A coral reef infested with cyanobacteria (dark). Photo courtesy of Jennifer Smith.            Seaweed may be a drug out of place In the pristine waters of Pu’uhonua o H’onauau National Historical Park off the Kona coast of Hawaii, a kind of seaweed consisting of blue-green cyanobacteria is considered a pest and bane to indigenous corals, which are smothered and killed by the rubbery, bulbous bacterial colonies.            But almost nothing nasty in nature is without its upside, a fact underscored again in findings by researchers at UC San Diego’s Scripps Institution of Oceanography and the Skaggs School of Pharmacy and Pharmaceutical Sciences, who found that the cyanobacterium – Leptolyngbya crossbyana – produces chemical compounds that may provide the basis for new anti-inflammatory medicines and anti-bacterial treatments.              Writing in the journal Chemistry & Biology, Hyukjae Choi, a postdoctoral researcher in the laboratory of William Gerwick and colleagues report that L. crossbyana secretes natural products known as honaucins, chemical compounds that control how and where the tiny algae grows and spreads.            If researchers can translate that natural talent into therapeutic drugs or treatments, they might be able to prevent at least some types of bacterial infections in humans or treat inflammation-related conditions like acne and arthritis.               “I think this finding is a nice illustration of how we need to look more deeply in our environment because even nuisance pests, as it turns out, are not just pests,” said Gerwick. “It’s a long road to go from this early-stage discovery to application in the clinic but it’s the only road if we want new and more efficacious medicines.”            You can read the entire UC San Diego news release here.
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A coral reef infested with cyanobacteria (dark). Photo courtesy of Jennifer Smith.
           
Seaweed may be a drug out of place

In the pristine waters of Pu’uhonua o H’onauau National Historical Park off the Kona coast of Hawaii, a kind of seaweed consisting of blue-green cyanobacteria is considered a pest and bane to indigenous corals, which are smothered and killed by the rubbery, bulbous bacterial colonies.           

But almost nothing nasty in nature is without its upside, a fact underscored again in findings by researchers at UC San Diego’s Scripps Institution of Oceanography and the Skaggs School of Pharmacy and Pharmaceutical Sciences, who found that the cyanobacterium – Leptolyngbya crossbyana – produces chemical compounds that may provide the basis for new anti-inflammatory medicines and anti-bacterial treatments.             

Writing in the journal Chemistry & Biology, Hyukjae Choi, a postdoctoral researcher in the laboratory of William Gerwick and colleagues report that L. crossbyana secretes natural products known as honaucins, chemical compounds that control how and where the tiny algae grows and spreads.           

If researchers can translate that natural talent into therapeutic drugs or treatments, they might be able to prevent at least some types of bacterial infections in humans or treat inflammation-related conditions like acne and arthritis.              

“I think this finding is a nice illustration of how we need to look more deeply in our environment because even nuisance pests, as it turns out, are not just pests,” said Gerwick. “It’s a long road to go from this early-stage discovery to application in the clinic but it’s the only road if we want new and more efficacious medicines.”           

You can read the entire UC San Diego news release here.

