Science topic

Depression - Science topic

Depressive states usually of moderate intensity in contrast with major depression present in neurotic and psychotic disorders.
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Hello,
The objective of one of my projects is to assess the overall mental health status of a specific population group. For that I have used DASS-21 to obtain the mental health status, i.e., symptoms of Depression, Anxiety, and Stress in binary form. That is, Depression - Yes / No; Anxiety - Yes / No; and Stress - Yes / No. Until this stage, we have followed some published literature for categorizing these symptoms in this way.
Now, we wanted to estimate our outcome variable, that is the coexistence of Depressive, Anxiety, and Stress symptoms in the following categories: 1. No symptoms at all, 2. At least one symptom, 3. At least two symptoms, 4. All 3 symptoms.
But we couldn't find any suitable literature yet that has applied the aforementioned coexisting categorizations directly.
Now, my questions are-
a) Is our categorization approach methodologically/conceptually sound?
b) Is there any available literature that can support our outcome variable categorization?
Thanks in advance.
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The categorization approach seems reasonable. Attachments provide some norms
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I am doing a research project on prolonged social media use and the mental well-being of college students. I want to compare time spent as well as gender to the results of the Beck Anxiety Inventory and the Beck Depression Inventory. How would I go about comparing these and what statistical test would I perform?
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It sounds like you want to do a pair of regression analyses with social media use and gender as your predictors in each. You might also want to include interaction effects to see if the effects of social media use differ by gender.
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I have to run a pearson correlation analysis between HPA axis markers- cortisol , ACTH and inflammatory marker IL-6(analysed through ELISA) and Depression anxiety questionnaires which were recorded at baseline and post interventions. I also need check the data for normality before running the analysis. If someone can provide an appropriate suggestion.
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Thank you so much Anna. Would like to ask when running a correlation analysis between hormones and questionnaire data for post-intervention do you correlate it directly with the post scores or first calculate the change score and then correlate it with hormones concentration ?
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Apologises I'm really confused and don't know how to do, appreciate any guidance you can give
Aim
1. To explore if anxiety is predicted by stress and treatment delay and whether this is moderated by Brief Cope strategies (Brief COPE) .
Design
1 continuous outcome variable – anxiety (let’s call this H)
2 continuous predictor variables (let’s call these D, S)
3 Continous Moderator - (lets call these BC - ef, bc pf and bc avoidant). These are inputted into SPSS as 3 separate variables as the questionnaire b-cope does NOT allow you to create a total score (by adding ef + pf + avoidant).
- D – delay
- S – Stress (measured by pss-10)
- BC pf - Brief Cope - 1 (consists of 4 questions with each questions represent a different factor)
- BC ef - Brief Cope – 2 (consists of 9 questions with each questions represent a different factor)
- BC avoidant - Brief Cope – 3 (consists of 4 questions which each questions represent a different factor)
To answer the aim I know i need to complete a hierarchial multiple regression but I don't know what to enter on what model or whether I need to do separate regressions and again what should be entered with what.
Q1. Can you please advise how my regression models would look as I can't work this out given my predictors, moderators and outcome variable listed below.
E.g. Model 1 ...
Model 2 ...
Q2. Do I need to look at interactions? If so which ones, how would this be put into SPSS ie in which models.
Possible Interaction examples ?
Stress x bc ef
Stress x bc pf
Stress x avoidant
Delay x bc ef
Delay x bc pf
Delay x avoidant
Q3. Do I need to run separate hierachial multiple regressions? If so can you please write how the model would look ie. Model 1 ..
Model 2...
To confirm I have completed only parametric tests. I have 1 group completing all predictor /moderators variables.
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It sounds like you would end up with a regression model in which you have a very large number of predictor (independent) variables as well as many interaction terms (since you have so many different COPE variables). My advice would be to first think about meaningful ways to reduce the number of COPE variables to be included in the model, for example, by aggregation (calculation of a summary COPE score), factor analysis, or simply selection of the theoretically most meaningful COPE variables. Otherwise you might run into various problems when entering all individual COPE items into the regression (e.g., potential collinearity, too many individual significance tests, large model with many predictors, loss of power to detect interaction and other effects).
Other than that, you could run a hierarchical regression model with only the main effects (predictors, no interaction terms) in the first model, then add the interaction terms in Model 2 to see if they add anything to the prediction of the outcome. But, once again, I would try to reduce the overall number of predictors first to avoid problems in the analysis.
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Hello,
I am using DASS-21 for a project. And, after getting the scores from 21 questions of the DASS-21 scale, you know, scores on the DASS-21 are multiplied by 2 to calculate the final score for each sub-scale and recorded according to its severity rating index. Depression, anxiety, and stress scores are calculated by adding up the scores of the items in each separate subscale, i.e.,
For Depression, the categories are-
No depression or normal (score: 0 - 9)
Mild (score: 10 - 13)
Moderate (score: 14 - 20)
Severe (score: 21 - 27)
Extremely severe (score: 28 and above)
**Anxiety, and Stress had similar types of categorie
Now, here these categories have been categorized/made after getting the scores from DASS-21. The respondents did not answer directly based on these categories.
So, are the variables of Depression, Anxiety, and Stress, obtained from DASS-21 can be considered 'Nominal data'?, or the 'Ordinal data'?
Thanks in advance.
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The main difference between Nominal and Ordinal numbers is that ordinal numerals are always used to demonstrate the order or rank of elements in a collection.  Nominal numerals are used to name or identify things. There’s no way to tell how many there are or how high they’re ranked.
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Depression is a mood disorder that involves a persistent feeling of sadness and loss of interest. What are the causes, effects and probable solutions to depression? Sharing is caring. Thanks!!!
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Depression is also a leading cause of disability globally and contributes greatly to the global burden of disease. Even though psychological and pharmacological treatments exist for depression, however, in low- and middle-income countries (LMIC), treatment and support services for depression are often absent. According to report from the World Health Organization, over 75% of individuals suffering from mental disorders in LMIC countries do not receive treatment. Depression is a serious public health challenge.
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I want to find the correlation coefficients between two signals and to plot the deference in values using matlab. I have two eeg.edf datasets with 20 electrodes each, of healthy and depressed subjects. I have to find the correlation coefficient between electrode Fp1 healthy and Fp1 depressed, F3 healthy and F3 depressed and so on..
Can anyone help me with the code? so far I used edfread to transform my datasets in timetable variables.
Thank you!
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You have 20 in each group, why not use Spearman rho = rs
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Any studies provide this?
