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Biology subjects

Moll, S.

Publications and source records attributed to Moll, S..

5 recordsLinked to original sources

Soil invertebrate biomass estimation from image-derived body area and contour length

1. Soil invertebrate biomass is closely linked to ecosystem processes, yet its routine quantification remains constrained by the effort required to weigh large numbers of small individuals. Length-mass relationships provide an indirect alternative, but body length can be difficult to standardise and extract automatically from images of curved, coiled or contracted organisms. Projected body area may provide a more tractable image-derived predictor, but its performance across diverse soil-faunal taxa and at the community scale remains insufficiently evaluated. 2. Here, we developed a framework using projected body area and contour length to estimate fresh and dry mass from measurements of 1,792 soil invertebrates representing 15 higher-level taxa. We fitted taxon-specific models for six well-represented groups and general models across taxa, and evaluated predictive performance using leave-one-out cross-validation. We then assessed cross-dataset transferability by comparing our data with those of Lemoine et al. (2026) and pooled the two datasets to derive combined models. Finally, we tested whether individual predictions could be scaled to independently measured community biomass. 3. Taxon-specific models generally reduced prediction error relative to general models, with mean absolute percentage error (MAPE) values of 6.9-37.3% for fresh mass and 7.6-30.2% for dry mass. General models retained MAPEs of 27.2% and 22.4%, respectively. Comparisons of our dataset with that of Lemoine et al. (2026) showed no detectable differences in six of eight taxon-by-mass slopes. Although intercepts frequently differed, no overall dataset effect was detected after accounting for taxa. Pooling both datasets broadened model development, while taxon-specific models generally retained lower error than the combined general model. Finally, community-level predictions tracked measured biomass across all model sets (R2 = 0.87-0.99), but absolute error varied among models and faunal groups (MAPE = 9.6-52.5%). 4. Body area and contour length extracted from images therefore provide a practical basis for scaling soil invertebrate biomass estimation from individuals to communities. Integration with automated imaging and segmentation tools such as flatbug, BIODISCOVER and CollembolAI could extend soil invertebrate monitoring at larger scales beyond abundance and taxonomic composition to biomass, while providing scalable inputs for analyses of food webs and general ecosystem ecology.

ecology↗

Tissular glucocorticoid reactivating enzyme 11beta-HSD1 drives pathogenic myofibroblast differentiation in chronic kidney disease

Chronic kidney disease (CKD) is a growing public health crisis, affecting over 10% of the global population and significantly increasing mortality and morbidity. Irrespective of its underlying cause, tubulointerstitial fibrosis (TIF) is a hallmark of CKD progression, with myofibroblasts being the primary effectors of renal fibrosis. Here, we show that 11beta-hydroxysteroid dehydrogenase type 1 (11{beta}-HSD1) is a critical driver of pathogenic myofibroblast differentiation and fibrosis in CKD. Using genetic deletion and pharmacological inhibition of 11{beta}-HSD1 in mouse models, we demonstrate a marked reduction in TIF severity and improved renal function, linked to the suppression of a regulatory myofibroblast (Reg-MF) subpopulation. Single-cell and spatial transcriptomics data reveal that 11{beta}-HSD1 is essential for the activation and expansion of Reg-MFs, which is conserved across species and predicts worse outcomes in CKD patients and kidney allograft recipients. These findings establish a direct link between 11{beta}-HSD1 activity and renal fibrogenesis, highlighting its role during the transition from pericytes to pathogenic Reg-MFs. Our results support 11{beta}-HSD1 inhibition as a promising therapeutic strategy to mitigate CKD progression, offering both mechanistic insights and translational potential for improving patient outcomes.

physiology↗

Claudin-4, a core component of the tight-junctional complex along the collecting system, is induced in nephrotic syndrome

