By adopting the Policy for Global Development (PGD) in 2003 the Swedish parliament established gender mainstreaming as a goal in development cooperation policy, thereby emphasizing women’s role as agents of empowerment in development. This has not always been the case. During most of the history of Swedish foreign aid women issues have been handled separately and development policy mainly based on a male perspective. A lot of research has focused on trends in the global debate over how to better integrate women in development process, but much less academic attention has focused on how Swedish development policy has addressed the issue and how women have been referred to in development policy since the origin of Swedish foreign aid. According to the theories of critical discourse analysis (CDA) our written and spoken language influence our view of the reality and how we understand society. Following that logic, how women are referred to in Swedish development policy influence how women are perceived by the actors of development cooperation. Through a critical discourse analysis of official Swedish governmental documents concerning foreign aid, such as government bills and letters of appropriation, this study aims to detect discourses of Swedish development policy regarding women in developing countries. Furthermore it aims to understand how these discourses have related to the global debate about women’s role in development. This study observes six discourses of women in developing countries in the material: Women as passive recipient, agent of empowerment, the savior, motherhood-women as mothers, the other woman, and the man as the norm. The analysis shows Sweden’s development policies following the global discussions fairly coherently during much of the period, with 80s as the only possible exception.

<p>The purpose of this study is to understand the situation concerning women and gender in relation to development, in the Mozambican district of Nacala Porto. The ambition is to identify present theoretical feminist perspectives in terms of perceived problems for women, their ability to solve them, focus areas for improvement and strategies for reaching development aims.</p><p>To enable an understanding of the situation concerning women and gender in relation to development, we have conducted an analytical framework consisting of three main theoretical feminist perspectives in international development policies. These were applied as analytical tools, which consisted of Ester Boserups perspective of Women’s role in economic development, Women In Development (WID) and Gender And Development (GAD).</p><p>The study displayed a discrepancy between the powerful women in the Mozambican parliament and the lack of social power described by the women in Nacala Porto. At the district level the results showed a dominating modernistic paradigm, similar to the situation identified by Boserup, who emphasised that the economical development did not benefit women equally. The subordination of women has been apparent in the district. The long-term strategy of transforming the gender structure has been met with support as well as resistance. The GAD-aim of mainstreaming gender showed a gap between international policy and practise in the district. The interventions that were WID-oriented have on the other hand shown progress regarding female representation, non-discriminatory legislation and increase of girls starting primary school. However, the WID-progress is limited without a gender perspective.</p><p>Three main areas were continuously discussed as means having to change, to potentially alleviate poverty and include women in the development process. These areas were the access to employment, sustainable education and functioning family relations. The interdependence of these areas also seemed to require an integration of the three theoretical feminist perspectives of Boserup, WID and GAD.</p>

Understanding the specificity of homeobox genes has been hampered by the lack of verified direct transcriptional targets. The Dlx family of homeobox genes is expressed in the ganglionic eminences of the developing forebrain. Dlx1/Dlx2 double knockout (DKO) mice die at birth. Phenotypic analyses demonstrate abnormal development of the basal telencephalon, including defects in neuronal differentiation in the basal ganglia, reduced expression of GABA in the basal telencephalon, and loss of migration of GABAergic inhibitory interneurons to the neocortex. The mechanisms underlying DLX protein regulation of differentiation and migration of GABAergic interneurons are poorly defined. We have successfully applied chromatin immunoprecipitation to identify potential direct transcriptional targets of DLX homeoproteins from embryonic tissues in vivo. Reporter gene assays demonstrated the transcriptional significance of the binding of DLX proteins to different downstream regulatory elements, which were confirmed in vitro by electrophoretic mobility shift assay and site-directed mutagenesis. The functional significance of DLX mediated transcriptional regulation of these targets was further elaborated through several series of loss-of-function assays including gene expression in Dlx1/2 knockout embryonic forebrain tissues, as well as siRNA or Lentiviral mediated shRNA knockdown experiments with primary forebrain cultures. Quantitative analysis of the regulatory effect of Dlx genes on various forebrain markers of differentiation and migration was performed using in situ hybridization, high-performance liquid chromatography coupled with cell counting. Neuronal migration was assessed by forebrain explants and diI labelling of migratory cells from ganglionic eminence to neocortex. We have demonstrated that DLX1 and DLX2 can transcriptionally activate (Gad1, Gad2) or repress (Nrp2) different downstream targets. In the Dlx1/2 DKO, reduction of GABA expression and failure of GABAergic interneurons to migrate to the neocortex is partly due to loss or aberrant expression of these DLX downstream targets. In the triple Dlx1/2; Nrp2KO, partial restoration of tangential migration of GABAergic interneurons from basal ganglia to the neocortex was successfully established signifying the importance of DLX regulation of Semaphorin-Neuropilin signalling during forebrain development.

