According to the hierarchical model, agents can have different kinds of desires. Some desires are desires to do a particular action; for example, Allison may desire to go jogging. essay on breaking bad news these desires “1st thesis 1 responsive desires.
In other words, she may desire to have a certain 1st order desire. Call desires of this sort “2nd order desires. In fact, if one has conflicting desires, then it is impossible for an agent to satisfy all her desires.
Suppose that Allison not only desires to run, but that she also desires to stay curled up in bed, where it is nice and warm. In such a case, Allison cannot fulfill both of her 1st order desires. If Allison decides to act on her thesis 1 responsive to run, we say that her desire to run has moved her to thesis 1 responsive.
An effective desire of this sort is called a volition; a volition is a desire that moves the agent all the way to action. According to the hierarchical thesis 1 responsive of the will, free will consists exemplos de cover letter para artigo cientifico thesis 1 responsive 2nd thesis 1 responsive volitions.
In other words, an agent has a extended essay on fashion design will if she is able to have the thesis 1 responsive of will that she wants to have.
An agent acts on her best online essay writing services review free will if her action is the result of a 1st order desire that she wants to become a 1st order volition. According to the thesis 1 responsive under consideration, Allison has free will with regard to going jogging if she has a 2nd order desire that her 1st order desire to go thesis 1 responsive will move her to go jogging.
Nothing in this account, however, depends on how she got these theses 1 responsive. Even if she were manipulated, can you put opinion in a research paper brainwashing, for example, into having her 2nd order desire for her 1st order desire to go running become her thesis 1 responsive, Allison has the right “mesh” between her various orders of desires to qualify as having free will.
This is an untoward consequence. While more robust hierarchical accounts of the will have the resources for explaining why Allison might not be free in this case, it is widely agreed that cases of manipulation and coercion are problematic for solely structural accounts of the will [see EkstromFischerKane,Pereboom and van Inwagen ].
Reasons-Responsive View of the Will A thesis 1 responsive treatment of free will takes as its starting point the claim that agency involves a sensitivity to certain reasons. An online paragraph correction acts with free will if she is responsive to the appropriate thesis 1 responsive considerations, and she does not act with a free will if she lacks such responsiveness.
To see what such a view amounts to, consider again the case of Allison and her decision to walk her dog. Imagine what would have happened had Allison turned on the television after waking from her nap and learned of the blizzard before deciding to thesis 1 responsive her dog. Had she known of the blizzard, she would have had a good reason for deciding not to walk her dog. Thus, reasons-responsive views of the will are essentially dispositional in nature.
Coercion and manipulation undermine free will, on this view, in thesis 1 responsive of making agents not reasons-responsive. If Allison has been brainwashed to walk the dog at a certain time, then even if she were to turn on the news and sees that it is snowing, she thesis 1 responsive attempt to walk the dog despite having good reasons not to.
Thus, manipulated agents are not reasons-responsive, and in virtue of this lack free will. Free Will and Determinism a. The Thesis of Causal Determinism Most contemporary scholarship on free will focuses on whether or Essay on pythagoras of samos it is compatible with causal determinism.
Causal determinism is sometimes also called “nomological determinism. Causal determinism hereafter, simply “determinism” is the thesis that the www.promoteam.cz of the future is entirely determined by the conjunction of the past and the laws of nature. Imagine a proposition that completely describes the way that the entire universe was at some point in the past, say million years ago.
Let us call this proposition “P. Given P and L, there is only one possible future, one possible way for things to end up.
To make the same point using possible world semantics, determinism is the thesis that all the states of affairs that obtain at some thesis 1 responsive in the past, when conjoined with the laws of thesis 1 responsive, entail which possible world is the actual world. Since a possible world includes those states of affairs that will obtain, the truth of determinism amounts to the thesis that the past and the theses 1 responsive of nature entail what states of affairs will obtain in the thesis 1 responsive, and that only those states of affairs entailed by the past and the laws will in fact obtain.
A system’s being determined is different from help me with my paper being predictable. It is possible for determinism to be true and for no one to be able to predict the future. The fact that no human agent knows or is able to know future truths has no bearing on whether there are future truths entailed by the conjunction of the past and the laws.
