Alleen diegenen met
ongeschonden bloed zal de vaccin/radiatie holocaust die tegen de mensheid wordt
losgelaten overleven ... het spike-eiwit in vaccins veroorzaakt genetische DESINTEGRATIE
Vrijdag 19 november 2021 door: Mike Adams
Tags: badcancer , badhealth , badmedicine , bloed , bloedkanker , bloedcellen , COVID , ontvolking , DNA , uitroeiing , genetische integriteit , genetica , genocide , mRNA , mutaties , NHEJ , pandemie , purebloods , vaccin
oorlogen , vaccins
( Natural News ) De podcast van vandaag is als een bom die inslaat en die iedereen moet
begrijpen die hoopt de vaccinholocaust te overleven, want het is echt een
"genetische bom" tegen de mensheid.
Het vaccin, door het natuurlijke DNA-herstelmechanisme in het lichaam te
onderdrukken - bekend als NHEJ of Non-Homologous End Joining - maakt mensen zeer vatbaar voor verwoestende,
kankerachtige mutaties, zelfs wanneer ze worden blootgesteld aan zeer lage niveaus van
ioniserende straling zoals blootstelling aan zonlicht of mammografie . Nu NHEJ wordt onderdrukt door het spike-eiwit , kan het lichaam
het beschadigde DNA niet langer herstellen, en cellen muteren uit de hand,
verwoesten het hele lichaam en veroorzaken genetische desintegratie van het
organisme.
De
studie die dit alles documenteert, werd gepubliceerd in het MDPI-tijdschrift
"Viruses" en werd uitgevoerd door wetenschappers van de
Universiteit van Stockholm, Zweden:
https://doi.org/10.3390/v13102056
De studie toont aan dat de NHEJ-efficiëntie
instort in de aanwezigheid van het mRNA covid-vaccin spike-eiwit:
Geen enkel levend organisme op de planeet kan
overleven zonder genetische integriteit . NHEJ maakt deel uit van elke cel in
elke levende plant, dier en mens op de planeet.
Het spike-eiwitvaccin is een aanval op de genetische integriteit van
mensen, en degenen die het vaccin nemen, zullen grotendeels niet in staat zijn
om zich voort te planten omdat hun baby's zichzelf zullen aborteren als
gevolg van genetische mutaties . Dit is de reden waarom 82% van de zwangere vrouwen die tijdens
hun eerste trimester van de zwangerschap covid-vaccins nemen, hun baby's
verliezen door spontane abortussen.
Hoe ontvolkingsglobalisten de
mutaties onder de gevaccineerden kunnen versnellen?
Belangrijk is dat, zodra de wezens op een planeet op grote schaal worden
geïnjecteerd met het covid-vaccin, globalisten een nucleair ongeval (of
nucleair terrorisme) kunnen ontketenen om straling over de planeet te
verspreiden. Zelfs een lage blootstelling aan cesium-137 (of strontium-91,
jodium-131, enz.) zal een golf van dodelijke kankers ontketenen onder degenen
die zijn gevaccineerd. Terwijl normale, gezonde mensen de DNA-schade
kunnen herstellen die wordt veroorzaakt door lage niveaus van blootstelling aan
ioniserende straling, kunnen gevaccineerde mensen de reparaties nauwelijks
uitvoeren (ze hebben ongeveer 90% onderdrukking van DNA-herstel).
Zo zullen de kankercijfers onder de gevaccineerden omhoogschieten, en
wanneer ze sterven, kunnen de sterfgevallen worden toegeschreven aan kanker in
plaats van aan de vaccins. Dus deze binaire wapenregeling stelt
vaccin-pooiers ook in staat om de schuld voor de vaccins te ontlopen. Het
verdoezelt sterfgevallen door vaccins door ze te categoriseren als sterfgevallen
door kanker.
Het enige wat ze nodig hebben is nog een Tsjernobyl-, Fukushima- of
nucleaire explosie ergens op het noordelijk halfrond - bijna overal - en de
wind zal de radio-isotopen over de halve planeet verspreiden, en de lage
niveaus van ioniserende straling bereiken die nodig zijn om gevaccineerde
mensen om te zetten in door kanker geteisterde mutanten met versnelde
sterfgevallen.
Het is zeer onwaarschijnlijk dat de gevaccineerde personen die niet door
de kankers worden gedood, levensvatbare nakomelingen kunnen produceren vanwege
DNA-beschadiging van sperma en eicellen.
