The thioredoxin interaction protein (TXNIP) has been reported to be closely related to cell oxidative stress, apoptosis and inflammation. TXNIP is involved in the regulation of oxidative stress in lung and renal injury. However, it is unclear as to whether it participates in the protective effects of sevoflurane preconditioning in cardiomyocyte injury caused by oxidative stress in ischemia. In the present study, H9c2 cardiomyocytes were cultured with 0, 1.5, 2, 3.5, 5 or 6% sevoflurane for 3 h, followed by exposure to oxygen and glucose deprivation. The results demonstrated that oxygen and glucose deprivation induced an increase in TXNIP expression, lactate dehydrogenase (LDH) release, caspase‑3 activity, reactive oxygen species and malondialdehyde production. Preconditioning of the H9c2 cells with 3.5% sevoflurane suppressed TXNIP expression, LDH leakage, caspase‑3 activity, reactive oxygen species and malondialdehyde production, and it promoted cell viability. TXNIP overexpression reversed ...
Full Text - Inducing cardiomyocyte proliferation is a hopeful approach for cardiac regeneration following myocardial infarction. Previous studies have shown that p21 inhibits the cardiomyocyte proliferation and cardiac regeneration. Deacetylation of p21 by Sirt1 deacetylase may reduce p21 abundance and remove p21-induced cell cycle arrest. However, whether p21 deacetylation and Sirt1 deacetylate control cardiomyocyte proliferation is unclear. Here, we show that acetylation of p21 induces cardiomyocyte proliferation arrest, whereas blocking the acetylation of p21 increases cardiomyocyte proliferation. P21 can be acetylated by Sirt1, and Sirt1 activate p21 ubiquitination through deacetylation. Additionally, overexpression of Sirt1 induces EdU-, pH3-, and Aurora B-positive cardiomyocytes in neonatal and adult mice. In contrast, depletion of Sirt1 reduces cardiomyocyte proliferation in vitro and in vivo. Moreover, Sirt1 protects cardiac function, reduces cardiac remodeling, inhibits
In vitro human embryonic stem cells (hESCs) and human induced pluripotent stem cells (hiPSCs) can differentiate into functional cardiomyocytes (CMs). Protocols for cardiac differentiation of hESCs and
Intracellular calcium (Ca) cycling plays a central role in cardiac excitation-contraction coupling.1,2 Ca alternans, a beat-to-beat alternation in intracellular Ca transient amplitude, is an important factor promoting T-wave alternans and pulsus alternans, markers conferring an increased risk of sudden cardiac death.3 Although Ca alternans has been widely studied in cardiac myocytes,4-13 the underlying mechanism remains controversial. Eisner et al4 were the first to propose that Ca alternans could be explained by a steep nonlinear dependence of sarcoplasmic reticulum (SR) Ca release on the diastolic SR Ca load immediately preceding the release (a steep fractional release-load relationship). This mechanism requires that diastolic SR Ca load alternate concomitantly with SR Ca release. Subsequent experimental6,7,9 and theoretical9,14,15 studies have provided evidence supporting this mechanism. However, later experimental studies in rabbit ventricular myocytes by Picht et al12 and in cat atrial ...
The present study demonstrates that (1) human PF has a greater trophic effect than human serum on cultured rat adult cardiac myocytes, which is likely due to a high concentration of FGF2, and (2) both serum and PF from patients with cardiac hypertrophy have additional effects on cardiac myocytes that are related to the increase in LV mass and that suggest the presence of a circulating growth factor(s) involved in the process of hypertrophy.. One of the major findings of the present study is that PF has a hypertrophic effect on cardiac myocytes, as indicated by (1) the increase of MyHC mRNA level, (2) increased rate of protein synthesis, and (3) increase in total protein content. This trophic effect is not associated with a shift in myosin isoforms, since both α- and β-MyHC mRNAs increase. Furthermore, PF does not seem to enhance apoptosis, since the percentage of cells dying in culture was the same under all experimental conditions (Table 1⇑).. The greater trophic effect of PF on cardiac ...
