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Addiction Research - Science topic

Addiction Research is an addiction biology, counseling, psychiatry, and psychology
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We have been working on smart glasses with multiple sensors and the research point is how to improve the battery usage while using streaming data from sensors all the time
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Dear Ahmed Ismail Ebada,
see my answer to this question:
How can I calculate using of energy by WSN node?
Maybe my answer to this question can help you a little.
Best regards
Anatol Badach
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1. Please suggest easy to use questionnaire.
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There are four kinds of tools available to measure social networking addiction.
1) Tools that measure generalized internet addiction such as Internet addiction scale (Young, 1998), Pathological Internet Use Scale (Morahan-Martin & Schumacher, 2000), Online Cognition Scale (Davis et al., 2002), and Internet-Related Problem Scale (Armstrong et al., 2000).
2) Since Facebook has recently been one of the most popular media, many measures have been developed to measure Facebook-related addiction (Çam & Isbulan, 2012; Andreassen et al., 2012b; Sofiah et al., 2011).
3) Two scales that assess generalized social media addiction are Bergen Social Media Addiction Scale (Andreassen et al., 2016) and Social media disorder (Van den Eijnden et al., 2016).
4) Tools that measure social networking addiction such as Addictive tendencies toward SNS (Wu et al., 2013) and Social networking addiction scale (Shahnawaz et al., 2013).
However, a closer look at these tools revealed that none measured social networking addiction except for the last two. The first category of tools measures generalized internet addiction while the second category of tools measures a very specific parameter that is Facebook. The third category of tools which are of recent origin measure social media addiction. In a review on social networking sites, Kuss and Griffiths (2017) categorically stated that “social networking and social media use have often been interchangeable in the scientific literature, but, they are not same” Also, they stated that “Facebook addiction is only one example of SNS addiction.”
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A country trying hard to its level best for making urbanization, industrialization and does not care about deforestation, pollution and its natural resources, what will be the end cause of that country in such a situation? and What is Sustainable Development?
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urbanization and industrialization are the end cause of urbanization and industrialization
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In which areas of science are adequate research carried out by research teams, and in which areas, scientific disciplines are research conducted by researchers more often? Do you know fields, disciplines in which research is usually conducted by research teams? Do team research projects have specific attributes that generate additional added value or do they have an advantage over research conducted individually by scientists?
Do you agree with me on the above matter?
What is your opinion on this topic?
Please reply.
I invite you to discussion and scientific cooperation.
Thank you very much.
Best wishes.
Dariusz Prokopowicz
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Dear Colleagues and Friends from RG,
In the context of the above discussion, I propose to add to our considerations the following important issue:
The impact of scientific conferences on the development of science.
Scientific conferences make it possible to make friends with other scientists and researchers. During the conference there are opportunities to conduct discussions and debates on interesting topics. Thanks to this, it is possible to undertake scientific cooperation and create international research teams and projects.
Do you agree with me on the above matter?
- What do you think about this topic?
- What is your opinion on this topic?
Please reply.
I invite you to discussion and scientific cooperation.
Thank you very much.
Best wishes.
Dariusz Prokopowicz
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Hello all!
I'm learning the ropes of cocaine self-administration, extinction, and cue-induced reinstatement in rats. My current group is almost finished with extinction, and will be ready for reinstatement soon. We use cue-induced reinstatement, where the house light, tone, and cue light are all functional but no drug infusion is delivered upon lever pressing. Another lab member runs each rat undergoing reinstatement alone, in its own separate session. He doesn't run all the reinstatement rats together as one session nor does he run the reinstatement rat with a drug group (though it is the same program with the drug pump turned off). He says that the tones from the other rats receiving either real or fake infusions will influence reinstatement. I can see where having one of the cues presented externally might trigger reinstatement at first, but is the effect large enough to warrant each rat having its own isolated session? What is the standard of practice in your lab? Any input anyone can provide would be greatly appreciated!
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It might be a good idea to run your extinction rats separately so to not interfere with their extinction learning, although I have run cue-reinstatement testing alongside extinction before within the same session (across different boxes) and didn't notice any issues. That being said, I don't see a problem running multiple rats for cue-reinstatement within the same session. The rats learn to self-administer drug (with the paired contingent cues) alongside all the other rats, and they are possibly hearing the cues from the other boxes during this learning process. This experience in and of itself could be a salient cue as well! I guess it could depend on the specific question you're trying to answer. For example, if you were trying to measure cue-dependent, second-by-second neurochemical recordings in real time during a reinstatement session, having potentially salient "background noise" coming from other boxes could introduce some variability perhaps. For most purposes though, I don't see why it would be a significant issue to run multiple reinstatement tests across different boxes within the same session.
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Lets say that you have two students with different dopamine neuron efficiency in their hypothalamus: one student has large efficient neurons and the other has small inefficient neurons. (Other hypothalamic hormone levels are identical for these two students.)
Which one of these students will more likely get addicted to drugs, display impulsive behavior, and fail in school (especially in math)?
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I think it should be the student with low of inefficient level of dopamine because band there will be reduction in some cognitive function and dopamine also excite the nerve fiber with low level this will be reduce leading to craving for stimulants
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My question is simple -
Do you want to help someone ?
Do you want to help change someones life for the better ?
Do you want to have an impact on lowering the suicide rate?
What would you do for someone you love? Anything..
The struggle of addiction and mental health is more prominent today than ever before. With suicide & mental health rates increasing everyday and the lack of information & resources out there required to help tackle and deal with these things are limited.
Granted that there are services out there that do help and do work but are not always easily accessible or in some cases to late. The world is changing and it is becoming more prominent that suicide and mental health are real issues that are being overlooked in some cases where they should not of been.
Change is needed to a better quality of service, information and care that is currently being provided.
Please help us with our research to understand more from holistic overview,
help us to help those that are indeed struggling but are not getting the attention that is required.
Link below is to the study :-
Thank You
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I took the survey to help. A good piece of work!
I think addictions treatment should not just focus on the old model of abstinence and 12 steps. There are many newer techniques including acupuncture and holistic approaches which should be integrated into the treatment protocol. The old approach of "confront, confront..." does not work with every addict. Use of the "Stages for Change" model ( Prochaska and DiClemente) along with a full blown assessment of where the client is and their support system and beliefs is vital.
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How to identify the research gaps for Mechanical Engineering in a country like Uganda?
If anyone can share any details about identifying research gap or identified research gaps in country Uganda?
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These graphs show the status of research in the area of engineering in the country of Uganda. These results are performed using Scopus. Scopus is a bibliographic database started in 2004, of abstracts and citations of articles from scientific journals. It covers areas of: science, technology, medicine and social sciences (including arts and humanities). It covers more than 35,000 titles from all areas. Apart from magazines, it has monographic series, conference proceedings, books (emptied at the book and chapter level) or patents (more than 39 million, emptied from five official offices: WIPO, EPO, United States, Japan and United Kingdom). Its temporary coverage is from 1996, although it sometimes reaches 1970.
The graphics appear as an attachment to this message.
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I have been diagnosed and medicated over twenty years with a psychiatric condition that medication works well for me.
