Adcetris (Brentuximab Vedotin) Gets Conditional European Marketing Authorization

Adcetris (Brentuximab Vedotin) Gets Conditional European Marketing Authorization31 Oct 2012-nbsp;-nbsp;-nbsp;

Adcetris (Brentuximab Vedotin) has been approved in the European Union for patients with certain types of lymphoma, Millennium announced today.

Adcetris has been approved in Europe for:

Adult patients with relapsed or refractory CD30 positive Hodgkin lymphoma after ASCT (autologous stem cell transplant), or after at least two previous treatments when ASCT or chemotherapy (multi-agent) is not an option for treatment.

Adults with relapsed/refractory sALCL (systemic anaplastic large cell lymphoma).



Adcetris was approved in the USA by the Food and Drug Administration in August 2011. Takeda says it plans to launch Adcetris across Europe within the next few weeks.

CHMP (Committee for Medicinal Products for Human Use) adopted a positive opinion for conditional marketing authorization of Adcetris on 19th July, 2012, after assessing the benefit-risk ratio for the above indications.

In the European Commission (EC), granting conditional marketing authorization means the drugmaker must provide more clinical data later on to confirm that the benefits outweigh the risks.

Professor Andreas Engert, M.D., University Hospital of Cologne, Germany, said:

"Adcetris has been shown to offer a high overall response rate, including durable complete responses in both of its indications. Conditional marketing authorization by the European Commission signifies an important advancement in the treatment of adult patients with these rare CD30 positive hematological cancers who are relapsed or refractory and previously had limited options."

Trevor Smith, Head of Commercial Operations, Europe - Canada, Takeda Pharmaceuticals, said:

"The European conditional marketing authorization of Adcetris represents a significant step in Takeda's oncology franchise commitment to developing innovative medicines that make a real difference to patients' lives. Adcetris is a new targeted therapeutic option for adult patients with relapsed or refractory Hodgkin lymphoma or relapsed or refractory systemic anaplastic large cell lymphoma, and Takeda looks forward to making it available in Europe."

Millenium (part of Takeda) and Seattle Genetics are developing brentuximab vedotin jointly. Seattle Genetics has Canadian and US commercialization rights, while the Takeda Group has the rest of the world. The two companies are paying equally towards the developing costs of brentuximab vedotin, except in Japan where Takeda pays for all of it.

About Adcetris (Brentuximab Vedotin)

Adcetris (brentuximab vedotin) is an ADC (antibody-drug conjugate) consisting of an anti-CD monoclonal antibody attached by a protease-cleavable linker to a MMAE (microtubule disrupting agent, monomethyl auristatin E).

The ADC uses a linker system that makes it stable in the bloodstream while releasing MMAE upon internalization into CD30-expressing tumor cells.

In a 2010 clinical trial, 34% of participants with refractory Hodgkin Lymphoma achieved complete remission, while another 40% had partial remission. 94% of patients experienced tumor reductions. 87% of patients with ALCL experienced tumor shrinkage of at least 50%, while 97% had some kind of tumor shrinkage.

A course of treatment with Adcetris may cost up to $100,000 in the USA.

Adcetris side effects include thrombocytopenia (low blood platelet levels), peripheral sensory neuropathy (nerve damage), neutropenia (drop in white blood cells), nausea, upper respiratory infection, diarrhea, vomiting, and anemia.

What is Hodgkin Lymphoma?

Lymphoma includes several cancers that start off in the lymphatic system. There are two main lymphoma categories:

Hodgkin lymphoma - this type has one characteristic type of cell which is not present in other lymphomas; "Reed-Sternberg cells". The Reed-Sternberg cell expresses CD30.

Non-Hodgkin lymphoma



What is Anaplastic Large Cell Lymphoma (ALCL)?
ALCL is a kind of aggressive T-cell lymphoma. Between 10% and 30% of all Non-Hodgkin lymphomas in children are of this type, and approximately 3% of adults. There are two types of ALCL: 1. Primary cutaneous ALCL. 2. Systemic ALCL (sALCL).


sALCL is the more aggressive one; it is systemic and mainly involves lymph nodes and expresses CD30.

Takeda bought Millennuim for $8.8 billion in 2008.

Written by Christian Nordvist
Copyright: Medical News TodayNot to be reproduced without permission of Medical News Today

Common Drugs Could Provide A New Way To Combat Dementia

Common Drugs Could Provide A New Way To Combat Dementia31 Oct 2012-nbsp;-nbsp;-nbsp;


Medications that are used to treat conditions such as diabetes, hypertension, and skin conditions could also be used for Alzheimer's within the next 10 years. An unprecedented new study has recognized four existing drugs and one group of drugs that could potentially decrease risk, or impede symptoms of the disease.

This groundbreaking study, published in Nature Reviews Drug Discovery, is a critical component of ongoing drug discovery work which targets to speed up the process of searching for a cure or medications for dementia by specifically looking at existing treatments.

The following drugs or groups have been identified as possible Alzheimer's treatments by the study:

High blood pressure medications - from the calcium channel inhibitors family. Research suggests these drugs may considerably decrease risk of dementia. (Example: Nilvadipine)

Diabetes medication (exenatide and liraglutide) - that arouse the brain and decrease the formation of plaques on the brain. (a key characteristic of dementia)

Minocycline - a tetracycline antibiotic used to treat acne.

Acitretin - a psoriasis drug, which researchers suggest have been seen to alter the way that proteins connect to dementia structure

The investigators of this study performed a systematic review of research on existing treatments that are already approved for conditions such as high blood pressure, diabetes, and hypertension. They put into order potential treatments for future study.

These recognized drugs have multiple actions which earlier research has shown us could be successful in treating the modifications that occur in the brian during Alzheimer's disease.

More studies to further the knowledge of how these drugs function and how they could be prescribed to treat Alzheimer's is currently underway, including research into liraglutide funded by Alzheimer's Society. The current study also looks at the big opportunity to review available drugs for other conditions to find even more unused treatments for Alzheimer's disease.

Progression of new treatments for Alzheimer's can take years and cost millions. The drugs that were looked at in this study are readily available, and therefore will be less expensive and faster to modify into dementia treatments if effective.

These treatments are extremely promising, but further research is required to know specifically how they could work for people with Alzheimer's. For now, people should not take these drugs for anything else other than the conditions they are prescribed for.

Dementia is caused by brain diseases and currently affects 800,000 people in the UK. It currently has no cure, and countless clinical trials of potential dementia medications have failed.

Lead author, Professor Clive Ballard who is Director of Research at Alzheimer's Society and Professor of Age Related Diseases at King's College London, said:

"Defeating dementia is one of the biggest challenges facing both medicine and society as a whole. Developing new drugs to treat the condition is incredibly important, but comes with a huge price tag and, for those affected by dementia, an unimaginable wait. This study identifies existing treatments and shows the potential to identify other similar drugs which are safe and if effective in clinical trials could be used to treat Alzheimer's disease in 10 years or less. We are urgently working to take this work forward to start making a difference to the lives of people with dementia."

These potential new uses of common medications could enable Alzheimer's patients to live a more satisfying and fuller life.

Written by Kelly Fitzgerald

Copyright: Medical News TodayNot to be reproduced without permission of Medical News Today

Chinese Food Bean May Protect Against Sepsis

Chinese Food Bean May Protect Against Sepsis31 Oct 2012-nbsp;-nbsp;-nbsp;

A bean commonly found in Chinese food protects people against the potentially fatal condition sepsis.

The finding, published in the current issue of Evidence-based Complementary and Alternative Medicine (eCAM), came from a team of experts at The Feinstein Institute for Medical Research.

HMGB1, a deoxyribonucleic acid (DNA) protein, is responsible for regulating inflammation. Inflammation is critical in order to have good health - it is the body's way of protecting itself. Without it, infections and woulds would not be able to heal.

On the other hand, if inflammation is persistent and constant, it can cause harm to tissue and organs and eventually result in diseases, including sepsis.

Each year, an estimated 750,000 people in the United States are affected by Sepsis, costing the country's health care system almost $17 billion. Unfortunately, the disease takes the lives of 28 to 50% of those people. Previous research showed that although sepsis is the leading cause of death in U.S. hospitals, 66% of Americans reported to never had heard of the word 'sepsis'.

Sepsis results when there is a complication of an infection or injury - when chemicals are let out into the bloodstream to try to kill the infection initiate inflammation throughout the body. The organs then become harmed, including the heart, lungs, liver, kidney, and even brain.


The organs may be irreparable if they are severely damaged. For this reason, it is critical to determine ways to stop persistent and constant inflammation.


People can be protected against this inflammation that causes harm to the body's tissue and organs if the protein HMGB1 is counteracted, the team noted.


Researcher leader Haichao Wang, Ph.D., and his team, including Shu Zhu, M.D. and Ph.D., and Andrew E. Sama, M.D., discovered that a bean native to India known as mung bean (Vigna radiate), commonly used in Chinese food and conventional medicine, significantly reduced the release of this protein.

After experimenting on mice, results showed that their survival rates increased from 29.4% to 70% (P

Dr. Wang concluded:

"Many traditional medicinal herbs have been successfully developed into effective therapies for various inflammatory ailments, and now we have validated the therapeutic potential of another medicinal product, mung bean extract.

Demonstrating that mung bean extract has a positive effect on septic mice shows promise that this bean can also have a positive effect on septic humans - of course, additional studies are required to prove the safe and effective use in humans."

