Yes, ICantSeeYou

Study : Positive attitude 'no cure for cancer'

THE belief that a positive attitude can help fight cancer has been debunked by Australian specialists who have proved a fighting spirit does not improve survival chances.

The researchers said they realised their findings, presented at a major cancer conference in Chicago today, might not impress the majority of patients who believed their outlook could help their diagnosis, but said it could be good news too.

"People often really beat themselves up and blame their attitude if their cancer relapses," said Professor Kelly-Anne Phillips, a medical oncologist at the Peter MacCallum Cancer Centre in Melbourne.

"We've shown absolutely that you're not at fault. You cannot influence your cancer with positive or negative thinking, depression, a fighting spirit, or any other factor.

"That should be reassuring, but I guess it could cut both ways."

The study involved 708 women in the Australian Breast Cancer Family Study who had been newly diagnosed with localised breast cancer and tracked them over eight years to see whether their cancer relapsed.

A quarter died over the period.

Levels of depression, anxiety and other factors like fatalist outlook, avoidance, anger, and feelings of hopelessness were also assessed.

"Essentially the bottom line is we didn't find any correlation at all between these issues and whether their cancer came back," Prof Phillips said.

"This goes against what the vast majority of patients believe."

Women who had an anxious preoccupation with their cancer were more likely to relapse but once the researchers adjusted for all the things known to cause recurrence, like size and grade of the tumour, this association disappeared, she said.

"The women who were anxiously preoccupied were the ones that had the worst tumours, so they were anxious and preoccupied for a reason," said Prof Phillips.

She said women may not like the news as it might make them feel like they have little control of their outcome, "but it's important to see the upside too".

Cancer Council Australia chief executive Professor Ian Olver said he had been involved in a smaller study in lung cancer that reached a similar conclusion.

"A positive attitude is great and it clearly helps quality of life when you're going through treatment but it makes an undetectable difference to disease," he said.

Tumor suppressor genes speed up and slow down aging in engineered mouse

ROCHESTER, Minn. -- Mayo Clinic researchers have developed an animal model that can test the function of two prominent tumor suppressor genes, p16 and p19, in the aging process. Scientists knew that both these genes were expressed at increased levels as humans and mice age, but their role in the aging process was not clear. Findings by the Mayo team show that p16 provides gas to accelerate cellular aging, while p19 stops that process.

The findings, to be published May 30 in the online issue of Nature Cell Biology, could help explain the development of some characteristics associated with aging, such as loss of muscle mass and strength or cataracts, and how they might be retarded.

"Scientists interested in aging have developed mice that lack p16 or p19, but these mice were not suitable for studies on aging because they all die of cancer before they even begin to age," says the study's first author, Darren Baker, a laboratory technician at Mayo Clinic and a doctoral candidate. "By crossing these mice with a mouse strain that ages five times faster than normal due to a mutation in the BubR1 gene, we were able to bypass this problem."

While other genes are involved in aging, the researchers firmly established that when too much p16 is produced, tissues start to age. Instead of driving aging, the p19 gene was found to counteract the effects of p16. This was completely unexpected, says Jan van Deursen, Ph.D., a molecular biologist at Mayo Clinic, because tissue culture experiments had predicted that p19 expression promotes aging.

Another important finding of the study is that initiation and progression of aging is caused, at least in part, by the accumulation of senescent or aging cells in tissues and organs. These senescent cells have an abnormal gene expression profile and secrete proteins that damage the surrounding cells, affecting tissue and organ function and aspects of aging.

Researchers clear up Alzheimer's plaques in mice

New Haven, Conn. – Blocking a common immune system response cleared up plaques associated with Alzheimer’s Disease and enabled treated mice to recover some lost memory, Yale University researchers report Friday in the journal Nature Medicine.

Researchers hope the new approach may one day overcome one of the biggest obstacles to development of new dementia medications – the difficulty in finding drugs that can safely cross the blood-brain barrier.

