Limited effect of management on apple pollination : a case study from an oceanic Island

Intensive agricultural practices leading to habitat degradation represent a major threat to pollinators. Diverse management practices are expected to influence wild pollinator abundance and richness on farms, although their effect in perennial crops is still unclear. In this study, we assessed the impact of management on apple (Malus domestica) pollination on an oceanic island, by comparing conventional (with and without herbicide application) and organic apple orchards. Pollinator visitation and pan trap surveys were carried out in six apple orchards in Terceira Island (Azores) and the landscape composition surrounding orchards was characterized. We also quantified fruit set, seed set and apple weight. We found no significant effect of management on insect visitation rates, whereas there was a negative association with increasing surrounding agricultural land. In contrast, management had an effect on species abundance, richness and diversity at the orchard level. Conventional orchards without herbicides showed higher abundance than the rest, but lower richness and diversity than conventional orchards with herbicides. Management had an effect on fruit set, but not on seed set or fruit weight. Our results suggest that management alone is insufficient for the overall improvement of apple pollination on an oceanic island, while landscape composition may play a relevant role.Regional Government of Extremadura in Spain (PO17006); ACORES-01-0145-FEDER-000073info:eu-repo/semantics/publishedVersio

Chronic eosinophilic leukemia with a FIP1L1-PDGFRα fusion: case report and literature review

Chronic eosinophilia is habitually associated with allergic, infectious, inflammatory, neoplastic and endocrine conditions and exposure to certain drugs and toxic agents. However, eosinophilic proliferation may be primary, without identifiable causes, or provoked by clonal hematopoietic stem cell proliferation. Gene fusions involving PDGFR-α, PDGFR-β, and FGFR1 predispose patients to rare conditions with chronic myeloproliferation or lymphoproliferation, alterations in peripheral blood and bone marrow and diffuse tissue injury due to the release of cytokines and humoral factors from eosinophilic granules. The presence of the PDGFR-α rearrangement is commonly related to chronic eosinophilic leukemia, with alterations in peripheral mastocytes and neutrophils, and rarely to acute myeloid leukemia or T lymphoblastic lymphoma with eosinophilia. The most prevalent PDGFR-α rearrangement is one resulting from an interstitial deletion in the long arm of chromosome 4, that allows the formation of a neogene from the fusion of the FIP1L1 and PDGFRα genes. This codes a constitutively active tyrosine kinase, which can be inhibited by imatinib mesylate. In 2002, the successful treatment of a patient using imatinib to treat hypereosinophilic syndrome was reported. Since then, this drug has been utilized with fast, complete and lasting clinical responses. Here we describe a case of chronic eosinophilic syndrome with expression of the FIP1L1-PDGFR-α rearrangement.A eosinofilia no sangue e em tecidos está habitualmente associada a condições alérgicas, infecciosas, inflamatórias, neoplásicas, endocrinológicas, uso de medicamentos e exposição a agentes tóxicos. No entanto, pode ocorrer proliferação eosinofílica primária, sem causa aparente ou por expansão clonal da célula-tronco hematopoética. As neoplasias mielo ou linfoproliferativas associadas a rearranjos gênicos como PDGFRα, PDGFRβ e FGFR1 constituem condições raras nas quais ocorre mieloproliferação crônica, alterações no sangue periférico e na medula óssea e lesão tecidual de diferentes órgãos, a partir da liberação de citocinas e fatores humorais pelos grânulos eosinofílicos. A presença do rearranjo PDGFRα relaciona-se comumente à leucemia eosinofílica crônica, com envolvimento de mastócitos e neutrófilos e, mais raramente, à leucemia mielóide aguda ou ao linfoma linfoblástico T, com eosinofilia. O rearranjo PDGFRα mais comum é aquele resultante da deleção intersticial no braço longo do cromossomo 4, que permite a formação de um neogene a partir da fusão dos genes FIP1L1 e PDGFRα. Este codifica uma tirosino-quinase constitutivamente ativa que é inibida pelo mesilato de imatinibe. Em 2002 foi relatado o uso bem sucedido de mesilato de imatinibe em baixas doses em um paciente com síndrome hipereosinofilica e, desde então, vem-se utilizando esta droga com respostas clínicas rápidas, completas e duradouras. Descrevemos um caso de LEC com expressão do rearranjo FIP1L1-PDGFRα.Universidade Federal de São Paulo (UNIFESP) EPMHospital do Servidor Público Municipal de São PauloHospital Guilherme Álvaro UNIFESPUNIFESPUNIFESP, EPMHospital Guilherme Álvaro UNIFESPSciEL

