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Study Design Retrospective cohort study using PearlDiver database.Objectives To evaluate the effect of prior thyroidectomy on complications of Anterior Cervical Discectomy and Fusion (ACDF) surgery.Methods PearlDiver was used to identify patients without prior dysphagia or dysphonia undergoing ACDF between the years 2010-2020Q1. Patients with and without prior thyroidectomy were matched by levels of fusion, alcohol use, and gastroesophageal reflux disease in a 1:5 ratio. Postoperative outcomes were assessed for each cohort with multivariable logistic regression, controlling for age, sex, and Elixhauser Comorbidity Index.Results Between 2010 and 2019, matched cohorts of 792 ACDF patients with prior thyroidectomy and 3960 ACDF only patients were included in the study. Of patients with previous thyroidectomy undergoing ACDF, 16.3% experienced dysphagia at 1-year compared with 10.6% for patients undergoing ACDF only (aOR=1.39, P=.004). Patients with previous thyroidectomy also had higher odds of dysphonia at 1-year following ACDF, as compared to patients with ACDF alone (2.7% vs 1.2%, aOR=1.74, P= .048). Patients undergoing ACDF with prior thyroidectomy did not have increased risk of revision at 1 year (aOR=1.10, P=.698), 2 years (aOR=1.16, P=.457), or 5 years (aOR=1.20, P=.255) following surgery. There were no differences in postoperative opioid utilization rates at 1 month (aOR=2.07, P=.138), 3 months (aOR=2.45, P=.095), 6 months (aOR=1.34, P=.520), and 12 months (aOR=1.69, P=.202). Prior thyroidectomy was not associated with reintubation following ACDF (P=.995).Conclusions Patients with prior thyroidectomy undergoing ACDF surgery experience increased odds of dysphagia and dysphonia at 1-year follow-up compared to those without prior thyroidectomy.

Drawing from possible selves theory (H. Markus & P. Nurius, 1986), this study explored the roles of peer beliefs about school and gender differences in the development of academic and [...]

This article summarizes 12 presentations in Group 7 of the 2007 joint symposium of the International Association for Educational and Vocational Guidance, Society' for Vocational Psychology, and National Career Development [...]

Sustainability science research conducted with Indigenous collaborators must be Indigenous-led and achieve impacts that are grounded in local values and priorities, both for ethical reasons and to achieve more robust outcomes. However, there has been limited focus on determining how best to evaluate the way research is used, shared and created to adaptively solve complex sustainable issues facing Indigenous lands. In this paper, we outline a collaborative and adaptive approach for conducting Indigenous-led evaluations of sustainability research and show how this approach was applied to evaluate cross-cultural knowledge co-production practice and impact in Australia’s jointly managed and World Heritage-listed Kakadu National Park. As part of an Indigenous-led research project, indicators were co-developed by Indigenous and non-Indigenous research team members to monitor the health of the knowledge-sharing and co-production practices that underpinned the design, management and success of the project’s research activities. The evaluations focused on determining whether research activities were providing negotiated benefits for local Indigenous people; helping to restore and protect agreed values in priority areas; and supporting Indigenous-led collaborative knowledge sharing and research practices. In Kakadu, we show how the Indigenous-led design of the research evaluation empowered the usability and benefits of knowledge which was negotiated, shared and co-created. The approach shows how sustainability science can be evaluated by Indigenous leaders to test if and how research practice and impact is responding to their priorities for their traditional estates.

Regulated cell death is an integral part of life, and has broad effects on organism development and homeostasis1. Malfunctions within the regulated cell death process, including the clearance of dying cells, can manifest in diverse pathologies throughout various tissues including the gastrointestinal tract2. A long appreciated, yet elusively defined relationship exists between cell death and gastrointestinal pathologies with an underlying microbial component3–6, but the direct effect of dying mammalian cells on bacterial growth is unclear. Here we advance a concept that several Enterobacteriaceae, including patient-derived clinical isolates, have an efficient growth strategy to exploit soluble factors that are released from dying gut epithelial cells. Mammalian nutrients released after caspase-3/7-dependent apoptosis boosts the growth of multiple Enterobacteriaceae and is observed using primary mouse colonic tissue, mouse and human cell lines, several apoptotic triggers, and in conventional as well as germ-free mice in vivo. The mammalian cell death nutrients induce a core transcriptional response in pathogenic Salmonella, and we identify the pyruvate formate-lyase-encoding pflBgene as a key driver of bacterial colonization in three contexts: a foodborne infection model, a TNF- and A20-dependent cell death model, and a chemotherapy-induced mucositis model. These findings introduce a new layer to the complex host–pathogen interaction, in which death-induced nutrient release acts as a source of fuel for intestinal bacteria, with implications for gut inflammation and cytotoxic chemotherapy treatment.

