Economics of Management Zone Delineation in Cotton Precision Agriculture

This paper develops a management zone delineation procedure based on a spatial clustering approach and evaluates its economic impact for the case of Texas cotton production. The results show that there is potential economic value in using a spatial approach to management zone delineation, but its value critically depends on the cost of collecting soil test information needed to delineate those zones.Management Zones, Exploratory Spatial Data Analysis, Site-Specific Nitrogen Management, Cotton Precision Agriculture, Crop Production/Industries, Q12,

Economics of Management Zone Delineation in Cotton Precision Agriculture

This paper develops a management zone delineation procedure based on a spatial statistics approach and evaluates its economic impact for the case of Texas cotton production. With the use of an optimization model that utilizes a yield response function estimated through spatial econometric methods, we found that applying variable N rates based on the management zones delineated would result in higher cotton yields and higher net returns, above Nitrogen cost, relative to uniformly applying a single N rate for the whole field. In addition, a variable rate N application using the delineated management zones produced higher net returns, above Nitrogen cost, relative to a variable N rate system where the zones are based solely on landscape position. This is indicative of the potential economic value of using a spatial statistics approach to management zone delineation.Management Zones, Exploratory Spatial Data Analysis, Site-Specific Nitrogen Management, Cotton Precision Agriculture., Crop Production/Industries, Q1, Q16,

Un análisis económico de la aproximación estadística para el establecimiento de zonas de manejo en agricultura de precisión: caso de algodón en Texas

Este artículo desarrolla un proceso para el establecimiento de zonas de manejo basado en una aproximación estadística espacial y evalúa su impacto económico para el caso de producción de algodón en Texas. Con el uso de un modelo de optimización que utiliza funciones de producción estimadas tomando en cuenta la autocorrelación espacial mediante métodos de econometría espacial, se encontró que al aplicar nitrógeno a una tasa variable, basada en las zonas de manejo delineadas, se obtienen rendimientos de algodón más altos comparados con los rendimientos obtenidos al aplicar una tasa uniforme de nitrógeno sobre toda la unidad productiva. Así mismo, se encontró que las aplicaciones de N a una tasa variable generan ingresos netos superiores comparados con los ingresos netos generados por la aplicación uniforme de N a la tasa agronómica sugerida, y retornos inferiores comparados con la aplicación uniforme derivada del óptimo económico. Adicionalmente, se encontró que niveles promedios de nitrógeno más bajos son requeridos con las aplicaciones de nitrógeno a una tasa variable para alcanzar rendimientos más altos comparados con la aplicación uniforme de nitrógeno.Zonas de manejo, análisis espacial exploratorio de datos, manejo espacial específico de nitrógeno, agricultura de precisión con aplicaciones en algodón.

Modifier loci condition autoimmunity provoked by Aire deficiency

Loss of function mutations in the autoimmune regulator (Aire) gene in autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy patients and mutant mice lead to autoimmune manifestations that segregate as a monogenic trait, but with wide variation in the spectrum of organs targeted. To investigate the cause of this variability, the Aire knockout mutation was backcrossed to mice of diverse genetic backgrounds. The background loci strongly influenced the pattern of organs that were targeted (stomach, eye, pancreas, liver, ovary, thyroid, and salivary gland) and the severity of the targeting (particularly strong on the nonobese diabetic background, but very mild on the C57BL/6 background). Autoantibodies mimicked the disease pattern, with oligoclonal reactivity to a few antigens that varied between Aire-deficient strains. Congenic analysis and a whole genome scan showed that autoimmunity to each organ had a distinctive pattern of genetic control and identified several regions that controlled the pattern of targeting, including the major histocompatibility complex and regions of Chr1 and Chr3 previously identified in controlling type 1 diabetes

Tumor Induction and Tissue Atrophy in Mice Lacking E2F-1

AbstractThe retinoblastoma tumor suppressor protein (pRB) is a transcriptional repressor that regulates gene expression by physically associating with transcription factors such as E2F family members. Although pRB and its upstream regulators are commonly mutated in human cancer, the physiological role of the pRB–E2F pathway is unknown. To address the function of E2F-1 and pRB/E2F-1 complexes in vivo, we have produced mice homozygous for a nonfunctional E2F-1 allele. Mice lacking E2F-1 are viable and fertile, yet experience testicular atrophy and exocrine gland dysplasia. Surprisingly, mice lacking E2F-1 develop a broad and unusual spectrum of tumors. Although overexpression of E2F-1 in tissue culture cells can stimulate cell proliferation and be oncogenic, loss of E2F-1 in mice results in tumorigenesis, demonstrating that E2F-1 also functions as a tumor suppressor

Distinct Malignant Behaviors of Mouse Myogenic Tumors Induced by Different Oncogenetic Lesions

