Biology subjects

Ferenczi, S.

Publications and source records attributed to Ferenczi, S..

5 recordsLinked to original sources

bioRxiv2025

The Cause of Most Common Antler Abnormality is Not a Fracture But an Osteomyelitis Like Disease the Pedunculitis Chronica Deformans

Climate change is increasing the incidence of certain diseases in wildlife, offering a deeper understanding of their underlying causes. Traditionally, the most common antler abnormalities have been attributed to trauma, based on their morphology. However, this explanation does not account for the epidemic-like spread of abnormalities in specific regions, suggesting that they might be a previously undescribed aspect of this anomaly. In fallow deer (Dama dama), using advanced medical diagnostic tools, we identified an osteomyelitis-like condition, Pedunculitis Chronica Deformans (PCD) which is also observed in other Cervidae. The incidence of this disease shows a strong correlation with the production of mycotoxins by molds that are becoming more prevalent with global warming. Mycotoxins can inhibit wound healing through scar formation after the antlers are cast, leading to the development of PCD. In this report we characterize PCD pathomorphology and introduce a scoring system to differentiate it from other deformities. Moreover, we argue that the most common anomalies such as fractures, antler losses, fatal meningoencephalitis and brain abscesses are complications of PCD. Our research underscores the potential of antlers to serve as biomarkers for mycotoxin exposure.

zoology↗

bioRxiv2024

Impact of Mycotoxins and Glyphosate residue on the Gut Microbiome and Resistome of European Fallow Deer

Mycotoxins and herbicides residue significant threats to animal health. This study investigated the impact of these toxins on the gut microbiome of the fallow deer, a valuable game species. We analyzed the intestinal contents of deer exposed to varying levels of zearalenone (ZEA) and other mycotoxins and toxic compounds such as aflatoxins, deoxynivalenol, fumonisin B1 and glyphosate residues. Metagenomic analysis revealed significant alterations in the bacterial community composition, particularly in the abundance of specific taxa. Higher ZEA levels were associated with decreased alpha diversity, whereas higher aflatoxin levels had the opposite effect. We also observed changes in the abundance of antibiotic resistance genes (ARGs), suggesting a potential link between mycotoxin exposure and antimicrobial resistance. Furthermore, five complete bacterial genomes were assembled from the metagenomic data. These findings highlight the complex interplay between environmental toxins, the gut microbiota, and animal health. Understanding these interactions is crucial for developing strategies to mitigate the negative effects of toxin exposure on wildlife populations.

genomics↗

bioRxiv2023

Novel Insights into the Aortic Mechanical Properties of Mice Modeling Hereditary Aortic Diseases

OBJECTIVEHereditary aortic diseases (hADs) increase the risk of aortic dissections and ruptures. Recently, we have established an objective approach to measure the rupture force of the murine aorta, thereby explaining the outcomes of clinical studies and assessing the added value of approved drugs in vascular Ehlers-Danlos syndrome (vEDS). Here, we applied our approach to six additional mouse hAD models. APPROACH AND RESULTWe used two mouse models of Marfan syndrome (MFS) as well as one smooth-muscle-cell-specific knockout (SMKO) of Efemp2 and three CRISPR/Cas9-engineered knock-in models (Ltbp1, Mfap4, and Timp1). One of the two MFS models was subjected to 4-week-long losartan treatment. Per mouse, three rings of the thoracic aorta were prepared, mounted on a tissue puller, and uniaxially stretched until rupture. The aortic rupture force of the SMKO and both MFS models was significantly lower compared with wild-type mice but in both MFS models higher than in mice modeling vEDS. In contrast, the Ltbp1, Mfap4, and Timp1 knock-in models presented no impaired aortic integrity. As expected, losartan treatment reduced aneurysm formation but surprisingly had no impact on the aortic rupture force of our MFS mice. CONCLUSIONSOur read-out system can characterize the aortic biomechanical integrity of mice modeling not only vEDS but also related hADs, allowing the aortic-rupture-force- focused comparison of mouse models. Furthermore, aneurysm progression alone may not be a sufficient read-out for aortic rupture, as antihypertensive drugs reducing aortic dilatation might not strengthen the weakened aortic wall. Our results may enable identification of improved medical therapies of hADs. HighlightsO_LIAssay to measure the aortic rupture force as read-out for the biomechanical integrity identified weakened murine thoracic aorta prior to micro- and macroscopic changes in Fbn1+/C1041G mice. C_LIO_LIDespite reducing aneurysm growth, losartan treatment did not have any impact on the aortic rupture force of Fbn1mgR/mgR mice modeling MFS. C_LIO_LISmooth-muscle-cell-knock-out of Efemp2 significantly impaired the rupture force of the murine ascending aorta. C_LIO_LIAortic rupture force measurements could clarify the causality of novel candidate gene(s)/variant(s) in mouse models of aortic diseases. C_LI Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=139 SRC="FIGDIR/small/553452v2_ufig1.gif" ALT="Figure 1"> View larger version (32K): org.highwire.dtl.DTLVardef@a29d79org.highwire.dtl.DTLVardef@10a272org.highwire.dtl.DTLVardef@19071forg.highwire.dtl.DTLVardef@122ab40_HPS_FORMAT_FIGEXP M_FIG C_FIG