Interessant is dat als het eenmaal duidelijk wordt dat gevaccineerde
individuen geen zonlicht kunnen verdragen zonder genetische mutaties, ze
het daglicht zullen mijden en nachtdieren zullen worden .
In culturele mythen zijn vampiers nachtdieren die onmiddellijk
uiteenvallen wanneer zonlicht hun huid raakt. In werkelijkheid zal de
desintegratie veel meer tijd kosten, maar het is een soortgelijk idee:
Covid-vaccins + zonlicht = genetische desintegratie .
Alleen volbloeden zullen zich
kunnen voortplanten, dus de toekomst van de mensheid behoort toe aan degenen
die mRNA-vaccins afwijzen
Degenen die covid-vaccins afwijzen, staan bekend als 'zuivere
bloeden'. Zij zijn de enigen die in staat zullen zijn de genetische
integriteit voor de komende generaties te behouden, wat
betekent dat de toekomst van de mensheid toebehoort aan degenen die
covid-vaccins afwijzen . (Mensen die spike-eiwit /
mRNA-covid-opnamen maken, winnen de Darwin Award ...)
Volgens God is via het Oude Testament het bloed waar het leven bestaat. Je
lichaam maakt elke minuut twee miljoen rode bloedcellen aan en deze worden in
je botten gemaakt. Dit is de reden waarom Genesis zegt
dat Eva werd gemaakt uit de rib van Adam. De botten zijn waar het DNA
bestaat om bloed te produceren, de essentie van het leven, en om het genetische
patroon te vinden dat de biologie van een nieuw wezen beschrijft.
Een persoon die aan genetische mutaties in het bloed lijdt, wordt
gediagnosticeerd met leukemie , in wezen bloedkanker. Dit
is een desintegratie van de genetische integriteit van hun
bloedproductietemplates, simpel gezegd, en geen enkel zoogdier is levensvatbaar
op de lange termijn wanneer de genetische integriteit van hun bloed wordt vernietigd.
Toch is dit precies wat de vaccins zullen bereiken wanneer ze gepaard
gaan met blootstelling aan lage ioniserende straling. Nogmaals vermeld:
Spike-eiwitten + Ioniserende straling =
DNA-mutaties / verlies van genetische integriteit
Degenen die de spike-eiwitinjecties namen, ervaren al een versnelde
groei van kankertumoren. Dit wordt breed uitgemeten onder
natuurgeneeskundige artsen en analisten. Hoewel het mogelijk is dat
DNA-mutaties een halt worden toegeroepen door een agressief voedingsontgiftingsprogramma
en een levenslange levensstijl tegen kanker, leiden de meeste mensen in feite
een pro-kankerlevensstijl via hun giftige voeding, giftige producten voor
persoonlijke verzorging en giftige woonomgevingen binnenshuis. . De meeste
mensen hebben bovendien een vitamine D-tekort, wat betekent dat ze in wezen
"kankerfabrieken" zijn, zelfs voordat er spike-eiwitinjecties kwamen.
Zo zijn we op het punt om een explosie in kanker wereldwijd te
zien als gevolg van covid vaccins. Dit zal echt versnellen in
2022, en we zullen in 2022 gemakkelijk meer dan een miljoen sterfgevallen door
kanker in de VS zien (hoewel de gegevens hoogstwaarschijnlijk pas in 2024
beschikbaar zullen zijn). In de komende tien jaar (2022 – 2032) zullen we
waarschijnlijk tientallen miljoenen sterfgevallen door kanker zien in de
Verenigde Staten.
Elke vrijgave van straling door globalisten zal deze aantallen alleen
maar versnellen en meer levens kosten. (Dat is het doel van de
globalisten.)
Ondertussen zullen degenen die de mRNA-spike-eiwitinjecties namen, gemuteerde
baby's baren die geen genetische levensvatbaarheid hebben, zelfs als
ze hun eigen mutaties overleven. Momenteel heeft ongeveer de helft van de
menselijke bevolking covid-prikken van een of andere soort genomen, wat
betekent dat de ontvolkingsglobalisten hun doel om de vruchtbaarheid /
genetische levensvatbaarheid voor een aanzienlijk deel van het menselijk ras te
vernietigen, al hebben bereikt.
