1,222 research outputs found

    Updated guidelines for gene nomenclature in wheat

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    The last decade has seen a proliferation in genomic resources for wheat, including reference- and pan-genome assemblies with gene annotations, which provide new opportunities to detect, characterise, and describe genes that influence traits of interest. The expansion of genetic information has supported growth of the wheat research community and catalysed strong interest in the genes that control agronomically important traits, such as yield, pathogen resistance, grain quality, and abiotic stress tolerance. To accommodate these developments, we present an updated set of guidelines for gene nomenclature in wheat. These guidelines can be used to describe loci identified based on morphological or phenotypic features or to name genes based on sequence information, such as similarity to genes characterised in other species or the biochemical properties of the encoded protein. The updated guidelines provide a flexible system that is not overly prescriptive but provides structure and a common framework for naming genes in wheat, which may be extended to related cereal species. We propose these guidelines be used henceforth by the wheat research community to facilitate integration of data from independent studies and allow broader and more efficient use of text and data mining approaches, which will ultimately help further accelerate wheat research and breeding.EEA PergaminoFil: Boden, S. A. University of Adelaide. Waite Research Institute. School of Agriculture, Food and Wine; AustraliaFil: McIntosh, R .A. University of Sydney. School of Life and Environmental Sciences. Plant Breeding Institute; AustraliaFil: Uauy, C. Norwich Research Park. John Innes Centre; Reino UnidoFil: Krattinger, S. G. King Abdullah University of Science and Technology. Biological and Environmental Science and Engineering Division. Plant Science Program; Arabia SauditaFil: Krattinger, S. G. The Wheat Initiative; AlemaniaFil: Dubcovsky, J. University of California. Department of Plant Science; Estados UnidosFil: Dubcovsky, J. The Wheat Initiative; AlemaniaFil: Rogers, W.J. Universidad Nacional del Centro de La Provincia de Buenos Aires. Facultad de Agronomía (CIISAS, CIC-BIOLAB AZUL, CONICET-INBIOTEC, CRESCA). Departamento de Biología Aplicada; ArgentinaFil: Rogers, W.J. The Wheat Initiative; AlemaniaFIL: Xia, X. C. Chinese Academy of Agricultural Sciences. National Wheat Improvement Centre. Institute of Crop Science; ChinaFil: Badaeva, E. D. Russian Academy of Sciences. N.I. Vavilov Institute of General Genetics; RusiaFil: Bentley, A. R. International Maize and Wheat Improvement Center (CIMMYT); MéxicoFil: Bentley, A. R. The Wheat Initiative; AlemaniaFil: Brown-Guedira, G. North Carolina State University. USDA-ARS Plant Science Research; Estados UnidosFil: Brown-Guedira, G. The Wheat Initiative; AlemaniaFil: González, Fernanda G. Instituto Nacional de Tecnología Agropecuaria (INTA). Estación Experimental Agropecuaria Pergamino. Sección Ecofisiología; ArgentinaFil: González, Fernanda G. Centro de Investigaciones y Transferencia del Noroeste de la Provincia de Buenos Aires (CITNOBA, CONICET-UNNOBA-UNSADA); ArgentinaFil: González, Fernanda G. The Wheat Initiative; AlemaniaFil: Zhang, Y. Fudan University. School of Life Sciences. Institute of Plant Biology. Collaborative Innovation Center of Genetics and Development. State Key Laboratory of Genetic Engineering; Chin

    Desialilación plaquetaria e influencia de los autoanticuerpos en la trombocitopenia del lupus eritematoso sistémico

