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That difference between VP and NAc suggests that NAc segregates hedonic gain of function versus loss of function into different anatomical sites of medial shell, whereas the VP hotspot combines both forms of hedonic causation together Ho and Berridge, The VP hotspot thus appears unique among brain sites for hedonic loss of function. The excessive disgust that follows these VP disruptions may be viewed as a release phenomenon, produced by disinhibition of negative-valenced circuitry in the remaining forebrain diencephalon Ho and Berridge, A disinhibition interpretation also fits a hierarchical view of how pleasure and displeasure are organized in the brain Hughlings Jackson, This NAc pattern resembles an affective keyboard arranged rostrocaudally within medial shell, which can generate intense desire or even dread as well as hedonic impact Reynolds and Berridge, ; Richard and Berridge, Figure 4.

The keyboard pattern is arranged from anterior to posterior ends of medial shell. At its anterior end, it generates predominantly positive-valenced motivations in response to localized neural events such as microinjections of a GABA agonist muscimol or of a glutamate AMPA antagonist DNQX : eating more than twice normal amounts of food, increasing appetitive seeking for food rewards Stratford and Kelley, ; Stratford and Wirtshafter, ; Wirtshafter et al.

However, as the microinjection site moves more caudally in NAc shell, appetitive behaviors decline. Top: A rostrocaudal keyboard pattern of generators in NAc for appetitive versus fearful behaviors, showing consequences of microinjections of either glutamate AMPA antagonist or GABA agonist microinjections at rostrocaudal sites in medial shell. The same antipredator behaviors occurs without any specific threat stimulus after DNQX or muscimol microinjections in posterior NAc: denoted by red dots.

Yellow sites released both desire and fearful behaviors in the same rats during the same 1-hr test. Just as a keyboard has many notes, bars reflect the many graded mixtures of affective desire-dread released as microinjection sites move rostrocaudal location in medial shell appetitive desire to eat at top; fearful dread reactions at bottom. Bottom: Environmental ambience retuned the NAc keyboard. A standard laboratory environment rebalances the keyboard into nearly equal halves for desire versus dread.

A stressfully over-stimulating sensory environment bright lights plus loud rock music tilted the causal keyboard toward dread, and shrank the zoned that generated appetitive desire. Squirrel photo by Cooke from Coss and Owings, Figure data modified from Richard et al. Of course, several other brain structures, from amygdala to hypothalamus, ventral pallidum or brainstem also known to mediate various aversive emotional reactions, including fear, pain or disgust Baliki et al.

The amygdala is especially crucial for fear-related learning of passive responses to threats, such as freezing to a Pavlovian cue that predicts footshock LeDoux, ; Maren et al. The posterior NAc instead produces a more active set of fearful coping reactions Faure et al. These defensive reactions are usually targeted toward stimuli the affected rat may perceive as potentially threatening, such as glittering transparent corners of the cage or experimenters visible beyond the transparent wall Coss and Owings, ; Reynolds and Berridge, The number of differently-valenced rostrocaudal keys contained in the nucleus accumbens shell is difficult to estimate, and in practice is defined somewhat arbitrarily by the size of the microinjections used to tap the keyboard.

But probably it contains more than two keys corresponding to mere positive vs negative valence: two keys would generate only two outputs, but the NAc shell generates many different incremental outputs of gradual variation depending on precise site. Just as a musical keyboard generates many distinct notes, the rostrocaudal affective keyboard generates multiple distinct quantities of appetitive versus fearful behaviors.

For example, as sites move from front to back, intense behaviors become gradually less appetitive, and incrementally more fearful, so that many different ratio mixtures are produced, just as moving a brick along a piano keyboard would generate many different mixtures of notes changing gradually in pitch. However, a causal caveat may be needed here. To say an appetitive mechanism is densest in the anterior half of NAc shell may really be to say that the anterior half is densest in neural mechanisms which ordinarily inhibit appetitive behavior — and which themselves must be inhibited by the rostral microinjection that produces the intense appetitive behavior.

