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And so these phosphatases can influence and shut down this protein, these proteins, these proteins and also these two structures here which are actually part of that EGF receptor. And finally we can terminate the pathway by inactivating that receptor of the pathway. And actually we already spoke about one way by which we can inactivate is by removing these phosphoryl groups. Another way is if these two ligands actually dissociate. When the two ligands dissociate, the entire diameter basically breaks apart into monomers and in that particular case it is not as active as in this particular case. And so what that means is that will decrease the activity of this signal transduction pathway. | Cancer and Termination of Signal Pathways .txt |
Another way is if these two ligands actually dissociate. When the two ligands dissociate, the entire diameter basically breaks apart into monomers and in that particular case it is not as active as in this particular case. And so what that means is that will decrease the activity of this signal transduction pathway. So this is the normal way by which the pathway actually is terminated. But what happens in the abnormal case? How can an abnormality in each one of these cases, one, two, three, actually lead to the production of tumors and eventually cancer? | Cancer and Termination of Signal Pathways .txt |
So this is the normal way by which the pathway actually is terminated. But what happens in the abnormal case? How can an abnormality in each one of these cases, one, two, three, actually lead to the production of tumors and eventually cancer? So let's focus on number one. So we said our cells can terminate by using these Gtpas activity G proteins. So this Rasp protein has a certain gene in the DNA that expresses it. | Cancer and Termination of Signal Pathways .txt |
So let's focus on number one. So we said our cells can terminate by using these Gtpas activity G proteins. So this Rasp protein has a certain gene in the DNA that expresses it. Now let's suppose the gene is a normal gene and that means this will be a normal protein. But what happens if that gene that encodes for this structure is actually mutated in some way? And let's suppose we mutate that gene in such a way so that this molecule loses its ability to basically hydrolyze the GTP back into GDP. | Cancer and Termination of Signal Pathways .txt |
Now let's suppose the gene is a normal gene and that means this will be a normal protein. But what happens if that gene that encodes for this structure is actually mutated in some way? And let's suppose we mutate that gene in such a way so that this molecule loses its ability to basically hydrolyze the GTP back into GDP. And so if there's a mutation that takes place in the Ras gene, and the mutation basically destroys the Gtpa's activity of this g protein, then once the protein is activated, it will remain in the on position. It will remain active. And that means it will continually stimulate these processes. | Cancer and Termination of Signal Pathways .txt |
And so if there's a mutation that takes place in the Ras gene, and the mutation basically destroys the Gtpa's activity of this g protein, then once the protein is activated, it will remain in the on position. It will remain active. And that means it will continually stimulate these processes. And the signal transduction pathway will continue the process of cell growth, cell division and cell proliferation. So we see that one way by which a signal transduction pathway may malfunction is if a gene encoding for a protein that is part of that pathway is actually mutated. For instance, the rat gene that codes for the Ras protein in the EGF pathway is the most commonly mutated gene that leads to tumor growth of epithelial and epidermal cells. | Cancer and Termination of Signal Pathways .txt |
And the signal transduction pathway will continue the process of cell growth, cell division and cell proliferation. So we see that one way by which a signal transduction pathway may malfunction is if a gene encoding for a protein that is part of that pathway is actually mutated. For instance, the rat gene that codes for the Ras protein in the EGF pathway is the most commonly mutated gene that leads to tumor growth of epithelial and epidermal cells. So a mutation in the gene might produce a Raspotee that is incapable of Atpa's activity, which basically means it cannot turn itself off after actually being activated. So this is essentially the off position and this is the on position. And so if we have a mutation that destroys the Atpa's activity of this structure, it will always remain on and always go on to activate Rap proteins which will contain these processes that essentially lead to self growth and division. | Cancer and Termination of Signal Pathways .txt |
So a mutation in the gene might produce a Raspotee that is incapable of Atpa's activity, which basically means it cannot turn itself off after actually being activated. So this is essentially the off position and this is the on position. And so if we have a mutation that destroys the Atpa's activity of this structure, it will always remain on and always go on to activate Rap proteins which will contain these processes that essentially lead to self growth and division. Now we see that these types of mutated genes that lead to the production of these cells that have cancer characteristics are known as oncology. So this is what an oncogene actually is. Now let's move on to two. | Cancer and Termination of Signal Pathways .txt |
Now we see that these types of mutated genes that lead to the production of these cells that have cancer characteristics are known as oncology. So this is what an oncogene actually is. Now let's move on to two. So if there is an abnormality in this process, how can that lead to cancer? So we said that phosphatases are these proteins which are used to reverse the effects of protein kinases and that essentially shuts down this process. Now, just like any other protein in our chromosomes, in our DNA, we have genes that code for phosphatases. | Cancer and Termination of Signal Pathways .txt |
So if there is an abnormality in this process, how can that lead to cancer? So we said that phosphatases are these proteins which are used to reverse the effects of protein kinases and that essentially shuts down this process. Now, just like any other protein in our chromosomes, in our DNA, we have genes that code for phosphatases. So for any given phosphatase, we have one gene that comes from the father and the other gene that comes from the mother. So let's suppose we have this homologous pair of chromosomes and this is the gene that let's say comes from the mother. And this is the gene showed in blue that comes from the father. | Cancer and Termination of Signal Pathways .txt |
So for any given phosphatase, we have one gene that comes from the father and the other gene that comes from the mother. So let's suppose we have this homologous pair of chromosomes and this is the gene that let's say comes from the mother. And this is the gene showed in blue that comes from the father. So we have the pair of alleles that code for that same type of. So this should be phosphatase, not phosphatase. Okay? | Cancer and Termination of Signal Pathways .txt |
So we have the pair of alleles that code for that same type of. So this should be phosphatase, not phosphatase. Okay? So let's change that real quick. We have phosphatase. So we have these genes that code for phosphatase. | Cancer and Termination of Signal Pathways .txt |
So let's change that real quick. We have phosphatase. So we have these genes that code for phosphatase. Now, if these two genes are normal, then there really will be no problem. In fact, if one of them is abnormal, the other one is normal. Usually the cell will be functional and will be able to actually shut down and terminate the process by using phosphatases. | Cancer and Termination of Signal Pathways .txt |
