12-03-2021, 02:11 PM
Czekam na glutamine a tymczasem wyglada na to ze naprawdę mamy już przyczynę
https://link.springer.com/article/10.118...20-01165-7
Some years ago, we discovered that in the presence of microbial cell wall components [28, 29], and in a variety of chronic, inflammatory diseases [30,31,32] (including sepsis [33]), blood fibrinogen can clot into an anomalous, amyloid form [34]. These forms are easily detected by a fluorogenic stain such as thioflavin T, or the so-called Amytracker stains [35]. In all cases, however, these experiments were performed in vitro using relevant plasma, with clotting being induced by the addition of thrombin. In our preliminary experiments this was also the case for plasma from COVID-19 patients, but the signals were so massive that they were essentially off the scale. However, as we report here, the plasma of COVID-19 patients carries a massive load of preformed amyloid clots (with no thrombin being added), and this therefore provides a rapid and convenient test for COVID-19.
I badanie które już wklejałem:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8381139/
We show that plasma samples from Long COVID/PASC still contain large anomalous (amyloid) deposits (microclots). We also show that these microclots in both acute COVID-19 and Long COVID/PASC plasma samples are resistant to fibrinolysis (compared to plasma from controls and T2DM), even after trypsinisation. After a second trypsinization, the persistent pellet deposits (microclots) were solubilized. We detected various inflammatory molecules that are substantially increased in both the supernatant and trapped in the solubilized pellet deposits of acute COVID-19 and Long COVID/PASC, versus the equivalent volume of fully digested fluid of the control samples and T2DM. Of particular interest was a substantial increase in α(2)-antiplasmin (α2AP), various fibrinogen chains, as well as Serum Amyloid A (SAA) that were trapped in the solubilized fibrinolytic-resistant pellet deposits.
Kurczę poszedłbym do lekarza po jakąś heparynę ale na tym etapie by mnie pewnie tylko wyśmiał. Z drugiej strony już kilka osób widziałem które mówią ze środki antyzakrzepowe znacznie poprawiły ich stan w długim covidzie, wiec jakiś lekarz im je zapisał, ale ciekawe na jakiej podstawie?
https://link.springer.com/article/10.118...20-01165-7
Some years ago, we discovered that in the presence of microbial cell wall components [28, 29], and in a variety of chronic, inflammatory diseases [30,31,32] (including sepsis [33]), blood fibrinogen can clot into an anomalous, amyloid form [34]. These forms are easily detected by a fluorogenic stain such as thioflavin T, or the so-called Amytracker stains [35]. In all cases, however, these experiments were performed in vitro using relevant plasma, with clotting being induced by the addition of thrombin. In our preliminary experiments this was also the case for plasma from COVID-19 patients, but the signals were so massive that they were essentially off the scale. However, as we report here, the plasma of COVID-19 patients carries a massive load of preformed amyloid clots (with no thrombin being added), and this therefore provides a rapid and convenient test for COVID-19.
I badanie które już wklejałem:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8381139/
We show that plasma samples from Long COVID/PASC still contain large anomalous (amyloid) deposits (microclots). We also show that these microclots in both acute COVID-19 and Long COVID/PASC plasma samples are resistant to fibrinolysis (compared to plasma from controls and T2DM), even after trypsinisation. After a second trypsinization, the persistent pellet deposits (microclots) were solubilized. We detected various inflammatory molecules that are substantially increased in both the supernatant and trapped in the solubilized pellet deposits of acute COVID-19 and Long COVID/PASC, versus the equivalent volume of fully digested fluid of the control samples and T2DM. Of particular interest was a substantial increase in α(2)-antiplasmin (α2AP), various fibrinogen chains, as well as Serum Amyloid A (SAA) that were trapped in the solubilized fibrinolytic-resistant pellet deposits.
Kurczę poszedłbym do lekarza po jakąś heparynę ale na tym etapie by mnie pewnie tylko wyśmiał. Z drugiej strony już kilka osób widziałem które mówią ze środki antyzakrzepowe znacznie poprawiły ich stan w długim covidzie, wiec jakiś lekarz im je zapisał, ale ciekawe na jakiej podstawie?