MedWorm: Arteriosclerosis

Q & A: Are All Plaques the Same?

NYT Health — Tue, 07 Feb 2012 00:08:44 +0100

Coronary plaque and eye plaque are directly related, while oral plaque is a different entity — but all of them can cause problems. (Source: NYT Health)

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Peritransplant kidney biopsies: comparison of pathologic interpretations and practice patterns of organ procurement organizations

Clinical Transplantation — Sun, 29 Jan 2012 05:00:00 +0100

Singh P, Farber JL, Doria C, Francos GC, Gulati R, Ramirez CB, Maley WR, Frank AM. Peritransplant kidney biopsies: comparison of pathologic interpretations and practice patterns of organ procurement organizations.  Clin Transplant 2012 DOI: 10.1111/j.1399‐0012.2011.01584.x.  © 2012 John Wiley & Sons A/S.Abstract: The preimplantation kidney biopsy affects utilization by diagnosing glomerulosclerosis, interstitial fibrosis (IF), arteriosclerosis, and arteriolar hyalinosis. Organ procurement organizations (OPOs) determine whether a donor warrants this biopsy and the donor hospital pathologists (DHPs) report on an OPO‐specific pathology interpretation form. Biopsy slides from 40 deceased donor kidneys transplanted at our institution were used to compare interpretations between ...

Targeting angiogenesis as treatment for obesity.

Arteriosclerosis, Thrombosis and Vascular Biology — Wed, 25 Jan 2012 07:09:18 +0100

Authors: Bruemmer D PMID: 22258895 [PubMed - in process] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Humanizing the problem of transplant vasculopathy.

Arteriosclerosis, Thrombosis and Vascular Biology — Wed, 25 Jan 2012 07:09:05 +0100

Authors: Méndez-Fernández YV, Major AS PMID: 22258896 [PubMed - in process] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Endothelial-to-Mesenchymal Transition and MicroRNA-21: The Game Is On Again.

Arteriosclerosis, Thrombosis and Vascular Biology — Wed, 25 Jan 2012 07:08:53 +0100

Authors: Cavarretta E, Latronico MV, Condorelli G PMID: 22258897 [PubMed - in process] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Intraplaque hemorrhage: an imaging marker for atherosclerotic plaque destabilization?

Arteriosclerosis, Thrombosis and Vascular Biology — Wed, 25 Jan 2012 07:08:41 +0100

Authors: Pasterkamp G, van der Steen AF PMID: 22258898 [PubMed - in process] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

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Life After GWAS: Functional Genomics in Vascular Biology.

Arteriosclerosis, Thrombosis and Vascular Biology — Wed, 25 Jan 2012 07:08:28 +0100

Authors: Lusis AJ PMID: 22258899 [PubMed - in process] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Strategies beyond genome-wide association studies for atherosclerosis.

Arteriosclerosis, Thrombosis and Vascular Biology — Wed, 25 Jan 2012 07:08:16 +0100

Authors: Maouche S, Schunkert H Abstract Atherosclerotic diseases, including coronary artery disease (CAD) and myocardial infarction (MI), are the leading causes of death in the world. The genetic basis of CAD and MI, which are caused by multiple interacting endogenous and exogenous factors, has gained considerable interest in the last years as genome-wide association studies (GWASs) have identified many new susceptibility loci for CAD and MI, and the underlying genes provide new insights into the genetic architecture of these diseases. Here we summarize the recent findings from GWASs of atherosclerosis and discuss their functional and biological implications. We also discuss the different post-GWAS strategies that are currently used for refining the location of causal variants, un...

The use of high-throughput technologies to investigate vascular inflammation and atherosclerosis.

Arteriosclerosis, Thrombosis and Vascular Biology — Wed, 25 Jan 2012 07:08:04 +0100

Authors: Döring Y, Noels H, Weber C Abstract The greatest challenge of scientific research is to understand the causes and consequences of disease. In recent years, great efforts have been devoted to unraveling the basic mechanisms of atherosclerosis (the underlying pathology of cardiovascular disease), which remains a major cause of morbidity and mortality worldwide. Because of the complex and multifactorial pathophysiology of cardiovascular disease, different research techniques have increasingly been combined to unravel genetic aspects, molecular pathways, and cellular functions involved in atherogenesis, vascular inflammation, and dyslipidemia to gain a multifaceted picture addressing this complexity. Thanks to the rapid evolution of high-throughput technologies, we are now ab...

Recent studies of the human chromosome 9p21 locus, which is associated with atherosclerosis in human populations.

Arteriosclerosis, Thrombosis and Vascular Biology — Wed, 25 Jan 2012 07:07:53 +0100

Authors: Holdt LM, Teupser D Abstract The chromosome 9p21 (Chr9p21) locus was discovered in 2007 by independent genome-wide association studies for coronary artery disease. Since then, the locus has been replicated numerous times and can be considered the most robust genetic marker of coronary artery disease today. Subsequent work has shown associations of Chr9p21 with a number of additional cardiovascular disease traits, such as carotid artery plaque, stroke, aneurysms, peripheral artery disease, heart failure, and cardiovascular mortality, suggesting a more general role in vascular pathology. Importantly, Chr9p21 lacks associations with common cardiovascular risk factors, such as lipids and hypertension, indicating that the locus exerts its effect through a completely novel mecha...

Beyond genome-wide association studies: the usefulness of mouse genetics in understanding the complex etiology of atherosclerosis.

Arteriosclerosis, Thrombosis and Vascular Biology — Wed, 25 Jan 2012 07:07:43 +0100

Authors: Welch CL Abstract The development of population-based genome-wide association studies has led to the rapid identification of large numbers of genetic variants associated with coronary artery disease (CAD) and related traits. Together with large-scale gene-centric studies, at least 35 loci associated with CAD per se have been identified with replication. The majority of these associations are with common single-nucleotide polymorphisms exhibiting modest effects on relative risk. The modest nature of the effects, coupled with ethical/practical constraints associated with human sampling, makes it difficult to answer important questions beyond gene/locus localization and allele frequency via human genetic studies. Questions related to gene function, disease-causing mechanism(s...

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Use of functional genomics to identify candidate genes underlying human genetic association studies of vascular diseases.

Arteriosclerosis, Thrombosis and Vascular Biology — Wed, 25 Jan 2012 07:07:32 +0100

Authors: Yang X Abstract Recent genome-wide association studies have identified hundreds of genetic loci as being associated with vascular diseases or traits and their risk factors. Many of the loci uncovered represent novel discoveries with no obvious candidate genes and molecular mechanisms, testifying to the complexity of vascular diseases. To understand the functional consequences of genetic variations and help pinpoint the underlying genes and mechanisms of common complex diseases, functional genomics that integrate genetic variations and intermediate molecular traits such as gene expression has been extensively studied in the past few years. This review summarizes the key concepts of functional genomics, the current state of the field, and its application in vascular diseases...

Indocyanine Green Angiography for Intra-operative Assessment in Vascular Surgery.

PubMed: Eur J Vasc Endovasc ... — Fri, 20 Jan 2012 05:00:00 +0100

CONCLUSION: HEMS angiography can accurately assess peripheral arterial perfusion in surgical cases with ASO and AAA. PMID: 22264591 [PubMed - as supplied by publisher] (Source: PubMed: Eur J Vasc Endovasc ...)

FGF19 Signaling Cascade Suppresses APOA Gene Expression.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 19 Jan 2012 05:00:00 +0100

CONCLUSIONS: These findings provide mechanistic insights in to the transcriptional regulation of human APOA by FGF19. Further studies in the human system are required to substantiate our findings and to design therapeutics for hyper lipoprotein(a). PMID: 22267484 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Identification of Galectin-1 and Galectin-3 as Novel Partners for Von Willebrand Factor.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 19 Jan 2012 05:00:00 +0100

CONCLUSIONS: We have identified galectin-1 and galectin-3 as novel partners for VWF, and these proteins may modulate VWF-mediated thrombus formation. PMID: 22267483 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Long Pentraxin 3/TSG-6 Interaction: A Biological Rheostat for Fibroblast Growth Factor 2-Mediated Angiogenesis.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 19 Jan 2012 05:00:00 +0100

CONCLUSIONS: TSG-6 reverts the inhibitory effects exerted by PTX3 on FGF2-mediated angiogenesis through competition of FGF2/PTX3 interaction. This may provide a novel mechanism to control angiogenesis in those pathological settings characterized by the coexpression of TSG-6 and PTX3, in which the relative levels of these proteins may fine-tune the angiogenic activity of FGF2. PMID: 22267482 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

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Antiatherosclerotic Effect of an Antibody That Binds to Extracellular Matrix Glycosaminoglycans.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 19 Jan 2012 05:00:00 +0100

CONCLUSIONS: These results support the use of anti-sulfated glycosaminoglycan antibody-based immunotherapy as a potential tool to prevent atherosclerosis. PMID: 22267481 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Site-Specific MicroRNA-92a Regulation of Kruppel-Like Factors 4 and 2 in Atherosusceptible Endothelium.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 19 Jan 2012 05:00:00 +0100

CONCLUSIONS: miR-92a coregulates KLF4 and KLF2 expression in arterial endothelium and contributes to phenotype heterogeneity associated with regional atherosusceptibility and protection in vivo. PMID: 22267480 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Anti-Inflammatory Effects of Nicotinic Acid in Human Monocytes Are Mediated by GPR109a Dependent Mechanisms.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 19 Jan 2012 05:00:00 +0100

CONCLUSIONS: NA displays a range of effects that are lipoprotein-independent and potentially antiatherogenic. These effects are mediated by GPR109a and are independent of prostaglandin pathways. They suggest a rationale for treatment with NA that is not dependent on levels of plasma cholesterol and possible applications beyond the treatment of dyslipidemia. PMID: 22267479 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Sympathetic Nervous System Regulates Bone Marrow-Derived Cell Egress Through Endothelial Nitric Oxide Synthase Activation: Role in Postischemic Tissue Remodeling.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 19 Jan 2012 05:00:00 +0100

CONCLUSIONS: These results unravel, for the first time, a major role for the sympathetic nervous system in BM-derived cell egress through stromal eNOS activation. PMID: 22267478 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Fractalkine: A Survivor's Guide: Chemokines as Antiapoptotic Mediators.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 12 Jan 2012 05:00:00 +0100

Authors: White GE, Greaves DR Abstract Chemokines are a family of low-molecular-weight proteins essential to the directed migration of cells under homeostatic and pathological conditions. Fractalkine (CX3CL1) is an unusual chemokine that can act as either a soluble or membrane-bound mediator and signals through the G protein-coupled chemokine receptor CX3CR1, expressed on monocytes, natural killer cells, T cells, and smooth muscle cells. Accumulating evidence suggests that fractalkine, in addition to its role in chemotaxis and adhesion of leukocytes, supports the survival of multiple cell types during homeostasis and inflammation. This review presents the evidence obtained from several disease models implying an antiapoptotic function for fractalkine and shows how this is relevant ...

