Posting has been light lately due to an overabundance of real life deadlines and responsibilities but we will be resuming our regularly scheduled programming shortly. Stay tuned.

~ The 3 Monkeys

Although this may seem to be a simple concept, skin functions in a complex way which is not easily mimicked.

Skin, Prof. Zilberman explains, serves a number of vastly different purposes. “Wound dressings must maintain a certain level of moisture while acting as a shield,” she says. “Like skin, they must also enable fluids from the wound to leave the infected tissue at a certain rate. It can’t be too fast or too slow. If too fast, the wound will dry out and it won’t heal properly. If too slow, there’s a real risk of increased contamination.”

Severe burns are a particularly nasty variety of dermal damage. About 70% of people with severe burns die from infections, not from their actual wounds. In a valiant effort to help patients survive the healing process nurses must change dressings often to prevent infection by cleaning the wounded areas. This new wound dressing can change all that by eliminating the need for constant redressing and by applying high levels of antibiotics precisely where they are needed.

Unlike oral antibiotics, locally-applied antibiotics can target and kill harmful bacteria before they enter the body to cause further infection, sepsis, or death. “People who suffer from large burns don’t usually die from the condition itself. The fatal culprits are the secondary bacterial infections that invade the body through these vulnerable burned areas,” says Prof. Zilberman.

The new TAU dressing inhibits bacterial growth and is biodegradable, which helps doctors avoid constant wound cleaning and  redressing, allowing the body to do the work on its own. “When administered at the wound, a doctor can give relatively high but local doses of antibiotics, avoiding any toxicity issues that arise when the same amount of antibiotic passes through the body,” explains Prof. Zilberman, who worked on this research with Jonathan Elsner, her Ph.D. student.

The only sad part of this news is how early in the development phase it is in right now.

Prof. Zilberman is now starting the early stages of clinical trials on animal models. So far, her wound dressing has passed physical and mechanical tests in vitro and in bacterial inhibition tests in the laboratory. She is also seeking a strategic partner to co-develop the research and take it to the commercial stage.

If this revolutionary new wound dressing survives the clinical stage then it may begin appearing in hospital near you within a few short years.

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Over a decade ago, the first part of this research led to some positive news as researchers found that certain mutations involved in the insulin pathways can greatly extend lifespan in worms.

“In the early 90s, we discovered mutations that could double the normal life span of worms,” Kenyon said. Those mutations effected insulin signals. Specifically, a mutation in a gene known as daf-2 slowed aging and doubled life span. That longer life depended on another “FOXO transcription factor” called DAF-16 and the heat shock factor HSF-1.

Unfortunately, the recent results show that adding sugar to the worm diet has the opposite effect.

By adding just a small amount of glucose to C. elegans usual fare of straight bacteria, they found the worms lose about 20 percent of their usual life span. They trace the effect to insulin signals, which can block other life-extending molecular players.

Here is the technical aspect of the results:

In fact, glucose makes no difference to the life span of worms that lack DAF-16 or HSF-1, they show. Glucose also completely prevents the life-extending benefits that would otherwise come with mutations in the daf-2 gene.Ultimately, worms fed a steady diet containing glucose show a reduction in aquaporin channels that transport glycerol, one of the ingredients in the process by which the body produces its own glucose. “If there is not enough glucose, the body makes it with glycerol,” Kenyon explained. That glycerol has to first get where it needs to go, which it does via the aquaporin channels.

There are a few ways in which the result from studying worms affects us as humans.

A diet with a low glycemic index seems like a safe bet for now. One of the scientists was alarmed enough with the data to make serious changes to her diet:

As an aside, Kenyon says she read up on low-carb diets and changed her eating habits immediately — cutting out essentially all starches and desserts — after making the initial discovery in worms. The discovery was made several years ago, but had not been reported in a peer-reviewed journal until now.

Another area of concern is medicine. Current drugs may be offering treatment which carry as of yet unknown long term side effects. Fortunately, as is the case with anti-depressant medication, science is continually advancing to make our lives better and this research will undoubtedly result in better life saving medicines.

