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Objective: Certain modifiable risk factors lead to higher health care costs and reduced worker productivity. A predictive return-on-investment (ROI) model was applied to an obesity management intervention to demonstrate the use of econometric modeling in establishing financial justification for worksite health promotion. Methods: Self-reported risk factors (n = 890) were analyzed using chi square and t test methods. Changes in risk factors, demographics, and financial measures comprised the model inputs that determined medical and productivity savings. Results: Over 1 year, 7 of 10 health risks decreased. Of total projected savings ($311,755), 59% were attributed to reduced health care expenditures ($184,582) and 41% resulted from productivity improvements ($127,173), a $1.17 to $1.00 ROI. Conclusions: Using an ROI model to project program savings is a practical way to provide financial justification for investment in worksite health promotion when risk reduction data are available. [ABSTRACT FROM AUTHOR]

The beneficial effects of blood transfusions have been described and widely accepted. Multiple factors, including shortages, costs, infectious risks, immunologic risks, and the risk/benefit ratio to the patient, have made the medical community reassess the guidelines for transfusion. Cardiac surgery presents a unique subset of patients, because intervention at multiple stages in the care of these patients is possible to decrease the need for transfusion. An algorithm for a cardiac surgery program was developed and a reassessment performed. Once it was seen that no detrimental effect on patient care occurred, the program was expanded, was enhanced, and subsequently has been offered to the rest of the health care system. This program has resulted in a decrease in cost while maintaining patient outcomes. The success of the program is believed to be a result of the multidisciplinary approach taken, with a commitment from all members of the blood reduction team being the key component of this success. [ABSTRACT FROM AUTHOR]

Objectives: One in 20 outpatients in the United States experiences a diagnostic error each year, but there are no validated methods for collecting feedback from patients on diagnostic safety. We examined patient experience surveys to determine whether patients' free text comments indicated diagnostic breakdowns. Our objective was to evaluate associations between patient-perceived diagnostic breakdowns reported in free text comments and patients' responses to structured survey questions., Methods: We conducted an exploratory mixed methods study using data from patient experience surveys collected from adult ambulatory care patients March 2020 to June 2020 in a large U.S. health system. Data analysis included content analysis of qualitative data and statistical analysis of quantitative data., Results: In 2525 surveys with negative comments, 619 patients (24.5%) identified diagnostic breakdowns, including issues with accuracy (n = 282, 46%), timeliness (n = 243, 39%), or communication (n = 290, 47%); some patients (n = 181) reported breakdowns in multiple categories. Patients who gave a low average score (50 or less on a 100-point scale) on provider questions were almost seven times more likely to perceive a diagnostic breakdown than patients who scored their provider higher. Similarly, patients who gave a low average score on practice-related questions were twice as likely to perceive a diagnostic breakdown., Conclusions: Patient feedback in routinely collected patient experience surveys is a valuable and actionable information source on diagnostic breakdowns in the ambulatory setting. The more easily monitored structured survey data provide a screening method to identify encounters that may have included a patient-perceived diagnostic breakdown and therefore require further examination., Competing Interests: The authors disclose no conflict of interest., (Copyright © 2024 The Author(s). Published by Wolters Kluwer Health, Inc.)

