Rr009 wrote:/.../Ja siis on vaid vähesed plussis, aga maht 2-3 triljonit tuleb kuidagi teist moodi katta./.../
Rr009 wrote:Pagan, ma tahaks küll seda hullu näha kes BC eest oma põllu või metsa ära annaks.. Mingi keskpanga stablecoini eest palun väga
The pooled incidence of total VTE according to the pharmacologic thromboprophylaxis received were as follows:
no prophylaxis 41.9% (95% CI: 28.1–57.2, I 2 = 76%),
standard-dose prophylaxis 19.8% (95% CI: 13.2–28.6, I 2 = 95%),
intermediate-dose prophylaxis 11.9% (95% CI: 4.3–28.6, I 2 = 91%), and
therapeutic-dose anticoagulants 10.5% (95% CI: 4.2–23.8, I 2 = 82%) ( p -value for between-group heterogeneity = 0.003;
The pooled incidence rates of arterial thrombosis according to the pharmacologic thromboprophylaxis received were as follows:
no prophylaxis 11.3% (95% CI: 5.2–23.0, I 2 = 0%),
standard-dose prophylaxis 2.5% (95% CI: 1.4–4.3, I 2 = 45%),
intermediate-dose prophylaxis 2.1% (95% CI: 0.5–7.7, I 2 = 45%), and
therapeutic-dose anticoagulants 1.3% (95% CI: 0.2–8.8, I 2 = 0) ( p -value for between-group heterogeneity = 0.009;
Current evidence suggests COVID-19 associated coagulopathy is a combination of low-grade DIC and pulmonary thrombotic microangiopathy, which could have a significant impact on organ dysfunction in most patients with severe disease.14
The presence of coagulopathy as part of the systemic inflammatory response syndrome is a common feature of severe COVID-19. Approximately 20%-50% of hospitalized patients with COVID-19 have hematologic changes in coagulation tests (elevated D-dimer, prolonged PT, thrombocytopenia, and/or low fibrinogen levels). This condition is characterized by more thrombotic than hemorrhagic events that are associated with coagulopathy (specifically venous thromboembolism [VTE]). On the other hand, endothelial dysfunction results in high levels of D-dimer, thrombin and fibrin degradation products, thrombocytopenia and prolonged clotting times, which leads to hypoxia and pulmonary congestion mediated by thrombosis and microvascular occlusion, in addition to thrombosis of central lines and catheters and vascular occlusive events (cerebrovascular events, limb ischemia, etc) that generally occur in the intensive care units.6 , 10 , 15 , 17, 18, 19
Fibrin and thrombin deposition occurs mainly in the pulmonary microvasculature, being a factor that contributes to acute respiratory distress syndrome and coagulopathy in patients who die from COVID-19. Furthermore, the hypoxia that occurs in severe COVID-19 can aggravate thrombosis not only by increasing the viscosity of the blood, but also through the hypoxia-inducible transcription factor-dependent signaling pathway.10 , 17 , 20
Similar to the endothelial dysfunction of sepsis induced coagulopathy (SIC), in which there is excessive thrombin generation and impaired fibrinolysis, there is a type of endotheliopathy that appears to contribute to the pathophysiology of microcirculatory changes in SARS-CoV-2 infection. The receptor for viral adhesion is an angiotensin-converting enzyme-2 receptor on endothelial cells, and viral replication causes inflammatory cell infiltration, endothelial apoptosis, and microvascular prothrombotic events. Viral inclusions within endothelial cells and mononuclear and polymorphonuclear cell infiltration have been observed, with evidence of endothelial apoptosis in postmortem analysis of SARS-Cov-2 infection. As a result of this, microcirculatory dysfunction contributes to the clinical sequelae of COVID-19 patients.6 , 10 Other abnormalities that may be relevant in the context of coagulopathy are decreased fibrinogen, elevated Lactate dehydrogenase (LDH), and, in some patients, markedly elevated serum ferritin values.20
Another important characteristic of COVID-19 infection is the procoagulant response in its acute phase, where acute phase reactants (such as Factor VIII, Von Willebrand Factor, and fibrinogen) are associated with an increased risk of thrombosis directly related to elevated levels of fibrinogen. In severe stages of the disease, there is an increase in inflammatory cytokines (tumor necrosis factor and interleukins, including interleukin 1 and interleukin 6). IL-6 induces expression of tissue factor in macrophages, which initiates the activation of coagulation and generation of thrombin. Tumor necrosis factor and IL-1 are the main mediators of the suppression of the endogenous coagulation cascade. In a group of severely compromised COVID-10 patients, a cytokine storm characterized by high concentrations of proinflammatory cytokines and chemokines may be found.12 , 14
spl wrote:https://majandus24.postimees.ee/7202920/hispaania-sundvoorandab-ja-jagab-tuhjalt-seisvad-korterid-vaestele
Ma tean, mis selle tulemus on, kas Hispaania riik ka
Korterid antakse vähekindlustatud peredele, nende seas immigrantidele
spl wrote:https://majandus24.postimees.ee/7202920/hispaania-sundvoorandab-ja-jagab-tuhjalt-seisvad-korterid-vaestele
Ma tean, mis selle tulemus on, kas Hispaania riik ka
Korterid antakse vähekindlustatud peredele, nende seas immigrantidele
spl wrote:td wrote: Lipiide korrigeerivat ravimit ma ei võta: arst tahab elada, apteeker tahab elada ja mina tahan ka elada.
Hahaa, seda üritab minu perearst mulle alati pähe määrida. Ma kutsun juba oma perearsti Tädi Kolesterool. Küsisin, noh kaua siis seda ravimit peab võtma....eluaeg![]()
See meenutab tarkvaramudelit, kui varem ostsid tarkvara ja said seda igavesti kasutada. Siis nüüd ostad ja maksad end oinaks, sisuliselt pead igavesti "rentima" tarkvara.
td wrote:Trombe leitakse sageli koroonaviirusesse surnutelt, eriti kopsudest. Üheks vallandavaks faktoriks võiks olla veresooni vooderdava sisekihi ehk endoteeli kahjustus (selle üks funktsioonidest ongi välistada vere hüübimist veresoontes). Kuna selle sisekihi rakkudel on samuti ACE-2 retseptorid, siis viirus meeleldi kinnitub ka sinna, seetõttu nende normaalne hüübimist takistav funktsioon väheneb (endoteeli rakud surevad, surnud rakke ründavad põletikurakud, mis toodavad hüübimise algatajaid jne). Erinevalt tavalistest trombidest tekkivad siis trombid kohapeal, seega ka kapillaarides ehk mikroveresoontes (veenitromboosi ja arterite tromboosi tavaline mehhanism on selline, et kuskilt suuremast veresoonest pääsevad trombitüklid liikuma ning liiguvad edasi, kuni jõuavad väiksemasse veresoonde, kust enam edasi ei pääse ning ummistavad selle). Seega, koroonaviiruse puhul on haaratud ka väikesed veresooned, kus moodustuvad trombid kohapeal.
hh wrote:Hästi tore Ringvaate klipp maalikunsti saladustest, 10 minutit:
Marten Esko: maalidel peituvad salasõnumid on sageli paljudele huvitavamad kui teos ise
https://menu.err.ee/1608144334/marten-e ... i-teos-ise
hh wrote:Ja eelneva jätkuks -- ÜLIVÕIMSA resolutsiooniga (saab hästi tugevalt suurendada)
Leonardo da Vinci "Viimane õhtusöömaaeg", fresko, asub Milanos
https://artsandculture.google.com/asset ... Swj5Pus85w
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