Données économiques sur la lutte biologique contre le scolyte des baies du caféier

La possibilité d'utiliser un parasitoïde, Cephalonomia stephanoderis Betrem, pour contrôler les populations de scolytes des baies a été démontrée. Cette étude économique en évalue les possibilités d'application dans les grandes exploitations familiales du sud-ouest du Guatemala. Cette innovation technique ne représente pas un investissement financier élevé. Son coût, essentiellement la main-d'oeuvre nécessaire au maintien des élevages du parasitoïde, est comparable à celui de la lutte chimique, soit 7% du coût total. Les petits exploitants qui rénovent leur caféière sont très favorables à l'adoption des techniques de lutte biologique, car ils peuvent se grouper pour les mettre en oeuvre. (Résumé d'auteurs

Pathogenic FAM83g palmoplantar keratoderma mutations inhibit the PAWS1::Ck1α association and attenuate wnt signalling

Background: Two recessive mutations in the FAM83G gene, causing A34E and R52P amino acid substitutions in the DUF1669 domain of the PAWS1 protein, are associated with palmoplantar keratoderma (PPK) in humans and dogs respectively. We have previously reported that PAWS1 associates with the Ser/Thr protein kinase CK1α through the DUF1669 domain to mediate canonical Wnt signalling. Methods: Co-immunoprecipitation was used to investigate possible changes to PAWS1 interactors caused by the mutations. We also compared the stability of wild-type and mutant PAWS1 in cycloheximide-treated cells. Effects on Wnt signalling were determined using the TOPflash luciferase reporter assay in U2OS cells expressing PAWS1 mutant proteins. The ability of PAWS1 to induce axis duplication in Xenopus embryos was also tested. Finally, we knocked-in the A34E mutation at the native gene locus and measured Wnt-induced AXIN2 gene expression by RT-qPCR. Results: We show that these PAWS1 A34E and PAWS1 R52P mutants fail to interact with CK1α but, like the wild-type protein, do interact with CD2AP and SMAD1. Like cells carrying a PAWS1 F296A mutation, which also abolishes CK1α binding, cells carrying the A34E and R52P mutants respond poorly to Wnt signalling to an extent resembling that observed in FAM83G gene knockout cells. Consistent with this observation, these mutants, in contrast to the wild-type protein, fail to induce axis duplication in Xenopus embryos. We also found that the A34E and R52P mutant proteins are less abundant than the native protein and appear to be less stable, both when overexpressed in FAM83G-knockout cells and when knocked-in at the native FAM83G locus. Ala 34 of PAWS1 is conserved in all FAM83 proteins and mutating the equivalent residue in FAM83H (A31E) also abolishes interaction with CK1 isoforms. Conclusions: We propose that mutations in PAWS1 cause PPK pathogenesis through disruption of the CK1α interaction and attenuation of Wnt signalling. </p

Csnk1a1 inhibition has p53-dependent therapeutic efficacy in acute myeloid leukemia

Despite extensive insights into the underlying genetics and biology of acute myeloid leukemia (AML), overall survival remains poor and new therapies are needed. We found that casein kinase 1 α (Csnk1a1), a serine-threonine kinase, is essential for AML cell survival in vivo. Normal hematopoietic stem and progenitor cells (HSPCs) were relatively less affected by shRNA-mediated knockdown of Csnk1a1. To identify downstream mediators of Csnk1a1 critical for leukemia cells, we performed an in vivo pooled shRNA screen and gene expression profiling. We found that Csnk1a1 knockdown results in decreased Rps6 phosphorylation, increased p53 activity, and myeloid differentiation. Consistent with these observations, p53-null leukemias were insensitive to Csnk1a1 knockdown. We further evaluated whether D4476, a casein kinase 1 inhibitor, would exhibit selective antileukemic effects. Treatment of leukemia stem cells (LSCs) with D4476 showed highly selective killing of LSCs over normal HSPCs. In summary, these findings demonstrate that Csnk1a1 inhibition causes reduced Rps6 phosphorylation and activation of p53, resulting in selective elimination of leukemia cells, revealing Csnk1a1 as a potential therapeutic target for the treatment of AML

L'adhésion thérapeutique dans l'hypertension artérielle résistante

peer reviewe

Carbon and biodiversity restoration potential in an artificial savanna in the Democratic Republic of the Congo