Background: Diagnostic errors are a global patient safety challenge. Over 75% of diagnostic errors in ambulatory care result from breakdowns in patient-clinician communication. Encouraging patients to speak up and ask questions has been recommended as one strategy to mitigate these failures., Objectives: The goal of the scoping review was to identify, summarize, and thematically map questions patients are recommended to ask during ambulatory encounters along the diagnostic process. This is the first step in a larger study to co-design a patient-facing question prompt list for patients to use throughout the diagnostic process., Methods: Medline and Google Scholar were searched to identify question lists in the peer-reviewed literature. Organizational websites and a search engine were searched to identify question lists in the gray literature. Articles and resources were screened for eligibility and data were abstracted. Interrater reliability (K = 0.875) was achieved., Results: A total of 5509 questions from 235 resources met inclusion criteria. Most questions (n = 4243, 77.02%) were found in the gray literature. Question lists included an average of 23.44 questions. Questions were most commonly coded along the diagnostic process categories of treatment (2434 questions from 250 resources), communication of the diagnosis (1160 questions, 204 resources), and outcomes (766 questions, 172 resources)., Conclusions: Despite recommendations for patients to ask questions, most question prompt lists focus on later stages of the diagnostic process such as communication of the diagnosis, treatment, and outcomes. Further research is needed to identify and prioritize diagnostic-related questions from the patient perspective and to develop simple, usable guidance on question-asking to improve patient safety across the diagnostic continuum., Competing Interests: The authors disclose no conflict of interest., (Copyright © 2024 The Author(s). Published by Wolters Kluwer Health, Inc.)

Imerslund-Gräsbeck syndrome is an autosomal recessive disorder of vitamin B12 malabsorption presenting with megaloblastic anemia and mild proteinuria in childhood. The disorder is caused by biallelic pathogenic variants in the CUBN or AMN genes, which encode proteins involved in B12 absorption. We present the case of a 17-month-old boy with failure to thrive, pancytopenia, and fevers. His megaloblastic anemia was overlooked leading to unnecessary invasive testing. Findings on bone marrow biopsy prompted investigation for genetic disorders of B12 metabolism. Exome sequencing uncovered 1 known pathogenic variant and 1 novel likely pathogenic variant in CUBN, confirming the diagnosis of Imerslund-Gräsbeck syndrome., (Copyright © 2021 Wolters Kluwer Health, Inc. All rights reserved.)

Background/purpose: To characterize the nature of posterior segment ocular injuries in combat trauma., Methods: Eyes in the Walter Reed Ocular Trauma Database were evaluated for the presence of posterior segment injury. Final visual outcomes in open-globe versus closed-globe injuries and by zone of injury and the types of posterior segment injuries in open-globe versus closed-globe injuries were assessed., Results: Four hundred fifty-two of 890 eyes (50.8%) had at least one posterior segment injury. The mechanism of injury was most commonly an improvised explosive device in 280 (62.0%) eyes. Sixty-one patients (13.5%) had a Zone I injury, 50 (11.1%) a Zone II injury, and 341 (75.4%) a Zone III injury. Patients with Zone I injuries were more likely to have a final visual acuity of 20/200 or better compared with patients with either a Zone II (P < 0.001) or Zone III injury (P = 0.007). Eyes with a closed-globe injury were more likely to have a final visual acuity of 20/200 or better compared with those with an open-globe injury (P < 0.001). Furthermore, closed-globe injury compared with open-globe injury had a lower risk of vitreous hemorrhage (odds ratio 0.32, P < 0.001), proliferative vitreoretinopathy (odds ratio 0.14, P < 0.001), and retinal detachment (odds ratio 0.18, P < 0.001) but a higher risk of chorioretinal rupture (odds ratio 2.82, P < 0.001) and macular hole (odds ratio 3.46, P = 0.004)., Conclusion: Patients with combat ophthalmic trauma had similar posterior segment injury patterns to civilian trauma in open-globe versus closed-globe injuries. Zone II and III injuries were associated with a worse visual prognosis.

Background: Methods to deliver diabetes education are needed to support patient safety and glycemic control in the transition from hospital to home., Purpose: This study examined barriers and facilitators of integrating web-based, iPad-delivered diabetes survival skills education (DSSE) into the nursing inpatient unit workflow., Methods: Nurses, nurse managers, and patient care technicians (PCTs) from 3 medical-surgical and 2 behavioral health units participated in semistructured interviews and focus groups., Results: Four themes emerged: educational program and content; platform usability; tablet feasibility (eg, theft prevention, infection control, and charging); and workflow considerations. Behavioral health unit-specific concerns were also identified. Findings indicated that nurses and PCTs were eager to find approaches to deliver DSSE., Conclusions: Implementation of a web-based DSSE program for inpatients needs adaptation to overcome challenges at the patient, care team, and process levels.

