What does it mean to be “prepared for work”? Perceptions of new engineers

Background: Engineering education seeks to prepare students for engineering practice, but the concept of preparedness is often ill-defined. Moreover, findings from studies of different populations or in different contexts vary regarding how well new graduates are prepared. These variations, coupled with the lack of clarity, suggest the need to better understand what it means to be prepared for engineering work. Purpose: This study contributes to research on workplace preparation by exploring how new graduates describe being prepared for engineering work. Method: Applying secondary analysis to data from the multi-institution Capstone To Work (C2W) project, we used thematic analysis to explore new engineers\u27 descriptions of preparedness. We analyzed written responses to structured questions about the school-to-work transition collected weekly during participants\u27 first 12 weeks of work; 105 graduates drawn from four universities provided 956 responses, with a mean of 9 (out of 12 possible) responses per participant. Results: Participants\u27 descriptions of preparedness included applying concrete skills, recognizing familiar situations, and having strategies for approaching challenging tasks even when they lacked relevant knowledge or skill. Conclusion: Our findings suggest that although many discussions about workplace preparation implicitly focus narrowly on mastery of skills and knowledge, that focus may not fully capture new graduates\u27 experiences, and may limit discussions about the ways in which school can (and cannot) prepare students for work. A more expansive understanding may better support both student learning and workplace onboarding, though more research is needed across stakeholders to establish shared understanding

Segmented filamentous bacteria-based treatment to elicit protection against Enterobacteriaceae in Layer chickens

IntroductionGut microbes like segmented filamentous bacteria (SFB) play a key role in gut maturation during early life, as demonstrated in humans and mice. Our previous study demonstrated oral inoculation of ileum-spores containing SFB to chickens after hatch increases early SFB gut colonization, which increases immune maturation and resistance to bacteria, like Salmonella, as tested in vitro; however, more studies are needed for treatment optimization and in vivo testing. The objectives of this study were to (1) test a treatment that includes both spores and filamentous SFB, (2) validate antimicrobial ability of the treatment in layer hens in vivo, and (3) elucidate its molecular mechanism.MethodsOne-day-old specific pathogen-free layers (n = 12 per group) were orally treated with either PBS (CON) or SFB-based treatment (SFB). At 4 days post-inoculation (DPI), both CON and SFB groups were orally challenged with Salmonella Typhimurium. Total Enterobacteriaceae and Salmonella were examined by plating and enumeration in feces at 7,10 and 14 dpi; and in the ileum, cecum, and spleen at 16 dpi in euthanized birds. The presence and levels of SFB were determined from ilea scrapings via microscopy and qPCR, respectively. Relative gene expression of host-derived antimicrobial peptides and cytokines in the distal ileum was determined by RT-qPCR.ResultsAt 10 and 14 dpi, a significant decrease in total Enterobacteriaceae was observed in the feces of the SFB group. At necropsy, the level of SFB was significantly higher in the SFB group than in the CON group, while a significant decrease in total Enterobacteriaceae and Salmonella was observed in the ceca of the SFB group. RT-qPCR revealed increased expression of β-defensin 14, and cytokines IL-10 and IFNγ.DiscussionThe introduction of SFB at hatch as a prophylactic treatment may benefit commercial partners as well as consumers by reducing the incidence of Enterobacteriaceae in food animals. Reduction of these bacteria in animals would, in turn, increase animal health, productivity, and safety for consumers. Studies to optimize the treatment for poultry industry applications are ongoing in our lab

NACHOS, a CubeSat-Based High-Resolution UV-Visible Hyperspectral Imager for Remote Sensing of Trace Gases: System Overview, Science Objectives, and Preliminary Results

The Nano-satellite Atmospheric Chemistry Hyperspectral Observation System (NACHOS) is a high-throughput (f/2.9), high spectral resolution (1.3 nm optical, 0.57 nm sampling) hyperspectral imager covering the 300-500 nm spectral region with 350 spectral bands. The combined 1.5U instrument payload and 1.5U spacecraft bus comprise a 3U CubeSat. Spectroscopically similar to NASA’s Ozone Monitoring Instrument (OMI), which provides wide-field coverage at ~20 km spatial resolution, NACHOS offers complementary targeted measurements at far higher spatial resolution of ~0.4 km/pixel from 500 km altitude over its 15 ̊ across-track field of view. NACHOS incorporates highly streamlined onboard gas-retrieval algorithms, alleviating the need to routinely downlink massive hyperspectral data cubes. This paper discusses the instrument design, requirements leading to it, preliminary results, and science goals, including monitoring NO2 as a proxy for anthropogenic greenhouse gases, low-level degassing of SO2 and halogen oxides at pre-eruptive volcanoes, and formaldehyde from wildfires. Aiming for an eventual many-satellite constellation providing both high spatial resolution and frequent target revisits, the current NACHOS project is launching two CubeSats, the first already launched to the International Space Station aboard the NG-17 Cygnus vehicle on February 19, 2022 and awaiting deployment to its final orbit in June, and the second launching June 29, 2022

Biology of advanced uveal melanoma and next steps for clinical therapeutics.