The results of the research surprised the scientists working in the lab of Richard Flavell, senior author of the paper, chairman of the Department of Immunobiology at Yale and investigator with the Howard Hughes Medical Institute. Flavell’s team originally thought that blocking the immune system molecule TGF-β(or transforming growth factor), might actually increase the buildup of amyloid plaques associated with Alzheimer’s Disease

Earlier studies had shown that Alzheimer’s patients tend to have elevated amounts of TGF-β, which plays a key role in activating immune system response to injury. Some had thought the presence of the molecule was simply an attempt to quiet the inflammatory response caused by a buildup of plaque.

Instead, the team found that as much as 90 percent of the plaques were eliminated from the brains of mice genetically engineered to block TGF-β in the peripheral immune cells.

It was like a vacuum cleaner had removed the plaques," Flavell said.

When the TGF-β pathway was interrupted in mice engineered to have Alzheimer’s, the mice showed an improved ability to perform some tests, including navigating mazes when compared to mice without TGF-β blocked. Scientists also found lower levels of other biological markers associated with the dementia.

When TGF-β was blocked, the immune system seemed to unleash immune cells known as peripheral macrophages. The macrophages passed through the blood-brain barrier and surrounded the neurons and plaques in the brains of mice. “If results from our study in mice engineered to develop Alzheimer’s-like dementia are supported by studies in humans, we may be able to develop a drug that could be introduced into the bloodstream to cause peripheral immune cells to target the amyloid plaques," said Terrence Town, lead author of the study.

Darpa's New Medical Treatment: Putty

When bombs shatter bones with compound fractures, it can take multiple surgeries and lots of rehab to set things right.  So Darpa, the Pentagon's premiere research shop, wants to "develop a dynamic putty-like material" that can be packed around a shattered bone, support the body while the patient heals -- and bio-degrade, once it's all over. 

If successful, this "Fracture Putty" could "rapidly restore a patient to ambulatory function while normal healing ensues, with dramatically reduced rehabilitation time and the elimination of infection and secondary fractures," the agency notes.

But, like all Darpa programs, it'll be tough. Challenges for the program include:

...novel bioresorbable adhesives which bond preferentially to bone vs. soft tissues, with bone-like mechanical properties, in the wet biological environment; load-bearing biomaterials with high mechanical strength and high porosity that match the mechanical properties of bone; biomaterials which create hierarchical bone-like internal structure; and biomaterials which adapt to biochemical cues.

There's a meeting on July 1 in Virginia, to kick off the program.

Doctors Using Pig Powder to Regrow a Soldier's Finger

Last week in an operating room in Texas, a wounded American soldier underwent a history-making procedure that could help him regrow the finger that was lost to a bomb attack in Baghdad, Iraq, last year.

Army Sgt. Shiloh Harris' doctors applied specially formulated powder to what's left of the finger in an effort to do for wounded soldiers what salamanders can do naturally: replace missing body parts.

If it sounds like science fiction, the lead surgeon agreed.

"It is. But science fiction eventually becomes true, doesn't it?" asked Dr. Steven Wolf of Brooke Army Medical Center.

Harris' surgery is part of a major medical study of "regenerative medicine" being pursued by the Pentagon and several of the nation's top medical facilities, including the University of Pittsburgh Medical Center and the Cleveland Clinic. Nearly $250 million has been dedicated to the research.

Air Force Tech. Sgt. Israel Del Toro is one of the wounded vets who might one day benefit from this research. He was injured by a bomb in Afghanistan. Both his hands were badly burned. On his left hand, what was left of his fingers fused together.

"You know, in the beginning, when I first got hurt, I told them, just cut it off. So I can get some function," Del Toro said. His doctors did not cut off his injured left arm. And since that injury, advancements in burn and amputation treatment mean he may one day be able to use his fingers again.

A key to the research dedicated to regrowing fingers and other body parts is a powder, nicknamed "pixie dust" by some of the people at Brooke. It's made from tissue extracted from pigs.

