Treatment for Your Mental Illness Based on Carl Jung's Method of Dream Interpretation

You are lucky because today you can easily learn Carl Jung's method of dream interpretation and find a free and safe treatment for your mental illness by translating the meaning of your own dreams. This is a spectacular alternative.

The wisdom of the unconscious mind that produces our dreams proves the existence of a superior creature. Your dreams are sent by God through the unconscious mind. However, you must learn the right way to translate the precious meaning of dreams if you want to understand the divine unconscious wisdom. Only Carl Jung could discover the mysterious meaning of the symbolic dream language, and only I had the courage to continue his dangerous research.

There is too much craziness in the human brain. Human beings are basically under-developed primates who must work changing their behavior in order to evolve.

If you suffer from a mental illness, you are not an exception. You are the confirmation of a tragic rule. Most people suffer from a mental illness without understanding that they don't control their thoughts and their behavior. They ignore the fact that they are controlled by their anti-conscience.

On the other hand, nobody really knows what should be considered normal or absurd on Earth. Many contrasting opinions and definitions couldn't prove to the world what it really means to be balanced or mentally ill.

The scientific method of dream interpretation that accurately translates the meaning of the unconscious messages in your dreams will help you understand the unconscious lessons. The unconscious mind will teach you what is good or bad. You'll have many explanations in dreams. The unconscious mind is a very generous teacher and doctor.

You'll find a treatment for your mental illness based on the unconscious wisdom. The unconscious mind will answer all your questions in dreams, and show you how to eliminate the influence of your anti-conscience. This is how you will stop being mentally ill, and find sound mental health that lasts for life.

The difference between balance and craziness is based on the absence or on the existence of sensitivity in your psyche. You will be balanced if you show compassion, and you always forgive your enemies. You will be balanced if you are always generous, humble, and sincere. Otherwise, the violent tendencies you have inherited into the biggest part of your brain will control your behavior and ruin your human personality.

Once you start following dream therapy you will stop having absurd thoughts, strange feelings, nightmares, and recurring dreams. The scientific method of dream interpretation is a bridge that unites you with your natural doctor; the divine unconscious mind. You learn how to interpret the meaning of the dream images based on the unconscious logic. You learn how to follow the wise unconscious guidance and improve your life.

After understanding the meaning of the dream language, you'll have the unconscious guidance forever showing you how to avoid all dangers, and always triumph.

For example, after seeing a fly in a dream, you will understand that something is bothering you, and you are not seeing obvious truths.

After seeing a river in a dream you will understand that you must study the content of your anti-conscience. You have to cross the river and learn what exists in the other side.

Many times only by seeing a dream symbol in a dream you will already understand how your future life will be, or what you have to do in order to prevent bad future results. You will understand how your brain works, and how to completely evolve, acquiring total consciousness.

You will also be able to practically read other people's minds by observing various revealing details in their behavior. You'll easily understand when someone is controlled by their anti-conscience, being able to avoid conspiracies against you.

The treatment you find when you translate the meaning of your dreams eliminates your mental illness, and transforms you into a balanced, calm, and wise human being. After passing through dream therapy you never let the evilness of the world affect your behavior. You are always kind, balanced, and wise, independently of the absurdity of your environment. You never lose control; you never use violence. You also help the world find balance thanks to your superior attitude.

Christina Sponias continued Carl Jung's research into the human psyche, discovering the cure for all mental illnesses, and simplifying the scientific method of dream interpretation that teaches you how to exactly translate the meaning of your dreams, so that you can find health, wisdom and happiness.

Learn more at: http://www.scientificdreaminterpretation.com/.

Click Here to download a Free Sample of the eBook Dream Interpretation as a Science (86 pages!).

View the original article here ezine.com

Depressed, pregnant women receive inconsistent treatment, have longer hospital stays

ScienceDaily (June 16, 2011) — Pregnant women who screen positive for depression are unlikely to receive consistent treatment, researchers say. That may translate to women spending more time in the hospital before babies are even born.

The Obstetric Clinics and Resources Study, published in General Hospital Psychiatry, tracked 20 health care providers in six Michigan clinics and revealed a lack of uniformity in addressing perinatal depression.