She says the findings may also have implications for drugs now in development for the treatment of diabetes, which are meant to block glucose production by inhibiting glycerol channels. The new findings “raise a flag” that glycerol channels might be doing something else, she says, and that drugs designed to block them might have a downside.

A long term study recently found a connection between consuming two servings of diet soda daily and a significant decline in kidney function. How do different types of artificial sugars factor into these results? Is there any connection between these two studies?

Aging in humans is far more complex than in worms.

“Although we do not fully understand the mechanism by which glucose shortens the life span of C. elegans, the fact that the two mammalian aquaporin glycerol-transporting channels are downregulated by insulin raises the possibility that glucose may have a life-span-shortening effect in humans, and, conversely, that a diet with a low glycemic index may extend human life span,” the researchers write. Kenyon also points to recent studies that have linked particular FOXO variants to longevity in several human populations, making the pathway the first with clear effects on human aging.

Glucose and the insulin signaling pathways are probably just one piece in a complex puzzle explaining the aging process. With every piece of the puzzle that gets illuminated and understood we come one step closer to allowing science an opportunity to stop aging.

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Julie Lin MD, MPH, FASN and Gary Curhan, MD, ScD, FASN of Brigham and Women’s Hospital studied more than 3,000 women participating in the Nurses’ Health Study to identify the impact of sodium and sweetened drinks on kidney function.

The information from the participating women, whose median age is 67, was from 1984, 1986, and 1990 and included data about kidney function. Over the course of the years from 1989 – 2000, the shocking data revealed that over 11% of the women suffered a decline of over 30% in their kidney function.

“Thirty percent is considered significant,” says researcher Julie Lin, MD, MPH, assistant professor of medicine at Harvard Medical School and a staff physician at Brigham and Women’s Hospital in Boston. That’s especially true, she says, because most study participants had well-preserved kidney function at the start of the study.

What those women had in common was a thirst for artificially sweetened sodas which exceeded two per day. Other factors were ruled out in reaching that conclusion, including age, caloric intake, obesity, high blood pressure, diabetes, cigarette smoking, physical activity, and cardiovascular disease.

Put another way: the women who drank two or more diet sodas a day had a decline in their glomerular filtration rate, a measure of kidney function, of 3 milliliters per minute per year. ”With natural aging, kidney function declines about 1 mL per minute per year after age 40,” Lin says. No link was found with the other beverages. And less than two sodas a day didn’t seem to hurt. “We didn’t see any association up to two artificially sweetened beverages a day,” Lin says.

”A serving was reported as either a glass, a can, or a bottle of a beverage,” Lin tells WebMD. ”It was not more specific than that.”

”The mechanisms aren’t clear,” Lin says of the association she found. In another study she presented at the meeting, she found higher salt intake is also associated with faster kidney function decline.

Understanding the mechanisms are important because it can help evaluate with certainty whether these results are applicable to men as well.

Unsurprisingly, an industry group remains skeptical of these findings:

Asked to review the study findings, Maureen Storey, senior vice president of science policy for the American Beverage Association, says in a prepared statement: “It’s important to remember that this is an abstract presented at an annual meeting.” She notes that the research needs further scrutiny by researchers.

She acknowledges that kidney disease is serious but that diabetes and high blood pressure account for the majority of kidney disease cases, ”not consumption of diet soda.”

When it comes to dieting and exercise there are no short cuts. Diet soda may help satisfy a craving for a sugary beverage without the caloric penalty, but there may be unintended consequences. For example, what if the body recognizes a discrepancy between the information sent by the tongue, “sugar incoming”, and the message processed by the other parts of the metabolism, “no sugar received”? Logically, if the discrepancy is processed, the body will increase the hunger drive as a way of compensating for the missing sugar, which may cause the person to consume more calories than they would have otherwise.

Even for those people who take the excellent first step towards getting healthy by exercising need to be keenly aware of the law of unintended consequences, because exercise can make you fatter.

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Writing in the journal Medical Hypotheses, researcher Dr Colin Hendrie from the University of Leeds said: ‘Female inoculation with a specific male’s cytomegalovirus is most efficiently achieved through mouth-to-mouth contact and saliva exchange, particularly where the flow of saliva is from the male to the typically shorter female.’

