]

Abstract: Transmit beamforming is a versatile technique for signal transmission from an array of antennas to one or multiple users [1]. In wireless communications, the goal is to increase the signal power at the intended user and reduce interference to nonintended users. A high signal power is achieved by transmitting the same data signal from all antennas but with different amplitudes and phases, such that the signal components add coherently at the user. Low interference is accomplished by making the signal components add destructively at nonintended users. This corresponds mathematically to designing beamforming vectors (that describe the amplitudes and phases) to have large inner products with the vectors describing the intended channels and small inner products with nonintended user channels.

Ketamine reduces muscle pain, temporal summation, and referred pain in fibromyalgia patients

Abstract: Central mechanisms related to referred muscle pain and temporal summation of muscular nociceptive activity are facilitated in fibromyalgia syndrome (FMS) patients. The present study assessed the ef ...

Hyperexcitability in fibromyalgia

Abstract: Objective. Spontaneous chronic widespread pain in combination with hyperalgesia to pressure stimuli is the hallmark of fibromyalgia (FM). We tested whether muscular hyperalgesia can exist in a muscle without spontaneous pain, which could indicate a generalized hyperexcitability of the nociceptive system in patients with FM. Methods. Twelve women with FM and 12 age matched female controls participated in this blind study. Patients had no spontaneous pain in the anterior tibial (AT) muscle. The pressure pain threshold was tested on the AT muscle. The pain threshold to electrical single and repeated stimulations of the skin and of the right AT muscle was assessed. Pain was evoked in the left AT muscle by infusion of sterile hypertonic saline (5.7%, 2.8 ml over 480 s). The saline induced muscle pain intensity and duration were assessed by continuous recordings on an electronic visual analog scale (VAS), and the distribution of pain was assessed on drawings. The sequence of electrical sensibility tests and the infusion of hypertonic saline was randomized. Results. Pressure pain thresholds were lower (p < 0.02) in patients with FM compared to controls. Thresholds for pain evoked by electrical stimulation at the skin were not significantly different in the 2 groups. The pain threshold to repeated intramuscular stimulation was significantly (p = 0.02) lower for the patients with FM compared to the control group, indicating that the temporal nociceptive summation was more pronounced in patients with FM. This is an indication of central sensitization (hyperexcitability). Infusion of hypertonic saline evoked muscle pain with a longer duration (p = 0.01) in patients with FM, and referred pain that spread to a larger area (p = 0.002) than in controls. This is an indication of central hyperexcitability. Conclusion. There is a state of central hyperexcitability in the nociceptive system in FM. This hyperexcitability can be revealed by excitation of intramuscular nociceptors in a muscle with no spontaneous pain.

Modeling of wide-band MIMO radio channels based on NLoS indoor measurements

Abstract: In this paper, we first verify a previously proposed Kronecker-structure-based narrow-band model for nonline-of-sight (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-input-single-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.

I and i

Abstract: There is, I think, something ethereal about i —the square root of minus one. I remember first hearing about it at school. It seemed an odd beast at that time—an intruder hovering on the edge of reality. Usually familiarity dulls this sense of the bizarre, but in the case of i it was the reverse: over the years the sense of its surreal nature intensified. It seemed that it was impossible to write mathematics that described the real world in …

Pattern Recognition and Machine Learning

Abstract: Probability Distributions.- Linear Models for Regression.- Linear Models for Classification.- Neural Networks.- Kernel Methods.- Sparse Kernel Machines.- Graphical Models.- Mixture Models and EM.- Approximate Inference.- Sampling Methods.- Continuous Latent Variables.- Sequential Data.- Combining Models.

Central sensitization: implications for the diagnosis and treatment of pain.

Abstract: Nociceptor inputs can trigger a prolonged but reversible increase in the excitability and synaptic efficacy of neurons in central nociceptive pathways, the phenomenon of central sensitization. Central sensitization manifests as pain hypersensitivity, particularly dynamic tactile allodynia, secondary punctate or pressure hyperalgesia, aftersensations, and enhanced temporal summation. It can be readily and rapidly elicited in human volunteers by diverse experimental noxious conditioning stimuli to skin, muscles or viscera, and in addition to producing pain hypersensitivity, results in secondary changes in brain activity that can be detected by electrophysiological or imaging techniques. Studies in clinical cohorts reveal changes in pain sensitivity that have been interpreted as revealing an important contribution of central sensitization to the pain phenotype in patients with fibromyalgia, osteoarthritis, musculoskeletal disorders with generalized pain hypersensitivity, headache, temporomandibular joint disorders, dental pain, neuropathic pain, visceral pain hypersensitivity disorders and post-surgical pain. The comorbidity of those pain hypersensitivity syndromes that present in the absence of inflammation or a neural lesion, their similar pattern of clinical presentation and response to centrally acting analgesics, may reflect a commonality of central sensitization to their pathophysiology. An important question that still needs to be determined is whether there are individuals with a higher inherited propensity for developing central sensitization than others, and if so, whether this conveys an increased risk in both developing conditions with pain hypersensitivity, and their chronification. Diagnostic criteria to establish the presence of central sensitization in patients will greatly assist the phenotyping of patients for choosing treatments that produce analgesia by normalizing hyperexcitable central neural activity. We have certainly come a long way since the first discovery of activity-dependent synaptic plasticity in the spinal cord and the revelation that it occurs and produces pain hypersensitivity in patients. Nevertheless, discovering the genetic and environmental contributors to and objective biomarkers of central sensitization will be highly beneficial, as will additional treatment options to prevent or reduce this prevalent and promiscuous form of pain plasticity.