This disinhibition interpretation arises because of the inhibitory nature of the GABA A agonist or glutamate antagonist microinjections that produce the intense behaviors. The drug microinjections either hyperpolarize NAc neurons i. A disinhibition interpretation suggests that reduced activity of NAc projection neurons, which themselves release mostly GABA, would release or disinhibit recipient neurons in target structures into relative excitation e.

Target excitations could be the final active mechanism to produce intense motivations. Output projections from particular rostrocaudal sites in NAc shell appear partly segregated from each other in target structures Thompson and Swanson, ; Zahm et al. Although some contrary evidence suggests that local NAc excitations also generate motivated behaviors Britt et al. Strikingly, the valence of desire-dread motivations generated by the NAc keyboard is not necessarily fixed by anatomical location, but can be powerfully retuned psychologically for many sites by emotional factors such as the valenced ambience of an environment Figure 4.

At least, dramatic psychological retuning occurs for the glutamate-related DNQX gradient that merely blocks local NAc excitation Reynolds and Berridge, ; Richard and Berridge, By comparison, the GABA-related muscimol gradient is more resistant to retuning, perhaps because it involves stronger neuronal NAc hyperpolarization Richard et al.

Retuning can completely reverse the valence generated at a site from desire to dread, or back from dread to desire. For example, the fear-generating zone of caudal shell expands in a stressfully bright and loud environment to invade rostral shell, while simultaneously shrinking the desire-generating zone to only the far-rostral tip of medial shell Reynolds and Berridge, ; Richard and Berridge, Conversely, a quiet home-like environment which rats prefer causes the NAc keyboard to expand its rostral desire-generating zone into the caudal half of shell, and shrink the fear-generating zone into merely the far-caudal tip.

Such remapping can actually flip many intermediate sites of shell into releasing opposite motivations in the different environments. Speculatively, it can be hypothesized that some pathological human conditions might induce more permanent retuning of NAc valence generators. For example, post-traumatic stress disorder might persistently retune NAc generation in a fearful direction in human patients, similarly to a stressful ambience.

Conversely, human addiction and mesolimbic sensitization might retune NAc generators in an appetitive direction, potentiating desire for addicted rewards. These possibilities could be explored by future research. For the glutamatergic keyboard in rats, the neurobiological mechanism of psychological retuning appears to rewire local neurobiological modes of neurochemical activation within the local NAc microdomain.

By contrast, generation of appetitive desire, even at the same NAc site, requires only D1 activity — not D2 activity Richard and Berridge, That pattern suggests that direct and indirect output paths of NAc may have different roles in this desire-dread generation. If so, that would be consistent with suggestions from others that a NAc D1 direct path dominates in appetitive motivation Xiu et al.

Finally, NAc keyboard tuning is regulated by corticolimbic top-down inputs from prefrontal limbic cortex Richard and Berridge, For example, raising local cortical excitations in infralimbic cortex, a medial prefrontal region homologous to human subgenual anterior cingulate cortex Area 25 , broadly suppressed the intensity of motivations otherwise produced by simultaneous NAc microinjections, regardless of valence Richard and Berridge, Thus corticolimbic regulation adjusts both the intensity and valence of motivations produced by NAc circuitry.

Beyond identifying brain mechanisms that cause subjective feelings of pleasure or objective hedonic reactions, progress in affective neuroscience is also aided by pruning away previous candidates for pleasure generators that have failed to live up to their initial hedonic promise. The mesolimbic dopamine system has been the most famous neurochemical candidate in the past half century for a pleasure generator in the brain. The mesolimbic system contains dopamine neurons originating in or near the ventral tegmental area VTA of the midbrain, which chiefly ascend to the NAc or ventral striatum, as well as to amygdala, prefrontal cortex and neostriatum.

