Chemical From Medicinal Plants May Be Used To Fight HIV

Like other kinds of cells, immune cells lose the ability to divide as they age because a part of their chromosomes known as a telomere becomes progressively shorter with cell division. As a result, the cell changes in many ways, and its disease fighting ability is compromised.

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But a new UCLA AIDS Institute study has found that a chemical from the Astragalus root, frequently used in Chinese herbal therapy, can prevent or slow this progressive telomere shortening, which could make it a key weapon in the fight against HIV.

"This has the potential to be either added to or possibly even replace the HAART (highly active antiretroviral therapy), which is not tolerated well by some patients and is also costly," said study co-author Rita Effros, a professor of pathology and laboratory medicine at the David Geffen School of Medicine at UCLA and member of the UCLA AIDS Institute.

A telomere is a region at the end of every cell chromosome that contains repeated DNA sequences but no genes; telomeres act to protect the ends of the chromosomes and prevent them from fusing together — rather like the plastic tips that keep shoelaces from unraveling. Each time a cell divides, the telomeres get shorter, eventually causing the cell to reach a stage called replicative senescence, when it can no longer divide. This seems to indicate that the cell has reached an end stage, but, in fact, the cell has changed into one with new genetic and functional characteristics.

A great deal of cell division must take place within the immune system for the system to function properly. For example, the so-called "killer" CD8 T-cells that help fight infection have unique receptors for particular antigens. When a virus enters the body, the killer T-cells whose receptors recognize that virus create, through division, versions of themselves that fight the invader.

Generally, the telomeres in cells are sufficiently long that they can divide many times without a problem. Moreover, when fighting infections, T-cells can turn on an enzyme called telomerase, which can prevent the telomeres from shortening.

"The problem is that when we're dealing with a virus that can't be totally eliminated from the body, such as HIV, the T-cells fighting that virus can't keep their telomerase turned on forever," Effros said. "They turn off, and telomeres get shorter and they enter this stage of replicative senescence."

Previous studies have shown that injecting the telomerase gene into T-cells can keep the telomeres from shortening, enabling them to maintain their HIV-fighting function for much longer. This gene-therapy approach, however, is not a practical way to treat the millions of people living with HIV.

For the present study, rather than utilizing gene therapy, the researchers used a chemical called TAT2, which was originally identified from plants used in traditional Chinese therapy and which enhances telomerase activity in other cell types.

They tested TAT2 in several ways. First, they exposed the CD8 T-cells from HIV-infected persons to TAT2 to see if the chemical not only slowed the shortening of the telomeres but improved the cells' production of soluble factors called chemokines and cytokines, which had been previously shown to inhibit HIV replication. It did.

They then took blood samples from HIV-infected individuals and separated out the CD8 T-cells and the CD4 T-cells — those infected with HIV. They treated the CD8 T-cells with TAT2 and combined them with the CD4 T-cells in the dish-and found that the treated CD8 cells inhibited production of HIV by the CD4 cells.

"The ability to enhance telomerase activity and antiviral functions of CD8 T-lymphocytes suggests that this strategy could be useful in treating HIV disease, as well as immunodeficiency and increased susceptibility to other viral infections associated with chronic diseases or aging," the researchers write.

In addition to Effros, researchers were Steven Russell Fauce, Beth D. Jamieson, Ronald T. Mitsuyasu, Stan T. Parish, Christina M. Ramirez Kitchen, and Otto O. Yang, all of UCLA, and Allison C. Chin and Calvin B. Harley of the Geron Corp.

The Geron Corp., TA Therapeutics Ltd., the National Institutes of Health and the Frank Jernigan Foundation funded this study.

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Journal reference:

1. . Telomerase-Based Pharmacologic Enhancement of Antiviral Function of Human CD8+ T Lymphocytes. Journal of Immunology, Nov. 15, 2008
   

Alzheimer's Disease

• Overview
  • Alternative Names
  • Causes
  • Symptoms
  • Exams and Tests
  • Treatment
  • Support Groups
  • Outlook (Prognosis)
  • Possible Complications
  • When to Contact a Medical Professional
  • Prevention
  • References

Coping With Alzheimer’s

A Descent Into Alzheimer's

Alzheimer's: Quest for Understanding

Alzheimer's: The Rarest Gene

Illustrations

• Aged Nervous Tissue

Alzheimer's disease (AD), one form of dementia, is a progressive, degenerative brain disease. It affects memory, thinking, and behavior.

Memory impairment is a necessary feature for the diagnosis of this or any type of dementia. Change in one of the following areas must also be present: language, decision-making ability, judgment, attention, and other areas of mental function and personality.

The rate of progression is different for each person. If AD develops rapidly, it is likely to continue to progress rapidly. If it has been slow to progress, it will likely continue on a slow course.

Alternative Names

Senile dementia/Alzheimer's type (SDAT)

The older you get, the greater your risk of developing AD, although it is not a part of normal aging. Family history is another common risk factor.

In addition to age and family history, risk factors for AD may include:

• Longstanding high blood pressure
• History of head trauma
• High levels of homocysteine (a body chemical that contributes to chronic illnesses such as heart disease, depression, and possibly AD)
• Female gender -- because women usually live longer than men, they are more likely to develop AD

There are two types of AD -- early onset and late onset. In early onset AD, symptoms first appear before age 60. Early onset AD is much less common, accounting for only 5-10% of cases. However, it tends to progress rapidly.

The cause of AD is not entirely known but is thought to include both genetic and environmental factors. A diagnosis of AD is made based on characteristic symptoms and by excluding other causes of dementia.

Prior theories regarding the accumulation of aluminum, lead, mercury, and other substances in the brain leading to AD have been disproved. The only way to know for certain that someone had AD is by microscopic examination of a sample of brain tissue after death.

The brain tissue shows "neurofibrillary tangles" (twisted fragments of protein within nerve cells that clog up the cell), "neuritic plaques" (abnormal clusters of dead and dying nerve cells, other brain cells, and protein), and "senile plaques" (areas where products of dying nerve cells have accumulated around protein). Although these changes occur to some extent in all brains with age, there are many more of them in the brains of people with AD.

The destruction of nerve cells (neurons) leads to a decrease in neurotransmitters (substances secreted by a neuron to send a message to another neuron). The correct balance of neurotransmitters is critical to the brain.

By causing both structural and chemical problems in the brain, AD appears to disconnect areas of the brain that normally work together.

About 10 percent of all people over 70 have significant memory problems and about half of those are due to AD. The number of people with AD doubles each decade past age 70. Having a close blood relative who developed AD increases your risk.

Early onset disease can run in families and involves autosomal dominant, inherited mutations that may be the cause of the disease. So far, three early onset genes have been identified.

Late onset AD, the most common form of the disease, develops in people 60 and older and is thought to be less likely to occur in families. Late onset AD may run in some families, but the role of genes is less direct and definitive. These genes may not cause the problem itself, but simply increase the likelihood of formation of plaques and tangles or other AD-related pathologies in the brain.

Symptoms »

In the early stages, the symptoms of AD may be subtle and resemble signs that people mistakenly attribute to "natural aging." Symptoms often include:

• Repeating statements
• Misplacing items
• Having trouble finding names for familiar objects
• Getting lost on familiar routes
• Personality changes
• Losing interest in things previously enjoyed
• Difficulty performing tasks that take some thought, but used to come easily, like balancing a checkbook, playing complex games (such as bridge), and learning new information or routines

In a more advanced stage, symptoms are more obvious:

• Forgetting details about current events
• Forgetting events in your own life history, losing awareness of who you are
• Problems choosing proper clothing
• Hallucinations, arguments, striking out, and violent behavior
• Delusions, depression, agitation
• Difficulty performing basic tasks like preparing meals and driving

At end stages of AD, a person can no longer survive without assistance. Most people in this stage no longer:

• Understand language
• Recognize family members
• Perform basic activities of daily living such as eating, dressing, and bathing

Exams and Tests »

The first step in diagnosing Alzheimer's disease is to establish that dementia is present. Then, the type of dementia should be clarified. A health care provider will take a history, do a physical exam (including a neurological exam), and perform a mental status examination.

Tests may be ordered to help determine if there is a treatable condition that could be causing dementia or contributing to the confusion of AD. These conditions include thyroid disease, vitamin deficiency, brain tumor, drug and medication intoxication, chronic infection, anemia, and severe depression.

