Les meules rotatives du site ibérique d'Alcorda Park (Calafell, Baix Penedès, Tarragona)

El jaciment ibèric d' Alorda Park està situat a la costa central de Catalunya, a uns 30 km al nordest de Tarragona. El jaciment, l'ocupació del qual es data principalment entre el s. VI i el III aC, ha estat excavat extensament des de 1983. Els treballs d'excavació han lliurat sis metae i disset catilli de molins rotatius, la major part dels quals han estat reutilitzats per a usos secundaris. D' altra banda, cap molí rotatiu ha estat trobat in situ a l'interior d'una casa, de manera que es dedueix que la molta amb aquests instruments era probablement una activitat practicada en instal·lacions communals o bé per especialistes. Pel que fa a la funcionalitat d'aquestes peces, les anàlisis de residus indiquen que eren utilitzades per a la molta de cereals i, en un sol cas, de faves. Pel que fa a la cronologia, el més antic d'aquests exemplars data de mitjan segle V aC, i la utilització dels molins de rotació continua fins a finals de l'ocupació de l'assentament. Al llarg d'aquests tres segles, els molins rotatius d' Alorda Park sofreixen una evolució morfològica els trets essencials de la qual han pogut ser establerts. Els exemplars presentats són morfologicament similars a altres molins iberics de la costa central de Catalunya, pero es diferencien considerablement dels models documentats al País Valencia, a Ullastret i a la Gal·lia meridional. Aquest fet sembla indicar l'existència de tradicions locals ben caracteritzades, que hauran de ser precisades per les recerques futures. Finalment, cal observar que, segons les analisis de residus, els altres instruments lítics o de triturat descoberts al jaciment (molins de vaivé, morters) han estat utilitzats per a la transformació de materies primeres.

Functional compensation of motor function in pre-symptomatic Huntington's disease.

Involuntary choreiform movements are a clinical hallmark of Huntington's disease. Studies in clinically affected patients suggest a shift of motor activations to parietal cortices in response to progressive neurodegeneration. Here, we studied pre-symptomatic gene carriers to examine the compensatory mechanisms that underlie the phenomenon of retained motor function in the presence of degenerative change. Fifteen pre-symptomatic gene carriers and 12 matched controls performed button presses paced by a metronome at either 0.5 or 2 Hz with four fingers of the right hand whilst being scanned with functional magnetic resonance imaging. Subjects pressed buttons either in the order of a previously learnt 10-item finger sequence, from left to right, or kept still. Error rates ranged from 2% to 7% in the pre-symptomatic gene carriers and from 0.5% to 4% in controls, depending on the condition. No significant difference in task performance was found between groups for any of the conditions. Activations in the supplementary motor area (SMA) and superior parietal lobe differed with gene status. Compared with healthy controls, gene carriers showed greater activations of left caudal SMA with all movement conditions. Activations correlated with increasing speed of movement were greater the closer the gene carriers were to estimated clinical diagnosis, defined by the onset of unequivocal motor signs. Activations associated with increased movement complexity (i.e. with the pre-learnt 10-item sequence) decreased in the rostral SMA with nearing diagnostic onset. The left superior parietal lobe showed reduced activation with increased movement complexity in gene carriers compared with controls, and in the right superior parietal lobe showed greater activations with all but the most demanding movements. We identified a complex pattern of motor compensation in pre-symptomatic gene carriers. The results show that preclinical compensation goes beyond a simple shift of activity from premotor to parietal regions involving multiple compensatory mechanisms in executive and cognitive motor areas. Critically, the pattern of motor compensation is flexible depending on the actual task demands on motor control.

Huntington ja monikulttuurisuus

Vastaus Panu Minkkisen arviointiin Samuel P. Huntingtonin Kulttuurien kamppailu-kirjasta (TT-lehdessä 7/2004)

Coloquialismo y humor en South Park: análisis del doblaje al español

Este trabajo es un estudio sobre la traducción del coloquialismo y el humor en productos audiovisuales. Tomando como referencia el doblaje al español de South Park, se analizan algunos errores habituales en obras similares y se plantean estrategias de traducción efectivas, tanto a nivel textual como oracional.

A pathogenic mechanism in Huntington"s disease involves small CAG-repeated RNAs with neurotoxic activity

Huntington's disease (HD) is an autosomal dominantly inherited disorder caused by the expansion of CAG repeats in the Huntingtin (HTT) gene. The abnormally extended polyglutamine in the HTT protein encoded by the CAG repeats has toxic effects. Here, we provide evidence to support that the mutant HTT CAG repeats interfere with cell viability at the RNA level. In human neuronal cells, expanded HTT exon-1 mRNA with CAG repeat lengths above the threshold for complete penetrance (40 or greater) induced cell death and increased levels of small CAG-repeated RNAs (sCAGs), of ≈21 nucleotides in a Dicer-dependent manner. The severity of the toxic effect of HTT mRNA and sCAG generation correlated with CAG expansion length. Small RNAs obtained from cells expressing mutant HTT and from HD human brains significantly decreased neuronal viability, in an Ago2-dependent mechanism. In both cases, the use of anti-miRs specific for sCAGs efficiently blocked the toxic effect, supporting a key role of sCAGs in HTT-mediated toxicity. Luciferase-reporter assays showed that expanded HTT silences the expression of CTG-containing genes that are down-regulated in HD. These results suggest a possible link between HD and sCAG expression with an aberrant activation of the siRNA/miRNA gene silencing machinery, which may trigger a detrimental response. The identification of the specific cellular processes affected by sCAGs may provide insights into the pathogenic mechanisms underlying HD, offering opportunities to develop new therapeutic approaches

Issue review : Cedar Rock State Park.

This issue review provides an overview of Cedar Rock State Park, that is part of Iowa's park system and managed by the Department of Natural Resources, or DNR.

