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Archive for the ‘Behavior’ Category

Socioeconomic factors involved in chronic illness

Posted in Behavior, Child and Adolescent Psychiatry, Cognition, Empathy, tagged , , , , , on November 25, 2015| Leave a Comment »

Socioeconomic factors involved in chronic illness

Larry H. Bernstein, MD, FCAP, Curator

LPBI

 

I have discussed a number of features of the health care system that are available to individuals and are becoming integrated over the last decade to a much greater extent than at the end of the last century.
Part of this has come because of an emergent view of health care markets and the patient base as a customer patient base.  Related to this view is the emergence over a quarter of a century of greater consolidation of heath care providers.  The first significant attempt to rationalize healthcare payments was with the development of diagnostic related groups by studies and proposals at Yale University School of Management under Robert Fetter. The first implementation was in New Jersey, prematurely supported by the Healthcare Financing Administration. As healthcare financing is usually predicated on HCFA, the insurance agencies, which includes negotiated for-profit entities follow suit.  However, it takes a large patient base to support any insurance provider, and with the not-for profit providers negotiating with large for-profit organizations, there is a tension and a balance that has to come with such a plan.  The existing system doesn’t support a fully nationalized system as exists elsewhere, and a two tiered system is almost inevitable.  In addition, our society, built by two centuries of immigration, and having a model system from the Kaiser Project in building the San Francisco bridge, that also influence IBM, employment-based insurance had a good start.  Government provision had to wait, with real success in the mid-twentieth century.

I have pointed out that the healthcare system has been in a remodeling process for the last quarter of a century aligned very much with business interests and the workforce. Even retirement insurance has been a worker innovation.  However, what is the underlying situation that arises from this arrangement.
The power of labor-unions has been eroded, which erodes an element of leverage.

At the beginning of the industrial revolution in England there was a seminal study that showed that the workers developed stress related illness that was not seen at the management level. In the US we have had streams of immigration and seemingly boundless innovation that has contributed to an impressive economic image of a country.  However, the story is also bimodal.  There is a strong cultural factor and family structure factor in both upward mobility and in resilience of the individual under stress.  This has been evident from observing the emergence of a former slavery descendent negro population and suppression of this people for a half century after the civil war, and more recently from migrations from Mexico, South America, and Cuba.  We have had a selective migration of educated people from India and Asia, being that they were of a more mobile class of achievers.  America, the home of the brave has been limited in representation.

What are the effects of this class disequilibrium?  As the country has growth and as companies have moved offshore for cheap labor, the power of labor declined, and the benefits of labor have been pushed down.  This resulted in a decline of the middle class, and levels of poverty and over the poverty line pushing families into considerable tension.  This is characterized by high divorce rates, and there are single mothers working two shifts, or both parents trying to balance the time available.

The problem here is like a compound fractured society.  The clustered neighborhoods are not just black, as a generation moved out and up, and property values dropped in once desirable neighborhoods.  The existence of a close community of common culture is workable as it is held together by common lineage. However, the fissures occur where the parents have no time for family, and the parents have no time to play with or read to their children.  This problem can be carried over from one generation to the next by failure in child development to gain basic living and society skills.  What we don’t happen to recognize is that as this multiplies, compounded by the highest level of incarceration in the Western world, there is uncontrolled violence, hatred, suicide, anger, and shortened lifespan.  This has a huge cost, and the cost weighs on the individuals affected and the communities they live in.  The cost includes the health burden.  Moreover, even though we have a large service sector with sports and exercise therapy, it may not be included in healthcare benefits, but is provided as add on to unreimbursed costs.

 

 

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An ambiguous course of psychosis

Posted in Behavior, Clinical & Translational, Curation, Empathy, Neuroscience, Patient Outlook, tagged on November 24, 2015| Leave a Comment »

An ambiguous course of psychosis

Larry H. Bernstein, MD, FCAP, Curator

LPBI

 

It is not always clear what the diagnosis is when a young person develops a psychosis, which is usually a clear break, but the features are not typical.  In the New York Times Opinion Page of Nov 17, 2015, Norman Ornstein describes the development of such in his son – How to help save the mentally ill from themselves.  He describes legislation in process to deal with the problem of when you institutionalize a potentially suicidal patient.  This was the situation that I described in the murder of Rabbi Adler on the podium by Richard Wishnetsky so many years ago.  In the case of Ornstein, his oldest son Mathhew died at 34 of carbon monoxide poisoning 10 years after his problem was discovered.

The son was a brilliant student, and he excelled in debating.  He was compassionate and empathetic.  This young man was a standup comedian and after graduating from Princeton wh went to Hollywood. The father describes his son’s condition as anosognosia, meaning lack of recognition of his illness.  I recall that a prominent cancer surgeon who was manic depressive psychotic and required lithium might have behaved that way when he failed to take his medication. He had a tragic surgical failure that ended his career when he was doing a rectal dissection and got into the posterior vascular bed and was in trouble, needing the assistance of the Chief of Urology.  The patient who died received over 100 units of blood. This very intelligent surgeon would throw the specimen he removed to the pathologist who entered the operating room in poor judgement.  I also recall a valued colleague of mine, a mathematical genius with MD and PhD tell me how the great surgeon and father of kidney transplantation could work tirelessly, but he died in a plane crash – himself as the pilot. I’m not in a position to disagree with Norman Ornstein’s conclusion that the son had a serious mood disorder, but the presentation he describes is similar to the two cases I mention.  In addition, I did not mention that my dear colleague was himself manic depressive, and he would work tirelessly, except when he was down and out.  He wrote an incredible program to diagnose heart attach from the serum enzymes for the IBM PC-XT in apl.  He sailed through difficult mathematics classes without taking notes.  He bacame interested in Shannon Information Theory when he heard a lecture by a microbiologist colleague who had done seminal work in classifying organisms by their biochemical features, which led to extending the use of feature extraction and combinatorial classes.

Ornstein points out that his son was over age 18, so that neither the family or professionals had any legal authority to make a decision about his hospitalization or related matters.  This is not quite like what I had seen with my brother.  But in my brother’s case, he was completely fractured, but he also was in no way belligerent.  In the case of Mathew Ornstein, he was never belligerent, but he was unkempt, kept himself poorly, and grew a beard.  He also becaame ultra religious.  The religiosity was also a feature of my own brother’s illness.  Matthew took a position that he could not take medication.  What is not clear is what medication he would have been on, which might be informative.

see more at – http://www.nytimes.com/2015/11/17/opinion/how-to-help-save-the-mentally-ill-from-themselves

 

 

 

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Philip Seymour Hoffman’s death

Posted in Behavior, Neurological Diseases, Neuroscience, Population Health Management, Stress Disorders on November 20, 2015| Leave a Comment »

Philip Seymour Hoffman’s death

Larry H. Bernstein, MD, FCAP, Curator

LPBI

 

 

 

Philip Seymour Hoffman, Actor of Depth, Dies at 46

By  FEB. 2, 2014 NEW York Times

Philip Seymour Hoffman, perhaps the most ambitious and widely admired American actor of his generation, who gave three­ dimensional nuance to a wide range of sidekicks, villains and leading men on screen and embraced some of the theater’s most burdensome roles on Broadway, died on Sunday at an apartment in Greenwich Village he was renting as an office. He was 46.

The death, from an apparent drug overdose, was confirmed by the police. Mr. Hoffman was found in the apartment by a friend who had become concerned after being unable to reach him. Investigators found a syringe in his arm and, nearby, an envelope containing what appeared to be heroin.

Mr. Hoffman was long known to struggle with addiction. In 2006, he said in an interview with “60 Minutes” that he had given up drugs and alcohol many years earlier, when he was 22. Last year he checked into a rehabilitation program for about 10 days after a reliance on prescription pills resulted in his briefly turning again to heroin.

“I saw him last week, and he was clean and sober, his old self,” said David Bar Katz, a playwright, and the friend who found Mr. Hoffman and called 911. “I really thought this chapter was over.

A stocky, often sleepy­looking man with blond, generally uncombed hair who favored the rumpled clothes more associated with an out­of­work actor than a star, Mr. Hoffman did not cut the traditional figure of a leading man, though he was more than capable of leading roles.

In his final appearance on Broadway, in 2012, he put his Everyman mien to work in portraying perhaps the American theater’s most celebrated protagonist — Willy Loman, Arthur Miller’s title character in “Death of a Salesman.” At 44, he was widely seen as young for the part — the casting, by the director Mike Nichols, was meant to emphasize the flashback scenes depicting a younger, pre­disillusionment Willy — and though the production drew mixed reviews, Mr. Hoffman was nominated for a Tony Award.

“Mr. Hoffman does terminal uncertainty better than practically anyone,” Ben Brantley wrote in The New York Times, “and he’s terrific in showing the doubt that crumples Willy just when he’s trying to sell his own brand of allAmerican optimism.”

In supporting roles, he was nominated three times for Academy Awards — as a priest under suspicion of sexual predation in “Doubt” (2008); as a C.I.A. agent especially eloquent in high dudgeon in “Charlie Wilson’s War” (2007); and as a charismatic cult leader in “The Master” (2012).

But he won in the best actor category for “Capote” (2005). As the eccentrically sociable, brilliantly probing and unflappably gay author of “In Cold Blood,” Mr. Hoffman flawlessly affected the real­life Truman Capote’s distinctly nasal, high­pitched voice and the naturally fey drama of his presence. Writing in The Times, A. O. Scott described the film as being about a writer’s relationship with his work.

“This makes for better drama than you might expect,” Mr. Scott wrote. “Capote’s human connections are, for the most part, secondary and instrumental, which makes Philip Seymour Hoffman’s performance all the more remarkable, since he must connect with the audience without piercing the membrane of his character’s narcissism.

“Not only does Mr. Hoffman achieve an impressive physical and vocal transformation — mimicking Capote’s chirpy drawl and appearing to shrink to his elfin stature — but he also conveys, with clarity and subtlety, the complexities of Capote’s temperament.”

Mr. Hoffman appeared in more than 50 films in a career that spanned less than 25 years; in the early 1990s he had small roles in “Leap of Faith,” which starred Steve Martin as a faith healer, and “Scent of a Woman,” in which he played a prep school classmate of Chris O’Donnell, the weekend escort of a blind former military officer on a New York City jaunt, played by Al Pacino, who won an Oscar for the role.

