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Purpose To use a mixed methods approach to investigate the patient waiting experience for a medically underserved population at an outpatient surgical clinic. Methods We used lean methodology to perform 96 time-tracked observations of the patient journey in clinic, documenting the duration of activities from arrival to departure. We also used human-centered design (HCD) to perform and analyze 43 semi-structured interviews to understand patients’ unmet needs. Results Patients spent an average of 68.5% of their total clinic visit waiting to be seen. While the average visit was 95.8 minutes, over a quarter of visits (27%) were over 2 hours. Patients waited an average of 24.4 minutes in the waiting room and 41.2 minutes in the exam room; and only spent 19.7% of their visit with an attending provider and 11.8% with a medical assistant. Interviews revealed that patients arrive to their visit already frustrated due to difficulties related to scheduling and attending their appointment. This is exacerbated during the visit due to long wait times, perceived information opacity, and an uncomfortable waiting room, resulting in frustration and anxiety. Conclusions While time tracking demonstrated that patients spend a majority of their visit waiting to be seen, HCD revealed that patient frustrations span the waiting experience from accessing the appointment to visit completion. These combined findings are crucial for intervention design and implementation for medically underserved populations to improve the quality and experience with healthcare and also address system inefficiencies such as long wait times.

Cell growth and/or proliferation may require the reprogramming of metabolic pathways, whereby a switch from oxidative to glycolytic metabolism diverts glycolytic intermediates towards anabolic pathways. Herein, we identify a novel role for TRIM32 in the maintenance of glycolytic flux mediated by biochemical interactions with the glycolytic enzymes Aldolase and Phosphoglycerate mutase. Loss of Drosophila TRIM32, encoded by thin (tn), shows reduced levels of glycolytic intermediates and amino acids. This altered metabolic profile correlates with a reduction in the size of glycolytic larval muscle and brain tissue. Consistent with a role for metabolic intermediates in glycolysis-driven biomass production, dietary amino acid supplementation in tn mutants improves muscle mass. Remarkably, TRIM32 is also required for ectopic growth - loss of TRIM32 in a wing disc-associated tumor model reduces glycolytic metabolism and restricts growth. Overall, our results reveal a novel role for TRIM32 for controlling glycolysis in the context of both normal development and tumor growth.

Chronic kidney disease (CKD) results in calcitriol deficiency and altered vitamin D metabolism. The objective of this study was to assess the 24-hydroxylation-mediated metabolism of 25(OH)D 3 and 1,25(OH) 2 D 3 in a cross-sectional analysis of participants with a range of kidney function assessed by precise measured GFR (mGFR) (N = 143) and in rats with the induction and progression of experimental kidney disease. Vitamin D metabolites were assessed with LC–MS/MS. Circulating measures of 24-hydroxylation of 25(OH)D 3 (24,25(OH) 2 D 3 :25(OH)D 3 ) precisely decreased according to mGFR in humans and progressively in rats with developing CKD. In contrast, the 1,24,25(OH)3D3: 1,25(OH) 2 D 3 vitamin D metabolite ratio increased in humans as the mGFR decreased and in rats with the induction and progression of CKD. Human participants taking cholecalciferol had higher circulating 1,24,25(OH) 3 D 3 , despite no increase of 1,25(OH) 2 D 3 . This first report of circulating 1,24,25(OH) 3 D 3 in the setting of CKD provides novel insight into the uniquely altered vitamin D metabolism in this setting. A better understanding of the uniquely dysfunctional catabolic vitamin D profile in CKD may guide more effective treatment strategies. The potential that 24-hydroxylated products have biological activity of is an important area of future research.

