A Field-Scale Decision Support System for Assessment and Management of Soil Functions

peer-reviewedAgricultural decision support systems (DSSs) are mostly focused on increasing the supply of individual soil functions such as, e.g., primary productivity or nutrient cycling, while neglecting other important soil functions, such as, e.g., water purification and regulation, climate regulation and carbon sequestration, soil biodiversity, and habitat provision. Making right management decisions for long-term sustainability is therefore challenging, and farmers and farm advisors would greatly benefit from an evidence-based DSS targeted for assessing and improving the supply of several soil functions simultaneously. To address this need, we designed the Soil Navigator DSS by applying a qualitative approach to multi-criteria decision modeling using Decision Expert (DEX) integrative methodology. Multi-criteria decision models for the five main soil functions were developed, calibrated, and validated using knowledge of involved domain experts and knowledge extracted from existing datasets by data mining. Subsequently, the five DEX models were integrated into a DSS to assess the soil functions simultaneously and to provide management advices for improving the performance of prioritized soil functions. To enable communication between the users and the DSS, we developed a user-friendly computer-based graphical user interface, which enables users to provide the required data regarding their field to the DSS and to get textual and graphical results about the performance of each of the five soil functions in a qualitative way. The final output from the DSS is a list of soil mitigation measures that the end-users could easily apply in the field in order to achieve the desired soil function performance. The Soil Navigator DSS has a great potential to complement the Farm Sustainability Tools for Nutrients included in the Common Agricultural Policy 2021–2027 proposal adopted by the European Commission. The Soil Navigator has also a potential to be spatially upgraded to assist decisions on which soil functions to prioritize in a specific region or member state. Furthermore, the Soil Navigator DSS could be used as an educational tool for farmers, farm advisors, and students, and its potential should be further exploited for the benefit of farmers and the society as a whole

Interleukin-6 is elevated in synovial fluid of patients with focal cartilage defects and stimulates cartilage matrix production in an in vitro regeneration model

Introduction: This study aimed to determine whether, as in osteoarthritis, increased levels of interleukin-6 (IL-6) are present in the synovial fluid of patients with symptomatic cartilage defects and whether this IL-6 affects cartilage regeneration as well as the cartilage in the degenerated knee.Methods: IL-6 concentrations were determined by ELISA in synovial fluid and in conditioned media of chondrocytes regenerating cartilage. Chondrocytes were obtained from donors with symptomatic cartilage defects, healthy and osteoarthritic donors. The effect of IL-6 on cartilage regeneration and on metabolism of the resident cartilage in the knee was studied by both inhibition of endogen

Interobserver variability between experienced and inexperienced observers in the histopathological analysis of Wilms tumors:a pilot study for future algorithmic approach

Contains fulltext : 236892.pdf (Publisher’s version ) (Open Access

Enterohepatic circulation of triiodothyronine (T3) in rats:Importance of the microflora for the liberation and reabsorption of T3 from biliary T3 conjugates