Now, if these two genes are normal, then there really will be no problem. In fact, if one of them is abnormal, the other one is normal. Usually the cell will be functional and will be able to actually shut down and terminate the process by using phosphatases. And by the way, because the phosphatases turn off the activity of these pathways and that essentially decreases the likelihood that tumor growth will actually take place, these genes that code for phosphatases are also known as tumor suppressing genes. And the phosphatase themselves are known as tumor suppressing molecules because it's a result of these molecules that tumors do not actually develop. So phosphatases are called tumor suppressing molecules because they inactivate proteins and enzymes that drive that signal transduction pathway. | Cancer and Termination of Signal Pathways .txt |
And by the way, because the phosphatases turn off the activity of these pathways and that essentially decreases the likelihood that tumor growth will actually take place, these genes that code for phosphatases are also known as tumor suppressing genes. And the phosphatase themselves are known as tumor suppressing molecules because it's a result of these molecules that tumors do not actually develop. So phosphatases are called tumor suppressing molecules because they inactivate proteins and enzymes that drive that signal transduction pathway. And for this reason, we call the genes that code for phosphatases tumor suppressing genes. Now, what happens if both of these genes are for some reason inactivate or for some reason mutated or blocked? So it could be some type of chromosomal abnormality, so a deletion, an insertion, a movement to some other chromosome, and so forth. | Cancer and Termination of Signal Pathways .txt |
And for this reason, we call the genes that code for phosphatases tumor suppressing genes. Now, what happens if both of these genes are for some reason inactivate or for some reason mutated or blocked? So it could be some type of chromosomal abnormality, so a deletion, an insertion, a movement to some other chromosome, and so forth. So when both of these genes in the allele pair and coding for a specific type of phosphatase that inactivates some specific type of molecule in this process are actually knocked out or destroyed, that may lead to tumor formation because the cell will not be able to correctly terminate that process by using these phosphatases. So we know how abnormality can lead to cancer here as well as here. What about this final case? | Cancer and Termination of Signal Pathways .txt |
So when both of these genes in the allele pair and coding for a specific type of phosphatase that inactivates some specific type of molecule in this process are actually knocked out or destroyed, that may lead to tumor formation because the cell will not be able to correctly terminate that process by using these phosphatases. So we know how abnormality can lead to cancer here as well as here. What about this final case? So we said that we could actually terminate the pathway by inactivating that receptor protein. In this case, it's the EGF receptor. Now, in some cases we see that over expression of these tyrosine kinase domains. | Cancer and Termination of Signal Pathways .txt |
So we said that we could actually terminate the pathway by inactivating that receptor protein. In this case, it's the EGF receptor. Now, in some cases we see that over expression of these tyrosine kinase domains. So the tyrosine kinase receptors like the EGF receptor here, if the cell actually builds too many of these proteins and inserts too many of these proteins into the membrane of that cell, what that will do is increase the likelihood that the cell will activate the pathway at an inappropriate time. And so this access number, the excess amount of these receptors, the access amount of these receptors in a cell membrane can basically lead to the production of these cancer cells. So, overexpression of tyrosine kinase receptors can also lead to cancer of the epithelial cells. | Cancer and Termination of Signal Pathways .txt |
So the tyrosine kinase receptors like the EGF receptor here, if the cell actually builds too many of these proteins and inserts too many of these proteins into the membrane of that cell, what that will do is increase the likelihood that the cell will activate the pathway at an inappropriate time. And so this access number, the excess amount of these receptors, the access amount of these receptors in a cell membrane can basically lead to the production of these cancer cells. So, overexpression of tyrosine kinase receptors can also lead to cancer of the epithelial cells. For instance, we have cancers like breast cancers, ovarian cancers, colorectal cancers and so forth. So any place we have these epithelial cells, this can actually cause this type of cancer. So, if a cell expresses too many receptors, that access receptors may stimulate growth at inappropriate times. | Cancer and Termination of Signal Pathways .txt |
For instance, we have cancers like breast cancers, ovarian cancers, colorectal cancers and so forth. So any place we have these epithelial cells, this can actually cause this type of cancer. So, if a cell expresses too many receptors, that access receptors may stimulate growth at inappropriate times. And actually by studying this specific type of mechanism, we were able to create different types of drugs which act as anticancer, anti tumor agents. And these drugs are essentially antibodies. So we were able to develop these antibodies in a laboratory that actually bind onto these EGF receptors. | Cancer and Termination of Signal Pathways .txt |
And actually by studying this specific type of mechanism, we were able to create different types of drugs which act as anticancer, anti tumor agents. And these drugs are essentially antibodies. So we were able to develop these antibodies in a laboratory that actually bind onto these EGF receptors. And once the antibody binds onto these pockets of the EGF receptor, that can basically inactivate these receptors. And by inactivating these receptors, that decreases the likelihood that this will lead to producing a cancer cell. And so one important drug that is basically used to treat individuals who have breast cancer is known as herceptin. | Cancer and Termination of Signal Pathways .txt |
And it uses those electrical signals to create the muscular contraction that is needed to move all that blood through the blood vessels of our body. In fact, physicians can actually study and analyze the way that the heart of the patient produces electrical signals. And they can determine different types of abnormalities that might exist within the heart simply by using this tool. So this tool is known as an electrocardiogram. An electrocardiogram is a graph that describes the electrical signal that is generated by the heart. Now, how do we actually obtain the electrocardiogram? | Introduction to Electrocardiogram .txt |
So this tool is known as an electrocardiogram. An electrocardiogram is a graph that describes the electrical signal that is generated by the heart. Now, how do we actually obtain the electrocardiogram? Well, we basically take special electrodes and we connect the electrodes onto the surface of the skin as special locations on the body. So six electrodes are usually placed around the heart. Two electrodes are placed on the arms and two electrodes are placed on the legs. | Introduction to Electrocardiogram .txt |
