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Jun 24
Smoking Linked To Brain Damage, New Study
Research led by scientists in India suggests there is a direct link between smoking and brain damage whereby a compound in tobacco that turns into a cancer-causing chemical once it has been through the body's metabolism, triggers white blood cells in the brain's immune system to attack healthy brain cells.

The study is the work of lead investigators Debapriya Ghosh and Dr Anirban Basu from the Indian National Brain Research Center (NBRC) and was published online on 2 June in the Journal of Neurochemistry.

NNK is a procarcinogen commonly found in tobacco. A procarcinogen is a chemical that becomes cancer-causing (carcinogenic) once it has been metabolised in the body.

While alcohol and many drugs used by drug abusers damages brain cells directly, the researchers believe NNK damages brain cells indirectly, by first causing inflammation in brain cells, similar to that which leads to disorders like Multiple Sclerosis.

For the study, Ghosh, Basu and colleagues carried out two types of test: one in the test tube and the other in live mice ( in vitro and in vivo).

Using a technique called Western blot analysis they showed that treatment with NNK led to significant increases in signalling and effector proteins that promote inflammation, as well as other stress-related proteins. They also found increased levels of proinflammatory cytokines, compounds that help cells communicate with each other.

The researchers suggest the NNK caused the brain's immune cells or microglia, which normally only destroy damaged or unhealthy cells, to overreact and attack healthy cells.

"Immunohistochemical staining of the brain sections of NNK-treated mice reveals massive microglial and astrocyte activation along with distinct foci of neuronal damage," they wrote and concluded that:

"Both in vitro and in vivo results provide strong indication that NNK causes significant upheaval of the inflammatory condition of brain and inflicts subsequent neuronal damage."

Basu said these findings prove that:

"Tobacco compound NNK can activate microglia significantly which subsequently harms the nerve cells."

NNK passes into the body not just through smoking tobacco, it can also pass into the body from chewing tobacco.

Second hand smoking or so called "passive" smoking is another way that NNK can enter the body since it is present in tobacco smoke. A smoke-filled room may contain as much as 26 nanograms of NNK, which is on a par with the amount of NNK found in cigarettes which ranges from 20 to 310 nanograms, said the authors.

Ghosh said this research helps us understand one way that people who smoke or consume tobacco regularly might end up with damaged nerve or brain cells.

According to research cited by the National Cancer Institute (NCI) and the US Centers for Disease Control and Prevention (CDC), cigarette smoke contains about 4,000 chemical agents, including over 60 carcinogens, many of which are also poisonous in their own right (eg carbon monoxide, tar, arsenic, and lead).

Jun 23
DNA Template Could Explain Evolutionary Shifts
Rearrangements of all sizes in genomes, genes and exons can result from a glitch in DNA copying that occurs when the process stalls at a critical point and then shifts to a different genetic template, duplicating and even triplicating genes or just shuffling or deleting part of the code within them, said researchers from Baylor College of Medicine in a recent report in the journal Nature Genetics. The report further elucidated the effect of the fork stalling and template switching mechanism involved in some forms of copy number variation.

"I think this is going to make people think very hard about copy number variation with respect to genome evolution, gene evolution and exon shuffling," said Dr. James R. Lupski, vice chair of molecular and human genetics at BCM and senior author of the report.

The mechanism not only represents a newly discovered method by which the genome generates copy number variation among genes, but it also demonstrates that copy number variation can occur at a different time in the life of a cell. DNA replication takes place as the cell is dividing and becoming two - a process known as mitosis.

Copy number variation involves structural changes in the human genome that result in the deletion of genes or parts of them or extra copies of genes. Often, this process is associated with disease or with evolution of the genome itself.

DNA (deoxyribonucleic acid) exists as two complementary strands that remain together because of the attraction between nucleotides. A, or adenine, is always attracted to T, or thymine. C, or cytosine, is always attracted to G, or guanine.

When a cell divides, it must reproduce its DNA so that each cell that results from the division has the same genetic code. That means it must replicate its DNA. During this process, an enzyme called a helicase separates the two strands, breaking the hydrogen bonds between the A - T and G - C base pairs. The two separating strands become the replication fork. On one strand, an enzyme called DNA polymerase reads the genetic material in the strand as a template and makes a strand of complementary DNA to pair to it. Again, the code is A to T and C to G. This process is continuous. On the lagging strand, the complementary strand is made in short, separated segments by a process that involves RNA and a series of enzymes.

