Wenn Palmer das als Haarspalterei empfindet, will ich nicht wissen, wie er peer review Prozesse bei APSB auffassen würde...
https://substack.com/profile/50562652-genervter-burger/note/c-299974075 (2 Anmerkungen)
https://substack.com/profile/50562652-genervter-burger/note/c-299974075 (2 Anmerkungen)
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Möge der Saft mit euch sein.
https://open.substack.com/pub/myrauk/p/lipid-nanoparticles-lnps-the-delivery
Thank you so much, Dr. Forster-van Hijfte, for this great article. ♥️
Thank you so much, Dr. Forster-van Hijfte, for this great article. ♥️
Substack
Lipid nanoparticles (LNPs): The Delivery System Under Scrutiny
Lipid nanoparticles (LNPs): The Delivery System Under Scrutiny
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Hab übrigens noch nen richtig hübschen Witz für euch:
Palmer meinte doch, als ich ihm die unterschiede zwischen LNP-modRNA und AZ demonstrierte, dass ja Beides zu nephrotischem Syndrom führte also gleicher Mechanismus, also egal:
mRNA-LNP cases (Comirnaty):
Case 1: Minimal-change disease (MCD) with nephrotic syndrome, proteinuria 14 g/day, cholesterol 244 mg/dL, LDL 170 mg/dL, triglycerides 159 mg/dL.
Case 3: FSGS-type podocytopathy with nephrotic syndrome, proteinuria UPCR 10.3 g/g, cholesterol 566 mg/dL, LDL 350 mg/dL, triglycerides 302 mg/dL. A detailed lipid profile was reported, including marked LDL and triglyceride elevation in Case 3.
Adenoviral vector case (Janssen):
Case 2: MCD with nephrotic syndrome, proteinuria up to 22.6 g/g, albumin 1,070 mg/dL, cholesterol 589 mg/dL. LDL and triglycerides were not reported. Therefore, the relevant observation is not a simple difference in "presence or absence" of hyperlipidemia.
Dormann H, Knüppel-Ruppert A, Amann K, Erley C. Nephrotic Syndrome After Vaccination Against COVID-19: Three New Cases From Germany. Dtsch Arztebl Int. 2021 Oct 1;118(39):662-663. doi: 10.3238/arztebl.m2021.0330. PMID: 34919048; PMCID: PMC8762589.
"Ashkarran et al.57 reported that the addition of small molecules such as glucose, triglycerides, or phosphatidylcholine to human plasma markedly altered the PC composition on polystyrene NPs. For instance, phosphatidylcholine interacted with albumin via hydrophobic interactions, hydrogen bonding, and water bridges, which consequently reduced the incorporation of albumin into the corona."
https://www.sciencedirect.com/science/article/pii/S2211383526003370
Was sind schon subklinisch relevante Unterschiede in einem Schweizeruhrwerk, wenn man als Kliniker mit nem Vorschlaghammer draufhauen kann, bis es ruhe gibt? Problem gelöst...
Palmer meinte doch, als ich ihm die unterschiede zwischen LNP-modRNA und AZ demonstrierte, dass ja Beides zu nephrotischem Syndrom führte also gleicher Mechanismus, also egal:
mRNA-LNP cases (Comirnaty):
Case 1: Minimal-change disease (MCD) with nephrotic syndrome, proteinuria 14 g/day, cholesterol 244 mg/dL, LDL 170 mg/dL, triglycerides 159 mg/dL.
Case 3: FSGS-type podocytopathy with nephrotic syndrome, proteinuria UPCR 10.3 g/g, cholesterol 566 mg/dL, LDL 350 mg/dL, triglycerides 302 mg/dL. A detailed lipid profile was reported, including marked LDL and triglyceride elevation in Case 3.
Adenoviral vector case (Janssen):
Case 2: MCD with nephrotic syndrome, proteinuria up to 22.6 g/g, albumin 1,070 mg/dL, cholesterol 589 mg/dL. LDL and triglycerides were not reported. Therefore, the relevant observation is not a simple difference in "presence or absence" of hyperlipidemia.
Dormann H, Knüppel-Ruppert A, Amann K, Erley C. Nephrotic Syndrome After Vaccination Against COVID-19: Three New Cases From Germany. Dtsch Arztebl Int. 2021 Oct 1;118(39):662-663. doi: 10.3238/arztebl.m2021.0330. PMID: 34919048; PMCID: PMC8762589.