Well, we basically take special electrodes and we connect the electrodes onto the surface of the skin as special locations on the body. So six electrodes are usually placed around the heart. Two electrodes are placed on the arms and two electrodes are placed on the legs. And that creates a closed electric circuit. And if we connect the wires to a special device, that device can read the electrical signal that is generated by our heart. So we basically create an electrocardiogram that is nothing more than an XY graph, where the X axis is the time and the Y axis is the voltage. | Introduction to Electrocardiogram .txt |
And that creates a closed electric circuit. And if we connect the wires to a special device, that device can read the electrical signal that is generated by our heart. So we basically create an electrocardiogram that is nothing more than an XY graph, where the X axis is the time and the Y axis is the voltage. So we see that the electrocardiogram is the fluctuations, the change in voltage that is produced by the heart. And this voltage is used to basically generate that muscular contraction that propels all that blood through the blood vessels of our body. Now, in this lecture, we're going to study the normal electrocardiogram. | Introduction to Electrocardiogram .txt |
So we see that the electrocardiogram is the fluctuations, the change in voltage that is produced by the heart. And this voltage is used to basically generate that muscular contraction that propels all that blood through the blood vessels of our body. Now, in this lecture, we're going to study the normal electrocardiogram. We're not going to discuss any abnormalities that might exist within the heart and that might be described by an abnormal electrocardiogram. So we're simply going to focus on the brief details of a normal electrocardiogram. So let's take a look. | Introduction to Electrocardiogram .txt |
We're not going to discuss any abnormalities that might exist within the heart and that might be described by an abnormal electrocardiogram. So we're simply going to focus on the brief details of a normal electrocardiogram. So let's take a look. By taking a cross section of our heart, we basically expose the four different chambers. So if we're examining the heart from this angle, we have the right side and the left side. So this is the right side of the heart, the left side of the heart, the right atrium, right ventricle, the left atrium and our left ventricle. | Introduction to Electrocardiogram .txt |
By taking a cross section of our heart, we basically expose the four different chambers. So if we're examining the heart from this angle, we have the right side and the left side. So this is the right side of the heart, the left side of the heart, the right atrium, right ventricle, the left atrium and our left ventricle. So let's begin by looking at the different sections of the lecture cardiogram. So we have a wave known as the P wave. We have an upside down Q wave, an upside down S wave. | Introduction to Electrocardiogram .txt |
So let's begin by looking at the different sections of the lecture cardiogram. So we have a wave known as the P wave. We have an upside down Q wave, an upside down S wave. We have this r wave. We also have a T and a U wave. Now, we also have points on the actual curve. | Introduction to Electrocardiogram .txt |
We have this r wave. We also have a T and a U wave. Now, we also have points on the actual curve. So we have the points shown in blue. We have point P and point R, and we have point S and point T. So let's discuss what each one of these segments and waves actually represents. Let's begin with wave P or the P wave. | Introduction to Electrocardiogram .txt |
So we have the points shown in blue. We have point P and point R, and we have point S and point T. So let's discuss what each one of these segments and waves actually represents. Let's begin with wave P or the P wave. So let's recall where the heart actually begins, where it generates that electrical signal. So within the right atrium, within the upper wall of the right atrium, we have a collection of specialized cells that collectively are called the sinoatrial node, or simply the SA node. So this is where the SA node is located. | Introduction to Electrocardiogram .txt |
So let's recall where the heart actually begins, where it generates that electrical signal. So within the right atrium, within the upper wall of the right atrium, we have a collection of specialized cells that collectively are called the sinoatrial node, or simply the SA node. So this is where the SA node is located. And the essay note contains cells where the membrane of those cells depolarize. And that creates an electrical potential difference. And that's exactly why we have an increase in the voltage taking place within this portion. | Introduction to Electrocardiogram .txt |
And the essay note contains cells where the membrane of those cells depolarize. And that creates an electrical potential difference. And that's exactly why we have an increase in the voltage taking place within this portion. So when the SA node generates that electrical signal, the action potential, it increases the voltage, it makes it more positive. And our electrical signal then propagates through these conduction channels shown in purple. And these conduction channels extend through the right atrium and through the left atrium. | Introduction to Electrocardiogram .txt |
So when the SA node generates that electrical signal, the action potential, it increases the voltage, it makes it more positive. And our electrical signal then propagates through these conduction channels shown in purple. And these conduction channels extend through the right atrium and through the left atrium. Now, when the voltage reaches its maximum, so at the peak of this wave, at the peak of the P wave, that is when these two atriums begin to contract simultaneously. So this ventricle, this atrium and this atrium begin to contract. And as they begin to contract, they cause these two valves, the tricuspid and the Bicuspid valve, to basically open. | Introduction to Electrocardiogram .txt |
Now, when the voltage reaches its maximum, so at the peak of this wave, at the peak of the P wave, that is when these two atriums begin to contract simultaneously. So this ventricle, this atrium and this atrium begin to contract. And as they begin to contract, they cause these two valves, the tricuspid and the Bicuspid valve, to basically open. And as they open, the blood begins to rush into the right ventricle and into our left ventricle. Now, at the same time that our two atrium begins to contract, that signal eventually reaches another specialized section known as the AV node, or the atrial ventricular node. And this note is located in the interatrial septum of the heart in the wall separating our two atrium. | Introduction to Electrocardiogram .txt |
And as they open, the blood begins to rush into the right ventricle and into our left ventricle. Now, at the same time that our two atrium begins to contract, that signal eventually reaches another specialized section known as the AV node, or the atrial ventricular node. And this note is located in the interatrial septum of the heart in the wall separating our two atrium. Now, when the signal arrives at the AV node, the AV node, what it does is it delays that signal by about zero of a second. And what that does is it gives the atria enough time to fully contract and move all that blood into the fully relaxed ventricles. So we see along our P waves, our atria begins to contract at the tip while the ventricles are actually fully relaxed. | Introduction to Electrocardiogram .txt |
Now, when the signal arrives at the AV node, the AV node, what it does is it delays that signal by about zero of a second. And what that does is it gives the atria enough time to fully contract and move all that blood into the fully relaxed ventricles. So we see along our P waves, our atria begins to contract at the tip while the ventricles are actually fully relaxed. Now let's move on to our PR segment. This PR segment basically has no voltage difference. We have a zero voltage difference. | Introduction to Electrocardiogram .txt |
