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Archive for the ‘Social Development’ Category


Yesterday and today are not the same

Larry H. Bernstein

LPBI

 

The New Generation Gap

https://www.project-syndicate.org/commentary/new-generation-gap-social-injustice-by-joseph-e–stiglitz-2016-03

Joseph E. Stiglitz

Joseph E. Stiglitz, recipient of the Nobel Memorial Prize in Economic Sciences in 2001 and the John Bates Clark Medal in 1979, is University Professor at Columbia University, Co-Chair of the High-Level Expert Group on the Measurement of Economic Performance and Social Progress at the OECD, and Chief Economist of the Roosevelt Institute. A former senior vice president and chief economist of the World Bank and chair of the US president’s Council of Economic Advisers under Bill Clinton, in 2000 he founded the Initiative for Policy Dialogue, a think tank on international development based at Columbia University. His most recent book is Rewriting the Rules of the American Economy.

NEW YORK – Something interesting has emerged in voting patterns on both sides of the Atlantic: Young people are voting in ways that are markedly different from their elders. A great divide appears to have opened up, based not so much on income, education, or gender as on the voters’ generation.

There are good reasons for this divide. The lives of both old and young, as they are now lived, are different. Their pasts are different, and so are their prospects.

The Cold War, for example, was over even before some were born and while others were still children. Words like socialism do not convey the meaning they once did. If socialism means creating a society where shared concerns are not given short shrift – where people care about other people and the environment in which they live – so be it. Yes, there may have been failed experiments under that rubric a quarter- or half-century ago; but today’s experiments bear no resemblance to those of the past. So the failure of those past experiments says nothing about the new ones.

Older upper-middle-class Americans and Europeans have had a good life. When they entered the labor force, well-compensated jobs were waiting for them. The question they asked was what they wanted to do, not how long they would have to live with their parents before they got a job that enabled them to move out.

That generation expected to have job security, to marry young, to buy a house – perhaps a summer house, too – and finally retire with reasonable security. Overall, they expected to be better off than their parents.

While today’s older generation encountered bumps along the way, for the most part, their expectations were met. They may have made more on capital gains on their homes than from working. They almost surely found that strange, but they willingly accepted the gift of our speculative markets, and often gave themselves credit for buying in the right place at the right time.

Today, the expectations of young people, wherever they are in the income distribution, are the opposite. They face job insecurity throughout their lives. On average, many college graduates will search for months before they find a job – often only after having taken one or two unpaid internships. And they count themselves lucky, because they know that their poorer counterparts, some of whom did better in school, cannot afford to spend a year or two without income, and do not have the connections to get an internship in the first place.

Today’s young university graduates are burdened with debt – the poorer they are, the more they owe. So they do not ask what job they would like; they simply ask what job will enable them to pay their college loans, which often will burden them for 20 years or more. Likewise, buying a home is a distant dream.

These struggles mean that young people are not thinking much about retirement. If they did, they would only be frightened by how much they will need to accumulate to live a decent life (beyond bare social security), given the likely persistence of rock-bottom interest rates.

In short, today’s young people view the world through the lens of intergenerational fairness. The children of the upper middle class may do well in the end, because they will inherit wealth from their parents. While they may not like this kind of dependence, they dislike even more the alternative: a “fresh start” in which the cards are stacked against their attainment of anything approaching what was once viewed as a basic middle-class lifestyle.

These inequities cannot easily be explained away. It isn’t as if these young people didn’t work hard: these hardships affect those who spent long hours studying, excelled in school, and did everything “right.” The sense of social injustice – that the economic game is rigged – is enhanced as they see the bankers who brought on the financial crisis, the cause of the economy’s continuing malaise, walk away with mega-bonuses, with almost no one being held accountable for their wrongdoing. Massive fraud was committed, but somehow, no one actually perpetrated it. Political elites promised that “reforms” would bring unprecedented prosperity. And they did, but only for the top 1%. Everyone else, including the young, got unprecedented insecurity.

These three realities – social injustice on an unprecedented scale, massive inequities, and a loss of trust in elites – define our political moment, and rightly so.

More of the same is not an answer. That is why the center-left and center-right parties in Europe are losing. America is in a strange position: while the Republican presidential candidates compete on demagoguery, with ill-thought-through proposals that would make matters worse, both of the Democratic candidates are proposing changes which – if they could only get them through Congress – would make a real difference.

Were the reforms put forward by Hillary Clinton or Bernie Sanders adopted, the financial system’s ability to prey on those already leading a precarious life would be curbed. And both have proposals for deep reforms that would change how America finances higher education.

But more needs to be done to make home ownership possible not just for those with parents who can give them a down payment, and to make retirement security possible, given the vagaries of the stock market and the near-zero-interest world we have entered. Most important, the young will not find a smooth path into the job market unless the economy is performing much better. The “official” unemployment rate in the United States, at 4.9%, masks much higher levels of disguised unemployment, which, at the very least, are holding down wages.

But we won’t be able to fix the problem if we don’t recognize it. Our young do. They perceive the absence of intergenerational justice, and they are right to be angry.

Read more at https://www.project-syndicate.org/commentary/new-generation-gap-social-injustice-by-joseph-e–stiglitz-2016-03#vxQE74VR3kfAWbf1.99

 

 

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Lifelong Contraceptive Device for Men: Mechanical Switch to Control Fertility on Wish

Reporter and Curator: Dr. Sudipta Saha, Ph.D.

There aren’t many options for long-term birth control for men. The most common kinds of male contraception include

  • condoms,
  • withdrawal / pulling out,
  • outercourse, and
  • vasectomy.

But, other than vasectomy none of the processes are fully secured, comfortable and user friendly. Another solution may be

  • RISUG (Reversible Inhibition of Sperm Under Guidance, or Vasalgel)

which is said to last for ten years and no birth control pill for men is available till date.

VIEW VIDEO

http://www.mdtmag.com/blog/2016/01/implanted-sperm-switch-turns-mens-fertility-and?et_cid=5050638&et_rid=461755519&type=cta

Recently a German inventor, Clemens Bimek, developed a novel, reversible, hormone free, uncomplicated and lifelong contraceptive device for controlling male fertility. His invention is named as Bimek SLV, which is basically a valve that stops the flow of sperm through the vas deferens with the literal flip of a mechanical switch inside the scortum, rendering its user temporarily sterile. Toggled through the skin of the scrotum, the device stays closed for three months to prevent accidental switching. Moreover, the switch can’t open on its own. The tiny valves are less than an inch long and weigh is less than a tenth of an ounce. They are surgically implanted on the vas deferens, the ducts which carry sperm from the testicles, through a simple half-hour operation.

