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To characterize the composition and specialty training of sideline medical providers present during National Collegiate Athletic Association (NCAA) Division I (Power 5) college football games. Cross-sectional survey study. Power 5 NCAA Division I football programs during the 2023 to 2024 season. Head team physicians from 69 institutions were contacted; 53 (76.8%) completed the survey.Intervention: A 25-question REDCap survey assessing on-site personnel during home and away football games, including physician specialties, emergency coverage, imaging availability, emergency medicines, and athletic training support. Presence, specialty training, and roles of medical providers on the sideline during football games. All responding programs had orthopedic surgeons (OS) on-site at home games, and all but 1 had a primary care sports medicine physician (SMP). SMPs most commonly trained in family medicine (54.2%), followed by emergency medicine (13.5%) and pediatrics (11.9%). OSs were most frequently fellowship-trained in sports medicine (68.6%). Emergency/airway management physicians were present at 37.7% of schools; neurotrauma-specific providers were present at 15.1%. Away game coverage was reduced, with fewer SMPs and OSs traveling. Athletic trainer coverage remained consistent. Only a minority of schools traveled with additional medical specialists. There is significant variability in sideline medical staffing across Power 5 college football programs. While all schools met or exceeded NCAA minimums, these findings highlight opportunities for standardization and alignment with professional sports models to optimize athlete safety.

The Erlang B equation is directly applicable to smaller hospital departments such as maternity and paediatrics departments. The bed occupancy margin is directly linked to size and not 'efficiency'. A figure of 0.1% turn-away has been recommended as a planning target, i.e., only 1 in a thousand admissions suffer a delay before a bed can be found. Two bed calculators are provided which can be used for paediatric, obstetric, maternity, midwife-led, birthing wards and neonatal/paediatric critical care capacity. The negative effects of turn-away are likely to be context specific, hence, critical care > theatres > birthing unit > maternity unit. The uncertainty regarding future births is discussed along with the variable nature of seasonality in births. For paediatrics, much of bed demand is also influenced by the trend in births. Weighted population density (WPD) is associated with the size distribution of hospitals/units within countries and regions. This influences the average cost per birth/admission. The USA has a low WPD and a significant problem with small hospitals/departments. Only 10% of countries have WPD higher than England. Some countries choose to operate with even more hospitals than needed and this acts to elevate costs. Suggestions are made for a pragmatic approach to bed planning, especially where a dispersed population dictates a need for small hospitals, and hence, issues regarding size and costs. For maternity/paediatrics admissions (and other relatively short-stay admissions) the majority of overhead/indirect costs and most staffing costs should be apportioned based on admissions, and not LOS. Apportionment based on LOS creates the spurious illusion that LOS is the major cost driver and that reducing LOS will immediately save costs. Below 20 beds, Poisson statistical variation plus environment-induced randomness in daily arrivals imply that staff costs may become increasingly fixed irrespective of LOS. Around >30 beds, it looks possible to save costs by reducing LOS. Allocating total organizational costs to individual units and then to patients is less precise than realized and can be done in different ways, which all heavily rely on the steady-state assumption. When bed availability is the bottleneck, then reducing LOS may increase throughput per bed and increase income; however, is this for the benefit of the patient or for the benefit of the organization, and does it lead to higher unanticipated total costs including patient harm? The older economy-of-scale literature has been demonstrated to be flawed, with a recent focus on economy of scale at the department level being entirely consistent with the application of the Erlang B equation. A list of nine catastrophic pitfalls is given for doctors to identify dubious capacity advice from managers and external experts.

