Harri Pennanen

Decentralized Minimum Power Multi-Cell Beamforming with Limited Backhaul Signaling

A decentralized solution is proposed for the coordinated multi-cell multi-antenna minimum power beamformer design problem with single-antenna users. The optimal minimum power beamformers can be obtained locally at each base station (BS) relying on limited backhaul information exchange between BSs. The original centralized problem is reformulated such that the BSs are coupled by real-valued inter-cell interference terms. The coupling is handled by taking local copies of the interference terms at each BS and enforcing consistency between them. The consistency constraints are then decoupled by a standard dual decomposition approach leading to a distributed algorithm. The proposed method is able to guarantee feasible solutions even if the interference information is outdated or incomplete. In addition, the proposed approach allows for a number of special cases, where the backhaul information exchange is reduced at the cost of somewhat sub-optimal performance. The performance of the proposed coordinated multi-cell transmission is compared with the coherent multi-cell beamforming and with inter-cell interference nulling in different scenarios with varying interference. A near-optimal performance can be achieved even with significantly reduced backhaul information exchange and with relatively high velocities and/or low backhaul signaling rates.

p38 Kinase rescues failing myocardium after myocardial infarction: evidence for angiogenic and anti-apoptotic mechanisms

As a leading cause of heart failure, postinfarction left ventricular remodeling represents an important target for therapeutic interventions. Mitogen‐activated protein kinases regulate critical cellular processes including stress response and survival, but their role in left ventricular remodeling is unknown. In the present study, rats were subjected to myocardial infarction by ligating the left anterior descending coronary artery. Western blot and kinase assay analysis revealed an inactivation of p38 kinase after myocardial infarction. Local adenovirus‐mediated cotransfection of wild‐type (WT) p38 kinase and constitutively active MKK3b reduced infarct size (26±3% vs. 47±4%, P<0.05 vs. LacZ‐treated control) associated with improved ejection fraction (66.9±5.5% vs. 44.4±4.0%, P<0.001), fractional shortening (30.2±2.1% vs. 19.7±2.2%, P<0.001), and decreased left ventricular diastolic diameter (8.5±0.4 mm vs. 9.5±0.2 mm, P<0.01). p38 kinase gene transfer increased capillary density (2423±107/mm2 vs. 1934±86/mm2, P<0.001) and resulted in microvessel enlargement in the ischemic border zone. Apoptosis (35±7 vs. 69±13 cells, P<0.01) and fibrosis (16±3% vs. 34±8%, P<0.05) were reduced, while the number of c‐kit positive cardiac stem‐like cells remained unchanged. These results indicate that reduced p38 signaling predisposes to adverse postinfarction remodeling. The rescue of failing myocardium with p38 kinase may be a potential new therapy for heart failure after myocardial infarction. —Tenhunen, O., Soini, Y., Ilves, M., Rysä, J., Tuukkanen, J., Serpi, R., Pennanen, H., Ruskoaho, H., Leskinen, H. p38 Kinase rescues failing myocardium after myocardial infarction: evidence for angiogenic and anti‐apoptotic mechanisms. FASEB J. 20, E1276‐E1286 (2006)

Decentralized Coordinated Downlink Beamforming via Primal Decomposition

This letter considers the design problem of coordinated downlink minimum power beamforming for a multiuser multi-cell network, where each multi-antenna base station (BS) serves multiple single antenna users. We propose a decentralized primal decomposition based algorithm where limited amount of information is exchanged between coupled BSs at each iteration. Algorithm converges to the globally optimal solution for a static scenario. Unlike most of the previous decentralized methods, a feasible set of beamformers is guaranteed at each iteration even when the exchanged backhaul information is outdated. Consequently, the proposed approach naturally lends itself to realistic time-correlated fading scenarios.

