Alzheimer's Prevented And Reversed With Natural Protein In Animal Models

Memory loss, cognitive impairment, brain cell degeneration and cell death were prevented or reversed in several animal models after treatment with a naturally occurring protein called brain-derived neurotrophic factor (BDNF). The study by a University of California, San Diego-led team – published in the February 8, 2009 issue of Nature Medicine – shows that BDNF treatment can potentially provide long-lasting protection by slowing, or even stopping the progression of Alzheimer's disease in animal models.

"The effects of BDNF were potent," said Mark Tuszynski, MD, PhD, professor of neurosciences at the UC San Diego School of Medicine and neurologist at the Veterans Affairs San Diego Health System. "When we administered BDNF to memory circuits in the brain, we directly stimulated their activity and prevented cell death from the underlying disease."

BDNF is normally produced throughout life in the entorhinal cortex, a portion of the brain that supports memory. Its production decreases in the presence of Alzheimer's disease. For these experiments, the researchers injected the BDNF gene or protein in a series of cell culture and animal models, including transgenic mouse models of Alzheimer's disease; aged rats; rats with induced damage to the entorhinal cortex; aged rhesus monkeys, and monkeys with entorhinal cortex damage.

In each case, when compared with control groups not treated with BDNF, the treated animals demonstrated significant improvement in the performance of a variety of learning and memory tests. Notably, the brains of the treated animals also exhibited restored BDNF gene expression, enhanced cell size, improved cell signaling, and activation of function in neurons that would otherwise have degenerated, compared to untreated animals. These benefits extended to the degenerating hippocampus where short-term memory is processed, one of the first regions of the brain to suffer damage in Alzheimer's disease.

The demonstration of the effectiveness and safety of BDNF administration in animals provides "a rationale for exploring clinical translation" to humans, the team concludes, suggesting that the protective and restorative effects of BDNF on damaged neurons and neuronal signaling may offer a new approach to treating Alzheimer's disease.

This work builds on previous studies by Tuszynski and others, demonstrating the therapeutic affects of nerve growth factor (NGF) administered to patients with Alzheimer's disease. In 2001, Tuszynski and his team at UC San Diego Medical Center performed the first surgical implants of NGF genes into the brains of Alzheimer's patients, with follow-up results showing these patients experienced a possible slowing in cognitive decline and increased metabolic function in the brain. The NGF studies continue today, with Phase 2, multi-center studies currently underway.

"NGF therapy aims to stimulate the function of specific cholinergic neurons, which are like the air traffic controllers of the brain, helping to direct the activities of cells in broad regions of the brain," Tuszynski explained. However, he added that the benefits of NGF therapy, if validated in ongoing trials, will not be curative. Eventually, the effect of the NGF "boost" will be countered by the widespread death of neurons in the cerebral cortex as a result of advancing Alzheimer's disease.

"In contrast, BDNF acts directly on dying cells in specific memory circuits of the brain," Tuszynski said. "In this series of studies, we have shown that BDNF targets the cortical cells themselves, preventing their death, stimulating their function, and improving learning and memory. Thus, BDNF treatment can potentially provide long-lasting protection by slowing, or even stopping disease progression in the cortical regions that receive treatment."

The protective and restorative effects of BDNF occurred independently of the build-up of amyloid, a protein that accumulates in the brain to form plaques in Alzheimer's disease. Many current experimental treatments for Alzheimer's disease target amyloid production, so the potential role of BDNF as an alternative protective intervention is of great potential interest, said Tuszynski. Because BDNF targets a different set of disease mechanisms than amyloid modulation, there is also potential to combine BDNF and amyloid-based treatments, theoretically providing a two-pronged attack on the disease.

The study was supported by the National Institutes of Health, the California Regional Primate Research Center, the Veterans Administration, the Alzheimer's Association, the State of California, the Dr. Miriam and Sheldon G. Adelson Medical Research Foundation and the Shiley Family Foundation. Tuszynski is scientific founder of Trophin Therapeutics, a company that may potentially benefit from the research results.

Study co-authors are Alan H. Nagahura, David A. Merrill, Shingo Tsukada, Brock E. Schroeder, Gideon M. Shaked, Ling Want, Armin Blesch, James M. Conner, Edward Rockenstein, Edward H. Koo, and Eliezer Masliah of the UC San Diego Department of Neurosciences, and Andrea A. Chiba of the UC San Diego Departments of Neurosciences and Cognitive Science. Giovanni Coppola and Daniel Geschwind of the Program in Neurogenetics, Department of Neurology at UCLA, and Albert Kim and Moses V. Chao, Skirball Institute of Biomolecular Medicine at New York University School of Medicine.