The treatment of intracellular bacterial infections such as Chlamydia remains a significant clinical challenge due to rising antibiotic resistance and persistent, immunopathology-driven tissue damage. Macrophages are essential for host defense; they can originate from both tissue-resident precursors and circulating monocytes. During infection, macrophages at infected sites are largely derived from monocytes that migrate and differentiate there, where they phagocytose pathogens and orchestrate immune responses. The chemokine receptor CCR2 is a key regulator of this process, yet its role beyond monocyte trafficking is not fully understood. Previous studies have shown that CCR2 deficiency impairs monocyte mobilization and exacerbates disease during Chlamydia infection, shifting immune responses away from protective Th1 immunity toward pathological Th2 and Th17 polarization. Here, we investigate how CCR2 regulates macrophage function to balance protective Th1 versus pathological Th2/Th17 immunity during Chlamydia respiratory infection. Our results show that CCR2 deficiency reduces pulmonary infiltration of Ly6Chi and Ly6Clow monocytes and shifts macrophage differentiation away from an M1-like toward an M2-like phenotype. Mechanistically, CCR2 deficiency compromises macrophage endocytosis and survival, elevates ROS production, and activates the NLRP3 inflammasome, leading to Caspase-3/GSDME-mediated pyroptosis with increased IL-1β and IL-18, while suppressing the Caspase-1/GSDMD pathway. These findings were recapitulated in vitro using C. muridarum-stimulated Ccr2-deficient bone marrow-derived macrophages (BMDMs), which also showed impaired migration, reduced M1-like polarization, diminished endocytosis, and enhanced ROS/NLRP3/pyroptosis. Furthermore, co-culture of these BMDMs with CD4+ T cells revealed that Th1 differentiation was inhibited, whereas Th2 and Th17 responses were promoted. Collectively, CCR2 orchestrates monocyte-macrophage function by driving M1-like polarization and inhibiting NLRP3/Caspase-3/GSDME pyroptosis to rebalance Th1/Th2/Th17 immunity, thereby enhancing bacterial clearance while mitigating immunopathological tissue damage during Chlamydia infection.

Organic molecular oxidation reactions are ideally regarded to be energy-saving alternative to replace oxygen evolution reaction (OER) for lowering the oxidation overpotential during green hydrogen production. However, the vast scale of hydrogen production is far beyond the fine chemical processes, inevitably resulting in substantial oxygen release. Here, we propose another type of coupled oxidation reactions to stably accommodate with high-current density hydrogen production, accompanied by easy separation. As taking benzylamine oxidation reaction (BOR) as a probe without other side reactions, we propose a bubble-assisted strategy by activating OER and utilizing the generated oxygen bubbles to timely take the insoluble product benzonitrile away from electrode surface, and effectively overcome the electrode poisoning issue. The assembled prototype water electrolyzer achieves a typical current density of 200 mA/cm2 and faradaic efficiency of 55% at 1.65 V for over 40 hours, diversify high-value chemical outputs. Such hybrid electrolysis within bubble-assisted strategy endows system flexibility for next-generation integrated electrochemical energy platforms.

Alzheimer's disease (AD) is characterized by the accumulation of amyloid-β (Aβ), yet the specific link between plaque burden and cognitive decline remains a subject of intense investigation. This paper presents a mathematical model that simulates the coupled dynamics of Aβ monomers, soluble oligomers, and fibrillar species in the brain tissue. By modifying existing governing equations to include a dedicated conservation equation for Aβ monomers, the model explores how various microscopic processes, such as primary nucleation, surface-catalyzed secondary nucleation, fibril elongation, and fragmentation, contribute to macroscopic disease progression. Central to this study is the concept of "accumulated neurotoxicity" as a surrogate marker of biological age, defined as the time-integrated concentration of soluble Aβ oligomers. Unlike plaque burden, accumulated neurotoxicity cannot be reversed, and the harm it causes depends critically on the sequence of events that produced it. Numerical results demonstrate that while plaque burden and neurotoxicity both increase over time, their relationship is non-linear and highly sensitive to the efficiency of protein degradation machinery. Specifically, impaired degradation causes biological age, defined in terms of accumulated neurotoxicity, to advance considerably faster than calendar age. The model further identifies oligomer dissociation and fibril fragmentation as potential protective mechanisms that can counterintuitively reduce neurotoxic burden by diverting monomers away from the soluble oligomer pool. These findings provide a quantitative basis for understanding why individuals with similar plaque burdens may experience vastly different cognitive outcomes, underscoring the importance of targeting soluble oligomers early in therapeutic interventions.