He appeared in big­budget Hollywood films — including “Mission: Impossible III” (2006), “Moneyball” (2011) and “The Hunger Games: Catching Fire” (2013) — and critically praised independent films, including “The Savages” (2007), in which he and Laura Linney, as his sister, struggle to care for their declining father; “Synecdoche, New York” (2008), Charlie Kaufman’s offbeat drama in which he played a moody theater director wrangling with his work and women; and “A Late Quartet,” about a violinist in the midst of dual crises, familial and musical.

But citing the highlights of Mr. Hoffman’s prolific work life — which included directing and acting in Off Broadway shows for the Labyrinth Theater Company, a New York City troupe, which he served for a time as artistic director — undervalues his versatility and his willingness, rare in a celebrity actor, to explore the depths of not just creepy or villainous characters, but especially unattractive ones. He was a chameleon of especially vivid colors in roles that called for him to be unappealing.

He played an obsequious sycophant in the Coen brothers’s cult comedy “The Big Lebowski” (1998); a former child star pathetically desperate to reclaim his celebrity in “Along Came Polly” (2004), a romantic comedy that starred Ben Stiller and Jennifer Aniston; a chronic masturbator in Todd Solondz’s portrait of suburban New Jersey, “Happiness” (1998); a snooty Princetonian in “The Talented Mr. Ripley” (1999); a weaselly tabloid reporter who gets his comeuppance (he’s glued to a wheelchair and set on fire) in “Red Dragon” (2002), an adaptation of one of Thomas Harris’s Hannibal Lecter novels; and in the role that brought him his first renown, he was Scotty J., a shy, overweight, gay boom operator on a pornographic film in “Boogie Nights” (1997).

In addition to “Death of a Salesman,” Mr. Hoffman appeared as the anguished and violent playwright, Konstantin, in Mr. Nichols’s production of “The Seagull” at the Delacorte Theater in Central Park in 2001, and on Broadway in two other long and difficult roles. In 2000, he and John C. Reilly were in “True West,” Sam Shepard’s harrowing comic drama about the reunion of two estranged brothers; each of the two roles is substantial, but in this production, directed by Matthew Warchus, the actors each played them both, switching roles in different performances.

And in 2003, he played James Tyrone, the doomed ­to ­alcoholism elder son of James and Mary Tyrone (Brian Dennehy and Vanessa Redgrave) in “Long Day’s Journey Into Night,” Eugene O’Neill’s portrait of an epic family demise.

“The theater was very difficult for him,” Robert Falls, the director of “Long Day’s Journey,” said in an interview Sunday. “It cost him; there was an emotional cost to the work, having to do it for eight performances a week, and having to rehearse. In ‘Long Day’s Journey,’ a role about an addict who would be dead in a number of years, who was filled with self­loathing, certainly Phil had access to those emotions. But I’m not talking about a method actor. He just brought every fiber of his being to the stage. He was there — with his depth of feeling, depth of humanity — and no other actor I’ve ever worked with ever brought it like that, not at that level.”

Mr. Hoffman was born on July 23, 1967, in Fairport, N.Y., a suburb of Rochester. His mother, the former Marilyn Loucks, is a former family court judge. His father, Gordon, worked for the Xerox Corporation. His parents, who divorced when Philip was young, survive him. In his acceptance speech at the Academy Awards in 2006, Mr. Hoffman thanked many people, but in particular his mother, now known as Marilyn O’Connor, who attended. He thanked her for raising him and his three siblings on her own and for taking him to see his first play.

“Be proud, Mom, ‘cause I’m proud of you, and we’re here tonight, and it’s so good,” he said with a smile.

Mr. Hoffman’s other survivors include a brother, Gordon, a screenwriter who wrote “Love Liza,” a 2002 film starring Mr. Hoffman as a man living through the aftermath of his wife’s suicide; and two sisters, Jill Hoffman DelVecchio and Emily Hoffman Barr; his longtime partner, Mimi O’Donnell, a costume designer who is the current artistic director of the Labyrinth Theater Company; and their three children, Cooper, Tallulah and Willa.

Mr. Hoffman became an actor in high school after a wrestling injury halted his athletic aspirations. He played Radar in a school production of “MASH,” a performance that was skilled enough that the school’s drama director decided to put on “Death of a Salesman”; in 1984, as a senior, he played Willy Loman. After graduating, he spent a summer at the Circle in the Square Theater School in Manhattan and later graduated from the New York University Tisch School of the Arts.

Mr. Hoffman’s other notable film roles included one of two brothers (Ethan Hawke was the other) who contrive to rob their parents’ jewelry store, a crime that goes grotesquely wrong, in Sidney Lumet’s 2007 thriller “Before the Devil Knows You’re Dead”; the renegade rock critic Lester Bangs in Cameron Crowe’s “Almost Famous” (2000); a rogue disc jockey in “Pirate Radio” (2009); and the campaign manager of a politician in “The Ides of March” (2011).

His principal works in progress were “The Hunger Games: Mockingjay Part 1” and “The Hunger Games: Mockingjay Part 2,” in which he plays the head game-­maker Plutarch Heavensbee. He had largely finished on the first film, but was scheduled for seven more shooting days on the second, according to a person who was briefed on the situation and spoke on condition of anonymity because of confidentiality strictures. The films, directed by Francis Lawrence, are set for release by Lionsgate, the first on Nov. 21 of this year, the second on Nov. 20, 2015. As a director, Mr. Hoffman worked with Stephen Adly Guirgis, a Labyrinth colleague, on several well­ received Off Broadway plays, including “In Arabia We’d All Be Kings,” “Jesus Hopped the A Train,” “Our Lady of 121st Street” and “The Little Flower of East Orange” — all tempestuous works about urban life — and a fantasy biblical discourse, “The Last Days of Judas Iscariot.”

Also for Labyrinth, he played the title role in Robert Glaudini’s “Jack Goes Boating,” about the tentative love life of a pot­smoking limousine driver; Mr. Hoffman reprised the role in a 2010 adaptation, a film he also directed. Labyrinth members were in a state of shock yesterday. “I had no indication at all,” the actor Felix Solis said in an interview. “He was our hero; he was our leader.”

On Sunday afternoon outside the building where Mr. Hoffman died, more than 100 people had gathered to mourn. The body was removed at about 6:40 p.m.; police officers formed a barricade to prevent people from taking pictures. “He’s a local — he’s a fixture in this neighborhood,” said Christian McCulloch, who said he lived nearby. “You see him with his kids in the coffee shops. He is so sweet. It’s desperately sad.”

Annie Correal, Emma G. Fitzsimmons, J. David Goodman, Patrick Healy, Dave Itzkoff and Michael Cieply contributed reporting. A version of this article appears in print on February 3, 2014, on page A1 of the New York edition with the headline: Actor of Depth, Fearless in His Choice of Roles.

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Robin Williams death

Posted in Behavior, Biological Networks, Cerebrovascular and Neurodegenerative Diseases, Clinical Diagnostics, Cognition, Curation, Empathy, Gene Regulation, Neurodegenerative Diseases, Neurological Diseases, Neuroscience, tagged , , , on November 20, 2015| Leave a Comment »

Robin Williams death

Larry H. Bernstein, MD, FCAP, Curator

LPBI

 

Lewy body: The ‘monster’ dementia blamed for Robin Williams’s death

Robin Williams , wife Susan Schneider and their daughter Zelda Williams at the premiere of "Happy Feet Two" in, November 2011.

Actor Robin Williams with wife Susan Schneider Williams in August 2009. Robin Williams had been planning to undergo neurological testing the week before he committed suicide last year, and likely only had three years to live his widow said earlier this month.  Robin Williams , wife Susan Schneider and their daughter Zelda Williams at the premiere of “Happy Feet Two” in, November 2011.

Robin Williams, then 63, had been seeking treatment for severe depression. But last week, his widow, Susan Schneider, revealed that her husband was suffering not only from Parkinson’s disease that had been diagnosed three months earlier, but also from Lewy body dementia (LBD), a progressively brutal illness that affects memory, movement and motor skills, and causes severe psychiatric symptoms.

Schneider says depression didn’t cause Williams’s death: “Lewy body dementia killed Robin. That’s what took his life.”

Strikingly, LBD – sometimes referred to as dementia with Lewy bodies or Parkinson’s with Lewy bodies, depending on symptoms – is the second-most common dementia after Alzheimer’s and affects more than 127,000 Britons. Yet most people have never heard of it.

Robin Williams who suffered from Lewy Body Dementia.

James Galvin, a neurology and psychiatry professor at Florida Atlantic University, says: “It’s the most common disease you’ve never heard of.”

“This disease is a sea monster with 50 tentacles of symptoms that show when they want,” Schneider said.

Williams suffered hallucinations, anxiety, depression, loss of motor control and problem-solving skills, sleep, balance and spatial awareness problems, and delusions.

Schneider describes one incident just weeks before Williams’s death, when she was in the shower and he was standing by the sink.

“Something didn’t seem right,” she recalls, so Schneider got out of the shower to find her husband’s head covered in blood. “He pointed to the door and I said, ‘Did you hit your head?’ and he nodded.” The incident confused her at the time. “But now, finding out all about Lewy body disease, lo and behold, their vision is affected, as is the ability to recognise and identify objects,” she says. “Now I get it.”

 

Lewy bodies are protein deposits in the brain, explains Professor David Burn, consultant neurologist and director of the biomedical research unit in LBD at the UK National Institute of Health Research (NIHR).

Discovered by Dr Frederic Lewy, a colleague of Dr Alzheimer’s, in 1912, the deposits develop inside nerve cells (neurons) in the brain, interrupting messaging and causing neurons to die. A patient’s symptoms will depend on which part of the brain is affected.

“When neurons die in the cortex, it causes dementia, but when it occurs in the brainstem, it causes motor symptoms (Parkinsonism),” says Burn.

“LBD patients face a rapid deterioration in their cognitive, physical and psychiatric function, and it tends to progress faster than other dementias,” he says.

When Paul Moynagh’s wife, Imogen, couldn’t find her way from a cafe table to the counter on a visit to a National Trust house in Devon in 2006, he thought little of it.Paul, 78, couldn’t have predicted the confusing set of symptoms that Imogen, 74, would experience. LBD is often misdiagnosed as Parkinson’s or Alzheimer’s, and it took doctors almost seven years to confirm her illness.

