Peru’s native potato revolution.

For the past half century, potato production has grown slowly in the Andean region of South America, where the potato originated and has long been a major staple food. The exception is Peru, where potato production has surged in recent years. Based on a review of official Peruvian statistics, this Innovation Brief documents trends in Peruvian potato production over the past half century, estimates production and marketing of native and improved potato varieties over the past decade, and identifies factors that have influenced these trends. The recent growth in Peru’s potato production reflects changes in both supply and demand. On the supply side, the rapid expansion of Peru’s road network, the increasing number and size of trucks, and the spread of cellphones have dramatically improved the links between highland farmers and dynamic urban markets and have reduced marketing costs. On the demand side, the image of the potato has changed from one of a “poor man’s food” to one of an under-exploited national treasure and source of pride. The Project for Potato Innovation and Competitiveness in Peru (INCOPA Project) has promoted the cultivation and use of native potatoes through public-private alliances that pursue: innovations in production and marketing, policy changes, and public awareness. This initiative appears to have stimulated demand for native and improved potatoes and it has also contributed to the supply of new production technology. Many small farmers, including those who cultivate native potatoes, have benefitted from the recent increases in potato production, sales, and farm-gate prices. The main benefits of market chain innovation and increased market demand for potatoes have accrued to early innovators characterized by higher levels of education, larger land holdings, better access to credit and input supplies and to markets for their products, and superior endowments of financial and social capital and entrepreneurial capabilities

La revolucion de la papa nativa en Peru. Resumen de innovacion 2 de Papa Andina

Durante el último medio siglo, la producción de la papa ha crecido lentamente en la región andina de América del Sur, donde tiene su centro de origen y donde constituye un alimento básico principal. La excepción es Perú, en donde la producción de papa ha crecido en los años recientes. En base a una revisión de las estadísticas peruanas oficiales, este documento muestra las tendencias en la producción de papa peruana en el último medio siglo, estima producción y comercialización de papas nativas y mejoradas en la última década, e identifica los factores que han influenciado esas tendencias. El crecimiento de la producción de papa en Perú refleja cambios tanto en la oferta como en la demanda. Por el lado de la oferta, la rápida expansión de la red de carreteras en Perú, el número creciente y tamaño de los camiones, y la diseminación de celulares, ha mejorado dramáticamente los vínculos entre los pequeños productores de la sierra rural y el mercado urbano dinámico, a la vez que ha reducido costos de comercialización. Por el lado de la demanda, la imagen de la papa ha cambiado de un “alimento para pobres” a un tesoro nacional subexplotado y un motivo de orgullo. El Proyecto para la Innovación y Competitividad de la Papa en el Perú (Proyecto INCOPA) ha promovido el cultivo y uso de papas nativas a través de alianzas público-privadas que buscan: innovaciones en la producción y la comercialización, cambios en las políticas, e incidencia pública

Local Glioma Cells Are Associated with Vascular Dysregulation

BACKGROUND AND PURPOSE: Malignant glioma is a highly infiltrative malignancy that causes variable disruptions to the structure and function of the cerebrovasculature. While many of these structural disruptions have known correlative histopathologic alterations, the mechanisms underlying vascular dysfunction identified by resting-state blood oxygen level-dependent imaging are not yet known. The purpose of this study was to characterize the alterations that correlate with a blood oxygen level-dependent biomarker of vascular dysregulation. MATERIALS AND METHODS: Thirty-two stereotactically localized biopsies were obtained from contrast-enhancing (n = 16) and nonenhancing (n = 16) regions during open surgical resection of malignant glioma in 17 patients. Preoperative resting-state blood oxygen level-dependent fMRI was used to evaluate the relationships between radiographic and histopathologic characteristics. Signal intensity for a blood oxygen level-dependent biomarker was compared with scores of tumor infiltration and microvascular proliferation as well as total cell and neuronal density. RESULTS: Biopsies corresponded to a range of blood oxygen level-dependent signals, ranging from relatively normal (z = -4.79) to markedly abnormal (z = 8.84). Total cell density was directly related to blood oxygen level-dependent signal abnormality (P = .013, R2 = 0.19), while the neuronal labeling index was inversely related to blood oxygen level-dependent signal abnormality (P = .016, R2 = 0.21). The blood oxygen level-dependent signal abnormality was also related to tumor infiltration (P = .014) and microvascular proliferation (P = .045). CONCLUSIONS: The relationship between local, neoplastic characteristics and a blood oxygen level-dependent biomarker of vascular function suggests that local effects of glioma cell infiltration contribute to vascular dysregulation