"Ashkarran et al.57 reported that the addition of small molecules such as glucose, triglycerides, or phosphatidylcholine to human plasma markedly altered the PC composition on polystyrene NPs. For instance, phosphatidylcholine interacted with albumin via hydrophobic interactions, hydrogen bonding, and water bridges, which consequently reduced the incorporation of albumin into the corona."
https://www.sciencedirect.com/science/article/pii/S2211383526003370
Was sind schon subklinisch relevante Unterschiede in einem Schweizeruhrwerk, wenn man als Kliniker mit nem Vorschlaghammer draufhauen kann, bis es ruhe gibt? Problem gelöst...
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Mutflash - Medizinische Argumentationen und Studiensammlungen
Hab übrigens noch nen richtig hübschen Witz für euch: Palmer meinte doch, als ich ihm die unterschiede zwischen LNP-modRNA und AZ demonstrierte, dass ja Beides zu nephrotischem Syndrom führte also gleicher Mechanismus, also egal: mRNA-LNP cases (Comirnaty):…
Es ist soviel schlimmer: Lest bitte aufmerksam meinen aktuellsten Kommentar:
As long as the biological hazard potential of LNPs is not investigated as an independent scientific question in a rational and mechanistic manner (see our work Lipid nanoparticles as active biointerfaces: From membrane interaction to systemic dysregulation), and downstream effectors such as spike protein or modRNA expression are treated as the only admissible explanatory models, any attempt to establish a complete causal chain will inevitably remain incomplete.
This becomes particularly problematic for pathologies whose development does not necessarily correlate with the local detection of spike protein or modRNA. Examples may include alterations of reproductive organs, cardiac micro-scarring, neurodegenerative processes, or other delayed sequelae whose pathogenesis may be shaped by systemic or early physicochemical and biological processes. Such mechanisms can neither be adequately investigated nor excluded by experimental approaches that focus exclusively on downstream effectors.
This creates a methodological circularity: only mechanisms that are actively investigated can be discovered. If spike protein or modRNA are defined a priori as the only admissible causal mechanisms, LNP-mediated processes become invisible by study design rather than being experimentally excluded. That is not evidence against such mechanisms; it is a consequence of the underlying investigative framework.
“mRNA-LNP cases (Comirnaty):
Case 1: Minimal-change disease (MCD) with nephrotic syndrome, proteinuria 14 g/day, cholesterol 244 mg/dL, LDL 170 mg/dL, triglycerides 159 mg/dL.
Case 3: FSGS-type podocytopathy with nephrotic syndrome, proteinuria UPCR 10.3 g/g, cholesterol 566 mg/dL, LDL 350 mg/dL, triglycerides 302 mg/dL. A detailed lipid profile was reported, including marked LDL and triglyceride elevation in Case 3.
Adenoviral vector case (Janssen):
Case 2: MCD with nephrotic syndrome, proteinuria up to 22.6 g/g, albumin 1,070 mg/dL, cholesterol 589 mg/dL. LDL and triglycerides were not reported. Therefore, the relevant observation is not a simple difference in "presence or absence" of hyperlipidemia.
Dormann H, Knüppel-Ruppert A, Amann K, Erley C. Nephrotic Syndrome After Vaccination Against COVID-19: Three New Cases From Germany. Dtsch Arztebl Int. 2021 Oct 1;118(39):662-663. doi: 10.3238/arztebl.m2021.0330. PMID: 34919048; PMCID: PMC8762589.
"Ashkarran et al.57 reported that the addition of small molecules such as glucose, triglycerides, or phosphatidylcholine to human plasma markedly altered the PC composition on polystyrene NPs. For instance, phosphatidylcholine interacted with albumin via hydrophobic interactions, hydrogen bonding, and water bridges, which consequently reduced the incorporation of albumin into the corona."*
Yu, X., Li, M., Zhou, Y., Shi, J. and Yu, W. (2026) ‘Tuning protein corona on nucleic acid nanodrugs for targeted delivery’, Acta Pharmaceutica Sinica B. doi: 10.1016/j.apsb.2026.06.007.
The demonstrated ability of lipid molecules such as triglycerides to mediate specific protein interactions provides a mechanistic rationale to consider that lipid-based nanoparticles may similarly engage lipid-responsive proteins or lipoprotein-associated factors within biological fluids.
However, Ashkarran et al. themselves highlighted a particularly striking point:
“Metabolites, lipids, vitamins, nutrition, and other types of small biomolecules present in the biological fluid can interact with proteins in these fluids and influence their behavior, including their adsorption onto NPs. For example, it was shown that the addition of glucose and cholesterol to plasma can alter the composition of protein corona on the surface of otherwise identical NPs. Small molecules can alter the protein corona of NPs, after interaction with plasma proteins, due to various mechanisms such as (i) their competition with proteins for binding to the surface of NPs; (ii) altering proteins’ binding affinities to NPs; and (iii) changing protein conformation.”
