Billericay Gazette published Dementia care centre to open in Billericay

A LEADING centre for people with dementia has been given the go-ahead in Billericay.

A specialist unit dedicated to patients suffering from the illness will be opened at Mountnessing Court from the autumn after being approved by the board of NHS South Essex.

approved: Ian Stidston from NHS South Essex, mental health commissioner Irene Lewsey and dementia foundation founder Caroline Dearson outside the new unit

The Mountnessing Road centre will encompass organisations involved in caring for people with dementia, bringing together medical, therapeutic, social care, and mental health staff, as well as workers from the Alzheimer's Society.

It will be supported by a consultant psychiatrist and a geriatrician.

The new centre will be a pilot project with initial results assessed in January next year.

Ian Stidston, director of primary care and partnership commissioning at NHS South Essex, said: "This unit will give people the choice to have intensive support away from hospital.

"We want to provide the necessary care they and their carers need so they can stay at home and live as independently as possible, for as long as possible, if that is their wish."

The 22-bed specialist unit, for dementia patients in south west Essex as well as Castle Point and Rochford, will provide rehabilitation seven days a week for up to eight weeks.

During this time, patients will receive intensive, expert care in an environment set up specifically for people with dementia.

Read the original post:
Billericay Gazette published Dementia care centre to open in Billericay

Do more for people with dementia, advocates urge

Dementia advocates are urging the province to do more for people with the disease after a man with Alzheimer's went missing for five days, leaving a nursing home in Stephenville and then travelling to New Brunswick. The man was found safe in Saint John.

The Alzheimer Society of Newfoundland and Labrador said the province needs to prepare for a growing population of people with Alzheimer's and other forms of dementia.

One of the greatest needs said executive director Shirley Lucas is additional housing.

"If we were to look at the baby boom population, we know that the existing care that we have out there isn't going to meet that demand," Lucas added.

She said new and innovative ways need to be found to provide proper care.

"It's time to look at different housing options, such as secured units for patients," said Lucas.

Because people with Alzheimer's and dementia experience many stages in their illness, there is no onefit solution, she added.

Read the original:
Do more for people with dementia, advocates urge

Finding Parkinson's clue offers unshakable hope

Lorraine Ho

Friday, August 10, 2012

Hope may be stirring for those suffering from an incurable brain disease that causes loss of muscle control.

Spinocerebellar Ataxia affects the cerebellum - a small but key region of the brain - killing nerve cells and triggering genetic diseases, such as Parkinson's and Huntington's.

SCA patients may suffer tremors, gradually lose fine motor skills, and have trouble keeping their balance or coordinating daily movements.

But a team of Chinese University researchers may have an answer to their suffering - as they have found exactly how the disease is triggered.

Toxic ribonucleic acids cause deterioration of the small brain by disrupting the production of proteins called ribosomes - claims the team's findings, published in the US journal Proceedings of the National Academy of Sciences.

"The lack of ribosomes eventually causes programmed cell death ... and leads to the development of SCAs," lead researcher and CUHK School of Life Sciences associate professor Edwin Chan Ho-yin said.

"In theory, therefore, finding a way to revive ribosome supply in patients suffering from SCAs may help in treating the disease."

The territory currently has about 300 patients with symptoms of SCAs, Chan said. DNA tests have shown a third to be confirmed cases.

Excerpt from:
Finding Parkinson's clue offers unshakable hope

Finding Parkinson’s clue offers unshakable hope

Lorraine Ho

Friday, August 10, 2012

Hope may be stirring for those suffering from an incurable brain disease that causes loss of muscle control.

Spinocerebellar Ataxia affects the cerebellum - a small but key region of the brain - killing nerve cells and triggering genetic diseases, such as Parkinson's and Huntington's.

SCA patients may suffer tremors, gradually lose fine motor skills, and have trouble keeping their balance or coordinating daily movements.

But a team of Chinese University researchers may have an answer to their suffering - as they have found exactly how the disease is triggered.

Toxic ribonucleic acids cause deterioration of the small brain by disrupting the production of proteins called ribosomes - claims the team's findings, published in the US journal Proceedings of the National Academy of Sciences.

"The lack of ribosomes eventually causes programmed cell death ... and leads to the development of SCAs," lead researcher and CUHK School of Life Sciences associate professor Edwin Chan Ho-yin said.

"In theory, therefore, finding a way to revive ribosome supply in patients suffering from SCAs may help in treating the disease."

The territory currently has about 300 patients with symptoms of SCAs, Chan said. DNA tests have shown a third to be confirmed cases.

Excerpt from:
Finding Parkinson's clue offers unshakable hope

Family starts fundraising to buy van for Lynn man suffering from ALS-like disease

Home > News Family starts fundraising to buy van for Lynn man suffering from ALS-like disease Originally Published on Thursday, August 09, 2012 By Cyrus Moulton / The Daily Item

LYNN Patrick Cogan said he doesn't like to ask for help.

