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Massive multi-user (MU) multiple-input multipleoutput (MIMO) systems are one possible key technology for next generation wireless communication systems. Claims have been made that massive MU-MIMO will increase both the radiated energy efficiency as well as the sum-rate capacity by orders of magnitude, because of the high transmit directivity. However, due to the very large number of transceivers needed at each basestation (BS), a successful implementation of massive MU-MIMO will be contingent on of the availability of very cheap, compact and power-efficient radio and digital-processing hardware. This may in turn impair the quality of the modulated radio frequency (RF) signal due to an increased amount of power-amplifier distortion, phase-noise, and quantization noise.In this paper, we examine the effects of hardware impairments on a massive MU-MIMO single-cell system by means of theory and simulation. The simulations are performed using simplified, well-established statistical hardware impairment models as well as more sophisticated and realistic models based upon measurements and electromagnetic antenna array simulations.

Olsenella umbonata sp. nov., a microaerotolerant anaerobic lactic acid bacterium from the sheep rumen and pig jejunum, and emended descriptions of Olsenella, Olsenella uli and Olsenella profusa Strain A2 is an anaerobic, variably Gram-stain-positive, non-spore-forming, small and irregularly rod-shaped bacterium from the ruminal fluid of a sheep that has been described informally as a representative of 'Olsenella (basonym Atopobium) oviles'. Three phenotypically similar bacterial strains (lac15, lac16 and lac31 T ) were isolated in concert with Veillonella magna lac18 T from the mucosal jejunum of a pig. A phylogenetic analysis based on 16S rRNA gene sequences revealed that strains A2, lac15, lac16 and lac31 T formed a genetically coherent group (100 % interstrain sequence similarity) within the bigeneric Olsenella-Atopobium branch of the family Coriobacteriaceae, class Actinobacteria. This group was most closely related to the type strains of the two recognized Olsenella species, namely Olsenella uli (sequence similarity of 96.85 %) and Olsenella profusa (sequence similarity of 97.20 %). The sequence similarity to the type strain of Atopobium minutum, the type species of the genus Atopobium, was 92.33 %. Unlike those of O. uli and O. profusa, outgrown colonies of strains A2, lac15, lac16 and lac31 T were opaque and greyish-white with an umbonate elevation on solid culture media. The four novel strains were characterized as being well-adapted and presumably indigenous to the gastrointestinal tract of homoeothermic vertebrates: they were mesophilic, microaerotolerant, neutrophilic and acidotolerant, bile-resistant, mucin-utilizing and markedly peptidolytic lactic acid bacteria. The results of DNA-DNA hybridizations, cellular fatty acid analysis and other differential phenotypic (physiological and biochemical) tests confirmed that strains A2, lac15, lac16 and lac31 T represent a novel species of the genus Olsenella. On the basis of the genotypic and phenotypic results, we therefore describe Olsenella umbonata sp. nov., with lac31 T (5CCUG 58604 T 5DSM 22620 T 5JCM 16156 T ) as the type strain and A2 (5CCUG 58212 5DSM 22619 5JCM 16157) as an additionally available reference strain. Also, based on our data, we propose emended descriptions of the genus Olsenella and the species Olsenella uli and Olsenella profusa.

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Staphylococcus aureus is the most common bacterial species found in association with nongonococcal bacterial arthritis in humans. We present here the first description of spontaneous bacterial arthritis and osteitis in mice. Clinically, the most obvious findings were swelling and/or ankylosis of hindpaws and nodose changes of the tail. The prevalence of arthritis and osteitis ranged from 0% to greater than 50% of the mice studied, depending on the mouse strain. The most prominent histopathologic feature of the arthritis was hypertrophy of the synovial tissue and destruction of cartilage and underlying bone. Most of the S aureus-infected mice displayed an identical phage type, which was also the only S aureus phage type found in skin isolates from clinically healthy mice. However, a few S aureus isolates were not typeable, indicating that an additional strain(s) might cause bacterial arthritis in mice.

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IL-1R-deficient mice (IL-1R−/−) and their wild-type controls (IL-1R+/+) were i.v. inoculated with 1 × 107 or 106 Staphylococcus aureus per mouse to mimic bacterial sepsis and septic arthritis. The disease outcome was severely worsened in the IL-1R−/− mice as compared with IL-1R+/+ mice. Indeed, 3 days after inoculation of 107 S. aureus per mouse 84% of IL-1R−/− mice displayed clinical signs of septicemia as compared with none of the IL-1R+/+ mice. On day 9 after inoculation with 106 S. aureus per mouse 75% of the IL-1R−/− mice were dead as compared with none of the IL-1R+/+ mice. Also, the number of staphylococci in circulation was 25- to 30-fold increased in IL-1R−/− mice as compared with IL-1R+/+ mice, the most probable reason for the outcome. The frequency and severity of septic arthritis were significantly increased in IL-1R−/− mice, as compared with IL-1R+/+ mice, following i.v. inoculation of staphylococci. This was probably due to an increased accumulation of bacteria in the joints of IL-1R−/− mice as compared with their wild-type controls. Interestingly, while serum levels of IL-18 in IL-1R−/− mice were significantly lower than in IL-1R+/+ mice 24 h after inoculation of S. aureus, both IL-18 and IL-1β were significantly increased in IL-1R−/− vs IL-1R+/+ mice 4 days after the bacterial inoculation. In conclusion, IL-1R signaling plays a crucial role in host protection during systemic S. aureus infection as seen by the fatal outcome of S. aureus sepsis and arthritis in IL-1R-deficient mice.

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