Image courtesy of the Alzheimer’s Reading Room Q&A with Dilip Jeste: cognitive decline and Alzheimer’s disease Every 70 seconds, someone in the United States is diagnosed with Alzheimer’s disease, a progressive neurological affliction that, some experts suggest, will eventually swamp the healthcare system if effective treatments are not found Last week, the Obama Administration announced a national plan to find solutions by 2025, among them expanded research and clinical trials. Toward that end, researchers at University of California, San Diego School of Medicine have just launched three randomized, double-blind, placebo-controlled clinical trials of new treatments for Alzheimer’s disease and a related disorder called Mild Cognitive Impairment. The trials investigate the purported cognitive beneficial effects of resveratrol, a compound found in red grapes, chocolate and tomatoes, and two drugs that target harmful accumulating plaques in the brain. For more information about the trials or to participate, call 858-246-1300 or email. That’s the good news. The bad news may be a study earlier this year in the British Medical Journal (BMJ) that suggests cognitive decline may begin earlier than previously thought, about age 45. We asked Dilip Jeste, MD, director of the Stein Institute for Research on Aging and a professor of psychiatry and neurosciences at UC San Diego, when folks should get worried. Q: Are you surprised at all by the BMJ study’s findings that cognitive abilities measurably decline after the age of 45? Is there any indication the decline might actually start even earlier in life? A: It’s really not a surprise.  Clinical and research experience suggests that, while notable cognitive decline may not be observed until late 50s or early 60s, at least subtle declines in some cognitive functions begin earlier. For example, mental processing speed starts slowing down as early as age 30.  Indeed, if we consider other systems in the body, degenerative changes in the knee cartilage appears at age 20. The news is not all bad, however. For one thing, aging is extremely heterogeneous. Different people age differently, and within the same person, different organs and tissues age at different rates. Similarly, not all cognitive abilities decline with age. Typically, vocabulary does not worsen with age until much later in life. There is also an interesting, not fully understood, but clear and consistent finding that subsequent birth cohorts tend to do better on cognitive tests. This is known as the “Flynn effect.” Thus, 30-year-olds tested in 2012 will tend to do better on a given cognitive test than 30-year-olds would have done on the same test several decades ago. (This may be, in part, because of improved nutrition and healthcare from younger age in recent birth cohorts.)  So, while decline in at least some cognitive domains begins well before “old age,” that rate may now be actually slower than it was in the past. Q: Everyone at any age can be forgetful or a little fuzzy in their thinking. What would be examples of signs indicating real or serious cognitive decline? Should we be looking for these signs in younger people? A: This is an important question, and one that our older patients are frequently concerned about: How do we distinguish normal forgetfulness from pathological memory loss or other cognitive decline? When the deficits are subtle, the only way to be certain about cognitive decline is through repeated cognitive testing with standardized and psychometrically validated measures, which allow one to take into account the normal effects of age, as well as differences attributable to education and other demographic factors. But in terms of potential warning signs that closer examination might be warranted, there are a couple of points to consider:  Things like remembering names of new acquaintances, or where one left the car keys or even minor word finding problems, these happen to all of us, and do tend to get subtly worse with age. But so-called recognition memory tends to be relatively spared.  So, if a person finds that he is having considerable difficulty recognizing something that he once knew well, that might be worth discussing with one’s physician. If other people notice that a middle-aged person is having progressive cognitive worsening, it may also be taken as a warning. Another example of a cognitive ability that tends to be relatively spared with aging is procedural memory – our ability to remember how to do things such as preparing a meal or writing a check or driving a car. When we lose this ability, it can be a sign of trouble, so again would be worth discussing with one’s physician.  As to whether physicians should routinely look for these signs in younger people, I do not believe that routine screening is in order. Investigation is needed when the changes are functionally relevant. Q: How do you slow age-related cognitive decline, especially the little, incremental stuff? A: We usually think of childhood as the period of growth and development, and old age as the period of deterioration. This view is simplistic. I like to say that aging begins at conception whereas some growth and development continue into old age. The well known adage of “use it or lose it” seems to have some scientific merit.  There is growing evidence at both the behavioral and neurobiological levels that an enriched /cognitively stimulating environment can benefit cognitive functioning. People who do daily crossword puzzles, read regularly, have an active social life, appear to be at a somewhat lower (although, unfortunately, not at zero) risk for dementia.  So staying mentally engaged is important. Other things that one can do include controlling cardiovascular risk factors.  By controlling blood pressure, watching one’s cholesterol, etc., one can reduce the risk of “micro infarcts” (tiny unnoticed strokes that, cumulatively, may impair cognitive function) as well as major strokes.  Exercise, reducing stress to the extent possible, a nutritionally balanced diet can all help with cognitive function. Risk factors for dementia include a strong family history of Alzheimer’s disease or other dementias, untreated or poorly treated diabetes or hypertension, head injuries. In people with such risk factors, signs of progressive cognitive decline should lead to a consultation with one’s physician. It is worth noting that stress, anxiety, or depression can worsen cognitive dysfunction. Therefore, these factors should also be considered in management. However, at present, there are no proven “cognitive enhancers” – i.e., drugs that would improve cognition and prevent dementia. The best strategy is healthy lifestyle.
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Image courtesy of the Alzheimer’s Reading Room

Q&A with Dilip Jeste: cognitive decline and Alzheimer’s disease

Every 70 seconds, someone in the United States is diagnosed with Alzheimer’s disease, a progressive neurological affliction that, some experts suggest, will eventually swamp the healthcare system if effective treatments are not found