Unlabelled: The innate immune response is generally considered to have an important role in tissue remodeling after resistance exercise., Purpose: The purpose of this study was to compare changes in markers of monocyte recruitment after an acute bout of high-intensity (HVY) versus high-volume (VOL) lower-body resistance exercise., Methods: Ten resistance-trained men (24.7 ± 3.4 yr, 90.1 ± 11.3 kg, 176.0 ± 4.9 cm) performed each protocol in a randomized, counterbalanced order. Blood samples were collected at baseline, immediately (IP), 30 min (30P), 1 h (1H), 2 h (2H), and 5 h (5H) postexercise. Plasma concentrations of monocyte chemoattractant protein 1 (MCP-1), tumor necrosis factor alpha (TNF-α), myoglobin, and cortisol were measured via assay. Tumor necrosis factor receptor 1 (TNFr1), macrophage-1 antigen (cluster of differentiation 11b [CD11b]), and C-C chemokine receptor 2 (CCR2) expression levels were measured using flow cytometry. TNFr1 and CD11b were assessed on CD14CD16 monocytes, whereas CCR2 was assessed on CD14 monocytes., Results: Plasma myoglobin concentrations were significantly greater after HVY compared with VOL (P < 0.001). Changes in plasma TNF-α, MCP-1, and expression levels of CCR2 and CD11b were similar between HVY and VOL. When collapsed across groups, TNF-α was significantly increased at IP, 30P, 1H, and 2H (P values < 0.05), whereas MCP-1 was significantly elevated at all postexercise time points (P values < 0.05). CCR2 expression on CD14 monocytes was significantly lower at IP, 1H, 2H, and 5H (P values < 0.05). CD11b expression on CD14 CD16 was significantly greater at IP (P < 0.014) and 1H (P = 0.009). TNFr1 expression did not differ from baseline at any time point. Plasma cortisol concentrations did not seem to be related to receptor expression., Conclusions: Results indicate that both HVY and VOL protocols stimulate a robust proinflammatory response. However, no differences were noted between resistance exercise training paradigms.

Background: Heart failure (HF) with preserved ejection fraction (HFpEF) accounts for ≈50% of all cases of HF and currently has no effective treatment. Diastolic dysfunction underlies HFpEF; therefore, elucidation of the mechanisms that mediate relaxation can provide new potential targets for treatment. Cardiac myosin-binding protein-C (cMyBP-C) is a thick filament protein that modulates cross-bridge cycling rates via alterations in its phosphorylation status. Thus, we hypothesize that phosphorylated cMyBP-C accelerates the rate of cross-bridge detachment, thereby enhancing relaxation to mediate diastolic function., Methods and Results: We compared mouse models expressing phosphorylation-deficient cMyBP-C(S273A/S282A/S302A)-cMyBP-C(t3SA), phosphomimetic cMyBP-C(S273D/S282D/S302D)-cMyBP-C(t3SD), and wild-type-control cMyBP-C(tWT) to elucidate the functional effects of cMyBP-C phosphorylation. Decreased voluntary running distances, increased lung/body weight ratios, and increased brain natriuretic peptide levels in cMyBP-C(t3SA) mice demonstrate that phosphorylation deficiency is associated with signs of HF. Echocardiography (ejection fraction and myocardial relaxation velocity) and pressure/volume measurements (-dP/dtmin, pressure decay time constant τ-Glantz, and passive filling stiffness) show that cMyBP-C phosphorylation enhances myocardial relaxation in cMyBP-C(t3SD) mice, whereas deficient cMyBP-C phosphorylation causes diastolic dysfunction with HFpEF in cMyBP-C(t3SA) mice. Simultaneous force and [Ca(2+)]i measurements on intact papillary muscles show that enhancement of relaxation in cMyBP-C(t3SD) mice and impairment of relaxation in cMyBP-C(t3SA) mice are not because of altered [Ca(2+)]i handling, implicating that altered cross-bridge detachment rates mediate these changes in relaxation rates., Conclusions: cMyBP-C phosphorylation enhances relaxation, whereas deficient phosphorylation causes diastolic dysfunction and phenotypes resembling HFpEF. Thus, cMyBP-C is a potential target for treatment of HFpEF., (© 2015 American Heart Association, Inc.)