I was on 100 mg of Seroquel for a long time with no problems, then had to be hospitalized.  The Dr. told me it wasn't a therapeutic dose, even though it had been working just fine for years.  He raised my dose to 300 mg.  When I went home I felt like I would die every time I went to sleep went back to the hospital then the same Dr. gave me Geodon, which did not even work at all and then I was threatened if I did not take an injection to go to court.  They messed my medication up, not me.
I understand the holistic approach, but requiring services the client does not want, does not benefit the client in any way other than someone to talk to.  I don't think Social Workers should be making diagnostic decisions anyway.  It is a waste of time and money and Paternalistic.
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The assumption is that the "social worker" or "therapist" or "counselor" (all of whom do not prescribe medication) can discern from the conversation signs of intellectual and emotional impairment. If you are just having challenges and difficulties in life that cause you discomfort then medication is not called for. If you are unable to deal with challenges due to mental or emotional impairment then you may need medication (or medication change). To save the medical doctor (psychiatrist) time the client is "screened" with this approach. It is to use the doctor (who is usually more expensive) only after it has been determined what your problem is (physiological or not physiological). A third option is to seek out practitioners who understand the emerging orthomolecular techniques that address the dysfunctional metabolic cycles that underlie various mental illnesses. This is more problematic if you have been on medication for 10 years or more but it may be worth consideration. I review a popular book "Nutrient Power" written for the non-expert on this approach that I think has great promise and quality researchers involved at:
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See above.
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Thank you so much for your thoughtful and useful answer. And for the time taken to respond. Kind wishes to you
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I have a Native American client who became extremely intoxicated .16 BAC from 4 beers.  Is there any research indicating Native Americans are impacted greater or quicker than others from alcohol intake.  Also, is there genetic support for the proposition that Native Americans are more susceptible to alcoholism?
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There is evidence to suggest that they, like Asians (see studies on Japanese) are more susceptible to ALCOHOL, in the sense that it takes less alcohol to create the equivalent or greater sense of intoxication, than, for example, someone of Scottish origin. There is NO EVIDENCE that I HAVE SEEN to suggest that Native Americans are more susceptible to ALCOHOLISM, more properly referred to as Alcohol Use Disorder (DSM-V). It is important to make this distinction.
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Hello everyone,
I am currently investigating which measures and variables I should include in a treatment outcome study at a residential addiction treatment facility. Any suggestions and guidance would be appreciated.
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Simple outcome measure:
Percent with a diagnosis of opioid use disorder who are discharged on medication-assisted treatment-
1. Percent discharged on oral suboxone (good) or oral methadone
2. Percent discharged on sublocade (best)
3. percent discharged on naltrexone/Vivitrol (okay)
4. percent discharged without any medication protection (poor)
Patients in category #4 are at HIGH RISK of relapse, overdose and death.
Patients in categories 1-3 have protection against the risk of death via overdose.
75,000 Americans died of opioid overdose last year. Treatment should PROTECT patients in the initial phase of recovery (year #1 at least) from death.
Other outcome measures are secondary.
Treatment centers that don't encourage patients to protect themselves from death with these life-saving medications are setting them up for failure and death after they live the highly structured and supportive environment.
On appropriate meds = lower risk
No meds = extremely high risk
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Nowadays, a lot of social media occupied the minds of PhD Scholars and as such most of their times are being devoted on this social media activities. Most scholars are being distracted at home by family activities. How did you do it that you finish as expected? What did you do to your times? How much time did you spend daily on your write up or your research? How did you prioritize your time? I heard of a Doctor saying that during his PhD Program that he deactivated his Facebook and Whatsapp just to ensure that he finish as designed by the university. In your own case, what method(s) did you apply that makes you finish on or before the time? I will appreciate your candid opinions. Thanks
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I read two very pertinent guide books at the beginning of my PhD. Try reading this one to start: https://www.amazon.com/Authoring-PhD-Doctoral-Dissertation-Palgrave-ebook/dp/B006UH4F12
Three things that I took from these guide books:
  1. Treat the PhD position as a paid job - follow normal workplace rules, start and finish times, scheduling breaks/leave/vacation throughout the year;
  2. Do not get distracted by 'helping' others' research, especially when it comes to research associated with your supervisor/advisor, academic department/faculty, friends, colleagues etch - remain focused on your own research;
  3. Start writing at the beginning of your PhD to practice/improve your writing skills. Conceive that everything you do, everything you write, is designed to succeed in your PhD oral examination - to convince your examiners that you are the expert in your field and that you deserve to pass.
I hope this advice helps you.
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I am looking for Researcher who are working in Alcohol & Nicotine addiction research in Europe. The review article (under preparation) mainly covers researcher mainly from US.
I shall appreciate if you suggest: Example L Eric J Nestler, George Koob, Nora volkow, Neal benowitz ( US region), Wolfang Sommer, Rainer Spanagel (Europe).
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Thanks Beatrice for sharing your article! You have interesting data from regression analysis & factors contributing to drug abuse. Apart from biological research, I also collaborate with Premium Business schools on IP policy / Pharma policy. I am currently working as CO-author with Premium B-school. I am happy to collaborate as co-author, if you have any interesting mix Research (Biology/chemistry)/IPR policy/Market research. Please email me, if interested!
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I am planning a study-project on emotionregulation and the bodily experience (bodily maps of emotions) of drug addicts. I am not sure, if I can mix useres of cannabis and useres of ecstasy for example in my sample. So I'm looking for literature/studies, wheather there are differences between users of stimulant drugs versus useres of sedating drugs regarding emotionregulation and/or the experience of emotions. I'm happy about any hints!
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Addiction may begin with attitudes towards addiction in early years. There was a time when, e.g., the Swedish king asked people to grow their own tobacco in their gardens! Here our take on attitudes in schools:
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I am a student researcher at the USC Leonard D. Schaeffer Center for Health Policy and Economics working on a project detailing the utilization drivers of Avastin (specifically, compounded Avastin intravitreal injections used off label for wet AMD) vs Lucentis, both drugs used to treat wet-AMD, in Medicare patients. Since 2008, we have seen a dramatic rise in the utilization of Lucentis (~$2000/dose) compared to compounded Avastin (~$20/dose) although the CATT report has shown the efficacy and side effect profiles of both drugs to be essentially the same. We are trying to figure out which drivers are influencing these pricing differentials by answering some of the following questions:
-Are there supply chain barriers in certain states that make it difficult or even prohibitive to obtain or use compounded Avastin?
-Are there state specific laws that make it difficult or even prohibitive to obtain or use compounded Avastin?
-How do physicians go about ordering/receiving compounded Avastin? Do they use purchasing groups? Do they compound the drug themselves in office? Do they use compounding pharmacies or outsourcing facilities?
-Are there any other influencers that may cause a physician to use one drug over the other?
Any information, data, charts, figures, or references related to the above topics would be greatly appreciated. Please feel free to contact me with any questions you may have.
Thanks for the help!
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Dear Holloway,
Doctors in Iran use hybrid pharmacies with outsourcing capabilities.
