Metformin-mediated mitochondrial protection post-cardiac arrest improves EEG activity and confers neuroprotection and survival benefit.

Cardiac arrest (CA) produces global ischemia/reperfusion injury resulting in substantial multiorgan damage. There are limited efficacious therapies to save lives despite CA being such a lethal disease process. The small population of surviving patients suffer extensive brain damage that results in substantial morbidity. Mitochondrial dysfunction in most organs after CA has been implicated as a major source of injury. Metformin, a first-line treatment for diabetes, has shown promising results in the treatment for other diseases and is known to interact with the mitochondria. For the treatment of CA, prior studies have utilized metformin in a preconditioning manner such that animals are given metformin well before undergoing CA. As the timing of CA is quite difficult to predict, the present study, in a clinically relevant manner, sought to evaluate the therapeutic benefits of metformin administration immediately after resuscitation using a 10 min asphxyial-CA rat model. This is the first study to show that metformin treatment post-CA (a) improves 72 h survival and neurologic function, (b) protects mitochondrial function with a reduction in apoptotic brain injury without activating AMPK, and (c) potentiates earlier normalization of brain electrophysiologic activity. Overall, as an effective and safe drug, metformin has the potential to be an easily translatable intervention for improving survival and preventing brain damage after CA.

ouR Space Commentary: Wellness Perspective From SABI's Early Career Committee.

ABSTRACT: Radiologists and members-in-training are experiencing higher (and escalating) rates of burnout, resulting in a profound impact on the health of physicians, patients, and the community. Lately, the radiology community has demonstrated a growing awareness of this phenomenon, which has led to emphasis on practicing and promoting wellness. With a myriad of factors contributing to burnout in radiology, a multifaceted approach is pivotal for counteracting burnout and fostering overall well-being, including efforts driven at both organizational and individual levels. This article discusses perspectives from the members of the Early Career Committee at the Society for Advanced Body Imaging (SABI); it explores their beliefs and practical strategies for maintaining personal well-being.

A Novel Approach to Delivering Evidence-based, High-quality Care in Psychiatry Through an Electronic Integrated Care Pathway (eICP) Pilot.

Integrated care pathways (ICPs) are evidence-based decision support tools intended to reduce variation and improve quality of care. Historically, adoption of ICPs has been difficult to measure, as the pathways were outside of the electronic health record (EHR), where care delivery documentation and orders were completed. This Technology Column describes the innovative development and implementation of a diagnosis specific electronic ICP that directly embeds pathway steps into an EHR to facilitate order sets, clinical decision-making, and usage tracking. The pathway was implemented at a seven-hospital academic medical center, and details the technology, team structure, early adoption results, and future directions. As such, the importance of investing and organizing resources to create an eICP (e.g., time, technology, and specialized teams) to provide a user-friendly experience to support early adoption is underscored. Preliminary findings show that the eICP had consistent use in the first year of implementation. This manuscript is intended to serve as a practical guide to build eICPs within behavioral health service areas across institutions.

Algorithmic Approach to the Splenic Lesion Based on Radiologic-Pathologic Correlation.

Splenic lesions are commonly discovered incidentally at imaging, without clinical signs or symptoms that may aid in diagnosis. As such, the differential diagnosis and subsequent management are based primarily on imaging characteristics. Much has been written about the myriad pathologic conditions that can occur in the spleen; however, there is little guidance on the approach to an incidental splenic mass. Applying an approach frequently used in imaging to the splenic mass-based on the number and consistency of lesions and refined by supplementary imaging features-allows formulation of a useful differential diagnosis. Solitary cystic masses include true cysts, pseudocysts, and parasitic cysts. When multiple cystic lesions are present, the differential diagnosis expands to include infectious lesions (abscess or microabscesses) and lymphangioma (a benign cystic neoplasm). Hemangioma is the most common solitary solid mass, although other vascular lesions (hamartoma, sclerosing angiomatoid nodular transformation) and nonvascular lesions (inflammatory pseudotumor, lymphoma) manifest as solitary and solid. When multiple solid masses are present, diffuse inflammatory disease (sarcoidosis), littoral cell angioma, and lymphoma should be considered. Malignancies, such as angiosarcoma or metastasis, can manifest as solitary or multiple and solid or cystic masses but are typically associated with symptoms or widespread primary malignancy. Careful assessment of the multimodality imaging characteristics of splenic lesions based on this approach aids the radiologist faced with the incidental splenic lesion. Online supplemental material is available for this article. Work of the U.S. Government published under an exclusive license with the RSNA.