But two years after being diagnosed with a debilitating and degenerative neuromuscular disease called Friedreich's Ataxia, the Cogan family is seeking help raising money for a van and a service dog to help Patrick and money to help provide dogs for other families.

"The time is going to come when I do need help but I'm going to do as much right now as I can," Patrick Cogan said at his apartment on Wednesday. "The goal is to raise money for a van." He said he already has a service dog, which was donated to the family, "but (the trainer) doesn't get any federal funding and so whatever we can give back to them we will."

Cogan said he was diagnosed with Friedreich's Ataxia in December 2010. He said he and the family believed for years that another and more benign disorder was causing the pain in his feet, and balance and coordination problems that had bedeviled him since childhood. But he went to see a neurologist at Massachusetts General Hospital after suffering several falls. He recalled the neurologist's advice when she gave him the diagnosis.

"'Don't Google it,' the neurologist told me, and gave me one website to visit to learn about the disease," he said. "So I Googled it, and it scared the crap out of me."

Patrick's mother Helen Cogan described Friedreich's Ataxia as "the evil cousin of Amyotrophic lateral sclerosis (ALS) or Lou Gehrig's disease," which she said is a similar but more well-known - and well-researched - disease.

The Cogans referred to the disease as "life-shortening," and Patrick Cogan said most patients eventually succumb to heart disease or lung problems as a result of the disease.

Patrick said he is thankful he is not at that stage.

But the disease has begun to impact his life. He reports difficulty typing and texting - unfortunate since he just got an unlimited texting plan on his phone, he joked. He increasingly uses a wheelchair since he feels safer in public in a chair than when he is using a walker or arm crutches.

Follow this link:
Family starts fundraising to buy van for Lynn man suffering from ALS-like disease

Local teen looks to take autism campaign national, make Lou. first in research

by Joe Arnold

WHAS11.com

Posted on August 9, 2012 at 6:47 PM

Updated yesterday at 7:01 PM

LOUISVILLE, Ky. (WHAS11) -- A local teenager who has spent years raising money and awareness for autism said she has a big dream - to make Louisville the home of autism research.

We first introduced you to Michaela Riggle eight years ago, then just 7-years-old and already battling to find a cure for her 4-year-old brother who was diagnosed with autism.

She started the Beading to Beat Autism campaign where she, along with help from others, sold hand-made beaded bracelets to raise money for autism research.

Michala is now 15-years-old and is still looking out for Evan. Evan has come a long way, but despite progress his family said autism still dominates their lives.

She started the Beading to Beat Autism campaign where she, along with help from others, sold hand-made beaded bracelets to raise money for autism research. After five years of selling bracelets, Michala is now taking her effort to the next level, a local campaign to raise $5 million to buy land and hire staff for a Louisville autism and research facility.

She's asking 60,000 of her Kentuckiana neighbors to pledge $7 per month for one year. But that's just the start. Michala hopes to take Campaign 7 national raise hundreds of millions of dollars and make Louisville the home of autism hope.

See the article here:
Local teen looks to take autism campaign national, make Lou. first in research

Autism research foundation looks to expand

Autism research foundation looks to expand

It began as a movement started by a 10-year-old girl to fight autism. Now, Michala Riggle is impacting the world of autism research yet again.

In 2007, Michala got national attention for selling homemade beaded bracelets for $3 each.

She wanted to raise $200,000 for an autism study her younger brother, Evan, was in, along with other autistic children at Kosair Children's Hospital.

Within six months, her Beading to Beat Autism campaign exceeded her goal.

"What we're here to announce today, we're going to kick off Campaign 7," said Riggle.

Five years and $500,000 later, Michala's mission has grown just like she has. Evan, now 12 years old, is doing well with his treatment. With their success, Michala and her family have set another goal, called Campaign 7.

"We're going to kick that off and we're going to try and get people to commit donating $7 a month for one year so we can raise the money to buy the land we want the center in and hire staff and kick off our national campaign to raise the money," said Riggle.

The center will be a world-class autism research and treatment facility built in Louisville. It will include an autism school and a bigger warehouse for the beading operation.

The facility, named the We Believe International Autism and Research Treatment Center, will be built on 40 acres in eastern Jefferson County.

Here is the original post:
Autism research foundation looks to expand

'Treating the whole person with autism' sets direction for parent-clinician collaboration

Public release date: 9-Aug-2012 [ | E-mail | Share ]

Contact: Jane E. Rubinstein jrubinstein@rubenstein.com 212-843-8287 Autism Speaks

NEW YORK, N.Y. (August 9, 2012) Over 400 attendees from across the U.S. and around the world participated in the first national conference for families and professionals, "Treating the Whole Person with Autism: Comprehensive Care for Children and Adolescents with ASD."

Autism Speaks, the world's leading autism science and advocacy organization, organized and hosted the conference in collaboration with educational partners at Nationwide Children's Hospital (NCH), The Ohio State University Wexner Medical Center, the American Academy of Pediatrics (AAP), and the Health Resources and Services Administration (HRSA).

