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Population ageing and international migration are two of the major societal trends challenging European elderly care regimes at present. Virtually no research has addressed how public discourses about the implications of these trends for elderly care are shaped in different countries. This article addresses this knowledge gap, examining how Swedish daily newspaper (SvD and DN) reporting on elderly care between 1995 and 2017 (N=370) depicts the impact of increased ethno-cultural diversity on this sector. Through content analysis, this article brings attention to the representations of migrants and culture that this reporting has deployed, and the rhetorical practices that the reporting has relied on (i.e. genre stratification, hegemonisation, homogenisation, normative referencing and idealisation/ diminishment). The article exposes how the ‘Othering’ of migrants is accomplished in Sweden’s daily newspaper reporting on elderly care, and problematizes the ethea of inclusiveness and equality of care with which we have come to associate this welfare sector.

In recent decades there has been a significant increase in diagnosing children and adults with Attention-Deficit/Hyperactivity Disorder (AD/HD), and in the use of pharmacological treatment with Ritalin, Concerta and Strattera for AD/HD. This development has given rise to scientific criticism, claiming that the pharmaceuticals prescribed by doctors are, to a large extent, ineffective or harmful. This study discusses media’s portrayal of treatment of AD/HD. The aim of the article is to develop a social constructionist perspective, highlighting how scientific critique of pharmaceuticals for AD/HD is handled in the mass media. The authors introduce the concept of “psychopharmacological extensibility,” which demonstrates the importance of collective definitional processes in society. Psychopharmacological extensibility reflects the fact that the perception of AD/HD agents as beneficial medicines or harmful drugs is open to interpretation and dependent on social factors related to context, power, rhetoric, and marketization. The empirical data are based on 211 articles from eight of the largest newspapers in Sweden, published between 2002 and 2021. The result shows that Swedish mass media, in numerous ways, neglects or undermines the scientific criticism made, thereby facilitating an increased use of the diagnosis and of psychotropic agents in society.

International migration and population aging have brought renewed attention to the ethics of care debate and the notion of caring democracy. This discussion problematizes the ways in which different statuses (based on gender, class and/or ethnicity) give people ‘passes’ out of caring responsibilities. This chapter uses this discussion as a backdrop while shedding light on the ways in which migrant status and culture are depicted in Swedish daily newspaper reporting on elder care. Through quantitative and qualitative analyses of all articles published between 1995 and 2017 (n = 370) in two national newspapers, this chapter shows the varying ways in which migration and culture are deployed in these media representations, and how care work is represented as a much needed but highly under-valued activity. Our analyses show that while older migrants are depicted as a burden to the elder care sector, migrant care workers are described as the solution par excellence to the staff crisis that this sector is experiencing, and are, as such, depicted as an asset. By bringing attention to these opposing representations, this chapter questions whether Sweden can be regarded as a caring democracy.

This article outlines a theoretical framework for understanding deviance and deviance-management in a social movement context. Such a deviance perspective is useful because in striving for social change, activists challenge existing social norms and may readily be defined by their environments as “outsiders” or deviants. However, activists also differ from traditional deviant groups. The article therefore conceptualizes activists as “entrepreneurial deviants,” combining features of both moral entrepreneurs and deviants in society, as presented in Howard Becker's classical theory. It is argued that in order to understand the strategies of deviance-management performed by activists, traditional notions of “passing,” “techniques of neutralization,” and “subculture” must be complemented by the concepts of “confronting,” “techniques of idealization,” and the forming of a “transformative subculture.” Empirically, the article builds on a case study of animal rights activism in Sweden and the ways in which the ac...

Social movement activism requires emotional motivation and entails emotional costs, and, because of this, activists tend to be deeply involved in the management of emotions – or emotion work – and not just in connection with protest events, but also on an everyday basis. Based on a case study of animal rights activism in Sweden, this article identifies five types of emotion work that animal rights activists typically perform: containing, ventilation, ritualization, micro-shocking and normalization of guilt. The emotion work performed by activists, it is argued, is best understood from a moral-sociological perspective building on Durkheim’s sociology of morality, based on which the article then outlines key elements of a comprehensive theoretical framework for the study of emotion work in social movements.