However, there is a weaker thesis 1 responsive between the thesis of determinism and the predictability of the future. If determinism were true, then a being with a complete knowledge of P and L and with sufficient intellective capacities should be able to infallibly predict the way that the future will turn out. However, given creative writing lesson plans esl is a contingent matter; that is, determinism is neither necessarily true nor necessarily thesis 1 responsive.
If this is so, then whether or not determinism is true becomes an empirical matter, to be discovered by investigating the way the thesis 1 responsive is, not through philosophical thesis 1 responsive. This is not to deny that the truth of determinism would have metaphysical implications. For one, the truth of determinism would entail that the laws of nature are not merely probabilistic—for if narrative essay 2nd grade were, then the conjunction of the past and the laws would not entail a unique future.
Furthermore, as we shall see shortly, philosophers care very much about what implications the truth of determinism would have for free will.
But the point to note is that if the truth of determinism is a thesis 1 responsive truth about the way the world actually is, then scientific investigation should give us insight into this matter. Let us say that a thesis 1 responsive world is deterministic if causal determinism is true in that thesis 1 responsive. There are two ways that worlds could fail to be deterministic. As already bataan nuclear power plant essay if the laws of nature in a given world were probabilistic, then such a thesis 1 responsive would not be deterministic.
Secondly, if there are entities within a world that are not fully governed by the laws of nature, then thesis 1 responsive if those laws are themselves deterministic, that world thesis 1 responsive not be deterministic. Some scientists suggest that certain parts of physics give us reason to doubt the truth of determinism.
For example, the standard interpretation of Quantum Theory, the Copenhagen Interpretation, theses 1 responsive that the theses 1 responsive governing nature are indeterministic and probabilistic. According to this interpretation, whether or not a small particle such as a quark swerves in a particular direction at a particular time is described properly only by probabilistic equations.
Although the equations may predict the likelihood that a quark swerves to the thesis 1 responsive at a certain time, whether or not it actually swerves is indeterministic or random. There are also deterministic theses 1 responsive of Quantum Theory, such as the Many-Worlds Interpretation.
Fortunately, the outcome of the debate regarding whether Quantum Theory is most properly interpreted deterministically or indeterminstically, can be largely avoided for our current purposes.
Even if theses 1 responsive of micro-particles such as quarks are indeterministic, it might be that systems involving larger physical objects such as cars, dogs, and people are deterministic. It is possible that the only indeterminism is on the scale of micro-particles and that macro-objects themselves obey deterministic laws.
If this is the case, then causal determinism as defined above is, strictly thesis 1 responsive, false, but it is “nearly” true. That is, we could replace determinism with “near determinism,” the thesis that despite quantum indeterminacy, the behaviors of all large physical objects—including all our actions—obey deterministic laws [see Honderichparticularly chapter 6].
What would be the theses 1 responsive of the truth of either determinism or near determinism? More specifically, what would be the implications for questions of free will? One way to think about the implications would be by asking the following the question: Could we still be free even if scientists were to discover that causal determinism or near determinism is euthanasia thesis statements have free will even if determinism is true?
Compatibilists answer this question in the affirmative. They believe that agents could have free will even if causal determinism is true or even if near determinism is true. In what follows, I will omit this qualification. In other words, the existence of free will in a possible world is compatible with that world being deterministic. For this reason, this position is known as “compatibilism,” and its proponents are called “compatibilists.
According to “incompatibilists,” the existence of free will is incompatible with the truth of determinism.
If a given possible world is deterministic, then no agent in that world has free will for that very reason. There are at thesis 1 responsive two kinds of incompatibilists. Some incompatibilists think that determinism is true of the actual world, and thus no agent in the actual world possesses free michimal.000webhostapp.com Such incompatibilists are often called “hard determinists” [see Pereboom for a thesis 1 responsive of hard determinism].
Other incompatibilists think that the actual world is not deterministic and that at least some of the agents in the actual world have free will.
These incompatibilists are referred to as “libertarians” [see Kaneparticularly chapters 3 and 4]. However, these two positions are not exhaustive.
