The psychological scars of burns in survivors and their partners

A burn can be a traumatic experience for both the survivor and the partner. This thesis aims to enhance our understanding of the traumatic impact of burn injuries on the quality of life of burn survivors and the psychological symptoms experienced by their partners. The research is divided into two main parts. In the first part, the focus is on the development and trajectory of PTSD symptoms in partners of burn survivors, examining how the interpersonal behavior of both partners influences these symptoms over time. The second part investigates the impact of the survivor’s PTSD symptoms on their health-related quality of life (HRQL) and fatigue. Additionally, the study explores different recovery patterns to pre-burn HRQL levels and compares the perspectives of survivors and their partners on the survivor’s pre-burn HRQL. The findings reveal significant insights into the mental well-being of burn survivors and their partners during the 18 months following the injury. Both survivors and their partners may experience post-traumatic stress symptoms. The study highlights the importance of couple dynamics, showing that partners who are more involved in the mental well-being of burn survivors can help reduce the survivors' traumatic stress. Conversely, it is crucial for the partners' own well-being that they do not suppress their feelings out of a desire to protect the survivor. Furthermore, early signs of post-traumatic stress in burn survivors are strong predictors of persistent symptoms and a long-term decline in quality of life, and increased fatigue. These results underscore the importance of early detection and continuous monitoring of psychological symptoms, both in the hospital and throughout the aftercare phase. The significant impact of post-traumatic stress symptoms supports the implementation of trauma-informed care, emphasizing early symptom recognition and the need for care practices that are aligned with the psychological needs of both patients and their families

A fast and robust method for whole genome sequencing of the Aleutian Mink Disease Virus (AMDV) genome

AbstractAleutian Mink Disease Virus (AMDV) is a frequently encountered pathogen associated with commercial mink breeding. AMDV infection leads to increased mortality and compromised animal health and welfare. Currently little is known about the molecular evolution of the virus, and the few existing studies have focused on limited regions of the viral genome.This paper describes a robust, reliable, and fast protocol for amplification of the full AMDV genome using long-range PCR. The method was used to generate next generation sequencing data for the non-virulent cell-culture adapted AMDV-G strain as well as for the virulent AMDV-Utah strain. Comparisons at nucleotide- and amino acid level showed that, in agreement with existing literature, the highest variability between the two virus strains was found in the left open reading frame, which encodes the non-structural (NS1–3) genes. This paper also reports a number of differences that potentially can be linked to virulence and host range.To the authors’ knowledge, this is the first study to apply next generation sequencing on the entire AMDV genome. The results from the study will facilitate the development of new diagnostic tools and can form the basis for more detailed molecular epidemiological analyses of the virus

Effect of Terbinafine on the Pharmacokinetics of Cyclosporin in Humans

Cyclosporin is largely metabolized by hepatic cytochrome P450 enzymes, and azole drugs that inhibit cytochrome P450 may precipitate cyclosporin toxicity. The allylamine terbinafine binds to a small subfraction of hepatic cytochrome P450 in type I fashion, and has no effect upon hepatic metabolism of cyclosporin in vitro. The purpose of this study was to determine whether oral terbinafine alters the pharmacokinetics of oral cyclosporin in vivo.Twenty male volunteers (age 19–44 years), were randomly allocated to two groups. The first group received three single oral doses of cyclosporin 300mg at intervals of 21 d. The second and third doses of cyclosporin were preceded by a 6-d course of oral terbinafine 250mg each morning. A further 250mg of terbinafine was taken with the second and third doses of cyclosporin. Blood levels of cyclosporin and terbinafine were monitored for 36h after each dose. The second group received a 7-d course of terbinafine 250mg each morning. On the seventh day a single dose of cyclosporin 300mg was taken together with the terbinafine. Blood levels of both cyclosporin and terbinafine were monitored for 36kh. Two further single doses of cyclosporin 300mg were given at intervals of 2 weeks and the cyclosporin levels again monitored. In both groups each cyclosporin dose was preceded by an 8-h fast.The mean peak blood concentration of cyclosporin when taken alone was 958 μg/I, and 822 when taken with terbinafine. The mean area under the curve for cyclosporin was 4207 μg/l/h when taken alone and 3665 when taken with terbinafine. The mean absorption half-life for cyclosporin when taken alone was 0.29 h, and 0.33 when taken with terbinafine. The mean time of maximum concentration and elimination half-life of cyclosporin were unaltered by terbinafine. The results suggest that terbinafine is likely to prove a safe systemic anti-fungal treatment for patients who are taking cyclosporin