The valves are made of PEEK OPTIMA, a medical-grade polymer that has long been employed as a material for implants. The device is patented back in 2000 and is scheduled to undergo clinical trials at the beginning of this year. The inventor claims that Bimek SLV’s efficacy is similar to that of vasectomy, it does not impact the ability to gain and maintain an erection and ejaculation will be normal devoid of the sperm cells. The valve’s design enables sperm to exit the side of the vas deferens when it’s closed without any semen blockage. Leaked sperm cells will be broken down by the immune system. The switch to stop sperm flow can be kept working for three months or 30 ejaculations. After switching on the sperm flow the inventor suggested consulting urologist to ensure that all the blocked sperms are cleared off the device. The recovery time after switching on the sperm flow is only one day, according to Bimek SLV. However, men are encouraged to wait one week before resuming sexual activities.

Before the patented technology can be brought to market, it must undergo a rigorous series of clinical trials. Bimek and his business partners are currently looking for men interested in testing the device. If the clinical trials are successful then this will be the first invention of its kind that gives men the ability to control their fertility and obviously this method will be preferred over vasectomy.

 

References:

 

https://www.bimek.com/this-is-how-the-bimek-slv-works/

 

http://www.mdtmag.com/blog/2016/01/implanted-sperm-switch-turns-mens-fertility-and?et_cid=5050638&et_rid=461755519&type=cta

 

http://www.telegraph.co.uk/news/worldnews/europe/germany/12083673/German-carpenter-invents-on-off-contraception-switch-for-sperm.html

 

http://www.discovery.com/dscovrd/tech/you-can-now-turn-off-your-sperm-flow-with-the-flip-of-a-switch/

 

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To reduce symptoms of mental illness and retrain the brain

Larry H. Bernstein, MD, FCAP, Curator

Leaders in Pharmaceutical Intelligence

Series E. 2; 5.11

Researchers have found that by specifically targeting a central signaling pathway in the brain, they can improve the innate behavioral response to stress in mice. Stress-induced behaviors in rodents reflect many of the symptoms that affect people suffering from major depression and other clinical conditions associated with stress. The findings, published July 20th online in the journalNature Neuroscience, suggest a new strategy for treating depression and other stress-associated disorders.

The study was led by James A. Bibb, Ph.D., at The University of Texas Southwestern Medical Center, who received NARSAD Young Investigator grants in 2000 and 2003, and lead authorFlorian Plattner, Ph.D. The scientific team also included Paul Greengard, Ph.D., a member of BBRF’s Scientific Council and a 1992, 2002, and 2008 Distinguished Investigator; Eric J. Nestler, M.D., Ph.D., a Scientific Council Member and a 1996 Distinguished Investigator; 2006 Young Investigator Kanehiro Hayashi, Ph.D.; 2007 Young Investigator Eunice Y. Yuen, Ph.D.; 1999 and 2004 Young Investigator Zhen Yan, Ph.D.; and 1999 Independent Investigator and 2006 Distinguished Investigator Angus C. Nairn, Ph.D.

The team’s findings are a result of a detailed investigation into a “signaling cascade,” called the cAMP/PKA pathway, which regulates a wide range of processes in the central nervous system. Disruption of the pathway has been linked with several mental disorders, including depression. Some existing antidepressant medications are known to boost cAMP signaling, but better understanding how this signaling network works could help researchers develop treatments that are more effective or cause fewer side effects.

Two new small-molecule compounds tested in mice can alleviate some symptoms of schizophrenia-like behaviors, including movement abnormalities, social avoidance, and cognitive performance. As reported in the July 1st issue of Neuropsychopharmacology, these research results may point the way toward new kinds of medications that treat specific aspects ofschizophrenia behaviors.

Current antipsychotic drugs used to treat the disorder target the dopamine D2 receptor, an important communication port for some neurons in the brain. These drugs are used primarily to treat schizophrenia “positive” symptoms such as delusions and hallucinations. They are less effective in treating “negative” symptoms such as a lack of pleasure in everyday life, or concentration and memory problems (“cognitive symptoms”), according to Duke University Medical Center scientists William C. Wetsel, Ph.D., a 1998 NARSAD Independent Investigator grantee, and Marc G. Caron, Ph.D., a Foundation Scientific Council member and 2005 NARSAD Distinguished Investigator grantee.

Current antipsychotic drugs were developed to bind to and block one specific type of communication pathway through dopamine D2 receptors, but the receptors are involved in more than one type of signaling pathway. Dr. Wetsel and colleagues decided to look for drug candidates that would block other pathways related to the dopamine D2 receptor, in the hope that this might reveal novel ways to treat a wider variety of schizophrenia symptoms.

They tested two dopamine D2 receptor-targeting compounds called UNC9975 and UNC9994 (developed by Jian Jin, Ph.D., of the University of North Carolina) that influence the beta-arrestin communication pathway, a different pathway than the one typically affected by antipsychotic drugs. The researchers showed that the compounds could normalize schizophrenia-like symptoms in mice by reducing their hyperactive movements, improving their memory for novel stimuli, and making them more social around other mice, among other improvements.

The new compounds also produced a much lower level of catalepsy—the rigid muscle, “trance-like” state that is sometimes a side effect of schizophrenic treatment—than traditional antipsychotic drugs such as haloperidol. Targeting different pathways connected to the dopamine D2 receptors, the researchers say, may increase the possibilities for treating people with schizophrenia in more individualized, fine-tuned ways that match their exact symptoms and vulnerabilities to side effects.

Effects of β-Arrestin-Biased Dopamine D2 Receptor Ligands on Schizophrenia-Like Behavior in Hypoglutamatergic Mice

Su M Park1, Meng Chen1, Claire M Schmerberg1, Russell S Dulman1, Ramona M Rodriguiz1,2, Marc G Caron3, Jian Jin4 and William C Wetsel1,2,3,5
Neuropsychopharmacology 2015; http://dx.doi.org:/10.1038/npp.2015.196

Current antipsychotic drugs (APDs) show efficacy with positive symptoms, but are limited in treating negative or cognitive features of schizophrenia. Whereas all currently FDA-approved medications target primarily the dopamine D2 receptor (D2R) to inhibit Gi/o-mediated adenylyl cyclase, a recent study has shown that many APDs affect not only Gi/o– but they can also influence β-arrestin- (βArr)-mediated signaling. The ability of ligands to differentially affect signaling through these pathways is termed functional selectivity. We have developed ligands that are devoid of D2R-mediated Gi/o protein signaling, but are simultaneously partial agonists for D2R/βArr interactions. The purpose of this study was to test the effectiveness of UNC9975 or UNC9994 on schizophrenia-like behaviors in phencyclidine-treated or NR1-knockdown hypoglutamatergic mice. We have found the UNC compounds reduce hyperlocomotion in the open field, restore PPI, improve novel object recognition memory, partially normalize social behavior, decrease conditioned avoidance responding, and elicit a much lower level of catalepsy than haloperidol. These preclinical results suggest that exploitation of functional selectivity may provide unique opportunities to develop drugs with fewer side effects, greater therapeutic selectivity, and enhanced efficacy for treating schizophrenia and related conditions than medications that are currently available.

