The Impacts of Climate and Social Changes on Cloudberry (Bakeapple) Picking: a Case Study from Southeastern Labrador

The traditional subsistence activities of Indigenous communities in Canada’s subarctic are being affected by the impacts of climate change, compounding the effects of social, economic and political changes. Most research has focused on hunting and fishing activities, overlooking berry picking as an important socio-cultural activity and contributor to the diversity of food systems. We examined the vulnerability of cloudberry (referred to as ‘bakeapple’ consistent with local terminology) picking to environmental changes in the community of Cartwright, Labrador using semi-structured interviews (n =?18), field surveys, and satellite imagery. We identified the components of vulnerability including: the environmental changes affecting the abundance, quality, and ripening time of bakeapples (i.e., exposure), the characteristics of the community that affect how these changes have local impacts (i.e., sensitivity), and the ways in which the community is responding to environmental changes (i.e., adaptive capacity). Our results confirm that environmental changes related to permafrost, vegetation, and water have occurred at the bakeapple picking grounds with observed impacts on bakeapples. It is becoming increasingly difficult for bakeapple pickers to respond to variable growth as in the past because of changes in summer settlement patterns that place families farther from their bakeapple patches. We conclude that harvesters in Cartwright have high adaptive capacity to respond to environmental changes due to their knowledge of their bakeapple patches, and at present, socioeconomic changes have had a greater impact than environmental changes on their harvesting capacity.     

Resting‐state functional connectivity measured by diffuse correlation spectroscopy

Near‐infrared diffuse correlation spectroscopy (DCS) is used to record spontaneous cerebral blood flow fluctuations in the frontal cortex. Nine adult subjects participated in the experiments, in which 8‐minute spontaneous fluctuations were simultaneously recorded from the left and right dorsolateral and inferior frontal regions. Resting‐state functional connectivity (RSFC) was measured by the temporal correlation of the low frequency fluctuations. Our data shows the RSFC within the dorsolateral region is significantly stronger than that between the inferior and dorsolateral regions, in line with previous observations with functional near‐infrared spectroscopy. This indicates that DCS is capable of investigating brain functional connectivity in terms of cerebral blood flow.      

TNF-alpha opens a paracellular route for HIV-1 invasion across the blood-brain barrier.

BACKGROUND: HIV-1 invades the central nervous system early after infection when macrophage infiltration of the brain is low but myelin pallor is suggestive of blood-brain-barrier damage. High-level plasma viremia is a likely source of brain infection. To understand the invasion route, we investigated virus penetration across in vitro models with contrasting paracellular permeability subjected to TNF-alpha. MATERIALS AND METHODS: Blood-brain-barrier models constructed with human brain microvascular endothelial cells, fetal astrocytes, and collagen I or fibronectin matrix responded in a dose-related fashion to cytokines and ligands modulating paracellular permeability and cell migration. Virus penetration was measured by infectious and quantitative HIV-1 RNA assays. Barrier permeability was determined using inulin or dextran. RESULTS: Cell-free HIV-1 was retained by the blood-brain barrier with close to 100% efficiency. TNF-alpha increased virus penetration by a paracellular route in a dose-dependent manner proportionately to basal permeability. Brain endothelial cells were the main barrier to HIV-1. HIV-1 with monocytes attracted monocyte migration into the brain chamber. CONCLUSIONS: Early after the infection, the blood-brain barrier protects the brain from HIV-1. Immune mediators, such as TNF-alpha, open a paracellular route for the virus into the brain. The virus and viral proteins stimulate brain microglia and macrophages to attract monocytes into the brain. Infiltrating macrophages cause progression of HIV-1 encephalitis.     

