Metabolic reprogramming of natural killer cells in obesity limits antitumor responses.

Up to 49% of certain types of cancer are attributed to obesity, and potential mechanisms include overproduction of hormones, adipokines, and insulin. Cytotoxic immune cells, including natural killer (NK) cells and CD8+ T cells, are important in tumor surveillance, but little is known about the impact of obesity on immunosurveillance. Here, we show that obesity induces robust peroxisome proliferator-activated receptor (PPAR)-driven lipid accumulation in NK cells, causing complete 'paralysis' of their cellular metabolism and trafficking. Fatty acid administration, and PPARα and PPARδ (PPARα/δ) agonists, mimicked obesity and inhibited mechanistic target of rapamycin (mTOR)-mediated glycolysis. This prevented trafficking of the cytotoxic machinery to the NK cell-tumor synapse. Inhibiting PPARα/δ or blocking the transport of lipids into mitochondria reversed NK cell metabolic paralysis and restored cytotoxicity. In vivo, NK cells had blunted antitumor responses and failed to reduce tumor growth in obesity. Our results demonstrate that the lipotoxic obese environment impairs immunosurveillance and suggest that metabolic reprogramming of NK cells may improve cancer outcomes in obesity.

Srebp-controlled glucose metabolism is essential for NK cell functional responses.

Activated natural killer (NK) cells engage in a robust metabolic response that is required for normal effector function. Using genetic, pharmacological and metabolic analyses, we demonstrated an essential role for Srebp transcription factors in cytokine-induced metabolic reprogramming of NK cells that was independent of their conventional role in the control of lipid synthesis. Srebp was required for elevated glycolysis and oxidative phosphorylation and promoted a distinct metabolic pathway configuration in which glucose was metabolized to cytosolic citrate via the citrate-malate shuttle. Preventing the activation of Srebp or direct inhibition of the citrate-malate shuttle inhibited production of interferon-γ and NK cell cytotoxicity. Thus, Srebp controls glucose metabolism in NK cells, and this Srebp-dependent regulation is critical for NK cell effector function.

Iron Is Critical for Mucosal-Associated Invariant T Cell Metabolism and Effector Functions.

Mucosal-Associated Invariant T (MAIT) cells are a population of innate T cells that play a critical role in host protection against bacterial and viral pathogens. Upon activation, MAIT cells can rapidly respond via both TCR-dependent and -independent mechanisms, resulting in robust cytokine production. The metabolic and nutritional requirements for optimal MAIT cell effector responses are still emerging. Iron is an important micronutrient and is essential for cellular fitness, in particular cellular metabolism. Iron is also critical for many pathogenic microbes, including those that activate MAIT cells. However, iron has not been investigated with respect to MAIT cell metabolic or functional responses. In this study, we show that human MAIT cells require exogenous iron, transported via CD71 for optimal metabolic activity in MAIT cells, including their production of ATP. We demonstrate that restricting iron availability by either chelating environmental iron or blocking CD71 on MAIT cells results in impaired cytokine production and proliferation. These data collectively highlight the importance of a CD71-iron axis for human MAIT cell metabolism and functionality, an axis that may have implications in conditions where iron availability is limited.

Determinants of Mortality and Mid-Term Outcomes After Transcarotid Artery Revascularization and Transfemoral Carotid Artery Stenting.

