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• W4254518056 abstract "HomeCirculation ResearchVol. 127, No. 2Circulation Research “In This Issue” Anthology Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticlePDF/EPUBCirculation Research “In This Issue” Anthology Ruth Williams and The Editors Ruth WilliamsRuth Williams Search for more papers by this author and The Editors Search for more papers by this author Originally published2 Jul 2020https://doi.org/10.1161/RES.0000000000000406Circulation Research. 2020;127:e48–e76is related toA Proinflammatory Gut Microbiota Increases Systemic Inflammation and Accelerates AtherosclerosisPATJ Low Frequency Variants Are Associated With Worse Ischemic Stroke Functional OutcomeATF6 Regulates Cardiac Hypertrophy by Transcriptional Induction of the mTORC1 Activator, RhebThe β-Adrenergic Agonist Albuterol Improves Pulmonary Vascular Reserve in Heart Failure With Preserved Ejection FractionTissue Resident CCR2− and CCR2+ Cardiac Macrophages Differentially Orchestrate Monocyte Recruitment and Fate Specification Following Myocardial InjuryAtrial-Specific Gene Delivery Using an Adeno-Associated Viral VectorWhole Exome Sequencing Reveals the Major Genetic Contributors to Nonsyndromic Tetralogy of FallotOxidative Stress Contributes to Microvascular Endothelial Dysfunction in Men and Women With Major Depressive DisorderAtherosclerotic Conditions Promote the Packaging of Functional MicroRNA-92a-3p Into Endothelial MicrovesiclesNHLBI-Sponsored Randomized Trial of Postconditioning During Primary Percutaneous Coronary Intervention for ST-Elevation Myocardial InfarctionDietary Fats in Relation to Total and Cause-Specific Mortality in a Prospective Cohort of 521 120 Individuals With 16 Years of Follow-UpMolecular Imaging Visualizes Recruitment of Inflammatory Monocytes and Macrophages to the Injured HeartAssociations of Monounsaturated Fatty Acids From Plant and Animal Sources With Total and Cause-Specific Mortality in Two US Prospective Cohort StudiesDNA Damage Response/TP53 Pathway Is Activated and Contributes to the Pathogenesis of Dilated Cardiomyopathy Associated With LMNA (Lamin A/C) MutationsSarcTrackHigh-Risk Human Papillomavirus Infection and the Risk of Cardiovascular Disease in Korean WomenDevelopment of Light-Responsive Liquid Crystalline Elastomers to Assist Cardiac ContractionNut Consumption in Relation to Cardiovascular Disease Incidence and Mortality Among Patients With Diabetes MellitusMitophagy Is Essential for Maintaining Cardiac Function During High Fat Diet-Induced Diabetic CardiomyopathyTEAD1 (TEA Domain Transcription Factor 1) Promotes Smooth Muscle Cell Proliferation Through Upregulating SLC1A5 (Solute Carrier Family 1 Member 5)-Mediated Glutamine Uptakeβ2-Adrenergic Stimulation Compartmentalizes β1 Signaling Into Nanoscale Local Domains by Targeting the C-Terminus of β1-AdrenoceptorsProtective Role of RNA Helicase DEAD-Box Protein 5 in Smooth Muscle Cell Proliferation and Vascular RemodelingEndothelial SIRT6 Is Vital to Prevent Hypertension and Associated Cardiorenal Injury Through Targeting Nkx3.2-GATA5 SignalingNdufs2, a Core Subunit of Mitochondrial Complex I, Is Essential for Acute Oxygen-Sensing and Hypoxic Pulmonary VasoconstrictionCRRL269Propentdyopents as Heme Degradation Intermediates Constrict Mouse Cerebral Arterioles and Are Present in the Cerebrospinal Fluid of Patients With Subarachnoid HemorrhageGut Microbial Associations to Plasma Metabolites Linked to Cardiovascular Phenotypes and RiskRelationship Between Serum Alpha-Tocopherol and Overall and Cause-Specific MortalityMitochondria Are a Subset of Extracellular Vesicles Released by Activated Monocytes and Induce Type I IFN and TNF Responses in Endothelial CellsMacrophage Smad3 Protects the Infarcted Heart, Stimulating Phagocytosis and Regulating InflammationNuclear Focal Adhesion Kinase Controls Vascular Smooth Muscle Cell Proliferation and Neointimal Hyperplasia Through GATA4-Mediated Cyclin D1 TranscriptionImpact of the 2017 ACC/AHA Guideline for High Blood Pressure on Evaluating Gestational Hypertension–Associated Risks for Newborns and MothersG-CSF for Extensive STEMILoss of SRSF3 in Cardiomyocytes Leads to Decapping of Contraction-Related mRNAs and Severe Systolic DysfunctionMetabolic