'Displaced in the name of Religion': Girl child abuse and community healthcare workers' response to women crying for help in IDP camps in North Central, Nigeria.

This study examines girl child abuse in an internally displaced people's camp in north-central Nigeria and the response of community health workers. The conflict in Benue State is caused by religious differences between the natives (Tiv people) and the invading Fulani herdsmen. During these conflicts, women and girls were displaced, and they were kept in internally displaced persons (IDPs) located in different parts of the state. Literature has been extensively written on internal displacement in Nigeria, but none has been able to elucidate the health needs of girls and the various abuses girls and women are suffering in IDP camps. In this study, literature was extended (1) to explore the environment of the girl child in IDP camps, (2) to identify reasons for the abuse of the girl child in IDP camps, (3) to investigate the impacts of the abuse on the girl child in IDP camps and (4) to investigate how healthcare workers could be used to alleviate the plight of girl children in IDP camps. This is a qualitative case study, with data obtained from relevant academic literature and personal observation. The data were analysed using content analysis. Findings reveal that the girl child is suffering from psychological, economic and health challenges due to the various forms of abuse they are going through. Following the devastation in Benue State, healthcare workers from the community relocated to neighbouring states. There is a need to recall those healthcare workers and provide them with the necessary materials to assist girls in IDP camps. Recommendations are discussed.

Centronuclear myopathy in Labrador retrievers: a recent founder mutation in the PTPLA gene has rapidly disseminated worldwide.

Centronuclear myopathies (CNM) are inherited congenital disorders characterized by an excessive number of internalized nuclei. In humans, CNM results from ~70 mutations in three major genes from the myotubularin, dynamin and amphiphysin families. Analysis of animal models with altered expression of these genes revealed common defects in all forms of CNM, paving the way for unified pathogenic and therapeutic mechanisms. Despite these efforts, some CNM cases remain genetically unresolved. We previously identified an autosomal recessive form of CNM in French Labrador retrievers from an experimental pedigree, and showed that a loss-of-function mutation in the protein tyrosine phosphatase-like A (PTPLA) gene segregated with CNM. Around the world, client-owned Labrador retrievers with a similar clinical presentation and histopathological changes in muscle biopsies have been described. We hypothesized that these Labradors share the same PTPLA(cnm) mutation. Genotyping of an international panel of 7,426 Labradors led to the identification of PTPLA(cnm) carriers in 13 countries. Haplotype analysis demonstrated that the PTPLA(cnm) allele resulted from a single and recent mutational event that may have rapidly disseminated through the extensive use of popular sires. PTPLA-deficient Labradors will help define the integrated role of PTPLA in the existing CNM gene network. They will be valuable complementary large animal models to test innovative therapies in CNM.

Prevalence of the MYBPC3-A31P mutation in a large European feline population and association with hypertrophic cardiomyopathy in the Maine Coon breed.

OBJECTIVES: The MYBPC3-A31P mutation has been identified in the USA in a colony of Maine Coon cats with an autosomal dominant hypertrophic cardiomyopathy (HCM). The objectives of this prospective study were: 1) to evaluate the prevalence of this mutation in a large feline population from Europe; 2) to compare these data with the prevalence of HCM in the Maine Coon breed. ANIMALS AND METHODS: 1) 3757 cats from different breeds including 2744 Maine Coon cats were screened for the mutation. 2) 164/2744 Maine Coon cats were subjected to echocardiography (Echo-Group, mean age = 2.6 years [0.3-11.5]). RESULTS: 1) In the whole study population, the mutation was only found in Maine Coon cats (prevalence = 41.5%), except for one British Longhair cat. 2) 55/164 (34%) cats from the Echo-Group carried the mutation while only 12/164 (7%; 5/48 heterozygous, 5/7 homozygous mutated, 2/109 homozygous wild-type cats) showed HCM. MYBPC3-A31P was associated with a significant increased risk of HCM (relative risk = 9.91). CONCLUSION: The MYBPC3-A31P mutation is highly prevalent in Maine Coon cats in Europe and appears to be breed specific with potential marginal events. Young unaffected mutated cats and affected homozygous wild-type cats illustrate the phenotypic and etiological heterogeneity of feline HCM, as demonstrated in humans.