Now let's move on to our PR segment. This PR segment basically has no voltage difference. We have a zero voltage difference. And that's why we have a slope that has a zero line that has a zero slope. And that's because within this section, what happens is our AV note essentially sends that electrical signal through the bundle of his and through our perkinji fibers. And within this segment, no contraction actually takes place. | Introduction to Electrocardiogram .txt |
And that's why we have a slope that has a zero line that has a zero slope. And that's because within this section, what happens is our AV note essentially sends that electrical signal through the bundle of his and through our perkinji fibers. And within this segment, no contraction actually takes place. So once the AV node delays the signal, it depolarizes and sends the electrical signal through the bundle of his and our PerkinsI fibers that essentially permeate through the walls of our two ventricles, as shown by these purple fibers within this diagram, this does not actually cause any contraction. Now let's move on to this segment, the QRS segment, which is commonly known as the QRS complex. And this complex actually consists of three individual waves. | Introduction to Electrocardiogram .txt |
So once the AV node delays the signal, it depolarizes and sends the electrical signal through the bundle of his and our PerkinsI fibers that essentially permeate through the walls of our two ventricles, as shown by these purple fibers within this diagram, this does not actually cause any contraction. Now let's move on to this segment, the QRS segment, which is commonly known as the QRS complex. And this complex actually consists of three individual waves. We have the Q wave, the R wave, and the S wave. Now, the Q wave and the Swave are known as the downward deflection waves because they actually decrease our voltage. They make it more negative. | Introduction to Electrocardiogram .txt |
We have the Q wave, the R wave, and the S wave. Now, the Q wave and the Swave are known as the downward deflection waves because they actually decrease our voltage. They make it more negative. But the R is known as our right side up, or the upward deflection wave because it increases the voltage, it makes it more positive now, what exactly takes place within the QRS? So here we have the electrical signal that permeated through the entire walls of our right and left ventricle. And now what begins to happen as soon as we reach the maximum point of the R way, this voltage here contraction of these ventricles begins to take place. | Introduction to Electrocardiogram .txt |
But the R is known as our right side up, or the upward deflection wave because it increases the voltage, it makes it more positive now, what exactly takes place within the QRS? So here we have the electrical signal that permeated through the entire walls of our right and left ventricle. And now what begins to happen as soon as we reach the maximum point of the R way, this voltage here contraction of these ventricles begins to take place. And as the ventricles begin to contract, there is an increase in hydrostatic pressure. And that forces these two valve, the tricuspid and the biconspid valve, to close. And when they shut close, that's exactly what causes that first sound that we hear when we listen to our heart via a stethoscope. | Introduction to Electrocardiogram .txt |
And as the ventricles begin to contract, there is an increase in hydrostatic pressure. And that forces these two valve, the tricuspid and the biconspid valve, to close. And when they shut close, that's exactly what causes that first sound that we hear when we listen to our heart via a stethoscope. So if we listen to our heart, we hear the love dub love dub sound. And the love is caused by the closure of these two valves during the QRS complex. Now, this is when the ventricles actually begin to contract. | Introduction to Electrocardiogram .txt |
So if we listen to our heart, we hear the love dub love dub sound. And the love is caused by the closure of these two valves during the QRS complex. Now, this is when the ventricles actually begin to contract. These valves closed and the right and left atrium are now relaxing. Now, the question is why exactly is the voltage difference here so high? Well, that's because this section of the heart, the ventricles, contain the thickest layer of myocardium. | Introduction to Electrocardiogram .txt |
These valves closed and the right and left atrium are now relaxing. Now, the question is why exactly is the voltage difference here so high? Well, that's because this section of the heart, the ventricles, contain the thickest layer of myocardium. They have the thickest layer of muscle cell. And so that means a much higher voltage difference is needed to cause the contraction of all these muscles found within our right and left ventricle. And that's exactly why this peak is such a high peak. | Introduction to Electrocardiogram .txt |
They have the thickest layer of muscle cell. And so that means a much higher voltage difference is needed to cause the contraction of all these muscles found within our right and left ventricle. And that's exactly why this peak is such a high peak. Now let's move on to the st segment. What exactly takes place within our st segment? So within the st segment, that contraction increases that hydrostatic pressure. | Introduction to Electrocardiogram .txt |
Now let's move on to the st segment. What exactly takes place within our st segment? So within the st segment, that contraction increases that hydrostatic pressure. And what that causes is these two semi lunar valves, our pulmonary semi lunar valve and our aortic semilunar valve, to basically open up. And as those valves open up, all that blood flows from the ventricles into our arteries. So the left ventricle sends that oxygenated blood into the order, while the right ventricle sends our deoxynated blood into the pulmonary arteries and eventually into our lungs. | Introduction to Electrocardiogram .txt |
And what that causes is these two semi lunar valves, our pulmonary semi lunar valve and our aortic semilunar valve, to basically open up. And as those valves open up, all that blood flows from the ventricles into our arteries. So the left ventricle sends that oxygenated blood into the order, while the right ventricle sends our deoxynated blood into the pulmonary arteries and eventually into our lungs. So within the st segment, all of the cells within the ventricles have been depolarized, and repolarization of those cells basically begin. Now, the semi lunar valves, both of them, actually open up and our blood begins to eject into these blood vessels. This takes place in this flat region, the st segment, where the voltage is basically flat. | Introduction to Electrocardiogram .txt |
So within the st segment, all of the cells within the ventricles have been depolarized, and repolarization of those cells basically begin. Now, the semi lunar valves, both of them, actually open up and our blood begins to eject into these blood vessels. This takes place in this flat region, the st segment, where the voltage is basically flat. Now let's move on to our T wave. And then let's take a look at the U wave. Now, what exactly happens within our T wave? | Introduction to Electrocardiogram .txt |
Now let's move on to our T wave. And then let's take a look at the U wave. Now, what exactly happens within our T wave? So within a T wave, we also have a slight increase in voltage. And what happens here is repolarization begins or repolarization continues. So repolarization begins in the st segment, but it continues and takes place fully within our T wave. | Introduction to Electrocardiogram .txt |