Syndrome Exacerbates Pulmonary Hypertension due to Left Heart DiseaseIdentification of Celastramycin as a Novel Therapeutic Agent for Pulmonary Arterial Hypertension15-Deoxy-Δ12,14-Prostaglandin J2 Reinforces the Anti-Inflammatory Capacity of Endothelial Cells With a Genetically Determined NO DeficitSingle-Cell Transcriptomics Reveals Chemotaxis-Mediated Intraorgan Crosstalk During CardiogenesisPlasma Peptidylarginine Deiminase IV Promotes VWF-Platelet String Formation and Accelerates Thrombosis After Vessel InjuryTranscriptomic Profiling of the Developing Cardiac Conduction System at Single-Cell ResolutionIncreased Activated Protein C Response Rates Reduce the Thrombotic Risk of Factor V Leiden Carriers But Not of Prothrombin 20210G>A CarriersEndothelial Foxp1 Suppresses Atherosclerosis via Modulation of Nlrp3 Inflammasome ActivationThe Human-Specific and Smooth Muscle Cell-Enriched LncRNA SMILR Promotes Proliferation by Regulating Mitotic CENPF mRNA and Drives Cell-Cycle Progression Which Can Be Targeted to Limit Vascular RemodelingCharacterization of Kcnk3-Mutated Rat, a Novel Model of Pulmonary HypertensionVariation in a Left Ventricle–Specific Hand1 Enhancer Impairs GATA Transcription Factor Binding and Disrupts Conduction System Development and FunctionInstantaneous Amplitude and Frequency Modulations Detect the Footprint of Rotational Activity and Reveal Stable Driver Regions as Targets for Persistent Atrial Fibrillation AblationReactive Vasodilation Predicts Mortality in Primary Systemic Light-Chain AmyloidosisDynamic Chromatin Targeting of BRD4 Stimulates Cardiac Fibroblast ActivationCoupling to Gq Signaling Is Required for Cardioprotection by an Alpha-1A-Adrenergic Receptor AgonistHIV-Nef Protein Transfer to Endothelial Cells Requires Rac1 Activation and Leads to Endothelial Dysfunction Implications for Statin Treatment in HIV PatientsMiro2 Regulates Inter-Mitochondrial Communication in the Heart and Protects Against TAC-Induced Cardiac DysfunctionCirculating Monocyte Chemoattractant Protein-1 and Risk of StrokeYin Yang 1 Suppresses Dilated Cardiomyopathy and Cardiac Fibrosis Through Regulation of Bmp7 and CtgfBody Mass Index Drives Changes in DNA MethylationLeptin Induces Hypertension Acting on Transient Receptor Potential Melastatin 7 Channel in the Carotid BodyDiversification and CXCR4-Dependent Establishment of the Bone Marrow B-1a Cell Pool Governs Atheroprotective IgM Production Linked to Human Coronary AtherosclerosisPeripheral Vasoconstriction During Mental Stress and Adverse Cardiovascular Outcomes in Patients With Coronary Artery DiseaseADAMTS8 Promotes the Development of Pulmonary Arterial Hypertension and Right Ventricular FailureAn Unbiased Proteomics Method to Assess the Maturation of Human Pluripotent Stem Cell–Derived CardiomyocytesRace, Natriuretic Peptides, and High-Carbohydrate ChallengeMigratory and Dancing Macrophage Subsets in Atherosclerotic LesionsMitochondrial Metabolic Reprogramming by CD36 Signaling Drives Macrophage Inflammatory ResponsesA20 in Myeloid Cells Protects Against Hypertension by Inhibiting Dendritic Cell-Mediated T-Cell ActivationIn This Issue pages highlight articles that the editors feel are particularly important by providing a short synopsis written in a language that can be understood by the nonspecialist. The purpose of this feature are two-fold: first, to call the attention of readers to important articles and, second, to enable all readers to grasp, easily and quickly, the significance of these papers. We believe that this initiative has been successful and, as a further service to our readers, provide below a compendium of these pages from the previous year, 2019. Each summary is accompanied by the corresponding citation, so that readers can easily find the entire article should they wish to read it. This remarkable anthology of outstanding articles attests to the diversity and depth of the work published in Circulation Research. — The EditorsCirculation Research, vol 124, 2019ATF6 Regulates Cardiac Growth (p 79)1Blackwood et al discover how pressure overload-induced protein misfolding leads to hypertrophy of cardiomyocytes.Download figureDownload PowerPointAn increase in protein synthesis puts pressure on the protein folding machinery