First Constraints on Heavy QCD Axions with a Liquid Argon Time Projection Chamber Using the ArgoNeuT Experiment.

We present the results of a search for heavy QCD axions performed by the ArgoNeuT experiment at Fermilab. We search for heavy axions produced in the NuMI neutrino beam target and absorber decaying into dimuon pairs, which can be identified using the unique capabilities of ArgoNeuT and the MINOS near detector. This decay channel is motivated by a broad class of heavy QCD axion models that address the strong CP and axion quality problems with axion masses above the dimuon threshold. We obtain new constraints at a 95% confidence level for heavy axions in the previously unexplored mass range of 0.2-0.9 GeV, for axion decay constants around tens of TeV.

Renal, but not platelet or skin, extracellular vesicles decrease oxidative stress, enhance nascent peptide synthesis, and protect from ischemic renal injury.

Acute kidney injury (AKI) is deadly and expensive, and specific, effective therapy remains a large unmet need. We have demonstrated the beneficial effects of transplanted adult tubular cells and extracellular vesicles (EVs; exosomes) derived from those renal cells on experimental ischemic AKI, even when administered after renal failure is established. To further examine the mechanisms of benefit with renal EVs, we tested the hypothesis that EVs from other epithelia or platelets (a rich source of EVs) might be protective, using a well-characterized ischemia-reperfusion model. When given after renal failure was present, renal EVs, but not those from skin or platelets, markedly improved renal function and histology. The differential effects allowed us to examine the mechanisms of benefit with renal EVs. We found significant decreases in oxidative stress postischemia in the renal EV-treated group with preservation of renal superoxide dismutase and catalase as well as increases in anti-inflammatory interleukin-10. In addition, we propose a novel mechanism of benefit: renal EVs enhanced nascent peptide synthesis following hypoxia in cells and in postischemic kidneys. Although EVs have been used therapeutically, these results serve as "proof of principle" to examine the mechanisms of injury and protection.NEW & NOTEWORTHY Acute kidney injury is common and deadly, yet the only approved treatment is dialysis. Thus, a better understanding of injury mechanisms and potential therapies is needed. We found that organ-specific, but not extrarenal, extracellular vesicles improved renal function and structure postischemia when given after renal failure occurred. Oxidative stress was decreased and anti-inflammatory interleukin-10 increased with renal, but not skin or platelet, exosomes. We also propose enhanced nascent peptide synthesis as a novel protective mechanism.

Impaired microvascular circulation in distant organs following renal ischemia.

Mortality in acute kidney injury (AKI) patients remains very high, although very important advances in understanding the pathophysiology and in diagnosis and supportive care have been made. Most commonly, adverse outcomes are related to extra-renal organ dysfunction and failure. We and others have documented inflammation in remote organs as well as microvascular dysfunction in the kidney after renal ischemia. We hypothesized that abnormal microvascular flow in AKI extends to distant organs. To test this hypothesis, we employed intravital multiphoton fluorescence imaging in a well-characterized rat model of renal ischemia/reperfusion. Marked abnormalities in microvascular flow were seen in every organ evaluated, with decreases up to 46% observed 48 hours postischemia (as compared to sham surgery, p = 0.002). Decreased microvascular plasma flow was found in areas of erythrocyte aggregation and leukocyte adherence to endothelia. Intravital microscopy allowed the characterization of the erythrocyte formations as rouleaux that flowed as one-dimensional aggregates. Observed microvascular abnormalities were associated with significantly elevated fibrinogen levels. Plasma flow within capillaries as well as microthrombi, but not adherent leukocytes, were significantly improved by treatment with the platelet aggregation inhibitor dipyridamole. These microvascular defects may, in part, explain known distant organ dysfunction associated with renal ischemia. The results of these studies are relevant to human acute kidney injury.

Cardiac effects of renal ischemia.