In normal rats, T3 glucuronide (T3G) is themajor biliary T3 metabolite, but excretion of T3 sulfate (T3S) isgreatly increased after inhibition of type I deiodinase, e.g. with6-propyl-2-thiouracil (PTU). In this study, the fate of the T3conjugates excreted with bile was studied to assess the significance of a putative enterohepatic circulation of T3 in rats.Conventional (CV) or intestine-decontaminated (ID) rats received iv [125I]T3G or [125I]T3S, the latter usually after pretreatment with PTU (1 mg/100 g BW). Radioactivity in plasma andbile or feces was analyzed by Sephadex LH-20 chromatographyand HPLC. Within 1 h, 88% of injected T3G was excreted inbile of CV or ID rats, independent of PTU. About 75% of theinjected T3S was excreted within 4 h in PTU-treated rats, incontrast to only 20% in controls. Up to 13 h after iv administration of T3G or T3S (+PTU) to intact ID and CV rats, fecalradioactivity consisted of more than 90% T3 in all CV rats, 95%of T3S in T3S-injected ID rats, and 30% T3 and 67% T3G inT3G-injected ID rats. In overnight-fasted CV rats injected withT3G, total plasma radioactivity rapidly declined until a nadir of0.10% dose/ml at about 2.5 h, but radioactivity reappeared witha broad maximum of 0.12% dose/ml between 5.5-10 h. In thelatter phase, plasma radioactivity consisted of predominantly I"and T3 in a ratio of 2:1. Reabsorption was diminished in fed CVrats and prevented in ID rats. Plasma T3 4-10 h after iv T3Ginjection to overnight-fasted CV rats was 12, 2, and 3 timeshigher than that in bile-diverted rats, fed CV rats, and ID rats,respectively, and similar to that 4 h after the injection of T3itself. Total plasma radioactivity as well as plasma T3 6-13 hafter iv administration T3S in PTU-treated rats were significantly increased in CV us. ID rats, e.g. T3 0.016% us. 0.005%dose/ml. These results demonstrate a significant enterohepaticcirculation of T3 in rats in which bacterial hydrolysis of T3conjugates excreted with bile plays an important role. {Endocrinology 125: 2822-2830,1989

PTH decreases in vitro human cartilage regeneration without affecting hypertrophic differentiation

Regenerated cartilage formed after Autologous Chondrocyte Implantation may be of suboptimal quality due to postulated hypertrophic changes. Parathyroid hormone-related peptide, containing the parathyroid hormone sequence (PTHrP 1-34), enhances cartilage growth during development and inhibits hypertrophic differentiation of mesenchymal stromal cells (MSCs) and growth plate chondrocytes. This study aims to determine the possible anabolic and/or hypertrophic effect of PTH on human articular chondrocytes. Healthy human articular cartilage-derived chondrocytes (n = 6 donors) were cultured on type II collagen-coated transwells with/without 0.1 or 1.0 μM PTH from day 0, 9, or 21 until the end of culture (day 28). Extracellular matrix production, (pre)hypertrophy and PTH signaling were assessed by RT-qPCR and/or immunohistochemistry for collagen type I, II, X, RUNX2, MMP13, PTHR1 and IHH and by determining glycosaminoglycan production and DNA content. The Bern score assessed cartilage quality by histology. Regardless of the concentration and initiation of supplementation, PTH treatment significantly decreased DNA and glycosaminoglycan content and reduced the Bern score compared with controls. Type I collagen deposition was increased, whereas PTHR1 expression and type II collagen deposition were decreased by PTH supplementation. Expression of the (pre)hypertrophic markers MMP13, RUNX2, IHH and type X collagen were not affected by PTH. In conclusion, PTH supplementation to healthy human articular chondrocytes did not affect hypertrophic differentiation, but negatively influenced cartilage quality, the tissues' extracellular matrix and cell content. Although PTH may be an effective inhibitor of hypertrophic differentiation in MSC-based cartilage repair, care may be warranted in applying accessory PTH treatment due to its effects on articular chondrocytes

On the enterohepatic circulation of triiodothyronine in rats: importance of the intestinal microflora.

Until 70 h after a single iv injection of I0 uCi [1251]trllodothyronine (T3) , normal rats excreted 15.8+2.8 % of the radioactivitywith the feces and 17.5+2.7 % with the--urlne, while in intestinedecontaminated rats fecal and urinary excretion over this periodamounted to 25.1+7.2 % and 23.6+4.0 % of administered radioactivity, respeetlvely--(mean~SD, n=4)~ In fecal extracts of decontaminated rats 11.5+6.8 % of the excreted radioactivity consisted of T 3glueuronide ~T3G) and 10.9+2.8 % of T 3 sulfate (T3S) , whereas noconjugates were detected ~n feces from normal rats. Until 26 hafter ig administration of I0 uCi [1251]T3, integrated radioactivity in blood of decontaminated rats was 1.5 times higher than thatin normal rats. However, after ig administration of I0 uCi[1251]T3G or [1251]T3S , radioactivity in blood of decontaminatedrats was 4.9- and 2.8-fold lower, respectively, than in normalrats. The radloactlvlty in tbe serum of control animals was composed of T 3 and iodide in proportions independent of the tracerinjected, while T 3 conjugates represented <I0 % of serum radloactivity. These results suggest an important role of the intestinalmicroflora in the enterohepatlc circulation of T 3 in rats