The estrogen-related drug raloxifene can improve attention and memory in men and women with schizophrenia, according to a new study published in the journal Molecular Psychiatry.

University of New South Wales researcher Cynthia S. Weickert, Ph.D., a 1999 and 2001 NARSAD Young Investigator and 2004 Independent Investigator grantee, and her colleagues say their raloxifene findings could help improve some cognitive problems related to schizophrenia that have been the most difficult to treat with drugs. Dr. Weickert’s research team included NARSAD Young Investigator grantees Rhoshel K. Lenroot, M.D., (2003), and Ans Vercammen, Ph.D., (2010), along with Independent Investigator grantee Jayashri Kulkarni, Ph.D., (2000), and her husband and first author Tom Weickert, Ph.D.

A growing body of evidence suggests that estrogen plays a beneficial role in the brain, supporting growth and protecting neurons from damage. From work supported by her NARSAD Young Investigator awards, Dr. Weickert and her colleagues found that brain estrogen receptors are altered in some people with schizophrenia, blunting their ability to respond to estrogen’s beneficial effects. Raloxifene stimulates estrogen receptors and can help overcome a blunted estrogen response. Raloxifene is probably best known as a treatment for osteoporosis in women, where it mimics estrogen’s beneficial action in bones. The drug also stimulates estrogen receptors in the brain and may guard against memory loss in aging, making it potentially useful for cognitive problems in schizophrenia patients.

The research team examined the drug’s effect in 98 people diagnosed with schizophrenia or schizoaffective disorder (which combines symptoms of schizophrenia and depression). All of the patients received a daily dose of raloxifene along with their usual antipsychotic medications in one phase of the clinical trial and a placebo in another phase.

After the first six-week period, patients taking raloxifene had improved scores on memory and attention, compared to those taking placebo. When considering all the people in the study during both phases, raloxifene treatment significantly improved attention and thought processing speed. Raloxifene didn’t reduce the severity of schizophrenia symptoms more than the placebo did, but both groups showed less symptoms overall during the study, and none of the patients had severe side effects from the treatment.

Dr. Weickert and colleagues did detect some signs that the positive impact of raloxifene lasted more than one month after the treatment stopped. Although the researchers do not know the exact reasons for the lasting effects, they note that stimulating estrogen receptors might protect neurons, reduce inflammation, and increase connections between nerve cells in the brain over a longer time frame than drugs working on other neurotransmitter receptors. In light of their findings, they suggest future studies should replicate these results in a larger group of schizophrenia patients and also determine how long the cognitive benefits of a six-week treatment with raloxifene may last.

An injectable antipsychotic medication whose effects last for three months has successfully delayed the return of schizophrenia symptoms, researchers have found. Taking the drug in this form may help people with schizophrenia who struggle to stay on treatment by enabling them to take medication less frequently.

The research team, which included Adam J. Savitz, M.D., Ph.D., recipient of a NARSAD Young Investigator Grant in 2001, examined use of the long-acting antipsychotic medication paliperidone palmitate (Invega) in treating symptoms of schizophrenia such as hallucinations, delusions, and strong feelings of suspicion. The research was published online March 29th inJAMA Psychiatry.

When a person with schizophrenia cannot maintain a daily medication schedule, the drug level in his or her body can dip too low to combat symptoms, leading to relapse (return of symptoms) and an increased risk of being hospitalized. This study aimed to determine whether a dosage that would only have to be taken once every three months, rather than every day, would effectively hold off symptoms. After starting with a once-monthly dosage, patients took a three-month dosage to maintain symptom prevention and then were given randomly either placebo or the same three-month dosage every 12 weeks to see whether the medication’s positive effects would persist. (A placebo is a look-alike with inactive ingredients.)

Significantly fewer people who got the second three-month dosage experienced symptom relapse during the experimental phase of the study, compared to those taking a placebo. During this phase, the placebo group also reported more severe symptoms, while the paliperidone palmitate group’s symptoms remained constant.

The two groups also showed different patterns of side effects. The more serious side effects occurred in the placebo group: anxiety and return of other symptoms of schizophrenia. The paliperidone palmitate group more frequently experienced headaches, weight gain, common colds, as well as so-called extrapyramidal symptoms, which involve disruptions to movement.

This study did not include people with a history of substance dependence, major active medical problems, or other serious mental disorders. More research is needed to know whether less frequent dosage of long-acting injectable medication like paliperidone palmitate can help prevent relapse in these groups.

Efficacy and Safety of the 3-Month Formulation of Paliperidone Palmitate vs Placebo for Relapse Prevention of Schizophrenia – A Randomized Clinical Trial

Joris Berwaerts, MD1; Yanning Liu, MS2; Srihari Gopal, MD, MHS1; Isaac Nuamah, PhD1; Haiyan Xu, PhD1; Adam Savitz, MD, PhD1; Danielle Coppola, MD1; Alain Schotte, PhD3; Bart Remmerie, Chem Eng3; Nataliya Maruta, MD, PhD4; David W. Hough, MD1
JAMA Psychiatry. 2015; 72(8):830-839. http://dx.doi.org:/10.1001/jamapsychiatry.2015.0241.

Design, Setting, and Participants  This randomized, multicenter trial conducted from April 26, 2012, through April 9, 2014, in 8 countries consisted of 4 phases: 3-week screening phase, flexible-dose 17-week open-label transition phase, 12-week open-label maintenance phase, and open-ended double-blind (DB) phase. Of the 506 patients enrolled (aged 18-70 years; DSM-IV-TR diagnosis of schizophrenia), 305 were randomized to 3-month paliperidone palmitate (n = 160) or placebo (n = 145) in the DB phase.

Interventions  Patients received once-monthly doses of the 1-month formulation of paliperidone palmitate (50, 75, 100, or 150 mg eq) during the transition phase, followed by a single dose of the 3-month formulation (3.5 times the stabilized dose of once-monthly paliperidone palmitate) during the maintenance phase. Stabilized patients were randomized to receive either a fixed dose of 3-month paliperidone palmitate (175, 263, 350, or 525 mg eq) or placebo once every 3 months during the DB phase.