SINR Balancing with Coordinated Multi-Cell Transmission

Coordinated multi-cell processing facilitates multi-user precoding techniques across distributed base station (BS) antenna heads. Hence, it can efficiently exploit the available spatial degrees of freedom in a multi-user multiple-input multiple-output (MIMO) channel. A generalised method for joint design of linear transceivers with coordinated multi-cell processing subject to per-BS/antenna power constraints is proposed. The system optimisation objective is to balance the weighted SINR across all the transmitted data streams. The method can accommodate a variety of scenarios from coherent multi-cell beamforming across a large virtual MIMO channel to single-cell beamforming with inter-cell interference coordination and beam allocation. The performance of different coherent/non-coherent and coordinated/noncoordinated multi-cell transmission methods with optimal and heuristic beam allocation algorithms is numerically compared in different scenarios with varying inter-cell interference. The coherent multi-cell beamforming greatly outperforms the non-coherent cases, especially at the cell edge and with a full spatial load. However, the coordinated single-cell transmission with interference avoidance and dynamic beam allocation performs considerably well with a partial spatial loading.

On the Value of Coherent and Coordinated Multi-Cell Transmission

Coordinated multi-cell processing facilitates multi- user precoding techniques across distributed base station (BS) antenna heads. This paper evaluates the performance of different coordinated multi-cell transmission methods with several channel allocation algorithms in different scenarios with varying inter- cell interference. A generalised method for joint design of linear transceivers with coordinated multi-cell processing subject to per-BS power constraints is provided for single antenna receivers. The method can accommodate a variety of scenarios from coherent multi-cell beamforming across a large virtual multiantenna broadcast channel to single-cell beamforming with inter-cell interference coordination and channel allocation. The system optimisation objectives are weighted SINR maximisation across all the transmitted data streams and weighted sum rate maximisation. The numerical examples demonstrate the value of the coherent multi-cell beamforming, which greatly outperforms the non-coherent cases especially at the cell edge. The coordinated single-cell transmission with interference avoidance and dynamic user allocation is also shown to perform relatively well with a partial spatial loading.

Distinct regulation of B-type natriuretic peptide transcription by p38 MAPK isoforms.

Persistent controversy underlies the functional roles of specific p38 MAPK isoforms in cardiac biology and regulation of hypertrophy-associated genes. Here we show that adenoviral gene transfer of p38β but not p38α increased B-type natriuretic peptide (BNP) mRNA levels in vitro as well as atrial natriuretic peptide mRNA levels both in vitro and in vivo. Overexpression of p38α, in turn, augmented the expression fibrosis-related genes connective tissue growth factor, basic fibroblast growth factor and matrix metalloproteinase-9 both in vitro and in vivo. p38β-induced BNP transcription was diminished by mutation of GATA-4 binding site, whereas overexpression of MKK6b, an upstream regulator of p38α and p38β, activated BNP transcription through both GATA-4 and AP-1. Overexpression of MKK3, upstream regulator of p38α, induced BNP transcription independently from AP-1 and GATA-4. These data provide new evidence for diversity in downstream targets and functional roles of p38 pathway kinases in regulation of hypertrophy-associated cardiac genes.

Distributed Coordinated Multi-Cell Transmission Based on Dual Decomposition

A distributed solution is proposed for the coordinated multi-cell multi-antenna minimum power beamformer design problem with single-antenna users. The minimum power beamformers are obtained locally at each base station (BS) relying on limited backhaul information exchange between adjacent BSs. The original centralised problem is reformulated such that the BSs are coupled by real-valued inter-cell interference terms. The coupled interference terms are handled by taking local copies of the terms at each BS and enforcing consistency between them. The consistency constraints are then decoupled by a standard dual decomposition approach leading to a distributed algorithm. The proposed method is able to guarantee feasible solutions even if the interference information is outdated or incomplete, at the possible cost of increased sum power. In addition, the proposed approach allows for a number of special cases, where the backhaul information exchange is reduced at the cost of somewhat sub-optimal performance. The performance of the proposed coordinated multi-cell transmission is compared with the coherent multi-cell beamforming, as well as, with inter-cell interference nulling in different scenarios with varying interference. The numerical examples demonstrate that a near-optimal performance can be achieved even with significantly reduced backhaul information exchange.

