scholarly journals Antibody‐mediated procoagulant platelet formation in COVID‐19 is AKT dependent

2021 ◽  
Author(s):  
Lisann Pelzl ◽  
Anurag Singh ◽  
Jonas Funk ◽  
Andreas Witzemann ◽  
Irene Marini ◽  
...  
Keyword(s):  
Platelet Formation

scholarly journals Impact of supervised beego, a traditional Chinese water-only fasting, on thrombosis and haemostasis

2021 ◽  
pp. bmjnph-2020-000183
Author(s):  
Yixuan Fang ◽  
Yue Gu ◽  
Chen Zhao ◽  
Yaqi Lv ◽  
Jiawei Qian ◽  
...  
Keyword(s):  
Biological Effects ◽  
Selective Reduction ◽  
Coagulation Factors ◽  
Normal Diet ◽  
Non Invasive ◽  
Cholesterol Levels ◽  
Thrombosis Risk ◽  
Abdominal Breathing ◽  
Mediated Reduction ◽  
Platelet Formation

Beego is a traditional Chinese complete water-only fasting practice initially developed for spiritual purposes, later extending to physical fitness purposes. Beego notably includes a psychological induction component that includes meditation and abdominal breathing, light body exercise and ends with a specific gradual refeeding program before returning to a normal diet. Beego has regained its popularity in recent decades in China as a strategy for helping people in subhealthy conditions or with metabolic syndrome, but we are unaware of any studies examining the biological effects of this practice. To address this, we here performed a longitudinal study of beego comprising fasting (7 and 14 day cohorts) and a 7-day programmed refeeding phase. In addition to detecting improvements in cardiovascular physiology and selective reduction of blood pressure in hypertensive subjects, we observed that beego decreased blood triacylglycerol (TG) selectively in TG-high subjects and increased cholesterol in all subjects during fasting; however, the cholesterol levels were normalised after completion of the refeeding program. Strikingly, beego reduced platelet formation, activation, aggregation and degranulation, resulting in an alleviated thrombosis risk, yet maintained haemostasis by sustaining levels of coagulation factors and other haemostatic proteins. Mechanistically, we speculate that downregulation of G6B and MYL9 may influence the observed beego-mediated reduction in platelets. Fundamentally, our study supports that supervised beego reduces thrombosis risk without compromising haemostasis capacity. Moreover, our results support that beego under medical supervision can be implemented as non-invasive intervention for reducing thrombosis risk, and suggest several lines of intriguing inquiry for future studies about this fasting practice (http://www.chictr.org.cn/index.aspx, number, ChiCTR1900027451).

scholarly journals Proplatelets and stress platelets

Blood ◽  
1987 ◽  
Vol 69 (2) ◽  
pp. 522-528 ◽  
Author(s):  
M Tong ◽  
P Seth ◽  
DG Penington
Keyword(s):  
Bone Marrow ◽  
Platelet Rich Plasma ◽  
Early Period ◽  
Platelet Volume ◽  
Plasma Exposure ◽  
Functional Characteristics ◽  
Platelet Production ◽  
Relationship Of ◽  
The Relationship ◽  
Platelet Formation

Abstract The process of platelet formation by the fragmentation of megakaryocyte pseudopodia, termed proplatelets, demonstrable in the marrow sinusoids is poorly understood. “Stress” platelets produced under conditions of stimulated platelet production differ from normal circulating platelets with respect to volume and a number of functional characteristics. To clarify the relationship of stress platelets to proplatelets, rats were injected with heterologous platelet antiserum. Nondiscoid platelet forms, some characteristically beaded in appearance, strongly resembling bone marrow proplatelets, can be recovered in the circulation of normal rats. During the early period of recovery from acute thrombocytopenia, there was a substantial increase in the proportion of these elongated platelets in the citrated platelet rich plasma. Exposure to EDTA rendered them spherical. Circulating proplatelets may contribute significantly to the prompt increase in platelet volume during recovery from acute thrombocytopenia at a time prior to significant increase in megakaryocyte size and ploidy.

