167 research outputs found

    Adults are expected to take responsibility for their problems, especially when those problems are congruent with traditional gender role expectations

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    Some research suggests that we attribute responsibility differently for men and women. For example, Reynolds et al. (2019) found women are more easily typecast as victims and men as perpetrators. The present study was a cross-sectional online survey of 408 male and female adults aged 18 to 65, stratified by UK region. Participants saw 14 vignettes depicting a wide variety of scenarios featuring either a male or female character (a man or woman, or a boy or girl), about which participants were asked to make attributions. The gender of the vignette character was randomly assigned for each vignette. There was no overall difference in total internal attribution of responsibility to boys compared to girls (Cohen’s d = –0.01, p < .862). For the vignettes about adults, there was a non-significant overall trend towards total internal attribution being higher for male characters (d = 0.061, p < .065). However, in terms of each vignette separately, participants agreed more strongly that: boys were more responsible for how depressed they feel (p < .013), and men were more responsibility for avoiding workplace accidents (p < .002) and finding work (p < .003). Girls were attributed as more responsible for being physically fit (p < .034), and women attributed as more responsible for making sure their children don’t have a playground accident (p < .034). Findings of this exploratory study are discussed about attributions of responsibility being based on traditional gender role expectations. Implications for social issues, for example, encouraging help-seeking for mental health problems by boys, are discussed

    A model of professional self-identity formation in student doctors and dentists: a mixed method study.

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    BACKGROUND: Professional self-identity [PSI] can be defined as the degree to which an individual identifies with his or her professional group. Several authors have called for a better understanding of the processes by which healthcare students develop their professional identities, and suggested helpful theoretical frameworks borrowed from the social science and psychology literature. However to our knowledge, there has been little empirical work examining these processes in actual healthcare students, and we are aware of no data driven description of PSI development in healthcare students. Here, we report a data driven model of PSI formation in healthcare students. METHODS: We interviewed 17 student doctors and dentists who had indicated, on a tracking questionnaire, the most substantial changes in their PSI. We analysed their perceptions of the experiences that had influenced their PSI, to develop a descriptive model. Both the primary coder and the secondary coder considered the data without reference to the existing literature; i.e. we used a bottom up approach rather than a top down approach. RESULTS: The results indicate that two overlapping frames of reference affect PSI formation: the students' self-perception and their perception of the professional role. They are 'learning' both; neither is static. Underpinning those two learning processes, the following key mechanisms operated: [1] When students are allowed to participate in the professional role they learn by trying out their knowledge and skill in the real world and finding out to what extent they work, and by trying to visualise themselves in the role. [2] When others acknowledge students as quasi-professionals they experience transference and may respond with counter-transference by changing to meet expectations or fulfil a prototype. [3] Students may also dry-run their professional role (i.e., independent practice of professional activities) in a safe setting when invited. CONCLUSIONS: Students' experiences, and their perceptions of those experiences, can be evaluated through a simple model that describes and organises the influences and mechanisms affecting PSI. This empirical model is discussed in the light of prevalent frameworks from the social science and psychology literature

    Familial deletion 18p syndrome: case report

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    BACKGROUND: Deletion 18p is a frequent deletion syndrome characterized by dysmorphic features, growth deficiencies, and mental retardation with a poorer verbal performance. Until now, five families have been described with limited clinical description. We report transmission of deletion 18p from a mother to her two daughters and review the previous cases. CASE PRESENTATION: The proband is 12 years old and has short stature, dysmorphic features and moderate mental retardation. Her sister is 9 years old and also has short stature and similar dysmorphic features. Her cognitive performance is within the borderline to mild mental retardation range. The mother also presents short stature. Psychological evaluation showed moderate mental retardation. Chromosome analysis from the sisters and their mother revealed the same chromosomal deletion: 46, XX, del(18)(p11.2). Previous familial cases were consistent regarding the transmission of mental retardation. Our family differs in this regard with variable cognitive impairment and does not display poorer verbal than non-verbal abilities. An exclusive maternal transmission is observed throughout those families. Women with del(18p) are fertile and seem to have a normal miscarriage rate. CONCLUSION: Genetic counseling for these patients should take into account a greater range of cognitive outcome than previously reported

    The Characterisation of Three Types of Genes that Overlie Copy Number Variable Regions