Breakthrough To Treat Malaria: Scientists Deactivate Malaria Parasite's Digestive Machinery

The research, performed in collaboration with Professor John Dalton at the University of Technology, Sydney, provides a new approach to treating and controlling the disease that is contracted by half a billion people and causes around 1 million deaths a year.

The team, based at the Monash University ARC Centre of Excellence in Structural and Functional Microbial Genomics, has been able to deactivate the final stage of the malaria parasite's digestive machinery, effectively starving the parasite of nutrients and disabling its survival mechanism. This process of starvation leads to the death of the parasite.

Professor Whisstock said the results had laid the scientific groundwork to further develop a specific class of drugs to treat the disease.
"About forty percent of the world's population are at risk of contracting malaria. It is only early days but this discovery could one day provide treatment for some of those 2.5 billion people across the globe," Professor Whisstock said.

"Drug-resistant malaria is an ever increasing problem, meaning that there is an urgent requirement to develop new therapeutic strategies."
Researchers used the Australian Synchrotron, located adjacent to Monash University's Clayton campus. The results are published today in the prestigious Proceedings of the National Academy of Sciences U.S.A.

Lead author of the research paper, Dr Sheena McGowan, from the Monash University NHMRC program on protease systems biology said their findings prove their concept.
"We had an idea as to how malaria could be starved and we have shown this, chemically, can be done," Dr McGowan said.

"A single bite from an infected mosquito can transfer the malaria parasite into a human's blood stream. The malaria parasite must then break down blood proteins in order to obtain nutrients. Malaria carries out the first stages of digestion inside a specialised compartment called the digestive vacuole – this can be considered to be like a stomach. However, the enzyme we have studied (known as PfA-M1), which is essential for parasite viability, is located outside the digestive vacuole meaning that it is easier to target from a drug perspective."

This breakthrough is in addition to existing malaria drug discovery research advances at Monash University. A new drug candidate which aims to provide a single dose cure, discovered by a major international project involving the Monash Institute of Pharmaceutical Sciences, is currently progressing to first human studies with support from the Medicines for Malaria

Venture, Geneva, Switzerland.

World faces threat from deadly diseases as scientists struggle to keep up

The world is facing deadly threat on the scale of Aids, Sars and Ebola within a decade, the world's leading authority on health said , as it warned that diseases were spreading more quickly than at any time in history.

(An electron micrograph showing the bird influenza virus strain H5N1)

New diseases are emerging at an unprecedented rate, of one a year, and are becoming more difficult to treat, says the World Health

Organisation's annual report. It paints a bleak picture of future health threats, with science struggling to keep up as diseases increasingly become drug resistant.

The authors point to passenger flights, now numbering more than 2bn a year, as being a chillingly efficient mechanism for spreading diseases rapidly across continents. New diseases that pose a sudden threat in one part of the world are only "a few hours away" from becoming a threat somewhere else, the WHO says.

"Profound changes have occurred in the way humanity inhabits the planet," said Margaret Chan, the director general of the WHO. "The disease situation is anything but stable. Population growth, incursion into previously uninhabited areas, rapid urbanisation, intensive farming practices, environmental degradation, and the misuse of anti-microbials, have disrupted the equilibrium of the microbial world. The rate of emergence of new diseases, at one year, was "historically unprecedented".

The report, A Safer Future, identifies 40 diseases unknown a generation ago, and reveals that during the past five years the WHO has verified more than 1,100 epidemic events worldwide. It says:

· Cholera, yellow fever and epidemic meningococcal diseases made a comeback in the last quarter of the 20th century.

· Severe acute respiratory syndrome and avian influenza in humans still have the potential to wreak havoc globally.

· Viral diseases such as Ebola, Marburg haemorrhagic fever and Nipah virus, pose threats to global public health security.

· The use of smallpox in bioterrorism is a particularly worrying threat. Authorities around the world should work together to combat the kind of bioterrorism that occurred with the letters warning of anthrax after September 11 2001.

· A flu pandemic would affect more than 1.5 billion people, or 25% of the world's population. Even if the disease were mild in itself the economic and social disruption would be "enormous".

The WHO report adds: "It would be extremely naive and complacent to assume that there will not be another disease like Aids, another Ebola, or another Sars, sooner or later."

To prepare for these events will take unprecedented global and political collaboration, it advises. "No single country, however capable, wealthy or technologically advanced, can alone prevent, detect and respond to all public health threats." The organisation is calling for renewed international efforts to share information.

The UK's Department of Health said it strongly supported "the approach of managing these risks through cooperation".

