Science topic

Biological Psychology - Science topic

Behavioral neuroscience, also known as biological psychology, biopsychology, or psychobiology is the application of the principles of biology (in particular neurobiology), to the study of physiological, genetic, and developmental mechanisms of behavior in human and non-human animals. It typically investigates at the level of nerves, neurotransmitters, brain circuitry and the basic biological processes that underlie normal and abnormal behavior.
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Hello,
I would love to receive some recommendations from experts in regards to the topic, whether there are valid findings in research on biological markers for anxiety disorders. I am trying to gain some stable insight and be able to argue in favor of the notion, that no anxiety disorder "comes from a malfunction/sickness of the brain".
Thank you in advance!
Best
Ivo
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Galvanic Skin Response (GSR) varies from person to person. How to set a baseline for GSR considering parameters such as probe-type, probe-material, skin moisture level, blood pressure, temperature and stress-level which can affect the result?
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Hi, in our recent research , we used zero affection pictures at start and end of target pictures , then we have plan to subtract GSR values as baseline, however our paper is not published yet, we may get some comments in review. Hope this helps
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To Whom It May Concern,
To Whom So Ever Interested..
We are a research group from different countries (Palestine, Jordan, India, Malaysia, Germany, Turkey, UK, USA) who are interested in investigating personality traits as well mental disorders from different perspectives, biological, psychological, and socio-cultural domains.
For those who find themselves having the potential to collaborate in data collection (in some cases already we have a plenty enough bulk of raw data), surveying and reviewing the related literature reviews, writing per the APA style, analyzing, interpreting results and drawing conclusions, etc..
Please, send your statement letter of interest to: wael.abuhasan@aaup.edu, and kindly determine where you are most fitting to play a role in such a research project.
Sincerely yours,
Wael M. F. Abuhasan
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Interested
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Biological Psychology
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Well, I do not know what kind of serotonin articles you would like, but in the mean time I found these. You may look them up in google for the full articles.
Berumen, L. C., Rodríguez, A., Miledi, R., & García-Alcocer, G. (2012). Serotonin receptors in hippocampus. The Scientific World Journal, 2012.
Brummelte, S., Mc Glanaghy, E., Bonnin, A., & Oberlander, T. F. (2017). Developmental changes in serotonin signaling: Implications for early brain function, behavior and adaptation. Neuroscience, 342, 212-231.
Shad, K. F. (2017). Introductory Chapter: Serotonin-The Most Ancient Neurotransmitter, Hormone and Trophic Factor. Serotonin: A Chemical Messenger Between All Types of Living Cells, 1.
Shad, K. F. (2017). Serotonin-A Chemical Messenger Between All Types of Living Cells.
Young, S. N. (2007). How to increase serotonin in the human brain without drugs. Journal of psychiatry & neuroscience: JPN, 32(6), 394.
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Slow breathing, usually at frequency of 0.1 Hz, is a method of relaxation and supposed to increase parasympathetic activity. Heart rate variability is used as a marker for autonomic response to such intervention. In the frequency domain of HRV analysis, the HF power is considered as a marker of vagal modulation of cardiac activity, the LF power for sympathetic influence with parasympathetic component, and LF:HF ratio as sympatho-vagal balance, though with controversy.
There is a concern about how to interpret frequency domain of the HRV analysis if respiration frequency is variable (not controlled). For example, as showed in the attached file, while time domain analysis of HRV indicates increased vagal activity in response to slow breathing (increase in SDNN, RMSSD, NN50, and pNN50), the frequency domain is complex; LF (and LFnu) and the LF:HF ratio are higher in slow breathing compared with normal breathing and also compared with breathing at frequency of 0.2 Hz. Also, HF is not significantly different between slow breathing and breathing with frequency of 0.2 Hz while HFnu is lower in slow breathing.
How frequency domain of HRV must be interpreted when the intervention itself is changing the frequency of respiration? Is the time domain a better analysis of autonomic response in such case?
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1- Let's read these papers more carefully. Laborde et al. has mentioned in the introduction that "we refer to parasympathetic activity as vagal tone" that means that they are mixing all types of PNS activities together and call it vagal tone. So when reading this review keep this in mind. Also, they have mentioned that ""in this paper we refer to cardiac vagal tone as assessed by HRV measurement" well we cannot define a concept by a surrogate measure and use it as a method of validation. We need to always look at the gold standards; neural blockade studies and pharmacological blockade studies.
2- Grossman et al indeed have mentioned that "RSA has been shown to often provide a reasonable reflection of cardiac vagal tone when the above-mentioned complexities are considered", but also have listed 6 issues above of this that "can lead to misinterpretation of cardiovascular autonomic mechanisms" and one is respiratory parameters, please also see others. These are mostly overlooked by many researchers in psychophysiology.
3- HF, LF, or SDNN or RMSSD interpretation as a measure of cardiac vagal modulation requires paying attention to the issues raised by Grossman et al. When respiratory frequency changes from HF to LF, HF no longer represents the respiratory modulation of cardiac vagal activity, but LF does, as was shown by pharmacological blockade study. This doesn't mean that under resting state and with respiratory frequency being in HF band, LF still can represent vagal activity, this also has been shown by pharmacological blockade studies.
4- To interpret HRV, you need to first look at the physiology of HR modulation by ANS at the level of the heart and at cell level, as well as interaction between SNS and PNS at central and peripheral levels. As mentioned by Laborde et al "ease of access [and of measuring HR] should not obscure the difficulty of interpretation of HRV findings that can be easily misconstrued". We have too many studies using HRV to measure ANS activity but too little studies on the validity of such measures.
Finally, that many researchers repeatedly mentioned something does not mean that is correct. This is the problem with HRV interpretation in psychophysiology literature, unfortunately, and we continue repeating that without asking ourselves based on what evidence and based on what valid or gold-standard measure? If you look at cardiovascular physiology literature you usually don't see such misinterpretations. Same with 'resonant breathing', nice phrase but no strong evidence.
