48 resultados para Domestic family model


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Background: Women and their babies are entitled to equal access to high quality maternity care. However, when women fit into two or more categories of vulnerability they can face multiple, compound barriers to accessing and utilising services. Disabled women are up to three times more likely to experience domestic abuse than non-disabled women. Domestic abuse may compromise health service access and utilisation and disabled people in general have suboptimal access to healthcare services. Despite this, little is known about the compounding effects of disability and domestic abuse on women’s access to maternity care.

Methods: The aim of the study was to identify how women approach maternity care services, their expectations of services and whether they are able to get the type of care that they need and want. We conducted a qualitative, Critical Incident Technique study in Scotland. Theoretically we drew on Andersen’s model of healthcare use. The model was congruent with our interest in women’s intended/actual use of maternity services and the facilitators and barriers
impacting their access to care. Data were generated during 2013 using one-to-one interviews.

Results: Five women took part and collectively reported 45 critical incidents relating to accessing and utilising maternity services. Mapped to the underpinning theoretical framework, our findings show how the four domains of attitudes; knowledge; social norms; and perceived control are important factors shaping maternity care experiences.

Conclusions: Positive staff attitude and empowering women to have control over their own care is crucial in influencing women’s access to and utilisation of maternity healthcare services. Moreover these are cyclical, with the consequences and outcomes of healthcare use becoming part of the enabling or disabling factors affecting future healthcare decisions.Further consideration needs to be given to the development of strategies to access and recruit women in these circumstances. This will provide an opportunity for under-represented and silenced voices to be heard.

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Background: The oro-facial region is densely innervated by the trigeminal nerve, which when stimulated can induce noxious pain sensation and contribute to neurogenic inflammation in local tissues. Recent research on the expression of specialised ion channels on the trigeminal nerve has highlighted the need to undertake more extensive studies on ion channel expression/functionality with the aim of elucidating their role in pain sensations. A major family of such ion channels is the transient receptor potential (TRP) channels which are activated by a wide variety of thermal, mechanical or chemical stimuli and merit investigation as possible druggable targets for future analgesics.
Objective: Study of TRP channel expression and regulation in oro-facial tissues is hindered by the fact that the cell bodies of neurons innervating these tissues are located in the trigeminal ganglion. Using dental pulp stem cells differentiated towards peripheral neuronal equivalents (PNEs), we sought to determine TRP channel expression, functionality and potential modulation by cytokines in this novel model.
Method: Dental pulp stem cells (DPSCs) were grown on substrate-coated tissue culture plates and differentiated towards a neuronal phenotype using neuronal induction media. Quantitative polymerase chain reaction (qPCR) was performed on PNEs +/-cytokine treatment. Ion channel functionality was investigated using whole cell patch clamping.
Result: qPCR analysis showed that PNEs expressed the TRP channels TRPA1, TRPV1, TRPV4 and TRPM8. TRPA1 was the most abundantly expressed TRP channel studied whereas TRPM8 was lowly expressed. TRP channel expression was shown to be regulated by treatment with inflammatory cytokines. Patch clamp studies using specific agonists and antagonists for TRPA1 and TRPV1 showed these channels were functional.
Conclusion: PNEs differentiated from DPSCs provide a suitable model for TRP channel expression, regulation, and sensistisation in oro-facial tissues. This human neuronal model has potential for use in pre-clinical studies of novel analgesics.

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Genome-wide association studies (GWAS) of schizophrenia have yielded more than 100 common susceptibility variants, and strongly support a substantial polygenic contribution of a large number of small allelic effects. It has been hypothesized that familial schizophrenia is largely a consequence of inherited rather than environmental factors. We investigated the extent to which familiality of schizophrenia is associated with enrichment for common risk variants detectable in a large GWAS. We analyzed single nucleotide polymorphism (SNP) data for cases reporting a family history of psychotic illness (N = 978), cases reporting no such family history (N = 4,503), and unscreened controls (N = 8,285) from the Psychiatric Genomics Consortium (PGC1) study of schizophrenia. We used a multinomial logistic regression approach with model-fitting to detect allelic effects specific to either family history subgroup. We also considered a polygenic model, in which we tested whether family history positive subjects carried more schizophrenia risk alleles than family history negative subjects, on average. Several individual SNPs attained suggestive but not genome-wide significant association with either family history subgroup. Comparison of genome-wide polygenic risk scores based on GWAS summary statistics indicated a significant enrichment for SNP effects among family history positive compared to family history negative cases (Nagelkerke's R(2 ) = 0.0021; P = 0.00331; P-value threshold <0.4). Estimates of variability in disease liability attributable to the aggregate effect of genome-wide SNPs were significantly greater for family history positive compared to family history negative cases (0.32 and 0.22, respectively; P = 0.031). We found suggestive evidence of allelic effects detectable in large GWAS of schizophrenia that might be specific to particular family history subgroups. However, consideration of a polygenic risk score indicated a significant enrichment among family history positive cases for common allelic effects. Familial illness might, therefore, represent a more heritable form of schizophrenia, as suggested by previous epidemiological studies.