The pixie dust powder itself doesn't regrow the missing tissue; it tricks the patient's body into doing that itself.

All bodies have stem cells. As we are developing in our mothers' wombs, those stem cells grow our fingers, toes, organs -- essentially, our whole body. The stem cells stop doing that around birth, but they don't go away. The researchers believe that the "pixie dust" can put those stem cells back to work growing new body parts.

The powder forms a microscopic "scaffold" that attracts stem cells and convinces them to grow into the tissue that used to be there.

"If it is next to the skin, it will start making skin. If it's next to a tendon, it will start making a tendon, and so that's the hope, at least in this particular project, that we can grow a finger," Wolf said.

It has worked in earlier experiments. "They have taken a uterus out of a dog, made one in the lab, put it back in and had puppies," Wolf said. Researchers have also regrown a human bladder and implanted it in a person, and it is working as nature intended.

Although the technique has incredible promise, doctors will be watching for unexpected side effects as they follow Harris' recovery. "It could grow a cancer," Wolf said. "We will be closely monitoring for that to make sure that doesn't happen."

If the military's most badly wounded start benefiting, so will civilians. "If we can pull this off in missing parts the next step is, OK, can we grow a pancreas? Can we grow and replace that in a diabetic? And can we do the same thing with a kidney and can we do the same thing with a heart?"

One day, he hopes, people with heart trouble will be told, "That's OK. We will just grow you another one."

"That is something that is real science fiction."

In a study that couldnt come too soon - Study: Premature ejaculation defined

Experts from 10 countries, including Australia, the United States, Germany and Egypt, say they have defined life-long premature ejaculation.

Co-author Dr. Chris G McMahon of the University of Sydney says they developed the first-ever evidence-based definition of lifelong premature ejaculation in the hope it will aid future diagnosis, treatment and research.

The definition was developed after lengthy critical evaluation of the evidence presented in more than 100 studies on the sexual problem published over the last 65 years. It was unanimously agreed by the experts that the definition of lifelong premature ejaculation should be a combination of three key factors:

-- Ejaculation that always or nearly always occurs prior to or within about one minute of vaginal penetration.

-- The inability to delay ejaculation on all or nearly all vaginal penetrations.

-- Negative personal consequences such as distress, bother, frustration and/or the avoidance of sexual intimacy.

The study, conducted by the Standards Committee of the International Society for Sexual Medicine, is published online in the BJU International and The Journal of Sexual Medicine.

Electric Implant Device Could Do Away With Gastric Bypass

A New Way to Treat Obesity

Researchers believe that they might be able to combat obesity by blocking a nerve that helps regulate digestion.

Stomach signals: In VBLOC therapy, two electrodes are surgically implanted at the top of the stomach to block signals from the vagus nerve. In the illustration above, green arrows indicate neural signals traveling from the brain to the digestive system, while blue arrows indicate signals traveling from the stomach and intestines to the brain. A small regulator (shown at right) that controls the frequency and amplitude of electrical signals is implanted beneath the skin and connected to the electrodes (shown here in gray) via wires. The electrical signals can be changed at the physician’s office via a wireless controller. The device is currently being tested in clinical trials and has not yet been approved by the FDA. Credit: Enteromedics

An implantable device that uses electrical signals to block the vagus nerve, which helps regulate digestion, has shown early success in clinical trials. The experimental therapy, developed by Enteromedics, a medical-device company based in St. Paul, MN, is part of a growing trend to develop alternatives to gastric bypass surgery, an often highly successful but invasive procedure to curb obesity.

"We need an approach to this that is safer than current alternatives and efficient to perform," says Christopher Thompson, a surgeon at Brigham and Women's Hospital who tests new surgical tools and methods.

As the obesity epidemic booms, so has the number of people undergoing gastric bypass surgery, a procedure in which the stomach is surgically reduced to about the size of a lemon. The American Society for Metabolic and Bariatric Surgery estimates that gastric bypass rates have doubled in the United States in the past five years, from about 100,000 in 2003 to approximately 200,000 in 2007.

