A FEW OCCURRENCES THAT HAPPENED TO ME ABOUT A WEEK AGO, I SHARED ALREADY ON TWITTER, BUT I WANT TO REPEAT THEM ON THIS BLOGPOST, WITH AN ADDITION.
11-10-2020 , LAST SUNDAY , MY PARTNER AND I PASSED THE DAY WITH A CLOSE RELATIVE IN THE VILLAGE WHERE I WAS BORN AND LIVED DURING MY YOUTH, AS USUAL ( AS 'CARETAKERS')
I WENT ON MY BIKE TO THE LOCAL SUPERMARKET TO DO SOME GROCERY SHOPPING. ( I FELT PERFECTLY FINE)
THE SUPERMARKET WASN'T CROWDED , AND THERE WAS ONE FAIRLY YOUNG MAN, STANDING AT THE END OF A ROW WITH PRODUCTS, LOOKING EXPLICITLY AT ME, IN THE EYES, AND SMILING VERY FRIENDLY , HE HAD 'KIND EYES'.
I HAD NEVER SEEN THIS MAN BEFORE, BUT (AUTOMATICALLY) I SMILED BACK.
A SHORT TIME AFTER THIS, IN THE ROW HEADING TO THE PAY DESK; I FELT THIS SLIGHT PAIN IN MY BACK WITH BREATHING AND THE NEXT MOMENT IT FELT AS IF MY LUNGS WERE 'BLOCKED'; NO AIR; TIGHTNESS ON CHEST: SO I THOUGHT: I CAN LEAVE THE SHOPPING -CART RIGHT HERE AND FLEE OUTSIDE, OR I TRY TO BREATH VERY CALM AND SUPERFICIALLY THROUGH MY NOSE AND MAKE IT PAST THE PAY DESK.
AS I WAS NEAR THE PAY DESK AND THERE WAS ONLY ONE PERSON IN THE LINE , I DECIDED FOR THE LATTER, AND I SAW THAT THIS MAN , WHO HAD LOOKED AND SMILED IN THIS FRIENDLY WAY CAME NEXT, BEHIND ME.
(WHEN IT WAS HIS TURN, THE CASHIER SAID THAT HE SHOULD HAVE TAKEN A MANDATORY SHOPPING CART, WHICH HE HADN'T, BUT HE DIDN'T UNDERSTAND WHAT SHE SAID, I SUPPOSE BECAUSE OF THE LANGUAGE. I LEFT THE SHOP, VERY HAPPY TO BE OUTSIDE, THOUGH THE TIGHTNESS ON MY CHEST STAYED FOR MANY HOURS.)
( A COUPLE OF DAYS BEFORE I HAD LIVED A SIMILAR EXPERIENCE , REGARDING THE TIGHTNESS AND THE SENSATION OF 'GETTING NO AIR': FROM ONE MOMENT TO THE NEXT , OCCURRING IN IKEA, WHILE, AGAIN, I HAD BEEN FINE BEFORE)
TODAY, AT THIS VILLAGE, I ASKED MY PARTNER TO COME WITH ME; I HADN'T TOLD HIM ABOUT THIS MAN IN THE SUPERMARKET BEFORE, SO , AT THE HOUSE , BEFORE GOING OUT, I TOLD HIM, AND I ASKED HIM TO COME WITH ME TO THIS SUPERMARKET, JUST IN CASE I WOULD EXPERIENCE THE SAME PHYSICAL NASTY PHENOMENA.
( THE DAY BEFORE I HAD ASKED MY PARTNER TO DO THE SHOPPING TODAY, BUT I CHANGED MY MIND, I DON'T WANT TO STAY IN THE HOUSE, WORRIED THAT SOMETHING SIMILAR WOULD HAPPEN AGAIN).
WE WERE BOTH INSIDE THE SUPERMARKET; HE WENT FOR SOME PRODUCTS AND I SEARCHED FOR SOME OTHER ONES. NOTHING 'HAPPENED', FORTUNATELY.
I KNOW THIS MAN THAT SUNDAY HAD SOMETHING TO DO WITH WHAT HAPPENED THAT DAY, (HE KNOWS I KNOW AS WELL)
ONLY A FEW, WHEN THEY READ THIS, WILL HAVE SOME IDEA., OR KNOW WHAT ( POSSIBLY) HAPPENED.