PTH decreases in vitro human cartilage regeneration without affecting hypertrophic differentiation

Regenerated cartilage formed after Autologous Chondrocyte Implantation may be of suboptimal quality due to postulated hypertrophic changes. Parathyroid hormone-related peptide, containing the parathyroid hormone sequence (PTHrP 1–34), enhances cartilage growth during development and inhibits hypertrophic differentiation of mesenchymal stromal cells (MSCs) and growth plate chondrocytes. This study aims to determine the possible anabolic and/or hypertrophic effect of PTH on human articular chondrocytes. Healthy human articular cartilage-derived chondrocytes (n = 6 donors) were cultured on type II collagen-coated transwells with/without 0.1 or 1.0 μM PTH from day 0, 9, or 21 until the end of culture (day 28). Extracellular matrix production, (pre)hypertrophy and PTH signaling were assessed by RT-qPCR and/or immunohistochemistry for collagen type I, II, X, RUNX2, MMP13, PTHR1 and IHH and by determining glycosaminoglycan production and DNA content. The Bern score assessed cartilage quality by histology. Regardless of the concentration and initiation of supplementation, PTH treatment significantly decreased DNA and glycosaminoglycan content and reduced the Bern score compared with controls. Type I collagen deposition was increased, whereas PTHR1 expression and type II collagen deposition were decreased by PTH supplementation. Expression of the (pre)hypertrophic markers MMP13, RUNX2, IHH and type X collagen were not affected by PTH. In conclusion, PTH supplementation to healthy human articular chondrocytes did not affect hypertrophic differentiation, but negatively influenced cartilage quality, the tissues’ extracellular matrix and cell content. Although PTH may be an effective inhibitor of hypertrophic differentiation in MSC-based cartilage repair, care may be warranted in applying accessory PTH treatment due to its effects on articular chondrocytes

PTH decreases in vitro human cartilage regeneration without affecting hypertrophic differentiation.

Regenerated cartilage formed after Autologous Chondrocyte Implantation may be of suboptimal quality due to postulated hypertrophic changes. Parathyroid hormone-related peptide, containing the parathyroid hormone sequence (PTHrP 1-34), enhances cartilage growth during development and inhibits hypertrophic differentiation of mesenchymal stromal cells (MSCs) and growth plate chondrocytes. This study aims to determine the possible anabolic and/or hypertrophic effect of PTH on human articular chondrocytes. Healthy human articular cartilage-derived chondrocytes (n = 6 donors) were cultured on type II collagen-coated transwells with/without 0.1 or 1.0 μM PTH from day 0, 9, or 21 until the end of culture (day 28). Extracellular matrix production, (pre)hypertrophy and PTH signaling were assessed by RT-qPCR and/or immunohistochemistry for collagen type I, II, X, RUNX2, MMP13, PTHR1 and IHH and by determining glycosaminoglycan production and DNA content. The Bern score assessed cartilage quality by histology. Regardless of the concentration and initiation of supplementation, PTH treatment significantly decreased DNA and glycosaminoglycan content and reduced the Bern score compared with controls. Type I collagen deposition was increased, whereas PTHR1 expression and type II collagen deposition were decreased by PTH supplementation. Expression of the (pre)hypertrophic markers MMP13, RUNX2, IHH and type X collagen were not affected by PTH. In conclusion, PTH supplementation to healthy human articular chondrocytes did not affect hypertrophic differentiation, but negatively influenced cartilage quality, the tissues' extracellular matrix and cell content. Although PTH may be an effective inhibitor of hypertrophic differentiation in MSC-based cartilage repair, care may be warranted in applying accessory PTH treatment due to its effects on articular chondrocytes