While gastric bypass often leads to dramatic weight loss, only a small percentage of people eligible for the surgery--those with a body mass index (BMI) of more than 35--actually choose to do it. That may be because the procedure comes with some serious risks and is irreversible, requiring permanent dietary restrictions and nutritional supplements. "Many people who really need the procedure don't seek out medical attention because they're worried about potential medical complications," says Thompson. "We're only treating a small fraction of eligible patients."

A new option is on the horizon. At a neurotechnology conference in Boston last week, Enteromedics described positive preliminary results from a European trial of its vagal blocking therapy, called VBLOC.

The device uses an electrical stimulator to block signals from the vagus nerve, which connects the brain to the gastrointestinal organs, regulating hormones and other factors involved in satiety and hunger. "It controls how the stomach expands when we start to eat," says Mark Knudson, chief executive officer at Enteromedics. "If it doesn't expand, we become full after a few bites."

In the procedure, two small electrodes are laparoscopically implanted next to vagal nerve fibers at the top of the stomach. A regulator implanted under the skin sends high-frequency pulses of electricity to the electrodes, which are thought to block the signals coming from the vagus nerve. While scientists don't know exactly how it works, they theorize that the device blocks signals that would normally tell the stomach to expand to accept food, as well as trigger the release of digestive enzymes and gastric acid, potentially slowing digestion. Many patients report feeling less hungry and feeling fuller earlier, says Knudson.

An analysis of nine patients who were among the first to receive the implant shows that they lost almost 30 percent of their excess body weight after nine months. And preliminary data from a larger group indicates that following the procedure, patients ate an average of 500 fewer calories per day. "That's less than you'd see for a lap band or a gastric bypass, but it's still pretty good," says Janey Pratt, a surgeon at Massachusetts General Hospital, in Boston.

If you're a hospital patient and a doctor refers to you as a "rock" it's probably not a compliment, but try not to take offense if a nurse mutters "S.O.B." in describing your condition.

If you're a hospital patient and a doctor refers to you as a "rock" it's probably not a compliment, but try not to take offense if a nurse mutters "S.O.B." in describing your condition.

Those are just two examples of the common slang and shorthand that reveal one of medicine's little secrets: Doctors and nurses gossip just like anyone else, and they're not above gossiping about the patients they serve.

Some of the jargon is harmless or even useful; for instance, "S.O.B." usually is an acronym for shortness of breath.

But medical educators are trying to curtail the use of more callous language that can lead doctors to think of their patients as obstacles to overcome, rather than human beings deserving of empathy.

Medical residents tend to pick up such terms quickly during training, and many said the lingo ranges from humorous to downright nasty. A patient not in obvious need of surgery may get the tag "lgfd" — short for "looks good from the door."

But a "rock" describes someone whose condition never seems to get better or worse, creating a hassle for doctors who often see their job as moving patients smoothly through the system.

"It's implying that these human lives, these suffering people, are no more than mere insults to you," said Dr. John Schumann, a professor of internal medicine at the University of Chicago Medical Center who tries to prevent medical students from adopting crude habits of speech.

Medical slang is always changing, but doctors say many of the terms in current use appeared a generation ago, when residents routinely endured seemingly endless shifts and a crushing workload that was supposed to prepare them for the rigors of medical practice.

Some residents said they still pick up slang terms from the influential 1978 novel The House of God, one doctor's fictionalized account of the absurdity and emotional churn of medical training. One of the most infamous words that book introduced was "gomer," short for "Get Out of My Emergency Room" — usually for elderly patients with difficult, chronic illnesses.

"Oh, we never use that word anymore," said Dr. Alexis Dunne, a third-year internal medicine resident at Northwestern University School of Medicine. "That's old school."

