Background: Organoid technology is emerging rapidly as a valuable tool for precision medicine, particularly in the field of Cystic Fibrosis (CF). However, biobank storage and use of patient-derived organoids raises specific ethical and practical challenges that demand sound governance. We examined the perspectives of professionals affiliated with CF or organoids on the ethical aspects of organoid biobanking for CF precision medicine. By conducting this study parallel to the process of innovation and development of organoid biobanking, its findings are valuable for the design of responsible governance frameworks.Methods: To identify relevant themes and attitudes we conducted 21 semi-structured qualitative interviews with professionals in the field of organoid technology, biobanking, or CF research and care. Results:We identified three key challenges, as well as the suggestions of professionals on how to address them: (1) The challenges associated with commercial involvement, trust, and ownership, (2) Navigating the blurring boundary between research and clinical care, (3) Appropriate approaches to the informed consent procedure. Conclusion:Sound governance of organoid biobanks aimed at precision medicine requires coming to terms with the fact that its stakeholders no longer belong to separate domains. Responsible governance should be aimed at finding a sound, context-sensitive balance between integration of ongoing co-operation and mutual consideration of interests, and maintaining a feasible and sustainable research climate.

Thermoregulatory behaviour enables ectotherms to maintain preferred body temperatures across a range of environmental conditions, and it may buffer individuals against the effects of climate warming. In lizards, the mechanism underlying variation in thermoregulatory behaviour has long been assumed to be phenotypic plasticity, and while this assumption has been difficult to test using wild populations in their natural habitat, it has critical implications as to how variation in thermoregulation is incorporated in models designed to predict outcomes of climate change on ectotherms. We continuously recorded one component of thermoregulatory behaviour, light‐environment use, by two wild populations of desert short‐horned lizards Phrynosoma hernandesi occurring at low (warm) and high (cool) elevations. We then reciprocally transplanted lizards and recorded their light‐environment use when exposed to a novel climate at the transplant site. Immediately following the reciprocal transplant to a novel climate, lizards from both populations adjusted their light‐environment use and matched the light‐environment use exhibited by local lizards at that site. This study provides direct empirical evidence that lizards can immediately adjust light‐environment use, one component of thermoregulatory behaviour, via phenotypic plasticity to match the local environment. Our results provide hope that lizards may have some capacity to buffer against climate change by adjusting their light‐environment use to compensate for warmer environmental temperatures. A http://onlinelibrary.wiley.com/doi/10.1111/1365-2435.13071/suppinfo is available for this article.

We examined white-footed mice (Peromyscus leucopus) from Minnesota for infection with the etiologic agent of human granulocytic ehrlichiosis (HGE). From April to September 1997, we collected P. leucopus from Washington County, Minnesota, an area enzootic for HGE. Blood was cultivated in HL60 cells for isolation of the HGE agent. Of 59 mice examined, only a single mouse was culture positive for the HGE agent. The 16S ribosomal DNA sequence of the isolate was determined to be identical to that of the HGE agent. The isolate was reactive with monoclonal antibodies to the 44-kDa antigen of the HGE agent and was infectious for laboratory mice.Human granulocytic ehrlichiosis (HGE) is a recently described granulocytotropic infection first identified in the upper midwestern United States in 1994 (3). HGE is an acute febrile disease that may present as fever, myalgia, arthralgia, headache, and rigors (1, 4). Infection with the etiologic agent of HGE usually responds rapidly to treatment with tetracyclines. However, despite effective therapy, severe cases and some fatalities have occurred (9).Sequences of 16S ribosomal DNA (rDNA) from the HGE agent are nearly identical to those of the granulocytotropic agents Ehrlichia equi and E. phagocytophila (7), which are responsible for zoonotic infections in horses and ruminants, respectively. Serological cross-reactivity between antibodies to the HGE agent and the antigens of E. phagocytophila and E. equi has been demonstrated (8). Infection of horses with the HGE agent follows a clinical course indistinguishable from that of equine granulocytic ehrlichiosis, and horses infected with the agent of HGE are protected against subsequent challenge with E. equi (5).A family of 42-to 49-kDa surface proteins, designated P44, are capable of eliciting immunologic responses in patients with HGE (2,11,19). Genes encoding P44 proteins are members of the granulocytic ehrlichia-MSP-2 multigene family (15) and are present in multiple copies dispersed throughout the genome (24). The expression of P44 homologs has been postulated to be regulated at the level of transcription to maintain antigenic variability (24). P44 sequences from several isolates have been published (10,15,24), and these sequences may suggest that antigenic diversity exists among the species causing HGE.Epidemiological, molecular, and transmission studies provide evidence that Ixodes scapularis is the vector of HGE in the central and eastern United States (14, 18, 22; K. D. Reed, P. D. Mitchell, D. H. Persing, C. P. Kolbert, and V. Cameron, Letter, JAMA 273:23, 1995). Although the natural history of granulocytic ehrlichiosis is not clear, the white-footed mouse, Peromyscus leucopus, has been implicated as a reservoir of the HGE agent. It has been shown that white-footed mice collected from the wild are capable of transmitting ehrlichial organisms to laboratory-reared ticks (22). Serologic and molecular evidence of infection with the E. phagocytophila genomic group has been demonstrated for P. leucopus collected from regions endem...

The p44 gene of the agent of human granulocytic ehrlichiosis (aoHGE) encodes a 44-kDa major outer surface protein. A technique was developed for the typing of the aoHGE based on the PCR amplification of the p44 gene followed by a multiple restriction digest with HindIII, EcoRV, and AspI to generate restriction fragment length polymorphism patterns. Twenty-four samples of the aoHGE were collected from geographically dispersed sites in the United States and included isolates from humans, equines, canines, small mammals, and ticks. Six granulocytic ehrlichiosis (GE) types were identified. The GE typing method is relatively simple to perform, is reproducible, and is able to differentiate among the various isolates of granulocytic ehrlichiae in the United States. These characteristics suggest that this GE typing method may be an important epizootiological and epidemiological tool.