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CD36 Ectodomain Phosphorylation Blocks Thrombospondin-1 Binding: Structure-Function Relationships and Regulation by Protein Kinase C.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 12 Jan 2012 05:00:00 +0100

CONCLUSIONS: New protein synthesis and trafficking through the Golgi are required for PMA-induced CD36 phosphorylation, suggesting that phosphorylation probably occurs intracellularly. These studies suggest a novel in vivo pathway for CD36 phosphorylation that modulates cellular affinity for thrombospondin-related proteins to blunt vascular cell signaling. PMID: 22247259 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

EphA2 Activation Promotes the Endothelial Cell Inflammatory Response: A Potential Role in Atherosclerosis.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 12 Jan 2012 05:00:00 +0100

CONCLUSIONS: The current data suggest that enhanced EphA2 signaling during endothelial cell activation perpetuates proinflammatory gene expression. Coupled with EphA2 expression in mouse and human atherosclerotic plaques, these data implicate EphA2 as a novel proinflammatory mediator and potential regulator of atherosclerotic plaque development. PMID: 22247258 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Nrf3-Pla2g7 Interaction Plays an Essential Role in Smooth Muscle Cell Differentiation From Stem Cells.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 12 Jan 2012 05:00:00 +0100

CONCLUSIONS: Our findings demonstrated that Pla2g7 plays a crucial physiological role in SMC differentiation from stem cells, and the fine interactions between Nrf3 and Pla2g7 are essential for SMC differentiation from stem cells. PMID: 22247257 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Prevalence of ANGPTL3 and APOB Gene Mutations in Subjects With Combined Hypolipidemia.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 12 Jan 2012 05:00:00 +0100

CONCLUSIONS: these results demonstrated that in a cohort of subjects with severe primary hypobetalipoproteinemia the prevalence of ANGPTL3 gene mutations responsible for a combined hypolipidemia phenotype is about 10%, whereas mutations of APOB gene are absent. PMID: 22247256 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Pro-Inflammatory Role of MicroRNA-200 in Vascular Smooth Muscle Cells From Diabetic Mice.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 12 Jan 2012 05:00:00 +0100

CONCLUSIONS: Disruption of the reciprocal negative regulatory loop between miR-200 and Zeb1 under diabetic conditions enhances proinflammatory responses of VSMC implicated in vascular complications. PMID: 22247255 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

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Dynamic Immune Cell Accumulation During Flow-Induced Atherogenesis in Mouse Carotid Artery: An Expanded Flow Cytometry Method.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 12 Jan 2012 05:00:00 +0100

CONCLUSIONS: This is the first quantitative description of leukocyte number and composition over the life span of murine atherosclerosis. These results show that disturbed flow induces rapid and dynamic leukocyte accumulation in the arterial wall during the initiation and progression of atherosclerosis. PMID: 22247254 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Socioeconomic Status, Cardiovascular Risk Factors, and Subclinical Atherosclerosis in Young Adults: The Cardiovascular Risk in Young Finns Study.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 05 Jan 2012 05:00:00 +0100

CONCLUSIONS: This study shows that high education in young adults is associated with favorable cardiovascular risk factor profile and 6-year change of risk factors. Most importantly, the progression of carotid atherosclerosis was slower among individuals with higher educational level. PMID: 22223734 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Mirtron MicroRNA-1236 Inhibits VEGFR-3 Signaling During Inflammatory Lymphangiogenesis.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 05 Jan 2012 05:00:00 +0100

CONCLUSIONS: Our data suggest that miR-1236 may function as a negative regulator of VEGFR-3 signaling during inflammatory lymphangiogenesis. PMID: 22223733 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

γ-Glutamyltransferase, Hepatic Enzymes, and Risk of Incident Heart Failure in Older Men.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 05 Jan 2012 05:00:00 +0100

CONCLUSIONS: Elevated GGT was associated with increased risk of HF in men aged <70 years. Additional studies are now needed to determine the mechanisms responsible. PMID: 22223732 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Inhibition of Bone Morphogenetic Protein Signaling Reduces Vascular Calcification and Atherosclerosis.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 05 Jan 2012 05:00:00 +0100

CONCLUSIONS: These results definitively implicate BMP signaling in atherosclerosis and calcification, while uncovering a previously unidentified role for BMP signaling in LDL cholesterol metabolism. BMP inhibition may be helpful in the treatment of atherosclerosis and associated vascular calcification. PMID: 22223731 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

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Tissue Factor Pathway Inhibitor Blocks Angiogenesis via Its Carboxyl Terminus.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 05 Jan 2012 05:00:00 +0100

CONCLUSIONS: These data demonstrate an inhibitory role for TFPI in angiogenesis that is, in part, mediated through peptides within its carboxyl terminus. In addition to its known role as a TF antagonist, TFPI, via its carboxyl terminus, may regulate angiogenesis by directly blocking VEGF receptor 2 activation and attenuating the migratory capacity of endothelial cells. PMID: 22223730 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Urotensin-II Signaling Mechanism in Rat Coronary Artery: Role of STIM1 and Orai1-Dependent Store Operated Calcium Influx in Vasoconstriction.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 05 Jan 2012 05:00:00 +0100

CONCLUSIONS: Here, we demonstrated that different critical players of SOCE signaling pathway are required for UII-induced vasoconstriction of rat coronary artery. PMID: 22223729 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Regulatory T-Cell Response to Apolipoprotein B100-Derived Peptides Reduces the Development and Progression of Atherosclerosis in Mice.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 05 Jan 2012 05:00:00 +0100

CONCLUSIONS: Subcutaneous infusion of adjuvant-free ApoB100-derived peptides to Apoe(-/-) mice reduces atherosclerosis through the induction of a specific Treg cell response. PMID: 22223728 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Oxidative DNA Damage Repair

Health News from Medical News Today — Thu, 29 Dec 2011 08:00:00 +0100

Oxidative stress is the cause of many serious diseases such as cancer, Alzheimer's, arteriosclerosis and diabetes. It occurs when the body is exposed to excessive amounts of electrically charged, aggressive oxygen compounds. These are normally produced during breathing and other metabolic processes, but also in the case of ongoing stress, exposure to UV light or X-rays. If the oxidative stress is too high, it overwhelms the body's natural defences. The aggressive oxygen compounds destroy genetic material, resulting in what are referred to as harmful 8-oxo-guanine base mutations in the DNA... (Source: Health News from Medical News Today)

The changing face and abbreviated lives of bone marrow cells in the heart.

Arteriosclerosis, Thrombosis and Vascular Biology — Sat, 24 Dec 2011 22:00:31 +0100

Authors: Robinson ST, Landázuri N, Taylor WR PMID: 22173974 [PubMed - in process] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

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Tissue Factor-Thrombin-PAR-1 Pathway: A Novel Link Between Bone Marrow and Blood Vessel.

Arteriosclerosis, Thrombosis and Vascular Biology — Sat, 24 Dec 2011 22:00:21 +0100

Authors: Delacroix S, Simari RD PMID: 22173975 [PubMed - in process] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Human neutrophil peptides mediate endothelial-monocyte interaction, foam cell formation, and platelet activation: correction.

Arteriosclerosis, Thrombosis and Vascular Biology — Sat, 24 Dec 2011 22:00:11 +0100

Authors: PMID: 22173976 [PubMed - in process] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Chemical pathology of homocysteine. V. Thioretinamide, thioretinaco, and cystathionine synthase function in degenerative diseases.

Annals of Clinical and Laboratory Science — Fri, 23 Dec 2011 21:54:02 +0100

Authors: McCully KS Abstract Hyperhomocysteinemia was first associated with degenerative disease by observation of accelerated arteriosclerosis in children with inherited disorders of cystathionine synthase, methionine synthase, and methylene tetrohydrofolate reductase. The metabolic blockade of sulfate synthesis from homocysteine thiolactone in malignant cells is ascribed to a deficiency of a chemopreventive derivative of homocysteine thiolactone that occurs in normal cells. Its chemical structure was elucidated by the organic synthesis of thioretinamide from retinoic acid and homocysteine thiolactone. Oxidation of the sulfur atom of homocysteine is inhibited in scorbutic guinea pigs, demonstrating ascorbate function in sulfate synthesis from homocysteine. Studies of homocysteine ...