Main Outcomes and Measures  Time from randomization to the first relapse event (time to relapse) in the DB phase.

Results  In the interim analysis, time to first relapse was significantly different in favor of the paliperidone palmitate group vs the placebo group (hazard ratio = 3.45; 95% CI, 1.73-6.88; P < .001); median time to relapse was 274 days for placebo but not estimable for 3-month paliperidone palmitate. An independent data monitoring committee recommended early study termination due to efficacy. In the DB phase, 183 of 305 patients (62% with 3-month paliperidone palmitate; 58% with placebo) had at least 1 treatment-emergent adverse event; those noted more frequently in the group receiving paliperidone palmitate than in the placebo group were headache (9% vs 4%), weight increased (9% vs 3%), nasopharyngitis (6% vs 1%), and akathisia (4% vs 1%).

Conclusions and Relevance  Compared with placebo, the 3-month formulation of paliperidone palmitate administered 4 times yearly significantly delayed time to relapse in patients with schizophrenia. The 3-month formulation was generally tolerable and has a safety profile consistent with other marketed paliperidone formulations.

Trial Registration  clinicaltrials.gov Identifier:NCT01529515

 

Tracking Down the Causes of Alzheimer’s

University of Basel
http://www.biosciencetechnology.com/news/2015/09/tracking-down-causes-alzheimers?et_cid=4792750&et_rid=535648082&location=top

 

Researchers from the University of Basel were able to show that memory function (image shows the hippocampus highlighted) depends on calcium-regulating genes. (Source: MCN University of Basel

http://www.biosciencetechnology.com/sites/biosciencetechnology.com/files/bt1509_basel_brain.jpg

Genes are not only important for regular memory performance, but also for the development of Alzheimer’s disease. Researchers at the University of Basel now identified a specific group of genes that plays a central role in both processes. This group of molecules controls the concentration of calcium ions inside the cell. Their results appear in the current issue of the journal JAMA Psychiatry.

Intact memory capacity is crucial for everyday life. This fact becomes apparent once a memory disorder has developed. Alzheimer’s disease is the most common cause of age-associated memory disorders. Due to increasing life expectancy, the disease is on the rise in Switzerland and worldwide. Unfortunately, there is no effective treatment to cure or even slow down Alzheimer’s yet. Thus, understanding the origins of this neurodegenerative disorder is key to the development of much needed treatments.

Scientists have known for some years now, that genes do not only play a crucial role in normal memory performance, but also in the development of Alzheimer’s. However, it was so far unclear if specific genes are involved in both these processes.

Researchers at the transfaculty research platform at the Psychiatric University Clinics Basel and the Faculty of Psychology at the University of Basel were now able to show in a large scale study that a specific group of genes controls several processes that are central for regular brain functions as well as for the development of Alzheimer. First author Dr. Angela Heck collected and analyzed data of over 57,000 participants for this study.

Calcium is crucial

The study identified genes responsible for the concentration of calcium ions in the cell as central players of physiological and disease processes in the brain. Calcium genes stand in mutual relationship with memory performance of young and older healthy adults as well as with the function of the hippocampus, a brain region that is central to intact memory. Furthermore, calcium genes correlate with the risk for Alzheimer disease. The results contribute to the understanding of the complex processes that lead to memory disorders, such as Alzheimer’s.

 

 

 

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To understand what happens in the brain to cause mental illness

Larry H Bernstein, MD, FCAP, Curator

Leaders in Pharmaceutical Intelligence

Series E. 2; 5.10

https://bbrfoundation.org/research/basic-research

Fernando Sampaio Goes, M.D., a 2008 NARSAD Young Investigator at Johns Hopkins School of Medicine, and his colleagues took an alternative approach to the ongoing genome-wide association studies (GWAS) that hunt for these factors by scouring the complete genomes of tens of thousands of individuals. The team––which included 2005 Young InvestigatorDimitrios Avramopoulos, M.D., Ph.D.; 2000 Young Investigator, 2008 Independent Investigator, and BBRF Scientific Council member James B. Potash, M.D., M.P.H.; and 2004 Young Investigator Peter P. Zandi, Ph.D.––conceived the study to detect rare genetic variations that GWAS are not designed to find.

Rather than scanning entire genomes for depression-associated variations, Goes’s team narrowed its search to a set of genes in which they already suspected alterations might contribute to depression: those that encode proteins found at or near the junctions between neurons, where cell-to-cell communication takes place. Based on previous surveys of these synaptic proteins, the scientists chose 1,742 genes to include in their analysis.

They compared the protein-coding sequences of that set of genes in 259 people with major depression to the same set in 334 unaffected individuals. To increase the chance of finding relevant genetic factors, all the patients with depression were selected based on the criterion of early-onset, recurrent depression, which is suspected by some to be a more heritable form of the illness. (An important component of depression causation is environmental, and reflects the particular life circumstances of those affected, who may or may not be naturally resilient when faced with stress and other environmental factors.)

The team’s analysis pointed to two sets of genes in which variations were linked with major depression. One includes genes that control the growth of dendritic spines (tiny knob-like protrusions from a neuron’s surface that receive inputs from other neurons). Other research has suggested that the size, density, and shape of these structures may be involved in mood disorders and other mental illnesses. The second gene set includes genes linked with the entry of calcium into neurons, which regulates a variety of processes, including the release of message-propagating neurotransmitters. Variations within this gene set have also been linked to autism and epilepsy.

Researchers have identified unique characteristics of emotional processing in young people with post-traumatic stress disorder (PTSD), showing for the first time how that processing might be disrupted at different ages.

Publishing their findings online August 5th in Neuropsychopharmacology, were 2012 NARSAD Young Investigator grantee Ryan J. Herringa, M.D., Ph.D., of the University of Wisconsin School of Medicine and Public Health and Richard C. Wolf, a Ph.D. candidate at the university. Together they  looked at brain activity during an emotion-related task in children aged 8 to 18, both with and without PTSD. The children with PTSD had experienced trauma such as sexual abuse, the death of a loved one, a physical accident, or witnessing violence.

The children viewed emotionally “threatening” and “neutral” pictures. During this task, the researchers used imaging to measure activity in brain regions associated in PTSD with an increased fear response and sense of threat. These regions include the amygdala, important for processing emotions; the dorsal anterior cingulate cortex (dACC), which helps to gauge threat levels; and the medial portion of the prefrontal cortex (PFC), crucial for dialing back fear responses and putting perceived threats in context.