The loss of traits that no longer contribute to fitness is widespread; however, the causative evolutionary mechanisms are poorly understood. Vestigialization could proceed through the fixation of selectively neutral degenerative mutations via genetic drift. Alternatively, selection may facilitate vestigialization if trait loss results in enhanced fitness. We tested these hypotheses using Decodon verticillatus, a clonal plant in which sexual sterility has arisen repeatedly in populations across the northern geographical range limit. We compared growth and survival of replicated genotypes from 7 sexually fertile and 18 sterile populations, over 3 years in a common environment. Survival of sterile genotypes was 53% greater than for fertile genotypes, but there was no difference in biomass accumulation. Almost all mortality, and hence increased performance of sterile genotypes, occurred during simulated overwinter dormancy. These observations suggest that selection has facilitated the vestigialization of sex, and thus do not support the neutral mutation hypothesis. The selective mechanism probably involves the relaxation of a genetic trade-off between sexual reproduction and survival: alleles that increase vegetative performance at the expense of sexual fertility are selected in geographically peripheral populations where sexual reproduction is suppressed by adverse environmental conditions.

Since the 1970s, avian populations have decreased by about 29% in North America, sparking concerns about their continued survival. Birds are essential to ecosystems for seed dispersal and fertilization, insect and rodent control, and as a food source, yet people often under-value them. Research increasingly shows that human empathy is essential to the sustainability of species. Past work indicates that animal photo portraiture can activate empathy, but researchers have primarily focused on charismatic mammals and have poorly measured empathy for others, especially birds. We extend this research by creating the Empathy for Animals Scale (EAS) and conducting an online survey experiment with 793 people from the United States to examine whether bird photo portraiture activates empathy for birds in the same way it does for mammals. We find that bird photo portraiture, compared to traditional wildlife images, more effectively activates empathy for birds and enhances people’s perception of animals in general. Our findings have important implications for avian conservation and sustainability, potentially helping photographers, organizations, and scholars address public perceptions in promoting the sustainability of birds.

The 24 kD form of secreted phosphoprotein (SPP-24), a cytokine-binding bone matrix protein with various truncated C-terminal products, is primarily synthesized by the liver. SPP-24 shares homology with fetuin-A, a potent vascular and soft tissue calcification inhibitor and SPP-24 is one component of calciprotein particles (CPPs), a circulating fetuin–mineral complex. The limited molecular evidence to date suggests that SPP-24 may also function as an inhibitor of bone formation and ectopic vascular calcification, potentially through bone morphogenic protein 2 (BMP-2) and Wnt-signaling mediated actions. The C-terminal products of SPP-24 bind to BMP-2 and attenuate BMP-2-induced bone formation. The aim of this study was to assess circulating SPP-24 in relation to kidney function and in concert with markers of mineral metabolism in humans. SPP-24 was measured in the serum of total of 192 subjects using ELISA-based measurements. Subjects were participants of one of two cohorts: (1) mGFR Cohort (n = 80) was participants of a study of measured GFR (mGFR) using inulin urinary clearance, recruited mostly from a chronic kidney disease clinic with low-range kidney function (eGFR 38.7 ± 25.0 mL/min/1.73 m2) and (2) CaMOS Cohort (n = 112) was a subset of randomly selected, community-dwelling participants of year 10 of the Canadian Multicentre Osteoporosis Study with eGFR in the normal range of 75.0 ± 15.9 mL/min/1.73 m2. In the combined cohort, the mean SPP-24 was 167.7 ± 101.1 ng/mL (range 33.4–633.6 ng/mL). The mean age was 66.5 ± 11.3, 57.1% female and mean eGFR (CKD-EPI) was 59.9 ± 27.0 mL/min/1.73 m2 (range 8–122 mL/min/1.73 m2). There was a strong inverse correlation between SPP-24 and eGFR (R = − 0.58, p < 0.001) that remained after adjustment for age. Following adjustment for age, eGFR, and sex, SPP-24 was significantly associated with phosphate (R = − 0.199), PTH (R = 0.298), and the Wnt-signaling inhibitor Dickkopf-related protein 1 (R = − 0.156). The results of this study indicate that SPP-24 is significantly altered by kidney function and is the first human data linking levels of SPP-24 to other biomarkers involved in mineral metabolism. Whether there is a role for circulating SPP-24 in bone formation and ectopic mineralization requires further study.