So within a T wave, we also have a slight increase in voltage. And what happens here is repolarization begins or repolarization continues. So repolarization begins in the st segment, but it continues and takes place fully within our T wave. So this is when the cells of the ventricle repolarized. During this stage, these ventricles essentially empty out all that blood into our blood vessels. And because the hydrostatic pressure now decreases within our ventricles, these two semi lunar valves close. | Introduction to Electrocardiogram .txt |
So this is when the cells of the ventricle repolarized. During this stage, these ventricles essentially empty out all that blood into our blood vessels. And because the hydrostatic pressure now decreases within our ventricles, these two semi lunar valves close. And when they shut close, that is the second sound that we normally hear in our lub dub. So lub is when our bicuspid and tricuspid valves close, but the dub takes place when our two semi lunar valves close. We have the pulmonary and the aortic semi lunar valve. | Introduction to Electrocardiogram .txt |
And when they shut close, that is the second sound that we normally hear in our lub dub. So lub is when our bicuspid and tricuspid valves close, but the dub takes place when our two semi lunar valves close. We have the pulmonary and the aortic semi lunar valve. So the QRS complex is when our bicuspid and tricuspid valves close, but the T wave is when these two valves right here actually close. Now, what about this last wave we call the U wave. So the U wave is usually a very small peaked wave that follows our T wave. | Introduction to Electrocardiogram .txt |
So the QRS complex is when our bicuspid and tricuspid valves close, but the T wave is when these two valves right here actually close. Now, what about this last wave we call the U wave. So the U wave is usually a very small peaked wave that follows our T wave. And what we believe the U wave actually describes is the repolarization of all the cells found within the wall separating our two ventricles. So this wall is known as our interventricular wall. And what the uWave is believed to describe is the repolarization of all the cells found within this particular segment. | Introduction to Electrocardiogram .txt |
And what we believe the U wave actually describes is the repolarization of all the cells found within the wall separating our two ventricles. So this wall is known as our interventricular wall. And what the uWave is believed to describe is the repolarization of all the cells found within this particular segment. So these are some of the segments and waves that one would normally find on a normal cardiogram. And this is exactly what they describe. They describe the propagation, the movement of our electrical signal as we have a change in voltage. | Introduction to Electrocardiogram .txt |
Now, so far we discussed three of these important factors. We discussed how intermolecular bonds can influence the final structure of that biological molecule. We discussed hydrogen bonds. We examined London dispersion forces, also sometimes known as vandalbal forces. And we also discussed the hydrophobic interactions and the hydrophobic effect. Now we also discussed how the solvent in which the reaction is in can influence the pathway of that reaction and the final structure of that molecule. | Formation of DNA Double Helix .txt |
We examined London dispersion forces, also sometimes known as vandalbal forces. And we also discussed the hydrophobic interactions and the hydrophobic effect. Now we also discussed how the solvent in which the reaction is in can influence the pathway of that reaction and the final structure of that molecule. For example, we said that the majority of the reactions that take place in nature and specifically in our body take place in water. So water is the universal natural solvent and the properties of water can influence the reaction pathway as we'll see in just a moment. We also spoke about thermodynamics and how in any reaction we always have to remember that that reaction has to obey the laws of thermodynamics. | Formation of DNA Double Helix .txt |
For example, we said that the majority of the reactions that take place in nature and specifically in our body take place in water. So water is the universal natural solvent and the properties of water can influence the reaction pathway as we'll see in just a moment. We also spoke about thermodynamics and how in any reaction we always have to remember that that reaction has to obey the laws of thermodynamics. So it has to obey the first law of thermodynamics that basically states that energy is never created, energy is never destroyed. Energy can only be transformed from one form to another. So the total amount of energy in our universe is always constant. | Formation of DNA Double Helix .txt |
So it has to obey the first law of thermodynamics that basically states that energy is never created, energy is never destroyed. Energy can only be transformed from one form to another. So the total amount of energy in our universe is always constant. We also have to remember the second law of thermodynamics which basically describes the fact that in any real biological process the change in entropy of the universe is always positive, it always increases. So we also have to consider the temperature and the conditions under which a reaction is taking place because under certain conditions a reaction might be spontaneous but under other conditions the reaction might not be spontaneous. And so we have to consider the gifts free energy of our reaction. | Formation of DNA Double Helix .txt |
We also have to remember the second law of thermodynamics which basically describes the fact that in any real biological process the change in entropy of the universe is always positive, it always increases. So we also have to consider the temperature and the conditions under which a reaction is taking place because under certain conditions a reaction might be spontaneous but under other conditions the reaction might not be spontaneous. And so we have to consider the gifts free energy of our reaction. Now, another factor that we haven't yet focused on is the PH of a solution. So in the next several lectures we're going to discuss how the PH of a solution can also influence the pathway of the reaction and the final structure of that biological molecule. So to demonstrate how these factors can influence a particular biological reaction let's take a look at a common reaction the formation of a double helix of DNA. | Formation of DNA Double Helix .txt |
Now, another factor that we haven't yet focused on is the PH of a solution. So in the next several lectures we're going to discuss how the PH of a solution can also influence the pathway of the reaction and the final structure of that biological molecule. So to demonstrate how these factors can influence a particular biological reaction let's take a look at a common reaction the formation of a double helix of DNA. So inside every nucleus of every cell in our body we have DNA. Now, the DNA doesn't exist as a single strand. It exists as a double helix. | Formation of DNA Double Helix .txt |
So inside every nucleus of every cell in our body we have DNA. Now, the DNA doesn't exist as a single strand. It exists as a double helix. Now, from basic biology we know that a double helix consists of these two single strands of DNA that run in an antipowerall direction opposite with respect to one another. Now, on the outside of the DNA we have the phosphate groups and we have the carbon backbone as well as the deoxyribosugars. And on the inside of that DNA double helix, we have the basis that pair with each other. | Formation of DNA Double Helix .txt |
