Biology subjects

Russ, H.

Publications and source records attributed to Russ, H..

5 recordsLinked to original sources

bioRxiv2025

2000-year fish bone record reveals transition to commercial fisheries during climatic change

Animal bones from archaeological contexts can reveal the interplay between past environments and human societies. Resource acquisition shaped many aspects of past societies and influenced the development of trade networks and migration. Fish have been a cornerstone of human subsistence for millennia, yet the rise of commercial fishing and trade was complex. Here, we synthesised a database of [~]1.9 million zooarchaeological fish records spanning 2000 years across Europe. Using machine-learning of catch compositions alongside fish thermal tolerances, we show that fisheries became less local over time, with homogenisation coinciding with Little Ice Age-associated cooling, a period of documented resource scarcity, concurring with growing trade. Moreover, increased proportions of marine taxa and more specialist marine fisheries were observed in the preceding Medieval Climate Anomaly, to sustain concurrent urban and population growth. Enhanced use of marine protein buffered food insecurity, whilst signalling the transition from localised to trans-regional trade networks.

ecology↗

bioRxiv2025

Low breeding propensity and success of European Turtle Doves in Germany

Understanding the breeding success of European Turtle Doves is crucial for their conservation, helping to address the threats they face, and optimizing the species prospects for future successful reproduction and survival. However, data on breeding success of this species in Germany are missing due to the low density and poor accessibility of nests and chance to disturb nesting efforts during direct nest searches. We therefore used two indirect methods to obtain data on breeding success. First, we analyzed field age ratios, i.e. the proportion of juveniles from Citizen Science data. We observed a marked decrease in observed fledglings from 1.28 in the years 1957-1989 to 0.44 in 1990-2009 and to 0.32 in 2010-2023. This suggests a sharp decline in breeding success. Very low juvenile numbers in July further suggest that first broods were especially affected. Second, nesting sites were determined from GPS data, and the breeding constancy was checked at these sites. Based on data from 32 GPS-marked birds representing 28 breeding pairs, we obtained values of maximum breeding success of 1.5 chicks per potential breeding pair at hatching and 0.7 chicks per potential breeding pair at fledging. This is an optimistic calculation for fledglings, as it assumes that two chicks per nest survive until fledging. Overall, these data highlight an urgent need to improve the habitat conditions in the breeding areas to conserve this once common species.

ecology↗

bioRxiv2025

Human Stem Cell-Derived β-cells Expressing An Optimized CD155 Reduce Cytotoxic Immune Cell Function for Application in Type 1 Diabetes

Insulin-producing {beta}-cell replacement therapies offers a potential treatment for type 1 diabetes (T1D) but faces challenges from donor shortages and immune rejection. Stem cell-derived {beta}-cells (sBC) provide a renewable source but remain vulnerable to immune attack. We engineered human pluripotent stem cells to express either the wildtype (WT) or a high-affinity mutant (Mut) variant (rs1058402, G>A; Ala67Thr) of the NK and T cell checkpoint inhibitor CD155 before differentiation into sBC. Modified sBC maintained upregulated CD155 expression and showed enhanced binding to co-receptor ligands. Co-culture studies revealed that CD155 Mut-expressing sBC suppressed CD8+ T cell and NK cell activation and proliferation by preferentially engaging the co-inhibitory receptor TIGIT. Both CD155 Mut sBC lines reduced autoreactive CD8+ T cell- and NK cell-mediated sBC destruction and cytotoxic molecule secretion. This protection was lost with TIGIT blockade, confirming the role of CD155-TIGIT signaling in antagonizing immune cell-mediated killing. Our findings suggest that high-affinity CD155 expression enhances immune evasion of sBC, improving their potential for restorative therapy in T1D. TeaserEngineered {beta}-cells with a mutant CD155 help evade immune attack, offering a promising therapeutic approach for type 1 diabetes.

immunology↗

bioRxiv2025

GAL-101 prevents amyloid beta-induced membrane depolarization in two different types of retinal cells

Glaucoma and age-related macular degeneration (AMD) are two of the major causes of progressive vision loss and ultimately blindness worldwide. Both retinopathies share several pathological features with Alzheimers disease (AD) such as: impairment of neuronal function, astrocytosis, and activation of immune-competent microglia and Muller cells. It also has been shown that these conditions are characterized by the presence of an elevated concentration of amyloid beta (A{beta}). Under pathological conditions, A{beta}1-42 tends to aggregate, forming toxic soluble oligomers, considered to be the most harmful amyloid species. One strategy adopted to prevent cell damage caused by these oligomers is to impair their aggregation. Here we studied GAL-101, a small molecule designed to modify the aggregation of A{beta}1-42. To assess the role of GAL-101 in the aggregation of A{beta}1-42, in vitro electrophysiological measurements on retinal ganglion cells (RGCs) and retinal pigment epithelial (RPE) cells were performed to determine the polarization of the resting membrane potential. Cells treated only with A{beta}1-42 oligomers showed a strong depolarization of the resting membrane potential, which is believed to be the main reason for retinal cells malfunctioning in neurodegenerative diseases of the eye. Pre-incubation with GAL-101 stabilized the cell resting potential to around -50mV during exposure to A{beta}1-42, in both RGCs and RPE cells. GAL-101 was able to prevent changes in resting membrane potential and thus would be expected to prevent impairment of retinal cell function. These results are supportive of evaluating GAL-101 as a potential treatment of A{beta}-associated retinopathies like glaucoma and dry AMD.

neuroscience↗

bioRxiv2021

Use of Induced Pluripotent Stem Cells to Build Isogenic Systems and Investigate Type 1 Diabetes

Type 1 diabetes is a disease that arises due to complex immunogenetic mechanisms. Key cell-cell interactions involved in the pathogenesis of T1D are activation of autoreactive T cells by dendritic cells (DC), migration of T cells across endothelial cells (EC) lining capillary walls into the islets of Langerhans, interaction of T cells with macrophages in the islets, and killing of {beta}-cells by autoreactive CD8+ T cells. Overall, pathogenic cell-cell interactions are likely regulated by the individuals collection of genetic T1D-risk variants. To accurately model the role of genetics, it is essential to build systems to interrogate single candidate genes in isolation during the interactions of cells that are essential for disease development. However, obtaining single-donor matched cells relevant to T1D is a challenge. Sourcing these genetic variants from human induced pluripotent stem cells (iPSC) avoids this limitation. Herein, we have differentiated iPSC from one donor into DC, macrophages, EC, and {beta}-cells. Additionally, we also engineered T cell avatars from the same donor to provide an in vitro platform to study genetic influences on these critical cellular interactions. This proof of concept demonstrates the ability to derive an isogenic system from a single donor to study these relevant cell-cell interactions. Our system constitutes an interdisciplinary approach with a controlled environment that provides a proof-of-concept for future studies to determine the role of disease alleles (e.g. IFIH1, PTPN22, SH2B3, TYK2) in regulating cell-cell interactions and cell-specific contributions to the pathogenesis of T1D.

immunology↗