Worries about the effects of international travel were underscored in June when an American national, Andrew Speaker, 31, who had a contagious and deadly strain of tuberculosis, took an international flight. US authorities tracked every passenger who had shared one of two transatlantic flights with Mr Speaker, who had fallen ill with the drug-resistant XDR form of TB while on honeymoon in Europe. He went back home via Montreal to avoid the US authorities, who had ordered him into quarantine, and would not have allowed him to fly, he believed.

In South Africa, the courts have considered forcibly detaining people who have the same form of TB to prevent its spread, amid fears that many more than those officially diagnosed are suffering and have not informed the authorities. The XDR strain of TB is a highly infectious disease spread by airborne droplets and kills 98% of those infected within about two weeks. Experts believe it emerged after inappropriate and overuse of antibiotics to treat TB.

DOUBLE YOLK EGGs

Most of us have had the experience of finding we have a double yolk egg. Depending on whether you're a yolk person or a white person it's either a bonus or a fault. Personally I think it's a bonus, but I love egg yolk more than white.

Double yolk eggs are actually fairly rare, about 1 in 1,000 for commercial eggs where consistency is required.

Rarer still are multiple yolk eggs, triples or even quadruples and apparently there has even been a nine yolk egg!

What Causes Double Yolk Eggs?

When an egg starts its journey inside the hen, the first thing formed is the ovum in the hen's ovary. This grows and the colour changes from pale grey to the yellow we know as the yolk colour.

Once it reaches full size, the yolk sac breaks away (ovulation) and begins a journey down the oviduct where the egg white (albumen) and the shell form around it. The process from ovulation to egg laying takes around 24-26 hours.

Normally, the next ovulation is triggered by the hen laying the egg but occasionally things go wrong and two yolks are released at the same time to travel down the oviduct together, being surrounded by one shell and giving us the double yolker.

Which Hens Lay Double Yolkers?

Most often double yolk eggs are laid by young hens of productive egg laying breeds. If you really like double yolked eggs then the highly productive breeds are more likely to reward you when young.

As they become more mature hens and their system settles down to correct production then the double yolks become less frequent to non-existent.

Since the double yolk egg cannot bring forth double chicks, genetically it is not possible to have a breed that consistently produces them. They'd die out! It is possible to develop a breed where the ratio of double to single yolk eggs is higher but I do not know of one.

SURGEONS USE MICROWAVE TECHNOLOGY TO DESTROY TUMORS

A new minimally-invasive option for treating liver tumors, called microwave ablation, is now available at UC San Diego Medical Center and Moores UCSD Cancer Center, the only hospitals in the region to offer this technology to patients.“A liver tumor can be removed in many ways,” said Marquis Hart, MD, transplant surgeon at UC San Diego Medical Center. “Now, patients at UC San Diego have a new option called ‘microwave ablation.’ Simply put, we zap and destroy liver tumors with heat derived from microwave energy. This is an important alternative, especially since the majority of liver cancers cannot be partially removed and not all patients are transplant candidates.”To perform the procedure, Hart accesses the tumor through the skin, or through a small laparoscopic port or open incision. With ultrasound guidance or a computed tomography (CT) scan, the tumor is located and then pierced with a thin antenna which emits microwaves. This energy spins the water molecules in the tumor producing friction which causes heat. Temperatures above 60 degrees Celsius (140 degrees Fahrenheit) cause cellular death, usually within 10 minutes.
“Microwave ablation causes the tumor to be quickly and precisely removed. If necessary, multiple tumors can be treated at the same time,” said Hart. “This method appears to be more efficient than other ablation techniques which translates to better tumor destruction and less time for the patient under general anesthesia.”
In addition to liver disease, microwave ablation has promising potential in the treatment of lung, kidney, and bone cancer.

Omega-6 Fatty Acids: Make Them Part Of Heart-healthy Eating

Omega-6 fatty acids – found in vegetable oils, nuts and seeds – are a beneficial part of a heart-healthy eating plan, according to a science advisory published in Circulation: Journal of the American Heart Association.

The association recommends that people aim for at least 5 percent to 10 percent of calories from omega-6 fatty acids. Most Americans actually get enough of these oils in the foods they are currently eating, such as nuts, cooking oils and salad dressings, the advisory reports. Recommended daily servings of omega-6 depend on physical activity level, age and gender, but range from 12 to 22 grams per day.

Omega-6, and the similarly-named omega-3 fatty acids (found in fattier fish such as tuna, mackerel and salmon), are called polyunsaturated fatty acids (PUFA), and can have health benefits when consumed in the recommended amounts, especially when used to replace saturated fats or trans fats in the diet. Omega-6 and omega-3 PUFA play a crucial role in heart and brain function and in normal growth and development. PUFA are “essential” fats that your body needs but can’t produce, so you must get them from food.

