History of adversity, health and psychopathology among prisoners: comparison between men and women

Adversity in childhood, risk behaviors and psychopathology are highly prevalent phenomena in inmate populations and have a strong impact on health. Knowing the differences in these variables between the sexes is most important in order to develop appropriate intervention strategies in a prison context. By administering the Socio-demographic and Life History Questionnaire and the Brief Symptoms Inventory, we sought to characterize adverse childhood experiences and relate them to risk behaviors and to psychopathological symptoms, and study the differences between the 65 male and 42 female detainees in Portuguese prison establishments. Men and women report a complex web of adversity in childhood. In a range of ten possible categories, a medium value of 5.05 (DP = 2.63) in total adversity for women and 2.63 (DP = 2.18) for men was encountered, with the prevalence being significantly higher within the female population (Z = -4.33; p = .000). A high prevalence of risk behaviors and psychopathological symptoms was found in both groups, the latter being higher among females. We concluded that the differences between men and women calls for in depth studies in order to provide guidelines for intervention projects in specific populations.Adversidade na infância, comportamentos de risco e psicopatologia são fenómenos muito prevalentes na população reclusa e com forte impacto na saúde. Conhecer as diferenças entre sexos, no que diz respeito a tais variáveis, é de elevada importância no sentido de adequar estraté- gias de intervenção em contexto prisional. Utilizando o Questionário Sociodemográfico e Histó- ria de Vida, o Questionário de Adversidade na Infância e o Brief Symptons Inventory, procuramos caracterizar a adversidade na infância, os comportamentos de risco e as dimensões psicopatológicas, e averiguar as diferenças entre 65 homens e 42 mulheres reclusos em estabelecimentos prisionais Portugueses. Homens e mulheres relatam um quadro complexo de adversidade na infância. Num total possível de dez categorias, verificamos uma média de adversidade total de 5.05 (DP = 2.63) para as mulheres e de 2.63 (DP = 2.18) para os homens, sendo a prevalência significativamente mais elevada junto da população feminina (Z = -4.33; p = .000). Foi ainda encontrada uma elevada prevalência de comportamentos de risco e de sintomatologia psicopatológica em ambos os grupos, sendo esta última superior nas mulheres. Concluímos que as diferenças entre sexos devem ser estudadas para guiarem a adequação dos projetos

Alternative splicing of exon 10 in the tau gene as a target for treatment of tauopathies

Tau aggregation is one of the major features in Alzheimer's disease and in several other tauopathies, including frontotemporal dementia with Parkinsonism linked to chromosome 17 (FTDP-17), and progressive supranuclear palsy (PSP). More than 35 mutations in the tau gene have been identified from FTDP-17 patients. A group of these mutations alters splicing of exon 10, resulting in an increase in exon 10 inclusion into tau mRNA. Abnormal splicing with inclusion of exon 10 into tau mRNA has also been observed in PSP and AD patients. These results indicate that abnormal splicing of exon 10, leading to the production of tau with exon 10, is probably one of the mechanisms by which tau accumulates and aggregates in tauopathic brains. Therefore, modulation of exon 10 splicing in the tau gene could potentially be targeted to prevent tauopathies. To identify small molecules or compounds that could potentially be developed into drugs to treat tauopathies, we established a cell-based high-throughput screening assay. In this review, we will discuss how realistic, specific biological molecules can be found to regulate exon 10 splicing in the tau gene for potential treatment of tauopathies

Development of carpels and ovules in Dialypetalanthus fuscescens Kuhlm. (Rubiaceae): an enigmatic taxon

ABSTRACT Dialypetalanthus is a monospecific genus that occurs in the Amazon Basin of Brazil, Bolivia and Peru and occupies a controversial position among the Rubiaceae. We continue this taxonomic discussion with the overall aim of clarifying the systematic position of D. fuscescens within the Rubiaceae. To accomplish this, we analyzed the ontogeny of its gynoecium, in particular the floral meristem, as well as the development of the carpels and cauline placentation. Gynosporogenesis and the differentiation of the carpellary septa and ovules were also described. Dialypetalanthus fuscescens was classified according to evolutionary diagrams found in the literature. The following characteristics were observed in D. fuscescens: 1) permanence of the floral meristem in the central basal part of the early flower bud; 2) dual origin of carpellary septum; 3) trizonate ovular primordia with only one fertile gynospore per ovule; and 4) cellular proliferation in the chalazal region. Embryological results confirm the classification of D. fuscescens in the subfamily Ixoroideae. These results are distinct from any others previously proposed in the evolutionary diagram. Therefore, we conclude that this study has presented evidence strongly suggesting that Dialypetalanthus possesses new morphological-type of ovule we refer to as the Dialypetalanthus-type

The competitive transport inhibitor L-trans-pyrrolidine-2, 4-dicarboxylate triggers excitotoxicity in rat cortical neuron-astrocyte co-cultures via glutamate release rather than uptake inhibition

We studied the early and late effects of L-trans-pyrrolidine-2,4-dicarboxylate (PDC), a competitive inhibitor of glutamate uptake with low affinity for glutamate receptors, in co-cultures of rat cortical neurons and glia expressing spontaneous excitatory amino acid (EAA) neurotransmission. At 100 or 200 microM, PDC induced different patterns of electrical changes: 100 microM prolonged tetrodotoxin-sensitive excitation triggered by synaptic glutamate release; 200 microM produced sustained, tetrodotoxin-insensitive and EAA-mediated neuronal depolarization, overwhelming synaptic activity. At 200 microM, but not at 100 microM, PDC caused rapid elevation of the glutamate concentration ([Glu]o) in the culture medium, resulting in NMDA receptor-mediated excitotoxic death of neurons 24 h later. The increase in [Glu]o was largely insensitive to tetrodotoxin, independent of extracellular Ca2+, and present also in astrocyte-pure cultures. By the use of glutamate transporters functionally reconstituted in liposomes, we showed directly that PDC activates carrier-mediated release of glutamate via heteroexchange. Glutamate release and delayed neurotoxicity in our cultures were suppressed if PDC was applied in a Na(+)-free medium containing Li+. However, replacement of Na+ with choline instead of Li+ did not result in an identical effect, suggesting that Li+ does not act simply as an external Na+ substitute. In conclusion, our data indicate that alteration of glutamate transport by PDC has excitotoxic consequences and that active release of glutamate rather than just uptake inhibition is responsible for the generation of neuronal injury

Prostaglandins stimulate calcium-dependent glutamate release in astrocytes

Astrocytes in the brain form an intimately associated network with neurons. They respond to neuronal activity and synaptically released glutamate by raising intracellular calcium concentration ([Ca2+]i), which could represent the start of back-signalling to neurons. Here we show that coactivation of the AMPA/kainate and metabotropic glutamate receptors (mGluRs) on astrocytes stimulates these cells to release glutamate through a Ca2+-dependent process mediated by prostaglandins. Pharmacological inhibition of prostaglandin synthesis prevents glutamate release, whereas application of prostaglandins (in particular PGE2) mimics and occludes the releasing action of GluR agonists. PGE2 promotes Ca2+-dependent glutamate release from cultured astrocytes and also from acute brain slices under conditions that suppress neuronal exocytotic release. When applied to the CA1 hippocampal region, PGE2 induces increases in [Ca2+]i both in astrocytes and in neurons. The [Ca2+]i increase in neurons is mediated by glutamate released from astrocytes, because it is abolished by GluR antagonists. Our results reveal a new pathway of regulated transmitter release from astrocytes and outline the existence of an integrated glutamatergic cross-talk between neurons and astrocytes in situ that may play critical roles in synaptic plasticity and in neurotoxicity