"There are a lot of barriers to translating information into everyday practice situations," said Dr. Christie Palladino, an obstetrician/gynecologist with Georgia Health Sciences University's Education Discovery Institute and principal investigator on the study. "We wanted to understand what it's like for prenatal care providers to deal with depression care."

Providers felt burdened having to make instant decisions about complex issues, the multidisciplinary research team found. And those decisions varied dramatically, even within the same clinic.

"There was no system-level support for providers," Palladino said. "They felt as if they were making decisions out on an island."

That sense of isolation, coupled with a lack of direction about how to treat pregnant women with depression, may explain why fewer than half of women who need treatment receive it.

Adding to the disconnect was providers' discomfort in talking about the disease with both patients and mental health care providers.

"In training, we tend to talk about how frequent a disease is, what the known causes are and the treatments that are available, but we don't address developing referral relationships," Palladino said. "We need to focus on not only knowledge of the disease, but also on the intrinsic motivations."

To address the problem, GHSU's Education Discovery Institute is conducting a pilot project to teach such skills. Residents and faculty in OB-GYN, psychiatry and pediatrics are collaborating to develop and test tailored educational interventions in perinatal depression care, in hopes of quickly implementing the content into clinical practice.

Palladino is applying for a Health Resources and Services Administration grant to test the curriculum and intervention at other locations as well.

An earlier study led by Palladino discovered that depressed women had significantly longer-than-average hospital stays: more than 24 hours prior to delivery.

"That's a long time for an otherwise healthy woman to be in the hospital before going into labor," Palladino said. "It has serious consequences for the mother, for the family and for the hospital system in terms of time and cost."

The study, published in the Journal of Women's Health and funded by the Robert Wood Johnson Foundation, also confirmed previous research linking depression to an increased risk of complications such as pre-term delivery, pre-eclampsia, premature membrane rupture and gestational diabetes.

"I was in a fantastic residency program, but treating depression during pregnancy wasn't even on the map at the time," Palladino said, noting that many OB-GYN residency programs still lack mental health training. "This has become my passion."

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Georgia Health Sciences University. The original article was written by Sharron Walls.

Journal Reference:

Christie Lancaster Palladino, Gina L. Fedock, Jane H. Forman, Matthew M. Davis, Erin Henshaw, Heather A. Flynn. OB CARES — The Obstetric Clinics and Resources Study: providers' perceptions of addressing perinatal depression — a qualitative study. General Hospital Psychiatry, 2011; 33 (3): 267 DOI: 10.1016/j.genhosppsych.2011.02.001

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here

Bioengineers identify the cellular mechanisms of traumatic brain injury; New hope for treatment of TBI in veterans wounded by explosions

ScienceDaily (July 25, 2011) — Bioengineers at Harvard have identified, for the very first time, the mechanism for diffuse axonal injury and explained why cerebral vasospasm is more common in blast-induced brain injuries than in brain injuries typically suffered by civilians.

The research addresses two major aspects of traumatic brain injury (TBI), with significant implications for the medical treatment of soldiers wounded by explosions.

Two papers, published in the journals Proceedings of the National Academy of Sciences (PNAS) and PLoS ONE, provide the most comprehensive explanation to date of how mechanical forces can be translated into subtly disastrous physiological changes within the brain's neurons and vasculature.

"These results have been a long time coming," says principal investigator Kevin Kit Parker, a Professor of Bioengineering at Harvard's School of Engineering and Applied Sciences (SEAS) and a major in the U.S. Army. "So many young men and women are returning from military service with brain injuries, and we just don't know how to help them."

When the brain encounters a jarring force, such as an exploding roadside bomb, the delicate tissue slams against the skull. The result, if the patient survives, can be a temporary concussion, a more dangerous hemorrhage, or long-term TBI, which can even lead to the early onset of Parkinson's or Alzheimer's diseases.

Inspired by Parker's own military experience, the Disease Biophysics Group (based at SEAS and at the Wyss Institute for Biologically Inspired Engineering at Harvard) has taken up the cause. Using cutting-edge tissue engineering techniques -- essentially creating a living brain on a chip -- biologists, physicists, engineers, and materials scientists collaborate to study brain injury and potential targets for treatment.

Now, researchers in his group have identified the cellular mechanism that initiates diffuse axonal injury, offering urgently needed direction for research in therapeutic treatments.