Last week, the Obama Administration announced a national plan to find solutions by 2025, among them expanded research and clinical trials. Toward that end, researchers at University of California, San Diego School of Medicine have just launched three randomized, double-blind, placebo-controlled clinical trials of new treatments for Alzheimer’s disease and a related disorder called Mild Cognitive Impairment. The trials investigate the purported cognitive beneficial effects of resveratrol, a compound found in red grapes, chocolate and tomatoes, and two drugs that target harmful accumulating plaques in the brain. For more information about the trials or to participate, call 858-246-1300 or email.

That’s the good news. The bad news may be a study earlier this year in the British Medical Journal (BMJ) that suggests cognitive decline may begin earlier than previously thought, about age 45. We asked Dilip Jeste, MD, director of the Stein Institute for Research on Aging and a professor of psychiatry and neurosciences at UC San Diego, when folks should get worried.

Q: Are you surprised at all by the BMJ study’s findings that cognitive abilities measurably decline after the age of 45? Is there any indication the decline might actually start even earlier in life?

A: It’s really not a surprise.  Clinical and research experience suggests that, while notable cognitive decline may not be observed until late 50s or early 60s, at least subtle declines in some cognitive functions begin earlier.

For example, mental processing speed starts slowing down as early as age 30.  Indeed, if we consider other systems in the body, degenerative changes in the knee cartilage appears at age 20.

The news is not all bad, however. For one thing, aging is extremely heterogeneous. Different people age differently, and within the same person, different organs and tissues age at different rates. Similarly, not all cognitive abilities decline with age. Typically, vocabulary does not worsen with age until much later in life. There is also an interesting, not fully understood, but clear and consistent finding that subsequent birth cohorts tend to do better on cognitive tests.

This is known as the “Flynn effect.” Thus, 30-year-olds tested in 2012 will tend to do better on a given cognitive test than 30-year-olds would have done on the same test several decades ago. (This may be, in part, because of improved nutrition and healthcare from younger age in recent birth cohorts.)  So, while decline in at least some cognitive domains begins well before “old age,” that rate may now be actually slower than it was in the past.

Q: Everyone at any age can be forgetful or a little fuzzy in their thinking. What would be examples of signs indicating real or serious cognitive decline? Should we be looking for these signs in younger people?

A: This is an important question, and one that our older patients are frequently concerned about: How do we distinguish normal forgetfulness from pathological memory loss or other cognitive decline?

When the deficits are subtle, the only way to be certain about cognitive decline is through repeated cognitive testing with standardized and psychometrically validated measures, which allow one to take into account the normal effects of age, as well as differences attributable to education and other demographic factors.

But in terms of potential warning signs that closer examination might be warranted, there are a couple of points to consider:  Things like remembering names of new acquaintances, or where one left the car keys or even minor word finding problems, these happen to all of us, and do tend to get subtly worse with age. But so-called recognition memory tends to be relatively spared.  So, if a person finds that he is having considerable difficulty recognizing something that he once knew well, that might be worth discussing with one’s physician. If other people notice that a middle-aged person is having progressive cognitive worsening, it may also be taken as a warning.

Another example of a cognitive ability that tends to be relatively spared with aging is procedural memory – our ability to remember how to do things such as preparing a meal or writing a check or driving a car. When we lose this ability, it can be a sign of trouble, so again would be worth discussing with one’s physician.  As to whether physicians should routinely look for these signs in younger people, I do not believe that routine screening is in order. Investigation is needed when the changes are functionally relevant.

Q: How do you slow age-related cognitive decline, especially the little, incremental stuff?

A: We usually think of childhood as the period of growth and development, and old age as the period of deterioration. This view is simplistic. I like to say that aging begins at conception whereas some growth and development continue into old age. The well known adage of “use it or lose it” seems to have some scientific merit.  There is growing evidence at both the behavioral and neurobiological levels that an enriched /cognitively stimulating environment can benefit cognitive functioning. People who do daily crossword puzzles, read regularly, have an active social life, appear to be at a somewhat lower (although, unfortunately, not at zero) risk for dementia.  So staying mentally engaged is important.