OBJECTIVES: The potential benefit of transcarotid artery revascularization (TCAR) over transfemoral carotid artery stenting (tfCAS) has been studied in the perioperative period with lower rates of stroke and death; however, data on mid-term outcomes are limited. We aimed to evaluate 3-year outcomes after TCAR and tfCAS and determine the primary predictors of 30-day and 1-year mortality following TCAR. METHODS: Data from the Vascular Quality Initiative for patients undergoing TCAR or tfCAS from January 2016 to December 2022 were analyzed. 1:1 propensity score matching using the nearest-neighbor method was used to adjust baseline demographics and clinical characteristics. Kaplan-Meier survival analysis and Cox Proportional Hazard Regression were used to evaluate long-term outcomes. Iterative stepwise multiple logistic regression analysis and Cox Proportional Hazard Regression were used to identify predictors of 30-day and 1-year mortality, respectively, based upon preoperative, intraoperative, and postoperative factors. RESULTS: A total of 70 237 patients were included in analysis (TCAR=58.7%, tfCAS=41.3%). Transcarotid artery revascularization patients were older and had higher rates of comorbid conditions and high-risk medical and anatomic features than tfCAS patients. Propensity score matching yielded 22 322 pairs with no major differences between groups except that TCAR patients were older (71.6 years vs 70.8 years). At 3 years, TCAR was associated with a 24% reduction in hazard of death compared with tfCAS (hazard ratio [HR]=0.76, 95% confidence interval [CI]=0.71-0.82, p<0.001), for both symptomatic and asymptomatic patients. This survival advantage was established in the first 6 months (HR=0.59, 95% CI=0.53-0.62, p<0.001), with no difference in mortality risk from 6 months to 36 months (HR=0.95, 95% CI=0.86-1.05, p=0.31). Transcarotid artery revascularization was also associated with decreased hazard for 3-year stroke (HR=0.81, 95% CI=0.66-0.99, p=0.04) and stroke or death (HR=0.81, 95% CI=0.76-0.87, p<0.001) compared with tfCAS. The top predictors for 30-day and 1-year mortality were postoperative complications. The primary independent predictor was the occurrence of postoperative stroke. CONCLUSIONS: Transcarotid artery revascularization had a sustained mid-term survival advantage associated over tfCAS, with the benefit being established primarily within the first 6 months. Notably, our findings highlight the importance of postoperative stroke as the primary independent predictor for 30-day and 1-year mortal. CLINICAL IMPACT: The ongoing debate over the superiority of TCAR compared to tfCAS and CEA has been limited by a lack of comparative studies examining the impact of pre-operative symptoms on outcomes. Furthermore, data are scarce on mid-term outcomes for TCAR beyond the perioperative period. As a result, it remains uncertain whether the initial benefits of stroke and death reduction observed with TCAR over tfCAS persist beyond one year. Our study addresses these gaps in the literature, offering evidence to enable clinicians to assess the efficacy of TCAR for up to three years. Additionally, our study seeks to identify risk factors for postoperative mortality following TCAR, facilitating optimal patient stratification.

Small Caliber Distal Cephalic Veins Undergo Significant Dilation under Anesthesia and Can Successfully Be Used for Arteriovenous Fistula Creation.

BACKGROUND: Successful arteriovenous fistula (AVF) maturation and use for dialysis is highly dependent on preoperative diameter. Small veins (<2 mm) exhibit high failure rates and are typically avoided. This study investigates the effects of anesthesia on the distal cephalic vein diameter as compared to preoperative outpatient vein mapping for the purpose of hemodialysis access creation. METHODS: One hundred eight consecutive procedures for dialysis access placement met inclusion criteria and were reviewed. All patients received preoperative venous mapping and postanesthesia ultrasound mapping (PAUS). All patients received either regional and/or general anesthesia. A multiple regression was conducted to determine predictors of venous dilatation. The independent variables included both demographical and operative-specific variables such as the type of anesthesia. Outcomes of fistula maturation (successful cannulation and dialysis) were analyzed. RESULTS: In this cohort, the mean preoperative vein diameter was 1.85 mm and the mean PAUS diameter was 3.45 mm, a 2.21× increase, with only 2 patient veins failing to increase in diameter. Smaller veins (<2 mm) exhibited significantly more dilation than larger veins after anesthesia (2.73 vs. 1.47×, P < 0.001). In the multiple regression analysis, smaller vein diameter was correlated with a significantly greater degree of dilation (P < 0.001). The degree of venous dilation was not affected by patient demographic-specific factors or by the type of anesthesia (regional block versus general) in the multiple regression analysis. 6 month follow-up data for fistula maturation was available for 75 of 108 patients. Small veins (<2 mm) on preoperative ultrasound matured at a similar rate as larger veins (90% vs. 91.4%, P = 0.833). CONCLUSIONS: Small caliber distal cephalic veins experience a significant degree of dilation under regional and general anesthesia and can successfully be used for AVF creation. Consideration should be made to perform a postanesthesia vein mapping for all patients undergoing access placement despite preoperative venous mapping results.

De novo polyamine synthesis supports metabolic and functional responses in activated murine NK cells.

