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Background: The accessibility, versatility and motivation provided by virtual reality technology (VRT) have fostered its rapid expansion as a rehabilitation technique to improve functional mobility. The aim of this study was to investigate the effectiveness of rehabilitation programmes using VRT, specific virtual reality technology (VRT-S) and non-specific virtual reality technology (VRT-NS), to improve functional mobility in individuals aged >60 years versus conventional treatment (CT) or no intervention., Methods: Nine databases (Cochrane Library, Scopus, PEDro, Medline, CSIC, Web of Science, OT Seeker, NGCH and CINAHL) were searched to identify randomised trials up to December 2019. Results of clinical trials that used VRT-S and VRT-NS in rehabilitation were combined, using a random effects model with inverse variance weighting of the studies. GRADE was used to assess the quality of evidence. The protocol was registered in PROSPERO: CRD42019131630. Overall, there was moderate quality of evidence for the functional mobility results, which means that the estimate of effect is likely to change., Results: Sixteen of the 18 studies selected (n = 568) provided data for the subgroup meta-analysis. VRT-NS was more effective in improving functional mobility than no intervention [standardised mean difference (SMD) = -1.02; 95% confidence interval (CI) -1,91 to -0,14). VRT-NS was also more effective than CT in improving resistance in ambulation (SMD = -1.20; 95% CI -1.93 to 0.46). No significant differences were found between VRT-S and CT or no intervention. Programmes in which >18 sessions were applied were more beneficial (SMD = -0.89; 95% CI -1.71 to -0.08; <0.001) than programmes with ≤18 sessions (SMD = 0.04; 95% CI -0.51 to 0.59) versus no intervention., Conclusions: Our results suggest that VRT is an effective intervention for improving functional mobility in older persons compared with CT. VRT-NS proved to be more effective than VRT-S. However, these results are still not conclusive due to the low methodological quality of the studies. Thus, new studies and analyses are required., (© The Author(s) 2020. Published by Oxford University Press on behalf of the British Geriatrics Society. All rights reserved. For permissions, please email: journals.permissions@oup.com.)

Neonicotinoid insecticides show high persistence in the environment, and standard biological approaches such as biopurification systems have shown mostly inefficient removal of such compounds. In this work, soil pre-exposed to imidacloprid was used to obtain presumptive imidacloprid-degrading consortia. Cometabolic enrichment yielded a microbial consortium composed of eight bacterial and one yeast strains, capable of degrading not only this compound, but also thiamethoxam and acetamiprid, as demonstrated in cross-degradation assays. The biological removal process was scaled-up to batch stirred tank bioreactors (STBR); this configuration was able to simultaneously remove mixtures of imidacloprid + thiamethoxam or imidacloprid + thiamethoxam + acetamiprid, reaching elimination of 95.8% and 94.4% of total neonicotinoids, respectively. Removal rates in the bioreactors followed the pattern imidacloprid > acetamiprid > thiamethoxam, including >99% elimination of imidacloprid in 6 d and 17 d (binary and ternary mixtures, respectively). A comprehensive evaluation of the detoxification in the STBR was performed using different biomarkers: seed germination (Lactuca sativa), bioluminescence inhibition (Vibrio fischeri), and acute oral tests in honeybees. Overall, ecotoxicological tests revealed partial detoxification of the matrix, with clearer detoxification patterns in the binary mixture. This biological approach represents a promising option for the removal of neonicotinoids from agricultural wastewater; however, optimization of the process should be performed before application in farms., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

Intracellular bacterial pathogens probably arose when their ancestor adapted from a free-living environment to an intracellular one, leading to clonal bacteria with smaller genomes and less sources of genetic plasticity. Still, this plasticity is needed to respond to the challenges posed by the host. Members of the Brucella genus are facultative-extracellular intracellular bacteria responsible for causing brucellosis in a variety of mammals. The various species keep different host preferences, virulence, and zoonotic potential despite having 97-99% similarity at genome level. Here, we describe elements of genetic variation in Brucella ceti isolated from wildlife dolphins inhabiting the Pacific Ocean and the Mediterranean Sea. Comparison with isolates obtained from marine mammals from the Atlantic Ocean and the broader Brucella genus showed distinctive traits according to oceanic distribution and preferred host. Marine mammal isolates display genetic variability, represented by an important number of IS711 elements as well as specific IS711 and SNPs genomic distribution clustering patterns. Extensive pseudogenization was found among isolates from marine mammals as compared with terrestrial ones, causing degradation in pathways related to energy, transport of metabolites, and regulation/transcription. Brucella ceti isolates infecting particularly dolphin hosts, showed further degradation of metabolite transport pathways as well as pathways related to cell wall/membrane/envelope biogenesis and motility. Thus, gene loss through pseudogenization is a source of genetic variation in Brucella, which in turn, relates to adaptation to different hosts. This is relevant to understand the natural history of bacterial diseases, their zoonotic potential, and the impact of human interventions such as domestication., (© The Author 2017. Published by Oxford University Press on behalf of the Society for Molecular Biology and Evolution.)