Diets containing inorganic phosphate additives are unbalanced with respect to calcium and these diets have been linked to the development of altered bone metabolism. Using 2 randomized cross-over studies in healthy humans, we (1) characterized the hormonal and urinary response to 2 meals with the same reported phosphorus amount (562–572 mg), where one was manufactured with inorganic phosphate additives and a comparatively lower Ca:P molar ratio (0.26 vs 0.48), and (2) assessed how acute homeostatic mechanisms adapt following 5-d exposure to recommended dietary phosphorus amount (~700 mg P/d) compared to a diet enriched with inorganic phosphate additives (~1100 mg P/d). Participants were then challenged with 500 mg of oral phosphorus in the form of inorganic phosphate after an overnight fast following each diet condition. Measurements included serum calcium, phosphate, PTH, and fibroblast growth factor 23 , vitamin D metabolites, and urine calcium and phosphate excretion. Following the meal containing inorganic phosphate additives with a low Ca:P ratio, serum phosphate was higher and more phosphate was excreted in the urine compared to the low additive meal. Although the Ca:P and calcium content was lower in the high additive meal, the same amount of calcium was excreted into the urine. Subsequently, increasing only dietary phosphate through additives resulted in lower 24-h excretion of calcium. The oral phosphate challenge promoted urinary calcium excretion, despite no consumption of calcium, which was attenuated when pre-acclimated to a high phosphate diet. These data suggest that ingestion of inorganic phosphate promotes calcium excretion, but homeostatic mechanisms may exist to reduce calcium excretion that are responsive to dietary intake of phosphate. Future studies are required to evaluate potential implication of diets enriched with inorganic phosphate additives on bone health. Lay Summary Excessive dietary phosphorus has been linked to the development of bone and vascular disorders. Further, highly bioavailable inorganic phosphate additives, which are unregulated, have been estimated to comprise approximately 50% of an individual’s consumed dietary phosphorus. Using 2 randomized cross-over studies in young healthy participants, we assessed (1) the hormonal and urinary response to 2 meals with the same reported phosphate amount, but one manufactured with inorganic phosphate additives, and (2) how acute homeostatic mechanisms adapt following 5-d of a diet supplemented with inorganic phosphate additives. The results suggest that ingestion of meals containing phosphate additives promotes excess calcium excretion, but homeostatic mechanisms in young healthy adults are sufficient to reduce calcium excretion in response to a 5-d dietary intake of these phosphate additives. These findings indicate an important role of inorganic phosphate additives on acute and chronic calcium homeostasis that will need to be carefully explored for potential implications on bone and/or vascular outcomes. Together these findings also indicate the critical importance of bioavailability of phosphate and the balance with calcium in dietary management. Graphical Abstract Graphical Abstract

The orientation of the mitotic spindle at metaphase determines the placement of the daughter cells. Spindle orientation in animals typically relies on an evolutionarily conserved biological machine comprised of at least four proteins - called Partner of Inscuteable (Pins), Gαi, Mushroom body defective (Mud), and Dynein in flies - that exert a pulling force on astral microtubules and reels the spindle into alignment. The canonical model for spindle orientation holds that the direction of pulling is determined by asymmetric placement of this machinery at the cell cortex. In most cell types, this placement is thought to be mediated by Pins, and a substantial body of literature is therefore devoted to identifying polarized cues that govern localized cortical enrichment of Pins. In Drosophila neuroblasts, for example, this cue is thought to be Inscuteable, which helps recruit Pins to the apical cell surface. In this study we revisit the canonical model. We find that spindle orientation in the follicular epithelium requires not only Pins localization but also activation, which relies on direct interaction between Pins and the multifunctional protein Discs large. This mechanism is distinct from the one mediated by Inscuteable, which we find also has an activating step. Together our results show that the canonical model is incomplete. Local enrichment of Pins is not sufficient to determine spindle orientation; an activation step is also necessary. Competing Interest Statement The authors have declared no competing interest.

In an attempt to wean itself off fossil fuels in the past, Vietnam developed an expansive footprint in wind and solar energy through a series of government-backed feed-in tariffs. Additionally, a lack of regulation and an insufficient power purchasing plan led to excesses in electricity generation, forcing Vietnam Electricity (EVN) to cut renewable energy production in 2021, bankrupting solar companies and halting new renewable projects. The cost of change will have to include low-carbon emitting fossil fuels like LNG, and this should not be considered a negative in developing countries like Vietnam.