Drawing on Durkheim's sociology of morality, which identifies ideals and norms as the key components of morality, this article outlines a theoretical model for understanding how social movements can bring about legitimate social change. Social movement activists, we propose, can be conceptualized as followers and pursuers of sacred ideals. As such, they frequently come into conflict with existing norms in society. To manage this dilemma, activists must downplay their role as norm breakers while emphasizing their identity as followers of ideals. This in turn requires moral reflexivity in the staging of collective action. The article shows how dramaturgical control (Goffman) is exercised towards this end among activists engaged in two social movements in Sweden: the Plowshares peace movement and Animal Rights Sweden. The article further examines the internal stratification, or ‘moral hierarchies’, within the two activist groups in the light of the proposed model. The closer the activists were able to adhere to the sacred ideal, the higher the social status they enjoyed within the group.

Elite athletes, body builders and adolescents misuse anabolic-androgenic steroids (AAS) in order to increase muscle mass or to enhance physical endurance and braveness. The high doses misused are associated with numerous adverse effects. The purpose of this study was to evaluate the impact of chronic supratherapeutic AAS treatment on circulating hormones and gene expression in peripheral tissues related to such adverse effects. Quantitative real-time PCR was used to measure expression levels of in total 37 genes (including peptide hormones, cell membrane receptors, nuclear receptors, steroid synthesising enzymes and other enzymes) in the pituitary, testes, adrenals, adipose tissue, kidneys and liver of male Sprague-Dawley rats after 14-day administration of the AAS nandrolone decanoate, 3 or 15 mg/kg. Plasma glucose and levels of adrenocorticotropic hormone (ACTH), adiponectin, corticosterone, ghrelin, insulin and leptin were also measured. We found several expected effects on the hypothalamic-pituitary-gonadal axis, while the treatment also caused a number of other not previously identified changes in circulating factors and gene transcription levels such as the dose-dependent reduction of the beta(3)-adrenergic receptor in adipose tissue, reduction of both circulating and mRNA levels of adiponectin, up-regulation of both hydroxymethylglutaryl-CoA-reductase, the rate-limiting enzyme in de novo synthesis of cholesterol, and the receptor for ACTH in the adrenals. The results provide evidence for wide ranging effects of AAS on the hypothalamic-pituitary-adrenal axis, adipose tissue and substrates of the renal control of blood pressure.

Anxiety has been implicated in obesity and in the overconsumption of highly palatable foods such as those high in fat, sugar, or both. Also, the novelty-seeking trait has been associated with failure in weight-loss programs. The aim of this study was to investigate the associations of experimental anxiety and the self-administration of sucrose and high fat pellets in non-food deprived rats across different operant schedules. Male Wistar rats were subjected to the elevated plus-maze test (EPM) of anxiety-like behavior. The rats were tested for fixed ratio 5 (FR5) and progressive ratio (PR) operant responding for 50% sucrose, 95% sucrose, and high-fat pellets. PR active lever press response for 95% sucrose, but not the other pellet types, was correlated to % time spent on open arms (P=0.019) in the EPM. On the FR5 schedule, activity (closed arm entries) was correlated to the self-administration of 50% sucrose (P=0.027) and high-fat (P=0.002). This indicates an association of novelty-induced activity and self-administration of palatable food in sated rats, as well as a specific association of PR lever press response for 95% sucrose and low anxiety-like behavior. It has been argued that such active lever press response on PR may be interpreted as craving for the reinforcer; thus, our findings indicate an inverse relationship of experimental anxiety and craving for sucrose. This connection may have implications for human situations, since anxiety and novelty-seeking have been associated with obesity and failure in weight-loss programs.

The aim of this study was to investigate whether the preference for a palatable high-fat diet (HFD) is associated with response to novelty and with anxiety-like behavior in rats and whether such fat preference correlates with gene expression of hypothalamic neuropeptides related to feeding. We subjected male rats to two tests of exploration of novel environments: the multivariate concentric square field (MCSF) and the elevated plus maze (EPM). The rats were then exposed to a 5-day test of preference for a palatable HFD versus reference diets. Messenger RNA (mRNA) levels of 21 neuropeptides were investigated by quantitative polymerase chain reaction. We found a strong positive correlation of HFD preference and open-arm activity in the EPM (% open-arm time, r(s) = 0.629, df = 26, P0.001). Thus, HFD preference was inversely associated with anxiety-like behavior. The same association was found for HFD preference and behavior in the MCSF (bridge entries, r(s) = 0.399, df = 23, P = 0.048). In addition, the HFD preference was positively correlated (r(s) = 0.433, df = 25, P = 0.021) with hypothalamic mRNA levels of urocortin 2 (Ucn 2). Moreover, behavior in the EPM was significantly correlated with expression levels of the receptor for Ucn 2, the corticotropin-releasing factor receptor 2, in the hypothalamus (r(s) = 0.382, df = 33, P = 0.022, pituitary (r(s) = 0.494, df = 31, P = 0.004) and amygdala (r(s) = 0.381, df = 30, P = 0.032). We conclude that preference for palatable HFD is inversely associated with anxiety and propose that Ucn 2 signaling may play a role in this association.