Mortality in acute kidney injury (AKI) remains very high, yet the cause of death is often failure of extrarenal organs. We and others have demonstrated remote organ dysfunction after renal ischemia. The term "cardiorenal syndrome" was first applied to the "cross talk" between the organs by the National Heart, Lung, and Blood Institute of the National Institutes of Health, and the clinical importance is being increasingly appreciated. Nevertheless, more information is needed to effectively address the consequences of renal injury on the heart. Since AKI often occurs in patients with comorbidities, we investigated the effect of renal ischemia in the setting of existing cardiac failure. We hypothesized that the cardiac effects of renal ischemia would be significantly amplified in experimental cardiomyopathy. Male Sprague-Dawley rats with preexisting cardiac and renal injury due to low-dose doxorubicin were subjected to bilateral renal artery occlusion. Cardiac structure and function were examined 2 days after reperfusion. Loss of functional myocardial tissue with decreases in left ventricular pressure, increases in apoptotic cell death, inflammation, and collagen, and greater disruption in ultrastructure with mitochondrial fragmentation were seen in the doxorubicin/ischemia group compared with animals in the groups treated with doxorubicin alone or following ischemia alone. Systemic inflammation and cardiac abnormalities persisted for at least 21 wk. These results suggest that preexisting comorbidities can result in much more severe distant organ effects of acute renal injury. The results of this study are relevant to human AKI.NEW & NOTEWORTHY Acute kidney injury is common, expensive, and deadly, yet morbidity and mortality are often secondary to remote organ dysfunction. We hypothesized that the effects of renal ischemia would be amplified in the setting of comorbidities. Sustained systemic inflammation and loss of functional myocardium with significantly decreased systolic and diastolic function, apoptotic cell death, and increased collagen and inflammatory cells were found in the heart after renal ischemia in the doxorubicin cardiomyopathy model (vs. renal ischemia alone). Understanding the remote effects of renal ischemia has the potential to improve outcomes in acute kidney injury.

Role of coagulation in persistent renal ischemia following reperfusion in an animal model.

Ischemic acute kidney injury is common, deadly, and accelerates the progression of chronic kidney disease, yet has no specific therapy. After ischemia, reperfusion is patchy with early and persistent impairment in regional renal blood flow and cellular injury. We tested the hypothesis that intrarenal coagulation results in sustained renal ischemia following reperfusion, using a well-characterized model. Markedly decreased, but heterogeneous, microvascular plasma flow with microthrombi was found postischemia by intravital microscopy. Widespread tissue factor expression and fibrin deposition were also apparent. Clotting was accompanied by complement activation and inflammation. Treatment with exosomes derived from renal tubular cells or with the fibrinolytic urokinase, given 24 h postischemia when renal failure was established, significantly improved microvascular flow, coagulation, serum creatinine, and histological evidence of injury. These data support the hypothesis that intrarenal clotting occurs early and the resultant sustained ischemia is a critical determinant of renal failure following ischemia; they demonstrate that the coagulation abnormalities are amenable to therapy and that therapy results in improvement in both function and postischemic inflammation.NEW & NOTEWORTHY Ischemic renal injury carries very high morbidity and mortality, yet has no specific therapy. We found markedly decreased, heterogeneous microvascular plasma flow, tissue factor induction, fibrin deposition, and microthrombi after renal ischemia-reperfusion using a well-characterized model. Renal exosomes or the fibrinolytic urokinase, administered after renal failure was established, improved microvascular flow, coagulation, renal function, and histology. Data demonstrate that intrarenal clotting results in sustained ischemia amenable to therapy that improves both function and postischemic inflammation.

MicroBooNE and the ν_{e} Interpretation of the MiniBooNE Low-Energy Excess.