Understanding the specificity of homeobox genes has been hampered by the lack of verified direct transcriptional targets. The Dlx family of homeobox genes is expressed in the ganglionic eminences of the developing forebrain. Dlx1/Dlx2 double knockout (DKO) mice die at birth. Phenotypic analyses demonstrate abnormal development of the basal telencephalon, including defects in neuronal differentiation in the basal ganglia, reduced expression of GABA in the basal telencephalon, and loss of migration of GABAergic inhibitory interneurons to the neocortex. The mechanisms underlying DLX protein regulation of differentiation and migration of GABAergic interneurons are poorly defined. We have successfully applied chromatin immunoprecipitation to identify potential direct transcriptional targets of DLX homeoproteins from embryonic tissues in vivo. Reporter gene assays demonstrated the transcriptional significance of the binding of DLX proteins to different downstream regulatory elements, which were confirmed in vitro by electrophoretic mobility shift assay and site-directed mutagenesis. The functional significance of DLX mediated transcriptional regulation of these targets was further elaborated through several series of loss-of-function assays including gene expression in Dlx1/2 knockout embryonic forebrain tissues, as well as siRNA or Lentiviral mediated shRNA knockdown experiments with primary forebrain cultures. Quantitative analysis of the regulatory effect of Dlx genes on various forebrain markers of differentiation and migration was performed using in situ hybridization, high-performance liquid chromatography coupled with cell counting. Neuronal migration was assessed by forebrain explants and diI labelling of migratory cells from ganglionic eminence to neocortex. We have demonstrated that DLX1 and DLX2 can transcriptionally activate (Gad1, Gad2) or repress (Nrp2) different downstream targets. In the Dlx1/2 DKO, reduction of GABA expression and failure of GABAergic interneurons to migrate to the neocortex is partly due to loss or aberrant expression of these DLX downstream targets. In the triple Dlx1/2; Nrp2KO, partial restoration of tangential migration of GABAergic interneurons from basal ganglia to the neocortex was successfully established signifying the importance of DLX regulation of Semaphorin-Neuropilin signalling during forebrain development.

O ácido metilmalônico (MMA) é um agente convulsivante endógeno que se acumula na acidemia metilmalônica, um erro inato no metabolismo caracterizado por disfunções neurológicas severas, predispondo ao aparecimento de convulsão. O mecanismo responsável pelas convulsões induzidas pelo MMA envolve a ativação do receptor NMDA. O envolvimento GABAérgico nas convulsões induzidas pelo MMA ainda não foi demonstrado. Desta forma, no presente estudo objetivou investigar o envolvimento de macanismos GABAérgicos nas convulsões induzidas pelo MMA. Ratos adultos foram injetados (i.c.v.) com muscimol (46 pmol/1 ml), baclofen (0.03, 0.1 and 0.3 mmol/1 ml), MK- 801 (6 nmol/1 ml), piridoxine (2 mmol/ 4 ml) ou salina (0.15 mmol/1 ml). Após trinta minutos, MMA (0.3, 0.1 and 3 mmol/1 ml) ou NaCl (6 mmol/1 ml, i.c.v.) eram injetados. Após estas injeções, os animais eram transferidos imediatamente para um campo aberto, sendo observado o aparecimento de convulsões. Após a avaliação comportamental, foi dosada a atividade glutamato descarboxilase (GAD) em homogeneizado de córtex cerebral, mensurando a quantidade de 14CO2 liberado do L-[14C]-glutamato. As convulsões foram confirmadas pelo estudo eletrencefalográfico. O MMA induziu convulsões do tipo crônicas de forma dose-dependente e reduziu a atividade da GAD no córtex cerebral ex vivo. A atividade da GAD correlacionou-se negativamente com a duração das convulsões (r=- 0.873, P<0.01), mas somente o MK-801 e a piridoxina reverteram à inibição da GAD pelo MMA. Estes resultados sugerem o envolvimento de mecanismos GABAérgicos nas convulsões induzidas pelo MMA, e que a inibição da GAD depende da ativação de receptores NMDA ou da proteção da enzima pela piridoxina. Por fim, o presente estudo propôs, de forma inovadora, o envolvimento do sistema GABAérgico nas convulsões induzidas pelo MMA e o envolvimento dos receptores NMDA na falha da transmissão GABAérgica. / Methylmalonic acid (MMA) is an endogenous convulsing compound that accumulates in methylmalonic acidemia, an inborn error of the metabolism characterized by severe neurological dysfunction, including seizures. The mechanisms by which MMA causes seizures involves the activation of the NMDA receptors, but whether GABAergic mechanisms are involved in the convulsions induced by MMA is not known. Therefore, in the current study we investigated the involvement of GABAergic mechanisms in the convulsions induced by MMA. Adult rats were injected (i.c.v.) with muscimol (46 pmol/1 ml), baclofen (0.03, 0.1 and 0.3 mmol/1 ml), MK-801 (6 nmol/1 ml), pyridoxine (2 mmol/ 4 ml) or physiological saline (0.15 mmol/1 ml). After thirty minutes, MMA (0.3, 0.1 and 3 mmol/1 ml) or NaCl (6 mmol/1 ml, i.c.v.) was injected. The animals were immediately transferred to an open field and observed for the appearance of convulsions. After behavioral evaluation, glutamate decarboxylase (GAD) activity was determined in cerebral cortex homogenates by measuring the 14CO2 released from L-[14C]-glutamic acid. Convulsions were confirmed by electroencephalographic recording in a subset of animals. MMA caused the appearance of clonic convulsions in a dose-dependent manner and decreased GAD activity in the cerebral cortex ex vivo. GAD activity negatively correlated with duration of MMA-induced convulsions (r=-0.873, P<0.01), in an individual basis. Muscimol, baclofen, MK-801 and pyridoxine prevented MMA-induced convulsions, but only MK-801 and pyridoxine prevented MMA-induced GAD inhibition. These data suggest GABAergic mechanisms are involved in the convulsive action of MMA, and that GAD inhibition by MMA depends on the activation of NMDA receptors or enzyme protection by pyridoxine. While in this study we present novel data about the role of the GABAergic system in MMAinduced convulsions, the central role of NMDA receptors in the neurochemical actions of MMA is further reinforced since they seem to trigger GABAergic failure.