ABSTRACTThe scholarship and practice of responsibly navigating the disruptive possibilities of new technologies has yet to fully consider Indigenous worldviews. We draw on Indigenous-led research in northern Australia’s Kakadu National Park to reflect on research practices for responsibly navigating the introduction of aerial drones as a tool for local Indigenous co-managers to monitor and manage this World Heritage Area. We co-developed protocols to guide Indigenous-led innovation – empowering Indigenous governance, developing ethical and trusted research relationships, and enabling on-going Indigenous-led technological innovation. The protocols were applied to negotiate and navigate the use of drone technology at Jarrangbarnmi, an important biocultural landscape in country owned by Jawoyn people in northern Australia. These protocols provide a way for Indigenous cultural responsibilities for knowledge sharing and stewardship of country to guide and authorise the co-design and application of technological innovations, which are increasingly being used to produce new knowledge to adaptively co-manage Indigenous people’s lands and seas.

Caspase-dependent apoptosis accounts for approximately 90% of homeostatic cell turnover in the body1, and regulates inflammation, cell proliferation, and tissue regeneration2–4. How apoptotic cells mediate such diverse effects is not fully understood. Here we profiled the apoptotic metabolite secretome and determined its effects on the tissue neighbourhood. We show that apoptotic lymphocytes and macrophages release specific metabolites, while retaining their membrane integrity. A subset of these metabolites is also shared across different primary cells and cell lines after the induction of apoptosis by different stimuli. Mechanistically, the apoptotic metabolite secretome is not simply due to passive emptying of cellular contents and instead is a regulated process. Caspase-mediated opening of pannexin 1 channels at the plasma membrane facilitated the release of a select subset of metabolites. In addition, certain metabolic pathways continued to remain active during apoptosis, with the release of only select metabolites from a given pathway. Functionally, the apoptotic metabolite secretome induced specific gene programs in healthy neighbouring cells, including suppression of inflammation, cell proliferation, and wound healing. Furthermore, a cocktail of apoptotic metabolites reduced disease severity in mouse models of inflammatory arthritis and lung-graft rejection. These data advance the concept that apoptotic cells are not inert cells waiting for removal, but instead release metabolites as ‘good-bye’ signals to actively modulate outcomes in tissues.

Apoptotic cell clearance (efferocytosis) elicits an anti-inflammatory response by phagocytes, but the mechanisms that underlie this response are still being defined. Here, we uncover a chloride-sensing signalling pathway that controls both the phagocyte ‘appetite’ and its anti-inflammatory response. Efferocytosis transcriptionally altered the genes that encode the solute carrier (SLC) proteins SLC12A2 and SLC12A4. Interfering with SLC12A2 expression or function resulted in a significant increase in apoptotic corpse uptake per phagocyte, whereas the loss of SLC12A4 inhibited corpse uptake. In SLC12A2-deficient phagocytes, the canonical anti-inflammatory program was replaced by pro-inflammatory and oxidative-stress-associated gene programs. This ‘switch’ to pro-inflammatory sensing of apoptotic cells resulted from the disruption of the chloride-sensing pathway (and not due to corpse overload or poor degradation), including the chloride-sensing kinases WNK1, OSR1 and SPAK—which function upstream of SLC12A2—had a similar effect on efferocytosis. Collectively, the WNK1–OSR1–SPAK–SLC12A2/SLC12A4 chloride-sensing pathway and chloride flux in phagocytes are key modifiers of the manner in which phagocytes interpret the engulfed apoptotic corpse.

A key process in central sensory circuit development involves activity-dependent pruning of exuberant terminals. Here, we studied gustatory terminal field maturation in the postnatal mouse nucleus of the solitary tract (NST) during normal development and in mice where their mothers were fed a low NaCl diet for a limited period soon after conception. Pruning of terminal fields of gustatory nerves in controls involved the complement system and is likely driven by NaCl-elicited taste activity. In contrast, offspring of mothers with an early dietary manipulation failed to prune gustatory terminal fields even though peripheral taste activity developed normally. The ability to prune in these mice was rescued by activating myeloid cells postnatally, and conversely, pruning was arrested in controls with the loss of myeloid cell function. The altered pruning and myeloid cell function appear to be programmed before the peripheral gustatory system is assembled and corresponds to the embryonic period when microglia progenitors derived from the yolk sac migrate to and colonize the brain.