Our understanding of the central regulation of food intake and body weight has increased tremendously through implication of a high number of neuropeptides. However, lack of all-embracing studies have made comparison difficult in the past. The objective of this study was to demonstrate the relative importance of the different neuropeptides in terms of involvement in appetite regulatory mechanisms. We quantified expression levels of 21 hypothalamic neuropeptides and circulating levels of leptin, insulin, corticosterone, adrenocorticotropic hormone, ghrelin and adiponectin in rats after acute food deprivation and chronic food restriction using validated quantitative real-time PCR and hormone measurements. Body weight, insulin and leptin were reduced whereas corticosterone was increased by both acute food deprivation and chronic food restriction. Our results confirmed the relative importance in body weight homeostasis of neuropeptide Y and proopiomelanocortin, which were increased and decreased as predicted. The expression of other neuropeptides previously attributed central roles in body weight homeostasis, e.g. melanin-concentrating hormone and orexin, appeared to be less affected by the treatments. Moreover, the expression of dynorphin, galanin-like peptide and neuropeptide B was dramatically reduced after both treatments. This suggests that the latter neuropeptides--although previously known to be involved in body weight homeostasis--may be of unexpected importance in states of negative energy balance.

Gene variants of the FTO (fatso) gene have recently been strongly associated with body mass index and obesity. The FTO gene is well conserved and found in a single copy in vertebrate species including fish and chicken, suggesting that the ancestor of this gene was present 450 million years ago. Surprisingly, the FTO gene is present in two species of algae but not in any other invertebrate species. This could indicate that this gene has undergone a horizontal gene transfer. Quantitative real-time PCR showed that the gene is expressed in many peripheral and central rat tissues. Detailed in situ hybridization analysis in the mouse brain showed abundant expression in feeding-related nuclei of the brainstem and hypothalamus, such as the nucleus of the solitary tract, area postrema, and arcuate, paraventricular, and supraoptic nuclei as well as in the bed nucleus of the stria terminalis. Colabeling showed that the FTO gene is predominantly expressed in neurons, whereas it was virtually not found in astrocytes or glia cells. The FTO was significantly up-regulated (41%) in the hypothalamus of rats after 48-h food deprivation. We also found a strong negative correlation of the FTO expression level with the expression of orexigenic galanin-like peptide, which is mainly synthesized in the arcuate nucleus. These results are consistent with the hypothesis that FTO could participate in the central control of energy homeostasis.

Self-administration of ethanol and food share many common features and Richter hypothesized that an increase in ethanol consumption would decrease feeding to balance the excess calories contained in the ethanol. Previously, we have shown that individual alcohol consumption correlates with neurotransmitter gene expression, especially in the prefrontal cortex. To test the hypothesis of Richter, we measured hypothalamic gene expression of receptors or neuropeptides of known relevance for the regulation of food intake using qPCR and correlated this to individual ethanol consumption in Wistar rats. For validation, gene expression was first correlated with body weight. We found a correlation of dynorphin, somatostatin, melanocortin-4 receptor and serotonin 5-HT(2C) with body weight and trends to correlation for CART, thus confirming the established role of the hypothalamus in the regulation of weight. For ethanol consumption, correlations were found for CRH receptors 1 and 2 and vasopressin while strong trends were observed for galanin receptor 1, orexin receptor 1, MCH and adrenoceptor alpha(1B). Therefore, alcohol consumption does seem to involve several hypothalamic systems which also mediate feeding responses and suggests that the hypothalamus, together with the prefrontal cortex, may determine the 'stopping point' of an individual.