Het afsterven is nu begonnen. Deze winter zal het aantal
sterfgevallen door kanker in heel Amerika exploderen, en het komende decennium
zullen ze omhoogschieten bij degenen die goedgelovig genoeg waren om te worden
geïnjecteerd met dodelijke biowapens met spike-eiwitten. Maak je klaar om
een vloedgolf van kankers te zien in Amerika, Europa, Australië, Canada en
elk ander land waar goedgelovige mensen zelfmoord hebben gepleegd door vaccins.
Ik behandel het volledige, verbazingwekkende verhaal van dit alles in de
Situation Update-podcast van vandaag:
Brighteon.com/fef16093-6fd9-43a1-a5cb-cdecb4c63e64
Vind elke dag een nieuwe podcast (samen met
krachtige interviews en ander commentaar) op het Health Ranger Report-kanaal op
Brighteon.com:
https://www.brighteon.com/channels/hrreport
-------
settings
Open Access Article
SARS–CoV–2 Spike Impairs
DNA Damage Repair and Inhibits V(D)J Recombination In Vitro
https://www.mdpi.com/1999-4915/13/10/2056/htm
by
Hui Jiang
1,2,* and
Ya-Fang Mei
2,*
1 Department
of Molecular Biosciences, The Wenner–Gren Institute, Stockholm University,
SE-10691 Stockholm, Sweden
2 Department
of Clinical Microbiology, Virology, Umeå University, SE-90185 Umeå, Sweden
* Authors
to whom correspondence should be addressed.
Academic Editor: Oliver Schildgen
Viruses 2021, 13(10),
2056; https://doi.org/10.3390/v13102056
Received: 20 August 2021 / Revised: 8 September
2021 / Accepted: 8 October 2021 / Published: 13 October
2021
(This article belongs to the Special Issue SARS-CoV-2 Host Cell Interactions)
Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS–CoV–2) has led to
the coronavirus disease 2019 (COVID–19) pandemic, severely affecting public
health and the global economy. Adaptive immunity plays a crucial role in
fighting against SARS–CoV–2 infection and directly influences the clinical
outcomes of patients. Clinical studies have indicated that patients with severe
COVID–19 exhibit delayed and weak adaptive immune responses; however, the
mechanism by which SARS–CoV–2 impedes adaptive immunity remains unclear. Here,
by using an in vitro cell line, we report that the SARS–CoV–2 spike protein
significantly inhibits DNA damage repair, which is required for effective V(D)J
recombination in adaptive immunity. Mechanistically, we found that the spike
protein localizes in the nucleus and inhibits DNA damage repair by impeding key
DNA repair protein BRCA1 and 53BP1 recruitment to the damage site. Our findings
reveal a potential molecular mechanism by which the spike protein might impede
adaptive immunity and underscore the potential side effects of full-length
spike-based vaccines.
Keywords: SARS–CoV–2; spike; DNA damage repair; V(D)J recombination; vaccine
1. Introduction
2. Materials and Methods
2.1. Antibodies and Reagents
2.2. Plasmids
2.3. Cells and Cell Culture
2.4. HR and NHEJ Reporter Assays
2.5. Cellular Fractionation and Immunoblotting
2.6. Comet Assay
2.7. Immunofluorescence
2.8. Analysis of V(D)J Recombination
2.9. Statistical Analysis
3.
Results
3.1.
