Analysis of eligibility criteria in Alzheimer's and related dementias clinical trials.

Overly restrictive clinical trial eligibility criteria can reduce generalizability, slow enrollment, and disproportionately exclude historically underrepresented populations. The eligibility criteria for 196 Alzheimer's Disease and Related Dementias (AD/ADRD) trials funded by the National Institute on Aging were analyzed to identify common criteria and their potential to disproportionately exclude participants by race/ethnicity. The trials were categorized by type (48 Phase I/II pharmacological, 7 Phase III/IV pharmacological, 128 non-pharmacological, 7 diagnostic, and 6 neuropsychiatric) and target population (51 AD/ADRD, 58 Mild Cognitive Impairment, 25 at-risk, and 62 cognitively normal). Eligibility criteria were coded into the following categories: Medical, Neurologic, Psychiatric, and Procedural. A literature search was conducted to describe the prevalence of disparities for eligibility criteria for African Americans/Black (AA/B), Hispanic/Latino (H/L), American Indian/Alaska Native (AI/AN) and Native Hawaiian/Pacific Islander (NH/PI) populations. The trials had a median of 15 criteria. The most frequent criterion were age cutoffs (87% of trials), specified neurologic (65%), and psychiatric disorders (61%). Underrepresented groups could be disproportionately excluded by 16 eligibility categories; 42% of trials specified English-speakers only in their criteria. Most trials (82%) contain poorly operationalized criteria (i.e., criteria not well defined that can have multiple interpretations/means of implementation) and criteria that may reduce racial/ethnic enrollment diversity.

HBS1L deficiency causes retinal dystrophy in a child and a mouse model associated with defective development of photoreceptor cells.

Inherited retinal diseases encompass a genetically diverse group of conditions caused by mutations in genes critical to retinal function, including handful of ribosome-associated genes. This study focuses on HBS1L gene which encodes for HBS1-like translational GTPase crucial for ribosomal rescue. We have reported a female child carrying biallelic HBS1L variants, manifesting with poor growth and neurodevelopmental delay. Here we describe the ophthalmologic findings in the patient and Hbs1ltm1a/tm1a hypomorph mice and describe the associated microscopic and molecular perturbations. The patient has impaired visual function, showing dampened amplitudes of a- and b-waves in both rod- and cone-mediated responses. Hbs1ltm1a/tm1a mice exhibited profound thinning of the entire retina, specifically of the outer photoreceptor layer, due to extensive photoreceptor cell apoptosis. Loss of HBS1L resulted in comprehensive proteomic alterations on mass spectrometry analysis, with 169 proteins increased and 480 decreased including rhodopsin and peripherin 2. GO biological process and GSEA analyses reveal that the downregulated proteins are primarily involved in phototransduction, cilium assembly, and photoreceptor cell development. These findings underscore the importance of ribosomal rescue proteins in maintaining retinal health, particularly in photoreceptor cells.

Revisiting the Preparation and Catalytic Performance of a Phosphine-Modified Co(II) Hydroformylation Precatalyst.

In light of recent conflicting reports regarding the hydroformylation catalytic activity derived from cationic Co(II) precatalysts of the form [Co(acac)(bis(phosphine))]BF4, the synthetic procedures and characterization of [Co(acac)(dppBz)]BF4, 1, are evaluated. Leveraging calibrated ESI-TOF MS methodologies, substantial quantities of Co(acac)2(dppBz), 2, were observed within samples of 1. The source of the impurity, 2, is determined to derive from incomplete protonolysis of the Co(acac)2 precursor and ligand scrambling occurring during the synthesis of 1. Revised synthetic procedures using lower temperature conditions and longer reaction times afford analytically pure samples of 1 based on ESI-TOF MS and NMR spectroscopic analysis. Complex 1 is demonstrated to act as a hydroformylation precatalyst for the conversion of 1-hexene to 1-heptanal under relatively mild conditions at 51.7 bar and 140 °C. The presence of impurity 2 is shown to dramatically decrease the catalytic performance derived from 1.

Coronary Microvascular Dysfunction is Associated with Augmented Lysosomal Signaling in Hypercholesterolemic Mice.