About half of the risk to develop alcoholism is related to genetic background and it is well known that alcohol consumption is highly individualized. In this study, we investigated how individual alcohol consumption behaviour in Wistar rats correlated with mRNA expression of 20 genes in the prefrontal cortex, hippocampus and amygdala. We found that the long-term alcohol consumption of an individual could be estimated by the mean of its consumption on Day 2 and 3. This short exposure minimized changes in gene expression induced by alcohol itself. We found a positive correlation in the prefrontal cortex of GABA(A) alpha5 (r=0.96), GABA(B1) (r=0.96), AMPA GluR1 (r=0.93), 5-HT(3A) (r=0.93) and the alpha adrenoceptors (alpha(1A)r=1.00, alpha(1B)r=0.93, alpha(2A)r=0.93) with consumption. In the hippocampus, we found negative correlations with the NMDA NR2A subunit (r=-0.86), the alpha(1A) adrenoceptor (r=-0.89) and the glucocorticoid receptor (r=-0.86). Finally, in the amygdala there was a negative correlation to NMDA NR2A (r= -0.79) and a positive correlation with serotonin 5-HT(2C) (r=0.79). In conclusion, we have used qPCR to identify specific genes in the brain that correlated to alcohol self-administration of an individual animal. This study suggests that alcohol consumption in the early stages of acquisition depends on the genetic background of the individual and that the prefrontal cortex is particularly important in this behaviour.

I artikeln undersöks hur Svenska Dagbladet framställt äldreomsorgssektorn i samband med etnicitets- och migrationsrelaterade frågor mellan 1995 och 2008. Studien behandlar vilka ämnen som rapporteringen har handlat om, vilka för- klaringar man använt sig av, vilka äldreomsorgsaktörer som varit i fokus och vilka som har fått uttala sig.

Dieting as a strategy to reduce body weight often fails as it causes food cravings leading to bingeing and weight regain. Evidence from several lines of research suggests the presence of shared elements for neural regulation of food and drug craving. We quantified the expression of eight genes involved in dopamine signalling in brain regions related to the mesolimbic and nigrostriatal dopamine system in male rats subjected to chronic food restriction using quantitative real-time polymerase chain reaction. Food restriction strongly increased mRNA levels of tyrosine hydroxylase and the dopamine transporter in the ventral tegmental area. Quantitative autoradiography indicated that the dopamine transporter was also upregulated at the protein level in the shell of the nucleus accumbens. However, these effects were not observed after acute food deprivation. We suggest that the results reflect a sensitization of the mesolimbic dopamine pathway characterized by increased clearance of extracellular dopamine in the nucleus accumbens shell. Such sensitization of the mesolimbic dopamine system may be one of the underlying causes for the food cravings that interfere with dietary compliance.

Food restriction is associated with a number of endocrine disturbances. We validated the experimental conditions for several house-keeping genes and determined the effects of 12 day 50% food restriction on hypothalamic and pituitary transcription of genes involved in different neuroendocrine systems, using real-time quantitative polymerase chain reaction (PCR). A total of 7 nuclear receptors and 12 neuropeptides and peptide hormones were investigated in the dorsal and ventral hypothalamus and the pituitary gland in rats. In the hypothalamus, food restriction reduced mRNA levels of estrogen receptor alpha (ERalpha), progesterone receptor, glucocorticoid receptor, thyroid hormone receptor alpha and beta, pro-opiomelanocortin (POMC), growth hormone-releasing factor (GHRF), corticotropin-releasing factor (CRF), thyrotropin-releasing factor (TRF), somatostatin, and increased that of neuropeptide Y (NPY). In the pituitary, the treatment reduced growth hormone (GH), luteinizing hormone beta (LHbeta) and thyrotropin beta, but increased ERalpha mRNA levels. The study provides a map of how food restriction affects the regulation of a number of transcripts involved in neuroendocrine control.

By use of the brain microdialysis technique we show that administration of gamma(1)-melanocyte stimulating hormone (gamma(1)-MSH) into the ventral tegmental area of anaesthetized rats causes an increase in the release of extracellular dopamine and its metabolite 3,4-dihydroxyphenylacetic acid in the nucleus accumbens, while gamma(2)-MSH causes the opposite effect. Moreover, gamma(2)-MSH pre-treatment considerably reduced the gamma(1)-MSH-induced effects. Our findings suggest an opposing action of two gamma-MSH-activated pathways on the mesolimbic dopaminergic system, which could be important in the maintenance of a balanced psychoactivation state.