Immune checkpoint inhibitors (ICIs) have reshaped the treatment landscape of cancer, yet their clinical benefit is accompanied by a distinct spectrum of immune-related toxicities. Among these, cardiotoxicity remains uncommon but clinically consequential because it can evolve quickly, presents with marked heterogeneity, and may result in fulminant myocarditis, malignant arrhythmia, or hemodynamic collapse. Key mechanistic drivers include T-cell clonality directed against cardiac autoantigens (e.g., α-myosin heavy chain), cytokine amplification via JAK/STAT signaling, and innate immune recruitment. Recent work has shifted the field away from viewing ICI-related cardiotoxicity as a nonspecific inflammatory complication. Instead, available data support a model in which immune checkpoint blockade perturbs a broader tumor-host ecosystem and exposes organ-specific vulnerabilities within the heart. T-cell clonality, loss of peripheral tolerance, cytokine amplification, endothelial activation, stromal remodeling, and metabolic rewiring all appear to contribute, although their relative importance likely varies across patients. This review examines ICI-associated cardiotoxicity through the lens of cellular pharmacology. We focus on how checkpoint signaling sustains cardiac immune homeostasis, how susceptibility emerges from interactions between tumor-derived cues and host immune context, and why resistance to toxicity-directed therapy remains clinically relevant. We also discuss evolving biomarker strategies-including high-sensitivity troponins, cardiac MRI, and emerging immune-state markers-and mechanism-based interventions that may help reduce cardiac injury without fully negating antitumor efficacy. By framing cardiotoxicity as a context-dependent extension of systemic immune modulation rather than an isolated adverse event, we highlight unresolved questions that are central to the development of predictive biomarkers and more selective therapeutic strategies. Finally, we briefly note that structured nursing surveillance and multidisciplinary team coordination remain essential for translating mechanistic advances into improved bedside outcomes.

Background: Despite the rise of endoscopic approaches, the direct brow lift remains one of the most effective procedures for correcting brow ptosis for both functional and cosmetic indications. It continues to offer superior control when correcting brow shape, height, and asymmetry. However, visible scarring remains a concern. This systematic review was conducted to synthesize recent evidence on strategies that minimize visible scarring in direct brow lift surgery. Methods: A systematic literature search was performed to retrieve English-language publications from the past decade, discussing scar-minimization strategies in direct brow lift. A total of 124 records were identified through database searches in Ovid MEDLINE and Embase. Records were screened manually according to predetermined criteria, and those not in English, not addressing scarring, or not focused on direct brow lift were excluded. After this process, ten publications were included in the final qualitative synthesis. Results: The qualitative synthesis of all included publications (together comprising data on approximately 900 patients) revealed several strategies for scar minimization. (1) Incision beveling: A shallow cranially directed bevel between 20° and 45° preserves brow hair follicles and allows hair regrowth through the scar, providing natural camouflage. (2) Undermining: Gentle subcutaneous undermining in a limited 1-2 cm field, while preserving subcutaneous fat, allows tension-free advancement and maintains brow volume. (3) Periosteal suspension: Anchoring the mobilized brow flap to the frontal periosteum redistributes tension away from the dermal closure, maintaining elevation and improving scar quality. (4) Layered closure: Two- or three-layered wound closure with deep dermal anchoring and fine everting skin sutures minimizes dermal traction and scar widening. (5) Adjunctive measures: Evidence for topical silicone gel was inconclusive, whereas postoperative laser therapy and perioperative neuromodulator use demonstrated improved scar appearance. Across studies, outcomes were consistent, with high patient satisfaction, inconspicuous scars in over 85% of cases, and low complication or revision rates. Conclusions: Direct brow lift has historically been criticized for conspicuous scarring, contributing to the popularity of endoscopic techniques. Nevertheless, the traditional direct brow lift remains a fundamental skill in the oculofacial plastic surgeon's armamentarium, offering unmatched accuracy in brow repositioning, reliability, and symmetry. Contemporary evidence demonstrates refinements that can markedly minimize scar visibility. This systematic review and qualitative synthesis allow us to continue to refine and improve our techniques to minimize scarring in direct brow lift to the benefit of our patients.

