Introduction to the issue on signal processing for exploiting interference toward energy efficient and secure wireless communications

INTERFERENCE has been the central focus for meeting the ever increasing requirements on quality of service in modern and future wireless communication systems, and has long been considered as a deleterious factor that limits the system capacity. In conventional communications systems, the design objective is to allow users to share a medium with minimum or no interference. Thus, great efforts are made to avoid, mitigate, and cancel interference. For instance, to support multiple users, orthogonal access methods in time, frequency, code well as spatial domains have been used in different generations of cellular systems. In future-generation heterogeneous cellular networks, due to the increasing number of uncoordinated lowpower nodes such as femtocells to improve the coverage and pacity, interferences need to be mitigated in multiple domains, rendering their management a challenge. Interference mitigation/avoidance techniques provide convenient mechanisms allow multiple users to share the wireless medium. However, they lead to inefficient use of wireless resources

Frequency data of exon 3 variants after extension of screening in alcoholic chronic pancreatitis (ACP) and idiopathic/hereditary chronic pancreatitis (ICP/HP) patients and in control subjects.

<p>Abbreviations: n.s. = not significant.</p

<i>GT</i>-repeat analysis in acute pancreatitis (AP), alcoholic chronic pancreatitis (ACP), idiopathic/hereditary chronic pancreatitis (ICP/HP), and alcoholic liver cirrhosis (ALC) patients and in controls.

<p>S-alleles were defined as <25 <i>GT</i>-repeats, whereas L-alleles represented ≥25 <i>GT</i>-repeats. Abbreviations: S = S-allele, L = L-alleles, n.s. = not significant.</p

Rare variants identified by sequencing of <i>HMOX1</i> in alcoholic chronic pancreatitis (ACP), idiopathic/hereditary chronic pancreatitis (ICP/HP), and alcoholic liver cirrhosis (ALC) patients and controls and their location within <i>HMOX1</i>.

<p>Abbreviations: n.s. = not significant.</p

Genotype data of SNP rs2071746 in acute pancreatitis (AP), alcoholic chronic pancreatitis (ACP), idiopathic/hereditary chronic pancreatitis (ICP/HP), and alcoholic liver cirrhosis (ALC) patients and in controls.

<p>Abbreviations: n.s. = not significant.</p

Genotype data of <i>PNPLA3</i> variant rs738409 in German and Dutch patients with alcoholic CP and in German and Dutch controls.

<p>Percentages are given in brackets. <i>P</i>-values were calculated for these groups in a dominant (CC vs. GC+GG) and recessive model (CC+GC vs. GG). Abbreviations: ACP = alcoholic CP, n.s. = not significant.</p

Genotype data of <i>PNPLA3</i> variant rs738409 in German (n = 128) and Dutch (n = 7) patients with alcoholic liver cirrhosis, German patients with idiopathic and hereditary CP and in German controls.

<p>Percentages are given in brackets. <i>P</i>-values were calculated for these groups in a dominant and recessive model. The <i>p</i>-value represents the result of the dominant model (CC vs. GC+CC). Abbreviations: ALC = alcoholic liver cirrhosis, ICP = idiopathic CP, HCP = hereditary CP, n.s. = not significant.</p