The second messenger cyclic adenosine monophosphate (cAMP) is the most important modulator of sympathetic control over cardiac contractility. In cardiac myocytes and many other cell types, however, cAMP transduces the signal generated upon stimulation of various receptors and activates different cellular functions, raising the issue of how specificity can be achieved. In the general field of signal transduction, the view is emerging that specificity is guaranteed by tight localization of signaling events. Here, we show that in neonatal rat cardiac myocytes, beta-adrenergic stimulation generates multiple microdomains with increased concentration of cAMP in correspondence with the region of the transverse tubule/junctional sarcoplasmic reticulum membrane. The restricted pools of cAMP show a range of action as small as approximately 1 micrometer, and free diffusion of the second messenger is limited by the activity of phosphodiesterases. Furthermore, we demonstrate that such gradients of cAMP specifically
The regenerative potential of the adult heart is very limited and insufficient to replace damaged muscle mass in the diseased heart. Recent advances in cardiac cell therapy and tissue engineering fuel new hope for the development of novel therapeutic approaches with the aim to trigger myocardial regeneration after injury. Stem cell-derived cardiomyocytes represent ideal candidates for cardiac cell-based therapeutic strategies, and current research focuses on the development of cardiac constructs for implantation. Despite the cardiogenic properties of the newly generated cardiomyocytes, these cells present a heterogeneous and immature phenotype, which is more comparable with cardiomyocytes of early developmental stages. However, successful employment of these new cardiomyocytes for myocardial repair demands that the physiological profile of stem cell-derived cardiomyocytes matches with the functional complexity of mature cardiomyocytes. This is currently not the case. We are interested in gaining ...
The regenerative potential of the adult heart is very limited and insufficient to replace damaged muscle mass in the diseased heart. Recent advances in cardiac cell therapy and tissue engineering fuel new hope for the development of novel therapeutic approaches with the aim to trigger myocardial regeneration after injury. Stem cell-derived cardiomyocytes represent ideal candidates for cardiac cell-based therapeutic strategies, and current research focuses on the development of cardiac constructs for implantation. Despite the cardiogenic properties of the newly generated cardiomyocytes, these cells present a heterogeneous and immature phenotype, which is more comparable with cardiomyocytes of early developmental stages. However, successful employment of these new cardiomyocytes for myocardial repair demands that the physiological profile of stem cell-derived cardiomyocytes matches with the functional complexity of mature cardiomyocytes. This is currently not the case. We are interested in gaining ...
Genetic regulation of the cell fate transition from lateral plate mesoderm to the specification of cardiomyocytes requires suppression of Wnt/β-catenin signaling, but the mechanism for this is not well understood. By analyzing gene expression and chromatin dynamics during directed differentiation of human embryonic stem cells (hESCs), we identified a suppressor of Wnt/β-catenin signaling, transmembrane protein 88 (TMEM88), as a potential regulator of cardiovascular progenitor cell (CVP) specification. During the transition from mesoderm to the CVP, TMEM88 has a chromatin signature of genes that mediate cell fate decisions, and its expression is highly upregulated in advance of key cardiac transcription factors in vitro and in vivo. In early zebrafish embryos, tmem88a is expressed broadly in the lateral plate mesoderm, including the bilateral heart fields. Short hairpin RNA targeting of TMEM88 during hESC cardiac differentiation increases Wnt/β-catenin signaling, confirming its role as a ...
To the Editor:. We read with interest the article by Hosoda et al,1 "Human Cardiac Stem Cell Differentiation Is Regulated by a Mircrine Mechanism." We are pleased to read that Hosoda et al were able to confirm our observations that miR-499 is involved in the differentiation of human cardiac-derived progenitor cells.2. Hosoda and colleagues acknowledged our previous observations in human cardiomyocyte progenitor cells (hCMPCs), but claimed that these cells were erroneously considered a class of cardiac progenitor cells. The authors suggest that our results demonstrated that miR-1 and 499 favor a more mature phenotype in fetal-neonatal cardiomyocytes. Although controversy still exists about different populations of progenitor and stem cells in the heart, we used an exceptionally profound characterized and well-documented cell population,3-5 both present in the fetal and adult human myocardium. hCMPCs do express progenitor markers and early cardiomyocyte-specific transcription factors, but not any ...
