Adapting Agriculture to Climate Change: A Synopsis of Coordinated National Crop Wild Relative Seed Collecting Programs across Five Continents

The Adapting Agriculture to Climate Change Project set out to improve the diversity, quantity, and accessibility of germplasm collections of crop wild relatives (CWR). Between 2013 and 2018, partners in 25 countries, heirs to the globetrotting legacy of Nikolai Vavilov, undertook seed collecting expeditions targeting CWR of 28 crops of global significance for agriculture. Here, we describe the implementation of the 25 national collecting programs and present the key results. A total of 4587 unique seed samples from at least 355 CWR taxa were collected, conserved ex situ, safety duplicated in national and international genebanks, and made available through the Multilateral System (MLS) of the International Treaty on Plant Genetic Resources for Food and Agriculture (Plant Treaty). Collections of CWR were made for all 28 targeted crops. Potato and eggplant were the most collected genepools, although the greatest number of primary genepool collections were made for rice. Overall, alfalfa, Bambara groundnut, grass pea and wheat were the genepools for which targets were best achieved. Several of the newly collected samples have already been used in pre-breeding programs to adapt crops to future challenges.info:eu-repo/semantics/publishedVersio

Repercussões do Sars-Cov-2 no âmbito da cirurgia geral e medicina de emergência: uma revisão

Na China, em dezembro de 2019, foram relatados os primeiros casos da patologia respiratória  COVID-19, doença causado pelo SARS-CoV-2, um RNA vírus. A propagação foi veloz e global, de maneira que a Organização Mundial de Saúde definiu como pandemia em março de 2020. A doença tem manifestação clínica variada, com enfermos assintomáticos ou manifestando quadro crítico, apresentando alta transmissibilidade e letalidade considerável. Simultaneamente, indivíduos com indicação cirúrgica, de origem traumática ou não, tiveram seus atendimentos eletivos paralisados e houve queda nos índices de intervenções de cunho emergencista, tanto devido o medo do indivíduo procurar um serviço de saúde e ser contaminado pelo coronavírus, quanto por outros fatores. Essa revisão teve como objetivo averiguar como a pandemia acometeu serviços de cirurgia geral de emergência, bem como elucidar os preditores e fatores que ocasionaram mudanças no manejo e intervenções cirúrgicas durante o surto de SARS-CoV-2

Rationale, study design, and analysis plan of the Alveolar Recruitment for ARDS Trial (ART): Study protocol for a randomized controlled trial

Background: Acute respiratory distress syndrome (ARDS) is associated with high in-hospital mortality. Alveolar recruitment followed by ventilation at optimal titrated PEEP may reduce ventilator-induced lung injury and improve oxygenation in patients with ARDS, but the effects on mortality and other clinical outcomes remain unknown. This article reports the rationale, study design, and analysis plan of the Alveolar Recruitment for ARDS Trial (ART). Methods/Design: ART is a pragmatic, multicenter, randomized (concealed), controlled trial, which aims to determine if maximum stepwise alveolar recruitment associated with PEEP titration is able to increase 28-day survival in patients with ARDS compared to conventional treatment (ARDSNet strategy). We will enroll adult patients with ARDS of less than 72 h duration. The intervention group will receive an alveolar recruitment maneuver, with stepwise increases of PEEP achieving 45 cmH(2)O and peak pressure of 60 cmH2O, followed by ventilation with optimal PEEP titrated according to the static compliance of the respiratory system. In the control group, mechanical ventilation will follow a conventional protocol (ARDSNet). In both groups, we will use controlled volume mode with low tidal volumes (4 to 6 mL/kg of predicted body weight) and targeting plateau pressure <= 30 cmH2O. The primary outcome is 28-day survival, and the secondary outcomes are: length of ICU stay; length of hospital stay; pneumothorax requiring chest tube during first 7 days; barotrauma during first 7 days; mechanical ventilation-free days from days 1 to 28; ICU, in-hospital, and 6-month survival. ART is an event-guided trial planned to last until 520 events (deaths within 28 days) are observed. These events allow detection of a hazard ratio of 0.75, with 90% power and two-tailed type I error of 5%. All analysis will follow the intention-to-treat principle. Discussion: If the ART strategy with maximum recruitment and PEEP titration improves 28-day survival, this will represent a notable advance to the care of ARDS patients. Conversely, if the ART strategy is similar or inferior to the current evidence-based strategy (ARDSNet), this should also change current practice as many institutions routinely employ recruitment maneuvers and set PEEP levels according to some titration method.Hospital do Coracao (HCor) as part of the Program 'Hospitais de Excelencia a Servico do SUS (PROADI-SUS)'Brazilian Ministry of Healt

