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Background In breeding herds, porcine reproductive and respiratory syndrome (PRRS) clinically manifests as increased abortions, number of stillbirths, and pre-weaning mortality, and as a direct consequence, results in a decrease of the number of piglets weaned per sow per year. Breeding farm classification according the PRRS virus (PRRSV) status (unstable or stable) is a key control strategy for this disease. The aim of this study was to evaluate the production improvement related to achieving a PRRSV stable status in breeding herds in Spain. For this purpose, epidemiological and productivity data were collected from a systematic PRRSV monitoring program in 35 breeding herds from a large integrated swine group in Spain. A comparative statistical analysis was conducted using four key production indicators (KPI) between different PRRSV status and a generalized linear mixed model: weekly abortions/1000 sows (ABTHS), born-alive rate (BAR), pre-weaning mortality rate (PWMR), and number of weaned piglets per 1000 sows (WPTHS). Results From the 35 monitored farms during a total period of 58 weeks, we collected 49 to 58 weeks of production data and PRRSV classification status for each study farm. This represented a total of 1997 (741 unstable and 1256 stable) weekly data collected that was eligible for the KPI comparative study. PRRSV stability was associated with significant improvement in BAR (+ 1.10 %, p  < 0.001), PWMR (-0.88 %, p  < 0.002) and WPTHS (+ 24.52, p  < 0.0001). Conclusions These results demonstrate for the first time the improved production due to achieving PRRSV stability in breeding herds under field conditions in a European country. Increased number of born-alive piglets and a reduction of piglet pre-weaning mortality represents an increase of 1.28 weaned piglets per sow per year if PRRSV stability was achieved and maintained for one-year period in a breeding farm.

Background Porcine Reproductive and Respiratory Syndrome (PRRS) is an endemic swine disease causing significant productive and economic losses. Knowledge of PRRS epidemiology is crucial to develop control strategies against this disease. In that regard, classifying farms according to PRRS virus (PRRSV) shedding and exposure, and understanding key drivers of change in status over time, provides great applied knowledge for developing disease control programs. In most European countries, PRRSV monitoring is performed most frequently at the individual farm level although criteria selected for monitoring varies among different regions and farms. The aim of this study was to implement a systematic monitoring program for PRRSV in Spanish sow farms. Breeding herds were classified according to a standardized PRRSV infection status using sampling programs and terminology currently adopted in the United States (US), which allowed an evaluation of PRRSV epidemiology in a large integrated Spanish group during a one-year study period (February 2017–March 2018). Results Fifteen farms achieved a stable PRRSV status after the first 4 consecutive samplings and 20 farms were classified as unstable. One of the farms maintained a stable status throughout the duration of the whole monitoring period. Among the 20 farms classified as unstable at the beginning of the monitoring protocol, 9 farms (45%) never reached the stable status and 11 farms (55%) reached stable status afterwards during the monitoring study period. From PRRSV PCR positive pools, there were 47 different PRRSV nucleotide sequences from 24 different farms. More than one PRRSV sequence was obtained from 15 farms. In the farms with more than one sequence detected, we observed recirculation of the same PRRSV field strain in 7 farms and introduction of a different PRRSV strain in 5 farms and both events in 3 farms. Conclusions Systematic monitoring for PRRSV in breeding herds established a basis of knowledge of PRRSV epidemiology at the farm level and provided key data to classify farms according to PRRSV exposure and shedding status. These data allow further evaluation of the impact of the PRRSV farm status on production and economic performance in breeding herds and additional investigation of factors related to PRRSV epidemiology.

A randomized clinical trial reveals that the antidiabetic effects of metformin are at least partially due to beneficial changes in the microbiota. Metformin is widely used in the treatment of type 2 diabetes (T2D), but its mechanism of action is poorly defined. Recent evidence implicates the gut microbiota as a site of metformin action. In a double-blind study, we randomized individuals with treatment-naive T2D to placebo or metformin for 4 months and showed that metformin had strong effects on the gut microbiome. These results were verified in a subset of the placebo group that switched to metformin 6 months after the start of the trial. Transfer of fecal samples (obtained before and 4 months after treatment) from metformin-treated donors to germ-free mice showed that glucose tolerance was improved in mice that received metformin-altered microbiota. By directly investigating metformin–microbiota interactions in a gut simulator, we showed that metformin affected pathways with common biological functions in species from two different phyla, and many of the metformin-regulated genes in these species encoded metalloproteins or metal transporters. Our findings provide support for the notion that altered gut microbiota mediates some of metformin's antidiabetic effects.

Here we present a draft genome sequence of the common chimpanzee ( Pan troglodytes ). Through comparison with the human genome, we have generated a largely complete catalogue of the genetic differences that have accumulated since the human and chimpanzee species diverged from our common ancestor, constituting approximately thirty-five million single-nucleotide changes, five million insertion/deletion events, and various chromosomal rearrangements. We use this catalogue to explore the magnitude and regional variation of mutational forces shaping these two genomes, and the strength of positive and negative selection acting on their genes. In particular, we find that the patterns of evolution in human and chimpanzee protein-coding genes are highly correlated and dominated by the fixation of neutral and slightly deleterious alleles. We also use the chimpanzee genome as an outgroup to investigate human population genetics and identify signatures of selective sweeps in recent human evolution.