Ashkarran AA, Gharibi H, Sadeghi SA, Modaresi SM, Wang Q, Lin TJ, Yerima G, Tamadon A, Sayadi M, Jafari M, Lin Z, Ritz D, Kakhniashvili D, Guha A, Mofrad MRK, Sun L, Landry MP, Saei AA, Mahmoudi M. Small molecule modulation of protein corona for deep plasma proteome profiling. Nat Commun. 2024 Nov 7;15(1):9638. doi: 10.1038/s41467-024-53966-z. PMID: 39511193; PMCID: PMC11544298.
https://substack.com/@genervter/note/c-300057777
This consideration suggests that nanoparticle behavior is not exclusively dictated by the nanoparticle formulation itself, but may also depend on the physiological state of the host. Since endogenous metabolites and lipids can influence protein–nanoparticle interactions and reshape the protein corona, interindividual differences in metabolic status, lipid composition, or nutritional state may contribute to variability in the biological identity, biodistribution, and cellular interactions of lipid-based nanoparticles.
*Note: While these observations have thus far been reported for polystyrene nanoparticles and not for LNPs, the general phenomenon of protein corona formation suggests that LNPs may likewise bind triglyceride-rich lipoproteins. This possibility cannot currently be excluded.
Conflating distinct pathogenic mechanisms on the basis of a shared clinical endpoint is not only scientifically unjustified but may also have direct therapeutic implications. Interventions directed at a common downstream phenotype may appear clinically effective while the upstream pathogenic processes remain unaddressed or are even unintentionally exacerbated. Mechanistic understanding is therefore not an academic luxury but a prerequisite for rational, effective, and safe medical practice.
As long as the biological hazard potential of LNPs is not investigated as an independent scientific question in a rational and mechanistic manner (see our work Lipid nanoparticles as active biointerfaces: From membrane interaction to systemic dysregulation), and downstream effectors such as spike protein or modRNA expression are treated as the only admissible explanatory models, any attempt to establish a complete causal chain will inevitably remain incomplete.
This becomes particularly problematic for pathologies whose development does not necessarily correlate with the local detection of spike protein or modRNA. Examples may include alterations of reproductive organs, cardiac micro-scarring, neurodegenerative processes, or other delayed sequelae whose pathogenesis may be shaped by systemic or early physicochemical and biological processes. Such mechanisms can neither be adequately investigated nor excluded by experimental approaches that focus exclusively on downstream effectors.
This creates a methodological circularity: only mechanisms that are actively investigated can be discovered. If spike protein or modRNA are defined a priori as the only admissible causal mechanisms, LNP-mediated processes become invisible by study design rather than being experimentally excluded. That is not evidence against such mechanisms; it is a consequence of the underlying investigative framework.
“mRNA-LNP cases (Comirnaty):
Case 1: Minimal-change disease (MCD) with nephrotic syndrome, proteinuria 14 g/day, cholesterol 244 mg/dL, LDL 170 mg/dL, triglycerides 159 mg/dL.
Case 3: FSGS-type podocytopathy with nephrotic syndrome, proteinuria UPCR 10.3 g/g, cholesterol 566 mg/dL, LDL 350 mg/dL, triglycerides 302 mg/dL. A detailed lipid profile was reported, including marked LDL and triglyceride elevation in Case 3.
Adenoviral vector case (Janssen):
Case 2: MCD with nephrotic syndrome, proteinuria up to 22.6 g/g, albumin 1,070 mg/dL, cholesterol 589 mg/dL. LDL and triglycerides were not reported. Therefore, the relevant observation is not a simple difference in "presence or absence" of hyperlipidemia.
Dormann H, Knüppel-Ruppert A, Amann K, Erley C. Nephrotic Syndrome After Vaccination Against COVID-19: Three New Cases From Germany. Dtsch Arztebl Int. 2021 Oct 1;118(39):662-663. doi: 10.3238/arztebl.m2021.0330. PMID: 34919048; PMCID: PMC8762589.
