CGIAR modeling approaches for resource-constrained scenarios: I. Accelerating crop breeding for a changing climate.

Crop improvement efforts aiming at increasing crop production (quantity, quality) and adapting to climate change have been subject of active research over the past years. But, the question remains 'to what extent can breeding gains be achieved under a changing climate, at a pace sufficient to usefully contribute to climate adaptation, mitigation and food security?'. Here, we address this question by critically reviewing how model-based approaches can be used to assist breeding activities, with particular focus on all CGIAR (formerly the Consultative Group on International Agricultural Research but now known simply as CGIAR) breeding programs. Crop modeling can underpin breeding efforts in many different ways, including assessing genotypic adaptability and stability, characterizing and identifying target breeding environments, identifying tradeoffs among traits for such environments, and making predictions of the likely breeding value of the genotypes. Crop modeling science within the CGIAR has contributed to all of these. However, much progress remains to be done if modeling is to effectively contribute to more targeted and impactful breeding programs under changing climates. In a period in which CGIAR breeding programs are undergoing a major modernization process, crop modelers will need to be part of crop improvement teams, with a common understanding of breeding pipelines and model capabilities and limitations, and common data standards and protocols, to ensure they follow and deliver according to clearly defined breeding products. This will, in turn, enable more rapid and better-targeted crop modeling activities, thus directly contributing to accelerated and more impactful breeding efforts.Online Version of Record before inclusion in an issue

Vitrectomy with complete posterior hyaloid removal for ischemic central retinal vein occlusion: Series of cases

BACKGROUND: Central retinal vein occlusion (CRVO) is a common retinal vascular disorder with potentially complications: (1) persistent macular edema and (2) neovascular glaucoma. No safe treatment exists that promotes the return of lost vision. Eyes with CRVO may be predisposed to vitreous degeneration. It has been suggested that if the vitreous remains attached to the macula owing to a firm vitreomacular adhesion, the resultant vitreous traction can cause inflammation with retinal capillary dilation, leakage and subsequent edema6. The roll of vitrectomy in ischemic CRVO surgical procedures has not been evaluated. CASE PRESENTATION: This is a non comparative, prospective, longitudinal, experimental and descriptive series of cases. Ten eyes with ischemic CRVO. Vitrectomy with complete posterior hyaloid removal was performed. VA, rubeosis, intraocular pressure (IOP), and macular edema were evaluated clinically. Multifocal ERG (m-ERG), fluorescein angiography (FAG) and optic coherence tomography (OCT) were performed. Follow-up was at least 6 months. Moderate improvement of visual acuity was observed in 60% eyes and stabilized in 40%. IOP changed from 15.7 ± 3.05 mmHg to 14.9 ± 2.69 mmHg post-operative and macular edema from 976 ± 196 μm to 640 ± 191 μm to six month. The P1 wave amplitude changed from 25.46 ± 12.4 mV to 20.54 ± 11.2 mV. CONCLUSION: A solo PPV with posterior hyaloid removal may help to improve anatomic and functional retina conditions in some cases. These results should be considered when analyzing other surgical maneuvers

Estratigrafía revisada de estratos neógenos en la cuenca de Cocinetas, La Guajira, Colombia

The Cocinetas Basin of Colombia provides a valuable window into the geological and paleontological history of northern South America during the Neogene. Two major findings provide new insights into the Neogene history of this Cocinetas Basin: (1) a formal re-description of the Jimol and Castilletes formations, including a revised contact; and (2) the description of a new lithostratigraphic unit, the Ware Formation (Late Pliocene). We conducted extensive fieldwork to develop a basin-scale stratigraphy, made exhaustive paleontological collections, and performed 87Sr/86Sr geochronology to document the transition from the fully marine environment of the Jimol Formation (ca. 17.9–16.7 Ma) to the fluvio-deltaic environment of the Castilletes (ca. 16.7–14.2 Ma) and Ware (ca. 3.5–2.8 Ma) formations. We also describe evidence for short-term periodic changes in depositional environments in the Jimol and Castilletes formations. The marine invertebrate fauna of the Jimol and Castilletes formations are among the richest yet recorded from Colombia during the Neogene. The Castilletes and Ware formations have also yielded diverse and biogeographically significant fossil vertebrate assemblages. The revised lithostratigraphy and chronostratigraphy presented here provides the necessary background information to explore the complete evolutionary and biogeographic significance of the excellent fossil record of the Cocinetas Basin