Accumulating evidence indicates that coronary microvascular dysfunction (CMD) caused by hypercholesterolemia can lead to myocardial ischemia, with or without obstructive atherosclerotic coronary artery disease (CAD). However, the molecular pathways associated with compromised coronary microvascular function prior to the development of myocardial ischemic injury remain poorly defined. In this study, we investigated the effects of hypercholesterolemia on the function and integrity of the coronary microcirculation in mice and the underlying mechanisms. Mice were fed with a hypercholesterolemic Paigen's diet (PD) for 8 weeks. Echocardiography data showed that PD caused CMD, characterized by significant reductions in coronary blood flow and coronary flow reserve (CFR), but did not affect cardiac remodeling or dysfunction. Immunofluorescence studies revealed that PD-induced CMD was associated with activation of coronary arterioles inflammation and increased myocardial inflammatory cell infiltration. These pathological changes occurred in parallel with the upregulation of lysosomal signaling pathways in endothelial cells (ECs). Treating hypercholesterolemic mice with the cholesterol-lowering drug ezetimibe significantly ameliorated PD-induced adverse effects, including hypercholesterolemia, steatohepatitis, reduced CFR, coronary EC inflammation, and myocardial inflammatory cell infiltration. In cultured mouse cardiac endothelial cells (MCECs), 7-ketocholesterol (7K) increased mitochondrial reactive oxygen species (ROS) and inflammatory responses. Meanwhile, 7K induced the activation of TFEB and lysosomal signaling in MCECs, whereas the lysosome inhibitor bafilomycin A1 blocked 7K-induced TFEB activation and exacerbated 7K-induced inflammation and cell death. Interestingly, ezetimibe synergistically enhanced 7K-induced TFEB activation and attenuated 7K-induced mitochondrial ROS and inflammatory responses in MCECs. These results suggest that CMD can develop and precede detectable cardiac functional or structural changes in the setting of hypercholesterolemia, and that upregulation of TFEB-mediated lysosomal signaling in ECs plays a protective role against CMD.

Comorbidity of bipolar disorder and borderline personality disorder: Phenomenology, course, and treatment considerations.

AIM: Bipolar disorder (BD) and borderline personality disorder (BPD) are both serious psychiatric conditions that elevate the risk for harmful outcomes. Although these conditions represent distinct diagnostic entities, existing research suggests that approximately 20% of individuals with BD meet the criteria for comorbid BPD. Individuals with comorbid BD/BPD appear to have a markedly more severe and phenomenologically distinct clinical course when compared with those with BD alone. However, treatments have generally not been tested in this specific population, and currently, no formal treatment guidelines exist for this subgroup of patients. METHOD: In the current paper, we review the epidemiological and descriptive research characterizing those with comorbid BD/BPD and discuss the impact of this comorbidity on psychosocial treatment. We also review current findings on evidence-based treatments for BD and BPD that show promise in treating those with comorbid BD/BPD. RESULTS: In our review of the literature, we highlight the importance of recognizing this comorbidity and discuss avenues for developing and integrating evidence-based treatment approaches for this understudied clinical population. CONCLUSIONS: Although formal trials of interventions targeted to comorbid BD/BPD are limited, there is promising evidence regarding the possibility of using or integrating existing evidence-based approaches for this population. There are also several areas of clinical practice improvement and future research directions that stem from this literature.

Globally distributed bacteriophage genomes reveal mechanisms of tripartite phage-bacteria-coral interactions.

Reef-building corals depend on an intricate community of microorganisms for functioning and resilience. The infection of coral-associated bacteria by bacteriophages can modify bacteria-host interactions, yet very little is known about phage functions in the holobiont. This gap stems from methodological limitations that have prevented the recovery of high-quality viral genomes and bacterial host assignment from coral samples. Here, we introduce a size fractionation approach that increased bacterial and viral recovery in coral metagenomes by 9-fold and 2-fold, respectively, and enabled the assembly and binning of bacterial and viral genomes at relatively low sequencing coverage. We combined these viral genomes with those derived from 677 publicly available metagenomes, viromes, and bacterial isolates from stony corals to build a global coral virus database of over 20 000 viral genomic sequences spanning four viral realms. The tailed bacteriophage families Kyanoviridae and Autographiviridae were the most abundant, replacing groups formerly referred to as Myoviridae and Podoviridae, respectively. Prophage and CRISPR spacer linkages between these viruses and 626 bacterial metagenome-assembled genomes and bacterial isolates showed that most viruses infected Alphaproteobacteria, the most abundant class, and less abundant taxa like Halanaerobiia and Bacteroidia. A host-phage-gene network identified keystone viruses with the genomic capacity to modulate bacterial metabolic pathways and direct molecular interactions with eukaryotic cells. This study reveals the genomic basis of nested symbioses between bacteriophage, bacteria, and the coral host and its endosymbiotic algae.

