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1. Keel bone damage, such as deformations and fractures, is a severe problem regarding animal welfare in layers. To identify risk factors under commercial conditions, 33 layer flocks (22 barn, 11 free range) with white (n = 18), brown (n = 11) and mixed (n = 4) genotypes were examined. 2. Keel bone status was frequently scored by palpation throughout the laying period. Data on housing and management conditions were collected. Multiple regression and Generalized Estimating Equations procedure were used for analysis. 3. At 65–74 weeks of age, the prevalence of keel bone damage ranged between 26% and 74%. White genotypes and those kept in multi-tier systems developed significantly (p < 0.05) more keel bone damage than brown genotypes or those kept in single-tier systems. Wing feather condition was associated with keel bone damage (p < 0.05), while other investigated variables regarding health, housing and management were not associated. 4. In conclusion, housing and management should be adapted to meet the birds' specific needs in multi-tier systems, which may vary for brown and white genotypes. Whether those differences result from genotype associated predispositions or other individual traits remains to be determined. [ABSTRACT FROM AUTHOR]

1. Within a triennial project, 34 layer flocks with untrimmed beaks were examined regularly throughout the laying period to broaden knowledge on the occurrence and development of severe feather pecking and cannibalism, as well as on factors influencing this non-desirable behaviour. 2. Flocks involved 850 to 27,183 hens of seven different genetics, kept in a barn or on free-range systems. Damage to the plumage and skin was assessed in individual hens during each visit and their body weights recorded. Correlations smaller than 0.8 between different body areas for damage indicated the necessity to consider them separately. Accounting for the risk of bias due to unevenly distributed factors, regression functions were used to assess associations between pecking damage, losses and performance, housing and management conditions. In addition, temporal pattern of pecking damage for flocks with severe, medium and little damage was modelled using these functions. 3. As expected, plumage damage increased with age, whereas the development of skin lesions was less consistent. From 30 weeks of age, pecking damage on the back increased remarkably in flocks with the most severe scores compared to those with medium and little damage, especially during the later laying period. Associations were found between pecking damage on the back of hens with plumage quality of pullets when entering the layer house (point of lay). Damage to the vent/cloacal region was more pronounced in white compared to brown layers. However, this did not deny the importance of factors not significant in this study. 4. The study identified factors related to genetics and status of hens when entering the layer house, particularly the influence of the rearing phase. [ABSTRACT FROM AUTHOR]

