Indigenous Guardianship and Moose Monitoring: Weaving Indigenous and Western Ways of Knowing

Increasing global rates of wildlife species extinctions, extirpations, and declines warrant improvements to population monitoring and management approaches. To address regional environmental and wildlife issues, Indigenous communities globally are re-establishing traditional roles as stewards of the land through emerging Indigenous Guardianship Programs (IGPs). By providing the opportunity for community-level participation in monitoring and management, IGPs help foster cohesive solutions for long-term conservation of species while promoting environmental stewardship at the community level. Addressing challenges in monitoring and management of wildlife is especially critical for species that are of cultural and ecological importance at both community and distribution-wide scales. Herein, we describe IGPs in Canada with a focus on moose (Alces alces), an important species to many Indigenous Peoples across the species’ distribution. We outline common Western approaches to moose monitoring applied across Canadian jurisdictions and discuss ways in which weaving Indigenous knowledge systems and information gathered through local participation from Indigenous communities enhances monitoring initiatives at regional levels. We elaborate on a case study on moose monitoring and co-management in the community of Gitanyow in British Columbia, Canada to highlight the value of Guardianship to communities and species conservation in relation to moose. Our study reveals how IGPs and the weaving of Indigenous and Western knowledge systems can contribute to the maintenance of both ecological and cultural integrity to strengthen wildlife monitoring and management under changing global environments

Sex differences in confidence influence patterns of conformity

The research was supported in part by an ERC Advanced Grant (EVOCULTURE, Ref.232823) awarded to KNL.Lack of confidence in one's own ability can increase the likelihood of relying on social information. Sex differences in confidence have been extensively investigated in cognitive tasks, but implications for conformity have not been directly tested. Here, we tested the hypothesis that, in a task that shows sex differences in confidence, an indirect effect of sex on social information use will also be evident. Participants (N = 168) were administered a mental rotation (MR) task or a letter transformation (LT) task. After providing an answer, participants reported their confidence before seeing the responses of demonstrators and being allowed to change their initial answer. In the MR, but not the LT, task, women showed lower levels of confidence than men, and confidence mediated an indirect effect of sex on the likelihood of switching answers. These results provide novel, experimental evidence that confidence is a general explanatory mechanism underpinning susceptibility to social influences. Our results have implications for the interpretation of the wider literature on sex differences in conformity.PostprintPeer reviewe

Troubled Worlds: A Course Syllabus about Information Work and the Anthropocene

The goal of this syllabus is to interrogate the material, and socioeconomic processes which underpin our everyday information work. In particular, we examine the relationships developing between contemporary information practices and what problematically gets configured as “nature”—that messy world of non-human entanglements that often exists beyond the purview of innovation work, whether digital software development or industrial engineering. Much recent work on the environmental conditions of computing has sought to break down technology-nature dualisms in order to expose the implication of information technology in broader social and material ecologies. Library and information professionals and researchers are well poised to deepen this inquiry by presenting alternative nature-technology epistemologies grounded in longstanding analyses of information resources and their consumption. The “Troubled Worlds” syllabus starts with a discussion of concerns most obviously germane to the work of most library and information science professionals: practices at the intersection of structuring information and computing. Building on this attention, we turn to humanistic approaches to thinking through the era of dominant human activities widely known as the “Anthropocene” by introducing poetic, artistic, and activist lenses. We explore how artistic objects representing an increasingly troubled natural world raise awareness of the challenges facing it, as well as how they may incorporate and reshape information for aesthetic ends. We then look to questions of disability justice and how it works in blended built and natural spaces as well as the many different ways in which bodies respond to the toxic environments produced by information technologies. We next consider the newer design approaches to library and information research, specifically asking how design perspectives on digital information objects get inscribed in the Anthropocene. Lastly, we consider paradigms of repair and making and analyze the different valences through which information researchers and professionals categorize and contextualize what is possible with them. This compilation does not provide a comprehensive review of the literature on the environment within the information fields. Instead, it extends this literature to promote experimental research and practice. The modules construct an interdisciplinary and provisional path through the related literature in a form that we hope may be continually adjusted, rearranged, and augmented. Pre-print first published online 03/15/202

