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Background: Point of care ultrasound (POCUS) education has grown significantly over the past two decades. Like most curricular items, POCUS education is siloed within individual graduate medical education (GME) programs. The purpose of this study was to evaluate the effectiveness of a shared GME POCUS curriculum between five GME programs at a single institution., Methods: Post-graduate-year-1 (PGY-1) residents from emergency medicine (EM), family medicine (FM), internal medicine (IM), combined internal medicine-pediatrics (IM-Peds) and combined emergency medicine-pediatrics (EM-Peds) residency programs were enrolled in a core POCUS curriculum. The curriculum included eleven asynchronous online learning modules and ten hands-on training sessions proctored by sonographers and faculty physicians with POCUS expertise. Data was gathered about the curriculum's effectiveness including participation, pre- and post-curricular surveys, pre- and post-knowledge assessments, and an objective skills assessment., Results: Of the 85 residents enrolled, 61 (72%) participated in the curriculum. Engagement varied between programs, with attendance at hands-on sessions varying the most (EM 100%, EM-Peds 100%, FM 40%, IM 22%, Med-Peds 11%). Pre- and post-knowledge assessment scores improved for all components of the curriculum. Participants felt significantly more confident with image acquisition, anatomy recognition, interpreting images and incorporating POCUS findings into clinical practice (p < 0.001) after completing the curriculum., Conclusion: In this shared GME POCUS curriculum, we found significant improvement in POCUS knowledge, attitudes, and psychomotor skills. This shared approach may be a viable way for other institutions to provide POCUS education broadly to their GME programs., (© 2024. The Author(s).)

A comprehensive field- and temperature-dependent examination of nuclear magnetic resonance paramagnetic relaxation enhancements (PREs) for the constitutive protons of [Co(Tpm) 2 ][BF 4 ] 2 is presented. Data for an apically substituted derivative clearly establish that bis-Tpm complexes of Co(II) undergo Jahn-Teller dynamics about the molecular threefold axis. PREs from the parent Tpm complex were used to numerically extract the electron relaxation times ( T 1e ). The Tpm complex showed field-dependent behavior, with an approximately 40% higher activation barrier than the related trispyrazolylborate (Tp) complex, based on fits to the T 1e vs T , B 0 data. Analysis of the field-dependent line widths revealed a surprisingly large contribution from susceptibility (Curie) relaxation (20-35% at the highest field), and a molecular radius (9.5 Å) that is consistent with a tightly associated counterion slowing rotation in solution. Density functional theory showed a shared vibration that is consistent with the Jahn-Teller and appears proportionately higher in energy in [Co(Tpm) 2 ] 2+ . Complete active-space self-consistent field calculations support ascribing electron relaxation to enhanced mixing of the two E g orbital sets that accompanies the tetragonal distortion and the differences in electron correlation times to the higher Jahn-Teller activation barrier in [Co(Tpm) 2 ] 2+ .