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    En estudios previos demostramos que la apoptosis y activación plaquetaria junto con la inhibición en la formación de proplaquetas (FPP) contribuyen a la trombocitopenia en el lupus eritematoso sistémico (LES). En el presente estudio evaluamos la pérdida de ácido siálico inducida por plasma de LES como un posible mecanismo adicional que favorece la eliminación periférica de plaquetas en esta entidad y la participación de los autoanticuerpos anti-plaquetarios en la inhibición de la FPP. Se obtuvieron muestras de plasma de 25 pacientes LES sin (PNT) y con trombocitopenia (PT) y 25 controles (C) y muestras de plaquetas normales por centrifugación diferencial. Las plaquetas normales se incubaron con plasmas LES o controles y se evaluó la desialinización de glicoproteínas plaquetarias por citometría de flujo a través de la unión de RCA (Ricinus communis agglutinin I) y PNA (peanut agglutinin), lectinas con afinidad por galactosa que queda expuesta tras la pérdida de ácido siálico. Los plasmas de LES indujeron la desialilación de las plaquetas (p<0.01, test t) siendo mayor el efecto observado en presencia de plasmas PT. Para evaluar el efecto de los autoanticuerpos anti-plaquetarios en la inhibición de la FPP, se seleccionaron 3 plasmas LES que previamente demostraron un marcado efecto inhibitorio sobre la trombopoyesis y se incubaron con plaquetas normales para inducir la unión de los autoanticuerpos presentes en los plasmas de LES a sus blancos antigénicos en plaquetas normales. Luego se separaron las plaquetas para obtener el plasma libre de autoanticuerpos (inmunodepletado). Posteriormente, se cultivaron progenitores hematopoyéticos CD34+ obtenidos de sangre de cordón umbilical normal en medio libre de plasma, hasta obtener megacariocitos maduros. Al día 12 de cultivo se les adicionó en pocillos independientes 10% de plasma LES o el mismo plasma inmunodepletado y se evaluó la trombopoyesis al día 15, observándose reversión de la inhibición en presencia de los plasmas inmunodepletados, lo que demuestra el rol fundamental de los autoanticuerpos en este proceso.Considerando en conjunto tanto las alteraciones descriptas anteriormente (apoptosis y activación plaquetaria, inhibición de trombopoyesis) como la desialilación, estas anormalidades fueron más frecuentes en pacientes con PT que en PNT y dentro de los PT, en aquellos con mayor actividad de la enfermedad (SLEDAI) (Fisher exact test, **p<0.01).Nuestros resultados sugieren que los mecanismos de trombocitopenia son variados y pueden ser concomitantes en un mismo paciente, y que la incidencia de los mismos está asociada con mayor severidad de la enfermedad.Fil: Baroni Pietto, Maria Constanza. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaFil: Lev, Paola Roxana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaFil: Glembotsky, Ana Claudia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaFil: Collado, V.. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaFil: Pisoni, C.. Centro de Educaciones Médicas e Investigación Clínica "Norberto Quirno"; ArgentinaFil: Gonzalez, J.. Gobierno de la Ciudad Autónoma de Buenos Aires. Hospital General de Agudos Carlos Durand; ArgentinaFil: Gomez, R.. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; ArgentinaFil: Gomez, G.. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaFil: Heller, Paula Graciela. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaFil: Goette, Nora Paula. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaFil: Marta, Rosana Fernanda. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaXIV Congreso Argentino de Hemostasia y Trombosis y V Curso Educacional de la ISTHbuenos airesArgentinaSociedad Argentina de Hemostasia y Trombosi

    SMAD3 rs17228212 Gene Polymorphism Is Associated with Reduced Risk to Cerebrovascular Accidents and Subclinical Atherosclerosis in Anti-CCP Negative Spanish Rheumatoid Arthritis Patients

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    Rheumatoid arthritis (RA) is a complex polygenic inflammatory disease associated with accelerated atherosclerosis and increased risk of cardiovascular (CV) disease. Previous genome-wide association studies have described SMAD3 rs17228212 polymorphism as an important signal associated with CV events. The aim of the present study was to evaluate for the first time the relationship between this gene polymorphism and the susceptibility to CV manifestations and its potential association with the presence of subclinical atherosclerosis assessed by the evaluation of carotid intima-media thickness (cIMT) in patients with RA

    [(18)F]FDG-PET/CT metabolic parameters as useful prognostic factors in cervical cancer patients treated with chemo-radiotherapy.