Comparison of platelet formation in hydrogen and helium-implanted silicon

2007 ◽  
Vol 262 (1) ◽  
pp. 24-28 ◽  
Author(s):  
X. Hebras ◽  
P. Nguyen ◽  
K.K. Bourdelle ◽  
F. Letertre ◽  
N. Cherkashin ◽  
...  
Keyword(s):  
Platelet Formation

Oxide platelet formation in tantalum single crystals

1962 ◽  
Vol 10 (2) ◽  
pp. 149-160 ◽  
Author(s):  
R.E Pawel ◽  
J.V Cathcart ◽  
J.J Campbell
Keyword(s):  
Single Crystals ◽  
Platelet Formation

scholarly journals Studies of the interaction of ticagrelor with the P2Y13 receptor and with P2Y13-dependent pro-platelet formation by human megakaryocytes

2016 ◽  
Vol 116 (12) ◽  
pp. 1079-1088 ◽  
Author(s):  
Anna Björquist ◽  
Christian A. Di Buduo ◽  
Eti A. Femia ◽  
Robert F. Storey ◽  
Richard C. Becker ◽  
...  
Keyword(s):  
Platelet Count ◽  
Cellular Response ◽  
P2y Receptors ◽  
Cell System ◽  
Experimental Models ◽  
Significant Activity ◽  
Label Free ◽  
Coronary Syndrome ◽  
Platelet Formation

SummaryTicagrelor is an antagonist of the platelet P2Y12 receptor for ADP, approved for the prevention of thromboembolic events in patients with acute coronary syndrome. Previous studies showed that ticagrelor has no significant activity versus P1 receptors for adenosine and other known P2Y receptors, with the exception of P2Y13, which was not tested. The P2Y12 antagonist cangrelor has been shown to also inhibit P2Y13 and to decrease the P2Y13-regulated capacity of megakaryocytes to produce pro-platelets. We tested whether or not ticagrelor inhibits P2Y13 signalling and function. The in vitro effects of ticagrelor, its active (TAM) and inactive (TIM) metabolites, cangrelor and the P2Y13 antagonist MRS2211 were tested in two experimental models: 1) a label-free cellular response assay in P2Y13-transfected HEK293 T-REx cells; and 2) pro-platelet formation by human megakaryocytes in culture. Ticagrelor, TAM, cangrelor and MRS2211, but not TIM, inhibited the cellular responses in P2Y13-transfected cells. In contrast, only MRS2211 and cangrelor, confirming previous results, inhibited pro-platelet formation by megakaryocytes in vitro. The platelet count of patients randomised to treatment with ticagrelor in the PLATO trial did not change during treatment and was comparable to those of patients randomised to clopidogrel. In conclusion, ticagrelor and TAM act as P2Y13 antagonists in a transfected cell system in vitro but this does not translate into any impact on pro-platelet formation in vitro or altered platelet count in patients.

Platelet Formation, Platelet Density and Platelet Ageing

1990 ◽  
pp. 109-143 ◽  
Author(s):  
K. G. Chamberlain ◽  
M. Tong ◽  
D. G. Penington
Keyword(s):  
Platelet Formation

scholarly journals Arachidonic acid and Docosahexanoic acid enhance platelet formation from human apheresis-derived CD34+ cells

Cell Cycle ◽  
2017 ◽  
Vol 16 (10) ◽  
pp. 979-990 ◽  
Author(s):  
Ankita Dhenge ◽  
Kedar Limbkar ◽  
Sameer Melinkeri ◽  
Vaijayanti Prakash Kale ◽  
Lalita Limaye
Keyword(s):  
Arachidonic Acid ◽  
Docosahexanoic Acid ◽  
Cd34 Cells ◽  
Platelet Formation

Modern approach to the diagnosis and treatment of thrombocytopenia

2021 ◽  
pp. 28-34
Author(s):  
Marina Leonidovna Kochieva
Keyword(s):  
Blood Test ◽  
Healthy Adult ◽  
Clinical Manifestations ◽  
Antithyroid Drugs ◽  
Modern Approach ◽  
Somatic Diseases ◽  
Immunodeficiency States ◽  
Test Treatment ◽  
Main Clinical Manifestation ◽  
Platelet Formation

Normally, the number of platelets in a healthy adult is in the range of 150-320 x 10⁹. A condition in which their number falls below 150x10⁹ is called thrombocytopenia. It can be both associated with a violation of the process of platelet formation in the bone marrow (in particular, with aplastic anemia, hemoblastosis, thrombocytopenic purpura), and be a concomitant pathology, for example, be a consequence of drug treatment of a number of somatic diseases. In the pathogenesis of thrombocytopenia, three main directions are distinguished: a decrease in platelet production, an acceleration of their decay and a violation of the distribution of the platelet pool with their sequestration in the spleen. Most often, drug thrombocytopenia develops against the background of the use of cytostatics, chloramphenicol, antithyroid drugs, NSAIDs. The decrease in the number of platelets can also be influenced by the regular use of alcohol, some infectious diseases, and immunodeficiency states. The main clinical manifestation of thrombocytopenia is hemorrhagic syndrome, proceeding as petechial rashes or ecchymosis, however, in some cases, clinical manifestations may be absent, and then the diagnosis is made on the basis of a clinical blood test. Treatment of thrombocytopenia is carried out taking into account the etiological factor that caused it.

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