“Looking back, it began with little signs – loss of spatial awareness is an early symptom –  but they were so inconsistent,” recalls Paul, a retired surgeon.

First, there was a minor trembling in Imogen’s hands, then severe sleepiness during the day, along with spasms that made her right foot turn in when she walked. Then she developed depression and suffered panic attacks.

“Imogen has a pragmatic personality,” says Paul. “She used to play sports, was a keen gardener, walked everywhere and looked after our two children, Mark and Rachel. Ten years ago, if you had told her she would be afraid of being left alone, she would have laughed.”

By 2010, Imogen’s reasoning and planning skills were suffering – a key sign of LBD.

A keen bridge player, Imogen recalls: “I stopped winning, so I knew something was wrong.” (Though her speech is now slow, her sense of humour remains.)

 

Like Schneider, Paul Moynagh was also baffled by his wife’s repeated falls in the years preceding her diagnosis. “She’d had nine different broken bones, breaking her wrist twice, her ankle, and once, when she’d fallen down some stairs, her elbow.”

Imogen, like Williams and many LBD sufferers, was initially diagnosed with Parkinson’s disease.

 “She began shuffling when she walked and her voice became weak, both symptoms of Parkinson’s,” says Paul. Meanwhile, her depression was getting worse, not least because Imogen was so aware of what was happening to her.

“It’s different from Alzheimer’s in that people know exactly what’s happening, and one day can be completely lucid and the next be experiencing terrible anxiety and delusions. The more Imogen is aware of her situation, the more she gets depressed.”

When Paul Moynagh’s wife began experiencing hallucinations – a tell-tale sign of LBD – he knew that there was more to her illness than Parkinson’s. “She would see people in the windows of the conservatory and in our floor – which we made look like natural stone – she saw figures speaking to her.

“In my desperation, I would spend hours Googling Imogen’s symptoms until I stumbled on Lewy body dementia,” he says.

Brown says Robert had paranoia and hallucinations – he was frightened by faces he would see in the windows of a summer house he had built at the bottom of the garden. “One evening we were watching the Baftas on television and the camera panned, settling on various stars, and Bob turned to me and said: ‘I think Judi saw us.’ He meant Dame Judi Dench. He thought we were there and became very distressed because he wasn’t correctly dressed.”

“I’m a doctor and I had never even heard of it, and the neurologist was reluctant to accept it, but Imogen ticked all the boxes.” By 2013, a locum psychiatrist finally diagnosed Imogen with LBD. “I went along with my Google list, and she finally made the diagnosis. Two months later, the neurologist finally agreed.”

 

June Brown, who plays Dot Cotton in EastEnders, lost her husband, actor Robert Arnold, to LBD in 2003.

In a moving video made for the charity Lewy Body Society, Brown recalls: “Bob knew what was happening to him and he hated it. He once said: ‘I never thought I would go like this.'”

Unlike Alzheimer’s sufferers, LBD patients often have lucid memories. “Bob never lost his memory for people’s names. It’s the most strange disease because he would have moments of confusion and moments of clarity. It’s worse than Alzheimer’s because of this awareness of what you’re going through.”

 

Now, the only way to know that someone had Lewy body dementia is when a post-mortem examination finds Lewy bodies in the brain.

According to LBD specialist Ian McKeith, professor of old age psychiatry at the Newcastle University Institute for Ageing, LBD often gets misdiagnosed because doctors don’t know which questions to ask. He is in the middle of a study funded by the NIHR to develop a diagnostic toolkit for use in NHS practices.

Although there is no cure for LBD, doctors can treat symptoms using drugs that work on the brain’s messaging system, says McKeith. But correct diagnosis is essential. “If antipsychotic or anti-Parkinson’s drugs are given to patients with LBD, they can be fatal,” he says.

“We were living a nightmare,” Susan Schneider said of Robin Williams’s final months.

McKeith says one study found that when carers looking after someone with LBD were asked to rate their quality of life on a scale of zero to one (where zero was as bad as it could be), one in four rated it as below zero.

Still, Paul Moynagh refuses to refer to life with Imogen as a nightmare. She now needs 24-hour attention and help feeding. They recently celebrated their 50th wedding anniversary. During our interview, she turns to her husband and says slowly, with the difficulty she now has in getting words out: “Without your care, I don’t know where I would be.”

“Underneath it all, she is still the lovely person that I married,” he says.

“We still love each other as much as we did before – that hasn’t changed. If anything, I love her more.”

 

 

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Studying Alzheimer’s biomarkers in Down syndrome

Posted in Alzheimer's Disease, Behavior, Behavioral Genetics, Biomarkers & Medical Diagnostics, Cerebrovascular and Neurodegenerative Diseases, Child and Adolescent Psychiatry, Clinical & Translational, Clinical Diagnostics, Curation, Diagnostics and Lab Tests, Disease Biology, Etiology, Gene Regulation, Genome Biology, Genomic Testing: Methodology for Diagnosis, Human aging, Innovations in Neurophysiology & Neuropsychology, Neurodegenerative Diseases, Neurological Diseases, Nuclear Medicine, tagged , on November 18, 2015| Leave a Comment »

Studying Alzheimer’s biomarkers in Down syndrome

Larry H. Bernstein, MD, FCAP, Curator

LPBI

 

NIH supports new studies to find Alzheimer’s biomarkers in Down syndrome

Groundbreaking initiative will track dementia onset, progress in Down syndrome volunteers

http://www.nih.gov/news-events/news-releases/nih-supports-new-studies-find-alzheimers-biomarkers-down-syndrome

 

The National Institutes of Health has launched a new initiative to identify biomarkers and track the progression of Alzheimer’s in people with Down syndrome. Many people with Down syndrome have Alzheimer’s-related brain changes in their 30s that can lead to dementia in their 50s and 60s. Little is known about how the disease progresses in this vulnerable group. The NIH Biomarkers of Alzheimer’s Disease in Adults with Down Syndrome Initiative will support teams of researchers using brain imaging, as well as fluid and tissue biomarkers in research that may one day lead to effective interventions for all people with dementia.

The studies will be funded by the National Institute on Aging (NIA) and the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), both part of NIH. The institutes are jointly providing an estimated $37 million over five years to two highly collaborative projects, which enlist a number of leading researchers to the effort. To advance Alzheimer’s research worldwide, the teams will make their data and samples freely available to qualified researchers.

“This is the first large-scale Alzheimer’s biomarker endeavor to focus on this high-risk group,” said Laurie Ryan, Ph.D., chief of the Dementias of Aging Branch in NIA’s Division of Neuroscience, which leads NIH research on Alzheimer’s.  “Much like the long-established Alzheimer’s Disease Neuroimaging Initiative, the goal of this initiative is to develop biomarker measures that signal the onset and progression of Alzheimer’s in people with Down syndrome. Hopefully, one day, we will also use these biomarkers to determine the effectiveness of promising treatments.”

The link between Alzheimer’s and Down syndrome is well-known. People with Down syndrome are born with an extra copy of chromosome 21, which contains the amyloid precursor protein gene. This gene plays a role in the production of harmful amyloid plaque, sticky clumps that build up outside neurons in Alzheimer’s disease. Having three copies of this gene is a known risk factor for early-onset Alzheimer’s that can occur in people in their 30s, 40s and 50s. By middle age, most but not all adults with Down syndrome develop signs of Alzheimer’s, and a high percentage go on to develop symptoms of dementia as they age into their 70s.

The initiative establishes funding for two research teams that will pool data and standardize procedures, increase sample size, and collectively analyze data that will be made widely available to the research community. The teams will employ an array of biomarkers to identify and track Alzheimer’s-related changes in the brain and cognition for over 500 Down syndrome volunteers, aged 25 and older. The measures include:

  • Positron emission tomography (PET) scans that track levels of amyloid and glucose (energy used by brain cells); MRI of brain volume and function; and levels of amyloid and tau in cerebrospinal fluid and blood;
  • Blood tests to identify biomarkers in blood, including proteins, lipids and markers of inflammation;
  • Blood tests to collect DNA for genome-wide association studies that identify the genetic factors that may confer risk, or protect against, developing Alzheimer’s;
  • Evaluations of medical conditions and cognitive and memory tests to determine levels of function and monitor any changes;
  • For the first time in people with Down syndrome, PET brain scans that detect levels of tau, the twisted knots of protein within brain cells that are a hallmark Alzheimer’s disease.

Aside from earlier onset, Alzheimer’s in people with Down syndrome is similar to Alzheimer’s in others. The first symptom may be memory loss, although people with Down syndrome initially tend to show behavior changes and problems with walking.

“Over the past 30 years, the average lifespan of people with Down syndrome has doubled to 60 years—a  bittersweet achievement when faced with the possibility of developing Alzheimer’s,” said Melissa Parisi, M.D., Ph.D., chief of the NICHD Intellectual and Developmental Disabilities Branch, which leads NIH’s Down syndrome research. “There is much to learn about Alzheimer’s in Down syndrome, and we’re hopeful that these new projects will provide some answers. One mystery we hope to solve is whether or not the disease progresses at a faster rate in this group.”

Parisi noted that research into Alzheimer’s in Down syndrome is a key focus of the National Plan to Address Alzheimer’s Disease(link is external), which calls for improved care for specific populations that are unequally burdened by the disease, including people with Down syndrome, and for increased research that may lead to possible Alzheimer’s therapies.

Benjamin Handen, Ph.D., Department of Psychiatry, University of Pittsburgh, heads a team that involves investigators and data from: Banner Alzheimer’s Institute, Phoenix; Cambridge University, England; Alzheimer’s Disease Cooperative Study, San Diego; Laboratory of Neuro Imaging, University of Southern California, Los Angeles. Nicole Schupf, Ph.D., Columbia University Medical Center, New York City, leads a team involving investigators at: University of California, Irvine; Kennedy Krieger Institute/Johns Hopkins University, Baltimore; Massachusetts General Hospital/Harvard University, Boston; and the University of North Texas Health Sciences Center, Fort Worth.

Learn more about this topic at https://www.nia.nih.gov/alzheimers/publication/alzheimers-disease-people-down-syndrome.

About the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD): The NICHD sponsors research on development, before and after birth; maternal, child, and family health; reproductive biology and population issues; and medical rehabilitation. For more information, visit the Institute’s website at http://www.nichd.nih.gov.