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Reading can help reduce the rate of depression
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Hello, I have a question related to the metabolism of Serotonin. I am studying its metabolism in case of stress and depression and I could not find out the relationship between serotonin and 5HIAA in this particular case. MAO-A (the enzyme which metabolizes the serotonin hormone) inhibition is usually the mechanism of a lot of anti deprdepressantgs, but I have found several articles where the concentration of 5HIAA was lowered in case of depression and also suggestive of a lower concentration of Serotonin itself. But it doesn't justify the mechanism of action of antidepressant drugs. so I am confused now and want an answer for the exact relation of Serotonin and 5HIAA.
If serotonin is metabolized in 5HIAA, then 5HIAA concentration increases and serotonin descreases, so as serotoni conc. decreases, depression will increase. Is it right or no?
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Hi,
The referenced article given below can clarify your doubt:
Jayamohananan H, Manoj Kumar MK, T P A. 5-HIAA as a Potential Biological Marker for Neurological and Psychiatric Disorders. Adv Pharm Bull. 2019 Aug;9(3):374-381. doi: 10.15171/apb.2019.044. Epub 2019 Aug 1. PMID: 31592064; PMCID: PMC6773935.
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Do I need to request permission to use Beck Depression Inventory and Beck Anxiety Inventory or I can simply use them since they are available in the public domain. How I can decide that any given survey is in the public domain or not ?!
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But there are certain scales where Authors/publishers require fee for providing the questionnaires??
BDI II requires fee, I wonder if older version BDI also require fee.
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Dear Researchers,
Greetings! Very recently, one of our research articles have published in BMS Geriatrics where we discussed about the malnutrition and other geriatric depression risk factors. Here, we used 600 (300 depressed as cases and 300 non-depressed) older adult, residents (aged ≥60 years) of three rural communities of Bangladesh (see attachment).
Findings:
The study found no significant difference in gender (male Vs. female) between depressed (44.0% Vs. 56.0%) and non-depressed (46.0% Vs. 54.0%) older individuals. The study revealed that malnutrition was significantly (p < 0.01) higher in depressed (56.0%) than in non-depressed (18.0%) rural older adults. The malnourished older adults had around three times (AOR = 3.155; 95% CI: 1.53–6.49, p = 0.002) more risk of having depression than the well-nourished older individuals. Older adults who were unemployed (AOR = 4.964; 95% CI: 2.361–10.440; p = 0.0001) and from lower and middle class (AOR = 3.654; 95% CI: 2.266–7.767; p = 0.001) were more likely to experience depression. Older adults having a ‘poor diet’ were more likely to experience depression (AOR = 3.384; 95% CI: 1.764–6.703; p = 0.0001). The rural older adults who were single (AOR = 2.368; 95% CI: 1.762–6.524; p = 0.001) and tobacco users (AOR = 2.332; 95% CI: 1.663–5.623; p = 0.003) were found more likely to experience depression.
Geriatric Health research in Bangladesh is not in a good position. There is still so many lacks in this sectors. It's time to take some national level investigation and proper health policy for this age group.
Dear Researchers,
You can also add more policy recommendation for this age group.
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I think it would be interesting to include the topic of frailty in the discussion, caused among other things by a sedentary lifestyle. Low functional capacity is an important factor related to cognition and depression...
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Dear colleagues in the filed of psychology and similar disciplines,
Do you know some open call for cross-cultural project regarding post-COVID effects (or what is happening after the 2 years of pandemic) on various aspects of mental health (life satisfaction, stress, anxiety, optimism...), emotional status, interpersonal relationships, risky behavior, conspiracy theories and other beliefs, etc.?
Thank you.
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Dear Prof. Dinić!
I found the following websites hoping you consider these of value:
1) Coronavirus and COVID-19 Related Funding Opportunities from Research Professional and Pivot, Research Professional News is part of Ex Libris Group. Available at:
In this list I noticed the following: CDC-RFA-IP22-2203 "Tracking the burden, distribution, and impact of Post COVID-19 conditions in diverse populations for children, adolescents, and adults (Track PCC)" Department of Health and Human Services, Centers for Disease Control - NCIRD
Current Closing Date for Applications: Mar 07, 2022  Electronically submitted applications must be submitted no later than 11:59 pm ET on the listed application due date. Estimated Total Program Funding:$45,000,000
Further details are available at:
I really think these funds are also available for EU institutions as well.
Yours sincerely, Bulcsu Szekely
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I am measuring the association between depression and some variables in my study. The study population is divided into cases and controls. Depression is measured as a secondary outcome. When conducting a bivariate correlation between depression and the variables of interest in the whole population it produces a strong significant correlation, however when measuring the same association in cases only or controls only, the correlation coefficients drop to non significant level. i.e controlling for the disease status, the association between depression and the other variables become non-significant. What is the correct interpretation in this case?
"Depression is associated with certain variables" or "Depression has no relation to those variables and the disease status was the main cause of change in these variables"?
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As cases and controls are completely different based on their inclusion/exclusion criteria, so correlation for specific parameters cannot be calculated for whole sample. The correlation that you find for whole sample not in cases and controls may sometimes mislead the readers for specific associations among the parameters.
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I have been able to access the 10-item clinician-administered version but am interested in using the self-report form. I'm able to find articles that cite its use and those testing its viability but none that include the actual measure.
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Looking for this as well. Have you found it?
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Would it harm if an MDD patient receives TMS sessions 6 days a week instead of 5?
On a different note, is it required for the patient to receive 5 sessions in a row, or a patient could have TMS sessions simply 5 days a week in any order. Thanking you in advance.
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Some references:
Lefaucheur JP, Aleman A, Baeken C, Benninger DH, Brunelin J, Di Lazzaro V, Filipović SR, Grefkes C, Hasan A, Hummel FC, Jääskeläinen SK, Langguth B, Leocani L, Londero A, Nardone R, Nguyen JP, Nyffeler T, Oliveira-Maia AJ, Oliviero A, Padberg F, Palm U, Paulus W, Poulet E, Quartarone A, Rachid F, Rektorová I, Rossi S, Sahlsten H, Schecklmann M, Szekely D, Ziemann U. Evidence-based guidelines on the therapeutic use of repetitive transcranial magnetic stimulation (rTMS): An update (2014-2018). Clin Neurophysiol. 2020 Feb;131(2):474-528. doi: 10.1016/j.clinph.2019.11.002
Yang LL, Zhao D, Kong LL, Sun YQ, Wang ZY, Gao YY, Li N, Lu L, Shi L, Wang XY, Wang YM. High-frequency repetitive transcranial magnetic stimulation (rTMS) improves neurocognitive function in bipolar disorder. J Affect Disord. 2019 Mar 1;246:851-856. doi: 10.1016/j.jad.2018.12.102. Epub 2018 Dec 25. PMID: 30795490.