"Autism Speaks' Autism Treatment Network (ATN) is a key initiative aimed at improving the health and well-being of individuals with ASD," remarked Daniel Coury, M.D., ATN medical director and chief of Developmental & Behavioral Pediatrics at Nationwide Children's Hospital. "It provides "whole person," family-centered medical care which aims to address the individual's and the family's unique set of needs and challenges. We're excited to build upon these efforts through this national conference with Autism Speaks and our other conference partners."

The conference provided a forum for both families and professionals to learn about current guidance for addressing associated medical issues, and developing approaches to care that integrate behavioral and medical approaches across the lifespan.

"The theme of this conference, treating the whole person, reflects our ultimate goal of helping individuals with ASD to have healthy and successful lives," stated Geraldine Dawson, Ph.D., chief science officer at Autism Speaks. These themes were highlighted by the two conference keynote speakers. Ricki Robinson, M.D., M.P.H., co-director of the Descanso Medical Center for Development and Learning, who served as the first speaker, encouraged practitioners to view individuals with ASD through a wide array of "lenses" that together paint a total picture of the child's life. These lenses include the child's physical and mental health, behaviors, intellectual interests and creative pursuits. By seeing the whole child, treatment and care plans can be tailored to address the individuals' needs.

Peter Gerhardt, Ed.D., director of the McCarton Upper School and chair of the Scientific Council for the Organization for Autism Research, emphasized the need to continually think of the changing care needs across the lifespan. Dr. Gerhardt stressed the importance of making optimizing adult outcomes a much higher research priority. In particular, he noted the need to identify and focus on meaningful knowledge and skills vital for independence and fulfillment. This emphasis on care across the lifespan was further supported in the presentation by Marsha Mailick Seltzer, Ph.D., professor and director of the Waisman Center at the University of Wisconsin. A key point was the importance for researchers, clinicians, and advocates to expand their view of autism beyond childhood and to consider individuals with ASD within the context of their families. Her team's research on adolescents and adults with ASD looks at how ASD symptoms change across the lifespan. They observed in their data that overall there is stability or some improvement in symptoms and behavior problems over time. However, they noted that there can be stage-related changes, a critical one being the exit from high school, after which improvement in symptoms slows. Moreover, after high school, income level becomes a risk factor in the worsening of problem behaviors with those in low income groups at greatest risk regardless of intellectual ability.

The conference included general science sessions providing recent developments on health-related issues for individuals with ASD, and concurrent sessions tailored to families and professionals, respectively, that provided practical examples and discussion on the identification, management and treatment of medical conditions often associated with ASD. The sessions addressed immune dysfunction in autism, metabolic dysfunction, gastrointestinal dysfunction including the GI microenvironment and impaired carbohydrate digestion, nutrition, sleep disorders, the prevalence and management of psychiatric disorders and challenging behaviors, an overview of cognitive behavioral therapies, and the trajectories of development during adolescence and adulthood. The meeting concluded with family perspectives on how to coordinate and provide care both at home and in the clinical setting.

Some highlights include the presentation by Alessio Fasano, M.D. which was focused on the relationship between genes and environment in the GI problems in individuals with ASD. Dr. Fasano, professor of pediatrics, medicine and physiology, and director of the Mucosal Biology Research Center and the Center for Celiac Research at the University of Maryland School of Medicine, noted that progress is being made in the field to better understand the biology of the gut environment but that to be effective in leading to treatments, it is going to be important to integrate the findings across these areas to "connect the dots" in building a full picture of the nature of GI disorders in ASD. Brent Williams, Ph.D., associate research scientist at Columbia University reported on his on-going research looking at impaired carbohydrate metabolism in individuals with ASD, which highlights that GI dysfunction may be attributable to distinct molecular and microbial mechanisms in individuals with ASD.

Read more here:
'Treating the whole person with autism' sets direction for parent-clinician collaboration

‘Treating the whole person with autism’ sets direction for parent-clinician collaboration

Public release date: 9-Aug-2012 [ | E-mail | Share ]

Contact: Jane E. Rubinstein jrubinstein@rubenstein.com 212-843-8287 Autism Speaks

NEW YORK, N.Y. (August 9, 2012) Over 400 attendees from across the U.S. and around the world participated in the first national conference for families and professionals, "Treating the Whole Person with Autism: Comprehensive Care for Children and Adolescents with ASD."

Autism Speaks, the world's leading autism science and advocacy organization, organized and hosted the conference in collaboration with educational partners at Nationwide Children's Hospital (NCH), The Ohio State University Wexner Medical Center, the American Academy of Pediatrics (AAP), and the Health Resources and Services Administration (HRSA).

"Autism Speaks' Autism Treatment Network (ATN) is a key initiative aimed at improving the health and well-being of individuals with ASD," remarked Daniel Coury, M.D., ATN medical director and chief of Developmental & Behavioral Pediatrics at Nationwide Children's Hospital. "It provides "whole person," family-centered medical care which aims to address the individual's and the family's unique set of needs and challenges. We're excited to build upon these efforts through this national conference with Autism Speaks and our other conference partners."