Until the 1990s, researchers studying reasons for genetic mutations or changes looked at molecular "typos" in this process, tiny changes in the As, Ts, Cs or Gs called single nucleotide polymorphism (SNPs). They changed the message of the gene. However, in the early 1990s, Lupski was one of the early champions of a newly discovered mechanism in which the structure of the DNA itself was grossly duplicated or deleted to change numbers of copies of a gene that occurred in the genetic material. This "copy number variation" wrote a new chapter in the understanding of human genetic variation.

In a previous report, Lupski and colleagues described how the process that copies DNA during cell division stalls when there is a problem with the genetic material. In some cases, the process seeks a different template, often copying another similar but significantly different stretch of DNA before it switches back to the appropriate area.

In this newer report, Lupski and colleagues describe how this process - called fork stalling and template switching (FoSTeS) in humans or microhomology-mediated break-induced replication (MMBIR) in simpler models - generated genomic rearrangements ranging in size from several megabases to a few hundred base pair during normal cell division, resulting in the duplication or even triplications of individual genes or the rearrangements of single exons (the coding region of genes).

"This phenomenon occurs throughout the genome," said Dr. Feng Zhang, a postdoctoral associate in Lupski's laboratory and the first author of the report.

In studies of subjects with abnormalities in the gene associated with Charcot-MarieTooth type 1A (PMP22), the researchers found that the fork stalling, template switching phenomenon explained the changes, from those that involved triplication of a gene to others that resulted from shuffling within an exon.

Studies of one family - two children and a mother - demonstrated that the event occurred during mitosis or cell division, a significant finding that further confirms the significance of the event.

The researchers noted that finding this mitotic rearrangement of the gene in the mother, who did not have the disorder, of two children with a neuropathy suggests that the mechanism might be considered in genetic counseling about the risk of having another child with the disorder.

The scientists wrote, "We propose that FoSTeS/MMBIR may be a key mechanism for generating structural variation, particularly nonrecurrent CNV (copy number variation), of the human genome. "

The observation of mosaicism for an apparent mitotically generated, FoSTeS/MMBIR-mediated complex PMP22 rearrangement in the unaffected mother of two children with neuropathy suggests this mechanism can have implications for genetic counseling regarding recurrence risk.

Jun 23
Fate In Fly Sensory Organ Precursor Cells Could Explain Human Immune Disorder
Notch signaling helps determine the fate of a number of different cell types in a variety of organisms, including humans. In an article that appears in the current issue of Nature Cell Biology, researchers at Baylor College of Medicine report that a new finding about the Notch signaling pathway in sensory organ precursor cells in the fruit fly could explain the mystery behind an immunological disorder called Wiskott-Aldrich syndrome.

"This finding provides a model for how Wiskott Aldrich syndrome - a form of selective immunodeficiency in children - occurs," said Dr. Hugo Bellen, professor of molecular and human genetics and director of the Program in Developmental Biology at BCM. He is also a Howard Hughes Medical Institute investigator.

It all begins with the Notch pathway, which controls cell fate.

In the fly peripheral nervous system, two daughter cells arise from a single sensory organ precursor mother cell. Among the daughter cells, Notch is activated in one and not in the other. This differential activation of signaling results in two different kinds of cells which arise from the same mother cell. Thus the fruit flies sensory organ precursor cell division has been used as a model to understand how Notch signaling is activated during asymmetric cell division.

In a screen of fruit fly mutants that have disrupted peripheral nervous system development, Akhila Rajan and An-chi Tien, two graduate students in Bellen's laboratory, identified a mutant with a cluster of neurons. This occurs when there is a problem in Notch signaling.

Ordinarily, the sensory organ progenitor cell uses the Notch pathway to specify the fate of two daughter cells called pIIa and pIIb, which arise from a single mother cell. The pIIa cells go on to become the shaft and socket cells on the exterior of the fly's external sensory organ. The pIIb, through two divisions, become the neuron and sheath - internal cells of the external sensory organ. These four types of cells become the sensory cluster.

When a cluster of neurons is observed, cell fate determination has gone wrong as too many cells of one kind are being made from the mother cell. Akhila and An-chi found that mutations in the Actin-related protein 3 (Arp3), a component of the seven protein Arp2/3 complex, resulted in the loss of Notch signaling.