Other things that one can do include controlling cardiovascular risk factors.  By controlling blood pressure, watching one’s cholesterol, etc., one can reduce the risk of “micro infarcts” (tiny unnoticed strokes that, cumulatively, may impair cognitive function) as well as major strokes.  Exercise, reducing stress to the extent possible, a nutritionally balanced diet can all help with cognitive function.

Risk factors for dementia include a strong family history of Alzheimer’s disease or other dementias, untreated or poorly treated diabetes or hypertension, head injuries. In people with such risk factors, signs of progressive cognitive decline should lead to a consultation with one’s physician.

It is worth noting that stress, anxiety, or depression can worsen cognitive dysfunction. Therefore, these factors should also be considered in management. However, at present, there are no proven “cognitive enhancers” – i.e., drugs that would improve cognition and prevent dementia. The best strategy is healthy lifestyle.

Staphylococcus aureus, magnified 50 thousand times. Hormone Plays Surprise Role in Fighting Skin InfectionsBoosts immune response when vitamin D levels are low Antimicrobial peptides (AMPs) are molecules produced in the skin to fend off infection-causing microbes. Vitamin D has been credited with a role in their production and in the body’s overall immune response, but scientists at the University of California, San Diego School of Medicine say a hormone previously associated only with maintaining calcium homeostasis and bone health is also critical, boosting AMP expression when dietary vitamin D levels are inadequate. The finding, published in the May 23, 2012 online issue of Science Translational Medicine, more fully explains how the immune system functions in different situations and presents a new avenue for treating infections, perhaps as an alternative to current antibiotic therapies. The immunological benefits of vitamin D are controversial. In cultured cell studies, the fat-soluble vitamin provides strong immunological benefits, but in repeated studies with humans and animal models, results have been inconsistent: People with low levels of dietary vitamin D do not suffer more infections. For reasons unknown, their immune response generally remains strong, undermining the touted immunological strength of vitamin D. Working with a mouse model and cultured human cells, Gallo and colleagues discovered why: When levels of dietary vitamin D are low (it’s naturally present in very few foods), production of parathyroid hormone (PTH), which normally helps modulate calcium levels in blood, is ramped up. More PTH or a related peptide called PHTrP spurs increased expression of AMPs, such as  cathelicidin, which kill a broad spectrum of harmful bacteria, fungi and viruses. “No one suspected a role for PTH or the PTH-related peptide in immunity,” said Richard L. Gallo, MD, PhD, professor of medicine and chief of UCSD’s Division of Dermatology and the Dermatology section of the Veterans Affairs San Diego Healthcare System. “This may help resolve some of the controversy surrounding vitamin D. It fills in the blanks.” More here
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Staphylococcus aureus, magnified 50 thousand times.

Hormone Plays Surprise Role in Fighting Skin Infections
Boosts immune response when vitamin D levels are low

Antimicrobial peptides (AMPs) are molecules produced in the skin to fend off infection-causing microbes. Vitamin D has been credited with a role in their production and in the body’s overall immune response, but scientists at the University of California, San Diego School of Medicine say a hormone previously associated only with maintaining calcium homeostasis and bone health is also critical, boosting AMP expression when dietary vitamin D levels are inadequate.

The finding, published in the May 23, 2012 online issue of Science Translational Medicine, more fully explains how the immune system functions in different situations and presents a new avenue for treating infections, perhaps as an alternative to current antibiotic therapies.

The immunological benefits of vitamin D are controversial. In cultured cell studies, the fat-soluble vitamin provides strong immunological benefits, but in repeated studies with humans and animal models, results have been inconsistent: People with low levels of dietary vitamin D do not suffer more infections. For reasons unknown, their immune response generally remains strong, undermining the touted immunological strength of vitamin D.

Working with a mouse model and cultured human cells, Gallo and colleagues discovered why: When levels of dietary vitamin D are low (it’s naturally present in very few foods), production of parathyroid hormone (PTH), which normally helps modulate calcium levels in blood, is ramped up. More PTH or a related peptide called PHTrP spurs increased expression of AMPs, such as  cathelicidin, which kill a broad spectrum of harmful bacteria, fungi and viruses.

“No one suspected a role for PTH or the PTH-related peptide in immunity,” said Richard L. Gallo, MD, PhD, professor of medicine and chief of UCSD’s Division of Dermatology and the Dermatology section of the Veterans Affairs San Diego Healthcare System. “This may help resolve some of the controversy surrounding vitamin D. It fills in the blanks.”

