White blood cells "scan" the bloodstream to cause cardiovascular damage

18 12 2014

A study published in Science and led by researchers at the CNIC discover that neutrophils scan actively blood within the vessels in search of activated platelets.

The study shows that many types of cardiovascular accidents, such as stroke or septic shock, they are caused by the action of white blood cells which are activated by this mechanism.

The study has important implications for understanding, and try to, cardiovascular accidents very broad in nature.

 

The IASB researchers have discovered that a subtype of the main defensive agents of the Agency, leukocytes or white blood cells, It carries out a "scanning" procedure within the blood vessels that triggers multiple types of cardiovascular accidents, including some as common as stroke, as published today in the journal Science.

If one were to ask a doctor that I predict you the probability that suffer a cardiovascular accident, for example, a stroke or myocardial infarction, This would answer you that the answer is not simple because it is not known exactly how these accidents are initiated. It will also say that there are certain markers that, However, they are highly predictive. One of these markers is the level of a specific type of white blood cells - neutrophils- in the blood. The other, It is the presence of platelet activated in the bloodstream, which are responsible for clotting and which have been developed as well known as aspirin drug. The question from the biological point of view is whether there is a merely casual relationship between both markers, or if it really is that both cell types, neutrophils and platelets, they cooperate to start a vascular accident.

In collaboration with groups from the complutense University, Department of advanced image of the CNIC, and groups in Germany, United States and Japan, the team of the Dr. Andres Hidalgo, researcher at the Department of atherosclerosis, Image and epidemiology of the IASB has discovered a surprising mechanism that explains how both types of cells, neutrophils and platelets, they cooperate to initiate cardiovascular accidents.

To scrutinize this phenomenon, researchers from the group have looked directly into blood vessels in living tissues with advanced microscopy techniques, which allow to see neutrophils and platelets individual during the inflammatory process. The first surprise that took was that neutrophils that stick to the inflamed vessel extend a kind of arm or cell protrusion toward the inside of the vessel in which a highly adhesive protein concentrates. The second unexpected observation is that some of the blood platelets fought to the protein present in this protrusion. Surprisingly, only platelets that were enabled (one of these predictive markers of cardiovascular accidents) they adhered to this structure. The last observation, Perhaps the most surprising, This adhesive protein is also able to send signals to the neutrophil to initiate an inflammatory response. This response is, in the end, the vascular damage responsible for.

To investigate as this process may underlie vascular accidents referred to above, the researchers induced strokes, septic shock or acute lung damage in mice in which the adhesive protein was absent or had blocked, and they found that in all of them the degree of damage to the affected tissues (brain, liver or lung) It was significantly reduced compared with untreated animals.

The work explains ancient clinical observations, and it has implications which can be immediate to understand how originate many types of cardiovascular accidents more prevalent in our society.

The work also illustrates how the use of cutting-edge techniques helps us discover the elegance of previously unknown biological processes, and that they can now be manipulated to prevent or treat diseases that otherwise can be devastating for human health.

Sreeramkumar V, Adrover JM, Ballesteros I, Cuartero MI, Rossaint J, Bilbao I, Nacher M, C Pitaval, Radovanovic I, Fukui and, McEver RP, Filippi MD, Lizasoain I, J Ruiz-Cabello, A Zarbock, MA and Hidalgo A Moro. Neutrophils scan for activated platelets to initiate inflammation. Science, In Press 2014.

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 Cnic.es [en línea] Madrid (ESP): CNic.es, 18 de diciembre de 2014 [REF. 05 in December of 2014] Available on Internet: https://www.cnic.es/ es/noticias/index.php?ID = 3923



Anticoagulants are safe in patients treated with warfarin after a stroke

16 08 2012

The medication that dissolves clots, called Tissue plasminogen activator (tPA, for its acronym in English), It is safe to use in patients with acute stroke, you are already in treatment with warfarin, According to researchers at the Duke Clinical Research Institute (DCRI).   

 

This study helps dispel concerns about tPA, as it was thought that it was too dangerous for use in patients already treated with anticoagulation, and that could cause life-threatening intracranial hemorrhages. The new research has been published in the magazine ‘JAMA‘.

“To date, There were no randomised trials or large cohort studies to guide us”, explains Dr Ying Xian, Professor of medicine at Duke, and lead author of the study. According to Xian, “our new study at national level did not find a statistically significant increased risk, which supports the use of intravenous tPA in patients treated with warfarin, If your INR is equal or less to 1.7″.

