Una metodología para el trabajo en mesoescala para la provincia de Córdoba

La provincia de Córdoba presenta ambientes de diferentes características según la topografía con un gradiente de valles y sierras lo que hace que se encuentren en ella, el paisaje serrano y el de la pampa donde tradicionalmente se ha practicado agricultura extensiva de secano. En el presente estudio se pretende, mediante el uso de una metodología sencilla aumentar la información ya existente, dado que a pesar de ser una región vastamente estudiada, presenta datos hidrometeorológicos insuficientes.Facultad de Humanidades y Ciencias de la Educació

Introducción al estudio bioclimático de la ciudad de Buenos Aires y conurbano

Se inicia con este trabajo una investigación acerca del clima de la ciudad de Buenos Aires y su conurbano, el análisis del impacto del mismo sobre la vida humana y vegetal y la posible influencia andrógena sobre las características fundamentales del medio ambiente. En esta primera parte del estudio se analizan las condiciones ambientales del verano. La metodología de trabajo se efectúa tomando en consideración dos fuentes: el estudio estadístico en función de series históricas y datos obtenidos mediante observaciones con equipos móviles. Finalmente, se efectúa un análisis comparativo primario de las condiciones estivales en la ciudad y en estaciones del conurbano bonaerense.This survey starts a research work about the climate of the city of Buenos Aires and its urban girdle, the analysis of its impact on human life and vegetation and the possible androgenic influence on basic characteristics of the local environment. In this first part of the survey the summer environmental conditions are analyzed. The working methodology is developed taking into consideration two data sources: the historical data series, through appropriate statistical treatment, and data obtained through observations made by mobile teams. Finally, an elementary comparative analysis of the simmer conditions in the city and in observing stations of the Buenos Aires urban girdle was made.Asociación Argentina de Geofísicos y Geodesta

Sirt1 inhibition promotes in vivo arterial thrombosis and tissue factor expression in stimulated cells

Aims The mammalian silent information regulator-two 1 (Sirt1) blunts the noxious effects of cardiovascular risk factors such as type 2 diabetes mellitus and obesity. Nevertheless, the role of Sirt1 in regulating the expression of tissue factor (TF), the key trigger of coagulation, and arterial thrombus formation remains unknown. Methods and results Human as well as mouse cell lines were used for in vitro experiments, and C57Bl/6 mice for in vivo procedures. Sirt1 inhibition by splitomicin or sirtinol enhanced cytokine-induced endothelial TF protein expression as well as surface activity, while TF pathway inhibitor protein expression did not change. Sirt1 inhibition further enhanced TF mRNA expression, TF promoter activity, and nuclear translocation as well as DNA binding of the p65 subunit of nuclear factor-kappa B (NFκB/p65). Sirt1 siRNA enhanced TF protein and mRNA expression, and this effect was reduced in NFκB/p65−/− mouse embryonic fibroblasts reconstituted with non-acetylatable Lys310-mutant NFκB/p65. Activation of the mitogen-activated protein kinases p38, c-Jun NH2-terminal kinase, and p44/42 (ERK) remained unaffected. In vivo, mice treated with the Sirt1 inhibitor splitomicin exhibited enhanced TF activity in the arterial vessel wall and accelerated carotid artery thrombus formation in a photochemical injury model. Conclusion We provide pharmacological and genetic evidence that Sirt1 inhibition enhances TF expression and activity by increasing NFκB/p65 activation in human endothelial cells. Furthermore, Sirt1 inhibition induces arterial thrombus formation in vivo. Hence, modulation of Sirt1 may offer novel therapeutic options for targeting thrombosi

Deletion of the ageing gene p66Shc reduces early stroke size following ischaemia/reperfusion brain injury

Aims Stroke is a leading cause of morbidity and mortality, and its incidence increases with age. Both in animals and in humans, oxidative stress appears to play an important role in ischaemic stroke, with or without reperfusion. The adaptor protein p66Shc is a key regulator of reactive oxygen species (ROS) production and a mediator of ischaemia/reperfusion damage in ex vivo hearts. Hence, we hypothesized that p66Shc may be involved in ischaemia/reperfusion brain damage. To this end, we investigated whether genetic deletion of p66Shc protects from ischaemia/reperfusion brain injury. Methods and results Transient middle cerebral artery occlusion (MCAO) was performed to induce ischaemia/reperfusion brain injury in wild-type (Wt) and p66Shc knockout mice (p66Shc−/−), followed by 24 h of reperfusion. Cerebral blood flow and blood pressure measurements revealed comparable haemodynamics in both experimental groups. Neuronal nuclear antigen immunohistochemical staining showed a significantly reduced stroke size in p66Shc−/− when compared with Wt mice (P < 0.05, n = 7-8). In line with this, p66Shc−/− mice exhibited a less impaired neurological function and a decreased production of free radicals locally and systemically (P < 0.05, n = 4-5). Following MCAO, protein levels of gp91phox nicotinamide adenine dinucleotide phosphate oxidase subunit were increased in brain homogenates of Wt (P < 0.05, n = 4), but not of p66Shc−/− mice. Further, reperfusion injury in Wt mice induced p66Shc protein in the basilar and middle cerebral artery, but not in brain tissue, suggesting a predominant involvement of vascular p66Shc. Conclusion In the present study, we show that the deletion of the ageing gene p66Shc protects mice from ischaemia/reperfusion brain injury through a blunted production of free radicals. The ROS mediator p66Shc may represent a novel therapeutical target for the treatment of ischaemic strok

