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تست روانشناسی سه بعدی موضوع: تست روانشناسی سه بعدی 4:52 این تصویر در حقیقت ثابت و بدون حرکت میباشد . اگر آنرا متحرک میبینید به فشارهای روانی شما مربوط میباشد هر چه سرعت حرکت در تصویر بیشتر دیده شود فشارهای روانی بیننده نیز بیشتر میباشد و بالعکس نوشته شده توسط حسین نجفی | لینک ثابت |
برنامه های بدون نیاز به نصب
(PORTABLE) از ویندوز گرفته تـــــــــــا یاهو در اینجا Free-portable.Blogfa.com نوشته شده توسط حسین نجفی | لینک ثابت |
مقاله در مورد (بحران هويت) An Identity Crisis? Examining IMF Financial Programming William Easterly Abstract: The IMF uses its well-known “financial programming” model to derive monetary and fiscal programs to achieve desired macroeconomic targets in countries undergoing crises or receiving debt relief. This paper considers under what conditions financial programming would work best, and then tests those conditions in the data. The key restrictions of financial programming are assumptions about exogeneity of some components of identities with respect to others, and the assumption of stable and “reasonable” parameters for some very simple behavioral relationships. In at least the literal applications of the framework, financial programming does not do well in forecasting the target variables, even when some components of the identity are known with certainty. Acknowledgements: I am grateful for comments by Maria Carkovic, Shanta Devarajan, Atish Ghosh, Chang-Tai Hsieh, Joshua Greene, John Karlik, George Kopits, Ross Levine, Jacques Polak, Lant Pritchett, Miguel Savastano, Sergio Schmukler, Charles Sisson, E. Tanner, Axel Van Trotsenburg , Jos Verbeek and three anonymous referees. One of the most widely used applied models in macroeconomics is the financial programming (FP) model of the International Monetary Fund. The IMF utilizes the monetary, balance of payments, and fiscal identities in its design of macroeconomic programs ادامه مطلب نوشته شده توسط حسین نجفی | لینک ثابت |
Telomere identity crisis(بحران هویت) Telomere identity crisis Bridget L. Baumgartner1,2 and Vicki Lundblad1,3 1Salk Institute for Biological Research, Biology, Baylor College of Medicine, Houston, Texas 77030, USA Cells are designed to be intolerant of breaks in DNA, yet it is critical that cells do not identify the ends of linear chromosomes, called telomeres, as damaged DNA ends. Telomeres therefore must somehow prevent the recognition and subsequent repair of chromosome ends as double-strand breaks (DSBs), although how this is achieved is poorly understood. Chromosomal breaks can occur as a result of ionizing radiation, DNA replication across nicked DNA, or as intermediates of recombination. Whether these breaks are induced by the cell—for example, due to V(D)J recombination during lymphocyte development—or arise as a consequence of spontaneous damage, it is imperative that such lesions be repaired in order to prevent genomic rearrangements or even outright chromosome loss (Bassing and Alt 2004). The cell avoids such deleterious consequences by mounting a response, called the DNA damage checkpoint, which pauses the cell cycle, thereby permitting the efficient recruitment of a highly conserved set of proteins to the break (Zhou and Elledge 2000; Nyberg et al. 2002). In the budding yeast Saccharomyces cerevisiae, this process has been studied extensively using an experimental system that allows the creation of a single DSB at high frequency at a defined site, through the action of a sequence-specific endonuclease, HO (Rudin and Haber 1988). The DNA damage checkpoint is alerted to the presence of the HO-generated break by recruitment of sensor proteins, such as Tel1/ATM and Mec1/ATR, to the site of damage (Lisby et al. 2004; Garber et al. 2005). These kinases activate downstream effector proteins, Rad53/CHK2, Rad9, and Dun1, which in turn facilitate the activation of repair proteins. Repair of DSBs requires the recognition of these broken ends by the Ku70/80 heterodimer and the Mre11–Rad50–Xrs2 complex (MRX, or MRN in humans). The cell then has a choice between two pathways for DNA repair. If DSBs are repaired through the nonhomologous end-joining pathway (NHEJ), DNA ligase 4 is brought in to seal the two ends together. If the repair is accomplished by homologous recombination, the DSB is first processed by an exonuclease to reveal a single-stranded 3_ overhang, which subsequently initiates recombination with homologous sequences present in the genome. Functional DNA damage checkpoints also act to inhibit cell cycle progression in the presence of damaged DNA. Even a single DSB is sufficient to cause the cell cycle to arrest until repair is completed (Sandell and Zakian 1993), thereby ensuring that cells do not progress through mitosis until the integrity of the genome has been restored. Despite the presence of a highly efficient machine for the recognition of DSBs, the ends of linear chromosomes are natural DNA termini that must somehow be masked from triggering the DNA damage checkpoint and subsequent repair events. This unique property of telomeres is owed to the sequence and structure of the telomere DNA itself, as well as to the proteins that localize to chromosome ends (Blackburn 2001; Smogorzewska and de Lange 2004). In most eukaryotes, telomeres are composed of tandem G-rich repeats that terminate with a 3_ singlestranded overhang of the G-rich strand, often referred to as a G-tail. Disruption of this G-tail structure, due to either loss of the G-tail itself or exposure of the C-strand to nucleolytic attack, is a lethal event for the cell. Thus, cells have developed a dynamic protein assembly that maintains a telomere “cap.” In budding yeast, this cap depends in part on the