AD usually has a characteristic pattern of symptoms and can be diagnosed by history and physical exam by an experienced clinician. Tests that are often done to evaluate or exclude other causes of dementia include computed tomography (CT), magnetic resonance imaging (MRI), and blood tests.

In the early stages of dementia, brain image scans may be normal. In later stages, an MRI may show a decrease in the size of the cortex of the brain or of the area of the brain responsible for memory (the hippocampus). While the scans do not confirm the diagnosis of AD, they do exclude other causes of dementia (such as stroke and tumor).

Treatment

Unfortunately, there is no cure for AD. The goals in treating AD are to:

• Slow the progression of the disease.
• Manage behavior problems, confusion, and agitation.
• Modify the home environment.
• Support family members and other caregivers.

The most promising treatments include lifestyle changes, medications, and antioxidant supplements like vitamin E and ginkgo biloba.

LIFESTYLE CHANGES

The following steps can help people with AD:

• Walk regularly with a caregiver or other reliable companion. This can improve communication skills and prevent wandering.
• Use bright light therapy to reduce insomnia and wandering.
• Listen to calming music. This may reduce wandering and restlessness, boost brain chemicals, ease anxiety, enhance sleep, and improve behavior.
• Get a pet dog.
• Practice relaxation techniques.
• Receive regular massages. This is relaxing and provides social interactions.

DRUG TREATMENT

Several drugs are available to try to slow the progression of AD and possibly improve the person's mental capabilities. Memantine (Namenda) is currently the only drug approved for the treatment of moderate-to-severe Alzheimer’s disease.

Other medicines include donepezil (Aricept), rivastigmine (Exelon), galantamine (Razadyne, formerly called Reminyl), and tacrine (Cognex). These drugs affect the level of a neurotransmitter in the brain called acetylcholine. They may cause nausea and vomiting. Tacrine also causes an elevation in liver enzymes and must be taken four times a day. It is now rarely used.

Aricept is taken once a day and may stabilize or even improve the person's mental capabilities. It is generally well tolerated. Exelon seems to work in a similar way. It is taken twice a day.

Other medicines may be needed to control aggressive, agitated, or dangerous behaviors. These are usually given in very low doses.

It may be necessary to stop any medications that make confusion worse. Such medicines may include pain killers, cimetidine, central nervous system depressants, antihistamines, sleeping pills, and others. Never change or stop taking any medicines without first talking to your doctor.

SUPPLEMENTS

Folate (vitamin B9) is critical to the health of the nervous system. Together with some other B vitamins, folate is also responsible for clearing homocysteine (a body chemical that contributes to chronic illnesses) from the blood. High levels of homocysteine and low levels of both folate and vitamin B12 have been found in people with AD. Although the benefits of taking these B vitamins for AD is not entirely clear, it may be worth considering them, particularly if your homocysteine levels are high.

Antioxidant supplements, like ginkgo biloba and vitamin E, scavenge free radicals. These products of metabolism are highly reactive and can damage cells throughout the body.

Vitamin E dissolves in fat, readily enters the brain, and may slow down cell damage. In at least one well-designed study of people with AD who were followed for 2 years, those who took vitamin E supplements had improved symptoms compared to those who took a placebo pill. Patients who take blood-thinning medications like warfarin (Coumadin) should talk to their doctor before taking vitamin E.

Ginkgo biloba is an herb widely used in Europe for treating dementia. It improves blood flow in the brain and contains flavonoids (plant substances) that act as antioxidants. Although many of the studies to date have been somewhat flawed, the idea that ginkgo may improve thinking, learning, and memory in those with AD has been promising. DO NOT use ginkgo if you take blood-thinning medications like warfarin (Coumadin) or a class of antidepressants called monoamine oxidase inhibitors (MAOIs).

If you are considering any drugs or supplements, you MUST talk to your doctor first. Remember that herbs and supplements available over the counter are NOT regulated by the FDA.

SUPPORT AT HOME

Someone with AD will need support in the home as the disease worsens. Family members or other caregivers can help by trying to understand how the person with AD perceives his or her world. Simplify the patient's surroundings. Give frequent reminders, notes, lists of routine tasks, or directions for daily activities. Give the person with AD a chance to talk about their challenges and participate in their own care.

OTHER PRACTICAL STEPS

The person with AD should have their eyes and ears checked. If problems are found, hearing aids, glasses, or cataract surgery may be needed.

Those with AD may have particular dietary requirements such as:

• Extra calories due to increased physical activity from restlessness and wandering.
• Supervised meals and help with feeding. People with AD often forget to eat and drink, and can become dehydrated as a result.

The Safe Return Program, implemented by the Alzheimer's Association, requires that a person with AD wear in identification bracelet. If he or she wanders, the caregiver can contact the police and the national Safe Return office, where information about the person is stored and shared nationwide.

Eventually, 24-hour monitoring and assistance may be necessary to provide a safe environment, control aggressive or agitated behavior, and meet physiologic needs. This may include in-home care, nursing homes, or adult day care.

For additional information and resources for people with Alzheimer's disease and their caregivers, see Alzheimer's disease support groups.

Outlook (Prognosis)

The probable outcome is poor. The disorder usually progresses steadily. Total disability is common. Death normally occurs within 15 years, usually from an infection or a failure of other body systems.

Possible Complications

• Loss of ability to function or care for self
• Bedsores, muscle contractures (loss of ability to move joints because of loss of muscle function), infection (particularly urinary tract infections and pneumonia), and other complications related to immobility during end-stages of AD
• Falls and broken bones
• Loss of ability to interact
• Malnutrition and dehydration
• Failure of body systems
• Reduced life span
• Harmful or violent behavior toward self or others
• Abuse by an over-stressed caregiver
• Side effects of medications

When to Contact a Medical Professional

Call your health care provider if someone close to you experiences symptoms of senile dementia/Alzheimer's type.

Call your health care provider if a person with this disorder experiences a sudden change in mental status. (A rapid change may indicate other illness.)

Discuss the situation with your health care provider if you are caring for a person with this disorder and the condition deteriorates to the point where you can no longer care for the person in your home.

Prevention »

Although there is no proven way to prevent AD, there are some practices that may be worth incorporating into your daily routine, particularly if you have a family history of dementia. Talk to your doctor about any of these approaches, especially those that involve taking a medication or supplement.

• Consume a low-fat diet.
• Eat cold-water fish (like tuna, salmon, and mackerel) rich in omega-3 fatty acids, at least 2 to 3 times per week.
• Reduce your intake of linoleic acid found in margarine, butter, and dairy products.
• Increase antioxidants like carotenoids, vitamin E, and vitamin C by eating plenty of darkly colored fruits and vegetables.
• Maintain a normal blood pressure.
• Stay mentally and socially active throughout your life.
• Consider taking nonsteroidal anti-inflammatory drugs (NSAIDs) like ibuprofen (Advil, Motrin), sulindac (Clinoril), or indomethacin (Indocin). Statin drugs, a class of medications normally used for high cholesterol, may help lower your risk of AD. Talk to your doctor about the pros and cons of using these medications for prevention.

In addition, early testing of a vaccine against AD is underway.

References »

Rakel P. Conn ’s Current Therapy 2005. 57th ed. Philadelphia, Pa: Saunders; 2005.

Moore DP, Jefferson JW. Handbook of Medical Psychiatry. 2nd ed. St. Louis, Mo: Mosby; 2004.

Goetz CG, Pappert EJ. Textbook of Clinical Neurology. 2nd ed. Philadelphia, Pa: Saunders; 2003.