Cytomegalovirus is likely to be only one of many germs which take advantage of kissing as a transfer system and which can confer benefits rather than harm to the recipient.

Cytomegalovirus, which lurks in saliva, normally causes no problems. But it can be extremely dangerous if caught while pregnant and can kill unborn babies or cause birth defects.

These can include problems ranging from deafness to cerebral palsy.

Kissing, over the course of several months and increasing in intensity, transfers small amounts of the virus each time. The result is a built up immunity to the virus, thereby cutting the risk of infection and potential damage to the fetus tremendously. Previous research had hypothesized that kissing was important because it conveyed fitness information about the individual through saliva. Given this new data and given that there are many other methods for determining fitness, kissing is not likely to have evolved as a means of determining fitness from an evolutionary perspective.

Dr Hendrie said: ‘Information concerning body tone, smell, reproductive condition, disease state and, of course, personal physical and oral hygiene can all be gained solely from close physical proximity.’

‘The small amount of additional information from kissing is an unlikely pressure for its development.’

People have subconsciously understood for a long time that germs can be transferred via kissing, hence that use of copious amounts of alcohol when strangers kiss. Clearly, it is being used as an antiseptic.

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It is no secret that anabolic steroids have all sorts of nasty side effects.

Anabolic steroids can cause many adverse effects. Most of these side effects are dose-dependent, the most common being elevated blood pressure, especially in those with pre-existing hypertension, and harmful changes in cholesterol levels: some steroids cause an increase in LDL cholesterol and a decrease in HDL cholesterol. Anabolic steroids have been shown to alter fasting blood sugar and glucose tolerance tests. Anabolic steroids such as testosterone also increase the risk of cardiovascular disease or coronary artery disease. Acne is fairly common among anabolic steroid users, mostly due to stimulation of the sebaceous glands by increased testosterone levels. Conversion of testosterone to dihydrotestosterone (DHT) can accelerate the rate of premature baldness for males who are genetically predisposed, but testosterone itself can produce baldness in females.

There is a whole bunch more (we left out some of the nastier bits) where that came from. Now we can include damage to kidneys as a side effect of abusing anabolic steroids too. In fact, the damage incurred is worse than what is seen in the kidneys of morbidly obese individuals.

The investigators studied a group of 10 bodybuilders who used steroids for many years and developed protein leakage into the urine and severe reductions in kidney function. Kidney tests revealed that nine of the ten bodybuilders developed a condition called focal segmental glomerulosclerosis, a type of scarring within the kidneys. This disease typically occurs when the kidneys are overworked. The kidney damage in the bodybuilders has similarities to that seen in morbidly obese patients, but appears to be even more severe.

However, some good news also comes from this study:

When the bodybuilders discontinued steroid use their kidney abnormalities improved, with the exception of one individual with advanced kidney disease who developed end-stage kidney failure and required dialysis. Also, one of the bodybuilders started taking steroids again and suffered a relapse of severe kidney dysfunction.

If stopped in time, kidney function can improve enough for daily functioning. Kidneys in particular are so vulnerable to the effects of anabolic steroids because they are affected both directly and indirectly:

The researchers propose that extreme increases in muscle mass require the kidneys to increase their filtration rate, placing harmful levels of stress on these organs. It’s also likely that steroids have direct toxic effects on the kidneys. “Athletes who use anabolic steroids and the doctors caring for them need to be aware of the potentially serious risks to the kidney,” said Dr. Herlitz.

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Michael LeBalanc, 40, was an healthy man who fainted one day. He began to get weaker and weaker as time passed and occasionally blacked out. It became obvious to doctors that something was wrong with his heart and they theorized that a virus may have caused his heart to weaken. One potential cause of a heart attack is a malfunctioning sinoatrial node, the heart’s natural pacemaker.

Brief biology lesson: The sinoatrial node is a clump of cells in the right atrium of the heart which generate the impulse controlling the heartbeat. Interestingly, these cells in the sinoatrial node are modified version of cardiac myocytes (human muscle cells), yet they do not contract.