A new generation of neutrino experiments is testing the 4.7σ anomalous excess of electronlike events observed in MiniBooNE. This is of huge importance for particle physics, astrophysics, and cosmology, not only because of the potential discovery of physics beyond the standard model, but also because the lessons we will learn about neutrino-nucleus interactions will be crucial for the worldwide neutrino program. MicroBooNE has recently released results that appear to disfavor several explanations of the MiniBooNE anomaly. Here, we show quantitatively that MicroBooNE results, while a promising start, unquestionably do not probe the full parameter space of sterile neutrino models hinted at by MiniBooNE and other data, nor do they probe the ν_{e} interpretation of the MiniBooNE excess in a model-independent way.

New Constraints on Tau-Coupled Heavy Neutral Leptons with Masses m_{N}=280-970 MeV.

A search for heavy neutral leptons has been performed with the ArgoNeuT detector exposed to the NuMI neutrino beam at Fermilab. We search for the decay signature N→νµ^{+}µ^{-}, considering decays occurring both inside ArgoNeuT and in the upstream cavern. In the data, corresponding to an exposure to 1.25×10^{20} POT, zero passing events are observed consistent with the expected background. This measurement leads to a new constraint at 90% confidence level on the mixing angle |U_{τN}|^{2} of tau-coupled Dirac heavy neutral leptons with masses m_{N}=280-970 MeV, assuming |U_{eN}|^{2}=|U_{µN}|^{2}=0.

New opportunities at the next-generation neutrino experiments I: BSM neutrino physics and dark matter.

The combination of the high intensity proton beam facilities and massive detectors for precision measurements of neutrino oscillation parameters including the charge-parity violating (CPV) phase will open the door to help make beyond the standard model (BSM) physics reachable even in low energy regimes in the accelerator-based experiments. Large-mass detectors with highly precise tracking and energy measurements, excellent timing resolution, and low energy thresholds will enable the searches for BSM phenomena from cosmogenic origin, as well. Therefore, it is also conceivable that BSM topics in the next-generation neutrino experiments could be the dominant physics topics in the foreseeable future, as the precision of the neutrino oscillation parameter and CPV measurements continue to improve.This paper provides a review of the current landscape of BSM theory in neutrino experiments in two selected areas of the BSM topics-dark matter and neutrino related BSM-and summarizes the current results from existing neutrino experiments to set benchmarks for both theory and experiment. This paper then provides a review of upcoming neutrino experiments throughout the next 10 to 15 year time scale and their capabilities to set the foundation for potential reach in BSM physics in the two aforementioned themes. An important outcome of this paper is to ensure theoretical and simulation tools exist to carry out studies of these new areas of physics, from the first day of the experiments, such as Deep Underground Neutrino Experiment in the U.S. and Hyper-Kamiokande Experiment in Japan.

Exploring the roles, functions, and background of patient navigators and case managers: A scoping review.

BACKGROUND: Patient navigators and case managers are health care workers who aim to provide individualized assistance to patients facing significant health concerns. Although these roles emerged from distinct historical need, the terms are often used interchangeably in the literature and are described to have overlapping functions. Differences in the way that these roles are conceptualized across countries has led to a lack of clarity regarding the exact functions that each offer to patients, caregivers, and the health care system. OBJECTIVES: To differentiate the functions and backgrounds of patient navigators and case managers across settings and disease contexts. DESIGN: This review was guided based on the PRISMA extension for scoping reviews using a five-step review process: identify the research questions; search and identify relevant studies; select studies based on a priori criterion; chart the data; and collate, summarize and report the results. DATA SOURCES: A search of the literature was undertaken in peer-reviewed databases (Medline, CINAHL, and PubMed) and the grey literature (Google and unpublished articles in online repositories). REVIEW METHODS: Extracted data included information on patient navigators and/or case managers related to their reported background, training, and/or knowledge; roles and/or specific functions; clinical setting; and targeted condition or disease type. RESULTS: The search strategy resulted in 10,523 articles. After applying the eligibility criteria during title and abstract evaluation, 468 full-text articles were reviewed, resulting in a total of 160 articles. Functions of patient navigators and case managers were organized into nine emerging categories: (1) advocacy; (2) care coordination; (3) case monitoring and patient needs assessment; (4) community engagement; (5) education; (6) administration and research activities; (7) psychosocial support; (8) navigation of services; and (9) reduction of barriers. The background and knowledge areas of each role were compared and contrasted, and three categories related to the practice context of each role were identified: (1) typical setting and care trajectory; (2) target patient population; and (3) mode of service delivery. CONCLUSIONS: The current study identified important differences in the functions between patient navigators and case managers. However, there remains significant ambiguity between the functions of these two roles. Standardized definitions detailing scope of practice, and allowing for inherent flexibility across different settings, are needed to improve service delivery.