Cellular metabolism is dynamically regulated in NK cells and strongly influences their responses. Metabolic dysfunction is linked to defective NK cell responses in diseases such as obesity and cancer. The transcription factors, sterol regulatory element binding protein (SREBP) and cMyc, are crucial for controlling NK cell metabolic and functional responses, though the mechanisms involved are not fully understood. This study reveals a new role for SREBP in NK cells in supporting de novo polyamine synthesis through facilitating elevated cMyc expression. Polyamines have diverse roles and their de novo synthesis is required for NK cell glycolytic and oxidative metabolism and to support optimal NK cell effector functions. When NK cells with impaired SREBP activity were supplemented with exogenous polyamines, NK cell metabolic defects were not rescued but these NK cells displayed significant improvement in some effector functions. One role for polyamines is in the control of protein translation where spermidine supports the posttranslational hypusination of translation factor eIF5a. Pharmacological inhibition of hypusination also impacts upon NK cell metabolism and effector function. Considering recent evidence that cholesterol-rich tumor microenvironments inhibit SREBP activation and drive lymphocyte dysfunction, this study provides key mechanistic insight into this tumor-evasion strategy.

Carotid stenosis patients with a remote history of cerebrovascular events have increased risk of major adverse events over asymptomatic patients.

INTRODUCTION: Asymptomatic patients with a remote history of transient ischemic attack (TIA) or stroke are not well studied as a separate population from asymptomatic patients with no prior history of TIA or stroke. We compared in-hospital outcomes after transcarotid artery revascularization (TCAR) and transfemoral carotid artery stenting (TFCAS) among symptomatic patients, patients with a remote history of neurologic symptoms, and asymptomatic patients. METHODS: Data from patients in the Vascular Quality Initiative database who underwent TCAR (January 2017 to April 2020) or TFCAS (May 2005 to April 2020) were analyzed. Symptomatic status was defined as TIA and/or stroke occurring within 180 days before the procedure. Asymptomatic status was divided into patients with no history of TIA/stroke (asymptomatic) and patients with a history of TIA/stroke occurring more than 180 days before the procedure (remote history of neurologic symptoms). The Student t-test and Pearson χ2 test were used to compare baseline patient characteristics and outcomes. Multivariate logistic regression was used to adjust for significant between-group differences in baseline characteristics. RESULTS: There were 7158 patients who underwent TCAR (symptomatic: 2574, asymptomatic: 3689, and asymptomatic with a remote history of neurologic symptoms: 895) and 18,023 patients who underwent TFCAS (symptomatic: 6195, asymptomatic: 10,333, and asymptomatic with a remote history of neurologic symptoms: 1495). Regardless of symptom status, the mean patient age was 73 years for TCAR and 69 years for TFCAS. A total of 64% of patients in the study were male and 36% of patients were female. The mean long-term follow-up data ranged between 208 and 331 days within the three patient groups. Carotid stenosis patients with a remote history of neurologic symptoms had higher rates of TIA, stroke, TIA/stroke, stroke/death, and stroke/death/myocardial infarction than asymptomatic patients, and these rates were similar to those of symptomatic patients. Comparing TCAR and TFCAS among patients with a remote history of neurologic symptoms, there were statistically significant reductions in the odds of stroke/death (odds ratio: 0.46, 95% confidence interval: 0.27-0.84, P = .011) and stroke/death/myocardial infarction (odds ratio: 0.51, 95% confidence interval: 0.30-0.87, P = .013) after TCAR. This was likely driven by the increased rate of death after TFCAS in patients with a remote history of neurologic symptoms (0.9%) compared with asymptomatic patients (0.6%). CONCLUSIONS: Asymptomatic patients with a remote history of TIA/stroke do not have the same outcomes as asymptomatic patients without a history of TIA/stroke and are at higher risk of adverse in-hospital events. Patients with a remote history of TIA/stroke have increased risk of in-hospital death after TFCAS and may benefit from TCAR.

Nutcracker Phenomenon as a Result of Celiomesenteric Trunk Aneurysm.

A common origin of the celiac trunk and superior mesenteric artery is exceedingly rare, and aneurysms of this common trunk are even rarer. According to our literature search, there are no reported cases of nutcracker syndrome or phenomenon involving this rare aneurysmal anomaly. Repair of such anomalies is standardly via open surgical approach with few reported cases of endovascular repair. We describe a patient with an aneurysm of the celiomesenteric trunk resulting in nutcracker phenomenon of the left renal vein. The celiomesenteric trunk aneurysm was repaired endovascularly, resulting in decreased surrounding inflammation and improvement of the left renal vein compression.

A Novel Approach for the Treatment of Nutcracker Syndrome: A Case Report.

We describe a case of nutcracker syndrome in a 35 year-old male that was treated with a left renal vein transposition via an open retroperitoneal approach. Our case highlights some of the advantages of the retroperitoneal approach, which may decrease the risk of postoperative complications when compared to the traditional midline abdominal transperitoneal approach. The patient agreed to publish the case details and images included below.