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I have some EDA data from a colleague's project that I want to analyze. Looking into the data, I discovered that the sampling rate is relatively low - it is only 2 Hz. However, the literature I read suggested that the sampling rate should be at least 200 Hz. So, it seems the sampling rate is not high enough for analyzing the phasic components of EDA. Still, as I am completely new in the field of EDA, I would like to ask for your opinion:
Can I still conduct meaningful analysis of phasic SCRs?
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Indeed it is a low sampling ratio but even VarioPort, which is used for multi-channel physiology recordings in laboratory and ambulatory setups, has 25Hz frequency for EDA. Empatica E4 which is medically certified has sampling rate 4Hz. So, I am wondering which device could provide such a high ratio for EDA. What is more, the quality of physiological measurements may be affected by many factors (filtering process, inappropriate placement of sensors, movements during recording, alcohol or caffeine consumption, etc) except from sampling ratio.
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Hi, I am a german university student (business administration and psychology) and I am going to write my bachelor thesis.
I would like to research a correlation between stress and the language. For the following therms I need your help:
- differently option for stress induction
- or unsolvable tasks for stress induction
- or questionnaire for stress induction
I know about the trier social stress test and the socially evaluative cold water stress test, so I need other options. The best way for me is, to have a computeraided stress test.
I hope you can help me and make my student life a little easier :-).
Best regards,
Timo Köhler
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We study several aspects of moral stress and distress when you are supposed to treat the patient in a way that compromise your conscience or you are afraid of eg mental disorders.. I can add some examples:
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I now have created a compact version of the ``theory of everything'' I am developing since several years, also including the biological and psychological extensions dealing with human body, human soul, and human mind, in the latter case, comprising mental disorders just like drugs applied to treat mental disorders. In particular, in the last chapter (``On the Quest of the Actual Nature of Being''), I there present formal boxes which compactly elucidate the central feature of all this, namely the interrelation of forces and fields in the context of macroscopic systems and microscopic systems, naturally incorporating gravitation, electromagnetism, and self-interaction, by way of example, also presenting the way to the notions ``weak interaction'' and ``strong interaction'' as used in quantum field theory. Please consult the copies ``Understanding Nature Truly'', part one, two, and three presented in RG in the context of my projects
``Theory of Everything'' (part one) and ``Human Soul as Mathematical Object ...'' (part two, three). Do these formal boxes contain enough information to show that the ``theory of everything'' I am developing since several years indeed works? Do these formal boxes contain enough information to show that ``theory of everything'' is not what people so far a looking for, but something completely different? Do these formal boxes contain enough information to show that exactly this is the problem preventing that people realize the way I am going as the right way?
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Not all of the neuron circuits in the brain are active from the beginning.
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Respiratory Sinus Arrhythmia (RSA) appears to relate to vagal tone.  Perhaps loss of RSA is a marker for PTSD. 
I hope to measure whether a variety of mind-body interventions for traumatized populations has an impact on RSA. It would also be interesting to ascertain if change in RSA correlates with clinical improvement.
This will be for adolescents and adults.
I am looking for insights as how to measure RSA in a research context.  This includes whether commercially available Apps are acceptable, what would be the cost, etc.
Thanks.
Kris Kaliebe
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There are a number of relatively easy methods to measure RSA  that produce equvalent results (e.g. see my comparison of 3 available methods from 1991; Grossman, van Beek and Wientjes, which can be downloaded at this site).  However, it is really important that one measures respiration rate and depth, as well as Heart period (60000/heart rate), since changes  particularly in respiration rate can profoundly distort within-person relations between RSA magnitude and cardiac vagal tone. Also regarding individual differences in cardiac vagal tone, we showed in another available paper that  resting heart period was a far better marker of cardiac vagal tone than RSA is (Grossman & Kollai, 1993), a finding that has gone ignored in the literature but which was replicated in another study by Kollai. Somewhat better than heart period, alone, were multiple regression prediction, using both heart period and RSA (including respiratory measures did not make a difference in these between-individual assessments. Please study the early RSA physiological literature to learn the caveats of RSA indexing of cardiac vagal tone. Respiration, and with- vs. between-individual difference, are but two relevant factors. 
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about a mechanism
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Dear Ennas,
Please check out the following paper:
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There's plenty research literature on the topic with adult subjects, but I find it difficult to find any studies that would report using the technique (or other HRV Biofeedback breathing) with peadiatric population.
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Rescalm is more simple with design for adolescents, but less scientific figures see english site of www.rescalm.com  . Stresseraser pro is more for scientific research. See stresseraserpro.com
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A vasovagal response may be observed with needle phobia upon insertion of the needle therefore reducing blood pressure, heart rate, stroke volume and cardiac output.
However a study (Finsterer, 2004) showed that needle EMG did not affect blood pressure or heart rate.
Can anyone provide any more evidence or explanation of what would happen?
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Terun,
In an attempt to mitigate the blood sampling stimulus from your study, you may want to place an intravenous catheter prior to your intervention. You will be able to obtain pre-intervention and post intervention blood sampling without the "needle phobia" neuronal input tainting your results since the stimulus will occur prior to your intervention.  
Regards,
Christopher
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but not sure how good it is (it looks DIY hack-y) to use this as a gold standard. We are interested in using EMG to detect breathing , and need a reliable device to measure ground truth. Any suggestion would be highly appreciated! 
thanks! 
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thanks. We are only interested at the moment in healthy people at rest, and when they are doing a range of normal daily activity (like walking, lying down, etc).
I am predominantly interested in detecting breathing events (inhale , exhale), with a possibility of detecting volume of air flow, using only surface EMG sensors.
Have you come across any relevant literature ?? 
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Hi everyone! I am interested in measuring the electrodermal activity (also known as galvanic skin response). I would like to implement a low-cost, easy-to-buid circuit for this purpose. Any suggestions? Thank you very much in advance!
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Dear James,
Thank you for the references. I've already implemented the circuit depicted in Fowles et al, (1981), which is based on a Wheatstone bridge. It didn't work.
Please let me check the other reference... I hope I can find it
Best regards!