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    Background: Due to the increased accuracy of Copy Number Variable region (CNV) break point mapping, it is now possible to say with a reasonable degree of confidence whether a gene (i) falls entirely within a CNV; (ii) overlaps the CNV or (iii) actually contains the CNV. We classify these as type I, II and III CNV genes respectively. Principal Findings: Here we show that although type I genes vary in copy number along with the CNV, most of these type I genes have the same expression levels as wild type copy numbers of the gene. These genes must, therefore, be under homeostatic dosage compensation control. Looking into possible mechanisms for the regulation of gene expression we found that type I genes have a significant paucity of genes regulated by miRNAs and are not significantly enriched for monoallelically expressed genes. Type III genes, on the other hand, have a significant excess of genes regulated by miRNAs and are enriched for genes that are monoallelically expressed. Significance: Many diseases and genomic disorders are associated with CNVs so a better understanding of the different ways genes are associated with normal CNVs will help focus on candidate genes in genome wide association studies

    Incontinence in Individuals with Rett Syndrome: A Comparative Study

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    Frequency and type of incontinence and its association with other variables were assessed in females with Rett Syndrome (RS) (n = 63), using an adapted Dutch version of the ‘Parental Questionnaire: Enuresis/Urinary Incontinence’ (Beetz et al. 1994). Also, incontinence in RS was compared to a control group consisting of females with non-specific (mixed) intellectual disability (n = 26). Urinary incontinence (UI) (i.e., daytime incontinence and nocturnal enuresis) and faecal incontinence (FI) were found to be common problems among females with RS that occur in a high frequency of days/nights. UI and FI were mostly primary in nature and occur independent of participants’ age and level of adaptive functioning. Solid stool, lower urinary tract symptoms and urinary tract infections (UTI’s) were also common problems in females with RS. No differences in incontinence between RS and the control group were found, except for solid stool that was more common in RS than in the control group. It is concluded that incontinence is not part of the behavioural phenotype of RS, but that there is an increased risk for solid stool in females with RS

    Mapping and identification of candidate loci responsible for Peromyscus hybrid overgrowth

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    Crosses between two recently diverged rodent species of the genus Peromyscus result in dramatic parent-of-origin effects on growth and development. P. maniculatus females crossed with P. polionotus males yield growth-retarded conceptuses, whereas the reciprocal cross results in overgrowth and lethality. These hybrid effects are particularly pronounced in the placenta. We previously detected linkage to two regions of the genome involved in the overgrowth effects. One locus, termed Peal, is a paternally expressed autosomal locus mapping to a domain whose house mouse equivalent contains several clusters of imprinted genes. The other locus, termed Mexl, maps to a gene-poor region of the X chromosome. Here we use an advanced intercross line to verify and narrow the regions of linkage and identify candidate genes for Mexl and Peal. While we have previously shown that Mexl affects both pre-and postnatal growth, we show here that Peal affects only prenatal growth. Utilizing criteria such as mutant phenotypes and allelic expression, we identify the loci encoding the homeobox protein Esx1 and the zinc-finger protein Pw1/Peg3 as candidates. Both loci exhibit expression changes in the hybrids

    Variable effect of co-infection on the HIV infectivity: Within-host dynamics and epidemiological significance

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    <p>Abstract</p> <p>Background</p> <p>Recent studies have implicated viral characteristics in accounting for the variation in the HIV set-point viral load (spVL) observed among individuals. These studies have suggested that the spVL might be a heritable factor. The spVL, however, is not in an absolute equilibrium state; it is frequently perturbed by immune activations generated by co-infections, resulting in a significant amplification of the HIV viral load (VL). Here, we postulated that if the HIV replication capacity were an important determinant of the spVL, it would also determine the effect of co-infection on the VL. Then, we hypothesized that viral factors contribute to the variation of the effect of co-infection and introduce variation among individuals.</p> <p>Methods</p> <p>We developed a within-host deterministic differential equation model to describe the dynamics of HIV and malaria infections, and evaluated the effect of variations in the viral replicative capacity on the VL burden generated by co-infection. These variations were then evaluated at population level by implementing a between-host model in which the relationship between VL and the probability of HIV transmission per sexual contact was used as the within-host and between-host interface.</p> <p>Results</p> <p>Our within-host results indicated that the combination of parameters generating low spVL were unable to produce a substantial increase in the VL in response to co-infection. Conversely, larger spVL were associated with substantially larger increments in the VL. In accordance, the between-host model indicated that co-infection had a negligible impact in populations where the virus had low replicative capacity, reflected in low spVL. Similarly, the impact of co-infection increased as the spVL of the population increased.</p> <p>Conclusion</p> <p>Our results indicated that variations in the viral replicative capacity would influence the effect of co-infection on the VL. Therefore, viral factors could play an important role driving several virus-related processes such as the increment of the VL induced by co-infections. These results raise the possibility that biological differences could alter the effect of co-infection and underscore the importance of identifying these factors for the implementation of control interventions focused on co-infection.</p
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