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I'm a physician doctor with an MD degree. My passion for teaching has always been appreciated by students with whom I have shared my knowledge. I'm a passionate teacher of medical biochemistry and would like to share my knowledge about this beautiful subject with all those who is interested to learn to understand the cellular metabolic events and to understand the metabolic disease process. I would like to learn new things by keeping myself updated with current research in the field. Let us share the knowledge each other!!

Friday, September 23, 2016

Biotin - A Brief Review

In this video I have explained in brief about water soluble vitamin biotin. I have touched upon biological functions, enzymes, causes for deficiency and deficiency manifestations.

Biotin is widely available vitamin. it is also significantly synthesized in the intestine by bacterial flora. main function of biotin is it acts as a CO2 carrier for carboxylase enzymes in carboxylation reactions.

Four carboxylases needs biotin as their coenzyme, they are:

  1. acetyl CoA carboxylase
  2. pyruvate carboxylase
  3. propionyl CoA carboxylase
  4. methylcrotonyl CoA carboxylase
Dietary deficiency of biotin is rare. 

Deficiency of biotin is seen in four conditions: 

  1. Prolonged use of antibiotics (which kill bacterial flora)
  2. Prolonged use of anticonvulsants (interfere with absorption) 
  3. Consumption of raw egg white (avidin binding with biotin).
  4. Biotidinase deficiency (decreased recycling). 

Clinical Manifestation:

Multiple carboxylase deficiency leads to dermatitis, alopecia, diarrhea, opportunistic infections like fungal infection, and central nervous system signs like confusion, depression.

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Wednesday, September 21, 2016

Hemoglobin Electrophoretic pattern in Different Hemoglobinopathies

In this video I have explained hemoglobin electrophoresis normal electrophoretic bands along with different hemoglobinopathies like sickle cell trait, sickle cell anemia, hemoglobin C trait, hemoglobin C disease, hemoglobin SC disease, beta-thalassemia minor and beta-thalassemia major.
Thanks to Rachael Daniela for helping me in recording this video! 

Hemoglobin electrophoresis is a blood test that can detect different types of hemoglobin. It uses the principles of gel electrophoresis to separate out the various types of hemoglobin and is a type of native gel electrophoresis. The test can detect abnormal levels of HbS, the form associated with sickle-cell disease, as well as other abnormal hemoglobin-related blood disorders, such as alpha thalassaemia and hemoglobin C. It can also be used to determine whether there is a deficiency of any normal form of hemoglobin, as in the group of diseases known as thalassemias. Different hemoglobins have different charges, and according to those charges and the amount, hemoglobins move at different speeds in the gel whether in alkaline gel or acid gel. The hemoglobin electrophoresis is also known to be thalessemia screening, this also can be helpful for the patient who is frequently need of fresh blood transfusion. The patient needs blood transfusion because the body is unable to produce enough hemoglobin to satisfy the body's requirement. Electrophoresis is done by the use of cellulose acetate. After running electrophoresis at 150 to 200 volt, stain the cellulose acetate gel with Ponceau red.Thalassemia major Hb F level and Hb A2 levels increase.
Source for the above text is https://en.wikipedia.org/wiki/Hemoglobin_electrophoresis

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Tuesday, September 20, 2016

Enzymes in clinical diagnosis

Which Plasma enzyme determination help to diagnose perforation of intestine?

Friday, August 5, 2016

Donors of Each Atom Present in Purine and Pyrimydine Rings

In this video I have explained about the donors for each atoms present in purine and pyrimydine ring. Purine ring has 9 atoms and pyrimydine ring has 6 atoms. Metabolic intermediates like aspartate, glutamine, CO2, glycine, M10-formyl THF contribute to atoms present in both purine and pyrimydine rings.

Why Jaundice is seen in Classic galactosemia?

In this video the biochemical mechanism for the presence of jaundice in classic galactosemia is explained. Classic galactosemia is due to defect in galactose 1-phosphate uridyltransferase enzyme. this leads to elevation of galactose 1-phosphate thereby trapping the inorganic phosphate which can lead to fasting hyperglycemia, mental retardation. Elevated galactose 1-phosphate acts negatively on phosphoglucomutase enzyme and decrease the availability of glucose 1-phosphate leading to decreased UDP-glucose and consequently decreased UDP-glucoronate. Decreased availability of UDP-glucoronate lead to decreased activity of UGT1A1. Decreased activity of UGT1A1 lead to decreased conjugation of bilirubin and hence elevated levels of unconjugated bilirubin leading to jaundice. bilateral cataract seen in classic galactosemia is due to increased galactitol formation.