Brain slows at 40, starts body decline

WASHINGTON - Think achy joints are the main reason we slow down as we get older? Blame the brain, too: The part in charge of motion may start a gradual downhill slide at age 40.
How fast you can throw a ball or run or swerve a steering wheel depends on how speedily brain cells fire off commands to muscles. Fast firing depends on good insulation for your brain's wiring.
Now new research suggests that in middle age, even healthy people begin to lose some of that insulation in a motor-control part of the brain - at the same rate that their speed subtly slows.
That helps explain why "it's hard to be a world-class athlete after 40," concludes Dr. George Bartzokis, a neurologist at the University of California, Los Angeles, who led the work.
And while that may sound depressing, keep reading. The research points to yet another reason to stay physically and mentally active: An exercised brain may spot fraying insulation quicker and signal for repair cells to get to work.
To Bartzokis, the brain is like the Internet. Speedy movement depends on bandwidth, which in the brain is myelin, a special sheet of fat that coats nerve fibres.
Healthy myelin - good thick insulation wound tightly around those nerve fibres - allows prompt conduction of the electrical signals the brain uses to send commands. Higher-frequency electrical discharges, known as "actional potentials," speed movement - any movement, from a basketball rebound to a finger tap.
Consider someone like Michael Jordan. "The circuitry that made him a great basketball player was probably myelinated better than most other mortals," Bartzokis notes.
But while myelin builds up during adolescence, when does production slow enough that we fall behind in the race to repair fraying, older insulation?
Enter the new research. First, Bartzokis recruited 72 healthy men, ages 23 to 80, to perform a simple test: How fast they tapped an index finger. Anyone can do this; it doesn't depend on strength or fitness.
Researchers counted how many taps the men made in 10 seconds, recording the two fastest of 10 attempts. Then, brain scans checked for myelin in need of repair in the region that orders a finger to tap.
Strikingly, tapping speed and myelin health both peaked at age 39. Then both gradually declined with increasing age, the researchers reported last month in the journal Neurobiology of Aging.
That doesn't mean the rest of the brain is equally affected. Bartzokis has some evidence that myelin starts to fray a decade or so later in brain regions responsible for cognitive functions - higher-level thinking - than in motor-control areas.
So back to his example of Jordan, who last played professionally at age 40: "Even he started getting older. That circuitry started breaking down a little," contends Bartzokis. "He can become Michael Jordan the big-shot businessman ... but not be Michael Jordan the super-duper basketball player anymore."
Bartzokis isn't looking to build a better athlete. His ultimate goal is to fight Alzheimer's disease. The connection: Building memories requires high-frequency electrical bursts, too, and Bartzokis' earlier research suggests an Alzheimer's-linked gene may thwart myelin repair.
But the new research has broader implications because it sheds light on normal aging, says Dr. Zoe Arvanitakis, a neurologist at Chicago's Rush University Medical Center.
"We knew at some age you peak and there's a sense it would disintegrate as you grow older. But we didn't have a sense of where that age would be," says Arvanitakis, who next wants to see if myelin and cognitive functions show a similar trajectory.
Bartzokis' research supports a recent report from German scientists, that with age comes a weakening of the system that's supposed to repair broken myelin, adds Dr. Bradley Wise of the National Institute on Aging.
"Any disruption in these neural circuits and networks will have problems for functioning," says Wise, who says the two reports are spurring increased interest into myelin's role in aging. Until recently, most myelin research has focused on multiple sclerosis, where myelin doesn't gradually degrade but disappears.
While much more research is needed, Bartzokis has some practical advice:
-Keeping active and treating high blood pressure, high cholesterol and diabetes already are deemed important for good brain health. But physical and mental activity also may stimulate myelin repair, while unused neural pathways wouldn't send out a "help" signal, he says.
"Remember, these are average people I tested," Bartzokis says. "Someone that's really practising could make it (myelin) last longer because you're sending the signals to repair, repair, repair."
-Stress hormones, however, may hurt myelin.
-He's also testing whether consumption of omega-3 fatty acids - the oils, found in fatty fish, already recommended for cardiovascular health - might help maintain myelin

Biologists Spy On The Secret Inner Life Of A Cell

The transportation of antibodies from a mother to her newborn child is vital for the development of that child's nascent immune system. Those antibodies, donated by transfer across the placenta before birth or via breast milk after birth, help shape a baby's response to foreign pathogens and may influence the later occurrence of autoimmune diseases.
Images from biologists at the California Institute of Technology (Caltech) have revealed for the first time the complicated process by which these antibodies are shuttled from mother's milk, through her baby's gut, and into the bloodstream, and offer new insight into the mammalian immune system.
Newborns pick up the antibodies with the aid of a protein called the neonatal Fc receptor (FcRn), located in the plasma membrane of intestinal cells. FcRn snatches a maternal antibody molecule as it passes through a newborn's gut; the receptor and antibody are enclosed within a sac, called a vesicle, which pinches off from the membrane. The vesicle is then transported to the other side of the cell, and its contents--the helpful antibody--are deposited into the baby's bloodstream.
Pamela Bjorkman, Max Delbrück Professor of Biology at Caltech and an investigator with the Howard Hughes Medical Institute, and her colleagues were able to watch this process in action using gold-labeled antibodies (which made FcRn visible when it picked up an antibody) and a technique called electron tomography. Electron tomography is an offshoot of electron microscopy, a now-common laboratory technique in which a beam of electrons is used to create images of microscopic objects. In electron tomography, multiple images are snapped while a sample is tilted at various angles relative to the electron beam. Those images can then be combined to produce a three-dimensional picture, just as cross-sectional X-ray images are collated in a computerized tomography (CT) scan.
"You can get an idea of movement in a series of static images by taking them at different time points," says Bjorkman, whose laboratory studies how the immune system recognizes its targets, work that is offering insight into the processes by which viruses like HIV and human cytomegalovirus invade cells and cause disease.
The electron tomography images revealed that the FcRn/antibody complexes were collected within cells inside large vesicles, called "multivesicular bodies," that contain other small vesicles. The vesicles previously were believed to be responsible only for the disposal of cellular refuse and were not thought to be involved in the transport of vital proteins.
The images offered more surprises. Many vesicles, including multivesicular bodies and other more tubular vesicles, looped around each other into an unexpected "tangled mess," often forming long tubes that then broke off into the small vesicles that carry antibodies through the cell. When those vesicles arrived at the blood-vessel side of the cell, they fused with the cell membrane and delivered the antibody cargo. The vesicles also appeared to include a coat made from a molecule called clathrin, which helps form the outer shell of the vesicles. Researchers previously believed that a vesicle's clathrin cage was completely shed before the vesicle fused with the cell membrane. The new results suggest that only a small section of that coating is sloughed off, which may allow the vesicle to more quickly drop its load and move on for another.
"We are now studying the same receptor in different types of cells in order to see if our findings can be generalized, and are complementing these studies with fluorescent imaging in live cells," Bjorkman says. "The process of receptor-mediated transport is fundamental to many biological processes, including detection of developmental decisions made in response to the binding of hormones and other proteins, uptake of drugs, signaling in the immune and nervous systems, and more. So understanding how molecules are taken up by and transported within cells is critical for many areas of basic and applied biomedical research," she adds.
The work was supported by the National Institutes of Health, a Max Planck Research Award, the Gordon and Betty Moore Foundation, the Agouron Institute, and National University of Singapore AcRF start-up funds

How Hepatitis C Replicates

The hepatitis C virus is a prolific replicator, able to produce up to a trillion particles per day in an infected person by hijacking liver cells in which to build up its viral replication machinery. Now new research — in which scientists have for the first time used fluorescent proteins to image hepatitis C virus replication in live cells — shows that the microscopic viral factories are a diverse mix of big, immobile structures and tiny replication complexes that zip zanily around inside the cell.
The scientists say their results offer new insights into how this difficult-to-treat virus, and perhaps others in its class, ensures efficient reproduction of itself — knowledge that could help design next-generation treatments.
“There is so much that we don’t know about this virus, so a better understanding of how the pathogen cleverly forms lots of large and small factories to reproduce itself so that it can infect new hosts may be of great benefit,” says study coauthor Benno Wölk, a former postdoctoral researcher in the Rockefeller University Laboratory of Virology and Infectious Disease. He is now a researcher and physician at Hannover Medical School in Germany.
An estimated 170 million people worldwide are chronically infected with hepatitis C, which is a major cause of liver cirrhosis and liver cancer. So progress in understanding and treating the infection is crucial, says the study’s senior investigator, Charles M. Rice, Maurice R. and Corinne P. Greenberg Professor in Virology and director of the Center for the Study of Hepatitis C. “There is no vaccine available for hepatitis C, and current therapies are not always effective because the virus fights back against drugs developed to block replication,” Rice says.
Scientists had until now believed that the virus’s replication process occurred in one or several large complexes inside a cell. It was hard to learn more because in order to see the virus it had to be killed. “Up to this study, researchers have only been able to look at infected cells when they were fixed and immobile,” Wölk says. “They found areas where the cell membrane was altered and found viral proteins in these structures that suggested that was where replication took place.”
To visualize the replication process, the researchers selected one of the proteins that the hepatitis C virus uses to make its replication factories and fused it to a green fluorescent protein, which emits a green glow when exposed to a specific wavelength of light. They were surprised to see that the small hepatitis C virus replication complexes were transported around the cell. “It’s remarkable that the virus hijacks the cell’s transport machinery to move the viral replication complex around,” Wölk says. “We also learned that for the first several hours after infection only small structures, like dots, formed, which were quickly spread all over the cell. Then the big structures took shape, and they didn’t move.”
The researchers theorize that the small structures are the actual sites of viral replication and that the big structures are clusters of the smaller factories — perhaps formed after the virus has already successfully settled in with the cell. “It is questionable whether the virus even needs the big structures to replicate. They could be performing other functions or they could just represent garbage cans of the cell,” Wölk says. “This is very different from the traditional view.”
Although they can’t say for sure, the group, which also includes Benjamin Büchele of the University of Freiburg in Germany, and Darius Moradpour of the University of Lausanne in Switzerland, suspects that these small, mobile, replication complexes are more efficient and elegant than large structures because they do two things: distribute the factories so that the integrity of the cell is maintained, and keep the complexity of the replication factories to independent, small, manageable units that are easier to control for the virus.
What the researchers discovered in the hepatitis C virus may also prove to be true for related single-strand RNA viruses in the Flaviviridae family, Wölk says. “If that is the case, then we may be able to find a new treatment target for not just one, but many viral infections.”

