Implications of albedo changes following afforestation on the benefits of forests as carbon sinks

Increased carbon storage with afforestation leads to a decrease in atmospheric carbon dioxide concentration and thus decreases radiative forcing and cools the Earth. However, afforestation also changes the reflective properties of the surface vegetation from more reflective pasture to relatively less reflective forest cover. This increase in radiation absorption by the forest constitutes an increase in radiative forcing, with a warming effect. The net effect of decreased albedo and carbon storage on radiative forcing depends on the relative magnitude of these two opposing processes. <br></br> We used data from an intensively studied site in New Zealand's Central North Island that has long-term, ground-based measurements of albedo over the full short-wave spectrum from a developing <i>Pinus radiata</i> forest. Data from this site were supplemented with satellite-derived albedo estimates from New Zealand pastures. The albedo of a well-established forest was measured as 13 % and pasture albedo as 20 %. We used these data to calculate the direct radiative forcing effect of changing albedo as the forest grew. <br></br> We calculated the radiative forcing resulting from the removal of carbon from the atmosphere as a decrease in radiative forcing of −104 GJ tC<sup>−1</sup> yr<sup>−1</sup>. We also showed that the observed change in albedo constituted a direct radiative forcing of 2759 GJ ha<sup>−1</sup> yr<sup>−1</sup>. Thus, following afforestation, 26.5 tC ha<sup>−1</sup> needs to be stored in a growing forest to balance the increase in radiative forcing resulting from the observed albedo change. Measurements of tree biomass and albedo were used to estimate the net change in radiative forcing as the newly planted forest grew. Albedo and carbon-storage effects were of similar magnitude for the first four to five years after tree planting, but as the stand grew older, the carbon storage effect increasingly dominated. Averaged over the whole length of the rotation, the changes in albedo negated the benefits from increased carbon storage by 17–24 %

Genistein Improves Neuropathology and Corrects Behaviour in a Mouse Model of Neurodegenerative Metabolic Disease

BACKGROUND: Neurodegenerative metabolic disorders such as mucopolysaccharidosis IIIB (MPSIIIB or Sanfilippo disease) accumulate undegraded substrates in the brain and are often unresponsive to enzyme replacement treatments due to the impermeability of the blood brain barrier to enzyme. MPSIIIB is characterised by behavioural difficulties, cognitive and later motor decline, with death in the second decade of life. Most of these neurodegenerative lysosomal storage diseases lack effective treatments. We recently described significant reductions of accumulated heparan sulphate substrate in liver of a mouse model of MPSIIIB using the tyrosine kinase inhibitor genistein. METHODOLOGY/PRINCIPAL FINDINGS: We report here that high doses of genistein aglycone, given continuously over a 9 month period to MPSIIIB mice, significantly reduce lysosomal storage, heparan sulphate substrate and neuroinflammation in the cerebral cortex and hippocampus, resulting in correction of the behavioural defects observed. Improvements in synaptic vesicle protein expression and secondary storage in the cerebral cortex were also observed. CONCLUSIONS/SIGNIFICANCE: Genistein may prove useful as a substrate reduction agent to delay clinical onset of MPSIIIB and, due to its multimodal action, may provide a treatment adjunct for several other neurodegenerative metabolic diseases

Australasia

Observed changes and impacts Ongoing climate trends have exacerbated many extreme events (very high confidence). The Australian trends include further warming and sea level rise sea level rise (SLR), with more hot days and heatwaves, less snow, more rainfall in the north, less April–October rainfall in the southwest and southeast and more extreme fire weather days in the south and east. The New Zealand trends include further warming and sea level rise (SLR), more hot days and heatwaves, less snow, more rainfall in the south, less rainfall in the north and more extreme fire weather in the east. There have been fewer tropical cyclones and cold days in the region. Extreme events include Australia’s hottest and driest year in 2019 with a record-breaking number of days over 39°C, New Zealand’s hottest year in 2016, three widespread marine heatwaves during 2016–2020, Category 4 Cyclone Debbie in 2017, seven major hailstorms over eastern Australia and two over New Zealand from 2014–2020, three major floods in eastern Australia and three over New Zealand during 2019–2021 and major fires in southern and eastern Australia during 2019–2020

Neuropathology in Mouse Models of Mucopolysaccharidosis Type I, IIIA and IIIB

Mucopolysaccharide diseases (MPS) are caused by deficiency of glycosaminoglycan (GAG) degrading enzymes, leading to GAG accumulation. Neurodegenerative MPS diseases exhibit cognitive decline, behavioural problems and shortened lifespan. We have characterised neuropathological changes in mouse models of MPSI, IIIA and IIIB to provide a better understanding of these events

Early Neurodegeneration Progresses Independently of Microglial Activation by Heparan Sulfate in the Brain of Mucopolysaccharidosis IIIB Mice