Mesolimbic dopamine systems clearly do play an important role in reward, but that role may not be as hedonic as once thought. However, today relatively few neuroscientists who study dopamine in reward appear to assert in print that dopamine causes pleasure. Even original proponents are no longer so enthusiastic. The decline in advocacy of the dopamine pleasure hypothesis stems from of a series of problems that arose in the past two decades.

The first problem specifically applied to the an hedonia versions that posited loss of pleasure. And human subjective ratings of drug pleasure e. Related questions have arisen recently about whether other types of clinical 'anhedonia' truly live up to their lack-of-pleasure label, such as in depression or of schizophrenia.

Conversely, dopamine stimulations do not reliably cause pleasure. The intensity of dopamine NAc surges even when evoked by addictive drugs e. Those intense motivations range from gambling to shopping, pornography, internet, hobbies, addictive drugs, or taking excessive medication in addictive fashion Callesen et al. Yet these cases typically do not report intense pleasure. An important goal in future for addiction neuroscience is to understand how intense motivation becomes narrowly focused on a particular target.

In addicts or agonist-stimulated patients, the repetition of dopamine-stimulation of incentive salience becomes attributed to particular individualized pursuits, such as taking the addictive drug or the particular compulsions. The control of this narrow directional focus for intense incentive salience may involve dopamine system interactions with learning-related structures, including amygdala-related circuitry Difeliceantonio and Berridge, ; Koob and Volkow, ; Mahler and Berridge, ; Robinson et al.

Another puzzle has been that if dopamine does not cause sensory pleasure, why are dopamine-promoting drugs such as cocaine or methamphetamine so pleasant? There are several potential answers, both psychological and neurobiological. That is, high incentive salience is just one component used to construct reward experiences together with high hedonic impact.

But on its own, elevated incentive salience induced by dopamine stimulation may to some extent be mistaken for pleasure itself. Drug enhancement of incentive salience could make other people, events or actions in the world all seem more attractive, and be powerfully enabling of engagement with them, which might well carry an aura of euphoria even if not truly hedonic. Viewed this way, subjective reward experience may be partly synthesized from motivation and cognitive appraisal components, similar to many other emotions Barrett et al.

This mistaken appraisal explanation may also apply to cases of electrode self-stimulation described below. A neural explanation for why cocaine is pleasant may be that cocaine and amphetamine also stimulate secondary recruitment of endogenous opioid and related neurobiological hedonic mechanisms, beyond directly raising dopamine release.

For instance, dopamine-stimulating drugs recruit elevation in nucleus accumbens of endogenous opioid and GABA signals Colasanti et al. However, hedonic effects might well change over time. A major alternative hypothesis is that dopamine acts as a teaching signal via prediction error or temporal difference computations to cause learning about rewards Schultz et al. In practice, it is often difficult to distinguish mesolimbic coding of reward learning from incentive motivation, because most studies rely purely on incremental learning to alter the motivation status of stimuli: learned predictive value and incentive value thus tend to co-vary together.

Further, a potential experimental confound present in many dopamine tracking experiments is that physiological state control of motivation is often clamped into a narrow constant range during all phases of the study e. By contrast, studies that allow relevant physiological states to fluctuate often do find consequent fluctuations in the motivational value of cues and in dopamine-related activity Cone et al. Future studies that incorporate fluctuation might better be able to assess if mesolimbic dopamine systems track motivational value more faithfully than learned prediction values.

Additional difficulties for the dopamine learning hypothesis comes from evidence questioning whether dopamine is actually needed for any particular type of reward learning, and conversely evidence that stimulation of dopamine does not reliably act as a causal teaching signal to establish new memories Berridge and Robinson, ; Eisenegger et al.

These issues have been discussed elsewhere, and no doubt will be discussed further in future, perhaps eventually producing clearer consensus on dopamine in reward learning Berridge, ; Berridge and O'Doherty, ; Collins and Frank, ; Schultz, Those were electrode sites that rats would work to activate or self-stimulate.

