Regulation of Fatty Acid Oxidation

In this video I have explained the regulation of fatty acid oxidation in the mitochondria. The regulation is mainly going on over outer mitochondrial membrane. The main regulatory molecule is malonyl CoA controlling the activity of CPT I or CAT I.

Carnitine Shuttle Mechanism

In this video I have explained the carnitine shuttle mechanism for transport of long chain fatty acids into the mitochondrial matrix for beta oxidation. Carnitine is synthesized in the liver using essential amino acids lysine and methionine. Carnitine shuttles back and forth between matrix and inter membrane space to transport LCFA into the matrix.

Beta Oxidation of a Fatty Acid

In this video I have explained all the reactions involved in beta-oxidation of even number saturated fatty acid. Beta oxidation of a fatty acid will take place in the mitochondrial matrix. Fatty acid will be oxidized into acetyl CoA which will undergo TCA cycle and ketone body synthesis. Oxidation of fatty acid needs sufficient riboflavin and niacin to maintain the coenzyme needs. Defect in oxidation can lead to impaired ATP generation under fasting condition. 

Introduction to Lipoproteins

In this video I have explained the basic points about lipoproteins. In introduction to lipoproteins I have explained the general structure of lipoproteins, the arrangement of most of the components of lipoproteins including apolipoproteins. Also I have explained the arrangement of lipoproteins according to the density, size, electrophoretic mobility, all the major apolipoproteins and other important apolipoproteins over lipoproteins.

Surfactant and Infant Respiratory Distress Syndrome (IRDS)

In this video I have explained about surfactant, composition of surfactant, differentiation of pneumocytes into type I pneumocytes and type II pneumocytes. Type of phospholipid in surfactant the major being dipalmitoyl phosphotidyl choline which is also called as dipalmitoyl lecithin. Deficiency of surfactant is seen in pre-mature babies and it will lead to infant respiratory distress syndrome which is seen shortly after birth with apnea, tachycardia, respiratory grunting, flaring of nostril, cyanosis, chest wall retraction, atelectasis, ground glass appearance with air branchogram. 

Essential Fructosuria and Hereditary Fructose Intolerance

In this video I have explained about two disorders related with fructose metabolism that is essential fructosuria and hereditary fructose intolerance. Essential fructosuria is due to fructokinase deficiency and hereditary fructose intolerance is due to aldolase B deficiency. Patients with hereditary fructose intolerance will have nausea, vomiting, diarrhea, intolerance to fructose, jaundice, liver damage, kidney damage, convulsion, seizures, coma. Essential fructosuria is asymptomatic condition with only elevated levels of fructose in blood and urine. 

One Carbon Metabolism

In this video I have explained about one carbon metabolism reactions and the donors and formation of one carbon derivatives. Tetrahydrofolate (THF) plays a central role in one carbon metabolism. Vitamin B12, B6 and B2 that is cobalamin, pyridoxine and riboflavin, respectively, helps in the formation of one carbon derivatives from THF. One carbon metabolism participates in synthesis of thymidylate monophosphate, C2 and C8 of purine ring, synthesis of glycine from serine and conversion of homocystienine into methionine. 

Why Electrons flow from NADH to O2 in Electron Transport Chain

In this video I have explained the fundamental basis of electron transport chain that is the redox potential of NADH which is a electron donor and O2 which is a final electron acceptor. Electron transport chain which also referred as oxidative phosphorylation or respiratory chain runs with the redox potential difference of 1140 mv between NADH and O2. This drives flow of electrons from NADH to O2 via complex I, CoQ, III, cytochrome C and complex IV. The energy in the flow of electrons helps in pumping of protons across the membrane. 

Pyruvate Dehydrogenase Complex - Regulation

In this video I have explained all the points related to regulation of pyruvate dehydrogenase enzyme complex. Pyruvate dehydrogenase enzyme complex is also written as PDH complex or simple PDC. It has feedback regulation, allosteric modulation, covalent modification mediated by insulin and glucagon. In fasting condition its activity will decrease and in fed condition its activity will increase. NADH, acetyl CoA have a negative effect on PDH, ADP and pyruvate and Ca2+ will have a positive effect on PDH complex.

