LA RAZÓN TRANSFORMADORA. REFLEXIONES SOBRE LA POSICIÓN DE SABER DE LOS ESTUDIOS CULTURALES

Examino aquí la presuposición de un saber específico que se atribuye a los practicantes de los estudios culturales latinoamericanos y que constituye su aportación específica en la arena política y defiendo la posición de que ese saber es posible, pero no está garantizado por el mero aval institucional. Para sustentar esta postura, discuto las concepciones de razón humana, episteme y epistemología y luego caracterizo la aportación fundacional del Centro de Birmingham en términos del principio materialista de subordinar toda práctica de conocimiento a los datos brindados por los seres humanos concretos en sus relaciones concretas. Desde esta perspectiva, analizo el riesgo idealista de los esencialismos y propongo algunas inquisiciones metodológicas que orientarían el trabajo en estudios culturales latinoamericanos con coherencia política y epistemológica

Flexibility properties in Complex Analysis and Affine Algebraic Geometry

In the last decades affine algebraic varieties and Stein manifolds with big (infinite-dimensional) automorphism groups have been intensively studied. Several notions expressing that the automorphisms group is big have been proposed. All of them imply that the manifold in question is an Oka-Forstneri\v{c} manifold. This important notion has also recently merged from the intensive studies around the homotopy principle in Complex Analysis. This homotopy principle, which goes back to the 1930's, has had an enormous impact on the development of the area of Several Complex Variables and the number of its applications is constantly growing. In this overview article we present 3 classes of properties: 1. density property, 2. flexibility 3. Oka-Forstneri\v{c}. For each class we give the relevant definitions, its most significant features and explain the known implications between all these properties. Many difficult mathematical problems could be solved by applying the developed theory, we indicate some of the most spectacular ones.Comment: thanks added, minor correction

Algebraic volume density property of affine algebraic manifolds

We introduce the notion of algebraic volume density property for affine algebraic manifolds and prove some important basic facts about it, in particular that it implies the volume density property. The main results of the paper are producing two big classes of examples of Stein manifolds with volume density property. One class consists of certain affine modifications of \C^n equipped with a canonical volume form, the other is the class of all Linear Algebraic Groups equipped with the left invariant volume form.Comment: 35 page

Affine modifications and affine hypersurfaces with a very transitive automorphism group

We study a kind of modification of an affine domain which produces another affine domain. First appeared in passing in the basic paper of O. Zariski (1942), it was further considered by E.D. Davis (1967). The first named author applied its geometric counterpart to construct contractible smooth affine varieties non-isomorphic to Euclidean spaces. Here we provide certain conditions which guarantee preservation of the topology under a modification. As an application, we show that the group of biregular automorphisms of the affine hypersurface $X \subset C^{k+2}$ given by the equation $uv=p(x_1,...,x_k)$ where $p \in C[x_1,...,x_k],$ acts $m-$transitively on the smooth part reg$X$ of $X$ for any $m \in N.$ We present examples of such hypersurfaces diffeomorphic to Euclidean spaces.Comment: 39 Pages, LaTeX; a revised version with minor changes and correction

An interpolation theorem for proper holomorphic embeddings

Given a Stein manifold X of dimension n>1, a discrete sequence a_j in X, and a discrete sequence b_j in C^m where m > [3n/2], there exists a proper holomorphic embedding of X into C^m which sends a_j to b_j for every j=1,2,.... This is the interpolation version of the embedding theorem due to Eliashberg, Gromov and Schurmann. The dimension m cannot be lowered in general due to an example of Forster

Epigenetic alterations in hippocampus of SAMP8 senescent mice and modulation by voluntary physical exercise