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hello,
we are working to find already known naturally occuring plants, funghi, microbiota and the like, showing gabapentinoid activity or aiding the effect or helping with the reduction and so forth in order to support the tapering of pregabaline and similar substances and helping to rebuild normal functionality after the cessation.
it doesn't need to be exclusively focussed on gapapentinoid modes of action as there is probably a plethora of possibilities to start inducing a slow and protected adaptation of receptor density and Gaba supply and to heal the other affected metabolic and functional cycles in order to meet the demands placed by sobriety on the brain's constitution. 
i'm thinking for example of the modes of action of ketamine and ibogaine and other nmda antagonists.
also, which minerals and vitamins need to be primarily replenished (like b1, b5, b6, b7 b11, b12,...) and which nutrients or active substances (like taurine or magnesium,..) do aid the restoration process? 
we also look forward to all lifestyle recommendations like living free of stress, regular exercise, ... 
we welcome any input, ideas, hints, papers and research and hope together we can help a many good people who stumbled into a miserable situation!
thank you all in advance,
patrick schimpl
chairman of project: kindergarten, non-profit organisation, 'because if the world's a garden for children it's paradise'
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There are many herbs used as calcium channel blockers. But whether they contain gabapentins etc is to be researched.....
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Some patients on opiate or opioid analgesics paradoxically react with hyperactivity, verbosity and insomnia. As a student (more than 50 years ago) this was demonstrated during the pharmacology lectures bij injecting a cat with morphine and show it a white mouse, whereupon the cat panicked and jumped up and down its cage. Our pharmacology professor then explained that 'a small percentage of the human population reacted like cats', and indeed, this is reported incidentally by patients.
Can anybody explain the incidence and mechanism of this paradoxical effect?
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Frederik A De Wolff 45.02  Leiden University
What is the incidence and mechanism of the excitatory effect of opiates in some humans?
Some patients on opiate or opioid analgesics paradoxically react with hyperactivity, verbosity and insomnia. As a student (more than 50 years ago) this was demonstrated during the pharmacology lectures bij injecting a cat with morphine and show it a white mouse, whereupon the cat panicked and jumped up and down its cage. Our pharmacology professor then explained that 'a small percentage of the human population reacted like cats', and indeed, this is reported incidentally by patients.
Can anybody explain the incidence and mechanism of this paradoxical effect?
What is the incidence and mechanism of the excitatory effect of opiates in some humans?. Available from: https://www.researchgate.net/post/What_is_the_incidence_and_mechanism_of_the_excitatory_effect_of_opiates_in_some_humans [accessed Jun 6, 2017].
 Charles Schaffer & I found evidence that nearly one-third of bipolar patients when taking mu-opiates would have a manic-like reaction that might last a day or two.  In some cases this was the subject[s first manic episode.  There is evidence of interaction between dopamine and opiate system and perhaps a large subset of bipolar patients might be overly sensitive to the DA-opiate interaction.  We published one report but not the second, which had incidence around 35 percent.  Thanks you.Tom Nordahl UCD
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I have a large (very large) Facebook data set which I used to write a paper on Facebook addiction. I am looking for people that would like to write joint papers using the data set. Here is an overview of the data available:
1. For 1200 people answers to a survey on Facebook addiction
2. 300 answers to a survey on Internet addiction
3. A follow-up study on motivations for Facebook usage (1100 people)
4. A test of friending decisions with a random group of unknown people sending invitations to each person (10 invitations were sent to each person)
5. Detailed information on the posting habits of 1500 people
6. Detailed information on the lifestyle and purchasing habits for 1500 people
The full data set is about 350 MB with a little over 4000 data fields
I recently finished a paper on a Facebook addiction measurement tool. This will be submitted soon
I am personally interested in writing papers on the following…
• What drives people to accept invitations from unknown people
• What are the correlates of Facebook addiction in terms of activity on Facebook ad general buying/lifestyle habits
If you would be interested in doing something together, please send me an email bcassady@vub.ac.be
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Dear Mr. Cassady,
I am interested in doing research and data analysis on facebook addiction. 
Are you still looking for collaborator?
i am expert in data analysis.
best regards
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Does increased nicotine addiction and increased cancer (tobacco related) prevalence in a specific community can be cited as an example of syndemic ?
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I think I know what you are asking. Syndemic according to medical dictionary is: A set of linked health problems involving two or more afflictions, interacting synergistically, and contributing to excess burden of disease in a population. Syndemics occur when health-related problems cluster by person, place, or time. For example, the SAVA syndemic is comprised of substance abuse, violence, and AIDS, three conditions that disproportionately afflict those living in poverty in US cities. To prevent a syndemic, one must prevent or control not only each affliction but also the forces that tie those afflictions together. From syn-, together + (epi)-demic.
So your connecting nicotine, tobacco and cancer does make sense. It is a new idea and worth debating and discussing.
Cheers
PS: Drinking Smoke by Mac Marshall, University of Hawaii Press might be of your interest
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Dear researchers, to the best of your knowledge, what are the most reliable diagnostic biomarkers for opiate misuse? Benzodiazepine misuse?Z-drug misuse?
Kind regards,
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For detecting 'any use' in the previous month (or two, or three) hair testing is generally more reliable and sensitive than body fluid testing. For skinhead hairstyles, pubic, leg or armpit hair are alternatives. If someone has a sudden total Brazilian body-waxing when told they have to give a hair sample in the next day or two, it looks rather suspicious. 
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I am interested in studying chronic effect of METH in rats 
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For rat and mouse,
The LD50 for METH with intraperitoneal (ip) administration is 55 and 57 mg/kg, in rat and mouse, respectively (Davis et al., 1987; Yamamoto, 1963). But temperature is very important eg. at 29oC 80% of rats were died with 9 mg/kg i.p. administration  just 4-5 degree above ambient temp.
For human, 
A lethal dose of methamphetamine varies depending on characteristics of the drug and the user. In fact, each person has a different sensitivity to a specific amount of methamphetamine due to personal tolerance to meth. Therefore, toxic levels are different for each individual. Meth overdose may also be complicated by other drugs the user may have taken. Diseases that the person may have developed also play a role due to the current health condition of the body.
Oral administration = ~ 150mg a day
Injection (iv)= ~100mg or higher
Smoking and snorting methamphetamine = ~50 mg or higher
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Longterm opioid pharmacotherapies can be associated with decreased sexual desire in both men and women. Specifically looking at methadone maintenance treatment for opioid use disorder, does anyone have any credible, evidence-based information or articles that address effective treatments or interventions to these issues (most often related to hypogonadism)?
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Thanks to you both!
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Usually after rehabilitation or any treatment morphine addiction might be reduced, however, after a time period ( short or long) the same person can be addicted as like as before rehabilitation.   
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nice Ayca
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Hi, I'm conducting an investigation on internet addiction, measured with IAT (Internet Addiction Test) by Young. I've done most part of the results but would like some feedback on the tests I've chosen and if they are indeed correct. 
So in overall the variables I've used are
Age - continuous 
Sex - nominal
Relationship status - single, married, "together"
Internet use for: Games - Never/Low/Medium/High
Internet use for: Social networks - Never/Low/Medium/High
Recreational time spent online a day - Less then 1/1-2/2-5/5-8/8+
NEO-FFI - personality
BSI - depression, hostility, anxiety and social problems
and finally IAT
For the most part I've used T-Tests for sex, age, relationship. And Pearson Correlation for IAT and BSI; for IAT and use of games, social networks and time spent online. Then partial correlation controlling time spent. 