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    To compare the prognostic value of different anatomical and functional metabolic parameters determined using [(18)F]FDG-PET/CT with other clinical and pathological prognostic parameters in cervical cancer (CC). Thirty-eight patients treated with standard curative doses of chemo-radiotherapy (CRT) underwent pre- and post-therapy [(18)F]FDG-PET/CT. [(18)F]FDG-PET/CT parameters including mean tumor standardized uptake values (SUV), metabolic tumor volume (MTV) and tumor glycolytic volume (TGV) were measured before the start of CRT. The post-treatment tumor metabolic response was evaluated. These parameters were compared to other clinical prognostic factors. Survival curves were estimated by using the Kaplan-Meier method. Cox regression analysis was performed to determine the independent contribution of each prognostic factor. After 37 months of median follow-up (range, 12-106), overall survival (OS) was 71 % [95 % confidence interval (CI), 54-88], disease-free survival (DFS) 61 % [95 % CI, 44-78] and loco-regional control (LRC) 76 % [95 % CI, 62-90]. In univariate analyses the [(18)F]FDG-PET/CT parameters unfavorably influencing OS, DFS and LRC were pre-treatment TGV-cutoff ≥562 (37 vs. 76 %, p = 0.01; 33 vs. 70 %, p = 0.002; and 55 vs. 83 %, p = 0.005, respectively), mean pre-treatment tumor SUV cutoff ≥5 (57 vs. 86 %, p = 0.03; 36 vs. 88 %, p = 0.004; 65 vs. 88 %, p = 0.04, respectively) and a partial tumor metabolic response after treatment (9 vs. 29 %, p = 0.0008; 0 vs. 83 %, p &lt; 0.0001; 22 vs. 96 %, p &lt; 0.0001, respectively). After multivariate analyses a partial tumor metabolic response after treatment remained as an independent prognostic factor unfavorably influencing DFS and LRC (RR 1:7.7, p &lt; 0.0001, and RR 1:22.6, p = 0.0003, respectively) while the pre-treatment TGV-cutoff ≥562 negatively influenced OS and DFS (RR 1:2, p = 0.03, and RR 1:2.75, p = 0.05). Parameters capturing the pre-treatment glycolytic volume and metabolic activity of [(18)F]FDG-positive disease provide important prognostic information in patients with CC treated with CRT. The post-therapy [(18)F]FDG-PET/CT uptake (partial tumor metabolic response) is predictive of disease outcome

    Duffy Negative Antigen Is No Longer a Barrier to Plasmodium vivax – Molecular Evidences from the African West Coast (Angola and Equatorial Guinea)

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    Recent reports of Plasmodium vivax infections, the most widely distributed species of human malaria, show that this parasite is evolving and adapting, becoming not only more aggressive but also more frequent in countries where it was not present in the past, becoming, therefore, a major source of concern. Thus, it is extremely important to perform new studies of its distribution in West and Central Africa, where there are few reports of its presence, due to the high prevalence of Duffy-negative individuals. The aim of this study was to investigate the presence of P. vivax in Angola and in Equatorial Guinea, using blood samples and mosquitoes. The results showed that P. vivax seems to be able to invade erythrocytes using receptors other than Duffy, and this new capacity is not exclusive to one strain of P. vivax, since we have found samples infected with two different strains: VK247 and classic. Additionally we demonstrated that the parasite has a greater distribution than previously thought, calling for a reevaluation of its worldwide distribution

    HOXA1 is overexpressed in oral squamous cell carcinomas and its expression is correlated with poor prognosis

