Fiscal Federalism and Tax Equalization: The potential for progressive local taxes

We construct an empirically informed computational model of fiscal federalism, testing whether horizontal or vertical equalization can solve the fiscal externality problem in an environment in which heterogeneous agents can move and vote. The model expands on the literature by considering the case of progressive local taxation. Although the consequences of progressive taxation under fiscal federalism are well understood, they have not been studied in a context with tax equalization, despite widespread implementation. The model also expands on the literature by comparing the standard median voter model with a realistic alternative voting mechanism. We find that fiscal federalism with progressive taxation naturally leads to segregation as well as inefficient and inequitable public goods provision while the alternative voting mechanism generates more efficient, though less equitable, public goods provision. Equalization policy, under both types of voting, is largely undermined by micro-actors' choices. For this reason, the model also does not find the anticipated effects of vertical equalization discouraging public goods spending among wealthy jurisdictions and horizontal encouraging it among poor jurisdictions. Finally, we identify two optimal scenarios, superior to both complete centralization and complete devolution. These scenarios are not only Pareto optimal, but also conform to a Rawlsian view of justice, offering the best possible outcome for the worst-off. Despite offering the best possible outcomes, both scenarios still entail significant economic segregation and inequitable public goods provision. Under the optimal scenarios agents shift the bulk of revenue collection to the federal government, with few jurisdictions maintaining a small local tax.

Influencia de la Ciencia Ficción en las TIC y las Telecomunicaciones

Desde el comienzo de la Historia, el ser humano ha pensado en su futuro, ya fuera por el hecho de preocuparse por su supervivencia o por razones más filosóficas, como el porvenir como especie. Pensar en el futuro es anticipación. El género de la ciencia ficción es el que más se basa en la anticipación. En muchos subgéneros de la ciencia ficción se tratan temas futuristas, viajes espaciales a otros planetas, inteligencia artificial, etc. Por otra parte, en la actualidad vivimos un período donde los cambios en las TIC (Tecnologías de la Información y Comunicación) son prácticamente diarios, aunque podría llegar a decirse que los cambios se producen hora a hora. A veces, muchos de estos avances nos parecen producto de la fantasía o la ciencia ficción, o salidos de alguna película futurista. Sin embargo, dichos avances son perfectamente posibles y explicables a través de la ciencia actual. A través de este proyecto se pretenden analizar estos avances, relacionándolos con distintas obras de ciencia ficción. Una gran cantidad de los avances tecnológicos tienen su origen en alguna obra de la ciencia ficción, ya sea literatura o cine. Otro objetivo es realizar un estudio de diferentes propuestas tecnológicas de diferentes obras de esta rama que no se hayan realizado todavía, y analizar su viabilidad, su utilidad y los posibles cambios sociológicos que produciría en el mundo en el que vivimos. El tercer objetivo es evaluar la aptitud y actitud de los ingenieros de telecomunicación en cuanto a la innovación y la proyección hacia el futuro de los estos posibles cambios tecnológicos. Abstract Since the beginning of History, humans have thought about their future, either concerned about survival or by philosophical reasons like the future as species. Thinking about the future is speculation. The science fiction genre is the one that is based on speculation. Sub-genres of science fiction covers futuristic themes like space travel to other planets, artificial intelligence, etc. Today we live in a period where changes in ICT (Information and Communication Technologies) are almost daily, although we should say that changes occur in a matter of hours. Sometimes, many of these advances seem a product of fantasy or science fiction, or coming out of a futuristic movie. However, these advances are perfectly possible and explainable by current science. Through this project the intention is to analyze these developments, relating them to various works of science fiction. A great number of this technological advancements have their origin in a work of science fiction, either literature or film. Another objective is to study different technological proposals of this genre that have not been done yet, and analyze their feasibility, usefulness and potential sociological changes that occur in the world we live in. The third objective is to evaluate the ability and attitude of telecommunication engineers in terms of innovation and future projection of these potential technological changes.