More here

To Test or Not to Test? Three questions about the new PSA guidelines A report published in Annals of Internal Medicine by the United States Preventive Services Task Force contained the following recommendation:  healthy men do not need an annual Prostate specific antigen blood test (PSA test). The recommendation is based on evidence that suggests these test do more harm than good as they often result in men undergoing aggressive and often unnecessary treatments. However, many physicians, including the American Urological Association, aren’t happy with the new guidelines. We’ve asked Kellogg Parsons, MD, associate professor of Surgery at UC San Diego Moores Cancer Center and urologic cancer expert, three questions about the PSA test and what these new guidelines mean for men’s health. Question:  How does a PSA test determine whether or not a man has prostate cancer? Answer: PSA stands for “prostate-specific antigen.” It is a blood test that acts as an early warning system for prostate cancer. It can indicate that a man has prostate cancer years before symptoms develop. This is an important concept because, by the time a man develops symptoms, it is often too late to completely cure the cancer. Q:  The article mentions that only men “exhibiting symptoms” should be screened.  What are symptoms of prostate cancer that men should be aware of? A: Symptoms of prostate cancer are very non-specific.  A good resource is the American Urological Association web site.  More importantly, men should talk to their doctors about any concerns they may have. Q: Men are notorious for skipping regular health checkups. By altering the PSA guidelines, do you think the new guidelines will do more harm than good? A: Many, if not most, prostate cancer experts agree that these new guidelines will do more harm than good. PSA is not a perfect test. It can be abnormal in men who do not have cancer. However, if used in a responsible way, PSA screening can significantly reduce a man’s chances of dying from prostate cancer, especially in men younger than 65 years of age. Over 30,000 men die each year of prostate cancer in the U.S. Men should talk to their doctor about what PSA testing can and cannot do for them as individuals. Photo from the American Urological Association
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To Test or Not to Test? Three questions about the new PSA guidelines

A report published in Annals of Internal Medicine by the United States Preventive Services Task Force contained the following recommendation:  healthy men do not need an annual Prostate specific antigen blood test (PSA test). The recommendation is based on evidence that suggests these test do more harm than good as they often result in men undergoing aggressive and often unnecessary treatments.

However, many physicians, including the American Urological Association, aren’t happy with the new guidelines. We’ve asked Kellogg Parsons, MD, associate professor of Surgery at UC San Diego Moores Cancer Center and urologic cancer expert, three questions about the PSA test and what these new guidelines mean for men’s health.

Question:  How does a PSA test determine whether or not a man has prostate cancer?

Answer: PSA stands for “prostate-specific antigen.” It is a blood test that acts as an early warning system for prostate cancer. It can indicate that a man has prostate cancer years before symptoms develop. This is an important concept because, by the time a man develops symptoms, it is often too late to completely cure the cancer.

Q:  The article mentions that only men “exhibiting symptoms” should be screened.  What are symptoms of prostate cancer that men should be aware of?

A: Symptoms of prostate cancer are very non-specific.  A good resource is the American Urological Association web site.  More importantly, men should talk to their doctors about any concerns they may have.

Q: Men are notorious for skipping regular health checkups. By altering the PSA guidelines, do you think the new guidelines will do more harm than good?

A: Many, if not most, prostate cancer experts agree that these new guidelines will do more harm than good. PSA is not a perfect test. It can be abnormal in men who do not have cancer. However, if used in a responsible way, PSA screening can significantly reduce a man’s chances of dying from prostate cancer, especially in men younger than 65 years of age. Over 30,000 men die each year of prostate cancer in the U.S. Men should talk to their doctor about what PSA testing can and cannot do for them as individuals.

Photo from the American Urological Association

The worm turns There are two main types of human intestinal parasite: Single-cell protozoa like giardia and cryptosporidium that live and multiply in the human gut, and multi-celled helminths, such as roundworms, pinworms and tapeworms (above). The latter may be appalling to look at, but at least in their adult form, they cannot multiply in the human body. And they tend to stay put. Perish the thought if, say, one had worms in the brain.
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The worm turns

There are two main types of human intestinal parasite: Single-cell protozoa like giardia and cryptosporidium that live and multiply in the human gut, and multi-celled helminths, such as roundworms, pinworms and tapeworms (above). The latter may be appalling to look at, but at least in their adult form, they cannot multiply in the human body. And they tend to stay put. Perish the thought if, say, one had worms in the brain.