Several species of Brucella are known to be zoonotic, but B. neotomae infection has been thought to be limited to wood rats. In 2008 and 2011, however, B. neotomae was isolated from cerebrospinal fluid of 2 men with neurobrucellosis. The nonzoonotic status of B. neotomae should be reassessed.

Although neuromyelitis optica initially described by Eugen Devic in 1897 was considered for many years as a variant of multiple sclerosis, clinical course, more aggressive from the start, progressive towards severe disability and poor visual prognosis, and a different response to treatment, clearly point to a different process. Anti-aquaporin 4 antibodies are a specific biomarker of the entity and, since their discovery, both the number of symptoms and the radiological data about the disease have progressively increased, and the concept of clinical spectrum of neuromyelitis optica has been defined.  To our knowledge it is the first reported case of encephalopathy and neuromyelitis optica in elderly patient.

Brucellosis is a bacterial infectious disease affecting a wide range of mammals and a neglected zoonosis caused by species of the genetically homogenous genus Brucella . As in most studies on bacterial diseases, research in brucellosis is carried out by using reference strains as canonical models to understand the mechanisms underlying host pathogen interactions. We performed whole genome sequencing analysis of the reference strain B. abortus 2308 routinely used in our laboratory, including manual curated annotation accessible as an editable version through a link at https://en.wikipedia.org/wiki/Brucella#Genomics. Comparison of this genome with two publically available 2308 genomes showed significant differences, particularly indels related to insertional elements, suggesting variability related to the transposition of these elements within the same strain. Considering the outcome of high resolution genomic techniques in the bacteriology field, the conventional concept of strain definition needs to be revised.

Canine brucellosis caused by Brucella canis is a disease of dogs and a zoonotic risk. B. canis harbors most of the virulence determinants defined for the genus, but its pathogenic strategy remains unclear since it has not been demonstrated that this natural rough bacterium is an intracellular pathogen. Studies of B. canis outbreaks in kennel facilities indicated that infected dogs displaying clinical signs did not present hematological alterations. A virulent B. canis strain isolated from those outbreaks readily replicated in different organs of mice for a protracted period. However, the levels of tumor necrosis factor alpha, interleukin-6 (IL-6), and IL-12 in serum were close to background levels. Furthermore, B. canis induced lower levels of gamma interferon, less inflammation of the spleen, and a reduced number of granulomas in the liver in mice than did B. abortus. When the interaction of B. canis with cells was studied ex vivo, two patterns were observed, a predominant scattered cell-associated pattern of nonviable bacteria and an infrequent intracellular replicative pattern of viable bacteria in a perinuclear location. The second pattern, responsible for the increase in intracellular multiplication, was dependent on the type IV secretion system VirB and was seen only if the inoculum used for cell infections was in early exponential phase. Intracellular replicative B. canis followed an intracellular trafficking route undistinguishable from that of B. abortus. Although B. canis induces a lower proinflammatory response and has a stealthier replication cycle, it still displays the pathogenic properties of the genus and the ability to persist in infected organs based on the ability to multiply intracellularly., (Copyright © 2015, American Society for Microbiology. All Rights Reserved.)

Decisions regarding sedation as part of End-of-life Care in Acute Geriatric Hospitals, especially considering their 10% mortality rate, require an extremely rigorous approach to ensure complete ethical and clinical conformity. Developing a sedation protocol which examines a series of ethical and clinical safeguards regarding the implementation of this therapeutic measure facilitates and improves the decision-making process and encourages reflection among the professionals involved. Here we examine whether the protocol established in our hospital for terminal sedation was appropriately applied for those patients who passed away over the course of one year in our unit, and who received sedation in their final days.

An atypical case of familial mediterranean fever is presented in a 55 year old male with neither family antecedents nor ethnic determinants. The patient presented isolated articular involvement and positive response in the metaraminol provocation and colchicine suppression test. It was associated with monoclonal type IgG kappa gammopathy which evolved over one year until obtaining criteria, although asymptomatic, for myeloma. The increase of the monoclonal component and the infiltration of the bone medulla by plasmatic cells were considered as signs of progression inducing the initiation of treatment despite the lack of symptoms. Both entities are discussed and a mechanism justifying their association is proposed: interleukin-6 produced by macrophages in the inflammatory articular foci due to the deficiency of the C5a inhibitor existing in familial mediterranean fever, may act on a plasmatic cell clone in which receptors for IL-6 exist as a paracrine growth factor.