And finally a multiple hierarchical regression. Block 1 - all the demographic and questions of use and time. Block 2 - personality. The problem with this one is that some of the groups go as low as 14 individuals. For example on the use of social networks only 14 never use them. 
Thank you
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Non parametric ANOVA
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This is a support assessment tool in relation to what we are currently studying now, about internet gaming addiction
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If you want to use this for research, I would consider using a validated instrument such as the Problem Gambling Severity Index of the Canadian Problem Gambling Index (Ferris & Wynne, 2001).  The problem with the DSM is that it changes, most recently with the omission of the criminality criterion. Other widely used instruments such as the SOGS (DSM-III) and NODS (DSM-IV) become obsolete with each new edition.  In contrast, the PGSI has been used across a wide variety of contexts and includes, arguably, the strongest behavioral and addition-based criteria of earlier instruments.  It's what we use in research studies as well as with clinical clients.  Best of all, it's only 9 questions.  With the DSM-5, you are limited to just asking the criteria questions at present as there is no validated instrument.  Hope this helps. 
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Hi,
Our research aims to identify possible differences between the short-term effects of alcohol on cognitive functioning and the long-term effects of alcohol. This means we're comparing the cognitive functioning of people when intoxicated (drunk) and addicts. We have two different datafiles, namely the Intoxication-file (containing 15 or so people, all high-educated, mid-age), and the Addiction-file (over 600 people, all kinds of education/age).
To be able to compare these two different data-sets, we need to make sure that the two files are as alike as can be. This means that only the people from the Addiction-file with a high-education (or at least, as high as possible) and mid-age should be included in the comparison. Hopefully, there will be approximately 15 people with an alcohol-addiction and a high education within that file. Moreover, we want to match on age and maybe gender as well. 
Is there a way to make this possible? I've read about a program called FUZZY (Python extensions), but I'm not familiar with this program, nor do I know how to work with it. Hopefully someone does!
Thank you in advance, 
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What do you mean when you say "matching"? Are you trying to match the two data sets or are you trying to merge the two data sets? If your question is to match the two data sets, then you can use the following syntax
update file = "D:\dataset1.sav"
/in = flag1
/file = "D:\dataset22.sav"
/by all.
exe.
save outfile "D:\combined.sav".
value labels flag1 0 'mismatch' 1 'match'.
freq var = flag1
I hope this helps
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Various forms of entrainment are being incorporated into treatment modalities, but only limited and dated empirical data is offered. My question is, what significant effect may these therapies have, do they impact glutamate receptors to influence or balance the relationship between serotonin and domaine transmitters, improve distribution, address CREBS and Delta-FosB protein alterations, or improve plasticity? Is there influence in pathway generation, or alteration of dendritic spines - these are some of the claims made by providers.
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There is excellent research on neural and pharmacological aspects of addiction. please see proceedings of last three years of addiction therapy and education conferences by OMICS  
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I'm starting a qualitative study of the processes experienced by families when one of its members use drugs. Attempt to investigate how care and what has connotations in family dynamics and processes of vulnerability / generativity
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Hola Ana, 
Si entendí correctamente tu pregunta, vos estás investigando la percepción, procesos y funcionalidades que tiene una familia hacia el cuidado de uno de los suyos, que es adicto. Si es así, siempre es útil realizar estudios cualitativos que involucren grupos focales y/o entrevistas semi-estructuradas para poder explorar los sentimientos de la familia, tan difíciles de medir con simples cuestionarios. Yo recomendaría comenzar por los grupos focales y continuar con entrevistas de profundización.
Cordial saludo desde Paraguay  
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I am attempting to compare governmental responses to drug addiction--during the 1970s, 80s, & early 90s--among various Southeast Asian countries (as they relate to the Indonesian government's notably harsh response to drug use and addiction), This is part of a larger study that will assess the history of Indonesian pain-management & drug addiction over the last two centuries. Any input on this project would be most welcome.
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 hallo I reaserch about medicin of islsm for exampel rasez, Avecina
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I want to know whether the concentration/dose in the references refers to methamphetamine hydrochloride or its active ingredient methamphetamine (without hydrochloric acid)?
As we know, the molecular weight of methamphetamine hydrochloride is 185.7 while the molecular weight of methamphetamine is 149.2. And usually, we purchase methamphetamine hydrochloride. Therefore, if the concentration/dose refers to the active ingredient methamphetamine, the rate of the two moecular weghts should be take into concideration we diluting methamphetamine. Who can tell me how to prepare the saline solution of methamphetamine?
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If a paper refers to a concentration, for example, 1 uM methamphetamine given by reverse dialysis, then you weigh extra into the solution to take into account the HCl salt, and use the 185.7 MW to give both 1 uM methamphetamine and 1 uM HCl.  If a paper says 2 mg/kg and that the dose refers to the weight of the salt, or specifically mentions the HCl with the dose, then 2 mg/kg refers to 1.6 mg/kg methamphetamine and 0.4 mg/kg HCl. You would calculate the concentration of methamphetamine in saline using 1.6 mg/kg, the dosing volume of saline in ml/kg, and the 149.2 MW. If a paper says the dose refers to the freebase, then 2 mg/kg would be 2 mg/kg methamphetamine and 0.5 mg/kg HCl. The concentration of methamphetamine would be calculated using 2 mg/kg, the dosing volume in ml/kg, and the 149.2 MW. If a paper doesn't clarify if the dose refers to the salt or freebase, then it is not clear how to exactly replicate their dose, but since the weight of HCl is relatively low, the deviation from their dose will be relatively low.
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I would like to know if there are documented studies on how Addiction (mainly alcohol and drugs) was perceived in the traditional African Society or research on the 'conceptualization of  addiction in Africa.
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Hi, as far as I know, for the traditional African Society there are some good books out there. One of the best ones on the history of drugs is in Italian unfortunately and cannot find the translation its called "Le Droghe, Enrico Malizia, Stefania Borgo" and has a whole section on African drug ritual, as well as impact on the African and other cultures as well as a great description on how some drugs in later days spread some diseases due to inefficient and unsanitary delivery methods. Another book I can suggest is "Food of the Gods: The Search for the Original Tree of Knowledge : a Radical History of Plants, Drugs and Human Evolution" by Terrence McKenna, which is mainly based on African societal and tribal rituals. As well, since I do sense you are trying to make a study that has some backbone foundations in history, I would also look up some old Medical Journals from Italian records in Ethiopia or Medical Journal records from some of what was once colonies, since they did keep record of tribal societies and indigenous population at the time. As well last but not least I would also work my way up and learn from hallucinogenic uses of various mixtures like acacia and fermented substances.
Even though this is just wiki and not really a "peer reviewed source" this is a good start:
I think if you follow the path of acacia and it's various mixtures and how society has changed you might find some good stuff on addiction and tribal ritualism in older days.