Mr. LeBlanc had an internal pacemaker implanted which would give his heart a brief jolt to correct any abnormality in its rhythm, thereby preventing a heart attack. That type of pacemaker is formally called an Implantable Cardioverter Defibrillator (ICD). Dr. Helen, a Knoxville based psychologist, suffered a heart attack at the tender age of 37 and an ICD is responsible for keeping her alive today. However, her heart problem was not properly diagnosed right away:

Despite the fact that I was short of breath and shaking like a leaf, the doctor decided I was allergic to something in the gym and gave me a shot of benadryl. Actually, I later learned that shortness of breath and a sense of impending doom or death were signs (especially in women) of heart problems. I felt ok once I left the hospital and even for a week or two later. I was on vacation in Charleston, South Carolina when I again got short of breath and could not walk. I was so dizzy, scared and light-headed that I spent the day in bed until finally that night, I went to an emergency room.

There is a whole lot more to the story, so go read the whole thing. Fortunately, it has a happy ending and is a strong endorsement for the effectiveness of ICDs.

Unfortunately for Mr. LeBlanc, his ICD was working a little too well because his heart was deteriorating too quickly:

To keep me going, I qualified for a defibrillator, which basically shocked me if my heart rhythm started to get worse,” Mr. LeBlanc said. “But as I got sicker, the defibrillator kept going off, and it was awful.”

Even with the defibrillator, Mr. LeBlanc suffered a heart attack in April, followed by a stroke in July. Luckily, he was able to get to an emergency room before the stroke did too much damage.

Since Mr. LeBlanc was in otherwise good health and relatively young, UT Southwestern Medical Center in Texas decided he would be a great candidate for the newest generation of implantable heart saving devices, the Left-Ventricular Assist Device (LVAD).

“Mr. LeBlanc has cardiomyopathy, which causes the heart to dilate. The muscle becomes weaker, and it can’t pump efficiently,” said Dr. Dan Meyer, professor of cardiovascular and thoracic surgery at UT Southwestern and Mr. LeBlanc’s surgeon. “UT Southwestern has always had a presence in studying new mechanical assist devices, so we were honored to be only one of two sites in the state selected to implant the HeartWare LVAD as part of a national clinical trial.”

The pump is designed to rest inside the patient’s chest. A small cable attached to the device exits the body and connects to an externally worn controller. The controller is powered by a battery pack. The HeartWare LVAD has only one moving part, which contributes to its diminutive size. The lack of mechanical bearings is expected to lead both to longer-term device reliability and to a reduced risk of physical damage to blood cells as they pass through the pump, said Dr. Meyer, also director of the mechanical support program at UT Southwestern.

“The size of the device means the incision is also smaller. The entire implantation surgery takes about four hours,” Dr. Meyer said. “Mr. LeBlanc is a really great patient. He’s otherwise very healthy, and we believe he will do very well with the LVAD until he can get a new heart.”

Ok, as promised, here is where the story takes a left turn into “unusual land”:

He’s still adjusting to some of the stranger side effects of his new device, including no pulse. The LVAD keeps blood moving continually with no pulsation, so he no longer has a palpable heart beat or traditionally measurable blood pressure.

Think of all the mischief you could get into with an LVAD. Apparently, the infamous castle of Vlad the Impaler (the inspiration for Bram Stoker’s Dracula) is up for sale. With the right outfit and a bit of makeup you could show up and simply claim ownership.

Habsburg: I own it.

You: No, I do.

Habsburg: Not unless you’re some kind of vampire.

You: Check my pulse.

Habsburg: AAAAAAAAAAAAAAAAAHHHHHHHHHH!!!!

Habsburg: ::: runs away :::

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Leber’s congenital amaurosis (LCA) causes sight to deteriorate beginning at birth and and resulting in complete blindness before the age of forty.

Children born with one form, LCA2, have defects in a gene called RPE65 that helps the retina’s light-sensing cells make rhodopsin, a pigment needed to absorb light. Without rhodopsin, the photoreceptor cells gradually die.