Written by Sarah Glynn

Copyright: Medical News TodayNot to be reproduced without permission of Medical News Today

How Do The Brain And Body Communicate To Maintain Healthy Weight?

How Do The Brain And Body Communicate To Maintain Healthy Weight?31 Oct 2012-nbsp;-nbsp;-nbsp;


A person's brain and body works together to maintain a healthy body weight using energy balance, a correspondence between calories eaten and calories burned. When this balance, which stems from an exchange between the brain's hypothalamus and neurobiological signaling, goes wrong, individuals may develop obesity or anorexia, according to a recent study conducted by researchers at BIDMC (Beth Israel Deaconess Medical Center).

Not much is known about the the workings of this complicated exchange, which is unfavorable considering the seriousness of these disorders. The new study, published in the journal Cell, has revealed new evidence which explains this complicated process.

According to a 2008 study, what we eat may actually alter the regions in the brain that maintain healthy body weight.

The report shows how the GABA neurotransmitter regulates how much energy is expended. It also helps explain how the fat-burning properties of brown fat function in neurocircuits.

Bradford Lowell, Md, PhD, a Professor of Medicine at BIDMC's Division of Endocrinology and Harvard Medical School said:

"Our group has built up a research program with the overall goal of unraveling the 'wiring diagram' by which the brain controls appetite and the burning of calories. To advance our understanding to this level, we need to know the function of specific subsets of neurons, and in addition, the upstream neurons providing input to, and the downstream neurons receiving output from, these functionally defined neurons. Until recently, such knowledge in the hypothalamus has been largely unobtainable."

The hypothalamus, an area in the brain about the size of a pearl which manages a great number of responsibilities in the body, is the control center of energy balance.

Energy balance occurs when the body sends feedback signals, which convey messages regarding the status of fuel stores, to the brain. The brain then combines this information with the input from the outside world, along with a person's emotional condition, in order to alter eating behavior and the output of energy.


During the trial, the investigators looked into a distinct population of neurons found at the bottom of the brain in the arcuate nucleus of the hypothalamus.

Lowell said, "We genetically engineered mice such that they have a specific defect that prevents these neurons from releasing the inhibitory neurotransmitter, GABA. Mice with this defect developed marked obesity and, remarkably, their obesity was entirely due to a defect in burning off calories." He continued that food consumption was completely unchanged.

Next, the experts engineered a different group of mice so that these particular neurons could be turned on when the researchers wanted them to be. Through this, they found that arcuate neurons perform by way of a sequence of neurons heading downstream, in order to prompt energy expenditure in brown fat.

Brown fat has been a topic of interest recently, due to the fact that research has unveiled that brown fat burns energy to produce heat, a process called thermogenesis.

Dong Kong, PhD, an Instructor in Medicine in Lowell's lab, commented: "Energy expenditure mediated by brown adipose tissue is critical in maintaining body weigh and prevents diet-induced obesity. Its brain-based regulatory mechanism, however, is still poorly understood. Our discovery of a hypothalamus-based neurocircuit that ultimately controls thermogenesis is an important advance."

The researchers also determined that when the neurons were activated, energy expenditure was completely reliant on the release of GABA. The findings show that when GABA is released from arcuate neurons, energy expenditure is prompted.

"Our findings have greatly advanced our understanding in the control of energy expenditure and have provided novel insights into the pathogenesis of obesity," continued Kong."

Characteristics of arcuate neurons are significant because they offer a chance to alter energy expenditure by the brain for experimental use. Neurons which receive "GABA-mediated" communication from arcuate neurons are apt to play an important part in managing energy expenditure, not food consumption.

"It is now important to fully delineate the upstream neurons that control these thermogenesis-regulating arcuate neurons, and also the downstream neurons that complete the 'circuit' to brown adipose tissue," concluded Lowell. He and his team have singled out many different kinds of neurons which act downstream of arcuate neurons, but much more evidence is necessary to completely understand this process. The work will pave the way for new opportunities for treatments of obesity and obesity-related conditions, such as heart disease and diabetes.

Written by Christine Kearney
Copyright: Medical News TodayNot to be reproduced without permission of Medical News Today

The Controversy Of The Global Malaria Program

The Controversy Of The Global Malaria Program31 Oct 2012-nbsp;-nbsp;-nbsp;

A group of 29 researchers, led by a team from the London School of Hygiene and Tropical Medicine, who evaluated a global malaria treatment subsidy - AMFm - reported in The Lancet that it has had a considerable impact in a brief space of time.

They acknowledged, however, that the program has been "highly controversial".

Oxfam, a major charity organization, last week described the Affordable Medicines Facility-Malaria as a "dangerous distraction from effective public health measures". It says that a program which was designed as a "silver bullet" to combat malaria may, in fact, be putting lives at risk.

Oxfam claims that the medications are being distributed by unqualified shopkeepers and hawkers, and not qualified health workers. Oxfam published a study titled "Salt, Sugar and Malaria pills".

The 29 researchers in this Lancet report say the scheme reduced the price of medications and led to more treatment for malaria. A large number of American experts say that the scheme should include data on outcomes.

Malaria is one of the major killers globally. Estimates for malaria mortality in May 2012 were doubled to 1.2 million deaths annually. For those who need it the most, the use of the best treatments for malaria continues to be inadequate. Experts are becoming concerned about the emergence of resistant malaria - malaria for which current treatments do not work. Some are becoming resistant to the most powerful anti-malarial drugs.

The Affordable Medicines Facility-malaria (AMFm) was launched by the Global Fund in 2010. It consists of a series of pilot programs that are applied nationally in each country, and is aimed at providing access to more people, including the use of quality-assured QAACTs (quality-assured artemisinin based combination therapies), and reduce artemisinin-alone therapies for treating malaria.

AMFm consists of the following :

Price negotiations with manufacturers
For each treatment bought, subsidies on the manufacturer price
Supporting interventions, including communications campaigns


The researchers focused on the effect of AMFm on QAACT price, availability and market share from 6 to 15 months after subsidized ACTs (artemisinin based combination therapies) were delivered in Tanzania, Uganda, Nigeria, Niger, Madagascar, Kenya and Ghana.

The authors gathered data from each country on nationally representative baseline and endpoint surveys of private and public sector outlets that kept stocks of antimalarial treatments. They used the Global Fund's quality assurance policy to identify QAACTs, while fluctuations in availability, price and market share were determined against specific efficacy benchmarks 12 months after AMFm started.

Below are some highlights of their findings:

There were large increases in QAACT availability in all pilot schemes, except for Niger and Madagascar
Market shares rose from 15.9 to 40.3 percentage points, mainly due to changes in the private-for-profit sector
Large price cuts for QAACTs per adult equivalent dose occurred in the private for-profit sector in six of the pilots. Price falls ranged from $1.28 to $4.82
Oral artemisinin monotherapy market share dropped in Nigeria and Zanzibar, the two countries where market share was over 5% at the beginning of the project


The authors concluded:

"Subsidies combined with supporting interventions can be effective in rapidly improving availability, price, and market share of QAACTs, particularly in the private for-profit sector. Decisions about the future of AMFm should also consider the effect on use in vulnerable populations, access to malaria diagnostics, and cost-effectiveness."

Counterfeit and poor quality malaria drugs, a huge problem

In sub-Saharan Africa and Southeast Asia, up to 42% of all anti-malaria drugs are either of poor quality or fake, researchers from the Fogarty International Center at the US National Institutes of Health in Bethesda, Maryland, reported in The Lancer (May 2012 issue).

The authors said that this problem is fueling the growth in drug resistant malaria.

Co-author, Dr Joel Breman, said "Poor quality antimalarial drugs are very likely to jeopardize the unprecedented progress and investments in control and elimination of malaria made in the past decade."

This latest study was funded by the Bill - Melinda Gates Foundation, and The Global Fund to Fight AIDS, Tuberculosis and Malaria.


Written by Christian Nordqvist
Copyright: Medical News TodayNot to be reproduced without permission of Medical News Today

Literacy, A Powerful Predictor To Pre-Teen Pregnancy

Literacy, A Powerful Predictor To Pre-Teen Pregnancy31 Oct 2012-nbsp;-nbsp;-nbsp;


Supporting previous research, it has been confirmed that independent of other influences, low literacy rates in pre-teen girls significantly predict child-bearing among teenagers in the US, according to a new study presented at the American Public Health Association's 140th Annual Meeting in San Francisco.

This is the first research of its kind to analyze the possible link with literacy among US pre-teens and teen child-bearing. The team of researchers, from the University of Pennsylvania, found a connection between 12,339 girls' seventh-grade reading scores enrolled in Philadelphia Public Schools, to subsequent birth records between 1996-2002.

Findings of their analysis showed that girls with less-than-average reading levels were two and a half times more likely to give birth in their earlier teens, compared with those that had average reading levels.

Twenty-one percent of girls with below-average reading levels had one live birth during the six-year examination period, while three percent of girls with below-average reading levels had two or more live births within that period.

On the other hand, only 12 percent of girls with average reading skills had one live birth and one percent had two or more live births. Of the girls with above average reading skills, five percent had one live birth and 0.4 percent had two or more live births.

This study also measured racial inconsistencies in literacy as a factor to teenage pregnancy. A higher percentage of African American and Hispanic girls had below-average reading skill group.