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I normally used a DAM 50 amplifier from WPI but it broke. We have an Axopatch 1D in the lab and I heard it could be used for field potential recordings (e.g. cerebellum slice from mice). Could someone help me on how to configure the Axopatch amplifier for this purpose?
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Hope this will be of help;
Leda Roggeri, Bruno Rivieccio, Paola Rossi, and Egidio D'Angelo:Tactile Stimulation Evokes Long-Term Synaptic Plasticity in the Granular Layer of Cerebellum The Journal of Neuroscience 2008, 28(25): 6354-6359; doi: 10.1523/JNEUROSCI.5709-07.2008
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I have found several stains for developing granule cells, but no distinct markers for mature ones. I could just use NeuN and use location, but would prefer a specific marker. Thanks
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PAX6
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A scale other than a known scale or instrument to measure depression.
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Lots of validated scales for depression.  Make sure that the scale you choose matches the population you are working with.  For general populations you can use something like the CES-D; for clinical populations, in general hospital or primary care outpatient settings you can try the GHQ or the PHQ9.  For clinical populations, where there are likely to be higher prevelance and intensities of depression, use a specific instrument such as the Beck or Hamilton depression scales.  for medically ill populations you can try the HADS.  The reasons for choosing the appropriate instrument are that the population instruments are prone to ceiling effects in clinical populations (depressed people often produce very high scores on such instruments which limit discriminability) and the clinical instruments face floor effects (too few/too insensitive to milder, dysphoric mood) . Medically ill groups often have higher levels of vegetative symptoms such as fatigue or sleep problems which can artificially inflate apparent prevalence of intensities of depression in medical populations.
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I am planning an experiment in which I want to compare baseline heart rate variability before and after an intervention. For saving the participants time I want to keep the ECG-recording sessions as short as possible. Yet, i still want data from which I can make a reliable conclusion about the participants baseline HRV.
I would like to analyze time- (SDNN, RMSSD) and frequency parameters (LF, HF, LF/HF ratio but not VLF).
So, how long should the recording be at least? And do you know of any literature supporting this?
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Dear Miguel,
thank you for your answer!
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I was speaking with our University's vet and she mentioned that live decap is the better route to take if you're planning on doing any histology after death. Does anyone have any further information on this/any sources that show this? 
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Most ethical requirements (from government or institutions) require justification for live decapitation. It depends on what you are measuring- you should look to see if a particular anesthesia is known to have an effect on your measurement, and if that exists it might be worth asking for permission to do live decapitation. But in all likelihood, you won't have permission to do so within your lab's existing ethical permissions (unless someone has asked for it already).
Another point to think about is this- will the stress of the live decapitation affect your measured target more than anesthesia? Acute stress is often a purposeful manipulation and is known to affect many brain parameters, so depending on what you're measuring you might be affecting things more by NOT using anesthesia. Really depends on what you're measuring.
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Is there any report on effect of blood pressure (SBP and DBP) on short-time perception/short-interval time estimation, a cognitive attribute in human?
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Dear Béatrice Marianne,
Thank you for the reply. It is really informative.
Regards,
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A colleague and I have been trying to decide which NIRS system to purchase and hope to get advice from those with experience. We have no experience with NIRS and have lots of ideas for how it may be used in our psychology/behavioral neuroscience department (we are not purchasing it for one particular research goal). We’d like to be able to record from any area of cortex (not just prefrontal) and we’d like something flexible and modular so that we can scale up when we get more funds. We think we’ll have 75 - 100k to work with for now. Do you have suggestions based on your own experiences with particular vendors and systems? Thank you.
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If you have the ability to spend that amount of money, have a look at the Antaris FT-IR instrument from Thermo. Why? Because it is very versatile, and from you question, I think that is exactly what you need! You can measure powders, liquids, solids, even tablets in transmission. And the instrument provides you with some good quality spectra. 
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From my understanding, under increased metabolic demand, heart rate (HR) and respiratory rate (RR) increase (i.e. they are positively correlated). Is this always true?
1. Is there any metabolic situation where HR would increase but RR would not (no correlation)?
2. Is there any metabolic situation where HR would increase and RR would decrease (HR and RR are negatively correlated)?
Kindest regards,
Onkar Marway
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No they are not always positively correllated. The example that comes to mind is respiratory failure in COPD. as the condition deteriorates ant the level of  consciousness decreases the respiratioy rate decreases  but there is usually a significant tachycardia. The same happens in many other conditions in which the respiratory failure  progresses initially respiratory rate increases initially but if the condition is not reversed reduced respiratory rate occurs initially wiith tachycardia. If untreated brady cardia occurs and low respiratory rate with low pulse rate often signals  omminent cardiac arrest if untreated.
Hope this  helps
Richard
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Are there guidelines or instructions posted (or published) on how to best extract respiratory parameters during amusement/humor tasks? Specifically, I am having trouble extracting respiration rate from tasks where laughter is involved. The signal is noisy, and the variability in respiratory depth makes it challenging for me to meaningfully isolate when a breath ends and another begins. I only appear to encounter this issue during amusement tasks.
I have attached a picture of a representative example of the issue.
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Different effects of intrathoracic pressure allow you to pull a reasonable estimation of respiration off an oximeter. It's *somewhat* straightforward, and probably not fully as accurate as a lot of other adjunct methods of measuring respiration.
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Do you believe that young maternal age affect the development of the child?  
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Current research shows that young mothers use far less rich language  interactions, use more   dictatorial controls and orders; do not show as much patience. .However, when a  teen Mom  realizes that she does not want her baby to grow up feeling all the difficult angry and unloved feelings that  the teen mom experienced, then her interactions are more appropriate and positive. See article  "Reflectivity: Key ingredient in  positive  adolescent parenting ( Journal of Primary Prevention,  vol 19 (3),  pp. 241-150,) for intervention research by Brophy--Herb and  Honig.
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I used Open field plus sucrose preferential. However, I receive this question when I'm presenting my stress-depression animal model. One of the questioner, a professor ask me this as he is using a substance that greatly affected the mouse prefrontal cortex and the mouse barely move. 