A large share of the global forest restoration potential is situated in unstable mesic African savannas, contributing about 23% to the global mismatch between potential and actual terrestrial carbon stocks. However, uncertainty on Central African forest recovery rates impedes science-informed implementation of forest restoration efforts. Here, we quantify the forest restoration success of 17 years of fire exclusion within a mesic artificial savanna patch in the Kongo Central province of the Democratic Republic of the Congo. Since 2005, the local community of the Manzonzi village has conserved an 88-ha artificial savanna with support from World Wildlife Fund. In 2010, we established 101 permanent plots (total area of 40.4 ha) and remeasured them (at the threshold of 10 cm DBH) in 2014 and 2022, by considering two species categories: savanna and forest specialists. Between 2010 and 2022, mean stem density switched from 122.3 ± 9.0 to 27.0 ± 3.8 tree/ha and from 45.8 ± 7.5 to 178.6 ± 10.1 tree/ha for savanna specialists (e.g. Hymenocardia acida and Maprounea africana), and forest specialists (e.g. Xylopia aethiopica and Albizia adianthifolia) respectively. We found that aboveground carbon (AGC) recovery of forest specialist after 17 years was on average 11.9 ± 0.2 Mg C ha&#8722;1. Using a model fitted to the data, we predicted that AGC stocks take 110 ± 3 years to recover to 90% of AGC stocks in old-growth forests. Applying this recovery trajectory, we show that unstable , artificial savannas across DRC, Congo, and Angola have a total carbon uptake potential of 13.5 ± 1.6 Gt C by 2100. Species richness recovered to 33.1% after 17 years and we predicted a 90% recovery at 57 ± 1 years. In contrast, the recovery of species composition was much slower, with an estimated 90% recovery after 125 ± 3 years. We conclude that carbon and biodiversity recovery trajectories are indispensable to developing policies promoting forest restoration in artificial African savannas. However, more long-term, in situ monitoring efforts are needed to quantify variation in carbon and diversity recovery owing to resource availability (rainfall and soil fertility), prior vegetation and land-use history, and surrounding forest cover

Protecting an artificial savanna as a nature-based solution for restoring carbon and biodiversity in the Democratic Republic of the Congo

A large share of the global forest restoration potential is situated in unstable mesic African savannas, contributing about 23% to the worldwide mismatch between potential and actual terrestrial carbon stocks. However, uncertainty regarding central African forest recovery rates impedes science-informed implementation of forest restoration efforts. Here, we quantify the forest restoration success of 17 years of fire exclusion within a mesic artificial savanna patch in the Kongo Central province of the DR Congo. We found a rapid increase in the stem density of pioneer forest species (e.g., Xylopia aethiopica and Albizia adianthifolia) and a significant decrease in the stem density of savanna species (e.g., Hymenocardia acida and Maprounea africana). On average, forest species above ground carbon (AGC) recovery was 11.97 ± 0.20 Mg C ha&#8722;1. We predicted that AGC stocks take 112 ± 3 years to recover to 90% of AGC stocks in old-growth forests. We showed that unstable artificial savannas across DR Congo, Congo, and Angola have a total carbon uptake potential of 12.13 ± 2.25 Gt C by 2100. Species richness recovered to 33.17% after 17 years, and we predicted a 90% recovery at 54 ± 2 years. In contrast, the recovery of species composition was much slower, with an estimated 90% recovery after 12 ± 3 years. We conclude that the relatively simple and cost-efficient measure of fire exclusion in artificial savannas is an effective Nature-based solution to climate change and biodiversity loss. However, more long-term and in situ monitoring efforts are needed to quantify variation in longterm carbon and diversity recovery pathways

Hypercalcemia after transplant nephrectomy in a hemodialysis patient: a case report

<p>Abstract</p> <p>Introduction</p> <p>Hypercalcemia is a complication often seen in chronic hemodialysis patients. A rare cause of this condition is sarcoidosis. Its highly variable clinical presentation is challenging. Especially in patients suffering chronic kidney graft failure the nonspecific constitutional symptoms of sarcoidosis like fever, weight loss, arthralgia and fatigue may be easily misleading.</p> <p>Case presentation</p> <p>A 51 year old male developed hypercalcemia, arthralgia and B-symptoms after explantation of his kidney graft because of suspected acute rejection. The removed kidney showed vasculopathy and tubulointerstitial nephritis, which had not been overt in the biopsy taken half a year earlier. Despite explantation and withdrawal of the immunosuppression the patient's general condition deteriorated progressively. A rapid rise in serum calcium finally provoked us to check for sarcoidosis. CT scans of the lungs, broncho-alveolar-lavage and further lab tests confirmed the diagnosis.</p> <p>Conclusion</p> <p>This case demonstrates that withdrawal of immunosuppressive drugs sometimes unmasks sarcoidosis. It should be considered as differential diagnosis even in hemodialysis patients, in whom other reasons for hypercalcemia are much more common.</p