Also, the results of low literacy on risk of giving birth as teenagers was greater in Hispanic and African American girls than those who identified themselves as white. The authors suggest that poor reading skills in early grades are much harder to change, and foretell later decisions to quit formal education.

Rosemary Frasso, PhD, researcher at the University of Pennsylvania School of Nursing, says:

"It is quite possible that adolescent girls who experience a daily sense of rejection in the classroom might feel as though they have little chance of achievement later on in life. Our findings underscore the role of literacy as its own social risk factor throughout the life-course."

The investigators conclude that health care professionals involved with pre-teen girls should evaluate literacy when giving contraceptive and other reproductive health services to this population. Previous studies have recommended prevention programs, such as sexual health education, contraceptive use, and the distribution of free condoms in schools.

This study will appear in the February 2013 addition of Contraception.

Written by Kelly Fitzgerald

Copyright: Medical News TodayNot to be reproduced without permission of Medical News Today

Adcetris (Brentuximab Vedotin) Gets Conditional European Marketing Authorization

Adcetris (Brentuximab Vedotin) Gets Conditional European Marketing Authorization31 Oct 2012-nbsp;-nbsp;-nbsp;

Adcetris (Brentuximab Vedotin) has been approved in the European Union for patients with certain types of lymphoma, Millennium announced today.

Adcetris has been approved in Europe for:

Adult patients with relapsed or refractory CD30 positive Hodgkin lymphoma after ASCT (autologous stem cell transplant), or after at least two previous treatments when ASCT or chemotherapy (multi-agent) is not an option for treatment.

Adults with relapsed/refractory sALCL (systemic anaplastic large cell lymphoma).



Adcetris was approved in the USA by the Food and Drug Administration in August 2011. Takeda says it plans to launch Adcetris across Europe within the next few weeks.

CHMP (Committee for Medicinal Products for Human Use) adopted a positive opinion for conditional marketing authorization of Adcetris on 19th July, 2012, after assessing the benefit-risk ratio for the above indications.

In the European Commission (EC), granting conditional marketing authorization means the drugmaker must provide more clinical data later on to confirm that the benefits outweigh the risks.

Professor Andreas Engert, M.D., University Hospital of Cologne, Germany, said:

"Adcetris has been shown to offer a high overall response rate, including durable complete responses in both of its indications. Conditional marketing authorization by the European Commission signifies an important advancement in the treatment of adult patients with these rare CD30 positive hematological cancers who are relapsed or refractory and previously had limited options."

Trevor Smith, Head of Commercial Operations, Europe - Canada, Takeda Pharmaceuticals, said:

"The European conditional marketing authorization of Adcetris represents a significant step in Takeda's oncology franchise commitment to developing innovative medicines that make a real difference to patients' lives. Adcetris is a new targeted therapeutic option for adult patients with relapsed or refractory Hodgkin lymphoma or relapsed or refractory systemic anaplastic large cell lymphoma, and Takeda looks forward to making it available in Europe."

Millenium (part of Takeda) and Seattle Genetics are developing brentuximab vedotin jointly. Seattle Genetics has Canadian and US commercialization rights, while the Takeda Group has the rest of the world. The two companies are paying equally towards the developing costs of brentuximab vedotin, except in Japan where Takeda pays for all of it.

About Adcetris (Brentuximab Vedotin)

Adcetris (brentuximab vedotin) is an ADC (antibody-drug conjugate) consisting of an anti-CD monoclonal antibody attached by a protease-cleavable linker to a MMAE (microtubule disrupting agent, monomethyl auristatin E).

The ADC uses a linker system that makes it stable in the bloodstream while releasing MMAE upon internalization into CD30-expressing tumor cells.

In a 2010 clinical trial, 34% of participants with refractory Hodgkin Lymphoma achieved complete remission, while another 40% had partial remission. 94% of patients experienced tumor reductions. 87% of patients with ALCL experienced tumor shrinkage of at least 50%, while 97% had some kind of tumor shrinkage.

A course of treatment with Adcetris may cost up to $100,000 in the USA.

Adcetris side effects include thrombocytopenia (low blood platelet levels), peripheral sensory neuropathy (nerve damage), neutropenia (drop in white blood cells), nausea, upper respiratory infection, diarrhea, vomiting, and anemia.

What is Hodgkin Lymphoma?

Lymphoma includes several cancers that start off in the lymphatic system. There are two main lymphoma categories:

Hodgkin lymphoma - this type has one characteristic type of cell which is not present in other lymphomas; "Reed-Sternberg cells". The Reed-Sternberg cell expresses CD30.

Non-Hodgkin lymphoma



What is Anaplastic Large Cell Lymphoma (ALCL)?
ALCL is a kind of aggressive T-cell lymphoma. Between 10% and 30% of all Non-Hodgkin lymphomas in children are of this type, and approximately 3% of adults. There are two types of ALCL: 1. Primary cutaneous ALCL. 2. Systemic ALCL (sALCL).


sALCL is the more aggressive one; it is systemic and mainly involves lymph nodes and expresses CD30.

Takeda bought Millennuim for $8.8 billion in 2008.

Written by Christian Nordvist
Copyright: Medical News TodayNot to be reproduced without permission of Medical News Today

Common Drugs Could Provide A New Way To Combat Dementia

Common Drugs Could Provide A New Way To Combat Dementia31 Oct 2012-nbsp;-nbsp;-nbsp;


Medications that are used to treat conditions such as diabetes, hypertension, and skin conditions could also be used for Alzheimer's within the next 10 years. An unprecedented new study has recognized four existing drugs and one group of drugs that could potentially decrease risk, or impede symptoms of the disease.

This groundbreaking study, published in Nature Reviews Drug Discovery, is a critical component of ongoing drug discovery work which targets to speed up the process of searching for a cure or medications for dementia by specifically looking at existing treatments.

The following drugs or groups have been identified as possible Alzheimer's treatments by the study:

High blood pressure medications - from the calcium channel inhibitors family. Research suggests these drugs may considerably decrease risk of dementia. (Example: Nilvadipine)

Diabetes medication (exenatide and liraglutide) - that arouse the brain and decrease the formation of plaques on the brain. (a key characteristic of dementia)

Minocycline - a tetracycline antibiotic used to treat acne.

Acitretin - a psoriasis drug, which researchers suggest have been seen to alter the way that proteins connect to dementia structure

The investigators of this study performed a systematic review of research on existing treatments that are already approved for conditions such as high blood pressure, diabetes, and hypertension. They put into order potential treatments for future study.

These recognized drugs have multiple actions which earlier research has shown us could be successful in treating the modifications that occur in the brian during Alzheimer's disease.

More studies to further the knowledge of how these drugs function and how they could be prescribed to treat Alzheimer's is currently underway, including research into liraglutide funded by Alzheimer's Society. The current study also looks at the big opportunity to review available drugs for other conditions to find even more unused treatments for Alzheimer's disease.

Progression of new treatments for Alzheimer's can take years and cost millions. The drugs that were looked at in this study are readily available, and therefore will be less expensive and faster to modify into dementia treatments if effective.

These treatments are extremely promising, but further research is required to know specifically how they could work for people with Alzheimer's. For now, people should not take these drugs for anything else other than the conditions they are prescribed for.

Dementia is caused by brain diseases and currently affects 800,000 people in the UK. It currently has no cure, and countless clinical trials of potential dementia medications have failed.

Lead author, Professor Clive Ballard who is Director of Research at Alzheimer's Society and Professor of Age Related Diseases at King's College London, said:

"Defeating dementia is one of the biggest challenges facing both medicine and society as a whole. Developing new drugs to treat the condition is incredibly important, but comes with a huge price tag and, for those affected by dementia, an unimaginable wait. This study identifies existing treatments and shows the potential to identify other similar drugs which are safe and if effective in clinical trials could be used to treat Alzheimer's disease in 10 years or less. We are urgently working to take this work forward to start making a difference to the lives of people with dementia."

These potential new uses of common medications could enable Alzheimer's patients to live a more satisfying and fuller life.

Written by Kelly Fitzgerald

Copyright: Medical News TodayNot to be reproduced without permission of Medical News Today

Chinese Food Bean May Protect Against Sepsis

Chinese Food Bean May Protect Against Sepsis31 Oct 2012-nbsp;-nbsp;-nbsp;

A bean commonly found in Chinese food protects people against the potentially fatal condition sepsis.

The finding, published in the current issue of Evidence-based Complementary and Alternative Medicine (eCAM), came from a team of experts at The Feinstein Institute for Medical Research.

HMGB1, a deoxyribonucleic acid (DNA) protein, is responsible for regulating inflammation. Inflammation is critical in order to have good health - it is the body's way of protecting itself. Without it, infections and woulds would not be able to heal.

On the other hand, if inflammation is persistent and constant, it can cause harm to tissue and organs and eventually result in diseases, including sepsis.

Each year, an estimated 750,000 people in the United States are affected by Sepsis, costing the country's health care system almost $17 billion. Unfortunately, the disease takes the lives of 28 to 50% of those people. Previous research showed that although sepsis is the leading cause of death in U.S. hospitals, 66% of Americans reported to never had heard of the word 'sepsis'.

Sepsis results when there is a complication of an infection or injury - when chemicals are let out into the bloodstream to try to kill the infection initiate inflammation throughout the body. The organs then become harmed, including the heart, lungs, liver, kidney, and even brain.


The organs may be irreparable if they are severely damaged. For this reason, it is critical to determine ways to stop persistent and constant inflammation.