The conference provided a forum for both families and professionals to learn about current guidance for addressing associated medical issues, and developing approaches to care that integrate behavioral and medical approaches across the lifespan.

"The theme of this conference, treating the whole person, reflects our ultimate goal of helping individuals with ASD to have healthy and successful lives," stated Geraldine Dawson, Ph.D., chief science officer at Autism Speaks. These themes were highlighted by the two conference keynote speakers. Ricki Robinson, M.D., M.P.H., co-director of the Descanso Medical Center for Development and Learning, who served as the first speaker, encouraged practitioners to view individuals with ASD through a wide array of "lenses" that together paint a total picture of the child's life. These lenses include the child's physical and mental health, behaviors, intellectual interests and creative pursuits. By seeing the whole child, treatment and care plans can be tailored to address the individuals' needs.

Peter Gerhardt, Ed.D., director of the McCarton Upper School and chair of the Scientific Council for the Organization for Autism Research, emphasized the need to continually think of the changing care needs across the lifespan. Dr. Gerhardt stressed the importance of making optimizing adult outcomes a much higher research priority. In particular, he noted the need to identify and focus on meaningful knowledge and skills vital for independence and fulfillment. This emphasis on care across the lifespan was further supported in the presentation by Marsha Mailick Seltzer, Ph.D., professor and director of the Waisman Center at the University of Wisconsin. A key point was the importance for researchers, clinicians, and advocates to expand their view of autism beyond childhood and to consider individuals with ASD within the context of their families. Her team's research on adolescents and adults with ASD looks at how ASD symptoms change across the lifespan. They observed in their data that overall there is stability or some improvement in symptoms and behavior problems over time. However, they noted that there can be stage-related changes, a critical one being the exit from high school, after which improvement in symptoms slows. Moreover, after high school, income level becomes a risk factor in the worsening of problem behaviors with those in low income groups at greatest risk regardless of intellectual ability.

The conference included general science sessions providing recent developments on health-related issues for individuals with ASD, and concurrent sessions tailored to families and professionals, respectively, that provided practical examples and discussion on the identification, management and treatment of medical conditions often associated with ASD. The sessions addressed immune dysfunction in autism, metabolic dysfunction, gastrointestinal dysfunction including the GI microenvironment and impaired carbohydrate digestion, nutrition, sleep disorders, the prevalence and management of psychiatric disorders and challenging behaviors, an overview of cognitive behavioral therapies, and the trajectories of development during adolescence and adulthood. The meeting concluded with family perspectives on how to coordinate and provide care both at home and in the clinical setting.

Some highlights include the presentation by Alessio Fasano, M.D. which was focused on the relationship between genes and environment in the GI problems in individuals with ASD. Dr. Fasano, professor of pediatrics, medicine and physiology, and director of the Mucosal Biology Research Center and the Center for Celiac Research at the University of Maryland School of Medicine, noted that progress is being made in the field to better understand the biology of the gut environment but that to be effective in leading to treatments, it is going to be important to integrate the findings across these areas to "connect the dots" in building a full picture of the nature of GI disorders in ASD. Brent Williams, Ph.D., associate research scientist at Columbia University reported on his on-going research looking at impaired carbohydrate metabolism in individuals with ASD, which highlights that GI dysfunction may be attributable to distinct molecular and microbial mechanisms in individuals with ASD.

Read more here:
'Treating the whole person with autism' sets direction for parent-clinician collaboration

Olympic Horse Used Stem Cell Therapy

Ravel, a horse competing at the 2012 London Olympics, underwent stem cell therapy treatment that helped heal a possibly career-ending injury to one of his legs, according to the Helen Woodward Animal Center in California.

Ravel, a regular client of Rodrigo Vazquez of Equine Surgical Services at the center, is believed to be the first Olympian to benefit from a stem cell-based treatment. Ravel is now the highest scoring horse on Team USA at the Olympics.

"Ravel is a high-impact athlete," Vazquez said. "He runs the same risks as any other athlete in a high performance sport and he gets hurt like any other athlete too. But he is something special. He works hard and he's focused and he thrives in his sport. He just didn't want to quit."

The 15-year-old equine athlete, owned by Akiko Yamazaki, was united with his rider Steffen Peters in late 2006. Since then, the team has made history, with Ravel excelling in dressage, which is one of three Olympic equestrian disciplines. It involves riding and training a horse in a manner that develops obedience, flexibility and balance.

Ravel and Peters were the highest placing American pair at the 2008 Beijing Olympics, and have won numerous competitions over the years, including the prestigious Rolex/FEI World Cup in dressage.

Before these victories, Ravel sustained the leg injury. Jessica Gercke, a spokesperson for the Helen Woodward Animal Center, told Discovery News that staff working with competitive horses like Ravel do not wish to reveal detailed information about medical conditions and treatments, since that might affect the perceptions of judges or others.