Hope this helped
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This is not as unlikely as it first seems, since a strong general factor has been found for intelligence (g), personality, adolescent psychopathology, etc, in addition to more specialized sub-factors.   Drug withdrawal syndromes also have a common thread running through them. Looking through the 7 large tomes and thousands of pages of Meyler's Side Effects of Drugs 2016, I can find no mention of this possibility.   Looking through its Index of Adverse Effects, the symptoms listed look far from being a random or representative sample of complaints that present to a GP.  Some may represent the differential susceptibility of certain organs to drugs, but if so, this is worthy of interest and should be flagged up.   However, the other explanation is that there is some general syndrome here, that there is some gateway system in the body that checks all drugs and has a corresponding recognizable "side effect" syndrome.   Has anyone else noted that some drug side effects are far commoner than others for no apparent reason?
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Thank you for your quick reply!
Not necessarily indeed--I was merely pointing out that, by your logic, it would be equally reasonable to propose a system that allows for drugs (perhaps even only at specific doses) to exert therapeutic effects. However, given what we know about pharmacology, I see no need to introduce a generic black box into the equation.
However, it's not like these ideas aren't testable. If there is such a system, it must surely exist at the molecular level (the same level upon which drugs act), as some sort of biochemical phenomenon.
The closest biological parallel that I can think of would be VDJ recombination in immunoglobulins (which is very individual, and possess far less confounding variables than hepatic metabolism). We already know that drugs sometimes form immunogenic adducts, which can induce an inflammatory response (the hapten-carrier effect). As an academic exercise, we can hypothesize that the immune system could act as the so-called "gateway," and effectively screen for exogenous chemicals the same way that it screens for pathogens (without carriers, most drugs would simply be too small to be immunogenic). Thus, in this hypothetical, adverse events are but the byproduct of something 'getting through the filter" of the immune system.
However, it would be very difficult to make the case that a failure of the immune system is responsible for most (if not all) adverse events. After all, the hapten-carrier effect itself is a pathological one (e.g. glomerulonephritis); hardly the basis for a protective system, whose evolutionary function is to "filter out" dangerous drugs (or doses). In addition, we already know that the wide majority of drugs are cleared from the blood by the liver (enzymatic degradation and conjugation) and kidneys (filtration, secretion), rather than an immunologic mechanism (e.g. relying upon the reticuloendothelial system in either organ, which has a very limited drug metabolism capability).
The best example of a true drug "filter" phenomenon in humans would be first-pass metabolism through the liver (note that this occurs before renal filtration), which depends upon the pharmacokinetic properties of the drug in question, as well as the individual patient's characteristics (e.g. comorbidities, genetics, other drugs on-board, etc). Indeed, the hepatic portal is truly the gateway to systemic circulation for many drugs, and their activity depends upon it. However, the liver is ignorant towards what drugs work or do not work, and will just as gladly hamper a live-saving drug's bioavailability (given PO) just as it would any other exogenous chemical. Perhaps even more powerful is the recognition that a person can experience a severe, life-threatening reaction to a life-saving medication (consider penicillin). Rather than be a "generic system that vets drugs...that are too powerful," the liver takes a "shot gun" approach, and attempts to eliminate whatever it can. That's what we actually observe, rather than the selective system you're proposing.
The differential susceptibility to adverse events with certain drugs is best explained by pharmacogenomics, or by any of the mechanisms I've presented previously. I suppose my question is this: why propose a new model when the current one will suffice? Do you see an error or logical gap within our current understanding of toxicology?
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What is a good metric for measuring consequences and problems from substance use? Is the PFSU scale (1999) still utilized and if not, what are some good ways to measure problems related to substance use?
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Dear Austin,
The Addiction Severity Index - ASI (McLellan, 1980) is a semi-structured interview for substance abuse assessment and treatment planning.
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I am looking for any peer reviewed articles that indicate a relationship between a client's positive personality traits and treatment outcomes. Does anyone have any suggestions? Thanks much,
Christine
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Hi Christine,
In addition to the excellent references provided by Beatrice and Harshvardhan, these resources may interest you:
  • Predictors in substance use disorders by D. A. Ciraulo, J. Piechniczek-Buczek, & E. N. Iscan.
  • Client Characteristics and Treatment Retention in an Outpatient Drug-Free Chemical Dependency Program by Jessica A. Thull
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Does anyone have this article? Mc Hugo, Drake are the authors. My school doesnt have any acess because we are a swedish university.
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Hi Alexandra,
If you you just want the scale you can download it here:
If you want to read the whole article, you can request the full text to the original author in researchgate:
Best regards,
Alejandro
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I am doing a study from a queue provided by an article in the "bmj" titled "Frequent Nut Consumption and Risk of Coronary Heart Disease in Women  ", 1998,Vol- 317, pages 1341-1345.in which it stated that a higher consumption of peanuts had an association with the change of smoking habits among the subjects of that study, though no statistical evidence was provided. And thus i would like to know if whether there is any biological association that can probably help me with my study or if there are any literature that could second my so far assumption
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have a look at pubmed
behavioral changes, motivational interwieving, clues ... 
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what is the best choice as a standard in alcohol induced hyperalgesia, Depression and Alcohol withdrawal syndrome ?
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Thanks Devin Hosea for reply...kindly guide me fo Dx and Tx...both
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Smoking rates are high (40-70%) in schizophrenia and psychosis and smoking habits begin early. Risk of psychosis is elevated in teens who smoke (cigarettes are as risky as cannabis see http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=9394986&fileId=S0033291714000531). My question is how can we reduce this risk, ideally by discouraging smoking in those who are asymptomatic or those with early prodromal symptoms? Thank you.
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Nicotine is very often used as self-treatment, even if symptoms are of psychiatric illness are unnamed/undefined. This is a sample abstract of an article which describes how this happens. In practise, I have seen psychotic symptoms which appeared to be a consequence of THC use, but not nicotine.
Encephale. 2008 Jun;34(3):299-305. doi: 10.1016/j.encep.2007.04.003. Epub 2007 Dec 26.
[Smoking and schizophrenia: epidemiological and clinical features].
[Article in French]
Dervaux A1, Laqueille X.
Author information
 
Abstract
FREQUENCY:
The prevalence of cigarette smoking is significantly higher among patients with schizophrenia (60-90%) than in the general population (23-30%). While tobacco smoking decreases in the general population (from 45% in the 1960's to 23-30% in the 2000's), smoking in patients with schizophrenia remains high. Patients with schizophrenia smoke more cigarettes than control subjects. Patients smoke more deeply, thereby increasing their exposure to the harmful elements in tobacco smoke.
IMPACT OF SMOKING IN SCHIZOPHRENIC PATIENTS:
As in the general population, smoking contributes to the reduced life expectancy in patients with schizophrenia. Patients with schizophrenia are at increased risk for cardiovascular disease due to high rates of cigarette smoking. In the Department of Mental Health of the commonwealth of Massachusetts, cardiovascular disease was the factor the most strongly associated with excess mortality. Cardiac deaths were elevated more than six-fold. Weight gain, insulin resistance, metabolic syndrome and diabetes mellitus are frequent in patients with schizophrenia, and may worsen the risk of cardiovascular diseases. It has been reported that the risk for lung cancer in patients with schizophrenia is lower than that of the general population, despite increased smoking. However, in a study conducted in Finland, a slightly increased cancer risk was found in patients with schizophrenia. Half of the excess cases were attributable to lung cancer.