essential single-strand telomerebinding protein Cdc13, along with several Cdc13-interacting factors. Loss of the Cdc13 complex exposes yeast telomeres to massive resection of the C-strand, with the resulting 20–30-kb region of exposed single-stranded DNA provoking arrest of the cell cycle (Weinert et al. 1994; Garvik et al. 1995; Booth et al. 2001). A second protein, Rap1, which is bound to duplex telomeric repeats, may aid in protection of the other strand of the telomere, the G-strand overhang: Depleting cells of Rap1 causes telomere fusions that are mediated through the NHEJ pathway (Pardo and Marcand 2005). Mammalian cells also possess a mechanism to protect the vulnerable G-tail, which similarly relies on a duplex telomere DNA-binding factor called TRF2. In TRF2-deficient cells, the integrity of the terminal G-strand overhang is disrupted, resulting in high frequencies of end-to-end fusions (van Steensel et al. 1998; Celli and de Lange 2005). This TRF2-mediated telomere capping activity may be aided by the ability of telomeres to fold into a looped structure, called the t-loop, wherein the 3_ overhang invades the duplex region of telomere repeats (Griffith et al. 1999). Not unexpectedly, normal telomeres rarely interact with DSBs. However, loss of telomere repeats can lead to “repair” of chromosome ends, through either recombination (Lundblad and Blackburn 1993; Bryan et al. 1995) or end-to-end fusions (Smogorzewska et al. 2002). The latter situation creates dicentric chromosomes, which are unstable in dividing cells. Dysfunctional telomeres can be created experimentally, through genetic manipulation of telomere-associated components or by altering the sequence of the telomere repeats themselves. Human cells, in which telomerase expression has been down-regulated, can also accumulate eroded telomeres as a consequence of continual cell division. In both cases, critically shortened telomeres trigger a damage response that prevents the cells from dividing in the absence of intact chromosome ends. Cells can, however, escape this block to proliferation (albeit at very low frequencies) and continue to divide in the absence of functional telomeres, but at a price: Such “escapees” display massive levels of chromosomal rearrangements, illustrating the importance of telomeres for genome stability. Given all this, it is tempting to assume that telomeres prevent components of DNA damage-responsive pathways from interacting with the ends of chromosomes. However, the situation is more complicated, as many of the genes required for DNA repair are also necessary for normal telomere maintenance (Maser and DePinho 2004). The intertwining of DSB repair and telomere maintenance extends to pathways involved in signaling damage, as well as to those responsible for the actual repair of damage. For example, the members of the NHEJ pathway are intimately involved in telomere maintenance. This is paradoxical considering it is the NHEJ pathway that causes the fusion of chromosomes when telomeres become dysfunctional, and yet, the components of this pathway affect multiple facets of telomere metabolism. In yeast, the Ku heterodimer exhibits a robust association with telomeres and is required for capping, modulation of subtelomeric gene expression, and even telomere length regulation as the result of a direct interaction with the telomerase holoenzyme (Bertuch and Lundblad 2003). Likewise, deletion of any of the MRX subunits leads to telomere shortening (Boulton and Jackson 1998), possibly because telomere-specific proteins such as Cdc13 fail to be recruited to telomeres in the absence of MRX function (Diede and Gottschling 2001; Takata et al. 2005)... ادامه مطلب نوشته شده توسط حسین نجفی | لینک ثابت |
Eye movement theory Eye movement theory
نوشته شده توسط حسین نجفی | لینک ثابت |
EMDR - Eye Movement Desensitization and Reprocessing
The treatment is fairly complex and includes elements from several different schools of therapy. There are eight stages to the treatment technique, and they draw from different approaches and orientations. The most unusual part of the treatment involves the therapist waving his or her fingers back and forth in front of the client's eyes, and the client tracking the movements while focusing on a traumatic event. The act of tracking while concentrating seems to allow a different level of processing to occur. The client is often able to review the event more calmly or more completely than before. EMDR also includes a strong cognitive-behavioral component. Clients are asked to come up with a negative belief about themselves which resulted from the trauma, and asked "What would you rather believe about yourself?" At various points the client rates their level of emotions and the extent to which they believe this new belief. How does it work? That's one of the mysteries. Shapiro proposes an "accelerated information processing theory" mechanism. In earlier writings she speculated on the relationship between the eye movements and the eye movements in REM sleep. Another interesting theory has been presented online in the paper "An Orienting Reflex/External Inhibition Model of EMDR and Thought Field Therapy" by Nathan R. Denny, Ph.D. Denny speculates that both EMDR and "Thought Field Therapy" work by a common mechanism. He states that the eye movements elicit the orienting reflex, and that this reflex is incompatible with the fight-or-flight response. I asked Dr. Shapiro about this theory in her online forum An EMDR Discussion with Francine Shapiro. This forum on Behavior Online is a fascinating opportunity to discuss these issues with the psychologist who developed the technique. A portion of her reply: The inhibition of a fight