Buchholtz PE, Ashkanian M, Hjerrild S, Hauptmann LK, Devantier TA, Jensen P, Wissing S, Thorgaard MV, Bjerager L, Lund J, Alrø AJ, Speed MS, Brund RBK, Videbech P. Low-frequency rTMS inhibits the anti-depressive effect of ECT. A pilot study. Acta Neuropsychiatr. 2020 Dec;32(6):328-338. doi: 10.1017/neu.2020.
Chou YH, Ton That V, Sundman M. A systematic review and meta-analysis of rTMS effects on cognitive enhancement in mild cognitive impairment and Alzheimer's disease. Neurobiol Aging. 2020 Feb;86:1-10. doi: 10.1016/j.neurobiolaging.2019.08.020
Kaur M, Michael JA, Fitzgibbon BM, Hoy KE, Fitzgerald PB. Low-frequency rTMS is better tolerated than high-frequency rTMS in healthy people: Empirical evidence from a single session study. J Psychiatr Res. 2019 Jun;113:79-82. doi: 10.1016/j.jpsychires.2019.03.015
Ribeiro JA, Marinho FVC, Rocha K, Magalhães F, Baptista AF, Velasques B, Ribeiro P, Cagy M, Bastos VH, Gupta D, Teixeira S. Low-frequency rTMS in the superior parietal cortex affects the working memory in horizontal axis during the spatial task performance. Neurol Sci. 2018 Mar;39(3):527-532. doi: 10.1007/s10072-017-3243-8.
Lefaucheur JP. Transcranial magnetic stimulation. Handb Clin Neurol. 2019;160:559-580. doi: 10.1016/B978-0-444-64032-1.00037-0
Zhang H, Sollmann N, Castrillón G, Kurcyus K, Meyer B, Zimmer C, Krieg SM. Intranetwork and Internetwork Effects of Navigated Transcranial Magnetic Stimulation Using Low- and High-Frequency Pulse Application to the Dorsolateral Prefrontal Cortex: A Combined rTMS-fMRI Approach. J Clin Neurophysiol. 2020 Mar;37(2):131-139. doi: 10.1097/WNP.0000000000000528
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I guess there must be some data collected regarding Covid and related to the field of psychology/psychiatry, considering its psychological impact. It might be gathered from the patients, family members or the society at large, either a public or private collection. Does anybody have any idea on how to access such data for research purposes?
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Dear Prof. Farhad Montazeri ,
For example, I saw of Lancet & Nature publications, just register, they will send updated data and research as you agreed to get updated - the ones you chose - to your email registered with them e.g.:
ABOUT THIS ALERT Access to article abstracts is open to all Alert recipients. Access to full-text articles is limited to subscribers who have activated their online access. Activate your online access to your subscriptions at (under elsevier):
@
the Lancet COVID-19 Resource Centre
@
Please add briefing@nature.com to your address book.
Enjoying this newsletter? You can use this form to recommend it* to a friend or colleague — thank you!
@
LitCovid is a curated literature hub for tracking up-to-date scientific information about the 2019 novel Coronavirus
@
Novel Coronavirus Information Center
Elsevier’s free health and medical research on the novel coronavirus (SARS-CoV-2) and COVID-19
@
COVID-19: Epidemiology, virology, and prevention
Hope I understand you correctly, dear Prof.
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Can you tell me "what are the different clinical stages of Mental Health among young boys. " Related to anxiety or depression...If so can you plz tell me those stages.
E. G
Stage 1
(a)
(b)
(C)
Stage(2)
Stage (3)
Stage (4)
Stage (5)
Stage(6)
----++++--
What are the characteristics of these stages?
How as a clinical practitioner do you define these characteristics.?
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As already indicated, the STAGES, according to the Natural History of both psychoptologies, would be AND IT IS unethical and antimoral to see how they appear and evolve WITHOUT INTERVENING IN THEM !; But the LEVELS or DEGREES or STAGES of SEVERITY are universally categorized or hierarchical, from less to more, as: a) ABSENT, b) MILD, c) MODERATE and d) SERIOUS -which is how they are hierarchized, for example, the BDI -Beck Depression Inventory- and BAI -Beck Anxiety Inventory-
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As said in the title, I'm looking for a journal related to my research Twitter Arabic Sentiment Analysis to Detect Depression Using Machine Learning
to publish it it's preferred to be Q1
please help me out.
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Joao Luiz Junho Pereira I don't think the journal you proposed is suitable for what Reem Ml is looking for. In fact the question was about a journal related to Twitter Arabic Sentiment Analysis to Detect Depression Using Machine Learning so it preferred to have a journal that deals with Machine Learning, Artificial Intelligence such as:
- Machine Learning with Applications not impacted but indexed (https://www.journals.elsevier.com/machine-learning-with-applications)
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What do you think are the most important psychological disorders associated with COVID-19?
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Los más comunes son depresión, estrés, miedo, ansiedad, desesperación, tristeza etc
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Friends and colleagues that use psychological questionnaires to measure depressive symptoms: what is your preference between the PHQ-9 and the BDI-II?
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The PHQ-9 has the advantage of being faster to apply because it has fewer items, but the BDI-II is more complete and, therefore, more reliable in addition to having more literature on it: in short, I advise -if you can choose between the two, the BDI-II.
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why the score value in research gate depresses with weekly updated, sometime?
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From my point of view, ResearchGate (RG) is the best attractive academic social networking portal for the scientific community. In practice, RG is one of the biggest social media networks for the scientific community. It is a platform and a gateway for sharing information and experiences between scientists, experts, researchers, and practitioners. Hence, I am grateful to the network opportunities offered by RG for having this access to a broad range of researchers, papers, projects, questions, and discussion threads that otherwise I can't find. In a nutshell, ResearchGate (RG) is a kind of social media with a strong academics/research emphasis.
But, let me point to the following issue. Recommend, Follow, Download an article is just social interaction. Despite it helps to increase the RG scores, it reflects neither the work quality nor the researcher position. This score depends on the institution where you work; this score in the institution where I work hasn't any remote feedback.
I know that the more you participate in various research activities, the more your research interest increases. Nevertheless, as we are researchers, the RG total research of interest shouldn't be our main goal in itself. We should do our job honestly, such as writing valuable articles, participate in the useful discussions that we are really interested in. If we don't bother with this metric, we will see that it will increase.
If we make this metric our goal, it will astray us and then we will jump over some fences to increase our metrics without real internal improvement.
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What are the pharmacological risks?
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Thanks you, Dr. Miky Timothy
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I am a Medical student working on a research concerning mental health on young people. I am looking for a scale with good properties for symptoms of depression and anxiety.
Since the questionnaire includes many other dimension, short version are particularly welcome!
Thanks in advance!
