Tuesday, June 28, 2022

"Baicalin can protect neonatal rat brains against hypoxic-ischemic injury."

So now we learn, or should I say, it's now being confirmed that COVID causes brain damage.  What type of damage, you ask?  I initially thought it was just your everyday brain shrinkage since the shrinkage accompanied muscle wasting.  But, no, not just brain shrinkage, but literal holes in the brain.  What parts of the brain?  Does it matter?  Is there any way to fix the holes in the brain?  Sure . . . but only if you get--wait for it--early treatment.  Didn't get early treatment?  Oh, too bad.  You're SOL.  Early treatment is only for those exclusive few who knew how to treat COVID or spike protein transmission.  Didn't know how to do that?  Didn't know that transmission could even occur, despite the obvious transmission from a family member?  Didn't get that in time to treat early?  Oh, you poor Schnoor.    

So, okay, besides the different kinds of brain damage in the various locations of the brain caused by COVID-19 and its GoF spike protein, are there any other horrors that await us, I mean besides the destruction of reproductive organs, alopecia [which from my view is connected to the reproductive hormones, like testosterone], brain shrinkage, muscle wasting, prion disease, destruction of the medulla . . . let's see have I forgotten anything? 

From the video interview with Dr. Mannan Baig: 

He is calling the nerve damage Neuro-COVID and Neural Damage.  Oh, boy.  That can't be good.  So we're looking for neuroprotective agents that Dr. Mannan Baig might recommend.  Okay, so he says that one can have neurological symptoms during acute phases of COVID.  I'd like a definition of that.  What happens with folks with "comorbidities" where all that COVID does is exacerbate those?  

Here is Dr. Abdul Amman Baig's website.

Once the virus is in the cell, it can cause the development of plaques, amyloids, and proteins.  

2:48  Is it possible to diagnose, after 3 months to 1 year, that possible neural inflammation is still going on?  Hypoxia can cause neuronal damage.  Therefore, one should take a fat-soluble B1, like Benfotiamine, Allathiamine, and others.  

He points to this list: 

Light chain neurofilaments.  What are these?

Protein S 100B

Neuron specific enolase

Lactate dehydrogenase

Creatine kinase

Glial fibrillary acid protein 

Symptoms he points to are:

Brain fog

Dizziness

Inability to concentrate

Shortness of breath

Chronic cough

Myocarditis or Palpitations

Gastrointestinal symptoms

Urinary bladder control 

Neutrophil Elastase creates super fibrils, perhaps those thick fibrin strands found by embalmers and coroners?   They assume the form of amyloid and T Pau protein?   The speed at which these amyloid plaques accumulate directly corresponds to the accelerated aging that you see in vaccinated individuals.  At the 7:10 mark, he says that COVID sets up apoptosis.  He's got an illustration of loss of brain mass.  B-12 restores the brain mass as do fish oils.  

One, his audio is terrible.  Two, his hesitations and thinking as he goes exacerbates problems with his accent.  Fine.  But then the wording on his screen is tiny.  He refers to the IMiDs or Immune-Mediated Inflammatory Diseases.  

An immune-mediated inflammatory disease (IMID) is any group of conditions or diseases that lack a definitive etiology, but which are characterized by common inflammatory pathways leading to inflammation, and which may result from, or be triggered by, a dysregulation of the normal immune response.  All IMIDs can cause end-organ damage and are associated with increased morbidity and/or mortality. 

So this is nothing to trifle with.  How, then, does one repair this?  He mentions Pomalidomide, which is a chemotherapy drug called Pomalyst. 

So what he is trying to relay here is a list of nutraceuticals that protect the nerves and the brain.  So far, he's listed

Hesperidin 

Rutin is anti-apoptotic.  

Piperine 

Baicalin  So, two things: target the virus AND the inflammatory pathways.  


DYSAUTONOMIA

it’s the inability of the body to adequately execute involuntary actions like regulating intestinal function, blood pressure, heart rate, pupil size, bronchial tone, renal blood flow, urinary bladder, and sexual functions, due to the dysfunctional sympathetic and parasympathetic nerves acting in concert.


Amyloid plaques can occlude blood vessels leading to hypoxia.  Again, fat-soluble B1s [Benfotiamine, Allithiamine, and others] treat hypoxia.  Partially blocks the blood flow to the brain, so that the blood flow to the brain gets limited.  The neurons can suffer hypoxic damage that you heard Stephanie and other speakers describe.  


TREATMENT APPROACHES: WHAT CAN BE DONE?  

16:00  Neural Stem Cell Therapy?  Didn't know there was such a thing.  


Okay, at the 17:43 mark, he has a list.  Lists are good.  He writes,

Findings suggest that Baicalin induces neuronal differentiation of C17.2 neural stem cells and that this is mediated by activation of Erk1/2.  Our work lays the foundation for exploring baicalin for the promotion of neural regeneration after injury or disease. 

Our findings provide the first evidence, to our knowledge that baicalin can protect neonatal rat brains against hypoxic-ischemic injury. 

These findings indicate that Piperine can enhance the antioxidant and anti-inflammatory properties of Quercetin and Quercetin in combination with piperine exhibits strong neuroprotective effects against MPTP-induced neurotoxicity. 

After administration of 1umol/L curcumin, synaptic growth improved. Curcumin is neuroprotective against gp 120 V3 loop-induced neuronal damage by inhibiting the activation of L-type calcium currents. 

Neural stem cell therapy in conjunction with curcumin loaded in niosomal nanoparticles enhanced recovery from traumatic brain injury.   

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