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Dear Hafiz,
Indeed, open-field test is carried out to show the locomotor activity of rodents before Forced Swimming Test (FST) to show that despite the normal locomotion of animals they are immobile in the FST test. I added some reviews that are useful to better understanding the immobility behavior in the FST. Under acute unpredictable and unavoidable stressful conditions, depressed people get despair and hopeless and, in fact, FST mimics similar conditions for rodents in which immobility time is considered as a depressive-like behavior. The Tail Suspension Test is similar to FST as well. Also, Climbing behavior in FST reflects the activity of adrenergic system and swimming is associated with serotonergic system activity.
Cryan, John F., and Andrew Holmes. "The ascent of mouse: advances in modelling human depression and anxiety." Nature reviews Drug discovery 4.9 (2005): 775-790.
Cryan, John F., Rita J. Valentino, and Irwin Lucki. "Assessing substrates underlying the behavioral effects of antidepressants using the modified rat forced swimming test." Neuroscience & Biobehavioral Reviews 29.4 (2005): 547-569.
Slattery, David A., and John F. Cryan. "Using the rat forced swim test to assess antidepressant-like activity in rodents." Nature protocols 7.6 (2012): 1009-1014.
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I am looking for questionnaires and tests that apply to clinical assessment of novel psychoactive substances addiction.  Is there visual analogue scale for craving?
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Dear Dr. Béatrice Marianne Ewalds-Kvist
Thank you very much!
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The induced gamma synchrony has to do with the inferior frontal junction and other brain areas. How does consciousness is "produced" by this phenomenon and what this penomenon is about?
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David,
The following are my opinions as a former brainwave researcher, and most should not be considered as facts. I hope they are helpful when considering the relationship, if any, between gamma waves and consciousness.
1. The burden for showing that any brainwave phenomenon "mediates", "correlates with", or "represents" consciousness is very, very high, since up until now no such clear relationship has been shown between consciousness and any phenomenon in the body (depending on our definition of "consciousness"). The way science works is that it is up to the researchers themselves to show or prove their hypothesis. This may be obvious, but I'm just stating it for completeness.
2. The word "consciousness" needs to be defined. Since some published opinion [http://beyond-advaita.blogspot.com/2011/05/gamma-wave-synchrony-by-junius.html] relates this gamma wave research with the active philosophy known as advaita (nonduality), the word "consciousness" may refer to pure awareness, or to a mixture of a thought and pure awareness, both of which are commonly called "consciousness" in the field of subjective knowledge known as advaita. There is a big difference between a specific thought (such as "I am thirsty"), which starts at the level of the body or subconscious and grows in concreteness until it is appreciated as a thought occurring in time by the mind, and pure awareness, which contains no concrete meaning and does not grow or change.
3. Any proposed correlation between body and mind, or between body and awareness, must be shown by specific experiment, such as those which link an action by a subject (such as pressing a button) with the subject's recognition that he or she has decided to take the action, or has taken the action. Speculation relating to consciousness based on observing brainwaves alone and speculating about connections between neurons or layers of neurons is not science. It is a first stage of science consisting mostly of speculation.
4. In observing gamma waves, the pattern appears to be that of many wavelets (amplitude-modulated pulses) overlapping one another. One mathematical analysis that suggests itself is to compute individual wavelets from the entire brainwave channel, making assumptions about periodicity. Alternatively, it may be possible to distinguish individual wavelets in two or three dimensions by cross-correlating pairs or triplets of spatial brainwave channels. This type of analysis is frequently done to visualize brainwave disruption during epileptic seizures.
5. Care must be taken when claiming synchrony among or between spatial brainwave channels. In the case of alpha waves, the group of cells that acts as their generator has long been known to occupy a localized place in the brain, with signal propagation happening mostly in the large, highly-conductive blood vessels of the brain, and therefore synchronization of alpha waveforms or wavelets across the cranium is unavoidable and constant (everywhere at zero phase).
6. The article referenced above states, "Even the authors admit that the gamma synchronization is just a correlate, and does not explain how consciousness actually arises." What is meant by "a correlate" must be understood carefully before even speculation can be done.
7. Studies of gamma correlation that make use of subjects practicing meditation must be interpreted carefully, as there is no standard mental state of meditation, and no standard technique or mental activity of meditation. Instead, there are many forms of meditation, which may produce subtle differences in physiological and other markers in the body. Knowing that some form of meditation increases brainwaves at some frequency tells us very little by itself. For example, again in alpha waves, closing the eyes (a typical first step in most forms of meditation) is the critical action that stops the inhibition of alpha waves by the visual processing system. Similarly, a reduction in gamma wave amplitude in subjects with schizophrenia tells us very little by itself.
8. In summary, "Whether or not gamma wave activity is related to subjective awareness is a very difficult question which cannot be answered with certainty at the present time," according to the article "Are neocortical gamma waves related to consciousness?" by C.H. Vanderwolf in Brain Research, 2000 [http://www.sciencedirect.com/science/article/pii/S0006899399023513].
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For my experiment participants are assigned to two different groups while they to a Go/NoGoTask. I recorded the EDA via electrodes attached on the left hand and now I wanted to compare the SCL between the groups.
Of course, I could just compare the "raw" SCL data, but shouldn't I do some kind of range correction too? But if I do that e.g. following the recommendation of Lykken and Venables (1971), wouldn't I dimminish any group differences? 
best,
Katharina
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 Dear Katharina: to properly answer your question I would need further information about the experimental design you used and the main hypothesis you posed. In any case, skin conductance  usually requires some pre-processing steps before you actually analyze your data set. Since this would take too long to explain in detail, I'm attaching a recently published paper that might come as handy. Hope that it helps.
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The animal environment is full of attractive and dangerous sources which influences the behavior of it. It seems, Lewin's field theory could describe the multiple sensorial inputs as forces to determine animal behavior. Not only bacteria, where the forces could be interpreted as gradient of substrate concentrations, but also in higher animals with a developed cerebral system follow this field of forces.
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Dear all,
Merry Christmas to you and a happy new year.