IMPROVEMENT OF COGNITIVE DEFICITS:
Patients with schizophrenia may use nicotine to reduce cognitive deficits and negative symptoms or neuroleptic side effects. Smoking may transiently alleviate negative symptoms in schizophrenic patients by increasing dopaminergic and glutamatergic neurotransmission in the prefrontal cortex. In patients with schizophrenia, nicotine improves some cognitive deficits: (1) sensory gating deficits and abnormalities in smooth pursuit eye movements associated with schizophrenia are transiently normalized with the administration of nicotine ; (2) high-dose nicotine transiently normalizes the abnormality in P50 inhibition in patients with schizophrenia and in their relatives; (3) in tasks that tax working memory and selective attention, nicotine may improve performance in schizophrenia patients by enhancing activation of and functional connectivity between brain regions that mediate task performance (Jacobsen et al. 2004; Paktar et al.2002); (4) cigarette smoking may selectively enhance visuospatial working memory and attentional deficits in smokers with schizophrenia. However, Harris et al., found that nicotine affects only the attention without effects of nicotine on learning, memory or visuospatial/constructional abilities. In addition, smoking could facilitate disinhibition in schizophrenic patients.
PMID:
18558153
[PubMed - indexed for MEDLINE]
Prevention of smoking would be the ideal, and unlikely to happen unless families are also involved. Achieving impulse control could be considered a major developmental task which is likely deemed desirable by the young people who wish to positively influence. A shared goal rather than an imposed one altering the locus of control may make all the difference.
Good luck.
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I'm looking for studies with a psychodynamics approach using the IIP. Our study is an RCT testing movement (exercise) as additional therapy for alcohol use disorder.
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 Dear Beatrice,
Thank you for your answer. I have met the Norwegian Group but not the paper from Belgium. 
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I have been thinking about using Clarity to compare the expression of specific protein before and after addictive drug treatment, to kind of visualizing aberrant plasticity at molecular level. But wondering if the resolution of Clarity would be good enough for this purpose, since the abnormal circuits are the primary reports from the Clarity methodology.
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Please update me guidelines for heroin doses equivalency in animal species for drug reward. 
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You will find this article useful.
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There are many treatments which treat drug abuse like Therapeutic Community, other than that which is better?
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A helpful resource is a book entitled, "The Heart and Soul of Change" edited by Duncan, Miller, Wampold, & Hubble (2010). The editors and contributors make a compelling case that common factors (e.g., therapeutic relationship/alliance, collaboration in goal setting, hope, empathy, etc.) are far more important than specific factors (i.e., techniques and interventions associated with treatment models such as CBT, MI, or 12 Step Facilitation). A chapter devoted to substance abuse and dependence treatment summarizes research from Project MATCH, COMBINE, and the Cannabis Youth Treatment Study and conclude, essentially, that all treatments are equally effective. My takeaway - Treatment effectiveness hinges less on which treatment is provided and more on establishing a collaborative relationship, seeking feedback about the effectiveness of interventions, and altering the treatment course based on the feedback.
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Substance abuse is a patterned consumption of a drug in amounts or with harmful methods  Studies shoes that the social support may be helpful to recovery or relapse from it. What is the social support impression on prevention or treatment of it?
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The particular research study am conducting research about the efficacy of the “strengths” component in treatment plans for substance abuse, particularly with adolescents. My research  focuses on 2 areas:
When and why did the inclusion of “strengths” in the treatment plan begin?
What research is out there to show if it is helping with outcomes or not?
I was wondering if anyone could point me in the direction of resources?
Many thanks
Christine Rhodes
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Hi Christine,
In addition to the AA (Alcoholic Anonymous) model and the CBT (Cognitive-behavioral therapy) approaches to the treatment of substance-related disorders, there are strengths-based approaches such as motivational interviewing (MI) and solution-focused brief therapy (SFBT), etc. They attempt to elicit the client's motivation, cooperation, and strengths from the very beginning in the treatment process. Please see the following links.
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I am also interested in ranking of severity family tech overuse/addiction, and if that changes treatment methodology.
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Dear Cris,
From what I have encountered from studying addiction in university is that all treatments of addiction starts with people realising they have a problem. For people to come to terms with this there is a need to have a talking strategy in place I.e. CBT and a coping mechanism also. There has been found to be links between internet addiction and impulse control disorders, of which CBT has had very positive. I have attached a paper from 2007 which talks about tests to identify the addiction and the treatment to go along with it. 
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Looking to do some research on this; any papers would be greatly appreciated. Would be preferable if they had a healthy comparison control group.
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I am searching for research supporting AA 12-step meetings during college years for those diagnosed with substance use disorders.
Thanks.
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Thank you Margaret.
The students I am referring are in a safe collegiate recovery program that includes a residence hall that is substance free. They are all in recovery and are required to attend meetings and have a sponsor. I am searching for evidence-based research that supports the requirements or presents alternative evidence.
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[Edited question:]
Sorry, I wasn't being specific enough in my original question (but thanks for your responses so far!). Things like personality and genetics don't really change from day to day, so they can't directly correlate with / predict / cause someone to drink on one day but not another. I'm looking for antecedent causal variables that can fluctuate from day to day, and thereby cause fluctuating behavior from day to day. There are some daily-drinking-diary studies out there on this kind of thing (e.g., daytime experiences of negative social interactions leading to more drinking that evening), and to achieve greater specificity I want to parse "more drinking" into the binary variable "if drank" and the interval variable "how much drank, provided drinking occurred." Different daytime events may be differentially stronger predictors of these two criterion variables, and I'm looking to learn what people know about this possibility. In any research, have these variables been parsed before with respect to the causes of a single drinking episode? Aside from established research, what are your best guesses? Thanks!
[Original question:]
I'm aware of the frequency/quantity literature on characterizing global drinking traits, but would like to hone in on what causes whether or not a person will drink on a given day versus how much they will drink on a given day, provided they have at least one drink. Studies on daily determinants of other kinds of potentially problematic behavior or experiential avoidance would also be useful (e.g., drug use, binge eating); I'm primarily interested in functional and methodological approaches to this kind of distinction. Thanks!   
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I would suggest looking at secondary analyses from Project MATCH or the COMBINE study. Then look at predictors of percentage of days abstinent (a marker of frequency) and drinks per drinking day.
We recently looked at this in a depressed alcohol dependent sample (Foulds et al, Alcohol and Alcoholism,doi: 10.1093/alcalc/agv122) and found the personality trait novelty seeking predicted more heavy drinking on drinking days. 
Personality measures are probably worth considering for your analyses.
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There is a lot of research out there about the self-administered versions but I cannot find an actual copy of one.
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The first question I have is for which purpose you plan to use the ASI. The ASI is not an appropriate intake tool. The only realistic use of the ASI is as a before and after measure of potential treatment impacts.
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As our study is looking for someone who overuse their smartphone, and we try to let them experience a period which can reduce their overuse habit.But somehow,  less some previours research, don't know 'how long' will much appropriate? what's name of the withdrawal addition process? can this process modified and apply to smartphone users?  Wish you can help us , and please provide some evidences and literatures. thanks a lot!!!