TCA Cycle - Regulation

In this video I have explained all the points related to regulation of TCA cycle. The main enzyme in regulation of TCA cycle or citric acid or Krebs cycle is isocitrate dehydrogenase. Other enzymes that are regulated are alpha-ketoglutarate dehydrogenase, malate dehydrogenase and citrate synthase. Main molecules regulating are ADP, Ca2+ and NADH+H. 

TCA cycle - Important Reactions and Applied Aspects

In this video I have explained all the high yield points about TCA cycle reactions. Macromolecules like carbohydrates, lipids and proteins ultimately converted to final common metabolic intermediate acetyl CoA. Acetyl CoA gets into citric acid cycle (TCA cycle or Krebs cycle) to release CO2 and the reducing equivalents NADH and FADH2 and GTP. 

Why Lactose is an End Product of Anaerobic Glycolysis?

In this video I have explained the reason for why lactate is the end product of glycolysis under anaerobic situation or in cell which do not have mitochondria like red blood cells (RBCs). I have also briefly explained glycolysis that is oxidation of glucose to pyruvate and the energy yield from oxidation of glucose to pyruvate. 

Vitamin K - High Yield Review

In this video I have explained all the high yield points about vitamin K. I have explained the sources of vitamin K1 phylloquinone, vitamin K2 menaquinone, vitamin K3 menadione. The major sources are green leafy vegetables like spinach, significant source of vitamin K is bacterial flora. Main function of vitamin K is post translational carboxylation of glutamate to make gla. Clotting factors activation, activation of protein C and protein S, matrix gla proteins, osteocalcin in osteobalsts. Vitamin K helps in clotting process, bone health, preventing atherosclerosis and thrombosis. Vitamin K deficiency can lead to hemorrhagic disease of newborn or excess bleeding adults. 

How to Differentiate Cobalamin Deficiency from Folate Deficiency

In this video I'm explaining one of the most important and high yiled concept that is to differentiate between folate and cobalamin deficiency. Both the deficiencies leads to megaloblastic anemia and macrocytic RBCs but the clinical sigens and laboratory test can differentiate both the deficiencies. While explaining that I have also briefly explained the causes for deficiency of folate and cobalamin like overcooking of greens, pernicious anemia, folate trap.

Role of Vitamins in Bone Health

In this video I have briefly explained the role of vitamins in bone health. Specially role of vitamin K I have explained little more than the role of vitamin D and vitamin C. Vitamin K is needed for the gamma-carboxylation of osteocalcin to increase bone density. Bone density is proportional to the levels of carboxylated osteocalcin in the blood. 

Vitamin D - Activation, Function, Regulation

In this video I have explained the activation of vitamin D in the liver and kidney by hydroxylation process. Regulation of active vitamin D3 by PTH (parathyroid hormone), 24-hydroxylase and active vitamin D itself. Main function of vitamin D is to regulate calcium and phosphate levels in the blood. Other functions of vitamin D have been revealed by recent research like its role in preventing tumor formation, immune mechanism, insulin sensitivity.
Sunlight exposure is the source of vitamin D from our skin.

Absorption of Monosaccharides

In this video I have explained the process of absorption of monosaccharides in the duodenum and jejunum. Two transporters absorb monosaccharides like glucose, galactose and fructose, they are SGLT-1 and GLUT 5. SGLT-1 works in a sodium dependent manner and GLUT 5 works in sodium independent manner. GLUT 2 on the basal side transport these monosaccharides out into portal vessel. Na-K ATPase on the basolateral side helps SGLT-1 to function optimally. Lactose intolerance can occur due to lactase deficiency leading to osmotic diarrhea, abdominal cramps and flatulence. Carbohydrate indigestion, and carbohydrate dumping could lead to osmotic diarrhea. 

Digestion of Carbohydrates

In this video I have explained all high yield points about the digestion of carbohydrates. The major carbohydrates in the diet are starch, lactose and sucrose. Salivary alpha-amylase digest starch in the mouth into alpha-dextrin. Alpha dextrin further digested into oligosaccharides, maltose and isomaltose by pancreatic alpha-amylase. Specific disaccharidases like maltase, isomlatase, lactase and sucrose will take care of maltose, isomaltose, lactose and sucrose, respectively. The oligosaccharides are digested by alpha-glucosidase into individual glucose molecules one at a time.

