Overlooked CV Researcher On Twitter, Must Read

[RealNeat]

His name is Sandeep Chakraborty.

Nuclease based gene-editing - a disaster waiting to happen
Sandeep Chakraborty - Google Scholar Citations

Some of his tweets at @sanchak74


Pinned Tweet

sandeep chakraborty
@sanchak74
·
Apr 13
And this is my hypothesis: 1. anaerobic antibiotics #doxycycline #metronidazole 2. Anticoagulants #heparin to remove the D-dimers which act as biofilm 3. Maybe repurpose Rdrp based anti-virals if you want to. I am not sure about HCQ.
Quote Tweet

sandeep chakraborty
@sanchak74
· Apr 7
1/ Ignoring bacterial infection is the bane of #Covid19 sandeep chakraborty on Twitter
The synergy between (anaerobic) bacteria and viruses deplete heme->iron->O2. so giving just O2 is counterproductive. sandeep chakraborty on Twitter Explains why children are safe sandeep chakraborty on Twitter
Show this thread

sandeep chakraborty
@sanchak74
·
5h
I hope this is true ! I will be happy and relieved, but not surprised. Pls ask to add anti-coagulants to the therapy, if you cant get in touch...
Quote Tweet

Oum Cali
@OumCali
· 5h
Replying to @sanchak74
In France, Dr Paliard-Franco cures 100% of his patients with antibiotics covid-traitement-macrolide-c3g

sandeep chakraborty
@sanchak74
·
6h
Change Azith to doxycycline (its better for anaerobic bacteria), add an anti-coagulant. I think you will be much better results !
Quote Tweet

Un Seigneur
@USeigneur
· Apr 14
Replying to @GregDemeure and @aragon_jb
L'hcl ne semble pas utile. L'#azithromycine + zinc est bien suffisante et sans effets secondaires. Article de l’Est Républicain du 11/04/2020. Test par 3 médecins de Moselle qui semble prometteur.


sandeep chakraborty
@sanchak74
·
6h
*have* To paraphrase the Godfather dialogue: "Leave the HCQ – take the Azith."


And hope this paper will make the idea complete. Prevotella binds to hemoglobin in the initial stages of the diseases - Sp02 reading go low, but patient doesnt have any symptoms. https://academic.oup.com/femsle/article/162/2/227/528018 Then its expressed heme-binding proteins, and then things get serious.

 

[md_a]

Bacterial endotoxin (lipopolysaccharide) has affinity for a number of cations, including iron.
Previous investigations have demonstrated that lipopolysaccharide can affect the oxidation rate of iron; heme-bound ferrous iron in hemoglobin is oxidized to ferric iron when hemoglobin binds lipopolysaccharide.

…

A series of sugars, starches and a preparation of purified O-chain polysaccharide (the carbohydrate portion of the lipopolysaccharide macromolecule) had no effect on the rate of iron oxidation, whereas phospholipid-enriched brain tissue extracts (similar to the lipid A component of lipopolysaccharide) stimulated oxidation.

We conclude that the lipid moiety of bacterial lipopolysaccharide is responsible for the stimulation of iron oxidation. This process may contribute to the ability of lipopolysaccharide to cause oxidation of heme-bound iron in hemoglobin.


INTRODUCTION

Iron appears to play a number of diverse roles in the promulgation of bacterial infection and sepsis. Iron is an essential nutrient for bacterial proliferation, and bacteria have high affinity siderophores in order to utilize host sources of iron. It has long been hypothesized that hypoferremia, a characteristic of infections and sepsis, represents a host response to limit bacterial proliferation.

Iron-containing hemoglobin is also a pathogenic factor in infection. Enhanced morbidity and mortality from infection has been documented in the settings of hemorrhagic peritonitis, hemoglobinemia secondary to hemolysis during sepsis, or when cell-free hemoglobin (a red blood cell substitute) is infused in the presence of sepsis. In these conditions, it is possible that heme-derived iron may become available for bacterial growth. Alternatively, a variety of mechanisms other than providing nutrient iron may be involved in the deleterious combination of hemoglobin and infection, including inhibition by iron of leukocyte anti-bacterial activity, depression of reticulo-endothelial cell system function, and enhancement of lipopolysaccharide-mediated toxicity.