O ácido metilmalônico (MMA) é um agente convulsivante endógeno que se acumula na acidemia metilmalônica, um erro inato no metabolismo caracterizado por disfunções neurológicas severas, predispondo ao aparecimento de convulsão. O mecanismo responsável pelas convulsões induzidas pelo MMA envolve a ativação do receptor NMDA. O envolvimento GABAérgico nas convulsões induzidas pelo MMA ainda não foi demonstrado. Desta forma, no presente estudo objetivou investigar o envolvimento de macanismos GABAérgicos nas convulsões induzidas pelo MMA. Ratos adultos foram injetados (i.c.v.) com muscimol (46 pmol/1 ml), baclofen (0.03, 0.1 and 0.3 mmol/1 ml), MK- 801 (6 nmol/1 ml), piridoxine (2 mmol/ 4 ml) ou salina (0.15 mmol/1 ml). Após trinta minutos, MMA (0.3, 0.1 and 3 mmol/1 ml) ou NaCl (6 mmol/1 ml, i.c.v.) eram injetados. Após estas injeções, os animais eram transferidos imediatamente para um campo aberto, sendo observado o aparecimento de convulsões. Após a avaliação comportamental, foi dosada a atividade glutamato descarboxilase (GAD) em homogeneizado de córtex cerebral, mensurando a quantidade de 14CO2 liberado do L-[14C]-glutamato. As convulsões foram confirmadas pelo estudo eletrencefalográfico. O MMA induziu convulsões do tipo crônicas de forma dose-dependente e reduziu a atividade da GAD no córtex cerebral ex vivo. A atividade da GAD correlacionou-se negativamente com a duração das convulsões (r=- 0.873, P<0.01), mas somente o MK-801 e a piridoxina reverteram à inibição da GAD pelo MMA. Estes resultados sugerem o envolvimento de mecanismos GABAérgicos nas convulsões induzidas pelo MMA, e que a inibição da GAD depende da ativação de receptores NMDA ou da proteção da enzima pela piridoxina. Por fim, o presente estudo propôs, de forma inovadora, o envolvimento do sistema GABAérgico nas convulsões induzidas pelo MMA e o envolvimento dos receptores NMDA na falha da transmissão GABAérgica. / Methylmalonic acid (MMA) is an endogenous convulsing compound that accumulates in methylmalonic acidemia, an inborn error of the metabolism characterized by severe neurological dysfunction, including seizures. The mechanisms by which MMA causes seizures involves the activation of the NMDA receptors, but whether GABAergic mechanisms are involved in the convulsions induced by MMA is not known. Therefore, in the current study we investigated the involvement of GABAergic mechanisms in the convulsions induced by MMA. Adult rats were injected (i.c.v.) with muscimol (46 pmol/1 ml), baclofen (0.03, 0.1 and 0.3 mmol/1 ml), MK-801 (6 nmol/1 ml), pyridoxine (2 mmol/ 4 ml) or physiological saline (0.15 mmol/1 ml). After thirty minutes, MMA (0.3, 0.1 and 3 mmol/1 ml) or NaCl (6 mmol/1 ml, i.c.v.) was injected. The animals were immediately transferred to an open field and observed for the appearance of convulsions. After behavioral evaluation, glutamate decarboxylase (GAD) activity was determined in cerebral cortex homogenates by measuring the 14CO2 released from L-[14C]-glutamic acid. Convulsions were confirmed by electroencephalographic recording in a subset of animals. MMA caused the appearance of clonic convulsions in a dose-dependent manner and decreased GAD activity in the cerebral cortex ex vivo. GAD activity negatively correlated with duration of MMA-induced convulsions (r=-0.873, P<0.01), in an individual basis. Muscimol, baclofen, MK-801 and pyridoxine prevented MMA-induced convulsions, but only MK-801 and pyridoxine prevented MMA-induced GAD inhibition. These data suggest GABAergic mechanisms are involved in the convulsive action of MMA, and that GAD inhibition by MMA depends on the activation of NMDA receptors or enzyme protection by pyridoxine. While in this study we present novel data about the role of the GABAergic system in MMAinduced convulsions, the central role of NMDA receptors in the neurochemical actions of MMA is further reinforced since they seem to trigger GABAergic failure.