or flight mechanism is intriguing. However, as I stipulated in the text, hypotheses regarding potential effects of the eye movements alone are insufficient to account for the wide range of treatment effects. For that one has to look at an interaction of the all the various procedural elements. (Shapiro, 1997) Suzanne Hurst and Natasha Milkewicz have written a review of the research in a paper entitled Eye Movement Desensitization and Reprocessing - A Controversial Treatment Technique. They conclude that EMDR deserves further research because of the surprisingly positive results from a number of studies. In their review they note that Shapiro has been criticized for insisting that all EMDR training be done by herself and a select group of people that she has trained. Her organization thus stands to profit from all of the training. Some of the criticism has been muted since she published Eye Movement Desensitization and Reprocessing : Basic Principles, Protocols, and Procedures in 1995. This book explains the technique in detail so that researchers can fully examine it. Clinicians are still encouraged to receive training in this complex procedure. I've been trained in EMDR and I use it at times in my practice. I have seen it work extremely well to relieve trauma symptoms in a short period of time, but it does not seem to work for everyone. We need more research and study to determine who this treatment works best for. نوشته شده توسط حسین نجفی | لینک ثابت |
Visual-motor transformations for smooth pursuit eye movements
When a small, smoothly moving object appears, primates are able to generate a smooth eye movement having a velocity nearly equal to the velocity of the target. The basic anatomical circuit for pursuit is known -- from retina to motoneuron. We are trying to understand how visual inputs related to moving targets are converted by the brain to commands for motor action. In the past 5 years, we have discovered that pursuit is a complex voluntary motor behavior that comprises many components. These include: the representation of target motion with respect to the eye, primarily in extrastriate area MT (Lisberger & Movshon 1999; Osborne et al 2004); pooling of the population response in MT to acquire good estimates of the direction and speed of target motion (Churchland & Lisberger 2001; Gardner et al 2004); an on-line volume control that regulates how strongly visual inputs are transmitted to the motor system (Tanaka & Lisberger 2001); the ability to choose targets based on a spatial window of motor attention under the control of orienting, saccadic eye movements (Gardner & Lisberger 2002); learning based on the recent history of target motions (Chou & Lisberger 2004; Medina & Lisberger 2005); and cerebellar compensation for the physical properties of the eye and orbit. Our work is currently focusing on two main concepts. 1) We are using theoretical approaches to exploit the variation in natural pursuit behavior and neural responses. Our goal is to correlate the variation in neural and motor behavior as a way of understanding how different groups of neurons contribute to pursuit behavior. Recent unpublished results have revealed that the variation in pursuit behavior can be understood in terms of errors in estimates of the direction, speed, and time of onset of target motion. The coordinate system of the variations implies pursuit operates at the precision to sensory coding, and that motor noise may arise primarily from sensory representations. By relating variations in sensory representation to variations in motor behavior, we will understand how neurons pool the sensory population response to generate eye movements. 2) We are using a combination of precise measurements of eye movement, electrical stimulation, and neural recordings to evaluate the neural basis for modulation of the strength of visual transmission to the motor system. We have evidence that the neural mechanism of this "gain" modulation is related to learning, target choice, and motor attention. Our goal is to identify the neural loci and mechanisms of gain modulation, learning, and target choice. نوشته شده توسط حسین نجفی | لینک ثابت |
Toward a Neurophysiologically-based Theory of Eye Movement Control During Reading Toward a Neurophysiologically-based Theory of Eye Movement Control During Reading
Yang & McConkie (Vision Research, in press) describe the beginnings of a theory of eye movement control during reading, based on a neurophysiological framework of eye movement control proposed by Findlay & Walker (1999, Brain & Behavior Science). This paper will develop the theory more fully, describing, in terms of activation and inhibition within the oculomotor system, the normal operation of eye movement control during reading, possible ways in which eye behavior is modified in response to task and stimulus characteristics, and how the system responds to processing difficulties. The paper will describe how certain puzzling observations can be explained within this theory (i.e., the many saccades that are uninfluenced by current stimulus characteristics, lack of a relation between fixation duration and whether a word is skipped, relatively flat hazard curve for longer fixation durations). It will also point out issues that arise within the frame of reference of this type of theory, such as the time course of the onset and dissipation of saccade inhibition when processing difficulties are encountered, and how activation and inhibition influence saccade length and direction. نوشته شده توسط حسین نجفی | لینک ثابت |
CAN EYE MOVEMENTS CURE MENTAL AILMENTS?
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Copyright 2006 - Designer: Penguin Network >Hessam Sedaghati