Transient changes to metabolic homeostasis initiate mitochondrial adaptation to endurance exercise.

Endurance exercise is well established to increase mitochondrial content and function in skeletal muscle, a process termed mitochondrial biogenesis. Current understanding is that exercise initiates skeletal muscle mitochondrial remodeling via modulation of cellular nutrient, energetic and contractile stress pathways. These subtle changes in the cellular milieu are sensed by numerous transduction pathways that serve to initiate and coordinate an increase in mitochondrial gene transcription and translation. The result of these acute signaling events is the promotion of growth and assembly of mitochondria, coupled to a greater capacity for aerobic ATP provision in skeletal muscle. The aim of this review is to highlight the acute metabolic events induced by endurance exercise and the subsequent molecular pathways that sense this transient change in cellular homeostasis to drive mitochondrial adaptation and remodeling.

Tissue factor pathway inhibitor-2 (TFPI-2)-an underappreciated partaker in cancer and metastasis.

The coagulation system is known to play an important role in cancer development and metastasis, but the precise mechanisms by which it does so remain incompletely understood. With this in mind, we provide an updated overview of the effects of TFPI-2, a protease inhibitor, on cancer development and metastasis. TFPI-2 interacts with the thrombin cascade and also employs other mechanisms to suppress cancer growth and dissemination, which include extracellular matrix stabilization, promotion of caspase-mediated cell apoptosis, inhibition of angiogenesis and transduction of intracellular signals. Down-regulation of TFPI-2 expression is well documented in numerous types of neoplasms, mainly via promoter methylation. However, the exact role of TFPI-2 in cancer progression and possible approaches to up-regulate TFPI-2 expression warrant further studies. Strategies to reactivate TFPI-2 may represent a promising direction for future anticancer studies and therapy development.

The Complex Role of Thrombin in Cancer and Metastasis: Focus on Interactions with the Immune System.

Thrombin, a pleiotropic enzyme involved in coagulation, plays a crucial role in both procoagulant and anticoagulant pathways. Thrombin converts fibrinogen into fibrin, initiates platelet activation, and promotes clot formation. Thrombin also activates anticoagulant pathways, indirectly inhibiting factors involved in coagulation. Tissue factor triggers thrombin generation, and the overexpression of thrombin in various cancers suggests that it is involved in tumor growth, angiogenesis, and metastasis. Increased thrombin generation has been observed in cancer patients, especially those with metastases. Thrombin exerts its effects through protease-activated receptors (PARs), particularly PAR-1 and PAR-2, which are involved in cancer progression, angiogenesis, and immunological responses. Thrombin-mediated signaling promotes angiogenesis by activating endothelial cells and platelets, thereby releasing proangiogenic factors. These functions of thrombin are well recognized and have been widely described. However, in recent years, intriguing new findings concerning the association between thrombin activity and cancer development have come to light, which justifies a review of this research. In particular, there is evidence that thrombin-mediated events interact with the immune system, and may regulate its response to tumor growth. It is also worth reevaluating the impact of thrombin on thrombocytes in conjunction with its multifaceted influence on tumor progression. Understanding the role of thrombin/PAR-mediated signaling in cancer and immunological responses is crucial, particularly in the context of developing immunotherapies. In this systematic review, we focus on the impact of the thrombin-related immune system response on cancer progression.

Who tests for lead and why? A 10-year analysis of blood lead screening, follow-up and CNS outcomes in a statewide US healthcare system.

OBJECTIVES: This study aims to determine (1) which providers in US healthcare systems order lead tests, why and at what frequency and (2) whether current patient population lead levels are predictive of clinical outcomes. METHODS: Retrospective medical record study of all blood lead tests in the Medical University of South Carolina healthcare system 2012-2016 and consequent evidence of central nervous system (CNS)-related disease across a potential 10-year window (2012-2022). RESULTS: Across 4 years, 9726 lead tests resulted for 7181 patients (49.0% female; 0-94 years), representing 0.2% of the hospital population. Most tests were for young (76.6%≤age 3) and non-Hispanic black (47.2%) and Hispanic (26.7%) patients. A wide variety of providers ordered tests; however, most were ordered by paediatrics, psychiatry, internal medicine and neurology. Lead levels ranged from ≤2.0 µg/dL (80.8%) to ≥10 µg/dL (0.8%; max 36 µg/dL). 201 children (3.1%) had initial lead levels over the reference value for case management at the time (5.0 µg/dL). Many high level children did not receive follow-up testing in the system (36.3%) and those that did often failed to see levels fall below 5.0 µg/dL (80.1%). Non-Hispanic black and Hispanic patients were more likely to see lead levels stay high or go up over time. Over follow-up, children with high lead levels were more likely to receive new attention-deficit/hyperactivity disorder and conduct disorder diagnoses and new psychiatric medications. No significant associations were found between lead test results and new CNS diagnoses or medications among adults. CONCLUSIONS: Hospital lead testing covers a small portion of patients but includes a wide range of ages, presentations and provider specialities. Lack of lead decline among many paediatric patients suggests there is room to improve provider guidance around when to test and follow-up.