of the endoplasmic reticulum and can lead to the build-up of misfolded proteins. In turn, this activates transcription factor ATF6, which ramps up expression of protein folding factors to assist with the increased demand. An increase in protein synthesis has been associated with cardiac hypertrophy; however, the role of ATF6 under such conditions has not been investigated. Now, Blackwood and colleagues report that ATF6 is activated in a mouse model of hypertrophy (induced by transverse aortic constriction [TAC]) and that deletion of ATF6 from cardiac myocytes ameliorates hypertrophy but impairs cardiac function. The authors also report that the gene for the protein, RHEB—itself an activator of the cell growth and proliferation factor mTOR—is a direct target of ATF6. Indeed, they found that, following aortic constriction, both RHEB and mTOR were upregulated in the heart of wild-type mice, but not in the heart of ATF6-null mice. These results link hypertrophic signaling via ATF6 and RHEB to mTOR-mediated cardiac myocyte growth, providing a novel mechanistic insight into the development of hypertrophy.Gut Microbiota, Inflammation, and Atherosclerosis (p 94)2A proinflammatory gut microbiota exacerbates atherosclerosis in mice, according to Brandsma et al.Download figureDownload PowerPointThe gut microbiome is known to influence the development of the host immune system and to regulate inflammation. Nevertheless, the extent to which the microbiome can influence atherosclerosis remains unknown. To find out, Brandsma and colleagues gave atherosclerosis-prone mice (Ldlr−/−) fecal transplants (via cohousing) from mice whose gut microbes had previously been shown to promote systemic inflammation. On a high-fat diet, the recipient Ldlr−/− mice displayed accelerated atherosclerosis compared with their control Ldlr−/− counterparts. The recipient mice had significantly larger arterial plaques and higher levels of circulating neutrophils and monocytes than controls. Moreover, the feces of the recipient mice contained fewer microbial taxa capable of producing short-chain fatty acids (SCFA), molecules thought to exert both anti-inflammatory and antiatherogenic effects. The mice also had lower levels of SCFAs in their intestines than control animals. Altogether, the work provides further evidence that favorable alterations in the gut microbiome could protect against systemic inflammation and cardiovascular disease.PATJ Variants and Ischemic Stroke Functional Outcome (p 114)3Polymorphisms at the gene PATJ influence outcomes after ischemic stroke, report Mola-Caminal et al.Download figureDownload PowerPointIschemic stroke is a major cause of death and disability worldwide. And, among those who survive such an event, recovery is highly variable, regardless of stroke severity or the burden of other cardiovascular risk factors. Indeed, individual responses to ischemic damage differ significantly. For example, some patients show evidence of new synapse formation around the infarct just days after the event, a response associated with better recovery, while others do not. To investigate potential genetic explanations underlying such variability, Mola-Caminal and colleagues performed the largest meta-analysis of ischemic stroke GWAS to date. With the statistical power offered by combining four GWAS cohorts, and the ability to stringently define the phenotype in question, the authors were able to identify 3 nucleotide variants (SNPs) at the PATJ (protein found at tight junctions) gene locus associated with poor recovery. The team then replicated their analysis in 3 additional cohorts and found SNPs at the PATJ gene in these cohorts as well. In fact, PATJ was the only significantly associated gene identified in the study. Elucidating how this gene might influence brain recovery is the next step.Atria-Specific Gene Delivery (p 256)4Ni et al have tweaked a viral gene-expression vector for use in atrium-specific applications.Download figureDownload PowerPointAdeno-associated viruses (AAVs) are commonly used for delivering genes into mammalian cells in both biomedical research and clinical gene therapy trials. Among the various AAV serotypes available, AAV9 is particularly efficient at transducing cardiac myocytes and therefore