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1.
PLoS One ; 11(10): e0164836, 2016.
Artigo em Inglês | MEDLINE | ID: mdl-27736997

RESUMO

Atherosclerosis is considered a chronic disease of the arterial wall and is the major cause of severe disease and death among individuals all over the world. Some recent studies have established the presence of bacteria in atherosclerotic plaque samples and suggested their possible contribution to the development of cardiovascular disease. The main objective of this preliminary pilot study was to better understand the bacterial diversity and abundance in human atherosclerotic plaques derived from common carotid arteries of individuals with atherosclerosis (Russian nationwide group) and contribute towards the further identification of a main group of atherosclerotic plaque bacteria by 454 pyrosequencing their 16S ribosomal RNA (16S rRNA) genes. The applied approach enabled the detection of bacterial DNA in all atherosclerotic plaques. We found that distinct members of the order Burkholderiales were present at high levels in all atherosclerotic plaques obtained from patients with atherosclerosis with the genus Curvibacter being predominant in all plaque samples. Moreover, unclassified Burkholderiales as well as members of the genera Propionibacterium and Ralstonia were typically the most significant taxa for all atherosclerotic plaques. Other genera such as Burkholderia, Corynebacterium and Sediminibacterium as well as unclassified Comamonadaceae, Oxalobacteraceae, Rhodospirillaceae, Bradyrhizobiaceae and Burkholderiaceae were always found but at low relative abundances of the total 16S rRNA gene population derived from all samples. Also, we found that some bacteria found in plaque samples correlated with some clinical parameters, including total cholesterol, alanine aminotransferase and fibrinogen levels. Finally, our study indicates that some bacterial agents at least partially may be involved in affecting the development of cardiovascular disease through different mechanisms.


Assuntos
Aterosclerose/microbiologia , Bactérias/genética , Placa Aterosclerótica/microbiologia , RNA Ribossômico 16S/metabolismo , Idoso , Aterosclerose/patologia , Bactérias/classificação , Bactérias/isolamento & purificação , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Análise de Componente Principal , RNA Ribossômico 16S/química , RNA Ribossômico 16S/isolamento & purificação , Federação Russa , Análise de Sequência de DNA
2.
Blood ; 127(1): 149-59, 2016 Jan 07.
Artigo em Inglês | MEDLINE | ID: mdl-26603837

RESUMO

Platelet-driven blood clot contraction (retraction) is thought to promote wound closure and secure hemostasis while preventing vascular occlusion. Notwithstanding its importance, clot contraction remains a poorly understood process, partially because of the lack of methodology to quantify its dynamics and requirements. We used a novel automated optical analyzer to continuously track in vitro changes in the size of contracting clots in whole blood and in variously reconstituted samples. Kinetics of contraction was complemented with dynamic rheometry to characterize the viscoelasticity of contracting clots. This combined approach enabled investigation of the coordinated mechanistic impact of platelets, including nonmuscle myosin II, red blood cells (RBCs), fibrin(ogen), factor XIIIa (FXIIIa), and thrombin on the kinetics and mechanics of the contraction process. Clot contraction is composed of 3 sequential phases, each characterized by a distinct rate constant. Thrombin, Ca(2+), the integrin αIIbß3, myosin IIa, FXIIIa cross-linking, and platelet count all promote 1 or more phases of the clot contraction process. In contrast, RBCs impair contraction and reduce elasticity, while increasing the overall contractile stress generated by the platelet-fibrin meshwork. A better understanding of the mechanisms by which blood cells, fibrin(ogen), and platelet-fibrin interactions modulate clot contraction may generate novel approaches to reveal and to manage thrombosis and hemostatic disorders.


Assuntos
Coagulação Sanguínea/fisiologia , Plaquetas/citologia , Plaquetas/fisiologia , Retração do Coágulo/fisiologia , Fibrina/metabolismo , Trombose/patologia , Cálcio/metabolismo , Reagentes de Ligações Cruzadas , Eritrócitos/metabolismo , Fator XIIIa/metabolismo , Hemostasia , Humanos , Cinética , Miosina não Muscular Tipo IIA/metabolismo , Complexo Glicoproteico GPIIb-IIIa de Plaquetas/metabolismo , Reologia , Trombina/metabolismo , Trombose/metabolismo
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