William Sandborn, MD, chief of gastroenterology, at UC San Diego Health System, discusses a clinical trial for a promising therapy for patients with ulcerative colitis that can be self-administered.

Entamoeba histolytica cyst. Drug Found for Parasite that is Major Cause of Death Worldwide Research by a collaborative group of scientists from UC San Diego School of Medicine, UC San Francisco and Wake Forest School of Medicine has led to identification of an existing drug that is effective against Entamoeba histolytica. This parasite causes amebic dysentery and liver abscesses and results in the death of more than 70,000 people worldwide each year. Using a high-throughput screen for drugs developed by the research team, they discovered that auranofin – a drug approved by the US Food and Drug Administration 25 years ago for rheumatoid arthritis – is very effective in targeting an enzyme that protects amebae from oxygen attack (thus enhancing sensitivity of the amebae to reactive oxygen-mediated killing). The results of the work, led by Sharon L. Reed, MD, professor in the UCSD Departments of Pathology and Medicine and James McKerrow, MD, PhD, professor of Pathology in the UCSF Sandler Center for Drug Discovery, will be published in the May 20, 2012 issue of Nature Medicine. Entamoeba histolytica is a protozoan intestinal parasite that causes human amebiasis, the world’s fourth leading cause of death from protozoan parasites. It is listed by the National Institutes of Health as a category B priority biodefense pathogen.  Current treatment relies on metronidazole, which has adverse effects, and potential resistance to the drug is an increasing concern. More here
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Entamoeba histolytica cyst.

Drug Found for Parasite that is Major Cause of Death Worldwide

Research by a collaborative group of scientists from UC San Diego School of Medicine, UC San Francisco and Wake Forest School of Medicine has led to identification of an existing drug that is effective against Entamoeba histolytica. This parasite causes amebic dysentery and liver abscesses and results in the death of more than 70,000 people worldwide each year.

Using a high-throughput screen for drugs developed by the research team, they discovered that auranofin – a drug approved by the US Food and Drug Administration 25 years ago for rheumatoid arthritis – is very effective in targeting an enzyme that protects amebae from oxygen attack (thus enhancing sensitivity of the amebae to reactive oxygen-mediated killing).

The results of the work, led by Sharon L. Reed, MD, professor in the UCSD Departments of Pathology and Medicine and James McKerrow, MD, PhD, professor of Pathology in the UCSF Sandler Center for Drug Discovery, will be published in the May 20, 2012 issue of Nature Medicine.

Entamoeba histolytica is a protozoan intestinal parasite that causes human amebiasis, the world’s fourth leading cause of death from protozoan parasites. It is listed by the National Institutes of Health as a category B priority biodefense pathogen.  Current treatment relies on metronidazole, which has adverse effects, and potential resistance to the drug is an increasing concern.

More here

The Skin You’re In:  three questions for our expert on melanoma Researchers at the Mayo Clinic have reported that melanoma rates are on the rise in 18 to 39 year olds. For years we have been bombarded with information about sun-safety and the importance of wearing sunscreen and limiting exposure – so why this increase?  We’ve asked Greg Daniels, PhD, MD, associate clinical professor of Medicine at the UC San Diego School of Medicine and coordinator of UC San Diego Moores Cancer Center’s clinical melanoma program three questions about the rise of melanoma and what people can do to protect themselves. Question: The Mayo study cites tanning bed exposure as one cause of this uptick in melanoma rates amongst younger patients but representatives for the tanning bed industry are denying that their beds are unsafe.  Are tanning beds harmful? Is there a safe way to tan? Answer: Melanoma is associated with intense intermittent exposure to UV. Tanning beds fit this description and melanoma incidence is higher in patients reporting tanning bed use. Q: The message to wear sunscreen has been strongly promoted by the health care industry for years.  How effective are sunscreens in preventing melanoma? A: Sunscreen protection depends upon the proper use and quality of the block. The new FDA labeling guidelines will help clarify for consumers the protection afforded by the sun screens. Sun screens prevent non-melanoma skin cancers and damage to normal skin. The amount of protection sun screens offer regarding melanoma is not well defined. Q:  Many people know to pay attention to suspicious moles or skin abnormalities.  Is there any one place where melanoma tends to show up on the body? A: Skin awareness saves lives. Melanoma occurs at any site on the skin. Complete skin exams are essential. While some melanomas follow the pattern of pigmented lesion, some melanomas are not pigmented. It is important to look for any lesion that is either new or changing, particularly if the skin lesion is different than the lesions around them.
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The Skin You’re In:  three questions for our expert on melanoma