( I ALWAYS REMEMBER THE WORDS, MENTALLY OVER- DISTANCE COMMUNICATED BY THE FORMER 'MINDHACKER'; THIS GOES FAR BEYOND YOUR IMAGINATION)
A SHORT, IN SOME WAY REVEALING VIDEO ABOUT THE ISOTOPE CARBON 12 ; EXISTING OF 6 PROTONS; 6 ELECTRONS AND 6 NEUTRONS; THAT WOULD CHANGE INTO CARBON 7...
SUPPOSEDLY DUE TO: ( ONLY?) THE SUN RADIATION.... (ELECTROMAGNETIC SPECTRUM!)
-INDUCED- 'NARRATIVES' THAT COULD KEEP SOME TRUTHS OUT OF SIGHT:
SPECIFIC DNA CHANGES WOULD BE TRANSLATED; INTERPRETED TO : -'ASCENSION' CONCEPT- 'LIGHT BEINGS' -TRANSFORMATION NARRATIVES - NEW-AGE MOVEMENT, NEW RELIGION (AND A LOT MORE DISTRACTING AND BLINDING 'RUBBISH', IN MY PERSPECTIVE)
THE AGENDA AND SCRIPT OF THE CULT(S), WITH THEIR 'HIDDEN' KNOWLEDGE AGAIN.
HIDDEN EUGENICS, WITHOUT CONSENT
A LINK WITH A SPECIFIC INTERPRETATION I WANT TO SHARE:
NOTE: THE NUMBER OF THE BEAST: 666 IN THE BIBLICAL TEXT BOOKS, AS A LOT OF CHRISTIANS KNOW IT, REFERS TO THE 'ANTICHRIST':
HOWEVER CLAIMED IS THAT MORE ANCIENT WRITTEN REVELATIONS TALK ABOUT: 616 AS THE NUMBER OF THE BEAST ( AS MENTIONED IN THE VIDEO), SO, IN THAT CASE, (MORE PLAUSIBLE TO ME) ONE COULD COME TO SOME POSSIBLE DEDUCTIONS...
- THE SCREENING OF GENES SENSITIVE TO LONG-TERM, LOW LEVEL MICROWAVE EXPOSURE AND BIOINFORMATIC ANALYSIS OF POTENTIAL CORRELATION TO LEARNING AND MEMORY. SCIENCEDIRECT:
MY OWN EXPERIENCES OUTSIDE MY HOUSE, THE LAST WEEK; IN 3 PLACES IN ANTWERP, WERE VERY NASTY, TO BE HONEST : IN IKEA, NEAR THE CASH DESKS SUDDENLY A PAIN IN MY UPPER BACK WITH BREATHING, TIGHTNESS IN CHEST AND THE FEELING OF NOT GETTING ENOUGH 'AIR' , IT TOOK A DAY AT HOME TO RECOVER A BIT; SOME DAYS LATER IN A SUPERMARKET: ALBERT HEIJN: AGAIN , NEAR THE CASH DESKS, SAME STORY, AND YESTERDAY IN THE 'KRUIDVAT'; LESS SEVERE THOUGH. THE MONTHS BEFORE I HAD SOME SYMPTOMS AS ITCHY THROAT, COUGH, HOARSE VOICE ETC. AFTER VISITING SOME BIG SUPERMARKETS.
( NOW IT HAS COME TO A POINT I DEFINITELY CAN'T GO TO SOME PLACES ANYMORE.)
I'LL FINISH WITH THIS BLOG ( THANKS TO THE WRITER!)
5G, 60 GHZ, OXYGEN ABSORPTION, YOU AND CORONAVIRUS:
I transcribed part of Dana Ashley’s video regarding the impact of 5G/60 GHz on the human body. The transcript is not word for word.
The impacts of 5G/60 GHz are not widely published. Here’s what we know from big telecom company promotional material: “60 GHz has a very distinct impact on none other than oxygen itself.” Yes, articles from companies touting benefits of 5G admit 60 GHz is absorbed by oxygen as seen by this graph.
Frequencies under 60 GHz are not impacted. Once it hits 60 GHz it spikes and becomes hugely absorbed by oxygen.