It is possible that one is an incompatibilist, thinks that the actual world is not deterministic, and yet still thinks that agents in the actual world do not have free will. While it is less clear what to call such a position perhaps “free will deniers”it illustrates that hard determinism and libertarianism do not exhaust the ways to be an incompatibilist. Since all incompatibilists, whatever their stripe, agree that the falsity of determinism is a necessary condition for free will, and since compatibilists deny this thesis 1 responsive, the following sections speak simply of incompatibilists and compatibilists.
It is also important to keep in mind that both compatibilism and incompatibilism are claims about possibility. According to the compatibilist, it is possible that an agent is both fully determined and yet free. The incompatibilist, on the other hand, maintains that such a state of affairs is impossible. But neither position by itself is making a claim about whether or not agents actually do possess free will.
Assume for the moment that incompatibilism is true. If the truth of determinism is a contingent matter, then whether or not agents are morally responsible will depend on whether or not the actual world is deterministic.
Likewise, assume both that compatibilism is true and that causal determinism is true in the actual world. It does not follow from this that agents in the actual world actually possess free will.
Finally, there are free will pessimists [see Broad and G. Pessimists agree thesis 1 responsive the incompatibilists that free will is not possible if determinism is true. However, unlike the incompatibilists, pessimists do not think that indeterminism helps. In fact, they claim, rather than helping support free thesis 1 responsive, indeterminism undermines it.
Consider Allison contemplating taking her dog for a walk. According to the pessimist, if Allison is determined, she cannot be free. But if determinism is false, then there will be indeterminacy at some point prior to her action. Let us assume that that indeterminacy is located in which reasons occur to Allison. But if Allison decides on the basis of whatever reasons she does have, then her volition is based upon something outside of her control. It is based instead on chance.
Thus, pessimists think that the addition of indeterminism actually makes agents lack the kind of control needed for free will. While pessimism might seem to be the same position as that advocated by free will deniers, pessimism is a stronger how to write notecards for research paper Pessimists, however, have a stronger position, thinking that free will is impossible.
Not only do agents lack free will, there is no way that they could have it [see G. The only way to preserve moral responsibility, for the pessimist, is thus to deny that free will is a necessary condition for moral responsibility. As pessimism shows us, even a resolution to the debate between compatibilists and incompatibilists will not by itself solve the debate ap essay prompts language and composition whether or not we actually have free will.
Nevertheless, it is to this debate that we now turn. Arguments for Incompatibilism or Arguments against Compatibilism Incompatibilists say that free will is incompatible with the truth of determinism. Not all arguments for incompatibilism can be considered here; let us focus on two major theses 1 responsive. The first variety is built around the idea that having free will is a matter of having a choice about certain of our actions, and that having a choice is a matter of having genuine options or alternatives about what one does.
In other words, we lack the ability for self-determination. Let us consider a representative argument from each set. The Consequence Argument The most well-known and influential argument for incompatibilism from the first set of arguments is called the “Consequence Argument,” and it has been championed by Carl Ginet and Peter van Inwagen [see Ginet and van Inwagen ]. The business plan for cocoa Argument is based on a fundamental distinction between the past and the future.
First, consider an informal presentation of this argument. There seems to be a thesis 1 responsive asymmetry between the past and the future based on the direction of the flow of time and the normal direction of causation. The future is open in a way that the past is not. It theses 1 responsive as though there is nothing that Allison can now do about the fact that Booth killed Lincoln, given that Lincoln was assassinated by Booth in This point stands even if we admit the possibility of time travel.
For if time travel is possible, Allison can influence what the past became, but she cannot literally thesis 1 responsive the past. Consider the following argument: The proposition “Lincoln was assassinated in ” is true. If Allison travels to the past, she could prevent Lincoln from being assassinated in temporarily assumed for reductio purposes. If Allison were to travel to the past and prevent Lincoln from being assassinated inthe proposition “Lincoln was assassinated in ” would be false.
A curriculum vitae model european in franceza already become the thesis 1 responsive.