Vazquez, however, did share that regular check-ups, vaccinations, dentistry and the "emergency treatment with a new technology based on stem cell therapy" helped to heal Ravel after an eight-month break in training.

Adult stem cells can reproduce and differentiate into different types of cells. They continue to be a focus of study for scientists hoping to treat a number of diseases in humans and non-human animals. In horses, to repair cartilage and tendon tissues, scientists have been looking into stem cells derived from bone.

"Bone derived cells in horses are most often obtained from an aspirate (material drawn by suction) of either the hip or sternum with apparent minimal discomfort" to the horse, according to David Frisbie, an associate professor at the Colorado State University College of Veterinary Medicine. "The procedure typically takes less than 15 minutes and can be done standing under light sedation."

Results of clinical studies on horses suggest that stem cell treatment can improve healing rates, overall outcomes, and decrease re-injury rates almost by half. Further studies are needed, however, to better determine dosage and timing specifics.

Here is the original post:
Olympic Horse Used Stem Cell Therapy

Summer school students help scientists advance stem cell research at USC

Listen Now [4 min 28 sec] Listen Now [4 min 28 sec]

For many Southern California high school students, summer is synonymous with surf, sand and sun. But, for some of Los Angeles' top math and science students, the lure of the beach and traditional summer fun fizzles fast when compared to microscopes, slide kits and real-life stem cell research.

Armed with little more than protective gear and enthusiasm, 20 overachieving teenagers have been clocking 40-hour weeks in the lab at USC's Eli and Edythe Broad Center for Regenerative Medicine and Stem Cell Research.

Among them is 17-year-old Brian Tom of Lincoln Heights.

Its fascinating because stem cells have all this potential to heal these degenerative diseases like Multiple Sclerosis and Alzheimer's," says Tom, a senior at Bravo Medical Magnet in Los Angeles. "It's amazing how you can create multiple tissues from one cell."

Stem cells offer promise as a treatment or cure for many diseases because they can be can induced to morph into other cell types such as brain, muscle or skin cells. Stem cells can also divide without limit, which gives them the potential to repair and replace damaged tissue.

You can just imagine the possibilities," says Sophie McAllister, a 17-year-old senior at Harvard-Westlake School in Los Angeles. McAllister works with a USC mentor on cardiac cell regeneration.

Two programs, one goal

McAllister and nine other students are in a program that's privately funded by two donors with ties to USC. Meanwhile, Tom and his summer school classmates are studying under a statewide program funded by the California Institute of Regenerative Medicine (CIRM), a voter-created agency that funds stem cell research throughout California.

CIRM has invested $1.7 million in nine high school summer programs statewide for three years.

Here is the original post:
Summer school students help scientists advance stem cell research at USC

International Stem Cell Corp Announces Second Quarter 2012 Financial Results

CARLSBAD, CA--(Marketwire -08/09/12)- International Stem Cell Corporation (ISCO) (www.internationalstemcell.com) ("ISCO" or "the Company"), a California-based biotechnology company focused on therapeutic and research products, today announced financial results for the three and six months ended June 30, 2012.

Three and Six Months Ended June 30, 2012

Revenue for the three months ended June 30, 2012 totaled $1.06 million compared to $1.11 million for the three months ended June 30, 2011. The decrease in revenue was due largely to lower sales generated from Lifeline Cell Technology (LCT). LCT and Lifeline Skin Care (LSC) each accounted for approximately 50% total revenue in the three months ended June 30, 2012 compared to 52% and 48%, respectively, in the corresponding periods the prior year. Revenue for the six months ended June 30, 2012 was $2.13 million compared to $2.63 million for the corresponding period in 2011. The decrease in revenue was due principally to fewer sales generated from LSC, partially offset by LCT's higher sales generated from larger distributors. For the six months ended June 30, 2012, LSC generated $1.07 million or 50% of total revenue, compared to $1.66 million or 63% of total revenue for the corresponding period in 2011. For the six months ended June 30, 2012, LCT generated $1.06 million or 50% of total revenue, compared to $0.97 million or 37% of total revenue for same period in 2011.

Research and development expenses (R&D) were $0.87 million for the three months ended June 30, 2012, representing a decrease of approximately 23% compared to the corresponding period in 2011. The decrease was due primarily to lower consulting expenses associated with various research projects, lower stock-based compensation expense, lower laboratory-related expenses, and lower personnel-related spending. The decrease was partially offset by higher stem cell line research and testing expenses. R&D expenses were $1.80 million for the six months ended June 30, 2012, compared to $2.13 million for the same period in 2011. The 15% decrease was due primarily to lower consulting expenses associated with various research projects, lower stock-based compensation expense, lower laboratory-related expenses, and reduced travel expenses, partially offset by higher stem cell line research and testing expenses and higher personnel-related spending associated with higher headcount and increased research activities.