Preequilibrium Asymmetries in the

The physical properties of neutrons emitted from neutron-induced fission are fundamental to our understanding of nuclear fission. However, while state-of-the-art fission models still incorporate isotropic fission neutron spectra, it is believed that the preequilibrium prefission component of these spectra is strongly anisotropic. The lack of experimental guidance on this feature has not motivated incorporation of anisotropic neutron spectra in fission models, though any significant anisotropy would impact descriptions of a fissioning system. In the present work, an excess of counts at high energies in the fission neutron spectrum of ^{239}Pu is clearly observed and identified as an excess of the preequilibrium prefission distribution above the postfission neutron spectrum. This excess is separated from the underlying postfission neutron spectrum, and its angular distribution is determined as a function in incident neutron energy and outgoing neutron detection angle. Comparison with neutron scattering models provides the first experimental evidence that the preequilibrium angular distribution is uncorrelated with the fission axis. The results presented here also impact the interpretation of several influential prompt fission neutron spectrum measurements.

Development of a variable-energy, high-intensity, pulsed-mode ion source for low-energy nuclear astrophysics studies.

The primary challenge in directly measuring nuclear reaction rates near stellar energies is their small cross sections. The signal-to-background ratio in these complex experiments can be significantly improved by employing high-current (mA-range) beams and novel detection techniques. Therefore, the electron cyclotron resonance ion source at the Laboratory for Experimental Nuclear Astrophysics underwent a complete upgrade of its acceleration column and microwave system to obtain high-intensity, pulsed proton beams. The new column uses a compression design with O-ring seals for vacuum integrity. Its voltage gradient between electrode sections is produced by the parallel resistance of channels of chilled, deionized water. It also incorporates alternating, transverse magnetic fields for electron suppression and an axially adjustable beam extraction system. Following this upgrade, the operational bremsstrahlung radiation levels and high-voltage stability of the source were vastly improved, over 3.5 mA of target beam current was achieved, and an order-of-magnitude increase in normalized brightness was measured. Beam optics calculations, structural design, and further performance results for this source are presented.

Human extracellular microvesicles from renal tubules reverse kidney ischemia-reperfusion injury in rats.

Hypoxic acute kidney injury, a major unresolved problem, initiates, or aggravates, renal functional and structural decline. There is no treatment for hypoxic acute renal injury and its sequelae. We tested the hypothesis that human kidney tubular cells, or their extracellular vesicles (exosomes), prevent renal injury when infused intravenously 24 hours after 50 minutes of bilateral renal ischemia in Nude rats. Cells and their exosomes were from harvested human kidneys declined for transplantation. Injections of either cells or exosomes, given after 24 and 48 hours of reperfusion, preserved renal function and structure in both treatment groups. However, exosomes were superior to cells; and maintained renal vascular and epithelial networks, prevented renal oxidant stress, and apoptosis; and restrained activation of pro-inflammatory and pro-fibrogenic pathways. Exosomes worked in 24 hours, consistent with functional rather than regenerative activity. Comprehensive proteomic analysis identified 6152 renal proteins from all cellular compartments; and 628 were altered by ischemia at all cell levels, while 377 were significantly improved by exosome infusions. We conclude that renal damage from severe ischemia was broad, and human renal exosomes prevented most protein alterations. Thus, exosomes seem to acutely correct a critical and consequential abnormality during reperfusion. In their absence, renal structure and cells transition to a chronic state of fibrosis and extensive renal cell loss.

