Lasers to combat AIDS..New developments in laser treatment

November 7, 2007 Current laser treatments for virus and disease can be more harmful than effective, sometimes causing damage to DNA and even skin cancer. Now groundbreaking research has developed a new technique that uses lasers to destroy viruses and bacteria, including AIDS and Hepatitis, without causing harm to the human cells of the infected person.

The research was conducted by Physicists from Arizona State University and published in the Institute of Physics' Journal of Physics: Condensed Matter. It discusses how pulses from an infrared laser can be fine-tuned to discriminate between problem microorganisms and human cells.

The research was based on putting femtosecond (one billionth of one millionth of a second.) laser pulses through a process which then produces lethal vibrations in the protein coat of microorganisms. In doing so, the vibrations destroy the microorganisms and thereby can work to disinfect blood and treat blood-borne diseases.

The physicists involved in the research believe the treatment destroys the virus but not the human cells due to the different structural compositions on the protein coats of the human cells and the bacteria and viruses. Beyond being a treatment for disease, the technique may also be effective in reducing the spread of infections such as MRSA in hospitals.

Starve yourself and live longer

Researchers at Mount Sinai School of Medicine have unraveled a molecular puzzle to reveal why a lower-calorie diet slows the development of some age-related conditions such as Alzheimer’s disease, as well as the aging process itself. In their search for an answer they discovered that it doesn’t seem to matter how the diet is restricted – whether fats, proteins or carbohydrates are cut – to produce protective effects against aging and disease.

A two-part study led by Charles Mobbs, PhD, Professor of Neuroscience and of Geriatrics and Palliative Medicine at Mount Sinai School of Medicine, indicates that a reduction of dietary intake blocks a person’s glucose metabolism, which contributes to oxidative stress - a cellular process that leads to tissue damage and also promotes cancer cell growth. Conversely, high calorie diet may accelerate age-related disease by promoting oxidative stress.
Dietary restriction induces a transcription factor called CREB-binding protein (CBP), which controls the activity of genes that regulate cellular function. By developing drugs that mimic the protective effects of CBP – those usually caused by dietary restriction – scientists may be able to extend lifespan and reduce vulnerability to age-related illnesses.
“We discovered that CBP predicts lifespan and accounts for 80 percent of lifespan variation in mammals,” said Dr. Mobbs. “Finding the right balance is key; only a 10 percent restriction will produce a small increase in lifespan, whereas an 80 percent restriction will lead to a shorter life due to starvation.”
The team found an optimal dietary restriction, estimated to be equivalent to a 30 percent caloric reduction in mammals, increased lifespan over 50 percent while slowing the development of an age-related pathology similar to Alzheimer’s disease.
The first part of the study looked at c. elegans, a species of roundworm, that were genetically altered to develop Alzheimer’s disease-like symptoms. Dr. Mobbs and his team reduced the roundworms’ dietary intake by diluting the bacteria the worms consume. They found that when dietary restriction was maintained throughout the worms’ adulthood, lifespan increased by 65 percent and the Alzheimer's disease-related paralysis decreased by about 50 percent.
In the second part of study, Dr. Mobbs and his team looked at the other end of this process: What happens to CBP in a high-calorie diet that has led to diabetes, a disease in which glucose metabolism is impaired? Researchers examined mice and found that diabetes reduces activation of CBP, leading Dr. Mobbs to conclude that a high-calorie diet that leads to diabetes would have the opposite effect of dietary restriction and would accelerate aging.
Interestingly, dietary restriction triggers CBP for as long as the restriction is maintained, suggesting that the protective effects may wear off if higher dietary intake resumes. CBP responds to changes in glucose within hours, indicating genetic communications respond quickly to fluctuations in dietary intake. “Our next step is to understand the exact interactions of CBP with other transcription factors that mediate its protective effects with age,” said Dr. Mobbs. “If we can map out these interactions, we could then begin to produce more targeted drugs that mimic the protective effects of CBP.”

New 3D Imaging technology promises early detection of Alzheimer’s and Dementia

The older people become, the greater risk they have of sharing the tragic fate of those who remain alive yet are increasingly unaware of the world around them. In industrialised countries, one to six percent of the population over the age of 65 and an even more alarming ten to twenty percent over the age of 80 suffer a progressive loss of their cognitive abilities. Alzheimer disease is the most common cause, affecting 50 to 60 percent of all cases, followed by circulatory disorders in small blood vessels, capillaries and venules (calcifications), which make up about 20 percent. These disorders cause ever larger parts of the brain to become necrotic due to an insufficient supply of blood.