O ácido metilmalônico (MMA) é um agente convulsivante endógeno que se acumula na acidemia metilmalônica, um erro inato no metabolismo caracterizado por disfunções neurológicas severas, predispondo ao aparecimento de convulsão. O mecanismo responsável pelas convulsões induzidas pelo MMA envolve a ativação do receptor NMDA. O envolvimento GABAérgico nas convulsões induzidas pelo MMA ainda não foi demonstrado. Desta forma, no presente estudo objetivou investigar o envolvimento de macanismos GABAérgicos nas convulsões induzidas pelo MMA. Ratos adultos foram injetados (i.c.v.) com muscimol (46 pmol/1 ml), baclofen (0.03, 0.1 and 0.3 mmol/1 ml), MK- 801 (6 nmol/1 ml), piridoxine (2 mmol/ 4 ml) ou salina (0.15 mmol/1 ml). Após trinta minutos, MMA (0.3, 0.1 and 3 mmol/1 ml) ou NaCl (6 mmol/1 ml, i.c.v.) eram injetados. Após estas injeções, os animais eram transferidos imediatamente para um campo aberto, sendo observado o aparecimento de convulsões. Após a avaliação comportamental, foi dosada a atividade glutamato descarboxilase (GAD) em homogeneizado de córtex cerebral, mensurando a quantidade de 14CO2 liberado do L-[14C]-glutamato. As convulsões foram confirmadas pelo estudo eletrencefalográfico. O MMA induziu convulsões do tipo crônicas de forma dose-dependente e reduziu a atividade da GAD no córtex cerebral ex vivo. A atividade da GAD correlacionou-se negativamente com a duração das convulsões (r=- 0.873, P<0.01), mas somente o MK-801 e a piridoxina reverteram à inibição da GAD pelo MMA. Estes resultados sugerem o envolvimento de mecanismos GABAérgicos nas convulsões induzidas pelo MMA, e que a inibição da GAD depende da ativação de receptores NMDA ou da proteção da enzima pela piridoxina. Por fim, o presente estudo propôs, de forma inovadora, o envolvimento do sistema GABAérgico nas convulsões induzidas pelo MMA e o envolvimento dos receptores NMDA na falha da transmissão GABAérgica. / Methylmalonic acid (MMA) is an endogenous convulsing compound that accumulates in methylmalonic acidemia, an inborn error of the metabolism characterized by severe neurological dysfunction, including seizures. The mechanisms by which MMA causes seizures involves the activation of the NMDA receptors, but whether GABAergic mechanisms are involved in the convulsions induced by MMA is not known. Therefore, in the current study we investigated the involvement of GABAergic mechanisms in the convulsions induced by MMA. Adult rats were injected (i.c.v.) with muscimol (46 pmol/1 ml), baclofen (0.03, 0.1 and 0.3 mmol/1 ml), MK-801 (6 nmol/1 ml), pyridoxine (2 mmol/ 4 ml) or physiological saline (0.15 mmol/1 ml). After thirty minutes, MMA (0.3, 0.1 and 3 mmol/1 ml) or NaCl (6 mmol/1 ml, i.c.v.) was injected. The animals were immediately transferred to an open field and observed for the appearance of convulsions. After behavioral evaluation, glutamate decarboxylase (GAD) activity was determined in cerebral cortex homogenates by measuring the 14CO2 released from L-[14C]-glutamic acid. Convulsions were confirmed by electroencephalographic recording in a subset of animals. MMA caused the appearance of clonic convulsions in a dose-dependent manner and decreased GAD activity in the cerebral cortex ex vivo. GAD activity negatively correlated with duration of MMA-induced convulsions (r=-0.873, P<0.01), in an individual basis. Muscimol, baclofen, MK-801 and pyridoxine prevented MMA-induced convulsions, but only MK-801 and pyridoxine prevented MMA-induced GAD inhibition. These data suggest GABAergic mechanisms are involved in the convulsive action of MMA, and that GAD inhibition by MMA depends on the activation of NMDA receptors or enzyme protection by pyridoxine. While in this study we present novel data about the role of the GABAergic system in MMAinduced convulsions, the central role of NMDA receptors in the neurochemical actions of MMA is further reinforced since they seem to trigger GABAergic failure.