But other trainees said the dread word still makes an appearance now and then. Dr. Mark Obermeyer of Loyola University Medical Center said his colleagues strive not to use offensive language around patients, but some amount of venting is only natural.

"A lot of this work is pretty morbid," said Obermeyer, a resident in internal medicine and pediatrics. "If you're working in an ICU with people who may die any day, you use different ways to keep your mood up."

Indoctrination into the finer points of slang is part of what many professors call the hidden curriculum of medical school and residency training. The official coursework requires reading textbooks and paying attention during medical rounds, but the rest comes from watching how older doctors and nurses actually deal with the sometimes overwhelming experience of caring for patients.

A common slip happens when doctors refer to a patient as his or her disease — as in, "the gall bladder in Room 602" or "the P.E. (short for pulmonary embolism) who was admitted last night."

Gregory Makoul, director of Northwestern's center for communication and medicine, said such references can make doctors forget the human dimension of their decisions.

"When you start labeling someone as a disease you can't help but see them as a problem and not as a person," Makoul said. "We try to get people to recognize that, the power and detriment of that sort of label."

Some residents note that medical privacy regulations have made doctors and nurses careful about using a patient's name, which can encourage shorthand such as referring to patients by their diseases

Many medical slang terms revolve around the struggle to get patients in and out of the hospital in as short a time as possible. Schumann said such concerns reached new heights in the 1980s, when Medicare and many insurance plans began paying hospitals fixed rates according to a patient's illness, putting a premium on wrapping up care quickly

A 17-year-old Ottawa high school student invents way to identify and cure the flu.

OTTAWA–It's not the long-sought cure for the common cold but a 17-year-old Ottawa high school student won a national science competition today by developing a novel way of identifying and perhaps even fighting flu infections.

Maria Merziotis, a Grade 12 student at Hillcrest High School, won a $5,000 first prize and a chance to take her discovery to an international competition in San Diego next month.

A team of three Toronto Grade 10 students, Jonathan Schneider, Josh Alman and Norman Yau from the University of Toronto School, won the $4,000 second prize for identifying genes that help a plant thrive in salty soil.

They will also go to San Diego.

Vandana Rawal, a 15-year-old from Montreal's Centennial Regional High School, won third place and $3,000 for discovering a human gene variation that may help in dealing with bipolar disorder.

Health Canada is already looking at Merziotis's work, which offers a new way of identifying, and perhaps even fighting different influenza strains.

The flu virus attacks human cells by binding to a compound called sialic acid, or sialyllactose, on the cell surface. Merziotis synthesized a floating form of the acid, which dupes the virus with an alternative attachment site.

She said her process can help with both diagnosis and treatment.

"It can be used to detect what strain of influenza is responsible for a specific infection," she said. "It can differentiate between human and avian strains.

"It may also be possible to interfere with the infection process by administering the floating sialyllactose through injection, nasal spray or lungs with a pump. The flu virus would attach to the artificial receptor rather than the human cell."

The teens were competing in the Sanofi-Aventis BioTalent Challenge, a competition jointly sponsored two leading drug companies, the National Research Council and several other government agencies.

"The students in this competition represent some of the brightest young scientists in Canada," said Roman Szumski, vice-president of life sciences at the NRC.

The Toronto team's work with the plant gene offers insights into developing crops resistant to salty soils.

Rawal's work found a human gene variation which may explain why lithium is effective for some but not all bipolar patients.

The competition, now in its 15th year, involved 14 regional winners, both individuals and teams, from across the country.

Their projects ranged from an investigation of the role that mercury-polluted snow may play in northern community cancer rates, to methods of improving the survival of frozen stem cells and a study of herbal medicines.

Imagine being able to tone down appetite and promote weight loss, while improving the body’s ability to handle blood sugar levels.

Blocked brain enzyme decreases appetite and promotes weight loss

“We believe we have identified an important drug development target that could potentially turn into a metabolic triple play: appetite control, weight loss and blood sugar management,“ said Means, who is the Nanaline H. Duke Professor and Chairman of Pharmacology and Cancer Biology.