Comparison of Transcarotid Artery Revascularization and Transfemoral Carotid Artery Stenting Based on High Risk Anatomic Characteristics.

BACKGROUND: Anatomic details affecting the adverse outcomes following carotid artery stenting have not been well characterized. We compared in-hospital outcomes following transcarotid artery revascularization (TCAR) and transfemoral carotid artery stenting (TFCAS) among symptomatic and asymptomatic patients stratified by degree of lesion calcification and aortic arch type. METHODS: Data from patients in the Society for Vascular Surgery's Vascular Quality Initiative database undergoing TCAR (January 2017 to April 2020) or TFCAS (May 2005 to April 2020) and had non-missing grading on carotid artery calcification or aortic arch type was analyzed. Degree of calcification was stratified into 3 groups: none, ≤ 50% calcification, and >50% calcification. Arch type was stratified as Type I, Type II, and Type III. RESULTS: A total of 9,868 patients (TCAR: 4,224; TFCAS: 5,644) were included in the calcification analysis. TCAR patients were generally older, white, smokers, and had more comorbidities than TFCAS patients. Among the symptomatic patients, there was no difference in rates of stroke, stroke/transient ischemic attack (TIA), and myocardial infarction (MI) by calcification severity between TCAR and TFCAS. However, there was a trend towards increased risk in all 3 events with higher calcification only after TFCAS. Symptomatic patients with severe (>50%) calcification had lower rates of death (TCAR: 0.9% vs. TFCAS: 2.8%, P = 0.013), stroke/death (TCAR: 2.7% vs. TFCAS: 5.8%, P = 0.006), stroke/death/MI (TCAR: 3.3% vs. TFCAS: 6.5%, P = 0.007), and postop complications (TCAR: 6.0% vs. TFCAS: 12.4%, P < 0.001) after TCAR compared to TFCAS. Furthermore, TCAR had lower risk of mortality at all degrees of calcification compared to TFCAS. Similar findings were noted among asymptomatic TCAR patients with >50% calcification, in which the rates of death (TCAR: 0.4% vs. TFCAS: 1.1%, P = 0.080) and stroke/death (TCAR: 1.5% vs. TFCAS: 3.1%, P = 0.029) were reduced. A comparison of TCAR to TFCAS by arch type showed that rates of stroke/death after TCAR were similar regardless of arch complexity (Type I: 2.6% vs. Type II: 2.8%), but increased after TFCAS with complex, high risk anatomy (Type I: 4.2% vs. Type II: 5.2%). CONCLUSIONS: While increased calcification increased rates of adverse events after TFCAS, this trend was not observed after TCAR, which also had lower rates of death and stroke/death among patients with severe calcification. Furthermore, TCAR had lower risk of mortality than TFCAS across all degrees of calcification. TFCAS was associated with increased risk of stroke/death with complex aortic arch anatomy, however, rates of stroke/death after TCAR were similar regardless of arch complexity. Our results suggests that TCAR should be preferentially considered in revascularization of patients with anatomy considered high-risk for TFCAS.

Rational design of cannabinoid type-1 receptor allosteric modulators: Org27569 and PSNCBAM-1 hybrids.

Allosteric modulation offers an alternate approach to target the cannabinoid type-1 receptor (CB1) for therapeutic benefits. Examination of the two widely studied prototypic CB1 negative allosteric modulators (NAMs) Org27569 and PSNCBAM-1 revealed structural resemblance and similar structure-activity relationships (SARs). In silico docking and dynamics simulation studies using the crystal structure of CB1 co-bound with CP55,940 and Org27569 suggested that Org27569 and PSNCBAM-1 occupied the same binding pocket and several common interactions were present in both series with the CB1 receptor. A new scaffold was therefore designed by merging the key structural features from the two series and the hybrids retained these binding features in the in silico docking studies. In addition, one such hybrid displayed similar functions to Org27569 in dynamic simulations by preserving a key R2143.50-D3386.30 salt bridge and maintaining an antagonist-like Helix3-Helix6 interhelical distance. Based on these results, a series of hybrids were synthesized and assessed in calcium mobilization, [35S]GTPγS binding and cAMP assays. Several compounds displayed comparable potencies to Org27569 and PSNCBAM-1 in these assays. This work offers new insight of the SAR requirement at the allosteric site of the CB1 receptor and provides a new scaffold that can be optimized for the development of future CB1 allosteric modulators.

Obesity Reduces mTORC1 Activity in Mucosal-Associated Invariant T Cells, Driving Defective Metabolic and Functional Responses.

