Explore the vast range of titles available.

Resource distribution, habitat structure, and predators greatly influence spatial and temporal landscape use by prey species. The “risky places” hypothesis establishes prey will proactively respond to predators' presence based on habitat cues, whereas the “risky times” hypothesis predicts prey will reactively respond by increasing vigilance in the presence of predators regardless of habitat cues. We fit a multiscale, Bayesian species interaction occupancy model with detection/non‐detection data to evaluate black‐tailed jackrabbit (Lepus californicus) and eastern cottontail rabbit (Sylvilagus floridanus) habitat use in the presence and absence of coyotes (Canis latrans), American badgers (Taxidea taxus), and swift foxes (Vulpes velox). We also evaluated how species‐specific predator presence modified temporal activity patterns of prey. Jackrabbits decreased habitat use in areas with greater forage and opted to use areas with greater visibility when coyotes or swift foxes were present. However, cottontails used habitat in open areas with greater visibility when American badgers were present and all other predators absent, suggesting dissimilar habitat‐use patterns dictated by predator‐specific risks. Both lagomorph species are nocturnal with segregated peaks of activity compared with predators, suggesting fine‐scale temporal use partitioning. Our results provide insights into predator–prey dynamics across heterogenous landscapes in a multi‐predator system.

Anthropogenic activities since the European colonization of the North American Great Plains have drastically altered landscape composition and configuration, subsequently affecting native biodiversity. These contemporary human-modified landscapes may affect mammal species’ distributions, diel activity patterns, habitat use, and interspecific interactions, though a better understanding of these effects on mammals occurring in remaining prairie landscapes is needed. To fill this gap, we surveyed 381 randomly selected sites in 2018, 2019, and 2020 using motion-sensing camera traps across the western part of the US state of Kansas (7,160,077 ha). Sites were separated by ≥2 km (x = 8.16 km, SD = 3.61), and cameras were secured to a metal post 40 cm above ground and randomly oriented toward the north or south. We placed an olfactory attractant (mixture of skunk essence and petroleum jelly) on a wooden stake 3 m in front of each camera. Cameras were in place at each site for 28 consecutive days for each year. We manually identified all mammal species detected at each site, collating these data into a database that included taxonomic information for 14 families of mammals (Antilocapridae, Bovidae, Canidae, Cervidae, Cricetidae, Dasypodidae, Didelphidae, Erethizontidae, Felidae, Heteromyidae, Leporidae, Mephitidae, Mustelidae, Procyonidae, Sciuridae, and Muridae) comprising 28 total species. We recorded 31,178 mammal photographs (nonindependent events) over 27,954 camera trap nights during 2018 (n = 10,351), 2019 (n = 9478), and 2020 (n = 8125). Additionally, we included the time and date of each photocapture. Moreover, we gathered survey-specific data useful for modeling species-specific detection along with site-level habitat composition data taken at each site each year. These data will be useful for examining habitat use, species distributions, diel activity patterns, and spatiotemporal interactions between species and across guilds of mammals occurring in a rapidly changing agro-prairie ecosystem. There are no copyright restrictions, but we ask researchers to cite this paper when using these data for publication.

Kidney disease is a leading cause of morbidity and mortality across the globe. Current interventions for kidney disease include dialysis and renal transplantation, which have limited efficacy or availability and are often associated with complications such as cardiovascular disease and immunosuppression. There is therefore a pressing need for novel therapies for kidney disease. Notably, as many as 30% of kidney disease cases are caused by monogenic disease and are thus potentially amenable to genetic medicine, such as cell and gene therapy. Systemic disease that affects the kidney, such as diabetes and hypertension, might also be targetable by cell and gene therapy. However, although there are now several approved gene and cell therapies for inherited diseases that affect other organs, none targets the kidney. Promising recent advances in cell and gene therapy have been made, including in the kidney research field, suggesting that this form of therapy might represent a potential solution for kidney disease in the future. In this Review, we describe the potential for cell and gene therapy in treating kidney disease, focusing on recent genetic studies, key advances and emerging technologies, and we describe several crucial considerations for renal genetic and cell therapies.Despite advances in cell and gene therapy for the treatment of disease, no such interventions currently target the kidney. Here, the authors review the potential for cell and gene therapies to be applied to kidney disease, highlighting recent genetic studies, key technical advances and considerations, and areas for further investigation.

At present, neither basic research nor clinical studies have revealed the exact biological functions or mechanisms of action of individual oligosaccharides during development or in adulthood. Thus, it remains largely unknown whether human milk oligosaccharides could serve as effective therapeutics for gastrointestinal-related diseases. Results from the present study uncover 2′-FL-driven alterations in bacterial metabolism and identify novel B. infantis -secreted metabolites following the consumption of 2′-FL, including pantothenol. This work further demonstrates a previously unrecognized role of pantothenate in significantly protecting the intestinal barrier against oxidative stress and mitigating colitis in adult mice. Remarkably, 2′-FL-enhanced bacterial metabolic pathways are found to be dysregulated in the fecal microbiota of ulcerative colitis patients. These novel metabolic pathways underlying the bioactivities of 2′-FL may lay a foundation for applying individual oligosaccharides for prophylactic intervention for diseases associated with impaired intestinal homeostasis.