The researchers found higher threat-related dACC activity in youths with PTSD, as well as weaker connections between the amygdala and mPFC. The findings suggest these brain regions contribute to the difficulty young people with PTSD have in assessing perceptions of threat.  The study also found that amygdala-PFC connections followed a different developmental path for youths with PTSD. Whereas those connections were stronger at older ages in those without PTSD, the same connections grew weaker for children with PTSD as they aged. This may reflect a progressive weakening in the ability of the PFC to reduce fear.

In research reported June 17th in the journal Neuron, scientists have shown that a protein called CPEB3 is critical for the stabilization and storage of long-term memories in mice. Three-timeNARSAD Distinguished Investigator and BBRF Scientific Council member Eric Kandel, M.D., led the research. Also on the team is 2013 NARSAD Young Investigator Pierre Trifilieff, Ph.D.

CPEB3 is a “prion-like” protein. Prions––infectious, misshapen proteins best known for the devastation they cause––clump together and lead to brain damage in people and animals with mad cow disease and related conditions. Similar protein-clumping mechanisms may also contribute to neurodegenerative diseases including Alzheimer’sParkinson’s, and amyotrophic lateral sclerosis. (Curiously, certain proteins with prion-like properties have an important role in the healthy brain.)

The new finding extends previous work showing that prion-like proteins are vital for the stabilization of long-term term memory in sea slugs and fruit flies. Although further work is needed to understand whether the same mechanism is at work in humans, humans do produce a protein similar to the mouse protein CPEB3.

Memories are stored in the connections between neurons, and proteins play a role in the long-term storage of the information. But since proteins degrade over time, scientists had wondered how a memory can persist long after a new experience triggers neurons to make memory-specific proteins. Prion-like proteins, which are self-perpetuating because they can convert normal proteins to their own misshapen form, appear to be the answer.

Genetic studies have recently yielded large numbers of “hits” for genes that subtly increase or decrease risk for disorders, including for schizophrenia. However, there have been no hits for major depression, perhaps because the studies are not yet large enough or because depression is less heritable. Estimates put the heritability of major depression at around 50%, with the remaining contribution coming from environmental and experiential causes.

However, a new approach has paid off: a study published online July 15th at the journal Natureidentifies two genomic regions that harbor genes that increase risk of major depression. A multinational collaboration employed a strategy of narrowing the pool of subjects to women in China with the most severe and stubborn form of depression, with the hope that a more homogenous population would yield results.

In an accompanying News and Views, 2014 Lieber Prizewinner for Outstanding Achievement in Schizophrenia Research,Patrick Sullivan, M.D., of the University of North Carolina, writes, “This first identification of replicable, significant genome-wide associations for MDD is exceptional.”

Qi Xu, Ph.D., of Peking Union Medical College and Jun Wang, Ph.D., of BGI-Shenzhen, who led the China components of the study, along with Foundation Scientific Council Member Kenneth Kendler, M.D., of Virginia Commonwealth University and 2007 NARSAD Distinguished Investigator Grantee Jonathan Flint, M.D., of the University of Oxford in the United Kingdom focused exclusively on women with severe, recurrent depression (an average of more than five episodes), building a sample of 5,303 cases and 5,337 controls. The results were replicated in a separate group of 3,231 Chinese women with major depression and 3,186 mixed male/female controls.

“I think this paper is groundbreaking because it really demonstrates that we can make progress in reducing genetic heterogeneity by paying attention to key clinical indicators,” said three-time NARSAD Grantee, Francis McMahon, M.D., of the National Institute of Mental Health (NIMH), who was not an author on the paper.

A team based at the University of Edinburgh analyzed data from thousands of Scottish adults to see whether they had genetic mutations either linked with obesity or major depressive disorder. They tested for relationships between those genetic profiles, the presence of depression or other psychological distress, and body mass index, a measure used to determine obesity. A genetic predisposition for obesity more strongly predicted actual obesity among those adults who were also depressed.

The findings were reported June 30th in Translational Psychiatry by a team including 2008NARSAD Distinguished Investigator Grantee David J. Porteous, Ph.D., and 2010 Independent Investigator Andrew M. McIntosh, Ph.D.

The study results show people becoming obese in part because of their depression, rather than becoming depressed because they are already obese. The experience of depression may drive disordered eating habits. It may also trigger chemical responses in the body (such as the release of the stress hormone cortisol) that promote weight gain, the researchers hypothesize.

The team also found some degree of association between a genetic profile linked to obesity and current psychological distress, even among individuals who were not obese. Obesity-linked genes also more closely predicted actual obesity among people experiencing distress even if they were not diagnosed with depression. This indicates that psychological strain, and not just depression per se, contributes to obesity.

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Outstanding Achievement in Schizophrenia Research

Larry H. Bernstein, MD, FCAP, Curator

Leaders in Pharmaceutical Innovation

Series E. 2; 5.9

2014 Prizewinner:
David Braff, M.D.
 – University of California, San Diego School of Medicine – Watch Video

David Braff M.D. named Lieber Prize winner

David Braff MD, Distinguished Professor at UCSD’s Department of Psychiatry has been named this year’s Lieber Prize winner by the National Brain and Behavior Research Foundation (NBBRF) and the National Association for Research in Schizophrenia and Depression (NARSAD). This Prize is given to an outstanding neuropsychiatric researcher who has enhanced our fundamental understanding of schizophrenia, a devastating no fault heritable clinical brain disorder affecting 1% of the world’s population. Schizophrenia causes psychosis, cognitive dysfunction and profound disability in many patients. It also affects the families of the patients, since the disability-often strikes early in young adult life. Past Lieber Prize winners include two Nobel Laureates and many other world leading distinguished neuroscientists. The Award will be presented at a scientific meeting, ceremony and dinner in New York at the NBBRF-NARSAD Annual Gala at Lincoln Center in late October.

Dr. Braff has pursued and extended our understanding of schizophrenia via a number of major research projects. The Consortium on the Genomics of Schizophrenia (COGS) is a 30 million-dollar 10 year NIMH-funded consortium on the neurocognitive, neurophysiological, neural circuit and dysfunctional genomic architecture of schizophrenia. Dr Braff has been Principal Scientist and Director of this 7-site study: COGS 1 examined clinical features, neurocognitive and neurophysiological, and other familial endophenotypes or biomarkers in schizophrenia patients and their families as well as healthy control subjects. The follow up COGS 2 is studying 2500 schizophrenia patients and case-control subjects. Genomic and related methods include extensive behavioral, candidate gene, genome wide association, sequencing, methylation and stem cell projects from COGS and UCSD grants. This has led to an increased understanding of both the neural network and underlying genomic network bases of schizophrenia and has enhanced our understanding of risk and vulnerability markers which may provide targets for very early intervention and even, in the longer run, prevention. This neurodevelopmental psychotic process starts early in life but usually manifests itself in late teenagers and young adults. In addition, because of the underlying complex neural and genomic networks that have been identified by this work and the studies of other scientific projects, we have hope of finding novel therapeutic targets for pharmacological and sensory training- cognitive behavioral therapies for this devastating disorder.