Artificial intelligence (AI) implementation within the National Health Service (NHS): the South West London AI Working Group experience.

In the rapidly evolving field of artificial intelligence (AI) for radiology, with a plethora of vendor options and use-cases and evidence claims to sift through, the pressing question is how to effectively implement the right tool for enhanced patient care? This article presents a structured approach to AI deployment, drawing from a comprehensive case study in South West London. We underscore the necessity of forming a dedicated AI team with a clear vision and assertive leadership to navigate such complexities. Central to our discussion is the significance of crafting an AI implementation plan, with an overarching aim to augment patient care, promote operational efficiency, and lay down standardized protocols for seamless AI adoption. By presenting a blueprint for AI implementation within the National Health Service (NHS), we intend to demystify the process for radiology departments across the UK, enabling them to make informed decisions and empowering their staff to embrace and leverage AI responsibly ensuring that patient welfare remains at the heart of innovation. Thus, having a framework to follow when implementing an AI solution that addresses a vision for scalable adoption, core team members with diversity of skillset, staff engagement and education, plan for vendor selection, and change management is crucial for success.

ATXN7L3 and ENY2 Coordinate Activity of Multiple H2B Deubiquitinases Important for Cellular Proliferation and Tumor Growth.

Histone H2B monoubiquitination (H2Bub1) is centrally involved in gene regulation. The deubiquitination module (DUBm) of the SAGA complex is a major regulator of global H2Bub1 levels, and components of this DUBm are linked to both neurodegenerative diseases and cancer. Unexpectedly, we find that ablation of USP22, the enzymatic center of the DUBm, leads to a reduction, rather than an increase, in global H2bub1 levels. In contrast, depletion of non-enzymatic components, ATXN7L3 or ENY2, results in increased H2Bub1. These observations led us to discover two H2Bub1 DUBs, USP27X and USP51, which function independently of SAGA and compete with USP22 for ATXN7L3 and ENY2 for activity. Like USP22, USP51 and USP27X are required for normal cell proliferation, and their depletion suppresses tumor growth. Our results reveal that ATXN7L3 and ENY2 orchestrate activities of multiple deubiquitinating enzymes and that imbalances in these activities likely potentiate human diseases including cancer.

Factors influencing hospital charges for tonsillectomy to treat obstructive sleep apnea in children.

PURPOSE: This study investigates the impact of patient characteristics and demographics on hospital charges for tonsillectomy as a treatment for pediatric obstructive sleep apnea (OSA). The aim is to identify potential disparities in hospital charges and contribute to efforts for equitable access to care. METHODS: Data from the 2016 Healthcare Cost and Utilization Project (HCUP) Kid Inpatient Database (KID) was analyzed. The sample included 3,304 pediatric patients undergoing tonsillectomy ± adenoidectomy for OSA. Variables such as age, race, length of stay, hospital region, residential location, payer information, and median household income were collected. The primary outcome variable was hospital charge. Statistical analyses, including t-tests, ANOVA, and multiple linear regression, were conducted. RESULTS: Among 3,304 pediatric patients undergoing tonsillectomy for OSA. The average total charges for tonsillectomy were $26,400, with a mean length of stay of 1.70 days. Significant differences in charges were observed based on patient race, hospital region, and payer information. No significant differences were found based on gender, discharge quarter, residential location, or median household income. Multiple linear regression showed race, hospital region, and residential location were significant predictors of total hospital charges. CONCLUSION: This study highlights the influence of patient demographics and regional factors on hospital charges for pediatric tonsillectomy in OSA cases. These findings underscore the importance of addressing potential disparities in healthcare access and resource allocation to ensure equitable care for children with OSA. Efforts should be made to promote fair and affordable treatment for all pediatric OSA patients, regardless of their demographic backgrounds.