The RNA binding protein IGF2BP2/IMP2 alters the cargo of cancer cell-derived extracellular vesicles supporting tumor-associated macrophages.

BACKGROUND: Tumor cells release extracellular vesicles (EVs) that contribute to the polarization of macrophages towards tumor-associated macrophages (TAMs). High expression levels of the RNA binding protein IGF2BP2/IMP2 are correlated with increased tumor cell proliferation, invasion, and poor prognosis in the clinic. However, there is a lack of understanding of whether IMP2 affects the cargo of cancer cell-derived EVs, thereby modulating macrophage polarization. METHODS: EVs were isolated from IMP2-expressing HCT116 parental cells (WT) and CRISPR/Cas9 IMP2 knockout (KO) cells. EVs were characterized according to MISEV guidelines, microRNA cargo was assessed by microRNA-Seq, and the protein cargo was analyzed by proteomics. Primary human monocyte-derived macrophages (HMDMs) were polarized by EVs, and the expression of genes and surface markers was assessed using qPCR and flow cytometry, respectively. Morphological changes of macrophages, as well as the migratory potential of cancer cells, were assessed by the Incucyte® system and macrophage matrix degradation potential by zymography. Changes in the metabolic activity of macrophages were quantified using a Seahorse® analyzer. For in vivo studies, EVs were injected into the yolk sac of zebrafish larvae, and macrophages were isolated by fluorescence-activated cell sorting. RESULTS: EVs from WT and KO cells had a similar size and concentration and were positive for 25 vesicle markers. The expression of tumor-promoting genes was higher in macrophages polarized with WT EVs than KO EVs, while the expression of TNF and IL6 was reduced. A similar pattern was observed in macrophages from zebrafish larvae treated in vivo. WT EV-polarized macrophages showed a higher abundance of TAM-like surface markers, higher matrix degrading activity, as well as a higher promotion of cancer cell migration. MicroRNA-Seq revealed a significant difference in the microRNA composition of WT and KO EVs, particularly a high abundance of miR-181a-5p in WT EVs, which was absent in KO EVs. Inhibitors of macropinocytosis and phagocytosis antagonized the delivery of miR-181a-5p into macrophages and the downregulation of the miR-181a-5p target DUSP6. Proteomics data showed differences in protein cargo in KO vs. WT EVs, with the differentially abundant proteins mainly involved in metabolic pathways. WT EV-treated macrophages exhibited a higher basal oxygen consumption rate and a lower extracellular acidification rate than KO EV-treated cells. CONCLUSION: Our results show that IMP2 determines the cargo of EVs released by cancer cells, thereby modulating the EVs' actions on macrophages. Expression of IMP2 is linked to the secretion of EVs that polarize macrophages towards a tumor-promoting phenotype.

Artificial Intelligence Methods for the Argenta Classification of Deformational Plagiocephaly to Predict Severity and Treatment Recommendation.

