Lloret de Mar : destruccions i resistencies d'un poble en mans del turisme

En aquest article es reflecteix l’estat actual d’una recerca socioantropològica en curs sobre les transformacions d’un poble de la Costa Brava sotmès a les pressions de signe divers, d’una enorme onada turística (més de 100.000 persones en el mes d’agost), de la immigració del sud d’Espanya i de la burgesia autòctona. Fins a quin punt el teixit social del poble s’esquerda i es trenca amb la destrucció de l’economia tradicional –el pas d’una activitat extractiva al domini del sector terciari– i la renovació de més de la meitat de la població estable? Una ruptura de les estructures productives engendra un canvi total de les relacions socials i ideològiques? La resposta no és senzilla. La societat de Lloret s’ha erosionat a causa de: 1) Una major dependència respecte d’un exterior no controlable (financer, operadors turístics, mà d’obra, producció per al consum, etc.) 2) Una alteració dels centres i de les formes de poder. 3) Una metamorfosi dels ritmes i les manifestacions de la vida natural i social. 4) Una pèrdua de funcionalitat d’institucions i grups abans importants, com la família, l’església, la vellesa. 5) Un divorci cada vegada més gran entre la quotidianitat i els valors tradicionals. L’estructura de les classes socials també s’ha modificat. Però, davant d’aquestes mutacions, l’edifici social ha trobat unes acomodacions econòmiques i ideològiques, ha reforçat els seus llaços interns, s’ha fet més complex. Per fi, ha resistit tractant de recolzar-se en els seus fonaments més profunds. El ressorgiment actual de les manifestacions populars catalanes a Lloret és en certa manera una sortida i una oposició a les tendències externes de dispersió i de disgregació. Aquesta reacció se sosté en unes arrels històriques no desmantellades, en la diferenciació lingüística, en una trama de pràctiques socials específiques, en una difusa consciència de pertinença a una comunitat nacional perseguida. Podria resumir-se la qüestió en aquests termes: davant l’imperialisme, resistència nacional popular? Massa simple per respondre a la complexitat de la realitat del Lloret de 1978

A Europa nas Trevas

Esta edição é uma versão revista e aumentada da edição original (Icaria Editorial, 2018)Este livro é um ensaio comparativo das políticas sociais que tiveram origem e foram aplicadas no nazismo, no fascismo italiano, no salazarismo e no franquismo. Nos quatro países, as ideias que levaram ao fascismo têm suas raízes no século XIX. A Primeira Guerra Mundial e a crise económica de 1929 aceleraram as políticas económicas, sociais e laborais numa tentativa de efetuar a integração interclassista, criar mecanismos corporativos e sindicais de assistência, reproduzir a força de trabalho e adaptar os sistemas de proteção social. A Beneficência, os Serviços Sociais e os Trabalhadores Sociais foram também afetados pelas mudanças introduzidas por esses regimes, alcançando altos níveis de consentimento controlado. Este trabalho dedica uma especial atenção à evolução dos dois países ibéricos e termina com um conjunto de reflexões sobre como enfrentar a fragilidade democrática atual. Como combater o fascismo e as crescentes formas de populismo que pairam sobre a Europa de hoje, se continuam nas trevas as condições que anteriormente as tornaram possíveis? Este livro é destinado a todos aqueles que não querem que a história se repita. Nesta versão portuguesa da edição catalã (Icaria Editorial, 2018, Barcelona), foram alterados alguns títulos e, sobretudo, reduzido um longo capítulo sobre a história da beneficência e da assistência na Catalunha e no Estado espanhol, nele inserindo, quando possível, comparações com a situação portuguesa. Foi ainda incluído um novo capítulo sobre o início da economia social em Portugal.info:eu-repo/semantics/publishedVersio

La configuración y las consecuencias del miedo en el espacio público desde la perspectiva de género

As various works show, fear is one of the most important limitations of women's access to public space. In this article we examine the configuration of fear and its consequences based on the empirical qualitative work conducted with 70 young men and women in three villages in the Basque Country. The aim is to analyse the perception of it from a gender and spatial perspective to understand how fear is configured, perceived and what kind of implications it has for women. Main results show that gender and age condition the perception of fear, that it is based on the public/private dichotomy and that this same dichotomy renders some kinds of violence against women invisible and perpetuates it.Como muestran numerosos estudios, el miedo es una de las limitaciones más importantes para el acceso de las mujeres al espacio público. En este artículo examinamos la configuración del mismo y sus consecuencias en base al trabajo empírico cualitativo realizado con 70 chicos y chicas jóvenes en tres localidades del País Vasco. El objetivo es analizar la percepción del miedo desde una perspectiva de género y espacial para comprender en qué se basa, cómo se percibe y qué implicaciones tiene para las mujeres. Los principales resultados muestran que el género y la edad condicionan la percepción del miedo, que este se fundamenta en la dicotomía público/privado y que la misma dicotomía es la que invisibiliza y perpetúa determinadas formas de violencia contra las mujeres

Genome-wide analysis of single nucleotide polymorphisms and copy number variants in fibromyalgia suggest a role for the central nervous system