"Ashkarran et al.57 reported that the addition of small molecules such as glucose, triglycerides, or phosphatidylcholine to human plasma markedly altered the PC composition on polystyrene NPs. For instance, phosphatidylcholine interacted with albumin via hydrophobic interactions, hydrogen bonding, and water bridges, which consequently reduced the incorporation of albumin into the corona."*
Yu, X., Li, M., Zhou, Y., Shi, J. and Yu, W. (2026) ‘Tuning protein corona on nucleic acid nanodrugs for targeted delivery’, Acta Pharmaceutica Sinica B. doi: 10.1016/j.apsb.2026.06.007.
The demonstrated ability of lipid molecules such as triglycerides to mediate specific protein interactions provides a mechanistic rationale to consider that lipid-based nanoparticles may similarly engage lipid-responsive proteins or lipoprotein-associated factors within biological fluids.
However, Ashkarran et al. themselves highlighted a particularly striking point:
“Metabolites, lipids, vitamins, nutrition, and other types of small biomolecules present in the biological fluid can interact with proteins in these fluids and influence their behavior, including their adsorption onto NPs. For example, it was shown that the addition of glucose and cholesterol to plasma can alter the composition of protein corona on the surface of otherwise identical NPs. Small molecules can alter the protein corona of NPs, after interaction with plasma proteins, due to various mechanisms such as (i) their competition with proteins for binding to the surface of NPs; (ii) altering proteins’ binding affinities to NPs; and (iii) changing protein conformation.”
Ashkarran AA, Gharibi H, Sadeghi SA, Modaresi SM, Wang Q, Lin TJ, Yerima G, Tamadon A, Sayadi M, Jafari M, Lin Z, Ritz D, Kakhniashvili D, Guha A, Mofrad MRK, Sun L, Landry MP, Saei AA, Mahmoudi M. Small molecule modulation of protein corona for deep plasma proteome profiling. Nat Commun. 2024 Nov 7;15(1):9638. doi: 10.1038/s41467-024-53966-z. PMID: 39511193; PMCID: PMC11544298.
https://substack.com/@genervter/note/c-300057777
This consideration suggests that nanoparticle behavior is not exclusively dictated by the nanoparticle formulation itself, but may also depend on the physiological state of the host. Since endogenous metabolites and lipids can influence protein–nanoparticle interactions and reshape the protein corona, interindividual differences in metabolic status, lipid composition, or nutritional state may contribute to variability in the biological identity, biodistribution, and cellular interactions of lipid-based nanoparticles.
*Note: While these observations have thus far been reported for polystyrene nanoparticles and not for LNPs, the general phenomenon of protein corona formation suggests that LNPs may likewise bind triglyceride-rich lipoproteins. This possibility cannot currently be excluded.
Conflating distinct pathogenic mechanisms on the basis of a shared clinical endpoint is not only scientifically unjustified but may also have direct therapeutic implications. Interventions directed at a common downstream phenotype may appear clinically effective while the upstream pathogenic processes remain unaddressed or are even unintentionally exacerbated. Mechanistic understanding is therefore not an academic luxury but a prerequisite for rational, effective, and safe medical practice.
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I have to actually thank Michael Palmer for this “discussion”:
His comparison of LNPs with adenoviral vector vaccines was intended as a dismissal, but ironically it exposed a much broader implication of the hypothesis than I had initially appreciated.
The fundamental mistake is reducing biological effects to the encoded protein alone. Delivery platforms are not biologically inert envelopes. Whether we are talking about lipid nanoparticles or viral vectors, the vehicle itself interacts with membranes, trafficking pathways, immune sensors, and cellular physiology.
The membrane is not a passive container: it is the interface where biology happens. Wherever such technologies interact with cells, there will be upstream effects determined by the properties of that interaction. You do not need to invoke a translated protein as the only possible source of biological consequences.
The amusing part is that by bringing adenoviral vectors into the discussion, Dr. Palmer inadvertently strengthened the very point he was trying to dismiss: if the relevant mechanism involves delivery systems, cellular targeting, membrane interactions, and biodistribution, then the question is much broader than a single antigen or protein product.
So, thank you, Dr. Palmer: this otherwise rather unproductive argument made the scope and potential transferability of the hypothesis much clearer than before. The comparison you offered may have been intended as a rebuttal, but it actually revealed a much larger conceptual framework.
https://substack.com/@genervter/note/c-301058812
His comparison of LNPs with adenoviral vector vaccines was intended as a dismissal, but ironically it exposed a much broader implication of the hypothesis than I had initially appreciated.
The fundamental mistake is reducing biological effects to the encoded protein alone. Delivery platforms are not biologically inert envelopes. Whether we are talking about lipid nanoparticles or viral vectors, the vehicle itself interacts with membranes, trafficking pathways, immune sensors, and cellular physiology.