Elderly patients are at increased risk for morbidity and mortality after injury or surgery in both the inpatient and postdischarge settings. The importance of discharge destination after the index hospitalization is increasingly recognized as a determinant of long-term survival, with discharge to a post–acute care facility portending a worse prognosis. Efforts to minimize discharge to post–acute care facilities should include early discharge planning. Communication among a multidisciplinary care team sets the groundwork for effective discharge planning and transitions of care. The elderly face several systematic, psychosocial, functional, and financial barriers that pose significant challenges to successful transitions of care.

Rheumatoid arthritis is characterized by progressive joint inflammation and affects ~1% of the human population. We noted single-nucleotide polymorphisms (SNPs) in the apoptotic cell–engulfment genes ELMO1, DOCK2, and RAC1linked to rheumatoid arthritis. As ELMO1 promotes cytoskeletal reorganization during engulfment, we hypothesized that ELMO1 loss would worsen inflammatory arthritis. Surprisingly, Elmo1-deficient mice showed reduced joint inflammation in acute and chronic arthritis models. Genetic and cell-biology studies revealed that ELMO1 associates with receptors linked to neutrophil function in arthritis and regulates activation and early neutrophil recruitment to the joints, without general inhibition of inflammatory responses. Further, neutrophils from the peripheral blood of human donors that carry the SNP in ELMO1associated with arthritis display increased migratory capacity, whereas ELMO1knockdown reduces human neutrophil migration to chemokines linked to arthritis. These data identify ‘noncanonical’ roles for ELMO1 as an important cytoplasmic regulator of specific neutrophil receptors and promoter of arthritis.

Development and routine tissue homeostasis require a high turnover of apoptotic cells. These cells are removed by professional and non-professional phagocytes via efferocytosis1. How a phagocyte maintains its homeostasis while coordinating corpse uptake, processing ingested materials and secreting anti-inflammatory mediators is incompletely understood1,2. Here, using RNA sequencing to characterize the transcriptional program of phagocytes actively engulfing apoptotic cells, we identify a genetic signature involving 33 members of the solute carrier (SLC) family of membrane transport proteins, in which expression is specifically modulated during efferocytosis, but not during antibody-mediated phagocytosis. We assessed the functional relevance of these SLCs in efferocytic phagocytes and observed a robust induction of an aerobic glycolysis program, initiated by SLC2A1-mediated glucose uptake, with concurrent suppression of the oxidative phosphorylation program. The different steps of phagocytosis2—that is, ‘smell’ (‘find-me’ signals or sensing factors released by apoptotic cells), ‘taste’ (phagocyte–apoptotic cell contact) and ‘ingestion’ (corpse internalization)—activated distinct and overlapping sets of genes, including several SLC genes, to promote glycolysis. SLC16A1 was upregulated after corpse uptake, increasing the release of lactate, a natural by-product of aerobic glycolysis3. Whereas glycolysis within phagocytes contributed to actin polymerization and the continued uptake of corpses, lactate released via SLC16A1 promoted the establishment of an anti-inflammatory tissue environment. Collectively, these data reveal a SLC program that is activated during efferocytosis, identify a previously unknown reliance on aerobic glycolysis during apoptotic cell uptake and show that glycolytic by-products of efferocytosis can influence surrounding cells.

Pulsed electric fields with microsecond pulse width (μsPEFs) are used clinically; namely, irreversible electroporation/Nanoknife is used for soft tissue tumor ablation. The μsPEF pulse parameters used in irreversible electroporation (0.5–1 kV/cm, 80–100 pulses, ∼100 μs each, 1 Hz frequency) may cause an internal field to develop within the cell because of the disruption of the outer cell membrane and subsequent penetration of the electric field. An internal field may disrupt voltage-sensitive mitochondria, although the research literature has been relatively unclear regarding whether such disruptions occur with μsPEFs. This investigation reports the influence of clinically used μsPEF parameters on mitochondrial respiration in live cells. Using a high-throughput Agilent Seahorse machine, it was observed that μsPEF exposure comprising 80 pulses with amplitudes of 600 or 700 V/cm did not alter mitochondrial respiration in 4T1 cells measured after overnight postexposure recovery. To record alterations in mitochondrial function immediately after μsPEF exposure, high-resolution respirometry was used to measure the electron transport chain state via responses to glutamate-malate and ADP and mitochondrial membrane potential via response to carbonyl cyanide-p-trifluoromethoxyphenylhydrazone. In addition to measuring immediate mitochondrial responses to μsPEF exposure, measurements were also made on cells permeabilized using digitonin and those with compromised cytoskeleton due to actin depolymerization via treatment with the drug latrunculin B. The former treatment was used as a control to tease out the effects of plasma membrane permeabilization, whereas the latter was used to investigate indirect effects on the mitochondria that may occur if μsPEFs impact the cytoskeleton on which the mitochondria are anchored. Based on the results, it was concluded that within the pulse parameters tested, μsPEFs alone do not hinder mitochondrial physiology but can be used to impact the mitochondria upon compromising the actin. Mitochondrial susceptibility to μsPEF after actin depolymerization provides, to our knowledge, a novel avenue for cancer therapeutics.