The senescence-accelerated SAMP8 mouse model displays features of cognitive decline and Alzheimer's disease. With the purpose of identifying potential epigenetic markers involved in aging and neurodegeneration, here we analyzed the expression of 84 mature miRNAs, the expression of histone-acetylation regulatory genes and the global histone acetylation in the hippocampus of 8-month-old SAMP8 mice, using SAMR1 mice as control. We also examined the modulation of these parameters by 8 weeks of voluntary exercise. Twenty-one miRNAs were differentially expressed between sedentary SAMP8 and SAMR1 mice and seven miRNAs were responsive to exercise in both strains. SAMP8 mice showed alterations in genes involved in protein acetylation homeostasis such as Sirt1 and Hdac6 and modulation of Hdac3 and Hdac5 gene exprssion by exercise. Global histone H3 acetylation levels were reduced in SAMP8 compared with SAMR1 mice and reached control levels in response to exercise. In sum, data presented here provide new candidate epigenetic markers for aging and neurodegeneration and suggest that exercise training may prevent or delay some epigenetic alterations associated with accelerated aging

Epigenetic alterations in hippocampus of SAMP8 senescent mice and modulation by voluntary physical exercise

The senescence-accelerated SAMP8 mouse model displays features of cognitive decline and Alzheimer's disease. With the purpose of identifying potential epigenetic markers involved in aging and neurodegeneration, here we analyzed the expression of 84 mature miRNAs, the expression of histone-acetylation regulatory genes and the global histone acetylation in the hippocampus of 8-month-old SAMP8 mice, using SAMR1 mice as control. We also examined the modulation of these parameters by 8 weeks of voluntary exercise. Twenty-one miRNAs were differentially expressed between sedentary SAMP8 and SAMR1 mice and seven miRNAs were responsive to exercise in both strains. SAMP8 mice showed alterations in genes involved in protein acetylation homeostasis such as Sirt1 and Hdac6 and modulation of Hdac3 and Hdac5 gene expression by exercise. Global histone H3 acetylation levels were reduced in SAMP8 compared with SAMR1 mice and reached control levels in response to exercise. In sum, data presented here provide new candidate epigenetic markers for aging and neurodegeneration and suggest that exercise training may prevent or delay some epigenetic alterations associated with accelerated aging

High dietary folate in pregnant mice leads to pseudo-MTHFR deficiency and altered methyl metabolism, with embryonic growth delay and short-term memory impairment in offspring

Methylenetetrahydrofolate reductase (MTHFR) generates methyltetrahydrofolate for methylation reactions. Severe MTHFR deficiency results in homocystinuria and neurologic impairment. Mild MTHFR deficiency (677C > T polymorphism) increases risk for complex traits, including neuropsychiatric disorders. Although low dietary folate impacts brain development, recent concerns have focused on high folate intake following food fortification and increased vitamin use. Our goal was to determine whether high dietary folate during pregnancy affects brain development in murine offspring. Female mice were placed on control diet (CD) or folic acid-supplemented diet (FASD) throughout mating, pregnancy and lactation. Three-week-old male pups were evaluated for motor and cognitive function. Tissues from E17.5 embryos, pups and dams were collected for choline/methyl metabolite measurements, immunoblotting or gene expression of relevant enzymes. Brains were examined for morphology of hippocampus and cortex. Pups of FASD mothers displayed short-term memory impairment, decreased hippocampal size and decreased thickness of the dentate gyrus. MTHFR protein levels were reduced in FASD pup livers, with lower concentrations of phosphocholine and glycerophosphocholine in liver and hippocampus, respectively. FASD pup brains showed evidence of altered acetylcholine availability and Dnmt3a mRNA was reduced in cortex and hippocampus. E17.5 embryos and placentas from FASD dams were smaller. MTHFR protein and mRNA were reduced in embryonic liver, with lower concentrations of choline, betaine and phosphocholine. Embryonic brain displayed altered development of cortical layers. In summary, high folate intake during pregnancy leads to pseudo-MTHFR deficiency, disturbed choline/methyl metabolism, embryonic growth delay and memory impairment in offspring. These findings highlight the unintended negative consequences of supplemental folic acid