Objective: The health effects of a supplemented Mediterranean diet (SMD) with extra-virgin olive oil (EVOO) and nuts are well documented in non-HIV-infected individuals. We hypothesised that the benefits of an SMD could be mediated by changes in the gut microbiota, even in those with an altered intestinal microbiota such as people living with HIV. Design: Individuals living with HIV (n = 102) were randomised to receive an SMD with 50 g/day of EVOO and 30 g/day of walnuts (SMD group) or continue with their regular diet (control group) for 12 weeks. Methods: Adherence to the Mediterranean diet was assessed using the validated 14-item MD-Adherence-Screener (MEDAS) from the PREDIMED study. A sub-study classifying the participants according to their MEDAS scores was performed. Results: The lipid profile was improved in the SMD group vs. that in the control group (delta-total cholesterol and delta-B-lipoprotein). The immune activation (CD4+HLADR+CD38+ and CD8+HLADR+CD38+ cells) and IFN-γ-producing T-cells significantly decreased at week 12 compared to the baseline in the SMD group but not in the control group. The gut microbiota in those from the high-adherence group presented significantly high diversity and richness at the end of the intervention. Succinivibrio and Bifidobacterium abundances were influenced by the adherence to the MD and significantly correlated with Treg cells. Conclusion: The Mediterranean diet improved metabolic parameters, immune activation, Treg function, and the gut microbiota composition in HIV-1-infected individuals. Further, Mediterranean diet increased the Bifidobacterium abundances after the intervention, and it was associated to a beneficial profile.

We present here a draft genome sequence of the red jungle fowl, Gallus gallus. Because the chicken is a modern descendant of the dinosaurs and the first non-mammalian amniote to have its genome sequenced, the draft sequence of its genome—composed of approximately one billion base pairs of sequence and an estimated 20,000–23,000 genes—provides a new perspective on vertebrate genome evolution, while also improving the annotation of mammalian genomes. For example, the evolutionary distance between chicken and human provides high specificity in detecting functional elements, both non-coding and coding. Notably, many conserved non-coding sequences are far from genes and cannot be assigned to defined functional classes. In coding regions the evolutionary dynamics of protein domains and orthologous groups illustrate processes that distinguish the lineages leading to birds and mammals. The distinctive properties of avian microchromosomes, together with the inferred patterns of conserved synteny, provide additional insights into vertebrate chromosome architecture.

The laboratory rat ( Rattus norvegicus ) is an indispensable tool in experimental medicine and drug development, having made inestimable contributions to human health. We report here the genome sequence of the Brown Norway (BN) rat strain. The sequence represents a high-quality ‘draft’ covering over 90% of the genome. The BN rat sequence is the third complete mammalian genome to be deciphered, and three-way comparisons with the human and mouse genomes resolve details of mammalian evolution. This first comprehensive analysis includes genes and proteins and their relation to human disease, repeated sequences, comparative genome-wide studies of mammalian orthologous chromosomal regions and rearrangement breakpoints, reconstruction of ancestral karyotypes and the events leading to existing species, rates of variation, and lineage-specific and lineage-independent evolutionary events such as expansion of gene families, orthology relations and protein evolution.

The sequence of the mouse genome is a key informational tool for understanding the contents of the human genome and a key experimental tool for biomedical research. Here, we report the results of an international collaboration to produce a high-quality draft sequence of the mouse genome. We also present an initial comparative analysis of the mouse and human genomes, describing some of the insights that can be gleaned from the two sequences. We discuss topics including the analysis of the evolutionary forces shaping the size, structure and sequence of the genomes; the conservation of large-scale synteny across most of the genomes; the much lower extent of sequence orthology covering less than half of the genomes; the proportions of the genomes under selection; the number of protein-coding genes; the expansion of gene families related to reproduction and immunity; the evolution of proteins; and the identification of intraspecies polymorphism.

Trichinella spiralis infection in rodents is a well-known model of intestinal inflammation associated with hypermotility and hypersecretion. Our aim was to use this experimental model to elucidate if iNOS was involved in the development of gastrointestinal hypermotility. Rats infected with Trichinella spiralis were treated for 4 days with the nitric oxide synthase inhibitors L-NAME or L-NIL. Treatment began either simultaneously with the infection or 3 days after infection when inflammation was already fully developed. In all cases, at day 10-12 after infection, anesthetized rats were prepared with strain gauges and electrodes in the small intestine to evaluate motor activity of the small intestine. In addition, histology and iNOS immunohistochemistry studies were performed. The results showed that both NOS inhibitors blocked iNOS expression in the intestine. None of the NOS inhibitors attenuated the inflammatory process. However, the preventive treatment with L-NIL reversed hypermotility. In contrast, the treatment with NOS inhibitors 3 days after infection was not so effective in reversing motor alterations. L-NAME, but not L-NIL, caused alterations on spontaneous motility. In conclusion, these results indicate that iNOS participates in the development of motor hypermotility in the gut.