TY - JOUR. T1 - The role of the tumor suppressor gene p53 in cardiomyocyte apoptosis. AU - Crow, Michael T.. AU - Long, Xilin. AU - Guglielmi, Mario B.. AU - Asai, Toshinobu. AU - Lakatta, Edward G.. PY - 1998/1/1. Y1 - 1998/1/1. N2 - The possibility that a significant fraction of cardiac myocyte loss in various disease states occurs through apoptosis has elicited considerable attention in recent years. Evidence from human studies as well as in vitro and animal models of disease has shown that cardiac myocyte apoptosis can be induced by a variety of stimuli and in a number of disease states, including hypoxia, ischemia-reperfusion, myocardial infarction, mechanical stretch, aortic constriction, and heart failure. Because adult cardiac myocytes are terminally differentiated cells, the effects of such loss can never be fully compensated. Interest in cardiomyocyte apoptosis has been fueled by the possibility that once the proximal and distal signals were defined that initiate this pathway of cell ...
Fingerprint Dive into the research topics of Generation of reentrant arrhythmias by dominant-negative inhibition of connexin43 in rat cultured myocyte monolayers. Together they form a unique fingerprint. ...
Adult zebrafish possess a significant ability to regenerate injured heart tissue through proliferation of pre-existing cardiomyocytes, which contrasts with the inability of mammals to do so after the immediate postnatal period. Zebrafish therefore provide a model system in which to study how an injured heart can be repaired. However, it remains unknown what important processes cardiomyocytes are involved in other than partial de-differentiation and proliferation. Here we show that migration of cardiomyocytes to the injury site is essential for heart regeneration. Ventricular amputation induced expression of cxcl12a and cxcr4b, genes encoding a chemokine ligand and its receptor. We found that cxcl12a was expressed in the epicardial tissue and that Cxcr4 was expressed in cardiomyocytes. We show that pharmacological blocking of Cxcr4 function as well as genetic loss of cxcr4b function causes failure to regenerate the heart after ventricular resection. Cardiomyocyte proliferation was not affected ...
Accumulating evidence supports the notion that the renin-angiotensin system exists not only in the blood circulation but also in cardiac tissues.34 35 Recently, it has been reported that Ang II induces hypertrophy of cultured cardiac myocytes from neonatal rats9 and embryonic chick8 and also causes the proliferation of cultured neonatal rat cardiac fibroblasts.9 Furthermore, very recently, using an in vitro model of load (stretch)-induced cardiac hypertrophy, Sadoshima et al10 have obtained evidence showing that mechanical stretch leads to release of Ang II from neonatal rat ventricular myocytes and the released Ang II acts as an initial mediator of the stretch-induced hypertrophic response. All these findings, obtained by in vitro studies,8 9 10 support the notion that autocrine release of Ang II from cardiac myocytes is involved in load (stretch)-induced growth of ventricular myocytes, thereby suggesting the central role of Ang II in cardiac hypertrophy and remodeling. However, it remains to ...
Author summary A molecular understanding of cardiomyocyte development is an essential goal for improving clinical approaches to CHD. While TBX20 is an essential transcription factor for heart development and its disease relevance is well established, many fundamental questions remain about the mechanism of TBX20 function. Principle among these is how TBX20 mutations associated with adult dilated cardiomyopathy circumvent (DCM) the essential embryonic requirement for TBX20 in heart development. Here we report using an integrated approach that TBX20 complexes with the cardiac transcription factor CASZ1 in vivo. We confirmed TBX20 and CASZ1 interact biochemically and genetically, and show mice heterozygous for both Tbx20 and Casz1 die, beginning at 4 to 8 weeks post birth, exhibiting hallmarks of DCM. Interestingly, the human mutant TBX20F256I bypasses the early essential requirement for TBX20 but leads to DCM. We report here that TBX20F256I disrupts the TBX20-CASZ1 interaction, ascribing clinical
Cardiac structure and functionare commonly studied using primary culture of neonatal and adult cardiac myocyte. However, their inability to divide and retain their differentiated phenotype in culture limits their use.. Established from a mouse atrial myocyte tumour, HL-1 cells share similar characteristics with primary cultures of cardiac myocytes. They have the ability to proliferate while keeping a differentiated cardiomyocyte phenotype in culture (this allows the use of specific molecular tools as RNA interference). However, there are concerns about their genetic stability and some studies have shown the cells to contain a functionally heterogeneous population.. The team from Imperial College isolated homogeneous and stable clones of HL-1 cell lines - thereby excluding any differences due to cellular heterogeneity of the original cell line - that display phenotypic characteristics consistent with cardiac cells.. Clones 3 and 6 appear to be most promising for cardiac research. These cells ...