This occurs because the ligand Delta - a protein that activates the Notch pathway - cannot travel properly within the sensory organ cells in the absence of Arp3 protein. In addition, they found that under normal conditions vesicles (tiny bubbles) containing the Notch activating protein Delta travel to the top of the daughter cell to a structure rich in actin. This specialized actin structure contains many membrane protrusions that increase the surface area of cells called microvilli. Under normal circumstances Delta containing vesicles traffic to the microvilli. In the Arp3 mutants, there are significantly fewer microvilli but, more important, the transport of Delta is compromised in Arp3 mutants, affecting the ability of Delta to activate Notch. This is an important part of their work.

"Normally, Delta is presented at the top of the actin structure," said Bellen. It is then encapsulated in the vesicles and travels to the basal, or bottom, of the structure. Delta then travels back to the top of the daughter cells.

Bellen and colleagues have found that the Arp2/3 complex and its activator WASp (Wiskott-Aldrich syndrome protein) function in these daughter cells to transport Delta vesicles to the apical region of the daughter cells. If this complicated trafficking of Delta does not occur, the ability of Delta to activate Notch is compromised.

"It is likely that whatever we have discovered here has a relationship to what is happening in the patients with Wiskott-Aldrich syndrome. The patients with Wiskott-Aldrich syndrome have mutations in a gene called WASp. WASp is an activator of the Arp2/3 complex. In our work we found that WASp is also required for the trafficking of Delta to the top of the actin structure," said Bellen.

Notch signaling is required for proper development, differentiation and activation of a class of immune cells called the T-cells. T-cell function is compromised in patients with Wiskott-Aldrich syndrome. Since the gene WASp is mutated in the patients with Wiskott-Aldrich syndrome, the work done by Bellen and his colleagues suggest that defects in the presentation of Delta could explain the loss and dysfunction of T-cells in patients with Wiskott-Aldrich syndrome.

Jun 23
London Surgeon Pioneering Scarless Abdominal Surgery Using Belly Button
A London surgeon is pioneering a new way to remove abdominal organs through the belly button using an approach called single incision laparoscopic surgery (SILS) which requires only a 10 mm cut in the navel to allow entry of a camera and all the surgical instruments and through which organs like the appendix and gall bladder can be removed.

Imperial College Healthcare NHS Trust consultant surgeon Paraskevas Paraskeva, who also lectures at Imperial College London, is the first UK surgeon to use SILS to remove an appendix and a gall bladder.

Before SILS the organs were removed using three cuts in the torso, as well as the belly button, which leaves the patient with abdominal scars.

But SILS uses only one 10 mm "single access port" through which the surgical instruments and a camera are inserted, and through which the excised organ is removed and then the belly button is sewn up.

The procedure takes about 20 minutes for an appendix and an hour for a gall bladder, and the patient generally goes home on the same day. Paraskeva said in a statement last month that:

"This technique further minimises minimally invasive surgery."

"Having a single access port minimises the discomfort to the patient, reduces the risk of infection and because the incision is through the belly button, the surgery is scarless," he added.

SILS is the product of research carried out by Paraskeva and his team at the department of biosurgery and surgical technology at Imperial College London.

Aberdeen Royal Infirmary (ARI) in Scotland has also been using SILS to remove appendices and gall bladders. They started to use the procedure after learning about urologists at the Cleveland clinic in the USA using it to remove part of a kidney and also after hearing about Paraskeva's work at Imperial College London.

ARI's consultant surgeon Irfan Ahmed said that when he offered this method to his patients they were "excited by the idea and delighted with the cosmetic results after surgery".

He said:

"Single-incision laparoscopic surgery still needs to be studied in an academic setting before it becomes widely available."

Ahmed said he thinks SILS will replace traditional laparoscopic procedures performed by surgeons and gynaecologists in selected conditions.

"I see it happening routinely in the next two years," he said.

Consultant general surgeon Geoffrey Glazer, who is based at Wellington Hospital in London, told the BBC that as well as helping with the healing process, SILS was a "technological step forward" which might appeal to people who don't want scars on their abdomen.

He said other methods are also being developed to remove organs through existing orifices so that extra incisions don't have to be made.

One such method for example uses the rectum as the "access port", but this carries a higher risk of contamination.

Jun 20
Indian Medical Travel Association (IMTA) launched
Indian Hospitals, Wellness and Medical Tourism players join forces to make India the Global Healthcare Destination - Indian Medical Travel Association (IMTA) launched.