Tocopherol (vitamin E) - All high yield points

In this video I have done a high yeild review on tocopherol the vitamin E. Vitamin E is a collective term for tocopherols and tocotrienols. Alpha tocopherol is biologically most active form of tocopherol and is a powerful reactive oxygen species scavenger, that is tocopherol has antioxidant property. tocopherol prevents lipid peroxidation. it prevents LDL oxidation and thereby atherosclerosis. Deficiency of tocopherol is seen in lipid malabsorption disorders like cystic fibrosis. Tocopherol deficiency leads to spinocerebellar ataxia, hemolytic anemia, skelatal myopathy, retinopathy, polyneuropathy.

Thiamine (vitamin B1) - All high yield points for exam

In this video I have done a high yield review about all the important points related to thiamine that is vitamin B1. Different types of beri beri the deficiency disease of thiamine were explained. the causes for thiamine deficiency is explained.

Pyridoxine (vitamin B6) - High yield review

In this video I have done a high yield review on pyridoxine vitamin B6 - it includes its forms, active form, biological functions, causes for deficiency, deficiency ,anifestation and the diseases where supplementing pyridoxine is beneficial. 

Niacin (vitamin B3) - All high yield points

In this video I have explained all high yield points about niacin vitamin B3. Niacin deficiency causes pellagra with 3 D's diarrhea, dermatitis and dementia. 

Riboflavin (vitamin B2) - High yield review

In this video I have explained all high yield points about riboflavin vitamin B2.
Riboflavin (vitamin B2) is part of the vitamin B group. It is the central component of the cofactors FAD and FMN and as such required for a variety of flavoprotein enzyme reactions including activation of other vitamins.

How to calculate Km and Vmax using Lineweaver Burk plot

In this video I have explained how to calculate Km and Vmax of an enzyme in Lineweaver Burk double reciprocal plot.

The Lineweaver–Burk plot was widely used to determine important terms in enzyme kinetics, such as Km and Vmax, before the wide availability of powerful computers and non-linear regression software. The y-intercept of such a graph is equivalent to the inverse of Vmax; the x-intercept of the graph represents −1/Km. It also gives a quick, visual impression of the different forms of enzyme inhibition.

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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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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Enzymes in clinical diagnosis

Which Plasma enzyme determination help to diagnose perforation of intestine?

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. 

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. 

Why Jaundice is seen in Classic galactosemia?

Primary Hyperoxaluria - Detailed Review

Cobalamin - Question and Brief Review

Homocysteinuria - A review of methionine metabolism, details on homocysteinurias

Melatonin synthesis - A Quick Review

Melatonin is synthesized in pineal gland and is responsible for maintaining the circadian rhythm. Tryptophan is converted to melatonin in the pineal gland. This process involves methylation and acetylation. 

Melatonin synthesis - A Quick Review

Atherosclerosis - Risk Factors - A Question and brief Explanation

Fatty Acid Synthesis - A Question and Brief Review

Blood Glucose Regulation under Fasting Condition - A Question and Brief Review

Pompe's Disease - A Question and Brief Review

Galactose metabolism and Galactosemia - A Brief Review

Importance of Glucokinase and Hexokinase

Alkaptonuria - A Question and Brief Review

ATP and NADH Calculation in Fatty Acid Synthesis and Beta-Oxidation

Phytanic Acid Oxidation - A Question and Brief Review

Fabry Disease - A Question and Brief Review

Gaucher's Disease - A Question and Brie Review

Gluconeogenesis Process - A Question and Brief Explanation

Gluconeogenesis - Question and Answer

In this video I have explained answer to one of my question on gluconeogenesis. I have also explained in brief about conversion of propionyl CoA to glucose while explaining the answer for this question.

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Gluconeogenesis - precursors and regulation

In this video I have explained how non-carbohydrate sources like lactate, alanine, propionyl CoA and glycerol are converted to glucose in gluconeogenesis process. All the important gluconeogenesis enzymes are explained with their function. Important enzymes fr each of the gluconeogenic precursors conversion into glucose is explained.