The Company continues to invest in its sales and marketing initiatives. Marketing expenses for the three months ended June 30, 2012 were $0.55 million, an increase of 58% from the same period in 2011. The increase was primarily driven by investments in marketing and promotion, advertising, higher shipping and logistic expenses, additions of sales and customer service staff, higher consulting expense and higher commission paid to various strategic partners. The increase was partially offset by a reduction in commission paid to a consultant who promoted, marketed, and sold skin care products through various proprietary mailings and employee stock-based compensation. For the six months ended June 30, 2012, marketing expenses amounted to $1.04 million, reflecting an increase of $0.38 million or 57%, as compared to $0.66 million for the corresponding period in 2011. The substantial increase was primarily driven by increased investments in marketing support, promotion, and advertising, higher consulting expense, higher shipping and logistic expenses, higher personnel-related expenses resulting from higher headcount in the sales and marketing of the skin care products, and higher commission paid to various strategic partners. The increase was partially offset by a reduction in sales commission paid to a consultant who promoted, marketed, and sold skin care products through various proprietary mailings and lower employee stock-based compensation.

General and administrative expenses for the three months ended June 30, 2012 were $1.76 million, down 18% compared to the same period in 2011, as a result of ongoing operational efficiency initiatives. The decrease resulted largely from lower employee stock-based compensation, reduced employee-related spending resulting from lower headcount, lower professional accounting fees, and lower corporate support expenses. The decrease was partially offset by higher legal fees relating to our corporate activities, and higher consulting expense. General and administrative expenses for the six months ended June 30, 2012 were $3.79 million, reflecting a decrease of $0.58 million or 13%, compared to $4.37 million for the same period in 2011. The decrease was primarily attributable to lower employee stock-based compensation, the absence of stock-based compensation incurred for services provided by a consultant, reduced employee-related spending resulting from lower headcount, and lower corporate support expenses. The decrease was partially offset by an increase in legal fees relating to our corporate expenses, higher consulting expense, and higher professional accounting fees related to Sarbanes-Oxley compliance efforts.

Cash and cash equivalents totaled $4.29 million at June 30, 2012 compared to $1.34 million as of December 31, 2011, due primarily to two financing transactions totaling approximately $6.9 million completed in the first six months of 2012 partially offset by normal business operations.

"We have made solid progress across our entire organization in the first half of this year," stated Dr. Andrey Semechkin, ISCO's CEO and Co-Chairman, "and I'm pleased to see that the operational efficiencies we implemented in the second quarter are resulting in lower administrative expenses. Going forward we will continue to look for further opportunities to improve our organization effectiveness and reduce expenses. As you may have read in my shareholder letter, following a detailed analysis of our research priorities, we concentrated our resources on the most promising therapeutic programs and this has already resulted in exciting achievements and progressed our programs closer to clinical development."

Q2 2012 Highlights:

Conference Call and Webcast Details:

Read the rest here:
International Stem Cell Corp Announces Second Quarter 2012 Financial Results

Premature Considerations of Immortality

For whatever reason, a number of public voices seem to be talking about immortality all of a sudden, largely meaning physical immortality in the sense of immunity to aging but vulnerability to fatal accidents. Topics ebb and flow like tides, I suppose, the signs of many hidden connections that underlie our culture - that grand conversation of innumerable threads held in the myriad communication channels available to us.

It's a big project so it's hard to summarize to its core being but I'd say we're investigating two different kinds of immortality. One would be the possibility of living forever without ever dying. The main questions there are whether it's technologically plausible or feasible for us, either by biological enhancement such as those described by Ray Kurzweil, or by some combination of biological enhancement and uploading our minds onto computers in the future. I think another more interesting and important question is would we choose to be immortal in that sense, or does death and finitude give life meaning?

And so forth, repeated in the echo chamber. Immortality can be a useful term - such as on the occasions on which you want to plant a flag a long way out in the discussion and make waves. It is, I think, becoming less useful with time, however. So many people use it without meaning or with so many varied and half-thought meanings that it is, like "anti-aging", becoming more harmful than helpful. Too much baggage, too many charlatans of various types hitching their carts to the bandwagon.

Putting in serious time and thought on physical immortality - $5 million here and $5 million there adds up pretty quickly - seems to me to be premature. There is a great deal of work that lies between here and first generation rejuvenation biotechnology, something that will allow us to live additional decades in good health, never mind what comes after that. The rise and rapid obsolescence of many massive industries in medicine will happen over the next fifty years in order to extend the outer limits of human health and life span far beyond the present century-and-a-bit. Each of those churning engines of progress will see millions of individuals working in hundreds of competing companies, a world of intricate detail.

The result of all of that? Possibly humans that can live for two centuries or more before hitting as-yet unknown limits to presently envisaged biological repair technologies. This is a drop in the ocean of time. But that will give a hundred years of grace in which to work feverishly on the next generations of technology: replacements for biological systems, improving on the ways to repair and rebuild our cells, merging with our machines as those machines become ever smaller and more capable. The world of a century and a half from now will be as distant and strange and capable to us as our tools and society would seem to a 18th century peasant.