Enoxaparin for primary thromboprophylaxis in ambulatory patients with coronavirus disease-2019 (the OVID study): a structured summary of a study protocol for a randomized controlled trial.

The OVID study will demonstrate whether prophylactic-dose enoxaparin improves survival and reduces hospitalizations in symptomatic ambulatory patients aged 50 or older diagnosed with COVID-19, a novel viral disease characterized by severe systemic, pulmonary, and vessel inflammation and coagulation activation. The OVID study is conducted as a multicentre open-label superiority randomised controlled trial. Inclusion Criteria 1. Signed patient informed consent after being fully informed about the study's background. 2. Patients aged 50 years or older with a positive test for SARS-CoV2 in the past 5 days and eligible for ambulatory treatment. 3. Presence of respiratory symptoms (i.e. cough, sore throat, or shortness of breath) or body temperature &gt;37.5° C. 4. Ability of the patient to travel to the study centre by private transportation, performed either by an accompanying person from the same household or by the patient themselves 5. Ability to comply with standard hygiene requirements at the time of in-hospital visit, including a face mask and hand disinfectant. 6. Ability to walk from car to study centre or reach it by wheelchair transport with the help of an accompanying person from the same household also complying with standard hygiene requirements. 7. Ability to self-administer prefilled enoxaparin injections after instructions received at the study centre or availability of a person living with the patient to administer enoxaparin. Exclusion Criteria 1. Any acute or chronic condition posing an indication for anticoagulant treatment, e.g. atrial fibrillation, prior venous thromboembolism (VTE), acute confirmed symptomatic VTE, acute coronary syndrome. 2. Anticoagulant thromboprophylaxis deemed necessary in view of the patient's history, comorbidity or predisposing strong risk factors for thrombosis: a. Any of the following events occurring in the prior 30 days: fracture of lower limb, hospitalization for heart failure, hip/knee replacement, major trauma, spinal cord injury, stroke, b. previous VTE, c. histologically confirmed malignancy, which was diagnosed or treated (surgery, chemotherapy, radiotherapy) in the past 6 months, or recurrent, or metastatic, or inoperable. 3. Any clinically relevant bleeding (defined as bleeding requiring hospitalization, transfusion, surgical intervention, invasive procedures, occurring in a critical anatomical site, or causing disability) within 30 days prior to randomization or sign of acute bleeding. 4. Intracerebral bleeding at any time in the past or signs/symptoms consistent with acute intracranial haemorrhage. 5. Haemoglobin &lt;8 g/dL and platelet count &lt;50 x 10 &lt;sup&gt;9&lt;/sup&gt; cells/L confirmed by recent laboratory test (&lt;90 days). 6. Subjects with any known coagulopathy or bleeding diathesis, including known significant liver disease associated with coagulopathy. 7. Severe renal insufficiency (baseline creatinine clearance &lt;30 mL/min calculated using the Cockcroft-Gault formula) confirmed by recent laboratory test (&lt;90 days). 8. Contraindications to enoxaparin therapy, including prior heparin-induced thrombocytopenia and known hypersensitivity. 9. Current use of dual antiplatelet therapy. 10. Participation in other interventional studies over the past 30 days. 11. Non-compliance or inability to adhere to treatment or lack of a family environment or support system for home treatment. 12. Cognitive impairment and/or inability to understand information provided in the study information. Patient enrolment will take place at seven Swiss centres, including five university hospitals and two large cantonal hospitals. Patients randomized to the intervention group will receive subcutaneous enoxaparin at the recommended dose of 4,000 IU anti-Xa activity (40 mg/0.4 ml) once daily for 14 days. Patients randomized to the comparator group will receive no anticoagulation. Primary outcome: a composite of any hospitalization or all-cause death occurring within 30 days of randomization. (i) a composite of cardiovascular events, including deep vein thrombosis (including catheter-associated), pulmonary embolism, myocardial infarction/myocarditis, arterial ischemia including mesenteric and extremities, acute splanchnic vein thrombosis, or ischemic stroke within 14 days, 30 days, and 90 days of randomization; (ii) each component of the primary efficacy outcome, within 14 days, 30 days, and 90 days of randomization; (iii) net clinical benefit (accounting for the primary efficacy outcome, composite cardiovascular events, and major bleeding), within 14 days, 30 days, and 90 days of enrolment; (iv) primary efficacy outcome, within 14 days, and 90 days of enrolment; (v) disseminated intravascular coagulation (ISTH criteria, in-hospital diagnosis) within 14 days, 30 days, and 90 days of enrolment. Patients will undergo block stratified randomization (by age: 50-70 vs. &gt;70 years; and by study centre) with a randomization ratio of 1:1 with block sizes varying between 4 and 8. Randomization will be performed after the signature of the informed consent for participation and the verification of the eligibility criteria using the electronic data capture software (REDCAP, Vanderbilt University, v9.1.24). In this open-label study, no blinding procedures will be used. The sample size calculation is based on the parameters α = 0.05 (2-sided), power: 1-β = 0.8, event rate in experimental group, pexp = 0.09 and event rate in control group, pcon = 0.15. The resulting total sample size is 920. To account for potential dropouts, the total sample size was fixed to 1000 with 500 patients in the intervention group and 500 in the control group. Protocol version 1.0, 14 April 2020. Protocol version 3.0, 18 May 2020 Recruiting start date: June 2020. Last Patient Last Visit: March 2021. ClinicalTrials.gov Identifier: NCT04400799 First Posted: May 26, 2020 Last Update Posted: July 16, 2020 FULL PROTOCOL: The full protocol is attached as an additional file, accessible from the Trials website (Additional file 1). In the interest in expediting dissemination of this material, the familiar formatting has been eliminated; this Letter serves as a summary of the key elements of the full protocol