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Previously to understand the concept of health disease medical model is applied, where health professional concerned about the disease, diagnosis and drugs, but now this model is replaced by the bio-psycho social model, in which we should include the psychology and social factors along with the biological as it is also the part of the nature.
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Dear Mohan, Nico and Marianne,
Thank you for revisiting these important issues!
I say this because the overlapping fields of psychosomatic medicine, behavioral medicine, health psychology and psychiatric epidemiology have evolved so much since I began my work many years ago. Engel was a pioneer who influenced all of these research areas. Indeed, Marianne's comments are very spot on.
Albee is another pioneer whom you may want to research. I like his work because he originally developed a model that I have found useful in my work on stress in medical students, spouse caregivers of persons with either Alzheimer's disease or schizophrenia, disasters, etc.
Albee formed a simple model that characterizes
Distress as a response to not only stressors, but also a person's unique vulnerabilities and resources.
Distress = (Exposure to Stress + Vulnerability)/Resources
I have found it useful, statistically, to multiply Exposure by Vulnerability because, the product makes it easier to use statistically than the addition.
I am not saying that this is a perfect model, but that it provides a theoretical framework for research in terms of identifying groups at high risk for deleterious responses to varying types of stressors. I do believe, as did Albee, that vulnerabilities are more hard wired (race, gender, developmental illnesses, personality, early trauma) than are resources, which are more flexible (coping, social supports, income).
My experience has been that Health Psychology embraces the other disciplines mentioned above and that it has focused on empirical analyses of theoretical models. Having gone to numerous conferences on psychosom medicine, behavioral medicine, health and physio psychology, I can tell you that it is difficult to talk about health psych in isolation without referencing its cousins. .
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Hi! We would like to present a series of affective pictures. What is the best time interval between two pictures so that we might analyze skin conductance responses in the right way? We would like to change from one picture to the other as quickly as possible to maintain the interest and provide constant affective stimulation. Thus, we are mostly interested in minimal acceptable intervals. What literature guidelines would you recommend? What is your personal experience? I will be grateful for any hint. Thank you!
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Some additional studies have investigated this question examining different quantification methods with some success for ISI between 2-4 seconds, although these methods are more sophisticated (see attached) 
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I am looking for literature about resting energy expenditure, activity-induced thermogenesis or total energy expenditure in anorectic subgroups! Are there papers reporting about differences between bulimic and restrictive anorexic patients in energy expenditure? Does anybody has recommendations? (P.S.: I have found the papers of Kaye 1988 reporting about differences in bulimic and restrictive anorexic patients during refeeding) Thank you for your help!
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Dear Maria,
maybe you can use the following papers...
Best wishes from Munich
Martin
____________________
de Zwaan M, Aslam Z, Mitchell JE. Research on energy expenditure in individuals with eating disorders: a review. Int J Eat Disord. 2002;32(2):127-34.
de Zwaan M, Aslam Z, Mitchell JE. Research on energy expenditure in individuals with eating disorders: a review. Int J Eat Disord. 2002;31(4):361-9.
Casper RC, Schoeller DA, Kushner R, Hnilicka J, Gold ST. Total daily energy expenditure and activity level in anorexia nervosa. Am J Clin Nutr. 1991;53(5):1143-50. http://ajcn.nutrition.org/content/53/5/1143.full.pdf+html
Bossu C, Galusca B, Normand S, Germain N, Collet P, Frere D, Lang F, Laville M, Estour B. Energy expenditure adjusted for body composition differentiates constitutional thinness from both normal subjects and anorexia nervosa. Am J Physiol Endocrinol Metab. 2007;292(1):E132-7. http://ajpendo.physiology.org/content/292/1/E132.full-text.pdf+html
Smitka K, Papezova H, Vondra K, Hill M, Hainer V, Nedvidkova J. The role of "mixed" orexigenic and anorexigenic signals and autoantibodies reacting with appetite-regulating neuropeptides and peptides of the adipose tissue-gut-brain axis: relevance to food intake and nutritional status in patients with anorexia nervosa and bulimia nervosa. Int J Endocrinol. 2013;2013:483145. http://www.hindawi.com/journals/ije/2013/483145/
Dostálová I, Sedlácková D, Papezová H, Nedvídková J, Haluzík M. Serum visfatin levels in patients with anorexia nervosa and bulimia nervosa. Physiol Res. 2009;58(6):903-7. http://www.biomed.cas.cz/physiolres/pdf/58/58_903.pdf
Monteleone P, Matias I, Martiadis V, De Petrocellis L, Maj M, Di Marzo V. Blood levels of the endocannabinoid anandamide are increased in anorexia nervosa and in binge-eating disorder, but not in bulimia nervosa. Neuropsychopharmacology. 2005;30(6):1216-21. http://www.nature.com/npp/journal/v30/n6/pdf/1300695a.pdf
Housova J, Anderlova K, Krizová J, Haluzikova D, Kremen J, Kumstyrová T, Papezová H, Haluzik M. Serum adiponectin and resistin concentrations in patients with restrictive and binge/purge form of anorexia nervosa and bulimia nervosa. J Clin Endocrinol Metab. 2005;90(3):1366-70. http://press.endocrine.org/doi/pdf/10.1210/jc.2004-1364
Zipfel S, Mack I, Baur LA, Hebebrand J, Touyz S, Herzog W, Abraham S, Davies PS, Russell J. Impact of exercise on energy metabolism in anorexia nervosa. J Eat Disord. 2013;1(1):37.
El Ghoch M, Calugi S, Pellegrini M, Milanese C, Busacchi M, Battistini NC, Bernabè J, Dalle Grave R.Measured physical activity in anorexia nervosa: features and treatment outcome. Int J Eat Disord. 2013;46(7):709-12. https://www.researchgate.net/publication/236948765_Measured_Physical_Activity_in_Anorexia_Nervosa_Features_and_Treatment_Outcome
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Hello! I have recently started collecting data using a Brain Products EEG system. I have been analyzing ERPs using the free software ERPlab. I also collect heart rate data during sessions using the Brain Products blood pulse sensor. I would like to analyze the HR data, preferably in a way that examines heart rate variability. I know it is possible to do so with Brain Vision Analyzer, however my lab does not own this software. Does anyone have a recommendation for how I can analyze these HRV data? Preferably using a free software package (I have access to matlab, R, and Python).