Leading Indian Hospitals, Healthcare providers (both Modern Medicine and Traditional Indian Medicine), Travel and Medical Tourism Industry providers have come together to form an industry association - Indian Medical Travel Association (IMTA) that aims to work together to make India the leading global healthcare destination.

The phenomenon now popularly known as Medical Tourism is often cited as the next big opportunity for India after the IT outsourcing to earn billions of dollars in forex earnings and create jobs in the healthcare sector. So far only a select group of Indian hospitals have been making valiant attempts to market their services in international arena. More than a million overseas patients already treated at top Indian corporate hospitals like Apollo, Fortis, Wockhardt, Max, Manipal and many others have already proved to the world that the clinical quality, technology and cost proposition offered by India is unmatched. The capacity in super specialty segment Indian hospitals is expanding fast and there is no waiting period for local or overseas patients.

CII Mc'Kinsey study first reported on medical tourism as the billion dollar opportunity for India way back in 2002 and the steady growth in overseas patient arrivals has validated the potential. With a large number of new private super specialty hospitals and even integrated health cities coming up in India's top ten cities, India has the potential to become the global leader in the Medical Travel/ Outsourcing industry. Indian doctors and professionals are world renowned for their skills and the country has abundance of all the inputs like talented young manpower, local high quality manufacturing base for pharmaceuticals, technology hardware and software that makes the Indian costs for high end surgical procedures so attractive. The challenge really is on the non medical side, primarily on the marketing front and also to create infrastructure and services to support the growth of medical tourism.

Indian Medical Travel Association (IMTA) - a non profit body and a unified voice of the Indian healthcare (modern medicine as well as traditional Indian medicine) and travel industry is aimed at preparing India for facing the challenges of global competition and actualise the tremendous opportunity for India to become a leading global healthcare destination. Modern medicine as well as India's 5000 year old traditional therapies like Ayurveda, Siddha and Yoga can offer to the world an unbeatable healing package.

"IMTA would strive to help its members reach out in a cost effective manner to millions of our potential global consumers who reside on the other side of the globe in a different time and cultural zone and make them aware of the tremendous value that Indian healthcare offers. The fact is that prior to choosing a hospital, the international patients first decide on the country or the destination. Therefore we all must join hands to aggressively promote INDIA as a preferred global healthcare destination," Says Pradeep Thukral, Executive Director, Indian Medical Travel Association (IMTA)

The Government of India and its various arms are actively supporting the growth of medical tourism to India. Two years ago the Government of India introduced a special category of Visa called M Visa for foreigners desirous of coming to India for medical treatment. India's Ministry of Tourism has achieved phenomenal success in last five years with its much acclaimed "Incredible India "campaign that has multiplied the arrival of foreign tourists to India. The current year 2009 is being promoted by Indian Ministry of Tourism as "Visit India'" year and the ministry is keen to promote Medical Tourism. It has recently notified the Market Development Assistance (MDA) Scheme to eligible Medical Tourism players which enables them to get financial support for participation in overseas promotional events.

About Indian Medical Travel Association.

A non profit body aimed at preparing India for facing the challenges of global competition in Medical Tourism space and actualise the tremendous opportunity for India to become a leading global healthcare destination. IMTA's membership has a diverse base of India's leading JCI, NABH accredited hospitals, Indian System of Medicine and Wellness service providers, travel industry, Insurance, Assistance and Medical Tourism facilitation companies.

For more details please contact :-

Mr Pradeep Thukral,

Executive Director,

Indian Medical Travel Association

Phone : 91 9810907151

Website :

Jun 18
Regular Exercise And A Healthy Diet Build Stronger Bones
June is National Osteoporosis Month and health experts from NHS Somerset are urging people to look after their bones by living well and eating well.

Osteoporosis is a disease where the inner honeycomb structure inside each bone becomes thinner and more fragile. It can affect any part of our body but the wrist, hip and spine are the most common areas.

Every bone in your body is alive - new cells are being created all the time to replace older ones - but when we are young this process tends to work faster enabling the skeleton to increase in density and strength.

The best way to build up your bones is by doing exercise and eating a healthy diet. During childhood, adolescence and early adulthood, when the skeleton is growing, you can 'bank' plenty of bone which puts the skeleton in a better position to hold out against the natural bone loss that occurs later in life.