Relationship between Magnesium and Clinical Biomarkers on Inhibition of Vascular Calcification.

American Journal of Nephrology — Thu, 15 Dec 2011 05:00:00 +0100

Conclusion: Elevated phosphate concentrations in the culture media induce ex vivo/in vitro medial calcification in intact rat aortic rings in the presence of alkaline phosphatase. Mg(2+) ions reduced ex vivo/in vitro vascular calcification despite increased phosphate concentration. This hypothesis is additionally based on the fact that CKD patients with high Mg(2) serum levels had significantly lower IMT and PWV values, which may result in a lower risk for cardiovascular events and mortality in these patients. Therefore, Mg(2+) supplementation may be an option for treatment and prevention of vascular calcification resulting in a reduction of cardiovascular events in CKD patients. PMID: 22179063 [PubMed - as supplied by publisher] (Source: American Journal of Nephrology)

Reciprocal Metabolic Perturbations in the Adipose Tissue and Liver of GPIHBP1-Deficient Mice.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 15 Dec 2011 05:00:00 +0100

CONCLUSIONS: Defective lipolysis in Gpihbp1-/- mice causes reciprocal metabolic perturbations in adipose tissue and liver. In adipose tissue, the essential fatty acid content of triglycerides is reduced and lipid biosynthetic gene expression is increased, whereas the opposite changes occur in the liver. PMID: 22173228 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

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Syndecan-1 Displays a Protective Role in Aortic Aneurysm Formation by Modulating T Cell-Mediated Responses.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 15 Dec 2011 05:00:00 +0100

CONCLUSIONS: These investigations identify cross-talk between Sdc-1-expressing macrophages and AAA-localized CD4(+) T cells, with Sdc-1 providing an important counterbalance to T-cell-driven inflammation in the vascular wall. PMID: 22173227 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Coronary Artery Calcification in Hemophilia A: No Evidence for a Protective Effect of Factor VIII Deficiency on Atherosclerosis.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 15 Dec 2011 05:00:00 +0100

CONCLUSIONS: The extent of coronary artery atherosclerosis is comparable between elderly men with and without hemophilia. Results from this study also underscore the importance of screening and treating atherosclerosis risk factors in hemophilia patients. PMID: 22173226 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Aldosterone Induces Vascular Insulin Resistance by Increasing Insulin-Like Growth Factor-1 Receptor and Hybrid Receptor.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 15 Dec 2011 05:00:00 +0100

ConclusionAldosterone induces vascular remodeling through IGF1R- and hybrid receptor-dependent vascular insulin resistance. Mineralocorticoid receptor blockade may attenuate angiopathy in hypertensive patients with hyperinsulinemia. PMID: 22173225 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Age estimation based on a combined arteriosclerotic index

International Journal of Legal Medicine — Mon, 12 Dec 2011 17:16:49 +0100

This study introduces a new quantity, the combined arteriosclerotic index (CAI), which is defined as the ratio between the diameter and the longitudinal prestrain of an artery. The longitudinal prestrain has been adopted as the ratio between the in situ length and the excised length of the abdominal aorta, and is a measure of arterial elasticity. During ageing, arteriosclerosis is manifested by the loss of pretension and by enlargement of the diameter of the artery. CAI combines these two effects. A sample of 61 female and 194 male autopsy measurements of human abdominal aortas shows that CAI correlates significantly with chronological age (R = 0.916/0.921; female/male). The sample had the following parameters: age 53 ± 19/48 ± 16 years; diameter of the abdominal a...

Preventive Effects of Exenatide on Endothelial Dysfunction Induced by Ischemia-Reperfusion Injury via KATP Channels.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 08 Dec 2011 05:00:00 +0100

CONCLUSIONS: The present study demonstrates that subcutaneous exenatide protects IR-induced endothelial dysfunction through opening of K(ATP) channels in human IR injury model. PMID: 22155457 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

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Genetic Variation in ABCG1 and Risk of Myocardial Infarction and Ischemic Heart Disease.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 08 Dec 2011 05:00:00 +0100

CONCLUSIONS: This is the first report of a functional variant in ABCG1 that associates with increased risk of MI and IHD in the general population. PMID: 22155456 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Urokinase-Type Plasminogen Activator Downregulates Paraoxonase 1 Expression in Hepatocytes by Stimulating Peroxisome Proliferator-Activated Receptor-γ Nuclear Export.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 08 Dec 2011 05:00:00 +0100

CONCLUSIONS: This study provides the first evidence that uPA interferes with PPARγ transcriptional activity in hepatocytes, resulting in downregulation of PON1 expression and its secretion to the medium. This may explain, at least in part, the prooxidative effect of uPA in the vascular wall. PMID: 22155455 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Resolution of Mitochondrial Oxidative Stress Rescues Coronary Collateral Growth in Zucker Obese Fatty Rats.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 08 Dec 2011 05:00:00 +0100

CONCLUSIONS: We conclude that mitochondrial oxidative stress and dysfunction play a key role in disrupting coronary collateral growth in obesity and the metabolic syndrome, and elimination of the mitochondrial oxidative stress with MQ or MT rescues collateral growth. PMID: 22155454 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Platelet Glycoprotein VI Dimerization, an Active Process Inducing Receptor Competence, Is an Indicator of Platelet Reactivity.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 08 Dec 2011 05:00:00 +0100

CONCLUSIONS: The rapid assembly of highly competent dimers of GPVI at sites of vascular lesion represents an important step in the sequence of events leading to platelet activation by collagen. GPVI dimers could represent a new marker to analyze platelet reactivity. PMID: 22155453 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Apolipoprotein B Secretion Is Regulated by Hepatic Triglyceride, and Not Insulin, in a Model of Increased Hepatic Insulin Signaling.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 08 Dec 2011 05:00:00 +0100

CONCLUSIONS: Either hepatic TG is the dominant regulator of apoB secretion or any inhibitory effects of hepatic insulin signaling on apoB secretion is very short-lived. PMID: 22155452 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

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The Proteoglycan Syndecan 4 Regulates Transient Receptor Potential Canonical 6 Channels via RhoA/ROCK Signaling.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 08 Dec 2011 05:00:00 +0100

CONCLUSIONS: Our results establish a previously unknown function of Sdc4 for regulation of TRPC6 channels and support the role of Sdc4 for the regulation of glomerular permeability. PMID: 22155451 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Extracorporeal assays of thrombosis.

Thrombosis and Haemostasis — Thu, 08 Dec 2011 00:06:44 +0100

Authors: Badimon L, Padro T, Vilahur G Abstract Platelet deposition, adhesion/aggregation, to the damaged vessel wall or atherosclerotic plaque components has shown to play a major role in hemostasis, thrombosis, and the development of atherosclerosis. Platelet-vessel wall interaction and thrombus formation is driven by blood flow rheology/hemodynamics (changes in local flow conditions), the nature of the flowing blood, and the characteristics of the triggering substrate (lesion type). An extracorporeal perfusion system (the Badimon chamber) was developed to investigate the dynamics of platelet deposition and thrombus formation on: (a) different surfaces (biological and synthetic); (b) under controlled blood flow conditions with varying degrees of stenosis mimicking various vascula...

Relationship between the catalase RS 769214 SNP and carotid plaques in a Caucasian cohort

Artery Research — Thu, 01 Dec 2011 05:00:00 +0100

In conclusion, our results indicate that CAT rs769214 SNP A allele may be a risk factor that contribute to carotid plaques in Caucasians. (Source: Artery Research)

Relation of mean and pulsatile blood pressure components to atherosclerosis and arteriosclerosis: A 10-year follow-up study

Artery Research — Thu, 01 Dec 2011 05:00:00 +0100

Background: Blood pressure (BP) can be separated into mean arterial pressure (MAP) and pulsatile (pulse pressure, PP) components which may relate differently to atherosclerosis and arteriosclerosis. The aim of the study was to examine the association between longitudinal measures of MAP and PP (central and peripheral) with measures of atherosclerosis and arterial stiffness. (Source: Artery Research)

Haemodialysis Access-induced Distal Ischaemia (HAIDI) is Caused by Loco-regional Hypotension but not by Steal

European Journal of Vascular and Endovascular Surgery — Mon, 28 Nov 2011 05:00:00 +0100

Conclusion: HAIDI is caused by too low forearm and hand blood pressures. Therapy should focus on attenuating the loss of arterial pressure including optimalisation of inflow arteries and/or ligation of the AVF’s venous side branches. Surgery aimed at access flow reduction or distal revascularisation is only indicated if these measures fail. (Source: European Journal of Vascular and Endovascular Surgery)

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Haemodialysis Access-induced Distal Ischaemia (HAIDI) is Caused by Loco-regional Hypotension but not by Steal.

PubMed: Eur J Vasc Endovasc ... — Fri, 25 Nov 2011 05:00:00 +0100

CONCLUSION: HAIDI is caused by too low forearm and hand blood pressures. Therapy should focus on attenuating the loss of arterial pressure including optimalisation of inflow arteries and/or ligation of the AVF's venous side branches. Surgery aimed at access flow reduction or distal revascularisation is only indicated if these measures fail. PMID: 22119228 [PubMed - as supplied by publisher] (Source: PubMed: Eur J Vasc Endovasc ...)

The influence of obesity on progression of coronary arteriosclerosis and clinical course after ST elevation acute myocardial infarction treated with primary coronary interventions.