Their studies show that integrins, receptor proteins embedded in the cell membrane, provide the crucial link between external forces and internal physiological changes.

Integrins connect the structural components within the cell (such as actin and other cytoskeletal proteins) with the extracellular matrix that binds cells together into tissue. Collectively, this network of structural and signaling components is referred to as the focal adhesion complex.

Parker's research has demonstrated that the forces unleashed by an explosion physically disrupt the structure of the focal adhesion complex, setting off a chain reaction of destructive molecular signals within the nerve cells of the brain.

Inside the neuron, integrins normally mediate the activation of the proteins RhoA and Rho kinase (ROCK). When the focal adhesion complex is disturbed, the Rho-ROCK signaling pathway goes haywire: it directs the motor protein actin to retract the cell's arm-like axons, disconnecting the neurons from each other and collapsing the cellular networks that constitute the brain.

"Our research has shown that abrupt mechanical forces, such as those from a blast wave and transduced by integrins, can result in neural injury," says Matthew A. Hemphill, who with Borna Dabiri (S.B. '07) and Sylvain Gabriele, is a lead author of the paper in PLoS One. Dabiri and Hemphill are currently graduate students at SEAS, and Gabriele is a former postdoctoral fellow in Parker's lab.

Adds Dabiri: "Encouragingly, we also found that treating the neural tissue with HA-1077, which is a ROCK inhibitor, within the first 10 minutes of injury, reduced the number of focal swellings. We think that further study of ROCK inhibition could lead to viable treatments within the near future."

A second direction of research in Parker's lab has solved another mystery in TBI, explaining why cerebral vasospasm, a dangerous remodeling of the brain's blood vessels, occurs more commonly in TBI caused by explosions than in other types of brain trauma.

"Until now, other researchers looking at TBI focused on ion channels and membrane poration, and it was generally accepted that cerebralvasospasm was only caused by hemorrhaging. It turns out that it's much morecomplicated than that," says Patrick W. Alford, a former postdoctoral fellow in Parker's lab and lead author of the paper in PNAS. "Integrins and Rho-ROCK signaling appear to be players in both diffuse axonal injury and cerebral vasospasm."

As reported in PNAS, the forces exerted on arteries are different during an explosive blast than during blunt force trauma. Subarachnoid hemorrhage, which can occur in very severe head injuries, is known to cause vasospasm, but Parker's new research shows that the unique force of an explosion can also cause vasospasm by itself.

The blast from an explosion creates a surge in blood pressure, which stretches the walls of the blood vessels in the brain. To study this, Parker's team of bioengineers built artificial arteries, made of living vascular cells, and used a specialized machine to rapidly stretch them, simulating an explosion. While this stretching did not overtly damage the cellular structure, it did cause an immediate hypersensitivity to the protein endothelin-1.

Endothelin-1 is known to stimulate vascular cells to absorb calcium ions, which affect actin -- the same protein involved in the retraction of axons.

In the 24 hours following the simulated blast, the vascular tissues hypercontract and undergo a complete phenotypic switch, disrupting the overall function of the tissue. Both of these behaviors are characteristic of cerebral vasospasm.

Most importantly, as in the neural tissue, the Rho-ROCK signaling pathway plays an important role in the behavior of actin and the cells' contraction. Parker's team found that inhibition of Rho soon after the injury can mitigate the harmful effects of the blast on the brain's vascular system.

"We have established a toe-hold as we try to climb up on top of this problem," says Parker. "In many ways, this work is just the beginning."

Parker's coauthors on the paper in PLoS One are Hemphill, currently at the University of Mons in Belgium; Dabiri, who beganworking in Parker's lab as an undergraduate; Gabriele, who is now at the University of Mons; Lucas Kerscher, a visiting student; Christian Franck, formerly a postdoctoral fellow at SEAS and now at Brown University; Josue A. Goss, a staff engineer at SEAS; and Alford, who is now at the University ofMinnesota.

Parker's coauthors on the paper in PNAS are Alford; Dabiri; Goss; Hemphill; and Mark D. Brigham, a graduate student at SEAS.

The Disease Biophysics Group received financial support from the Defense Advanced Research Projects Agency (DARPA) Preventing Violent Explosive Neurologic Trauma (PREVENT) Program, the Department of Defense, and the Harvard School of Engineering and Applied Sciences (SEAS).