Self-stimulation sites typically were in the lateral hypothalamus LH or other points along the mesolimbic path, where electrodes can elicit surges in NAc dopamine release among other mechanisms Gallistel, ; Hernandez et al. However, Olds himself later revisited the question of whether actual pleasure was produced in the final publication of his career.

It deserves further study. We have been drawn to re-examine the literature on pleasure electrodes, and to question whether most electrodes actually produced pleasure. This finding arose from an investigation by one of us with Elliot Valenstein on the motivation versus hedonic properties of LH electrodes Berridge and Valenstein, One explanatory hypothesis at the time for why LH electrodes were not only self-stimulated, but also evoked intense spontaneous motivation directed at a natural reward, such as eating food, was that the stimulation essentially made the food or other reward more pleasant Hoebel, Still, of course, the electrodes might themselves have generated an internal pleasure state, regardless of any lack of effects on external hedonic stimuli.

The first were patients implanted in the s—s, who received electrode implants while institutionalized for depression, schizophrenia or other psychiatric conditions. B was never actually quoted as saying the stimulation felt pleasurable per se. Nor was he said to show behavioral signs of pleasure or to exclaim anything like "Oh -- that feels nice!

The electrode stimulation certainly never served as a substitute for sex. What it did instead was to make him want to engage more in sex -- just as it made him want the stimulation more, and to press the button so avidly. For both rat and humans, electrode sites would now be recognized to be located in or near the nucleus accumbens. Thick line shows electrode shaft, and red dots show stimulation points. In human brain, representation of ventral pallidum has been moved forward into the coronal plane of the electrode to show relative positions of NAc and VP.

Modified from Smith et al. Deep brain stimulation has resurged in the new millennium as a therapeutic technique for disorders ranging from chronic pain to depression, obsessive-compulsive disorder, and Parkinson's disease Boccard et al. Contemporary target sites for deep brain electrodes often include the nucleus accumbens and the subthalamic nucleus, the subgenual cingulate cortex, and fibers descending from prefrontal cortex through the internal capsule.

A woman with a deep brain electrode in the subthalamic nucleus was reported, upon initial activation of her electrode, to act "in love with two neurologists, and tried to embrace and kiss people" Herzog et al. Subsequently she became motivationally focused on intense shopping, to the point of engaging in binges of "unrestrained buying of clothes". However, rather than this being a purely happy exhilaration, the continued subthalamic stimulation increasingly made her more suspicious, tense and hostile.

She developed a "delusion that her sons were conspiring against her, and she said that they tried to get her money by threat of force" all p. At sites in the nucleus accumbens, deep brain stimulation has been reported to produce sudden feelings of desire to engage in a particular activity, such as visiting a nearby landmark or taking up again an old hobby Schlaepfer et al. Indeed, the patients were usually unable to tell even whether their NAc electrode was on or off.

Whether these activities actually would be made more pleasurable by NAc stimulation remains unknown. We remain open on this question, and acknowledge that a lack of evidence in cases above does not mean that no electrode ever causes pleasure.

It is just that most published cases appear to not be very pleasant in our view. It would be valuable to have more studies of contemporary deep brain stimulation effects on human pleasure. Finally, we do not doubt that some electrodes may at least reduce negative affect, producing escape from distress or pain Mayer et al. One of us MLK has witnessed dramatic relief in chronic pain patients when deep brain stimulation is turned on in targets such as the periaqueductal gray and anterior cingulate cortex Kringelbach et al.

Similarly, relief from anxiety or depression may be produced by some deep brain stimulations of NAc or prefrontal cortex, resulting in positive engagement in social or leisure activities Bewernick et al. Thus it may well be that part of the mood-enhancing effects of much brain stimulation comes from alleviation of unpleasant affective states Boccard et al. Deep brain stimulation and neuropharmacological dopamine activations seem to dissociate this natural constellation, engaging only one or two of the three components.