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For Anxiety the "BAI" (Beck Anxiety Inventory) and, for Depression, the "BDI" (Beck Depression Inventory) ... Idem Hamilton
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What are the factors that predispose patients to treatment-resistant depression?
What are the advances that predict antidepressant treatment response for depression?
Two articles about prediction of antidepressant treatment response by using artificial intelligence technology and machine learning algorithms:
  • An electroencephalographic signature predicts antidepressant response in major depression (doi:10.1038/s41587-019-0397-3)
  • Brain regulation of emotional conflict predicts antidepressant treatment response for depression (doi:10.1038/s41562-019-0732-1)
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Because it depends on several causes:
-The type and intensity of such Depression
-The one that, in addition, there is also an Anxiety Chart (Mixed Depressive / Anxious Disorder)
-Whoever is male or female
-The type of Antidepressant used: An MAOI is not the same as a Tricyclic type, an SSRI or a Selective Serotonin and Noradrenaline Reuptake Inhibitor or Epinephrine (SSNRI)
-The one who receives a Combined Treatment with, in addition to Antidepressants, Psychotherapy, eminently Cognitive Behavioral.
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I am working on a paper on unemployment on psychological health of youth. Please in what order can input the following predictors variables using age as the control variable?
Perseverance
Irrational behaviour
Low self esteem
Depression and
Suicidal ideation
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It probably depends on your hypotheses and your design. I'd look at inter correlations between them, to see if multicollinearity might become a problem, but in the end theory and predictions should dictate the order.
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To understand the gut microbiome-brain axis
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It seems yes. I read a study just last week that found that microbiota were associated with depression. Unfortunately, I deleted the source so I can't give you the reference :-( Sorry!
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Many people suffering from Typ one diabetes mellitus, could be identify as almost depressive as well.
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@bettina berger, i agree with you. Diabetes is usually associated with many psychiatric and psychological manifestations, apart from just depression. So it will be great to screen all diabetic patients with atleast all major psychological problems besides depression.
This might not be possible in all the LMIC , but general physicians should be very vigilant for identifying , diagnosiing these disorders
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I have done EIS of SDC (Sm doped ceria) electrolyte from 550 to 750C. I observed the formation of a depressed semicircle. Also the diameter of semicircle decreases with increasing temperature with a decrease in resistance. What could be the possible reasons for formation of depressed semicircle? I am attaching the figure below.
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Thanks, I will study the article you referred. I have tried to construct an equivalent circuit using Zview but it simply leads to Rt(QRep), which is not very helpful to reveal the true information.
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how many of us undergo the Stress of being a researcher ? does it motivates only or it does Depresses at Times ?
please do write your views on it.
Best regards
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It can be nerve-racking at times, but can provide the necessary impetus to create something meaningful.....something that makes a good contribution to the field.
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Hey, all! I'm conducting research including a depression screening as one of our measures - the Centers for Epidemiological Studies Depression scale (CES-D). This tool has cutoff scores: ≥16 indicates clinically relevant symptoms and ≥27 indicates moderate to severe symptomology.
Our team is discussing how to disclose to participants if they had a positive score after our research concludes. We want to inform subjects of anything clinically relevant but not cause harm. How do you all handle this?
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NEVER !: it is an investigation not a clinical practice ... but also, if the anonymity of the participants in it has been rigorously guarded - as required by the APA, the "Lex Artis" and common sense, so that the subjects fill in The Tests - how can the researcher / s know who each Test is or are and their results?
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I do not know if this is a merely coincidence, but over the last number of years doing research, I have seen hundreds of Junior Researchers (either undergrad, master of PhD students) suffering from blood- and energy-suckers coordinators. Perhaps, this is a consequence of multiple factors (such as history of academic world and labor western culture). The fact is, as a Senior Researcher or Project Coordinator, what do you do to avoid or to alleviate mental illness amongst your students?
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The psychological stability has a great impact on the educational level, because it increases his desire for education, which in turn reflects positively on his comprehension and educational attainment, and vice versa if the student's psychological state is disturbed or has a feeling of anxiety, this will lead to poor concentration and a lack of comprehension in general.
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I need a stack of black and white .jpeg/.tiff/.jpg/.png images across time of either action potentials, neurons firing, or brain scans (comparing disease and normal brain, disease progression, etc.) that I can colorize and overlay for a project in a data visualization course. It wouldn't be published and only for submission to the instructor.
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Something like this for action potentials ?
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I'm doing a research with my team on Depression in India. We need a dataset of social media posts of Indian people. We want to do Sentiment Analysis on these posts and find out some insights which are India specific.
  • We have tried Facebook(but its very hard to scrape data from it).
  • We have tried Reddit(but got very less posts, also it doesn't tell the country)
  • We looked twitter, but not fruitful.
It is possible that we can get data from the above three more efficiently, but do not know how?
If there is any forum related to depression, or mental health, it will also work.
We've also posted related question here:
  1. https://www.reddit.com/r/redditdev/comments/k2stws/getting_post_from_a_subreddit_only_from_users_of/
  2. https://www.reddit.com/r/datasets/comments/k2tx96/looking_for_social_media_posts_of_indian_people/
TL;DR: Looking for Indian dataset of social media posts of depresses/anxious people.
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Mohamed Elhadad Thanks for your suggestion, will sure look into that.
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Dear colleagues
I'm interesting in vermiculture and vermicompost technology. However, I noticed that there were some negative impact effects of adding vermicompost to soil, and depressing growth rate of plants.
Is there any one noticed that or face problems with using vermicompost as organic fertilizers
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M.K. Tripathi
I do agreed with Dr. M.K. Tripathi sir
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Hi,
for a facial emotion recognition detection project, a friend asked me if I know where he could find a dataset with faces of depressed people.
I found this deep learning facial emotion recognition project:
based on theDexter Miranda’s photo project, "The Face We Make":
But, the photos are not specifically about "depressive faces" (more about emotions).
On Kaggle, I found a better dataset:
And the JAFFE dataset:
So, I would like to know if there are "scientific or psychological dataset" with photos of faces expressing different emotions with depressive symptoms?
Thanks,
Laurent Berry
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Thanks a lot...
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I am interested in the literary origins of noir crime writing.
Can anyone recommend the very best, or 'must read', works on either the novelist Ernest Hemingway or the subject of the 'Forgotten Man' (that is American veterans of WWI and the mass unemployed of the Great Depression)?
Many Thanks!
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Its a pity this has not heretofore been answered. I do not know of essays etc but there were a number of writers who filled in the gap but not necessarily by alluding to the war as such or in depth. Scott Fitzgerald's stories of social and personal dissociation demonstrate the effects of the conflict.
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Dear Colleauges,
What is the rationale for studying dopamine’s role in Major Depressive Disorder?