Multi-Cell Beamforming With Decentralized Coordination in Cognitive and Cellular Networks

This paper considers a downlink beamforming problem in a cognitive radio network where multiple primary and secondary cells coexist. Each multiantenna primary and secondary transmitter serves its own set of single antenna users. The optimization objective is to minimize the sum transmission power over secondary transmitters while guaranteeing the minimum SINR for each secondary user and satisfying the maximum aggregate interference power constraint for each primary user. We propose a decentralized beamforming algorithm where the original centralized problem is decomposed via primal decomposition method into two levels, i.e., transmitter-level subproblems managed by a network-level master problem. The master problem is solved independently at each secondary transmitter using a projected subgradient method requiring limited backhaul signaling among secondary transmitters. To solve the independent transmitter-level subproblems, we propose three alternative approaches which are based on second order cone programming, semidefinite programming and uplink-downlink duality. Special emphasis is put on the last approach, which is also considered in a multi-cell MISO cellular network. Numerical results show that the proposed algorithm achieves close to optimal solution even after a few iterations in quasi-static channel conditions. Moreover, near centralized performance is demonstrated in time-correlated channels.

Distributed implementation of coordinated multi-cell beamforming

A distributed implementation of coordinated multi-cell beamforming with single-antenna users in a time-correlated fading scenario is considered. The minimum power beamformers are obtained locally at each base station (BS) relying on limited backhaul information exchange between adjacent BSs. The original centralised problem is reformulated such that the BSs are coupled by real-valued inter-cell interference terms. The problem is then decoupled by a standard dual decomposition approach leading to a distributed algorithm. The method is able to guarantee feasible solutions even if the interference information is incomplete or outdated. Occasional high peaks in the transmitted power due to outdated interference terms are alleviated by switching to interference nulling mode when necessary. The performance of the proposed coordinated multi-cell transmission is compared with the coherent multi-cell beamforming, as well as, with interference nulling in different time-correlated fading scenarios with varying interference. The numerical examples demonstrate that a near-optimal performance can be achieved even with significantly reduced backhaul information exchange and with relatively high velocities and/or low signalling rates.

Characterization of the Regulatory Mechanisms of Activating Transcription Factor 3 by Hypertrophic Stimuli in Rat Cardiomyocytes

Aims Activating transcription factor 3 (ATF3) is a stress-activated immediate early gene suggested to have both detrimental and cardioprotective role in the heart. Here we studied the mechanisms of ATF3 activation by hypertrophic stimuli and ATF3 downstream targets in rat cardiomyocytes. Methods and Results When neonatal rat cardiomyocytes were exposed to endothelin-1 (ET-1, 100 nM) and mechanical stretching in vitro, maximal increase in ATF3 expression occurred at 1 hour. Inhibition of extracellular signal-regulated kinase (ERK) by PD98059 decreased ET-1– and stretch–induced increase of ATF3 protein but not ATF3 mRNA levels, whereas protein kinase A (PKA) inhibitor H89 attenuated both ATF3 mRNA transcription and protein expression in response to ET-1 and stretch. To characterize further the regulatory mechanisms upstream of ATF3, p38 mitogen-activated protein kinase (MAPK) signaling was investigated using a gain-of-function approach. Adenoviral overexpression of p38α, but not p38β, increased ATF3 mRNA and protein levels as well as DNA binding activity. To investigate the role of ATF3 in hypertrophic process, we overexpressed ATF3 by adenovirus-mediated gene transfer. In vitro, ATF3 gene delivery attenuated the mRNA transcription of interleukin-6 (IL-6) and plasminogen activator inhibitor-1 (PAI-1), and enhanced nuclear factor-κB (NF-κB) and Nkx-2.5 DNA binding activities. Reduced PAI-1 expression was also detected in vivo in adult rat heart by direct intramyocardial adenovirus-mediated ATF3 gene delivery. Conclusions These data demonstrate that ATF3 activation by ET-1 and mechanical stretch is partly mediated through ERK and cAMP-PKA pathways, whereas p38 MAPK pathway is involved in ATF3 activation exclusively through p38α isoform. ATF3 activation caused induction of modulators of the inflammatory response NF-κB and Nkx-2.5, as well as attenuation of pro-fibrotic and pro-inflammatory proteins IL-6 and PAI-1, suggesting cardioprotective role for ATF3 in the heart.