Such a person is likely to be confused by the unfamiliar decoupling among reward components, and may fail to recognize what is happening. This hypothesis could be probed by more sophisticated studies of pleasure during brain stimulation.

Reversing the hedonic valence of the experience would not necessarily disrupt its motivating power. The idea that incentive motivation can be distressing is not new. In other words, mesolimbic motivation can be plastic in hedonic valence. Motivational salience is never neutral, but its valence is not fixed. Fearful salience makes the percept equally attention-grabbing yet perceived as potential threat.

Yet the hedonic valence of the entire experience can be ambiguous. Incentive salience can occur either as eager anticipation, or as negative frustration as in Tantalus. In other situations, the overall hedonic experience of fearful salience might flip to positive, as in roller coasters or horror movies. Our approach to the affective neuroscience of pleasure has combined perspectives from human and animal studies, aiming to recognize both subjective feelings and objective hedonic reactions, and to give a more accurate mapping between brain circuitry and affective processes.

We believe such new insights are emerging, as described above. Time will further assess the validity of these new conclusions, and if confirmed, we think they may aid in better understanding of both normal pleasures and affective psychopathologies. Eventually the goal is to contribute to more effective and safer treatments for affective disorders, as well as understanding of affective wellbeing.

Finally, evidence gained may inspire future affective neuroscientists to further refine the search for the neural underpinnings of pleasure, which remains an important motivating factor for many people and without which life too often becomes meaningless. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication.

As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

Author manuscript; available in PMC May 6. Kent C. Berridge 1 and Morten L. Kringelbach 2, 3. Morten L. Author information Copyright and License information Disclaimer. Copyright notice. The publisher's final edited version of this article is available at Neuron. See other articles in PMC that cite the published article. Abstract Pleasure is mediated by well-developed mesocorticolimbic circuitry, and serves adaptive functions.

Open in a separate window. Figure 1. Evolutionary origins of brain systems for hedonic reactions The ultimate explanation for why pleasure encompasses both objective and subjective levels of reaction likely lies in evolutionary history. Mapping pleasure in the brain The experience of one pleasure often seems very different from another. Figure 2. Three-dimensional comparison of hedonic sites in rat brain left and human brain right A. Figure 3.

Hedonic coding in the human orbitofrontal cortex OFC In humans, the orbitofrontal cortex is an important hub for pleasure coding, albeit heterogeneous, where different sub-regions are involved in different aspects of hedonic processing. Mapping brain pleasure generators? Causal hedonic hotspots for hedonic enhancements Yet hedonic gains of function can be produced by neural events in several forebrain structures, resulting in intense pleasure reactions.

Hotspots at top and bottom of the brain? Interaction between hotpot site and neurochemical stimulation Hotspots generate hedonic enhancement through an interaction between their specific anatomical site and their particular neurochemical state or mode of stimulation. Figure 4. Multiple anatomical modules in NAc shell The number of differently-valenced rostrocaudal keys contained in the nucleus accumbens shell is difficult to estimate, and in practice is defined somewhat arbitrarily by the size of the microinjections used to tap the keyboard.

Retuning the affective keyboard Strikingly, the valence of desire-dread motivations generated by the NAc keyboard is not necessarily fixed by anatomical location, but can be powerfully retuned psychologically for many sites by emotional factors such as the valenced ambience of an environment Figure 4. Mesolimbic dopamine and the an hedonia hypothesis The mesolimbic dopamine system has been the most famous neurochemical candidate in the past half century for a pleasure generator in the brain.