The bioconversion of CO2‑derived methanol into higher‑value chemicals offers an attractive route for hybrid catalytic-biotechnological carbon capture and utilization (CCU). Clostridium luticellarii is one of the few acetogens able to produce isobutyric acid. However, operational and metabolic factors driving its production are poorly understood. This work investigates how CO2 availability shapes the product spectrum of C. luticellarii during methylotrophic growth and assesses whether CO2 supply can be used as a process lever to promote isobutyric acid formation. Batch experiments with varying initial bicarbonate concentrations revealed that conditions leading to CO2 limitation (i.e., DIC depletion at ≤ 30 mM NaHCO3) redirected carbon and electron fluxes away from acetic acid toward butyric and isobutyric acids, with the latter accounting for up to 41% of total products. This metabolic switch was not observed when CO2 was in excess (>45 mM). High acetic acid supplementation (100 mM) triggered isobutyric acid production even while CO2 was still available, indicating a combined regulation of dissolved inorganic carbon (DIC) and acetic acid availability. Net acetic acid consumption took place in all isobutyric acid-producing experiments. These observations were reproduced in 3-L bioreactors and further exploited through a fed‑batch strategy in which an initial acetic‑acid‑accumulating phase was followed by CO2‑limited feeding. This approach achieved complete conversion of methanol and CO2 and yielded an isobutyric acid titer of 2.70 ± 0.04 g·L-1. Controlling CO2 availability is a viable operational tool to steer C. luticellarii metabolism toward isobutyric acid production, in interaction with electron acceptor availability.

The nervous system constitutes a highly ordered, integrated network of cells. Understanding this neuroanatomical architecture in vitro is fundamental to elucidating the cellular computations underlying functional network formation. Neuronal connectivity orchestrated through axonal pathfinding arises from an interplay of biochemical signals and electromechanical properties of the growth substrate. Our study focuses on how neurons' morphology and spatial organization are affected by the periodic, micrometer-scale patterned stripes of two electrically contrasting polymers-poly(vinylidenefluoride-trifluoroethylene) (PVDF-TrFE) and poly(3,4-ethylenedioxythiophene)-poly(styrene sulfonate) (PEDOT:PSS). This periodic confinement provides a length-scale-driven cue, which unfolds as a self-organized, spatial guidance phenomenon. Primary cortical cultures on these patterned substrates reveal significant differences-with more elaborate neurite outgrowth and morphological complexity on the PVDF-TrFE stripe. The features observed at the stripe boundaries, along with the network dependence on stripe width, suggest that the neurons exhibit a preference to remain confined within the PVDF-TrFE region, with growth cones deflecting away from the PEDOT:PSS regions. These morphological observations demonstrate a proof-of-concept substrate design for future development of a functional bioinstructive template capable of directing axonal growth, with potential implications for early models of connectivity disorders in vivo.