Isn’t that nice. They don’t want your first shooter video games to lag, and most of us know from mainstream releases promoting 5G that things like water and trees are going to get in the way of this frequency. So how does this even make sense unless their intentions are something besides faster speeds?
02:13 mins Knowing this frequency impacts oxygen, why mess with absorption of oxygen in the human body?
The way 60 GHz impacts oxygen is this. From the book ‘Magnetobiology’, Underlying Physical Problems, Effects of electromagnetic fields on living organisms:
Oxygen the atom is O. Oxygen the molecule is 02. Two atoms together.
These two atoms form the oxygen molecule and share some electrons. 60 GHz causes electrons surrounding oxygen molecules to spin, akin to how high-powered microwaves running on 2.4 impact molecules in food such as water. They’re heating, in part, by impacting those molecules to rotate or oscillate with each wave. The movement energy from the rotation of these super tiny water molecules helps heat the rest of the food.
In a similar way that 2.4 causes H20 to oscillate, 5G/60 GHz even at low power causes electrons on oxygen molecules to spin, changes to the spin frequencies on oxygen electrons impact human biology.
When you breathe air into your lungs it gets oxygen into your blood, brain, tissues etc. and oxygen entering your lungs gets picked up by a very important iron containing protein called hemoglobin in your blood.
The impact of oxygen molecules spinning the electrons is that it makes the hemoglobin unable to uptake the oxygen and get it to the rest of your body.
Shouldn’t the fact that 60 GHz fundamentally interacts with oxygen, the most abundant and arguably most important element to all biological life, be headline news that stops everything until we deeply test the implications? https://youtu.be/y5C3-IYtdjc
What about people quarantined at sea? Many of them elderly, many of them with preexisting health conditions, many of them who had the flu shot making them more susceptible to this season’s flu. Did they experience microwave sickness? https://doctormurray.com/does-the-flu-shot-increase-covid-19-risk/
About 5G and Oxygen. We created this video to help you understand the concerns scientists have regarding 5G and to help you form your own opinion
Please share to raise awareness so people take responsibility for their own lives and the lives of family. Thank you.
Sincerely, Doreen A Agostino Without Prejudice and Without Recourse http://freetobewealthy.net Sent via hardwired computer All wireless turned off to safeguard life
An addition, searching about the possible healing effects of the ( right) intake of sodiumbicarbonate I, found this article:
Baking soda (or sodium bicarbonate) is the monosodium salt of carbonic acid, and it forms sodium and bicarbonate ions. This ion formation increases plasma bicarbonate and buffers excess hydrogen ion concentration, resulting in a raised blood pH.
It turns to carbon dioxide (CO2) when it reaches the stomach acid. You can experiment by squeezing a fresh lemon onto a little bit of baking soda — you will instantly see it bubble and turn to carbon dioxide.
Sodium bicarbonate, or rather carbon dioxide, is the key to oxygen in our body. Oxygen is incredibly dangerous, even deadly, without carbon dioxide. So carbon dioxide is actually not a waste product; doctors like to think of it as metabolic waste, but when we exercise we actually create a lot of carbon dioxide — which is very healthy and beneficial, and that’s the reason why exercise is very healthy.
The more carbon dioxide we have, the more the blood vessels dilate, blood flow increases, and more oxygen is delivered to the different parts of the body. If we do not pay attention to our breathing then we can get rid of too much carbon dioxide. The levels then go down in the blood and the blood vessels constrict, making it more difficult for oxygen to get delivered to all the tissues in in the same concentration.
And a pdf in Dutch: de genezende werking van baking soda.
WOODWARD TV: THE IMPLICATIONS OF A CHANGING ATMOSPHERE ON THE BODY
VERY INTERESTING (AND ALARMING);
SOME QUESTIONS:
IN HOW FAR DO THE IMPLEMENTED ELECTROMAGNETIC FIELDS; RADIATION INFLUENCE THE ATMOSPHERE?
LIKE E.G. INCREASING LOW GROUND OZONE GAS ? AIR PRESSURE?