Microbial communities are essential for the maintenance of human health, and when these communities are altered, hosts can become susceptible to inflammation and disease. Dysbiosis contributes to gastrointestinal cancers, and specific bacterial species are associated with this phenotype. This study uses a robust and reproducible animal model to demonstrate that H. pylori infection induces gastric dysbiosis in a cagA -dependent manner and further that dysbiosis and altered microbial community structure parallel the severity of H. pylori -induced gastric injury. Ultimately, such models of H. pylori infection and cancer that can effectively evaluate multiple determinants simultaneously may yield effective strategies for manipulating the gastric microbiota to prevent the development of gastric cancer. Helicobacter pylori is the strongest risk factor for gastric adenocarcinoma; however, most infected individuals never develop this malignancy. Strain-specific microbial factors, such as the oncoprotein CagA, as well as environmental conditions, such as iron deficiency, augment cancer risk. Importantly, dysbiosis of the gastric microbiota is also associated with gastric cancer. To investigate the combinatorial effects of these determinants in an in vivo model of gastric cancer, Mongolian gerbils were infected with the carcinogenic cag + H. pylori strain 7.13 or a 7.13 cagA isogenic mutant, and microbial DNA extracted from gastric tissue was analyzed by 16S rRNA sequencing. Infection with H. pylori significantly increased gastric inflammation and injury, decreased α-diversity, and altered microbial community structure in a cagA- dependent manner. The effect of iron deficiency on gastric microbial communities was also investigated within the context of infection. H. pylori -induced injury was augmented under conditions of iron deficiency, but despite differences in gastric pathology, there were no significant differences in α- or β-diversity, phyla, or operational taxonomic unit (OTU) abundance among infected gerbils maintained on iron-replete or iron-depleted diets. However, when microbial composition was stratified based solely on the severity of histologic injury, significant differences in α- and β-diversity were present among gerbils harboring premalignant or malignant lesions compared to gerbils with gastritis alone. This study demonstrates that H. pylori decreases gastric microbial diversity and community structure in a cagA- dependent manner and that as carcinogenesis progresses, there are corresponding alterations in community structure that parallel the severity of disease. IMPORTANCE Microbial communities are essential for the maintenance of human health, and when these communities are altered, hosts can become susceptible to inflammation and disease. Dysbiosis contributes to gastrointestinal cancers, and specific bacterial species are associated with this phenotype. This study uses a robust and reproducible animal model to demonstrate that H. pylori infection induces gastric dysbiosis in a cagA -dependent manner and further that dysbiosis and altered microbial community structure parallel the severity of H. pylori -induced gastric injury. Ultimately, such models of H. pylori infection and cancer that can effectively evaluate multiple determinants simultaneously may yield effective strategies for manipulating the gastric microbiota to prevent the development of gastric cancer.

This paper characterizes the actual science performance of the James Webb Space Telescope (JWST), as determined from the six month commissioning period. We summarize the performance of the spacecraft, telescope, science instruments, and ground system, with an emphasis on differences from pre-launch expectations. Commissioning has made clear that JWST is fully capable of achieving the discoveries for which it was built. Moreover, almost across the board, the science performance of JWST is better than expected; in most cases, JWST will go deeper faster than expected. The telescope and instrument suite have demonstrated the sensitivity, stability, image quality, and spectral range that are necessary to transform our understanding of the cosmos through observations spanning from near-earth asteroids to the most distant galaxies.

All models are wrong but data sharing and better reporting could improve this

In healthy people, blood glucose levels are maintained within a narrow range by several physiological mechanisms. Key among them is the release of the hormone insulin by pancreatic β cells, which occurs when glucose levels rise after a meal. In response to insulin, blood glucose is taken up by tissues that need fuel, such as muscle. β cells can anticipate the body's varying demand for insulin throughout the 24-hour day because they have their own circadian clock. How this clock controls insulin release has been unclear. Perelis et al. now show that the activity of transcriptional enhancers specific to β cells regulates the rhythmic expression of genes involved in the assembly and trafficking of insulin secretory vesicles (see the Perspective by Dibner and Schibler). Science , this issue p. 10.1126/science.aac4250 ; see also p. 628 Circadian control of insulin release is mediated by transcriptional enhancers active specifically in pancreatic β cells. [Also see Perspective by Dibner and Schibler ] The mammalian transcription factors CLOCK and BMAL1 are essential components of the molecular clock that coordinate behavior and metabolism with the solar cycle. Genetic or environmental perturbation of circadian cycles contributes to metabolic disorders including type 2 diabetes. To study the impact of the cell-autonomous clock on pancreatic β cell function, we examined pancreatic islets from mice with either intact or disrupted BMAL1 expression both throughout life and limited to adulthood. We found pronounced oscillation of insulin secretion that was synchronized with the expression of genes encoding secretory machinery and signaling factors that regulate insulin release. CLOCK/BMAL1 colocalized with the pancreatic transcription factor PDX1 within active enhancers distinct from those controlling rhythmic metabolic gene networks in liver. We also found that β cell clock ablation in adult mice caused severe glucose intolerance. Thus, cell type–specific enhancers underlie the circadian control of peripheral metabolism throughout life and may help to explain its dysregulation in diabetes.