The earlier these disorders and their causes are detected, the more effective the therapies can be for preventing the disease or at least substantially slowing down its progress. Increasingly higher-resolution imaging techniques making major contributions to early detection are now being presented at the European Congress of Radiology (ECR 2007), held in Vienna from March 9 to 13, 2007, and attended by some 16,000 participants from 92 countries. University Professor Dr. Daniela Prayer from the Clinical Department for Neuroradiology at the Vienna University of Medicine states, “Although we cannot yet depict individual cells, we can image ultra-tiny bundles of fibre with high resolution. That is a spectacular breakthrough!”
Voxel-based morphometry allows for the volume of grey matter and white matter in the brain to be determined to the nearest cubic millimetre.
A reduction in brain mass (atrophy) in certain areas indicates Alzheimer’s disease and in other areas, other forms of dementia, according to Professor Prayer. An MR study by Professor Dr. Riccardo della Nave and his colleagues at the University of Florence, for instance, found that certain degenerative phenomena occurring in the left thalamus and in a zone in the left cerebral cortex are the first signs of family-related Alzheimer’s disease. “These findings are quite valuable. They enable us not only to differentiate precisely but also to detect the patterns of the disease before symptoms even occur and to check the efficacy of new drugs, namely, whether they can really stop the loss of brain mass.”
Another advance allows insights into the circuitry architecture of individual bundles of cerebral fibre. It is based on special techniques applicable with modern magnetic resonance devices to render visible the movements of water molecules in the space between fibres. Professor Prayer explains, “Wherever protons change direction, there has to be an obstacle, a cell wall or a fibre connection. Applying the reverse conclusion, we obtain a picture of these structures and see early on where swelling occurs or cells die off.”
No less fascinating are the prospects opened up by magnetic resonance spectroscopy (MRS). It allows a non-contact x-ray view of biochemical processes within the regions of the brain under examination.
All in all, Professor Prayer notes, “the new methodological advances of magnetic resonance technology provide us with a hopeful view of the future in terms of the early diagnosis and efficacy testing of therapies for dementias. If this happens in the near future, the spectre of old-age dementia will lose much of its threatening effect.”

Early detection of Alzheimer’s disease using x-rays!!

A highly detailed x-ray imaging technique previously been used to examine tumors in breast tissue and cartilage in knee and ankle joints could used for early diagnosis of Alzheimer’s disease. Researchers at the U.S. Department of Energy’s (DOE) Brookhaven National Laboratory are the first to test the technique’s ability to visualize a class of minuscule plaques that are a hallmark feature of Alzheimer’s disease.
Scientists have long known that Alzheimer’s disease is associated with plaques - areas of dense built-up proteins in the affected brain. Many also believe that these plaques actually cause the disease. Before drug therapies that remove the plaques from the brain can be tested, researchers need a non-invasive, safe, and cost-effective way to track the plaques’ number and size.

That is no easy task as the plaques are on the micrometer scale, or one millionth of a meter. Conventional techniques such as computed tomography (CT) poorly distinguish between the plaques and other soft tissue such as cartilage or blood vessels. The new technique developed at Brookhaven, called diffraction-enhanced imaging (DEI), might provide the extra imaging power researchers crave.
DEI, which makes use of extremely bright beams of x-rays available at synchrotron sources such as Brookhaven’s National Synchrotron Light Source, is used to visualize not only bone, but also soft tissue in a way that is not possible using standard x-rays. In contrast to conventional sources, synchrotron x-ray beams are thousands of times more intense and extremely concentrated into a narrow beam. The result is typically a lower x-ray dose with a higher image quality.

In their study study, researchers from Brookhaven and Stony Brook University used DEI in a high-resolution mode called micro-computed tomography to visualize individual plaques in a mouse-brain model of Alzheimer’s disease. The results not only revealed detailed images of the plaques, but also proved that DEI can be used on whole brains to visualize a wide range of anatomical structures without the use of a contrast agent. The images are similar to those produced by high-resolution magnetic resonance imaging (MRI), with the potential to even exceed MRI pictures in resolution.
Although the radiation dose used for the study is too high to safely image individual plaques in humans, it did show that images could be produced from live animal brains to learn how the plaques grow. The ultimate goal for the researchers is to find a way to develop a safe imaging technique for humans.

Human blood stem cells engineered to kill HIV

A proof-of-principle study has demonstrated that it is possible to engineer human blood stem cells into cells that can target and kill HIV-infected cells. The result is the equivalent of a genetic vaccine which is not only good news in the fight against HIV - the process could also be used against a range of chronic viral diseases.

In the study researchers from the UCLA AIDS Institute and colleagues took the “killer” T cells that help fight infection, known as CD8 cytotoxic T lymphocytes, from an HIV-infected individual. The researchers then identified the molecule known as the T-cell receptor – the molecule that guides the T cell in recognizing and killing HIV-infected cells. Although these cells are able to destroy HIV-infected cells, they do not exist in enough quantities to clear the virus from the body. So the researchers cloned the receptor and genetically engineered human blood stem cells, then placed the stem cells into human thymus tissue that had been implanted in mice, allowing them to study the reaction in a living organism.

The engineered stem cells developed into a large population of mature, multifunctional HIV-specific CD8 cells that could specifically target cells containing HIV proteins. The researchers also found that HIV-specific T-cell receptors have to be matched to an individual in much the same way that an organ is matched to a transplant patient.
The next step is to test this strategy in a more advanced model to determine if it would work in the human body, said co-author Jerome A. Zack, UCLA professor of medicine in the division of hematology and oncology and associate director of the UCLA AIDS Institute. And with the results of the study suggesting the strategy could be an effective weapon in the fight against AIDS, the researchers also hope to expand the range of viruses against which this approach could be used.

"We have demonstrated in this proof-of-principle study that this type of approach can be used to engineer the human immune system, particularly the T-cell response, to specifically target HIV-infected cells," said lead investigator Scott G. Kitchen, assistant professor of medicine in the division of hematology and oncology at the David Geffen School of Medicine at UCLA and a member of the UCLA AIDS Institute. "These studies lay the foundation for further therapeutic development that involves restoring damaged or defective immune responses toward a variety of viruses that cause chronic disease, or even different types of tumors."