Major Depressive Disorder (depression) is a multifactorial, biologically and symptomatically heterogeneous condition. Amongst the numerous—and potentially equally valid—proposals concerning its aetiology (e.g., inflammation, genetics, stress-related mechanisms, etc.), one of the longest-standing ideas is the “monoamine hypothesis” stating that one or more dysfunctional monoamine systems are key contributors in the development of this psychiatric disorder. Historically, most of the research focus has been on the role of serotonin and noradrenalin. Although this might not be “The” biological explanation for depression, a dysfunctional monoamine system, dopamine system in particular, is likely to contribute to the emergence of the two “sine qua non” symptoms associated with depression: on one hand, depressed mood and reduced motivation/perseverance and on the other, anhedonia and loss of interest in what were previously pleasurable activities. There is growing interest in dopamine’s role in clinical depression, especially, in the way it works as a modulator of the brain’s reward systems. Furthermore, there is pre-clinical evidence that A10 dopaminergic neurons projecting from the midbrain ventral tegmental area to the nucleus accumbens and dorsolateral prefrontal cortical areas over several routes are associated with motivation, exploration, appetitive learning, reward-driven behaviours, and a depressive-like phenotype in experimental models of depression. The reward systems might also be implicated in aversive stimuli, a recent notion which needs to be further explored.
This Special Issue of Brain Sciences aims to bring together some of the current ideas on the function or dysfunction of dopamine and dopaminergic transmission in depression, by examining the most recent evidence from advanced clinical and experimental research. It will gather insights from well-acclaimed experts in the field towards answering the ultimate question: what is the true role of dopamine in Major Depression?
For more information on contributing to this Special Issue, please go to:
Thank You!
Dr. Màté D. Döbrössy Guest Editor
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Нехватка дофамина и повышение глутаминергические рецепторы увеличивают риск болезни Паркинсона, на механизм развитие депрессии основной роль играет серотонинергические медиаторы
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Are feelings of emptiness commonly experienced even within non-clinical populations? If so, are these experiences less salient due to a lack of personal awareness about the problem? Or, are people reluctant to disclose this feeling due to societal stigma?
In other words, is emptiness a major problem in modern society, and, if so, why is it so inconspicuous?
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Different believes have different meaning for "Emptiness". In Buddhism, Emptiness is the kernel of everything, living or non-living. All human feelings are illusion, and only emptiness is essential and eternal.
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Why the number of secondary depressions on existing chromosomes varies?
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Thank you dear hadeel.
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As millions are getting depressed losing health and job and loniliness ,anew hope is begining to build up.really we need to this encouragement.we need all hygene ,distant physically to immune ourself from epidemic .this is new oxygen and new life really.so How can we fight depression and fear?lets hope that vwe recovered from deadly disease ,to get new life ,freedom and happiness.
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Once people can master (balance) their ego (materialistic desires) and turn to their soul (creative purpose), happiness and bliss will set in.
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Evidence is accumulating that glutamate abnormalities may also play a role in depression. But how does the glutamate level change? In chronic mild unexpected stress models, the glutamate level is decreased. But in the early stress, the glutamate level is increased. In my opinion, the early stress results in the increased glutamate, which leads to glutamate-mediated toxicity and damage the neurons. Later, the loss of neurons lead to decreased glutamate.
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I have worked a lot with mice and must say that they are surprisingly good models for the human being. One evolutionistic theory claims that the rat is our closest cousin, not the ape.
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Anyone has a pdf form of Children''s Depression Inventory 2 (CDI2)
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Children's Depression Inventory (CDI and CDI 2)
  • January 2015
  • DOI:
  • 10.1002/9781118625392.wbecp419
  • In book: The Encyclopedia of Clinical Psychology
  • 📷Maria Kovacs
  • request fulltext from here on RG
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Hello everyone! I am researching the molecular mechanisms which drive depression in the context of gut microbiota. From what I know, depression's pathogenesis primarily relies on Tryptophan metabolism. On one hand, the pathway is perturbed to the kynurenic pathway which leads to the formation of kynurenic metabolites (KYNA, QA, XA, etc). These kynurenic metabolites exert neurotoxic effects which ultimately drive depression phenotypes. They are also able to affect the enteric nervous system, the gut millieu, and immune system which contribute to depression.
On the other hand, Tryptophan metabolism can also be driven towards serotonin synthesis. Inflammatory bowel disease and its likes (Crohn's disease, colitis) have been shown to have increased serotonin (evidenced by increased TPH expression) and decreased SERT expression. Serotonin has been shown to be pro-inflammatory and this supports the inflammatory theory of depression.
While these explanations do not completely contradict each other and that they may simultaneously contribute to depression, an "irony" still exist that one says a perturbation towards kynurenine while the other is towards serotonin. Either way, Tryptophan is consumed and surely leads towards an increased bias to one pathway (ie. increased serotogenic or increased kynurenic). Hence, do you know of any articles which settle this apparent contradiction? Or perhaps there is something I incorrectly understand?
Thank you!
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Simon N Young thank you for your response.
1. Yes, they cannot cross the BBB but kynurenine and tryptophan can. Trp can be converted by microglia and astrocytes using IDO to kynurenine. From thereon, they can be metabolized into these acids. Is this not a mechanism which kynurenine metabolites exert negative effects on the brain?
2. Thank you for this. I , too, am more familiar with the low serotonin associated with depression. I just asked about high serotonin and IBS because it conflicts this explanation. Perhaps inflammation and other factors caused by IBS influence increased depression incidence found in patients.
And yes, MDD is indeed multifactorial. I am interested in how gut microbiota possibly exert influence in the etiology of depression via Trp metabolism.
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Hi all,
I am doing a longitudinal study using depressive score as my DV. It is an observational study. No variables are manipulated. I have currently collected baseline (Time 1) and first follow-up (Time 2) data. I have a number of variables as predictors of the depressive score and I would like to identify what hypothesized variables collected at baseline would predict the Time 2 depressive score, and possibly be significant predictors for depressive scores at other time points in the future.
Do I
1) put predictors at baseline as IV, change score of depressive score as DV in the multiple regression model?
or
2) put predictors at baseline and baseline (Time 1) depressive score as IV, and Time 2 depressive score as DV in the multiple regression model?
I have actually tried both methods, it ended up that while using method 1, the predictors of change score are the same as those of Time 1 depressive score.
Whlie using method 2, no predictors (not even baseline depressive score) at baseline are significant predictors of Time 2 depressive score.
I wonder how I should have analyzed and interpreted the data. Thanks a lot!
Anna
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Remember, especially with no manipulation, correlation does not equal causation. So, "predicttion" may be a bit of a stretch.