Dr. Braff also has conducted longstanding translational (TRANS) and genomic studies over 30 years of continuously funded projects supported by NIMH, NARSAD and the Brain and Behavior Foundation. This research, conducted with many essential colleagues, including TRANS Co-PIs Mark Geyer, Ph.D. and Neal Swerdlow, M.D. Ph.D., has led to cross-species translational advances in understanding the neurobiology of schizophrenia and created powerful tools for screening candidate antipsychotic compounds to treat schizophrenia. Braff has also Directed the VA VISN 22 Mental Illness Research Center Clinical Neuroscience and Genomics Project, which provides crucial infrastructure and intellectual support for this work.

In recent years, Dr. Braff, a NARSAD Distinguished Investigator, has consistently been ranked by “ISI” in the top half of the top percent of all cited neuropsychiatric researchers based on the frequency with which his 300 publications are cited. He has also been awarded the Warren Award from the International Congress of Schizophrenia, the Inspiration Pioneer Research Award from NAMI, the Dean Award from the American College of Psychiatrists and the Marmor Award from the American Psychiatric Association, all given to honor an outstanding neuropsychiatric researcher. Dr. Braff’s colleagues at UCSD have included crucial contributions and context from TRANS Co-PIs, Mark Geyer Ph.D. and Neal Swerdlow MD Ph.D., Department Vice Chair (Also Deputy Director of COGS) as well as more recent faculty appointees Gregory Light, Ph.D (UCSD COGS Director and San Diego VA VISN 22 MIRECC Director) and Tiffany Greenwood, Ph.D. (Genetics And Statistical Genetics Lead Scientist) and many others.

Dr. Igor Grant, Chair of the Department commented, “Professor David Braff has been at the forefront of research into the neurobiology of schizophrenia. Beginning with observations on neurophysiologic biomarkers related to aberrant attentional and other cognitive mechanisms in those afflicted with schizophrenia, his work has progressed to linking such biomarkers to genetic underpinnings of this serious disorder, which affects 1% of our population, and causes great disruptions both for the person affected, and their families and loved ones. Professor Braff’s innovative work has opened better understanding of the interplay of genetic and neurodevelopmental factors in the evolution of schizophrenia, as well as promise of specific diagnostic markers that may help with early identification of people vulnerable to this disorder, at a time when preventive strategies may be most useful. As such his work will inform both improved treatment and prevention. Dr. Braff has also been a generative mentor to younger scientists, a fine educator, and helped the Department establish a modern inpatient psychiatric unit to care for people with severe mental disorders. The Department is very proud that Professor Braff was recognized with the Lieber Prize, reserved for the very finest psychiatrist scientists.”

https://youtu.be/c1_FtkMLJc4

“We are entering a new era of the neuropsychiatric and genomic revolutions, where advanced bioinformatics and other evolving technologies will help us to integrate brain, behavioral and genomic data about schizophrenia that we only imagined was possible in the past. Receiving this prize will serve to enhance all of our endeavors.”

 

Patrick F. Sullivan, M.D., Karolinska Institutet & University of North Carolina – Watch Video

Patrick F. Sullivan Awarded 2014 Lieber Prize for Outstanding Achievement in Schizophrenia Research

Patrick F. Sullivan, MD, FRANZCP, M. Hayworth & Family Distinguished Professor of Psychiatry and Professor of Genetics and Psychiatry at the University of North Carolina School of Medicine, is one of two researchers awarded the 2014 Lieber Prize for Outstanding Achievement in Schizophrenia Research.

The $50,000 cash award from the Brain & Behavior Research Foundation is given in recognition of a research scientist who has made distinguished contributions to the understanding of schizophrenia. It rewards past achievement and provides further incentive for an outstanding working scientist to continue to do exceptional research into the causes, prevention, and treatment of schizophrenia.

“The 2014 Outstanding Achievement Prize winners have dedicated their lives to solving some of the most intractable psychiatric problems in order to improve the lives of millions of people and their families,” said Jeffrey Borenstein, MD, CEO of the Brain & Behavior Research Foundation. “We applaud their past and future accomplishments.”

As a psychiatric geneticist, Dr. Sullivan works to decode the molecular and cellular consequences of genetic variations underlying schizophrenia. He heads large, multinational projects across a range of disorders, dividing his time between Sweden, where he is a Professor at the Karolinska Institutet, and UNC, where he is the Director of the Center for Psychiatric Genomics.

As founder and lead investigator of the Psychiatric Genomics Consortium (PGC), Dr. Sullivan directs 300 scientists from 70 institutions in 19 countries who are conducting mega-analyses, involving 90,000 participants, of genetic risk for schizophrenia, depression, autism, bipolar disorder and attention-deficit hyperactivity disorder. He is also the principal investigator for a Swedish genetic study of 10,000 patients with schizophrenia and bipolar disorder, one of the few projects looking into the impact of environmental factors in these disorders.

http://www.youtube.com/watch%3Fv%3DPzoEgKv5yKQ    Feb 5, 2015

A Stockholm Psychiatry Lecture held at Karolinska Institutet Feb 3 2015 by Prof. Patrick F Sullivan, UNC and KI.

http://www.dana.org/Briefing_Papers/Schizophrenia__Q_A_with_Patrick_F__Sullivan/Jul 14, 2015

Baby steps may become giant steps in the next ten years for schizophrenia, an illness which impacts an estimated 2.4 million Americans

 https://youtu.be/uJmA0gGTUnk 

“It is my deep hope that the work that led to my selection of this prize will continue so that we can greatly expand our knowledge of the genetic basis of schizophrenia so that these new findings will, in turn, lead to advances that improve the lives of people living with schizophrenia and other serious mental disorders.”

SIDNEY R. BAER, JR. PRIZE FOR INNOVATIVE AND PROMISING SCHIZOPHRENIA RESEARCH

Gregory Light, Ph.D.
University of California, San Diego

https://youtu.be/XqtcBkyz7vE

“This award strengthens my resolve to continue to develop treatment strategies that will ameliorate, prevent, and perhaps even cure schizophrenia and related psychotic illnesses in the next stages of my career.”

Stephan Ripke, M.D.
Broad Institute

https://youtu.be/nMfKsWFdM-k

“As a result of the immense collaborative efforts of the PGC, I believe that we are now on the path towards making seminal discoveries into the biology of this devastating disease. New therapeutic targets are imminent and the support of this prize will have a great impact on realizing this goal.”

