Directional Movement Index

AppId is over the quota
AppId is over the quota

The Directional Movement Index (also known as DMI) is a momentum indicator that was developed by J. Welles Wilder. It is calculated using the price, compares the current price with the previous price range, and displays the result as an upward movement line (+DI), and a downward movement line (-DI), between 0 and 100. The DMI also calculates the strength of the upward or downward movement, and displays the result as a trend strength line (ADX). The DMI is displayed on its own chart, separate from the price bars, and is the lower section in the chart shown above.

Description: The DMI is the ratio of exponential moving averages of the greater of the upward (U) and downward (D) price movements, and the true range (TR). Calculation:
U = Hn - Hn-1
D = Ln-1 - Ln
TR = (Hn - Ln) | (Hn - Cn-1) | (Cn-1 - Ln)
EMAUP = EMAUn-1 + ((2 / (n + 1)) * (Un - EMAUn-1))
EMADOWN = EMADn-1 + ((2 / (n + 1)) * (Dn - EMADn-1))
EMATR = EMATRn-1 + ((2 / (n + 1)) * (TRn - EMATRn-1))
+DI = EMAUP / EMATR
-DI = EMADOWN / EMATR

    DX = ABS(+DI - -DI) / (+DI + -DI)
ADX = EMADXn-1 + ((2 / (n + 1)) * (DXn - EMADXn-1))

The Directional Movement Index can be used in both ranging and trending markets. In general, when the +DI line is above the -DI line, the market is moving upwards, and when the -DI line is above the +DI line, the market is moving downwards. The ADX line shows the strength of the move, and the market is considered to be trending when the ADX line is above 30, and ranging when the ADX line is below 30. There are several trading systems that use the DMI, so there are several alternative uses of both the DI lines, and the ADX line.

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Does abnormal non-rapid eye movement sleep impair declarative memory consolidation? Disturbed thalamic functions in sleep and memory processing

a Yeshiva University: Ferkauf Graduate School of Psychology, Rousso Building, 1165 Morris Park Avenue, Bronx, NY 10461, United Statesb Department of Psychiatry and Psychotherapy, University Hospital Schleswig-Holstein, University of Kiel, GermanyReceived 10 July 2010. Revised 30 July 2011. Accepted 1 August 2011. Available online 1 September 2011.View full text Non-rapid eye movement (NREM) sleep has recently garnered support for its role in consolidating hippocampus-based declarative memories in humans. We provide a brief review of the latest research on NREM sleep activity and its association with declarative memory consolidation. Utilizing empirical findings from sleep studies on schizophrenia, Alzheimer’s disease, and fibromyalgia, we argue that a significant reduction of slow-wave sleep and sleep spindle activity contribute to the development of deficits in declarative memory consolidation along with concomitant sleep disturbances commonly experienced in the aforementioned disorders. A tentative model is introduced to describe the mediating role of the thalamocortical network in disruptions of both declarative memory consolidation and NREM sleep. The hope is to stimulate new research in further investigating the intimate link between these two very important functions.

prs.rt("abs_end");NREM sleep; Sleep spindles; Slow-wave sleep; Declarative memory consolidation; Hippocampus; Thalamocortical network; Schizophrenia; Alzheimer’s disease; Fibromyalgia syndrome

Figures and tables from this article:

Fig. 1. During NREM sleep, abnormal thalamocortical structures may be unable to generate sufficient slow oscillations to drive the reactivation of hippocampal memory traces. These same structures may also be unable to facilitate normal spindle activity, preventing efficient declarative memory consolidation due to an absence in cortical plastic changes. Decreases in spindle activity lead to failure in inhibiting sensory information from reaching the neocortex. Thus, the individual is awakened and kept awake by sensory information, consequently experiencing disturbed NREM sleep.

View Within ArticleCopyright © 2011 Elsevier Ltd. All rights reserved.

