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Why Immunization Against Covid-19 Causes Heart Attack?

The so called protective function of the vaccine against Covid-19 is based on the fact that the Spyke protein of Covid-19 coming into contact with our immune system causes the production of antibodies which react with this spyke protein. The human macrophage incorporates this spyke protein on its cell membrane and presents it to the B-cells which produce antibodies against it. Of course we should not forget that this spyke protein has a structure which responds to the ACE-2 receptor. This means that those Macrophages could connect themselves directly with the corresponding ACE-2 receptor through the spyke protein which is expressed on their cell membrane, causing a quick non-specific immune reaction directly against vascular endothelial cells in the heart and kidneys, but also in respiratory epithelia and in the gastrointestinal tract. Perhaps this is the cause of the very quick and sharpened reaction of many people to the vaccine against Covid-19 which is often connected with late
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CoViD-19 and ACE inhibitors

  The disease is often moderate or even asymptomatic. However, severe courses can occur, usually manifesting as pneumonia. In some of the seriously ill patients, severe cardiovascular damage is also observed. For people with heart disease, the disease - which is caused by the SARS-CoV-2 virus - thus appears to be particularly dangerous. Angiotensin-converting enzyme 2 (ACE2) plays a major role in the body's water balance. ACE inhibitors lower blood pressure and reduce afterload - which also makes them very useful in treating heart failure disease. ACE2 are particularly abundant in the heart and lungs. Currently, attention is focused on this enzyme because ACE2 has been identified as a functional receptor for the coronaviruses SARS-CoV and SARS-CoV-2. It appears that the amount of ACE2 increases by taking ACE2 inhibitors in response. Thus, the body responds to inhibition of these receptors by increasing potential docking sites. It has not yet been proven whether this mec
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Angiotensin converting enzyme 2

Angiotensin converting enzyme 2, or ACE2, is an exopeptidase expressed primarily by vascular endothelial cells in the heart and kidneys, but also in respiratory epithelia[1] and in the gastrointestinal tract. It is the target of several coronaviruses, including SARS-CoV and SARS-CoV-2. 2 Biochemistry ACE2 is a transmembrane metallocarboxypeptidase composed of 805 amino acids. Zinc and chloride ions act as cofactors. The extracellular region consists of two domains, a zinc metallopeptidase domain and a C-terminal collectrin homology domain. The enzyme exhibits homology to angiotensin converting enzyme (ACE). ACE2 is encoded by the ACE2 gene on the X chromosome (gene locus Xp22.2). In addition to being expressed as a transmembrane protein, a soluble form exists in serum. 3 Function ACE2 cleaves angiotensin II into angiotensin (1-7), which has anti-inflammatory and lung protective effects via MAS and AT2 receptors. 4 Clinical 4.1 Infectiology ACE2 serves as a major entry p
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New Look on Antihypertensive Therapy

  Angiotensin converting enzyme 2   Angiotensin converting enzyme 2, or ACE2, is an exopeptidase expressed primarily by vascular endothelial cells in the heart and kidneys, but also in respiratory epithelia[1] and in the gastrointestinal tract. It is the target of several coronaviruses, including SARS-CoV and SARS-CoV-2. 2 Biochemistry ACE2 is a transmembrane metallocarboxypeptidase composed of 805 amino acids. Zinc and chloride ions act as cofactors. The extracellular region consists of two domains, a zinc metallopeptidase domain and a C-terminal collectrin homology domain. The enzyme exhibits homology to angiotensin converting enzyme (ACE). ACE2 is encoded by the ACE2 gene on the X chromosome (gene locus Xp22.2). In addition to being expressed as a transmembrane protein, a soluble form exists in serum. 3 Function ACE2 cleaves angiotensin II into angiotensin (1-7), which has anti-inflammatory and lung protective effects via MAS and AT2 receptors. 4 Clinical 4.1 Infec
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Receptors for SARS-CoV and How This Knowledge could Help?

Medical studies prove that corona viruses enter the human cells through a receptor called Angiotensin Converting Enzyme 2. ACE2 is an exopeptidase which is found on the cell membrane of vessels of the heart or kidneys, also in respiratory cells epithelium and gastrointestinal tract cells. ACE-blockers are long known in medicine and are used for  antihypertensive therapy. Could those antihypertensive drugs be used in the treatment of covid is a question that makes us curious. Until now there are not enough studies that could answer this question, but the therapy with ACE-blockers, angiotensin 2 receptor blockers, ASS and betablockers for heart patients with covid infection is considered to be protective.  Could we use ACE-blockers as virostatic therapy for covid? In my opinion we should at least try.
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Die Fünfte Art der Ausscheidung von Arsen

Von Tanya Georgieva Ivanova   Nach der Definition Ausscheidung ist : Die Tat oder der Prozess der Entladung Abfallstoffe aus dem Blut , Geweben oder Organen. Die Ausscheidung von exogenen Giften und / oder deren Metaboliten erfolgt über : - Nieren - durch Prozesse der Diffusion und aktiven Transport   -Lungen- (flüchtige Stoffe, die in einem freien Zustand sind - wie Alkohol , organische Lösungsmittel und andere ..   - Magen-Darm- System - die Galle ( Kot und / oder Reverse Resorption)   - Schweiß, Speichel , Milch.   Kumulierung ( Depot ) Nach grossem Penetration oder nach längerer Exposition   eine Reihe von Giften kumulieren in bestimmten Geweben oder Organen ( Fettgewebe - DDT , Knochen - die Blei , Nieren - . Cadmium, Haarfollikel – Arseny.   Hauptmerkmal der Akkumulation ist dass unter bestimmten Bedingungen die akkumulierte Substanz aus dem Organ in dem die akkumuliert ist in das Blut freigesetzt werden kann und zu der Symptome einer akuten Vergiftung führen
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Versteht Trampuz überhaupt von Medizin?

https://www.pro-implant-foundation.org/images/material/Renz_Perka_Trampuz_Management_PI_des_Kniegelenks.pdf Periprothetische Infektionen treten nach primärem Gelenkersatz in 2 bis 3% auf [1]. Bei Wechseloperationen liegt die Infektionsrate deutlich höher (3–10%) [2, 3]. Die tatsächliche Inzidenz von Infektionen wird aufgrund von unerkannten chronischen (s.g. „low-grade“) Infektionen unterschätzt, welche typischerweise in den ersten 2–3 Jahren nach Implantation auftreten. Das Infektionsrisiko wird auf 0,5% pro Jahr innerhalb der ersten zwei Jahre nach Implantation geschätzt, in den folgenden Jahren beträgt die Infektionsrate 0,2% pro Jahr. Aus diesem Grund sind Kenntnisse von diagnostischen und therapeutischen Konzepten essenziell. In diesem Beitrag werden aktuelle Erkenntnisse und die neuesten Empfehlungen hinsichtlich Diagnostik und Therapie von periprothetischen Infektion des Kniegelenkes zusammengefasst. Pathogenese Die Gelenkprothese kann auf drei Wege besiedelt werden (. Tab. 1).
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