The researchers also gratefully acknowledge the use of facilities at the Harvard Center for Nanoscale Systems, a member of the National Nanotechnology Infrastructure Network (NNIN), which is funded by the National Science Foundation (NSF).

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Harvard University, via EurekAlert!, a service of AAAS.

Journal References:

P. W. Alford, B. E. Dabiri, J. A. Goss, M. A. Hemphill, M. D. Brigham, K. K. Parker. Blast-induced phenotypic switching in cerebral vasospasm. Proceedings of the National Academy of Sciences, 2011; DOI: 10.1073/pnas.1105860108Matthew A. Hemphill, Borna E. Dabiri, Sylvain Gabriele, Lucas Kerscher, Christian Franck, Josue A. Goss, Patrick W. Alford, Kevin Kit Parker. A Possible Role for Integrin Signaling in Diffuse Axonal Injury. PLoS ONE, 2011; 6 (7): e22899 DOI: 10.1371/journal.pone.0022899

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here

Scientists discover potential stroke treatment that may extend time to prevent brain damage

ScienceDaily (July 25, 2011) — A naturally occurring substance shrank the size of stroke-induced lesions in the brains of experimental mice -- even when administered as much as 12 hours after the event, Stanford University School of Medicine researchers have shown. The substance, alpha-B-crystallin, acts as a brake on the immune system, lowering levels of inflammatory molecules whose actions are responsible for substantial brain damage above and beyond that caused by the initial oxygen deprivation of a stroke.

The finding, which will be published online July 25 in Proceedings of the National Academy of Sciences, is of great potential significance. Every year brings nearly 800,000 new stroke patients in North America. "That's one every 40 seconds," said Gary Steinberg, MD, PhD, director of Stanford's Institute for Neuro-Innovation and Translational Neurosciences and one of the study's two senior authors. Steinberg is also the Bernard and Ronni Lacroute-William Randolph Hearst Professor of Neurosurgery and the Neurosciences, and chair of neurosurgery at the medical school.

The largest single cause of severe neurological disability and the third-leading cause of death in the United States, stroke accounts for an estimated $74 billion annually in related costs, including treatment and additional assistance for the three of every four stroke patients whose ability to perform the activities of daily life is impaired. Strokes are caused by a sudden drop in the flow of blood to the brain resulting from a clot or, less often, bleeding. One of every three stroke patients is under the age of 65. In all, there are 5.4 million stroke survivors in the United States and 15 million worldwide.

The only currently approved drug for stroke -- tissue plasminogen activator, or tPA -- dissolves clots that keep oxygenated blood from reaching brain tissue. To be effective, tPA must be administered within about 4.5 hours after the stroke. But patients' brains must first be scanned to rule out the possibility that the stroke was caused by bleeding, which tPA would exacerbate, rather than by blockage.

Moreover, tPA does nothing to counter the stroke's insidious inflammatory aftershock: a flood of noxious chemicals secreted by angry immune cells that rush in to the affected area, causing significant further damage.

Alpha-B-crystallin appears to act as a sponge, sopping up those bad actors and stopping inflammation from making a bad situation worse.

Alpha-B-crystallin is a major structural protein in the eye's lens. It is also constantly made in the heart. In other tissues, including the brain, its production can be triggered by stressful events, such as oxygen deprivation or excessive heat or cold. Growing evidence suggests that alpha-B-crystallin can help curb inflammatory activity in the brain.

"The brain doesn't roll over and play dead when it's under attack," said Lawrence Steinman, MD, the other senior author of the new study, who is the George A. Zimmermann Professor of Neurology and Neurological Sciences and Pediatrics as well as chair of Stanford's interdepartmental program in immunology.

In an earlier study, published in Nature in 2007, Steinman and his colleagues found that the presence of alpha-B-crystallin could help reduce the severity of brain damage caused by multiple sclerosis, a chronic, debilitating autoimmune disease of the brain. Other studies published this year by his group have shown that alpha-B-crystallin limits the damage caused by blood-supply cutoffs to heart tissue and the retina.

