Biochar is a carbonized biomass that can be used as a soil amendment. However, the exclusive use of biochar may present some limitations, such as the lack of nutrients. Thus, biochar enrichment ...techniques have made it possible to obtain biochar-based fertilizers (BCFs), with great potential to improve soil fertility. Nevertheless, there is still a lack of information about the description, advantages, and limitations of the methods used for biochar enrichment. This review provides a comprehensive overview of the production methods of enriched biochar and its performance in agriculture as a soil amendment. Studies demonstrate that the application of BCF is more effective in improving soil properties and crop yields than the exclusive application of pure biochar or other fertilizers. The post-pyrolysis method is the most used technique for enriching biochar. Future studies should focus on understanding the mechanisms of the long-term application of BCFs.
Enriched biochar; Organomineral fertilizer; Agriculture; Soil fertility.
The marked cardiovascular risk in autoimmune diseases is only partly explained. The capacity of high-density lipoproteins (HDL) to promote cell cholesterol efflux is a property with a well-known ...anti-atherogenic significance, but is also involved in functional modulation of endothelial and immune cells. The aim of this work was to evaluate HDL functionality with respect to cell cholesterol efflux in rheumatoid arthritis (RA) and systemic lupus erythemathosus (SLE) patients.
We evaluated serum cholesterol efflux capacity (CEC) of apoB-depleted serum, which mainly reflects HDL activity, from 30 RA and 30 SLE patients, and from 30 healthy controls by radioisotopic ex-vivo systems discriminating between the specific pathways of cholesterol efflux.
RA patients presented impairment of ATP-binding cassette G1-mediated CEC that correlated with disease activity. SLE patients showed a more complex pattern of modifications unrelated to disease activity, with marked reduction of ATP-binding cassette G1-mediated CEC and impairment of ATP-binding cassette A1-mediated CEC. The relationship between specific pathways of CEC values and serum total HDL differed between groups and there was no relationship with autoantibody profile or current therapy.
CEC is impaired in RA and SLE, with a specific mechanism pattern in each disease not depending on serum HDL levels. These findings provide a new mechanism for the increased atherosclerotic risk in RA and SLE patients.
Abstract Organic production systems are increasingly gaining market share; however, there are still few studies on their influence on the activity of soil microorganisms in sugarcane. Arbuscular ...mycorrhizal fungi are extremely sensitive to environmental changes, and their activity can be used as a parameter of comparison and quality between organic and conventional systems. The objective of this work was to evaluate mycorrhizal activity in different varieties of sugarcane under two production systems. This work was carried out in a commercial plantation of the Jalles Machado plant in the municipality of Goianésia in Goiás, Brazil. The values of spore density in the soil, mycorrhizal colonization rate in the roots and easily extractable glomalin were evaluated, and the associated fungal species were identified. There was no effect of sugarcane variety on the number of spores or the glomalin content in the soil. The conventional system presented significantly lower mycorrhizal colonization rates than did the organic system. The varieties cultivated under the conventional planting system showed a greater diversity of arbuscular mycorrhizal fungi, where 12 of the 13 different species of mycorrhizal fungi found in both cultivation systems occurred.
Altered control of T follicular helper (Tfh) cells can lead to generation of autoantibodies and autoimmune manifestations. Signaling pathways that selectively limit pathogenic responses without ...affecting the protective function of Tfh cells are unknown. Here we show that the ATP-gated ionotropic P2X7 receptor restricts the expansion of aberrant Tfh cells and the generation of self-reactive antibodies in experimental murine lupus, but its activity is dispensable for the expansion of antigen-specific Tfh cells during vaccination. P2X7 stimulation promotes caspase-mediated pyroptosis of Tfh cells and controls the development of pathogenic ICOS
IFN-γ-secreting cells. Circulating Tfh cells from patients with systemic lupus erythematosus (SLE) but not primary antiphospholipid syndrome (PAPS), a nonlupus systemic autoimmune disease, were hyporesponsive to P2X7 stimulation and resistant to P2X7-mediated inhibition of cytokine-driven expansion. These data point to the P2X7 receptor as a checkpoint regulator of Tfh cells; thus, restoring P2X7 activity in SLE patients could selectively limit the progressive amplification of pathogenic autoantibodies, which deteriorate patients' conditions.