Renal Tubular Cell-Derived Extracellular Vesicles Accelerate the Recovery of Established Renal Ischemia Reperfusion Injury.

Ischemic renal injury is a complex syndrome; multiple cellular abnormalities cause accelerating cycles of inflammation, cellular damage, and sustained local ischemia. There is no single therapy that effectively resolves the renal damage after ischemia. However, infusions of normal adult rat renal cells have been a successful therapy in several rat renal failure models. The sustained broad renal benefit achieved by relatively few donor cells led to the hypothesis that extracellular vesicles (EV, largely exosomes) derived from these cells are the therapeutic effector in situ We now show that EV from adult rat renal tubular cells significantly improved renal function when administered intravenously 24 and 48 hours after renal ischemia in rats. Additionally, EV treatment significantly improved renal tubular damage, 4-hydroxynanoneal adduct formation, neutrophil infiltration, fibrosis, and microvascular pruning. EV therapy also markedly reduced the large renal transcriptome drift observed after ischemia. These data show the potential utility of EV to limit severe renal ischemic injury after the occurrence.

Improved Structure and Function in Autosomal Recessive Polycystic Rat Kidneys with Renal Tubular Cell Therapy.

Autosomal recessive polycystic kidney disease is a truly catastrophic monogenetic disease, causing death and end stage renal disease in neonates and children. Using PCK female rats, an orthologous model of autosomal recessive polycystic kidney disease harboring mutant Pkhd1, we tested the hypothesis that intravenous renal cell transplantation with normal Sprague Dawley male kidney cells would improve the polycystic kidney disease phenotype. Cytotherapy with renal cells expressing wild type Pkhd1 and tubulogenic serum amyloid A1 had powerful and sustained beneficial effects on renal function and structure in the polycystic kidney disease model. Donor cell engraftment and both mutant and wild type Pkhd1 were found in treated but not control PCK kidneys 15 weeks after the final cell infusion. To examine the mechanisms of global protection with a small number of transplanted cells, we tested the hypothesis that exosomes derived from normal Sprague Dawley cells can limit the cystic phenotype of PCK recipient cells. We found that renal exosomes originating from normal Sprague Dawley cells carried and transferred wild type Pkhd1 mRNA to PCK cells in vivo and in vitro and restricted cyst formation by cultured PCK cells. The results indicate that transplantation with renal cells containing wild type Pkhd1 improves renal structure and function in autosomal recessive polycystic kidney disease and may provide an intra-renal supply of normal Pkhd1 mRNA.

Prior cold water swim stress alters immobility in the forced swim test and associated activation of serotonergic neurons in the rat dorsal raphe nucleus.

Prior adverse experience alters behavioral responses to subsequent stressors. For example, exposure to a brief swim increases immobility in a subsequent swim test 24h later. In order to determine if qualitative differences (e.g. 19°C versus 25°C) in an initial stressor (15-min swim) impact behavioral, physiological, and associated neural responses in a 5-min, 25°C swim test 24h later, rats were surgically implanted with biotelemetry devices 1 week prior to experimentation then randomly assigned to one of six conditions (Day 1 (15 min)/Day 2 (5 min)): (1) home cage (HC)/HC, (2) HC/25°C swim, (3) 19°C swim/HC, (4) 19°C swim/25°C swim, (5) 25°C swim/HC, (6) 25°C swim/25°C swim. Core body temperature (Tb) was measured on Days 1 and 2 using biotelemetry; behavior was measured on Day 2. Rats were transcardially perfused with fixative 2h following the onset of the swim on Day 2 for analysis of c-Fos expression in midbrain serotonergic neurons. Cold water (19°C) swim on Day 1 reduced Tb, compared to both 25°C swim and HC groups on Day 1, and, relative to rats exposed to HC conditions on Day 1, reduced the hypothermic response to the 25°C swim on Day 2. The 19°C swim on Day 1, relative to HC exposure on Day 1, increased immobility during the 5-min swim on Day 2. Also, 19°C swim, relative to HC conditions, on Day 1 reduced swim (25°C)-induced increases in c-Fos expression in serotonergic neurons within the dorsal and interfascicular parts of the dorsal raphe nucleus. These results suggest that exposure to a 5-min 19°C cold water swim, but not exposure to a 5-min 25°C swim alters physiological, behavioral and serotonergic responses to a subsequent stressor.