…

DISCUSSION

…

We believe that the processes of iron binding to LPS, with subsequent oxidation, may have relevance to bacterial infections. Bacterial virulence is enhanced by administration of iron, and bacteria, as well as other organisms, require iron for growth. Since the solubility of iron at physiological pH is very limited, it is logical that microorganisms have evolved sophisticated mechanisms for iron sequestration. Many micro-organisms synthesize and secrete chelators that can bind iron and maintain its solubility at physiological pH. However, these chelators have not been reported to associate with, or bind to, endotoxin. In addition, bacterial cell membranes have been demonstrated to have metal binding sites that serve as transmembrane redox systems, and LPS could be part of such a system.

…


CONCLUSIONS

In conclusion, bacterial LPS-dependent oxidation of Fe2+ is likely to occur through a variety of mechanisms, including simple iron ‘auto-oxidation’ as well as free radical formation. In previous studies, we have demonstrated that the binding of iron to endotoxin decreased the biological activity of LPS and, if endotoxin undergoes free radical attack during iron binding and oxidation, perhaps its chemical structure, composition, or aggregation state is altered. Finally, an interaction between iron and the LPS in the membrane of Gram-negative bacteria may directly contribute to bacterial virulence.


SAGE Journals: Your gateway to world-class research journals

 

[RealNeat]

Bacterial endotoxin (lipopolysaccharide) has affinity for a number of cations, including iron.
Previous investigations have demonstrated that lipopolysaccharide can affect the oxidation rate of iron; heme-bound ferrous iron in hemoglobin is oxidized to ferric iron when hemoglobin binds lipopolysaccharide.

…

A series of sugars, starches and a preparation of purified O-chain polysaccharide (the carbohydrate portion of the lipopolysaccharide macromolecule) had no effect on the rate of iron oxidation, whereas phospholipid-enriched brain tissue extracts (similar to the lipid A component of lipopolysaccharide) stimulated oxidation.

We conclude that the lipid moiety of bacterial lipopolysaccharide is responsible for the stimulation of iron oxidation. This process may contribute to the ability of lipopolysaccharide to cause oxidation of heme-bound iron in hemoglobin.


INTRODUCTION

Iron appears to play a number of diverse roles in the promulgation of bacterial infection and sepsis. Iron is an essential nutrient for bacterial proliferation, and bacteria have high affinity siderophores in order to utilize host sources of iron. It has long been hypothesized that hypoferremia, a characteristic of infections and sepsis, represents a host response to limit bacterial proliferation.

Iron-containing hemoglobin is also a pathogenic factor in infection. Enhanced morbidity and mortality from infection has been documented in the settings of hemorrhagic peritonitis, hemoglobinemia secondary to hemolysis during sepsis, or when cell-free hemoglobin (a red blood cell substitute) is infused in the presence of sepsis. In these conditions, it is possible that heme-derived iron may become available for bacterial growth. Alternatively, a variety of mechanisms other than providing nutrient iron may be involved in the deleterious combination of hemoglobin and infection, including inhibition by iron of leukocyte anti-bacterial activity, depression of reticulo-endothelial cell system function, and enhancement of lipopolysaccharide-mediated toxicity.

…

DISCUSSION

…

We believe that the processes of iron binding to LPS, with subsequent oxidation, may have relevance to bacterial infections. Bacterial virulence is enhanced by administration of iron, and bacteria, as well as other organisms, require iron for growth. Since the solubility of iron at physiological pH is very limited, it is logical that microorganisms have evolved sophisticated mechanisms for iron sequestration. Many micro-organisms synthesize and secrete chelators that can bind iron and maintain its solubility at physiological pH. However, these chelators have not been reported to associate with, or bind to, endotoxin. In addition, bacterial cell membranes have been demonstrated to have metal binding sites that serve as transmembrane redox systems, and LPS could be part of such a system.