Advances in Medical Sciences — Fri, 25 Nov 2011 05:00:00 +0100

Conclusions: Results of our prospective study indicate that in obese patients, there is a significantly greater number of atherosclerotic lesions in coronary arteries found during PCI, as compared to those with normal body weight or overweight. We proved that overweight and obesity did not result in significantly greater damage to the myocardium and left ventricular dysfunction, both in the acute phase and 6 months after myocardial infarction treated with primary coronary intervention, as compared to those with normal body weight. In addition correlation was found between BNP concentration profile and body mass index in the 6-month follow-up after STEMI treated with PCI and bare metal stent implantation. PMID: 22119914 [PubMed - as supplied by publisher] (Source: Advances in Medical Sc...

Primary Aldosteronism and Metabolic Syndrome

Hormone and Metabolic Research — Thu, 24 Nov 2011 05:00:00 +0100

This article reviews current knowledge regarding the prevalence and characteristics of the metabolic syndrome in primary aldosteronism, and discusses a possible pathophysiological link between aldosterone and its individual components other than hypertension. An abnormal glucose metabolism due to insulin resistance appears to be linked to aldosterone overproduction, and seems the major contributor to metabolic dysfunction in primary aldosteronism. Impairment of insulin action may be also due to concurrent environmental factors (hypokalemia?), and/or it might occur in compartments other than fat tissue (liver? skeletal muscle?). Higher rates of cardiovascular events reported in primary aldosteronism could be due in part to the increased prevalence of the metabolic syndrome in this disorder....

2011 nobel prize in physiology or medicine: toll-like receptors, dendritic cells, and their roles in atherosclerosis.

Arteriosclerosis, Thrombosis and Vascular Biology — Sat, 19 Nov 2011 21:37:37 +0100

Authors: Tedgui A, Owens AP, Mackman N PMID: 22096091 [PubMed - in process] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

The controversial role of the urokinase system in abdominal aortic aneurysm formation and rupture.

Arteriosclerosis, Thrombosis and Vascular Biology — Sat, 19 Nov 2011 21:37:27 +0100

Authors: Rein CM, Cardenas JC, Church FC PMID: 22096092 [PubMed - in process] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

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Smooth muscle cells for vascular engineering.

Arteriosclerosis, Thrombosis and Vascular Biology — Sat, 19 Nov 2011 21:37:16 +0100

Authors: Chen YE, Xie C, Hamblin M PMID: 22096093 [PubMed - in process] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

We Can Do It Together: PAR1/PAR2 Heterodimer Signaling in VSMCs.

Arteriosclerosis, Thrombosis and Vascular Biology — Sat, 19 Nov 2011 21:37:05 +0100

Authors: Pawlinski R, Holinstat M PMID: 22096094 [PubMed - in process] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Calcific aortic valve disease: cellular origins of valve calcification.

Arteriosclerosis, Thrombosis and Vascular Biology — Sat, 19 Nov 2011 21:36:55 +0100

Authors: Rajamannan NM PMID: 22096095 [PubMed - in process] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Cell death in cardiovascular disease.

Arteriosclerosis, Thrombosis and Vascular Biology — Sat, 19 Nov 2011 21:36:45 +0100

Authors: Bennett MR PMID: 22096096 [PubMed - in process] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Cell death, damage-associated molecular patterns, and sterile inflammation in cardiovascular disease.

Arteriosclerosis, Thrombosis and Vascular Biology — Sat, 19 Nov 2011 21:36:34 +0100

Authors: Zheng Y, Gardner SE, Clarke MC Abstract Cell death and inflammation are ancient processes of fundamental biological importance in both normal physiology and pathology. This is evidenced by the profound conservation of mediators, with ancestral homologues identified from plants to humans, and the number of diseases driven by aberrant control of either process. Apoptosis is the most well-studied cell death, but many forms exist, including autophagy, necrosis, pyroptosis, paraptosis, and the obscure dark cell death. Cell death occurs throughout the cardiovascular system, from initial shaping of the heart and vasculature during development to involvement in pathologies, including atherosclerosis, aneurysm, cardiomyopathy, restenosis, and vascular graft rejection. However, dete...

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Autophagy in atherosclerosis: a potential drug target for plaque stabilization.

Arteriosclerosis, Thrombosis and Vascular Biology — Sat, 19 Nov 2011 21:36:24 +0100

Authors: Schrijvers DM, De Meyer GR, Martinet W Abstract Evidence is accumulating that autophagy occurs in advanced atherosclerotic plaques. Although there is an almost relentless discovery of molecules that are involved in autophagy, studies of selective autophagy induction or inhibition using knockout mice are just now beginning to reveal its biological significance. Most likely, autophagy safeguards plaque cells against cellular distress, in particular oxidative injury, by degrading the damaged intracellular material. In this way, autophagy is protective and contributes to cellular recovery in an unfavorable environment. Pharmacological approaches have recently been developed to stabilize vulnerable, rupture-prone lesions through induction of autophagy. This approach has proven ...

Mechanisms of ER Stress-Induced Apoptosis in Atherosclerosis.

Arteriosclerosis, Thrombosis and Vascular Biology — Sat, 19 Nov 2011 21:36:13 +0100

Authors: Scull CM, Tabas I Abstract Endoplasmic reticulum (ER) stress is triggered by perturbations in ER function such as those caused by protein misfolding or by increases in protein secretion. Eukaryotic cells respond to ER stress by activating 3 ER-resident proteins, activating transcription factor-6, inositol requiring protein-1, and protein kinase RNA-like ER kinase (PERK). These proteins direct signaling pathways that relieve ER stress in a process known as the unfolded protein response (UPR). In pathological settings, however, prolonged UPR activation can promote cell death, and this process has recently emerged as an important concept in atherosclerosis. We review here the evidence for UPR activation and cell death in macrophages, smooth muscle cells, and endothelial cells...

Absence of arteriosclerosis in intramyocardial coronary arteries: a mystery to be solved?

Revista Brasileira de Cirurgia Cardiovascular — Fri, 18 Nov 2011 11:23:26 +0100

Several studies show that portions of intramyocardial coronary arteries are spared of arteriosclerosis, involving morphological, embryological, biochemical and pathophysiological aspects. Endothelial function is significantly affected in the segment of transition, as estimated by the vasoactive response to Ach. These findings suggest that myocardial bridge can provide protection against arteriosclerosis by counteracting the negative effects of endothelial dysfunction. The intramyocardial portion's protection phenomenon deserves further scientific research on all research fronts. Improved morphological, biomechanical and especially physiological and embryological knowledge may be the key to a future window of opportunity for chronic arterial disease therapy and prevention. In addition, this...

Transforming Growth Factor-β-Induced Endothelial-to-Mesenchymal Transition Is Partly Mediated by MicroRNA-21.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 17 Nov 2011 05:00:00 +0100

CONCLUSIONS: TGF-β-mediated EndMT is regulated at least in part by miR-21 via the phosphatase and tensin homolog/Akt pathway. In vivo, antifibrotic effects of miR-21 antagonism are partly mediated by blocking EndMT under stress conditions. PMID: 22095988 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Apolipoprotein B-100-Containing Lipoprotein Metabolism in Subjects With Lipoprotein Lipase Gene Mutations.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 17 Nov 2011 05:00:00 +0100

CONCLUSIONS: Our results confirm that hypertriglyceridemia is a key feature of familial LPL deficiency. This is due to impaired VLDL- and IDL-apoB-100 catabolism and VLDL-to-IDL conversion. Single-allele mutations of the LPL gene result in modest to elevated plasma triglycerides. The changes in plasma triglycerides and apoB-100 kinetics are attributable to the effects of the LPL genotype. PMID: 22095987 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

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NADPH Oxidase 4 Mediates Monocyte Priming and Accelerated Chemotaxis Induced by Metabolic Stress.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 17 Nov 2011 05:00:00 +0100

CONCLUSIONS: By increasing actin-S-glutathionylation and remodeling, metabolic stress primes monocytes for chemoattractant-induced transmigration and recruitment to sites of vascular injury. This Nox4-dependent process provides a novel mechanism through which metabolic disorders promote atherogenesis. PMID: 22095986 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Regulation of Peroxisome Proliferator-Activated Receptor-γ by Angiotensin II Via Transforming Growth Factor-β1-Activated p38 Mitogen-Activated Protein Kinase in Aortic Smooth Muscle Cells.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 17 Nov 2011 05:00:00 +0100

CONCLUSIONS: These findings suggest that Ang II decreases PPARγ abundance in cultured VSMCs via an angiotensin type 1 receptor-dependent secretion of TGF-β1 via phosphorylation of p38 mitogen-activated protein kinase and histone deacetylase 3. PMID: 22095985 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Association of Testosterone Levels With Endothelial Function in Men: Results From a Population-Based Study.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 17 Nov 2011 05:00:00 +0100

CONCLUSIONS: Lower serum total and free testosterone levels are associated with impaired endothelial function in this population-based sample of men. PMID: 22095984 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Xanthine Oxidoreductase Is Involved in Macrophage Foam Cell Formation and Atherosclerosis Development.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 17 Nov 2011 05:00:00 +0100

CONCLUSIONS: These results strongly suggest XOR activity and/or its expression level to contribute to macrophage foam cell formation. Thus, XOR inhibitors may be useful for preventing atherosclerosis. PMID: 22095983 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Pharmacological Suppression of Hepcidin Increases Macrophage Cholesterol Efflux and Reduces Foam Cell Formation and Atherosclerosis.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 17 Nov 2011 05:00:00 +0100

CONCLUSIONS: These data suggest that pharmacological manipulation of iron homeostasis may be a promising target to increase macrophage reverse cholesterol transport and limit atherosclerosis. PMID: 22095982 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

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Inhibition of MicroRNA-29 Enhances Elastin Levels in Cells Haploinsufficient for Elastin and in Bioengineered Vessels.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 17 Nov 2011 05:00:00 +0100

CONCLUSIONS: miR-29 antagonism may promote increased ELN levels during conditions of ELN deficiencies. PMID: 22095981 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

S100A8 and S100A9 in Cardiovascular Biology and Disease.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 17 Nov 2011 05:00:00 +0100

Authors: Averill MM, Kerkhoff C, Bornfeldt KE Abstract There is recent and widespread interest in the damage-associated molecular pattern molecules S100A8 and S100A9 in cardiovascular science. These proteins have a number of interesting features and functions. For example, S100A8 and S100A9 (S100A8/A9) have both intracellular and extracellular actions, they are abundantly expressed in inflammatory and autoimmune states, primarily by myeloid cells but also by other vascular cells, and they modulate inflammatory processes, in part through Toll-like receptor 4 and the receptor for advanced glycation end products. S100A8/A9 also have anti-inflammatory and immune regulatory actions. Furthermore, increased plasma levels of S100A8/A9 predict cardiovascular events in humans, and deletion o...