has great utility for heart-based applications. However, there are instances when atrium-specific gene transfer is desirable, such as for studies of atrial fibrillation, which is the most common form of cardiac arrhythmia. To target genes to the atrium, Ni and colleagues developed a version of AAV9 that contains a promoter from the Nppa gene, which drives gene expression specifically in atrial myocytes. In their proof-of-principle experiments, they found that injection of the vector into live mice resulted in atrium-specific expression of a GFP (green fluorescent protein) and of Cre-recombinase—the latter being used for effective atrial knockdown of a floxed gene. Use of such atrium-specific AAV9 vectors will not only enable greater insight into atrial biology but also assist in the identification and modification of potential targets for the treatment of atrial fibrillation and other atrial diseases.Tissue Resident Macrophages and Myocardial Injury (p 263)5Bajai et al examine the monocyte-recruiting potential of distinct subsets of cardiac macrophages after injury.Download figureDownload PowerPointAlthough recruitment of circulating monocytes helps clear damaged cells after tissue injury, after a myocardial infarction, an over abundance of these cells can exacerbate the damage and worsen the deterioration in heart function. Indeed, in mice, chemical inhibition of monocyte recruitment reduces inflammation after infarction and prevents functional deterioration of the heart. However, not all monocyte populations may be equally detrimental. To examine the role of specific monocyte populations, Bajpai and colleagues examined the effects of depleting different monocytes on cardiac inflammation. They found in mice that depletion of cells expressing CCR2—a surface protein essential for recruitment of immune cells—reduced inflammatory monocyte recruitment after heart injury and resulted in better heart function. However, depletion of CCR2-heart macrophages led to increased monocyte recruitment and inferior heart function compared with controls. These results indicate that suppressing the activity of CCR2+ macrophages, which are also present in human hearts, might be one way to reduce inflammation and improve outcomes after cardiac injuries.Albuterol and Pulmonary Vascular Reserve in HFpEF (p 306)6Albuterol improves pulmonary vasodilation in patients with heart failure, report Reddy et al.Download figureDownload PowerPointPatients with heart failure with preserved ejection fraction (HFpEF) are at risk of developing vascular disease of the lungs. This may begin with reduced pulmonary artery dilation during exercise but can progress to more prolonged pulmonary hypertension and resultant right ventricle dysfunction. Recent studies in patients with HFpEF have shown that intravenous delivery of a β-adrenergic agonist can promote pulmonary artery vasodilation at rest. However, intravenous administration is not practicable for chronic use. To investigate whether inhaled β-adrenergic agonist would be effective as well, Reddy and colleagues gave albuterol or placebo to HFpEF patients via a nebulizer, in a double-blind randomized trial. After baseline hemodynamic assessments at rest and after exercise, study participants received albuterol or placebo, and their hemodynamic responses were again measured at rest and after exercise. They found that patients given albuterol had improved pulmonary resistance under both conditions. The treated patients also had reduced right atrial and pulmonary artery pressure compared with controls. They also showed reduced right atrial and pulmonary artery pressure compared with controls. Given the availability, safety, and low cost of albuterol, the authors say that larger trials of the drug in HFpEF patients are warranted.Major Genetic Contributors to Tetralogy of Fallot (p 553)7Page et al perform whole exome sequencing and identify genetic links to a common heart defect.Download figureDownload PowerPointTetralogy of Fallot (TOF), a form of congenital heart defect, affects ≈1 in 3000 newborns. It is characterized by ventricular septal defect, pulmonary stenosis, right ventricular hypertrophy, and an overriding aorta. The condition is treated by surgery, which enables most patients to