…


CONCLUSIONS

In conclusion, bacterial LPS-dependent oxidation of Fe2+ is likely to occur through a variety of mechanisms, including simple iron ‘auto-oxidation’ as well as free radical formation. In previous studies, we have demonstrated that the binding of iron to endotoxin decreased the biological activity of LPS and, if endotoxin undergoes free radical attack during iron binding and oxidation, perhaps its chemical structure, composition, or aggregation state is altered. Finally, an interaction between iron and the LPS in the membrane of Gram-negative bacteria may directly contribute to bacterial virulence.


SAGE Journals: Your gateway to world-class research journals

Covid-19 : la piste du microbiote, vers un nouveau paradigme ?

 

[RealNeat]

sandeep chakraborty
@sanchak74
·
18h
Another marker of #Covd19 - anaerobic respiration, Lactate dehydrogenase - LDH. "If the flow of O2 is not sufficient, however, the pipeline of energy production gets stopped up at the end of glycolysis. LDH is the way that cells solve this problem.." https://pdb101.rcsb.org/motm/102
Quote Tweet

sandeep chakraborty
@sanchak74
· Apr 16
287 patients, 55 with AKI AKI patients were predominantly older/male present with hypoxia higher levels of WBC/D-dimer,lactate dehydrogenase, procalcitonin Why are they ignoring procalcitonin, produced in response to bacterial infections? NYC.. sandeep chakraborty on Twitter
https://twitter.com/outbreaksci/st

 

[RealNeat]

sandeep chakraborty
@sanchak74
·
18h
Another marker of #Covd19 - anaerobic respiration, Lactate dehydrogenase - LDH. "If the flow of O2 is not sufficient, however, the pipeline of energy production gets stopped up at the end of glycolysis. LDH is the way that cells solve this problem.." https://pdb101.rcsb.org/motm/102
Quote Tweet

sandeep chakraborty
@sanchak74
· Apr 16
287 patients, 55 with AKI AKI patients were predominantly older/male present with hypoxia higher levels of WBC/D-dimer,lactate dehydrogenase, procalcitonin Why are they ignoring procalcitonin, produced in response to bacterial infections? NYC.. sandeep chakraborty on Twitter
https://twitter.com/outbreaksci/st

the proofs in the PUFA? @haidut

 

[evanjones]

Sandeep tweeted:
> giving O2 (alone, and not antibiotics) will exacerbate the breathing problems (low Sp02 levels) - if my theory is true.

Ray Peat says this too, though I think he attributes the dangers of giving patients pure O2 to Bohr's Law

 

[RealNeat]

Sandeep tweeted:
> giving O2 (alone, and not antibiotics) will exacerbate the breathing problems (low Sp02 levels) - if my theory is true.

Ray Peat says this too, though I think he attributes the dangers of giving patients pure O2 to Bohr's Law

Sandeep says this is most likely caused by the anaerobic bacteria (like Prevotella) releasing more heme binding proteins to mitigate the oxygenation for its own survival. Hence the need for antibiotics.

this theory may still be downstream however as this was Rays response to me when asked about a similar phenomenon:

Ray, "I have seen some articles talking about the hypoxia that occurs as a problem with the hemoglobin, but I don’t know of any evidence for that, while it’s well known that the virus infects both the intestine and the lung, and bowel inflammation leads to impaired lung function and the other things associated with the virus. The antiinflammatory things work on the actual causes of the sickness—endotoxin, serotonin, histamine, vascular leakiness." 4/16

 

[RealNeat]

Sandeep seems like a very honest person who tries his best to get to the truth. His tweets are on point and educated. Nice to know we have researchers and scientists like this in the mainstream. His latest rebuttal to the claim that unvaccinated people in India filling up ICUs.


View: https://twitter.com/sanchak74/status/1435442755568746497?s=20