Mycobacterium leprae induces a tolerogenic profile in monocyte‐derived dendritic cells via TLR2 induction of IDO

The enzyme IDO‐1 is involved in the first stage of tryptophan catabolism and has been described in both microbicidal and tolerogenic microenvironments. Previous data from our group have shown that IDO‐1 is differentially regulated in the distinctive clinical forms of leprosy. The present study aims to investigate the mechanisms associated with IDO‐1 expression and activity in human monocyte‐derived dendritic cells (mDCs) after stimulation with irradiated Mycobacterium leprae and its fractions. M. leprae and its fractions induced the expression and activity of IDO‐1 in human mDCs. Among the stimuli studied, irradiated M. leprae and its membrane fraction (MLMA) induced the production of proinflammatory cytokines TNF and IL‐6 whereas irradiated M. leprae and its cytosol fraction (MLSA) induced an increase in IL‐10. We investigated if TLR2 activation was necessary for IDO‐1 induction in mDCs. We observed that in cultures treated with a neutralizing anti‐TLR2 antibody, there was a decrease in IDO‐1 activity and expression induced by M. leprae and MLMA. The same effect was observed when we used a MyD88 inhibitor. Our data demonstrate that coculture of mDCs with autologous lymphocytes induced an increase in regulatory T (Treg) cell frequency in MLSA‐stimulated cultures, showing that M. leprae constituents may play opposite roles that may possibly be related to the dubious effect of IDO‐1 in the different clinical forms of disease. Our data show that M. leprae and its fractions are able to differentially modulate the activity and functionality of IDO‐1 in mDCs by a pathway that involves TLR2, suggesting that this enzyme may play an important role in leprosy immunopathogenesis.Graphical AbstractMycobacterium leprae and its fractions are able to differentially modulate the activity and functionality of Indoleamine 2,3 dioxygenase in human monocyte‐derived dendritic cells via a pathway that involves TLR2.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/168373/1/jlb10827_am.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/168373/2/jlb10827.pd

Pterocarpanquinone LQB-118 Induces Apoptosis in Leishmania (Viannia) braziliensis and Controls Lesions in Infected Hamsters

Made available in DSpace on 2015-05-04T16:34:30Z (GMT). No. of bitstreams: 2 license.txt: 1914 bytes, checksum: 7d48279ffeed55da8dfe2f8e81f3b81f (MD5) eduardo_santosetal_IOC_2014.pdf: 661284 bytes, checksum: 28c8f5b253df75e3d946ff31a14aebe4 (MD5) Previous issue date: 2014Universidade do Estado do Rio de Janeiro. Departamento de Microbiologia, Imunologia e Parasitologia. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Hanseníase. Rio de Janeiro, RJ, Brasil.Universidade do Estado do Rio de Janeiro. Departamento de Microbiologia, Imunologia e Parasitologia. Laboratório de Bioquímica de Protozoários e Imunofisiologia do Exercício. Rio de Janeiro, RJ, Brasil.Universidade do Estado do Rio de Janeiro. Departamento de Microbiologia, Imunologia e Parasitologia. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Bioquímica de Tripanossomatídeos. Rio de Janeiro, RJ, BrasilFundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Bioquímica de Tripanossomatídeos. Rio de Janeiro, RJ, BrasilUniversidade Federal do Rio de Janeiro. Núcleo de Pesquisas de Produtos Naturais. Laboratório de Catálise Orgânica. Rio de Janeiro, RJ, Brasil.Universidade Federal do Rio de Janeiro. Núcleo de Pesquisas de Produtos Naturais. Laboratório de Química Bioorgânica. Rio de Janeiro, RJ, Brasil.Universidade do Estado do Rio de Janeiro. Departamento de Microbiologia, Imunologia e Parasitologia. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ, Brasil.Previous results demonstrate that the hybrid synthetic pterocarpanquinone LQB-118 presents antileishmanial activity against Leishmania amazonensis in a mouse model. The aim of the present study was to use a hamster model to investigate whether LQB-118 presents antileishmanial activity against Leishmania (Viannia) braziliensis, which is the major Leishmania species related to American tegumentary leishmaniasis. The in vitro antileishmanial activity of LQB-118 on L. braziliensis was tested on the promastigote and intracellular amastigote forms. The cell death induced by LQB-118 in the L. braziliensis promastigotes was analyzed using an annexin V-FITC/PI kit, the oxidative stress was evaluated by 29,79-dichlorodihydrofluorescein diacetate (H2DCFDA) and the ATP content by luminescence. In situ labeling of DNA fragments by terminal deoxyribonucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) was used to investigate apoptosis in the intracellular amastigotes. L. braziliensis-infected hamsters were treated from the seventh day of infection with LQB-118 administered intralesionally (26 mg/kg/day, three times a week) or orally (4,3 mg/kg/day, five times a week) for eight weeks. LQB-118 was active against the L. braziliensis promastigotes and intracellular amastigotes, producing IC50 (50% inhibitory concentration) values of 3,460,1 and 7,560,8 mM, respectively. LQB-118 induced promastigote phosphatidylserine externalization accompanied by increased reactive oxygen species production and ATP depletion. Intracellular amastigote DNA fragmentation was also observed, without affecting the viability of macrophages. The treatment of L. braziliensisinfected hamsters with LQB-118, either orally or intralesionally, was effective in the control of lesion size, parasite load and increase intradermal reaction to parasite antigen. Taken together, these results show that the antileishmanial effect of LQB- 118 extends to L. braziliensis in the hamster model, involves the induction of parasite apoptosis and shows promising therapeutic option by oral or local routes in leishmaniasis