La ciudad radical : el radical ciudad : tentativa de catálogo

“La ciudad radical” es una tentativa de catálogo de ciudades radicales, un atlas abierto de los límites imaginarios de la convivencia colectiva. Llamo al catálogo “tentativa” porque un catálogo siempre es abierto. Abierto en un doble sentido, en sentido de inacabado, siempre caben futuras revisiones, adiciones, modificaciones, alteraciones de orden… y en el sentido de permitir multitud lecturas y posibilidades abiertas de interpretación. El tema central de este trabajo es, el imaginario, lo imaginario, la fantasía, la ficción…como condición fundamental de creación en el ámbito social. En lo imaginario, y en el imaginario, reside la infinita y reiterativa capacidad de la sociedad para inventarse y re-inventarse, para crearse y re-crearse en el mundo, a través de la ciudad. Ciudad radical es una ciudad extremada, en la que una de sus rasgos ha sido llevado al extremo. Pero radical (del latín radix) también quiere decir raíz, origen, fundamento. El objeto del catálogo también es doble. Por un lado, el interés de generar un compendio de ciudades radicales, extremadas, acumuladas en la historia. Por otro lado, el objeto del catálogo es aproximarnos a la idea que nos hemos hecho, a lo largo de la historia, de nuestra gran “obra” en la tierra, el artificio esencialmente humano que es la ciudad. El análisis de las ciudades radicales sirve de método para la aproximación a la idea de ciudad y para desentrañar las metáforas urbanas que nos habitan, aquellas que nos hacen pensar la ciudad y en las que la ciudad nos piensa. En última instancia esta tesis pretender encontrar indicios que nos ayuden en la respuesta de una pregunta esencial, por qué ciudades, qué fuerzas nos empujan hacia los otros bajo la forma de la ciudad, desde los orígenes. La historia de nuestras sociedades es la historia de nuestras ciudades. La historia de la ciudad, es nuestra historia. La ciudad es la gran creación humana en la tierra, el objeto y el sujeto de la convivencia, del hábitat social. En este sentido la radicalización nos acerca a la esencia humana, desde el extremo llegamos al centro, al origen. Pensamos la ciudad, la ciudad nos piensa. Creamos la ciudad, la ciudad nos crea. La ciudad es radical en un doble sentido, está en el extremo y está en el origen, que es también el fin. ABSTRACT “The radical city” is an attempt to catalogue radical cities throughout history, it aims to be an open atlas of the imaginary limits of coexistence and the living together. I call this work an “attempt” of catalogue due to the implied open nature of catalogues. Open in the sense of unfinished, there is always space for adding, reviewing, modifying, altering…but also open in the sense of multiple readings and several possibilities for interpretation, which this work allows. The main background theme underlying this catalogue, providing context to the way of understanding human beings, is the imaginary, imagination, fantasy, and fiction as the fundamental condition for social creation. The imaginary is where the endless and reiterative capacity for societies to invent and re-invent themselves, to create and re-create themselves through the city, lies in. Radical city is an extreme city, which one of the features has been pushed to the limit. Radical, (from the Latin form, radix) also means root, origin and fundament. The object of this catalogue is double as well. On the one hand, the intention of putting together, as accumulating, a whole range of radical and extreme cities throughout history. On the other hand, the intention of the catalogue is approaching the idea, the way we, as humans, envision our own creation on Earth, the city as a purely and essentially human invention. In this sense, the analysis of radically produced cities helps as a means to understand, or at least, to get closer to the idea of the city itself; to figure out the urban metaphors envisioning “us” as living in cities, those metaphors determining the way we envision “inhabiting” as an essential need, and which set up the imaginary limits within we, as social individuals, dream of the city or the way in which the city, as the radix, “dreams of ourselves”. Ultimately, this work aims to approach the answer to a fundamental question, why cities? Which forces push us towards the others in the form of the city since forever? The history of our societies is the history of our cities. The history of our cities is our own history. Cities are our greatest invention, object and subject of coexistence, radical trigger for the living together. In this sense, radicalization helps us to get closer to human essence, is by approaching the limits that we can we reach the centre, the origin. We envision the city and¬¬¬ the city envisions us. The city is radical in a double way, is both origin and limits, origin and end.