A glutaminase isoform switch drives therapeutic resistance and disease progression of prostate cancer.

Cellular metabolism in cancer is significantly altered to support the uncontrolled tumor growth. How metabolic alterations contribute to hormonal therapy resistance and disease progression in prostate cancer (PCa) remains poorly understood. Here we report a glutaminase isoform switch mechanism that mediates the initial therapeutic effect but eventual failure of hormonal therapy of PCa. Androgen deprivation therapy inhibits the expression of kidney-type glutaminase (KGA), a splicing isoform of glutaminase 1 (GLS1) up-regulated by androgen receptor (AR), to achieve therapeutic effect by suppressing glutaminolysis. Eventually the tumor cells switch to the expression of glutaminase C (GAC), an androgen-independent GLS1 isoform with more potent enzymatic activity, under the androgen-deprived condition. This switch leads to increased glutamine utilization, hyperproliferation, and aggressive behavior of tumor cells. Pharmacological inhibition or RNA interference of GAC shows better treatment effect for castration-resistant PCa than for hormone-sensitive PCa in vitro and in vivo. In summary, we have identified a metabolic function of AR action in PCa and discovered that the GLS1 isoform switch is one of the key mechanisms in therapeutic resistance and disease progression.

Patient characteristics of pediatric inpatients with sensorineural hearing loss: Insights from the 2016 KID database.

This study examines how patient demographics impact pediatric sensorineural hearing loss (SNHL) prevalence using the 2016 Kids' Inpatient Database (KID). By analyzing age, gender, race, income, insurance, and region, the study provides insights for early intervention and diagnosis. Multivariate regression analysis reveals associations between these factors and SNHL occurrence. OBJECTIVE: This study aims to assess the influence of patient demographics on pediatric SNHL prevalence, offering guidance for early detection and intervention strategies. STUDY DESIGN: Using 2016 KID data, this retrospective analysis investigates how patient factors like age, gender, race, income, insurance, and region relate to SNHL prevalence. Multivariate regression is employed to control for potential confounders. METHODS: Data from 6,266,285 patient discharges, including 9997 hearing loss cases, are analyzed. SNHL prevalence is calculated, and demographic variables are examined. Weighted odds ratios and multivariate regression are used to assess associations. RESULTS: The study finds an overall SNHL prevalence of 101.67 cases per 100,000 discharges in 2016. Non-Hispanic White patients show the highest prevalence. Black patients are more likely to be diagnosed, while Hispanic patients are less likely. Multivariate analysis highlights race, income, insurance, region, age, and sex as significant confounders. CONCLUSION: This study underscores the impact of patient demographics on pediatric SNHL prevalence. Factors like race, income, insurance, and region play a role. These findings aid in risk assessment, early identification, and tailored interventions. Further research can uncover socioeconomic disparities and underlying mechanisms.

Understanding pediatric inpatient conductive hearing loss: An analysis of patient demographics.

OBJECTIVE: Hearing loss is a common sensory impairment in children that affects quality of life and development. Early intervention, such as hearing aids and communication therapies, can help children overcome these challenges and lessen the impact on their development. The objective of this study was to identify specific patient demographic factors correlated with the prevalence of pediatric conductive hearing loss. STUDY DESIGN: The study utilized the Kids' Inpatient Database (KID) by the Agency for Healthcare Research and Quality which collects inpatient information from hospitals for patients under 21 years old. We included all patients discharged in 2016 diagnosed with conductive hearing loss, and excluded neonatal patients discharged within 28 days of birth. METHODS: Statistical analyses were performed using R Studio and IBM SPSS Statistics. Weighted odds ratios were calculated for conductive hearing loss in relation to race and income, and a multivariate regression analysis examined associations between demographic variables and race categories in conductive hearing loss. RESULTS: The prevalence of conductive hearing loss (CHL) in pediatric patients in 2016 was 51.62 cases per 100,000 patients. Non-Hispanic White patients had the highest prevalence, while Black patients had the highest likelihood of CHL compared to the overall population. Lower income levels were associated with a decreased probability of CHL diagnosis. After adjusting for age, sex, hospital region, insurance, and income on multivariate analysis, White and Black patients were less likely to be diagnosed with CHL. Furthermore, patients in specific income quartiles also had lower CHL likelihood compared to the general population. CONCLUSION: While Black patients had a higher likelihood of being diagnosed with CHL than the general population, socioeconomic factors such as income greatly influenced the likelihood of CHL diagnosis. Other significant factors included income, region of the country, sex, and age. Further research is needed to better understand and address healthcare disparities related to pediatric hearing loss.