Effect of Nuclear–Localized SARS–CoV–2 Viral Proteins on DNA Damage Repair
DNA damage repair
occurs mainly in the nucleus to ensure genome stability. Although SARS–CoV–2
proteins are synthesized in the cytosol [1], some viral proteins are also
detectable in the nucleus, including Nsp1, Nsp5, Nsp9, Nsp13, Nsp14, and Nsp16
[19]. We investigated whether these
nuclear-localized SARS–CoV–2 proteins affect the host cell DNA damage repair
system. For this, we constructed these viral protein expression plasmids
together with spike and nucleoprotein expression plasmids, which are generally
considered cytosol–localized proteins. We confirmed their expression and
localization by immunoblotting and immunofluorescence (Figure 1A and Figure S1A). Our results were consistent with
those from previous studies [19]; Nsp1, Nsp5, Nsp9, Nsp13, Nsp14, and
Nsp16 proteins are indeed localized in the nucleus, and nucleoproteins are
mainly localized in the cytosol. Surprisingly, we found the abundance of the
spike protein in the nucleus (Figure 1A). NHEJ repair and homologous
recombination (HR) repair are two major DNA repair pathways that not only
continuously monitor and ensure genome integrity but are also vital for
adaptive immune cell functions [9]. To evaluate whether these viral
proteins impede the DSB repair pathway, we examined the repair of a
site-specific DSB induced by the I–SceI endonuclease using the direct
repeat–green fluorescence protein (DR–GFP) and the total-NHEJ-GFP (EJ5–GFP)
reporter systems for HR and NHEJ, respectively [15,16]. Overexpression of Nsp1, Nsp5, Nsp13,
Nsp14, and spike proteins diminished the efficiencies of both HR and NHEJ
repair (Figure 1B–E and Figure S2A,B). Moreover, we also found that Nsp1,
Nsp5, Nsp13, and Nsp14 overexpression dramatically suppressed proliferation
compared with other studied proteins (Figure S3A,B). Therefore, the inhibitory effect of
Nsp1, Nsp5, Nsp13, and Nsp14 on DNA damage repair may be due to secondary
effects, such as growth arrest and cell death. Interestingly, overexpressed
spike protein did not affect cell morphology or proliferation but significantly
suppressed both HR and NHEJ repair (Figure 1B–E, Figures S2A,B and
S3A,B).
Figure 1. Effect of severe acute respiratory
syndrome coronavirus 2 (SARS–CoV–2) nuclear-localized proteins on DNA damage
repair. (A) Subcellular distribution of the SARS–CoV–2 proteins.
Immunofluorescence was performed at 24 h after transfection of the plasmid
expressing the viral proteins into HEK293T cells. Scale bar: 10 µm. (B)
Schematic of the EJ5-GFP reporter used to monitor non-homologous end joining
(NHEJ). (C) Effect of empty vector (E.V) and SARS–CoV–2 proteins on NHEJ
DNA repair. The values represent the mean ± standard deviation (SD) from three
independent experiments (see representative FACS plots in Figure S2A). (D) Schematic of the DR-GFP
reporter used to monitor homologous recombination (HR). (E) Effect of
E.V and SARS–CoV–2 proteins on HR DNA repair. The values represent the mean ±
SD from three independent experiments (see representative FACS plots in Figure S2B). The values represent the mean ±
SD, n = 3. Statistical significance
was determined using one-way analysis of variance (ANOVA) in (C,E).
** p < 0.01, *** p < 0.001, **** p < 0.0001.
3.2.
SARS–CoV–2 Spike Protein Inhibits DNA Damage Repair
Because spike
proteins are critical for mediating viral entry into host cells and are the
focus of most vaccine strategies [20,21], we further investigated the role of
spike proteins in DNA damage repair and its associated V(D)J recombination.
Spike proteins are usually thought to be synthesized on the rough endoplasmic
reticulum (ER) [1]. After posttranslational modifications
such as glycosylation, spike proteins traffic via the cellular membrane
apparatus together with other viral proteins to form the mature virion [1]. Spike protein contains two major
subunits, S1 and S2, as well as several functional domains or repeats [22] (Figure 2A). In the native state, spike proteins
exist as inactive full–length proteins. During viral infection, host cell
proteases such as furin protease activate the S protein by cleaving it into S1
and S2 subunits, which is necessary for viral entry into the target cell [23]. We further explored different
subunits of the spike protein to elucidate the functional features required for
DNA repair inhibition. Only the full–length spike protein strongly inhibited
both NHEJ and HR repair (Figure 2B–E and Figure S4A,B). Next, we sought to determine whether
the spike protein directly contributes to genomic instability by inhibiting DSB
repair. We monitored the levels of DSBs using comet assays. Following different
DNA damage treatments, such as γ–irradiation, doxorubicin treatment, and
H2O2 treatment, there is less repair in
the presence of the spike protein (Figure 2F,G). Together, these data demonstrate
that the spike protein directly affects DNA repair in the nucleus.
Figure 2. Severe acute respiratory syndrome
coronavirus 2 (SARS–CoV–2) spike protein inhibits DNA damage repair. (A)
Schematic of the primary structure of the SARS–CoV–2 spike protein. The S1
subunit includes an N–terminal domain (NTD, 14–305 residues) and a
receptor–binding domain (RBD, 319–541 residues). The S2 subunit consists of the
fusion peptide (FP, 788–806 residues), heptapeptide repeat sequence 1 (HR1,
912–984 residues), HR2 (1163–1213 residues), TM domain (TM, 1213–1237
residues), and cytoplasm domain (CT,1237–1273 residues). (B,C)
Effect of titrated expression of the spike protein on DNA repair in HEK–293T
cells. (D,E) Only full-length spike protein inhibits
non-homologous end joining (NHEJ) and homologous recombination (HR) DNA repair.