Gene therapy works by using a modified virus as a delivery system to get specific genes into specific areas. (Take a look at our article Is Chronic Fatigue Syndrome Caused By A Virus? for some background about how viruses work explained in plain English). Researchers first tested the therapy on dogs and found they could partially restore sight by using a virus loaded with the RPE65 gene. Then the researchers conducted a limited study on six young adult humans, which also resulted in sight improvements.

But the Penn researchers knew from their studies in animals that children should improve even more because they have more intact retinal tissue than adults do. Today in an online paper in The Lancet, their team and collaborators in Europe report full study results for three of the adults they treated earlier and nine more patients, including four children ages 8 to 11. The children gained more light sensitivity than the adults did–their light sensitivity increased as much as four orders of magnitude, versus one–and they made far fewer mistakes in an obstacle course.

This is one of those good news/bad news stories.

The bad news:

• Older individuals with this disorder have lost more tissue, and therefore the therapy can be significantly less effective.
• This therapy only applies to blindness caused by a specific defective gene, and will not benefit someone suffering from any other type of blindness.

Now, the good news:

• Gene therapy sounds great in theory but has had few successes in real life applications. The success of this study will serve as boost to continue research into gene therapy.
• Other vision diseases are caused by genetic defects. In the near future it may be possible to do a simple blood test to determine which defective gene a child has and then apply the appropriate therapy to prevent a loss of vision from occurring in the first place.

There is a lot of excitement in the air because of the successful results. Take a look here to see a video of one of the patients, Cory Haas, breezing through an obstacle course a mere three months after therapy.

The LCA2 trials are a rare success for the field of gene therapy, which has also cured children with the immune disorder known as bubble boy disease. And they should pave the way for treating more vision disorders. “It’s an incredible launching pad to be able to target other diseases,” says Penn gene therapy researcher Jean Bennett, who led the study.

Showing that the LCA2 gene therapy treatment works best in children is “a big step” for inherited blindness, says geneticist Frans Cremers of Radboud University Nijmegen Medical Center in the Netherlands, who wrote an accompanying commentary in The Lancet. He notes that eight other vision diseases, including retinitis pigmentosa, have now been treated in mice and are ready to be tested in people. The challenge, he says, will be to expand genetic testing of people with blindness so as to find enough eligible patients for clinical trials of these rare disorders.

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There are two prevailing theories about the causes of depression. One is that depression can be caused by stressful life events and the second is that depression results from an imbalance in neurotransmitters. However, medications based on those theories are treating effects, not causes.

Most animal models that are used by scientists to test antidepressants are based on the hypothesis that stress causes depression. “They stress the animals and look at their behavior,” she said. “Then they manipulate the animals’ behavior with drugs and say, ‘OK, these are going to be good anti-depressants.’ But they are not treating depression; they are treating stress.”

That is one key reason why current antidepressants aren’t doing a great job, Redei noted. She is now looking at the genes that differ in the depressed rat to narrow down targets for drug development.

She said another reason current antidepressants are often ineffective is that they aim to boost neurotransmitters based on the popular molecular explanation of depression, which is that it’s the result of decreased levels of the neurotransmitters serotonin, norepinephrine and dopamine. But that’s wrong, Redei said.

Redei examined the genes involved in both stress and depression. Of the 254 genes related to stress and the 1275 genes related to depression there is an overlap of only 5 genes.

“This overlap is insignificant, a very small percentage,” Redei said. “This finding is clear evidence that at least in an animal model, chronic stress does not cause the same molecular changes as depression does.”

If current medications are only treating effects then research should be focused on finding and treating the causes.

In the second part of the study, Redei found strong indications that depression actually begins further up in the chain of events in the brain. The biochemical events that ultimately result in depression actually start in the development and functioning of neurons.

“The medications have been focusing on the effect, not the cause,” she said. “That’s why it takes so long for them to work and why they aren’t effective for so many people.”

Her animal model of depression did not show dramatic differences in the levels of genes controlling neurotransmitters functions. “If depression was related to neurotransmitter activity, we would have seen that,” she said.

Unfortunately, although we now know those theories are wrong, we still do not have a theory that is right.

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