My point is that many transformative, world-sweeping changes brought by advancing technology will occur in the decades between now and even a mere hard-fought doubling of the human life span. We'll be starting in earnest to settle the Moon and Mars by then. Our machines will be able to think for themselves. Desktop and motile nanofactories will be capable of fabricating everything from houses to gene therapies from raw materials. A sea of historical and cultural manuscripts will be written on those changes, and still fail to easily capture the scope of the way in which the world changes.

And then it starts over again, ever building new and greater edifices as we push on to overcome the next set of limits to the human condition. All of this grand and complex near future of increasing longevity and massive change seems far more worthy of thought than immortality, given the length of the road between here and there, and how much has to be done to even start talking seriously about lives of tens of thousands of years.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

The Brain is Plastic For Life

We have a great deal more control over the age-related decline of the brain than was once thought - "use it or lose it", and the ability to affect change through challenging the mind. Yet it remains the case that new biotechnology and medicine will be required to get to where we want to be, a world without the risk of dementia, fuzzy memory, and slow cognition. Still, the plasticity of the aging brain is encouraging: "There is growing evidence that, beyond what was previously believed, the adult human brain is remarkably malleable and capable of new feats - even in the last decades of life. In fact, new experiences can trigger major physical changes in the brain within just a few days, and certain conditions can accelerate this physical, chemical and functional remodeling of the brain. ... We used to think that the brain was completely formed by development and its basic structure didn't change much in adults, but as research went on we discovered that wasn't true, at least in the cerebral cortex. We now know that an underlying portion of the brain called the thalamus, which feeds the cortex information from our senses, is also remarkably plastic. ... There is no evidence that there is any part of the adult brain that is not plastic. But studies indicate that some aspects of musical training, such as the ability to perceive temporal patterns, require the brain to be trained during early developmental periods when its primed for certain types of stimuli. For other aspects of musical development, such as the ability to perceive and repeat a sequence of tones, it's irrelevant whether you've had that experience and training early in life. ... The brain is plastic for life. The fundamental thing that determines how much [persons with brain disorders] will improve is the level of their initial impairment, but not their age."

Link: http://www.newswise.com/articles/researchers-find-the-brain-more-malleable-than-believed

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Yet Another Theory to Explain Gender Differences in Longevity

There is no shortage of theories as to why women live longer than men - an apparently simple question, but one balanced on such a mountain of complex data and partial knowledge that it cannot be definitively answered at the present time. Here is another theory for the stack: "Mitochondria are inherited only from mothers, never from fathers, so there is no way to weed out mutations that damage a male's prospects. ... [Researchers] analysed the mitochondria of 13 different groups of male and female fruit flies. Mitochondria, which exist in almost all animal cells, convert food into the energy that powers the body. ... the results point to numerous mutations within mitochondrial DNA that affect how long males live, and the speed at which they age. ... Intriguingly, these same mutations have no effects on patterns of ageing in females. All animals possess mitochondria, and the tendency for females to outlive males is common to many different species. Our results therefore suggest that the mitochondrial mutations we have uncovered will generally cause faster male ageing across the animal kingdom. ... They suggest this is because there is no evolutionary reason for the faults that affect males to be picked up - because mitochondria are passed down by females. ... If a mitochondrial mutation occurs that harms fathers, but has no effect on mothers, this mutation will slip through the gaze of natural selection, unnoticed. Over thousands of generations, many such mutations have accumulated that harm only males, while leaving females unscathed."

Link: http://www.bbc.co.uk/news/health-19093442

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

What is Aging?

A recent open access commentary by researcher Michael Rose and colleagues looks at the following question: what, exactly, is aging? Much like art, we might know it if we see it, but there's plenty of room for debate over the details.

What is Aging?

In 1991, the book Evolutionary Biology of Aging offered the following definition of aging: a persistent decline in the age-specific fitness components of an organism due to internal physiological deterioration (Rose, 1991). This definition has since been used by others a number of times. However, it was only a modest generalization of a definition proffered by Alex Comfort over three editions (1956-1979) of his key book The Biology of Senescence (Comfort, 1979): "a progressive increase throughout life, or after a given stadium, in the likelihood that a given individual will die, during the next succeeding unit of time, from randomly distributed causes."

...

Yet a mere definition does not necessarily tell a scientist what causally underlies the phenomenon that is so defined. The latter issue is much broader, implicitly raising fundamental scientific questions regarding mechanisms.