Fibromyalgia (FM) is a highly disabling syndrome defined by a low pain threshold and a permanent state of pain. The mechanisms explaining this complex disorder remain unclear, and its genetic factors have not yet been identified. With the aim of elucidating FM genetic susceptibility factors, we selected 313 FM cases having low comorbidities, and we genotyped them on the Illumina 1 million duo array. Genotypic data from 220 control women (Illumina 610k array) was obtained for genome-wide association scan (GWAS) analysis. Copy number variants in FM susceptibility were analyzed by array comparative genomic hybridization (aCGH) experiments on pooled samples using the Agilent 2 × 400K platform. No single nucleotide polymorphism (SNP) reached GWAS association threshold, but 21 of the most associated SNPs were chosen for replication in 952 cases and 644 controls. Four of the SNPs selected for replication showed a nominal association in the joint analysis, and rs11127292 (MYT1L) was found to be associated to FM with low comorbidities (P = 4.28 × 10−5, odds ratio [95% confidence interval] = 0.58 [0.44-0.75]). aCGH detected 5 differentially hybridized regions. They were followed up, and an intronic deletion in NRXN3 was demonstrated to be associated to female cases of FM with low levels of comorbidities (P = .021, odds ratio [95% confidence interval] = 1.46 [1.05-2.04]). Both GWAS and aCGH results point to a role for the central nervous system in FM genetic susceptibility. If the proposed FM candidate genes were further validated in replication studies, this would highlight a neurocognitive involvement in agreement with latest reports

The V617F mutation of JAK2 is very uncommon in patients with thrombosis

Given that many cases of thrombosis do not have a clear cause, a myeloproliferative disease could be involved. We investigated the V617F mutation of the JAK2 gene in 295 patients with thrombosis. Only one case was positive. Therefore, the study of this mutation is not necessary in all patients with idiopathic thrombosis

Traffic-related air pollution, oxidative stress genes, and asthma (ECHRS)

BACKGROUND: Traffic-related air pollution is related with asthma, and this association may be modified by genetic factors. OBJECTIVES: We investigated the role of genetic polymorphisms potentially modifying the association between home outdoor levels of modeled nitrogen dioxide and asthma. METHODS: Adults from 13 cities of the second European Community Respiratory Health Survey (ECRHS II) were included (n = 2,920), for whom both DNA and outdoor NO(2) estimates were available. Home addresses were geocoded and linked to modeled outdoor NO(2) estimates, as a marker of local traffic-related pollution. We examined asthma prevalence and evaluated polymorphisms in genes involved in oxidative stress pathways [gluthatione S-transferases M1 (GSTM1), T1 (GSTT1), and P1 (GSTP1) and NAD(P)H:quinine oxidoreductase (NQO1)], inflammatory response [tumor necrosis factor alpha (TNFA)], immunologic response [Toll-like receptor 4 (TLR4)], and airway reactivity [adrenergic receptor beta2 (ADRB2)]. RESULTS: The association between modeled NO(2) and asthma prevalence was significant for carriers of the most common genotypes of NQO1 rs2917666 [odds ratio (OR) = 1.54; 95% confidence interval (CI), 1.10-2.24], TNFA rs2844484 (OR = 2.02; 95% CI, 1.30-3.27). For new-onset asthma, the effect of NO(2) was significant for the most common genotype of NQO1 rs2917666 (OR = 1.52; 95% CI, 1.09-2.16). A significant interaction was found between NQO1 rs2917666 and NO(2) for asthma prevalence (p = 0.02) and new-onset asthma (p = 0.04). CONCLUSIONS: Genetic polymorphisms in the NQO1 gene are related to asthma susceptibility among persons exposed to local traffic-related air pollution. This points to the importance of antioxidant pathways in the protection against the effects of air pollution on asthm

Transgenic mice overexpressing the full-length neurotrophin receptor TrkC exhibit increased catecholaminergic neuron density in specific brain areas and increased anxiety-like behavior and panic reaction

Accumulating evidence has suggested that neurotrophins participate in the pathophysiology of mood disorders. We have developed transgenic mice overexpressing the full-length neurotrophin-3 receptor TrkC (TgNTRK3) in the central nervous system. TgNTRK3 mice show increased anxiety-like behavior and enhancement of panic reaction in the mouse defense test battery, along with an increase in the number and density of catecholaminergic (tyrosine hydroxylase positive) neurons in locus coeruleus and substantia nigra. Furthermore, treatment of TgNTRK3 mice with diazepam significantly attenuated the anxiety-like behaviors in the plus maze. These results provide evidence for the involvement of TrkC in the development of noradrenergic neurons in the central nervous system with consequences on anxiety-like behavior and panic reaction. Thus, changes in TrkC expression levels could contribute to the phenotypic expression of panic disorder through a trophic effect on noradrenergic neurons in the locus coeruleus. Our results demonstrate that the elevated NT3-TrkC tone via overexpression of TrkC in the brain may constitute a molecular mechanism for the expression of anxiety and anxiety

Missense mutations in TENM4, a regulator of axon guidance and central myelination, cause essential tremor

