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Influence of different processing methods on anti-trypsin activity in bovine colostrum
(2025) Trzebiatowski, Lukas; Georgiev, Plamen; Büttner, Kathrin; Wehrend, Axel
Trypsin-inhibitory activity represents a general characteristic of the first bovine colostrum. The objectives of this study were to establish a test to determine anti-trypsin activity and test the hypothesis that freezing, acidification, and heat treatment would alter anti-trypsin activity compared with untreated bovine colostrum. A photometric assay was established to determine anti-trypsin activity. The activity was expressed in milligrams of inhibited trypsin per milliliter of colostrum. In experiment 1, anti-trypsin activity was compared in untreated and frozen colostrum of the same sample. In 40 untreated colostrum samples, the trypsin-inhibition (0.80 mg/mL) corresponded to that observed in frozen samples (0.79 mg/mL). In experiment 2, we compared the antitrypsin activity of 99 samples of frozen colostrum (0.85 mg/mL) with aliquots subjected to acidification (0.84 mg/mL), heat treatment at 60°C for 60 min (0.65 mg/mL), and heat treatment at 63.5°C for 30 min (0.61 mg/mL). Acidification did not significantly affect trypsin inhibition. Both heat treatment protocols significantly reduced anti-trypsin activity.
Bakta Web : rapid and standardized genome annotation on scalable infrastructures
(2025) Beyvers, Sebastian; Jelonek, Lukas; Goesmann, Alexander; Schwengers, Oliver
The Bakta command line application is widely used and one of the most established tools for bacterial genome annotation. It balances comprehensive annotation with computational efficiency via alignment-free sequence identifications. However, the usage of command line software tools and the interpretation of result files in various formats might be challenging and pose technical barriers. Here, we present the recent updates on the Bakta web server, a user-friendly web interface for conducting and visualizing annotations using Bakta without requiring command line expertise or local computing resources. Key features include interactive visualizations through circular genome plots, linear genome browsers, and searchable data tables facilitating the interpretation of complex annotation results. The web server generates standard bioinformatics outputs (GFF3, GenBank, EMBL) and annotates diverse genomic features, including coding sequences, non-coding RNAs, small open reading frames (sORFs), and many more. The development of an auto-scaling cloud-native architecture and improved database integration led to substantially faster processing times and higher throughputs. The system supports FAIR principles via extensive cross-reference links to external databases, including RefSeq, UniRef, and Gene Ontology. Also, novel features have been implemented to foster sharing and collaborative interpretation of results. The web server is freely available at https://bakta.computational.bio.
The EPPO/OLAF compendium of national procedures: Lithuania
(2026) Hauck, Pierre; Schneider, Jan-Martin; Karakocaoğlu, Nur Sena; Laird, Alastair Alexander
This Lithuanian EPPO/OLAF volume covers the procedures of the European Public Prosecutor's Office (EPPO) in Lithuania, including EU fraud typologies and relevant case law. The volume also contains information and provisions for defence lawyers working against the EPPO in cases of customs, financial, tax, or subsidy fraud. The second part is a guide to OLAF investigations in Lithuania, focusing on information controls and the relationship between national partners and external investigations. An anonymous person has acted as the publication’s national expert.
The EPPO/OLAF compendium of national procedures: Slovakia
(2026) Hauck, Pierre; Schneider, Jan-Martin; Karakocaoğlu, Nur Sena; Meyer, Sophie; Laird, Alastair Alexander
This Slovakian EPPO/OLAF volume contains the relevant legislation, EU law and Slovak law, as well as the measures taken by the regional offices of the European Public Prosecutor's Office (EPPO) in criminal investigations into EU fraud offences. In addition, possible measures of the EPPO in Slovakia and EU fraud typologies are discussed. The second part of the volume deals with the investigative missions of the European Anti-Fraud Office (OLAF) in Slovakia, including the Slovak national scenery and the AFCOS structure. Prof Dr Libor Klimek has acted as the publication’s national expert.
Preclinical studies on susceptibility to viral infection driving lung injury and disruptions to lung development in neonates with bronchopulmonary dysplasia
(2025) Gunjak, Miša
Bronchopulmonary dysplasia (BPD) is the most common complication of preterm birth, with significant morbidity and mortality, and is experimentally modelled by exposure of newborn mice to hyperoxia to mimic oxygen supplementation of preterm infants. Infants with BPD have a higher risk of acquiring a respiratory virus infection and have a worse disease course. The pathophysiological mechanisms underlying this increased risk of infection and more severe pathology have not been clarified, but include oxygen creating a more permissive environment for virus infection, or oxygen modulating the lung inflammatory response to virus infection. When neonatal mice were exposed to hyperoxia (85% O2) from birth, and then challenged with pneumonia virus of mice (PVM) on postnatal day (P)4, all hyperoxia-exposed pups infected at a 1:1,000 dilution of viral stock exhibited 100% mortality by P12. In contrast, mice maintained in room air survive PVM infection over a range of virus doses (1,1000, 1:2,500, or 1:5,000), highlighting a stark, dose-dependent synergy between oxygen toxicity and viral challenge. By P11, lungs from hyperoxia-exposed mice, with or without PVM infection, exhibit pronounced alveolar simplification, with enlarged airspaces and diminished septation. The PVM infection under conditions of hyperoxia provokes marked inflammatory infiltration, whereas lungs infected under conditions of normoxia (21% O2) retain normal architecture. Whole-body plethysmography revealed a dose-dependent decline in tidal volume, expiratory volume, minute volume, and breathing frequency in hyperoxia-infected mice. Despite identical early viral replication across both oxygen conditions, the addition of hyperoxia before and concomitant with virus infection reshapes inflammatory signaling and tissue remodeling. Gene expression in lung homogenates indicated early increases of Ccl2, Cxcl10, and Ccl3 mRNA transcript abundance under hyperoxia. Antibody microarrays revealed a shift from homeostatic chemokines (CCL2, IL-25) to pro-inflammatory and fibrotic mediators (IL-6, IL-8, TGF-β1-3) upon infection, with prior and concomitant hyperoxia magnifying CCL17, IL-15, and lung fibrosis pathways. Immune cell profiling using single-cell RNA sequencing revealed that hyperoxia depleted tissue-resident alveolar macrophages (TR-AM) and expanded exudate macrophages, dendritic cells, and neutrophils. Under normoxia, PVM infection enriches a virus-responsive TR-AM subset (AM_PVM), while hyperoxia completely eliminates these protective responses. Single-cell transcriptomics confirmed the loss of AM_HYX (a stress-adapted macrophage subset) and AM_PVM cells in hyperoxia-infected mice, with extensive dendritic cell expansion. Intranasal clodronate liposome–mediated TR-AM depletion in normoxia-treated, virus-infected animals mimicked the lethal phenotype noted in hyperoxia-infected animals, with 100% mortality by P15. These mice exhibited excessive lung inflammation, impaired respiratory function, and a hyperoxia-like proteomic signature, even as viral loads reduced. Therefore, TR-AM dysfunction and skewed inflammatory chemokine signaling, and not viral load, were associated with fatal outcome. Together, these findings reveal that hyperoxia disrupts macrophage-mediated immune regulation in the newborn mouse lung, converting a balanced antiviral defense into maladaptive inflammation. Strategies to preserve or restore TR-AM function may therefore protect preterm infants from severe respiratory viral disease. These novel findings might explain the predisposition of BPD patients to a high risk of respiratory virus infection and worse clinical outcomes.