Atrial Fibrillation and Older Age Predict Serum Brain-Derived Neurotrophic Factor Levels Among Patients With Heart Failure.

BACKGROUND: Predictors have not been determined of serum brain-derived neurotrophic factor (BDNF) levels among patients with heart failure (HF). OBJECTIVE: The primary purpose was to evaluate history of atrial fibrillation, age, gender, and left ventricular ejection fraction as predictors of serum BDNF levels at baseline, 10 weeks, and 4 and 8 months after baseline among patients with HF. METHODS: This study was a retrospective cohort analyses of 241 patients with HF. Data were retrieved from the patients' health records (coded history of atrial fibrillation, left ventricular ejection fraction), self-report (age, gender), and serum BDNF. Linear multiple regression analyses were conducted. RESULTS: One hundred three patients (42.7%) had a history of atrial fibrillation. History of atrial fibrillation was a significant predictor of serum BDNF levels at baseline (ß = -0.16, P = .016), 4 months (ß = -0.21, P = .005), and 8 months (ß = -0.19, P = .015). Older age was a significant predictor at 10 weeks (ß = -0.17, P = .017) and 4 months (ß = -0.15, P = .046). CONCLUSIONS: Prospective studies are needed to validate these results. Clinicians need to assess patients with HF for atrial fibrillation and include treatment of it in management plans.

Developing Folate-Conjugated miR-34a Therapeutic for Prostate Cancer: Challenges and Promises.

Prostate cancer (PCa) remains a common cancer with high mortality in men due to its heterogeneity and the emergence of drug resistance. A critical factor contributing to its lethality is the presence of prostate cancer stem cells (PCSCs), which can self-renew, long-term propagate tumors, and mediate treatment resistance. MicroRNA-34a (miR-34a) has shown promise as an anti-PCSC therapeutic by targeting critical molecules involved in cancer stem cell (CSC) survival and functions. Despite extensive efforts, the development of miR-34a therapeutics still faces challenges, including non-specific delivery and delivery-associated toxicity. One emerging delivery approach is ligand-mediated conjugation, aiming to achieve specific delivery of miR-34a to cancer cells, thereby enhancing efficacy while minimizing toxicity. Folate-conjugated miR-34a (folate-miR-34a) has demonstrated promising anti-tumor efficacy in breast and lung cancers by targeting folate receptor α (FOLR1). Here, we first show that miR-34a, a TP53 transcriptional target, is reduced in PCa that harbors TP53 loss or mutations and that miR-34a mimic, when transfected into PCa cells, downregulated multiple miR-34a targets and inhibited cell growth. When exploring the therapeutic potential of folate-miR-34a, we found that folate-miR-34a exhibited impressive inhibitory effects on breast, ovarian, and cervical cancer cells but showed minimal effects on and targeted delivery to PCa cells due to a lack of appreciable expression of FOLR1 in PCa cells. Folate-miR-34a also did not display any apparent effect on PCa cells expressing prostate-specific membrane antigen (PMSA) despite the reported folate's binding capability to PSMA. These results highlight challenges in the specific delivery of folate-miR-34a to PCa due to a lack of target (receptor) expression. Our study offers novel insights into the challenges and promises within the field and casts light on the development of ligand-conjugated miR-34a therapeutics for PCa.

Development of a Topological-Insulator-Based Quantum Resistance Standard.

This paper describes the characterization of the quantum anomalous Hall (QAH) effect resistor with Chromium-doped Bismuth Antimony Telluride with the efforts in coupling directly to a programmable Josephson voltage standard (PJVS) at zero magnetic field. The precision measurement of the QAH resistance was performed under the presence of microwave signal biased to the PJVS. Understanding such effect will help to improve the experimental set-up for integrating multiple quantum electrical standards in a single system.

Strategies of improving adherence to lipid-lowering therapy in patients with atherosclerotic cardiovascular disease.