It seemed logical to see if this protein could mitigate the effects of a stroke. "We made a jump from its relevance in inflammatory diseases such as multiple sclerosis," Steinberg said. "To my knowledge, nobody had looked at concentrations of alpha-B-crystallin after a stroke, either in people or in an experimental animal model before."

So, along with first authors Ahmet Arac, MD, a postdoctoral scholar in Steinberg's lab, and Steinman's former graduate student Sarah Brownell, PhD, Steinberg and Steinman turned to a standard animal model: the laboratory mouse. They found that, in mice bioengineered to lack alpha-B-crystallin, experimentally induced stroke lesions were more massive than those induced in otherwise genetically similar mice whose cells were capable of making the protein. The alpha-B-crystallin-deficient mice had worse neurological function after the stroke than did the normal mice.

The researchers also found that supplying synthetic alpha-B-crystallin to the deficient mice reduced brain-lesion sizes after a stroke, even when the substance was administered 12 hours after the stroke was induced. And they saw elevated alpha-B-crystallin levels in blood plasma from both human patients and mice after a stroke. (The human samples were obtained from study co-author Gregory Albers, MD, the Coy Foundation Professor of Neurology and Neurological Sciences and the director of the Stanford Stroke Center).

"In younger patients, the larger the stroke, the higher the concentration of alpha-B-crystallin," said Steinberg. Interestingly, increased alpha-B-crystallin levels were not detected in plasma from patients over the age of 80, whose strokes typically have worse consequences than those affecting younger patients.

Finally, the investigators demonstrated that alpha-B-crystallin-treated mice produce fewer inflammatory immune-signaling molecules and more anti-inflammatory ones than untreated mice.

At the doses given to the mice in this study, alpha-B-crystallin appeared to be nontoxic. "This is a naturally occurring molecule the body is already producing, although maybe just not enough of it," said Steinberg. "We're just supplementing it." If further studies by other labs and in other models confirm and extend the findings, alpha-B-crystallin may be an excellent candidate for clinical trials in stroke, Steinman and Steinberg both said.

"This is the first demonstration of an efficacious brain-protecting agent that targets the inflammatory aspect of stroke in a novel way, and it can be given at quite a delay," said Thomas Carmichael, MD, PhD, professor and vice chair of neurology at the David Geffen School of Medicine at UCLA. Carmichael, a stroke expert, did not participate in the study but is familiar with its methodology and results. "Tissue plasminogen activator has a fairly narrow risk-to-benefit ratio. The longer you wait, the more likely it is to stimulate a hemorrhage."

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Stanford University Medical Center. The original article was written by Bruce Goldman.

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here

Cognitive behavioral therapy may benefit patients in residential substance abuse treatment programs

ScienceDaily (June 6, 2011) — Patients in residential treatment programs for drug and alcohol abuse may benefit from cognitive behavioral therapy for depressive symptoms, according to a report in the June issue of Archives of General Psychiatry, one of the JAMA/Archives journals.

The article notes, as background information, that depression and substance abuse often co-occur, but that individuals with both disorders are not always treated for both. "The consequences of this unmet need are great," report the authors. "The interactive nature of the two disorders leads to poorer depression and substance abuse treatment outcomes compared with the outcomes when only one disorder is treated."

Katherine E. Watkins, M.D., M.S.H.S., from RAND Corporation, Santa Monica, Calif., and colleagues conducted the study at four Behavioral Health Services facilities in Los Angeles County, Calif. Between August 2006 and January 2009, the sites alternated every four months between usual care for substance abuse and usual care plus cognitive behavioral therapy as modeled in the Building Recovery by Improving Goals, Habits, and Thoughts (BRIGHT) study. The intervention comprised 16 two-hour BRIGHT sessions over the course of eight weeks.

Initially, 1,262 patients were screened for participation in the study. The researchers enrolled 140 patients in the intervention group and 159 patients in the control group. On average, participants scored in the clinically severe range on a scale of depression symptoms and nearly half (45.8%) had a past 12-month depressive disorder.

On the depression-symptom instrument used in the study, at three months patients receiving the intervention generally had mild symptoms and patients receiving usual care alone generally had moderate symptoms. At three months, 55.8 percent of patients in the BRIGHT group had minimal symptoms, compared with 33.6 percent in the control group; at six months, these numbers increased to 63.9 percent and 43.8 percent, respectively. Among patients no longer living in a treatment center at the six-month mark, those in the intervention group had fewer days of problem substance abuse and fewer drinking days than did those in the usual care group.