Adolescent males currently employ anabolic-androgenic steroids (AAS) to become intoxicated, besides the traditional desires of an improved physical appearance and enhanced sports performance. Several studies indicate that AAS affect the brain reward system. Recently chronic administration with nandrolone decanoate to male rats has been shown to increase the dopamine transporter (DAT) density in the striatum visualised in vivo by positron emission tomography. The present study aimed to investigate if the increased DAT density could be confirmed using in vitro autoradiography following a comparable regimen of nandrolone treatment. Specific binding of 50 pM [125I] RTI-55 in the presence of 1 microM citalopram was used to label DAT. Two weeks of nandrolone decanoate administration at the supra-therapeutic doses 1, 5 and 15 mg/kg per day increased DAT density in the caudate putamen at all three doses. In conclusion, this study confirms that chronic nandrolone administration increases dopamine transporter density in the CPU and therefore supports the theory that AAS affects the dopamine system in the male rat brain.

The aim of this study was to characterise the expression of the melanocortin system in the normal and injured rat visual system. Using real-time polymerase chain reaction and immunohistochemistry, we detected melanocortin MC(3), MC(4) and MC(5) receptors and proopiomelanocortin in adult retina and superior colliculus. Melanocortin MC(4) receptor mRNA was the most abundant receptor. Melanocortin MC(3), MC(4) and MC(5) receptors were localised to the ganglion cell and inner nuclear layers and the melanocortin MC(3) and MC(4) receptors were localised to retinal ganglion cells. Transection of the optic nerve leads to ganglion cell death and both melanocortin receptor and proopiomelanocortin expression decreased in superior colliculus after transection whereas the expression was unchanged or even increased in the retina. alpha-Melanocyte-stimulating hormone elicited neurite outgrowth from embryonic retinal explants. Together, these data implicate a role for the melanocortin system in the adult rat retina and that melanocortins can stimulate neurite growth from retinal neurons.

Some adolescent and young males are engaged in misuse of anabolic–androgenic steroids (AASs) in connection with multiple drug use, in order to become intoxicated and brave, apart from currently known motives connected to sports performance and physical appearance. Recent studies suggest that alterations in neurobiological circuits implicated in the regulation of reward-related learning, aggression and motoric behavior underlie the behavioral changes associated with AAS misuse. We have previously shown that AASs induce alterations in dopamine receptor densities. The aim of the present study was to investigate if these effects could be attributed to altered mRNA content for tyrosine hydroxylase, l -amino acid decarboxylase, dopamine D1- and dopamine D2-receptor as measured by in situ hybridisation. Male Sprague–Dawley rats were subjected to 2 weeks of treatment with daily intramuscular injections of the AAS nandrolone decanoate at three different doses (1, 5 and 15 mg/kg/day). Results of the in situ hybridization showed that the mRNA content of the dopamine D1-receptor subtype was significantly reduced at all doses in the caudate putamen and at the highest doses in the nucleus accumbens shell. The mRNA expression of the dopamine D2-receptor was significantly increased at the two lowest doses in the caudate putamen and the nucleus accumbens shell. In conclusion, nandrolone has been shown to affect the expression of gene transcripts of dopaminergic receptors possibly implicated in underlying mechanisms of reward-related behavioral changes among AAS misusers.

Strong evidence suggests a functional link between the melanocortin and dopamine systems. alpha-Melanocyte stimulating hormone (alpha-MSH) induced grooming behaviour, which can be blocked by dopamine receptor antagonists, is associated with increased dopaminergic transmission in the striatal regions. Whether this effect is mediated specifically by melanocortin (MC) receptors has not previously been established. Using in vivo microdialysis on anesthesized rats we have shown that alpha- MSH administered into the ventral tegmental area induced a significant increase in dopamine and DOPAC levels in the nucleus accumbens. This increase was completely blocked by pre-treatment with the MC4 receptor selective antagonist HS131, indicating that the effects of alpha-MSH on dopamine transmission may be mediated by the MC4 receptor.