This interdisciplinary longitudinal study examines the association between PM2.5 levels at sites downwind of a coal-fired thermal power plant (TPP) near the India-Bangladesh border and respiratory health in the exposed population, assessed using spirometry and fractional exhaled nitric oxide levels. Pulmonary function tests indicate significantly worse lung health at downwind sites in both India and Bangladesh compared with an upwind location. With averaged forced expiratory volume in one second (FEV1) values&#x2009;<&#x2009;80% of predicted, evidence of preserved ratio impaired spirometry (PRISm), and significantly lower forced expiratory flow between 25% and 75% of vital capacity (FEF25-75), the population at the Indian downwind site is clearly at risk of developing obstructive pulmonary and related diseases. Although PM2.5 concentrations decline sharply during the monsoon across all sites, this does not translate into a recovery in lung health at the downwind location, consistent with chronic, irreversible effects potentially related to long-term exposure to TPP-associated PM2.5. Moreover, poorer socioeconomic conditions and exposure to emissions from biomass-based indoor cooking are associated with exacerbated respiratory effects. Overall, the study advocates transitioning to cleaner fuels for power generation and household use and recommends locating power plants away from densely populated areas to minimize health impacts.

Preadipocyte commitment to the adipogenic lineage declines markedly with advancing age, while triglyceride accumulation in hypertrophied existing adipocytes persists or expands. This creates a dissociation between adipogenic capacity and lipid-buffering demand, progressively weakening depot metabolic competence and contributing to systemic insulin resistance. This review examines the molecular mechanisms linking impaired adipose tissue plasticity during ageing to metabolic decline, and appraises therapeutic strategies that may restore adipose progenitor competence or limit downstream metabolic dysfunction. Ageing adipose tissue is characterized by four interlocking defects. First, transcriptional reprogramming, including induction of the inhibitory CCAAT/enhancer-binding protein &#x3b2;-LIP isoform through CUG triplet repeat-binding protein 1, together with reduced C/EBP&#x3b1; and peroxisome proliferator-activated receptor &#x3b3; activity, shifts progenitors away from differentiation and toward hypertrophic lipid storage. Second, SIRT7 opposes SIRT1 in regulating adipogenic commitment, implicating sirtuin and NAD+ dysregulation in the age-related adipogenic deficit. Third, nuclear lamina remodelling restricts chromatin accessibility at adipogenic loci. Fourth, senescent cells accumulate in ageing depots and generate a senescence-associated secretory phenotype enriched in interleukin-6, tumour necrosis factor-&#x3b1;, and matrix metalloproteinases, sustaining local inflammation and inhibiting preadipocyte differentiation. These changes occur alongside redistribution of fat from subcutaneous depots toward visceral, hepatic, muscular, and perivascular compartments, accelerating insulin resistance, Type 2 diabetes, and cardiovascular disease. Sex-specific depot trajectories diverge, and rodent models reproduce these patterns only partly. Senolytics, NAD+ precursors, and incretin-based agents, including GLP-1 and dual GIP/GLP-1 receptor agonists, are reviewed together with still-preclinical stem cell and CRISPR approaches, ranked by translational readiness. Restoring adipose progenitor competence while preserving depot-specific metabolic identity may help slow age-related metabolic deterioration and prolong healthspan.

The ability to discriminate sensory stimuli is fundamental to sensory-guided behavior. Sensory discrimination by neural populations is constrained by the magnitude of trial-to-trial spiking variability, or noise, and its geometric alignment with the stimulus encoding directions of the population response. Computational models predict that cortical inhibition shapes the noise geometry, but causal evidence from primate cortex is lacking. We used optogenetic stimulation of parvalbumin-expressing inhibitory interneurons (PV-cells) combined with high-density extracellular recordings in primary visual cortex of awake marmoset monkeys to test this prediction. Stimulating PV-cells improved the discriminability of V1 population responses, without expanding the stimulus-related signal magnitude. Instead, PV-cell activation compressed shared trial-to-trial variability and rotated it away from the stimulus-coding direction. Our results establish a causal role for inhibition in shaping the geometry of neural population responses to improve sensory discrimination in the primate visual cortex.

