Roger Seheult
MedCram Videos
Roger Seheult is a physician, educator, and co-founder of MedCram Videos who has treated patients during the COVID-19 pandemic. His published research includes cost-effectiveness evaluations of vilobelimab for mechanically ventilated COVID-19 patients. Additionally, his work has examined the physiological effects of prophylactic bosentan on pulmonary artery pressure and exercise capacity at high altitude.
49 claims checked on air: 3 context 3 contradicted 2 overstated 33 supported 8 unverified 5 flagged
What they said on air - context
Aspirin was discovered in 1899 by the German company Bayer.
"Aspirin had just been discovered in 1899 uh by the German company Bayer." (said at 1:23:33)
The year 1899 marks when the German company Bayer registered the trademark "Aspirin" and launched the drug commercially, rather than its chemical discovery. The compound, acetylsalicylic acid, was first synthesized in 1853 by French chemist Charles Frédéric Gerhardt, and pure acetylsalicylic acid was synthesized at Bayer's laboratories on August 10, 1897.
- context: One hundred years of aspirin (Medical History 1999) · cited 32x in the literature
"Acetylsalicylic acid was synthesized by Gerhardt in 1853... on 10 August 1897 he synthesized acetylsalicylic acid... On 23 January 1899 they decided to give this substance the brand name of Aspirin and finally, on 6 March 1899, this was registered at the Kaiserlichen Patentsamt Berlin." (abstract)
openalexfull study (doi) - context: The discovery of aspirin: a reappraisal (BMJ 2000) · cited 246x in the literature
"Hoffmann, a chemist in the pharmaceutical laboratory of the German dye manufacturer Friedrich Bayer & Co in Elberfeld, consulted the chemical literature and came across the synthesis of acetylsalicylic acid and then prepared the first sample of pure acetylsalicylic acid on 10 August 1897. This was marketed in 1899 under the registered trademark of Aspirin." (abstract, passage verified)
openalexfull study (doi)
Vasoconstriction caused by cold exposure triggers demargination of leukocytes into the circulation.
"when you just like we know when you take a cold shower that vasoconstriction causes demargination of leukocytes and that causes the amount of leukocytes in solution if you will or in the in the vasculature to go through find the viral particles and report to their lymph nodes" (said at 1:32:23)
Acute cold exposure (such as cold-water immersion or cold ambient air) triggers sympathetic nervous system activation, resulting in surges of catecholamines (norepinephrine and epinephrine) and cortisol that cause a transient mobilization (demargination) and increase in circulating leukocytes and granulocytes. However, this demargination is primarily mediated by catecholamine signaling and hemodynamic shear forces acting on vascular endothelial adhesion molecules, rather than peripheral vasoconstriction itself directly dislodging white blood cells. Furthermore, while circulating immune cell counts transiently rise following cold stress, clinical evidence does not demonstrate that taking a cold shower meaningfully enhances antiviral surveillance or active viral clearance in lymph nodes.
- supports: Immune changes in humans during cold exposure: effects of prior heating and exercise. (Journal of applied physiology (Bethesda, Md. : 1985) 1999) · cited 163x in the literature
"Subsequent cold exposure induced a leukocytosis and granulocytosis, an increase in natural killer cell count and activity, and a rise in circulating levels of interleukin-6. Pretreatment with exercise in 18 degrees C water augmented the leukocyte, granulocyte, and monocyte response. These results indicate that acute cold exposure has immunostimulating effects and that, with thermal clamping, pretreatment with physical exercise can enhance this response. Increases in levels of circulating norepinephrine may account for the changes observed during cold exposure and their modification by changes in initial status." (abstract, results, passage verified)
pubmedfull study (doi) - supports: Residual effects of short-term whole-body cold-water immersion on the cytokine profile, wh… (International journal of hyperthermia : the official journal of European Society for Hyperthermic Oncology, North American Hyperthermia Group 2021) · cited 52x in the literature
"CWI also induced the marked release of the stress hormones Epi, NE, and cortisol. The change in IL-6 concentration after CWI was delayed and TNF-α production was decreased, but IL-1β was not affected within 48 h after CWI. A delayed increase in neutrophil percentage and decrease in lymphocyte percentage occurred after CWI." (abstract, results, passage verified)
pubmedfull study (doi)
N-acetylcysteine (NAC) functions as an antioxidant and recycles the glutathione peroxidase system to mitigate oxidative stress.
"NAC is a great antioxidant. It's packed with antioxidants and it it's recycles that the the glutathione peroxidase system which is helpful in dealing with oxidative stress." (said at 1:54:40)
N-acetylcysteine (NAC) functions as an antioxidant and precursor for intracellular glutathione (GSH) synthesis, helping cells counteract oxidative stress. However, the claim's description of its mechanism needs qualification: NAC is a single amino acid derivative (a cysteine prodrug) rather than something "packed with antioxidants," and it does not directly recycle the glutathione peroxidase enzyme. Glutathione peroxidase utilizes reduced glutathione (GSH) to detoxify peroxides, producing glutathione disulfide (GSSG), which is subsequently reduced back to GSH by glutathione reductase. NAC supports this system by supplying cysteine to replenish GSH pools rather than directly recycling the peroxidase system.
- supports: The Multifaceted Therapeutic Role of N-Acetylcysteine (NAC) in Disorders Characterized by … (Current neuropharmacology 2021) · cited 284x in the literature
"The sulfhydryl-containing tripeptide glutathione (GSH), which is synthesized and maintained at high concentrations in all cells, is one of the mechanisms by which cells protect themselves from oxidative stress." (abstract, passage verified)
pubmedfull study (doi) - context: The mechanism of action of N-acetylcysteine (NAC): The emerging role of H 2 S and sulfane … (Pharmacology & therapeutics 2021) · cited 468x in the literature
"Conventionally, it is assumed that NAC acts as (i) a reductant of disulfide bonds, (ii) a scavenger of reactive oxygen species and/or (iii) a precursor for glutathione biosynthesis." (abstract, passage verified)
pubmedfull study (doi) - context: N-acetylcysteine Pharmacology and Applications in Rare Diseases-Repurposing an Old Antioxi… (Antioxidants (Basel, Switzerland) 2023) · cited 94x in the literature
"N-acetylcysteine (NAC), a precursor of cysteine and, thereby, glutathione (GSH), acts as an antioxidant through a variety of mechanisms, including oxidant scavenging, GSH replenishment, antioxidant signaling, etc." (abstract, passage verified)
pubmedfull study (doi)
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