Comprehensive genomic profiling in diabetic nephropathy reveals the predominance of proinflammatory pathways.

Despite advances in the treatment of diabetic nephropathy (DN), currently available therapies have not prevented the epidemic of progressive chronic kidney disease (CKD). The morbidity of CKD, and the inexorable increase in the prevalence of end-stage renal disease, demands more effective approaches to prevent and treat progressive CKD. We undertook next-generation sequencing in a rat model of diabetic nephropathy to study in depth the pathogenic alterations involved in DN with progressive CKD. We employed the obese, diabetic ZS rat, a model that develops diabetic nephropathy, characterized by progressive CKD, inflammation, and fibrosis, the hallmarks of human disease. We then used RNA-seq to examine the combined effects of renal cells and infiltrating inflammatory cells acting as a pathophysiological unit. The comprehensive systems biology analysis of progressive CKD revealed multiple interactions of altered genes that were integrated into morbid networks. These pathological gene assemblies lead to renal inflammation and promote apoptosis and cell cycle arrest in progressive CKD. Moreover, in what is clearly a major therapeutic challenge, multiple and redundant pathways were found to be linked to renal fibrosis, a major cause of kidney loss. We conclude that systems biology applied to progressive CKD in DN can be used to develop novel therapeutic strategies directed to restore critical anomalies in affected gene networks.

Development of a scalable image formation pipeline for multiscale gigapixel photography.

We report on the image formation pipeline developed to efficiently form gigapixel-scale imagery generated by the AWARE-2 multiscale camera. The AWARE-2 camera consists of 98 "microcameras" imaging through a shared spherical objective, covering a 120° x 50° field of view with approximately 40 microradian instantaneous field of view (the angular extent of a pixel). The pipeline is scalable, capable of producing imagery ranging in scope from "live" one megapixel views to full resolution gigapixel images. Architectural choices that enable trivially parallelizable algorithms for rapid image formation and on-the-fly microcamera alignment compensation are discussed.

The effectiveness and cost of single and multi-factorial cardiovascular risk factor modification to guideline targets in type 2 diabetes.

AIMS: Cardiovascular disease is the main cause of morbidity and mortality in type 2 diabetes (T2DM), at huge cost to the NHS. We investigated the potential effect on population cardiovascular risk and associated costs of single and multi-factorial intervention, to target levels, in individuals with T2DM. METHODS: Baseline population means and proportions for cardiovascular risk factors were calculated for 159 patients with T2DM from 3 general practices. Predicted 10year cardiovascular risk, and associated costs were calculated using the LIP2687 risk calculator, based on Framingham and UKPDS equations. Systolic blood pressure, HbA(1C), total cholesterol and HDL-cholesterol were altered to NICE and SIGN target levels and the model run again. The difference in outcomes was observed. RESULTS: 45%, 76% and 38% of patients met NICE targets for cholesterol, systolic blood pressure and HbA1c, respectively. As expected, comparing the two guidelines, fewer patients met the 'stricter' targets (P=0.0001). Treatment-to-target produced no significant difference in cardiovascular risk or costs, although greater reductions in outcomes were seen with multi-factorial intervention. CONCLUSION: This small study suggests that intervention in only those patients with the highest cardiovascular risk brings little reduction in population cardiovascular risk and associated health costs. Multi-factorial intervention in all patients with T2DM, regardless of baseline values, is likely to bring greater reductions. This raises the question as to whether the current emphasis on treatment to target should be modified to encourage multi-factorial intervention in all patients with T2DM, even those with baseline values below target levels.