Background: Heart failure is a leading cause of morbidity and mortality in the USA and is closely associated with diabetes mellitus. The molecular link between diabetes mellitus and heart failure is incompletely understood. We recently demonstrated that insulin receptor substrates 1, 2 (IRS1, 2) are key components of insulin signaling and loss of IRS1 and IRS2 mediates insulin resistance, resulting in metabolic dysregulation and heart failure, which is associated with downstream Akt inactivation and in turn activation of the forkhead transcription factor Foxo1., Methods and Results: To determine the role of Foxo1 in control of heart failure in insulin resistance and diabetes mellitus, we generated mice lacking Foxo1 gene specifically in the heart. Mice lacking both IRS1 and IRS2 in adult hearts exhibited severe heart failure and a remarkable increase in the β-isoform of myosin heavy chain (β-MHC) gene expression, whereas deletion of cardiac Foxo1 gene largely prevented the heart failure and resulted in a decrease in β-MHC expression. The effect of Foxo1 deficiency on rescuing cardiac dysfunction was also observed in db/db mice and high-fat diet mice. Using cultures of primary ventricular cardiomyocytes, we found that Foxo1 interacts with the promoter region of β-MHC and stimulates gene expression, mediating an effect of insulin that suppresses β-MHC expression., Conclusions: Our study suggests that Foxo1 has important roles in promoting diabetic cardiomyopathy and controls β-MHC expression in the development of cardiac dysfunction. Targeting Foxo1 and its regulation will provide novel strategies in preventing metabolic and myocardial dysfunction and influencing MHC plasticity in diabetes mellitus., (© 2014 American Heart Association, Inc.)

Objective: To develop a checklist for use during pediatric trauma resuscitation and test its effectiveness during simulated resuscitations., Background: Checklists have been used to support a wide range of complex medical activities and have effectively reduced errors and improved outcomes in different medical settings. Checklists have not been evaluated in the domain of trauma resuscitation., Methods: A focus group of trauma specialists was organized to develop a checklist for pediatric trauma resuscitation. This checklist was then tested in simulated trauma resuscitations to evaluate its impact on team performance. Resuscitations conducted with and without the checklist were compared using the Advanced Trauma Life Support (ATLS) performance score, designed to measure adherence to ATLS protocol, and surveys of team members' subjective workload., Results: The focus group generated a checklist with 56 items divided into 5 sections corresponding to different phases of trauma resuscitation. In simulation testing, the total ATLS performance score was 4.9 points higher with a checklist than without (P < 0.001), with most of this difference related to improvement in performance of the secondary survey (+3.3 points, P < 0.001). Overall, workload scores were not affected by the addition of the checklist., Conclusions: Implementing a checklist during simulated pediatric trauma resuscitation improves adherence to the ATLS protocol without increasing the workload of trauma team members.

Objective: To examine first-year results from a workplace environmental obesity prevention program at The Dow Chemical Company., Methods: A quasi-experimental cohort study was conducted among employees at nine treatment worksites (n = 8013) who received environmental weight management interventions and three control worksites (n = 2269). Changes in employees' weight, body mass index (BMI), and other health risks were examined using chi2 and t-tests., Results: After 1 year, a modest treatment effect was observed for weight and BMI largely because the control group subjects gained weight; however, no effect was observed for overweight and obesity prevalence. Other risk factors (tobacco use, high blood pressure, and systolic and diastolic blood pressure values) decreased significantly, although blood glucose (high risk prevalence and values) increased., Conclusions: Environmental changes to the workplace can achieve modest improvements in employees' health risks, including weight and BMI measures, in 1 year.

