A hisztériával kapcsolatos diskurzusok tanulságai a szomatizációs jelenségek és a betegségmagatartás megértéséhez = The relevance of discourses about hysteria in the understanding of somatization phenomena and illness behaviour

Napjainkban a magatartástudományok képviselőinek egyszerre kell számolniuk a betegségekkel kapcsolatos bizonyosság és tudás konfliktusait előhívó medikalizációs-technicizációs orvostudományi tendenciákkal és a társadalomtudományok ezekre reflektáló, kritikai és „posztmodern” megközelítéseivel. Ebből adódóan igen fontos kihívásként jelentkezik az interdiszciplináris megközelítés szükségessége. Különösen így van ez a nehezen definiálható betegségek - a szomatizációs és pszichoszomatikus zavarok - esetében, ahol a betegségmagatartás gyakorlati problémái, továbbá a tünetek, a diagnózisok és a szenvedés „valódiságának” episztemológiai kérdései egyszerre vannak jelen. Az utóbbi másfél évtized kritikai társadalomtudományi kutatásaiban rendkívüli figyelmet kapott a szomatizációs zavarok és a klasszikus pszichoszomatikus kórképek elődjének számító hisztéria kérdésköre. A tanulmány a szakmai és laikus szóhasználatban nem hivatalosan máig tovább élő betegséggel kapcsolatos társadalomtudományi és orvosi megközelítések közül azokat mutatja be, amelyek szempontokkal szolgálhatnak a szomatizációs és pszichoszomatikus kórképek, valamint a velük kapcsolatos érzelmi és viselkedéses reakciók elemzéséhez és megértéséhez

Defining and measuring gender: A social determinant of health whose time has come

This paper contributes to a nascent scholarly discussion of sex and gender as determinants of health. Health is a composite of biological makeup and socioeconomic circumstances. Differences in health and illness patterns of men and women are attributable both to sex, or biology, and to gender, that is, social factors such as powerlessness, access to resources, and constrained roles. Using examples such as the greater life expectancy of women in most of the world, despite their relative social disadvantage, and the disproportionate risk of myocardial infarction amongst men, but death from MI amongst women, the independent and combined associations of sex and gender on health are explored. A model for incorporating gender into epidemiologic analyses is proposed

Chromosome Painting Reveals Asynaptic Full Alignment of Homologs and HIM-8–Dependent Remodeling of X Chromosome Territories during Caenorhabditis elegans Meiosis

During early meiotic prophase, a nucleus-wide reorganization leads to sorting of chromosomes into homologous pairs and to establishing associations between homologous chromosomes along their entire lengths. Here, we investigate global features of chromosome organization during this process, using a chromosome painting method in whole-mount Caenorhabditis elegans gonads that enables visualization of whole chromosomes along their entire lengths in the context of preserved 3D nuclear architecture. First, we show that neither spatial proximity of premeiotic chromosome territories nor chromosome-specific timing is a major factor driving homolog pairing. Second, we show that synaptonemal complex-independent associations can support full lengthwise juxtaposition of homologous chromosomes. Third, we reveal a prominent elongation of chromosome territories during meiotic prophase that initiates prior to homolog association and alignment. Mutant analysis indicates that chromosome movement mediated by association of chromosome pairing centers (PCs) with mobile patches of the nuclear envelope (NE)–spanning SUN-1/ZYG-12 protein complexes is not the primary driver of territory elongation. Moreover, we identify new roles for the X chromosome PC (X-PC) and X-PC binding protein HIM-8 in promoting elongation of X chromosome territories, separable from their role(s) in mediating local stabilization of pairing and association of X chromosomes with mobile SUN-1/ZYG-12 patches. Further, we present evidence that HIM-8 functions both at and outside of PCs to mediate chromosome territory elongation. These and other data support a model in which synapsis-independent elongation of chromosome territories, driven by PC binding proteins, enables lengthwise juxtaposition of chromosomes, thereby facilitating assessment of their suitability as potential pairing partners

Differential Localization and Independent Acquisition of the H3K9me2 and H3K9me3 Chromatin Modifications in the Caenorhabditis elegans Adult Germ Line

Histone methylation is a prominent feature of eukaryotic chromatin that modulates multiple aspects of chromosome function. Methyl modification can occur on several different amino acid residues and in distinct mono-, di-, and tri-methyl states. However, the interplay among these distinct modification states is not well understood. Here we investigate the relationships between dimethyl and trimethyl modifications on lysine 9 of histone H3 (H3K9me2 and H3K9me3) in the adult Caenorhabditis elegans germ line. Simultaneous immunofluorescence reveals very different temporal/spatial localization patterns for H3K9me2 and H3K9me3. While H3K9me2 is enriched on unpaired sex chromosomes and undergoes dynamic changes as germ cells progress through meiotic prophase, we demonstrate here that H3K9me3 is not enriched on unpaired sex chromosomes and localizes to all chromosomes in all germ cells in adult hermaphrodites and until the primary spermatocyte stage in males. Moreover, high-copy transgene arrays carrying somatic-cell specific promoters are highly enriched for H3K9me3 (but not H3K9me2) and correlate with DAPI-faint chromatin domains. We further demonstrate that the H3K9me2 and H3K9me3 marks are acquired independently. MET-2, a member of the SETDB histone methyltransferase (HMTase) family, is required for all detectable germline H3K9me2 but is dispensable for H3K9me3 in adult germ cells. Conversely, we show that the HMTase MES-2, an E(z) homolog responsible for H3K27 methylation in adult germ cells, is required for much of the germline H3K9me3 but is dispensable for H3K9me2. Phenotypic analysis of met-2 mutants indicates that MET-2 is nonessential for fertility but inhibits ectopic germ cell proliferation and contributes to the fidelity of chromosome inheritance. Our demonstration of the differential localization and independent acquisition of H3K9me2 and H3K9me3 implies that the trimethyl modification of H3K9 is not built upon the dimethyl modification in this context. Further, these and other data support a model in which these two modifications function independently in adult C. elegans germ cells

Meiotic mutants that cause a polar decrease in recombination on the X chromosome in Caenorhabditis elegans

Recessive mutations in three autosomal genes, him-1, him-5 and him-8, cause high levels of X chromosome nondisjunction in hermaphrodites of Caenorhabditis elegans, with no comparable effect on autosomal disjunction. Each of the mutants has reduced levels of X chromosome recombination, correlating with the increase in nondisjunction. However, normal or elevated levels of recombination occur at the end of the X chromosome hypothesized to contain the pairing region (the left end), with recombination levels decreasing in regions approaching the right end. Thus, both the number and the distribution of X chromosome exchange events are altered in these mutants. As a result, the genetic map of the X chromosome in the him mutants exhibits a clustering of genes due to reduced recombination, a feature characteristic of the genetic map of the autosomes in non-mutant animals. We hypothesize that these him genes are needed for some processive event that initiates near the left end of the X chromosome