Effects of omega-3 polyunsaturated fatty acid supplementation in patients with chronic chagasic cardiomyopathy: study protocol for a randomized controlled trial

Made available in DSpace on 2015-09-21T17:25:41Z (GMT). No. of bitstreams: 2 license.txt: 1914 bytes, checksum: 7d48279ffeed55da8dfe2f8e81f3b81f (MD5) andrea_souza_etal_IOC_2013.pdf: 291802 bytes, checksum: 582ea7aebb2a6b7052e66b9340fdf0cd (MD5) Previous issue date: 2013Fundação Oswaldo Cruz. Instituto de Pesquisa Clínica Evandro Chagas. Serviço de Nutrição. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto de Pesquisa Clínica Evandro Chagas. Laboratório de Pesquisa Clínica em Doença de Chagas. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Inovações em Terapias, Ensino e Bioprodutos. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto de Pesquisa Clínica Evandro Chagas. Serviço de Nutrição. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto de Pesquisa Clínica Evandro Chagas. Serviço de Nutrição. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto de Pesquisa Clínica Evandro Chagas. Serviço de Nutrição. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto de Pesquisa Clínica Evandro Chagas. Laboratório de Pesquisa Clínica em Doença de Chagas. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto de Pesquisa Clínica Evandro Chagas. Laboratório de Pesquisa Clínica em Doença de Chagas. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Hanseníase. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto de Pesquisa Clínica Evandro Chagas. Laboratório de Pesquisa Clínica em Doença de Chagas. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto de Pesquisa Clínica Evandro Chagas. Laboratório de Pesquisa Clínica em Doença de Chagas. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto de Pesquisa Clínica Evandro Chagas. Laboratório de Pesquisa Clínica em Doença de Chagas. Rio de Janeiro, RJ, Brasil.Background: Chronic chagasic cardiomyopathy is an inflammatory disease that occurs in approximately 30% of patients infected by the protozoan Trypanosoma cruzi, and it has a profile of high morbidity and mortality. The worst prognosis and the progression of this cardiomyopathy are associated with an exacerbated immune response and the production of proinflammatory cytokines, which also occur in other cardiomyopathies. Some nutrients, including omega-3 polyunsaturated fatty acids (PUFAs), promote the inhibition and/or stimulation of cytokine production. The objective of this trial is to study the effects of omega-3 PUFA supplementation on the inflammatory response and lipid profile in patients with chronic chagasic cardiomyopathy. Methods/Design: This is a parallel, randomized, placebo-controlled, double-blind clinical trial with 40 patients that will be conducted at a reference unit for Chagas disease patients, where the patients will be selected. The study will include patients with chronic chagasic cardiomyopathy who are 18 years of age or older. The exclusion criteria are (a) ongoing diarrheal disease, (b) inflammatory bowel disease, (c) diabetes or other endocrine disease, (d) use of fibrates, niacin, or statins, (e) use of anti-inflammatory drugs, (f) pregnant and lactating women, (g) use of vitamin, mineral, or omega-3 supplementation during the previous 30 days, (h) hospital admission during the study, and (i) other associated cardiomyopathies. The intervention will be treatment with omega-3 PUFAs at a dose of 3 g/day for 8 weeks, compared to placebo (corn oil). The primary endpoints will be the concentrations of inflammatory markers (interleukin (IL)-1, IL-2, IL-4, IL-6, IL-10, tumor necrosis factor (TNF)α, interferon (IFN)γ, and transforming growth factor (TGF)β). Secondary endpoints will be the fasting glucose, lipid, and anthropometric profiles. For statistical analysis, we plan to run either a t test or Wilcoxon test (numerical variables) and Pearson’s χ2 or Fisher’s exact test (categorical data), as appropriate. Discussion: Evidence suggests that the anti-inflammatory action of omega-3 PUFAs may have beneficial effects on chronic chagasic cardiomyopathy, as shown for other cardiomyopathies, due to improved control of the inflammatory response. At the end of the study, we predict that patients will have lower inflammatory markers and an improved metabolic and anthropometric profile