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Energy Sources During Fasting and Starvation

Biochemical Changes in Chronic Alcoholism

Answer to a Question on Uncoupler of Electron Transport Chain

In this video I have explained a question on uncouplers of electron transport chain. Chemical uncouplers are 2,4-Dinitrophenol, dinitrocresol, pentachlorophenaol. Physiological uncouplers are thermogenin, uncoupling proteins UCP1, UCP2, UCP3, UCP4, UCP5. All are present in various tissues like brown adipose tissue, skeletal muscle, brain, neurons, other tissues. Uncouplers increase BMR, body temperature, metabolic rate, increased rate of electron transport, increased O2 consumption, increased respiratory rate.

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Key words:
electron transport chain
uncouplers
2,4-dinitrophenol
thermogenin
T3 and T4
pentachlorophenol
temperature
basal metabolic rate
ATP synthesis
ATP synthase
redox potential
NADH
FADH2
complex I
complex II
cytochrome oxidase
ubiquionone
brown adipose tissue
BAT
UCP
O consumption
NAD
FAD
USMLE
step-1
Kaplan
biochemistry
Review video
Mungli

• Category

• 
  

Pyruvate Dehydrogenase Complex and Other Similar Enzyme Complexes.

In this video I have explained pyruvate dehydrogenase enzyme complex along with other two enzyme complexes that is alpha-ketoglutarate dehydrogenase complex and branched chain alpha-ketoacid dehydrogenase complex. I have specially emphasized on the E1, E2, and E3 subunits.

Thanks to my student Natalia Adorno Carvajal for meticulously recording this video.

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Key words:
pyruvate dehydrogenase complex
alpha-ketoglutarate dehydrogenase complex
branched chain alpha-ketoacid dehydrogenase complex
lipoate
pantothenate
thiamine pyrophosphate
NAD
FAD
Pyruvate
alpha-ketoglutarate
alpha ketoacid
USMLE
step-1
Kaplan
biochemistry
Review video
Mungli

Answer to a Question on Pentose Phosphate Pathway

In this video I have briefly explained a diseases related to pentose phosphate pathway (which is also referred as hexose monophosphate shunt). This disease in question is glucose 6-phosphate dehydrogenase deficiency (G6PD deficiency) which causes hemolytic anemia due to deficiency of NADPH. NADPH deficiency leads to decreased GSH (reduced glutathione) which leads to increased presence of reactive oxygen species (ROS). 

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Key words:
Glucose 6-phosphate
G6PD deficiency
species
ribose 5 phosphate
NADPH
GSH
glutathione
GSSG
ROS
Heinz bodies
hemolytic anemia
Beutler florescence
bite cells
quick review
Mungli
UMHS
antimalarial
sulfonamides
napthalene
hemolytic crisis
fava beans
favism
USMLE
step-1
Kaplan
biochemistry
Review video
Mungli

Pentose Phosphate Pathway - A Quick Review

In this video Im brief in explaining pentose phosphate pathway which is also referred as hexose monophosphate shunt. both oxidative and non oxidative phases are explained in brief. importance of both the phases are explained. Different cell scenarios are considered to explain the pathway.

Many thanks to my student Luis Andres Acosta for recording this video for me.

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Key words:
Glucose 6-phosphate
G6PD deficiency
species
ribose 5 phosphate
NADPH
GSH
glutathione
USMLE
step-1
Kaplan
biochemistry
Review video
Mungli
pentose
phosphate pathway
ribose 5 phosphate
nucleotide
detoxification
oxidative phase
transketolase
transaldolase
purine
pyrimidine
PRPP

Lipoprotein Abnormality - Dyslipidemia - A Quick Review

In this video I have briefly explained all lipoprotein abnormalities according to Freiderickson's classification of lipoprotein abnromality or dyslipidemia. Different types of lipoprotein abnormalitis (dyslipedemias) are explained using the case stem based question, the format of it is like USMLE step-1 style.
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Key words:
Lipase
lipoprotein
hepatic lipase
LDL
VLDL
IDL
Chylomicron
lipoprotein
chylomicronemia
hypertriglycerademia
hypercholesterolemia
LDL receptor
atherosclerosis
familial
lipoprotein
deficiency
combined
hyperlipidemia
dysbetalipoproteinemia
LCAT
CETP
HDL
Apo B
Apo A1
Apo CII
endothelium
usmle
step-1
Dr Mungli
Lipoprotein
metabolism

Answer and discuss the Question below.