Now, from basic biology we know that a double helix consists of these two single strands of DNA that run in an antipowerall direction opposite with respect to one another. Now, on the outside of the DNA we have the phosphate groups and we have the carbon backbone as well as the deoxyribosugars. And on the inside of that DNA double helix, we have the basis that pair with each other. So the question is how do intermolecular bonds, how does the reaction solvent and how does thermodynamics basically influence this reaction, the formation of the double helix of DNA. So let's begin with the intermolecular interaction. So the question is how exactly do these intermolecular interactions drive the formation of the double helix? | Formation of DNA Double Helix .txt |
So the question is how do intermolecular bonds, how does the reaction solvent and how does thermodynamics basically influence this reaction, the formation of the double helix of DNA. So let's begin with the intermolecular interaction. So the question is how exactly do these intermolecular interactions drive the formation of the double helix? So let's take a look at the following diagram that basically describes a portion of our double helix. So this is the deoxyribo sugar, and for simplification purposes, I've omitted the hydroxyl group. So no hydroxyl groups are found on these sugar molecules. | Formation of DNA Double Helix .txt |
So let's take a look at the following diagram that basically describes a portion of our double helix. So this is the deoxyribo sugar, and for simplification purposes, I've omitted the hydroxyl group. So no hydroxyl groups are found on these sugar molecules. So we have the sugar that is attached to our phosphate. And the sugar and phosphate is basically on the outside of that DNA. So this is the outside portion of the DNA that interacts with the solvent. | Formation of DNA Double Helix .txt |
So we have the sugar that is attached to our phosphate. And the sugar and phosphate is basically on the outside of that DNA. So this is the outside portion of the DNA that interacts with the solvent. In this case, water. Why water? Well, because in the nucleus we have water that predominates and that's why it acts as a solvent. | Formation of DNA Double Helix .txt |
In this case, water. Why water? Well, because in the nucleus we have water that predominates and that's why it acts as a solvent. Now on the inside of the DNA we have these bases. The question is why exactly does this interaction actually take place? Why is it favorable from the inter molecular perspective, from the intermolecular interaction perspective? | Formation of DNA Double Helix .txt |
Now on the inside of the DNA we have these bases. The question is why exactly does this interaction actually take place? Why is it favorable from the inter molecular perspective, from the intermolecular interaction perspective? Well, number one is on the inside of the DNA molecule we have these bases that are able to form hydrogen bonds. So we have one base that interacts with a complementary base on the other single strand molecule and that forms our hydrogen bond. So in this case, this is hydrogen bonding and this is also hydrogen bonding. | Formation of DNA Double Helix .txt |
Well, number one is on the inside of the DNA molecule we have these bases that are able to form hydrogen bonds. So we have one base that interacts with a complementary base on the other single strand molecule and that forms our hydrogen bond. So in this case, this is hydrogen bonding and this is also hydrogen bonding. So we can say hydrogen bonding and this is also hydrogen bonding or simply age bonding. Okay? So a base on one DNA strand interacts with via hydrogen bonds with a complementary base on the other DNA molecule. | Formation of DNA Double Helix .txt |
So we can say hydrogen bonding and this is also hydrogen bonding or simply age bonding. Okay? So a base on one DNA strand interacts with via hydrogen bonds with a complementary base on the other DNA molecule. And so when these single strand molecules approach one another, these hydrogen bonds that are formed, that is a stabilizing effect. Now what about the second type of interaction, the London Dispersion forces. So notice that these base pairs are essentially parallel with respect to one another. | Formation of DNA Double Helix .txt |
And so when these single strand molecules approach one another, these hydrogen bonds that are formed, that is a stabilizing effect. Now what about the second type of interaction, the London Dispersion forces. So notice that these base pairs are essentially parallel with respect to one another. So they lie along the same exact plane. So they're essentially stacked on top of one another. Now remember, when they are stacked on top of one another, there are instantaneous dipole moments that exist within our bases. | Formation of DNA Double Helix .txt |
So they lie along the same exact plane. So they're essentially stacked on top of one another. Now remember, when they are stacked on top of one another, there are instantaneous dipole moments that exist within our bases. And those instantaneous dipole moments will interact with one another via the London dispersion forces. So not only do we have hydrogen bonding between the complementary adjacent bases, but we have the Vanderbilt forces, these London dispersion forces, between our bases stacked on top of one another. So these are H bonds, but these Brown bonds are essentially our London forces, the London Dispersion forces. | Formation of DNA Double Helix .txt |
And those instantaneous dipole moments will interact with one another via the London dispersion forces. So not only do we have hydrogen bonding between the complementary adjacent bases, but we have the Vanderbilt forces, these London dispersion forces, between our bases stacked on top of one another. So these are H bonds, but these Brown bonds are essentially our London forces, the London Dispersion forces. So we have these two important types of intermolecular bonds that play a role in forming our DNA double helix. Now not only that, but because the bases are essentially non polar, notice what happened. So the entire DNA molecule is swimming around in the solvent, in water, inside the nucleus of the cell. | Formation of DNA Double Helix .txt |
So we have these two important types of intermolecular bonds that play a role in forming our DNA double helix. Now not only that, but because the bases are essentially non polar, notice what happened. So the entire DNA molecule is swimming around in the solvent, in water, inside the nucleus of the cell. And water is a polar molecule. So what that means is these bases which are predominantly non polar, will not once interact with that polar water solvent. And what this double helix structure ensures is that all these non polar bases are found inside the structure of the double helix and away from the polar water molecules. | Formation of DNA Double Helix .txt |
And water is a polar molecule. So what that means is these bases which are predominantly non polar, will not once interact with that polar water solvent. And what this double helix structure ensures is that all these non polar bases are found inside the structure of the double helix and away from the polar water molecules. And so that is known as the hydrophobic effect. And these base cells will interact via the hydrophobic interactions and that will be a stabilizing effect. So we see that we have hydrogen bonds, we have London dispersion forces and we have the hydrophobic effect. | Formation of DNA Double Helix .txt |
And so that is known as the hydrophobic effect. And these base cells will interact via the hydrophobic interactions and that will be a stabilizing effect. So we see that we have hydrogen bonds, we have London dispersion forces and we have the hydrophobic effect. That basically ensures that the double helix is a favorable structure. Now the only type of nonfavorable interaction is basically the interaction between the phosphate groups. So notice that this phosphate group has a negative charge, this phosphate group also has a negative charge. | Formation of DNA Double Helix .txt |