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In your personal experience,How do you manage your life and make a balance between work, family and other related sections!?:)
I would be thrilled to have your points!
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Equally, dear Dr. Hossein
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After being affected with that viruse , most of the patients feel depressed and sad . How can we , psychologically, encourage them ?
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Interested discussion. Please follow up....👍
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please guide me about the sample size calculation for this study
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Hi! It depends on whether the researcher is using probability or non probability sampling and the population size. Usually the sources used to decide the sample size is following Hair et al 2010, G power calculator etc.
Reading the following material could be helpful as well. Thanks
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I am trying to discern whether, in the brain (structure & function) of people with bipolar disorder/MDD/schizophrenia who experienced childhood trauma, there are:
1. already differences in children's brain structure & function that trauma further modifies and the person develops a mental illness OR (genetics first then trauma)
2. trauma changes the structure and function of the brain that the child's genetics further modifies and the person develops a mental illness (trauma first then genetics)
Has anyone researched this & if so, can you please share your findings or references you know of?
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Thank you for your insightful comment. I have read Cassiers et al (2018) as well as 3 other insightful articles: 1) Nemeroff CB.(2016). Paradise Lost: The Neurobiological and Clinical Consequences of Child Abuse and Neglect. In Neuron; 2) Aas M et al. (2019) Childhood maltreatment and polygenic risk in bipolar disorders. In Bipolar Disorders; and 3) Stevelink et al. (2019) Childhood abuse and white matter integrity in bipolar disorder patients and healthy controls. In European Neuropsychopharmacology.
  1. In Cassiers et al (2018), their review of the literature supports the hypothesis that the brain changes are a protective adaptation in response to abuse, they did not discuss the genetic components that may be predisposing to or responsive to abuse so it doesn't directly answer the question.
  2. In Nemeroff (2016), he suggests (based on my assessment) some brain changes are due to the moderating effects of genetics (so genetics first) (eg, carriers of 1 or 2 copies of the "short" allele of the serotonin transporter promoter polymorphism have greater rates of depression vs those with the "long" allele homozygotes with equal childhood trauma) and other changes are in response to the trauma and predispose the person to the mental illness (eg, reduced hippocampal volume in depressed women with a history of childhood maltreatment but not in equally depressed women without maltreatment).
  3. Aas M et al (2019) reported that polygenic risk score (PRS) and CTQ were inversely correlated so those with lower PRS reported more severe abuse and vice versa, so the based on this (my interpretation) is that in a brain/body with more "imbalances" due to genetics (brain structure/function and physiology that is predisposed to BD), abuse does not need to be severe to make the changes sufficient to cause BD wherein people with low PRS have brain structures and physiology is more "balanced", greater severity of abuse is needed to sufficiently change the brain structures and physiology to cause BD. They did not also look at brain or physiology so we can only infer based on genetics.
  4. In Stevelink et al (2019), their study findings suggest "that childhood abuse results in poor white matter integrity in a subset of people who are then possibly more vulnerable to development of psychiatric disorders, including bipolar disorder" and "that childhood abuse, in particular, is associated with FA, possibly due to its effects on HPA-axis activity." But as pointed out in the limitations, their cross-sectional study design does not allow for establishing causation "Based on our results, we cannot differentiate whether decreased integrity of white matter in patients is caused by childhood abuse, or whether this decreased integrity was already present prior to experiencing childhood abuse."
I am interested in causation and the interplay of genetics and childhood trauma as I am trying to write a book on childhood trauma and how the different types of trauma at different times explains the behaviors of survivors, the mental health challenges caused by childhood trauma and toxic stress, and how people can "overcome" (I hate this word but can't think of another) trauma. My story of childhood trauma, developing several mental illnesses including bipolar disorder, and how I was able to get a PhD and have a successful career while growing and healing is being used as the backdrop to tell the scientific story to a lay audience.
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Hi Everyone,
I want to analyse how well two scales agree for detecting changes in wellbeing. I look at the Bland-Altman Method. One scale is a simple score from 0 - 10 for wellbeing. The other scale is the well established Beck’s Depression Inventory-II (goes from 0 - 63) . I wonder how to analyse the agreement?
Thanks!
Fred
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Hello,
This link talk about: Agreement Between Two Ratings with Different Ordinal Scale
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I am a physician and visiting research scientist at yale and together with my coauthors have published several studies in the field of psychology through Network Modeling and related analyses using r packages like bootnet, qgraph, NetworkComparisonTest, etc. I thought it might be a good idea to discuss different subjects related to this field, in a group. I am also interested in collaboration with other teams working in the field. Let's share our ideas, questions and suggestions in this group.
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Makes sense. Thanks for letting me know.
I hope followers of this discussion forum check your study and package,
which address an interesting topic in network analysis. Let's keep in touch!
Best Wishes,
Farhad
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I have a student conducting research on coping mechanisms used by males with partners suffering from Post Part Depression. It has been very difficult getting participants to complete the survey. Any suggestions on where this can best be posted to improve participation?
Already tried social media sites and groups focused on male issues with limited response.
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Hi. I think you will have constant challenges getting validated data with a health topic relating to women, but studying it from a partner/male perspective.
All the best, though.
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With everyone having their own struggle and a different definition of being 'stressed'. Does problems of 23 years old smaller than that of 46 years?
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The uniqueness of depression is that the base of depression, on the basis of which depression occurs, is present in 99% of the population. 99% of the population are susceptible to depression, since the cause of depression is a violation of certain physiological processes in the human body, which of course are common to all people (all people in the body have the same physiological processes). Therefore, at 10, 20 or 40 years, depression is one and the same basic disorder, which can manifest itself in different ways due to different stresses at different ages (stresses are triggers of depression at any age).
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I am currently working on a database and I have tried various methods of machine learning and deep learning, all leads to poor classification/prediction. However, this might show that the two groups have no significant difference. For example, the database I have is a collection of audio speech and their associated depression level. I am assuming that the culture of where I am from and the strong religious believe, prevented the society from going too deep into depression. However, I need to find some literature to back up this statement. But, it seems that there are no significant difference between the acoustics of depressed and non depressed. Can I write these poor results in a paper? Any tips?
Thank you
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Hello Dr Nik, Yes sure you can write a paper and publish it in Scopus journals...
I can present some tips for you:
1- You can change the Chunk size of the voice sample and then check the results again (Usually when the chunk size (sec) is big, the results will increase (accuracy). While when the Chunk size is small, it sounds like a challenge to get high results.
2- Also, when the databases are equal (e.g., depressed and non depressed databases), the results often become higher
2- Give some significant points in the conclusion section in terms of this area.
3- Write the paper in very good English.