Thank you so much!
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Thank you everyone, for all your help! I've been working through some data and it is going well. 
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There are some excellent open access resources available for teaching psychology such as NOBA Psychology: http://nobaproject.com/
Would anyone have any similar recommendations for teaching biological psychology and cognitive neuroscience in particular? 
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I will also be testing the mothers but believe saliva to be the best way to do this. I am thinking that urine samples may be a way forward. Does anyone have any thoughts?
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Hi Jacquie - I'm also planning a study where I measure salivary oxytocin.  You need a relatively large volume of saliva (approx 5 mL) and to do purification steps before the oxytocin assay. 
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I would like to record ECG, EMG and respiration (with a chest belt) data in humans and have a general question about the filter settings. The recommended filter settings for my study are ECG 1-35 Hz, RSP DC-1 Hz and EMG 10-500 Hz. One expert recommends to apply the filters real-time during acquisition and the other one to apply filters after data acquisition. I searched former literature and couldn't find a general suggestion. Is there any disadvantage in applying post-aquisition filters and no real-time filters during the acquisition?
Thanks for sharing your thoughts and suggestions.
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The only analogue filter you should apply in real-time (at aquisition) is an antialiasing filter, as it is not possible to remove aliasing afterwards. All other filters can (and should) only be applied afterwards. This assures you have the most original signal possible. Once you apply anotther filter at acquisition time (say you apply a low-pass at 35 Hz as you are hinting) that smooths the ECG and seriously attenuates high frequencies, an effect that cannot be reversed afterwards if you (or a colleague) wants to use your ECG recordings to do something else where frequencies above 35 Hz might be useful.
Best wishes.
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Dear all,
There is an expectation that understanding the neural substrates of mental disorders will revolutionize the field of psychiatry, in terms of improving diagnostics and treatment. However, the clinical value of neurobiological research into mental disorders has so far been minimal.
What are your opinion on this matter?
Do you agree that an understanding of the biology of psychiatric disorders (genetics, molecular, brain circuits etc) will lead to improved diagnostics and treatment, or are the expectations of a ”revolution” exaggerated?
I’m interested in hearing your opinions on this matter.
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I think that there is indeed a great deal of potential for a "revolution," but that what has held back the field back is the decidedly non-biological approach that has traditionally characterized psychiatric genetics, neuroscience, and related fields.  That is, the object of study is biological, but the approach and assumptions are not (or only so in a very limited way).  That is, there has been a general lack of anything resembling a systems or organismic approach when it comes to matters of the mind.  Brains nonetheless don't exist in vacuums (or vats) and will never be understood purely in reference to themselves and the occasional stimulus that impinges upon some sensory organ.  Zing Yang Kuo and Jaques Le Magnen are notable, past critics of the mainstream, dualistic (and reductionistic) approach.  For recent reviews hammering on this issue in the domain of depression, read:
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We have observed a large noise increase in facial EMG recording when skin conductance electrodes (GSR) are applied. This seems to be caused by the fact that GSR amplifier produces currents that are captured by fEMG sensors. This is a serious problem because this noise (of about 200 microVolts) is usually stronger than the electrical signal from facial muscles. I wonder whether you might provide me some feedback whether you encounterd the same problem while simmulatenous EMG and SC recordings, and how you managed to handle it. We use ADInstruments Powerlab with BioAmp and GSR Amp. Thank you!
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If you can do impedance measurements at a high frequency rather than galvanic response at low frequency or DC, then you will be able to filter it easily from your EMG signal. EMG is typically well below 500Hz and it should be reliable (and possibly more accurate) to measure tissue impedance above 5kHz. Measuring at high frequencies eliminates a large portion of the motion noise artifacts from the measurement.
If it is not possible to switch to higher frequencies then you can turn it around at lower frequencies. There is rarely any EMG signal with frequencies under about 5Hz so if you can do DC or low frequency GSR, you can run a 5Hz long pass on the EMG signal.
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I am looking to develop a Social and Cultural Complexity Quotient. This will be built on Prof Clare W Graves' Biological, Psychological, Social System framework and include introvert extrovert, analogue digital thinking, various change states as a core. To develop the quotient further I feel I would need to include life conditions. Has anyone come across Complexity Quotient being used in this Social and Cultural settings? Welcome suggestions and ideas.
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I have just started research on this and complexity is very hard to define for example is a cucumber more complex than a Boeing aircraft? Currently in the assessments I use to uncover the 'hidden' coping mechanisms within an indivdual,  add digital analogue thinking, states of change, introvert extrovert and so on. Social and cultural structures being complex and open involving systems which become more complex as you try to measure additional parameters.  If I add in Ken Wilber's All Quadrant  All Levels  (AQAL) model then thing become more complex. Then we have the interplay between the coping mechanisms and the biological.
So for example would a society based around tribal coping mechanism have a lower complexity quotient than a humanistic, consensus based community structure? Each system Graves uncovered was the way we handle every increasing complexity to survive. He suggested that because the brain is 'smart' we only do whatever is necessary to survive in a given set of life conditions. The states of change measure this equilibrium. Today how much does being introvert or an analogue thinker in complex society add to a complexity quotient? 
Coping mechanisms (I define as meme complexes or memeplexes) have with life conditions have a two way effect for example on health. How can these be factored into the quotient? Or should we even try? Is it too reductionist?
I feel this is too broad at the moment and I need to go back to basics to define how I can put a factor onto the various elements and what would a quotient look like. At the moment I am surfing the wave between chaos and order.
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If a person fills out scale A multiple times, can we include all their attempts at that scale in calculating internal consistency or do we only have to select one attempt of that scale (e.g. the first attempt)?
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Internal consistency refers to the reliability of a test based on the consistency of its items. So, you should use data obtained through the same test. The inclusion of other attempts may affect the reliability index because of participant's learning effect during different attempts.