The purpose of this study is to understand the situation concerning women and gender in relation to development, in the Mozambican district of Nacala Porto. The ambition is to identify present theoretical feminist perspectives in terms of perceived problems for women, their ability to solve them, focus areas for improvement and strategies for reaching development aims. To enable an understanding of the situation concerning women and gender in relation to development, we have conducted an analytical framework consisting of three main theoretical feminist perspectives in international development policies. These were applied as analytical tools, which consisted of Ester Boserups perspective of Women’s role in economic development, Women In Development (WID) and Gender And Development (GAD). The study displayed a discrepancy between the powerful women in the Mozambican parliament and the lack of social power described by the women in Nacala Porto. At the district level the results showed a dominating modernistic paradigm, similar to the situation identified by Boserup, who emphasised that the economical development did not benefit women equally. The subordination of women has been apparent in the district. The long-term strategy of transforming the gender structure has been met with support as well as resistance. The GAD-aim of mainstreaming gender showed a gap between international policy and practise in the district. The interventions that were WID-oriented have on the other hand shown progress regarding female representation, non-discriminatory legislation and increase of girls starting primary school. However, the WID-progress is limited without a gender perspective. Three main areas were continuously discussed as means having to change, to potentially alleviate poverty and include women in the development process. These areas were the access to employment, sustainable education and functioning family relations. The interdependence of these areas also seemed to require an integration of the three theoretical feminist perspectives of Boserup, WID and GAD.

Syftet med denna uppsats var att undersöka behandlingseffekten av studentledd psykoterapi på Umeå Universitets psykologmottagning gällande depressions- och ångestsymptom. Mer specifikt var syftet även att jämföra de två behandlingsmetoder som praktiseras på mottagningen; kognitiv beteendeterapi (KBT) och psykodynamisk terapi (PDT), samt jämföra de självskattningsinstrument för depression och ångest som ingår i mottagningens testbatteri (Patient Health Questionnaire 9-items, PHQ-9; Hospital Anxiety and Depression scale, HADS; General Anxiety Disorder 7-item scale, GAD-7). Ett ytterligare delsyfte var att beskriva mottagningens klientpopulation. Stickprovet bestod av 61 deltagare (72.1 procent kvinnor, 49.2 procent studenter, medianålder 23 år) som behandlats med antingen KBT eller PDT. För att undersöka effekterna av behandling jämfördes deltagarnas symptomskattningar före och efter behandling uppdelat på behandlingsmetod med hjälp av två-vägs variansanalys (ANOVA). Resultaten visade stora effektstorlekar för behandling gällande depression och ångest. Inga signifikanta skillnader observerades mellan behandlingsmetoder, vilket kan bero på bristande power. Diskrepans mellan instrumentens förmåga att identifiera deltagare med symptom på depression och ångest kunde ses, i synnerhet gällande depressionssymptom. I linje med rådande forskning visar studiens resultat att studentledd behandling har effekt på depression och ångest. Validiteten för de instrument som används på Psykologmottagningen bör dock undersökas närmare. Sammantaget belyser resultaten i denna studie vikten av att välja mätinstrument anpassade för den tilltänkta populationen för att kunna utvärdera behandlingseffekt.

No description available.