For many years, scientists have been identifying and testing every step of the appetite stimulation and suppression pathways in search of a target. Such research is considered critical to finding ways for people to better control their weight and minimize their risk of developing diabetes, heart disease and other health conditions.

Activation of the enzyme CaMKK2 is just one step in the appetite stimulation pathway located in the hypothalamus section of the brain. An empty stomach releases the hormone ghrelin, which launches a cascade of signals that ultimately results in increased appetite.

Means and colleagues believed that CaMKK2 in the ghrelin pathway might be a likely candidate for study, because it activates AMPK, an enzyme that stimulates animals to eat and gain weight. They tested their theory in several ways, the results of which are published in the May issue of Cell Metabolism. The work was funded by NIH grants, as well as by the Australian Research Council, National Heart Foundation, and the National Health and Medical Research Council of Australia.

First they blocked CaMKK2 in mice with a specialized molecule inhibitor and then measured food intake. These mice ate significantly less food than untreated mice during the six days in which they were evaluated, and also lost body weight, which led the scientists to think they might be on to something.

Next they studied a group of mice that normally do not make CaMKK2 and found that the molecule inhibitor did not change feeding behavior or reduce weight. “The fact that blocking CaMKK2 worked in normal mice to make them eat less and lose weight, but not in mice missing the enzyme, provides compelling evidence that CaMKK2 signaling is a requirement for appetite control,” Means said.

They also studied both normal mice and mice missing CaMKK2 to learn how these types responded to low-fat and high-fat diets. After nearly 30 weeks on the specific diets, the normal mice on the high-fat diet became diabetic – they were unable to respond to insulin and weren’t able to manage blood sugar levels well. In contrast, the normal mice on a low-fat diet stayed healthy.

In mice missing CaMKK2, the scientists found that they stayed healthy regardless of whether they were on a low-fat or high-fat diet. The CAMKK2-negative mice apparently were protected from changes that lead to diabetes in a high-fat diet.

“Remarkably, we find that blocking CaMKK2 in the brain prevents the deposits of fat in liver and skeletal muscle that are characteristic of obese, diabetic patients,” Means said. “We find this very exciting and are trying to understand the mechanism responsible for this protective effect, as well as to identify more potent drugs to inhibit CaMKK2.”

Woman Suffers From Disease That Causes Fish Odor (video)

The man who grew a finger

The man who grew a finger

                                                                

The man who grew a finger

            In every town in every part of this sprawling country you can find a faceless sprawling strip mall in which to do the shopping.

 

Rarely though would you expect to find a medical miracle working behind the counter of the mall's hobby shop.

That however is what Lee Spievak considers himself to be.

"I put my finger in," Mr Spievak says, pointing towards the propeller of a model airplane, "and that's when I sliced my finger off."

       

                                 

I think that within ten years that we will have strategies that will re-grow the bones, and promote the growth of functional tissue around those bones                                                           Dr Dr Stephen Badylak University of Pittsburgh

   

It took the end right off, down to the bone, about half an inch.

"We don't know where the piece went."

The photos of his severed finger tip are pretty graphic. You can understand why doctors said he'd lost it for good.

Today though, you wouldn't know it. Mr Spievak, who is 69 years old, shows off his finger, and it's all there, tissue, nerves, nail, skin, even his finger print.

'Pixie dust'

How? Well that's the truly remarkable part. It wasn't a transplant. Mr Spievak re-grew his finger tip. He used a powder - or pixie dust as he sometimes refers to it while telling his story.

Mr Speivak's brother Alan - who was working in the field of regenerative medicine - sent him the powder.

For ten days Mr Spievak put a little on his finger.

"The second time I put it on I already could see growth. Each day it was up further. Finally it closed up and was a finger.

"It took about four weeks before it was sealed."

Now he says he has "complete feeling, complete movement."