Calpains Contribute to Vascular Repair in Rapidly Progressive Form of Glomerulonephritis: Potential Role of Their Externalization.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 17 Nov 2011 05:00:00 +0100

CONCLUSIONS: This study demonstrates that externalized calpains participate in angiogenesis and vascular repair, partly by promoting fibronectin cleavage and thereby amplifying vascular endothelial growth factor efficiency. Thus, manipulation of calpain externalization may have therapeutic implications to control angiogenesis. PMID: 22095979 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Arteriolar Function in Visceral Adipose Tissue Is Impaired in Human Obesity.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 17 Nov 2011 05:00:00 +0100

CONCLUSIONS: Our findings provide clinical evidence that the visceral microenvironment may be intrinsically toxic to arterial health providing a potential mechanism by which visceral adiposity burden is linked to atherosclerotic vascular disease. Our findings also support the evolving concept that both adipose tissue quality and quantity may play significant roles in shaping cardiovascular phenotypes in human obesity. PMID: 22095978 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

G Protein-Coupled Receptor Kinase-5 Attenuates Atherosclerosis by Regulating Receptor Tyrosine Kinases and 7-Transmembrane Receptors.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 17 Nov 2011 05:00:00 +0100

CONCLUSIONS: GRK5 attenuates atherosclerosis through multiple cell type-specific mechanisms, including reduction of SMC and endothelial cell NF-κB activity and desensitization of receptor-specific signaling through the monocyte CCR2, macrophage CSF-1R, and the SMC platelet-derived growth factor receptor-β. PMID: 22095977 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

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Hartmann’s operation: how often is it reversed and at what cost? A multicentre study

Colorectal Disease — Thu, 10 Nov 2011 10:36:37 +0100

Conclusion Hartmann’s reversal was performed in a small percentage of patients, mostly including those with benign disease. It had a significant morbidity. (Source: Colorectal Disease)

Competing Risk of Atherosclerotic Risk Factors for Arterial and Venous Thrombosis in a General Population: The Tromso Study.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 10 Nov 2011 05:00:00 +0100

CONCLUSIONS: Our findings imply that traditional atherosclerotic risk factors, such as smoking, hypertension, dyslipidemia, and diabetes mellitus are not shared by arterial and venous thrombosis. PMID: 22075253 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Inhibitor of Differentiation-3 Mediates High Fat Diet-Induced Visceral Fat Expansion.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 10 Nov 2011 05:00:00 +0100

CONCLUSIONS: Results identify Id3 as an important regulator of HFD-induced visceral adipose VEGFA expression, microvascular blood volume, and depot expansion. Inhibition of Id3 may have potential as a therapeutic strategy to limit visceral adiposity. PMID: 22075252 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Relationships Between Recent Intraplaque Hemorrhage and Stroke Risk Factors in Patients With Carotid Stenosis: The HIRISC Study.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 10 Nov 2011 05:00:00 +0100

CONCLUSIONS: Our findings support the potential link between recent IPH and risk of ipsilateral stroke in symptomatic disease but also imply that prognostic studies should adjust for known stroke risk factors in multivariate analyses. In asymptomatic stenosis, the potential predictive value of recent IPH is less likely to be confounded by stroke risk factors. PMID: 22075251 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Rap1-Rac1 Circuits Potentiate Platelet Activation.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 10 Nov 2011 05:00:00 +0100

CONCLUSIONS: We demonstrate important crosstalk between Rap1 and Rac1 downstream of GPVI. Whereas Rap1 signaling directly controls sustained Rac1 activation, Rac1 affects CalDAG-GEFI- and P2Y12-dependent Rap1 activation via its role in calcium mobilization and granule/ADP release, respectively. PMID: 22075250 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

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Clinical and Genetic Association of Serum Ceruloplasmin With Cardiovascular Risk.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 10 Nov 2011 05:00:00 +0100

CONCLUSIONS: In stable cardiac patients, serum Cp provides independent risk prediction of long-term adverse cardiac events. Genetic variants at the CP locus that modestly affect serum Cp levels are not associated with prevalent or incident risk of coronary artery disease in this study population. PMID: 22075249 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Transsignaling of Interleukin-6 Crucially Contributes to Atherosclerosis in Mice.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 10 Nov 2011 05:00:00 +0100

CONCLUSIONS: These data clarify, for the first time, the critical involvement of, in particular, the transsignaling of IL-6 in CAD and warrant further investigation of sgp130Fc as a novel therapeutic for the treatment of CAD and related diseases. PMID: 22075248 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Objectively Assessed Physical Activity, Sedentary Time, and Coronary Artery Calcification in Healthy Older Adults.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 10 Nov 2011 05:00:00 +0100

CONCLUSIONS: Our results confirm no association between objectively assessed physical activity and CAC. Because CAC measures cannot identify more vulnerable lesions, additional studies are required to examine whether physical activity can promote plaque stability. PMID: 22075247 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Dynamic Synchrotron Imaging of Diabetic Rat Coronary Microcirculation In Vivo.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 10 Nov 2011 05:00:00 +0100

CONCLUSIONS: Synchrotron imaging provides a novel method to investigate coronary microvascular function in vivo at all levels of the arterial tree. Furthermore, we have shown that early-stage diabetes is associated with localized coronary microvascular endothelial dysfunction. PMID: 22075246 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Urokinase Receptor Associates With Myocardin to Control Vascular Smooth Muscle Cells Phenotype in Vascular Disease.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 10 Nov 2011 05:00:00 +0100

CONCLUSIONS: These findings reveal the transcriptional activity of uPAR, controlling the differentiation of VSMCs in a vascular disease model. They also suggest a new role for uPAR as a therapeutic target and as a marker for VSMC phenotyping on prosthetic biomaterials. PMID: 22075245 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

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Effect of Ionizing Radiation Induced Damage of Endothelial Progenitor Cells in Vascular Regeneration.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 10 Nov 2011 05:00:00 +0100

CONCLUSIONS: The results of the present study suggest that suppression of p53 would be clinically applicable to (1) minimize the functional defects in EPCs in order to prevent the onset of vascular diseases caused by radiation therapy or radiation exposure and also to (2) provide novel insight into the mechanisms of IR-induced vascular damage and a possible strategy to minimize vascular damage by IR. PMID: 22075244 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Complement system activation and endothelial dysfunction in patients with age‐related macular degeneration (AMD): possible relationship between AMD and atherosclerosis

Acta Ophthalmologica — Tue, 08 Nov 2011 05:00:00 +0100

Abstract.Age‐related macular degeneration (AMD) shares several pathological and epidemiological similarities with systemic atherosclerosis (AS). First, an association between AS and AMD is apparent from the analyses of the histological and biochemical structure of atherosclerotic plaques in the vascular walls and retinal drusen, the hallmark of AMD. Second, there is considerable evidence implicating endothelial dysfunction in the pathogenesis of both disorders, and cellular oxidative stress appears to be a common denominator underlying this process. Moreover, there are observations that the complement system (CS) triggering inflammatory response contributes to the onset and advancement of both diseases. The CS plays a role in the generation of drusen and neovascularization in AMD as well...

ApoE Suppresses Atherosclerosis by Reducing Lipid Accumulation in Circulating Monocytes and the Expression of Inflammatory Molecules on Monocytes and Vascular Endothelium.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 03 Nov 2011 04:00:00 +0100

CONCLUSIONS: Our findings suggest that apoE reduces atherosclerosis in the setting of hyperlipidemia by increasing plasma apoA1-HDL that likely contribute to reduce intracellular lipid accumulation and thereby the activation of circulating leukocytes and the vascular endothelium. PMID: 22053073 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Reperfusion Injury Intensifies the Adaptive Human T Cell Alloresponse in a Human-Mouse Chimeric Artery Model.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 03 Nov 2011 04:00:00 +0100

CONCLUSIONS: We developed a new human-mouse chimeric model demonstrating interactions of reperfusion injury and alloimmunity using human cells and tissues that may be adapted to study other forms of nonimmune injury and other types of adaptive immune responses. PMID: 22053072 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Deleted in Malignant Brain Tumors 1 is Present in the Vascular Extracellular Matrix and Promotes Angiogenesis.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 03 Nov 2011 04:00:00 +0100

CONCLUSIONS: Taken together, the results of this study indicate that DMBT1 functions as an important endothelium-derived ECM protein that is able to bind angiogenic factors and promote adhesion, migration, proliferation, and angiogenesis as well as vascular repair. Mechanistically, DMBT1 interacts with galectin-3 and modulates the Notch signaling pathway as well as the differential expression of ephrin-B2 and EphB4. PMID: 22053071 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

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Determinants of Microvascular Network Topologies in Implanted Neovasculatures.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 03 Nov 2011 04:00:00 +0100

CONCLUSIONS: Here we show that network topology resulting from implanted microvessel precursors is independent from prepatterning of precursors but can be influenced by a patterning stimulus involving tissue deformation during postangiogenesis remodeling and maturation. PMID: 22053070 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Novel therapeutic approach based on recent understanding of the development of metabolic syndrome.