INTRODUCTION: Deformational plagiocephaly (DP) can be classified into 5 severity types using the Argenta scale (AS). Patients with type III or higher require referral to craniofacial surgery for management. Primary care pediatricians (PCPs) are often the first to encounter patients with DP, but current screening methods are subjective, increasing the risk of bias, especially for clinicians with little exposure to this population. The authors propose the use of artificial intelligence (AI) to classify patients with DP using the AS and to make recommendations for referral to craniofacial surgery. METHODS: Vertex photographs were obtained for patients diagnosed with unilateral DP from 2019 to 2020. Using the photographs, an AI program was created to characterize the head contour of these infants into 3 groups based on the AS. The program was trained using photographs from patients whose DP severity was confirmed clinically by craniofacial surgeons. To assess the accuracy of the software, the AS predicted by the program was compared with the clinical diagnosis. RESULTS: Nineteen patients were assessed by the AI software. All 3 patients with type I DP were correctly classified by the program (100%). In addition, 4 patients with type II were correctly identified (67%), and 7 were correctly classified as type III or greater (70%). CONCLUSIONS: Using vertex photographs and AI, the authors were able to objectively classify patients with DP based on the AS. If converted into a smartphone application, the program could be helpful to PCPs in remote or low-resource settings, allowing them to objectively determine which patients require referral to craniofacial surgery.

Why partial heart transplantation could be regulated as organ transplantation.

Partial heart transplant (PHT) is a recent clinical innovation involving the transplantation of a segment of the heart (valves) directly from the deceased donor into the recipient patient. This procedure holds out the possibility of significant benefit, especially for pediatric patients because these grafts show growth potential after transplant, reducing or eliminating the current need for repeat procedures. The clinical process for donation and transplant of partial heart (PH) grafts generally follows an organ clinical pathway; however, the Food and Drug Administration has recently stated its intent to regulate PH as tissues, raising a host of regulatory considerations. PHT requires donor testing and eligibility determinations within a short, clinically viable timeframe and, similar to organ transplant, involves donor-recipient matching. Waitlist allocation policies that are a regulatory focus of the Organ Procurement and Transplantation Network including equity and efficiency may become relevant. Oversight of PHT by the Organ Procurement and Transplantation Network could be accomplished through interpretation of the vascular composite allograft definition or through designation by the US Department of Health and Human Services of PH grafts as organs. While some clinical questions remain unanswered, it is important to carefully address these regulatory considerations to support the emergence of this innovation and ensure the continued trust of the donating public and the patients who may benefit from PHT.

The heterogeneity of intimate partner violence and its associations with distressed couples' emotional communication.

To understand the ways in which heterogeneous aspects of intimate partner violence (IPV) differentially influence partners' emotional expression during the conflict, the present study examined the unique and interactive effects among (a) types of IPV (psychological and/or physical), (b) directionality of IPV (unilateral or bilateral), and (c) couples' conversation topic (initiated by men or women) on the trajectories of emotional arousal in distressed, different-gender couples (N = 106). Vocally encoded emotional arousal (f0) was measured during couples' recorded conversations. Findings from growth-curve analyses demonstrated that the level of IPV, directionality of IPV, and conversation topic were associated with different patterns of emotional arousal. First, during the discussion of the woman's topic, escalation was observed among recipients of violence in relationships with high levels of unilateral IPV, while their partners-that is, perpetrators of IPV-demonstrated stable, flat trajectories. Second, during men's conversations, stable levels of arousal were predominantly observed among both partners in relationships with men's unilateral IPV and with bilateral psychological and physical IPV. Finally, for partners who engaged in low levels of IPV, men and women both showed escalating arousal across women's conversations; however, when discussing the man's topic, they demonstrated different patterns, with men escalating linearly and women maintaining stable levels of arousal. These findings converge to suggest a picture in which distressed partners who either engage in or experience IPV use "all-or-nothing" approaches to emotional expression during conflict-not only escalating but also containing or controlling their emotional arousal across various contexts. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Antibiotic Stewardship in the Neonatal Intensive Care Unit.

Antibiotic stewardship is a multidisciplinary, evidence-based approach to optimize antibiotic use and mitigate development of antibiotic resistance. Neonates have high rates of antibiotic exposure, particularly those born preterm and admitted to the NICU, and mounting evidence describes the adverse consequences of such exposures in the absence of infection. Here, we review the general principles of antibiotic stewardship and how they can be applied in NICUs. The unique characteristics of NICUs and patients cared for in this setting, which warrant unique implementation strategies and special considerations are discussed. We summarize current antibiotic use metrics for assessment of responses to stewardship interventions and changes over time, and review evidence-based infection prevention practices in the NICU. Current recommendations for empiric antibiotic use in the NICU and the utility of infection biomarkers are summarized. Lastly, given the growing global threat of increasing antibiotic resistance, specific threats in the NICU are highlighted.