Evolution Of Genes That Trigger The Body's Immune Response To Viral Infection

Virginia Commonwealth University Institute of Molecular Medicine researchers have traced the evolutionary origin of two genes that serve as primary cellular sensors of infection with RNA viruses, such as influenza, poliovirus, West Nile virus, and HIV, which may ultimately provide researchers with insight into a possible new pathway for the development of innate immunity.
Recent studies by other investigators have provided information on exactly how humans respond to virus infection and the role of innate immunity in protection from viral pathogenesis. Induction of innate immunity is closely associated with the production of type I interferons. Interferons are a class of proteins that are secreted by the body in response to a viral infection such as rhinovirus, the cause of the common cold.
In the study, published online in the Early Edition of the Proceedings of the National Academy of Sciences the week of October 20-24, the VCU team reported that melanoma differentiation associated gene-5 (MDA-5) and retinoic acid inducible gene-I (RIG-I) originated specifically in mammals. These genes induce the production of type I interferons.
“Understanding how these unique genes developed and evolved provides a unique opportunity to understand the origins of innate immunity and to develop ways of exploiting this process to develop new types of therapies for pathogenic viruses,” said lead investigator Paul B. Fisher, M.Ph., Ph.D., professor and chair of the Department of Human and Molecular Genetics and director of the VCU Institute of Molecular Medicine in the VCU School of Medicine.
According to Fisher, MDA-5, but not RIG-I, orthologs are found in fish, indicating that MDA-5 might have evolved before RIG-I. The unique domain arrangement of MDA-5 and RIG-I evolved independently by domain grafting and not by a simple gene-duplication event of the entire four-domain arrangement. This process may have been initiated by differential sensitivity of these proteins to viral infection.
“Our studies provide insights into the shuffling of gene regions, which culminated in a unique mechanism for protection against viral infection. Additionally, our phylogenetic analyses of these domains provides one of the first direct insights into the temporal pathways of development of innate immunity,” said Fisher.
According to Fisher, expression of both MDA-5 and RIG-I can limit viral replication post-entry in cells. In this context, identifying drugs that can effectively turn on either or both of these genes offers promise for decreasing virus-induced pathogenesis.
In related work, the team has identified the promoter region, which controls expression of MDA-5 and RIG-I. Studies are now under way at the VCU Institute of Molecular Medicine and the Burnham Institute for Medical Research in La Jolla, Calif., to use these promoters as part of a screening paradigm to identify small molecules that can be developed into drugs to treat infectious diseases.
This work was supported by grants from the National Institutes of Health.

Weight Gain In Pregnancy Linked To Overweight In Kids

Pregnant women who gain excessive or even appropriate weight, according to current guidelines, are four times more likely than women who gain inadequate weight to have a baby who becomes overweight in early childhood. These findings are from a new study at the Department of Ambulatory Care and Prevention of Harvard Medical School and Harvard Pilgrim Health Care and are published in the April issue of the American Journal of Obstetrics and Gynecology.
"Maternal weight gain during pregnancy is an important determinant of birth outcomes," says lead author Emily Oken, MD, MPH, instructor in the Department of Ambulatory Care and Prevention. "These findings suggest that pregnancy weight gain can influence child health even after birth and may cause the obstetric community to rethink current guidelines."
Oken and colleagues examined data from 1,044 mother-child pairs in Project Viva, a prospective study of pregnant women and their children based at the Department of Ambulatory Care and Prevention's Obesity Prevention Program. The authors studied whether pregnancy weight gain within or above the recommended range increased the risk of a child being overweight at age 3 years.
In 1990, the Institute of Medicine (IOM) published guidelines for gestational weight gain ("Nutrition During Pregnancy") that were motivated by evidence that low weight gain in pregnant women may cause low birth weight. These guidelines call for smaller gains in mothers with a higher body mass index (BMI) and generally permit greater gains than previous recommendations.
The IOM report remains the standard for clinical recommendations regarding gestational weight gain. However, some have questioned whether evidence is sufficient that greater gains promote better birth outcomes in modern developed nations. More weight gain may cause undesirable birth outcomes, such as increased rates of babies born at high birth weight and cesarean section, and is associated with higher postpartum weight retention and later risk of maternal obesity.
In this study, 51 percent of women gained excessive weight, 35 percent gained adequate weight, and 14 percent gained inadequate weight, according to the IOM guidelines. Women with adequate or excessive gain were approximately four times more likely than those with inadequate gain to have an overweight child, as measured at age 3. The authors defined overweight as a BMI greater than the 95th percentile for the child's age and sex.
"Our study shows that excessive weight gain during pregnancy was directly associated with having an overweight child," says Oken. "Just like adults, children who are overweight are at higher risk for a number of health conditions such as high blood pressure, diabetes, and high cholesterol."
The likelihood of having a baby that was heavy for gestational age was greater in women with excessive gain. Children of mothers who gained more weight also had somewhat higher systolic blood pressure, a cardiovascular risk factor related to weight even in young children.
The authors calculated total gestational weight gain as the difference between the last weight recorded before delivery and self-reported prepregnancy weight. The authors categorized women as having gained inadequate, adequate, or excessive weight according to the IOM guidelines. These guidelines recommend that women with a prepregnancy BMI between 19.8 and 26 kg/m2, (considered normal by the IOM guidelines) should gain 11.5 to 16kg (25 to 35 pounds); that women with a BMI of less than 19.8 kg/m2 (considered underweight by the IOM guidelines) should gain 7 to 11.5 kg (15 to 25 pounds); and that women with a BMI of more than 29 kg/m2 (considered obese by the IOM guidelines) should gain at least 6 kg (13 pounds).
Gestational weight gain may be linked to child overweight through several potential pathways. Mothers who gain weight readily because of genetic, dietary, or other behavioral factors may have children who are more likely to gain weight. Also, the amount of weight gained during pregnancy may alter the intrauterine environment, not only influencing fetal growth but also possibly resulting in persistent programming of child weight.
"Because childhood obesity is increasing in prevalence and effective treatment remains elusive, preventing childhood obesity remains critical," says Oken. "The IOM may need to reevaluate its recommendations for gestational weight gain, considering not only birth outcomes but also risk of obesity for both mother and child. While our study signals the potential need to adjust guidelines, further studies will need to occur to determine just what the appropriate weights should be."
Like the United States population as whole, many mothers and their children in this study were overweight. Even mothers with adequate gain according to the IOM guidelines had a substantially higher risk than mothers with inadequate weight gain of having overweight children, with no difference in risk of undesirable birth outcomes, such as small or large size for gestational age or birth by cesarean section.
"It has been 17 years since the IOM came out with its last set of recommendations, before the obesity epidemic hit with full force," says Matthew Gillman, MD, associate professor in the Department of Ambulatory Care and Prevention and senior author of the study. "Now, women are coming into pregnancy at higher weights and likely gaining excessively more than they used to. We need to find out how to counter this trend--but not go too far back in the other direction when women were gaining too little weight."
The Project Viva team is currently evaluating the children in this study who are now age seven.
This work was supported by the National Institutes of Health, Harvard Medical School, and the Harvard Pilgrim Health Care Foundation.