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View the original article here

Does abnormal non-rapid eye movement sleep impair declarative memory consolidation? Disturbed thalamic functions in sleep and memory processing

a Yeshiva University: Ferkauf Graduate School of Psychology, Rousso Building, 1165 Morris Park Avenue, Bronx, NY 10461, United Statesb Department of Psychiatry and Psychotherapy, University Hospital Schleswig-Holstein, University of Kiel, GermanyReceived 10 July 2010. Revised 30 July 2011. Accepted 1 August 2011. Available online 1 September 2011.View full text Non-rapid eye movement (NREM) sleep has recently garnered support for its role in consolidating hippocampus-based declarative memories in humans. We provide a brief review of the latest research on NREM sleep activity and its association with declarative memory consolidation. Utilizing empirical findings from sleep studies on schizophrenia, Alzheimer’s disease, and fibromyalgia, we argue that a significant reduction of slow-wave sleep and sleep spindle activity contribute to the development of deficits in declarative memory consolidation along with concomitant sleep disturbances commonly experienced in the aforementioned disorders. A tentative model is introduced to describe the mediating role of the thalamocortical network in disruptions of both declarative memory consolidation and NREM sleep. The hope is to stimulate new research in further investigating the intimate link between these two very important functions.

prs.rt("abs_end");NREM sleep; Sleep spindles; Slow-wave sleep; Declarative memory consolidation; Hippocampus; Thalamocortical network; Schizophrenia; Alzheimer’s disease; Fibromyalgia syndrome

Figures and tables from this article:

Fig. 1. During NREM sleep, abnormal thalamocortical structures may be unable to generate sufficient slow oscillations to drive the reactivation of hippocampal memory traces. These same structures may also be unable to facilitate normal spindle activity, preventing efficient declarative memory consolidation due to an absence in cortical plastic changes. Decreases in spindle activity lead to failure in inhibiting sensory information from reaching the neocortex. Thus, the individual is awakened and kept awake by sensory information, consequently experiencing disturbed NREM sleep.

View Within ArticleCopyright © 2011 Elsevier Ltd. All rights reserved.

prs.rt('data_end');

View the original article here

Does abnormal non-rapid eye movement sleep impair declarative memory consolidation? Disturbed thalamic functions in sleep and memory processing

a Yeshiva University: Ferkauf Graduate School of Psychology, Rousso Building, 1165 Morris Park Avenue, Bronx, NY 10461, United Statesb Department of Psychiatry and Psychotherapy, University Hospital Schleswig-Holstein, University of Kiel, GermanyReceived 10 July 2010. Revised 30 July 2011. Accepted 1 August 2011. Available online 1 September 2011.View full text Non-rapid eye movement (NREM) sleep has recently garnered support for its role in consolidating hippocampus-based declarative memories in humans. We provide a brief review of the latest research on NREM sleep activity and its association with declarative memory consolidation. Utilizing empirical findings from sleep studies on schizophrenia, Alzheimer’s disease, and fibromyalgia, we argue that a significant reduction of slow-wave sleep and sleep spindle activity contribute to the development of deficits in declarative memory consolidation along with concomitant sleep disturbances commonly experienced in the aforementioned disorders. A tentative model is introduced to describe the mediating role of the thalamocortical network in disruptions of both declarative memory consolidation and NREM sleep. The hope is to stimulate new research in further investigating the intimate link between these two very important functions.

prs.rt("abs_end");NREM sleep; Sleep spindles; Slow-wave sleep; Declarative memory consolidation; Hippocampus; Thalamocortical network; Schizophrenia; Alzheimer’s disease; Fibromyalgia syndrome

Figures and tables from this article:

Fig. 1. During NREM sleep, abnormal thalamocortical structures may be unable to generate sufficient slow oscillations to drive the reactivation of hippocampal memory traces. These same structures may also be unable to facilitate normal spindle activity, preventing efficient declarative memory consolidation due to an absence in cortical plastic changes. Decreases in spindle activity lead to failure in inhibiting sensory information from reaching the neocortex. Thus, the individual is awakened and kept awake by sensory information, consequently experiencing disturbed NREM sleep.

View Within ArticleCopyright © 2011 Elsevier Ltd. All rights reserved.

prs.rt('data_end');

View the original article here