4- Moreover, check out these articles may help you in this area:
Thesis ''Automatic assessment of depression from speech: paralinguistic analysis, modelling and machine learning''
And all the best (:
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Hello, I am working with the Beck Depression Inventory and Beck Anxiety Inventory. I am trying to establish cut points for depressed/not depressed and anxious/not anxious. I know that I need to use an ROC curve to find the cut points, but I am not sure of the process to get there. Can anyone provide directions on going from survey questions/answers (I have 22 participants who have completed both surveys; no missing data) to establishing the ROC curve?
Thank you very much
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ROC (Receiver Operating Characteristic) analysis (Hajian-Tilaki, 2013) is a graphical representation of the effectiveness of the prediction model by drawing the characteristics of qualitative binary classifiers created from the model using many different cut-off points. Calculate the Youden Index for best sensitivity and specificity values.
One (mine) example of use of ROC Analysis in research:
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It is believed that there are several depressed people of COVID-19 lockdown. How a psychologist could support them amid the lockdown?
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E-questionnaire to the family & the cases. I think that is may be help. psychiatrist and psychotherapist can help more.
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I would like to enrol into a master's program at one of these universities and write my master's thesis on a topic involving the above three components.
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Following.
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Is there any physiological value or index that show us a stress or anxiety level? For example in an experimental reseach, when we want to find out computer games effect on stress, depression or anxiety, How can we detect these disorders level by using with physiological indicators?
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Yes you can detect stress, anxiety and depression by using those parameters. Here is a paper on detecting stress by machine learning techniques using ECG.
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corona pandemic is worldwide issue and during the lockdown period people are getting depressed. so let all discuss their way of handling stress
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Strive to maintain a normal biological rhythm despite the quarantine
Exercise appropriately (without exaggerating) and, if possible, in contact with nature.
Maintain important emotional ties, take advantage of the quarantine to restore neglected ones due to the stress of busy life
Be creative and productive in what you like (work, art, readings or whatever you want)
Learn to be a little fatalistic and not to blame anyone for the problems you are facing
Think concretely about solutions for your problems.
Ask for help if you need it
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Dear all
Hope you are all safe and healthy. We are doing a study on Phubbing and its association with depression, anxiety, and couple satisfaction. Phubbing is an under-researched area despite the increasing prevalence of problematic internet use and the associated mental health consequences. Since we need a large number of respondents, we are posting here and requesting you all to kindly spare a couple of minutes to go through it.
We assure that it will only take a few minutes to complete the questions.
We also encourage you to share the study.
Feel free to contact us for any doubts
Here is the link:
PS: It can be filled by singles too, as couple satisfaction is only a part of the study.
Best regards
Pooja
Karthick
Bigya
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Neil Dagnall Thank you for your interest in our study. Please feel free to participate and share . This is the link
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Most of the commentary about the current COVID-19 induced economic challenges use either the 2008 global financial crisis (GFC) or the 1929 Great Depression (https://www.bbc.com/news/business-52236936) as reference points. The reference points most relate to; 1) the severity of the economic challenges and; b) the time it will take to recover from the current challenge, in relation to either 1929 or 2008.
In the outlook for the recovery period, it assumed that the recovery will either be in the form of V shape or an L Shape compared to previous recovery shapes.
The questions are as follows:
  1. Are there parallels between either the 2008 GFC or the 1929 Great Depression and the COVID-19 induced economic challenges? Can we possibly draw any parallels?
  2. If there is, in what way are these the same and in what way are they different, except for the obvious and "well documented" drivers and causes.
  3. What shape do you think the recovery will take/assume? V or L?
  4. How long will the recovery take, either as measured in number of years, quarters or months? and Why?
For ease of reference, see some of the links below
NB: The significance of the BBC reference is the quote (s) attributed to the MD of the International Monetary Fund (IMF).
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Well Dear Prof. Kheepe Lawrence Moremi
In 2008 vzla didn´t feel any finantial crisis (oil barrel ~ 100 US $) so for me 2008 GFC is not a reference point. Now happens the same, we don´t feel any crisis, since our internal hyperinflation started 3 years ago & the venezuelan oil industry was already brought to its knees at that time. So I take as a temporal reference the 1929 GD.
Interesting to see an hyperinflation chart poweder by Prof. Hanke:
Our hyperinflationary misfortune is a little more than a year ahead of the rest of the world according to Prof. Hanke chart (02/2019 we had a peak). But I can tell you something for sure: humankind can live only with 1/3 pound of white rice & a cooked green banana daily per person. No toothpaste & teeth falling out, all alive until a lack of medications, either the bug, kill the mayority.
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I am writing a research proposal on psychological aspects of IBD (anxiety/depression...) what should I use as my themes for my lit review?
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look at the idea emphasized in the literature review of the disease
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HI,
this is Farhana, currently studying Bachelor of Science in Computer Science and Engineering in BRAC University in Bangladesh.
My thesis project is on "Depression and normal condition" and I wanna find a clean EEG data set about Depression and normal condition. is it possible for you to share your data set with me?
Thank you
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Depression, also called major depressive disorder or clinical depression, is a mood disorder that causes a persistent feeling of sadness and loss of interest.
Have you ever struggle with depression? Please advise how depression can be overcome?
Thank you in advance for sharing your knowledge and experience.
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"Yoga" and "meditation" are the best ways to overcome depression.
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We are in the middle of a crisis, in the quarantines. Irresponsible behavior has brought us to our current state. We did not learn any lessons learned from viruses that preceded and resembled the COVID-19 virus. Today's topic is not the reason that led us to this situation but commenting on the measures we have taken. The study of (Bishwajit et al., 2017) examined the effects of physical activity on depression. Their study had a representative number of middle- and older-aged subjects (7204). They concluded that a lower frequency of vigorous physical activity was significantly associated with higher rates of depression diagnosed. Depression symptoms and physical inactivity are factors that are closely correlated with obesity (Garimella et al., 2016). The elderly population has a prevalence of anxiety and depression around 10 and 12 %, these findings are caused as a consequence of different factors. Health-related quality of life and physical function play an important role in depression and anxiety (Sousa et al., 2017). The logical conclusion is that physical activity can reduce the levels of depression. Many studies have addressed this topic. Throughout history, our race has evolved. From the beginning of the cognitive, through the agricultural and industrial revolution to the present, we can observe a trend of decline in physical activity. This trend was accompanied by the appearance of metabolic and chronic diseases. Chronic diseases are major killers in the modern era. Physical inactivity is the primary cause of most chronic diseases. (Booth et al., 2011). Physical activity primarily prevents, or delays, chronic diseases, implying that chronic disease need not be an inevitable outcome during life.
This brief introduction is just a small overview of the literature that has examined the topics of physical inactivity, depression, and chronic illnesses.