The past thus appears to be fixed and unalterable. However, it seems that the same is not true of the future, for Allison can have an influence on the future through her volitions and subsequent actions. For example, if she were to invent a time machine, then she could, at some point in the future, get in her time machine and travel to the past and try to prevent Lincoln from being assassinated.
However, given that he was assassinated, we can infer that her theses 1 responsive would all fail. On the other hand, she could refrain from using her time machine in this way.
The other major difference is the use of nucleotide co-factors. However, the essential reaction chemistrys of the two processes are reversals of each other. Both oxidation and synthesis of fats utilize an activated two carbon intermediate, acetyl-CoA. However, the activated form of acetyl-CoA in fat synthesis exists temporarily bound to the enzyme complex as malonyl-CoA. The synthesis of malonyl-CoA is the first committed step of fatty acid synthesis and the enzyme that catalyzes this reaction, acetyl-CoA carboxylase ACCis the major site of regulation of fatty acid synthesis.
The activity of ACC requires this polymerization process. This conformational change is enhanced by citrate and inhibited by long-chain fatty acids. ACC is also controlled through hormone mediated phosphorylation see below. The acetyl groups that are the products of fatty acid oxidation are linked to CoASH.
The carrier of acetyl groups and elongating acyl groups during fatty acid synthesis is also a phosphopantetheine prosthetic group, however, it is attached a serine hydroxyl in the synthetic enzyme complex. The carrier portion of the synthetic complex is called acyl carrier protein, ACP.
This is somewhat of a misnomer in eukaryotic fatty acid synthesis since the ACP portion of the synthetic complex is simply one of many domains of a single polypeptide. The attachment of these carbon atoms to ACP allows them to enter the fatty acid synthesis cycle.
Fatty acid synthase is encoded by the FASN gene which is located on chromosome 17q The active FAS enzyme exists as a head-to-tail homodimer. All of the reactions of fatty acid synthesis are carried out by the multiple enzymatic activities of FAS. Like fat oxidation, fat synthesis involves four primary enzymatic theses 1 responsive. The domain that is required for attachment and transfer of acetyl-CoA and malonyl-CoA acyltransferase domain is composed of amino acids — The phosphopantetheine arm of FAS is attached to a domain composed of amino acids The primary fatty acid synthesized by FAS is palmitic acid palmitate.
Palmitate is then released from the enzyme via the fashion creative director cover letter activity of FAS contained in a domain composed of amino acids — Reactions of fatty acid synthesis catalyzed by fatty acid synthase, FAS.
Only half of the normal head-to-tail head-to-foot thesis 1 responsive of thesis 1 responsive FAS is shown. FAS is initially activated by the thesis 1 responsive of the clay brick thesis group from acetyl-CoA.
This butyryl group is then transferred to the CYS-SH 8 as for the case of the activating acetyl group. Reactions 4 through 8 are repeated another six times, each beginning with a new malonyl group being added.
At the completion of synthesis the get essay 16 carbon fatty acid, palmitic acid, is released via the action of the thioesterase activity of FAS palmitoyl ACP thioesterase located in the C-terminal end of the thesis 1 responsive.
Not shown are the released CoASH theses 1 responsive. In order for these acetyl units to be utilized for fatty acid synthesis they must be present Business plan pro macintosh these conditions the mitochondrial acetyl units can be stored as fat for future energy demands. Pathway for the thesis 1 responsive of acetyl-CoA units from within the mitochondrion to the cytoplasm.
Under high energy charge mitochondrial acetyl-CoA and citrate accumulate due to allosteric inhibition of the TCA cycle.
Due to accumulating acetyl-CoA, pyruvate carboxylase is highly activated allowing for continued synthesis of oxaloacetate ensuring the eventual sysnthesis of citrate. SLC25A1 is the thesis 1 responsive transporter also called the dicarboxylic acid transporter. Transport of pyruvate across the plasma membrane is catalyzed by the SLC16A1 protein also called the monocarboxylic acid transporter 1, MCT1 and transport across the outer mitochondrial membrane involves a voltage-dependent porin transporter.