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Thanks Prof  Lewis,Prof  Susana  and Prof John!
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I am searching for data on the prevalence of IDU in the USA, by state if possible.  Does this exist?  So far all I have been able to find is estimates from 1992-2002, and I would say the climate has changed since then. 
(Not necessarily looking for heroin use rates, as it can be used without needles and other drugs can be used with needles, etc.)
If you have any leads on this I would greatly appreciate you sharing!  Thanks.
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Not easy to find, I know.  This article does a meta-analysis to estimate rates:
Estimating the Number of Persons Who Inject Drugs in the United States by Meta-Analysis to Calculate National Rates of HIV and Hepatitis C Virus Infections  http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0097596
SAMHSA estimates for 2014 put at 1.6% of the population, or 4,256, 000. Down slightly from 2013:
SAMHSA may break it down by state.  Check the main page to see:
John
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I'm looking for a questionnaire or scale about measuring stigma in substance or drug abusers (adults).
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Dear Giti
       you may can use the stigma scale after modification. I use it in my dissertation with schizophrenic patients. try it. Best of luck
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I am looking at public policy dealing with child abuse and neglect, specifically the role of DCF in dealing with opiate-dependent parents. What I am wanting to show is that long term abstinence-based recovery is linked to an improvement in socioeconomic status if the treatment is comprehensive. And that recovery improves not only the person and their family, but that recovery helps lift families out of poverty.
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I would suggest looking at landmark work by George Vaillant. 
eg Addiction Volume 98, Issue 8, pages 1043–1051, August 2003
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I'm interested in SAST (or any version.. SAST-R etc.) in language other than English and Polish.
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Thanks gals and guys!
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I am looking for a long term outcomes study comparing outcomes of taper-to-abstinence vs replacement with either no timeline or patient defined timelines.
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Re: Your chapter. The RCT difficulty- I feel like the RCT issue could be overcome with moderate suspension of the insistence on psychological measurement  must resemble medical trials. My opinion is that psychology tries to fit itself as a square peg into a round hole by the insistence (fetish) with empirical measurement. To me that misses the larger point of psychology- which is to examine, treat, and understand the subjective psychological experience.
One salient point you made about the "morality" of dosages- that by reducing the overall intake to maintain thresholds, administered responsibly by a third party (or even in the case of self-dosing), which does show effectiveness- has essentially been subject to moral argument rather than scientific ones.
I see this as well. I think most people in the field see this. However, my observational experience with the transformative effects of abstinence-based recovery (when done in full) really moves the discussion into the social and moral realm. Since the "problem is removed" from the lives of the sufferer in 12-Step work (anecdotal), then that would seem to be preferable (and ethical) over giving an addict just enough that they are neither intoxicated nor in withdrawal, which seems somewhat cruel when juxtaposed, to the radical improvements those in abstinence based recovery seem to undergo when done completely. At the same time, one cannot (truly) account for readiness and willingness to change, which is likely the single best determinant of outcomes, no matter what treatment is used.
I can see the basis of the moral argument. We could stop terrorism by implanting a chip in every human and monitoring them, but we don't, and shouldn't, though empirically, it would fix the problem. Thus morality is a consideration. In the end, the basic question still remains- Can we adequately compare, or should we really try to compare the two? After reading your work, I can more clearly define what the inherent problems of such a comparison would be beyond the RCT issue.
I really do like your point about having treatment options which are informed, which allow for the person receiving service to choose  the option which best fits (like family planning and BC). I wish we could do this in substance abuse. Unfortunately, too many people come in for services unwillingly, and thus would choose only the most comfortable choice, which may not be the best for him. I think a lot more work could be done at the intake level of substance abuse which could reduce or eliminate this phenomena. 
Thank you again. 
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I am conducting a research on impact of social networking sites on psychologial well being of adults.
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Do you know the IAT (Internet Addiction Test, do not mix it with Implicit Association Test)? it may helps you if you decide to create one specific for your research
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We are trying to identify the types of drugs and substances commonly used by students and prevalence rates.
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 We  use structural, validated  questonirare
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I agree that the choice of self-medication might have some genetic relationship to that of the parents because what works for them might also work for the offspring, but the reason for needing self-medication has a lot more to do with overwhelming experiences in very early childhood and the lack of models for how to cope with them.  I have a sense that something very complex is being reduced to an overly simplistic model.  Also where does nicotine exposure come in, both prenatally (passive and active) and growing up.  Are you counting nicotine use in the model?
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Since you are not one of the PIs could you forward this question to someone who can answer it?
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Cross addiction refers to the presence of two or more addictions - a common trait among addicts. Many cross addicted patients develop secondary dependencies in an effort to deal with their Cross addiction refers to the presence of two or more addictions - a common trait among addicts. Many cross addicted patients develop secondary dependencies in an effort to deal with their primary addiction..
What are the somatic and psychological factors that cause a cross addiction after primary addiction?
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A different take on addiction is delivered by Bruce Alexander in his 2008 book "The Globalization of Addiction". While he does not directly address cross-addiction in his book, it's easy to see how it would fit within his theory.
Here is the link to a speech Alexander gave that contains salient points of the book. Maybe you find it interesting.http://www.brucekalexander.com/articles-speeches/277-rise-and-fall-of-the-official-view-of-addiction-6
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Is information available on the number of nurses, non-professional workers etc in the drug treatment sector in the UK ?
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Hi Ian
You may found some information on 
Regards
Paulo Seabra
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Does anyone have any guidance regarding nursing / physician attitudes of patient drug abuse and if attitude or stigmatization of that population can affect patient outcomes? 
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Absolutely; in fact, a recent paper in the Canadian Journal of Psychiatry concluded that stigmatization was the NUMBER ONE predictor of relapse.  I would guide you to the work of Michel Perrault at McGill (a co-author on the recent CJP article - 2014) and to that of Sarah Wakeman at Harvard, who wrote an article also in 2014 in the Journal of American Medicine -- and see my short comment in the American Journal of Public Health published July 2014.  Stigmatization in general is highly detrimental to recovery from substance use disorders; stigmatization from caregivers (MDs, RNs, etc) is bordering on unethical -- patients need empathy and understanding in their treatment, not disdain and scorn -- I think this is pretty obvious, and the vast majority of caregivers I know do not hold their pts in low regard because they have a psychiatric illness.  I don't think there is a study out there on MD/RN's stigmatizing their pts illness because there aren't many who do.  But if we are to take the results of the CJP study and apply simple induction, it's pretty obvious that stigmatization by caregivers would have an even more negative effect on remission rates than stigmatization by society at large.
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I have searched extensively for a scale that allows me to detect the amount a person partakes in behaviours such as sex, alcohol, shopping, exercise.
The shorter PROMIS is close but it's too long.  any suggestions???
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Promis Shorter Questionnaire examines addictive tendencies across a whole range of behaviours
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I am interested to conduct a baseline survey (and aimed to extend it), however to accomplish this task I haven't acquired any purposeful literature. If anyone ll provide me literature of self-regulation in relation with health regulation, that would be more appreciable.
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Well dear aging is nature but nature has no aging :)
In our Punajbi culture we used to say that Heart should be young, aging is useles!!