NOTE: IT DOESN'T ONLY DEPEND ON THE HEALTH OF A VICTIM, OR AFFECTED BODY: IT JUST AS MUCH CAN DEPEND ON A ( HIGH) SENSITIVITY FOR CERTAIN EXTERNAL ATMOSPHERIC INFLUENCES ON A , IN NORMAL CONDITIONS, HEALTHY BODY.
A PUBLISHED STUDY OF THE SIMILARITIES OF THE PATHOLOGY OF
DECOMPRESSION SICKNESS: DCS ( CAISSON ) AND THE PATHOLOGY OF COVID-19:
A study by Saraiva et al. (2011) demonstrated the presence of Angiotensin II receptors on the erythrocyte membrane. This little-known information should be deemed as crucial as the SARS-CoV-2 relationships with oxygen saturation and the Renine Angiotensin System but it currently remains unexploited.
The pulmonary and cardiovascular systems are involved in any typical complications of COVID-19 but numerous other unrelated symptoms may occur. To fill the gap, we shall first emphasize some similarities between the complications of this infectious disease and Decompression Illness (DCI), which involves bubble formation.
We theorized that the Angiotensin II clearance by the red blood cells could trigger the release of its oxygen content in the bloodstream. The resulting foam would worsen the widespread endotheliitis, worsen the gas exchange, trigger the coagulation process, the inflammation process and the complement pathway as typically occurs in DCI. At the end, we propose a plausible mechanism.
Keywords: COVID-19, Decompression illness, Angiotensin II, SARS-CoV, Oxygen, Red blood cells
According to Kuba et al. in 2006, one mystery of SARS-CoV is why, in contrast to the other coronaviruses infecting humans, infections with the SARS-CoV trigger severe lung disease with such high mortality [1]. Eighteen years after the SARS outbreak, this assumption unfortunately remains true for SARS-CoV-2. We shall therefore propose a novel hypothesis to better understand the COVID-19 pathophysiology. As a matter of fact, an astounding amount of similarities between Decompression Illness (DCI) and COVID-19-related complications have attracted our attention.
In occupational medicine, we deal with specific work conditions such as caisson workers. DCI (or caisson disease) covers both arterial gas embolism, in which alveolar gas or venous gas emboli are introduced into the arterial circulation, and decompression sickness, which is caused by in-situ bubble formation from dissolved inert gas. Both syndromes can occur in divers, compressed air workers, aviators, and astronauts, but arterial gas embolism also arises from iatrogenic causes unrelated to decompression [2].
Symptoms of pulmonary DCI are similar to those of a thrombotic pulmonary embolus; specifically, substernal pain, cough, and dyspnea, which may progress quickly to pulmonary edema, respiratory failure, right ventricular dysfunction, and cardiovascular collapse [3].
The patients with Covid-19 pneumonia, fulfilling the Berlin criteria of ARDS, present an atypical form of the syndrome [4]. The cardiovascular system is also affected, with complications including myocardial injury, myocarditis, acute myocardial infarction, heart failure, dysrhythmias, venous thromboembolic events [5] and stroke [6]. Both large and small vessels are affected with manifestations ranging from pulmonary embolism to purpuric lesions on extremities [7].
There are several hypotheses as to the mechanism of cardiovascular symptoms. SARS-CoV-2 infection facilitates the induction of a widespread endothelium dysfunction such as endotheliitis in several organs as a direct consequence of viral involvement [8].
Interestingly, there is evidence of endothelial dysfunction in diving [9] as in decompression bubbles in animals. In addition to mechanically obstructing blood flow through the pulmonary vasculature, vascular bubbles may directly contact and damage the vascular endothelium [10]. After hyperbaric decompression, bubbles in the body may be located within tissues or carried along with the bloodstream [11]. The interface between the blood and the bubbles produces red cell sludging in the microcirculation, causes protein denaturation, increases platelet adhesiveness, and promotes the formation of lipid emboli [12]. Vascular bubbles may cause direct blockage, aggregate platelets and red blood cells, and trigger the coagulation process, causing local and downstream clotting [13].
Vascular bubbles activate the inflammatory cascade, which can result in or contribute to pulmonary edema and pulmonary hypertension [14]. Mesenteric injury and organ infarction such as stroke are typical sequelae of severe DCI [3], [15].