Researchers at the Mayo Clinic have reported that melanoma rates are on the rise in 18 to 39 year olds. For years we have been bombarded with information about sun-safety and the importance of wearing sunscreen and limiting exposure – so why this increase? 

We’ve asked Greg Daniels, PhD, MD, associate clinical professor of Medicine at the UC San Diego School of Medicine and coordinator of UC San Diego Moores Cancer Center’s clinical melanoma program three questions about the rise of melanoma and what people can do to protect themselves.

Question: The Mayo study cites tanning bed exposure as one cause of this uptick in melanoma rates amongst younger patients but representatives for the tanning bed industry are denying that their beds are unsafe.  Are tanning beds harmful? Is there a safe way to tan?

Answer: Melanoma is associated with intense intermittent exposure to UV. Tanning beds fit this description and melanoma incidence is higher in patients reporting tanning bed use.

Q: The message to wear sunscreen has been strongly promoted by the health care industry for years.  How effective are sunscreens in preventing melanoma?

A: Sunscreen protection depends upon the proper use and quality of the block. The new FDA labeling guidelines will help clarify for consumers the protection afforded by the sun screens. Sun screens prevent non-melanoma skin cancers and damage to normal skin. The amount of protection sun screens offer regarding melanoma is not well defined.

Q:  Many people know to pay attention to suspicious moles or skin abnormalities.  Is there any one place where melanoma tends to show up on the body?

A: Skin awareness saves lives. Melanoma occurs at any site on the skin. Complete skin exams are essential. While some melanomas follow the pattern of pigmented lesion, some melanomas are not pigmented. It is important to look for any lesion that is either new or changing, particularly if the skin lesion is different than the lesions around them.

“Birth of DNA (Epigenetics)” by Zdenko Herceg Deciphering DNA’s hidden code Reading the genetic “Book of Life” is not easy, an observation scientists learn all of the time. Consider the well-known nucleobases that comprise DNA. There are only four: adenine, thymine, guanine and cytosine (plus uracil, which is found in RNA).  It turns out, however, that cytosine comes in two modified forms: 5-methylcytosine (5-mc) and 5-hydroxymethlcytosine (5-hmC). The versions look almost alike, but affect genes in very different ways. In a paper published in the journal Cell today, researchers at the University of Chicago, the Ludwig Institute for Cancer Research  at UC San Diego and Emory University describe a new technique for reading the particular differences in cytosine, an achievement that has ramifications for better understanding fundamental life processes. These two modifications of cytosine “regulate gene expression that has broad impact on stem cell development, various human diseases such as cancer, and potentially neurodegenerative disease,” said Chuan He, a professor of chemistry at the University of Chicago. “They may even shape the development of the human brain.” He, with Bing Ren, PhD, head of the Laboratory of Gene Regulation at the Ludwig Institute for Cancer Research at UC San Diego, and colleagues developed a method called TAB-Seq that directly measures 5-hmC and produced the first map of the entire genome of 5-hmC at single-base resolution. Ren applied TAB-Seq to human embryonic stem cells; Peng Jin of Emory applied the method  to mouse embryonic stem cells. The work is expected to have a significant impact upon the field of epigenetics, which looks at changes in gene expression caused by factors other than alterations in the actual DNA. 5-mC and 5-hmC appear to be major epigenetic players. 5-mC is generally found on genes that are turned off; it helps silence genes that aren’t supposed to be turned on. Conversely, 5-hmC appears to be abundant on active genes, especially in brain cells. “This is a major breakthrough in that TAB-Seq allows precise mapping of all 5-hydroxymethylcytosine sites in a mammalian genome using well-established, next-generation DNA sequencing methods,” said Joseph Ecker, a professor at the Salk Institute for Biological Studies, who was not involved in the Cell study. “The study showed very clearly that deriving useful knowledge about this poorly understood epigenetic regulator requires determination of the exact locations of 5-hmC with base-level accuracy. I expect that their new method will immediately become widely adopted.”
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“Birth of DNA (Epigenetics)” by Zdenko Herceg