survive to age 30, but complications are common, as is premature death. The understanding of the pathology of TOF, however, is hindered by the fact that, in most cases, the underlying cause is unknown. Indeed, even though 15% of patients have a chromosomal deletion at 22q11.2 (often affecting the gene TBX1), 80% are nonsyndromic with generally no identifiable basis. Hence, to gain insight into additional underlying genetic contributors in TOF, Page and colleagues performed whole exome sequencing in 829 patients. Although they identified a large number of genetic variants in the participants’ DNA, strong associations were observed with only 2 particular genes—NOTCH1 and FLT4. Potentially pathological variations in NOTCH1, for example, were found in 4.5% of patients, and those in FLT4 were found in 2.5%. Interestingly, like TBX1, both NOTCH1 and FLT4 are important for blood vessel development, suggesting the root cause of TOF may be linked to problems with angiogenesis.Oxidant Stress and Endothelial Dysfunction in MDD (p 564)8Greaney et al gather insights into depression-associated vascular dysfunction.Download figureDownload PowerPointDepression afflicts somewhere between 10% and 15% of the US population and is associated with a higher prevalence of cardiovascular disease (CVD), independent of traditional CVD risk factors. Nevertheless, the link between CVD risk and depression is unclear. Recent evidence suggests that major depressive disorder (MDD) is associated with heightened oxidative stress, as reflected by an increase in blood biomarkers of oxidative damage, reduced plasma levels of NO metabolites and endothelial dysfunction. To gain additional insights into the mechanisms underlying vascular dysfunction in depression, Greaney and colleagues examined 24 otherwise healthy MDD patients and 20 healthy controls. As expected, they found that biomarkers of oxidative stress were elevated in patients with MDD, but even though their vascular conductance (the ratio of blood flow to arterial pressure) in the cutaneous circulation was unaffected, both NO-dependent and -independent vascular dilation was blunted in MDD subjects. They also found that scavenging of superoxide, or inhibiting the production of reactive oxygen species, improved dilation in MDD patients. These finding suggest that strategies that target vascular oxidative stress may be a clinical option for reducing CVD risk in MDD.MicroRNA-92a-3p in Endothelial Microvesicles (p 575)9MicroRNA-containing microvesicles alter endothelial cell function in atherosclerosis, report Liu et al.Download figureDownload PowerPointCoronary artery disease, resulting from atherosclerosis, is the leading cause of mortality worldwide. Among the many pathophysiological features of atherosclerosis is an increased abundance in the blood stream of microvesicles—small, cell-produced, membrane-bound packages containing proteins, messenger RNAs, and regulatory microRNAs that are thought to be important for cell-to-cell communication. To investigate the nature of these atherosclerosis-associated vesicles, Liu and colleagues compared circulating microvesicles from individuals with or without the condition. They found that microvesicles from individuals with atherosclerosis had higher levels of microRNA-92a-3b, than those from controls. Moreover, in their in vitro studies, they found that atherosclerotic stimuli promoted the production of miR-92a–filled microvesicles. These vesicles were also found to boost migration and proliferation of recipient endothelial cells. Indeed, knockdown of miR-92a-3b prevented such increased proliferation and migration, as well as vessel formation. The authors suggest that, in atherosclerosis, microvesicles containing miR-92a- may have regenerative potential that could be harnessed for therapeutic purposes.Human Papillomavirus and Cardiovascular Disease (p 747)10Joo et al link human papillomavirus infection to cardiovascular disease risk.Download figureDownload PowerPointApproximately 20% of patients with cardiovascular disease (CVD) do not have any of the conventional risk factors, such as obesity, high blood pressure, or diabetes, suggesting other contributors have yet to be discovered. One possible candidate is infection with high-risk strains