For the first time, thought and opinion leaders from two of the world's leading centers of aesthetic surgery, Brazil and the United States, will be meeting to share scientific updates, procedural knowledge and clinical information at the inaugural American-Brazilian Aesthetic Meeting.

Faculty for the meeting includes some of the most recognized names in organized plastic surgery from two continents, including:

- Ricardo Riberio, MD, Brazil, Meeting Co-Chair
Plastic Surgeon from Rio de Janiero, Brazil
- Renato Saltz, MD, Meeting Co-Chair and President-Elect, American Society for Aesthetic Plastic Surgery -- Plastic Surgeon from Park City, UT
- Jose Carlos Sampaio Goes, MD, Past-President, International Society of Aesthetic Plastic Surgery
Plastic Surgeon from Sao Paulo, Brazil
- Alan Gold, MD, President, the American Society for Aesthetic Plastic Surgery
Plastic Surgeon from Great Neck, NY
- Foad Nahai, MD, President, International Society of Aesthetic Plastic Surgery and Past-President, the American Society for Aesthetic Plastic Surgery -- Plastic Surgeon from Atlanta, GA
- Mark Jewell, MD, Past-President, the American Society for Aesthetic Plastic Surgery
Plastic Surgeon from Eugene, OR

The attendees for the meeting includes residents, fellows, nurses, aestheticians and physicians from the US, South America, Europe and Asia. The topics include aesthetic surgery, cosmetic medicine, patient safety (a full morning), breast and skin cancer reconstruction -- all related to aesthetic plastic surgery. The meeting is endorsed/sponsored by the American Society for Aesthetic Plastic Surgery (http://www.asaps.org) and the International Society of Aesthetic Plastic Surgery (http://www.isaps.org).

Researchers in the US studying mice with and without amyloid-beta plaques in their brains (the plaques that are characteristic of Alzheimer's disease) found that contrary to current thinking, the plaques don't just damage the neurons they are close to but may well affect signalling in other parts of the brain through their influence on extensive networks of astrocyte brain cells.

The study was the work of researchers from the MassGeneral Institute for Neurodegenerative Disease (MGH-MIND) at Massachusetts General Hospital in Charlestown, and is published in the 27 February online issue of Science.

Simply speaking, mammals have two main types of brain cell: neurons that send electrical and chemical signals and glia cells that support, control, and look after them. An astrocyte is a type of star-shaped glia cell that not only provides passive support to neurons, but as scientists discovered in the 1990s, they also send signals using calcium ions that move from cell to cell like waves, and these waves can travel a long way in the brain.

Astrocytes are found everywhere in the brain and they account for about half the volume of it.

Plaques are left over bits of cell that clump together and stick to neurons, disrupting their ability to send signals; they are more common in older brains and one of the hallmarks of Alzheimer's disease.

The authors explained in their background information that although we already know that senile plaques disrupt the neurons they stick to (focal disruption), we don't know much about how astrocytes behave in Alzheimer's disease. With this study they showed that senile plaques make astrocytes hyperactive; not just the ones nearby, but also others quite far away from the focal neuron site.

Lead author Kishore Kuchibhotla of MGH-MIND told the press:

"Our work suggests that amyloid plaques might have a more complex role in altering brain function than we had thought."

"Plaques develop rapidly and have been shown to cause relatively acute, localized neuro-toxicity," he added, explaining that their work shows astrocytes "could provide a network mechanism that may stretch the impact of plaques to more distant areas of the brain."

For this study Kuchibhotla and colleagues used a method called "multiphoton fluorescence lifetime imaging microscopy" to measure and trace the calcium waves travelling along astrocyte networks in the brains of gentically altered laboratory mice with and without some of the hallmarks of Alzheimer's disease, such as the amyloid-beta plaques. (Using a dye they "labelled" astrocytes so that when they were active they lit up and when they switched off they went dark).

They found that resting calcium levels were high throughout the astrocyte network in mice with plaques, not just where they happened to be near individual plaques.

Using time-lapsed images they found that changes in calcium waves in astrocytes were more frequent and synchronized across long distances and uncoupled from what was happening near the neurons.

The researchers also found some rare calcium waves travelling between cells: these were only present in mice with amyloid-beta plaques and the waves appeared to start near plaques and spread radially from them for at least 200 micrometers.

They concluded that:

"Although neurotoxicity is observed near amyloid-[beta] deposits, there exists a more general astrocyte-based network response to focal pathology."

Kuchibhotla said that:

"This is the first clear evidence in a live animal model that amyloid plaques perturb calcium signaling across the astrocyte network via a neuron-independent mechanism."

"It has been suggested that these intercellular calcium waves, which previously had been observed only in response to some sort of external stimulus, indicate the existence of or response to a traumatic insult," he added, explaining that while their results support this idea, what we still don't know is whether the calcium signals they observed actually protect or harm cells.

"We've only begun to scratch the surface of how plaque deposition impacts astrocyte function," said Kuchibhotla.

An important question for future research will be how the increased activity of astrocytes affects the ways neurons work, and another will be whether it increases or limits the formation of plaques.

An on-line training module for GP's and healthcare professionals to increase awareness of Parkinson's disease, has attracted over 3,000 participants from as far away as New Zealand.

Parkinsons' Disease Society's (PDS) 2007 membership survey showed that 50% of people with Parkinson's believed there was a lack of understanding from GP's and professionals about how to spot and treat the condition.

As a result the PDS commissioned BMJ Learning to produce an on-line module to help users increase their knowledge and skills in how to care for patients, and how to increase knowledge and skills to assess and refer people with suspected Parkinson's Disease.