Rachel Levenson, Associate Director of Nursing and Patient Safety for NHS Somerset said: "Your skeleton will grow stronger if you do regular weight-bearing exercise such as jogging, aerobics, tennis, dancing and brisk walking.

"As you get older, you may need to be careful of vigorous, high impact exercise but it's still very important to stay active and find something you enjoy doing. Swimming, gardening, walking or golf can all help reduce your risk of falling and breaking a bone," said Ms Levenson.

She added: "Eating a normal varied diet of bread, potatoes, fruit and vegetables, milk, meat, fish and foods containing fat and sugar will provide all you need to maintain a healthy skeleton. Our bodies contain 1kg of calcium, 99% of which is stored in our bones so we need to make sure our diet includes calcium-rich foods as well as other vitamins and minerals.

"If you can, try to give up smoking and reduce your alcohol intake. Don't let your weight drop too low - being overweight is not good for general health but being underweight increases the risk of broken bones when you fall.

Ms Levenson said: "Many older people fall in the home, so it is important to try and reduce the hazards that could cause you to trip and fall. Make sure you take your time using stairs and hold onto the rail. Tidy up any loose rugs or carpets, trailing wires, slippery floor surfaces and anything else that might cause you to fall over."

As you get older ask for help if feel you are at risk of falling or falling frequently. A referral to a physiotherapist may be helpful for advice about exercises to help with balance and co-ordination.

Jun 18
What Is Swine Flu? How Is Swine Flu Treated?
Swine flu (swine influenza) is a disease of pigs. It is a highly contagious respiratory disease caused by one of many Influenza A viruses. Approximately 1% to 4% of pigs that get swine flu die from it. It is spread among pigs by direct and indirect contact, aerosols, and from pigs that are infected but do not have symptoms. In many parts of the world pigs are vaccinated against swine flu.

Most commonly, swine flu is of the H1N1 influenza subtype. However, they can sometimes come from the other types, such as H1N2, H3N1, and H3N2.

The current outbreak of swine flu that has infected humans is of the H1N1 type - this type is not as dangerous as some others.
Avian Influenza (Bird Flu) can also infect pigs
Avian flu and human seasonal flu viruses can infect pigs, as well as swine influenza. The H3N2 influenza virus subtype, a virulent one, is thought to have come from pigs - it went on to infect humans.

It is possible for pigs to be infected with more than one flu virus subtype simultaneously. When this happens the genes of the viruses have the opportunity to mingle. When different flu subtypes mix they can create a new virus which contains the genes from several sources - a reassortant virus.

Although swine influenza tends to just infect pigs, they can, and sometimes do, jump the species barrier and infect humans.
What is the risk for human health?
Outbreaks of human infection from a virus which came from pigs (swine influenza) do happen and are sometimes reported. Symptoms will generally be similar to seasonal human influenzas - this can range from mild or no symptoms at all, to severe and possibly fatal pneumonia.

As swine flu symptoms are similar to typical human seasonal flu symptoms, and other upper respiratory tract infections, detection of swine flu in humans often does not happen, and when it does it is usually purely by chance through seasonal influenza surveillance. If symptoms are mild it is extremely unlikely that any connection to swine influenza is found - even if it is there. In other words, unless the doctors and experts are specifically looking for swine flu, it is rarely detected. Because of this, we really do not know what the true human infection rate is.
Examples of known swine flu infecting humans
Since the World Health Organization's (WHO's) implementation of IHR (2005) in 2007, they have been notified of swine influenza cases from the USA and Spain.

In March/April 2009 human cases of influenza A swine fever (H1N1) were first reported in California and Texas. Later other states also reported cases. A significant number of human cases during the same period have also been reported in Mexico - starting just in Mexico City, but now throughout various parts of the country. More cases are being reported in Canada, Europe, and New Zealand - mainly from people who have been in Mexico.
How does a human catch swine influenza?