About the National Institute on Aging: The NIA leads the federal government effort conducting and supporting research on aging and the health and well-being of older people. It provides information on age-related cognitive change and neurodegenerative disease specifically at its Alzheimer’s Disease Education and Referral (ADEAR) Center at www.nia.nih.gov/alzheimers.

About the National Institutes of Health (NIH): NIH, the nation’s medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.

 

 

NATIONAL PLAN TO ADDRESS ALZHEIMER’S DISEASE: 2015 UPDATE

pdf-document/national-plan-address-alzheimer%E2%80%99s-disease-2015-update (58 PDF pages)

Introduction

Vision Statement

National Alzheimer’s Project Act

Alzheimer’s Disease and Related Dementias

The Challenges

Framework and Guiding Principles

Goals as Building Blocks for Transformation

2015 Update

 

The Connection between Down Syndrome and Alzheimer’s Disease

Many, but not all, people with Down syndrome develop Alzheimer’s disease when they get older. Alzheimer’s is an irreversible, progressive brain disorder that slowly destroys memory and thinking skills and, eventually, the ability to carry out simple tasks.

Alzheimer’s disease is the most common cause of dementia among older adults. Dementia is the loss of cognitive functioning—thinking, remembering, and reasoning—and behavioral abilities to such an extent that it interferes with a person’s daily life and activities.

People with Down syndrome are born with an extra copy of chromosome 21, which carries the APP gene. This gene produces a specific protein called amyloid precursor protein (APP). Too much APP protein leads to a buildup of protein clumps called beta-amyloid plaques in the brain. By age 40, almost all people with Down syndrome have these plaques, along with other protein deposits, called tau tangles, which cause problems with how brain cells function and increase the risk of developing Alzheimer’s dementia.

However, not all people with these brain plaques will develop the symptoms of Alzheimer’s. Estimates suggest that 50 percent or more of people with Down syndrome will develop dementia due to Alzheimer’s disease as they age into their 70s.

Alzheimer’s Disease Symptoms

Many people with Down syndrome begin to show symptoms of Alzheimer’s disease in their 50s or 60s. But, like in all people with Alzheimer’s, changes in the brain that lead to these symptoms are thought to begin at least 10 years earlier. These brain changes include the buildup of plaques and tangles, the loss of connections between nerve cells, the death of nerve cells, and the shrinking of brain tissue (called atrophy).

The risk for Alzheimer’s disease increases with age, so it’s important to watch for certain changes in behavior, such as:

  • increased confusion
  • short-term memory problems (for example, asking the same questions over and over)
  • reduction in or loss of ability to do everyday activities

Other possible symptoms of Alzheimer’s dementia are:

  • seizures that begin in adulthood
  • problems with coordination and walking
  • reduced ability to pay attention
  • behavior and personality changes, such as wandering and being less social
  • decreased fine motor control
  • difficulty finding one’s way around familiar areas

Currently, Alzheimer’s disease has no cure, and no medications have been approved to treat Alzheimer’s in people with Down syndrome.

Down Syndrome and Alzheimer’s Disease Research

Alzheimer’s can last several years, and symptoms usually get worse over time.  Scientists are working hard to understand why some people with Down syndrome develop dementia while others do not. They want to know how Alzheimer’s disease begins and progresses, so they can develop drugs or other treatments that can stop, delay, or even prevent the disease process.

Research in this area includes:

  • Basic studies to improve our understanding of the genetic and biological causes of brain abnormalities that lead to Alzheimer’s
  • Observational research to measure cognitive changes in people over time
  • Studies of biomarkers (biological signs of disease), brain scans, and other tests that may help diagnose Alzheimer’s—even before symptoms appear—and show brain changes as people with Down syndrome age
  • Clinical trials to test treatments for dementia in adults with Down syndrome. Clinical trials are best the way to find out if a treatment is safe and effective in people.

 

Alzheimers Disease Neuroimaging Initiative (ADNI)

A public-private partnership, the purpose of ADNI is to develop a multisite, longitudinal, prospective, naturalistic study of normal cognitive aging, mild cognitive impairment (MCI), and early Alzheimer’s disease as a public domain research resource to facilitate the scientific evaluation of neuroimaging and other biomarkers for the onset and progression of MCI and Alzheimer’s disease.

Dr. Laurie Ryan of the NIA gives a brief overview of ADNI in this video:

https://youtu.be/0rBVe0Fwnik

Dr. Thomas Obisesan of Howard University, an ADNI study participant, and a study companion describe ADNI and what it’s like to be involved in the study

https://youtu.be/rK1yWvvHHl8

Learn more about this topic at https://www.nia.nih.gov/alzheimers/publication/alzheimers-disease-people-down-syndrome.

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Targeting Neuropathologies with GSK33 Inhibitor

Posted in Behavior, Biochemical pathways, Cancer and Current Therapeutics, Cell Biology, Signaling & Cell Circuits, Clinical & Translational, Curation, Disease Biology, Disease Biology, Small Molecules in Development of Therapeutic Drugs, FDA Regulatory Affairs, Innovations, Innovations in Neurophysiology & Neuropsychology, Metabolism, Neurodegenerative Diseases, Neuroscience, Patents, Pharmaceutical Analytics, Pharmaceutical Drug Discovery, Regulated Clinical Trials: Design, Methods, Components and IRB related issues, tagged , , on November 17, 2015| Leave a Comment »

Targeting Neuropathologies with GSK33 Inhibitor

Larry H. Bernstein, MD, FCAP,  Curator

LPBI

 

 

New 5-​Substituted-​N-​(piperidin-​4-​ylmethyl)​-​1H-​indazole-​3-​carboxamides: Potent Glycogen Synthase Kinase-​3 (GSK-​3) Inhibitors in Model of Mood Disorders

by DR ANTHONY MELVIN CRASTO Ph.D

str1

 

CAS 1452582-16-9, 428.47, C23 H26 F2 N4 O2

1H-​Indazole-​3-​carboxamide, 5-​(2,​3-​difluorophenyl)​-​N-​[[1-​(2-​methoxyethyl)​-​4-​piperidinyl]​methyl]​-

Aziende Chimiche Riunite Angelini Francesco A.C.R.A.F. S.P.A.

 

1 H-indazole-3-carboxamide compounds acting as glycogen synthase kinase 3 beta (GSK-33) inhibitors and to their use in the treatment of GSK-33-related disorders such as (i) insulin-resistance disorders; (ii) neurodegenerative diseases; (iii) mood disorders; (iv) schizophrenic disorders; (v) cancerous disorders; (vi) inflammation, (vii) substance abuse disorders; (viii) epilepsies; and (ix) neuropathic pain.

Protein kinases constitute a large family of structurally related enzymes, which transfer phosphate groups from high-energy donor molecules (such as adenosine triphosphate, ATP) to specific substrates, usually proteins. After phosphorylation, the substrate undergoes to a functional change, by which kinases can modulate various biological functions.

In general, protein kinases can be divided in several groups, according to the substrate that is phosphorylated. For example, serine/threonine kinase phosphorylates the hydroxyl group on the side chain of serine or threonine aminoacid.

Glycogen synthase kinases 3 (GSK-3) are constitutively active multifunctional enzymes, quite recently discovered, belonging to the serine/threonine kinases group.

Human GSK-3 are encoded by two different and independent genes, which leads to GSK-3a and GSK-33 proteins, with molecular weights of about 51 and 47 kDa, respectively. The two isoforms share nearly identical sequences in their kinase domains, while outside of the kinase domain, their sequences differ substantially (Benedetti et al., Neuroscience Letters, 2004, 368, 123-126). GSK-3a is a multifunctional protein serine kinase and GSK-33 is a serine-threonine kinase.

It has been found that GSK-33 is widely expressed in all tissues, with widespread expression in the adult brain, suggesting a fundamental role in neuronal signaling pathways (Grimes and Jope, Progress in Neurobiology, 2001, 65, 391-426). Interest in glycogen synthase kinases 3 arises from its role in various physiological pathways, such as, for example, metabolism, cell cycle, gene expression, embryonic development oncogenesis and neuroprotection (Geetha et al., British Journal Pharmacology, 2009, 156, 885-898).

GSK-33 was originally identified for its role in the regulation of glycogen synthase for the conversion of glucose to glycogen (Embi et al., Eur J Biochem, 1980, 107, 519-527). GSK-33 showed a high degree of specificity for glycogen synthase.

Type 2 diabetes was the first disease condition implicated with GSK- 3β, due to its negative regulation of several aspects of insulin signaling pathway. In this pathway 3-phosphoinositide-dependent protein kinase 1 (PDK-1 ) activates PKB, which in turn inactivates GSK-33. This inactivation of GSK-33 leads to the dephosphorylation and activation of glycogen synthase, which helps glycogen synthesis (Cohen et al., FEBS Lett, 1997, 410, 3-10). Moreover, selective inhibitors of GSK-33 are expected to enhances insulin signaling in prediabetic insulin- resistant rat skeletal muscle, thus making GSK-33 an attractive target for the treatment of skeletal muscle insulin resistance in the pre-diabetic state (Dokken et al., Am J. Physiol. Endocrinol. Metab., 2005, 288, E1 188-E1 194).

GSK-33 was also found to be a potential drug target in others pathological conditions due to insulin-resistance disorders, such as syndrome X, obesity and polycystic ovary syndrome (Ring DB et al., Diabetes, 2003, 52: 588-595).

It has been found that GSK-33 is involved in the abnormal phosphorylation of pathological tau in Alzheimer’s disease (Hanger et al., Neurosci. Lett, 1992, 147, 58-62; Mazanetz and Fischer, Nat Rev Drug Discov., 2007, 6, 464-479; Hong and Lee, J. Biol. Chem., 1997, 272, 19547- 19553). Moreover, it was proved that early activation of GSK-33, induced by apolipoprotein ApoE4 and β-amyloid, could lead to apoptosis and tau hyperphosphorylation (Cedazo-Minguez et al., Journal of Neurochemistry, 2003, 87, 1 152- 1 164). Among other aspect of Alzheimer’s disease, it was also reported the relevance of activation of GSK-33 at molecular level (Hernandez and Avila, FEBS Letters, 2008, 582, 3848-3854).

Moreover, it was demonstrated that GSK-33 is involved in the genesis and maintenance of neurodegenerative changes associated with Parkinson’s disease (Duka T. et al., The FASEB Journal, 2009; 23, 2820- 2830).