People can be protected against this inflammation that causes harm to the body's tissue and organs if the protein HMGB1 is counteracted, the team noted.


Researcher leader Haichao Wang, Ph.D., and his team, including Shu Zhu, M.D. and Ph.D., and Andrew E. Sama, M.D., discovered that a bean native to India known as mung bean (Vigna radiate), commonly used in Chinese food and conventional medicine, significantly reduced the release of this protein.

After experimenting on mice, results showed that their survival rates increased from 29.4% to 70% (P

Dr. Wang concluded:

"Many traditional medicinal herbs have been successfully developed into effective therapies for various inflammatory ailments, and now we have validated the therapeutic potential of another medicinal product, mung bean extract.

Demonstrating that mung bean extract has a positive effect on septic mice shows promise that this bean can also have a positive effect on septic humans - of course, additional studies are required to prove the safe and effective use in humans."

Written by Sarah Glynn

Copyright: Medical News TodayNot to be reproduced without permission of Medical News Today

How Do The Brain And Body Communicate To Maintain Healthy Weight?

How Do The Brain And Body Communicate To Maintain Healthy Weight?31 Oct 2012-nbsp;-nbsp;-nbsp;


A person's brain and body works together to maintain a healthy body weight using energy balance, a correspondence between calories eaten and calories burned. When this balance, which stems from an exchange between the brain's hypothalamus and neurobiological signaling, goes wrong, individuals may develop obesity or anorexia, according to a recent study conducted by researchers at BIDMC (Beth Israel Deaconess Medical Center).

Not much is known about the the workings of this complicated exchange, which is unfavorable considering the seriousness of these disorders. The new study, published in the journal Cell, has revealed new evidence which explains this complicated process.

According to a 2008 study, what we eat may actually alter the regions in the brain that maintain healthy body weight.

The report shows how the GABA neurotransmitter regulates how much energy is expended. It also helps explain how the fat-burning properties of brown fat function in neurocircuits.

Bradford Lowell, Md, PhD, a Professor of Medicine at BIDMC's Division of Endocrinology and Harvard Medical School said:

"Our group has built up a research program with the overall goal of unraveling the 'wiring diagram' by which the brain controls appetite and the burning of calories. To advance our understanding to this level, we need to know the function of specific subsets of neurons, and in addition, the upstream neurons providing input to, and the downstream neurons receiving output from, these functionally defined neurons. Until recently, such knowledge in the hypothalamus has been largely unobtainable."

The hypothalamus, an area in the brain about the size of a pearl which manages a great number of responsibilities in the body, is the control center of energy balance.

Energy balance occurs when the body sends feedback signals, which convey messages regarding the status of fuel stores, to the brain. The brain then combines this information with the input from the outside world, along with a person's emotional condition, in order to alter eating behavior and the output of energy.


During the trial, the investigators looked into a distinct population of neurons found at the bottom of the brain in the arcuate nucleus of the hypothalamus.

Lowell said, "We genetically engineered mice such that they have a specific defect that prevents these neurons from releasing the inhibitory neurotransmitter, GABA. Mice with this defect developed marked obesity and, remarkably, their obesity was entirely due to a defect in burning off calories." He continued that food consumption was completely unchanged.

Next, the experts engineered a different group of mice so that these particular neurons could be turned on when the researchers wanted them to be. Through this, they found that arcuate neurons perform by way of a sequence of neurons heading downstream, in order to prompt energy expenditure in brown fat.

Brown fat has been a topic of interest recently, due to the fact that research has unveiled that brown fat burns energy to produce heat, a process called thermogenesis.

Dong Kong, PhD, an Instructor in Medicine in Lowell's lab, commented: "Energy expenditure mediated by brown adipose tissue is critical in maintaining body weigh and prevents diet-induced obesity. Its brain-based regulatory mechanism, however, is still poorly understood. Our discovery of a hypothalamus-based neurocircuit that ultimately controls thermogenesis is an important advance."

The researchers also determined that when the neurons were activated, energy expenditure was completely reliant on the release of GABA. The findings show that when GABA is released from arcuate neurons, energy expenditure is prompted.

"Our findings have greatly advanced our understanding in the control of energy expenditure and have provided novel insights into the pathogenesis of obesity," continued Kong."

Characteristics of arcuate neurons are significant because they offer a chance to alter energy expenditure by the brain for experimental use. Neurons which receive "GABA-mediated" communication from arcuate neurons are apt to play an important part in managing energy expenditure, not food consumption.

"It is now important to fully delineate the upstream neurons that control these thermogenesis-regulating arcuate neurons, and also the downstream neurons that complete the 'circuit' to brown adipose tissue," concluded Lowell. He and his team have singled out many different kinds of neurons which act downstream of arcuate neurons, but much more evidence is necessary to completely understand this process. The work will pave the way for new opportunities for treatments of obesity and obesity-related conditions, such as heart disease and diabetes.

Written by Christine Kearney
Copyright: Medical News TodayNot to be reproduced without permission of Medical News Today

The Controversy Of The Global Malaria Program

The Controversy Of The Global Malaria Program31 Oct 2012-nbsp;-nbsp;-nbsp;

A group of 29 researchers, led by a team from the London School of Hygiene and Tropical Medicine, who evaluated a global malaria treatment subsidy - AMFm - reported in The Lancet that it has had a considerable impact in a brief space of time.

They acknowledged, however, that the program has been "highly controversial".

Oxfam, a major charity organization, last week described the Affordable Medicines Facility-Malaria as a "dangerous distraction from effective public health measures". It says that a program which was designed as a "silver bullet" to combat malaria may, in fact, be putting lives at risk.

Oxfam claims that the medications are being distributed by unqualified shopkeepers and hawkers, and not qualified health workers. Oxfam published a study titled "Salt, Sugar and Malaria pills".

The 29 researchers in this Lancet report say the scheme reduced the price of medications and led to more treatment for malaria. A large number of American experts say that the scheme should include data on outcomes.

Malaria is one of the major killers globally. Estimates for malaria mortality in May 2012 were doubled to 1.2 million deaths annually. For those who need it the most, the use of the best treatments for malaria continues to be inadequate. Experts are becoming concerned about the emergence of resistant malaria - malaria for which current treatments do not work. Some are becoming resistant to the most powerful anti-malarial drugs.

The Affordable Medicines Facility-malaria (AMFm) was launched by the Global Fund in 2010. It consists of a series of pilot programs that are applied nationally in each country, and is aimed at providing access to more people, including the use of quality-assured QAACTs (quality-assured artemisinin based combination therapies), and reduce artemisinin-alone therapies for treating malaria.

AMFm consists of the following :

Price negotiations with manufacturers
For each treatment bought, subsidies on the manufacturer price
Supporting interventions, including communications campaigns


The researchers focused on the effect of AMFm on QAACT price, availability and market share from 6 to 15 months after subsidized ACTs (artemisinin based combination therapies) were delivered in Tanzania, Uganda, Nigeria, Niger, Madagascar, Kenya and Ghana.

The authors gathered data from each country on nationally representative baseline and endpoint surveys of private and public sector outlets that kept stocks of antimalarial treatments. They used the Global Fund's quality assurance policy to identify QAACTs, while fluctuations in availability, price and market share were determined against specific efficacy benchmarks 12 months after AMFm started.

Below are some highlights of their findings:

There were large increases in QAACT availability in all pilot schemes, except for Niger and Madagascar
Market shares rose from 15.9 to 40.3 percentage points, mainly due to changes in the private-for-profit sector
Large price cuts for QAACTs per adult equivalent dose occurred in the private for-profit sector in six of the pilots. Price falls ranged from $1.28 to $4.82
Oral artemisinin monotherapy market share dropped in Nigeria and Zanzibar, the two countries where market share was over 5% at the beginning of the project


The authors concluded:

"Subsidies combined with supporting interventions can be effective in rapidly improving availability, price, and market share of QAACTs, particularly in the private for-profit sector. Decisions about the future of AMFm should also consider the effect on use in vulnerable populations, access to malaria diagnostics, and cost-effectiveness."

Counterfeit and poor quality malaria drugs, a huge problem

In sub-Saharan Africa and Southeast Asia, up to 42% of all anti-malaria drugs are either of poor quality or fake, researchers from the Fogarty International Center at the US National Institutes of Health in Bethesda, Maryland, reported in The Lancer (May 2012 issue).

The authors said that this problem is fueling the growth in drug resistant malaria.

Co-author, Dr Joel Breman, said "Poor quality antimalarial drugs are very likely to jeopardize the unprecedented progress and investments in control and elimination of malaria made in the past decade."

This latest study was funded by the Bill - Melinda Gates Foundation, and The Global Fund to Fight AIDS, Tuberculosis and Malaria.


Written by Christian Nordqvist
Copyright: Medical News TodayNot to be reproduced without permission of Medical News Today

Literacy, A Powerful Predictor To Pre-Teen Pregnancy

Literacy, A Powerful Predictor To Pre-Teen Pregnancy31 Oct 2012-nbsp;-nbsp;-nbsp;


Supporting previous research, it has been confirmed that independent of other influences, low literacy rates in pre-teen girls significantly predict child-bearing among teenagers in the US, according to a new study presented at the American Public Health Association's 140th Annual Meeting in San Francisco.