Immunomodulation by glucocorticoid-induced leucine zipper in macrophages: enhanced phagocytosis, protection from pyroptosis, and altered mitochondrial function.

Glucocorticoids, which have long served as fundamental therapeutics for diverse inflammatory conditions, are still widely used, despite associated side effects limiting their long-term use. Among their key mediators is glucocorticoid-induced leucine zipper (GILZ), recognized for its anti-inflammatory and immunosuppressive properties. Here, we explore the immunomodulatory effects of GILZ in macrophages through transcriptomic analysis and functional assays. Bulk RNA sequencing of GILZ knockout and GILZ-overexpressing macrophages revealed significant alterations in gene expression profiles, particularly impacting pathways associated with the inflammatory response, phagocytosis, cell death, mitochondrial function, and extracellular structure organization activity. GILZ-overexpression enhances phagocytic and antibacterial activity against Salmonella typhimurium and Escherichia coli, potentially mediated by increased nitric oxide production. In addition, GILZ protects macrophages from pyroptotic cell death, as indicated by a reduced production of reactive oxygen species (ROS) in GILZ transgenic macrophages. In contrast, GILZ KO macrophages produced more ROS, suggesting a regulatory role of GILZ in ROS-dependent pathways. Additionally, GILZ overexpression leads to decreased mitochondrial respiration and heightened matrix metalloproteinase activity, suggesting its involvement in tissue remodeling processes. These findings underscore the multifaceted role of GILZ in modulating macrophage functions and its potential as a therapeutic target for inflammatory disorders, offering insights into the development of novel therapeutic strategies aimed at optimizing the benefits of glucocorticoid therapy while minimizing adverse effects.

Dietary intervention rescues a bone porosity phenotype in a murine model of Neurofibromatosis Type 1 (NF1).

Neurofibromatosis type 1 (NF1) is a complex genetic disorder that affects a range of tissues including muscle and bone. Recent preclinical and clinical studies have shown that Nf1 deficiency in muscle causes metabolic changes resulting in intramyocellular lipid accumulation and muscle weakness. These can be subsequently rescued by dietary interventions aimed at modulating lipid availability and metabolism. It was speculated that the modified diet may rescue defects in cortical bone as NF1 deficiency has been reported to affect genes involved with lipid metabolism. Bone specimens were analyzed from wild type control mice as well as Nf1Prx1-/- (limb-targeted Nf1 knockout mice) fed standard chow versus a range of modified chows hypothesized to influence lipid metabolism. Mice were fed from 4 weeks to 12 weeks of age. MicroCT analysis was performed on the cortical bone to examine standard parameters (bone volume, tissue mineral density, cortical thickness) and specific porosity measures (closed pores corresponding to osteocyte lacunae, and larger open pores). Nf1Prx1-/- bones were found to have inferior bone properties to wild type bones, with a 4-fold increase in the porosity attributed to open pores. These measures were rescued by dietary interventions including a L-carnitine + medium-chain fatty acid supplemented chow previously shown to improve muscle histology function. Histological staining visualized these changes in bone porosity. These data support the concept that lipid metabolism may have a mechanistic impact on bone porosity and quality in NF1.

Review of factors affecting virus inactivation in aerosols and droplets.

The inactivation of viruses in aerosol particles (aerosols) and droplets depends on many factors, but the precise mechanisms of inactivation are not known. The system involves complex physical and biochemical interactions. We reviewed the literature to establish current knowledge about these mechanisms and identify knowledge gaps. We identified 168 relevant papers and grouped results by the following factors: virus type and structure, aerosol or droplet size, temperature, relative humidity (RH) and evaporation, chemical composition of the aerosol or droplet, pH and atmospheric composition. These factors influence the dynamic microenvironment surrounding a virion and thus may affect its inactivation. Results indicate that viruses experience biphasic decay as the carrier aerosols or droplets undergo evaporation and equilibrate with the surrounding air, and their final physical state (liquid, semi-solid or solid) depends on RH. Virus stability, RH and temperature are interrelated, but the effects of RH are multifaceted and still not completely understood. Studies on the impact of pH and atmospheric composition on virus stability have raised new questions that require further exploration. The frequent practice of studying virus inactivation in large droplets and culture media may limit our understanding of inactivation mechanisms that are relevant for transmission, so we encourage the use of particles of physiologically relevant size and composition in future research.