Accordingly to these experimental observations, inhibitors of GSK-33 may find applications in the treatment of the neuropathological consequences and the cognitive and attention deficits associated with tauopathies; Alzheimer’s disease; Parkinson’s disease; Huntington’s disease (the involvement of GSK-33 in such deficits and diseases is disclosed in Meijer L. et al., TRENDS Pharm Sci, 2004; 25, 471 -480); dementia, such as, but not limited to, vascular dementia, post-traumatic dementia, dementia caused by meningitis and the like; acute stroke; traumatic injuries; cerebrovascular accidents; brain and spinal cord trauma; peripheral neuropathies; retinopathies and glaucoma (the involvement of GSK-33 in such conditions is disclosed in WO 2010/109005).

The treatment of spinal neurodegenerative disorders, like amyotrophic lateral sclerosis, multiple sclerosis, spinal muscular atrophy and neurodegeneration due to spinal cord injury has been also suggested in several studies related to GSK-33 inhibition, such as, for example in Caldero J. et al., “Lithium prevents excitotoxic cell death of motoneurons in organotypic slice cultures of spinal cord”, Neuroscience. 2010 Feb 17;165(4):1353-69, Leger B. et al., “Atrogin-1 , MuRF1 , and FoXO, as well as phosphorylated GSK-3beta and 4E-BP1 are reduced in skeletal muscle of chronic spinal cord-injured patients”, Muscle Nerve, 2009 Jul; 40(1 ):69-78, and Galimberti D. et al., “GSK33 genetic variability in patients with Multiple Sclerosis”, Neurosci Lett. 201 1 Jun 1 5;497(1 ):46- 8. Furthermore, GSK-33 has been linked to the mood disorders, such as bipolar disorders, depression, and schizophrenia.

Inhibition of GSK-33 may be an important therapeutic target of mood stabilizers, and regulation of GSK-33 may be involved in the therapeutic effects of other drugs used in psychiatry. Dysregulated GSK-33 in mood disorder, bipolar disorder, depression and schizophrenia could have multiple effects that could impair neural plasticity, such as modulation of neuronal architecture, neurogenesis, gene expression and the ability of neurons to respond to stressful, potentially lethal conditions (Jope and Ron, Curr. Drug Targets, 2006, 7, 1421- 1434).

The role of GSK-33 in mood disorder was highlighted by the study of lithium and valproate (Chen et al., J. Neurochem., 1999, 72, 1327- 1330; Klein and Melton, Proc. Natl. Acad. Sci. USA, 1996, 93, 8455-8459), both of which are GSK-33 inhibitors and are used to treat mood disorders. There are also existing reports from the genetic perspective supporting the role of GSK-33 in the disease physiology of bipolar disorder (Gould, Expert. Opin. Ther. Targets, 2006, 10, 377-392).

It was reported a decrease in AKT1 protein levels and its phosphorylation of GSK-33 at Serine-9 in the peripheral lymphocytes and brains of individuals with schizophrenia. Accordingly, this finding supports the proposal that alterations in AKT1 -GSK-33 signaling contribute to schizophrenia pathogenesis (Emamian et al., Nat Genet, 2004, 36, 131- 137).

Additionally, the role of GSK-33 in cancer is a well-accepted phenomenon.

The potential of small molecules that inhibit GSK-33 has been evidenced for some specific cancer treatments (Jia Luo, Cancer Letters, 2009, 273, 194-200). GSK-33 expression and activation are associated with prostate cancer progression (Rinnab et al., Neoplasia, 2008, 10, 624-633) and the inhibition of GSK3b was also proposed as specific target for pancreatic cancer (Garcea et al., Current Cancer Drug Targets, 2007, 7, 209-215) and ovarian cancer (Qi Cao et al., Cell Research, 2006, 16 671 -677). Acute inhibition of GSK-33 in colon-rectal cancer cells activates p53-dependent apoptosis and antagonizes tumor growth (Ghosh et al., Clin Cancer Res 2005, 1 1 , 4580-4588).

The identification of a functional role for GSK-33 in MLL-associated leukaemia suggests that GSK-33 inhibition may be a promising therapy that is selective for transformed cells that are dependent on HOX overexpression (Birch et al., Cancer Cell, 2010, 1 7, 529-531 ).

GSK-33 is involved in numerous inflammatory signalling pathways, for example, among others GSK-33 inhibition has been shown to induce secretion of the anti-inflammatory cytokine IL-1 0. According to this finding, GSK-33 inhibitors could be useful to regulate suppression of inflammation (G. Klamer et al., Current Medicinal Chemistry, 2010, 17(26), 2873-2281, Wang et al., Cytokine, 2010, 53, 130-140).

GSK-33 inhibition has been also shown to attenuate cocaine-induced behaviors in mice. The administration of cocaine in mice pretreated with a GSK-33 inhibitor demonstrated that pharmacological inhibition of GSK3 reduced both the acute behavioral responses to cocaine and the long- term neuroadaptations produced by repeated cocaine (Cocaine-induced hyperactivity and sensitization are dependent on GSK3, Miller JS et al. Neuropharmacology. 2009 Jun; 56(8):1 1 16-23, Epub 2009 Mar 27).

The role of GSK-33 in the development of several forms of epilepsies has been demonstrated in several studies, which suggest that inhibition of GSK-33 could be a pathway for the treatment of epilepsy (Novel glycogen synthase kinase 3 and ubiquitination pathways in progressive myoclonus epilepsy, Lohi H et al., Hum Mol Genet. 2005 Sep 15;14(18):2727-36 and Hyperphosphorylation and aggregation of Tau in laforin-deficient mice, an animal model for Lafora disease, Purl R et al., J Biol Chem. 2009 Aug 21 ;284(34) 22657-63). The relationship between GSK-33 inhibition and treatment of neuropathic pain has been demonstrated in Mazzardo-Martins L. et al., “Glycogen synthase kinase 3-specific inhibitor AR-A014418 decreases neuropathic pain in mice: evidence for the mechanisms of action”, Neuroscience. 2012 Dec 13;226, and Xiaoping Gu et al., “The Role of Akt/GSK33 Signaling Pathway in Neuropathic Pain in Mice”, Poster A525, Anesthesiology 2012 October 13-17, 2012 Washington.

A review on GSK-33, its function, its therapeutic potential and its possible inhibitors is given in “GSK-33: role in therapeutic landscape and development of modulators” (S. Phukan et al., British Journal of Pharmacology (2010), 160, 1- 19).

WO 2004/014864 discloses 1 H-indazole-3-carboxamide compounds as selective cyclin-dependant kinases (CDK) inhibitors. Such compounds are assumed to be useful in the treatment of cancer, through a mechanism mediated by CDK2, and neurodegenerative diseases, in particular Alzheimer’s disease, through a mechanism mediated by CDK5, and as anti-viral and anti-fungine, through a mechanism mediated by CDK7, CDK8 and CDK9.

Cyclin-dependant kinases (CDKs) are serine/threonine kinases, first discovered for their role in regulating the cell cycle. CDKs are also involved in regulating transcription, mRNA processing, and the differentiation of nerve cells. Such kinases activate only after their interaction and binding with regulatory subunits, namely cyclins.

Moreover, 1 H-indazole-3-carboxamide compounds were also described as analgesics in the treatment of chronic and neuropathic pain (see, for example, WO 2004/074275 and WO 2004/101 548) and as 5-HT4 receptor antagonists, useful in the treatment of gastrointestinal disorders, central nervous system disorders and cardiovascular disorders (see, for example, WO 1994/101 74).

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Supportive Treatments: Hold the Mind Strong During Cancer

Posted in Behavior, CANCER BIOLOGY & Innovations in Cancer Therapy, Cell Biology, Signaling & Cell Circuits, Clinical & Translational, Clinical Diagnostics, Cognition, Neurological Diseases, Neuroscience, tagged , , on November 3, 2015| Leave a Comment »

Supportive Treatments: Hold the Mind Strong During Cancer

Demet Sag, PhD

 

Psychiatric treatments

Cancer is described under a general terminology of uncontrolled cell proliferation and changes that results in out of control development. Thus, correcting the cell division and immune control are the two focus areas. Yet, on the other side of the coin like any given terminal diseases there is another big factor that needs to be resolved that is mental health. This is usually not well discussed among many. After all fighting with a disease is a game of strength. I think that is one of the reason we say congrats to many cancer survivors since they won not only with their treatment but also with their psychological strength. However, it is like a balloon after the disease the battle is still on.

mind games

Here are the few articles discussing mainly advanced cancer patient’s psychiatric conditions, their clinical treatments, and training of the healthcare givers including oncologists, nurses, social workers, and other ancillary staff.

 

Last fifty years there is an improvement to cure mental illnesses yet there are many unresolved issues like passing blood brain barrier or specificity etc.  Many of these drugs also used for the adjuvant treatment of cancer-related symptoms. Some of these are pain, hot flashes, pruritus, nausea and vomiting, fatigue, and cognitive impairment.  However, the condition of cancer patient requires making psychopharmacology to improve quality life of cancer patients.

 

There new drugs with less side-effects and safer pharmacological profiles, has been a major advance in clinical psycho-oncology.

Since at least 25-30% of patients with cancer and an even higher percentage of patients in an advanced phase of illness meet the criteria for a psychiatric diagnosis, including depression, anxiety, stress-related syndromes, adjustment disorders, sleep disorders and delirium.

 

About 50% of patients with advanced cancer meet criteria for a psychiatric disorder, the most common being adjustment disorders (11%-35%) and major depression (5%-26%).

 

At least 30-40% of patients with cancer and even a higher percentage of patients in an advanced phase of illness.

 

 

In addition, age is a big issue since the outcomes and treatments changes based on expectations and challenges in their life. It is now possible to diagnose early and treat more means tolerance level to aggressive treatments also increases.  In older patients aging and cancer and in younger patient’s career and relationships broken. This is not just a longevity but improving the quality of life of a patient after cancer’s transition from likely death to survival.  Therefore, it is equally important to give their life back fully so there is an increased awareness on psychosocial issues and quality of life.

 

For example, there is a Psycho-oncology group in National Cancer Center. They are now conducting several clinical studies such as biological studies (neuro-imaging studies), studies to establish novel treatment strategy (n-3 poly unsaturated fatty acid), and multi-faceted intervention study (screening and individually tailored psychotherapy and pharmacotherapy). Hope to see more studies combining not only treat the physiological symptoms but psychological factors.