A novel type of adhering junction in an epithelioid tumorigenic rat cell culture line

Two major types of plaque-bearing adhering junctions are commonly distinguished: the actin microfilament-anchoring adhaerens junctions (AJs) and the desmosomes anchoring intermediate-sized filaments (IFs). Both types of junction usually possess the common plaque protein, plakoglobin, whereas the other plaque proteins and the transmembrane cadherins are mutually exclusive. For example, AJs contain E-, N-, or P-cadherin in combination with α- and β-catenin, vinculin and α-actinin, whereas in desmosomes, desmogleins and desmocollins are associated with desmoplakin and one or several of the plakophilins (PP1–3). Here we describe a novel type of adhering junction comprising proteins of both AJs and desmosomes and the tight junction (TJ) plaque protein, ZO-1, in a newly established, liver-derived tumorigenic rat cell line (RMEC-1). By immunofluorescence microscopy, cell-cell contacts are characterized by mostly continuous-appearing lines which are usually resolved by electron microscopy as extended arrays of closely spaced small plaque subunits. These plaque-covered regions are positive for plakoglobin, α- and β-catenin, the arm-repeat protein p120, vinculin, desmoplakin and protein ZO-1. They are positive for E-cadherin in cultures early on in passaging, but tend to turn negative for all known cadherins in densely grown cultures. On immunoblotting SDS-PAGE-separated proteins from dense-grown cell monolayers, “pan-cadherin” antibodies have reacted with a band at ～140 kDa, identified as N-cadherin by peptide fingerprinting of the immunoprecipitated protein, which for reasons not yet clear is modified or masked in immunolocalization experiments. The exact histological derivation of RMEC-1 cells is not known. However, the observations of several endothelial markers and the fact that all cells are rich in IFs containing vimentin and/or desmin, while only subpopulations also reveal IFs containing CKs 8 and 18, is suggestive of a mesenchymal, probably endothelial origin. We discuss the molecular relationship of this novel type of extended junction with other types of adhering junctions.     

Reproductive biology of the endemic goby, Lentipes concolor, from Makamaka'ole Stream, Maui and Waikolu Stream, Moloka'i

Constant pressure in Hawai'i to use limited freshwater resources has resulted in increasing concern for the future of the native stream fauna. Hawaiian freshwater gobies have an amphidromous life cycle with a marine larva period and require streams which flow continuously to the ocean for the critical reproductive periods and during recruitment. As such, the stream fauna is particularly sensitive to any anthropogenic perturbations which disrupt the continuity of stream flows. The objective of this 2-year study was to compare the life cycles of the goby, Lentipes concolor, from a heavily diverted stream on Moloka'i and a relatively undisturbed stream on Maui. In Makamaka'ole Stream, Maui, the population of L. concolor was reproductively active all year with females potentially spawning 2–3 times annually. The timing of spawning did not occur consistently during the wet or dry season but coincided with high stream flow conditions regardless of time-of-year. In Waikolu Stream, Moloka'i, the reproductive pattern was more variable with the number of reproductively active females ranging from 0% to 100%. In general the number of eggs was greater and egg size smaller for female L. concolor in Waikolu Stream than in Makamaka'ole Stream. However, female reproductive condition of L. concolor from Maui was consistently higher than from fish on Moloka'i. Reproduction of L. concolor in Makamaka'ole Stream was correlated with the seasonal pattern of flow rates with peaks in female reproductive condition associated with periods of elevated discharge. No correlation between reproduction and discharge occurred in Waikolu Stream. There were considerable differences between the magnitude of discharge in the two streams. Waikolu Stream experienced prolonged periods of extremely low flows which have become common since the Moloka'i Irrigation System began diverting water from the stream in 1960. In Makamaka'ole Stream, L. concolor was capable of reproducing throughout the year and adjusting fecundity in response to stream flow conditions. In contrast, the population in Waikolu Stream appeared to have a ‘boom or bust’ reproductive pattern; the population had reduced or no reproduction when stream flow conditions reached extreme low levels, but the population succesfully reproduced during higher flow months. The diversion structure in Waikolu Stream has dampened the natural seasonal discharge cycle, exacerbated natural low flow conditions, and increased the likelihood of prolonged periods of extremely low flow. Stream management practices in the Hawaiian Islands must take into account the complex life cycles and sensitivity to variable stream flow conditions of the native fauna. This revised version was published online in July 2006 with corrections to the Cover Date.     