PURPOSE OF REVIEW: Lowering LDL-C has been shown to reduce ASCVD events, yet many ASCVD patients do not achieve their guideline-directed LDL-C goals leaving patients at increased risk of another ASCVD event. This review discusses implementation strategies to improve guideline-directed lipid management in patients with ASCVD focusing on the provider, patient, and system level. RECENT FINDINGS: At a provider level, under-prescribing of statin intensity due most often to statin intolerance, clinical inertia, insufficient monitoring of LDL-C levels, and the difficulty and cost of prescribing other lipid-lowering therapies such as the PCSK9 inhibitors leads to suboptimal cholesterol management in ASCVD patients. Patients concerns about medication side effects and lack of understanding of their ASCVD risk are causes of poor adherence to their lipid-lowering therapy as are barriers at a system level. SUMMARY: To improve cholesterol management in ASCVD patients will require an integrated approach targeting the provider, the patient and the system. There is a need for further education of clinicians on the importance of intensive LDL-C lowering in ASCVD patients and greater use of nonstatin LDL-C-lowering therapies for those patients on a maximally tolerated statin who have not achieved their guideline-directed LDL-C goal. This will require shared decision-making with a focus on patient education and patient-clinician communication so that the clinician's goals and aims align with that of the patient.

Understanding and targeting prostate cancer cell heterogeneity and plasticity.

Prostate cancer (PCa) is a prevalent malignancy that occurs primarily in old males. Prostate tumors in different patients manifest significant inter-patient heterogeneity with respect to histo-morphological presentations and molecular architecture. An individual patient tumor also harbors genetically distinct clones in which PCa cells display intra-tumor heterogeneity in molecular features and phenotypic marker expression. This inherent PCa cell heterogeneity, e.g., in the expression of androgen receptor (AR), constitutes a barrier to the long-term therapeutic efficacy of AR-targeting therapies. Furthermore, tumor progression as well as therapeutic treatments induce PCa cell plasticity such that AR-positive PCa cells may turn into AR-negative cells and prostate tumors may switch lineage identity from adenocarcinomas to neuroendocrine-like tumors. This induced PCa cell plasticity similarly confers resistance to AR-targeting and other therapies. In this review, I first discuss PCa from the perspective of an abnormal organ development and deregulated cellular differentiation, and discuss the luminal progenitor cells as the likely cells of origin for PCa. I then focus on intrinsic PCa cell heterogeneity in treatment-naïve tumors with the presence of prostate cancer stem cells (PCSCs). I further elaborate on PCa cell plasticity induced by genetic alterations and therapeutic interventions, and present potential strategies to therapeutically tackle PCa cell heterogeneity and plasticity. My discussions will make it clear that, to achieve enduring clinical efficacy, both intrinsic PCa cell heterogeneity and induced PCa cell plasticity need to be targeted with novel combinatorial approaches.

Slow-cycling (dormant) cancer cells in therapy resistance, cancer relapse and metastasis.

It is increasingly appreciated that cancer cell heterogeneity and plasticity constitute major barriers to effective clinical treatments and long-term therapeutic efficacy. Research in the past two decades suggest that virtually all treatment-naive human cancers harbor subsets of cancer cells that possess many of the cardinal features of normal stem cells. Such stem-like cancer cells, operationally defined as cancer stem cells (CSCs), are frequently quiescent and dynamically change and evolve during tumor progression and therapeutic interventions. Intrinsic tumor cell heterogeneity is reflected in a different aspect in that tumors also harbor a population of slow-cycling cells (SCCs) that are not in the proliferative cell cycle and thus are intrinsically refractory to anti-mitotic drugs. In this Perspective, we focus our discussions on SCCs in cancer and on various methodologies that can be employed to enrich and purify SCCs, compare the similarities and differences between SCCs, CSCs and cancer cells undergoing EMT, and present evidence for the involvement of SCCs in surviving anti-neoplastic treatments, mediating tumor relapse, maintaining tumor dormancy and mediating metastatic dissemination. Our discussions make it clear that an in-depth understanding of the biological properties of SCCs in cancer will be instrumental to developing new therapeutic strategies to prevent tumor relapse and distant metastasis.

LRIG1, a regulator of stem cell quiescence and a pleiotropic feedback tumor suppressor.