Swim stress activates serotonergic and nonserotonergic neurons in specific subdivisions of the rat dorsal raphe nucleus in a temperature-dependent manner.

Physical (exteroceptive) stimuli and emotional (interoceptive) stimuli are thought to influence stress-related physiologic and behavioral responses through different neural mechanisms. Previous studies have demonstrated that stress-induced activation of brainstem serotonergic systems is influenced by environmental factors such as temperature. In order to further investigate the effects of environmental influences on stress-induced activation of serotonergic systems, we exposed adult male Wistar rats to either home cage control conditions or a 15-min swim in water maintained at 19 °C, 25 °C, or 35 °C and conducted dual immunohistochemical staining for c-Fos, a marker of immediate-early nuclear activation, and tryptophan hydroxylase (TPH), a marker of serotonergic neurons. Changes in core body temperature were documented using biotelemetry. As expected, exposure to cold (19 °C) swim, relative to warm (35 °C) swim, increased c-Fos expression in the external lateral part of the parabrachial nucleus (LPBel), an important part of the spinoparabrachial pathway involved in sensation of cold, cutaneous stimuli, and in serotonergic neurons in the raphe pallidus nucleus (RPa), an important part of the efferent mechanisms controlling thermoregulatory warming responses. In addition, exposure to cold (19 °C) swim, relative to 35 °C swim, increased c-Fos expression in the dorsal raphe nucleus, ventrolateral part/periaqueductal gray (DRVL/VLPAG) and dorsal raphe nucleus, interfascicular part (DRI). Both of these subregions of the dorsal raphe nucleus (DR) have previously been implicated in thermoregulatory responses. Altogether, the data are consistent with the hypothesis that midbrain serotonergic neurons, possibly via activation of afferents to the DR by thermosensitive spinoparabrachial pathways, play a role in integration of physiologic and behavioral responses to interoceptive stress-related cues involved in forced swimming and exteroceptive cues related to cold ambient temperature.

The impact of the World Trade Center attack on FDNY firefighter retirement, disabilities, and pension benefits.

BACKGROUND: Our goal was to examine the effect of the World Trade Center (WTC) attack and subsequent New York City Fire Department (FDNY) rescue/recovery activities on firefighter retirements. We also analyzed the financial impact associated with the increased number and proportion of service-connected "accidental" disability retirements on the FDNY pension system. METHODS: A total of 7,763 firefighters retired between 9/11/1994 and 9/10/2008. We compared the total number of retirements and the number and proportion of accidental disability retirements 7 years before and 7 years after the WTC attack. We categorized WTC-related accidental disability retirements by medical cause and worked with the New York City Office of the Actuary to approximate the financial impact by cause. RESULTS: In the 7 years before 9/11 there were 3,261 retirements, 48% (1,571) of which were accidental disability retirements. In the 7 years after 9/11, there were 4,502 retirements, 66% (2,970) were accidental disability retirements, of which 47% (1,402) were associated with WTC-related injuries or illnesses. After 9/11, the increase in accidental disability retirements was, for the most part, due to respiratory-related illnesses. Additional increases were attributed to psychological-related illnesses and musculoskeletal injuries incurred at the WTC site. Pension benefits associated with WTC-related accidental disability retirements have produced an increased financial burden of over $826 million on the FDNY pension system. CONCLUSIONS: The WTC attacks affected the health of the FDNY workforce resulting in more post-9/11 retirements than expected, and a larger proportion of these retirees with accidental disability pensions.