 

Colvin Prize for Outstanding Achievement in Mood Disorders Research:

Wayne C. Drevets, M.D.
Janssen Pharmaceutica

https://youtu.be/xs7c3u3_pjk

“This prize not only affirms the significance of our past work, it also inspires and invigorates our current and future research, which we hope will improve the lives of people affected by bipolar disorder by leading to the discovery and development of new treatments.”

Fritz A. Henn, M.D., Ph.D.
Cold Spring Harbor Laboratory

https://youtu.be/-HVF-Lxpx14

“That my peers feel our work merits recognition is the greatest reward after a lifetime of work aimed at understanding and better treating major mental illness.”

2013 Marc G. Caron, Ph.D.
Video Clip
Duke University School of Medicine
2012 Michael J. Owen, M.D., Ph.D.
Video Clip
Cardiff University
2012 Michael O’Donovan, M.D., Ph.D.
Video Clip
Cardiff University
2011 Carol A. Tamminga, M.D.
Video Clip
UT Southwestern Medical Center at Dallas
2011 Joel E. Kleinman, M.D., Ph.D.
Video Clip
National Institute of Mental Health (NIMH)
2010 Ming T. Tsuang, M.D., Ph.D., D.Sc.
Video Clip

 

Goldman-Rakic Prize for Outstanding Achievement in Cognitive Neuroscience

2014 Prizewinner:

Richard L. Huganir, Ph.D. – The Johns Hopkins University School of Medicine – Watch Video

Department Affiliation: Primary: Neuroscience; Secondary: Biological Chemistry; Howard Hughes Medical Institute
Degree: Ph.D., Cornell University
Rank: Professor/Director, Department of Neuroscience

Regulation of Neurotransmitter Receptors and Brain Function in Heath and Disease

Neurotransmitter receptors mediate signal transduction at the postsynaptic membrane of synaptic connections between neurons in the nervous system. We have been studying the molecular mechanisms in the regulation of neurotransmitter receptor function. Recently we have focused on glutamate receptors, the major excitatory receptors in the brain. Glutamate receptors can be divided into two major classes: AMPA and NMDA receptors. AMPA receptors mediate rapid excitatory synaptic transmission while NMDA receptors play important roles in neuronal plasticity and development. Studies in our laboratory have found that both AMPA and NMDA receptors are multiply phosphorylated by a variety of protein kinases. Phosphorylation regulates several functional properties of these receptors including conductance and membrane targeting. Recent studies in our lab have demonstrated that the phosphorylation of AMPA receptors is regulated during cellular models of learning and memory such as long-term potentiation (LTP) and long-term depression (LTD). Moreover, phosphorylation of the AMPA receptor GluR1 subunit is required for the expression of these forms of plasticity and for the retention of spatial memory and also regulates emotional memory formation and erasure.

We have also been examining the mechanisms of the subcellular targeting and clustering of glutamate receptors at synapses. We have recently identified a variety of proteins that directly or indirectly interact with AMPA and NMDA receptors. We have found a novel family of proteins that we call GRIPs (Glutamate Receptor Interacting Proteins) that directly bind to the C-termini of the GluR2/3 subunits of AMPA receptors. GRIPs contain seven PDZ domains, protein-protein interaction motifs, which crosslink AMPA receptors to each other or link them to other proteins. In addition, we have found that the C-termini of GluR2 also interacts with the PDZ domain of PICK1, a protein kinase C-binding protein that is found at excitatory synapses. The GluR2 subunit also interacts with the NSF protein, a protein involved in the regulation of membrane fusion events. These AMPA receptor interacting proteins are critical in the proper membrane trafficking and synaptic targeting of these receptors. We have shown that the binding of PICK1 and GRIP is required for a specific form of LTD in the cerebellum that is a cellular model for motor learning. Moreover, we have found that this receptor complex is critical for hippocampal LTP and LTD and spatial learning.

In addition to these studies on AMPA receptors, we have been characterizing a separate NMDA receptor associated protein complex that is important in synaptic targeting and downstream signaling of NMDA receptors. We have identified an excitatory synapse specific rasGAP, which we call synGAP that regulates synaptic Ras signaling and has profound effects on synaptic plasticity.

Importantly, recent evidence has implicated glutamate receptor associated complexes in several neurological and psychiatric disorders including Alzheimer’s disease, schizophrenia, autism, mental retardation as well as in chronic pain and drug addiction.

In summary, we have examined the molecular mechanisms underlying the regulation of neurotransmitter receptor function. Our studies have suggested that regulation of receptor function may be a major mechanism for the regulation of synaptic plasticity in the nervous system in health and disease and may be an important determinant of animal behavior.

Representative Publications:

  • Volk, L.J., Bachman, J.L., Johnson, R., Yu, Y., Huganir, R.L. (2013) PKM-Z is not required for hippocampal synaptic plasticity, learning and memory. Nature 493(7432): 420-3. Pub Med Reference
  • Thomas, G.M., Hayashi, T., Chiu, S.L., Chen, C.M., Huganir, R.L. (2012) Palmitoylation by DHHC5/8 targets GRIP1 to dendritic endosomes to regulate AMPA-R trafficking. Neuron73(3):482-96. Pub Med Reference
  • Makuch, L., Volk, L., Anggono, V., Johnson, R.C., Yu, Y., Duning, K., Kremerskothen, J., Xia, J., Takamiya, K., Huganir, R.L. (2011) Regulation of AMPA receptor function by the human memory-associated gene KIBRA. Neuron 71(6):1022-9. Pub Med Reference
  • Makino, Y., Johnson, R.C., Yu, Y., Takamiya, K., Huganir, R.L. (2011) Enhanced synaptic plasticity in mice with phosphomimetic mutation of the GluA1 AMPA receptor. Proc Natl Acad Sci USA. 108(20):8450-5. Epub 2011 May 2. Pub Med Reference
  • Mejias, R., Adamczyk, A., Anggono, V., Niranjan, T., Thomas, G.M., Sharma, K., Skinner, C., Schwartz, C.E., Stevenson, R.E., Fallin, M.D., Kaufmann, W., Pletnikov, M., Valle, D.,Huganir, R.L., Wang, T.  (2011) Gain-of-function glutamate receptor interacting protein 1 variants alter GluA2 recycling and surface distribution in patients with autism. Proc Natl Acad Sci USA. 108(12):4920-5. Pub Med Reference 
  • Clem, R. and Huganir, R.L. (2010) Calcium-permeable AMPA receptor dynamics mediate fear memory erasure, Science 330(6007): 1108-12.  Pub Med Reference
  • Hayashi, T., Thomas, G., Huganir, R.L. (2009) Dual palmitoylation of NR2 subunits regulates NMDA receptor trafficking. Neuron 64(2): 213-226. Pub Med Reference
  • Lin, D.T., Makino, Y., Sharma, K., Hayashi, T., Neve, R., Takamiya, K., Huganir, R.L. (2009) Regulation of AMPA receptor GluR1 subunit extrasynaptic insertion events by 4.1N, phosphorylation and palmitoylation. Nat. Neurosci. 12(7): 879-87.� PMCID:� PMC2712131. Pub Med Reference
  • Sia, G.-M., Beique, J.-C., Rumbaugh, G., Cho, R., Worley, P.F., Huganir, R.L. (2007) Interaction of the N-terminal domain of the AMPA Receptor GluR4 subunit with the Neuronal Pentraxin NP1 mediates GluR4 synaptic recruitment. Neuron 55(1): 87-102. Pub Med Reference
  • Steinberg, J.P., Takamiya, K., Shen, Y., Xia, J., Rubio, M.E., Yu, S., Jin, W., Thomas, G.M., Linden, D.J., Huganir, R.L. (2006) Targeted In Vivo Mutations of the AMPA Receptor Subunit GluR2 and its Interacting Protein PICK1 Eliminate Cerebellar Long-Term Depression.Neuron. 49(6): 845-60. Pub Med Reference
  • Chung, H.J., Steinberg, J.P., Huganir, R.L. and Linden, D.J. Requirement of AMPA receptor GluR2 phosphorylation for cerebellar long-term depression. Science 300:1751-1755, 2003.Pub Med Reference
  • Lee, H-K., Takamiya, K., Han, J-S., Man, H., Kim, C.-H., Rumbaugh, G., Yu, S., Ding, L., He, C., Petralia, R.S., Wenthold, R.J., Gallagher, M., and Huganir, R.L. (2003) Phosphorylation of the AMPA receptor GluR1 subunit is required for synaptic plasticity and retention of spatial memory. Cell 112:631-643.  Pub Med Reference
  • Lee, H.K., Barbarosie, M., Kameyama, K., Bear, M.F., and Huganir, R.L. (2000) Regulation of distinct AMPA receptor phosphorylation sites during bidirectional synaptic plasticity. Nature405:955-959. Pub Med Reference
  • Ehlers, M.D., Zhang, S., Bernhardt, J.P., and Huganir R.L. (1996) Inactivation of NMDA receptors by direct interaction of calmodulin with NR1 subunit. Cell 84:745-755. Chung, H.J., Steinberg, J.P., Huganir, R.L. and Linden, D.J. Requirement of AMPA receptor GluR2 phosphorylation for cerebellar long-term depression. Science 300:1751-1755, 2003. Pub Med Reference

GOLDMAN-RAKIC PRIZE FOR OUTSTANDING ACHIEVEMENT IN COGNITIVE NEUROSCIENCE

https://youtu.be/4alesBVcM3s

“This has been my life long career goal—to understand how memory is encoded in the brain and how these mechanisms are disrupted in cognitive disorders. I am honored to be associated with Dr. Goldman- Rakic’s legacy.”

2013 Karl Deisseroth, M.D., Ph.D.
Video Clip
Stanford University
2012 Larry R. Squire, Ph.D.
Video Clip
University of California, San Diego
2011 Michael E. Goldberg, M.D.
Video Clip
Columbia University/NYSPI
2010 Robert Malenka, M.D., Ph.D.
Video Clip
Stanford University

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Addendum to LPBI’s Vision

Curators:

Stephen J Williams, PhD,

Adam Sonnenberg, BSc and

Aviva Lev-Ari, PhD, RN

 

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Our Team

Our Open Access Online Journal

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is a scientific, medical and business, multi-expert authoring environment for information syndication in several domains of Life Sciences, Medicine, Pharmaceutical and Healthcare Industries, BioMedicine, Medical Technologies & Devices. Scientific critical interpretations and original articles are written by PhDs, MDs, MD/PhDs, PharmDs, Technical MBAs as Experts, Authors, Writers (EAWs) on an Equity Sharing basis.

Journal Content Descriptors on 6/29/2015

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Slide2

For more information about our Team please see our site at https://pharmaceuticalintelligence.com/contributors-biographies/

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For more information of LPBI Deals and Partnerships please see our site at https://pharmaceuticalintelligence.com/joint-ventures/

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For more information about our BioMed E-Series please see our site at https://pharmaceuticalintelligence.com/biomed-e-books/

E-Book Titles by LPBI

LPBI book titles slide

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For more information on Real-Time Conference Coverage including a full list of Conferences Covered by LPBI please go to https://pharmaceuticalintelligence.com/press-coverage/

For more information on Real-Time Conference Coverage and a full listing of Conferences Covered by LPBI please go to:

https://pharmaceuticalintelligence.com/press-coverage/

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Leaders in Pharmaceutical Intelligence Presentation at The Life Sciences Collaborative

Curator: Stephen J. Williams, Ph.D. Website Analytics: Adam Sonnenberg, BSc Leaders in Pharmaceutical Intelligence presented their ongoing efforts to develop an open-access scientific and medical publishing and curation platform to The Life Science Collaborative, an executive pharmaceutical and biopharma networking group in the Philadelphia/New Jersey area.

Our Team

Slide1

For more information on the Vision, Funding Deals and Partnerships please see our site at https://pharmaceuticalintelligence.com/vision/

Slide2

For more information about our Team please see our site at https://pharmaceuticalintelligence.com/contributors-biographies/

Slide5

For more information of LPBI Deals and Partnerships please see our site at https://pharmaceuticalintelligence.com/joint-ventures/

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For more information about our BioMed E-Series please see our site at https://pharmaceuticalintelligence.com/biomed-e-books/

E-Book Titles by LPBI

LPBI book titles slide Slide8Slide3

Slide6

For more information on Real-Time Conference Coverage including a full list of Conferences Covered by LPBI please go to https://pharmaceuticalintelligence.com/press-coverage/

For more information on Real-Time Conference Coverage and a full listing of Conferences Covered by LPBI please go to:

https://pharmaceuticalintelligence.com/press-coverage/ Slide7

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The Pennsylvania (PA) and New Jersey (NJ) Biotech environment had been hit hard by the recession and loss of anchor big pharma companies however as highlighted by our interviews in “The Vibrant Philly Biotech Scene” and other news outlets, additional issues are preventing the PA/NJ area from achieving its full potential (discussions also with LSC)

Slide9Download the PowerPoint slides here: Presentationlsc

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