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See this article in JAMA Psych - http://app.jamanetwork.com/?doi=10.1001/jamapsychiatry.2015.0546&utm_source=email&utm_medium=app&utm_campaign=share  -- raises the obvious question of whether cycloserine can be a useful medication, with or without CBT.  I am wondering if any addiction docs have Rx-ed cycloserine as part of psychopharmacology for SUD pts.  Thank you.
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Recent have seen individuals with opiate addiction who are presenting ER with severe rhabdo after being clean.  They are presenting with negative urine drug screens.  Any ideas on what the causative agent(s) might be?
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You have to check the diff diagnosis as there are many potential causative agents for rhabdomylosis, ranging from statins to SSRIs to autoimmune issues.  My guess is that you will find, as suggested above, that it is not opioid use directly causing rhabdo, but rather secondary effects, such as Hep-C, etc.  What do you mean by "severe" rhabdo?  Some sort of really acute muscular deterioration occurring in a very short time period?  How long do the patients wait to present?  Do you run blood tests to confirm the urine tests?  I think this is a very interesting finding, but it's hard to guess as to whether it is related to pt SUD without a full differential diagnosis.
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Thanks in advance for your replies.
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I worked voluntarily with an adult chronic alcoholic when the services seemed to fail him and attitudes in the hospitals etc were harmful. I simply worked a motivational program whereby he felt it safe to move from behind the mask of addiction. Harrowing but sober now eight years.
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What is the evidence that sheds any light in the function of Dopamine (for example) in the hippocampus (behavioral, cellular, molecular) ?
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I attach the entire list of references from my database about any involvement of hippocampus in drug self-administration. If you prefer I can send you these references as Reference Manager or EndNote file.
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Does anybody have a valid questionnaire to evaluate staff attitudes toward methadone maintenance treatment and effects of their attitude on successful rate of treatment?
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I would consider adjusting the SAAPPQ (short alcohol and alcohol problems perception questionnaire, Gorman 1991). Well-used to capture staff attitudes.
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I am a 6th year Clinical Psychology graduate student (PsyD) that is currently working on finishing my dissertation proposal, but am having some trouble finding recent research (5-10 years - or even any research from 2002 and up) on my population. My research method & approach is qualitative/phenomenological. I want to go about things from a Positive Psychology framework, therefore, I will be exploring other factors within population such as resiliency, Posttraumatic Growth (PTG theory), & protective/risk factors etc. Any and all answers & comments are greatly appreciated. Thanks!!
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The National Scientific Council on the Developing Child is a working group based at Harvard doing extensive work in examining resilience for adverse childhood events in general.  This includes the chaotic home environments that can be experienced by children of parents with substance use issues, rather than specific adverse experiences.  The research focuses on the mechanisms of resilience and how to promote resilience in children; however, the findings are equally relevent for adults.  
Individuals need strong social interaction, coping and stress management skill sets, as well as warm, supportive relationships to navigate life and thrive. Individuals growing up in homes with substance abuse and many other parental challenges often do not receive adequate warmth and nurturing within their family of origin because of the ways that parental substance use alter family systems.  Adaptive social interaction and coping skills are frequently absent in adult children of substance users as well, as the opportunities to learn those skills from parents can be infrequent or absent.  
Through supportive mentoring relationships through work, education, softball leagues, what have you, as well as counseling and various other experiences adults can build these skills and capacities over time and be resilient.
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I am particularly interested in the neurological aspects.
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Do you mean "cross addiction" as in addiction to one substance leading to addiction to other substances, or do you mean "cross addiction" in the sense of substance addiction (or the cessation of same) leading to other behavioral addictions, such as sex/gambling addiction?
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Hi
I work with self-administration, and, as you know, performing a patency test by injecting methohexital (Brevital) into the catheter is essential. The problem is that this ultrashort- barbiturate is very difficult to find if you don't have a DEA license. Is there a similar compound that can do the same thing? or maybe another technique to verify that the catheter is working? I hope someone can give me suggestions! Thank you!
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I've used xylazine (Anased) to test catheter patency in the past and it has worked well. It's not scheduled so it should be easier to get. For rats, we would give IV administration of 0.05 ml of xylazine (20 mg/ml) and if we saw motor ataxia within 5 seconds, the catheter would be considered patent. I'm not sure if you're using mice or rats but it should work for both.
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Delta-fos-b, the truncated form of fosB, is accumulated after stimulation with drugs of abuse, among other stimulus. Manipulation of its levels has been made, to my klnowedge, via transgenci mice or viral vectors. I was wondering if there is a way to pharmacologically inhibit its acumulation. Thanks
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I don't think you can PHARMACOLOGICALLY inhibit fosB accumulation as the stimulant effects a transcription change that increases fosB.  That's why the viral/genetic vectors work - I am not aware of a medication or compound/enzyme (in the pharmacopeia) that would reduce fosB accumulations once the RNA transcription is engendered by the stimulant.  You'd have to simply reverse the transcription with a viral vector - which you already know.  
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Research on the etiology of problem gambling from the pathological perspective has shown that elements responsible for addiction (and also the risk factors) lie in both the biological makeup of the individual and the external environment – including the structural characteristics of the games – in which the gaming activities take place. Still, the largest portion of the research on prevention and treatment in the last decade has focused on the biological makeup of the individual, ignoring among other things the complexities of the games. What would explain that bias? I myself see two possible reasons and invite my colleagues to disprove them or add others:
1. The majority of researchers in problem gambling are medical doctors or psychologists. The other type of research would involve other disciplines – for instance, mathematics – whose final results must contribute to the same biological/social sciences, and such interdisciplinary collaboration is difficult.
2. I don’t give much credence to this “practical” reason, but I’ll take it as possible: Most of the funds granted for research come – directly or indirectly – from the gaming industry’s revenue. Given this funding source, is it possible that game developers tacitly impose the focus of the research toward biological factors because the possible results from a gaming focus could affect their business?
The lack of research on the non-biological aspects prevents us from objectively weighting the importance the two types of research offer toward prevention and treatment of pathological gambling. In the absence of this weighting and also of other relations between the two types of research, I pose the basic question:
3. Is any individual predisposed genetically to gambling addiction, which would manifest under certain conditions and for certain profiles when the individual interacts with a game of chance?
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The fallacy that pathological gambling is a "brain disease" has spread like an axiom driven by psychiatry interested in “pathologize”, to give drugs and obtain benefits for it. The brain changes that are attributed to addiction (either to the game or to substances) are not necessarily evidence of disease, but sometimes vulnerabilities, being pre-addiction and favoring their establishment and maintenance. As Kevin and Paul said, the experiment of rat park, replicated countless times over the last decade in the paradigm of environmental enrichment, definitely rejects the concept of "disease" and places addictive behaviours in an evolutionary context in which the learning history, experience, alternatives, cultural conditionants and much other environmental elements interact with the biology of the individual in lead to a loss of control and automated compulsive behavior. It is time to reject old dogmas and study phenomena from scientific knowledge. Addiction is not, in any case, a disease but a complex behavioral framework that results in changes in the structure and brain function, as in many other cases that no one would call "disease" (i.e., romantic infatuation).