 

 

 

 

Table 1. Prevalence of Psychiatric Disorders in Advanced Cancer
  Advanced disease Terminal illness Caregivers
Adjustment disorder 14%–34.7% 10.6%–16.3% —
Anxiety disorders
 Generalized anxiety 3.2%–5.3% 5.80% 3.50%
 Panic disorder 4.20% 5.50% 8.00%
 Post-traumatic stress 2.40% 0% 4.00%
 Unspecified — 4.70% —
 Any 6%–8.2% 13.90% —

 

 

table 2 Psychiatric medication

 

 

References:

PMID: 26012508

Mehta RD1, Roth AJ2. Psychiatric considerations in the oncology setting. CA Cancer J Clin. 2015 Jul-Aug;65(4):300-14. doi: 10.3322/caac.21285. Epub 2015 May 26.

 

PMID:23949568

Caruso R1, Grassi L, Nanni MG, Riba M. Psychopharmacology in psycho-oncology. Curr Psychiatry Rep. 2013 Sep;15(9):393. doi: 10.1007/s11920-013-0393-0.

 

PMID: 24716500

Grassi L1, Caruso R, Hammelef K, Nanni MG, Riba M.  Efficacy and safety of pharmacotherapy in cancer-related psychiatric disorders across the trajectory of cancer care: a review.  Int Rev Psychiatry. 2014 Feb;26(1):44-62. doi: 10.3109/09540261.2013.842542.

 

PMID: 17847017

Miovic M1, Block S. Psychiatric disorders in advanced cancer. Cancer. 2007 Oct 15;110(8):1665-76.

 

PMID: 15387268

Akechi T1, Nakano T, Uchitomi Y. [Scientific background of psycho-oncology].  Seishin Shinkeigaku Zasshi. 2004;106(6):764-71. [Article in Japanese]

 

PMID: 25417593

Thekdi SM1, Trinidad A, Roth A. Psychopharmacology in cancer.

Curr Psychiatry Rep. 2015 Jan;17(1):529. doi: 10.1007/s11920-014-0529-x.

 

References for the table treatment:

Holland JC,Morrow GR,Schmale A, et al. A randomized clinical trial of alprazolam versus progressive muscle relaxation in cancer patients with anxiety and depressive symptoms. J Clin Oncol. 1991; 9: 1004–1011.

 

Razavi D,Kormoss N,Collard A,Farvacques C,Delvaux N. Comparative study of the efficacy and safety of trazodone versus clorazepate in the treatment of adjustment disorders in cancer patients: a pilot study. J Int Med Research. 1999; 27: 264–272.

 

Pugliese P,Perrone M,Nisi E, et al. An integrated psychological strategy for advanced colorectal cancer patients. Health Qual Life Outcomes. 2006; 4: 9.

 

Kornblith AB,Dowell JM,Herndon JE2nd, et al. Telephone monitoring of distress in patients aged 65 years or older with advanced stage cancer: a cancer and leukemia group B study. Cancer. 2006; 107: 2706–2714.

 

Goodwin PJ,Leszcz M,Ennis M, et al. The effect of group psychosocial support on survival in metastatic breast cancer. N Engl J Med. 2001; 345: 1719–1726. Web of Science® Times Cited: 249

 

Classen C,Butler LD,Koopman C, et al. Supportive-expressive group therapy and distress in patients with metastatic breast cancer: a randomized clinical intervention trial. Arch Gen Psychiatry. 2001; 58: 494–501. Web of Science® Times Cited: 156

 

Pirl WF,Siegel GI,Goode MJ,Smith MR. Depression in men receiving androgen deprivation therapy for prostate cancer: a pilot study. Psychooncology. 2002; 11: 518–523. Web of Science® Times Cited: 43

 

Chochinov HM,Wilson KG,Enns M, et al. Desire for death in the terminally ill. Am J Psychiatry. 1995; 152: 1185–1191.  Web of Science® Times Cited: 309

 

CA Cancer J Clin. 2015 Jul-Aug;65(4):300-14. doi: 10.3322/caac.21285. Epub 2015 May 26.

Hanna A,Sledge G,Mayer ML, et al. A phase II study of methylphenidate for the treatment of fatigue. Support Care Cancer. 2006;14: 210–215. Web of Science® Times Cited: 18

 

Dalton SO,Johansen C,Mellemkjaer L, et al. Antidepressant medications and risk for cancer. Epidemiology. 2000; 11: 171–176.PubMed,Web of Science® Times Cited: 31

 

Pitman RK,Lanes DM,Williston SK, et al. Psychophysiologic assessment of posttraumatic stress disorder in breast cancer patients.Psychosomatics. 2001; 42: 133–140.  Web of Science® Times Cited: 21

 

Derogatis LR,Morrow GR,Fetting J, et al. The prevalence of psychiatric disorders among cancer patients. JAMA. 1983; 249:751–757.PubMed, Web of Science® Times Cited: 837

 

Travado L,Grassi L,Gil F,Ventura C,Martins C;Southern European Psycho-Oncology Study Group. Physician-patient communication among Southern European cancer physicians: the influence of psychosocial orientation and burnout.Psychooncology. 2005; 14: 661–670.  Web of Science® Times Cited: 16

 

“CREATE Trial Providing Valuable Information on Epoetin Treatment for Anemia.” Hematology Week August 25, 2003: 10.

 

“Doubts Over Epoetin in Cancer.” SCRIP World Pharmaceutical News October 24, 2003: 24.

 

“Researcher Working on Medical Patch to Deliver Marijuanalike Drug.” Cancer Weekly September 9, 2003: 126.

 

 

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Advances in acoustics and in learning

Posted in Behavior, Biological Networks, Cell Biology, Signaling & Cell Circuits, Cerebrovascular and Neurodegenerative Diseases, Clinical & Translational, Curation, Human Sensation and Cellular Transduction: Physiology and Therapeutics, Innovations, Innovations in Neurophysiology & Neuropsychology, Neurodegenerative Diseases, Neurological Diseases, Neuroscience, tagged , , , , on October 31, 2015| Leave a Comment »

Advances in acoustics and in learning

Larry H. Brnstein, MD, FCAP, Curator

LPBI

 

Controlling acoustic properties with algorithms and computational methods

http://www.kurzweilai.net/controlling-acoustic-properties-with-algorithms-and-computational-methods

October 28, 2015

Computer scientists at Columbia Engineering, Harvard, and MIT have demonstrated that acoustic properties — both sound and vibration — can be controlled by 3D-printing specific shapes.

They designed an optimization algorithm and used computational methods and digital fabrication to alter the shape of 2D and 3D objects, creating what looks to be a simple children’s musical instrument — a xylophone with keys in the shape of zoo animals.

Practical uses

“Our discovery could lead to a wealth of possibilities that go well beyond musical instruments,” says Changxi Zheng, assistant professor of computer science at Columbia Engineering, who led the research team.

“Our algorithm could lead to ways to build less noisy computer fans and bridges that don’t amplify vibrations under stress, and advance the construction of micro-electro-mechanical resonators whose vibration modes are of great importance.”

Zheng, who works in the area of dynamic, physics-based computational sound for immersive environments, wanted to see if he could use computation and digital fabrication to actively control the acoustical property, or vibration, of an object.

Zheng’s team decided to focus on simplifying the slow, complicated, manual process of designing “idiophones” — musical instruments that produce sounds through vibrations in the instrument itself, not through strings or reeds.

The surface vibration and resulting sounds depend on the idiophone’s shape in a complex way, so designing the shapes to obtain desired sound characteristics is not straightforward, and their forms have so far been limited to well-understood designs such as bars that are tuned by careful drilling of dimples on the underside of the instrument.

Optimizing sound properties

To demonstrate their new technique, the team settled on building a “zoolophone,” a metallophone with playful animal shapes (a metallophone is an idiophone made of tuned metal bars that can be struck to make sound, such as a glockenspiel).

 

What happens in the brain when we learn

http://www.kurzweilai.net/what-happens-in-the-brain-when-we-learn

Findings could enhance teaching methods and lead to treatments for cognitive problems
October 28, 2015

A Johns Hopkins University-led research team has proven a working theory that explains what happens in the brain when we learn, as described in the current issue of the journal Neuron.

More than a century ago, Pavlov figured out that dogs fed after hearing a bell eventually began to salivate when they heard the bell ring. The team looked into the question of how Pavlov’s dogs (in “classical conditioning”) managed to associate an action with a delayed reward to create knowledge. For decades, scientists had a working theory of how it happened, but the team is now the first to prove it.

“If you’re trying to train a dog to sit, the initial neural stimuli, the command, is gone almost instantly — it lasts as long as the word sit,” said neuroscientist Alfredo Kirkwood, a professor with the university’s Zanvyl Krieger Mind/Brain Institute. “Before the reward comes, the dog’s brain has already turned to other things. The mystery was, ‘How does the brain link an action that’s over in a fraction of a second with a reward that doesn’t come until much later?’ ”

Eligibility traces

The working theory — which Kirkwood’s team has now validated experimentally — is that invisible “synaptic eligibility traces” effectively tag the synapses activated by the stimuli so that the learning can be cemented with the arrival of a reward. The reward is a neuromodulator* (neurochemical) that floods the dog’s brain with “good feelings.” Though the brain has long since processed the “sit” command, eligibility traces in the synapse respond to the neuromodulators, prompting a lasting synaptic change, a.k.a. “learning.”

The team was able to prove the eligibility-traces theory by isolating cells in the visual cortex of a mouse. When they stimulated the axon of one cell with an electrical impulse, they sparked a response in another cell. By doing this repeatedly, they mimicked the synaptic response between two cells as they process a stimulus and create an eligibility trace.

When the researchers later flooded the cells with neuromodulators, simulating the arrival of a delayed reward, the response between the cells strengthened (“long-term potentiation”) or weakened (“long-term depression”), showing that the cells had “learned” and were able to do so because of the eligibility trace.

“This is the basis of how we learn things through reward,” Kirkwood said, “a fundamental aspect of learning.”

In addition to a greater understanding of the mechanics of learning, these findings could enhance teaching methods and lead to treatments for cognitive problems, the researchers suggest.