of human papillomavirus (HPV)—those with the potential to cause cancer. A recent health survey demonstrated a link between such infections and myocardial infarction or stroke. However, because the data was based on self-reported conditions and self-collected vaginal swabs for HPV analysis, validation with a controlled study was necessary. Joo and colleagues have done just that, studying the health and HPV status of 63 411 Korean women. During their 5-year study period, they found that there were 1122 cases of new-onset CVD, and these were shown to disproportionately afflict subjects with HPV—even after controlling for body mass index, smoking status, alcohol intake, and exercise. Association between HPV and CVD was, however, stronger in individuals with obesity and metabolic syndrome. These findings identify HPV as an novel risk factor for cardiovascular disease, and suggest that HPV vaccination, in addition to protecting against cancer, may also be beneficial for cardiovascular health.Dietary Fats and Mortality in General Population (p 757)11Zhuang et al examine the impact of assorted dietary fats on long-term health in a super-scale study.Download figureDownload PowerPointDietary guidelines recommend low-fat diet, because accumulation of excess lipids in the bloodstream can lead to the development of atherosclerosis. The current guidelines suggest limiting intake of saturated fats and trans-fatty acids and ideally replacing them with unsaturated fats. However, recent studies question these recommendations, and there is little evidence to support these long-held recommendations. To address conflicting results, Zhuang and colleagues have examined self-reported dietary data from more than half a million North Americans for whom they have follow-up mortality data covering the past 16 years. The participants, 129 328 of whom have now died, completed detailed questionnaires on lifestyle and diet in the mid nineties. Analyses of the data has revealed that dietary intake of saturated fats, trans-fatty acids, alpha-linolenic acid, and arachidonic acid were all associated with higher mortality, while polyunsaturated fatty acids (PUFAs), linoleic acid, and marine omega-3 PUFAs were associated with lower mortality. The findings indicate that the existing dietary recommendations are indeed still worth following.Postconditioning Improves LV Remodeling (p 769)12A modified reperfusion technique may offer long-term protection against myocardial remodeling, say Traverse et alRapid restoration of blood flow after a myocardial infarction is critical for saving heart muscle function and reducing the risk of development of heart failure. However, restoration of blood flow could lead to reperfusion injury—an increase in inflammation and oxidative stress that damages the very tissue in need of preserving. One possible approach to reduce the risk of injury is postconditioning (PostC)—a modified reperfusion technique in which the blood flow is restored in a stop-start manner by repeatedly occluding and reperfusing the artery for 30 seconds at a time. In dogs, this approach was shown to reduce infarct size by 44%. To examine the efficacy of this procedure in humans, Traverse and colleagues have tested the procedure in 65 patients with ST-elevation myocardial infarction. They found that after 2 days there was no discernable difference between PostC and control subjects. However, after 1 year, PostC patients displayed improved left ventricle remodeling and, for a subset of patients who exhibited microvascular occlusion, the improvement was particularly evident. The results hint that PostC may have hitherto unappreciated long-term benefits for recovery and suggest that future trials should include extended follow-up periods.DDR/TP53 Activation in DCM Caused by LMNA Mutations (p 856)13Chen et al find a link between laminopathy and cardiomyopathy.Download figureDownload PowerPointLaminopathies are a range of diseases caused by mutations to LMNA, a structural component of the nuclear membrane. The dysfunctional protein affects cells in a variety of ways, and is particularly problematic for cells subjected to repeated mechanical stress, such as those of the heart and muscles. Indeed, dilated cardiomyopathy is a major cause of death