New tunnel diode for zero-bias direct detection for millimeter-wave imagers

High-resolution passive millimeter wave imaging cameras require per pixel detector circuitry that is simple, has high sensitivity, low noise, and low power. Detector diodes that do not require bias or local oscillator input, and have high cutoff frequencies are strongly preferred. In addition, they must be manufacturable in large quantities with reasonable uniformity and reproducibility. Such diodes have not been obtainable for W-band and above. We are developing zero-bias square-law detector diodes based on InAs/Alsb/GaAlSb heterostructures which for the first time offer a cost-effective solution for large array formats. The diodes have a high frequency response and are relatively insensitive to growth and process variables. The large zero- bias non-linearity in current floor necessary for detection arises from interband tunneling between the InAs and the GaAlSb layers. Video resistance can be controlled by varying an Alsb tunnel barrier layer thickness. Our analysis shows that capacitance can be further decreased and sensitivity increased by shrinking the diode area, as the diode can have very high current density. DC and RF characterization of these devices and an estimate of their ultimate frequency performance in comparison with commercially available diodes are presented

Intracranial injection of AAV expressing NEP but not IDE reduces amyloid pathology in APP+PS1 transgenic mice

The accumulation of β-amyloid peptides in the brain has been recognized as an essential factor in Alzheimer\u27s disease pathology. Several proteases, including Neprilysin (NEP), endothelin converting enzyme (ECE), and insulin degrading enzyme (IDE), have been shown to cleave β-amyloid peptides (Aβ). We have previously reported reductions in amyloid in APP+PS1 mice with increased expression of ECE. In this study we compared the vector-induced increased expression of NEP and IDE. We used recombinant adeno-associated viral vectors expressing either native forms of NEP (NEP-n) or IDE (IDE-n), or engineered secreted forms of NEP (NEP-s) or IDE (IDE-s). In a six-week study, immunohistochemistry staining for total Aβ was significantly decreased in animals receiving the NEP-n and NEP-s but not for IDE-n or IDE-s in either the hippocampus or cortex. Congo red staining followed a similar trend revealing significant decreases in the hippocampus and the cortex for NEP-n and NEP-s treatment groups. Our results indicate that while rAAV-IDE does not have the same therapeutic potential as rAAV-NEP, rAAV-NEP-s and NEP-n are effective at reducing amyloid loads, and both of these vectors continue to have significant effects nine months post-injection. As such, they may be considered reasonable candidates for gene therapy trials in AD

Histone deacetylase 6 inhibition improves memory and reduces total tau levels in a mouse model of tau deposition

INTRODUCTION: Tau pathology is associated with a number of age-related neurodegenerative disorders. Few treatments have been demonstrated to diminish the impact of tau pathology in mouse models and none are yet effective in humans. Histone deacetylase 6 (HDAC6) is an enzyme that removes acetyl groups from cytoplasmic proteins, rather than nuclear histones. Its substrates include tubulin, heat shock protein 90 and cortactin. Tubastatin A is a selective inhibitor of HDAC6. Modification of tau pathology by specific inhibition of HDAC6 presents a potential therapeutic approach in tauopathy. METHODS: We treated rTg4510 mouse models of tau deposition and non-transgenic mice with tubastatin (25 mg/kg) or saline (0.9%) from 5 to 7 months of age. Cognitive behavior analysis, histology and biochemical analysis were applied to access the effect of tubastatin on memory, tau pathology and neurodegeneration (hippocampal volume). RESULTS: We present data showing that tubastatin restored memory function in rTg4510 mice and reversed a hyperactivity phenotype. We further found that tubastatin reduced the levels of total tau, both histologically and by western analysis. Reduction in total tau levels was positively correlated with memory improvement in these mice. However, there was no impact on phosphorylated forms of tau, either by histology or western analysis, nor was there an impact on silver positive inclusions histologically. CONCLUSION: Potential mechanisms by which HDAC6 inhibitors might benefit the rTg4510 mouse include stabilization of microtubules secondary to increased tubulin acetylation, increased degradation of tau secondary to increased acetylation of HSP90 or both. These data support the use of HDAC6 inhibitors as potential therapeutic agents against tau pathology

