I haven't heard the story about toxin itself- there are some strain of Corynebacterium that are pathogenic (Corynebacterium diphteriae), but their pathogenicity is due to the genes that are acquired from bacteriophage (tox gene). Others may be part of the normal flora. These bacteria are called lysogenic. AB toxin has 2 units- A one which has 1 region which is called C region (c for catalytic activity) and its function is explained, and B subunit contains 2 regions- R region (receptor-binding region) and T region (translocation region). R region will bind to the HB-EGF precursor and endocytosis will occur. T region will release A subunit into the cell cytoplasm. Toxin won't be produced constantly. Bacteria needs Fe,so if its concentration is high, toxin won't be produced. But if there is a low concentration of Fe, bacteria will release toxin in order to destroy host cells and take their Fe storage. All of this is regulated by dtxR protein that regulates transcription of the toxin genes.
I was looking for the local effects. like the clinical symptom of the fibrin coating when fibrinogen comes in contact with thromboplastin from necrotizing cells, the inflammatory effect (hyperemia, swelling, and microcirculatory disturbances) and if there are more I am missing.
This is a nice but somewhat superficial run through. An advise could be to do the drawing video first and then add commentary afterwards, because as of right now you use a lot of time to say the same words over and over again. But thank you for the video never the less.
I haven't heard the story about toxin itself- there are some strain of Corynebacterium that are pathogenic (Corynebacterium diphteriae), but their pathogenicity is due to the genes that are acquired from bacteriophage (tox gene). Others may be part of the normal flora. These bacteria are called lysogenic. AB toxin has 2 units- A one which has 1 region which is called C region (c for catalytic activity) and its function is explained, and B subunit contains 2 regions- R region (receptor-binding region) and T region (translocation region). R region will bind to the HB-EGF precursor and endocytosis will occur. T region will release A subunit into the cell cytoplasm.
Toxin won't be produced constantly. Bacteria needs Fe,so if its concentration is high, toxin won't be produced. But if there is a low concentration of Fe, bacteria will release toxin in order to destroy host cells and take their Fe storage. All of this is regulated by dtxR protein that regulates transcription of the toxin genes.
I was looking for the local effects. like the clinical symptom of the fibrin coating when fibrinogen comes in contact with thromboplastin from necrotizing cells, the inflammatory effect (hyperemia, swelling, and microcirculatory disturbances) and if there are more I am missing.
Dunja T , Hello please need your help?
You did not mention T domain?
ya man. you have to do the video first and then you can add the audio later. that make your videos way better. But other than that, good videos
please allow this to have captions or subtitle I cannot understand some of the words
thank you
This is a nice but somewhat superficial run through. An advise could be to do the drawing video first and then add commentary afterwards, because as of right now you use a lot of time to say the same words over and over again. But thank you for the video never the less.
Thank you
You're welcome
Thanks sir
Nice explaintion but please stop putting all of these adds it's realy annoying
awesome
SOU BRASILEIRA COMO VOU ENTENDER A RESPEITO DA DOENÇA DIFTERIA