Scientific review of the impact of climate change on plant pests: a global challenge to prevent and mitigate plant pest risks in agriculture, forestry and ecosystems.

Climate change represents an unprecedented challenge to the world?s biosphere and to the global community. It also represents a unique challenge for plant health. Human activities and increased market globalization, coupled with rising temperatures, has led to a situation that is favourable to pest movement and establishment. This scientific review assesses the potential effects of climate change on plant pests and consequently on plant health. The evidence assessed strongly indicates that climate change has already expanded some pests? host range and geographical distribution, and may further increase the risk of pest introduction to new areas. This calls for international cooperation and development of harmonized plant protection strategies to help countries successfully adapt their pest risk management measures to climate change.bitstream/item/224381/1/Scientific-review-of-the-impact-of-climate-2021.pd

Acute kidney injury promotes development of papillary renal cell adenoma and carcinoma from renal progenitor cells.

Acute tissue injury causes DNA damage and repair processes involving increased cell mitosis and polyploidization, leading to cell function alterations that may potentially drive cancer development. Here, we show that acute kidney injury (AKI) increased the risk for papillary renal cell carcinoma (pRCC) development and tumor relapse in humans as confirmed by data collected from several single-center and multicentric studies. Lineage tracing of tubular epithelial cells (TECs) after AKI induction and long-term follow-up in mice showed time-dependent onset of clonal papillary tumors in an adenoma-carcinoma sequence. Among AKI-related pathways, NOTCH1 overexpression in human pRCC associated with worse outcome and was specific for type 2 pRCC. Mice overexpressing NOTCH1 in TECs developed papillary adenomas and type 2 pRCCs, and AKI accelerated this process. Lineage tracing in mice identified single renal progenitors as the cell of origin of papillary tumors. Single-cell RNA sequencing showed that human renal progenitor transcriptome showed similarities to PT1, the putative cell of origin of human pRCC. Furthermore, NOTCH1 overexpression in cultured human renal progenitor cells induced tumor-like 3D growth. Thus, AKI can drive tumorigenesis from local tissue progenitor cells. In particular, we find that AKI promotes the development of pRCC from single progenitors through a classical adenoma-carcinoma sequence

Summary for policymakers of the scientific review of the impact of climate change on plant pests: a global challenge to prevent and mitigate plant pest risks in agriculture, forestry and ecosystems.

Climate change represents an unprecedented challenge to the world?s biosphere and to the global community. It also represents a unique challenge for plant health. Human activities and increased market globalization, coupled with rising temperatures, has led to a situation that is favourable to pest movement and establishment. This summary for policy makers drawn from the FAO scientific review on the impact of climate change on plant pests, and by extension, on plant health provides concrete recommendations for decision makers on how to address the impact of climate change on plant health. The evidence assessed strongly indicates that climate change has already expanded some pests? host range and geographical distribution, and may further increase the risk of pest introduction to new areas. Increased international cooperation and development of harmonized plant protection strategies are crucial to help countries successfully adapt their pest risk management measures to climate change.bitstream/item/224382/1/Summary-for-policymakers-of-the-2021.pd

Modification of standard ISHAGE methodology for CD34+ cells count on thawed Cord Blood Units: results from a multi-center Eurocord/Netcord study

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Only hyperuricemia with crystalluria, but not asymptomatic hyperuricemia, drives progression of chronic kidney disease

BACKGROUND: The roles of asymptomatic hyperuricemia or uric acid (UA) crystals in CKD progression are unknown. Hypotheses to explain links between UA deposition and progression of CKD include that (1) asymptomatic hyperuricemia does not promote CKD progression unless UA crystallizes in the kidney; (2) UA crystal granulomas may form due to pre-existing CKD; and (3) proinflammatory granuloma-related M1-like macrophages may drive UA crystal-induced CKD progression. METHODS: MALDI-FTICR mass spectrometry, immunohistochemistry, 3D confocal microscopy, and flow cytometry were used to characterize a novel mouse model of hyperuricemia and chronic UA crystal nephropathy with granulomatous nephritis. Interventional studies probed the role of crystal-induced inflammation and macrophages in the pathology of progressive CKD. RESULTS: Asymptomatic hyperuricemia alone did not cause CKD or drive the progression of aristolochic acid I-induced CKD. Only hyperuricemia with UA crystalluria due to urinary acidification caused tubular obstruction, inflammation, and interstitial fibrosis. UA crystal granulomas surrounded by proinflammatory M1-like macrophages developed late in this process of chronic UA crystal nephropathy and contributed to the progression of pre-existing CKD. Suppressing M1-like macrophages with adenosine attenuated granulomatous nephritis and the progressive decline in GFR. In contrast, inhibiting the JAK/STAT inflammatory pathway with tofacitinib was not renoprotective. CONCLUSIONS: Asymptomatic hyperuricemia does not affect CKD progression unless UA crystallizes in the kidney. UA crystal granulomas develop late in chronic UA crystal nephropathy and contribute to CKD progression because UA crystals trigger M1-like macrophage-related interstitial inflammation and fibrosis. Targeting proinflammatory macrophages, but not JAK/STAT signaling, can attenuate granulomatous interstitial nephritis

Regenerative potential of embryonic renal multipotent progenitors in acute renal failure

Bone marrow-and adult kidney-derived stem/progenitor cells hold promise in the development of therapies for renal failure. Here is reported the identification and characterization of renal multipotent progenitors in human embryonic kidneys that share CD24 and CD133 surface expression with adult renal progenitors and have the capacity for self-renewal and multilineage differentiation. It was found that these CD24+CD133+ cells constitute the early primordial nephron but progressively disappear during nephron development until they become selectively localized to the urinary pole of Bowman's capsule. When isolated and injected into SCID mice with acute renal failure from glycerol-induced rhabdomyolysis, these cells regenerated different portions of the nephron, reduced tissue necrosis and fibrosis, and significantly improved renal function. No tumorigenic potential was observed. It is concluded that CD24+CD133+ cells represent a subset of multipotent embryonic progenitors that persist in human kidneys from early stages of nephrogenesis. The ability of these cells to repair renal damage, together with their apparent lack of tumorigenicity, suggests their potential in the treatment of renal failure