We suggest that previous infectious endotheliitis might be amplified by bubbles. Finally, in COVID-19, stroke, acute myocardial infarction, findings of thrombi in small pulmonary arterioles of lung parenchyma and exudative/proliferative diffuse alveolar damage are consistent with the above findings in DCI.
Radiological findings
The radiological findings in COVID-19 are ground-glass opacity [16] and bilateral patchy shadows. In severe form of DCI of chest involvement, radiological results are similar [17].
Biological findings
Numerous biological anomalies affect COVID-19 patients. Complete blood counts revealed lymphocytopenia in most hospitalized cases. According to researchers, multiple mechanisms work together to cause lymphopenia [18]. Less common are elevated levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), creatine kinase (CK), and d-dimer [19]. Acute decompression stress (in rats) has also been shown to cause a transient lymphocytic leucopenia [20] and to result in significantly increased ALT values [21]. There is also evidence of rhabdomyolysis (high CK levels) secondary to arterial gas embolism in skeletal muscles [22].
Finally, COVID-19 and DCI biological features share a number of anomalies.
Immune system and inflammatory features
The pathogenesis in the later stages of SARS-CoV and SARS-CoV-2 infections results not only from direct viral toxicity but also from immune dysregulation and hyperactivity (IL-6, TNF-α) [23]. Furthermore, the complement system plays a vital role in the host immune response to SARS-CoV infection [24].
Interestingly, the lung tissue mRNA levels of TNF-α, Il-1β and Il-6 were significantly increased at 0.5 h after simulated fast buoyancy ascent escape in an animal experiment [25]. In vitro, plasma samples incubated with air bubbles activated complement pathway (C3a and C5a) [26].
Eventually, there is an argument that the COVID-19-related “cytokine storm” [23] might be related to a nucleation of bubbles in the blood (foaming process). Moreover, there is evidence that bubbles activate the inflammatory cascade [25], which could explain COVID-19 hyper-inflammation.
Vascular and vasculitic skin changes including petechiae, purpura, ecchymosis, livedoid lesions, have been described in mostly pediatric COVID-19 patients. COVID-19 may show signs of small blood vessel occlusion such as petechiae or tiny bruises [27]. It is noteworthy that livedoid eruptions and rashes are typical skin manifestations seen in divers [3]. Hence, nucleation of bubbles in the skin microvasculature could be involved in COVID skin manifestations.
The COVID-19-related complications and decompression illness strikingly bear shared features. We have revealed an astounding amount of similarities regarding the clinical but also radiological, biological, immunological and finally humoral features. We believe that the vascular abnormalities and the hyper-inflammatory parameters measured in various COVID-19 organs may be related to the systemic toxic effects of bubbles in the bloodstream elicited by SARS-CoV2 infection. Hereafter, we shall provide a possible mechanism in order to explain how bubbling could occur in COVID-19 as it is obvious that no decompression arises.
Methemoglobinemia occurs when the redox balance of the iron in the heme group is disturbed. In this condition, the patient might experience a “refractory hypoxemia” and COVID-19 critical cases also experience refractory hypoxemia [28]. The analogy with methemoglobinemia suggests that the complication stage of COVID-19 would be secondary to a disturbance in hemoglobin. We shall consequently put forward the hypothesis of a deregulation in the affinity of COVID-19 patient hemoglobin.
Firstly, there is evidence that red cells express Angiotensin II receptors (AT1 and AT2) [29]. This little-kown information should be deemed as crucial as the SARS-CoV-2 relationships with oxygen saturation and the Renine Angiotensin System [23] but it currently remains unexploited. Thus and according to Nobre et al. in 2019, there are no studies deciphering the effect of Angiotensin II and its receptors on the red blood cell membrane [30].
SARS-CoV and SARS-CoV-2 bind to ACE2, a metalloenzyme normally responsible for the degradation of Angiotensin II, which downregulates ACE2 expression and therefore disturbs Angiotensin II clearance. In an animal study, spike protein of former SARS-CoV in mice led to a significant increase in Angiotensin II levels in the lung tissue [1] and recent findings indicate that it is also true in SARS-CoV-2 human infection. Red cells might therefore carry out the clearance of Angiotensin II during the course of the illness.