Comparison of Prostate Imaging and Reporting Data System V2.0 and V2.1 for Evaluation of Transition Zone Lesions: A 5-Reader 202-Patient Analysis.

OBJECTIVE: The aim of the study was to compare the distribution of Prostate Imaging and Reporting Data System (PI-RADS) scores, interreader agreement, and diagnostic performance of PI-RADS v2.0 and v2.1 for transition zone (TZ) lesions. METHODS: The study included 202 lesions in 202 patients who underwent 3T prostate magnetic resonance imaging showing a TZ lesion that was later biopsied with magnetic resonance imaging/ultrasound fusion. Five abdominal imaging faculty reviewed T2-weighted imaging and high b value/apparent diffusion coefficient images in 2 sessions. Cases were randomized using a crossover design whereby half in the first session were reviewed using v2.0 and the other half using v2.1, and vice versa for the 2nd session. Readers provided T2-weighted imaging and DWI scores, from which PI-RADS scores were derived. RESULTS: Interreader agreement for all PI-RADS scores had κ of 0.37 (v2.0) and 0.26 (v2.1). For 4 readers, the percentage of lesions retrospectively scored PI-RADS 1 increased greater than 5% and PI-RADS 2 score decreased greater than 5% from v2.0 to v2.1. For 2 readers, the percentage scored PI-RADS 3 decreased greater than 5% and, for 2 readers, increased greater than 5%. The percentage of PI-RADS 4 and 5 lesions changed less than 5% for all readers. For the 4 readers with increased frequency of PI-RADS 1 using v2.1, 4% to 16% were Gleason score ≥3 + 4 tumor. Frequency of Gleason score ≥3 + 4 in PI-RADS 3 lesions increased for 2 readers and decreased for 1 reader. Sensitivity of PI-RADS of 3 or greater for Gleason score ≥3 + 4 ranged 76% to 90% (v2.0) and 69% to 96% (v2.1). Specificity ranged 32% to 64% (v2.0) and 25% to 72% (v2.1). Positive predictive value ranged 43% to 55% (v2.0) and 41% to 58% (v2.1). Negative predictive value ranged 82% to 87% (v2.0) and 81% to 91% (v2.1). CONCLUSIONS: Poor interreader agreement and lack of improvement in diagnostic performance indicate an ongoing need to refine evaluation of TZ lesions.

Increased plasma disequilibrium between pro- and anti-oxidants during the early phase resuscitation after cardiac arrest is associated with increased levels of oxidative stress end-products.

BACKGROUND: Cardiac arrest (CA) results in loss of blood circulation to all tissues leading to oxygen and metabolite dysfunction. Return of blood flow and oxygen during resuscitative efforts is the beginning of reperfusion injury and is marked by the generation of reactive oxygen species (ROS) that can directly damage tissues. The plasma serves as a reservoir and transportation medium for oxygen and metabolites critical for survival as well as ROS that are generated. However, the complicated interplay among various ROS species and antioxidant counterparts, particularly after CA, in the plasma have not been evaluated. In this study, we assessed the equilibrium between pro- and anti-oxidants within the plasma to assess the oxidative status of plasma post-CA. METHODS: In male Sprague-Dawley rats, 10 min asphyxial-CA was induced followed by cardiopulmonary resuscitation (CPR). Plasma was drawn immediately after achieving return of spontaneous circulation (ROSC) and after 2 h post-ROSC. Plasma was isolated and analyzed for prooxidant capacity (Amplex Red and dihydroethidium oxidation, total nitrate and nitrite concentration, xanthine oxidase activity, and iron concentration) and antioxidant capacity (catalase and superoxide dismutase activities, Total Antioxidant Capacity, and Iron Reducing Antioxidant Power Assay). The consequent oxidative products, such as 4-Hydroxyl-2-noneal, malondialdehyde, protein carbonyl, and nitrotyrosine were evaluated to determine the degree of oxidative damage. RESULTS: After CA and resuscitation, two trends were observed: (1) plasma prooxidant capacity was lower during ischemia, but rapidly increased post-ROSC as compared to control, and (2) plasma antioxidant capacity was increased during ischemia, but either decreased or did not increase substantially post-ROSC as compared to control. Consequently, oxidation products were increased post-ROSC. CONCLUSION: Our study evaluated the disbalance of pro- and anti-oxidants after CA in the plasma during the early phase after resuscitation. This disequilibrium favors the prooxidants and is associated with increased levels of downstream oxidative stress-induced end-products, which the body's antioxidant capacity is unable to directly mitigate. Here, we suggest that circulating plasma is a major contributor to oxidative stress post-CA and its management requires substantial early intervention for favorable outcomes.