Cell proliferation is regulated by the balance between cyclin-dependent kinases (CDKs) and CDK inhibitors such as p27. In neonatal cardiomyocytes, p27 is a key inhibitor of cell proliferation (6) and cyclin D1 is important for cell cycle progression (36). To delineate the pathway through which TIMP-3 inhibits neonatal cardiomyocyte proliferation, the effect of TIMP-3 on cyclin D1 and p27 expression was investigated. Our data showed that cyclin D1 was increased in TIMP-3−/− cardiomyocytes and decreased in rTIMP-3-treated cells as compared with WT. Consistent with these results, p27 expression was decreased in the TIMP-3−/− cardiomyocytes and neonatal hearts as compared with WT. This decrease in p27 expression resulted in an increase in cardiomyocyte proliferation both in vitro and in vivo. Furthermore, treatment of cardiomyocytes with rTIMP-3 resulted in a significant increase in p27 expression, which led to a significant decrease in cardiomyocyte proliferation. Our data suggest that ...
It is believed that in embryonic cardiomyocytes the myocardial contraction is predominantly dependent on transsarcolemmal Ca2+ influx (26, 36). Therefore, it is expected that in embryonic cardiomyocytes, NCX might be a prominent Ca2+ remover and even more important than SERCA. However, it has been recently shown that in murine embryonic cardiomyocytes 8.5-9.5 days old, the majority of Ca2+ removal (∼74%) is accomplished by SERCA (32). The studies on mESCMs showed that the SERCA is the major Ca2+ remover in 17-day-old mESCMs (16). Here, we provided evidence showing that the contribution of SERCA to Ca2+ removal is upregulated with the time of mESCMs differentiation, accompanied with a downregulation of NCX to Ca2+ removal, a similar pattern as reported by Kapur and Banach (16). The functional changes with differentiation also coincide with the gene expression pattern of SERCA and NCX during embryonic development (21, 32) or mESCMs differentiation (12). Moreover, our data demonstrated that ...
We appreciate the interest of Drs Li and Shen in our study,1 which emphasizes the critical role that the insulin-like growth factor-1 (IGF-1) and IGF-1 receptor system has in defining the growth properties of human cardiac stem cells (hCSCs). We shared their view that IGF-1 positively interferes with the consequences of diabetes mellitus and dyslipidemia, and possibly with other cardiovascular pathologies. Based on our interest in IGF-1, a transgenic mouse model with cardiomyocyte-restricted overexpression of IGF-1 was developed.2 With this strategy, an increase in the number of ventricular myocytes was obtained, resulting in a significantly lower systolic and diastolic stress at the cellular level, together with an enhanced ability of the myocardium to sustain increases in pressure or volume loads.. Overexpression of IGF-1 prevents the manifestation of the diabetic myopathy and is associated with a better survival rate of the animals,3 consistent with the observations collected in the ...
Previous studies have reported that immature cardiomyocytes have characteristics of Ca2+-regulatory proteins which are different from that of mature cardiomyocytes [22-25]. During normal cardiac development in rabbits and rats, NCX expression is maximal near the time of birth and then declines postnatally [22, 25]. Conversely, SERCA2a expression levels increased during this period [23-25]. The characteristics of Ca2+-regulatory proteins in immature cardiomyocytes during hypertrophy with or without hypoxia has not been studied extensively, however the results of research will be beneficial for choosing an optimal time of therapy and interpreting the development process of cardiomyocytes in children with CHD.. To our knowledge, this study could be the first effort specifically dedicated to the evaluation of the gene and protein expression of Ca2+-regulatory proteins on human immature cardiomyocytes from RV. There were three major findings in this study. We found that SERCA2a, as a key regulator of ...