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My background is in mental health, however I am new to the study of asthma. What are the key conversations regarding the interaction of these two elements should I get myself up to speed on?
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On the epidemiology side, one of the important issues concerns the bidirectional (one could even say pluripotential) nature of the associations. As with many long-term medical conditions, asthma has mental health consequences. On the other hand, mood and anxiety disorders may increase the incidence of asthma (see General Hospital Psychiatry. Volume 30, Issue 5, Pages 407–413.). 
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In my experiment I would like to include a questionnaire or implicit measure that would allow me to distinguish among intrinsic, extrinsic and reputational pro-social motivation.
This concept was developed by Bénabou and Tirole (2003, Available at: http://idei.fr/doc/by/tirole/incentives_prosocial.pdf).
However, I have not found any measurement that could be applied in an experiment on pro-social behavior.
What would you recommend?
Thanks a lot in advance!
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I would  agree that motivation cannot be dissected meaningfully with regard to intrinsic vs extrinsic motivators...  in all cases one acts to serve oneself, even if it's to enhance or diminish perceived rewards or punishments derived from external sources. Pro-social behavior is a great example of how good "I" will feel if I do something nice for someone else (honest self-assessments required); extrapolating that to much larger efforts or groups would enhance my own "world" as well as theirs - not a truly altruistic endeavor. It's not that such behavior is not laudable (when genuine), it is, however, what one who emits the behavior  would get from it, not merely the recipient(s) of the largesse, when describing the motivation to do so.  
More to the point, self-perceptions of personal gain and/or loss accrue to acts driven internally,  externally, or more likely some combination thereof, without the consequence(s) of any particular act having universally objective and verifiable value - from a psychological perspective. Yesterday's election is a grand experiment in the psychology of motivation - tally the votes and relate them to both the stated, as well as the obscured (if you can), reasons for seeking office - you'd be hard pressed to make the case for even a single case of self-denial for both candidates and voters.   
Much work in the psychology of personality has gone into "locus of control" studies to determine the degree to which one is self-directed vs being at the mercy of one's environment, but even there the issue again is self-perception of the degree to which one meets internal/external expectations so as to achieve gain(s) or mitigate/eliminate loss. Many research techniques and scales have been advanced in this area.
Perhaps a more fruitful domain in which to search for research materials of a sort that might be helpful would be Microeconomics. Economists are wont to create measures for describing the "value" that one might expect from exhibiting some behavior, including measures of the expected "fruits" resulting from the behavior. In particular, theory and studies of "marginal utility" provide more quantitative approaches to defining and measuring perceived gain/loss in specific circumstances, i.e., the situations for which you seek to identify and quantify "motivators."    
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Hi all,
I am currently analysing data from an fMRI study, with a 2x2 between-within design. Patients vs controls reflect the between factor, and congruent and incongruent trials reflect the within factor (this is a Stroop task).
After seeing an interaction effect between the two factors in several brain clusters, I wanted to extract the beta-weights from these clusters to explore the underlying effects.
I used Marsbar to extract the raw beta-weights from congruent and incongruent trials, separately (so no contrast between conditions performed), and plotted the results for my two groups.
Many of the resulting beta-weights are negative, and I wonder what this means? Does it reflect a sort of 'deactivation'?  
Any input will be highly appreciated!
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Most likely, in your case, when you run a general linear model (GLM) analysis, you are attempting to predict the voxel signal using a vector of onsets convolved with some hemodynamic response function. It's fundamentally the same as when you are carrying out any other linear regression: You are predicting some variable (Y) as a function of a predictor variable (X): Y = B(X)+E -- Y is a function of X, plus some variance, (E). B is simply the coeffcient of the predictor variable that leads to the best estimate of Y. In the case of fMRI, X is the idealized time course for the onsets of a particular condition. When B is high for a voxel, that means that the activation for that voxel closely follows the idealized time course for that condition. If B is near 0, that means there is little to no relationship between voxel activity and the idealized time course. B can also be negative, meaning that it is inversely related (e.g, whenever that particular condition occurs, activation actually decreases).
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A lot of us are investigating the pathophysiology associated with mental disorders. One popular method is fMRI, which would be one example of measuring macro properties of the brain, at the regional / circuit level.
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Bassett, D. S., and Gazzaniga, M. S. (2011). Understanding complexity in the human brain. Trends in Cognitive Sciences, 15, 200-209. doi:10.1016/j.tics.2011.03.006 provided an interesting discussion along these lines. We have now published a series of articles suggesting the appropriate level to understand higher cortical functions is based on dynamic cortical columns that are in circuits. These in turn interact with subcortical structures, consistent with Luria's views that higher functions can only be understood as whole brain activity. The same theory provides information on serious neuropsychiatric disorders, depression/anxiety, the metatraits of plasticity and stability of the Big 5, the process variables in psychotherapy, and a structured approach in dealing with influential relationship-based negative emotional memories. I have attached one article from June that discussed the microcircuitry allowing the theorized manner of column formation. The other articles are available at my page, with the first being in 2006.
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I have conducted an fMRI study comparing recovered anorexia nervosa patients to healthy controls on an emotional stroop task. The task consists of fearful and happy faces, overlaid with either the word 'fear' or 'happy'. Thus, a given trial can either be congruent (face and word match) or incongruent (face and word mismatch). The task was to designate if the face was happy or fearful, ignoring the word. Reaction time data showed that it takes longer to respond to incongruent trials compared to congruent trials, which we expected.
However, the fMRI analysis shows that, for the control group, participants had more bilateral amygdala activation during congruent compared to incongruent trials (as shown by the extracted beta weights from left and right amygdala). I expected more amygdala activation for incongruent trials (thinking that an emotional conflict conveys more saliency). I am struggling to understand our observation. 
Does anyone have any comments regarding this finding? All comments are highly appreciated!
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Emotional processing is attenuated when task-demands are high (high cognitive load conditions) and during tasks that recruit executive control processes such as conflict resolution and inhibitory control.