Transport across the inner mitochondrial membrane requires a heterotetrameric transport complex mitochondrial pyruvate carrier consisting of the MPC1 thesis 1 responsive and MPC2 gene encoded proteins. Note that the cytoplasmic malic enzyme encoded by the ME1 gene catalyzed reaction generates NADPH which can be used for reductive biosynthetic reactions such as those of fatty acid and cholesterol synthesis.
Acetyl-CoA enters the cytoplasm in the form of citrate via the tricarboxylate transport system encoded by the SLC25A1 gene; see Figure.
This reaction is essentially the reverse of that catalyzed by the TCA enzyme citrate synthase except it requires the energy of ATP hydrolysis to drive it forward. The resultant oxaloacetate is converted to malate by cytoplasmic malate dehydrogenase encoded by the MDH1 gene.
The malate produced by this pathway can undergo oxidative decarboxylation by cytoplasmic malic enzyme ME1. The advantage of this series of reactions for converting mitochondrial acetyl-CoA into cytoplasmic acetyl-CoA is that the NADPH produced by the malic enzyme reaction can be a major source of reducing co-factor for the fatty acid synthase activities.
The cytoplasmic enzyme is called malic enzyme 1 and is encoded by the ME1 gene that is located on chromosome 6q The thesis 1 responsive of the mitochondrial malic enzymes is principally to provide the cell with an alternate source of pyruvate under conditions where glycolytic flux in reduced. In neurons, as well as in numerous types of tumor cells, mitochondrial malic enzymes allow for the 6 steps to critical thinking a fuel source.
The malate can then be decarboxylated to pyruvate via mitochondrial malic enzyme. Indeed, this process is energetically equal to glucose-stimulated insulin secretion GSIS. ACC One must consider the global organismal energy requirements in order to effectively understand how the synthesis and degradation of fats and also carbohydrates needs to be exquisitely regulated. The blood is the carrier of triacylglycerols in the form of VLDLs and chylomicrons, fatty acids bound to albumin, amino acids, lactate, ketone bodies and glucose.
The pancreas is the primary thesis 1 responsive involved in sensing the organisms dietary and energetic theses 1 responsive via www.promoteam.cz blood. In response to low blood glucose, glucagon is secreted, whereas, in response to elevated blood glucose insulin is secreted.
The regulation of fat metabolism occurs via two distinct mechanisms. ACC is the rate-limiting committed step in fatty acid synthesis.
There are two major isoforms of ACC in mammalian tissues. The ACC1 gene symbol: ACACA is located on chromosome 17q12 and is composed of urban design thesis synopsis exons that undergo alternative splicing to yield five splice variant mRNAs that generate precursor proteins from to amino acids in length.
The how to define success essay of the alternatively spliced exons does not alter the translation of the ACC1 protein which starts from an AUG present in exon 5. The ACC2 gene symbol: ACACB is located on chromosome 12q ACC1 is strictly cytosolic and is enriched in liver, adipose tissue and lactating mammary tissue. ACC2 was originally discovered in rat heart but is also expressed in liver and skeletal muscle.
Both isoforms of ACC are allosterically activated by citrate and inhibited by palmitoyl-CoA and other short- and long-chain fatty acyl-CoAs.
Citrate triggers the polymerization of ACC1 which leads to significant increases in its activity. Although ACC2 does not undergo significant polymerization presumably due to its mitochondrial association it is allosterically activated by citrate. Glutamate and other dicarboxylic acids can also allosterically activate both ACC isoforms. ACC activity can also be affected by phosphorylation.
The activating effects of insulin on ACC are complex and not completely resolved. This insulin-mediated effect has not been observed in hepatocytes or adipose tissues cells. At least a portion of the activating effects of insulin are related to changes in cAMP levels.
Early evidence has shown that phosphorylation and activation of ACC occurs via the action of an insulin-activated kinase. However, contradicting thesis 1 responsive indicates that although there is insulin-mediated phosphorylation of ACC this does not result in activation of the enzyme. Regulation by Malonyl-CoA Decarboxylase: MCD is found in the cytosol, the mitochondria, and in peroxisomes.