The presence of serotonin in cigarette smoke – a possible mechanistic link to 5-HT-induced airway inflammation

We previously reported the involvement of serotonin (5-HT) metabolism in cigarette smoke-induced oxidative stress in rat lung in vivo. Here, we report cigarette smoke as a source of serotonin (5-HT) to the airways and aim at investigating the effects of 5-HT on oxidative stress and inflammation in human bronchial epithelial cells (BEAS-2B). A 5-HT analog was identified to be present in aqueous phase cigarette smoke using the LC-MS/MS approach, which was later confirmed by a 5-HT enzyme-linked immune assay (EIA). Furthermore, exposure to 5-HT caused a time-dependent elevation of intracellular ROS level, which was blocked in the presence of apocynin (a NOX inhibitor). In support, the immunoblot analysis indicated that there was an increase in the expression of NOX2 time-dependently. 5-HT-induced elevation of IL-8 at both mRNA and protein levels was observed, which was inhibited by TEMPOL (a free radical scavenger), and inhibitors for p38 MAPK (SB203580) and ERK (U0126), in line with the time-dependent phosphorylation of p38 MAPK and ERK. In conclusion, our findings suggest that 5-HT presented in bronchial epithelium of smokers may be involved in cigarette smoke-induced oxidative stress and inflammation via activation of p38 MAPK and ERK pathway after the formation of free radicals.     

Chl1 and Ctf4 are required for damage-induced recombinations

Deletion mutants of CHL1 or CTF4, which are required for sister chromatid cohesion, showed higher sensitivity to the DNA damaging agents methyl methanesulfonate (MMS), hydroxyurea (HU), phleomycin, and camptothecin, similar to the phenotype of mutants of RAD52, which is essential for recombination repair. The levels of Chl1 and Ctf4 associated with chromatin increased considerably after exposure of the cells to MMS and phleomycin. Although the activation of DNA damage checkpoint did not affected in chl1 and ctf4 mutants, the repair of damaged chromosome was inefficient, suggesting that Chl1 and Ctf4 act in DNA repair. In addition, MMS-induced sister chromatid recombination in haploid cells, and, more importantly, MMS-induced recombination between homologous chromosomes in diploid cells were impaired in these mutants. Our results suggest that Chl1 and Ctf4 are directly involved in homologous recombination repair rather than acting indirectly via the establishment of sister chromatid cohesion.     

A field guide to cultivating computational biology

Evolving in sync with the computation revolution over the past 30 years, computational biology has emerged as a mature scientific field. While the field has made major contributions toward improving scientific knowledge and human health, individual computational biology practitioners at various institutions often languish in career development. As optimistic biologists passionate about the future of our field, we propose solutions for both eager and reluctant individual scientists, institutions, publishers, funding agencies, and educators to fully embrace computational biology. We believe that in order to pave the way for the next generation of discoveries, we need to improve recognition for computational biologists and better align pathways of career success with pathways of scientific progress. With 10 outlined steps, we call on all adjacent fields to move away from the traditional individual, single-discipline investigator research model and embrace multidisciplinary, data-driven, team science.

Do you want to attract computational biologists to your project or to your department? Despite the major contributions of computational biology, those attempting to bridge the interdisciplinary gap often languish in career advancement, publication, and grant review. Here, sixteen computational biologists around the globe present "A field guide to cultivating computational biology," focusing on solutions.

Biology in the digital era requires computation and collaboration. A modern research project may include multiple model systems, use multiple assay technologies, collect varying data types, and require complex computational strategies, which together make effective design and execution difficult or impossible for any individual scientist. While some labs, institutions, funding bodies, publishers, and other educators have already embraced a team science model in computational biology and thrived [1–7], others who have not yet fully adopted it risk severely lagging behind the cutting edge. We propose a general solution: “deep integration” between biology and the computational sciences. Many different collaborative models can yield deep integration, and different problems require different approaches (Fig 1).Open in a separate windowFig 1Supporting interdisciplinary team science will accelerate biological discoveries.Scientists who have little exposure to different fields build silos, in which they perform science without external input. To solve hard problems and to extend your impact, collaborate with diverse scientists, communicate effectively, recognize the importance of core facilities, and embrace research parasitism. In biologically focused parasitism, wet lab biologists use existing computational tools to solve problems; in computationally focused parasitism, primarily dry lab biologists analyze publicly available data. Both strategies maximize the use and societal benefit of scientific data.In this article, we define computational science extremely broadly to include all quantitative approaches such as computer science, statistics, machine learning, and mathematics. We also define biology broadly, including any scientific inquiry pertaining to life and its many complications. A harmonious deep integration between biology and computer science requires action—we outline 10 immediate calls to action in this article and aim our speech directly at individual scientists, institutions, funding agencies, and publishers in an attempt to shift perspectives and enable action toward accepting and embracing computational biology as a mature, necessary, and inevitable discipline (Box 1).Box 1. Ten calls to action for individual scientists, funding bodies, publishers, and institutions to cultivate computational biology. Many actions require increased funding support, while others require a perspective shift. For those actions that require funding, we believe convincing the community of need is the first step toward agencies and systems allocating sufficient support