Scientists at the University of Texas at Houston and the University of California, Davis were also involved in the research, which was supported by grants from JHU’s Science of Learning Institute and National Institutes of Health.

* The neuromodulators tested were norepinephrine, serotonin, dopamine, and acetylcholine, all of which have been implicated in cortical plasticity (ability to grow and form new connections to other neurons).

Abstract of Distinct Eligibility Traces for LTP and LTD in Cortical Synapses

In reward-based learning, synaptic modifications depend on a brief stimulus and a temporally delayed reward, which poses the question of how synaptic activity patterns associate with a delayed reward. A theoretical solution to this so-called distal reward problem has been the notion of activity-generated “synaptic eligibility traces,” silent and transient synaptic tags that can be converted into long-term changes in synaptic strength by reward-linked neuromodulators. Here we report the first experimental demonstration of eligibility traces in cortical synapses. We demonstrate the Hebbian induction of distinct traces for LTP and LTD and their subsequent timing-dependent transformation into lasting changes by specific monoaminergic receptors anchored to postsynaptic proteins. Notably, the temporal properties of these transient traces allow stable learning in a recurrent neural network that accurately predicts the timing of the reward, further validating the induction and transformation of eligibility traces for LTP and LTD as a plausible synaptic substrate for reward-based learning.

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Holographic sonic tractor beam lifts and moves objects using soundwaves

Another science-fiction idea realized
October 27, 2015

British researchers have built a working Star-Trek-style “tractor beam” — a device that can attract or repel one object to another from a distance. It uses high-amplitude soundwaves to generate an acoustic hologram that can grasp and move small objects.

The technique, published in an open-access paper in Nature Communications October 27, has a wide range of potential applications, the researchers say. A sonic production line could transport delicate objects and assemble them, all without physical contact. Or a miniature version could grip and transport drug capsules or microsurgical instruments through living tissue.

The device was developed at the Universities of Sussex and Bristol in collaboration with Ultrahaptics.

https://youtu.be/wDzhlW-rKvM
University of Sussex | Levitation using sound waves

The researchers used an array of 64 miniature loudspeakers. The whole system consumes just 9 Watts of power, used to create high-pitched (40Khz), high-intensity sound waves to levitate a spherical bead 4mm in diameter made of expanded polystyrene.

The tractor beam works by surrounding the object with high-intensity sound to create a force field that keeps the objects in place. By carefully controlling the output of the loudspeakers, the object can be held in place, moved, or rotated.

Three different shapes of acoustic force fields work as tractor beams: an acoustic force field that resembles a pair of fingers or tweezers; an acoustic vortex, the objects becoming trapped at the core; and a high-intensity “cage” that surrounds the objects and holds them in place from all directions.

Previous attempts surrounded the object with loudspeakers, which limits the extent of movement and restricts many applications. Last year, the University of Dundee presented the concept of a tractor beam, but no objects were held in the ray.

The team is now designing different variations of this system. A bigger version aims at levitating a soccer ball from 10 meters away and a smaller version aims at manipulating particles inside the human body.

https://youtu.be/g_EM1y4MKSc
Asier Marzo, Matt Sutton, Bruce Drinkwater and Sriram Subramanian | Acoustic holograms are projected from a flat surface and contrary to traditional holograms, they exert considerable forces on the objects contained within. The acoustic holograms can be updated in real time to translate, rotate and combine levitated particles enabling unprecedented contactless manipulators such as tractor beams.

Abstract of Holographic acoustic elements for manipulation of levitated objects

Sound can levitate objects of different sizes and materials through air, water and tissue. This allows us to manipulate cells, liquids, compounds or living things without touching or contaminating them. However, acoustic levitation has required the targets to be enclosed with acoustic elements or had limited maneuverability. Here we optimize the phases used to drive an ultrasonic phased array and show that acoustic levitation can be employed to translate, rotate and manipulate particles using even a single-sided emitter. Furthermore, we introduce the holographic acoustic elements framework that permits the rapid generation of traps and provides a bridge between optical and acoustical trapping. Acoustic structures shaped as tweezers, twisters or bottles emerge as the optimum mechanisms for tractor beams or containerless transportation. Single-beam levitation could manipulate particles inside our body for applications in targeted drug delivery or acoustically controlled micro-machines that do not interfere with magnetic resonance imaging.

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A drug-delivery technique to bypass the blood-brain barrier

http://www.kurzweilai.net/a-drug-delivery-technique-to-bypass-the-blood-brain-barrier

Could benefit a large population of patients with neurodegenerative disorders
October 26, 2015

Researchers at Massachusetts Eye and Ear/Harvard Medical School and Boston University have developed a new technique to deliver drugs across the blood-brain barrier and have successfully tested it in a Parkinson’s mouse model (a line of mice that has been genetically modified to express the symptoms and pathological features of Parkinson’s to various extents).

Their findings, published in the journal Neurosurgery, lend hope to patients with neurological conditions that are difficult to treat due to a barrier mechanism that prevents approximately 98 percent of drugs from reaching the brain and central nervous system.

“Although we are currently looking at neurodegenerative disease, there is potential for the technology to be expanded to psychiatric diseases, chronic pain, seizure disorders, and many other conditions affecting the brain and nervous system down the road,” said senior author Benjamin S. Bleier, M.D., of the department of otolaryngology at Mass. Eye and Ear/Harvard Medical School.

The nasal mucosal grafting solution

Researchers delivered glial derived neurotrophic factor (GDNF), a therapeutic protein in testing for treating Parkinson’s disease, to the brains of mice. They showed that their delivery method was equivalent to direct injection of GDNF, which has been shown to delay and even reverse disease progression of Parkinson’s disease in pre-clinical models.

Once they have finished the treatment, they use adjacent nasal lining to rebuild the hole in a permanent and safe way. Nasal mucosal grafting is a technique regularly used in the ENT (ear, nose, and throat) field to reconstruct the barrier around the brain after surgery to the skull base. ENT surgeons commonly use endoscopic approaches to remove brain tumors through the nose by making a window through the blood-brain barrier to access the brain.

The safety and efficacy of these methods have been well established through long-term clinical outcomes studies in the field, with the nasal lining protecting the brain from infection just as the blood brain barrier has done.

By functionally replacing a section of the blood-brain barrier with nasal mucosa, which is more than 1,000 times more permeable than the native barrier, surgeons could create a “screen door” to allow for drug delivery to the brain and central nervous system.

The technique has the potential to benefit a large population of patients with neurodegenerative disorders, where there is still a specific unmet need for blood-brain-penetrating therapeutic delivery strategies.

The study was funded by The Michael J. Fox Foundation for Parkinson’s Research (MJFF).

Abstract of Heterotopic Mucosal Grafting Enables the Delivery of Therapeutic Neuropeptides Across the Blood Brain Barrier

BACKGROUND: The blood-brain barrier represents a fundamental limitation in treating neurological disease because it prevents all neuropeptides from reaching the central nervous system (CNS). Currently, there is no efficient method to permanently bypass the blood-brain barrier.

OBJECTIVE: To test the feasibility of using nasal mucosal graft reconstruction of arachnoid defects to deliver glial-derived neurotrophic factor (GDNF) for the treatment of Parkinson disease in a mouse model.

METHODS: The Institutional Animal Care and Use Committee approved this study in an established murine 6-hydroxydopamine Parkinson disease model. A parietal craniotomy and arachnoid defect was repaired with a heterotopic donor mucosal graft. The therapeutic efficacy of GDNF (2 [mu]g/mL) delivered through the mucosal graft was compared with direct intrastriatal GDNF injection (2 [mu]g/mL) and saline control through the use of 2 behavioral assays (rotarod and apomorphine rotation). An immunohistological analysis was further used to compare the relative preservation of substantia nigra cell bodies between treatment groups.

RESULTS: Transmucosal GDNF was equivalent to direct intrastriatal injection at preserving motor function at week 7 in both the rotarod and apomorphine rotation behavioral assays. Similarly, both transmucosal and intrastriatal GDNF demonstrated an equivalent ratio of preserved substantia nigra cell bodies (0.79 +/- 0.14 and 0.78 +/- 0.09, respectively, P = NS) compared with the contralateral control side, and both were significantly greater than saline control (0.53 +/- 0.21; P = .01 and P = .03, respectively).

CONCLUSION: Transmucosal delivery of GDNF is equivalent to direct intrastriatal injection at ameliorating the behavioral and immunohistological features of Parkinson disease in a murine model. Mucosal grafting of arachnoid defects is a technique commonly used for endoscopic skull base reconstruction and may represent a novel method to permanently bypass the blood-brain barrier.

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Creating an artificial sense of touch by electrical stimulation of the brain

http://www.kurzweilai.net/creating-an-artificial-sense-of-touch-by-electrical-stimulation-of-the-brain

DARPA-funded study may lead to building prosthetic limbs for humans using a direct brain-electrode interface to recreate the sense of touch
October 26, 2015

Neuroscientists in a project headed by the University of Chicago have determined some of the specific characteristics of electrical stimuli that should be applied to the brain to produce different sensations in an artificial upper limb intended to restore natural motor control and sensation in amputees.

The research is part of Revolutionizing Prosthetics, a multi-year Defense Advanced Research Projects Agency (DARPA).

For this study, the researchers used monkeys, whose sensory systems closely resemble those of humans. They implanted electrodes into the primary somatosensory cortex, the area of the brain that processes touch information from the hand. The animals were trained to perform two perceptual tasks: one in which they detected the presence of an electrical stimulus, and a second task in which they indicated which of two successive stimuli was more intense.

The sense of touch is made up of a complex and nuanced set of sensations, from contact and pressure to texture, vibration and movement. The goal of the research is to document the range, composition and specific increments of signals that create sensations that feel different from each other.

To achieve that, the researchers manipulated various features of the electrical pulse train, such as its amplitude, frequency, and duration, and noted how the interaction of each of these factors affected the animals’ ability to detect the signal.

Of specific interest were the “just-noticeable differences” (JND),” — the incremental changes needed to produce a sensation that felt different. For instance, at a certain frequency, the signal may be detectable first at a strength of 20 microamps of electricity. If the signal has to be increased to 50 microamps to notice a difference, the JND in that case is 30 microamps.*

“When you grasp an object, for example, you can hold it with different grades of pressure. To recreate a realistic sense of touch, you need to know how many grades of pressure you can convey through electrical stimulation,” said Sliman Bensmaia, PhD, Associate Professor in the Department of Organismal Biology and Anatomy at the University of Chicago and senior author of the study, which was published today (Oct. 26) in the Proceedings of the National Academy of Sciences. “Ideally, you can have the same dynamic range for artificial touch as you do for natural touch.”