See for example the opinion paper by Okon-Singer, Lichtenstein-Vidne, & Cohen, Biological Psychology, 2013
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We are designing a neuroimaging study to test hypothesised circadian moderation of reward function in humans. Seems like our hypothesis is best tested using resting state methods, ideally with the hypothalamic suprachiasmatic nucleus as a 'seed region' to investigate correlations with brain reward centres (particularly ventral striatum).
I understand that small, deep brain centres are difficult to image.
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Hi Greg,
Interesting idea. In theory, almost any brain region can be used as a seed region for resting-state functional connectivity studies. In practice, I think the SCN is going to be tricky. Maybe not impossible, but certainly difficult.
Your two main problems are going to be:
1. Localisation - getting an accurate SCN ROI for each of your subjects. I'm only aware of one paper which tried to localise the SCN in humans (http://onlinelibrary.wiley.com/doi/10.1111/j.1460-9568.2008.06582.x/abstract;jsessionid=1DDF475BBC25A93E627D75AD61392F59.f04t04?deniedAccessCustomisedMessage=&userIsAuthenticated=false) and they did it basically by anatomical means - using the optic chiasm as a landmark. Since the SCN is so small (about 2mm^3) they admitted in the paper that their ROI probably included bits of the surrounding structures i.e. the anterior hypothalamus. I would imagine that this is probably the only option for such a small structure. Functional localisation would be extremely difficult given that typical fMRI resolutions are 3mm^3 - you'd be looking at a single voxel. Possibly you could try a functional localiser (i.e. a visual stimulus) with some very small voxels (2mm or 1.5mm) and just a few slices in that region, but you'd be losing so much signal that you might have to scan your subjects for hours to get anything reliable. Which leads me on to...
2. Signal-to-noise. You're right in saying that small, deep structures like this are difficult to image. The SCN in particular is right on the bottom of the hypothalamus, next to a pocket of CSF - this means you're going to get some pretty nasty magnetic susceptibility artefacts and partial-voluming effects, which will essentially serve to reduce your signal and inflate the noise. Plus, it's a very small area, so even if you localise anatomically (and manage to do it accurately) you're probably only going to be looking at a handful (5-10?) of functional voxels that are forming your ROI - this will give you a noisy estimate of the time-course of that area, which means when you feed that in to a functional connectivity analysis, your power to detect results will be reduced.
One solution might be to go the other way around, and localise the reward areas to be used as the seed region in your FC analysis - this can be pretty easily accomplished either anatomically, or using a functional localiser like the MID task.
Hope that helps!
M.
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We know about the effects of long winters and dark days on human psychology. Is there SAD in reverse ? What treatment do people get when depressed in summer,lose their energy, cannot take the heat even warm weathers and sunshine (other than photo-phobia in general)and rather want to hibernate when spring comes until fall ? (like me!)
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Maybe we might relate it to 'workoholism'. People who are busy in winter months and fail to socialise otherwise, might also find it difficult to cope with 'holiday and having fun' atmosphere which dominates the summer for many. I could remember , in high school years, I had been rather sleeping all day to have the days past. Now that I am working at an ESL college where it's busier summers, I feel much better dealing with approaching summer. However the '[burning sun' of Vancouver which is for some reason hotter and harsher than the one in Middle East (my Saudi students also confirm it) still makes me jump from shadow to shadow and feel awful when it touches my skin. I was able to sun bathe in younger years a bit (beauty suffers:)
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Many studies have shown a high comorbidity between depression and anxiety. Is it more likely that one of these conditions causes, or makes more likely, the other? Or do both depression and anxiety arise from a common source, either genetic or environmental?
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There is a high risk for depression as it maybe a genetic link, but often environmental due to habitual thoughts. Thus cognitive behavior therapy works very well with both of these illnesses. Anxiety overtime may actually be a causal link to later recurring depression. Often, chemicals and adrenaline can weaken the body , thus producing a more fatigued, less responsive immune system. Depression is a direct result of continuous negative affect and overall response to decisions that are made during periods of intense rumination. Similarly, phobias and other recurrent negative thoughts produce staying isolated which is a habitual, repetitive avoidance tactic to avoid anxiety inducing situations. Thus, the link between anxiety and depression is a common comorbidity that is often somewhat successfully treated with cognitive behavior therapy and psychiatric referral for medication. This thinking pattern is often cyclical and repeats itself. Turning the negative thinking cycle off is like "turning a barge around" (Diamond, Brad, 2012)
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I need resting state multi channel EEGs or fMRI recordings from people with bipolar depression and healthy control
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Dear Cheryl,
Thank you for your kind attention
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Before transferring to research, I did psychotherapy for @ 15 yrs. While certainly imperfect, the DSM provided a common lexicon, and facilitated treatment planning. I'm cynical about this initiative, and wonder what might have been accomplished if the minds, that were occupied with creating this nosology, had been applied to treatment or research.
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Hi, do you have the idea to answer this question?
"When monkeys with Kluver-Bucy syndrome pick up lighted matches and snakes, we do not know whether they are displaying an emotional deficit or an inability to identify the object. What kind of research method might help answer the question?"
Thank you
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The question is directed towards two of the symptoms of the KB syndrome, i.e., emotional deficits (Placidity/Tameness) and visual agnosia (inability to recognize familiar objects or people). So, what kind of research method would answer the question asked. Since it is clear that by asking specifically about the emotional deficits or recognition deficits, the author has, in other words, specifically pointed out to two distinct areas of the brain that are affected by the KB syndrome and also have been implicated in emotional deficits (amygdalae) and recognition deficits (temporal lobe areas implicated in visual agnosia). Also, another thing to remember is that it is bilateral temporal lesions that produce this syndrome. Now, according to my understanding, answer shall be, that controlled experimental research with lab animals shall answer this question in which one group shall have inactive (by e.g., infusing amobarbitol) or lesioned amygdalae whereas other group shall have inactive or lesioned area that is responsible for visual recognition. With such groups at hand, one can develop experimental tasks specific to assess emotional reactions as well as visual recognition tests to answer such questions.
Hope this helps...