1. Respect collaborators’ specific research interests and motivationsProblem: Researchers face conflicts when their goals do not align with collaborators. For example, projects with routine analyses provide little benefit for computational biologists.Solution: Explicit discussion about interests/expertise/goals at project onset.Opportunity: Clearly defined expectations identify gaps, provide commitment to mutual benefit.
2. Seek necessary input during project design and throughout the project life cycleProblem: Modern research projects require multiple experts spanning the project’s complexity.Solution: Engage complementary scientists with necessary expertise throughout the entire project life cycle.Opportunity: Better designed and controlled studies with higher likelihood for success.
3. Provide and preserve budgets for computational biologists’ workProblem: The perception that analysis is “free” leads to collaborator budget cuts.Solution: When budget cuts are necessary, ensure that they are spread evenly.Opportunity: More accurate, reproducible, and trustworthy computational analyses.
4. Downplay publication author order as an evaluation metric for computational biologistsProblem: Computational biologist roles on publications are poorly understood and undervalued.Solution: Journals provide more equitable opportunities, funding bodies and institutions improve understanding of the importance of team science, scientists educate each other.Opportunity: Engage more computational biologist collaborators, provide opportunities for more high-impact work.
5. Value software as an academic productProblem: Software is relatively undervalued and can end up poorly maintained and supported, wasting the time put into its creation.Solution: Scientists cite software, and funding bodies provide more software funding opportunities.Opportunity: More high-quality maintainable biology software will save time, reduce reimplementation, and increase analysis reproducibility.
6. Establish academic structures and review panels that specifically reward team scienceProblem: Current mechanisms do not consistently reward multidisciplinary work.Solution: Separate evaluation structures to better align peer review to reward indicators of team science.Opportunity: More collaboration to attack complex multidisciplinary problems.
7. Develop and reward cross-disciplinary training and mentoringProblem: Academic labs and institutions are often insufficiently equipped to provide training to tackle the next generation of biological problems, which require computational skills.Solution: Create better training programs aligned to necessary on-the-job skills with an emphasis on communication, encourage wet/dry co-mentorship, and engage younger students to pursue computational biology.Opportunity: Interdisciplinary students uncover important insights in their own data.
8. Support computing and experimental infrastructure to empower computational biologistsProblem: Individual computational labs often fund suboptimal cluster computing systems and lack access to data generation facilities.Solution: Institutions can support centralized compute and engage core facilities to provide data services.Opportunity: Time and cost savings for often overlooked administrative tasks.
9. Provide incentives and mechanisms to share open data to empower discovery through reanalysisProblem: Data are often siloed and have untapped potential.Solution: Provide institutional data storage with standardized identifiers and provide separate funding mechanisms and publishing venues for data reuse.Opportunity: Foster new breed of researchers, “research parasites,” who will integrate multimodal data and enhance mechanistic insights.
10. Consider infrastructural, ethical, and cultural barriers to clinical data accessProblem: Identifiable health data, which include sensitive information that must be kept hidden, are distributed and disorganized, and thus underutilized.Solution: Leadership must enforce policies to share deidentifiable data with interoperable metadata identifiers.Opportunity: Derive new insights from multimodal data integration and build datasets with increased power to make biological discoveries.

     

Species traits and channel architecture mediate flow disturbance impacts on invertebrate drift

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