Yakugaku Zasshi : Journal of the Pharmaceutical Society of Japan — Wed, 02 Nov 2011 12:05:02 +0100

Authors: Hosoi T Abstract Obesity is associated with metabolic syndrome, a cluster of symptoms including diabetes, hyperlipidemia, hypertension and arteriosclerosis, which can cause serious health problems. Accumulating evidence suggests that endoplasmic reticulum stress (ER stress) is associated with metabolic syndrome. Leptin is an anti-obesity hormone, which is secreted from adipose tissue. Circulating leptin acts at the brain hypothalamus and reduces food intake. As most forms of obesity indicate a state of leptin resistance, elucidation of the mechanisms of leptin resistance would be an important subject. We and other groups have recently suggested that leptin resistance may be derived from ER stress. These results raised the possibility that attenuating ER stress would be eff...

History of discovery: platelet-derived growth factor.

Arteriosclerosis, Thrombosis and Vascular Biology — Tue, 01 Nov 2011 04:00:00 +0100

Authors: Bowen-Pope DF, Raines EW Abstract A growth-promoting activity released from activated platelets, the platelet-derived growth factor, was discovered and characterized while the cellular and molecular mechanisms underlying the formation of the lesions of atherosclerosis were being investigated. This review provides a personal account of the different challenges we faced 3 decades ago in this undertaking and describes how our path was influenced by our focus on a disease process and by the evolving general understanding of the molecular effectors of cell proliferation. PMID: 22011752 [PubMed - in process] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Circulating MicroRNAs: Biomarkers or Mediators of Cardiovascular Diseases?

Arteriosclerosis, Thrombosis and Vascular Biology — Tue, 01 Nov 2011 04:00:00 +0100

Authors: Fichtlscherer S, Zeiher AM, Dimmeler S Abstract MicroRNAs (miRs) are small, noncoding RNAs that posttranscriptionally control gene expression by inhibiting protein translation or inducing target mRNA destabilization. Besides their intracellular function, recent studies demonstrate that miRs can be exported or released by cells and circulate with the blood in a remarkably stable form. The discovery of circulating miRs opens up intriguing possibilities to use the circulating miR patterns as biomarker for cardiovascular diseases. Cardiac injury as it occurs after acute myocardial infarction increases the circulating levels of several myocardial-derived miRs (eg, miR-1, miR-133, miR-499, miR-208), whereas patients with coronary artery disease or diabetes showed reduced levels ...

MicroRNA Modulation of Cholesterol Homeostasis.

Arteriosclerosis, Thrombosis and Vascular Biology — Tue, 01 Nov 2011 04:00:00 +0100

Authors: Fernández-Hernando C, Moore KJ Abstract Although the roles of the sterol response element binding protein-1 (SREBP1) and SREBP2 transcription factors in regulating fatty acid and cholesterol synthesis and uptake have been known for some time, it was recently discovered that 2 related microRNAs (miRs), miR-33a and miR-33b, are embedded in these genes. Studies indicate that miR-33a and miR-33b act with their host genes, Srebp2 and Srebp1, respectively, to reciprocally regulate cholesterol homeostasis and fatty acid metabolism in a negative feedback loop. miR-33 has been shown to posttranscriptionally repress key genes involved in cellular cholesterol export and high-density lipoprotein metabolism (Abca1, Abcg1, Npc1), fatty acid oxidation (Crot, Cpt1a, Hadhb, Ampk), and glu...

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Micromanaging vascular smooth muscle cell differentiation and phenotypic modulation.

Arteriosclerosis, Thrombosis and Vascular Biology — Tue, 01 Nov 2011 04:00:00 +0100

Authors: Davis-Dusenbery BN, Wu C, Hata A Abstract The phenotype of vascular smooth muscle cells (VSMCs) is dynamically regulated in response to various stimuli. In a cellular process known as phenotype switching, VSMCs alternate between a contractile and synthetic phenotype state. Deregulation of phenotype switching is associated with vascular disorders such as atherosclerosis, restenosis after angioplasty, and pulmonary hypertension. An important role for microRNAs (miRNAs) in VSMC development and phenotype switching has recently been uncovered. Individual miRNAs are involved in promoting both contractile and synthetic VSMC phenotype. In this review, we summarize recent advances in the understanding of miRNA function in the regulation of VSMC phenotype regulation. PMID: 22011...

MicroRNA Regulation of Cardiovascular Functions.

Arteriosclerosis, Thrombosis and Vascular Biology — Tue, 01 Nov 2011 04:00:00 +0100

Authors: Sessa WC PMID: 22011748 [PubMed - in process] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

MicroRNAs Looping Around Angiogenesis.

Arteriosclerosis, Thrombosis and Vascular Biology — Tue, 01 Nov 2011 04:00:00 +0100

Authors: Fiedler J, Thum T PMID: 22011747 [PubMed - in process] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Blood coagulation and blood vessel development: is tissue factor the missing link?

Arteriosclerosis, Thrombosis and Vascular Biology — Tue, 01 Nov 2011 04:00:00 +0100

Authors: Mackman N, Davis GE PMID: 22011746 [PubMed - in process] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

The clock is ticking as the clot thickens.

Arteriosclerosis, Thrombosis and Vascular Biology — Tue, 01 Nov 2011 04:00:00 +0100

Authors: Conway EM PMID: 22011745 [PubMed - in process] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

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Can the Occurrence of Gastrointestinal Bleeding in Nonpulsatile Left Ventricular Assist Device Patients Provide Clues for the Reversal of Arteriosclerosis?

Cardiology Clinics — Tue, 01 Nov 2011 04:00:00 +0100

This article is written not only to explore the deleterious effects of nonpulsatile flow (namely, gastrointestinal [GI] bleeding), but also to propose the novel concept that deliberate induction of nonpulsatile flow might be harnessed to produce beneficial remodeling in arteriosclerotic arteries. Continuous-flow left ventricular assist devices have proven their efficacy in the treatment of end-stage heart disease. They are a reliable option in bridge-to-transplant and destination therapy. An enigmatic consequence of this therapy has been occult GI bleeding. (Source: Cardiology Clinics)

Editorial Comment on “Can the Occurrence of GI Bleeding in Non-Pulsatile LVAD Patients Provide Clues for the Reversal of Arteriosclerosis?”

Cardiology Clinics — Tue, 01 Nov 2011 04:00:00 +0100

The authors of “Can the Occurrence of GI Bleeding in Non-Pulsatile LVAD Patients Provide Clues for the Reversal of Arteriosclerosis?” (Drs John A. Elefteriades and Louis H. Stein) make the point that arterial morphology is highly dependent on mechanical loading, especially the pulse pressure of the arterial waveform. With nonpulsatile flow of axial LVADs, the mechanical loading is light and the arterial wall involutes, thinning and losing smooth muscle cells. This observation may provide a mechanism for stopping or reversing arteriosclerosis via LVAD therapy in the future. (Source: Cardiology Clinics)

Transforming Growth Factor Beta Expression by Human Vascular Cells Inhibits Interferon Gamma Production and Arterial Media Injury by Alloreactive Memory T Cells

American Journal of Transplantation — Fri, 28 Oct 2011 05:32:19 +0100

Arteriosclerosis is characterized by the local activation of effector T cells leading to production of proinflammatory cytokines, such as IFN (interferon)‐γ and IL‐17, within the vessel wall. Conversely, the production of antiinflammatory cytokines, for example, TGF‐β, by regulatory lymphocytes is known to inhibit both the differentiation of naïve T cells into effector T cells and the development of arteriosclerosis in murine models. We investigated the role of TGF‐β on the alloreactivity of human effector memory T cells (Tem). Quiescent vascular cells, but not Tem, expressed TGF‐β. Blockade of TGF‐β activity in cocultures of CD4+ Tem with allogeneic endothelial cells significantly increased IFN‐γ, but not IL‐17, secretion. Additionally, serologic neutralization of T...