The INR (International Normalized Ratio), It measures the speed at which blood coagulates in patients taking blood thinning drugs, like warfarin.

 

The Duke researchers also noted that almost half of the patients treated with warfarin, that there may be a benefit from treatment with tPA, they did not receive this treatment. According to Eric Peterson, main author of the article “a substantial proportion of patients taking warfarin, did not receive tPA After his stroke”.

Warfarin is an anticoagulant which reduces the rate of stroke in patients with atrial fibrillation - irregular beats of the heart. If treatment with warfarin fails, and the patient suffers a stroke, the tPA is the only effective treatment. However, It also carries an increased risk of symptomatic intracranial hemorrhage. The guidelines of the American Heart Association says that the tPA, in patients treated with warfarin, It can be used if the INR is less than or equal to 1,7, but few studies support these guidelines.

 

The new observational study of Duke included to 23.437 patients with Ictus, of 1.203 hospitals, analyzing the use of tPA, en pacientes en tratamienfo with warfarin, and in patients not taking this anticoagulant. While warfarin-treated patients had slightly higher rates of intracranial hemorrhage than the patients not treated with warfarin (5,7% vs 4,6%), these patients also had an older. After making adjustments for age, the severity of the stroke, and other factors, the risk of intracranial hemorrhage was similar.

“This study provides support for the current treatment guidelines”, says Xian, (e) indicates that a portion of the population is being sub-tratada. On the other hand, According to the researcher, “more studies are needed to analyze the use of tPA in patients with one INR greater of 1.7, as well as those who are taking one of the new alternative to warfarin anticoagulants (dabigatran and rivaroxiban)”.

 

Diariosalud.NET [en línea] Montevideo(URU): diariosalud.NET, 16 in August of 2012 [REF. 30 in June of 2012] Available on Internet: http://diariosalud.NET/index.php?option = com_content&task = view&ID = 24713&Itemid = 413



Revelan el mecanismo de protección cerebral durante un ictus

25 08 2011

Neurologists of the University of Bristol they have identified the mechanism of natural protection of some of the nerve cells of the brain during the start of a stroke. Results, published in the magazine ‘Journal of Neuroscience‘, they could be used to develop treatments to protect other types of nerve cells responsible for speech and movement.

The stroke - the third cause of death in the United Kingdom- It causes the interruption of the blood supply to the brain, nerve cells deprived of oxygen and nutrients. This leads to the death of nerve cells and the consequent loss of cognitive functions of the brain such as speech and movement. However, not all nerve cells are equally susceptible to stroke-induced damage.

Research, directed by the doctor Jack Mellor the University of Bristol, It examined two types of nerve cells in a part of the brain called the hippocampus – the region linked to memory and orientation. One of these types of cells, CA1 cells, It is highly susceptible to damage after a stroke, While the other, CA3 cells, It is much more resistant while there are many similarities between the two types.

In the words of Dr. Mellor, “If we can understand why some nerve cells are resistant to damage caused by a stroke, We may be able to develop strategies to protect sensitive cells”.

The researchers noted that CA3 cells have a mechanism to reduce their vulnerability during, (e) immediately after a stroke, According to a model of laboratory. According to this mechanism, CA3 cells become less sensitive to the neurotransmitter glutamate (It is released in large amounts during a stroke), through the Elimination of glutamate of the cell surface receptor proteins.

The Elimination of glutamate receptor is activated by adenosine A3 receptors, He turns to very high levels of the neurotransmitter adenosine — only during a stroke. Curiously, CA1 cells that are susceptible to damage from stroke have no adenosine A3 receptors and do not respond to the model of elimination of glutamate receptors during stroke. The results reveal that CA3 cells possess a neural protection mechanism.

Dr. Mellor added that “Historically, the stroke has been very difficult to treat because of its unpredictable nature and the need for medications within a few minutes of your home. Our research does not solve these problems, but it highlights the natural protection that offer some nerve cells, useful knowledge to develop treatments and protect other cell types”.

VALIDADO POR LA SRA. ALBA CALLS.

Europapress.es [en línea] Madrid (Spain): europapress.es, 25 de agosto de 2011 [REF. 17 in August of 2011] Available on Internet:

http://www.europapress.es/salud/noticia-revelan-mecanismo-proteccion-cerebral-ictus-20110817110210.html