pathology↗

bioRxiv2022

Recruitment of Corticotropin-releasing Hormone CRH Neurons in response ton Categorically Distinct Stress Challenges in the Mouse Brain

1.Corticotropin-releasing hormone (CRH) neurons in the paraventricular hypothalamic nucleus (Pa) are in the position to integrate stress-related information and initiate adaptive neuroendocrine-, autonomic-, metabolic- and behavioral responses. In addition to hypophyseotropic cells, CRH is widely expressed in the CNS, however their involvement in organization of the stress response is not fully understood. In these experiments, we took the advantage of recently available Crh-IRES-Cre; Ai9 mouse line to study the recruitment of hypothalamic and extrahypothalamic CRH neurons in categorically distinct, acute stress reactions. Reporter mice were exposed to restraint, ether, high salt and lipopolisacharide stress. The induced activation of CRH neurons was detected by colocalization of immediate early gene c-Fos in Td tomato expressing cells. We found differential activation of CRH neurons in central amygdaloid nucleus (Ce), bed nucleus stria terminalis lateral division, ventral posterior (BSTLVP), medial preoptic nucleus (MPO), ventromedial hypothalamic nucleus (VMH), premammillary nucleus (PM) and prepositus hypoglossal nucleus (Pr) in response to physiological (ether, high salt and LPS) and psychological (restraint) stressors. CRH positive cells in Pa became activated, however in the Barringtons nucleus and locus coeruleus no actiovation could be observed due to most tested stressors. Furthermore no CRH neuron activation occured in dorsal (BSTLD) and posterior (BSTLP) region of lateral division of bed nucleus stria terminalis after restraint stress. In the inferior olive only ether exposition resulted in CRH neuron activation. These results confirm activation of CRH neurons in the Pa, reveals new subset of stress-related CRH cells through the mouse brain and disprove the recruitment of CRH cells in the SOL and in the Barringtons nucleus to acute psychological stress in mice.

neuroscience↗

bioRxiv2019

Efficient treatment of a preclinical inflammatory bowel disease model with engineered bacteria

We developed an engineered bacterium based, RNA interference mediated therapeutic method to significantly reduce the symptoms in the most frequently used animal model of inflammatory bowel disease. This transkingdom RNA interference strategy was based on the non-pathogenic E. coli MDS42 strain, which was engineered to constitutively produce invasin and histeriolysin cytolysin. These proteins enabled the bacteria first to invade the colon epithelium and then degrade in the phagosome. This allowed the delivery of a plasmid encoding shRNA targeting TNF alpha into the cytoplasm of the target cells. The expression levels of TNF alpha and other cytokines significantly decreased and the inflammatory symptoms were significantly reduced. With further safety modifications this method could serve as a safe and side-effect free alternative to biologicals targeting TNF-alpha.

synthetic biology↗