In Vivo Functional and Transcriptional Profiling of Bone Marrow Stem Cells After Transplantation Into Ischemic Myocardium.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 27 Oct 2011 04:00:00 +0100

CONCLUSION-: Collectively, these data suggest that BMMC therapy, in its present iteration, may be less efficacious than once thought. Additional refinement of existing cell delivery protocols should be considered to induce better therapeutic efficacy. PMID: 22034515 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Calcified Atherosclerosis in Different Vascular Beds and the Risk of Mortality.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 27 Oct 2011 04:00:00 +0100

CONCLUSION-: The associations between calcified atherosclerosis and mortality differ by vascular bed, suggesting that the location and severity of calcification in different vascular beds provide unique information for mortality. PMID: 22034514 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

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Transglutaminase 2-Mediated Activation of β-Catenin Signaling Has a Critical Role in Warfarin-Induced Vascular Calcification.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 27 Oct 2011 04:00:00 +0100

CONCLUSION-: TG2 is a critical mediator of warfarin-induced vascular calcification that acts through the activation of β-catenin signaling in VSMCs. Inhibition of canonical β-catenin pathway or TG2 activity prevents warfarin-regulated calcification, identifying the TG2/β-catenin axis as a novel therapeutic target in vascular calcification. PMID: 22034513 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Inhibition of Thrombin Receptor Signaling on α-Smooth Muscle Actin+ CD34+ Progenitors Leads to Repair After Murine Immune Vascular Injury.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 27 Oct 2011 04:00:00 +0100

CONCLUSION-: Specific inhibition of thrombin generation or PAR-1 signaling on α-SMA CD34 cells inhibits IH and promotes regenerative repair despite ongoing immune-mediated damage. PMID: 22034512 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

The Scaffolding Protein EBP50 Promotes Vascular Smooth Muscle Cell Proliferation and Neointima Formation by Regulating Skp2 and p21cip1.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 27 Oct 2011 04:00:00 +0100

CONCLUSION-: EBP50 is critical for neointima formation and induces VSMC proliferation by decreasing S-phase kinase protein 2 stability, thereby accelerating the degradation of the cell cycle inhibitor p21. PMID: 22034511 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Aging Enhances the Basal Production of IL-6 and CCL2 in Vascular Smooth Muscle Cells.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 27 Oct 2011 04:00:00 +0100

CONCLUSION-: Aging induces a proinflammatory phenotype in VSMC due in part to increased signaling of TLR4 and MyD88. Our results provide a potential explanation as to why aging leads to chronic inflammation and enhanced atherosclerosis. PMID: 22034510 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Renal histological lesions and outcome in liver transplant recipients

Clinical Transplantation — Sun, 23 Oct 2011 04:00:00 +0100

Conclusion: Renal histology is variable and not limited to CNI toxicity in OLT recipients referred for KB. Whether management based on KB findings can directly improve outcomes remains unclear. (Source: Clinical Transplantation)

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Overexpression of Tissue Inhibitor of Metalloproteinase 3 in Macrophages Reduces Atherosclerosis in Low-Density Lipoprotein Receptor Knockout Mice.

Arteriosclerosis, Thrombosis and Vascular Biology — Fri, 21 Oct 2011 04:00:00 +0100

CONCLUSION-: Our study confirmed that macrophage-specific overexpression of TIMP3 decreases the inflammatory content and the amplitude of atherosclerotic plaques in mice. PMID: 22015660 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Mean Platelet Volume and Integrin Alleles Correlate With Levels of Integrins αIIbβ3 and α2β1 in Acute Coronary Syndrome Patients and Normal Subjects.

Arteriosclerosis, Thrombosis and Vascular Biology — Fri, 21 Oct 2011 04:00:00 +0100

CONCLUSION-: MPV is the major effector of platelet αIIbβ3 level, whereas the ITGA2 rs1126643 alleles influence α2β1 level more than MPV does. The rs1126643 minor allele, associated with lower MPV, likely exerts this effect via the influence of α2β1 on megakaryocyte maturation. Because of the hyperactivity of larger platelets, MPV is an accurate metric of risk for adverse outcome in ACS. PMID: 22015659 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Disruption of Endothelial Peroxisome Proliferator-Activated Receptor γ Accelerates Diet-Induced Atherogenesis in LDL Receptor-Null Mice.

Arteriosclerosis, Thrombosis and Vascular Biology — Fri, 21 Oct 2011 04:00:00 +0100

CONCLUSION-: Endothelial PPARγ plays an important protective role in atherogenesis. PMID: 22015658 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Lysophosphatidic Acid Signaling Protects Pulmonary Vasculature From Hypoxia-Induced Remodeling.

Arteriosclerosis, Thrombosis and Vascular Biology — Fri, 21 Oct 2011 04:00:00 +0100

CONCLUSION-: Our findings indicate that LPA may negatively regulate pulmonary vascular pressure through LPA1 and LPA2 receptors and that in the absence of LPA signaling, upregulation in the endothelin system favors remodeling. PMID: 22015657 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Stent Coated With Antibody Against Vascular Endothelial-Cadherin Captures Endothelial Progenitor Cells, Accelerates Re-Endothelialization, and Reduces Neointimal Formation.

Arteriosclerosis, Thrombosis and Vascular Biology — Fri, 21 Oct 2011 04:00:00 +0100

CONCLUSION-: VE-cad stents captured EPC successfully in vitro, accelerated endothelial recovery on stent, and eventually reduced neointimal formation in vivo. PMID: 22015656 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

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Relationship between carotid intima-media thickness, cytokines, atherosclerosis extent and a two-year cardiovascular risk in patients with arteriosclerosis.

Kardiologia Polska — Thu, 20 Oct 2011 12:35:03 +0100

Conclusions: Levels of hs-CRP, IL-6, IL-10 are independently associated with atherosclerosis extent, while TNF-α and NT- -proBNP are mostly related to a two-year CV event risk. The CIMT 〉 1.3 mm seems to be a clinically relevant marker associated with atherosclerosis extent and CV risk, although CV event risk is primarily related to the baseline stenosis location. Kardiol Pol 2011; 69, 10: 1024-1031. PMID: 22006602 [PubMed - in process] (Source: Kardiologia Polska)

Biomarkers Associated With Pulse Pressure in African-Americans and Non-Hispanic Whites.

American Journal of Hypertension — Thu, 20 Oct 2011 04:00:00 +0100

ConclusionsOur results suggest that hemodynamic stress, vascular inflammation and calcification, and matrix remodeling may have a role in the pathogenesis and/or adverse consequences of increased pulse pressure.American Journal of Hypertension (2011). doi:10.1038/ajh.2011.193. PMID: 22012208 [PubMed - as supplied by publisher] (Source: American Journal of Hypertension)

Endoplasmic Reticulum Stress and Glycogen Synthase Kinase-3β Activation in Apolipoprotein E-Deficient Mouse Models of Accelerated Atherosclerosis.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 13 Oct 2011 04:00:00 +0100

CONCLUSION: These findings support the existence of a common mechanism of accelerated atherosclerosis involving ER stress signaling through activation of GSK3β. Furthermore, our results suggest that atherosclerosis can be attenuated by modulating GSK3β phosphorylation. PMID: 21998135 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Geranylgeranylacetone, Heat Shock Protein 90/AMP-Activated Protein Kinase/Endothelial Nitric Oxide Synthase/Nitric Oxide Pathway, and Endothelial Function in Humans.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 13 Oct 2011 04:00:00 +0100

CONCLUSION: These findings suggest that GGA-induced activation of Hsp90/AMPK significantly increased NO-mediated vasodilation in healthy subjects, as well as in smokers. The use of GGA may be a new therapeutic approach for improving endothelial dysfunction. PMID: 21998134 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Crucial Role of CD40 Signaling in Vascular Wall Cells in Neointimal Formation and Vascular Remodeling After Vascular Interventions.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 13 Oct 2011 04:00:00 +0100

CONCLUSION: CD40 signaling through TRAF6 in vascular SMCs seems to be centrally involved in neointimal formation in a NF-κB-dependent manner. Modulating CD40 signaling on local vascular wall may become a new therapeutic target against vascular restenosis. PMID: 21998133 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

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Tissue-intrinsic dysfunction of circadian clock confers transplant arteriosclerosis [Medical Sciences]

Proceedings of the National Academy of Sciences — Tue, 11 Oct 2011 04:00:00 +0100

The suprachiasmatic nucleus of the brain is the circadian center, relaying rhythmic environmental and behavioral information to peripheral tissues to control circadian physiology. As such, central clock dysfunction can alter systemic homeostasis to consequently impair peripheral physiology in a manner that is secondary to circadian malfunction. To determine the impact of circadian clock function in organ transplantation and dissect the influence of intrinsic tissue clocks versus extrinsic clocks, we implemented a blood vessel grafting approach to surgically assemble a chimeric mouse that was part wild-type (WT) and part circadian clock mutant. Arterial isografts from donor WT mice that had been anastamosed to common carotid arteries of recipient WT mice (WT:WT) exhibited no pathology in th...

Spatial Distribution and Mechanical Function of Elastin in Resistance Arteries: A Role in Bearing Longitudinal Stress.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 06 Oct 2011 04:00:00 +0100

CONCLUSION-: These results indicate the importance of elastin in bearing longitudinal stress in the arteriolar wall and that these fibers constrain vascular smooth muscle cells. Differences between skeletal muscle and cerebral small arteries may reflect differences in the local mechanical environment, such as exposure to longitudinal stretch. PMID: 21979438 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Abcc6 Deficiency Causes Increased Infarct Size and Apoptosis in a Mouse Cardiac Ischemia-Reperfusion Model.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 06 Oct 2011 04:00:00 +0100

CONCLUSION-: These data identify Abcc6 as a novel modulator of cardiac myocyte survival after I/R. This cardioprotective mechanism may involve inhibition of the BMP signaling pathway, which modulates apoptosis. PMID: 21979437 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Heparin Strongly Induces Soluble fms-Like Tyrosine Kinase 1 Release In Vivo and In Vitro.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 06 Oct 2011 04:00:00 +0100

CONCLUSION-: Heparin releases sFlt1 by displacing the sFlt1 heparin-binding site from heparan sulfate proteoglycans. Heparin could induce an antiangiogenic state. PMID: 21979436 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Transforming Growth Factor-β Signaling in Myogenic Cells Regulates Vascular Morphogenesis, Differentiation, and Matrix Synthesis.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 06 Oct 2011 04:00:00 +0100

CONCLUSION-: TGF-β signaling in SMCs controls differentiation, matrix synthesis, and vascular morphogenesis. Effects of TGF-β on SMC gene expression appear to differ depending on the location of SMCs in the aorta. PMID: 21979435 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

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Macrophage Polarization by Angiotensin II-Type 1 Receptor Aggravates Renal Injury-Acceleration of Atherosclerosis.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 06 Oct 2011 04:00:00 +0100