From here the piece heads off into a discussion of late life plateaus in aging, for example in flies where it is observed that the chance of death per unit time stops rising at advanced ages - in other words the flies stop aging by one definition of the term, left with a high but steady mortality rate. There are some arguments for this phenomenon to exist in humans, but the data is sparse and other results argue the opposite conclusion. Still, the researchers here argue that the demonstrated existence of this phenomenon in lower animals requires further thought to be directed towards how to define aging:

it appears that the cessation of aging occurs at the individual level, and is not just an artifact of population structure. Yet this is clearly paradoxical, if we think of the machinery of aging in terms of such physiological processes as steadily cumulative damage. If it is supposed that some process of cumulative damage or disharmony is supposed to underlie aging, why should that process abruptly stop at the very point, late in adult life, when it has greatly reduced the ability of the surviving individuals to sustain life and reproduction?

...

These results call for some fundamental re-thinking of what aging is: [that] aging is not inevitably a cumulative and unremitting process of deterioration. Instead, aging might be best conceived as a facet of [evolutionary] adaptation ... under sufficiently benign environmental conditions, individuals from species as disparate as humans and fruit flies can survive a protracted aging period and reach a subsequent late-life respite in which fitness-component deterioration stops, a phase permitted by the complete attenuation of the forces of natural selection relative to the effects of genetic drift.

The details of the way in which these researchers put forward their hypothesis to reconcile the late-life plateau in aging with existing ideas on the evolution of aging is not conceptually straightforward or easy to understand - but is interesting. As they put it:

This vision of what underlies aging may be off-putting for some, given its theoretical complexities and difficulties for experimental design. No doubt many physicists felt the same way about the destruction of the elegant late nineteenth Century version of Newtonian mechanics by the advent of relativistic and quantum mechanics, in the period from 1905 to 1945. But paradigm transitions in science are generally like that, requiring that we abandon comfortable theories in favor of those that are significantly less wrong.

It remains to be seen whether this view of aging merits comparison with the signature physics of the 20th century, but it is certainly true that a lot of new theorizing on evolution and aging is taking place these days - no doubt driven by an increasing interest in the biology of aging and the prospects of new medicine to intervene in the aging process.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Engineering Viruses to Make a Better Targeted Cancer Therapy

Some viruses show promise in terms of preferentially attacking cancer cells - but they can be engineered to be far more effective in the role of therapeutic agent: "Parvoviruses specifically kill cancer cells and are already in the clinical trial stage for treating malignant brain tumors. However, they can also infect normal cells - without doing any harm to them - so a large portion of viruses is lost during therapy. [Researchers] have now modified parvoviruses in such a way that they initially lose their ability to infect cells. In a second step, they equipped the viruses with a molecular key for infecting cancer cells. ... the researchers chose H1 parvoviruses, which normally infect rodents but are also infectious for human cells. H1 viruses kill tumor cells on the basis of their natural properties, i.e., their genetic material does not need to be modified for them to do so. ... The viruses exclusively destroy cancer cells. But with the same efficiency that they infect cancer cells, they also infect healthy cells. There they do not cause any damage and cannot replicate, but we lose a large portion of therapeutic viruses every time ... To solve this problem, the researchers [first] modified the genetic material of the virus in such a way that it loses its ability to infect cells. In a second step, this non-infectious virus was equipped with a molecular key for cancer cells. ... This is first evidence that it is basically possible to modify properties of H1 according to a plan. We will surely need several more attempts in order to target the viruses more specifically to cancer cells in the second step. We also already have ideas how to further enhance the infectious capacity and the potential to destroy cancer cells."

Link: http://www.kurzweilai.net/tailor-made-viruses-for-enhanced-cancer-therapy

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Unnatural Selection: Muscles, Genes and Genetic Cheats

Take a close look at the athletes competing in this year's Summer Olympic Games in London --their musculature will tell you a lot about how they achieved their elite status. Endless hours of training and commitment to their sport played a big role in building the bodies that got them to the world's premier athletic competition. Take an even closer look--this one requires microscopy--and you'll see something else, something embedded in the genetic blueprints of these young men and women that's just as important to their success. [More]

Add to digg
Add to StumbleUpon
Add to Reddit
Add to Facebook
Add to del.icio.us
Email this Article


Source:
http://rss.sciam.com/sciam/topic/gene-therapy

AIDS: Genetic Clues from HIV Elite Controllers Could Lead to Better Vaccines, Cancer Treatments (preview)

One day in early 1995 a man named bob massie walked into my office at the outpatient clinic of Massachusetts General Hospital in Boston. Massie told me he had been infected with HIV--the virus that causes AIDS--for 16 years and yet had never shown any symptoms. My physical examination confirmed he was healthy, in stark contrast to all other patients I saw that day. At that time, a new combination of drugs was being tested that would eventually slow the progressive decline in immune function that HIV caused. In 1995, however, most people who had been infected with HIV for a decade or more had already progressed to AIDS--the stage marked by the inability to fight off other pathogens. The young man standing before me had never taken anti-HIV medication and strongly believed that if I learned the secret to his good fortune, the information could help others to survive what was then generally thought to be a uniformly fatal disease.

[More]

Add to digg
Add to StumbleUpon
Add to Reddit
Add to Facebook
Add to del.icio.us
Email this Article


Source:
http://rss.sciam.com/sciam/topic/gene-therapy