Angiotensin II, the effector peptide of the renin-angiotensin system, regulates cellular growth in response to developmental, physiological, and pathological processes. The identification of renin-angiotensin system components and angiotensin II receptors in cardiac tissue suggests the existence of an autocrine/paracrine system that has effects independent of angiotensin II derived from the circulatory system. To be functional, a local renin-angiotensin system should produce sufficient amounts of the autocrine and/or paracrine factor to elicit biological responses, contain the final effector (angiotensin II receptor), and respond to humoral, neural, and/or mechanical stimuli. In this review, we discuss evidence for a functional cardiac renin-angiotensin system.

Case studies are presented on three organizational models for immunization registries in local communities: agency-based, facility-based, and population-based systems. The strengths and limitations of the respective approaches are highlighted. Each model faces three similar challenges: generating "real-time" information on the status of children who fall behind on their immunizations, assuring confidentiality of registrants and medical information, and maintaining operations amidst adverse social conditions that are at the root of underimmunization of children. With sufficient resources and cooperation among many private and public interests, registries have considerable potential to increase vaccination coverage among our population.

Angiotensin II has been reported to be a hormonal stimulus of cardiac growth, a response that may involve myocyte hypertrophy as well as growth of nonmyocytes. This study was designed to determine whether neonatal rat cardiac fibroblasts have an angiotensin II receptor that is coupled with hypertrophic and/or proliferative growth. Competitive radioligand binding studies showed that cardiac fibroblasts have a single class of high-affinity (IC50, 1.0 nM) angiotensin II binding sites (Bmax, 778 fmol/mg protein) that are sensitive to the competitive nonpeptide AT1 receptor antagonist losartan (IC50, 13 nM). Other angiotensin peptides competed for [125I]angiotensin II binding in the following rank order: angiotensin II > angiotensin III > angiotensin I > > [des-Asp1-des-Arg2]angiotensin II. A nonhydrolyzable analogue of guanosine triphosphate increased the dissociation rate of bound [125I]angiotensin II and decreased hormone binding to the receptor at equilibrium. The angiotensin II receptor was coupled with increases in intracellular calcium. Incorporation of precursors into protein, DNA, and RNA in response to angiotensin II was determined. In serum-deprived cultures, a 24-hour exposure to 1 microM [Sar1]angiotensin II increased rates of phenylalanine, thymidine, and uridine incorporation by 58%, 103%, and 118%, respectively. These increases were blocked by the noncompetitive AT1 receptor antagonist EXP3174. After 48 hours, [Sar1]angiotensin II increased total protein and DNA of cardiac fibroblasts by 23% and 15%, respectively, with no change in the protein/DNA ratio. [Sar1]Angiotensin II increased cell number by 138% after a 24-hour exposure, without affecting cell area. In summary, cardiac fibroblasts have G protein-linked AT1 receptors that are coupled with proliferative growth. These results suggest that angiotensin II-induced cardiac hypertrophy is, in part, secondary to stimulated increases in nonmyocyte cellular growth.

The octapeptide, angiotensin II, elicits a positive inotropic response in myocardial tissue by activating slow calcium channels. Pharmacological studies suggest that the inotropic action of angiotensin II is receptor mediated. The current investigation was performed to characterize the binding of 125I-angiotensin II to the putative receptor in a plasma membrane-sarcoplasmic reticulum preparation of the rabbit left ventricle. In experiments performed at 18 degrees C, steady state binding occurred at 45 minutes and saturable binding was 80-85% of the total binding. Analysis of the binding data indicated that the 125I-angiotensin II interacted with a single class of sites with a Kd = 4.5 +/- 0.8 nM and exhibited a binding capacity of 53.5 +/- 8 fmol/mg protein. The potency order for the competitive binding of analogues and antagonists of angiotensin II paralleled that observed for in vitro contractile force development in bioassay systems utilizing left atrial tissue. The binding of 125I-angiotensin II was stimulated 2-fold in the presence of the divalent cations of calcium and magnesium (10 mM). Guanine nucleotides modified the binding of 125I-angiotensin II to the rabbit myocardial particulate fraction. Guanine triphosphate and nonhydrolyzable analogues of guanine triphosphate increased the dissociation rate of the bound 125I-angiotensin II and decreased hormone binding to the receptor at equilibrium. In the absence of magnesium, guanine nucleotides had no effect on the dissociation rate of 125I-angiotensin II. 125I-Angiotensin II binding to a rabbit myocardial particulate fraction was found to have high affinity, to be saturable, reversible, specific, and modulated by guanine nucleotides.(ABSTRACT TRUNCATED AT 250 WORDS)