Revised stratigraphy of Neogene strata in the Cocinetas Basin, La Guajira, Colombia

The Cocinetas Basin of Colombia provides a valuable window into the geological and paleontological history of northern South America during the Neogene. Two major findings provide new insights into the Neogene history of this Cocinetas Basin: (1) a formal re-description of the Jimol and Castilletes formations, including a revised contact; and (2) the description of a new lithostratigraphic unit, the Ware Formation (Late Pliocene). We conducted extensive fieldwork to develop a basin-scale stratigraphy, made exhaustive paleontological collections, and performed 87Sr/86Sr geochronology to document the transition from the fully marine environment of the Jimol Formation (ca. 17.9?16.7 Ma) to the fluvio-deltaic environment of the Castilletes (ca. 16.7?14.2 Ma) and Ware (ca. 3.5?2.8 Ma) formations. We also describe evidence for short-term periodic changes in depositional environments in the Jimol and Castilletes formations. The marine invertebrate fauna of the Jimol and Castilletes formations are among the richest yet recorded from Colombia during the Neogene. The Castilletes and Ware formations have also yielded diverse and biogeographically significant fossil vertebrate assemblages. The revised lithostratigraphy and chronostratigraphy presented here provides the necessary background information to explore the complete evolutionary and biogeographic significance of the excellent fossil record of the Cocinetas Basin.Fil: Moreno, F.. Smithsonian Tropical Research Institute; Estados Unidos. Corporación Geológica ARES; Colombia. University of Rochester; Estados UnidosFil: Hendy, A. J. W.. Natural History Museum of Los Angeles County; Estados Unidos. Florida Museum of Natural History; Estados UnidosFil: Quiroz, L.. Smithsonian Tropical Research Institute; Estados Unidos. University of Saskatchewan; CanadáFil: Hoyos, N.. Smithsonian Tropical Research Institute; Estados Unidos. Corporación Geológica ARES; Colombia. Universidad del Norte; ColombiaFil: Jones, D. S.. Florida Museum of Natural History; Estados UnidosFil: Zapata, V.. Smithsonian Tropical Research Institute; Estados Unidos. Ecopetrol S.A.; ColombiaFil: Zapata, S.. Smithsonian Tropical Research Institute; Estados UnidosFil: Ballen, G. A.. Smithsonian Tropical Research Institute; Estados UnidosFil: Cadena, E.. Smithsonian Tropical Research Institute; Estados Unidos. Senckenberg Museum; AlemaniaFil: Cárdenas, A. L.. Smithsonian Tropical Research Institute; Estados Unidos. Corporación Geológica ARES; Colombia. Universidad del Norte; ColombiaFil: Carrillo Briceño, J. D.. Smithsonian Tropical Research Institute; Estados Unidos. Universitat Zurich; SuizaFil: Carrillo, J. D.. Smithsonian Tropical Research Institute; Estados Unidos. Universitat Zurich; SuizaFil: Delgado Sierra, D.. Universidad Eafit; ColombiaFil: Escobar, J.. Smithsonian Tropical Research Institute; Estados Unidos. Universidad del Norte; ColombiaFil: Martínez, J. I.. Universidad Eafit; ColombiaFil: Martínez, C.. Smithsonian Tropical Research Institute; Estados Unidos. Cornell University; Estados UnidosFil: Montes, C.. Universidad de los Andes; ColombiaFil: Moreno, J.. Smithsonian Tropical Research Institute; Estados Unidos. Universidad de Nebraska - Lincoln; Estados UnidosFil: Pérez, N.. Smithsonian Tropical Research Institute; Estados Unidos. Universidad de los Andes; ColombiaFil: Sánchez, R.. Smithsonian Tropical Research Institute; Estados UnidosFil: Suarez Gomez, Sandra Catalina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Smithsonian Tropical Research Institute; Estados Unidos. Universidad Nacional de La Plata. Facultad de Ciencias Naturales y Museo; ArgentinaFil: Vallejo Pareja, M. C.. Smithsonian Tropical Research Institute; Estados UnidosFil: Jaramillo, Carlos. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Smithsonian Tropical Research Institute; Estados Unido

Mouse hepatic oval cells require Met-dependent PI3K to impair TGF-β-Induced oxidative stress and apoptosis.