Post-ischaemic silencing of p66Shc reduces ischaemia/reperfusion brain injury and its expression correlates to clinical outcome in stroke

In light of the limited repertoire of therapeutical options available for the treatment of ischaemic stroke, the identification of novel potential targets is vital; in this respect, the present study demonstrates that the adaptor protein p66Shc holds this potential as an adjunct therapy to thrombolysis. Post-ischaemic silencing of p66Shc protein yielded beneficial effects in a mouse model of I/R brain injury underlying an interesting translational perspective for this target protein. Further, in proof-of-principle clinical experiments using PBMs, we demonstrate that p66Shc gene expression is transiently increased and that its levels correlate to short-term outcome in ischaemic stroke patients. Although these latter experiments are not directly relevant to the experiments performed in mice and in human endothelial cells, they provide novel important information about p66Shc regulation in stroke patients and set the basis for further investigations aimed at assessing the potential for p66Shc to become a novel therapeutic target as an adjunct of thrombolysis for the management of acute ischaemic strok

Una metodología para el trabajo en mesoescala para la provincia de Córdoba

Fil: Scarpati, Olga Eugenia. Universidad Nacional de La Plata. Facultad de Humanidades y Ciencias de la Educación; Argentina

Una metodología para el trabajo en mesoescala para la provincia de Córdoba

Fil: Scarpati, Olga Eugenia. Universidad Nacional de La Plata. Facultad de Humanidades y Ciencias de la Educación; Argentina

Una metodología para el trabajo en mesoescala para la provincia de Córdoba

Fil: Scarpati, Olga Eugenia. Universidad Nacional de La Plata. Facultad de Humanidades y Ciencias de la Educación; Argentina

Impacto del ENOS sobre los rendimientos de maíz en la región pampeana argentina

El fenómeno de “El Niño - Oscilación del Sur” (ENOS) es uno de los principales responsables de la variabilidad climática inter-anual, con influencia sobrela región pampeana argentina. El objetivo de este trabajo fue analizar el impacto del ENOS sobre las variaciones anuales de la producción de maíz. La región fue dividida en 10 zonas en las cuales los rendimientos tienen una variabilidad inter anual homogénea. Se utilizaron diferentes índices del ENOS. Los resultados indicaron que, en la mayor parte de la región, los desvíos de los rendimientos son, en general, positivos durante eventos “El Niño” y negativos durante “La Niña”. Sin embargo, el impacto es muy fuerte al norte y centro de la región analizada, y se debilita hacia el sur. En el sudeste de la provincia de Buenos Aires el comportamiento es diferente que en el resto. Los índices promediados de mayo a julio son, en general, un buen indicador de la influencia del ENOS sobre la productividad de los cultivos, y brindan una adecuada información para la toma de decisiones de la empresa agropecuaria, con suficiente anticipación respecto del comienzo de la campaña