Resolving the cocaine puzzle? Dopamine and reward learning? Figure 5. False pleasure electrodes? Modern Deep Brain Stimulation Deep brain stimulation has resurged in the new millennium as a therapeutic technique for disorders ranging from chronic pain to depression, obsessive-compulsive disorder, and Parkinson's disease Boccard et al. Conclusion: Building a fruitful affective neuroscience of pleasure Our approach to the affective neuroscience of pleasure has combined perspectives from human and animal studies, aiming to recognize both subjective feelings and objective hedonic reactions, and to give a more accurate mapping between brain circuitry and affective processes.

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Food deprivation does not potentiate glucose taste reactivity responses of chronic decerebrate rats. As the action is sampled from the generated policy, QF-TraderNet adopts a soft profit-and-loss control strategy rather than the deterministic TP and SL. An equivalent way to interpret our strategy is that our model trades with long buy if the decision is made in positive QPL. In reverse, short sell transactions will be delivered. Once the trading direction is decided, the target QPL with the maximum probability will be considered as the soft target price S-TP , and the soft stop loss line will be the QPL with the highest probability in the opposite trading direction.

One exemplification is presented in Figure 4. A case study illustrates our profit-and-loss control strategy. The trading policy is uniformly distributed initially. It will think whether there is a better target price for settlement in the entire action space. We conduct the empirical evaluation for our QF-TraderNet in various types of financial datasets.

In our experiment, eight datasets from 4 categories are used, including 1 foreign exchange product: Great Britain Pounds vs. The evaluation is conducted from the perspective of earning profits; and the robustness when agents face the unexpected change of market states. We also investigate the impact of different settings of our proposed QPL based action space search for RL trader, and the ablation study of our model. All datasets utilized in experiments are fetched from the free and opened historical data center in MetaTrader 4 , which is a professional trading platform for the FOREX, financial indices, and other securities.

The rest will be utilized as out-of-sample verification, i. To be noticed, the evaluation period has covered the recent fluctuations in the global financial market caused by the COVID pandemic, which could be utilized as the robustness test when the trading agent is handling the unforeseen market fluctuations.

The size of look-back window is set at 3, and the metrics regarding price return and Sharpe ratio is daily calculated. In the backtest, initial capital is set to the corresponding currency or asset with a value of 10,, at a transaction cost with 0. To compare our model with the traditional methods, we select the forecasting based trading model and other state-of-the-art reinforcement learning-based trading agents as the baseline.

This strategy is used to measure the overall performance of the market during this period T , by holding the product consistently. Following the idea of Deep Direct Reinforcement, but we apply the principal component analysis PCA to denoise and composes data. It trades with a Buy-Winner-Sell-Loser strategy. This model could be admitted as our model without the deep feature representation block.

A state-of-the-art direct reinforcement RL trader following the one-product trading, by using the fuzzy representation and deep autoencoder to extract the features. The size of action space is 3. Regarding the training settings, the Adaptive Moment Estimation ADAM optimizer with 1, training epochs is used for all iterative optimization models at a 0. The reason is that our experimental results show our model can perceive the market state good enough in these settings. For the sake of computational complexity, we remove the extra input features.

The CPR is formulated with,. The result of Market denotes that the market is in a downtrend with high volatility in the evaluating interval, due to the recent global economic fluctuation. The price range in testing is not fully covered in training data in some datasets crude oil and AUDUSD , which tests the models in an unseen environment. QFTN-L is also comparable to the baselines.

It signifies the profitability and robustness of our QF-TraderNet. The ablation study in Table 2 also presents the contribution of each component in detail Supervised counts from the average of Rf and Fcm , where the QPL actions dramatically contribute to the Sharpe Ratio of our full model. These demonstrates the benefit of trading with QPL to gain considerable profitability and efficient risk-control ability. It is the only strategy for earning a positive profit on almost all datasets, which is because the day-trading strategy are less affected by the market trend, compared with other strategies in long, neutral, and short setting.

We also find that the performance of our model in FOREX datasets is significantly better than others. FOREX contains more noise and fluctuations, which indicates the advantages of our models in highly fluctuated products. QFTN-7 might have multiple ground truths, as the payoff might be the same while settlement in varied QPLs, thus we only report the accuracy.