This is the first research of its kind to analyze the possible link with literacy among US pre-teens and teen child-bearing. The team of researchers, from the University of Pennsylvania, found a connection between 12,339 girls' seventh-grade reading scores enrolled in Philadelphia Public Schools, to subsequent birth records between 1996-2002.

Findings of their analysis showed that girls with less-than-average reading levels were two and a half times more likely to give birth in their earlier teens, compared with those that had average reading levels.

Twenty-one percent of girls with below-average reading levels had one live birth during the six-year examination period, while three percent of girls with below-average reading levels had two or more live births within that period.

On the other hand, only 12 percent of girls with average reading skills had one live birth and one percent had two or more live births. Of the girls with above average reading skills, five percent had one live birth and 0.4 percent had two or more live births.

This study also measured racial inconsistencies in literacy as a factor to teenage pregnancy. A higher percentage of African American and Hispanic girls had below-average reading skill group.

Also, the results of low literacy on risk of giving birth as teenagers was greater in Hispanic and African American girls than those who identified themselves as white. The authors suggest that poor reading skills in early grades are much harder to change, and foretell later decisions to quit formal education.

Rosemary Frasso, PhD, researcher at the University of Pennsylvania School of Nursing, says:

"It is quite possible that adolescent girls who experience a daily sense of rejection in the classroom might feel as though they have little chance of achievement later on in life. Our findings underscore the role of literacy as its own social risk factor throughout the life-course."

The investigators conclude that health care professionals involved with pre-teen girls should evaluate literacy when giving contraceptive and other reproductive health services to this population. Previous studies have recommended prevention programs, such as sexual health education, contraceptive use, and the distribution of free condoms in schools.

This study will appear in the February 2013 addition of Contraception.

Written by Kelly Fitzgerald

Copyright: Medical News TodayNot to be reproduced without permission of Medical News Today

Common Drugs Could Provide A New Way To Combat Dementia

Common Drugs Could Provide A New Way To Combat Dementia31 Oct 2012-nbsp;-nbsp;-nbsp;


Medications that are used to treat conditions such as diabetes, hypertension, and skin conditions could also be used for Alzheimer's within the next 10 years. An unprecedented new study has recognized four existing drugs and one group of drugs that could potentially decrease risk, or impede symptoms of the disease.

This groundbreaking study, published in Nature Reviews Drug Discovery, is a critical component of ongoing drug discovery work which targets to speed up the process of searching for a cure or medications for dementia by specifically looking at existing treatments.

The following drugs or groups have been identified as possible Alzheimer's treatments by the study:

High blood pressure medications - from the calcium channel inhibitors family. Research suggests these drugs may considerably decrease risk of dementia. (Example: Nilvadipine)

Diabetes medication (exenatide and liraglutide) - that arouse the brain and decrease the formation of plaques on the brain. (a key characteristic of dementia)

Minocycline - a tetracycline antibiotic used to treat acne.

Acitretin - a psoriasis drug, which researchers suggest have been seen to alter the way that proteins connect to dementia structure

The investigators of this study performed a systematic review of research on existing treatments that are already approved for conditions such as high blood pressure, diabetes, and hypertension. They put into order potential treatments for future study.

These recognized drugs have multiple actions which earlier research has shown us could be successful in treating the modifications that occur in the brian during Alzheimer's disease.

More studies to further the knowledge of how these drugs function and how they could be prescribed to treat Alzheimer's is currently underway, including research into liraglutide funded by Alzheimer's Society. The current study also looks at the big opportunity to review available drugs for other conditions to find even more unused treatments for Alzheimer's disease.

Progression of new treatments for Alzheimer's can take years and cost millions. The drugs that were looked at in this study are readily available, and therefore will be less expensive and faster to modify into dementia treatments if effective.

These treatments are extremely promising, but further research is required to know specifically how they could work for people with Alzheimer's. For now, people should not take these drugs for anything else other than the conditions they are prescribed for.

Dementia is caused by brain diseases and currently affects 800,000 people in the UK. It currently has no cure, and countless clinical trials of potential dementia medications have failed.

Lead author, Professor Clive Ballard who is Director of Research at Alzheimer's Society and Professor of Age Related Diseases at King's College London, said:

"Defeating dementia is one of the biggest challenges facing both medicine and society as a whole. Developing new drugs to treat the condition is incredibly important, but comes with a huge price tag and, for those affected by dementia, an unimaginable wait. This study identifies existing treatments and shows the potential to identify other similar drugs which are safe and if effective in clinical trials could be used to treat Alzheimer's disease in 10 years or less. We are urgently working to take this work forward to start making a difference to the lives of people with dementia."

These potential new uses of common medications could enable Alzheimer's patients to live a more satisfying and fuller life.

Written by Kelly Fitzgerald

Copyright: Medical News TodayNot to be reproduced without permission of Medical News Today

Chinese Food Bean May Protect Against Sepsis

Chinese Food Bean May Protect Against Sepsis31 Oct 2012-nbsp;-nbsp;-nbsp;

A bean commonly found in Chinese food protects people against the potentially fatal condition sepsis.

The finding, published in the current issue of Evidence-based Complementary and Alternative Medicine (eCAM), came from a team of experts at The Feinstein Institute for Medical Research.

HMGB1, a deoxyribonucleic acid (DNA) protein, is responsible for regulating inflammation. Inflammation is critical in order to have good health - it is the body's way of protecting itself. Without it, infections and woulds would not be able to heal.

On the other hand, if inflammation is persistent and constant, it can cause harm to tissue and organs and eventually result in diseases, including sepsis.

Each year, an estimated 750,000 people in the United States are affected by Sepsis, costing the country's health care system almost $17 billion. Unfortunately, the disease takes the lives of 28 to 50% of those people. Previous research showed that although sepsis is the leading cause of death in U.S. hospitals, 66% of Americans reported to never had heard of the word 'sepsis'.

Sepsis results when there is a complication of an infection or injury - when chemicals are let out into the bloodstream to try to kill the infection initiate inflammation throughout the body. The organs then become harmed, including the heart, lungs, liver, kidney, and even brain.


The organs may be irreparable if they are severely damaged. For this reason, it is critical to determine ways to stop persistent and constant inflammation.


People can be protected against this inflammation that causes harm to the body's tissue and organs if the protein HMGB1 is counteracted, the team noted.


Researcher leader Haichao Wang, Ph.D., and his team, including Shu Zhu, M.D. and Ph.D., and Andrew E. Sama, M.D., discovered that a bean native to India known as mung bean (Vigna radiate), commonly used in Chinese food and conventional medicine, significantly reduced the release of this protein.

After experimenting on mice, results showed that their survival rates increased from 29.4% to 70% (P

Dr. Wang concluded:

"Many traditional medicinal herbs have been successfully developed into effective therapies for various inflammatory ailments, and now we have validated the therapeutic potential of another medicinal product, mung bean extract.

Demonstrating that mung bean extract has a positive effect on septic mice shows promise that this bean can also have a positive effect on septic humans - of course, additional studies are required to prove the safe and effective use in humans."

Written by Sarah Glynn

Copyright: Medical News TodayNot to be reproduced without permission of Medical News Today

How Do The Brain And Body Communicate To Maintain Healthy Weight?

How Do The Brain And Body Communicate To Maintain Healthy Weight?31 Oct 2012-nbsp;-nbsp;-nbsp;


A person's brain and body works together to maintain a healthy body weight using energy balance, a correspondence between calories eaten and calories burned. When this balance, which stems from an exchange between the brain's hypothalamus and neurobiological signaling, goes wrong, individuals may develop obesity or anorexia, according to a recent study conducted by researchers at BIDMC (Beth Israel Deaconess Medical Center).

Not much is known about the the workings of this complicated exchange, which is unfavorable considering the seriousness of these disorders. The new study, published in the journal Cell, has revealed new evidence which explains this complicated process.

According to a 2008 study, what we eat may actually alter the regions in the brain that maintain healthy body weight.

The report shows how the GABA neurotransmitter regulates how much energy is expended. It also helps explain how the fat-burning properties of brown fat function in neurocircuits.

Bradford Lowell, Md, PhD, a Professor of Medicine at BIDMC's Division of Endocrinology and Harvard Medical School said:

"Our group has built up a research program with the overall goal of unraveling the 'wiring diagram' by which the brain controls appetite and the burning of calories. To advance our understanding to this level, we need to know the function of specific subsets of neurons, and in addition, the upstream neurons providing input to, and the downstream neurons receiving output from, these functionally defined neurons. Until recently, such knowledge in the hypothalamus has been largely unobtainable."

The hypothalamus, an area in the brain about the size of a pearl which manages a great number of responsibilities in the body, is the control center of energy balance.

Energy balance occurs when the body sends feedback signals, which convey messages regarding the status of fuel stores, to the brain. The brain then combines this information with the input from the outside world, along with a person's emotional condition, in order to alter eating behavior and the output of energy.


During the trial, the investigators looked into a distinct population of neurons found at the bottom of the brain in the arcuate nucleus of the hypothalamus.

Lowell said, "We genetically engineered mice such that they have a specific defect that prevents these neurons from releasing the inhibitory neurotransmitter, GABA. Mice with this defect developed marked obesity and, remarkably, their obesity was entirely due to a defect in burning off calories." He continued that food consumption was completely unchanged.

Next, the experts engineered a different group of mice so that these particular neurons could be turned on when the researchers wanted them to be. Through this, they found that arcuate neurons perform by way of a sequence of neurons heading downstream, in order to prompt energy expenditure in brown fat.