Targeting HOX transcription factors in prostate cancer

YesBackground: The HOX genes are a family of transcription factors that help to determine cell and tissue identity during early development, and which are also over-expressed in a number of malignancies where they have been shown to promote cell proliferation and survival. The purpose of this study was to evaluate the expression of HOX genes in prostate cancer and to establish whether prostate cancer cells are sensitive to killing by HXR9, an inhibitor of HOX function. Methods: HOX function was inhibited using the HXR9 peptide. HOX gene expression was assessed by RNA extraction from cells or tissues followed by quantitative PCR, and siRNA was used to block the expression of the HOX target gene, cFos. In vivo modelling involved a mouse flank tumour induced by inoculation with LNCaP cells. Results: In this study we show that the expression of HOX genes in prostate tumours is greatly increased with respect to normal prostate tissue. Targeting the interaction between HOX proteins and their PBX cofactor induces apoptosis in the prostate cancer derived cell lines PC3, DU145 and LNCaP, through a mechanism that involves a rapid increase in the expression of cFos, an oncogenic transcription factor. Furthermore, disrupting HOX/PBX binding using the HXR9 antagonist blocks the growth of LNCaP tumours in a xenograft model over an extended period. Conclusion: Many HOX genes are highly over-expressed in prostate cancer, and prostate cancer cells are sensitive to killing by HXR9 both in vitro and in vivo. The HOX genes are therefore a potential therapeutic target in prostate cancer.The authors gratefully acknowledge the support of the Prostate Project charity (UK)

CCL2 Overexpression in the Brain Promotes Glial Activation and Accelerates Tau Pathology in a Mouse Model of Tauopathy

Innate immune activation is a major contributor to Alzheimer’s Disease (AD) pathophysiology, although the mechanisms involved are poorly understood. Chemokine C-C motif ligand (CCL) 2 is produced by neurons and glial cells and is upregulated in the AD brain. Transgene expression of CCL2 in mouse models of amyloidosis produces microglia-induced amyloid β oligomerization, a strong indication of the role of these activation pathways in the amyloidogenic processes of AD. We have previously shown that CCL2 polarizes microglia in wild type mice. However, how CCL2 signaling contributes to tau pathogenesis remains unknown. To address this question, CCL2 was delivered via recombinant adeno-associated virus serotype 9 into both cortex and hippocampus of a mouse model with tau pathology (rTg4510). We report that CCL2 overexpression aggravated tau pathology in rTg4510 as shown by the increase in Gallyas stained neurofibrillary tangles as well as phosphorylated tau-positive inclusions. In addition, biochemical analysis showed a reduction in the levels of detergent-soluble tau species followed by increase in the insoluble fraction, indicating a shift toward larger tau aggregates. Indeed, increased levels of high molecular weight species of phosphorylated tau were found in the mice injected with CCL2. We also report that worsening of tau pathology following CCL2 overexpression was accompanied by a distinct inflammatory response. We report an increase in leukocyte common antigen (CD45) and Cluster of differentiation 68 (CD68) expression in the brain of rTg4510 mice without altering the expression levels of a cell-surface protein Transmembrane Protein 119 (Tmem119) and ionized calcium-binding adaptor molecule 1 (Iba-1) in resident microglia. Furthermore, the analysis of cytokines in brain extract showed a significant increase in interleukin (IL)-6 and CCL3, while CCL5 levels were decreased in CCL2 mice. No changes were observed in IL-1α, IL-1β, TNF-α. IL-4, Vascular endothelial growth factor-VEGF, IL-13 and CCL11. Taken together our data report for the first time that overexpression of CCL2 promotes the increase of pathogenic tau species and is associated with glial neuroinflammatory changes that are deleterious. We propose that these events may contribute to the pathogenesis of Alzheimer’s disease and other tauopathies