Because we are in quarantine, and our movement is restricted and in some environments disabled we face many difficulties. Speaking personally and listening to people from my surroundings, from a psychological point of view, quarantine has a rather negative impact on people. With this, the media and the internet, which is full of misinformation, make people panic.
The following questions are:
  • Is quarantine an ethical solution?
  • How will this inactivity affect people?
  • How will inactivity affect obesity, chronic diseases, and ultimately, mortality?
Reference:
Bishwajit, G., O’Leary, D. P., Ghosh, S., Yaya, S., Shangfeng, T., & Feng, Z. (2017). Physical inactivity and self-reported depression among middle-and older-aged population in South Asia: World health survey. BMC geriatrics, 17(1), 100.
Booth, Frank W., Christian K. Roberts, and Matthew J. Laye. "Lack of exercise is a major cause of chronic diseases." Comprehensive Physiology 2, no. 2 (2011): 1143-1211.
Garimella, R. S., Sears, S. F., & Gehi, A. K. (2016). Depression and physical inactivity as confounding the effect of obesity on atrial fibrillation. The American journal of cardiology, 117(11), 1760-1764.
Sousa, R. D. D., Rodrigues, A. M., Gregório, M. J., Branco, J. D. C., Gouveia, M. J., Canhão, H., & Dias, S. S. (2017). Anxiety and depression in the Portuguese older adults: prevalence and associated factors. Frontiers in medicine, 4, 196.
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You have touched on an interesting problem of long-term and epidemic-related effects. No one is dealing with them right now because of the current situation but in a few months, we will see a terrifying summary of what happens.
Patients have worse control of chronic diseases due to difficult access to health care and almost not existing private health care sector. Quarantine is associated with a lack of physical activity, social life and developing bad eating habits. It will result in a higher suicide rate, higher chronic diseases mortality.
In my opinion, two weeks of restricted quarantine won't lead to increased obesity. Although the quarantine should last as long as the pandemic will end, and we don't know how long it'll take...
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Treatment of Bipolar Depression
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Cognitive behavioral therapy as well as somebody who walks with them is also helpful if you fear that an antidepressant will provoke mania. The more physical training and talking the better. These patients are usually rather alone while relatives and friends are tired and burdened from their ups and downs. Already group therapy is helpful.
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During test of cycle_gate, we ask people to walk, then they pay attention to it and their way of walking is changed, also darkness can change it too.
but that is question, whether mental illness such as depression change the cycle_gate?that could help us to find therapies for these diseases.
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Yes,affects,Of course it affect our cycle_gate. Depression (major depressive disorder) is a common and serious medical illness that negatively affects our feels. Depression causes feelings of sadness and/or a loss of interest in activities once enjoyed. It can lead to a variety of emotional and physical problems and can decrease a person’s ability to function at work and at home.
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Planning an intervention for infertile depressed and anxious people, for guidence purpose I want to go through those interventions if you know any. thank You
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Logotherapy is a successful intervention. Finding the present meaning in life, can be short-term or long-term. Resolving the fear of death by finding a lasting faith. Social support, love, which a man suggested should be available in the pharmacy,
and insight and acceptance that there are things that exceeds our understanding.
A very quick and effective intervention is listening to classic music.
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Is there a scale available free of cost and without copyright issues to evaluate self-efficacy for primary health workers ?
Similarly , are they scales available for evaluating change in social , health and economic outcome in depressed individuals located in low middle income countries ?
If the scales are not available , on constructing these scales can we develop a structured questionnaire assessing social , health and economic outcome in depressed individuals ? If so , what constructs should we undertake ?
Thank you
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http://userpage.fu-berlin.de/~health/selfscal.htm here is the page to self-efficacy scales in many different languages
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I am currently starting to write a literature review for my Doctoral Thesis. As I am writing, I am wondering about the acceptability of using only three books as references for a chapter (not the whole discussion) in my literature review.
The reason why I am doing because I found these three books are recent (2012, 2014, & 2015) and already consist of abundant information for the chapter.
I am writing a chapter about Depression and these three books has already given me information about 1) Types of Depression 2) Causes of Depression (from Biopsychosocial aspect) 3) Effect of Depression 4) Best Available Treatments 5) Prognosis of Depression. Furthermore, for me, these sub-chapters are already enough for one chapter only. Considering that there are still many to come.
Any critique or suggestions are welcome.
Thank you
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Dear Wisnu
Whilst it is good that you have a solid reading base from the books you have mentioned, it is often the case that books have taken some time to produce and therefore have older primary sources. I think it would be good for you to conduct a scoping search as well, you may identify some of the latest literature from a quick search. It is always good to look for any current systematic reviews or commentary reviews that fit your topic in general (i.e. search of topic names + systematic review, review), in addition look for the latest papers as they may be useful and can often signpost you to other relevant literature. In addition books tend to have their own overall narrative that reflects the thinking of an author (or authors), whereas it would be expected that you would take a more critical and objective stance and this would be helped by a wider search of the literature.
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I need to apply LiDAR for fault growth analysis project to study the presence of Strike-slip faults in strain linkage extensional regime.
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Try to see the following publication: Magmatic cycles pace tectonic and morphological expression of rifting (Afar depression, Ethiopia)S. Medynski, Raphaël Pik, Pete Burnard, S Dumont, Raphael Grandin, Alice Williams, Pierre-Henri Blard, Irene Schimmelpfennig, C Vye-Brown, Lyderic France, et al.
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I've seen at symposia that some people have success recruiting for research studies on subreddits like r/depression or r/anxiety. Does anyone have experience with this? I have an upcoming study where I think this recruitment method would be useful. Has anyone run into IRB issues with this recruitment method? If you've had success with this recruitment method, how did you go about making your posts?
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I've used the "subreddit" r/samplesize for recruitment, its dedicated directly for this purpose (instructions on how to post, etc., are contained in the sidebar). I got about 200 participants in of a month using this approach, and my IRB did not ask any questions.
I think posting recruitment ads on other subreddits (related to disease states, etcc) is at the discretion of the moderators. I asked about one and was told no.
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I would like to write an academic essay on Depression among youth using Participatory Action Research and its applicability in our country but I dont have the idea how to make my ideas flow. Im starting to build an outline but it seems lacking and disastrous. Do u have any idea what are the essential information and data to include so that my paper will be clear and convincing? You can also include suggests readings that I could review. I highly appreciate any form of help.
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Two other articles of mine might help:
`Action research in graduate management research programs', Higher Education, vol. 23, pp. 195-208, March 1992. With O. Zuber-Skerritt.
Zuber-Skerritt, O. and Perry, C. 2002, ‘Action research within organisations and university thesis writing’ Organisational Learning, vol. 9, no. 4, pp. 171-179.
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