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    <p>Abstract</p> <p>Background</p> <p>HOX genes encode homeodomain-containing transcription factors involved in the regulation of cellular proliferation and differentiation during embryogenesis. However, members of this family demonstrated oncogenic properties in some malignancies. The present study investigated whether genes of the HOXA cluster play a role in oral cancer.</p> <p>Methods</p> <p>In order to identify differentially expressed HOXA genes, duplex RT-PCR in oral samples from healthy mucosa and squamous cell carcinoma was used. The effects of HOXA1 on proliferation, apoptosis, adhesion, invasion, epithelial-mesenchymal transition (EMT) and anchorage-independent growth were assessed in cells with up- and down-regulation of HOXA1. Immunohistochemical analysis using a tissue microarray (TMA) containing 127 oral squamous cell carcinomas (OSCC) was performed to determine the prognostic role of HOXA1 expression.</p> <p>Results</p> <p>We showed that transcripts of HOXA genes are more abundant in OSCC than in healthy oral mucosa. In particular, HOXA1, which has been described as one of the HOX members that plays an important role in tumorigenesis, was significantly more expressed in OSCCs compared to healthy oral mucosas. Further analysis demonstrated that overexpression of HOXA1 in HaCAT human epithelial cells promotes proliferation, whereas downregulation of HOXA1 in human OSCC cells (SCC9 cells) decreases it. Enforced HOXA1 expression in HaCAT cells was not capable of modulating other events related to tumorigenesis, including apoptosis, adhesion, invasion, EMT and anchorage-independent growth. A high number of HOXA1-positive cells was significantly associated with T stage, N stage, tumor differentiation and proliferative potential of the tumors, and was predictive of poor survival. In multivariate analysis, HOXA1 was an independent prognostic factor for OSCC patients (HR: 2.68; 95% CI: 1.59-2.97; p = 0.026).</p> <p>Conclusion</p> <p>Our findings indicate that HOXA1 may contribute to oral carcinogenesis by increasing tumor cell proliferation, and suggest that HOXA1 expression might be helpful as a prognostic marker for patients with OSCC.</p

    The impact of SARS-CoV-2 in dementia across Latin America : A call for an urgent regional plan and coordinated response

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    The SARS-CoV-2 global pandemic will disproportionately impact countries with weak economies and vulnerable populations including people with dementia. Latin American and Caribbean countries (LACs) are burdened with unstable economic development, fragile health systems, massive economic disparities, and a high prevalence of dementia. Here, we underscore the selective impact of SARS-CoV-2 on dementia among LACs, the specific strain on health systems devoted to dementia, and the subsequent effect of increasing inequalities among those with dementia in the region. Implementation of best practices for mitigation and containment faces particularly steep challenges in LACs. Based upon our consideration of these issues, we urgently call for a coordinated action plan, including the development of inexpensive mass testing and multilevel regional coordination for dementia care and related actions. Brain health diplomacy should lead to a shared and escalated response across the region, coordinating leadership, and triangulation between governments and international multilateral networks

    Development and validation of a simple questionnaire for the identification of hereditary breast cancer in primary care

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    <p>Abstract</p> <p>Background</p> <p>Breast cancer is a significant public health problem worldwide and the development of tools to identify individuals at-risk for hereditary breast cancer syndromes, where specific interventions can be proposed to reduce risk, has become increasingly relevant. A previous study in Southern Brazil has shown that a family history suggestive of these syndromes may be prevalent at the primary care level. Development of a simple and sensitive instrument, easily applicable in primary care units, would be particularly helpful in underserved communities in which identification and referral of high-risk individuals is difficult.</p> <p>Methods</p> <p>A simple 7-question instrument about family history of breast, ovarian and colorectal cancer, FHS-7, was developed to screen for individuals with an increased risk for hereditary breast cancer syndromes. FHS-7 was applied to 9218 women during routine visits to primary care units in Southern Brazil. Two consecutive samples of 885 women and 910 women who answered positively to at least one question and negatively to all questions were included, respectively. The sensitivity, specificity and positive and negative predictive values were determined.</p> <p>Results</p> <p>Of the 885 women reporting a positive family history, 211 (23.8%; CI95%: 21.5–26.2) had a pedigree suggestive of a hereditary breast and/or breast and colorectal cancer syndrome. Using as cut point one positive answer, the sensitivity and specificity of the instrument were 87.6% and 56.4%, respectively. Concordance between answers in two different applications was given by a intra-class correlation (ICC) of 0.84 for at least one positive answer. Temporal stability of the instrument was adequate (ICC = 0.65).</p> <p>Conclusion</p> <p>A simple instrument for the identification of the most common hereditary breast cancer syndrome phenotypes, showing good specificity and temporal stability was developed and could be used as a screening tool in primary care to refer at-risk individuals for genetic evaluations.</p