Brown fat has been a topic of interest recently, due to the fact that research has unveiled that brown fat burns energy to produce heat, a process called thermogenesis.

Dong Kong, PhD, an Instructor in Medicine in Lowell's lab, commented: "Energy expenditure mediated by brown adipose tissue is critical in maintaining body weigh and prevents diet-induced obesity. Its brain-based regulatory mechanism, however, is still poorly understood. Our discovery of a hypothalamus-based neurocircuit that ultimately controls thermogenesis is an important advance."

The researchers also determined that when the neurons were activated, energy expenditure was completely reliant on the release of GABA. The findings show that when GABA is released from arcuate neurons, energy expenditure is prompted.

"Our findings have greatly advanced our understanding in the control of energy expenditure and have provided novel insights into the pathogenesis of obesity," continued Kong."

Characteristics of arcuate neurons are significant because they offer a chance to alter energy expenditure by the brain for experimental use. Neurons which receive "GABA-mediated" communication from arcuate neurons are apt to play an important part in managing energy expenditure, not food consumption.

"It is now important to fully delineate the upstream neurons that control these thermogenesis-regulating arcuate neurons, and also the downstream neurons that complete the 'circuit' to brown adipose tissue," concluded Lowell. He and his team have singled out many different kinds of neurons which act downstream of arcuate neurons, but much more evidence is necessary to completely understand this process. The work will pave the way for new opportunities for treatments of obesity and obesity-related conditions, such as heart disease and diabetes.

Written by Christine Kearney
Copyright: Medical News TodayNot to be reproduced without permission of Medical News Today

Literacy, A Powerful Predictor To Pre-Teen Pregnancy

Literacy, A Powerful Predictor To Pre-Teen Pregnancy31 Oct 2012-nbsp;-nbsp;-nbsp;


Supporting previous research, it has been confirmed that independent of other influences, low literacy rates in pre-teen girls significantly predict child-bearing among teenagers in the US, according to a new study presented at the American Public Health Association's 140th Annual Meeting in San Francisco.

This is the first research of its kind to analyze the possible link with literacy among US pre-teens and teen child-bearing. The team of researchers, from the University of Pennsylvania, found a connection between 12,339 girls' seventh-grade reading scores enrolled in Philadelphia Public Schools, to subsequent birth records between 1996-2002.

Findings of their analysis showed that girls with less-than-average reading levels were two and a half times more likely to give birth in their earlier teens, compared with those that had average reading levels.

Twenty-one percent of girls with below-average reading levels had one live birth during the six-year examination period, while three percent of girls with below-average reading levels had two or more live births within that period.

On the other hand, only 12 percent of girls with average reading skills had one live birth and one percent had two or more live births. Of the girls with above average reading skills, five percent had one live birth and 0.4 percent had two or more live births.

This study also measured racial inconsistencies in literacy as a factor to teenage pregnancy. A higher percentage of African American and Hispanic girls had below-average reading skill group.

Also, the results of low literacy on risk of giving birth as teenagers was greater in Hispanic and African American girls than those who identified themselves as white. The authors suggest that poor reading skills in early grades are much harder to change, and foretell later decisions to quit formal education.

Rosemary Frasso, PhD, researcher at the University of Pennsylvania School of Nursing, says:

"It is quite possible that adolescent girls who experience a daily sense of rejection in the classroom might feel as though they have little chance of achievement later on in life. Our findings underscore the role of literacy as its own social risk factor throughout the life-course."

The investigators conclude that health care professionals involved with pre-teen girls should evaluate literacy when giving contraceptive and other reproductive health services to this population. Previous studies have recommended prevention programs, such as sexual health education, contraceptive use, and the distribution of free condoms in schools.

This study will appear in the February 2013 addition of Contraception.

Written by Kelly Fitzgerald

Copyright: Medical News TodayNot to be reproduced without permission of Medical News Today

Brain Can't Empathize And Analyze At Same Time, New Study

Brain Can't Empathize And Analyze At Same Time, New Study31 Oct 2012-nbsp;-nbsp;-nbsp;


Scientists have discovered that the brain circuits we engage when we think about social matters, such as considering other people's views, or moral

issues, inhibit the circuits that we use when we think about inanimate, analytical things, such as working on a physics problem or making sure the numbers add

up when we balance our budget. And they say, the same happens the other way around: the analytic brain network inhibits the social network.

Perhaps the study, led by researchers at Case Western Reserve University in Cleveland, Ohio, in the US, and reported early online on 27 October in the journal

NeuroImage, explains why some business leaders sometimes overlook the public relations consequences of their cost-cutting exercises.

The authors suggest their findings help increase understanding of disorders like autism, ADHD and schizophrenia.


Empathic and Analytic Thinking are Mutually Exclusive

The study is believed to be the first to show that humans have a built in neural constraint that stops us thinking empathically and analytically at the same

time.

When not doing anything in particular, our brains switch between social and analytic networks. But, when working on a goal-directed task, healthy adults

engage the appropriate neural pathways, say the researchers.

Lead author Anthony Jack, an assistant professor of cognitive science at Case Western Reserve, says in a news blog on the university's website, that "this is the

cognitive structure we've evolved":

"Empathetic and analytic thinking are, at least to some extent, mutually exclusive in the brain," says Jack.


Two Networks in Tension

Before this study, from previous research, scientists already thought there were two large networks in the brain that were in tension, one called the default mode

network and the other called the task positive network. However, there are different views on what drives them.

One view proposes that one network is deployed in goal-directed tasks, and when this happens, the other one allows the mind to wander.

Another view proposes that one network engages in external attention, while the other is for internal attention.

The new study suggests a new explanation: both networks focus on external stimuli, but one is for social problems and the other is for analytical problems, and

when the one concerned with one type of problem is engaged, the neural pathways for the other type are repressed.



The Study

For their study, Jack and colleagues recruited 45 healthy volunteers, all college students.

The participants each spent 10 minutes at a time inside a fMRI brain scanner while a screen in front of them presented them with random selections of 20 written

and 20 video problems where they had to think about how other people might feel, and another random selection of 20 written and 20 video problems where

they had to use knowledge of physics to solve.

After reading a written problem or viewing a video one, each participant then had to give a yes or no answer to a question within 7 seconds.

During each session in the scanner, the participants also underwent rest periods lasting 27 seconds, and there were also various timed delays between each test,

some lasting 1 second, others lasting 3 or 5 seconds. During the rest breaks the participants were asked to relax and look at a red cross on the screen.

The Results

When they examined the results of the fMRI brain scans, the researchers found that when the participants were presented with social problems, the brain regions

associated with analytical thinking were deactivated and the regions associated with empathy and social thinking were active.

And this was also the same the other way around: when presented with physics questions, the analytic regions were active and the empathy regions were

inactivated.

These findings were the same for written and video versions of problems.

But when the participants were in the resting state, that is not challenged to solve any problems, the activity cycled naturally between the two

networks.

"This tells us that it's the structure of the adult brain that is driving this, that it's a physiological constraint on cognition," says Jack.

The Explanatory Gap

Jack says the study was inspired by one of the eternal philosophical questions surrounding the nature of cosciousness:

"Why can we describe the workings of a brain, but that doesn't tell us what it's like to be that person?"

Something that intrigues scientists interested in this field is what they call the "explanatory gap", which Jack describes as the "disconnect between experiential

understanding and scientific understanding".

He explains how in 2006 he and Philip Robbins, an associate professor of philosophy at the University of Missouri, boldly proposed that the explanatory gap is

driven by our neural structure.

Looking back on that time after completing this new study, Jack says, "I was genuinely surprised to see how powerfully these findings fit that theory".

Perceptual Rivalry

The results from this latest study appear to suggest that the same brain mechanisms drive the explanatory gap as that which become engaged when we look

at a visual illusion known as the "duck-rabbit", a drawing that can be seen in one of two ways. When you look at it you either see a duck facing one way or a rabbit

facing the other way, but you never see both at the same time.

Jack says that phenomenon is known as "perceptual rivalry", which occurs because of neural inhibition between the two representations.

"What we see in this study is similar, but much more wide-scale. We see neural inhibition between the entire brain network we use to socially, emotionally and

morally engage with others, and the entire network we use for scientific, mathematical and logical reasoning," he explains.

He suggests this means scientific explanations "really do leave something out - the human touch".

Jack says a major challenge for scientists of the mind is how better to translate between the "cold and distant mechanical descriptions that neuroscience

produces, and the emotionally engaged intuitive understanding which allows us to relate to one another as people".


Implications

The researchers suggest their findings have implications for a number of disorders that have a social dysfunction component, from anxiety, depression and

ADHD to schizophrenia.

They propose their ideas are particularly relevant to development disabilities such as autism and Williams syndrome. For instance autistic people tend to be very

good at solving visuospatial problems, but have poor social skills. And people with Williams syndrome are the other way around: they come across as warm and

friendly, but don't do well on visuospatial tests.

"Treatment needs to target a balance between these two networks," suggests Jack.

Current methods, including rehabilitation and education, appear to work mostly on strengthening the analytic network.

"Yet, we found more cortex dedicated to the social network," says Jack.