The antihypertensive effects of captopril and enalapril maleate were studied over a 10-week period in 24 hypertensive patients randomized into captopril or enalapril treatment groups. Prestudy blood pressure was 171 +/- 4/109 +/- 1 mm Hg and after 4 weeks of hydrochlorothiazide 160 +/- 4/103 +/- 1 (p less than 0.05). With the addition of converting enzyme inhibitor to hydrochlorothiazide the blood pressure decreased at 3 h to 132 +/- 3/87 +/- 2 in the subjects. The diastolic blood pressure decreased acutely more with captopril (-24) than with enalapril (-17) (p less than 0.05). After 10 weeks of combined therapy the depressor response was maintained (134 +/- 3/83 +/- 1) and there was no difference between the diastolic blood pressure in the two groups treated with captopril and enalapril. Acute and chronic responses of plasma renin activity, plasma aldosterone, and converting enzyme to the angiotensin-converting enzyme inhibitor were determined. There was a significant correlation between the acute fall in diastolic blood pressure and rise in plasma renin activity in patients treated with captopril but not with enalapril. In conclusion, there is an acute depressor response with converting enzyme inhibition which is more pronounced with captopril than with enalapril and which correlates with an increase in plasma renin activity. With more prolonged treatment, the two drugs show equivalent efficacy in reducing blood pressure, inhibiting angiotensin-converting enzyme, reducing aldosterone, and stimulating plasma renin activity.

Angiotensin II elicits a receptor-mediated positive inotropic response in cardiac tissue from most mammalian species by activating voltage-sensitive slow Ca2+ channels. In the guinea pig, we confirm there is no in vitro contractile force development in bioassay systems using isolated hearts or left atrial tissue in response to angiotensin peptides. However, 125I-angiotensin II binding sites that have the characteristics of a membrane receptor were identified in ventricular (myocardial) and atrial membrane preparations from guinea pigs. In ventricles, saturation-binding data yielded an optimal fit to a two-site model with a high-affinity site Kd1 = 3.6 +/- 0.7 nM and a low-affinity site Kd2 = 433 +/- 126 nM and binding capacities of 66 +/- 10 and 821 +/- 49 fmol/mg protein, respectively. In atria, saturation binding data yielded an optimal fit to a two-site model with a high-affinity site Kd1 = 1.6 nM and a low-affinity site Kd2 = 300 nM and capacities of 145 and 752 fmol/mg protein, respectively. The ventricular binding of 125I-angiotensin II was stimulated approximately twofold in the presence of the divalent cations calcium and magnesium (10 mM). Nonhydrolyzable analogues of guanosine triphosphate increased the dissociation rate of the bound 125I-angiotensin II and decreased hormone binding to the receptor at equilibrium. Competition for 125I-angiotensin II binding by an agonist-antagonist analogue series correlated with previous studies obtained in the rabbit, a mammal in which inotropic responses to angiotensin II were demonstrated. The data indicate the presence of angiotensin II myocardial and atrial receptors and a G-type coupling protein in guinea pig. Although this species lacks an inotropic response to angiotensin peptides, there is a dose-dependent increase in inositol-1-phosphate production in response to angiotensin II, and this response is blocked by the selective angiotensin II antagonist [Sar1,Ile8]angiotensin II.(ABSTRACT TRUNCATED AT 250 WORDS)