Replies to post #33516 on Revive Therapeutics Ltd (RVVTF)

[Ecomike]

Wow, the MDs I know's heads would explode on page one of 59 of that document, and they would ask me what it says LOL

They still have no solutions, just 59 pages of how bad it is... and how many symptoms there are...

They need to hire some RA specialists (and MS/Lupus, et al specialists) that have dealt with this kind of chronic immune system problem, all the symptoms it causes already. Problem is they all work in their own bubbles and few of them know how to navigate such massive data and information across the specialty fields.

Googles AI is likely way ahead of them (I saw evidence of it 2 years ago, but nothing since), and Google is not in the FDA/MD medical field yet..

The medical field is still focused on one dimension, one variable analysis in a world that has infinite variables..., which is why so much of the junk drugs do as much or more damage than they fix... They were designed to reduce one problem, for profit... and never mind the other problems they cause....over time..

50 years ago, I gave up on car stealerships for car repairs, they always broke stuff and never fixed what I took in to get fixed.... I have done all my own family vehicle repairs for decades now. And I mean all of it...That way I know it is fixed..

Rant over... for now. I need another nickle please , LOL

[Ecomike]

$RVVTF applications news:

https://www.msn.com/en-us/news/politics/decreased-lung-function-from-covid-persists-in-children/ar-AA125UDP

https://medicalxpress.com/news/2022-09-lung-children-teens-covid.html

" September 21, 2022
Lasting lung damage seen in children and teens after COVID"

Children and adolescents who have either recovered from COVID-19 or have long COVID show persistent lung damage on MRI, according to a study published in Radiology.

COVID-19 is an infectious disease caused by the SARS-CoV-2 virus. Since emerging in late 2019, it has killed more than 5 million people worldwide. The lungs are the primary target for the virus.

Study of the disease's long-term effects has accelerated as the number of COVID survivors climbs and more people are diagnosed with long COVID. The World Health Organization defines long COVID as involving symptoms that persist for a minimum of 12 weeks and other factors, such as symptoms that result in a new health limitation or worsening of a pre-existing underlying medical condition.

The researchers looked at changes in lung structure and function in 54 children and adolescents (mean age 11 years) with previous SARS-CoV-2 infection. Of the 54 patients, 29 had recovered, and 25 had long COVID. All but one of the patients had been unvaccinated at the time of original infection.

and Covid19 is not the only problem:

https://www.cbsnews.com/video/respiratory-virus-cases-rise-among-children/

[Ecomike]

Lots of new end points are possible. Here is one!!!!

https://neurosciencenews.com/covid-microglia-21676/

COVID-19 Linked to Excessive Destruction of Connections Between Nerve Cells
FeaturedNeurologyNeuroscience
·October 19, 2022

Summary: COVID-19 infection causes microglia to excessively engulf synaptic structures and the upregulation of factors involved in phagocytosis.

Source: Karolinska Institute

Researchers at Karolinska Institutet have in a new study used cellular reprogramming to create human three-dimensional brain models and infected these models with SARS-CoV-2.

In infected models, the brain immune cells excessively eliminated synapses and acquired a gene expression pattern mimicking what has been observed in neurodegenerative disorders.

The findings could help to identify new treatments against persistent cognitive symptoms after a COVID-19 infection.

Multiple studies have reported persistent cognitive symptoms after a COVID-19 infection but the underlying mechanisms for this remains unknown.

The researchers behind the study, published as an Immediate Communication in the journal Molecular Psychiatry, have from human induced pluripotent stem (iPS) cells created three-dimensional models of the brain in a dish—so-called brain organoids.

The model differs from previous organoid models as the researchers also included the brain immune cells—microglia—in the model.

In the infected models, microglia excessively engulfed synaptic structures and displayed upregulation of factors involved in phagocytosis. The developed model and the findings in the study could help to guide future efforts to target cognitive symptoms in the aftermath of COVID-19 and other neuroinvasive viral infections.

Cognitive deficits after the infection

“Interestingly, our results to a large extent mimic what has recently been observed in mouse models infected with other neuroinvasive RNA viruses such as the West Nile virus. These viruses are also linked to residual cognitive deficits after the infection, and a persisting activation of microglia leading to an excessive engulfment of synapses, which has been suggested to drive these symptoms.

“Multiple studies have now also reported remaining cognitive symptoms after a COVID-19 infection, as well as an increased risk of receiving a diagnosis of a disorder characterized by cognitive symptoms,” says co-first author of the study Samudyata, postdoctoral fellow in Sellgren lab at the Department of Physiology and Pharmacology at Karolinska Institutet.

Connections to Parkinson’s and Alzheimer’s disease

Microglia are the resident immune cells of the brain but also carries out important regulatory functions of the neuronal circuitries in the developing and adult brain. One of these crucial functions is to engulf unwanted synapses, a process that is believed to improve and maintain cognitive functions.

However, excessive engulfment of synapses has been linked to both neurodevelopmental disorders, such as schizophrenia, as well as to neurodegenerative disorders including Alzheimer’s disease.

By sequencing genes in single cells, the authors could also study how different cell types in the model responded to the virus.

“Microglia displayed a distinct gene signature largely characterized by an upregulation of interferon-responsive genes, and included pathways previously linked to neurodegenerative disorders such as Parkinson’s and Alzheimer’s disease.

“This signature was also observed at a later time-point when the virus load was minimal,” says co-author of the study Susmita Malwade, doctoral student in Sellgren lab at the Department of Physiology and Pharmacology at Karolinska Institutet.

The researchers will now study how different pharmacological approaches can reverse the observed changes in the infected models.