TY - JOUR. T1 - Targeted Sprouty1 overexpression in cardiac myocytes does not alter myocardial remodeling or function. AU - Charles, Nathan J.. AU - Huebert, Robert C.. AU - Lee, Sangjin. AU - Adhikari, Neeta. AU - Polster, Sean. AU - Rider, James E.. AU - Braunlin, Elizabeth. AU - Mariash, Ami. AU - Robledo, Maggie. AU - Schuweiler, David. AU - Hall, Jennifer L.. PY - 2010/9/1. Y1 - 2010/9/1. N2 - The mitogen activated protein kinase (MAPK) signaling pathway regulates multiple events leading to heart failure including ventricular remodeling, contractility, hypertrophy, apoptosis, and fibrosis. The regulation of conserved intrinsic inhibitors of this pathway is poorly understood. We recently identified an up-regulation of Sprouty1 (Spry1) in a targeted approach for novel inhibitors of the MAPK signaling pathway in failing human hearts following reverse remodeling. The goal of this study was to test the hypothesis that up-regulated expression of Spry1 in cardiac myocytes would be sufficient to ...
The findings herein advance a strategy for inducing myocardial repair in pediatric patients. Myocardial regeneration experiments in neonatal mice were not feasible until the recent introduction of techniques for inducing myocardial injury (15, 17, 41). LAD ligation (16, 17) and amputation injury (15, 42) in neonatal mice were reported to lead to scarless repair, although these results are controversial (43, 44). Here, we verify that cryoinjury is a technically feasible method that produces scar formation and dysfunction, which is in line with the scar formation and delayed repair process observed in zebrafish (31-33) and neonatal mice (35, 36) after cryoinjury. We also show that cryoinjury in neonatal mice is a useful model for human infants with heart disease because it recapitulates the scar formation, dysfunction, and decrease in cardiomyocyte cell cycle activity frequently seen in young patients with heart disease. The observed decrease in cardiomyocyte proliferation after cryoinjury ...
Lijun Liu is the author of these articles in the Journal of Visualized Experiments: A Model for Perineural Invasion in Head and Neck Squamous Cell Carcinoma, Isolation and Culture of Adult Mouse Cardiomyocytes for Cell Signaling and in vitro Cardiac Hypertrophy
In the studies reported in the American Journal of Pathology, Dr. Charles Murry and his colleagues at the University of Washington, in collaboration with scientists at Geron Corporation, produced cardiomyocytes from hESCs and injected the cells into the left ventricular wall of normal healthy rats. The transplant was examined one and four weeks after injection and human cells were detected in the rat myocardium at both timepoints. At the four week timepoint, the grafted human cardiomyocytes were identified using characteristic markers including sarcomeric actin, alpha and beta-myosin heavy chain, and myosin light chain 2v. Approximately 10% of the cardiomyocytes at the four week timepoint retained proliferative capacity, thereby potentially enhancing engraftment. Both host and graft derived angiogenesis (new blood vessel formation) was observed, critical to sustaining the viability of the graft. No evidence of tumor formation was seen ...
This method - tested in a mouse heart attack model - doubled the engraftment rate of injected stem cell-derived cardiomyocytes. Ram KannappanThe heart cannot regenerate muscle tissue after a heart attack has killed part...
Activation of mammalian sterile 20-like kinase 1 (Mst1) by genotoxic compounds is known to stimulate apoptosis in some cell types. The importance of Mst1 in cell death caused by clinically relevant pathologic stimuli is unknown, however. In this study, we show that Mst1 is a prominent myelin basic protein kinase activated by proapoptotic stimuli in cardiac myocytes and that Mst1 causes cardiac myocyte apoptosis in vitro in a kinase activity-dependent manner. In vivo, cardiac-specific overexpression of Mst1 in transgenic mice results in activation of caspases, increased apoptosis, and dilated cardiomyopathy. Surprisingly, however, Mst1 prevents compensatory cardiac myocyte elongation or hypertrophy despite increased wall stress, thereby obscuring the use of the Frank-Starling mechanism, a fundamental mechanism by which the heart maintains cardiac output in response to increased mechanical load at the single myocyte level. Furthermore, Mst1 is activated by ischemia/reperfusion in the mouse heart ...
This study was initiated with the original aim of assessing the consequences of the expression of the functional α2-subunit of the rat Na+-K+-ATPase in the neonatal rat cardiac myocytes lacking this isoform. It soon became evident, however, that only a truncated α2-subunit not likely to be functional was overexpressed in these cells. Because enzyme and receptor fragments may often act like inactive mutant variants and cause dominant negative inhibition (2, 10, 12, 23, 27, 36) we attempted to determine whether the expression of the α2-fragment impaired the function of endogenous Na+-K+-ATPase in the neonatal myocytes. Our findings clearly show that the ion transport function of Na+-K+-ATPase is indeed inhibited concomitant with the expression of the truncated α2-isoform and that this is accompanied by a significant reduction of the α1-protein content of the neonatal myocyte. Because the induced reduction of the α3-protein content is small, if any, and because it is established that α1 ...