With the study, the authors hope to address a gap in the substance abuse treatment system, particularly in the public sector. They note that the BRIGHT intervention involved substance abuse counselors, as opposed to other mental health professionals and resources that some substance abuse programs cannot access. "The study demonstrates that it is possible to develop the capacity of substance abuse programs to deliver evidence-based mental health care by enhancing the skills and expanding the clinical roles of substance abuse counselors," the researchers state. This is important, they add, because "Lack of access to efficacious depression treatment for substance abusers is an important public health problem."

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by JAMA and Archives Journals.

Journal Reference:

K. E. Watkins, S. B. Hunter, K. A. Hepner, S. M. Paddock, E. de la Cruz, A. J. Zhou, J. Gilmore. An Effectiveness Trial of Group Cognitive Behavioral Therapy for Patients With Persistent Depressive Symptoms in Substance Abuse Treatment. Archives of General Psychiatry, 2011; 68 (6): 577 DOI: 10.1001/archgenpsychiatry.2011.53

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here

New 'chemical pathway' in the brain for stress: Breakthrough offers hope for targeted treatment of stress-related disorders

ScienceDaily (Apr. 20, 2011) — A team of neuroscientists at the University of Leicester, UK, in collaboration with researchers from Poland and Japan, has announced a breakthrough in the understanding of the 'brain chemistry' that triggers our response to highly stressful and traumatic events.

The discovery of a critical and previously unknown pathway in the brain that is linked to our response to stress is published in the journal Nature. The advance offers new hope for targeted treatment, or even prevention, of stress-related psychiatric disorders.

About 20% of the population experience some form of anxiety disorder at least once in their lives. The cumulative lifetime prevalence of all stress-related disorders is difficult to estimate but is probably higher than 30%.

Dr Robert Pawlak, from the University of Leicester who led the UK team, said: "Stress-related disorders affect a large percentage of the population and generate an enormous personal, social and economic impact. It was previously known that certain individuals are more susceptible to detrimental effects of stress than others. Although the majority of us experience traumatic events, only some develop stress-associated psychiatric disorders such as depression, anxiety or posttraumatic stress disorder. The reasons for this were not clear."

Dr Pawlak added that a lack of correspondence between the commonness of exposure to psychological trauma and the development of pathological anxiety prompted the researchers to look for factors that may make some individuals more vulnerable to stress than others.

"We asked: What is the molecular basis of anxiety in response to noxious stimuli? How are stress-related environmental signals translated into proper behavioural responses? To investigate these problems we used a combination of genetic, molecular, electrophysiological and behavioural approaches. This resulted in the discovery of a critical, previously unknown pathway mediating anxiety in response to stress."

The study found that the emotional centre of the brain -- the amygdala -- reacts to stress by increasing production of a protein called neuropsin. This triggers a series of chemical events which in turn cause the amygdala to increase its activity. As a consequence, a gene is turned on that determines the stress response at a cellular level.

"We then examined behavioural consequences of the above series of cellular events caused by stress in the amygdala," said Dr Pawlak. "Studies in mice revealed that upon feeling stressed, they stayed away from zones in a maze where they felt unsafe. These were open and illuminated spaces they avoid when they are anxious."

"However when the proteins produced by the amygdala were blocked -- either pharmacologically or by gene therapy -- the mice did not exhibit the same traits. The behavioural consequences of stress were no longer present. We conclude that the activity of neuropsin and its partners may determine vulnerability to stress."

Neuropsin was previously discovered by Professor Sadao Shiosaka, a co-author of the paper. This research, for which the bioinformatics modelling was done by Professor Ryszard Przewlocki and his team, has for the first time characterized its mechanism of action in controlling anxiety in the amygdala.