Abstract
Objectives
The impact of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in patients with SLE remains unclear and data on clinical manifestations after infection are lacking. ...The aim of this multicentre study is to describe the effect of SARS-CoV-2 in SLE patients.
Methods
SLE patients referring to four Italian centres were monitored between February 2020 and March 2021. All patients with SARS-CoV-2 infection were included. Disease characteristics, treatment, disease activity and SARS-CoV-2-related symptoms were recorded before and after the infection.
Results
Fifty-one (6.14%) SLE patients were included among 830 who were regularly followed up. Nine (17.6%) had an asymptomatic infection and 5 (9.8%) out of 42 (82.6%) symptomatic patients developed interstitial pneumonia (no identified risk factor). The presence of SLE major organ involvement (particularly renal involvement) was associated with asymptomatic SARS-CoV-2 infection (P = 0.02). Chronic corticosteroid therapy was found to be associated with asymptomatic infection (P = 0.018). Three SLE flares (5.9%) were developed after SARS-CoV-2 infection: one of them was characterized by MPO-ANCA-positive pauci-immune crescentic necrotizing glomerulonephritis and granulomatous pneumonia.
Conclusions
SARS-CoV-2 infection determined autoimmune flares in a small number of patients. Our data seem to confirm that there was not an increased risk of SARS-CoV-2 in SLE. Patients with asymptomatic SARS-CoV-2 infections were those having major SLE organ involvement. This may be explained by the high doses of corticosteroids and immunosuppressive agents used for SLE treatment.
Evidence about the relevance of the complement system, a highly conserved constituent of the innate immunity response that orchestrates the elimination of pathogens and the inflammatory processes, ...has been recently accumulated in many different rheumatologic conditions. In rheumatoid arthritis, complement, mainly the classical pathway, contributes to tissue damage especially in seropositive subjects, with complement activation occurring in the joint. Data about complement pathways in psoriatic arthritis are dated and poorly consistent; among patients with Sjögren syndrome, hypocomplementemia exerts a prognostic role, identifying patients at risk of extra-glandular manifestations. Hints about complement involvement in systemic sclerosis have been recently raised, following the evidence of complement deposition in affected skin and in renal samples from patients with scleroderma renal crisis. In vasculitides, complement plays a dual role: on one hand, stimulation of neutrophils with anti-neutrophil cytoplasmic antibodies (ANCA) results in the activation of the alternative pathway, on the other, C5a induces translocation of ANCA antigens, favouring the detrimental role of antibodies. Complement deposition in the kidneys identifies patients with more aggressive renal disease; patients with active disease display low serum levels of C3 and C4. Even though in dermatomyositis sC5b-9 deposits are invariably present in affected muscles, data on C3 and C4 fluctuation during disease course are scarce. C3 and C1q serum levels have been explored as potential markers of disease activity in Takayasu arteritis, whereas data in Behçet disease are limited to
observations. Pregnancies in women with rheumatologic conditions are still burdened by a higher rate of pregnancy complications, thus the early identification of women at risk would be invaluable. A fine-tuning of complement activation is required from a physiological progression of pregnancy, from pre-implantation stages, through placentation to labour. Complement deregulation has been implicated in several pregnancy complications, such as recurrent abortion, eclampsia and premature birth; low complement levels have been shown to reliably identify women at risk of complications. Given its physiologic role in orchestrating pregnancy progression and its involvement as pathogenic effector in several rheumatologic conditions, complement system is an attractive candidate biomarker to stratify the obstetric risk among women with rheumatologic conditions.
Objective
It has been suggested that only antibodies against domain 1 (D1) of β2‐glycoprotein I (β2GPI) are pathogenic and diagnostic. The role of antibodies against other β2GPI domains is still ...debated. This study was undertaken to evaluate the clinical relevance of domain specificity profiling of anti‐β2GPI IgG antibodies in antiphospholipid syndrome (APS) patients and in control groups of patients with systemic autoimmune rheumatic diseases and in asymptomatic antiphospholipid antibody (aPL) carriers.