Rhabdomyosarcomas (RMS) are heterogeneous cancers with myogenic differentiation features. The cytogenetic and mutational aberrations in RMS are diverse. This study examined differences in the malignant behavior of two genetically distinct and disease-relevant mouse myogenic tumor models. Kras; p1619null myogenic tumors, initiated by expression of oncogenic Kras in p16p19null mouse satellite cells, were metastatic to the lungs of the majority of tumor-bearing animals and repopulated tumors in seven of nine secondary recipients. In contrast, SmoM2 tumors, initiated by ubiquitous expression of a mutant Smoothened allele, did not metastasize and repopulated tumors in 2 of 18 recipients only. In summary, genetically distinct myogenic tumors in mice exhibit marked differences in malignant behavior

Targeted disruption of ATM leads to growth retardation, chromosomal fragmentation during meiosis, immune defects, and thymic lymphoma

ATM, the gene mutated in the inherited human disease ataxia-telangiectasia, is a member of a family of kinases involved in DNA metabolism and cell-cycle checkpoint control. To help clarify the physiological roles of the ATM protein, we disrupted the ATM gene in mice through homologous recombination. Initial evaluation of the ATM knockout animals indicates that inactivation of the mouse ATM gene recreates much of the phenotype of ataxia-telangiectasia. The homozygous mutant (ATM-/-) mice are viable, growth-retarded, and infertile. The infertility of ATM-/- mice results from meiotic failure. Meiosis is arrested at the zygotene/pachytene stage of prophase I as a result of abnormal chromosomal synapsis and subsequent chromosome fragmentation. Immune defects also are evident in ATM-/- mice, including reduced numbers of B220+CD43- pre-B cells, thymocytes, and peripheral T cells, as well as functional impairment of T-cell-dependent immune responses. The cerebella of ATM-/- mice appear normal by histologic examination at 3 to 4 months and the mice have no gross behavioral abnormalities. The majority of mutant mice rapidly develop thymic lymphomas and die before 4 months of age. These findings indicate that the ATM gene product plays an essential role in a diverse group of cellular processes, including meiosis, the normal growth of somatic tissues, immune development, and tumor suppression

The fibrinolytic system facilitates tumor cell migration across the blood-brain barrier in experimental melanoma brain metastasis

BACKGROUND: Patients with metastatic tumors to the brain have a very poor prognosis. Increased metastatic potential has been associated with the fibrinolytic system. We investigated the role of the fibrinolytic enzyme plasmin in tumor cell migration across brain endothelial cells and growth of brain metastases in an experimental metastatic melanoma model. METHODS: Metastatic tumors to the brain were established by direct injection into the striatum or by intracarotid injection of B16F10 mouse melanoma cells in C57Bl mice. The role of plasminogen in the ability of human melanoma cells to cross a human blood-brain barrier model was studied on a transwell system. RESULTS: Wild type mice treated with the plasmin inhibitor epsilon-aminocaproic acid (EACA) and plg(-/- )mice developed smaller tumors and survived longer than untreated wild type mice. Tumors metastasized to the brain of wild type mice treated with EACA and plg(-/- )less efficiently than in untreated wild type mice. No difference was observed in the tumor growth in any of the three groups of mice. Human melanoma cells were able to cross the human blood-brain barrier model in a plasmin dependent manner. CONCLUSION: Plasmin facilitates the development of tumor metastasis to the brain. Inhibition of the fibrinolytic system could be considered as means to prevent tumor metastasis to the brain

The Oncogenic Lung Cancer Fusion Kinase CD74-ROS Activates a Novel Invasiveness Pathway through E-Syt1 Phosphorylation

Patients with lung cancer often present with metastatic disease and therefore have a very poor prognosis. The recent discovery of several novel ROS receptor tyrosine kinase molecular alterations in non–small cell lung cancer (NSCLC) presents a therapeutic opportunity for the development of new targeted treatment strategies. Here, we report that the NSCLC-derived fusion CD74-ROS, which accounts for 30% of all ROS fusion kinases in NSCLC, is an active and oncogenic tyrosine kinase. We found that CD74-ROS–expressing cells were highly invasive in vitro and metastatic in vivo. Pharmacologic inhibition of CD74-ROS kinase activity reversed its transforming capacity by attenuating downstream signaling networks. Using quantitative phosphoproteomics, we uncovered a mechanism by which CD74-ROS activates a novel pathway driving cell invasion. Expression of CD74-ROS resulted in the phosphorylation of the extended synaptotagmin-like protein E-Syt1. Elimination of E-Syt1 expression drastically reduced invasiveness both in vitro and in vivo without modifying the oncogenic activity of CD74-ROS. Furthermore, expression of CD74-ROS in noninvasive NSCLC cell lines readily conferred invasive properties that paralleled the acquisition of E-Syt1 phosphorylation. Taken together, our findings indicate that E-Syt1 is a mediator of cancer cell invasion and molecularly define ROS fusion kinases as therapeutic targets in the treatment of NSCLC.National Institutes of Health (U.S.) (Grant NCI U01 CA141556