BackgroundBovine mastitis is a common disease of dairy cattle causing major economic losses due to reduced yield and poor quality of milk worldwide. The current investigation aimed to gain insight into the genetic diversity, antimicrobial resistance profiles and virulence associated factors of Staphylococcus (S.) aureus isolated from clinical bovine mastitis in dairy farms in Thuringia, Germany.MethodsForty Staphylococcus aureus isolates collected from clinical bovine mastitis cases from 17 Thuringian dairy farms were phenotyped and genetically characterized using whole genome sequencing.ResultsOut of 40 S. aureus, 30 (75%) were confirmed as methicillin resistant isolates. The isolates showed elevated antimicrobial resistance against penicillin, tetracycline and oxacillin, i.e., 77.5, 77.5, and 75%, respectively. Lower resistance rates were found against moxifloxacin, ciprofloxacin, gentamicin and trimethoprim/sulfamethoxazole, i.e., 35, 35, 30, and 22.5%, respectively. While resistance against clindamycin and erythromycin was rarely found (5 and 2.5%, respectively). All isolates were susceptible to linezolid, teicoplanin, vancomycin, tigecycline, fosfomycin, fusidic acid and rifampicin. These isolates were further allocated into five different sequence types: ST398 (n = 31), ST1074 (n = 4), ST504 (n = 3), ST582 (CC15) (n = 1) and ST479 (n = 1). These isolates were also assigned to seven clusters with up to 100 SNP which has facilitated geographical mapping and epidemiological distribution in Thuringia. Strains belonging to ST398 were classified into clusters 1, 2, 3, 4 and 7. The isolates of ST504 were of cluster 5, those of ST1074 were belonging to cluster 6. Resistance genes blaZ, blaI and blaR associated with penicillin resistance were found in 32 (80%) strains, all except one were belonging to ST398. Methicillin resistance associated mecA was identified in 30 (96.8%) isolates of ST398. All tetracycline and erythromycin resistant isolates were of ST398, and all harbored both tetM and ermA. About 90.3% of tetracycline resistant isolates assigned to ST398 were also carrying tetK gene. The point mutations parC_S80F, gyrA_S84L and parC_S80Y in gyrA and parC associated with quinolone resistance were found in all phenotypically resistant isolates to ciprofloxacin and moxifloxacin (n = 14). Sixty-eight virulence genes were identified among isolates. Both lukD/E and lukM/F-PV-P83 were identified in 22.5% of isolates, all were non-ST398.ConclusionIn this study, ST398 had the highest potential to cause disease and had a massive prevalence in bovine mastitis cases. Five different sequence types and seven clusters were identified in the federal state of Thuringia. The circulation of some clusters in the same region over several years shows the persistence of cluster-associated infection despite the intensive veterinary care. On the other hand, some regions had different clusters at the same year or in different consecutive years. Different sequence types and associated different clusters of S. aureus were geographically widely distributed among dairy farms in Thuringia. The findings of this study show that various clusters have the potential to spread over a large geographical scale. The detection of LA-MRSA on dairy farms, which is known for cabapility to widely spread among different groups of animals, humans and their environment urges for the implementation of national wide strategic programs. The identification of CA-MRSA among the isolates such as ST398 poses a significant risk for the transmission of such strains between animals and humans on dairy farms.

Glioblastoma (GBM) still presents as one of the most aggressive tumours in the brain, which despite enormous research efforts, remains incurable today. As many theories evolve around the persistent recurrence of this malignancy, the assumption of a small population of cells with a stem-like phenotype remains a key driver of its infiltrative nature. In this article, we research Chordin-like 1 (CHRDL1), a secreted protein, as a potential key regulator of the glioma stem-like cell (GSC) phenotype. It has been shown that CHRDL1 antagonizes the function of bone morphogenic protein 4 (BMP4), which induces GSC differentiation and, hence, reduces tumorigenicity. We, therefore, employed two previously described GSCs spheroid cultures and depleted them of CHRDL1 using the stable transduction of a CHRDL1-targeting shRNA. We show with in vitro cell-based assays (MTT, limiting dilution, and sphere formation assays), Western blots, irradiation procedures, and quantitative real-time PCR that the depletion of the secreted BMP4 antagonist CHRDL1 prominently decreases functional and molecular stemness traits resulting in enhanced radiation sensitivity. As a result, we postulate CHRDL1 as an enforcer of stemness in GSCs and find additional evidence that high CHRDL1 expression might also serve as a marker protein to determine BMP4 susceptibility.

Abstract Background The evasion of apoptosis is a hallmark of cancer. Understanding this process holistically and overcoming apoptosis resistance is a goal of many research teams in order to develop better treatment options for cancer patients. Efforts are also ongoing to personalize the treatment of patients. Strategies to confirm the therapeutic efficacy of current treatments or indeed to identify potential novel additional options would be extremely beneficial to both clinicians and patients. In the past few years, system medicine approaches have been developed that model the biochemical pathways of apoptosis. These systems tools incorporate and analyse the complex biological networks involved. For their successful integration into clinical practice, it is mandatory to integrate systems approaches with routine clinical and histopathological practice to deliver personalized care for patients. Results We review here the development of system medicine approaches that model apoptosis for the treatment of cancer with a specific emphasis on the aggressive brain cancer, glioblastoma. Conclusions We discuss the current understanding in the field and present new approaches that highlight the potential of system medicine approaches to influence how glioblastoma is diagnosed and treated in the future.