BackgroundNephrotic syndrome (NS) is characterized by massive sodium chloride retention. Along the kidney tubule, sodium and chloride reabsorption are coupled via a combination of transcellular and paracellular transport pathways. The mechanism of sodium retention in NS has been extensively studied, but the associated chloride transport pathway has not been elucidated. MethodsTo investigate the pathway of chloride retention in NS, we assessed the expression levels of both paracellular and transcellular components of chloride transport in the CD of POD-ATTAC mice and PAN rats, two rodent models of NS. We also used cultured mouse cortical collecting duct cells to see how overexpression or silencing of claudin-4 affect paracellular permeability. Finally, human renal biopsies were used to confirm our in vivo results. ResultsIn control animals, claudin-4 was expressed at low levels in collecting duct (CD). In POD-ATTAC mice and PAN rats, claudin-4 expression was strongly increased in CD beta-intercalated cells (B-IC) and to a lesser extent in CD principal cells and was also induced in connecting tubules. Similarly, we found that claudin-4 was expressed at low levels in normal human kidneys and was dramatically increased in CD cells of nephrotic human kidneys (focal and segmental glomerulosclerosis). In parallel, the expression of pendrin, which exchanges chloride for bicarbonates in B-IC, was decreased in nephrotic compared to control animals. However, the increase in claudin-4 expression observed in NS is likely independent of pendrin abundance. Increased claudin-4 abundance is coupled with increased ENaC-dependent sodium transport. Overexpression or silencing of claudin-4 in mCCDcl1 cells confirmed the preferential permeability of claudin-4 to chloride over sodium. ConclusionsThese results suggest that during NS, transcellular Cl-/HCO - transport decreases while paracellular chloride transport via claudin-4 may increase along the collecting system. Paracellular chloride permeability may constitute a chloride shunt that favors Na+ reabsorption and opposes K+ secretion along the CD in NS. Significance StatementNephrotic syndrome is a common disease characterized by massive proteinuria, hypoalbuminemia and edema due to renal sodium-chloride retention. We demonstrate for the first time an induction of claudin-4 expression indicating a partial shift from transcellular to paracellular chloride transport in the renal collecting system of nephrotic rodents. We confirmed the increased expression of claudin-4 in kidney biopsies of nephrotic patients, highlighting the translational significance of these results. Whether the paracellular pathway may represent a novel target to treat edema in nephrotic syndrome remains to be elucidated.

physiology↗

Single-cell profiling in COVID-19 associated acute kidney injury reveals patterns of tubule injury and repair in human

The cellular mechanisms of kidney tubule repair are poorly characterized in human. Here, we applied single-nucleus RNA sequencing to analyze the kidney in the first days after acute injury in 5 critically ill patients with COVID-19. We identified abnormal proximal tubule cell states associated with injury, characterized by altered functional and metabolic profiles and by pro-fibrotic properties. Tubule repair involved the plasticity of mature tubule cells in a process of cell de-differentiation and re-differentiation, which displayed substantial similarities between mouse and man. In addition, in man we identified a peculiar tubule reparative response determining the expansion of progenitor-like cells marked by PROM1 and following a differentiation program characterized by the sequential activation of the WNT, NOTCH and HIPPO signaling pathways. Taken together, our analyses reveal cell state transitions and fundamental cellular hierarchies underlying kidney injury and repair in critically ill patients.

pathology↗

Impact of an intra-abdominal cooling device during open kidney transplantation in pigs

BackgroundKidney transplantation using deceased donors still suffers from high post-operative dysfunction rate. During implantation into the recipient, the kidney rewarms. This second warm ischemia time, which is not monitored, is harmful especially if prolonged. We recently developed an intra-abdominal cooling device that efficiently prevents kidney rewarming during robotic transplantation, and prevent ischemia-reperfusion injuries. Here, we tested the benefits of this cooling device during open kidney transplantation in pigs.\n\nMaterialsKidneys were procured from large pigs by open bilateral nephrectomy. Following procurement, kidneys were flushed with 4{degrees}C Institut Georges Lopez-1 preservation solution, and placed on ice for 128.5 {+/-} 23.2 min. The cooling device was used to continuously cool down the kidney during the vascular anastomosis time.\n\nMethodsAnimals underwent double sequential autologous open renal transplantation with (n = 7) and without (n = 6) intra-abdominal cooling. Renal cortex temperature and urine output were monitored. The severity of the ischemia reperfusion lesions was analyzed by histology (modified Goujon score).\n\nResultsMean anastomosis time was similar between groups (43.9 {+/-} 13 min). At reperfusion, the renal cortex temperature was lower in the group with cooling (4.3 {+/-} 1.1{degrees}C vs 26.5 {+/-} 5.5{degrees}C p <0.001). The cooled kidneys tended to be protected from injury, including some histopathological ischemia-reperfusion lesions. With the device, kidneys had a better immediate post-operative urine output (p=0.05).\n\nConclusionsOur results indicate that the intra-abdominal cooling device significantly reduces second warm ischemic time during transplantation, is technically safe, and does not prolong anastomotic time.

physiology↗