allergies may protect against certain types of cancer

A new article provides strong evidence that allergies are much more than just an annoying immune malfunction. They may protect against certain types of cancer.
The article, by researchers Paul Sherman, Erica Holland and Janet Shellman Sherman from Cornell University, suggests that allergy symptoms may protect against cancer by expelling foreign particles, some of which may be carcinogenic or carry absorbed carcinogens, from the organs most likely to come in with contact them. In addition, allergies may serve as early warning devices that let people know when there are substances in the air that should be avoided.
Medical researchers have long suspected an association between allergies and cancer, but extensive study on the subject has yielded mixed, and often contradictory, results. Many studies have found inverse associations between the two, meaning cancer patients tended to have fewer allergies in their medical history. Other studies have found positive associations, and still others found no association at all.
In an attempt to explain these contradictions, the Cornell team reexamined nearly 650 previous studies from the past five decades. They found that inverse allergy-cancer associations are far more common with cancers of organ systems that come in direct contact with matter from the external environment—the mouth and throat, colon and rectum, skin, cervix, pancreas and glial brain cells. Likewise, only allergies associated with tissues that are directly exposed to environmental assaults—eczema, hives, hay fever and animal and food allergies—had inverse relationships to cancers.
Such inverse associations were found to be far less likely for cancers of more isolated tissues like the breast, meningeal brain cells and prostate, as well as for myeloma, non-Hodgkins lymphoma and myelocytic leukemia.
The relationship between asthma and lung cancer, however, is a special case. A majority of the studies that the Cornell team examined found that asthma correlates to higher rates of lung cancer. "Essentially, asthma obstructs clearance of pulmonary mucous, blocking any potentially prophylactic benefit of allergic expulsion," they explain. By contrast, allergies that affect the lungs other than asthma seem to retain the protective effect.
So if allergies are part of the body's defense against foreign particle invaders, is it wise to turn them off with antihistamines and other suppressants? The Cornell team says that studies specifically designed to answer this question are needed.
"We hope that our analyses and arguments will encourage such cost/benefit analyses," they write. "More importantly, we hope that our work will stimulate reconsideration…of the current prevailing view … that allergies are merely disorders of the immune system which, therefore, can be suppressed with impunity."

Global Warming Is Killing Frogs And Salamanders

Frogs and salamanders, those amphibious bellwethers of environmental danger, are being killed in Yellowstone National Park. The predator, Stanford researchers say, is global warming.
Biology graduate student Sarah McMenamin spent three summers in a remote area of the park searching for frogs and salamanders in ponds that had been surveyed 15 years ago. Almost everywhere she looked, she found a catastrophic decrease in the population.
The amphibians need the ponds for their young to hatch, but high temperatures and drought are drying up the water. The frogs and salamanders lay eggs that have a gelatinous outer layer—basically "jelly eggs," McMenamin says—that leaves them completely unsuitable for gestation on land. If the ponds dry up, so do the eggs. "If there isn't any water, then the animals simply don't breed," she said.
Biology Associate Professor Elizabeth Hadly, McMenamin's graduate adviser and co-author of a research paper published this week on the website of the Proceedings of the National Academy of Sciences, has worked in Yellowstone since 1981 and has witnessed the ponds going dry. "They're just blinking off," she said. "It's depressing."
"Precipitous declines of purportedly unthreatened amphibians in the world's oldest nature reserve indicate that the ecological effects of global warming are even more profound and are happening more rapidly than previously anticipated," the researchers wrote.
The disappearing ponds lie in picturesque northern Yellowstone, specifically the lower Lamar Valley, which holds dozens of small fishless ponds where the habitat has been ideal for the breeding and larval development of blotched tiger salamanders, boreal chorus frogs and Colombia spotted frogs. As the world's first national park, it is one of the most environmentally protected areas in the world.
The researchers studied climate and water records going back a century, ranging from handwritten logs of water flow in the Lamar River to satellite imagery, and could find no cause for the drying ponds other than a persistent change in temperature and precipitation. "It's the cumulative effects of climate," Hadly said.
During the summers of 2006 through 2008, McMenamin, wearing hip waders and carrying a dip net, cataloged the amphibian life—or lack thereof—in and around 42 ponds that had been surveyed in 1992-1993. In that earlier survey, involving 46 ponds, 43 supported amphibian populations for at least one of the two years. But in the recent inspection, only 38 of those same ponds even contained water in summer.
In their fieldwork, the researchers were able to visit 31 of the 38 wet ponds (the remainder were off limits, to protect nesting trumpeter swans). Only 21 of them supported amphibian populations for even one of the three years they were checked, 2006-2008. In 15 years the number of ponds with frogs and salamanders had dropped drastically.
"That's when we really got alarmed, because the data just showed such a huge difference," Hadly said.
Historically, the ponds—as small as backyard fish ponds, as large as small lakes—have been recharged during the summer by the groundwater in the soil. But the water table is dropping, the researchers say, as human-induced climate change produces a deadly combination of higher temperatures and less rain and snow. Moreover, the seasonal wetlands near the ponds, usually ideal amphibian habitat, are evaporating earlier in the spring, the result of an earlier snowmelt.
During the course of their study, the researchers witnessed the loss of four amphibian communities because of pond drying. Each event left hundreds of dried tiger salamander corpses behind. The ponds had dried rapidly, over just a few days, too fast for larvae to metamorphose and adults to migrate.
"Everybody can identify with the loss of glaciers, but in Yellowstone the decrease in lakes and ponds and wetlands has been astounding," John Varley, the former chief scientist for Yellowstone, told New West. "What were considered permanent bodies of water, meaning reference was given to them in the 1850s, '60s and '70s, and bestowed with a name as a lake, are now gone. Some wetlands that were considered permanent ponds are no longer there. Some lakes have become ephemeral."
The problem is not going to go away, McMenamin said. "It's extremely depressing and there aren't any evident solutions that come to mind. It's a symptom of a much, much larger problem."

linke bet. stress and acne severity

The largest study ever conducted on acne and stress reveals that teenagers who were under high levels of stress were 23 percent more likely to have increased acne severity, according to researchers from Wake Forest University School of Medicine and colleagues.
"Acne significantly affects physical and psychosocial well-being, so it is important to understand the interplay between the factors that exacerbate acne," said Gil Yosipovitch, M.D., lead author and a professor of dermatology. "Our study suggests a significant association between stress and severity of acne."
The results of the study, which involved 94 adolescents from Singapore, are reported today in Acta Derm Venereol, a Swedish medical journal.
While psychological stress had been identified among many factors that can worsen acne, there has been little research to understand the mechanisms behind this relationship. The current study looked at whether levels of sebum, the oily substance that coats the skin and protects the hair, increase in times of stress and are related to acne severity. Hormone levels, sebum production and bacteria are all known to play major roles in acne.
The study involved secondary school students in Singapore with a mean age of 14.9 years. The students' self-reported stress levels and acne severity were measured at two different times -- just before mid-year exams and during summer break. Students' long-term career prospects are influenced by the results of the examinations and they are known to induce psychological stress.
Stress levels were measured using the Perceived Stress Scale, a 14-item, self-questionnaire that is widely used in stress research. Acne severity was measured using a system that classifies acne based on type and number of lesions. Ninety-two percent of the girls and 95 percent of the boys reported having acne.
Acne is an inflammatory disease of the skin caused by changes in the hair follicle and the sebaceous glands of the skin that produce sebum. The oily substance plugs the pores, resulting in whiteheads or blackheads (acne comedonica) and pimples (acne papulopustulosa).
The researchers suspected that stress increases the quantity of sebum, which leads to increased acne severity. However, the results showed that sebum production didn't differ significantly between the high-stress and low-stress conditions.
The researchers did find that students reporting high stress were 23 percent more likely to have increased severity of acne papulopustulosa. Levels of stress were not linked to severity of acne comedonica.
"Our research suggests that acne severity associated with stress may result from factors others than sebum quantity," said Yosipovitch. "It's possible that inflammation may be involved."
Singapore was selected as the study location because sebum production is known to fluctuate with variations in temperature and humidity. In Singapore's tropical climate, temperature and humidity are consistent throughout the year.
The research was funded by the National Medical Research Council of Singapore.
Co-researchers were Aerlyn Dawn, M.D., from Wake Forest, Mark Tang, M.D., Chee Leok Goh, M.D., and Yiong Hauk Chan, Ph.D., all from National Skin Center and National University of Singapore, and Lim Fong Seng, M.D., from National Healthcare Group Polyclinics, Singapore.