Objectives: Detecting reduced left ventricular ejection fraction (LVEF) by an emergency physician (EP) is an important skill. The subjective ultrasound assessment of LVEF by EPs correlates with comprehensive echocardiogram (CE) results. Mitral annular plane systolic excursion (MAPSE) is an ultrasound measure of vertical movement of the mitral annulus, which correlates to LVEF in the cardiology literature, but has not been studied when measured by an EP. Our objective is to determine whether EP measured MAPSE can accurately predict LVEF <50% on CE., Methods: This is a prospective observational single center study using a convenience sample to evaluate the use of a focused cardiac ultrasound (FOCUS) for patients with possible decompensated heart failure. The FOCUS included standard cardiac views to estimate LVEF, MAPSE, and E-point septal separation (EPSS). Abnormal MAPSE was defined as <8 mm and abnormal EPSS as >10 mm. The primary outcome assessed was the ability of an abnormal MAPSE to predict an LVEF <50% on CE. MAPSE also was compared to EP estimated LVEF and EPSS. Inter-rater reliability was determined by two investigators performing independent blinded review., Results: We enrolled 61 subjects, 24 (39%) had an LVEF <50% on a CE. MAPSE <8 mm had a 42% sensitivity (95% CI 22-63), 89% specificity (95% CI 75-97), and accuracy of 71% for detecting LVEF <50%. MAPSE demonstrated lower sensitivity than EPSS (79% sensitivity [95% CI 58-93], and 76% specificity [95% CI 59-88]) and higher specificity than estimated LVEF (100% sensitivity [95% CI 86-100], 59% specificity [95% CI 42-75]). PPV and NPV for MAPSE was 71% (95% CI 47-88) and 70% (95% CI 62-77) respectively. The ROC for MAPSE <8 mm is 0.79 (95% CI 0.68-0.9). MAPSE measurement interrater reliability was 96%., Conclusions: In this exploratory study evaluating MAPSE measurements by EPs, we found the measurement was easy to perform with excellent agreement across users with minimal training. A MAPSE value <8 mm had moderate predictive value for LVEF <50% on CE and was more specific for reduced LVEF than qualitative assessment. MAPSE had high specificity for LVEF <50%. Further studies are needed to validate these results on a larger scale., Competing Interests: Declaration of Competing Interest We confirm that the authors have no conflicts of interest to disclose., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Patients with end stage renal disease (ESRD) suffer high mortality from arrhythmias linked to fibrosis, but are contraindicated to late gadolinium enhancement magnetic resonance imaging (MRI). We present a quantitative method for gadolinium-free cardiac fibrosis imaging using magnetization transfer (MT) weighted MRI, and probe correlations with widely used surrogate markers including cardiac structure and contractile function in patients with ESRD. In a sub-group of patients who returned for follow-up imaging after one year, we examine the correlation between changes in fibrosis and ventricular structure/function. Quantification of changes in MT revealed significantly greater fibrotic burden in patients with ESRD compared to a healthy age matched control cohort. Ventricular mechanics, including circumferential strain and diastolic strain rate were unchanged in patients with ESRD. No correlation was observed between fibrotic burden and concomitant measures of either circumferential or longitudinal strains or strain rates. However, among patients who returned for follow up examination a strong correlation existed between initial fibrotic burden and subsequent loss of contractile function. Gadolinium-free myocardial fibrosis imaging in patients with ESRD revealed a complex and longitudinal, not contemporary, association between fibrosis and ventricular contractile function.

Paramagnetic resonance studies (EPR, ESEEM, ENDOR, and NMR) of a series of cobalt(II) bis-trispyrazolylmethane tetrafluoroborates are presented. The complexes studied include the parent, unsubstituted ligand (Tpm), two pyrazole-substituted derivatives (4Me and 3,5-diMe), and tris(1-pyrazolyl)ethane (Tpe), which includes a methyl group on the apical carbon atom. NMR and ENDOR establish the magnitude of 1 H hyperfine couplings, while ESEEM provides information on the coordinated 14 N. The data show that the pyrazole 3-position is more electron rich in the Tpm analogues, that the geometry about the apical atom influences the magnetic resonance, and that apical atom geometry appears more fixed in Tpm than in Tp. NMR and ENDOR establish that the BF 4 - counterion remains associated in fluid solution. In the case of the Tpm 3,5Me complex, it appears to associate in solution, in the same position it occupies in the X-ray structure.

For a long time, the study of heart failure focused on single heart chamber disease. There is, instead, growing attention on the interplay between the atria and the ventricles during the cardiac cycle and on the consequences of an altered chamber coupling on global heart performance and heart failure. This review aimed to explore the principles of atrioventricular (AV) function and coupling of the left heart and the consequences that their disruption could have in several diseases. Furthermore, we will examine echocardiographic tips for analyzing the chamber function and the AV coupling. Finally, we will explore the most recent pharmacological acquisitions and the device therapies we have for use. [ABSTRACT FROM AUTHOR]

Although angiotensin converting enzyme (ACE) inhibitors are considered useful for the treatment of human heart failure, some experimental failing-heart models have shown little beneficial effect of ACE inhibitors in animals with poor oral health, particularly periodontitis. In this study, we examined the effects of the ACE inhibitor captopril (Cap; 0.1 mg/mL in drinking water) on cardiac dysfunction in mice treated with Porphyromonas gingivalis lipopolysaccharide (PG-LPS) at a dose (0.8 mg/kg/day) equivalent to the circulating level in patients with periodontal disease. Mice were divided into four groups: 1) Control, 2) PG-LPS, 3) Cap, and 4) PG-LPS + Cap. After1 week, we evaluated cardiac function by echocardiography. The left ventricular ejection fraction was significantly decreased in PG-LPS-treated mice compared to the control (from 66 ± 1.8 to 59 ± 2.5%), while Cap ameliorated the dysfunction (63 ± 1.1%). The area of cardiac fibrosis was significantly increased (approximately 2.9-fold) and the number of apoptotic myocytes was significantly increased (approximately 5.6-fold) in the heart of PG-LPS-treated group versus the control, and these changes were suppressed by Cap. The impairment of cardiac function in PG-LPS-treated mice was associated with protein kinase C δ phosphorylation (Tyr-311), leading to upregulation of NADPH oxidase 4 and xanthine oxidase, and calmodulin kinase II phosphorylation (Thr-286) with increased phospholamban phosphorylation (Thr-17). These changes were also suppressed by Cap. Our results suggest that the renin-angiotensin system might play an important role in the development of cardiac diseases induced by PG-LPS. [ABSTRACT FROM AUTHOR]