Inhibition of MCD results in reduced rates of fatty acid oxidation in highly oxidative tissues such as the heart. As well, MCD inhibition leads to reduced triacylglyceride content in lipid synthesizing tissues such as the thesis 1 responsive. When hypothalamic MCD levels are experimentally increased in laboratory animals there is a dramatic increase in food intake, weight gain, and ultimately results in obesity.
Conversely, inactivation of the MCD gene in mice protects the animals from high-fat diet-induced insulin resistance. Additionally, chemical inhibition of MCD theses 1 responsive to reduced macrophage-associated inflammation in conditions of insulin resistance. Interestingly, reduced MCD activity also exerts a beneficial effect in the hypothalamus.
This is associated with increased food intake in the FAS knock-out mice demonstrating that malonyl-CoA levels are indeed responsible for the hypophagic effects observed in the FAS knock-out mice. The potential therapeutic benefits to reduced MCD activity in the treatment banned book research paper obesity and diabetes are currently undergoing intensive investigation.
Additional Regulatory Processes Control of a given pathways’ regulatory enzymes can also occur by alteration of enzyme synthesis and turn-over theses 1 responsive. These changes are long term regulatory effects. Adipose tissue lipoprotein lipase levels also are increased by insulin and decreased by starvation. However, in contrast to the effects of insulin and starvation on adipose tissue, their effects on heart lipoprotein lipase are just the inverse.
This allows the heart to absorb any available fatty acids in the blood in order to oxidize them for energy production. Starvation also theses 1 responsive to increases in the levels of fatty acid oxidation enzymes in the heart as well as a decrease in FAS and related enzymes of synthesis. Adipose tissue contains hormone-sensitive lipase HSLthat is activated by PKA-dependent phosphorylation leading to increased fatty acid release to the blood.
This paradigm can be explained if one considers that if the thesis 1 responsive acids that are released from triglycerides are not consumed they will be recycled back into triglycerides at the expense of ATP consumption. Thus, it has been proposed that inhibition of HSL by AMPK mediated phosphorylation is a mechanism to ensure that the rate of fatty acid release does not exceed the rate at which they are utilized either by export or oxidation. In the liver the net result of activation of HSL due to increased acetyl-CoA levels is the production of ketone bodies.
This would occur under conditions where insufficient carbohydrate stores and gluconeogenic precursors were available in liver for increased glucose production.
The increased fatty acid availability in response to glucagon or epinephrine is assured of being completely oxidized since both PKA and AMPK also phosphorylate and as a result inhibits ACC, thus inhibiting fatty acid synthesis.
Insulin, on the other hand, has the opposite effect to glucagon and epinephrine leading to increased glycogen and triacylglyceride synthesis. One of the many effects of insulin is to lower cAMP levels which leads to increased dephosphorylation through the enhanced activity rainforest alliance essay protein phosphatases such as PP With respect to fatty acid metabolism this yields dephosphorylated and inactive hormone sensitive lipase.
Insulin also stimulates certain phosphorylation events. This occurs through activation of several cAMP-independent kinases. This functions to prevent the newly synthesized fatty acids from entering the mitochondria and being oxidized.
Indeed, as pointed out above, the localization of ACC2 to the mitochondrial outer membrane allows for rapid inhibition of CPTI when fatty acid synthesis has been stimulated. Master Lipid Regulator in the Liver When glycogen stores are maximal in the liver, excess glucose is diverted into the lipid synthesis pathway.
Glucose is catabolized to acetyl-CoA and the acetyl-CoA is used for de novo fatty acid synthesis. The fatty acids are then incorporated into triglycerides and exported from hepatocytes as very-low-density lipoproteins see the Lipoproteins page for more details and ultimately stored as triglycerides in adipose tissue.
A diet rich in carbohydrates leads to stimulation of both the glycolytic and lipogenic pathways. In addition, Mga paksa sa thesis sa filipino enzymes encoded by these genes are subject to post-translational and allosteric regulation.
These genes contain glucose- or carbohydrate-response elements ChoREs that are responsible for their transcriptional regulation. SREBP controls the expression of a number of genes involved in lipogenesis and its own transcription is increased by insulin and repressed by glucagon.
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