LRIG1, leucine-rich repeats and immunoglobulin-like domains protein 1, was discovered more than 20 years ago and has been shown to be downregulated or lost, and to function as a tumor suppressor in several cancers. Another well-reported biological function of LRIG1 is to regulate and help enforce the quiescence of adult stem cells (SCs). In both contexts, LRIG1 regulates SC quiescence and represses tumor growth via, primarily, antagonizing the expression and activities of ERBB and other receptor tyrosine kinases (RTKs). We have recently reported that in treatment-naïve human prostate cancer (PCa), LRIG1 is primarily regulated by androgen receptor (AR) and is prominently overexpressed. In castration-resistant PCa (CRPC), both LRIG1 and AR expression becomes heterogeneous and, frequently, discordant. Importantly, in both androgen-dependent PCa and CRPC models, LRIG1 exhibits tumor-suppressive functions. Moreover, LRIG1 induction inhibits the growth of pre-established AR+ and AR- PCa. Here, upon a brief introduction of the LRIG1 and the LRIG family, we provide an updated overview on LRIG1 functions in regulating SC quiescence and repressing tumor development. We further highlight the expression, regulation and functions of LRIG1 in treatment-naïve PCa and CRPC. We conclude by offering the perspectives of identifying novel cancer-specific LRIG1-interacting signaling partners and developing LRIG1-based anti-cancer therapeutics and diagnostic/prognostic biomarkers.

Analysis of orphan designation status for FDA approved drugs, and case studies in oncology, neuroscience and metabolic diseases.

Many new drugs have been approved over the past decade for rare or orphan diseases. The passage of the Orphan Drug Act (ODA) in 1983 has provided key economic and regulatory incentives to provide medicines for patients who are suffering from rare diseases that may not be commercially attractive for research and development. We have analyzed 497 novel drugs approved from 2010 - June 13, 2022, of which 220 were given orphan designation status. We discuss trends over this time period, potential risks for long development times, and provide example case studies of successful development and launch of novel drugs for rare diseases.

Structural insight into allosteric modulation of protease-activated receptor 2.

Protease-activated receptors (PARs) are a family of G-protein-coupled receptors (GPCRs) that are irreversibly activated by proteolytic cleavage of the N terminus, which unmasks a tethered peptide ligand that binds and activates the transmembrane receptor domain, eliciting a cellular cascade in response to inflammatory signals and other stimuli. PARs are implicated in a wide range of diseases, such as cancer and inflammation. PARs have been the subject of major pharmaceutical research efforts but the discovery of small-molecule antagonists that effectively bind them has proved challenging. The only marketed drug targeting a PAR is vorapaxar, a selective antagonist of PAR1 used to prevent thrombosis. The structure of PAR1 in complex with vorapaxar has been reported previously. Despite sequence homology across the PAR isoforms, discovery of PAR2 antagonists has been less successful, although GB88 has been described as a weak antagonist. Here we report crystal structures of PAR2 in complex with two distinct antagonists and a blocking antibody. The antagonist AZ8838 binds in a fully occluded pocket near the extracellular surface. Functional and binding studies reveal that AZ8838 exhibits slow binding kinetics, which is an attractive feature for a PAR2 antagonist competing against a tethered ligand. Antagonist AZ3451 binds to a remote allosteric site outside the helical bundle. We propose that antagonist binding prevents structural rearrangements required for receptor activation and signalling. We also show that a blocking antibody antigen-binding fragment binds to the extracellular surface of PAR2, preventing access of the tethered ligand to the peptide-binding site. These structures provide a basis for the development of selective PAR2 antagonists for a range of therapeutic uses.

A preliminary examination of sexual and physical victimization 6 months after recent rape.

One in four US women will experience a completed or attempted rape in their lifetime, and more than 50% of survivors will experience two or more rapes. Rape and physical violence also co-occur. Multiple experiences of sexual and physical violence are associated with elevated mental and physical health problems. This secondary analysis examined the prevalence and correlates of experiencing sexual or physical violence within 6 months of a sexual assault medical forensic exam (SAMFE). Between May 2009 and December 2013, 233 female rape survivors aged 15 and older were enrolled in a randomized controlled trial during a SAMFE in the emergency department (ED). Demographics, rape characteristics, distress at the ED, and pre-rape history of sexual or physical victimization were assessed. New sexual and physical victimization was assessed 6 months after the SAMFE via telephone interview. Six months after the exam, 21.7% reported a new sexual or physical victimization. Predictors of revictimization during follow-up included sexual or physical victimization prior to the index rape, making less than $10,000 annually, remembering the rape well, life threat during the rape, and higher distress at the ED. In adjusted models, only pre-rape victimization and making less than $10,000 annually were associated with revictimization. Factors assessed at the ED can inform subsequent victimization risk. More research is needed to prevent revictimization among recent rape victims. Policies to provide financial support to recent rape victims and/or targeted prevention for those with pre-rape victimization at the SAMFE could reduce revictimization risk. TRIAL REGISTRATION: NCT01430624.