The study took four years to complete, during which scientists from the Department of Cell Physiology and Pharmacology collaborated with colleagues from the Medical Research Council Toxicology Unit at the University of Leicester, the Department of Molecular Neuropharmacology, Polish Academy of Sciences in Krakow, Poland and Nara Institute of Science and Technology in Japan. The work was supported by the European Union, the Medical Research Council and Medisearch -- the Leicestershire Medical Research Foundation. The first author, Benjamin Attwood, sponsored by Medisearch, took 3 years off from his medical studies curriculum to complete the necessary experiments. He commented: "It has been a thoroughly absorbing project to uncover how our experiences can change the way we behave. Hopefully this will lead to help for people that have to live with the damaging consequences of traumatic experiences."

Dr Pawlak added: "We are tremendously excited about these findings. We know that all members of the neuropsin pathway are present in the human brain. They may play a similar role in humans and further research will be necessary to examine the potential of intervention therapies for controlling stress-induced behaviours."

"Although research is now needed to translate our findings to the clinical situation, our discovery opens new possibilities for prevention and treatment of stress-related psychiatric disorders such as depression and posttraumatic stress disorder."

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by University of Leicester, via EurekAlert!, a service of AAAS.

Journal Reference:

Benjamin K. Attwood, Julie-Myrtille Bourgognon, Satyam Patel, Mariusz Mucha, Emanuele Schiavon, Anna E. Skrzypiec, Kenneth W. Young, Sadao Shiosaka, Michal Korostynski, Marcin Piechota, Ryszard Przewlocki, Robert Pawlak. Neuropsin cleaves EphB2 in the amygdala to control anxiety. Nature, 2011; DOI: 10.1038/nature09938

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here

Cognitive behavioral therapy may benefit patients in residential substance abuse treatment programs

ScienceDaily (June 6, 2011) — Patients in residential treatment programs for drug and alcohol abuse may benefit from cognitive behavioral therapy for depressive symptoms, according to a report in the June issue of Archives of General Psychiatry, one of the JAMA/Archives journals.

The article notes, as background information, that depression and substance abuse often co-occur, but that individuals with both disorders are not always treated for both. "The consequences of this unmet need are great," report the authors. "The interactive nature of the two disorders leads to poorer depression and substance abuse treatment outcomes compared with the outcomes when only one disorder is treated."

Katherine E. Watkins, M.D., M.S.H.S., from RAND Corporation, Santa Monica, Calif., and colleagues conducted the study at four Behavioral Health Services facilities in Los Angeles County, Calif. Between August 2006 and January 2009, the sites alternated every four months between usual care for substance abuse and usual care plus cognitive behavioral therapy as modeled in the Building Recovery by Improving Goals, Habits, and Thoughts (BRIGHT) study. The intervention comprised 16 two-hour BRIGHT sessions over the course of eight weeks.

Initially, 1,262 patients were screened for participation in the study. The researchers enrolled 140 patients in the intervention group and 159 patients in the control group. On average, participants scored in the clinically severe range on a scale of depression symptoms and nearly half (45.8%) had a past 12-month depressive disorder.

On the depression-symptom instrument used in the study, at three months patients receiving the intervention generally had mild symptoms and patients receiving usual care alone generally had moderate symptoms. At three months, 55.8 percent of patients in the BRIGHT group had minimal symptoms, compared with 33.6 percent in the control group; at six months, these numbers increased to 63.9 percent and 43.8 percent, respectively. Among patients no longer living in a treatment center at the six-month mark, those in the intervention group had fewer days of problem substance abuse and fewer drinking days than did those in the usual care group.

With the study, the authors hope to address a gap in the substance abuse treatment system, particularly in the public sector. They note that the BRIGHT intervention involved substance abuse counselors, as opposed to other mental health professionals and resources that some substance abuse programs cannot access. "The study demonstrates that it is possible to develop the capacity of substance abuse programs to deliver evidence-based mental health care by enhancing the skills and expanding the clinical roles of substance abuse counselors," the researchers state. This is important, they add, because "Lack of access to efficacious depression treatment for substance abusers is an important public health problem."

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by JAMA and Archives Journals.

Journal Reference:

K. E. Watkins, S. B. Hunter, K. A. Hepner, S. M. Paddock, E. de la Cruz, A. J. Zhou, J. Gilmore. An Effectiveness Trial of Group Cognitive Behavioral Therapy for Patients With Persistent Depressive Symptoms in Substance Abuse Treatment. Archives of General Psychiatry, 2011; 68 (6): 577 DOI: 10.1001/archgenpsychiatry.2011.53

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here