Somatic SLC35A2 variants in the brain are associated with intractable neocortical epilepsy

ObjectiveSomatic variants are a recognized cause of epilepsy-associated focal malformations of cortical development (MCD). We hypothesized that somatic variants may underlie a wider range of focal epilepsy, including nonlesional focal epilepsy (NLFE). Through genetic analysis of brain tissue, we evaluated the role of somatic variation in focal epilepsy with and without MCD.MethodsWe identified somatic variants through high-depth exome and ultra-high-depth candidate gene sequencing of DNA from epilepsy surgery specimens and leukocytes from 18 individuals with NLFE and 38 with focal MCD.ResultsWe observed somatic variants in 5 cases in SLC35A2, a gene associated with glycosylation defects and rare X-linked epileptic encephalopathies. Nonsynonymous variants in SLC35A2 were detected in resected brain, and absent from leukocytes, in 3 of 18 individuals (17%) with NLFE, 1 female and 2 males, with variant allele frequencies (VAFs) in brain-derived DNA of 2 to 14%. Pathologic evaluation revealed focal cortical dysplasia type Ia (FCD1a) in 2 of the 3 NLFE cases. In the MCD cohort, nonsynonymous variants in SCL35A2 were detected in the brains of 2 males with intractable epilepsy, developmental delay, and magnetic resonance imaging suggesting FCD, with VAFs of 19 to 53%; Evidence for FCD was not observed in either brain tissue specimen.InterpretationWe report somatic variants in SLC35A2 as an explanation for a substantial fraction of NLFE, a largely unexplained condition, as well as focal MCD, previously shown to result from somatic mutation but until now only in PI3K-AKT-mTOR pathway genes. Collectively, our findings suggest a larger role than previously recognized for glycosylation defects in the intractable epilepsies. Ann Neurol 2018

Somatic SLC35A2

ObjectiveSomatic variants are a recognized cause of epilepsy-associated focal malformations of cortical development (MCD). We hypothesized that somatic variants may underlie a wider range of focal epilepsy, including nonlesional focal epilepsy (NLFE). Through genetic analysis of brain tissue, we evaluated the role of somatic variation in focal epilepsy with and without MCD.MethodsWe identified somatic variants through high-depth exome and ultra-high-depth candidate gene sequencing of DNA from epilepsy surgery specimens and leukocytes from 18 individuals with NLFE and 38 with focal MCD.ResultsWe observed somatic variants in 5 cases in SLC35A2, a gene associated with glycosylation defects and rare X-linked epileptic encephalopathies. Nonsynonymous variants in SLC35A2 were detected in resected brain, and absent from leukocytes, in 3 of 18 individuals (17%) with NLFE, 1 female and 2 males, with variant allele frequencies (VAFs) in brain-derived DNA of 2 to 14%. Pathologic evaluation revealed focal cortical dysplasia type Ia (FCD1a) in 2 of the 3 NLFE cases. In the MCD cohort, nonsynonymous variants in SCL35A2 were detected in the brains of 2 males with intractable epilepsy, developmental delay, and magnetic resonance imaging suggesting FCD, with VAFs of 19 to 53%; Evidence for FCD was not observed in either brain tissue specimen.InterpretationWe report somatic variants in SLC35A2 as an explanation for a substantial fraction of NLFE, a largely unexplained condition, as well as focal MCD, previously shown to result from somatic mutation but until now only in PI3K-AKT-mTOR pathway genes. Collectively, our findings suggest a larger role than previously recognized for glycosylation defects in the intractable epilepsies. Ann Neurol 2018