The acceptability of a novel procedure service run by PAs and NPs.

BACKGROUND: Hospitalist physicians are performing fewer procedures because of multiple reasons, including expanded responsibilities beyond their patient panel. A procedure service that offloads hospitalists could expedite these necessary services. An opportunity exists for physician assistants (PAs) and NPs to fill this gap. OBJECTIVE: To describe the implementation of a PA- and NP-run procedure service at a large academic hospital. METHODS: This is a retrospective cohort study of procedures by the procedure service at one institution from 2015 to 2019. RESULTS: Over 5 years, 7,002 procedures were performed, with requests increasing over time. The most frequent procedures were venous access, lumbar puncture, paracentesis, and placement of nasogastric or nasojejunal tubes. Requesting services included hospitalists and residents from internal medicine, surgery, and neurology. CONCLUSIONS: A PA- and NP-run procedure service is well accepted at a large academic hospital despite the lack of involvement by attending physicians. Future directions are focused on augmenting coverage and procedures offered.

Lipid-cytokine-chemokine cascade drives neutrophil recruitment in a murine model of inflammatory arthritis.

A large and diverse array of chemoattractants control leukocyte trafficking, but how these apparently redundant signals collaborate in vivo is still largely unknown. We previously demonstrated an absolute requirement for the lipid chemoattractant leukotriene B(4) (LTB(4)) and its receptor BLT1 for neutrophil recruitment into the joint in autoantibody-induced arthritis. We now demonstrate that BLT1 is required for neutrophils to deliver IL-1 into the joint to initiate arthritis. IL-1-expressing neutrophils amplify arthritis through the production of neutrophil-active chemokines from synovial tissue cells. CCR1 and CXCR2, two neutrophil chemokine receptors, operate nonredundantly to sequentially control the later phase of neutrophil recruitment into the joint and mediate all neutrophil chemokine activity in the model. Thus, we have uncovered a complex sequential relationship involving unique contributions from the lipid mediator LTB(4), the cytokine IL-1, and CCR1 and CXCR2 chemokine ligands that are all absolutely required for effective neutrophil recruitment into the joint.

Transfer is not a transition - voices of Jamaican adolescents with HIV and their health care providers.

Increasing access to antiretroviral therapy in resource-limited settings (RLS) has resulted in the survival of perinatally HIV-infected children into adulthood. We characterized the transition process from pediatric to adult care by conducting semi-structured interviews of HIV-infected adolescents and health care providers in Jamaica. Using an inductive content analytic approach, four themes emerged: (1) Transition should be holistic and a process; (2) Pediatric clinics were like families; (3) Rootedness in the pediatric clinic; and (4) Need for adolescent-centered services to bridge the gap between pediatric and adult-centered services. Adolescent informed- and centered-transition approach may result in better outcomes for HIV-infected adolescents.

Association of in-hospital resource utilization with post-acute spending in Medicare beneficiaries hospitalized for acute myocardial infarction: a cross-sectional study.