In recent years a male group of anabolic-androgenic steroid misusers has been identified to share socio-demographic and personality related background factors with misusers of psychotropic substances, as well as being involved in habits of multiple drug use. The present study aimed to assess whether anabolic-androgenic steroids (AAS) would affect the density of the dopamine receptors in areas implicated in reward and behaviour in the male rat brain. The effects of 2 weeks of treatment with i.m. injections of nandrolone decanoate (15 mg/kg/day) on the expression of the D(1)-like and D(2)-like receptors were evaluated by autoradiography. Specific binding of D(1)-like receptors was significantly down regulated in the caudate putamen, the nucleus accumbens core and shell. D(2)-like receptor densities were down regulated in the nucleus accumbens shell, but up regulated in the caudate putamen, the nucleus accumbens core and the ventral tegmental area. These results are compatible with nandrolone induced neuroadaptive alterations in dopamine circuits associated with motor functions and behavioural paradigms known to be affected following AAS misuse.

Knowledge of melanocortins and their receptors has increased tremendously over the last few years. The cloning of five melanocortin receptors, and the discovery of two endogenous antagonists for these receptors, agouti and agouti-related peptide, have sparked intense interest in the field. Here we give a comprehensive review of the pharmacology, physiology and molecular biology of the melanocortins and their receptors. In particular, we review the roles of the melanocortins in the immune system, behaviour, feeding, the cardiovascular system and melanoma. Moreover, evidence is discussed suggesting that while many of the actions of the melanocortins are mediated via melanocortin receptors, some appear to be mediated via mechanisms distinct from melanocortin receptors.

The melanocortin (MC) 4 receptor is important for food intake and weight homeostasis as it mediates the orexigenic and anorexigenic effects of the MCs. OLETF (Otsuka–Long–Evans–Tokushima–Fatty) rats are a selective inbred strain of polygenic variant rats which overeat and develop obesity with elevated leptin levels. We investigated by autoradiography if the expression of MC receptors were altered in ovariectomized estradiol-replaced female OLETF rats compared to their controls (Long–Evans–Tokushima–Otsuka (LETO) rats). We found that OLETF rats show a reduction in total [ 125 I ]NDP-MSH MC receptor binding in the ventromedial hypothalamic nucleus, perhaps reflecting an increased release of MC peptides in this region. The levels of MC receptors in the arcuate nucleus and the paraventricular hypothalamic nucleus were not changed. Interestingly, the OLETF rats also showed reduced MC-receptor binding in areas such as the nucleus accumbens shell, and the ventral tegmental area, both of which are believed to be involved in reward systems. Similarities in the changes of MC receptor expression in obese animals and in animals treated with opiates may suggest a neurobiological link between food intake mediated through the MC receptors and reward.

In the present study we examined the distribution of alpha 2A- and alpha 2C-adrenoceptors in tissue slices from the rat cervical spinal cord and from brain slices collected at the level of the striatum. To differentiate between alpha 2A- and alpha 2C-adrenoceptors, the slices were incubated with [3H]MK912 in the presence of graded concentrations of the alpha 2A-selective drug, BRL44408, or the alpha 2C-selective drug, spiroxatrine. Computer analysis of the autoradiograms indicated that 0.4 nM [3H]MK912 plus 185 nM BRL44408 selectively labeled alpha 2C-adrenoceptors, while 0.4 nM [3H]MK912 plus 220 nM spiroxatrine selectively labeled alpha 2A-adrenoceptors. Using this approach, alpha 2C-adrenoceptors were detected in the striatum, while alpha 2A-adrenoceptors predominated in the cortical layers 1-4, the spinal cord distal dorsal horn, the septum and the endopiriform nucleus.

The alpha2C-adrenoceptor preferring radioligand [3H]-MK912 was used for labelling alpha2A- and alpha2C-adrenoceptors in the rat striatum, in the cervical, thoracic and lumbar parts of the spinal cord, and in the dorsal and ventral halves of the spinal cord. In addition, guanfacine was used as a tool to delineate the alpha2A- and alpha2C-adrenoceptors. In the striatum the sites were 72% alpha2A- and 28% alpha2C-adrenoceptors, while in all regions of the spinal cord the proportions of the sites were about 96% alpha2A- and 4% alpha2C-adrenoceptors. A multi-curve experimental design and computer analysis was used in order to enable the accurate quantification of the alpha2A- and alpha2C-adrenoceptors in the striatum and spinal cord.