That basically ensures that the double helix is a favorable structure. Now the only type of nonfavorable interaction is basically the interaction between the phosphate groups. So notice that this phosphate group has a negative charge, this phosphate group also has a negative charge. And when we have two light charges in close proximity, they will create a repulsive force. And so the only type of electric force, the only type of intermolecular force that tends to separate these single strands are these negative charges on these adjacent phosphate groups. So the negatively charged phosphate groups lead to electric repulsive forces. | Formation of DNA Double Helix .txt |
And when we have two light charges in close proximity, they will create a repulsive force. And so the only type of electric force, the only type of intermolecular force that tends to separate these single strands are these negative charges on these adjacent phosphate groups. So the negatively charged phosphate groups lead to electric repulsive forces. Now normally under room temperature or in body temperature, at body temperature, these attractive forces overpower these repulsive forces. And so that's exactly why the double helix structure remains. Now let's move on to the reaction solvent. | Formation of DNA Double Helix .txt |
Now normally under room temperature or in body temperature, at body temperature, these attractive forces overpower these repulsive forces. And so that's exactly why the double helix structure remains. Now let's move on to the reaction solvent. How exactly do the properties of water, the solvent found in the nucleus, affect the structure of that DNA molecule? How does it lead to a double helix formation? So basically, outside this DNA molecule are a bunch of water molecules. | Formation of DNA Double Helix .txt |
How exactly do the properties of water, the solvent found in the nucleus, affect the structure of that DNA molecule? How does it lead to a double helix formation? So basically, outside this DNA molecule are a bunch of water molecules. So this is a water molecule, this is a water molecule and so forth. Now this is the oxygen and these are the age groups. So we know that the age groups, because of the polarity of water, the age groups will be partially positive and our oxygen groups will be partially negative. | Formation of DNA Double Helix .txt |
So this is a water molecule, this is a water molecule and so forth. Now this is the oxygen and these are the age groups. So we know that the age groups, because of the polarity of water, the age groups will be partially positive and our oxygen groups will be partially negative. So what that means is these polar water molecules will orient themselves in such a way as to interact with the phosphate groups that are pointing to the outside on the double helix DNA molecule and that will be a stabilizing interaction. So once again we see that not only do we have hydrogen bonds that exist between the bases, but we also have these hydrogen bonds that exist between our water molecules and these phosphate groups. And that will be a very stabilizing effect. | Formation of DNA Double Helix .txt |
So what that means is these polar water molecules will orient themselves in such a way as to interact with the phosphate groups that are pointing to the outside on the double helix DNA molecule and that will be a stabilizing interaction. So once again we see that not only do we have hydrogen bonds that exist between the bases, but we also have these hydrogen bonds that exist between our water molecules and these phosphate groups. And that will be a very stabilizing effect. And so we see that the fact that water is the solvent, the properties of water that acts as a solvent in the formation of the DNA molecule actually favorably leads to the formation of that double helix DNA. And finally let's discuss how the thermodynamics of this reaction is also favorable. So let's suppose that this is our system and everything outside this box, everything outside our system are the surroundings. | Formation of DNA Double Helix .txt |
And so we see that the fact that water is the solvent, the properties of water that acts as a solvent in the formation of the DNA molecule actually favorably leads to the formation of that double helix DNA. And finally let's discuss how the thermodynamics of this reaction is also favorable. So let's suppose that this is our system and everything outside this box, everything outside our system are the surroundings. And let's suppose that the temperature at which our reaction takes place is either room temperature or we can also say it's a body temperature. So it's either 25 degrees Celsius or a body temperature 37 degrees Celsius. Now, before the reaction takes place, we have these single strands of DNA. | Formation of DNA Double Helix .txt |
And let's suppose that the temperature at which our reaction takes place is either room temperature or we can also say it's a body temperature. So it's either 25 degrees Celsius or a body temperature 37 degrees Celsius. Now, before the reaction takes place, we have these single strands of DNA. So we have three of these blue strands and three of these complementary red strands. Now, when this reaction takes place, what do we form? Well, we form three of these DNA molecules that are in their double helix form. | Formation of DNA Double Helix .txt |
So we have three of these blue strands and three of these complementary red strands. Now, when this reaction takes place, what do we form? Well, we form three of these DNA molecules that are in their double helix form. Now, what can we say about the entropy of this system and this system after the reaction? Well, before the reaction took place, the entropy of the system was greater than the entropy of the system after the reaction. Why? | Formation of DNA Double Helix .txt |
Now, what can we say about the entropy of this system and this system after the reaction? Well, before the reaction took place, the entropy of the system was greater than the entropy of the system after the reaction. Why? Well, because in this case, we have much more order in our system as in this case. So actually, in this reaction, the entropy of this system decreases. It becomes negative. | Formation of DNA Double Helix .txt |
Well, because in this case, we have much more order in our system as in this case. So actually, in this reaction, the entropy of this system decreases. It becomes negative. So the Delta S of our system is negative. Now, we know, according to thermodynamics this is only possible if this reaction releases enough energy to compensate for that decrease in entropy. And this is exactly what happens at room temperature or at body temperature inside our cells. | Formation of DNA Double Helix .txt |
So the Delta S of our system is negative. Now, we know, according to thermodynamics this is only possible if this reaction releases enough energy to compensate for that decrease in entropy. And this is exactly what happens at room temperature or at body temperature inside our cells. This reaction is actually spontaneous because even though the entropy of the system decreases, there's so much heat, so much energy released into the surroundings that that increases the entropy of the surroundings by a greater amount than the decrease of the entropy of the system. And so what that means is the change in entropy of the Universe is positive. Because if this is greater than this, then this is a positive value. | Formation of DNA Double Helix .txt |