BACKGROUND: In mucopolysaccharidosis type IIIB, a lysosomal storage disease causing early onset mental retardation in children, the production of abnormal oligosaccharidic fragments of heparan sulfate is associated with severe neuropathology and chronic brain inflammation. We addressed causative links between the biochemical, pathological and inflammatory disorders in a mouse model of this disease. METHODOLOGY/PRINCIPAL FINDINGS: In cell culture, heparan sulfate oligosaccharides activated microglial cells by signaling through the Toll-like receptor 4 and the adaptor protein MyD88. CD11b positive microglial cells and three-fold increased expression of mRNAs coding for the chemokine MIP1alpha were observed at 10 days in the brain cortex of MPSIIIB mice, but not in MPSIIIB mice deleted for the expression of Toll-like receptor 4 or the adaptor protein MyD88, indicating early priming of microglial cells by heparan sulfate oligosaccharides in the MPSIIIB mouse brain. Whereas the onset of brain inflammation was delayed for several months in doubly mutant versus MPSIIIB mice, the onset of disease markers expression was unchanged, indicating similar progression of the neurodegenerative process in the absence of microglial cell priming by heparan sulfate oligosaccharides. In contrast to younger mice, inflammation in aged MPSIIIB mice was not affected by TLR4/MyD88 deficiency. CONCLUSIONS/SIGNIFICANCE: These results indicate priming of microglia by HS oligosaccharides through the TLR4/MyD88 pathway. Although intrinsic to the disease, this phenomenon is not a major determinant of the neurodegenerative process. Inflammation may still contribute to neurodegeneration in late stages of the disease, albeit independent of TLR4/MyD88. The results support the view that neurodegeneration is primarily cell autonomous in this pediatric disease

Myeloid/Microglial driven autologous hematopoietic stem cell gene therapy corrects a neuronopathic lysosomal disease

Mucopolysaccharidosis type IIIA (MPSIIIA) is a lysosomal storage disorder caused by mutations in N-sulfoglucosamine sulfohydrolase (SGSH), resulting in heparan sulfate (HS) accumulation and progressive neurodegeneration. There are no treatments. We previously demonstrated improved neuropathology in MPSIIIA mice using lentiviral vectors (LVs) overexpressing SGSH in wild-type (WT) hematopoietic stem cell (HSC) transplants (HSCTs), achieved via donor monocyte/microglial engraftment in the brain. However, neurological disease was not corrected using LVs in autologous MPSIIIA HSCTs. To improve brain expression via monocyte/microglial specificity, LVs expressing enhanced green fluorescent protein (eGFP) under ubiquitous phosphoglycerate kinase (PGK) or myeloid-specific promoters were compared in transplanted HSCs. LV-CD11b-GFP gave significantly higher monocyte/B-cell eGFP expression than LV-PGK-GFP or LV-CD18-GFP after 6 months. Subsequently, autologous MPSIIIA HSCs were transduced with either LV-PGK-coSGSH or LV-CD11b-coSGSH vectors expressing codon-optimized SGSH and transplanted into MPSIIIA mice. Eight months after HSCT, LV-PGK-coSGSH vectors produced bone marrow SGSH (576% normal activity) similar to LV-CD11b-coSGSH (473%), but LV-CD11b-coSGSH had significantly higher brain expression (11 versus 7%), demonstrating improved brain specificity. LV-CD11b-coSGSH normalized MPSIIIA behavior, brain HS, GM2 ganglioside, and neuroinflammation to WT levels, whereas LV-PGK-coSGSH partly corrected neuropathology but not behavior. We demonstrate compelling evidence of neurological disease correction using autologous myeloid driven lentiviral-HSC gene therapy in MPSIIIA mice. © The American Society of Gene & Cell Therapy

L'actine cytosquelettique et ses protéines associées. Quelques exemples chez les protistes

La mise en œuvre de multiples processus biologiques nécessite des changements du cytosquelette riche en actine. Tel est le cas de la motilité cellulaire qui résulte de l'assemblage et désassemblage des filaments d'actine, une activité régulée par l'action de nombreuses protéines liant l'actine. Les organismes unicellulaires sont des modèles de choix pour l'étude des régulations engendrant les remaniements du cytosquelette car leur manipulation aisée s'adapte à diverses technologies. Lors de la XXXVe réunion annuelle du Groupement des Protistologues de Langue Française (GPLF), un symposium concernant « L'actine cytosquelettique et ses protéines associées chez les protistes » a été organisé. Ce colloque reflète l'intérêt du GPLF pour le développement en France des thèmes de recherche concernant des protistes pathogènes pour l'homme et ceux, pathogènes ou non, servant de modèles d'analyse cellulaire. Un compte rendu de ce colloque est présenté dans cet article

Evaluation of NT-proBNP in Inflammatory Bowel Disease

International audienc

Evaluation of NT-proBNP in Inflammatory Bowel Disease

International audienc