Methods
We evaluated 159 subjects with persistently positive, medium or high‐titer anti‐β2GPI IgG, including 56 patients with thrombotic (obstetric or nonobstetric) primary APS, 31 women with obstetric primary APS, 42 aPL‐positive patients with systemic autoimmune rheumatic diseases, and 30 asymptomatic aPL carriers. One hundred healthy donors were included. Anti‐β2GPI D1 and D4/5 IgG were tested on research enzyme‐linked immunosorbent assays containing recombinant β2GPI domains.
Results
As compared to other groups, aPL carriers displayed higher frequency/titer of anti‐D4/5 IgG. Unlike anti‐D4/5, anti‐D1 IgG antibodies were more frequent and at higher titer in triple than in single or double aPL‐positive subjects. An anti‐D1 to anti‐D4/5 ratio of ≥1.5 was predictive of systemic autoimmunity (odds ratio 3.25 95% confidence interval 1.45–7.49, P = 0.005). Neither anti‐D1 nor anti‐D4/5 antibodies were associated with APS clinical criteria.
Conclusion
Anti‐D1 IgG is the preferential specificity not only in vascular and obstetric primary APS, but also in patients with systemic autoimmune rheumatic disease with no clinical features of APS. Conversely, aPL carriers do not have a polarized profile toward D1. Combined testing for anti‐β2GPI IgG with different domain specificity allows a more accurate aPL profiling, with polarization toward anti‐D1 IgG as a possible fingerprint of systemic autoimmunity.
Antiphospholipid syndrome (APS) is an acquired autoimmune disease characterized by thromboembolic events, pregnancy morbidity, and the presence of antiphospholipid (aPL) antibodies. There is sound ...evidence that aPL act as pathogenic autoantibodies being responsible for vascular clots and miscarriages. However, the exact mechanisms involved in the clinical manifestations of the syndrome are still a matter of investigation. In particular, while vascular thrombosis is apparently not associated with inflammation, the pathogenesis of miscarriages can be explained only in part by the aPL-mediated hypercoagulable state and additional non-thrombotic effects, including placental inflammation, have been described. Despite this difference, evidence obtained from animal models and studies in APS patients support the conclusion that complement activation is a common denominator in both vascular and obstetric APS. Tissue-bound aPL rather than circulating aPL-beta2 glycoprotein I immune complexes seem to be responsible for the activation of the classical and the alternative complement pathways. The critical role of complement is supported by the finding that complement-deficient animals are protected from the pathogenic effect of passively infused aPL and similar results have been obtained blocking complement activation. Moreover, elevated levels of complement activation products in the absence of abnormalities in regulatory molecules have been found in the plasma of APS patients, strongly suggesting that the activation of complement cascade is the result of aPL binding to the target antigen rather than of a defective regulation. Placental complement deposits represent a further marker of complement activation both in animals and in patients, and there is also some suggestive evidence that complement activation products are deposited in the affected vessels. The aim of this review is to analyze the state of the art of complement involvement in the pathogenesis of APS in order to provide insights into the role of this system as predictive biomarker for the clinical manifestations and as therapeutic target.
Beta-2 glycoprotein I (β
2
GPI) is the main antigenic target for antiphospholipid antibodies (aPL), the serological markers of antiphospholipid syndrome (APS). Domain I (DI) of β
2
GPI has lately ...been identified as the main epitope targeted by antibodies reacting against β
2
GPI. DI is a cryptic epitope, becoming available for autoantibody binding when β
2
GPI opens from a circular to a fish-hook configuration. Antibodies targeting β
2
GPI-DI are more frequently detected in patients with a full-blown syndrome than in asymptomatic aPL carriers or in patients with infectious diseases that have reactivity toward the whole molecule. Interestingly, anti-DI antibodies are strongly positively correlated with thrombotic and pregnancy manifestations, enabling identification of patients at higher risk of clinical events. However, available tests to detect anti-DI antibodies still lack standardization. Moreover, some APS patients develop antibodies reacting against β
2
GPI epitopes other than DI, suggesting that other anti-β
2
GPI antibody subsets may be clinically relevant. Available evidence on anti-DI antibodies in APS is herein critically reviewed.
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