Why do you see Dyslipidemia in Thyroid Disorders - A Quick Review

Do you know why dyslipidemia is seen in thyroid disorders? Please watch the video to know why!

Explanation to USMLE style Biochemistry Question on Hypothyroidism

Please watch the video to know the question details and also each choice is right or wrong!

Note: in the initial part of the video I said the diagnosis is hypoparathydoidism by mistake, read it as HYPOTHYROIDISM.

Review on Cobalamin for USMLE Step-1

In this video I have reviewed all high yield points about cobalamin: source, functions, causes for deficiency, deficiency manifestation of cobalamin.

Explanation for a Kaplan Question on Enzyme Kinetics

In the following video I have explained in detail about the correct answer to a Kaplan question on enzyme kinetics and also I have explained why other choices are wrong. I have touched up on the concepts like Km, Vmax, affinity-Km relation, non-competitive inhibition and effect of enzyme concentration on the reaction.

Kaplan Question for you on Enzymes!

Why do you think the choice you have chosen is correct? 

Discuss in the comments section below!

Omega 6 and Omega 3 PUFAs in relation to inflammation

I would like to bring to your attention about Comparison between omega 6 and omega 3 PUFAs with respect to inflammation. 

We are debating here on good vs good, both omega 6 and omega 3 are good for our body in their own way. As we all know inflammation is a good thing but not always, controlled inflammation is a good thing, when inflammation goes uncontrolled that leads to acute and chronic inflammatory diseases. All this mediated by inflammatory mediators which are largely from our two class of PUFAs. Omega 6 and omega-3. 

As you might be knowing we need to get these omega FAs from plant source as linoleic acid (omega 6) and linoleic acid (omega3), in our body linoleic acid is converted arachidonic acid (omeg6) whereas linoleic acid into DHA and EPA (omega3) which are incorporated into membrane. 

In response to injury there will be activation of phospholipase A2 which breaks and release these membrane lipids and further they go on to make inflammatory mediators. 

Arachidonic acid (omega6) largely form pro-inflammatory mediators and increases inflammation including platelet aggregation, it also makes pro-resolving mediators like lipoxins. 

Whereas DHA and EPA will form predominantly anti-inflammatory, pro-resolving and cytoprotectants like E series resolvins, D-series resolvins, protectins, neuroprotectins, meresins which all participate in resolving the inflammation and protecting the cell. 

So by adequately consuming omega3 PUFAs we are trying to keep things in balance and protect from uncontrolled inflammation which could lead to variety of disease conditions include thromboembolism. 

Hence it is all about keeping homeostasis by consuming omega6, omega3, MUFA and saturated fatty acids all in balance because we need all of them but in balance. 

Hope this explanation helps some of you to understand this very important concept.

Bohr Shift and Haldane Effect

In this video I have explained about the Bohr Shift and Haldane effect on the interaction of hemoglobin with O2 and H+ with the help of a question. Watch the video to know the answer to the question and also to learn abut Bohr shift and Haldane effect.

Biochemistry USMLE Style Question

Explain your answer why do you think you the choice you have chosen is correct.

A Quick Review on Oxygen Dissociation Curve for USMLE Step-1

In this video I have explained the oxygen dissociation curve for hemoglobin and myoglobin. While explaining that I have touched upon the mechanism of oxygen dissociation, function of these two molecules and their affinities for oxygen.

A Quick Review on Amino Acids (structure and all types of classifications for USMLE Step-1

In this video I have explained the basic structure of amino acids, pH and Pka relation, various types of classification of amino acids. 

Explanation for a question on Prion disease

In this video I'm explaining the answer to one of my question on Prion disease. You can pause the video to answer yourself to this question. You can continue to play the video to know in brief about Prion disease and the explanation for the question.

Explanation for a Question on Beta Bends of a Protein Molecule

In the following video I have briefly explained on protein folding process and the structural organization of a protein molecules. I have given explanation to one of my question on beta bends of a protein molecule. 

Metabolism of HDL

Metabolism of VLDL