Research on welfare regimes and migration regimes has shown that Sweden and Finland have similar elderly care regimes but different migration regimes. It is against this backdrop that we set out to study what Swedish and Finnish daily press focusing on elderly care has written about ethnic minorities, migrants and migration. The study uses quantitative content analysis to analyze 241 daily newspaper articles published between 1995 and 2008. This article presents the themes that have been discussed, the elderly care actors that have been in focus (i.e. whether the focus has been on elderly care recipients, elderly care providers or informal caregivers), the ethnic backgrounds that these actors have had (i.e. whether the focus has been on the ethnic majority or on ethnic minorities) and the type of explanatory frameworks that the newspaper articles in focus have used. On the basis of this, we problematize the representations of ethnic minorities, migrants and migration that the newspaper articles in question put forth and the fact that the Swedish and Finnish daily press treats the issues at hand as if migration is mostly an issue that can be relegated to the periphery of the elderly care sectors’ agenda.

The abuse of anabolic androgenic steroids (AASs) at supratherapeutic doses is a problem not only in the world of sports, but also among non-athletes using AASs to improve physical appearance and to become more bold and courageous. Investigations of the possible neurochemical effects of AAS have focused partially on the monoaminergic systems, which are involved in aggressive behaviours and the development of drug dependence. In the present study, we administered nandrolone decanoate (3 or 15 mg/kg/day for 14 days) and measured mRNA expression of dopaminergic and serotonergic receptors, transporters and enzymes in the male rat brain using quantitative real-time polymerase chain reaction. Expression of the dopamine D1-receptor transcript was elevated in the amygdala and decreased in the hippocampus while the transcript level of the dopamine D4-receptor was increased in the nucleus accumbens. No changes in transcriptional levels were detected among the serotonin-related genes examined in this study. The altered mRNA expression of the dopamine receptors may contribute to some of the behavioural changes often reported in AAS abusers of increased impulsivity, aggression and drug-seeking.

Anabolic androgenic steroids (AAS) are known as doping agents within sports and body-building, but are currently also abused by other groups in society in order to promote increased courage and aggression. We previously showed that 14 days of daily intramuscular injections of the AAS nandrolone decanoate (15 mg/kg) reduced the extracellular levels of the dopaminergic metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) in the nucleus accumbens shell using microdialysis. The aim of the present study was to investigate whether the same dose regimen of nandrolone decanoate may affect the activities of the dopamine-metabolizing enzymes monoamine oxidases A and B (MAO-A and MAO-B). A radiometric assay was used to determine the activities of MAO-A and MAO-B in rat brain tissues after 14 days of daily i.m. nandrolone decanoate injections at the doses 3 and 15 mg/kg. Gene transcript contents of MAO-A, MAO-B and cathecol-O-methyltransferase (COMT) were measured with quantitative real-time reverse transcription PCR. 3 mg/kg of nandrolone decanoate significantly reduced the activity of both MAO-A and -B in the caudate putamen. 15 mg/kg of nandrolone decanoate significantly reduced the activity of MAO-A in the amygdala and increased the gene transcript level of MAO-B in the substantia nigra. In conclusion, imbalanced MAO activities may contribute to explain the impulsive and aggressive behaviour often described in AAS abusers. The reduced MAO activities observed are in line with our previously presented findings of decreased extracellular levels of DOPAC and HVA in the rat brain, indicating decreased monoaminergic activity following repeated AAS administration.

The solute carrier family 22 (SLC22) is a large family of organic cation and anion transporters. These are transmembrane proteins expressed predominantly in kidneys and liver and mediate the uptake and excretion of environmental toxins, endogenous substances, and drugs from the body. Through a comprehensive database search we identified six human proteins not yet cloned or annotated in the reference sequence databases. Five of these belong to the SLC22 family, SLC22A20, SLC22A23, SLC22A24, SLC22A25, and SPNS3, and the sixth gene, SVOPL, is a paralog to the synaptic vesicle protein SVOP. We identified the orthologs for these genes in mouse and rat and additional homologous proteins and performed the first phylogenetic analysis on the entire SLC22 family in human, mouse, and rat. In addition, we performed a phylogenetic analysis which showed that SVOP and SV2A-C are, in a comparison with all vertebrate proteins, most similar to the SLC22 family. Finally, we performed a tissue localization study on 15 genes on a panel of 30 rat tissues using quantitative real-time polymerase chain reaction.