We visualize the reward in the training process and the actions made in testing as shown in Figure 6. We analyze that the better performance of QFTN-U is due to the more accurate judgment of trading direction see their accuracy in the trading direction classification. When the agent perceives changes in the market environment confidently, it can select the QPL farther than the ground state as the target price for order closing, rather than only the first positive or negative QPL, thereby obtaining more potential payoff, although the action might not be optimal.

In this section, we compare the average CPR and SR among 8 datasets versus different settings of the action space size in Figure 7. We observe that when the size of the action space is less than 7, increasing this parameter has a positive effect on system performance. Especially, Figure 5 shows that our lite model fails in the HSI dataset but the ultra one achieves strong performance. We argue this is because the larger action space can potentially contribute to trading with complex strategies.

We analyze as that the action space of the daytrade model should cover the optimal settlement QPL global ground truth within the daily price range ideally. However, if the action space has covered the ground truth already, it is meaningless to continue to expand the action space. On the contrary, a large number of candidate actions can make the decision to be more difficult.

We report the results for each dataset in the supplementary. With a QPL inspired probabilistic loss-and-profit control for the order settlement, our model substantiate the profitability and robustness in the intraday trading task. Experiments reveal our QF-TraderNet outperforms other baselines. To perform intraday trading, we assumed the ground state in t -th day is available for QF-TraderNet in this work. One interesting future work will be combining QF-TraderNet with the state-of-the-art forecasters to perform real-time trading by a predictor-trader framework in which a forecaster predicts the opening price in t -th day for our QF-TraderNet to perform trading.

Writing and Editing. YQ: Implementation and Experiment, Editing. YY: Visualization. Implementation and Experiment. ZC: Implementation and Experiment. RL: Supervision, Reviewing and Editing. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers.

Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher. Chen, C. Google Scholar. Chen, J. Expert Syst. Colby, R. The Encyclopedia of Technical Market Indicators. Dempster, M. Deng, Y. IEEE Trans. Neural Netw. Gers, F. Learning to Forget: Continual Prediction with Lstm. Neural Comput. Giudici, P. Libra or Librae? Finance Res.

Huang, D. Data Eng. Lee, R. Fuzzy Syst. Singapore: Springer. Li, Z. Marques, N. Meng, X. Physica A: Stat. Mohan, S. Moody, J. Learning to Trade via Direct Reinforcement. Neely, C. Pagnottoni, P. Peralta, G. A Network Approach to Portfolio Selection. Empirical Finance 38, — Pichler, A. Financial Stab. Resta, M. Risks 8, Sutton, R. Reinforcement Learning: An Introduction.

Tran, D. Vella, V. Wang, J. Wei, B. Plos One 12, e

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Is the price of gold going down Committees of the Board. Risks 8, However, a causal caveat may be needed here. We currently intend to retain future earnings, if any, to finance the expansion of our business. A familiar adult can employ this responsiveness to build up play sequences predictably progressing from smiling, through giggling, to laughter and great excitement on the part of the child. Fair values were assumed to approximate carrying values for cash and payables because they are short term in nature and their carrying amounts approximate fair values or they are payable on demand. In such event, any commissions received by the broker-dealers or agents and any profit on the resale of the shares purchased by them may be deemed source be underwriting commissions or discounts under the Securities Act.
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Bruce greenwald in his book value investing Any of these factors could cause our stock price to decline and result in our stockholders losing a portion or all of their investments. If we are unable to fund our business through operations or raise sufficient additional funds, we will have to develop and implement a plan to further extend payables, reduce overhead, or scale back our current business plan until sufficient additional capital is raised to support increased operations. The trading policy is uniformly distributed initially. Expenses, Indemnification. Huang, D. In this event, our stockholders could lose some or all of their investment.

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