Depression as a determinant of frailty in late life

Objectives Accumulating evidence shows depression as a risk factor for frailty, but studies are mainly population-based and widely differ in their assessment of either depression or frailty. We investigated the association between depression and frailty among geriatric outpatients using different assessment instruments for both conditions. Method Among 315 geriatric outpatients (mean age 72.1 years, 68.3% female sex) participating the MiMiCS-FRAIL cohort study, major and subthreshold depression were measured with psychiatric diagnostic interview according to DSM-5 criteria (SCID-5) as well as with instruments to screen and measure severity of depressive symptoms (GDS-15 and PHQ-9). Frailty was assessed according to a screening instrument (FRAIL-BR) and a multidimensional Frailty Index (FI-36 items). Multiple logistic and linear regression were performed to assess the association between depression (independent variable) and frailty (dependent variable) adjusted for confounders. Results Frailty prevalence in patients with no, subthreshold or major depressive disorder increases from either 14.5%, 46.5% to 65.1% when using the FRAIL-BR questionnaire, and from 10.2%, 20.9%, to 30.2% when using the FI-36 index. These association remain nearly the same when adjusted for covariates. Both the FRAIL-BR and the FI-36 were strongly associated with major depressive disorder, subthreshold depression, and depressive symptoms by PHQ-9 and GDS-15. Conclusion Late life depression and frailty are associated in a dose-dependent manner, irrespective of the used definitions. Nonetheless, to avoid residual confounding, future research on underlying biological mechanisms should preferably be based on formal psychiatric diagnoses and objectively assessment frailty status

Methyl donor nutrients in chronic kidney disease: impact on the epigenetic landscape

Epigenetic alterations, such as those linked to DNA methylation, may potentially provide molecular explanations for complications associated with altered gene expression in illnesses, such as chronic kidney disease (CKD). Although both DNA hypo- and hypermethylation have been observed in the uremic milieu, this remains only a single aspect of the epigenetic landscape and, thus, of any biochemical dysregulation associated with CKD. Nevertheless, the role of uremia-promoting alterations on the epigenetic landscape regulating gene expression is still a novel and scarcely studied field. Although few studies have actually reported alterations of DNA methylation via methyl donor nutrient intake, emerging evidence indicates that nutritional modification of the microbiome can affect one-carbon metabolism and the capacity to methylate the genome in CKD. In this review, we discuss the nutritional modifications that may affect one-carbon metabolism and the possible impact of methyl donor nutrients on the microbiome, CKD, and its phenotype

Dogs are resistant to prion infection, due to the presence of aspartic or glutamic acid at position 163 of their prion protein