“This study gets us to the point where we can actually create real algorithms that work. It gives us the parameters as to what we can achieve with artificial touch, and brings us one step closer to having human-ready algorithms.”

Researchers from the University of Pittsburgh and Johns Hopkins University were also involved in the DARPA-supported study.

* The study also has important scientific implications beyond neuroprosthetics. In natural perception, a principle known as Weber’s Law states that the just-noticeable difference between two stimuli is proportional to the size of the stimulus. For example, with a 100-watt light bulb, you might be able to detect a difference in brightness by increasing its power to 110 watts. The JND in that case is 10 watts. According to Weber’s Law, if you double the power of the light bulb to 200 watts, the JND would also be doubled to 20 watts.

However, Bensmaia’s research shows that with electrical stimulation of the brain, Weber’s Law does not apply — the JND remains nearly constant, no matter the size of the stimulus. This means that the brain responds to electrical stimulation in a much more repeatable, consistent way than through natural stimulation.

“It shows that there is something fundamentally different about the way the brain responds to electrical stimulation than it does to natural stimulation,” Bensmaia said.

Abstract of Behavioral assessment of sensitivity to intracortical microstimulation of primate somatosensory cortex

Intracortical microstimulation (ICMS) is a powerful tool to investigate the functional role of neural circuits and may provide a means to restore sensation for patients for whom peripheral stimulation is not an option. In a series of psychophysical experiments with nonhuman primates, we investigate how stimulation parameters affect behavioral sensitivity to ICMS. Specifically, we deliver ICMS to primary somatosensory cortex through chronically implanted electrode arrays across a wide range of stimulation regimes. First, we investigate how the detectability of ICMS depends on stimulation parameters, including pulse width, frequency, amplitude, and pulse train duration. Then, we characterize the degree to which ICMS pulse trains that differ in amplitude lead to discriminable percepts across the range of perceptible and safe amplitudes. We also investigate how discriminability of pulse amplitude is modulated by other stimulation parameters—namely, frequency and duration. Perceptual judgments obtained across these various conditions will inform the design of stimulation regimes for neuroscience and neuroengineering applications.

references:

  • Sungshin Kim, Thierri Callier, Gregg A. Tabot, Robert A. Gaunt, Francesco V. Tenore, and Sliman J. Bensmaia. Behavioral assessment of sensitivity to intracortical microstimulation of primate somatosensory cortex. PNAS 2015; doi:10.1073/pnas.1509265112

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This Algorithm Is Better At Predicting Human Behavior Than Humans Are

Posted in Artificial Intelligence - Breakthroughs in Theories and Technologies, Artificial Intelligence - General, Behavior on October 27, 2015| Leave a Comment »

This Algorithm Is Better At Predicting Human Behavior Than Humans Are

 

Reporter: Aviva Lev-Ari, PhD, RN

 

You’re so predictable.

Sourced through Scoop.it from: www.fastcodesign.com

See on Scoop.it – Cardiovascular and vascular imaging

This Algorithm Is Better At Predicting Human Behavior Than Humans Are

BY MEG MILLER 1 MINUTE READ

Analyzing big data sets in order to forecast trends or predict customer behavior usually relies on both computers and humans. Computer algorithms are advanced enough to rapidly comb through numbers and find useful patterns, and humans are still necessary for setting the parameters and analyzing the results. But an algorithm created by two MIT researchers suggest we could take out the human factor all together.

Conceived by Max Kanter, a MIT graduate student in computer science, and his advisor, Kalyan Veeramachaneni, the Data Science Machine can approximate human “intuition” when it comes to data analysis. Using raw datasets to make models that predict things like when a student is most at risk of dropping a course, or whether a retail customer will turn into a repeat buyer, its creators claim it can do it faster and with more accuracy than its human counterparts.

To test the system prototype, the researchers pitted the Data Science Machine against human teams at three data science competitions. While the algorithm didn’t get the top score in any of the competitions, it did beat out a whopping 615 of the 906 human teams competing. In two of the competitions, it created models that were 94% and 96% as accurate as the winning teams. Whereas the teams of humans required months to build their prediction algorithms, the Data Science Machine did it in 2 to 12 hours.

The researchers don’t view the algorithm as a replacement for human intelligence, but do recognize that it could prove useful for helping analyze the huge amount of data with less manpower. It could also be an important tool for user-centered design–if a machine can comb through massive amounts of data with much less manpower and in record time, it could also help companies better understand their customer base and design with future behavior in mind.

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NIMHD welcomes nine new members to the National Advisory Council on Minority Health and Health Disparities

Posted in Behavior, Clinical Diagnostics, Diabetes Mellitus, Disease Biology, FDA, Health Economics and Outcomes Research, Healthcare costs and reimbursement, HealthCare IT, Healthcare Reform, Infectious Disease & New Antibiotic Targets, Infectious Disease Immunodiagnostics, Pain: Etiology, Genetics & Innovations in Treatment, Patient Experience: Personal Memories of Invasive Medical Intervantion, Patient’s Voice: Personal Experience with Invasive Medical Procedures, tagged , , , , , , , , , , , , , , , , , , on September 10, 2015| Leave a Comment »

NIMHD welcomes nine new members to the National Advisory Council on Minority Health and Health Disparities

Reporter: Stephen J. Williams, Ph.D.

The National Institute on Minority Health and Health Disparities (NIMHD) has announced the appointment of nine new members to the National Advisory Council on Minority Health and Health Disparities (NACMHD), NIMHD’s principal advisory board. Members of the council are drawn from the scientific, medical, and lay communities, so they offer diverse perspectives on minority health and health disparities.

The NACMHD, which meets three times a year on the National Institutes of Health campus, Bethesda, Maryland, advises the secretary of Health and Human Services and the directors of NIH and NIMHD on matters related to NIMHD’s mission. The council also conducts the second level of review of grant applications and cooperative agreements for research and training and recommends approval for projects that show promise of making valuable contributions to human knowledge.

The next meeting of the NACMHD will be held on Thursday, Sept. 10, 8:30 a.m.-5:00 p.m. on the NIH campus. The meeting will be available on videocast at http://www.videocast.nih.gov.

NIMHD Director Eliseo J. Pérez-Stable, M.D., is pleased to welcome the following new members

Margarita Alegría, Ph.D., is the director of the Center for Multicultural Mental Health Research at Cambridge Health Alliance and a professor in the department of psychiatry at Harvard Medical School, Boston. She has devoted her career to researching disparities in mental health and substance abuse services, with the goal of improving access to and equity and quality of these services for disadvantaged and minority populations.

Maria Araneta, Ph.D., a perinatal epidemiologist, is a professor in the Department of Family and Preventive Medicine at the University of California, San Diego. Her research interests include maternal/pediatric HIV/AIDS, birth defects, and ethnic health disparities in type 2 diabetes, regional fat distribution, cardiovascular disease, and metabolic abnormalities.

Judith Bradford, Ph.D., is director of the Center for Population Research in LGBT Health and she co-chairs The Fenway Institute, Boston. Dr. Bradford has participated in health research since 1984, working with public health programs and community-based organizations to conduct studies on lesbian, gay, bisexual, and transgender people and racial minority communities and to translate the results into programs to reduce health disparities.

Linda Burhansstipanov, Dr.P.H., has worked in public health since 1971, primarily with Native American issues. She is a nationally recognized educator on cancer prevention, community-based participatory research, navigation programs, cultural competency, evaluation, and other topics. Dr. Burhansstipanov worked with the Anschutz Medical Center Cancer Research Center — now the University of Colorado Cancer Research Center — in Denver for five years before founding Native American Cancer Initiatives, Inc., and the Native American Cancer Research Corporation.

Sandro Galea, M.D., a physician and epidemiologist, is the dean and a professor at the Boston University School of Public Health. Prior to his appointment at Boston University, Dr. Galea served as the Anna Cheskis Gelman and Murray Charles Gelman Professor and chair of the Department of Epidemiology at the Columbia University Mailman School of Public Health, New York City. His research focuses on the causes of brain disorders, particularly common mood and anxiety disorders, and substance abuse.

Linda Greene, J.D., is Evjue Bascom Professor of Law at the University of Wisconsin–Madison Law School. Her teaching and academic scholarship include constitutional law, civil procedure, legislation, civil rights, and sports law. Most recently, she was the vice chancellor for equity, diversity, and inclusion at the University of California, San Diego.

Ross A. Hammond, Ph.D., a senior fellow in the Economic Studies Program at the Brookings Institution, Washington, D.C., is also director of the Center on Social Dynamics and Policy. His primary area of expertise is using mathematical and computational methods from complex systems science to model complex dynamics in economic, social, and public health systems. His current research topics include obesity etiology and prevention, tobacco control, and behavioral epidemiology.

Hilton Hudson, II, M.D., is chief of cardiothoracic surgery at Franciscan Healthcare, Munster, Indiana and a national ambassador for the American Heart Association. He also is the founder of Hilton Publishing, Inc., a national publisher dedicated to producing content on solutions related to health, wellness, and education for people in underserved communities. Dr. Hilton’s book, “The Heart of the Matter: The African American Guide to Heart Disease, Heart Treatment and Heart Wellness” has impacted at-risk patients nationwide.

Brian M. Rivers, Ph.D., M.P.H., currently serves on the research faculty at the H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida. He is also an assistant professor in the Department of Oncologic Sciences at the University of South Florida College of Medicine, Tampa. Dr. Rivers’ research efforts include examination of unmet educational and psychosocial needs and the development of communication tools, couple-centered interventions, and evidence-based methods to convey complex information to at-risk populations across the cancer continuum.

NIMHD is one of NIH’s 27 Institutes and Centers. It leads scientific research to improve minority health and eliminate health disparities by conducting and supporting research; planning, reviewing, coordinating, and evaluating all minority health and health disparities research at NIH; promoting and supporting the training of a diverse research workforce; translating and disseminating research information; and fostering collaborations and partnerships. For more information about NIMHD, visit http://www.nimhd.nih.gov.

About the National Institutes of Health (NIH): NIH, the nation’s medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.

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