Uveal melanoma is the most common intraocular malignancy although it is a rare subset of all melanomas. Uveal melanoma has distinct biology relative to cutaneous melanoma, with widely divergent patient outcomes. Patients diagnosed with a primary uveal melanoma can be stratified for risk of metastasis by cytogenetics or gene expression profiling, with approximately half of patients developing metastatic disease, predominately hepatic in location, over a 15-yr period. Historically, no systemic therapy has been associated with a clear clinical benefit for patients with advanced disease, and median survival remains poor. Here, as a joint effort between the Melanoma Research Foundation\u27s ocular melanoma initiative, CURE OM and the National Cancer Institute, the current understanding of the molecular and immunobiology of uveal melanoma is reviewed, and on-going laboratory research into the disease is highlighted. Finally, recent investigations relevant to clinical management via targeted and immunotherapies are reviewed, and next steps in the development of clinical therapeutics are discussed

Long-term correction of diabetes in rats after lentiviral hepatic insulin gene therapy

Aims/hypothesis: Type 1 diabetes results from the autoimmune destruction of pancreatic beta cells. Exogenous insulin therapy cannot achieve precise physiological control of blood glucose concentrations, and debilitating complications develop. Lentiviral vectors are promising tools for liver-directed gene therapy. However, to date, transduction rates in vivo remain low in hepatocytes, without the induction of cell cycling. We investigated long-term transgene expression in quiescent hepatocytes in vitro and determined whether the lentiviral delivery of furin-cleavable insulin to the liver could reverse diabetes in rats. Materials and methods: To improve transduction efficiency in vitro, we optimised hepatocyte isolation and maintenance protocols and, using an improved surgical delivery method, delivered furin-cleavable insulin alone or empty vector to the livers of streptozotocin-induced diabetic rats by means of a lentiviral vector. Rats were monitored for changes in body weight and blood glucose, and intravenous glucose tolerance tests were performed. Expression of insulin was determined by RT-PCR, immunohistochemistry and electron microscopy. Results: We achieved long-term transgene expression in quiescent hepatocytes in vitro (87 ± 1.2% transduction efficiency), with up to 60 ± 3.2% transduction in vivo. We normalised blood glucose for 500 days-a significantly longer period than previously reported-making this the first successful study using a lentiviral vector. This procedure resulted in the expression of genes encoding several beta cell transcription factors, some pancreatic endocrine transdifferentiation, hepatic insulin storage in granules, and restoration of glucose tolerance. Liver function tests remained normal. Importantly, pancreatic exocrine transdifferentiation did not occur. Conclusions/interpretation: Our data suggest that this regimen may ultimately be employed for the treatment of type 1 diabetes

Evolutionary ecology of intraspecific brain size variation: a review

The brain is a trait of central importance for organismal performance and fitness. To date, evolutionary studies of brain size variation have mainly utilized comparative methods applied at the level of species or higher taxa. However, these studies suffer from the difficulty of separating causality from correlation. In the other extreme, studies of brain plasticity have focused mainly on within-population patterns. Between these extremes lie interpopulational studies, focusing on brain size variation among populations of the same species that occupy different habitats or selective regimes. These studies form a rapidly growing field of investigations which can help us to understand brain evolution by providing a test bed for ideas born out of interspecific studies, as well as aid in uncovering the relative importance of genetic and environmental factors shaping variation in brain size and architecture. Aside from providing the first in depth review of published intraspecific studies of brain size variation, we discuss the prospects embedded with interpopulational studies of brain size variation. In particular, the following topics are identified as deserving further attention: (i) studies focusing on disentangling the contributions of genes, environment, and their interactions on brain variation within and among populations, (ii) studies applying quantitative genetic tools to evaluate the relative importance of genetic and environmental factors on brain features at different ontogenetic stages, (iii) apart from utilizing simple gross estimates of brain size, future studies could benefit from use of neuroanatomical, neurohistological, and/or molecular methods in characterizing variation in brain size and architecture

Organogenesis relies on SoxC transcription factors for the survival of neural and mesenchymal progenitors

During organogenesis, neural and mesenchymal progenitor cells give rise to many cell lineages, but their molecular requirements for self-renewal and lineage decisions are incompletely understood. In this study, we show that their survival critically relies on the redundantly acting SoxC transcription factors Sox4, Sox11 and Sox12. The more SoxC alleles that are deleted in mouse embryos, the more severe and widespread organ hypoplasia is. SoxC triple-null embryos die at midgestation unturned and tiny, with normal patterning and lineage specification, but with massively dying neural and mesenchymal progenitor cells. Specific inactivation of SoxC genes in neural and mesenchymal cells leads to selective apoptosis of these cells, suggesting SoxC cell-autonomous roles. Tead2 functionally interacts with SoxC genes in embryonic development, and is a direct target of SoxC proteins. SoxC genes therefore ensure neural and mesenchymal progenitor cell survival, and function in part by activating this transcriptional mediator of the Hippo signalling pathway

Copy number variants as modifiers of breast cancer risk for BRCA1/BRCA2 pathogenic variant carriers

The risk of germline copy number variants (CNVs) in BRCA1 and BRCA2 pathogenic variant carriers in breast cancer is assessed, with CNVs overlapping SULT1A1 decreasing breast cancer risk in BRCA1 carriers.The contribution of germline copy number variants (CNVs) to risk of developing cancer in individuals with pathogenic BRCA1 or BRCA2 variants remains relatively unknown. We conducted the largest genome-wide analysis of CNVs in 15,342 BRCA1 and 10,740 BRCA2 pathogenic variant carriers. We used these results to prioritise a candidate breast cancer risk-modifier gene for laboratory analysis and biological validation. Notably, the HR for deletions in BRCA1 suggested an elevated breast cancer risk estimate (hazard ratio (HR) = 1.21), 95% confidence interval (95% CI = 1.09-1.35) compared with non-CNV pathogenic variants. In contrast, deletions overlapping SULT1A1 suggested a decreased breast cancer risk (HR = 0.73, 95% CI 0.59-0.91) in BRCA1 pathogenic variant carriers. Functional analyses of SULT1A1 showed that reduced mRNA expression in pathogenic BRCA1 variant cells was associated with reduced cellular proliferation and reduced DNA damage after treatment with DNA damaging agents. These data provide evidence that deleterious variants in BRCA1 plus SULT1A1 deletions contribute to variable breast cancer risk in BRCA1 carriers.Peer reviewe