We recently reported a positive relationship between occlusal disharmony and cardiovascular disease via activation of β-adrenergic signaling in mice. Furthermore, inhibition of type 5 adenylyl cyclase (AC5), a major cardiac subtype in adults, protects the heart against oxidative stress. Here, we examined the role of AC5 in the development of occlusal-disharmony-induced cardiovascular disease in bite-opening (BO) mice, prepared by cementing a suitable appliance onto the mandibular incisor. We first examined the effects of BO treatment on cardiac function in mice treated or not treated for 2 weeks with vidarabine, which we previously identified as an inhibitor of cardiac AC. Cardiac function was significantly decreased in the BO group compared to the control group, but vidarabine ameliorated the dysfunction. Cardiac fibrosis, myocyte apoptosis and myocyte oxidative DNA damage were significantly increased in the BO group, but vidarabine blocked these changes. The BO-induced cardiac dysfunction was associated with increased phospholamban phosphorylation at threonine-17 and serine-16, as well as increased activation of the Ca2+-calmodulin-dependent protein kinase II/receptor-interacting protein 3 signaling pathway. These data suggest that AC5 inhibition with vidarabine might be a new therapeutic approach for the treatment of cardiovascular disease associated with occlusal disharmony. [ABSTRACT FROM AUTHOR]

Oral infections, particularly periodontitis, are a well-established risk factor for cardiovascular diseases, although the molecular mechanisms involved remain elusive. The aims of the present study were to investigate the effects of lipopolysaccharide derived from Porphyromonas gingivalis (PG-LPS) on cardiac function in mice, and to elucidate the underlying mechanisms. Mice (C57BL/6) were injected with PG-LPS (0.8 mg/kg/day) with or without an inhibitor of Toll-like receptor 4 (TLR4) signaling (TAK-242, 0.8 mg/kg/day) for 4 weeks. Left ventricular ejection function was significantly decreased at 1 week (from 67 ± 0.5 to 58 ± 1.2%) and remained low at 4 weeks (57 ± 1.0%). The number of apoptotic myocytes was increased (approximately 7.4-fold), the area of fibrosis was increased (approximately 3.3-fold) and the number of 8-hydroxydeoxyguanosine-positive myocytes, a sensitive indicator of oxidative DNA damage, was increased (approximately 7.6-fold) at 4 weeks in the heart of PG-LPS treated mice. However, levels of various serum pro-inflammatory cytokines in PG-LPS-treated mice were similar to those in control mice. The impairment of cardiac function in PG-LPS-treated mice appears to involve activation of TLR4-NADPH oxidase (NOX) 4 signaling, leading to abundant production of reactive oxygen species and Ca2+ leakage from sarcoplastic reticulumn induced by calmodulin kinase II (CaMKII)-mediated phosphorylation of phospholamban (at Thr-17) and ryanodine receptor 2 (at Ser-2448). Pharmacological inhibition of TLR4 with TAK-242 attenuated the changes in cardiac function in PG-LPS-treated mice. Our results indicate that TLR4-NOX4 signaling may be a new therapeutic target for treatment of cardiovascular diseases in patients with periodontitis. [ABSTRACT FROM AUTHOR]