Essential tremor (ET) is a common movement disorder with an estimated prevalence of 5% of the population aged over 65 years. In spite of intensive efforts, the genetic architecture of ET remains unknown. We used a combination of whole-exome sequencing and targeted resequencing in three ET families. In vitro and in vivo experiments in oligodendrocyte precursor cells and zebrafish were performed to test our findings. Whole-exome sequencing revealed a missense mutation in TENM4 segregating in an autosomal-dominant fashion in an ET family. Subsequent targeted resequencing of TENM4 led to the discovery of two novel missense mutations. Not only did these two mutations segregate with ET in two additional families, but we also observed significant over transmission of pathogenic TENM4 alleles across the three families. Consistent with a dominant mode of inheritance, in vitro analysis in oligodendrocyte precursor cells showed that mutant proteins mislocalize. Finally, expression of human mRNA harboring any of three patient mutations in zebrafish embryos induced defects in axon guidance, confirming a dominant-negative mode of action for these mutations. Our genetic and functional data, which is corroborated by the existence of a Tenm4 knockout mouse displaying an ET phenotype, implicates TENM4 in ET. Together with previous studies of TENM4 in model organisms, our studies intimate that processes regulating myelination in the central nervous system and axon guidance might be significant contributors to the genetic burden of this disorde

Variants at APOE influence risk of deep and lobar intracerebral hemorrhage

Objective Prior studies investigating the association between APOE alleles ε2/ε4 and risk of intracerebral hemorrhage (ICH) have been inconsistent and limited to small sample sizes, and did not account for confounding by population stratification or determine which genetic risk model was best applied. Methods We performed a large-scale genetic association study of 2189 ICH cases and 4041 controls from 7 cohorts, which were analyzed using additive models for ε2 and ε4. Results were subsequently meta-analyzed using a random effects model. A proportion of the individuals (322 cases, 357 controls) had available genome-wide data to adjust for population stratification. Results Alleles ε2 and ε4 were associated with lobar ICH at genome-wide significance levels (odds ratio [OR] = 1.82, 95% confidence interval [CI] = 1.50–2.23, p = 6.6 × 10 −10 ; and OR = 2.20, 95%CI = 1.85–2.63, p = 2.4 × 10 −11 , respectively). Restriction of analysis to definite/probable cerebral amyloid angiopathy ICH uncovered a stronger effect. Allele ε4 was also associated with increased risk for deep ICH (OR = 1.21, 95% CI = 1.08–1.36, p = 2.6 × 10 −4 ). Risk prediction evaluation identified the additive model as best for describing the effect of APOE genotypes. Interpretation APOE ε2 and ε4 are independent risk factors for lobar ICH, consistent with their known associations with amyloid biology. In addition, we present preliminary findings on a novel association between APOE ε4 and deep ICH. Finally, we demonstrate that an additive model for these APOE variants is superior to other forms of genetic risk modeling previously applied. ANN NEUROL 2010Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/78478/1/22134_ftp.pd

Genetic Variants of the FADS Gene Cluster and ELOVL Gene Family, Colostrums LC-PUFA Levels, Breastfeeding, and Child Cognition

Introduction: Breastfeeding effects on cognition are attributed to long-chain polyunsaturated fatty acids (LC-PUFAs), but controversy persists. Genetic variation in fatty acid desaturase (FADS) and elongase (ELOVL) enzymes has been overlooked when studying the effects of LC-PUFAs supply on cognition. We aimed to: 1) to determine whether maternal genetic variants in the FADS cluster and ELOVL genes contribute to differences in LC-PUFA levels in colostrum; 2) to analyze whether these maternal variants are related to child cognition; and 3) to assess whether children's variants modify breastfeeding effects on cognition. Methods: Data come from two population-based birth cohorts (n = 400 mother-child pairs from INMA-Sabadell; and n = 340 children from INMA-Menorca). LC-PUFAs were measured in 270 colostrum samples from INMA-Sabadell. Tag SNPs were genotyped both in mothers and children (13 in the FADS cluster, 6 in ELOVL2, and 7 in ELOVL5). Child cognition was assessed at 14 mo and 4 y using the Bayley Scales of Infant Development and the McCarthy Scales of Children"s Abilities, respectively. Results: Children of mothers carrying genetic variants associated with lower FADS1 activity (regulating AA and EPA synthesis), higher FADS2 activity (regulating DHA synthesis), and with higher EPA/AA and DHA/AA ratios in colostrum showed a significant advantage in cognition at 14 mo (3.5 to 5.3 points). Not being breastfed conferred an 8- to 9-point disadvantage in cognition among children GG homozygote for rs174468 (low FADS1 activity) but not among those with the A allele. Moreover, not being breastfed resulted in a disadvantage in cognition (5 to 8 points) among children CC homozygote for rs2397142 (low ELOVL5 activity), but not among those carrying the G allele. Conclusion: Genetically determined maternal supplies of LC-PUFAs during pregnancy and lactation appear to be crucial for child cognition. Breastfeeding effects on cognition are modified by child genetic variation in fatty acid desaturase and elongase enzymes