among laminopathy patients. To examine the link between LMNA mutation and heart dysfunction, Chen and colleagues engineered mice to express mutant LMNA in their cardiac myocytes, and then compared gene expression in these and control animals. By ≈1 month of age, mice carrying the LMNA mutation died from heart malformations. But, before that, at 2 weeks of age, they displayed ≈6000 differently expressed genes—many involved in apoptosis, cell cycle control, and DNA damage response (DDR). Indeed, TP53—a DDR transcription factor—was among the top differently regulated genes. Expression of TP53 and its downstream targets was increased in mutant mice. These changes were also observed in humans with mutant LMNA and cardiomyopathy. Moreover, deletion of the TP53 gene in the engineered mice partially rescued the cardiac phenotype. These results suggest that targeting TP53/DDR might alleviate laminopathy-associated cardiac dysfunction.Imaging Inflammatory Monocytes and Macrophages (p 881)14Heo et al develop a PET tracer for visualizing inflammatory monocytes and macrophages in the heart.Download figureDownload PowerPointHigh levels of myocardial inflammation after infarction are associated with poorer prognoses. Yet there are no methods for real-time monitoring of the cells that are largely responsible for that inflammation, namely infiltrating monocytes expressing CCR2 protein. A CCR2 tracer that contains radioactive copper (64Cu) has been used to monitor such cells in the lungs of live animals. But 64Cu is not only difficult to produce (it requires a cyclotron) it also has a long half-life, posing safety problems. Heo et al have, therefore, developed an alternative CCR2 tracer using radioactive gallium (68Ga), which has a much shorter half-life and is far easier to produce. Using this tracer for PET imaging of mice after myocardial infarction, the team observed a peak signal in the animals’ hearts 4 days after injury. CCR2–/– mice showed no such pattern, confirming the tracer’s specificity. The team also found that the tracer could detect CCR2+ cells in injured human heart tissue. The development of this tracer, and its applicability to human tissue, could enable further translational work to study myocardial inflammation, and to identify patients in need of inflammation-suppressing therapies.Nut Intake, CVD Risk, and Mortality Among Diabetes (p 920)15Patients with diabetes may benefit from eating more nuts, say Liu et al.Download figureDownload PowerPointNuts contain a variety of nutrients, such as unsaturated fats, fiber, vitamins, and minerals, which are considered beneficial to health. And frequent nut consumption has been associated with lower risk of cardiovascular disease, hypertension, and cancer. The health benefits of nut consumption is further supported by clinical trials suggesting that nut consumption improves lipid profiles and decreases the levels of oxidative stress. However, it is unclear whether people with diabetes, who are especially prone to cardiovascular disease, might benefit from more nuts in their diet. Liu and colleagues examined health and diet data from more than 16000 US men and women who either had or developed diabetes between the 1980s and 2014. The team’s analysis of the data, based on questionnaires every 2 to 4 years of the study period, revealed that higher consumption of nuts, especially tree nuts, was linked to a lower risk of cardiovascular disease, coronary artery disease, and death, even after controlling for established risks such as body mass index and lifestyle. Furthermore, increasing nut intake even after diabetes diagnosis was also linked to lower health risks. These findings suggest that increasing dietary consumption of nuts could help prevent cardiovascular complications in people with diabetes.SarcTrack: High-Fidelity Probing of Sarcomeres (p 1172)16Toepfer et al create image analysis software for monitoring sarcomeres in any muscle cell.Download figureDownload PowerPointSarcomeres are the fundamental units of contractility in muscle cells. However, studying their biology and disease-induced dysfunction is limited by tools optimized for analyzing uniform, linearly aligned sarcomeres—the sort fo" @default.
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