Written by Catharine Paddock PhD








Copyright: Medical News TodayNot to be reproduced without permission of Medical News Today

SMi's Lyophilisation Conference - Freeze-Drying In Pharmaceuticals And Biopharmaceuticals, 25-26 February 2013, London

Enormous Potential For Digital Healthcare Services - Interview With Alexander Schachinger

Roche Under More Pressure To Release Tamiflu Trial Data

Roche Under More Pressure To Release Tamiflu Trial Data31 Oct 2012-nbsp;-nbsp;-nbsp;

The makers of Tamiflu (oseltamivir), Roche, should honor their promise made nearly three years ago and release trial data on Tamiflu for independent scrutiny, R. Fiona Godlee, BMJ Editor-in-Chief has urged.

Dr. Godlee wrote in an open letter to Professor Sir John Bell, company director "Billions of pounds of public money have been spent on (Tamiflu) and yet the evidence on its effectiveness and safety remains hidden from appropriate and necessary independent scrutiny."

EMA (European Medicines Agency) has already initiated infringement proceedings against Roche to investigate failures in the reporting of safety data, which includes not releasing 80,000 reports on adverse drug reactions.

An open letter was also published in The Times (of London), urging pharmaceutical companies to "come clean" and release all clinical trial data on drugs that are currently used so that healthcare professionals have open access. Dr. Godlee, along with 27 others signed the letter.

British politicians are also beginning to apply pressure. Sarah Wollaston, a GP and Conservative MP (Member of Parliament), brought up the issue of missing data in Parliament. Norman Lamb, UK Health Minister has agreed to meet experts and talk about the issue of access to clinical trial data.

After a major investigation by the BMJ, in December 2009, Roche publicly pledged to release full clinical trial data on Tamiflu (oseltamivir), its antiviral medication. The BMJ investigation was carried out by Tom Jefferson and Peter Doshi from the Cochrane Collaboration.

According to the investigation, there is no compelling evidence demonstrating that Tamiflu prevents pneumonia, or other complications in healthy people. The authors expressed serious concern regarding access to drug data, the use of ghost writers in human trials, and the drug approval process.

The Cochrane investigators say they have received some further data from Roche, but as yet, not the full set as promised.

At least 123 clinical trials involving Tamiflu have been carried out, the Cochrane reviewers say. However, about 60% of patient data from Roche Phase 3 completed treatment trials have not yet been released.

The reviewers are concerned about "the likely overstating of effectiveness and the apparent under-reporting of potentially serious adverse effects."

Tamiflu has made a lot of money for Roche. It is included in the WHO (World Health Organization) list of "essential medicines".

Dr. Godlee urges Professor Bell:

"..to bring your influence to bear on your colleagues on Roche's board. In refusing to release these data of enormous public interest, you put Roche outside the circle of responsible pharmaceutical companies. Releasing the data would do a great deal to restore confidence in your company and its board of directors."

Professor Bell responded, saying he has referred the matter to Roche and awaits a response.

In an Accompanying Editorial, Dr. Godlee explains that the open correspondence "aims to hold specific individuals and organizations to account. Their actions are preventing independent scrutiny of the results of clinical trials and putting patients' lives at risk. We also hope it will contribute to a sea change in the public mood."

Last week, bmj.com asked who people thought is mainly at fault for denying access to negative clinical trial results. 569 respondents voted as follows:

Pharma - 69%
Regulators - 13.5%
Legislators - 9%

The BMJ says it has plans to launch further campaigns urging more openness in clinical trial results.
Dr. Godlee's open letter is published alongside correspondence by the Cochrane team with Roche, the CDC (Centers for Disease Control and Prevention, USA), and WHO, as part of an open data campaign urging Roche to provide doctors and patients access to complete data on Tamiflu.
Written by Christian Nordqvist
Copyright: Medical News TodayNot to be reproduced without permission of Medical News Today

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Accurate HIV Sensor Ten Times Cheaper Than Any Other

Accurate HIV Sensor Ten Times Cheaper Than Any Other30 Oct 2012-nbsp;-nbsp;-nbsp;

Scientists have developed an ultra-sensitive sensor for doctors to detect viral infections, such as HIV, as well as cancers in their early stages, with the naked eye.

The researchers, from Imperial College London, reported on their prototype sensor in Nature Nanotechnology.

According to the authors, their sensor is ten times more sensitive at measuring biomarkers than anything available today for current gold standard practice.

The sensors are extremely cheap and easy to use, and will be useful in countries where sophisticated equipment is in short supply.

The prototype's great advantages are twofold:

Price - it costs about one tenth of anything else on the market today.

It can detect diseases early on, so that patients can be treated in the early stages.



Cheap saliva tests are already available for detecting HIV infection. However, they can only detect the virus when blood concentrations are high.

A trial was carried out to see how well the sensor could detect p24 in blood samples. P24 is a biomarker which points towards HIV infection.

Professor Molly Stevens, who works at the Department of Materials and Bioengineering, Imperial College London, said:

"It is vital that patients get periodically tested in order to assess the success of retroviral therapies and check for new cases of infection. Unfortunately, the existing gold standard detection methods can be too expensive to be implemented in parts of the world where resources are scarce.

Our approach affords for improved sensitivity, does not require sophisticated instrumentation and it is ten times cheaper, which could allow more tests to be performed for better screening of many diseases."

They also tested for PSA (Prostate Specific Antigen), a biomarker which is commonly used for helping doctors diagnose prostate cancer.

It is possible to reconfigure the sensor, the scientists say, so that it can be used for detecting other diseases and viruses.

The prototype sensor analyzes serum, derived from blood, which is placed in a disposable container. Serum is a clear fluid derived from blood samples.

If the marker is present in the serum, it alters the course of a chemical reaction. If the samples contain p24, a chemical reaction takes place which makes tiny gold particles clump together irregularly, giving a distinctive blue color to the solution in the container. If PSA or p24 levels are not abnormal, the nanoparticles separate into little balls, creating a reddish color.

In both cases, positive and negative results, the reactions in the container can be seen with the naked eye - all you have to do is look at the color of the liquid.

Even in cases where HIV infected patients had low viral loads of p24, the sensor detected them - this is not possible with existing tests, such as ELISA (Enzyme-linked Immunosorbent Assay), nor with the nucleic acid based test.

Co-author, Dr. Roberto de la Rica, said that their prototype will hopefully be able to detect previously undetectable HIV infections and indicators of cancer. If people can be diagnosed sooner and treated sooner, their prognosis improves considerably. Dr de la Rica said "this could pave the way for more widespread use of HIV testing in poorer parts of the world."

The team will be looking for funding from not-for-profit global health organizations. Their aim is to enable low income countries to have access to this extremely economical and accurate sensor.

Written by Christian Nordqvist
Copyright: Medical News TodayNot to be reproduced without permission of Medical News Today

New Strategy To Prevent Ear Infections From Recurring

New Strategy To Prevent Ear Infections From Recurring30 Oct 2012-nbsp;-nbsp;-nbsp;

Recurrence of middle ear infection can be prevented by boosting levels of antimicrobial proteins that are already there, as well as eliminating bacteria's DNA


The finding came from a team in The Research Institute at Nationwide Children's Hospital who set out to observe how an immune defense protein commonly found in the middle ear communicates with a structure that secures a community of bacteria.


The bacterium is called nontypeable Haemophilus influenza (NTHI) and is responsible for a variety of diseases of both the lower and upper airways, such as middle ear infection.


Similar to other microorganisms, NTHI can create a strong colony of bacteria, known as a biofilm. This permits the bacteria to avoid the person's immune system, while keeping safe from antibiotics and other treatments that try to destroy them.


Gram-positive and Gram-negative bacteria can be killed by an antimicrobial defense protein, called human beta-defensin-3, that is expressed in the middle ear of humans and other mammals. According to prior studies, the host's ability to control the bacteria in the upper airway changes if the expression of beta-defensis is disrupted, and the infection gets even worse.


Human beta-defensin-3 might lose its strength to destroy NTHI if it gets stuck within the extracellular DNA that makes up a biofilm's outer layer, stopping its connection with bacteria within the biofilm, the team hypothesized.


Lauren O. Bakaletz, Ph.D., director of the Center for Microbial Pathogenesis, explained:
"Antimicrobial host defense proteins, like human beta-defensin-3, have been shown to bind to non-host DNA. This interaction has an impact on the defense protein's ability to function."


While analyzing the animal model of middle ear infection, Dr. Bakaletz and his colleagues discovered that in the biofilms that were created during infection, the animal's defense peptides and bacterial DNA were found together. The team also realized that the defense peptide was mainly co-localized with the extracellular DNA of the biofilm.


When a concentration of human-beta defensin-3, which is normally found in a child's middle ear with an active infection, was released to the bacteria that cause ear infections, the peptide destroyed 100% of the NTHI. However, the destruction ended when extracellular DNA was presented to the response.



"These data support the conclusion that the killing activity of the antimicrobial defense protein was decreased in an NTHI-induced biofilm due to its interaction with eDNA," said Dr. Bakaletz, leading author and professor of Pediatrics and Otolaryngology at The Ohio State University College of Medicine.


After taking away the extracellular DNA from the biofilm, the team found that it recovered the killing activity of the defense peptide.

"The ability to restore antimicrobial defense protein activity is encouraging, since biofilms are resistant to most treatments, including traditional antibiotics," Dr. Bakaletz said.


This research should encourage scientists to create a new treatment regimen that can aim for biofilms created by NTHI during middle ear infection.