CONCLUSION-: AT1 receptor of bone marrow-derived macrophages worsens the extent and complexity of renal injury-induced atherosclerosis by shifting the macrophage phenotype to more M1 and less M2 through mechanisms that include increased apoptosis and impaired efferocytosis. PMID: 21979434 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

The β-Chain of Cell Surface F0F1 ATPase Modulates ApoA-I and HDL Transcytosis Through Aortic Endothelial Cells.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 06 Oct 2011 04:00:00 +0100

CONCLUSION-: Binding of apoA-I to ectopic F0F1 ATPase triggers the generation of ADP, which via activation of the purinergic receptor. P2Y12 stimulates the uptake and transport of HDL and initially lipid-free apoA-I by endothelial cells. PMID: 21979433 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

New Approach To Keeping Coronary Arteries Open After Angioplasties

Health News from Medical News Today — Mon, 03 Oct 2011 07:00:00 +0100

Research at Loyola University Chicago Stritch School of Medicine could help lead to new ways to prevent coronary arteries from reclogging after balloon angioplasties. The latest in a series of studies in this effort is published online ahead of print in Arteriosclerosis, Thrombosis and Vascular Biology, a journal of the American Heart Association. Senior author is Allen M. Samarel, MD, and first author is Yevgeniya E. Koshman, PhD. In an angioplasty, a tiny balloon is inflated to open a clogged coronary artery... (Source: Health News from Medical News Today)

[Rosuvastatin improves myocardial function and arteriosclerosis plaque in patients with ST-segment elevation after acute myocardial infarction and percutaneous coronary intervention].

Journal of Southern Medical University — Sat, 01 Oct 2011 04:00:00 +0100

CONCLUSION: Rosuvastatin therapy in addition to conventional medications can significantly reduce IMT and improve the functions of the surviving myocardium in patients with STEMI after PCI. PMID: 22027793 [PubMed - in process] (Source: Journal of Southern Medical University)

The great cholesterol myth; unfortunate consequences of Brown and Goldstein's mistake

QJM — Fri, 23 Sep 2011 04:00:00 +0100

Following their Nobel Prize-winning discovery of the defective gene causing familial hypercholesterolaemia, Brown and Goldstein misunderstood the mechanism involved in the pathogenesis of the associated arterial disease. They ascribed this to an effect of the high levels of cholesterol circulating in the blood. In reality, the accelerated arterial damage is likely to be a consequence of more brittle arterial cell walls, as biochemists know cholesterol to be a component of them which modulates their fluidity, conferring flexibility and hence resistance to damage from the ordinary hydrodynamic blood forces. In the absence of efficient receptors for LDL cholesterol, cells will be unable to use this component adequately for the manufacture of normally resilient arterial cell walls, resulting i...

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Adverse Effects of Bone Marrow Stromal Cell Treatment of Stroke in Diabetic Rats.

Stroke — Thu, 22 Sep 2011 04:00:00 +0100

CONCLUSIONS: BMSC therapy in T1DM-MCAO rats does not improve functional outcome. On the contrary, it increases blood-brain barrier leakage and cerebral artery neointimal formation, and arteriosclerosis, which possibly is due to increased expression of angiogenin. Thus, BMSC treatment starting 24 hours after MCAO may not be beneficial for diabetic subjects with stroke. PMID: 21940967 [PubMed - as supplied by publisher] (Source: Stroke)

Targeting inhibitor of apoptosis proteins to block vascular inflammation.

Arteriosclerosis, Thrombosis and Vascular Biology — Tue, 20 Sep 2011 08:21:24 +0100

Authors: Luong le A, Evans PC PMID: 21918207 [PubMed - in process] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

BMPing Up Angiogenesis via BMPER.

Arteriosclerosis, Thrombosis and Vascular Biology — Tue, 20 Sep 2011 08:21:15 +0100

Authors: Prosdocimo DA, Jain MK PMID: 21918208 [PubMed - in process] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Osteocalcin: a novel vascular metabolic and osteoinductive factor?

Arteriosclerosis, Thrombosis and Vascular Biology — Tue, 20 Sep 2011 08:21:07 +0100

Authors: Kapustin AN, Shanahan CM PMID: 21918209 [PubMed - in process] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Qualitative score of systemic arteriosclerosis by vascular ultrasonography as a predictor of coronary artery disease in type 2 diabetes

Atherosclerosis — Tue, 20 Sep 2011 04:00:00 +0100

Abstract: Objective: Patients with type 2 diabetes mellitus (T2DM) are at risk of polyvascular comorbidities and poor prognosis. Non-invasive techniques for early prediction of coronary artery disease (CAD) are desirable to prevent cardiovascular events in these patients. The aim of the present study was to investigate the association between CAD and systemic arteriosclerosis by qualitative vascular ultrasonography.Methods: The study subjects were 102 consecutive outpatients with T2DM [males/females=60/42, age: mean±SD 67±9 (range, 40–85) years] evaluated by vascular ultrasonography for arteriosclerosis in the abdominal aorta, carotid, renal, and common iliac arteries. The total number of detected arteriosclerotic vascular lesions in the four arteries was determined. CAD was diagnosed ...

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Novel associations for coronary artery disease derived from genome wide association studies are not associated with increased carotid intima-media thickness, suggesting they do not act via early atherosclerosis or vessel remodeling

Atherosclerosis — Mon, 19 Sep 2011 04:00:00 +0100

Conclusions: We found no evidence that SNPs associated with CAD on GWAS are also associated with carotid IMT. This suggests these genetic associations are not acting via early vessel remodeling or early arteriosclerosis. (Source: Atherosclerosis)

Variations in Platelet Proteins Associated With ST-Elevation Myocardial Infarction: Novel Clues on Pathways Underlying Platelet Activation in Acute Coronary Syndromes.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 15 Sep 2011 04:00:00 +0100

CONCLUSIONS: CrkL, the active form of Src, and GPVI signaling are upregulated in platelets from STEMI patients. PMID: 21921262 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

N-Terminal Pro-Brain Natriuretic Peptide and Risk of Cardiovascular Events in a Japanese Community: The Hisayama Study.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 15 Sep 2011 04:00:00 +0100

CONCLUSIONS: Elevated NT-proBNP levels were shown to be a significant risk factor for the development of CVD and its subtypes in a general Japanese population, independently of other cardiovascular risk factors. PMID: 21921261 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Serum Lipid Levels and the Risk of Intracerebral Hemorrhage: The Rotterdam Study.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 15 Sep 2011 04:00:00 +0100

CONCLUSIONS: Low serum triglyceride levels were associated with an increased risk of intracerebral hemorrhage and with the presence of deep or infratentorial cerebral microbleeds. This provides novel insights into the role of lipid fractions, particularly triglycerides, in the etiology of intracerebral hemorrhage. PMID: 21921260 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Decrease in VEGF Expression Induces Intussusceptive Vascular Pruning.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 15 Sep 2011 04:00:00 +0100

CONCLUSIONS: Diminution of VEGF level induces vascular tree regression by intussusceptive vascular pruning. This observation may allude to the mechanism underlying the "normalization" of tumor vasculature if treated with antiangiogenic drugs. The described mechanism gives new insights into the understanding of the processes of vasculature regression and hence provides new and potentially viable targets for antiangiogenic and/or angio-modulating therapies during various pathological processes. PMID: 21921259 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

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Heparan Sulfate Proteoglycans Mediate the Angiogenic Activity of the Vascular Endothelial Growth Factor Receptor-2 Agonist Gremlin.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 15 Sep 2011 04:00:00 +0100

CONCLUSIONS: HSPGs act as functional gremlin coreceptors in ECs, affecting its productive interaction with VEGFR2 and angiogenic activity. This has allowed the identification of the biotechnological K5-N,OS(H) as a novel angiostatic gremlin antagonist. PMID: 21921258 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Clot Architecture Is Altered in Abdominal Aortic Aneurysms and Correlates With Aneurysm Size.

Arteriosclerosis, Thrombosis and Vascular Biology — Thu, 15 Sep 2011 04:00:00 +0100

CONCLUSIONS: Patients with AAA form denser, smaller pored plasma clots that are more resistant to fibrinolysis, and these characteristics correlate with aneurysm size. Clot structure may play a role in AAA development and concomitant cardiovascular disease. PMID: 21921257 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)

Accelerated aging syndromes, are they relevant to normal human aging?

Aging — Wed, 14 Sep 2011 04:00:00 +0100

Authors: Dreesen O, Stewart CL Abstract Hutchinson-Gilford Progeria (HGPS) and Werner syndromes are diseases that clinically resemble some aspects of accelerated aging. HGPS is caused by mutations in theLMNA gene resulting in post-translational processing defects that trigger Progeria in children. Werner syndrome, arising from mutations in the WRN helicase gene, causes premature aging in young adults. What are the molecular mechanism(s) underlying these disorders and what aspects of the diseases resemble physiological human aging? Much of what we know stems from the study of patient derived fibroblasts with both mutations resulting in increased DNA damage, primarily at telomeres. However, in vivo patients with Werner's develop arteriosclerosis, among other pathologies. In HGPS pati...

Chlamydia in Canine or Feline Coronary Arteriosclerotic Lesions

BMC Research Notes — Fri, 09 Sep 2011 04:00:00 +0100

Conclusions: These findings suggest that there is no obvious correlation between canine and feline coronary arteriosclerosis and the presence of Chlamydia. In order to draw final conclusions about the correlation between Chlamydia and canine atherosclerosis, examination of more samples is required. (Source: BMC Research Notes)