This reaction is actually spontaneous because even though the entropy of the system decreases, there's so much heat, so much energy released into the surroundings that that increases the entropy of the surroundings by a greater amount than the decrease of the entropy of the system. And so what that means is the change in entropy of the Universe is positive. Because if this is greater than this, then this is a positive value. For example, if, let's say, this is negative ten, but this is positive 20, that means this value will be a positive value. And whenever our delta S of the Universe is a positive value, that means at that particular temperature, the Delta G that gives free energy will be a negative value. And so our reaction will be spontaneous, it will be favorable, and the product molecule will be formed. | Formation of DNA Double Helix .txt |
For example, if, let's say, this is negative ten, but this is positive 20, that means this value will be a positive value. And whenever our delta S of the Universe is a positive value, that means at that particular temperature, the Delta G that gives free energy will be a negative value. And so our reaction will be spontaneous, it will be favorable, and the product molecule will be formed. And in this case, that double helix DNA molecule will, in fact, form. So this is basically what we have to do, what we have to think about every time we examine a reaction in biochemistry. We have to think about how these different types of factors will influence that reaction pathway and the final structure of that final molecule. | Formation of DNA Double Helix .txt |
And that involves studying things like Gibbs free energy which involves enthalpy and entropy, as well as studying things like activation energy of that chemical reaction. Now, because enzymes act on chemical reactions, if we are are to actually understand how enzymes behave and act on those chemical reactions, we also have to study the GIBS free energy and the activation energy of that chemical reaction. So let's begin by discussing gifts free energy. Then we'll look at activation energy and we'll finish off with how the enzyme actually affects these two quantities. So let's begin by supposing that we have the following hypothetical reaction. So we have reactants being transformed into products. | Enzymes’ Effect on Activation Energy and Free Energy .txt |
Then we'll look at activation energy and we'll finish off with how the enzyme actually affects these two quantities. So let's begin by supposing that we have the following hypothetical reaction. So we have reactants being transformed into products. Now, we're going to assume that the reaction has not reached equilibrium. And what that basically means is the reaction can either have a negative gives free energy or a positive Gibbs free energy. So what is gives free energy? | Enzymes’ Effect on Activation Energy and Free Energy .txt |
Now, we're going to assume that the reaction has not reached equilibrium. And what that basically means is the reaction can either have a negative gives free energy or a positive Gibbs free energy. So what is gives free energy? Well, the gives free energy, loosely speaking, describes how much energy can be used in that chemical reaction. So let's suppose we have the following graph. So the y axis is the energy value and the x axis is the reaction progress. | Enzymes’ Effect on Activation Energy and Free Energy .txt |
Well, the gives free energy, loosely speaking, describes how much energy can be used in that chemical reaction. So let's suppose we have the following graph. So the y axis is the energy value and the x axis is the reaction progress. So these are the reactants here and the energy value of the reactant is somewhere here. Now, the products have a free energy value that is equal to somewhere here. And notice that the products have a lower free energy than the reactants. | Enzymes’ Effect on Activation Energy and Free Energy .txt |
So these are the reactants here and the energy value of the reactant is somewhere here. Now, the products have a free energy value that is equal to somewhere here. And notice that the products have a lower free energy than the reactants. Now, to calculate mathematically the gives free energy of this reaction, all we have to do is take the free energy of the products and subtract the free energy of the reactants. And that gives us the gives free energy given by Delta G. So this quantity here is how much energy is going to be released in this reaction. And it's basically how much energy we can use in some process. | Enzymes’ Effect on Activation Energy and Free Energy .txt |
Now, to calculate mathematically the gives free energy of this reaction, all we have to do is take the free energy of the products and subtract the free energy of the reactants. And that gives us the gives free energy given by Delta G. So this quantity here is how much energy is going to be released in this reaction. And it's basically how much energy we can use in some process. Now, for this particular case, this reaction describes an exergonic reaction. And exergonic reactions always have a negative Delta G. That means energy is released in this reaction and the reaction is said to be spontaneous. So a chemical reaction is said to be exergonic and spontaneous if the Delta G is negative. | Enzymes’ Effect on Activation Energy and Free Energy .txt |
Now, for this particular case, this reaction describes an exergonic reaction. And exergonic reactions always have a negative Delta G. That means energy is released in this reaction and the reaction is said to be spontaneous. So a chemical reaction is said to be exergonic and spontaneous if the Delta G is negative. And one example of a spontaneous reaction in nature is combustion. So combustion reactions are examples of exergonic reactions where the Delta G value is negative. Now, what about the opposite? | Enzymes’ Effect on Activation Energy and Free Energy .txt |
And one example of a spontaneous reaction in nature is combustion. So combustion reactions are examples of exergonic reactions where the Delta G value is negative. Now, what about the opposite? Well, if we read this reaction going backwards, if this is the reactant and this is the product that if we subtract a high free energy from a low free energy, we're going to get a positive Delta G. And a positive Delta G means the reaction is endergonic and non spontaneous. And that means it will not take place unless we input a certain amount of energy. And one example of an endorganic reaction that is not spontaneous is the synthesis of ATP molecules inside our body. | Enzymes’ Effect on Activation Energy and Free Energy .txt |
Well, if we read this reaction going backwards, if this is the reactant and this is the product that if we subtract a high free energy from a low free energy, we're going to get a positive Delta G. And a positive Delta G means the reaction is endergonic and non spontaneous. And that means it will not take place unless we input a certain amount of energy. And one example of an endorganic reaction that is not spontaneous is the synthesis of ATP molecules inside our body. So to synthesize ATP, we have to actually input energy. And the ATP molecules, when they break down, that is an exergonic reaction and energy is released. And every time we break down ATP molecules inside our body, energy is released. | Enzymes’ Effect on Activation Energy and Free Energy .txt |
So to synthesize ATP, we have to actually input energy. And the ATP molecules, when they break down, that is an exergonic reaction and energy is released. And every time we break down ATP molecules inside our body, energy is released. And we can use that energy to basically power different types of processes that take place inside our body that require those ATP molecules. So on the other hand, a chemical reaction is said to be endergonic and non spontaneous if a delta g is positive. And ATP synthesis is an example of such an endergonic reaction. | Enzymes’ Effect on Activation Energy and Free Energy .txt |