Daiga Heisters, PDS National Education Adviser, comments:

"We were delighted with the response to the training. The target of 400 participants to complete the module in the first 6 months was exceeded with over 3,000 completing in the first 5 months. This reflects the interest health care professionals have in increasing their knowledge on the management of Parkinson's and the effectiveness of BMJ Learning's marketing campaign".

Alveena Igbal, from Derby City PCT who took the course, said:

"As our elderly population increases so does the challenge to deal with chronic disabling conditions like Parkinsonism. In this context I have found the BMJ Learning module very useful."

Dr Amal Paul from Pudsey, Leeds, adds:

'' As a G.P. I have to look after a few patients with Parkinson's disease, and the need for further care management was more imperative for me when someone close to me was diagnosed. The module was very interesting, designed for adult learning, interactive, and educational. My knowledge and skills have definitely improved and the module was a big impetus for further study''.

This module complements the work of the PDS Education Training Officers currently working with GPs and other healthcare professionals throughout the UK at a local level.

Due to the success of the pilot, a second learning module is being launched, focusing on non- motor symptoms of Parkinson's such as depression and sleep disorders.

Scientists from the US and Australia are using cells from yeast and mammals to learn about how environment and genes affect whether a person gets Parkinson's disease or not.

Many aspects of the way yeast cells work are the same in animal and human cells, and since it is only possible to get hold of cells diseased with Parkinson's after a person is dead, having a similar more easily accessible cell to work with helps scientists study the early development of the disease and scan and test the thousands of genes that might be involved.

One such example is the subject of a study published this week in Nature Genetics, where Antony Cooper from Sydney's Garvan Institute of Medical Research in Australia and colleagues have for the first time found a way to connect three pieces of the Parkinson's disease jigsaw: sensitivity to manganese, and the behaviour of two genes, alpha-synuclein and PARK9 (also known as ATP13A2).

Alpha-synuclein and PARK9 have already been separately associated with forms of Parkinson's, and manganese poisoning can cause Parkinson-like symptoms in miners and welders exposed to high levels of the metal.

Parkinson's disease is where neurons that produce the neurotransmitter dopamine degenerate, and scientists have also known for some time that this is associated with an overexpression of the protein alpha-synuclein which autopsies have found in abundance in affected regions of the brain.

A European team also previously found that PARK9, already known to be involved in a hereditary form of Parkinson's, was in much greater abundance in the brains of people who had died of sporadic (ie not inherited) forms of the disease compared to the same parts of the brain in people who did not have the disease.

Cooper suspects that PARK9 was actually protecting the neurons and may explain why many of them surrounded by PARK9 survived.

What Cooper and colleagues found was that PARK9 appears also to diminish the toxic effects of alpha-synuclein, and it may also act as a manganese pump that is potentially capable of removing excess amounts of the metal from cells.

Cooper and colleagues were able to study the effect of PARK9 in yeast because it contains an equivalent gene.

An important and puzzling question in Parkinson's research is whether there is a single or cluster of genetic factors that cause the degeneration of neurons that produce dopamine.

As Cooper explained:

"We would love to be able to link all the genes that we know have something to do with Parkinson's disease."

"If you discover there's a central pathway involved, it provides much better potential for finding a successful treatment," he added, explaining that so far they have linked PARK9, alpha-synuclein and manganese, and this is no coincidence.

"They're likely to be affecting a pathway and we suspect it's a central pathway. To confirm that would be very exciting indeed," said Cooper.

Cooper has been working for some years, with co-authors Dr Susan Lindquist, from the Whitehead Institute for Biomedical Research and Dr Aaron Gitler, from the University of Pennsylvania School of Medicine, to find how alpha-synuclein might cause cell damage.

They teamed up with associate professor Guy Caldwell, of the University of Alabama, and associate professor Jean-Christophe Rochet from the University of Purdue in Indiana, to check their results using other models of Parkinson's disease.

In the most extensive review of cancer patterns among an American Indian tribal group, Roswell Park Cancer Institute (RPCI) researchers analyzed cancer patterns within the Seneca Nation of Indians for the period from 1955 through 2004. The study, led by Arthur Michalek, PhD, FACE, Senior Vice President for Educational Affairs, and Martin C. Mahoney, MD, PhD, Associate Professor of Oncology, Departments of Medicine and Health Behavior, RPCI, was published in a recent issue of the journal Cancer.

The retrospective study examined patterns of cancer incidence in 3,935 males and 4,193 females who were registered tribal members of the Seneca Nation of Indians. Cancer incidence rates were based on data collected through a computer match with the New York State Cancer Registry.

"Among the unique strengths of this study was the reliance on tribal roll books to identify enrolled tribal members and the ability to conduct a comprehensive study over 50 years, leading to the accrual of more than 120,000 person-years of observation. These parameters helped to overcome the issue of limited-sized populations, which has challenged studies among American Indian tribal groups in the past," said Dr. Michalek. "Additionally, the leaders of the Seneca Nation demonstrated their trust in Roswell Park researchers and a commitment to the health of their members by allowing researchers access to information required for this comprehensive analysis."

The study that found overall, no specific type of cancer was significantly elevated - and, in fact, both male and female tribal members demonstrated significantly reduced incidences for all cancers combined. Additionally, no specific age group showed significantly elevated incidence. A total of 233 primary cancers were diagnosed among Seneca males, with colorectal (20%) and prostate cancers (17%) the most common. Among female members, 256 cancers were diagnosed, with lung (20%) and breast cancer (16%) reported as the most common malignancies.

Dr. Mahoney continued, "Cancer remains a relatively rare diagnosis among tribal members, which places some limitation on the interpretation of these results. However, these unique cancer patterns are of extraordinary value to the Seneca Nation leaders as they determine health policy and cancer prevention strategies."