Changes in the ΔΨ_m of macrophage.

<p>Peritoneal hamster macrophages (2×10⁶ cells/mL) were cultured in the presence of LQB-118 for 48 h at 37°C/5%CO₂. The cells were incubated for 10 min with JC-1 and analysed fluorometrically. Results are presented as means ± standard error; <i>n</i> = 3. *<i>P</i><0.05; **<i>P</i><0.01.</p

Activity of LQB-118 on golden hamsters infected with <i>L. braziliensis</i>.

<p>Golden hamsters (5/group) infected with <i>L. braziliensis</i> (10⁷) were treated on the seventh day of infection with LQB-118 intralesional (26 µg/kg/day) three times/week or orally (4,3 mg/kg/day) five times/week during eight weeks. Controls were untreated, treated with intralesional DMSO three times/week or Glucantime five times/week by intraperitoneal route. <b>A</b>) Lesion thickness was measured for nine weeks. The arrow indicates the start of treatment. Mean ± SD, # P<0.002 (in relation to untreated group). <b>*</b> p<0.001 (in relation to intralesional DMSO group); <b>B</b>) Intradermal reaction at <i>L. braziliensis</i> antigen was evaluated on the contralateral foot pad on eight week of infection. The swelling was measured 48 h later in the antigen-injected footpads. * p<0,04; ** p<0,01. Each point represents one animal and the horizontal bar indicates the mean. <b>C</b>) Parasite burden was assessment by limiting dilution at the end of treatment. *** p<0,001. il, intralesional/subcutaneous; ip, intraperitoneal.</p

Evaluation of LQB118 inducing apoptosis on <i>L. braziliensis</i> – A) and B) Phosphatidylserine exposure on promastigotes.

<p>Promastigotes were incubated with 3,5 or 20 µM LQB118 to 24 or 48 h/28°C and then stained with Annexin V-FITC+propidium iodide and analyzed by flow cytometer. Controls were promastigotes incubated with 60 µM Miltefosine or the culture medium supplemented with 20% fetal bovine serum. In <b>A</b> only treatment at 48 h and in <b>B</b> quantitative evaluation of cells stained with annexin V-FITC at 24 and 48 h. (mean ± SD, n = 3). * P<0.05 ** P<0.01. <b>C) ROS generation and D) impairment of ATP production in LQB-118-treated promastigotes</b>. Promastigotes of <i>L. braziliensis</i> were incubated for 48 h in the presence of LQB-118 in Schneider's insect medium plus 10% HIFCS. <b>A</b>) ROS generation was quantified using H₂DCFDA, <b>B</b>) Cellular ATP concentration was measured by bioluminescence assay. Results are presented as means ± standard error; <i>n</i> = 3. *<i>P</i><0.05; **<i>P</i><0.01. <b>E) </b><b><i>In situ</i></b><b> DNA fragmentation of intracellular amastigote</b>. Infected monolayers of hamsters peritoneal macrophages were treated with the indicated concentrations of LQB118 for 48 h. Monolayers were labeled using TUNEL and observated using fluorescence microscopy. Highlight the cells in 400× magnification. Legend Arrows indicate intracellular amastigotes, N – Macrophage nucleus.</p