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Background and Objectives: As demand for infusion therapy increases due to an aging population and growing rates of chronic illness, effective resource management in scheduling becomes more critical to serve patients in ambulatory infusion centers. The wide range of treatment types, lengths, and nursing requirements, as well as capacity constraints, makes infusion scheduling challenging to effectively manage patient flow and resource utilization. Despite efforts to improve scheduling efficiency, the lack of practice implication and feasibility remains. This study aims to develop a tool that delivers data- and algorithm-driven recommendations for appointment scheduling decisions to improve resource management. Methods: We introduce a real-time decision support tool that simultaneously accounts for (1) existing nursing workload and space utilization and (2) the nursing time and infusion chairs required for upcoming patients. The tool interface is presented, and the functions of each element are described. The appointment time selection algorithm was developed to provide schedulers with options for scheduling, constrained by nursing and chair availability. The tool also provides schedulers with the flexibility to deviate from recommendations and receive dynamic feedback on patient volume and nursing needs based on their decisions. Results: The implementation results show a significant reduction in distributing nurses’ workload in terms of time mismatching between patients’ needs and nursing availability by 45.5%, P < .001, while the chair utilization remained consistent. The feedback from both the scheduling team and nurses was positive, which provided strong evidence for how this tool addressed and targeted their scheduling needs. In addition, key practice behaviors and implementation challenges that impact operations efficiency are discussed for further improvement. Conclusions: The proposed tool offers a streamlined, interactive, and adaptable scheduling approach for better resource utilization and ultimately reduces the time schedulers spend on making manual decisions.

BACKGROUND: Myocardial infarction with nonobstructive coronary arteries (MINOCAs) and angina with nonobstructive coronary arteries (ANOCAs) present diagnostic and therapeutic challenges. We assessed the frequency of coronary microvascular disease (CMD) and its subtypes in MINOCA compared with ANOCA and evaluated long-term cardiovascular outcomes. METHODS: Patients with nonobstructive coronary arteries undergoing invasive coronary function testing from 2012 to 2022 were prospectively enrolled and retrospectively classified as MINOCA or ANOCA (reference group). Myocardial infarction due to atherothrombosis, myocarditis, and Takotsubo syndrome were excluded. Invasive provocation testing was performed. CMD was classified as endothelium-independent (coronary flow reserve <2.5 with adenosine) and endothelium-dependent (<50% increase in coronary blood flow with acetylcholine). Major adverse cardiovascular events (cardiac death, nonfatal myocardial infarction, heart failure hospitalization, urgent revascularization, stroke) were recorded over 8 years. RESULTS: Of 622 patients, 73 (12%) had MINOCA (69% female, median age 56 years) and 549 (88%) ANOCA (72% female, median age 53 years). CMD was common in both groups (71% versus 64%; P =0.271), while endothelium-independent CMD was more frequent in MINOCA (41% versus 21%; P <0.001). Over a median follow-up of 4.5 years, major adverse cardiovascular events occurred more often in MINOCA (40% versus 11%; adjusted hazard ratio, 2.4; P =0.001). CMD predicted higher major adverse cardiovascular events in both MINOCA (hazard ratio, 3.6 [95% CI, 1.1–12.0]; P =0.038) and ANOCA (hazard ratio, 7.9 [95% CI, 2.9–21.8]; P <0.001). CONCLUSIONS: CMD is common in both MINOCA and ANOCA. The higher prevalence of endothelium-independent CMD in MINOCA suggests a potential mechanistic role in infarction. Patients with MINOCA have a worse prognosis than ANOCA, particularly when CMD is present.

ABSTRACT Tissue-resident macrophages adapt to local environments to support organ-specific functions, but whether their regulation differs across regions of the same organ is poorly understood. The gastrointestinal tract provides an ideal system to address this question because its anatomically distinct regions perform specialized physiological functions and contain different cellular environments. Here, we found that intestinal muscularis macrophages (MMs) exhibited distinct regional trophic requirements and neuroimmune functions across the gut. Small-intestinal MMs were highly sensitive to CSF1 neutralization but recovered robustly, whereas colonic MMs were less sensitive to CSF1 depletion yet showed limited recovery. Disruption of CSF1-dependent MMs selectively reduced nitrergic neurons and altered motility in the small intestine, whereas the colonic neuronal compartment was comparatively preserved. Csf1 was enriched in small-intestinal nNOS + neurons, and neuron-specific Csf1 deletion reduced both MMs and nitrergic neurons and altered small-intestinal transit, with limited effects in the colon. Together, these findings reveal that macrophage trophic requirements and neuroimmune functions are regionally specialized within the intestine and identify neuronal CSF1 as a key component of the trophic relationship between nitrergic neurons and MMs in the small intestine.

Abstract Immune cell function is tightly coupled to cellular metabolism, with glycolysis, oxidative phosphorylation, and amino acid and lipid metabolism governing activation, differentiation, survival, and effector responses. In rheumatoid arthritis (RA), an autoimmune disease characterized by destructive joint inflammation, metabolic checkpoints have emerged as critical regulators of immune-cell behavior and drivers of tissue pathology. RA CD4+ T cells undergo profound metabolic reprogramming: glycolysis is suppressed, and glucose is redirected into the pentose phosphate pathway, resulting in NADPH accumulation, reduced ROS levels, and a highly reductive intracellular environment. Concurrent defects in mitochondrial DNA repair and electron transport chain function compromise mitochondrial fitness, leading to NAD+ depletion, altered tricarboxylic acid cycle activity, and metabolic exhaustion. The resulting accumulation of citrate and acetyl-CoA promotes lipogenesis and protein acetylation, driving membrane remodeling, tissue invasiveness, and proinflammatory effector functions. Depletion of oxaloacetate and aspartate limits NAD+ regeneration, inducing endoplasmic reticulum expansion and enhanced tumor necrosis factor production. Defective lysosomal coordination of AMPK and mTORC1 signaling uncouples energy sensing from anabolic programs, enabling cellular activation and proliferation despite metabolic insufficiency. Macrophage fate and function are similarly shaped by metabolic state. In synovial macrophages, GLUD1-dependent glutamine oxidation sustains mitochondrial respiration and ATP production, enabling survival under nutrient-deprived conditions while promoting antigen presentation. Conversely, metabolic stress in MerTK+ macrophages activates the NAD+ hydrolase SARM1, triggering NAD+ depletion, mitochondrial collapse, and PANoptotic cell death. Together, these findings identify NAD+ availability, mitochondrial fitness, and organelle-based signaling as central metabolic gatekeepers linking bioenergetic stress to immune-cell dysfunction and chronic inflammation in RA.

Abstract Renal cortical hemosiderosis is the accumulation of iron in the renal cortex. On MRI, this can be inferred by marked cortical T2 hypointensity and loss of signal on in-phase imaging relative to opposed-phase imaging. Although classically associated with paroxysmal nocturnal hemoglobinuria, renal hemosiderosis can be seen in a variety of pathologic conditions associated with acute or chronic renal injury. We present a case of a 59-year-old female that developed acute kidney injury while hospitalized for management of hydronephrosis and hepatic abscess with imaging features on MR angiography and renal parenchymal biopsy consistent with renal cortical hemosiderosis. Combined with other laboratory results, this finding expedited the diagnosis of atypical hemolytic uremic syndrome, a condition with poor prognosis for which timely treatment is essential. Thus, recognition of renal cortical hemosiderosis on imaging may facilitate appropriate clinical workup and timely management.