RESUMEN
The study aimed to evaluate the mediating roles of patient experiences on patient loyalty. The data were collected through an electronic questionnaire regarding feedback from 5732 patients received outpatient clinics. Patient loyalty was evaluated using the Net Promoter Score (NPS11) that patients were asked whether they would like to recommend the hospital to their relatives or friends. Patient experiences with physicians, nurses, and waiting times were also asked in the questionnaire. After preliminary analysis, mediation analyses were performed to evaluate direct and indirect causal effects among variables for NPS11. While patient experiences are used as possible mediators, Branch Groups in the first and Admission Time in the second model are independent variables. In the analyses, Surgical Medical Science (p = 0.019) and Day Shift (p = 0.000) have a direct mediating effect on NPS11. Nursing care experiences were found to be a mediator variable for NPS11 in both models (p = 0.000 for both). Patient loyalty was associated with Surgical Medical Science and Day Shift primarily whereas Nursing care experience had a mediating role.
RESUMEN
Hereditary sensory and autonomic neuropathy type IV (HSAN IV), or congenital insensitivity to pain with anhidrosis, is an autosomal recessive disorder characterized by insensitivity to noxious stimuli, anhidrosis from deinnervated sweat glands, and delayed mental and motor development. Mutations in the neurotrophic tyrosine kinase receptor type 1 (NTRK1), a receptor in the neurotrophin signaling pathway phosphorylated in response to nerve growth factor, are associated with this disorder. We identified six families from Northern Central Turkey with HSAN IV. We screened the NTRK1 gene for mutations in these families. Microsatellite and single nucleotide polymorphism (SNP) markers on the Affymetrix 250K chip platform were used to determine the haplotypes for three families harboring the same mutation. Screening for mutations in the NTRK1 gene demonstrated one novel frameshift mutation, two novel nonsense mutations, and three unrelated kindreds with the same splice-site mutation. Genotyping of the three families with the identical splice-site mutation revealed that they share the same haplotype. This report broadens the spectrum of mutations in NTRK1 that cause HSAN IV and demonstrates a founder mutation in the Turkish population.