One strategy may be to disrupt bacertial DNA by administering a therapeutic agent along with human beta-defensin-3 to the middle ear of a child with chronic, recurrent infection. The same pathway could be used that doctors use to target the middle ear during ear tube surgery (a therapy for chronic ear infections).


Dr. Bakaletz concluded:
"This approach would likely bolster the ability of the innate immune system to manage NTHI-induced biofilms, avoiding the need for antibiotics or empowering the use of antibiotics we already have in our arsena. Doing so could help diminish the recurrent nature of middle ear infection."

Written by Sarah Glynn
Copyright: Medical News TodayNot to be reproduced without permission of Medical News Today

ALS Treatment Target Found With Help From Yeast

ALS Treatment Target Found With Help From Yeast30 Oct 2012-nbsp;-nbsp;-nbsp;

With the help of baker's yeast, a tiny one-celled organism, scientists in the US say they have found a "chink in the armor" of the currently incurable

disease Amyotrophic Lateral Sclerosis (ALS), also known as Lou Gehrig's disease. They suggest their finding offers a new target for therapies, bringing fresh

hope to patients with a devastatingly cruel disorder that robs them of the ability to move, speak and in the end, breathe.

The researchers write about their discovery in the 28 October online issue of Nature Genetics.

Co-senior author Aaron Gitler is an associate professor in the department of genetics at Stanford University School of Medicine in California. He says in a press

statement:

"Even though yeast and humans are separated by a billion years of evolution, we were able to use the power of yeast genetics to identify an unexpected

potential drug target for ALS."


Protein Clumps

Many disorders like ALS, Parkinson's and Alzheimer's that gradually destroy the brain, show a particular type of clumping or misfolding of proteins in the

cytoplasm of brain cells or neurons (the cytoplasm being the internal gel that holds the various components of cells). The protein clumping or misfolding is

thought either to cause or contribute to the disease.

"We are trying to figure out why these proteins aggregate in neurons in the brain and spinal cord, and what happens when they do," explains Gitler.

While the cause of ALS is not clear, recent studies suggest an RNA-binding protein called TDP-43 may play a role. In many people with ALS, the protein forms

clumps inside neurons of the spinal cord, and some people with ALS also have mutations in this protein.

The Value of a Yeast Model

Previous work by Gitler and another study author, Robert Farese Jr, a senior investigator at the Gladstone Institutes in San Francisco, California, shows it is

possible to mimic ALS in yeast by expressing TDP-43 at higher levels than normal: the result is the protein forms deadly clumps in the cytoplasm of the

yeast cells.

Gitler explains the value of the yeast model:

"In humans, the progression of the disease can take years before symptoms arise. But in yeast, we see protein clumping in the cytoplasm within two days and

the cells rapidly begin to die."

Having developed the yeast model, Gitler and Farese decided to see if changing the behavior of some of the other proteins in the cell could protect the yeast cells

from the clumping damage.

What They Found

After tinkering with various proteins in the yeast cells, the researchers eventually found blocking the production of a protein called Dbr1, an enzyme involved in

RNA processing, prevented the clumping that results from TDP-43 over-expression, allowing the cells to lead a normal existence.

Farese says they went about their search systematically: they made no prior assumptions about how TDP-43 injures cells, but instead "screened the whole yeast

genome to find genes that might prevent the toxicity".

He says his lab and Gitler's lab came to the same conclusion about Dbr1 independently.

They then tested and proved blocking Dbr1 worked by repeating the results in lab-cultured human nerve cells and in rat neurons over-expressing TDP-43.


Mopping Up Excess TDP-43

The researchers found that blocking Dbr1 causes a buildup of "lariats" in the cytoplasm. These are unwanted "loops" of RNA left over from coding DNA into

proteins. Dbr1 cuts open the loops to make it easier for the cellular clean up tools to take them away for disposal and recycling.

Blocking Dbr1 causes uncut lariats to accumulate, which appear to mop up the excess TDP-43 so it doesn't form clumps. The researchers proved this was the

case by creating lariats with a binding site for a fluorescent tracking protein.

First author Maria Armakola, also of the department of genetics at Stanford's School of Medicine, says normally TDP-43 stays in the nucleus, but in diseased cells

it collects in the cytoplasm and forms clumps.

"We developed a novel way to track where these lariats go in living cells, and we saw that when Dbr1 is missing, the lariats act as a sink to sequester TDP-

43," she explains.


Treatment Targets

The researchers aren't exactly sure what is causing the cells to die in ALS: is it because the defective TDP-43 pulls essential RNA molecules that should be busy

helping to read DNA to make proteins out of the nucleus into the cytoplasm, or because the defectiive TDP-43 is not working as it should, which is to bind to

RNA in the nucleus? Perhaps it's a bit of both, they suggest.

Whichever it is, because of the promising results from the yeast, human and rodent cell experiments, the researchers recommend more studies should now

investigate the potential for blocking Dbr1, or creating artificial lariats to snare the defective TDP-43, as a potential target for drugs to treat

ALS.

Armakola says they now want to look at what happens when you block Dbr1 in flies, worms and rodents.

"We're also interested in identifying small molecule inhibitors of Dbr1," she adds.



Written by Catharine Paddock PhD









Copyright: Medical News TodayNot to be reproduced without permission of Medical News Today

Babies Born To Mothers After Bariatric Surgery Have Healthier Hearts

Babies Born To Mothers After Bariatric Surgery Have Healthier Hearts30 Oct 2012-nbsp;-nbsp;-nbsp;


Investigators have found that babies born to obese mothers who lost weight after bariatric surgery have less cardiovascular risk factors compared to siblings born before the surgery.

The bodily changes and weight loss that occur as a result of the surgery, positively effect inflammatory disease-related genes in the offspring, according to new research presented at the Canadian Cardiovascular Congress, co-hosted by the Heart and Stroke Foundation and the Canadian Cardiovascular Society.

The authors found that maternal obesity affects the genes of the offspring. Therefore, these characteristics can be changed to better impact the child. Eliminating obesity in the mother can lead to a favorable health outcome for the offspring.

This study focused on epigenetics, how our genes turn on and off by environmental factors. The new part of this study is the fact that scientists explored how these changes can influence the DNA of our children, without having to alter the DNA sequence.

How Can Two Different People With The Same DNA Have Different States Of Health?

Originally, it was thought that DNA structure caused genetic variation. However, now we know that genes can be expressed, and several processes can influence them to turn on or off.

One of these processes causes small molecules to bind to DNA. These molecules are made by one's own body and their binding to DNA is regulated by the environment (from food or toxins).

Molecules called methyl groups are responsible for turning genes on and off, a process known as DNA methylation. This process alters the gene expression but does not change the gene sequence. Normally, more methylation means a gene is turned off and less means it is turned on.

Maternal obesity can lead to significant pediatric obesity through genetic, environmental and epigenetic influences. Obesity while pregnant increases the likelihood of the offspring to develop lifelong weight problems and increases risk of heart disease.

Children Born To Non-Obese Mothers Show Improvements In Health

Bariatric surgeons and researchers at Laval University have discovered that children born after their mother had weight loss surgery, called bilio-pancreatic bypass surgery, were less likely to be obese, had better insulin resistance, lower blood pressure, and a decrease in risk for cardiovascular disease.

Dr. Frédéric Guénard, a post-doctoral fellow under the supervision of Dr. Marie-Claude Vohl of the Functional Food Institute at Laval University and a recipient of a Heart and Stroke Foundation Research Fellowship, and his team of researchers decided to investigate as to why there is an improvement in heart disease risk.

They took blood samples from 25 children of 20 mothers who were born before their mothers underwent the bilio-pancreatic bypass surgery, and blood samples from 25 of their siblings who were born after the surgery.

The children ranged in age from 2 to 24 years. The average BMI of the mothers was 45 before weight loss surgery and 27 after. Bariatric surgery is recommended for people with a BMI of 40 or greater, or a BMI of 35 or greater combined with conditions such as diabetes and are of low surgical risk.

DNA from the blood samples was tested using the Infinium HumanMethylation450 BeadChip to identify any alterations in the genes caused by methylation.

The researchers found that the methylation levels were extremely different in the children born to mothers before bypass surgery from those who were born after.

Particularly, the authors found that more than 5,500 known genes with differential methylation in the babies born before their mothers underwent surgery compared to children born after the surgery.

Dr. Guénard says:

"Our findings show that maternal bariatric surgery results in significant metabolic effects to the methylation profiles of inflammatory disease-related genes. The bariatric surgery and weight loss experienced by the mothers created an in utero environment that favorably changed the gene methylation levels of the fetus."

In simple words, this study shows that maternal obesity affects the weight and cardiovascular risk of children. Therefore, weight loss can better the cardiovascular health of children.

Heart and Stroke Foundation spokesperson Dr. Beth Abramson explains:

"We know our genetic makeup influences our children's risks, but so can our environment. For example, if a disease runs in a family, we know to watch out for it in the children as they age. This study shows that external factors also influence our risk for heart disease, and that of our offspring by switching genes on or off in our DNA; providing a glimpse as to why this occurs. This is why lifestyle behaviors are so important."

Dr. Abramson and Dr. Guénard both say this study verifies how important it is to maintain a healthy weight during all stages of life. More genetics studies are recommended to examine if weight loss can change the methylation profile of the genes of children of mothers who have lost weight by other means.

Written by Kelly Fitzgerald
Copyright: Medical News TodayNot to be reproduced without permission of Medical News Today