stress may make you itch

Stress May Make You Itch
Current research suggests that stress may activate immune cells in your skin, resulting in inflammatory skin disease.
Skin provides the first level of defense to infection, serving not only as a physical barrier, but also as a site for white blood cells to attack invading bacteria and viruses. The immune cells in skin can over-react, however, resulting in inflammatory skin diseases such as atopic dermatitis and psoriasis.
Stress can trigger an outbreak in patients suffering from inflammatory skin conditions. This cross talk between stress perception, which involves the brain, and the skin is mediated the through the "brain-skin connection". Yet, little is know about the means by which stress aggravates skin diseases.
Researchers lead by Dr. Petra Arck of Charité, University of Medicine Berlin and McMaster University in Canada, hypothesized that stress could exacerbate skin disease by increasing the number of immune cells in the skin. To test this hypothesis, they exposed mice to sound stress. Dr. Arck's group found that this stress challenge resulted in higher numbers of mature white blood cells in the skin. Furthermore, blocking the function of two proteins that attract immune cells to the skin, LFA-1 and ICAM-1, prevented the stress-induced increase in white blood cells in the skin.
Taken together, these data suggest that stress activates immune cells, which in turn are central in initiating and perpetuating skin diseases. Fostered by the present observation, the goal of future studies in Dr. Arck's group is to prevent stress-triggered outbreaks of skin diseases by recognizing individuals at risk and identifying immune cells suitable to be targeted in therapeutic interventions.
This work was supported by grants from the German Research Foundation and the Charité .
Journal reference:
Joachim RA, Handjiski B, Blois SM, Hagen E, Paus R, Arck PC. Stress-induced neurogenic inflammation in murine skin skews dendritic cells towards maturation and migration: key role of ICAM1/LFA-1 interactions. Am J Pathol, 2008 173:1379-1388

how plants know to send roots down and leaves up?

VIB researchers at Ghent University discovered how the transport of an important plant hormone is organized in a way that the plant knows in which direction its roots and leaves have to grow. They discovered how the needed transport protein turns up at the underside of plant cells. The discovery helps explain how plants grow, and how they organize themselves in order to grow.
Versatile hormone
It is known for a long time that the plant hormone auxin is transmitted from the top to the bottom of a plant, and that the local concentration of auxin is important for the growth direction of stems, the growth of roots, the sprouting of shoots. To name a few things; auxin is also relevant to, for instance, the ripening of fruit, the clinging of climbers and a series of other processes. Thousands of researchers try to understand the different roles of auxin.
In many instances the distribution of auxin in the plant plays a key role, and thus the transport from cell to cell. At the bottom of plant cells, so-called PIN proteins are located on the cell membrane, helping auxin to flow through to the lower cell. However, no one thoroughly understood why the PIN proteins only showed up at the bottom of a cell.
Endocytosis
An international group of scientists from labs in five countries, headed by Jirí Friml of the VIB-department Plant Systems Biology at Ghent University, revealed a rather unusual mechanism. PIN proteins are made in the protein factories of the cell and are transported all over the cell membrane. Subsequently they are engulfed by the cell membrane, a process called endocytosis.
The invagination closes to a vesicle, disconnects and moves back into the cell. Thus the PIN proteins are recycled and subsequently transported to the bottom of the cell, where they are again incorporated in the cell membrane. It is unclear why plants use such a complex mechanism, but a plausible explanation is this mechanism enables a quick reaction when plant cells feel a change of direction of gravity, giving them a new ‘underside’.
Gene technology
To see the path of the protein, the researchers used gene technology to make cells in which the PIN protein was linked to fluorescent proteins. (This technology was rewarded with the Nobel Prize 2008 for chemistry.) Subsequently they produced cells in which the endocytosis was disrupted in two different ways. The PIN proteins showed up all over the cell membrane. When the researchers proceeded from single cells to plant embryos, the embryos developed deformations, because the pattern of auxin concentrations in the embryo was distorted. When these plants with disrupted endocytosis grew further, roots developed where the first leaflet should have been

new strategy in treatment of common infection

Researchers at Georgetown University Medical Center (GUMC)

have successfully tested a genetic strategy designed to improve treatment of human infections caused by the yeast Candida albicans, ranging from diaper rash, vaginitis, oral infections (or thrush which is common in HIV/AIDS patients), as well as invasive, blood-borne and life-threatening diseases.
Their findings confirm that inhibiting a key protein could provide a new drug target against the yeast, which inhabits the mucous membranes of most humans. The research was presented today at the 48th Annual Interscience Conference on Antimicrobial Agents and Chemotherapy/46th Annual Meeting of the Infectious Diseases Society of America (ICAAC/IDSA) in Washington, DC.
"This is a genetically intelligent approach to target identification and drug design," says the study's lead author, Richard Calderone, PhD, professor and chair of the department of microbiology and immunology and co-director of the PhD program in the global infectious disease program at GUMC.
"Candida infections are often treatable, however, in patients that are immunocompromised following cancer chemotherapy, bone marrow transplantation, or surgery, diagnosis is often delayed, postponing therapy," he says. "Also when drug-resistant yeast pathogens cause the infection, clinical management of the patient becomes a problem."
Candida invasive, blood-borne infections are the fourth most common hospital-acquired infection in the United States, costing the healthcare system about $1.8 billion each year, Calderone says.
"More drug resistance is being seen clinically, so there is significant room for improvement in the therapies used today," he says
This study continues research in which Calderone and his colleagues identified a protein, the product of the Ssk1 gene that Candida needs to infect its host. To date, this protein has not been found in humans or in animals, which means it could be "targeted" with a novel drug without producing toxicity because such an agent should only attack the fungus.
The researchers found that if the Ssk1 gene is deleted from Candida albicans, the "triazole" drugs that are now used to treat these diseases are much more effective in the laboratory. "This allows the triazole drugs to do their job," Calderone says. "We propose that this finding might lead to other, possibly more effective, treatment options."
In this study, the researchers used a gene microarray analysis to further understand what knocking out the Ssk1 gene does to the organism, and they discovered that the gene is critical to the pathogenic nature of the fungi.
What this means is that an Ssk1 inhibitor might work in synergy with a triazole or perhaps as an effective stand-alone drug to treat Candida infections, the researchers say. If it works in Candida, it may have broader activity in other pathogens because Ssk1p is found in other fungi.
"Using the genome of the organism to find genes to target is a logical approach to drug design," he says. The researchers are now working with other groups to find the right agent to target the Ssk1protein.
Neeraj Chauhan, PhD, assistant research professor in the department of microbiology and immunology at GUMC, is co-author on the study. The authors report no disclosures. This research was funded by the National Institutes of Allergy & Infectious Diseases of the NIH.

cancer

Cancer is the uncontrolled growth of abnormal cells in the body. Cancerous cells are also called malignant cells.