Learning to perform instrumental tasks is an ability of all animals. In a population of rats, not all individuals will acquire an operant response for reward. We hypothesized that there could be a genetic explanation for differences between High Consumers (those that acquired the lever press response) and Low Consumers (lever press response is low). Additionally, we proposed that this genetic difference could produce measurable changes in response to novelty. Wistar rats were trained to lever press for a 0.2% saccharin reward and on the 10th day they were placed in a novel open field for 30 min to record locomotor activity. The prefrontal cortex and hippocampus were dissected and qPCR was used to measure mRNA expression. A significant difference (p=.048; 2-way ANOVA) in gene expression was observed between Low and High Consumers. A principal component analysis (PCA), to cluster which genes represent this difference, identified 4 genes; 5-HT2A and mGlu1 in the hippocampus and AMPA GluR1 and adrenergic alpha2A in the prefrontal cortex. Response to a novel open field also differed since Low Consumers displayed a higher Total Distance in comparison to High Consumers. Additionally, Low Consumers could be subdivided into Low-Lever (with lever press response only when water deprived) and Low-Non-Lever (lever press response is low throughout training). PCA with this subdivision identified an additional nine genes differing within the divisions; NMDA NR2B and GABAAalpha3 in the prefrontal cortex and adrenergic alpha2B and alpha2A, AMPA GluR1, GluR2 and GluR3, 5-HT1B and GABAAalpha5 in the hippocampus.

Tremendous amount of primary sequence information has been made available from the genome sequencing projects, although a complete annotation and identification of all genes is still far from being complete. Here, we present the identification of two new human genes from the pharmacologically important family of transporter proteins, solute carriers family 6 (SLC6). These were named SLC6A17 and SLC6A18 by HUGO. The human repertoire of SLC6 proteins now consists of 19 functional members and four pseudogenes. We also identified the corresponding orthologues and additional genes from mouse and rat genomes. Detailed phylogenetic analysis of the entire family of SLC6 proteins in mammals shows that this family can be divided into four subgroups. We used Hidden Markov Models for these subgroups and identified in total 430 unique SLC6 proteins from 10 animal, one plant, two fungi, and 196 bacterial genomes. It is evident that SLC6 proteins are present in both animals and bacteria, and that three of the four subfamilies of mammalian SLC6 proteins are present in Caenorhabditis elegans, showing that these subfamilies are evolutionary very ancient. Moreover, we performed tissue localization studies on the entire family of SLC6 proteins on a panel of 15 rat tissues and further, the expression of three of the new genes was studied using quantitative real-time PCR showing expression in multiple central and peripheral tissues. This paper presents an overall overview of the gene repertoire of the SLC6 gene family and its expression profile in rats.

We have previously shown that treatment of rats with the anabolic androgen steroid nandrolone decreased the density of alpha1B-adrenoceptors in the rat kidney [Uhlen, S., Lindblom, J., Kindlundh, A., Muhisha, P., Nyberg, F., (2003). Nandrolone treatment decreases the level of rat kidney alpha1B-adrenoceptors. Naunyn-Schmiedeberg's Arch. Pharmacol. 368, 91-98]. This effect may have been caused either by decreased de novo synthesis of alpha1B-adrenoceptors or by increased degradation of alpha1B-adrenoceptors [corrected] In the present study, we show that treatment of rats with nandrolone decreases the level of mRNA for the alpha1B-adrenoceptor in the kidneys, implying decreased synthesis of alpha1B-adrenoceptors. On the other hand, nandrolone did not decrease the density of alpha1B-adrenoceptors in Madin-Darby Canine Kidney (MDCK) cells, even though the sub-cell line tested, MDCK-D1, expresses both the androgen receptor and the alpha1B-adrenoceptor. It is concluded that the regulation of alpha1B-adrenoceptor expression by anabolic androgenic steroids is intricate and cell-type specific.

In this paper, Gaussian mixture (GM) models are used to design variable-dimension quantizers according to a weighted distortion criterion. A general method for combining a variable-to-fixed dimension transform, with GM modeling and quantization, is proposed. The method provides a convenient and efficient way to encode the amplitudes in a sinusoidal speech coder. Quantizers designed according to the proposed scheme are evaluated both according to weighted distortion criteria, and with respect to a high-rate bound approximation of the distortion. Informal listening tests suggest that the amplitudes can be encoded without subjective loss in a wideband harmonic coder, at a rate around 40 bits per frame (for the amplitudes only).