BACKGROUND: Efforts to decrease hospitalization costs could increase post-acute care costs. This effect could undermine initiatives to reduce overall episode costs and have implications for the design of health care under alternative payment models. METHODS: Among Medicare fee-for-service beneficiaries aged ≥65 years hospitalized with acute myocardial infarction (AMI) between July 2010 and June 2013 in the Premier Healthcare Database, we studied the association of in-hospital and post-acute care resource utilization and outcomes by in-hospital cost tertiles. RESULTS: Among patients with AMI at 326 hospitals, the median (range) of each hospital's mean per-patient in-hospital risk-standardized cost (RSC) for the low, medium, and high cost tertiles were $16,257 ($13,097-$17,648), $18,544 ($17,663-$19,875), and $21,831 ($19,923-$31,296), respectively. There was no difference in the median (IQR) of risk-standardized post-acute payments across cost-tertiles: $5014 (4295-6051), $4980 (4349-5931) and $4922 (4056-5457) for the low (n = 90), medium (n = 98), and high (n = 86) in-hospital RSC tertiles (p = 0.21), respectively. In-hospital and 30-day mortality rates did not differ significantly across the in-hospital RSC tertiles; however, 30-day readmission rates were higher at hospitals with higher in-hospital RSCs: median = 17.5, 17.8, and 18.0% at low, medium, and high in-hospital RSC tertiles, respectively (p = 0.005 for test of trend across tertiles). CONCLUSIONS: In our study of patients hospitalized with AMI, greater resource utilization during the hospitalization was not associated with meaningful differences in costs or mortality during the post-acute period. These findings suggest that it may be possible for higher cost hospitals to improve efficiency in care without increasing post-acute care utilization or worsening outcomes.

Case Records of the Mass General Hospital. Case 7-2015: A 25-year-old man with oral ulcers, rash, and odynophagia.

A 25-year-old man presented with oral ulcers and odynophagia. On examination, there were scattered pink papules and plaques on the trunk, thighs, and buttocks and multiple raised, erythematous nodules on both shins. A diagnostic procedure was performed.

The role of tissue resident cells in neutrophil recruitment.

Neutrophils are first responders of the immune system, rapidly migrating into affected tissues in response to injury or infection. To effectively call in this first line of defense, strategically placed cells within the vasculature and tissue respond to noxious stimuli by sending out coordinated signals that recruit neutrophils. Regulation of organ-specific neutrophil entry occurs at two levels. First, the vasculature supplying the organ provides cues for neutrophil egress out of the bloodstream in a manner dependent upon its unique cellular composition and architectural features. Second, resident immune cells and stromal cells within the organ send coordinated signals that guide neutrophils to their final destination. Here, we review recent findings that highlight the importance of these tissue-specific responses in the regulation of neutrophil recruitment and the initiation and resolution of inflammation.

Therapeutic Hypothermia Provides Variable Protection against Behavioral Deficits after Neonatal Hypoxia-Ischemia: A Potential Role for Brain-Derived Neurotrophic Factor.

BACKGROUND: Despite treatment with therapeutic hypothermia (TH), infants who survive hypoxic ischemic (HI) encephalopathy (HIE) have persistent neurological abnormalities at school age. Protection by TH against HI brain injury is variable in both humans and animal models. Our current preclinical model of hypoxia-ischemia (HI) and TH displays this variability of outcomes in neuropathological and neuroimaging end points with some sexual dimorphism. The detailed behavioral phenotype of this model is unknown. Whether there is sexual dimorphism in certain behavioral domains is also not known. Brain-derived neurotrophic factor (BDNF) supports neuronal cell survival and repair but may also be a marker of injury. Here, we characterize the behavioral deficits after HI and TH stratified by sex, as well as late changes in BDNF and its correlation with memory impairment. METHODS: HI was induced in C57BL6 mice on postnatal day 10 (p10) (modified Vannucci model). Mice were randomized to TH (31°C) or normothermia (NT, 36°C) for 4 h after HI. Controls were anesthesia-exposed, age- and sex-matched littermates. Between p16 and p39, growth was followed, and behavioral testing was performed including reflexes (air righting, forelimb grasp and negative geotaxis) and sensorimotor, learning, and memory skills (open field, balance beam, adhesive removal, Y-maze tests, and object location task [OLT]). Correlations between mature BDNF levels in the forebrain and p42 memory outcomes were studied. RESULTS: Both male and female HI mice had an approximately 8-12% lower growth rate (g/day) than shams (p ≤ 0.01) by p39. TH ameliorated this growth failure in females but not in males. In female mice, HI injury prolonged the time spent at the periphery (open field) at p36 (p = 0.004), regardless of treatment. TH prevented motor impairments in the balance beam and adhesive removal tests in male and female mice, respectively (p ≤ 0.05). Male and female HI mice visited the new arm of the Y-maze 12.5% (p = 0.05) and 10% (p = 0.03) less often than shams, respectively. Male HI mice also had 35% lower exploratory preference score than sham (p ≤ 0.001) in the OLT. TH did not prevent memory impairments found with Y-maze testing or OLT in either sex (p ≤ 0.01) at p26. At p42, BDNF levels in the forebrain ipsilateral to the HI insult were 1.7- to 2-fold higher than BDNF levels in the sham forebrain, and TH did not prevent this increase. Higher BDNF levels in the forebrain ipsilateral to the insult correlated with worse performance in the Y-maze in both sexes and in OLT in male mice (p = 0.01). CONCLUSIONS: TH provides benefit in specific domains of behavior following neonatal HI. In general, these benefits accrued to both males and females, but not in all areas. In some domains, such as memory, no benefit of TH was found. Late differences in individual BDNF levels may explain some of these findings.