Harmonic Monads : Reading Contemporary Scottish Fiction through the Enlightenment

Peer reviewed

Very Chicago : Mary Borden and the Art of Fiction

Peer reviewed

Potentially predictive and manipulable blood serum correlates of aging in the healthy human male: Progressive decreases in bioavailable testosterone, dehydroepiandrosterone sulfate, and the ratio of insulin-like growth factor 1 to growth hormone

A cross-sectional survey was made in 56 exceptionally healthy males, ranging in age from 20 to 84 years. Measurements were made of selected steroidal components and peptidic hormones in blood serum, and cognitive and physical tests were performed. Of those blood serum variables that gave highly significant negative correlations with age (r > −0.6), bioavailable testosterone (BT), dehydroepiandrosterone sulfate (DHEAS), and the ratio of insulin-like growth factor 1 (IGF-1) to growth hormone (GH) showed a stepwise pattern of age-related changes most closely resembling those of the age steps themselves. Of these, BT correlated best with significantly age-correlated cognitive and physical measures. Because DHEAS correlated well with BT and considerably less well than BT with the cognitive and physical measures, it seems likely that BT and/or substances to which BT gives rise in tissues play a more direct role in whatever processes are rate-limiting in the functions measured and that DHEAS relates more indirectly to these functions. The high correlation of IGF-1/GH with age, its relatively low correlation with BT, and the patterns of correlations of IGF-1/GH and BT with significantly age-correlated cognitive and physical measures suggest that the GH–IGF-1 axis and BT play independent roles in affecting these functions. Serial determinations made after oral ingestion of pregnenolone and data from the literature suggest there is interdependence of steroid metabolic systems with those operational in control of interrelations in the GH–IGF-1 axis. Longitudinal concurrent measurements of serum levels of BT, DHEAS, and IGF-1/GH together with detailed studies of their correlations with age-correlated functional measures may be useful in detecting early age-related dysregulations and may be helpful in devising ameliorative approaches.

Inhibition of human telomerase in immortal human cells leads to progressive telomere shortening and cell death

The correlation between telomerase activity and human tumors has led to the hypothesis that tumor growth requires reactivation of telomerase and that telomerase inhibitors represent a class of chemotherapeutic agents. Herein, we examine the effects of inhibition of telomerase inside human cells. Peptide nucleic acid and 2′-O-MeRNA oligomers inhibit telomerase, leading to progressive telomere shortening and causing immortal human breast epithelial cells to undergo apoptosis with increasing frequency until no cells remain. Telomere shortening is reversible: if inhibitor addition is terminated, telomeres regain their initial lengths. Our results validate telomerase as a target for the discovery of anticancer drugs and supply general insights into the properties that successful agents will require regardless of chemical type. Chemically similar oligonucleotides are in clinical trials and have well characterized pharmacokinetics, making the inhibitors we describe practical lead compounds for testing for an antitelomerase chemotherapeutic strategy.

Ablation of P/Q-type Ca2+ channel currents, altered synaptic transmission, and progressive ataxia in mice lacking the α1A-subunit

The Ca2+ channel α1A-subunit is a voltage-gated, pore-forming membrane protein positioned at the intersection of two important lines of research: one exploring the diversity of Ca2+ channels and their physiological roles, and the other pursuing mechanisms of ataxia, dystonia, epilepsy, and migraine. α1A-Subunits are thought to support both P- and Q-type Ca2+ channel currents, but the most direct test, a null mutant, has not been described, nor is it known which changes in neurotransmission might arise from elimination of the predominant Ca2+ delivery system at excitatory nerve terminals. We generated α1A-deficient mice (α1A−/−) and found that they developed a rapidly progressive neurological deficit with specific characteristics of ataxia and dystonia before dying ≈3–4 weeks after birth. P-type currents in Purkinje neurons and P- and Q-type currents in cerebellar granule cells were eliminated completely whereas other Ca2+ channel types, including those involved in triggering transmitter release, also underwent concomitant changes in density. Synaptic transmission in α1A−/− hippocampal slices persisted despite the lack of P/Q-type channels but showed enhanced reliance on N-type and R-type Ca2+ entry. The α1A−/− mice provide a starting point for unraveling neuropathological mechanisms of human diseases generated by mutations in α1A.