Purpose of the Review: Cardiorenal syndrome (CRS), defined as concomitant heart and kidney disease, has been a focus of attention for nearly a decade. As more patients survive severe acute and chronic heart and kidney diseases, CRS has emerged as an "epidemic" of modern medicine. Significant advances have been made in unraveling the complex mechanisms that underlie CRS based on classification of the condition into five pathophysiologic subtypes. In types 1 and 2, acute or chronic heart disease results in renal dysfunction, while in types 3 and 4, acute or chronic kidney diseases are the inciting factors for heart disease. Type 5 CRS is defined as concomitant heart and kidney dysfunction as part of a systemic condition such as sepsis or autoimmune disease. Recent Findings: There are ongoing efforts to better define subtypes of CRS based on historical information, clinical manifestations, laboratory data (including biomarkers), and imaging characteristics. Systematic evaluation of CRS by advanced cardiac imaging, however, has been limited in scope and mostly focused on type 4 CRS. This is in part related to lack of clinical trials applying advanced cardiac imaging in the acute setting and exclusion of patients with significant renal disease from studies of such techniques in chronic HF. Summary: Advanced cardiac nuclear imaging is well poised for assessment of the pathophysiology of CRS by offering a myriad of molecular probes without the need for nephrotoxic contrast agents. In this review, we examine the current or potential future application of advanced cardiac imaging to evaluation of myocardial perfusion, metabolism, and innervation in patients with CRS. [ABSTRACT FROM AUTHOR]

In skeletal muscle, the major isoform of β-adrenergic receptor (β-AR) is β2-AR and the minor isoform is β1-AR, which is opposite to the situation in cardiac muscle. Despite extensive studies in cardiac muscle, the physiological roles of the β-AR subtypes in skeletal muscle are not fully understood. Therefore, in this work, we compared the effects of chronic β1- or β2-AR activation with a specific β1-AR agonist, dobutamine (DOB), or a specific β2-AR agonist, clenbuterol (CB), on masseter and cardiac muscles in mice. In cardiac muscle, chronic β1-AR stimulation induced cardiac hypertrophy, fibrosis and myocyte apoptosis, whereas chronic β2-AR stimulation induced cardiac hypertrophy without histological abnormalities. In masseter muscle, however, chronic β1-AR stimulation did not induce muscle hypertrophy, but did induce fibrosis and apoptosis concomitantly with increased levels of p44/42 MAPK (ERK1/2) (Thr-202/Tyr-204), calmodulin kinase II (Thr-286) and mammalian target of rapamycin (mTOR) (Ser-2481) phosphorylation. On the other hand, chronic β2-AR stimulation in masseter muscle induced muscle hypertrophy without histological abnormalities, as in the case of cardiac muscle, concomitantly with phosphorylation of Akt (Ser-473) and mTOR (Ser-2448) and increased expression of microtubule-associated protein light chain 3-II, an autophagosome marker. These results suggest that the β1-AR pathway is deleterious and the β2-AR is protective in masseter muscle. These data should be helpful in developing pharmacological approaches for the treatment of skeletal muscle wasting and weakness. [ABSTRACT FROM AUTHOR]

Numerous studies have reported that the long non-coding RNA (lncRNA) small nucleolar RNA host gene 6 (SNHG6; ENSG00000245910) participates in the development of malignant tumors. However, the underlying mechanism of SNHG6 in the development of melanoma remains unknown. Thus, the present study aimed to investigate the biological role of SNHG6 in the progression of melanoma. SNHG6 expression in melanoma tissues and cells was assessed using a bioinformatics approach and reverse transcription-quantitative PCR analysis. Cell viability was determined using the Cell Counting Kit-8 and colony formation assays. The correlation between microRNA (miR)-101-3p, SNHG6 and RAP2B expression levels was assessed using Pearson's correlation analysis. Bioinformatic analysis and luciferase reporter assay were utilized to confirm the interaction between miR-101-3p and SNHG6 or RAP2B. The Transwell assay was conducted to examine the migratory and invasive activities of melanoma cells. In the present study, SNHG6 expression was upregulated in melanoma tissues and cell lines, and SNHG6 silencing suppressed melanoma cell viability, migration and invasion. SNHG6 was directly bound to miR-101-3p, which interacted with RAP2B. In addition, miR-101-3p expression was negatively correlated with SNHG6 or RAP2B expression. miR-101-3p silencing partially abrogated the suppressive effect of SNHG6-knockdown on RAP2B expression. Moreover, the data demonstrated that RAP2B overexpression reversed the inhibitory effects on melanoma cell proliferation, migration and invasion induced by SNHG6 silencing. In conclusion, the present study identified that SNHG6 accelerated melanoma progression via regulating the miR-101-3p/RAP2B axis. Thus, the SNHG6/miR-101-3p/RAP2B signaling pathway may be a novel therapeutic target for melanoma. [ABSTRACT FROM AUTHOR]