“Of course, as with any news about a single nutrient, it’s important to remember to focus on an overall healthy dietary pattern – one nutrient or one type of food isn’t a cure-all,” said William Harris, Ph.D., lead author of the advisory. “Our goal was simply to let Americans know that foods containing omega-6 fatty acids can be part of a healthy diet, and can even help improve your cardiovascular risk profile.”

The American Heart Association’s dietary recommendations suggest a broadly defined healthy eating pattern over time – with an emphasis on fruits, vegetables, high-fiber whole grains, lean meat, poultry, and fish twice a week. Diets rich in fruits, vegetables and whole grains have been associated in a large number of studies with reduced cardiovascular risk.

Linoleic acid (LA) is the main omega-6 fatty acid in foods, accounting for 85 percent to 90 percent of the dietary omega-6 PUFA.

There has been some debate within the nutrition community regarding the benefits of omega-6 based on the belief that they may promote inflammation, thus increasing cardiovascular risk. “That idea is based more on assumptions and extrapolations than on hard data,” said Harris, a research professor for the Sanford School of Medicine at the University of South Dakota and director of the Metabolism and Nutrition Research Center at Sanford Research/USD.

The linking of omega-6 intake to inflammation stems from the fact that arachidonic acid (AA), which can be formed from LA, is involved in the early stages of inflammation. However, the advisory explains that AA and LA also give rise to anti-inflammatory molecules.

For example, in the cells that form the lining of blood vessels, omega-6 PUFA have anti-inflammatory properties, suppressing the production of adhesion molecules, chemokines and interleukins — all of which are key mediators of the atherosclerotic process. “Thus, it is incorrect to view the omega-6 fatty acids as ‘pro-inflammatory,’” Harris explained. “Eating less LA will not lower tissue levels of AA (the usual rationale for reducing LA intakes) because the body tightly regulates the synthesis of AA from LA.”

The advisory reviewed a meta-analysis of randomized, controlled trials, and more than two dozen observational, cohort, case/control and ecological reports.

Observational studies showed that people who ate the most omega-6 fatty acids usually had the least heart disease. Other studies examined blood levels of omega-6 in heart patients compared with healthy people and found that patients with heart disease had lower levels of omega-6 in their blood.

In controlled trials in which researchers randomly assigned people to consume diets containing high versus low levels of omega-6 and then recorded the number of heart attacks over several years, those assigned to the higher omega-6 diets had less heart disease.

A meta-analysis of several trials indicated that replacing saturated fats with PUFA lowered risk for heart disease events by 24 percent. “When saturated fat in the diet is replaced by omega-6 PUFA, the blood cholesterol levels go down,” Harris said. “This may be part of the reason why higher omega-6 diets are heart-healthy.”

Co-authors are: Dariush Mozaffarian, M.D.; Eric Rimm, D.Sc.; Penny Kris-Etherton, Ph.D.; Lawrence Rudel, Ph.D.; Lawrence Appel, M.D.; Marguerite Engler, Ph.D.; Mary Engler, Ph.D.; and Frank Sacks, M.D. Author disclosures are on the manuscript.

HOUSE DUST MITES

Dust mite is a microscopic multicellular animal.

Dust mites are a major cause of allergies for a lot of people. The are in every home even though we cannot see them. They live primarily on skin cells and scales, most call dander from humans and pets.
Dust mites can be found in areas where we like to lounge, and in mattresses, carpet, furniture and even window drapes. How many are there you say, well a typical mattress could have as many as ten thousand to 10 million dust mites. How about the carpet, well about 100,000 could live in one square yard.
We are not allergic to the mite itself, but what it leaves behind. Mites are said to produce about 20 waste droppings each day. Which contain a protein that many people are allergic too. Reactions can range from itchy eyes to asthma attacks. And did you know that about 80% of the stuff you see floating in a sunbeam are skin flakes.

HOW TO CONTROL IT

Ok here is what we can do to help control them. The number one thing we can focus on is “dust control”. This can be done by putting a plastic cover over your mattress. It is also said that fitted sheets help prevent skin scales from building up. Vaccuum the pillows on the bed and area around the bed. You should wash your sheets and blankets in really hot water (130 degrees) at least every 2 weeks, and your pillow every week. For things that can’t be washed and if small can be placed in the freezer for 24 to 48 hours to kill the mites. Try and dust weekly with a damp rag and mop. Why not go buy a spray to kill the little suckers. Well that is because there are no pesticides at this time for killing dust mites. These are just a few tips at prevention which will aid in keeping the dust mite population down and hopefully allergies to a minimum.