Behavioural disorders are a major reason for euthanasia and sheltering of pet dogs. The prevention and treatment of behavioural disorders requires a better understanding of the underlying causes. Early life experiences, such as maternal care, attachment and socialisation, have long lasting and serious consequences for the behavioural and physiological development of an individual. The complex interplay between these factors is likely to have consequences for the future dog-owner bond and the vulnerability to develop behavioural disorders. Here, we summarise the current literature on the interactions between maternal care, attachment formation, and the sensitive socialisation period and their potential consequences on adult dog behaviour. Based on the findings we highlight gaps in knowledge and provide suggestions for future research which are necessary to formulate recommendations for pet dog breeding and socialisation.

Current methods that assay hemoglobin beta-globin chain variants can have limited clinical sensitivity when applied techniques identify only a predefined panel of mutations. Even sequence-based assays may be limited depending on which gene regions are investigated. We sought to develop a clinically practical yet inclusive molecular assay to identify beta-globin mutations in multicultural populations. We highlight the beta-globin mutation detection assay (beta-GMDA), an extensive gene sequencing assay. The polymerase chain reaction (PCR) primers are located to encompass virtually all hemoglobin beta locus (HBB) mutations. In addition, this assay is able to detect, by gap PCR, a common large deletion (Delta619 base pair), which would be missed by sequencing alone. We describe our 5-year experience with the beta-GMDA and indicate its capability for detecting homozygous, heterozygous, and compound heterozygous sequence changes, including previously unknown HBB variants. The beta-GMDA offers superior sensitivity and ease of use with comprehensive detection of HBB mutations that result in beta-globin chain variants.

No abstract

No abstract

A point mutation in the JAK2 gene, a member of the tyrosine kinase family, was recently identified and shown to be associated with several myeloproliferative disorders. Several studies identified the same JAK2 point mutation (1,849G>T), resulting in the substitution of a valine to phenylalanine at codon 617 (V617F). We developed a simple and sensitive method to detect this mutation via polymerase chain reaction and probe dissociation analysis using the LightCycler platform, and we compared this method to existing restriction fragment-length polymorphism, direct sequencing, and amplification refractory mutation system methods. We found that the LightCycler method offered advantages of speed, reliability, and more straightforward interpretation over the restriction fragment-length polymorphism and sequencing approaches.