This study aimed to investigate the role of anatomical factors on the outcomes of lateral sinus floor augmentation with simultaneous implant placement using cone-beam computed tomography (CBCT) images. This retrospective study evaluated 80 patients who underwent a sinus lift procedure with simultaneous implant placement and Bio-Oss particles using the lateral window approach. The patients underwent CBCT scans preoperatively, immediately, and 6 months after surgery. CBCT images were used to measure bone graft changes and anatomical features, including sinus width (SW), sinus angle, Schneiderian membrane thickness (Tm), and sinus floor morphology. Descriptive statistics and multiple linear regression models were used to investigate the correlations between these features. The linear changes in apical bone grafts are shown below: apical bone grafts height loss of the implant (aBGHL, median [interquartile range, IQR]: 1.00 [1.53] mm), bone and bone grafts height loss 2 mm away from the implant root horizontally (BGHL, median [IQR]: 1.14 [1.61] mm), apical bone grafts width loss of the implant (aBGWL, median [IQR]: 1.60 [4.15] mm), and bone grafts width loss 2 mm below the implant root (BGWL, median [IQR]: 0.80 [2.00] mm). Both aBGHL and BGHL were positively correlated with SW and Tm, while aBGWL and BGWL were primarily correlated with SW in a series of sequentially adjusted multivariable models. During the early bone remodelling phase, SW plays a pivotal role in the linear resorption of bone grafts, while Tm primarily influences the loss of bone graft height. The results suggest that sinuses with a wide bucco-palatal bony wall distance and a thick Schneiderian membrane are more likely to experience greater bone substitute loss after sinus floor augmentation. These findings will aid clinicians in the selection of implant sites, as well as determining the type and quantity of bone grafting materials.

The landscape of child and adolescent mental health has become increasingly complex, moving away from solely child-focused approaches to more holistic, systemic models that consider youth development within the context of the family environment [...].

Particulate-reinforced polymer composites (PRPCs) are susceptible to cracking under tensile loading, severely limiting their service life. Here, we propose a pressure-gradient-driven infiltration method that rapidly repairs narrow (<10 &#x3bc;m) cracks in a highly filled PRPC (95 wt.% BaSO4/5 wt.% fluororubber). Microstructural evidence confirms that the adhesive completely fills the tortuous crack and forms a continuous adhesive-matrix interface capable of supporting load transfer. Semi-circular bend (SCB) testing demonstrates a substantially higher peak load and increased apparent structural stiffness after repair under the present semi-circular bend configuration, indicating apparent mechanical enhancement beyond simple load-bearing recovery. Digital image correlation (DIC) and fracture morphology show that repair suppresses notch-tip strain localization, reduces the strain concentration factor, shifts the failure-controlling zone away from the original notch tip, and deflects the crack propagation path. Phase-field simulations further show that the post-repair load-bearing capacity is governed by the adhesive-matrix interfacial strength; once this strength approaches or exceeds the tensile strength of the intact PRPC (~8.3 MPa), the repaired crack path is stabilized, enabling peak-load enhancement while suppressing damage localization along the original crack path and shifting failure to adjacent weaker regions. Overall, this work establishes a promising crack repair approach for highly filled PRPCs, while the underlying interface-controlled mechanism provides guidance for adhesive selection and repair design.

We describe our experience in placing a tunneled femoral central venous catheter using a single-dermatotomy, image-guided technique in a preterm neonate&#x2024; Compared to the conventional approach of using 2 skin incisions' this technique utilizes a single small incision in the mid lateral thigh through which the catheter is advanced and tunneled subcutaneously into the common femoral vein&#x2024; This is an appealing approach because the catheter exit site is away from the contaminated diaper/groin area, and we hypothesize that this may reduce infection risk, although this single case demonstrates feasibility rather than proving reduction. In this case report' the procedure was technically successful with stable catheter function over a 14 day period without early complications of infection or dislodgment&#x2024; This case report confirms the feasibility of neonate tunneled central venous catheter placement using a single-dermatotomy technique and suggests the procedure may possibly be a safer option for central venous access&#x2024;.