The pathophysiology of heart failure is complex, but mitochondrial dysfunction is an emerging therapeutic target to improve cardiac function. In this Consensus Statement, insights into the mechanisms of mitochondrial dysfunction in heart failure are presented, along with an overview of emerging treatments with the potential to improve the function of the failing heart by targeting mitochondria.

Although commercial grazing can degrade natural habitats, sustainably grazed land may be effective for wildlife conservation. Thus, land condition frameworks that assess the landscape quality of grazed land may also be useful for assessment of habitat quality for wildlife. However, the relationship between the condition of grazed land and native biodiversity is mostly unknown, and this knowledge gap must be addressed to adequately balance commercial production and conservation. In the present case study we determined the relevance of a widely used grazing land condition scale to understanding native vertebrate species richness and abundance (birds, reptiles, amphibians, mammals and all these vertebrate classes grouped) in grazed rangelands in northern Australia (~24–13°S; annual rainfall ranging from >1200 to <400mm), sampled over approximately 10 years from 17 unique sites, containing 381 1-ha study plots. We defined the land condition scale relative to climate and comprehensive assessment of habitat attributes, and then described the relationships between land condition, habitat and biodiversity. The land condition scale partially explained richness and abundance patterns only for mammals (especially rodents), which tended to be higher in better-condition pasture. For other vertebrate groups, the scale was a very poor descriptor of richness and abundance. The land condition scale was not useful to assess wildlife diversity primarily because ‘woody thickening’ (increases in woody vegetation on grazed land, including shrubs and trees) lowers the ‘grazing value’ of land while also generally promoting vertebrate diversity. In line with this, biodiversity decreased with increasing bare ground and erosion, together with, and in the absence of, vegetation cover (i.e. desertification), consistent with grazing land degradation. The present study supports observations that land clearing and reductions in woody vegetation on grazed rangelands are particularly detrimental to native vertebrates.

The article focuses on advancements in the multicolor laser systems with benefits from scanning systems and advanced software programmability. Topics discussed include enhanced laser light experience delivered by galvanometer-based optical scanners; a high-precision position detector incorporated by galvanometer scanners; and development of moving-magnet scanners with rotor made up of a cylindrical magnet.

Justin Perry Chicago Let's put it this way, Justin: A walk through nature can be like a trip to Home Depot. Animals everywhere seem to be poking, pulling, and banging [...]

Installing conservation fences to prohibit feral animal access to wetlands can become a barrier for non‐target species of interest. We collected 161 turtles (Chelodina rugosa, Emydura subglobosaworrelli, Myuchelys latisternum) from twenty floodplain and riverine wetlands during post‐wet (June–August) and late‐dry season (November–December) surveys (2015–2018) in northern Australia. Wetlands were fenced (150 × 150 mm square, 1.05 m high wire mesh) or unfenced around the wet perimeter. Ninety‐seven percent of individuals caught in either fenced or unfenced wetlands had a shell carapace width greater than mesh width, of these 44 (46%) were captured inside fenced wetlands, while 50 were caught in unfenced wetlands. The remaining 35 turtles were smaller than 150 mm and would likely pass easily through fence mesh. Sixty‐five turtles partook in a fencing manipulative experiment. Turtles with carapace widths wider than mesh often successfully escaped through fences by lifting one side of their shell and passing diagonally through the mesh. In a second experiment where a piece of vertical wire (1500 × 300 mm) was removed, turtles located ‘gates' after prospecting and fitting through meshing areas that were too small to pass. Ninety‐two percent of turtles were able to locate and pass through gates, while 8% failed to locate a gate after 2 h. Gates applied every 4 m showed an 83% passage rate, every 2 m was 91%, and every 1 m was 100%. Combing field and manipulative experiments revealed that large turtles will prospect and move along a fence until they find suitable passage, which has important consequences when considering that gates could be easily retrofitted to existing sites, as well in new fencing programs, which has enormous positive conservation benefits for turtles in an already challenging and changing floodplain environment.