Audit report on the City of University Park, Iowa for the year ended June 30, 2014

Audit report on the City of University Park, Iowa for the year ended June 30, 2014

Ledges State Park, 1925.

This booklet, no. 1 in the Park Booklet Series, contains general information, features, history, geology and photos of Ledges State Park.

Islam político en Europa: un análisis actual de las teorías de S. P. Huntington : El paradigma español

Análisis actual sobre las teorías de S. P. Huntington aplicadas al contexto de la Unión Europea, respecto al islam político. Comparativa del islam primitivo con otros sistemas totalitarios y argumentación para la convivencia del islam actual en las sociedades modernas del marco europeo.

1210-007IJ Central Park Lake Final Report

The Central Park Lake Watershed Assessment and Management Plan identified four categories where improvements are needed to remove the 23 acre lake from the impaired waters list. These include the wastewater system, runoff from surrounding lands, in-lake nutrient re-suspension and runoff from hard surfaces within the park. The lake is currently impaired for bacteria, algae and pH. Through outcomes of the Watershed Assessment and Management Plan, this proposal includes for abandonment and reclamation of the single cell wastewater lagoon site, replacement with three conventional septic systems and construction of two wetlands. One of the wetlands is located on the same site as the reclaimed lagoon and the other is located to intercept sediment and trap nutrients transported by tile lines. The prescribed wastewater system improvements are based on assessment by grab samples test by the State Hygienic Lab, development of a Preliminary Engineering Report, soil analysis and communication with IDNR wastewater officials. The two wetland sites were assessed by officials from IDALS and the Jones County SWCD. This project is part of $1.7 million lake restoration effort to reclaim the 47 year old lake. The lake has a positive economic impact of more than $7.6 million annually and supports an average annual visitation of 58,145, according to the Iowa Lakes Valuation Project, conducted by Iowa State University.

U.S. 61 From Memorial Park Road in Burlington North to 1 Mile North of IA 78 in Louisa County. Des Moines & Louisa County, Iowa NHS-061-2(50) - 19-58, 2015

Iowa Department of Transportation (Iowa DOT) has re-initiated planning and preliminary design studies to improve U.S. 61 from Memorial Park Road in Burlington north to 1-mile north of IA 78 in Louisa County. The proposed project consists of improving approximately 18 miles of roadway from 2-lanes to 4-lanes and evaluating a potential bypass around Mediapolis.

Effectiveness of anti-psychotics and related drugs in the Huntington French-speaking group cohort.

PURPOSE: Huntington's disease is a rare condition. Patients are commonly treated with antipsychotics and tetrabenazine. The evidence of their effect on disease progression is limited and no comparative study between these drugs has been conducted. We therefore compared the effectiveness of antipsychotics on disease progression. METHODS: 956 patients from the Huntington French Speaking Group were followed for up to 8 years between 2002 and 2010. The effectiveness of treatments was assessed using Unified Huntington's Disease Rating Scale (UHDRS) scores and then compared using a mixed model adjusted on a multiple propensity score. RESULTS: 63% of patients were treated with antipsychotics during the survey period. The most commonly prescribed medications were dibenzodiazepines (38%), risperidone (13%), tetrabenazine (12%) and benzamides (12%). There was no difference between treatments on the motor and behavioural declines observed, after taking the patient profiles at the start of the drug prescription into account. In contrast, the functional decline was lower in the dibenzodiazepine group than the other antipsychotic groups (Total Functional Capacity: 0.41 ± 0.17 units per year vs. risperidone and 0.54 ± 0.19 vs. tetrabenazine, both p<0.05). Benzamides were less effective than other antipsychotics on cognitive evolution (Stroop interference, Stroop color and Literal fluency: p<0.05). CONCLUSIONS: Antipsychotics are widely used to treat patients with Huntington's disease. Although differences in motor or behavioural profiles between patients according to the antipsychotics used were small, there were differences in drug effectiveness on the evolution of functional and cognitive scores.

The JAK/STAT3 Pathway Is a Common Inducer of Astrocyte Reactivity in Alzheimer's and Huntington's Diseases.

Astrocyte reactivity is a hallmark of neurodegenerative diseases (ND), but its effects on disease outcomes remain highly debated. Elucidation of the signaling cascades inducing reactivity in astrocytes during ND would help characterize the function of these cells and identify novel molecular targets to modulate disease progression. The Janus kinase/signal transducer and activator of transcription 3 (JAK/STAT3) pathway is associated with reactive astrocytes in models of acute injury, but it is unknown whether this pathway is directly responsible for astrocyte reactivity in progressive pathological conditions such as ND. In this study, we examined whether the JAK/STAT3 pathway promotes astrocyte reactivity in several animal models of ND. The JAK/STAT3 pathway was activated in reactive astrocytes in two transgenic mouse models of Alzheimer's disease and in a mouse and a nonhuman primate lentiviral vector-based model of Huntington's disease (HD). To determine whether this cascade was instrumental for astrocyte reactivity, we used a lentiviral vector that specifically targets astrocytes in vivo to overexpress the endogenous inhibitor of the JAK/STAT3 pathway [suppressor of cytokine signaling 3 (SOCS3)]. SOCS3 significantly inhibited this pathway in astrocytes, prevented astrocyte reactivity, and decreased microglial activation in models of both diseases. Inhibition of the JAK/STAT3 pathway within reactive astrocytes also increased the number of huntingtin aggregates, a neuropathological hallmark of HD, but did not influence neuronal death. Our data demonstrate that the JAK/STAT3 pathway is a common mediator of astrocyte reactivity that is highly conserved between disease states, species, and brain regions. This universal signaling cascade represents a potent target to study the role of reactive astrocytes in ND.