Carcinoma; Malignant tumor
Causes
Cells are the building blocks of living things. Cancer grows out of normal cells in the body. Normal cells multiply when the body needs them, and die when the body doesn't need them. Cancer appears to occur when the growth of cells in the body is out of control and cells divide too quickly. It can also occur when cells “forget” how to die.
There are many different kinds of cancers. Cancer can develop in almost any organ or tissue, such as the lung, colon, breast, skin, bones, or nerve tissue.
There are many causes of cancers, including:
Benzene and other chemicals
Certain poisonous mushrooms and a type of poison that can grow on peanut plants (aflatoxins)
Certain viruses
Radiation
Sunlight
Tobacco
However, the cause of many cancers remains unknown.
The most common cause of cancer-related death is lung cancer.
The three most common cancers in men in the United States are:
Prostate cancer
Lung cancer
Colon cancer
In women in the U.S., the three most common cancers are:
Breast cancer
Colon cancer
Lung cancer
Some cancers are more common in certain parts of the world. For example, in Japan, there are many cases of gastric cancer, but in the U.S. this type of cancer is pretty rare. Differences in diet may play a role.
Some other types of cancers include:
Brain cancer
Cervical cancer
Hodgkin's lymphoma
Kidney cancer
Leukemia
Liver cancer
Non-Hodgkin's lymphoma
Ovarian cancer
Skin cancer
Testicular cancer
Thyroid cancer
Uterine cancer
Symptoms
Symptoms of cancer depend on the type and location of the tumor. For example, lung cancer can cause coughing, shortness of breath, or chest pain. Colon cancer often causes diarrhea, constipation, and blood in the stool.
Some cancers may not have any symptoms at all. In certain cancers, such as gallbladder cancer, symptoms often do not start until the disease has reached an advanced stage.
The following symptoms can occur with most cancers:
Chills
Fatigue
Fever
Loss of appetite
Malaise
Night sweats
Weight loss
Exams and Tests
Like symptoms, the signs of cancer vary based on the type and location of the tumor. Common tests include the following:
Biopsy of the tumor
Blood chemistries
Bone marrow biopsy (for lymphoma or leukemia)
Chest x-ray
Complete blood count (CBC)
CT scan
Most cancers are diagnosed by biopsy. Depending on the location of the tumor, the biopsy may be a simple procedure or a serious operation. Most patients with cancer have CT scans to determine the exact location and size of the tumor or tumors.
A cancer diagnosis is difficult to cope with. It is important, however, that you discuss the type, size, and location of the cancer with your doctor when you are diagnosed. You also will want to ask about treatment options, along with their benefits and risks.
It's a good idea to have someone with you at the doctor's office to help you get through the diagnosis. If you have trouble asking questions after hearing about your diagnosis, the person you bring with you can ask them for you.
Treatment
Treatment also varies based on the type of cancer and its stage. The stage of a cancer refers to how much it has grown and whether the tumor has spread from its original location.
If the cancer is confined to one location and has not spread, the most common goals for treatment are surgery and cure. This is often the case with skin cancers, as well as cancers of the lung, breast, and colon.
If the tumor has spread to local lymph nodes only, sometimes these can also be removed.
If surgery cannot remove all of the cancer, the options for treatment include radiation, chemotherapy, or both. Some cancers require a combination of surgery, radiation, and chemotherapy.
Although treatment for cancer can be difficult, there are many ways to keep up your strength.
If you have radiation treatment, know that:
Radiation treatment is painless.
Treatment is usually scheduled every weekday.
You should allow 30 minutes for each treatment session, although the treatment itself usually takes only a few minutes.
You should get plenty of rest and eat a well-balanced diet during the course of your radiation therapy.
Skin in the treated area may become sensitive and easily irritated.
Side effects of radiation treatment are usually temporary. They vary depending on the area of the body that is being treated.
If you are going through chemotherapy, you should eat right. Chemotherapy causes your immune system to weaken, so you should avoid people with colds or the flu. You should also get plenty of rest, and don't feel as though you have to accomplish tasks all at once.
It will help you to talk with family, friends, or a support group about your feelings. Work with your health care providers throughout your treatment. Helping yourself can make you feel more in control.
Support Groups
A cancer diagnosis often causes a lot of anxiety and can affect your entire quality of life. Several support groups for cancer patients can help you cope.
Outlook (Prognosis)
The outlook depends on the type of cancer. Even among people with one type of cancer, the outcome varies depending on the stage of the tumor when they are diagnosed.
Some cancers can be cured. Some cancers that are not curable can still be treated well. And some patients can live for many years with their cancer. Other tumors are quickly life-threatening.
Possible Complications
One complication is that the cancer may spread. Other complications vary with the type and stage of the tumor.
When to Contact a Medical Professional
Contact your health care provider if you develop symptoms of cancer.
Prevention
One of the best ways to prevent cancer is to not smoke or chew tobacco. Many cancers can be prevented by avoiding risk factors such as excessive exposure to sunlight and heavy drinking.
Cancer screenings, such as mammography and breast examination for breast cancer and colonoscopy for colon cancer, may help catch these cancers at their early stages when they are most treatable. Some people at high risk for developing certain cancers can take medication to reduce their risk.
More Information on This Topic
News & Features
Review Date: 8/2/2008Reviewed By: David C. Dugdale, III, MD, Professor of Medicine, Division of General Medicine, Department of Medicine, University of Washington School of Medicine. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M., Inc.A.D.A.M., Inc. is accredited by URAC, also known as the American Accreditation HealthCare Commission (www.urac.org). URAC's accreditation program is an independent audit to verify that A.D.A.M. follows rigorous standards of quality and accountability. A.D.A.M. is among the first to achieve this important distinction for online health information and services. Learn more about A.D.A.M.'s editorial policy, editorial process and privacy policy. A.D.A.M. is also a founding member of Hi-Ethics and subscribes to the principles of the Health on the Net Foundation (www.hon.ch). A.D.A.M. CopyrightThe information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition. A licensed medical professional should be consulted for diagnosis and treatment of any and all medical conditions. Call 911 for all medical emergencies. Links to other sites are provided for information only -- they do not constitute endorsements of those other sites. © 1997- 2008 A.D.A.M., Inc. Any duplication or distribution of the information contained herein is strictly prohibited.

asthma

Asthma is an inflammatory disorder of the airways, which causes attacks of wheezing, shortness of breath, chest tightness, and coughing.
Asthma is caused by inflammation in the airways. When an asthma attack occurs, the muscles surrounding the airways become tight and the lining of the air passages swell. This reduces the amount of air that can pass by, and can lead to wheezing sounds.
Most people with asthma have wheezing attacks separated by symptom-free periods. Some patients have long-term shortness of breath with episodes of increased shortness of breath. Still, in others, a cough may be the main symptom. Asthma attacks can last minutes to days and can become dangerous if the airflow becomes severely restricted.
In sensitive individuals, asthma symptoms can be triggered by breathing in allergy-causing substances (called allergens or triggers). Triggers include pet dander, dust mites, cockroach allergens, molds, or pollens. Asthma symptoms can also be triggered by respiratory infections, exercise, cold air, tobacco smoke and other pollutants, stress, food, or drug allergies. Aspirin and other non-steroidal anti-inflammatory medications (NSAIDS) provoke asthma in some patients.
Approximately 20.5 million Americans currently have asthma. Many people with asthma have an individual or family history of allergies, such as hay fever (allergic rhinitis) or eczema. Others have no history of allergies.
exams and tests
persistent asthma. Common allergens include pet dander, dust mites, cockroach allergens, molds, and pollens. Common respiratory irritants include tobacco smoke, pollution, and fumes from burning wood or gas.
The doctor will use a stethoscope to listen to the lungs. Asthma-related sounds may be heard. However, lung sounds are usually normal between asthma episodes.
Tests may include:
Lung function tests
Peak flow measurements
Chest x-ray
Blood tests, including eosinophil count (a type of white blood cell)
Arterial blood gas In-Depth Diagnosis »
TopSymptoms
Wheezing
Usually begins suddenly
Comes in episodes
May be worse at night or in early morning
Gets worse with cold aira, exercise, and heartburn (reflux)
May go away on its own
Is relieved by bronchodilators (drugs that open the airways)
Cough with or without sputum (phlegm) production
Shortness of breath that gets worse with exercise or activity
Intercostal retractions (pulling of the skin between the ribs when breathing)
Emergency symptoms:
Extreme difficulty breathing
Bluish color to the lips and face
Severe anxiety due to shortness of breath
Rapid pulse
Sweating
Decreased level of alertness, such as severe drowsiness or confusion, during an asthma attack
Additional symptoms that may be associated with this disease:
Nasal flaring
Chest pain
Tightness in the chest
Abnormal breathing pattern --breathing out takes more than twice as long as breathing in
Breathing temporarily stops
The stress caused by illness can often be helped by joining a support group, where members share common experiences and problems. See asthma and allergy - support group.
Treatment is aimed at avoiding known allergens and respiratory irritants and controlling symptoms and airway inflammation through medication.
There are two basic kinds of medication for the treatment of asthma:
Long-term control medications are used on a regular basis to prevent attacks, not for treatment during an attack. Types include:
Inhaled steroids (such as Azmacort, Vanceril, AeroBid, Flovent) prevent inflammation
Leukotriene inhibitors (such as Singulair and Accolate)
Anti-IgE therapy (Xolair), a medicine given by injection to patients with more severe asthma
Long-acting bronchodilators (such as Serevent) help open airways
Cromolyn sodium (Intal) or nedocromil sodium
Aminophylline or theophylline (not used as frequently as in the past)
Sometimes a combination of steroids and bronchodilators are used, using either separate inhalers or a single inhaler (such as Advair Diskus).
Quick relief, or rescue, medications are used to relieve symptoms during an attack. These include:
Short-acting bronchodilators (inhalers), such as Proventil, Ventolin, Xopenex, and others.
Corticosteroids, such as prednisone or methylprednisolone) given by mouth or into a vein
Persons with mild asthma (infrequent attacks) may use quick relief medication as needed. Those with persistent asthma should take control medications on a regular basis to prevent symptoms. A severe asthma attack requires a medical evaluation and may require a hospital stay, oxygen, and intravenous medications.
A peak flow meter, a simple device to measure lung volume, can be used at home to help you "see an attack coming" and take the appropriate action, sometimes even before any symptoms appear. If you are not monitoring asthma on a regular basis, an attack can take you by surprise.
Peak flow measurements can help show when medication is needed, or other action needs to be taken. Peak flow values of 50-80% of an individual’s personal best results indicate a moderate asthma attack, while values below 50% indicate a severe attack.There is no cure for asthma, though symptoms sometimes decrease over time. With proper self management and medical treatment, most people with asthma can lead normal lives.
Possible Complications
Respiratory fatigue
Side effects of asthma medications
Pneumothorax
Death
When to Contact a Medical Professional
Call for an appointment with your health care provider if you or your child experience mild asthma symptoms (to discuss treatment options).
Call your health care provider (or go to the emergency room) for moderate shortness of breath (shortness of breath with talking, peak flow 50-80% of personal best), if symptoms worsen or do not improve with treatment, or an attack requires more medication than recommended in the prescription.
Go to the emergency room for severe shortness of breath (shortness of breath at rest, peak flow less than 50% of personal best), if drowsiness or confusion develops, or for severe chest pain.
Prevention
Asthma symptoms can be substantially reduced by avoiding known allergens and respiratory irritants. If someone with asthma is sensitive to dust mites, exposure can be reduced by encasing mattresses and pillows in allergen-impermeable covers, removing carpets from bedrooms, and by vacuuming regularly. Exposure to dust mites and mold can be reduced by lowering indoor humidity.
If a person is allergic to an animal that cannot be removed from the home, the animal should be kept out of the patient's bedroom. Filtering material can be placed over the heating outlets to trap animal dander. Exposure to cigarette smoke, air pollution, industrial dusts, and irritating fumes should also be avoided.
Allergy desensitization may be helpful in reducing asthma symptoms and medication use, but the size of the benefit compared with other treatments is not known.
Guidelines for the Diagnosis and Management of Asthma -- Update on Selected Topics 2002. Bethesda, MD. 2003 June. National Asthma