Species are largely predicted to shift poleward as global temperatures increase, with this fingerprint of climate change being already observed across a range of taxonomic groups and, mostly temperate, geographic locations. However, the assumption of uni-directional distribution shifts does not account for complex interactions among temperature, precipitation and species-specific tolerances, all of which shape the direction and magnitude of changes in a species’ climatic niche. We analysed 60 years of past climate change on the Australian continent, assessing the velocity of changes in temperature and precipitation, as well as changes in climatic niche space for 464 Australian birds. We show large magnitude and rapid rates of change in Australian climate over the past 60 years resulting in high-velocity and multi-directional, including equatorial, shifts in suitable climatic space for birds (ranging from 0.1 to 7.6 km yr−1, mean 1.27 km yr−1). Overall, if measured only in terms of poleward distribution shifts, the fingerprint of climate change is underestimated by an average of 26% in temperate regions of the continent and by an average of 95% in tropical regions. We suggest that the velocity of movement required by Australian species to track their climatic niche may be much faster than previously thought and that the interaction between temperature and precipitation changes will result in multi-directional distribution shifts globally.

In this study (N= 137), although 70.8% of participants reported no current substance use and 42.3% reported never using, the Adolescent Substance Abuse Subtle Screening Inventory (SASSI‐A2; Miller & Lazowski, 2001) screened 39.41% of the participants for a high level of probability of having a substance‐related disorder. SASSI‐A2 classified more females in our sample as having a high probability of substance‐related disorder than males. Among African American participants, male adolescents had substantially higher levels of drug use and significantly lower levels of alcohol use than did female adolescents. Implications, limitations, and future directions are provided.

Determining which residues within a multiple alignment of protein sequences are most responsible for protein function is a difficult and important task in bioinformatics. Here, we show that this task is an application of the standard Feature Selection (FS) problem. We show the comparison of standard FS techniques with more specialised algorithms on a range of data sets backed by experimental evidence, and find that some standard algorithms perform as well as specialised ones. We also discuss how considering the discriminating power of combinations of residue positions, rather than the power of each position individually, has the potential to improve the performance of such algorithms.

A versatile method for the creation of multitier hierarchical structured surfaces is reported, which optimizes both antiviral and hydrophobic (easy-clean) properties. The methodology exploits the availability of surface-active chemical groups while also manipulating both the surface micro- and nanostructure to control the way the surface coating interacts with virus particles within a liquid droplet. This methodology has significant advantages over single-tier structured surfaces, including the ability to overcome the droplet-pinning effect and in delivering surfaces with high static contact angles (>130°) and good antiviral efficacy (log kill >2). In addition, the methodology highlights a valuable approach for the creation of mechanically robust, nanostructured surfaces which can be prepared by spray application using nonspecialized equipment.

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The synthesis, solution complexation behaviour and solvent extraction ability of related chelating mono-and bis-(benzimidazole)phosphinate ligands 8 and 9 has been assessed. 31P NMR, fluorescence and absorption spectroscopy and electrospray mass spectrometry revealed preferential formation of 1:1 complexes with the divalent ions Zn, Co and Ni, and ML2 complex formation with the bidentate ligand. Extraction studies showed that 9 extracted Zn>CoNi with no extraction of copper(II), but avid extraction of copper(I), generated insitu, consistent with the ligand's preference for the binding of tetrahedrally-coordinating metal ions.

Alkyl cholates 2and 3have been shown to bind tridentate oxoanions using 1H NMR and solubilisation measurements in C 6D 6and benzene-hexane mixtures respectively. Recognition is presumed to occur through hydrogen bonding to the three hydroxyl groups on the α face of the steroid nucleus.

Knockout or inhibition of the channel and kinase TRPM7 increases the number of regulatory T cells in mice.

The present study explored the causal relationship between self-esteem and school belongingness among a sample of urban youth. Based on a longitudinal cross-lagged panel design, the results offered initial support for the personal agency perspective of growth in self-esteem leading to growth in school belongingness. We discuss the implications for school counselors and the study’s limitations and directions for future research.

Daclizumab inhibition of inflammation in human autoimmunity is associated with blockade of lymphoid tissue inducer cell development.

ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 100 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a “Full Text” option. The original article is trackable via the “References” option.

No relevant conflicts of interest to declare.