An evaluation of the impact of social and structural determinants of health on forgone care during the COVID-19 pandemic in Baltimore, Maryland.

Evidence suggests that reductions in healthcare utilization, including forgone care, during the COVID-19 pandemic may be contributing towards excess morbidity and mortality. The objective of this study was to describe individual and community-level correlates of forgone care during the COVID-19 pandemic. We conducted a cross-sectional, secondary data analysis of participants (n = 2,003) who reported needing healthcare in two population-representative surveys conducted in Baltimore, MD in 2021 and 2021-2022. Abstracted data included the experience of forgone care, socio-demographic data, comorbidities, financial strain, and community of residence. Participant's community of residence were linked with data acquired from the Baltimore Neighborhood Indicators Alliance relevant to healthcare access and utilization, including walkability and internet access, among others. The data were analyzed using weighted random effects logistic regression. Individual-level factors found to be associated with increased odds for forgone care included individuals age 35-49 (compared to 18-34), female sex, experiencing housing insecurity during the pandemic, and the presence of functional limitations and mental illness. Black/African American individuals were found to have reduced odds of forgone care, compared to any other race. No community-level factors were significant in the multilevel analyses. Moving forward, it will be critical that health systems identify ways to address any barriers to care that populations might be experiencing, such as the use of mobile health services or telemedicine platforms. Additionally, public health emergency preparedness planning efforts must account for the unique needs of communities during future crises, to ensure that their health needs can continue to be met. Finally, additional research is needed to better understand how healthcare access and utilization practices have changed during versus before the pandemic.

Characteristics of Intracranial Injuries in Pediatric Patients Following Blunt Head Trauma.

OBJECTIVES: Pediatric head trauma is a frequent reason for presentation to the emergency department. Despite this, there are few reports on specific characteristics and injury patterns in head injured children. The goal of this study was to evaluate head injury patterns in children with blunt head injury and their prevalence by age group. METHODS: This is a planned secondary analysis of the NEXUS II Head CT validation study. Consecutive patients with blunt head trauma were enrolled between 2006 and 2015. Demographics and criteria from 2 clinical decision instruments (NEXUS and Canadian Head CT rules) were gathered at the time of enrollment. We abstracted and cataloged injuries for pediatric patients based on radiologist report. Frequencies of injuries and severity were analyzed by developmental age group. RESULTS: A total of 1018 pediatric patients were enrolled, 128 (12.6%) of whom had an injury on computed tomography scan. Median age was 11.9 (Interquartile range 4.5-15.5) for all patients and 12 (4.8-15.5) for injured patients. Of injured patients, 49 (38.3%) had a significant injury, and 27 (21.1%) received an intervention. Teenagers had the highest rate of significant injury (50%) and intervention (30%). Injuries were most frequently noted in the temporal (46.1%), frontal (45.3%), and parietal (45.3%) regions. Subarachnoid hemorrhage (29.7%) and subdural hematoma (28.9%) were the most common injuries observed.Intraparenchymal hemorrhage and cerebral edema were more prevalent in older age groups. The most common injury mechanism overall was fall from height (24.7%). Motor vehicle accidents and nonmotorized wheeled vehicle accidents were more common in older patients. CONCLUSIONS: Serious injuries requiring intervention were rarely encountered in pediatric patients experiencing blunt head trauma. Mechanisms of injury, type of injury, and rates of intervention varied between developmental age groups.

Interstitial Lung Disease and Progressive Pulmonary Fibrosis: a World Trade Center Cohort 20-Year Longitudinal Study.

