Lipopolysaccharide induces platelet activation in HIV patients: the role of different viral load patterns

HIV Medicine ◽  
2021 ◽  
Author(s):  
Cristina Nocella ◽  
Ivano Mezzaroma ◽  
Vittoria Cammisotto ◽  
Valentina Castellani ◽  
Cinzia Milito ◽  
...  
Keyword(s):  
Viral Load ◽  
Platelet Activation ◽  
Hiv Patients

On The Mechanism Of Heparin-Induced Potentiation Of Platelet Aggregation

1981 ◽  
Author(s):  
M Yamamoto ◽  
K Watanabe ◽  
Y Ando ◽  
H Iri ◽  
N Fujiyama ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Platelet Activation ◽  
Coagulation Factors ◽  
Marked Enhancement ◽  
Matrix Bound ◽  
Induced Aggregation ◽  
Aggregation Of Platelets ◽  
Plasma Heparin

It has been suggested that heparin caused potentiation of aggregation induced by ADP or epinephrine. The exact mechanism of heparin-induced platelet activation, however, remained unknown. In this paper, we have investigated the role of anti-thrombin III ( AT ) in heparin-induced platelet activation using purified AT and AT depleted plasma. When ADP or epinephrine was added to citrated PRP one minute after addition of heparin ( 1 u/ml, porcine intestinal mucosal heparin, Sigma Co. USA ), marked enhancement of platelet aggregation was observed, compared with the degree of aggregation in the absence of heparin. However, in platelet suspensions prepared in modified Tyrode’s solution, heparin exhibited no potentiating effect on platelet aggregation induced by epinephrine or ADP. Potentiation of epinephrine- or ADP-induced platelet aggregation by heparin was demonstrated when purified AT was added to platelet suspensions at a concentration of 20 μg/ml. AT depleted plasma, which was prepared by immunosorption using matrix-bound antibodies to AT, retained no AT, while determination of α1-antitrypsinα2- macroglobulin and fibrinogen in AT depleted plasma produced values which corresponded to those of the original plasma when dilution factor was taken into account. The activities of coagulation factors were also comparable to those of the original plasma. Heparin exhibited potentiating effect on ADP- or epinephrine-induced aggregation of platelets in original plasma, but no effect in AT depleted plasma. When purified AT was added back to AT depleted plasma at a concentration of 20 μg/ml, potentiation of platelet aggregation by heparin was clearly demonstrated.Our results suggest that effect of heparin on platelet aggregation is also mediated by anti-thrombin III.

Role of Calcium in Platelet Activation: Novel Insights and Pharmacological Implications

2016 ◽  
Vol 12 (2) ◽  
pp. 131-138 ◽  
Author(s):  
Periklis Davlouros ◽  
Ioanna Xanthopoulou ◽  
Nikolaos Mparampoutis ◽  
Georgios Giannopoulos ◽  
Spyridon Deftereos ◽  
...  
Keyword(s):  
Platelet Activation

scholarly journals Histopathological Features of Symptomatic and Asymptomatic Honeybees Naturally Infected by Deformed Wing Virus

Pathogens ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 874
Author(s):  
Karen Power ◽  
Manuela Martano ◽  
Gennaro Altamura ◽  
Nadia Piscopo ◽  
Paola Maiolino
Keyword(s):  
Viral Load ◽  
Asymptomatic Group ◽  
Deformed Wing Virus ◽  
Stage Of Development ◽  
Pathogenic Action ◽  
Degenerative Alterations ◽  
Flight Muscles ◽  
Asymptomatic Individuals ◽  
Histopathological Results

Deformed wing virus (DWV) is capable of infecting honeybees at every stage of development causing symptomatic and asymptomatic infections. To date, very little is known about the histopathological lesions caused by the virus. Therefore, 40 honeybee samples were randomly collected from a naturally DWV infected hive and subjected to anatomopathological examination to discriminate between symptomatic (29) and asymptomatic (11) honeybees. Subsequently, 15 honeybee samples were frozen at −80° and analyzed by PCR and RTqPCR to determinate the presence/absence of the virus and the relative viral load, while 25 honeybee samples were analyzed by histopathological techniques. Biomolecular results showed a fragment of the expected size (69bp) of DWV in all samples and the viral load was higher in symptomatic honeybees compared to the asymptomatic group. Histopathological results showed degenerative alterations of the hypopharyngeal glands (19/25) and flight muscles (6/25) in symptomatic samples while 4/25 asymptomatic samples showed an inflammatory response in the midgut and the hemocele. Results suggest a possible pathogenic action of DWV in both symptomatic and asymptomatic honeybees, and a role of the immune response in keeping under control the virus in asymptomatic individuals.