The values represent the mean ± SD from three independent experiments (see
representative FACS plots in Figure S4A,B). (F) Full–length spike (S–FL)
protein–transfected HEK293T cells exhibited more DNA damage than empty vector-,
S1–, and S2–transfected cells under different DNA damage conditions. For
doxorubicin: 4 µg/mL, 2 h. For γ–irradiation: 10 Gy, 30 min. For H2O2: 100 µM, 1 h. Scale bar: 50 µm. (G)
Corresponding quantification of the comet tail moments from 20 different fields
with n > 200 comets of three
independent experiments. Statistical significance was assessed using a two-way
analysis of variance (ANOVA). NS (Not Significant): * p > 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.
3.3.
Spike Proteins Impede the Recruitment of DNA Damage Repair Checkpoint Proteins
To confirm the
existence of spike protein in the nucleus, we performed subcellular fraction
analysis and found that spike proteins are not only enriched in the cellular
membrane fraction but are also abundant in the nuclear fraction, with
detectable expression even in the chromatin–bound fraction (Figure 3A). We also observed that the spike has
three different forms, the higher band is a highly glycosylated spike, the
middle one is a full–length spike, and the lower one is a cleaved spike
subunit. Consistent with the comet assay, we also found the upregulation of the
DNA damage marker, γ–H2A.X, in spike protein–overexpressed
cells under DNA damage conditions (Figure 3B). A recent study suggested that spike
proteins induce ER stress and ER–associated protein degradation [24]. To exclude the possibility that the
spike protein inhibits DNA repair by promoting DNA repair protein degradation,
we checked the expression of some essential DNA repair proteins in NHEJ and HR
repair pathways and found that these DNA repair proteins were stable after
spike protein overexpression (Figure 3C). To determine how the spike protein
inhibits both NHEJ and HR repair pathways, we analyzed the recruitment of BRCA1
and 53BP1, which are the key checkpoint proteins for HR and NHEJ repair,
respectively. We found that the spike protein markedly inhibited both BRCA1 and
53BP1 foci formation (Figure 3D–G). Together, these data show that the
SARS–CoV–2 full–length spike protein inhibits DNA damage repair by hindering
DNA repair protein recruitment.
Figure 3. Severe acute respiratory syndrome
coronavirus 2 (SARS–CoV–2) spike protein impedes the recruitment of DNA damage
repair checkpoint proteins. (A) Membrane fraction (MF), cytosolic
fraction (CF), soluble nuclear fraction (SNF), and chromatin-bound fraction
(CBF) from HEK293T cells transfected with SARS–CoV–2 spike protein were
immunoblotted for His-tag spike and indicated proteins. (B) Left:
Immunoblots of DNA damage marker γH2AX in empty vector (E.V)– and spike
protein–expressing HEK293T cells after 10 Gy γ-irradiation. Right: corresponding
quantification of immunoblots in left. The values represent the mean ± SD (n = 3). Statistical significance was
determined using Student’s t-test.
**** p < 0.0001. (C)
Immunoblots of DNA damage repair related proteins in spike protein–expressing
HEK293T cells. (D) Representative images of 53BP1 foci formation in E.V–
and spike protein-expressing HEK293 cells exposed to 10 Gy γ–irradiation.
Scale bar: 10 µm. (E) Quantitative analysis of 53BP1 foci per nucleus.
The values represent the mean ± SEM, n =
50. (F) BRCA1 foci formation in empty vector- and spike
protein-expressing HEK293 cells exposed to 10 Gy γ–irradiation. Scale bar: 10 µm. (G).
Quantitative analysis of BRCA1 foci per nucleus. The values represent the mean
± SEM, n = 50. Statistical
significance was determined using Student’s t-test.
**** p <
0.0001.