    Intraperitoneal but Not Intravenous Cryopreserved Mesenchymal Stromal Cells Home to the Inflamed Colon and Ameliorate Experimental Colitis

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    BACKGROUND AND AIMS: Mesenchymal stromal cells (MSCs) were shown to have immunomodulatory activity and have been applied for treating immune-mediated disorders. We compared the homing and therapeutic action of cryopreserved subcutaneous adipose tissue (AT-MSCs) and bone marrow-derived mesenchymal stromal cells (BM-MSCs) in rats with trinitrobenzene sulfonic acid (TNBS)-induced colitis. METHODS: After colonoscopic detection of inflammation AT-MSCs or BM-MSCs were injected intraperitoneally. Colonoscopic and histologic scores were obtained. Density of collagen fibres and apoptotic rates were evaluated. Cytokine levels were measured in supernatants of colon explants. For cell migration studies MSCs and skin fibroblasts were labelled with Tc-99m or CM-DiI and injected intraperitonealy or intravenously. RESULTS: Intraperitoneal injection of AT-MSCs or BM-MSCs reduced the endoscopic and histopathologic severity of colitis, the collagen deposition, and the epithelial apoptosis. Levels of TNF-α and interleukin-1β decreased, while VEGF and TGF-β did not change following cell-therapy. Scintigraphy showed that MSCs migrated towards the inflamed colon and the uptake increased from 0.5 to 24 h. Tc-99m-MSCs injected intravenously distributed into various organs, but not the colon. Cm-DiI-positive MSCs were detected throughout the colon wall 72 h after inoculation, predominantly in the submucosa and muscular layer of inflamed areas. CONCLUSIONS: Intraperitoneally injected cryopreserved MSCs home to and engraft into the inflamed colon and ameliorate TNBS-colitis

    Immunological Basis for the Gender Differences in Murine Paracoccidioides brasiliensis Infection

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    This study aimed to investigate the immunological mechanisms involved in the gender distinct incidence of paracoccidioidomycosis (pcm), an endemic systemic mycosis in Latin America, which is at least 10 times more frequent in men than in women. Then, we compared the immune response of male and female mice to Paracoccidioides brasiliensis infection, as well as the influence in the gender differences exerted by paracoccin, a P. brasiliensis component with carbohydrate recognition property. High production of Th1 cytokines and T-bet expression have been detected in the paracoccin stimulated cultures of spleen cells from infected female mice. In contrast, in similar experimental conditions, cells from infected males produced higher levels of the Th2 cytokines and expressed GATA-3. Macrophages from male and female mice when stimulated with paracoccin displayed similar phagocytic capability, while fungicidal activity was two times more efficiently performed by macrophages from female mice, a fact that was associated with 50% higher levels of nitric oxide production. In order to evaluate the role of sexual hormones in the observed gender distinction, we have utilized mice that have been submitted to gonadectomy followed by inverse hormonal reconstitution. Spleen cells derived from castrated males reconstituted with estradiol have produced higher levels of IFN-γ (1291±15 pg/mL) and lower levels of IL-10 (494±38 pg/mL), than normal male in response to paracoccin stimulus. In contrast, spleen cells from castrated female mice that had been treated with testosterone produced more IL-10 (1284±36 pg/mL) and less IFN-γ (587±14 pg/mL) than cells from normal female. In conclusion, our results reveal that the sexual hormones had a profound effect on the biology of immune cells, and estradiol favours protective responses to P. brasiliensis infection. In addition, fungal components, such as paracoccin, may provide additional support to the gender dimorphic immunity that marks P. brasiliensis infection
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