Deciphering DNA’s hidden code

Reading the genetic “Book of Life” is not easy, an observation scientists learn all of the time. Consider the well-known nucleobases that comprise DNA. There are only four: adenine, thymine, guanine and cytosine (plus uracil, which is found in RNA).  It turns out, however, that cytosine comes in two modified forms: 5-methylcytosine (5-mc) and 5-hydroxymethlcytosine (5-hmC). The versions look almost alike, but affect genes in very different ways.

In a paper published in the journal Cell today, researchers at the University of Chicago, the Ludwig Institute for Cancer Research  at UC San Diego and Emory University describe a new technique for reading the particular differences in cytosine, an achievement that has ramifications for better understanding fundamental life processes.

These two modifications of cytosine “regulate gene expression that has broad impact on stem cell development, various human diseases such as cancer, and potentially neurodegenerative disease,” said Chuan He, a professor of chemistry at the University of Chicago. “They may even shape the development of the human brain.”

He, with Bing Ren, PhD, head of the Laboratory of Gene Regulation at the Ludwig Institute for Cancer Research at UC San Diego, and colleagues developed a method called TAB-Seq that directly measures 5-hmC and produced the first map of the entire genome of 5-hmC at single-base resolution. Ren applied TAB-Seq to human embryonic stem cells; Peng Jin of Emory applied the method  to mouse embryonic stem cells.

The work is expected to have a significant impact upon the field of epigenetics, which looks at changes in gene expression caused by factors other than alterations in the actual DNA. 5-mC and 5-hmC appear to be major epigenetic players. 5-mC is generally found on genes that are turned off; it helps silence genes that aren’t supposed to be turned on. Conversely, 5-hmC appears to be abundant on active genes, especially in brain cells.

“This is a major breakthrough in that TAB-Seq allows precise mapping of all 5-hydroxymethylcytosine sites in a mammalian genome using well-established, next-generation DNA sequencing methods,” said Joseph Ecker, a professor at the Salk Institute for Biological Studies, who was not involved in the Cell study. “The study showed very clearly that deriving useful knowledge about this poorly understood epigenetic regulator requires determination of the exact locations of 5-hmC with base-level accuracy. I expect that their new method will immediately become widely adopted.”

Child brides in Rayer Bazar, Dhaka, Bangladesh. Images courtesy of MH Kawsar

Girl Child Marriages Decline In South Asia, But Only Among Youngest
Findings mixed in India, Nepal, Pakistan and Bangladesh

Each year, more than 10 million girls under the age of 18 marry, usually under force of local tradition and social custom. Almost half of these compulsory marriages occur in South Asia. A new study suggests that more than two decades of effort to eliminate the practice has produced mixed results.

Writing in the May 16, 2012 issue of Journal of the American Medical Association, Anita Raj, PhD, professor of medicine in the University of California, San Diego School of Medicine, and colleagues, report that marriage rates for girls under the age of 14 in India, Nepal, Pakistan and Bangladesh – the South Asian countries with the highest historical rates – have significantly declined since 1991. Conversely, the rate among girls aged 16 and 17 continues largely unchanged or, in the case of Bangladesh, has increased 36 percent.

Childhood marriage, which mostly involves girls, is widely condemned as a violation of individual human rights. Numerous studies have found that child brides are more likely to die young, suffer from serious health problems, live in poverty and remain illiterate.  

“There is a global effort to eliminate girl child marriage,” said Raj. “Our findings are heartening in terms of eliminating the practice among very young girls, but not among older girls. There needs to be a greater focus on prevention of marriage among later adolescents. If we cannot impact reduction of marriage in this age group, we’ll continue to see inadequate change on reduction of girl child marriage as a whole.”

Raj and colleagues examined randomized cluster samples from multiple demographic, health and nutrition surveys taken between 1991 and 2007 in India, Nepal, Pakistan and Bangladesh, where the prevalence of girl child marriages has historically reached or exceeded 20 percent.

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