Heart attacks are a leading cause of mortality in the United States, responsible for over 500,000 deaths annually. Despite advancing treatments for acute heart attack, 5-year mortality exceeds 50% as the organ fails to heal the resulting scar. Recent studies revealed modest cardiac regeneration occurring throughout life and accelerating (albeit insufficiently) post-injury. However, the magnitude is contested with some studies indicating low cardiomyocyte formation and others indicating rapid formation of increasingly inferior cardiomyocytes. Resolving this question determines the needed strategy for repair augmentation. Chapter 3 scrutinizes current apparently-paradoxical studies and offers a unified estimate of cardiomyocyte turnover via a hybrid-model software platform. As limited engraftment (|2%) was cited as a primary impediment in bone marrow cell (BMC) infusion clinical trials, Chapter 4 recapitulates these trials in an intact-organ murine model--the isolated perfused heart. Flow cytometry
Tissue regeneration without tumor formation may soon be within reach, at least for heart repair. On page 405, Behfar et al. report that embryonic stem (ES) cells preprogrammed to mature into cardiomyocytes can fix injured hearts in vivo without seeding tumors.. Directing ES cells to become a particular tissue type in vivo is an inefficient process. Consequently, transplanted ES cell populations may give rise to tumors in recipient hosts. Behfar et al. reasoned that delivery of partially differentiated ES cells may result in safe outcome provided that a modulator of differentiation shuts down troublesome tumor pathways.. When ES cells are delivered in vivo, their tumorigenicity is reduced in mice that suffer heart attacks. This is associated with TNF production. But TNF had not been tested for its ability to direct cardiomyocyte differentiation, although ES cells do express receptors for TNF. So the authors wondered whether TNF-driven signaling would be enough to guide cells into a ...
J:169706 Abdul-Ghani M, Dufort D, Stiles R, De Repentigny Y, Kothary R, Megeney LA, Wnt11 promotes cardiomyocyte development by caspase-mediated suppression of canonical Wnt signals. Mol Cell Biol. 2011 Jan;31(1):163-78 ...
New research shows that statins, drugs which lower cholesterol, cause heart disease. These drugs cause calcified plaques to form in coronary arteries in humans, thus causing or worsening heart disease.
It�s hard to read or watch the news without hearing of new things that could, apparently, cause heart disease. But can you believe what you read? We explain.
Heart failure is a costly and deadly disease, affecting over 23 million patients worldwide, 5.8 million patients in America, half of which die within 5 years of...
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Cardiac Nursing, Cardiac Nurses can use this section to network, discuss, and share trends and practices with other Cardiac Nursing Professionals. Cardiac nursing deals with... - pg. 3
Our cardiac care at home service is for patients recovering from cardiac-related surgeries or those who are living with chronic cardiac disease
MURF1 inhibits adrenergic agonist-induced cardiac gene expression. (A) NRVM were infected with Ad.GFP or Ad.MURF1 for 24 h followed by induction with PE for 48
The goal of this study was to determine whether beta(1)-adrenergic receptor (AR) and beta(2)-AR differ in regulating cardiomyocyte survival and apoptosis and, if so, to explore underlying mechanisms. One potential mechanism ...
... of or relating to the heart: cardiac disease. of or relating to the esophageal portion of the stomach. Medicine/Medical. a cardiac remedy. a person sufferi
Watch this training video from Cellular Dymanics International to learn about the storage, thawing, seeding, plating and maintainance of iCell Cardiomyocytes prior to performing you intended assay. Follow these techniques to maximize cell viability and ensure your success.
Viability of cardiomyocytes was examined using the MTT assay. The cell viability of the control was adjusted to 100%. The data presented are expressed as the me
J:170963 Heallen T, Zhang M, Wang J, Bonilla-Claudio M, Klysik E, Johnson RL, Martin JF, Hippo pathway inhibits Wnt signaling to restrain cardiomyocyte proliferation and heart size. Science. 2011 Apr 22;332(6028):458-61 ...
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