Unlike other species, prion disease has never been described in dogs even though they were similarly exposed to the bovine spongiform encephalopathy (BSE) agent. This resistance prompted a thorough analysis of the canine PRNP gene and the presence of a negatively charged amino acid residue in position 163 was readily identified as potentially fundamental as it differed from all known susceptible species. In the present study, the first transgenic mouse model expressing dog prion protein (PrP) was generated and challenged intracerebrally with a panel of prion isolates, none of which could infect them. The brains of these mice were subjected to in vitro prion amplification and failed to find even minimal amounts of misfolded prions providing definitive experimental evidence that dogs are resistant to prion disease. Subsequently, a second transgenic model was generated in which aspartic acid in position 163 was substituted for asparagine (the most common in prion susceptible species) resulting in susceptibility to BSE‐derived isolates. These findings strongly support the hypothesis that the amino acid residue at position 163 of canine cellular prion protein (PrPC) is a major determinant of the exceptional resistance of the canidae family to prion infection and establish this as a promising therapeutic target for prion diseases.MINECO/FEDER. Grant Numbers: AGL2015‐65046‐C2‐1‐R, AGL2008‐05296‐C02 Interreg. Grant Number: POCTEFA EFA148/1

Transgenic Mouse Bioassay : Evidence That Rabbits Are Susceptible to a Variety of Prion Isolates

Interspecies transmission of prions is a well-established phenomenon, both experimentally and under field conditions. Upon passage through new hosts, prion strains have proven their capacity to change their properties and this is a source of strain diversity which needs to be considered when assessing the potential risks associated with consumption of prion contaminated protein sources. Rabbits were considered for decades to be a prion resistant species until proven otherwise recently. To determine the extent of rabbit susceptibility to prions and to assess the effects of passage of different prion strains through this species a transgenic mouse model overexpressing rabbit PrPC was developed (TgRab). Intracerebral challenges with prion strains originating from a variety of species including field isolates (ovine SSBP/1 scrapie, Nor98- scrapie; cattle BSE, BSE-L and cervid CWD), experimental murine strains (ME7 and RML) and experimentally obtained ruminant (sheepBSE) and rabbit (de novo NZW) strains were performed. On first passage TgRab were susceptible to the majority of prions (Cattle BSE, SheepBSE, BSE-L, de novo NZW, ME7 and RML) tested with the exception of SSBP/1 scrapie, CWD and Nor98 scrapie. Furthermore, TgRab were capable of propagating strain-specific features such as differences in incubation periods, histological brain lesions, abnormal prion (PrPd) deposition profiles and proteinase-K (PK) resistant western blotting band patterns. Our results confirm previous studies proving that rabbits are not resistant to prion infection and show for the first time that rabbits are susceptible to PrPd originating in a number of other species. This should be taken into account when choosing protein sources to feed rabbits

The gut microbiota of people with asthma influences lung inflammation in gnotobiotic mice

The gut microbiota in early childhood is linked to asthma risk, but may continue to affect older patients with asthma. Here, we profile the gut microbiota of 38 children (19 asthma, median age 8) and 57 adults (17 asthma, median age 28) by 16S rRNA sequencing and find individuals with asthma harbored compositional differences from healthy controls in both adults and children. We develop a model to aid the design of mechanistic experiments in gnotobiotic mice and show enterotoxigeni

Author Correction: Cryptic inoviruses revealed as pervasive in bacteria and archaea across Earth's biomes.

An amendment to this paper has been published and can be accessed via a link at the top of the paper

An amino acid substitution found in animals with low susceptibility to prion diseases confers a protective dominant-negative effect in prion-infected transgenic mice

While prion diseases have been described in numerous species, some, including those of the Canidae family, appear to show resistance or reduced susceptibility. A better understanding of the factors underlying prion susceptibility is crucial for the development of effective treatment and control measures. We recently demonstrated resistance to prion infection in mice overexpressing a mutated prion protein (PrP) carrying a specific amino acid substitution characteristic of canids. Here, we show that coexpression of this mutated PrP and wild-type mouse PrP in transgenic mice inoculated with different mouse-adapted prion strains (22 L, ME7, RML, and 301C) significantly increases survival times (by 45 to 113%). These data indicate that this amino acid substitution confers a dominant-negative effect on PrP, attenuating the conversion of PrPC to PrPSc and delaying disease onset without altering the neuropathological properties of the prion strains. Taken together, these findings have important implications for the development of new treatment approaches for prion diseases based on dominant-negative proteins