Obesity underpins the development of numerous chronic diseases, such as type II diabetes mellitus. It is well established that obesity negatively alters immune cell frequencies and functions. Mucosal-associated invariant T (MAIT) cells are a population of innate T cells, which we have previously reported are dysregulated in obesity, with altered circulating and adipose tissue frequencies and a reduction in their IFN-γ production, which is a critical effector function of MAIT cells in host defense. Hence, there is increased urgency to characterize the key molecular mechanisms that drive MAIT cell effector functions and to identify those which are impaired in the obesity setting. In this study, we found that MAIT cells significantly upregulate their rates of glycolysis upon activation in an mTORC1-dependent manner, and this is essential for MAIT cell IFN-γ production. Furthermore, we show that mTORC1 activation is dependent on amino acid transport via SLC7A5. In obese patients, using RNA sequencing, Seahorse analysis, and a series of in vitro experiments, we demonstrate that MAIT cells isolated from obese adults display defective glycolytic metabolism, mTORC1 signaling, and SLC7A5 aa transport. Collectively, our data detail the intrinsic metabolic pathways controlling MAIT cell cytokine production and highlight mTORC1 as an important metabolic regulator that is impaired in obesity, leading to altered MAIT cell responses.

Physical activity and quality of life in African American cancer survivors: The Detroit Research on Cancer Survivors study.

BACKGROUND: The benefit of regular exercise in improving cancer outcomes is well established. The American Cancer Society (ACS) released a recommendation that cancer survivors should engage in at least 150 minutes of moderate to vigorous physical activity (PA) per week; however, few report meeting this recommendation. This study examined the patterns and correlates of meeting ACS PA recommendations in the Detroit Research on Cancer Survivors (ROCS) cohort of African American cancer survivors. METHODS: Detroit ROCS participants completed baseline and yearly follow-up surveys to update their health and health behaviors, including PA. This study examined participation in PA by select characteristics and reported health-related quality of life (HRQOL) as measured with the Functional Assessment of Cancer Therapy and Patient-Reported Outcomes Measurement Information System instruments. RESULTS: Among the first 1500 ROCS participants, 60% reported participating in regular PA, with 24% reporting ≥150 min/wk. Although there were no differences by sex, prostate cancer survivors were the most likely to report participating in regular PA, whereas lung cancer survivors were the least likely (P = .022). Survivors who reported participating in regular PA reported higher HRQOL (P < .001) and lower depression (P = .040). CONCLUSIONS: Just 24% of African American cancer survivors reported meeting the ACS guidelines for PA at the baseline, but it was encouraging to see increases in activity over time. Because of the established benefits of regular exercise observed in this study and others, identifying and reducing barriers to regular PA among African American cancer survivors are critical for improving outcomes and minimizing disparities.

Phosphatidylinositol-3-OH kinase and nutrient-sensing mTOR pathways control T lymphocyte trafficking.

Phosphatidylinositol-3-OH kinase (PI(3)K) and the nutrient sensor mTOR are evolutionarily conserved regulators of cell metabolism. Here we show that PI(3)K and mTOR determined the repertoire of adhesion and chemokine receptors expressed by T lymphocytes. The key lymph node-homing receptors CD62L (L-selectin) and CCR7 were highly expressed on naive T lymphocytes but were downregulated after immune activation. CD62L downregulation occurred through ectodomain proteolysis and suppression of gene transcription. The p110delta subunit of PI(3)K controlled CD62L proteolysis through mitogen-activated protein kinases, whereas control of CD62L transcription by p110delta was mediated by mTOR through regulation of the transcription factor KLF2. PI(3)K-mTOR nutrient-sensing pathways also determined expression of the chemokine receptor CCR7 and regulated lymphocyte trafficking in vivo. Hence, lymphocytes use PI(3)K and mTOR to match metabolism and trafficking.

Protein kinase B controls transcriptional programs that direct cytotoxic T cell fate but is dispensable for T cell metabolism.

In cytotoxic T cells (CTL), Akt, also known as protein kinase B, is activated by the T cell antigen receptor (TCR) and the cytokine interleukin 2 (IL-2). Akt can control cell metabolism in many cell types but whether this role is important for CTL function has not been determined. Here we have shown that Akt does not mediate IL-2- or TCR-induced cell metabolic responses; rather, this role is assumed by other Akt-related kinases. There is, however, a nonredundant role for sustained and strong activation of Akt in CTL to coordinate the TCR- and IL-2-induced transcriptional programs that control expression of key cytolytic effector molecules, adhesion molecules, and cytokine and chemokine receptors that distinguish effector versus memory and naive T cells. Akt is thus dispensable for metabolism, but the strength and duration of Akt activity dictates the CTL transcriptional program and determines CTL fate.