Body temperature, 2,3-BPG level, and PCO2 are well-known parameters that modulate hemoglobin affinity. We propose that a high level of Angiotensin II suddenly shifts the dissociation curve of hemoglobin to the right during the red cell transit in the lungs, through an unknown molecular mechanism. In lungs, the oxygen load would be normal but the Angiotensin-II-mediated shift would lead to an early (and pathological) oxygen release. For a limited fraction of blood volume, the release would therefore occur in the arterial tree (lungs, heart, brain, liver, kidneys) and not in the capillary beds. The blood would be locally supersaturated and would eventually bubble.
The median time from first symptom to hospital admission (7·0 days) and to ARDS (8·0 days) [31] is consistent with a time-dependent accumulation of foam in the vasculature and onto the endothelium areas.
In other tissues that exhibit ACE2 receptors, the sudden shift in the dissociation curve would produce a surge in free O2, giving rise to DCI-like symptoms. The same effect could result in a foaming process in any ACE2-containing tissue (see picture) Fig. 1 .
In a tissue experiencing a sustained oxygen demand (contractile bowels, active skeletal muscles, myocardic muscle, metabolically active brain and renal tissues), we depicted a blood vessel during an Ang 1–7 – mediated endothelium vasorelaxation (MAS receptor). Ang 1–7 is produced as a result of endothelial ACE2 peptidase activity on Ang II.
Ang II binds to the red blood cell ACE2. We propose that it triggers a shift on the dissociation curve of hemoglobin to the right. This speculative mechanism would provide a supply in free O2 in the cell free capillaries, a process called “plasma skimming”, which results in a reduced hematocrit on the downstream vessels from the first bifurcation.
B. COVID-19 condition (hypothesis).
In a tissue infected by SARS-CoV-2, virus particles are attached to endothelial ACE2 and downregulate ACE2 expression, reducing Ang II clearance.
When the tissue is at rest, capillary beds are more or less shut and the remaining vessels carry a high load of red cells (high hematocrit). As Ang II is not cleared, it could bind to the red cell Ang II receptors. As explained above, we propose that it triggers a shift on the dissociation curve of hemoglobin to the right. This speculative mechanism would provide an overload in free O2 but would occur in a blood flow overwhelmed with fully oxygenated red cells, moreover in a tissue at rest (vasoconstriction). This would involve oxygen supersaturation hence the bubble nucleation. Foaming would worsen the widespread (infectious) endotheliitis (depicted as endothelial dysfunction), worsen the gas exchange, trigger the coagulation process, the inflammation process and the complement pathway, as occurs in decompression illness.
Last, COVID-19 patients with hypertension comorbidity who are taking Angiotensin II Receptor Blockers (ARBs) as anti-hypertension drugs may be less likely to develop severe lung disease compared to patients who take no anti-hypertension drugs [32]. This observation is consistent with the suggested mechanism.
A case study [33] recently reported successful applications of hyperbaric oxygen treatments (HBOTs) in COVID-19, HBOT being the standard treatment in DCI. We suggest that future controlled-clinical trials explore the potential usefulness of HBOT among COVID-19 patients with respiratory conditions.
This paper deals with the theoretical potential possibility of a critical biophysical event during COVID-19, namely bubble nucleation or foaming.
Doppler ultrasonography and echocardiography are valuable tools for researching into venous gas emboli and are urgently needed to assess the previous assumptions. At the end, spectrophotometry assays of Angiotensin II-binding red cells are needed to assert the above assumptions.
We would like to thank the editor for putting this hypothesis forward in publishing this paper. It is the authors’ sincere hope and intent that this novel and original theoretical point of view be largely shared.
The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
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The TECOM Technology Symposium in 1997 concluded on non-lethal weapons, "determining the target effects on personnel is the greatest challenge to the testing community", primarily because "the potential of injury and death severely limits human tests".[62]
Also, "directed-energy weapons that target the central nervous system and cause neurophysiological disorders may violate the Certain Conventional Weapons Convention of 1980. Weapons that go beyond non-lethal intentions and cause 'superfluous injury or unnecessary suffering' may also violate the Protocol I to the Geneva Conventions of 1977."[63]
Some common bio-effects of non-lethal electromagnetic weapons include:
