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Background Methods Results Conclusions The advent of novel biologics has led to an increase in biologic‐switching as patients and clinicians pursue improved clinical outcomes. However, guidance on treatment sequencing in an Australian setting is sparse. This study examines the patterns of care across two tertiary centres in Australia and characterizes the factors contributing to biologic‐switching.A retrospective study of patients who attended the outpatient Dermatology biologic clinics across two tertiary hospitals was conducted. Data on treatment sequencing and patients' PASI at every visit from April 2006 to December 2020 were collected. Patterns of biologic‐switching were examined. The speed of treatment response for each biologic was determined by the time to achieve PASI‐90 and ‐100 for each treatment course.A total of 440 treatment courses were analysed. Ustekinumab and adalimumab were the most frequently prescribed first‐line biologics. The highest proportion of biologic‐switching was observed among patients on TNF‐α inhibitors (63.8%). After 2015, more patients were prescribed IL‐12/23 and IL‐17 inhibitors in favour of TNF‐α inhibitors. IL‐17 inhibitors demonstrated the most rapid treatment response and low PASI scores relative to other biologics. Patients who did not switch biologics had lower rates of psoriatic arthritis and lower BMI, compared to patients who switched biologics. The median PASI on discontinuation generally exceeded 3.0, while on continuation, it was less than 1.2, reflecting patients' and clinicians' thresholds for biologic‐switching.This study demonstrates an increased uptake of more novel biologics as they become available, due to improved safety profiles and clinical outcomes. [ABSTRACT FROM AUTHOR]

Background: Drug survival, which refers to the time from treatment initiation to discontinuation, provides a surrogate measure of the effectiveness of a biologic in a real‐world setting (J Invest Dermatol, 2015, 135, 1). The aim of this study was to determine the drug survival of biologics that are currently available in Australia. We also analysed the treatment efficacy of these biologics and reasons for discontinuation. Methods: Retrospective data from outpatient Dermatology biologic clinics in Westmead Hospital and Royal Prince Alfred Hospital (Sydney, Australia) from April 2006 to December 2020 were collected. Kaplan–Meier analysis was used to calculate drug survival. Results: A total of 306 patients who underwent 566 treatment courses were analysed. Guselkumab was observed to have the longest drug survival, with cumulative drug survival rates of 94.2% ± 4.0 at 1‐ and 5‐years. This was followed by ixekizumab which had a 1‐year survival rate of 87.2% ± 4.5 and 5‐year survival rate of 59.4% ± 9.5. Ixekizumab and guselkumab were also noted to have superior treatment efficacy compared with other biologics, with PASI‐75 rates of 94.9% and 93.8%, respectively. The most common reasons for treatment discontinuation were a lack of initial efficacy to treatment and a loss of efficacy over time despite an initial response, respectively. Conclusion: To our knowledge, this is the first Australian study to report on outcomes of multiple new biologics that are currently in use for the treatment of chronic plaque psoriasis. Overall, this study provides insight into patterns of care from a local experience that may help guide the management of moderate‐to‐severe psoriasis. [ABSTRACT FROM AUTHOR]

This paper presents coupled and decoupled multi‐autonomous underwater vehicle (AUV) motion planning approaches for maximizing information gain. The work is motivated by applications in which multiple AUVs are tasked with obtaining video footage for the photogrammetric reconstruction of underwater archeological sites. Each AUV is equipped with a video camera and side‐scan sonar. The side‐scan sonar is used to initially collect low‐resolution data to construct an information map of the site. Coupled and decoupled motion planning approaches with respect to this map are presented. Both planning methods seek to generate multi‐AUV trajectories that capture close‐up video footage of a site from a variety of different viewpoints, building on prior work in single‐AUV rapidly exploring random tree (RRT) motion planning. The coupled and decoupled planners are compared in simulation. In addition, the multiple AUV trajectories constructed by each planner were executed at archeological sites located off the coast of Malta, albeit by a single‐AUV due to limited resources. Specifically, each AUV trajectory for a plan was executed in sequence instead of simultaneously. Modifications are also made by both planners to a baseline RRT algorithm. The results of the paper present a number of trade‐offs between the two planning approaches and demonstrate a large improvement in map coverage efficiency and runtime. [ABSTRACT FROM AUTHOR]

Histopathology of a case of Hailey-Hailey Disease, punch biopsy skin sample taken from the groin. Vesiculobullous Hailey-Hailey's disease with scarring mimicking a subepidermal autoimmune blistering disease and its management with retinoids Dear editor, Hailey-Hailey disease (HHD) is a rare autosomal-dominant genodermatosis.1 It is caused by a mutation in the ATPase calcium-transporting type 2C member 1 (ATP2C1) gene, which leads to the dysregulation of calcium homeostasis in epidermal keratinocytes.2 These cellular changes lead to the characteristic finding of vesicles, blistering and erosive lesions that tend to affect intertriginous areas.1 Friction, heat and sweat tend to exacerbate the disease.1 A 47-year-old European man with a background of classic, biopsy-proven HHD of the bilateral groin and thighs since his twenties, presented with a new widespread blistering eruption over his trunk. [Extracted from the article]

FRDA (Friedreich's ataxia) is a debilitating mitochondrial disorder leading to neural and cardiac degeneration, which is caused by a mutation in the frataxin gene that leads to decreased frataxin expression. The most common cause of death in FRDA patients is heart failure, although it is not known how the deficiency in frataxin potentiates the observed cardiomyopathy. The major proposed biochemical mechanisms for disease pathogenesis and the origins of heart failure in FRDA involve metabolic perturbations caused by decreased frataxin expression. Additionally, recent data suggest that low frataxin expression in heart muscle of conditional frataxin knockout mice activates an integrated stress response that contributes to and/or exacerbates cardiac hypertrophy and the loss of cardiomyocytes. The elucidation of these potential mechanisms will lead to a more comprehensive understanding of the pathogenesis of FRDA, and will contribute to the development of better treatments and therapeutics. [ABSTRACT FROM AUTHOR]