Progressive entorhinal cortex lesions accelerate hippocampal sprouting and spare spatial memory in rats

Accelerating hippocampal sprouting by making unilateral progressive lesions of the entorhinal cortex spared the spatial memory of rats tested for retention of a learned alternation task. Subsequent transection of the sprouted crossed temporodentate pathway (CTD), as well as a simultaneous CTD transection and progressive entorhinal lesion, produced a persistent deficit on the memory task. These results suggest that CTD sprouting, which is homologous to the original perforant path input to the dentate gyrus of the hippocampus, is behaviorally significant and can ameliorate at least some of the memory deficits associated with hippocampal deafferentation.

Mutations in a NIMA-related kinase gene, Nek1, cause pleiotropic effects including a progressive polycystic kidney disease in mice

We previously have described a mouse model for polycystic kidney disease (PKD) caused by either of two mutations, kat or kat2J, that map to the same locus on chromosome 8. The homozygous mutant animals have a latent onset, slowly progressing form of PKD with renal pathology similar to the human autosomal-dominant PKD. In addition, the mutant animals show pleiotropic effects that include facial dysmorphism, dwarfing, male sterility, anemia, and cystic choroid plexus. We previously fine-mapped the kat2J mutation to a genetic distance of 0.28 ± 0.12 centimorgan between D8Mit128 and D8Mit129. To identify the underlying molecular defect in this locus, we constructed an integrated genetic and physical map of the critical region surrounding the kat2J mutation. Cloning and expression analysis of the transcribed sequences from this region identified Nek1, a NIMA (never in mitosis A)-related kinase as a candidate gene. Further analysis of the Nek1 gene from both kat/kat and kat2J/kat2J mutant animals identified a partial internal deletion and a single-base insertion as the molecular basis for these mutations. The complex pleiotropic phenotypes seen in the homozygous mutant animals suggest that the NEK1 protein participates in different signaling pathways to regulate diverse cellular processes. Our findings identify a previously unsuspected role for Nek1 in the kidney and open a new avenue for studying cystogenesis and identifying possible modes of therapy.

The cellular ecology of progressive neoplastic transformation: A clonal analysis

A comparison was made of the competence for neoplastic transformation in three different sublines of NIH 3T3 cells and multiple clonal derivatives of each. Over 90% of the neoplastic foci produced by an uncloned transformed (t-SA′) subline on a confluent background of nontransformed cells were of the dense, multilayered type, but about half of the t-SA′ clones produced only light foci in assays without background. This asymmetry apparently arose from the failure of the light focus formers to register on a background of nontransformed cells. Comparison was made of the capacity for confluence-mediated transformation between uncloned parental cultures and their clonal derivatives by using two nontransformed sublines, one of which was highly sensitive and the other relatively refractory to confluence-mediated transformation. Transformation was more frequent in the clones than in the uncloned parental cultures for both sublines. This was dramatically so in the refractory subline, where the uncloned culture showed no overt sign of transformation in serially repeated assays but increasing numbers of its clones exhibited progressive transformation. The reason for the greater susceptibility of the pure clones is apparently the suppression of transformation among the diverse membership that makes up the uncloned parental culture. Progressive selection toward increasing degrees of transformation in confluent cultures plays a major role in the development of dense focus formers, but direct induction by the constraint of confluence may contribute by heritably damaging cells. In view of our finding of increased susceptibility to transformation in clonal versus uncloned populations, expansion of some clones at the expense of others during the aging process would contribute to the marked increase of cancer with age.