Canonical TGF-ß Signaling Pathway Represses Human NK Cell Metabolism.

Cytokines stimulate rapid metabolic changes in human NK cells, including increases in both glycolysis and oxidative phosphorylation pathways. However, how these are subsequently regulated is not known. In this study, we demonstrate that TGF-ß can inhibit many of these metabolic changes, including oxidative phosphorylation, glycolytic capacity, and respiratory capacity. TGF-ß also inhibited cytokine-induced expression of the transferrin nutrient receptor CD71. In contrast to a recent report on murine NK cells, TGF-ß-mediated suppression of these metabolic responses did not involve the inhibition of the metabolic regulator mTORC1. Inhibition of the canonical TGF-ß signaling pathway was able to restore almost all metabolic and functional responses that were inhibited by TGF-ß. These data suggest that pharmacological inhibition of TGF-ß could provide a metabolic advantage to NK cells that is likely to result in improved functional responses. This has important implications for NK cell-based cancer immunotherapies.

Iliac Remote Endarterectomy to Restore Circulation in a Patient with Infected Aorto-Femoral and Axillo-Bifemoral Bypasses.

We report a case of a patient who underwent a 2-stage operation that included a right obturator bypass with left iliac remote endarterectomy followed by removal of an infected, previously failed aorto-right-femoral and right axillo-bifemoral bypass reconstructions.

Nutrient sensing, signal transduction and immune responses.

Most cells in the body have a constant supply of nutrients, which are required to sustain cellular metabolism and functions. In contrast, cells of the immune system can encounter conditions with a limited nutrient supply during the course of an immune response. Cells of the immune system frequently operate in complex nutrient restricted microenvironments such as tumour or inflammatory sites. The concentrations of key nutrients such as glucose and certain amino acids, can be low at these sites, and this can have an impact upon immune cell function. Nutrient sufficiency is important to supply the metabolic and biosynthetic pathways of immune cells. In addition nutrients can also act as important cues that influence immunological signalling pathways to affect the function of immune cells. This review will describe the various nutrient sensing signalling pathways and discuss the evidence that nutrients are critical signals that shape immune responses.

Not all lightweight lead aprons and thyroid shields are alike.

OBJECTIVE: With the explosion of minimally invasive surgery, the use of fluoroscopy has significantly increased. Concurrently, there has been a demand for lighter weight aprons. The industry answered this call with the development of lightweight aprons. Our goal was to see whether lighter weight garments provide reduced protection. METHODS: Dry laboratory testing was performed in a standard X-ray room, using a standard fluoroscopy table and standard acrylic blocks. A commercial-grade pressurized ion chamber survey meter (Ludlum Model 9DP; Ludlum Measurements, Inc, Sweetwater, Tex) was used to detect gamma rays and X-rays above 25 keV. Nonlead aprons from several manufacturers were tested for scatter radiation penetration above the table at a fixed distance (3 feet) and compared with two standard 0.5-mm lead aprons of different manufacturers. RESULTS: Scatter measurements were made at 60 kVp and 70 kVp for pure lead (0.5 mm), mixed, and nonlead protective garments. Scatter penetration for the nonlead blends and barium aprons was 292% and 258%, respectively, at 60 kVp compared with the pure lead apron. At the higher beam quality of 70 kVp, the scatter penetration was 214% and 233% for the blend and barium aprons, respectively, compared with the pure lead apron. Our measurements demonstrate a noticeable difference in scatter reduction between pure lead and nonlead garments. Pure barium aprons and nonlead aprons from certain companies demonstrated scatter penetration that is inconsistent with the 0.5 mm of lead equivalence as claimed on the label. In addition, there was an incidental finding of a handful of lightweight aprons with significant tears along the seams, leaving large gaps in protection. Our study also demonstrates that several companies rate their lightweight garments as 0.5 mm lead equivalent, when actually only a small area on the chest and abdomen where the garment overlapped was 0.5 mm, leaving the rest of the garment with half the protection at 0.25 mm. CONCLUSIONS: Our reliance on protective lead garments to shield us from the biologic effects of radiation exposure and the inferiority of some lightweight garments necessitate a streamlining of the testing methods and transparency in data reporting by manufacturers.