We have previously shown that oval cells harboring a genetically inactivated Met tyrosine kinase (Met−/− oval cells) are more sensitive to TGF-β-induced apoptosis than cells expressing a functional Met (Metflx/flx), demonstrating that the HGF/Met axis plays a pivotal role in oval cell survival. Here, we have examined the mechanism behind this effect and have found that TGF-β induced a mitochondria-dependent apoptotic cell death in Metflx/flx and Met−/− oval cells, associated with a marked increase in levels of the BH3-only proteins Bim and Bmf. Bmf plays a key role during TGF-β-mediated apoptosis since knocking down of BMF significantly diminished the apoptotic response in Met-/- oval cells. TGF-β also induced oxidative stress accompanied by NADPH oxidase 4 (Nox4) mRNA up-regulation and decreased protein levels of antioxidant enzymes. Antioxidants inhibit both TGF-β-induced caspase 3 activity and Bmf up-regulation, revealing an oxidative stress-dependent Bmf regulation by TGF-β. Notably, oxidative stress-related events were strongly amplified in Met−/− oval cells, emphasizing the critical role of Met in promoting survival. Pharmacological inhibition of PI3K did impair HGF-driven protection from TGF-β-induced apoptosis and increased sensitivity of Metflx/flx oval cells to TGF-ß by enhancing oxidative stress, reaching apoptotic indices similar to those obtained in Met−/− oval cells. Interestingly, both PI3K inhibition and/or knockdown itself resulted in caspase-3 activation and loss of viability in Metflx/flx oval cells, whereas no effect was observed in Met−/− oval cells. Altogether, results presented here provide solid evidences that both paracrine and autocrine HGF/Met signaling requires PI3K to promote mouse hepatic oval cell survival against TGF-β-induced oxidative stress and apoptosis

Mouse hepatic oval cells require Met-dependent PI3K to impair TGF-β-Induced oxidative stress and apoptosis.

We have previously shown that oval cells harboring a genetically inactivated Met tyrosine kinase (Met−/− oval cells) are more sensitive to TGF-β-induced apoptosis than cells expressing a functional Met (Metflx/flx), demonstrating that the HGF/Met axis plays a pivotal role in oval cell survival. Here, we have examined the mechanism behind this effect and have found that TGF-β induced a mitochondria-dependent apoptotic cell death in Metflx/flx and Met−/− oval cells, associated with a marked increase in levels of the BH3-only proteins Bim and Bmf. Bmf plays a key role during TGF-β-mediated apoptosis since knocking down of BMF significantly diminished the apoptotic response in Met-/- oval cells. TGF-β also induced oxidative stress accompanied by NADPH oxidase 4 (Nox4) mRNA up-regulation and decreased protein levels of antioxidant enzymes. Antioxidants inhibit both TGF-β-induced caspase 3 activity and Bmf up-regulation, revealing an oxidative stress-dependent Bmf regulation by TGF-β. Notably, oxidative stress-related events were strongly amplified in Met−/− oval cells, emphasizing the critical role of Met in promoting survival. Pharmacological inhibition of PI3K did impair HGF-driven protection from TGF-β-induced apoptosis and increased sensitivity of Metflx/flx oval cells to TGF-ß by enhancing oxidative stress, reaching apoptotic indices similar to those obtained in Met−/− oval cells. Interestingly, both PI3K inhibition and/or knockdown itself resulted in caspase-3 activation and loss of viability in Metflx/flx oval cells, whereas no effect was observed in Met−/− oval cells. Altogether, results presented here provide solid evidences that both paracrine and autocrine HGF/Met signaling requires PI3K to promote mouse hepatic oval cell survival against TGF-β-induced oxidative stress and apoptosis