An expanded population of pathogenic regulatory T cells in giant cell arteritis is abrogated by IL-6 blockade therapy.

OBJECTIVES: Randomised-controlled trials have recently proven the efficacy of the interleukin (IL)-6 receptor antagonist tocilizumab (TCZ) in giant cell arteritis (GCA). However, the mechanism of action of IL-6 blockade in this disease is unknown. Moreover, the role of regulatory T (Treg) cells in the pathogenesis of GCA remains underexplored. Given the plasticity of Tregs and the importance of IL-6 in their biology, we hypothesised that TCZ might modulate the Treg response in GCA. We therefore characterised the Treg compartment of patients with GCA treated with TCZ. METHODS: We classified 41 patients with GCA into three groups: active disease (aGCA, n=11), disease remission on corticosteroids (rGCA-CS, n=19) and disease remission on TCZ (rGCA-TCZ, n=11). Healthy controls (HCs) were included for comparison. We determined the frequency, phenotype and function of peripheral blood Tregs. RESULTS: Patients with aGCA demonstrated a hypoproliferating Treg compartment enriched in IL-17-secreting Tregs (IL-17+Tregs). Tregs in patients with aGCA disproportionally expressed a hypofunctional isoform of Foxp3 that lacks exon 2 (Foxp3Δ2). Foxp3Δ2-expressing Tregs coexpressed CD161, a marker commonly associated with the Th17 linage, significantly more often than full-length Foxp3-expressing Tregs. Compared with those of HCs, GCA-derived Tregs demonstrated impaired suppressor capacity. Treatment with TCZ, in contrast to CS therapy, corrected the Treg abnormalities observed in aGCA. In addition, TCZ treatment increased the numbers of activated Tregs (CD45RA-Foxp3high) and the Treg expression of markers of trafficking (CCR4) and terminal differentiation (CTLA-4). CONCLUSIONS: TCZ may exert its therapeutic effects in GCA by increasing the proliferation and activation of Tregs, and by reverting the pathogenic Treg phenotype seen during active disease.

Tropomodulin3-null mice are embryonic lethal with anemia due to impaired erythroid terminal differentiation in the fetal liver.

Tropomodulin (Tmod) is a protein that binds and caps the pointed ends of actin filaments in erythroid and nonerythoid cell types. Targeted deletion of mouse tropomodulin3 (Tmod3) leads to embryonic lethality at E14.5-E18.5, with anemia due to defects in definitive erythropoiesis in the fetal liver. Erythroid burst-forming unit and colony-forming unit numbers are greatly reduced, indicating defects in progenitor populations. Flow cytometry of fetal liver erythroblasts shows that late-stage populations are also decreased, including reduced percentages of enucleated cells. Annexin V staining indicates increased apoptosis of Tmod3(-/-) erythroblasts, and cell-cycle analysis reveals that there are more Ter119(hi) cells in S-phase in Tmod3(-/-) embryos. Notably, enucleating Tmod3(-/-) erythroblasts are still in the process of proliferation, suggesting impaired cell-cycle exit during terminal differentiation. Tmod3(-/-) late erythroblasts often exhibit multilobular nuclear morphologies and aberrant F-actin assembly during enucleation. Furthermore, native erythroblastic island formation was impaired in Tmod3(-/-) fetal livers, with Tmod3 required in both erythroblasts and macrophages. In conclusion, disruption of Tmod3 leads to impaired definitive erythropoiesis due to reduced progenitors, impaired erythroblastic island formation, and defective erythroblast cell-cycle progression and enucleation. Tmod3-mediated actin remodeling may be required for erythroblast-macrophage adhesion, coordination of cell cycle with differentiation, and F-actin assembly and remodeling during erythroblast enucleation.