benefits of garlic in cancer

Written by Gloria Tsang, RDlast updated: October 2004
Health benefits of garlic are often reported. The most commonly known benefits of garlic are its potential role in heart disease and cancer. Read Benefits of Garlic in Heart Disease.
Benefits of Garlic: Cancer Prevention
Indeed, the first scientific report to study garlic and cancer was performed in the 1950s. Scientists injected allicin, an active ingredient from garlic, into mice suffering from cancer. Mice receiving the injection survived more than 6 months whereas those which did not receive the injection only survived 2 months.
Many studies showed that the organic ingredient of garlic, allyl sulfur, another active ingredient in garlic, are effective in inhibiting or preventing cancer development. Many observational studies in human being also investigated the association of using garlic and allyl sulfur and cancer. Out of the 37 studies, 28 studies showed evidence that garlic can prevent cancer. The evidence is particularly strong in prevention of prostate and stomach cancers. This particular study looking at the risk of stomach cancer was especially interesting. This study was conducted in China. Researchers found that smokers with high garlic intake have a relatively lower stomach cancer risk than smokers with low garlic intake.
A large-scale epidemiological Iowa Women's Health Study looked at the garlic consumption in 41,000 middle-aged women. Results showed that women who regularly consumed garlic had 35% lower risk of developing colon cancer.
It is thought that the allyl sulfur compounds in garlic prevent cancer by slowing or preventing the growth of the cancer tumor cells.
Garlic Key Message: In order to maximize the health benefits of garlic, it is suggested to wait 15 minutes between peeling and cooking garlic to allow the enzymatic reaction to occur to retain some health benefits of garlic. If you use garlic supplements, use the enteric coated tablets so that the healthy ingredients can survive the stomach and be absorbed into the bloodstream in the small intestines Please be cautious if you are taking garlic supplements and blood thinners such as aspirin and warfarin at the same time. Garlic supplements will further thin your blood. In addition, it is suggested to discontinue garlic supplementation at least 7 days prior to surgery.

acid reflux diet

Written by Gloria Tsang, RDPublished in Nov 2004; updated in Sept 2006
Many people take over-the-counter antacids for a quick ease of acid reflux, but for most people, a proper diet is the best solution for overcoming acid reflux.
Acid Reflux Diet Myth
Myth 1: Drink milkA lot of people try drinking milk to ease acid reflux before sleep. But often, milk ends up causing acid reflux during sleep. To understand the whole situation, we have to realize that the problem roots from eating too much at dinner time. Eating a big meal at dinner causes excess stomach acid production. Drinking milk could be a quick fix to the acid reflux problem. Unfortunately, milk has a rebound action and would eventually encourage secretion of more stomach acid, which causes the acid reflux. To solve the problem, try adjusting your diet by eating a small meal at dinner and have a small snack such as crackers before sleep.
Myth 2: Avoid coffee, citrus fruits and Spicy foodWe have been told for years that coffee, acidic fruit as well as spicy foods can aggravate acid reflux. Therefore, we should avoid these in our daily diet in order to reduce acid reflux. A recent study published in the Archives of Internal Medicine in May 2006 showed that none of these myths hold true. Researchers from the Stanford University found that the only two behavioral changes can reduce symptoms of acid reflux - eating less and elevate your head while sleeping.
Acid Reflux Diet
First of all, try to eat small, frequent meals instead of three big meals a day. Small amounts of food each time would exert less workload on the stomach and therefore requires less acid secretion for digestion. Make sure to include foods that are high in complex carbohydrates in each meal. These foods, such as rice, breads and pasta, are able to tie up excess stomach acid and are often easy on the stomach.
Avoid high-fat meals such as those from the fast food chains. High fat foods will remain in the stomach longer, thus causing the need for more stomach acid in order to digest them.
But remember, don't overeat! Eating too much of any foods will stimulate the stomach to secret more acids for digestion.
Avoid or limit alcohol.
Maintain upright position during and at least 45 minutes after eating.
Try elevating the head of bed six to eight inches when lying down.
Don't think that beverages just quickly flow through your stomach without affecting acid production. Surprisingly, a lot of beverages stimulate acid secretion such as beer, wine and pop. The worst of all is beer. It could double your stomach acid within an hour.

antioxidants 101

Written by Gloria Tsang, RDPublished in Dec 2005; Updated in Aug 2007
What are Antioxidants? Benefits of Antioxidants
Antioxidants are substances or nutrients in our foods which can prevent or slow the oxidative damage to our body. When our body cells use oxygen, they naturally produce free radicals (by-products) which can cause damage. Antioxidants act as "free radical scavengers" and hence prevent and repair damage done by these free radicals. Health problems such as heart disease, macular degeneration, diabetes, cancer etc are all contributed by oxidative damage. Indeed, a recent study conducted by researchers from London found that 5 servings of fruits and vegetables reduce the risk of stroke by 25 percent. Antioxidants may also enhance immune defense and therefore lower the risk of cancer and infection.
Most Commonly Known Antioxidants

Vitamin A and Carotenoids
Carrots, squash, broccoli, sweet potatoes, tomatoes, kale, collards, cantaloupe, peaches and apricots (bright-colored fruits and vegetables!)

Vitamin C
Citrus fruits like oranges and lime etc, green peppers, broccoli, green leafy vegetables, strawberries and tomatoes

Vitamin E
Nuts & seeds, whole grains, green leafy vegetables, vegetable oil and liver oil

Selenium
Fish & shellfish, red meat, grains, eggs, chicken and garlic
Other Common Antioxidants
Some common phytochemicals
Flavonoids / polyphenols
soy
red wine
purple grapes or Concord grapes
pomegranate
cranberries
tea
Lycopene
Tomato and tomato products
pink grapefruit
watermelon
Lutein
dark green vegetables such as kale, broccoli, kiwi, brussels sprout and spinach
Lignan
flax seed
oatmeal
barley
rye
Vitamin-like Antioxidants:
Coenzyme Q10 (CoQ10)
Glutathione
Antioxidant enzymes made by the body:
superoxide dismutase (SOD)
catalase
glutathione peroxidase
Message: Antioxidants are found abundant in beans, grain products, fruits and vegetables. Look for fruits with bright color - lutein in some of the yellow pigments found in corn; orange in cantaloupe, butternut squash and mango; red from lycopene in tomatoes and watermelon, and purple and blue in berries. So enjoy eating a variety of these products. It is best to obtain these antioxidants from foods instead of supplements. In addition, minimize the exposure of oxidative stress such as smoking and sunburn.