The membrane is not a passive container: it is the interface where biology happens. Wherever such technologies interact with cells, there will be upstream effects determined by the properties of that interaction. You do not need to invoke a translated protein as the only possible source of biological consequences.
The amusing part is that by bringing adenoviral vectors into the discussion, Dr. Palmer inadvertently strengthened the very point he was trying to dismiss: if the relevant mechanism involves delivery systems, cellular targeting, membrane interactions, and biodistribution, then the question is much broader than a single antigen or protein product.
So, thank you, Dr. Palmer: this otherwise rather unproductive argument made the scope and potential transferability of the hypothesis much clearer than before. The comparison you offered may have been intended as a rebuttal, but it actually revealed a much larger conceptual framework.
https://substack.com/@genervter/note/c-301058812
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https://www.sciencedirect.com/science/article/pii/S2211383526004235
Es ist daaa! Die "corrected" Version!
Es ist daaa! Die "corrected" Version!
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https://substack.com/@michaelpalmer/note/c-301706859
LOL! Sorry... Aber ich hab dem Typen echt nicht mehr (mehr) zu sagen. 🤡
LOL! Sorry... Aber ich hab dem Typen echt nicht mehr (mehr) zu sagen. 🤡
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Forwarded from Seiji Draven
"Court of Appeal cited the Prep Act to waive @AstraZeneca responsibility to compensate & care for @BrianneDressen, an injured participant of their COV-19 trial!
Morally wrong & makes absolutely no sense!
Dismissing obvious vaccine injuries destroys trust in vaccination programs!
Not the only case:
Pfizer trial:
Augusto Roux (@RouxAugusto)
Maddie de Garay (@shdegaray73)
Moderna trial:
Olivia Tesinar
AZ trial:
Brianne Dressen
Steve De Mitri
Kleiton Lewis
@NIHDirector_Jay @RobertKennedyJr @AaronSiriSG"
https://fixupx.com/RetsefL/status/2081081334542262725
Morally wrong & makes absolutely no sense!
Dismissing obvious vaccine injuries destroys trust in vaccination programs!
Not the only case:
Pfizer trial:
Augusto Roux (@RouxAugusto)
Maddie de Garay (@shdegaray73)
Moderna trial:
Olivia Tesinar
AZ trial:
Brianne Dressen
Steve De Mitri
Kleiton Lewis
@NIHDirector_Jay @RobertKennedyJr @AaronSiriSG"
https://fixupx.com/RetsefL/status/2081081334542262725
FixupX
Retsef Levi (@RetsefL)
Court of Appeal cited the Prep Act to waive @AstraZeneca responsibility to compensate & care for @BrianneDressen, an injured participant of their COV-19 trial!
Morally wrong & makes absolutely no sense!
Dismissing obvious vaccine injuries destroys trust…
Morally wrong & makes absolutely no sense!
Dismissing obvious vaccine injuries destroys trust…
Forwarded from henning rosenbusch - Channel
Der seinerzeit amtierende Weltcup-Sieger Sivert Bakken erkrankte im Frühjahr 2022 nach einem Corona-Booster an einer Herzmuskelentzündung (Myokarditis) und musste daraufhin eine lange sportliche Pause einlegen.
Im Dezember 25 starb er, während eines Trainingslagers in Italien, im Alter von nur 27 Jahren. Die Todesursache bleibt bis heute, sieben Monate später, unbekannt, obwohl die Ergebnisse der Autopsie im März 2026 bekannt gegeben hätten werden sollen.
Nur in Norwegen wird noch - verschämt - über das Schicksal des Sportstars gesprochen.
Um nochmal zum FC Bayern zu kommen, da es Kritik unter dem Post gab:
Der Münchner Verein zahlte seinen ungeimpften Spielern (u.a. Kimmich) teilweise kein Gehalt.
t.me/Rosenbusch
Im Dezember 25 starb er, während eines Trainingslagers in Italien, im Alter von nur 27 Jahren. Die Todesursache bleibt bis heute, sieben Monate später, unbekannt, obwohl die Ergebnisse der Autopsie im März 2026 bekannt gegeben hätten werden sollen.
Nur in Norwegen wird noch - verschämt - über das Schicksal des Sportstars gesprochen.
Um nochmal zum FC Bayern zu kommen, da es Kritik unter dem Post gab:
Der Münchner Verein zahlte seinen ungeimpften Spielern (u.a. Kimmich) teilweise kein Gehalt.
t.me/Rosenbusch