The transcriptional repressor BLIMP1 curbs host defenses by suppressing expression of the chemokine CCL8.

The transcriptional repressor B lymphocyte-induced maturation protein 1 (BLIMP1) is a master regulator of B and T cell differentiation. To examine the role of BLIMP1 in innate immunity, we used a conditional knockout (CKO) of Blimp1 in myeloid cells and found that Blimp1 CKO mice were protected from lethal infection induced by Listeria monocytogenes. Transcriptome analysis of Blimp1 CKO macrophages identified the murine chemokine (C-C motif) ligand 8, CCL8, as a direct target of Blimp1-mediated transcriptional repression in these cells. BLIMP1-deficient macrophages expressed elevated levels of Ccl8, and consequently Blimp1 CKO mice had higher levels of circulating CCL8, resulting in increased neutrophils in the peripheral blood, promoting a more aggressive antibacterial response. Mice lacking the Ccl8 gene were more susceptible to L. monocytogenes infection than were wild-type mice. Although CCL8 failed to recruit neutrophils directly, it was chemotactic for γ/δ T cells, and CCL8-responsive γ/δ T cells were enriched for IL-17F. Finally, CCL8-mediated enhanced clearance of L. monocytogenes was dependent on γ/δ T cells. Collectively, these data reveal an important role for BLIMP1 in modulating host defenses by suppressing expression of the chemokine CCL8.

Understanding Lay Assessments of Alcohol Use Disorder: Need for Treatment and Associated Stigma.

AIMS: Three-quarters of people with an alcohol use disorder in the USA never receive treatment. Our understandings of who receives care are informed by sociological perspectives, theories and models, each of which discuss the role of lay people's understanding of illness. However, comparatively little work has been done to unpack the cognitive processes underlying lay assessment. In the context of the Framework Integrating Normative Influences on Stigma (FINIS), we aim to understand key factors guiding lay people's stigmatizing attitudes, perceptions and assessments of alcohol use disorder behaviors. METHODS: Lay people read a vignette depicting a male or female adult with a diagnosable alcohol use disorder, along with either a causal life-event explanation for the alcohol use disorder behaviors or no explanation. They then made judgments of the need for treatment, psychological abnormality and the stigma they felt toward the person depicted. RESULTS: Causal life-event explanations decreased lay judgments of the need for treatment, psychological abnormality and stigma. CONCLUSIONS: The results suggest that the availability of a causal life-event explanation may have a complex effect on lay judgments, decreasing the likelihood of recommending treatment for alcohol use disorders, yet simultaneously reducing stigmatizing perceptions (and presumably social distance).

An administrative claims measure of payments made for Medicare patients for a 30-day episode of care for acute myocardial infarction.

BACKGROUND: Understanding both cost and quality across institutions is a critical first step to illuminating the value of care purchased by Medicare. Under contract with the Centers for Medicare and Medicaid Services, we developed a method for profiling hospitals by 30-day episode-of-care costs (payments for Medicare beneficiaries) for acute myocardial infarction (AMI). METHODS: We developed a hierarchical generalized linear regression model to calculate hospital risk-standardized payment (RSP) for a 30-day episode for AMI. Using 2008 Medicare claims, we identified hospitalizations for patients 65 years of age or older with a discharge diagnosis of ICD-9 codes 410.xx. We defined an AMI episode as the date of admission plus 30 days. To reflect clinical care, we omitted or averaged payment adjustments for geographic factors and policy initiatives. We risk-adjusted for clinical variables identified in the 12 months preceding and including the AMI hospitalization. Using combined 2008-2009 data, we assessed measure reliability using an intraclass correlation coefficient and calculated the final RSP. RESULTS: The final model included 30 variables and resulted in predictive ratios (average predicted payment/average total payment) close to 1. The intraclass correlation coefficient score was 0.79. Across 2382 hospitals with ≥ 25 hospitalizations, the unadjusted mean payment was $20,324 ranging from $11,089 to $41,897. The mean RSP was $21,125 ranging from $13,909 to $28,979. CONCLUSIONS: This study introduces a claims-based measure of RSP for an AMI 30-day episode of care. The RSP varies among hospitals, with a 2-fold range in payments. When combined with quality measures, this payment measure will help profile high-value care.