scholarly journals Adapting the role of handheld echocardiography during the COVID-19 pandemic: A practical guide

Perfusion ◽  
2021 ◽  
pp. 026765912098653
Author(s):  
Hafiz Naderi ◽  
Shaun Robinson ◽  
Martin J Swaans ◽  
Nina Bual ◽  
Wing-See Cheung ◽  
...  
Keyword(s):  
Viral Load ◽  
Potential Role ◽  
Assessment Tool ◽  
High Viral Load ◽  
First Line ◽  
Scanning Time ◽  
Contagious Disease ◽  
Core Dataset ◽  
Clinical Questions

The COVID-19 pandemic has altered our approach to inpatient echocardiography delivery. There is now a greater focus to address key clinical questions likely to make an immediate impact in management, particularly during the period of widespread infection. Handheld echocardiography (HHE) can be used as a first-line assessment tool, limiting scanning time and exposure to high viral load. This article describes a potential role for HHE during a pandemic. We propose a protocol with a reporting template for a focused core dataset necessary in delivering an acute echocardiography service in the setting of a highly contagious disease, minimising risk to the operator. We cover the scenarios typically encountered in the acute cardiology setting and how an expert trained echocardiography team can identify such pathologies using a limited imaging format and include cardiac presentations encountered in those patients acutely unwell with COVID-19.

scholarly journals The Role of Endogenously Formed Diacylglycerol in the Propagation and Termination of Platelet Activation

1989 ◽  
Vol 264 (6) ◽  
pp. 3274-3285 ◽  
Author(s):  
D de Chaffoy de Courcelles ◽  
P Roevens ◽  
H Van Belle ◽  
L Kennis ◽  
Y Somers ◽  
...  
Keyword(s):  
Platelet Activation

scholarly journals The (Patho)Biology of SRC Kinase in Platelets and Megakaryocytes

Medicina ◽  
2020 ◽  
Vol 56 (12) ◽  
pp. 633
Author(s):  
Lore De Kock ◽  
Kathleen Freson
Keyword(s):  
Platelet Activation ◽  
Knockout Mice ◽  
Missense Variant ◽  
Surface Receptors ◽  
Src Signaling ◽  
Normal Platelet ◽  
Fibrinogen Binding ◽  
Cellular Environment ◽  
Proplatelet Formation

Proto-oncogene tyrosine-protein kinase SRC (SRC), as other members of the SRC family kinases (SFK), plays an important role in regulating signal transduction by different cell surface receptors after changes in the cellular environment. Here, we reviewed the role of SRC in platelets and megakaryocytes (MK). In platelets, inactive closed SRC is coupled to the β subunit of integrin αIIbβ3 while upon fibrinogen binding during platelet activation, αIIbβ3-mediated outside-in signaling is initiated by activation of SRC. Active open SRC now further stimulates many downstream effectors via tyrosine phosphorylation of enzymes, adaptors, and especially cytoskeletal components. Functional platelet studies using SRC knockout mice or broad spectrum SFK inhibitors pointed out that SRC mediates their spreading on fibrinogen. On the other hand, an activating pathological SRC missense variant E527K in humans that causes bleeding inhibits collagen-induced platelet activation while stimulating platelet spreading. The role of SRC in megakaryopoiesis is much less studied. SRC knockout mice have a normal platelet count though studies with SFK inhibitors point out that SRC could interfere with MK polyploidization and proplatelet formation but these inhibitors are not specific. Patients with the SRC E527K variant have thrombocytopenia due to hyperactive SRC that inhibits proplatelet formation after increased spreading of MK on fibrinogen and enhanced formation of podosomes. Studies in humans have contributed significantly to our understanding of SRC signaling in platelets and MK.

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