3.4. Spike Protein Impairs
V(D)J Recombination In vitro
DNA damage repair,
especially NHEJ repair, is essential for V(D)J recombination, which lies at the
core of B and T cell immunity [9]. To date, many approved SARS–CoV–2
vaccines, such as mRNA vaccines and adenovirus–COVID–19 vaccines, have been
developed based on the full–length spike protein [25]. Although it is debatable whether
SARS–CoV–2 directly infects lymphocyte precursors [26,27], some reports have shown that infected
cells secrete exosomes that can deliver SARS–CoV–2 RNA or protein to target
cells [28,29]. We further tested whether the spike
protein reduced NHEJ–mediated V(D)J recombination. For this, we designed an in
vitro V(D)J recombination reporter system according to a previous study [18] (Figure S5). Compared with the empty vector, spike
protein overexpression inhibited RAG–mediated V(D)J recombination in this in
vitro reporter system (Figure 4).
Figure 4. Spike protein impairs V(D)J
recombination in vitro. (A) Schematic of the V(D)J reporter system. (B)
Representative plots of flow cytometry show that the SARS–CoV–2 spike protein
impedes V(D)J recombination in vitro. (C) Quantitative analysis of
relative V(D)J recombination. The values represent the mean ± SD, n = 3. Statistical
significance was determined using Student’s t-test.
**** p < 0.0001.
4. Discussion
Our findings
provide evidence of the spike protein hijacking the DNA damage repair machinery
and adaptive immune machinery in vitro. We propose a potential mechanism by
which spike proteins may impair adaptive immunity by inhibiting DNA damage
repair. Although no evidence has been published that SARS–CoV–2 can infect
thymocytes or bone marrow lymphoid cells, our in vitro V(D)J reporter assay
shows that the spike protein intensely impeded V(D)J recombination. Consistent
with our results, clinical observations also show that the risk of severe illness
or death with COVID–19 increases with age, especially older adults who are at
the highest risk [22]. This may be because SARS–CoV–2 spike
proteins can weaken the DNA repair system of older people and consequently
impede V(D)J recombination and adaptive immunity. In contrast, our data provide
valuable details on the involvement of spike protein subunits in DNA damage
repair, indicating that full–length spike–based vaccines may inhibit the
recombination of V(D)J in B cells, which is also consistent with a recent study
that a full–length spike–based vaccine induced lower antibody titers compared
to the RBD–based vaccine [28]. This suggests that the use of
antigenic epitopes of the spike as a SARS–CoV–2 vaccine might be safer and more
efficacious than the full–length spike. Taken together, we identified one of
the potentially important mechanisms of SARS–CoV–2 suppression of the host
adaptive immune machinery. Furthermore, our findings also imply a potential
side effect of the full–length spike–based vaccine. This work will improve the
understanding of COVID–19 pathogenesis and provide new strategies for designing
more efficient and safer vaccines.
Supplementary Materials
The following are available online
at https://www.mdpi.com/article/10.3390/v13102056/s1, Figure S1: Expression of
nuclear–localized SARS–CoV–2 proteins in human cells, Figure S2: Effect of
nuclear SARS–CoV–2 proteins on NHEJ– and HR–DNA repair pathway, Figure S3:
Nsp1, Nsp5, Nsp13, Nsp14 but not spike inhibit cell proliferation, Figure S4:
Effect of SARS–CoV–2 spike mutants on NHEJ– and HR– DNA repair pathway, Figure
S5: In vitro V(D)J recombination assay.
Author Contributions
H.J. conceived and designed the study.
H.J. and Y.-F.M. supervised the study, performed experiments, and interpreted
the data. Writing—original draft preparation, H.J.; Writing—review and editing,
H.J. and Y.-F.M.; funding acquisition, Y.-F.M. All authors have read and agreed
to the published version of the manuscript.
Funding
This work was supported by Umeå University,
Medical Faculty’s Planning grants for COVID–19 (research project number: 3453
16032 to Y.F.M.); the Lion’s Cancer Research Foundation at Umeå University
(grants: LP 17–2153, AMP 19–982, and LP 20–2256 to Y.F.M.), and the base unit’s
ALF funds for research at academic healthcare units and university healthcare
units in the northern healthcare region (ALF–Basenheten: 2019, 2020, 2021 to
Y.F.M.).
Institutional Review
Board Statement
Not applicable, because of this study
not involving humans or animals.
Informed Consent
Statement
Not applicable, because of this study
not involving humans.
Data Availability
Statement
The data presented in this study are
available in the main text and Supplementary
Materials.
Conflicts of Interest
The authors have declared that no
competing interests exist. The funders had no role in study design, data
collection and analysis, decision to publish, or preparation of the manuscript.
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