* From contact with infected pigs (most common way)
* From contact with infected humans (much less common way)

In cases when humans have infected other humans close contact was necessary with the infected person, and they nearly always occurred in closed groups of people.
Can I eat pork meat and pork products?
If the pork meat and pork food products have been handled properly transmission of swine influenza to humans is not possible. Cooking pork meats to a temperature of 70C (160F) kills the virus. So the answer is YES, pork meat and pork food products are safe to eat.
Where have pigs been infected?
As swine influenza infection among pigs is not an internationally notifiable disease we cannot be completely sure. Swine influenza infection among pigs is known to be endemic in the USA. Outbreaks have also occurred in other parts of North America, South American, Europe, Africa, China, Japan, and other parts of Asia.
Is there a pandemic risk?
People who are not in close contact with pigs generally have no immunity to the swine influenza viruses - they are less likely to be able to prevent a virus infection. If the virus infects enough people in a given area, the risk of an influenza pandemic is significantly greater. Experts say it is very hard to predict what impact a flu pandemic caused by a swine influenza virus would have on the global human population. This would depend on how virulent the virus is, what existing immunity among humans there already is, plus several other factors.
Do we have a specific swine flu vaccine?
No - not for humans.
Will current human flu vaccines help protect people from swine influenza infection?
We really don't know. Influenza viruses are adapting and changing all the time. If a vaccine was made, it would have to be specifically for a current strain that is circulating for it to be effective. The WHO says it needs access to as many viruses as possible so that it can isolate the most appropriate candidate vaccine.
What are the signs and symptoms of swine influenza in humans?
They are similar to those of regular flu, and include:

* Body aches
* Chills
* Cough
* Diarrhea (less common)
* Headache
* Sore throat
* Temperature (fever)
* Tiredness (fatigue)
* Vomiting (less common)

What medications are there?
There are some drugs around that can effectively treat swine flu infection in humans - and many types of flu infections in humans. There are two main types:

* adamantanes (amantadine and remantadine)
* inhibitors of influenza neuraminidase (oseltamivir and zanamivir)

Most previous swine influenza human cases recovered completely without the need for medical attention.
What can I do to protect myself?

* Wash your hands regularly with soap
* Try to stay healthy
* Get plenty of sleep
* Do plenty of exercise
* Try to manage your stress
* Drink plenty of liquids
* Eat a well balanced diet
* Refrain from touching surfaces which may have the virus
* Do not get close to people who are sick
* Stay away from crowded areas if there is a swine flu outbreak in your area

If I am infected, how can I stop others from becoming infected?

* Limit your contact with other people
* Do not go to work or school
* When you cough or sneeze cover your mouth with a tissue. If you do not have a tissue, cover your mouth and nose.
* Put your used tissues in a waste basket
* Wash your hands and face regularly
* Keep all surfaces you have touched clean
* Follow your doctor's instructions

Jun 18
Cooking Carrots Whole Preserves More Anti-Cancer Properties
A new study by UK scientists showed that cooking carrots whole preserves their anti-cancer properties better than cooking them sliced or diced.

The study was the work Dr Kirsten Brandt and researcher Ahlam Rashed at the University of Newcastle Upon Tyne and is being presented today at the NutrEvent nutrition and health conference that is taking place in Lille, France.

Brandt and colleagues found that carrots boiled before cutting had 25 per cent more of the anti-cancer chemical falcarinol than those that were cut up before boiling.

They also found uncut cooked carrots had higher concentrations of the naturally occurring sugars that give them their distinctive flavour.

Brandt, who is based at the School of Agriculture, Food and Rural Development and the Human Nutrition Research Centre at Newcastle University said that:

"Chopping up your carrots increases the surface area so more of the nutrients leach out into the water while they are being cooked."

"By cooking them whole and chopping them up afterwards you are locking in both taste and nutrients so the carrot is better for you all round," she added.

Working with colleagues at the University of Southern Denmark, Brandt and her team at Newcastle discovered the health properites of falcarinol in carrots four years ago.

They showed that feeding rats a diet containing either raw carrots or isolated falcarinol reduced their risk of developing tumors by one third compared with rats in a control group.

Since then the researchers have been looking at the health benefits of raw and cooked carrots, comparing different varieties of the vegetable, and how their properties change with heat.

They found that cooking a carrot kills its cells so they can't hold water and this increases the concentration of falcarinol. But heat also softens the walls of the cells so sugar, vitamin C and other compounds such as falcarinol leach out more readily.

Cutting the carrot into pieces before boiling increases the surface area which allows more of the nutrients to leach out of the cell walls into the boiling water.

The scientists also asked 100 people to wear a blindfold and compare the taste of carrots that had been cut before cooking and carrots that had been cut after cooking. More than 80 per cent said the carrots that were cut after cooking tasted better.