PURPOSE: World Trade Center (WTC) exposure is associated with obstructive airway diseases and sarcoidosis. There is limited research regarding the incidence and progression of non-sarcoidosis interstitial lung diseases (ILD) after WTC-exposure. ILD encompasses parenchymal diseases which may lead to progressive pulmonary fibrosis (PPF). We used the Fire Department of the City of New York's (FDNY's) WTC Health Program cohort to estimate ILD incidence and progression. METHODS: This longitudinal study included 14,525 responders without ILD prior to 9/11/2001. ILD incidence and prevalence were estimated and standardized to the US 2014 population. Poisson regression modeled risk factors, including WTC-exposure and forced vital capacity (FVC), associated with ILD. Follow-up time ended at the earliest of incident diagnosis, end of study period/case ascertainment, transplant or death. RESULTS: ILD developed in 80/14,525 FDNY WTC responders. Age, smoking, and gastroesophageal reflux disease (GERD) prior to diagnosis were associated with incident ILD, though FVC was not. PPF developed in 40/80 ILD cases. Among the 80 cases, the average follow-up time after ILD diagnosis was 8.5 years with the majority of deaths occurring among those with PPF (PPF: n = 13; ILD without PPF: n = 6). CONCLUSIONS: The prevalence of post-9/11 ILD was more than two-fold greater than the general population. An exposure-response gradient could not be demonstrated. Half the ILD cases developed PPF, higher than previously reported. Age, smoking, and GERD were risk factors for ILD and PPF, while lung function was not. This may indicate that lung function measured after respirable exposures would not identify those at risk for ILD or PPF.

"Understanding why she had to leave me": The roles of religion and spirituality in narratives of parents grieving the loss of a child to cancer.

Religion and spirituality often influence how people experience illness, death, and grief. The roles of religion and spirituality for parents who have lost a child to cancer remain underexplored. This study aimed to describe how cancer-bereaved parents talk about religion and spirituality when reflecting on their experiences. Participants whose children died of cancer one to six years prior to participation completed a one-on-one semi-structured interview. Interview transcripts underwent qualitative analysis. Content pertaining to religion and/or spirituality underwent subsequent in-depth analysis to identify themes. Of 30 interviews analyzed, 28 contained religion/spirituality content. Four themes arose: (1) life after death, (2) divine control, (3) evolution of faith after loss, and (4) religious and spiritual interactions within the medical community. The absence of supports for religious and spiritual needs represents a gap in bereavement care. Future work should clarify needs and explore potential interventions.

Extending the concept of moral distress to parents of infants hospitalized in the NICU: a qualitative study in Greece.

BACKGROUND: The hospitalization of infants in the neonatal intensive care unit (NICU) is an ethically challenging situation. A limited number of studies have extended the concept of moral distress to parents of infants hospitalized in the NICU. This topic requires further investigation. METHODS: The present prospective qualitative study was conducted from February 2023 to May 2023. Data were collected through semistructured in-depth interviews, which were conducted in-person with fifteen parents of infants who were hospitalized in the NICU at the time of the interviews. Purposive sampling was used. The data were classified and analyzed using thematic analysis. RESULTS: Three themes emerged from the data analysis performed for this empirical study. One intrapersonal dimension featuring two aspects (one dynamic and one static) and another interpersonal dimension focusing on parental moral distress emerged from the data analysis. Furthermore, seven subthemes emerged across these themes: (1) self-directed negative feelings were experienced by parents due to their inability to fulfill their caregiving/parental roles; (2) intense internal conflict was experienced by parents in response to a moral dilemma that was difficult, which was perceived as irresolvable; (3) objectively unjustified, self-directed negative feelings of guilt or failure were experienced by parents; (4) parents experienced moral distress due to the poor image of the ill infants; (5) inadequate information may predispose parents to experience moral distress (6) neonatologists' caring behaviors were unduly perceived by parents as paternalistic behaviors; (7) reasonable or justified institutional rules were unduly perceived by parents as constraint. CONCLUSIONS: In general, the results of this study support the integrated definition of parental moral distress proposed by Mooney-Doyle and Ulrich. Furthermore, the present study introduces new information. The study distinguishes between the dynamic and static aspects of the intrapersonal dimension of the phenomenon of parental moral distress. Moreover, participants experienced moral distress because they unduly perceived certain situations as causing moral distress. In addition, inadequate information may predispose parents to experience moral distress. The findings of this study may contribute promote family-centered care in the NICU context.