Jun 15
Physicians To Discuss Health Consequences Of Climate Change
Physician representatives will gather in Copenhagen in September to discuss the health consequences of climate change to ensure that the medical profession's voice is heard when a new global climate treaty to replace the Kyoto accord is considered two months later.

The seminar will be held by the World Medical Association on September 1, when physician leaders and climate change experts will highlight the health impact of climate change and suggest the role physicians can play in alerting the world to the increased risks of disease.

Dr. Otmar Kloiber, Secretary General of the WMA, said: 'It is vital that health is fully considered in current global debates and that physicians are provided with accurate information and awareness raising tools to advocate action at a national level.

'The WMA is preparing major new policy for physicians in areas such as advocacy, capacity building and collaboration. We hope to adopt this at our annual General Assembly in New Delhi in October so that it can be fed into the United Nations climate change conference being held in Copenhagen in December'.

Jun 15
Cancer May Be Stopped In Its Tracks By MicroRNA Replacement Therapy
A new study suggests that delivering small RNAs, known as microRNAs, to cancer cells could help to stop the disease in its tracks. microRNAs control gene expression and are commonly lost in cancerous tumors. Researchers have shown that replacement of a single microRNA in mice with an extremely aggressive form of liver cancer can be enough to halt their disease, according to a report in the June 12 issue of the journal Cell, a Cell Press publication.

They delivered the microRNA to the mice using a virus that has been applied in other forms of gene therapy. That so-called adeno-associated virus (AAV) is particularly good at targeting new genetic material to the liver.

"Mice given the control virus showed no change in the growth rate of their tumors and within three weeks, the cancer had taken over," said Joshua Mendell of Johns Hopkins University School of Medicine. "When we gave them the microRNA-carrying virus, some animals showed essentially complete regression of their tumors." In other cases, he said, the tumors were much smaller and far fewer.

Mendell said his team, which included his father Jerry Mendell at The Research Institute at Nationwide Children's Hospital, was hopeful the strategy would work based on previous evidence. Nonetheless, he added, "it is always surprising to see results this striking."

They were also amazed by how specifically the microRNA affected cancer cells, while leaving normal cells unscathed. "We found that the tumor cells are exquisitely sensitive [to microRNA replacement]--they not only stopped proliferating, but they actually died," he said. Meanwhile, the mice showed no evidence of any damage to their normal liver tissue.

MicroRNAs are important regulators of gene activity, the researchers explained, and a single microRNA can have far-reaching effects. That's because an individual microRNA can influence hundreds of gene transcripts to coordinate complex programs of gene expression and affect global changes in the physiology of a cell. A growing body of evidence shows that microRNAs are essential for normal development and to keep cells in balance. By the same token, when microRNAs get out of whack, they can lead to disease.

In the last five years, researchers have discovered a particularly important role for microRNAs in cancer. "Virtually all examined tumor types are characterized by globally abnormal microRNA expression patterns," Mendell said. Some microRNAs lead to cancer when they reach levels that are higher than normal. But in most instances, microRNA levels are found to decline in cancerous tumors compared to normal tissue.

Earlier studies have begun to suggest that methods to replace those lost microRNAs might hold particular promise for therapy. For one thing, reducing the level of microRNAs can actually drive the transformation of normal cells into cancerous ones. And, in the case of lymphoma, Mendell's group showed that a single microRNA could suppress the growth of cancer cells.

The new study is the first to show that the strategy might work in a living animal.

First, they showed that primary liver cancers, known as hepatocellular carcinomas (HCC), have a dramatic reduction in a specific microRNA designated as miR-26a. miR-26a is found at high levels in many tissues throughout the body. When they introduced the microRNA back into cancer cells, those cells stopped progressing through the cell cycle. Likewise, mice with the liver cancer that were given the virus-delivered microRNA therapy were protected from the disease as their cancer cells stopped proliferating and underwent a programmed cell death.

There is a dire need for new strategies to combat HCC, which the researchers said is the third leading cause of cancer deaths and the fifth most common malignancy worldwide. HCC is often diagnosed at an advanced and incurable stage. Even when it is caught earlier, other characteristics of the disease tend to make it a challenge to treat with currently available drugs.

The promising strategy for HCC is also likely to work in other cancers as well. The researchers chose mice with liver cancer as a test bed in part because the liver is readily targeted by AAV, but they said that they don't think there is anything special about liver cancer that makes it more sensitive to microRNA replacement therapy.

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