The "pixie dust" comes from the University of Pittsburgh, though in the lab Dr Stephen Badylak prefers to call it extra cellular matrix.

Pig's bladder

The process he has been pioneering over the last few years involves scraping the cells from the lining of a pig's bladder.

The remaining tissue is then placed into acid, "cleaned" of all cells, and dried out.

It can be turned into sheets, or a powder.

How it works in detail

It looks like a simple process, but of course the science is complex.

"There are all sorts of signals in the body," explains Dr Badylak.

"We have got signals that are good for forming scar, and others that are good for regenerating tissues.

"One way to think about these matrices is that we have taken out many of the stimuli for scar tissue formation and left those signals that were always there anyway for constructive remodelling."

In other words when the extra cellular matrix is put on a wound, scientists believe it stimulates cells in the tissue to grow rather than scar.

If they can perfect the technique, it might mean one day they could repair not just a severed finger, but severely burnt skin, or even damaged organs.

Clinical trial

They hope soon to start a clinical trial in Buenos Aires on a woman who has cancer of the oesophagus.

The normal procedure in such cases is often deadly. Doctors remove the cancerous portion and try to stretch the stomach lining up to meet the shortened oesophagus.

In the trial they will place the extra cellular matrix inside the body from where the portion of oesophagus has been removed, and hope to stimulate the cells around it to re-grow the missing portion.

So could limbs be re-grown? Dr Badylak is cautious, but believes the technology is potentially revolutionary.

"I think that within ten years that we will have strategies that will re-grow the bones, and promote the growth of functional tissue around those bones. And that is a major step towards eventually doing the entire limb."

That kind of talk has got the US military interested.

They are just about to start trials to re-grow parts of the fingers of injured soldiers.

Skin burns

They also hope the matrix might help veterans like Robert Henline re-grow burnt skin.

He was almost killed in an explosion while serving in Iraq. His four colleagues travelling with him in the army Humvee were all killed.

He suffered 35% burns to his head and upper body. His ears are almost totally gone, the skin on his head has been burnt to the bone, his face is a swollen raw mess.

So far he has undergone surgery 25 times. He reckons he has got another 30 to go.

Anything that could be done in terms of regeneration would be great he says.

"Life changing! I think I'm more scared of hospitals than I am of going back to Iraq again."

Like any developing technology there are many unknowns. There are worries about encouraging cancerous growths by using the matrix.

Doctors though believe that within the so called pixie dust lies an amazing medical discovery.

Male menopause? Yes, it’s real

Waning testosterone in your aging partner could cause mood changes

Is there really such a thing as "male menopause"? Conventional wisdom says that menopause is a "woman's condition," but as men advance into their 40s they also experience a progressive decline in hormone levels, namely testosterone. The result can be andropause, which is estimated to affect about 5 million American men.

The hormonal decline that men experience isn't nearly as abrupt as it is in women — it's more like walking down a hill than jumping off a cliff. However, waning testosterone is likely to make a guy moody, irritable and depressed.

(Upon hearing this list of symptoms, one woman joked of her husband, "Is it possible he's had menopause since he was 20?") A decrease in available testosterone also increases a man’s risk for heart disease, and makes him more prone to injury because of decreasing bone density

Let's be clear: Andropause is not the same as a mid-life crisis, which is a psycho-social issue. And not all guys who experience aging — and the inevitable decline in testosterone that comes along with it — can be qualified as having andropause.

Andropause is a medical condition, diagnosed with a blood test by a physician that reveals testosterone levels below a certain level. If a diagnosis of andropause is warranted, treatment with testosterone replacement may be an option, depending on a man’s health history. Just as there are various hormone replacement therapies for women, there's also testosterone replacement therapy for men — and research is still ongoing into potential side effects.

However, the biggest, and most misunderstood, symptom of declining testosterone is a decrease in libido. Testosterone is truly the hormone that stokes the flames of desire. Many men confuse andropause with erectile dysfunction (ED), because they often occur around the same time. These men often turn to an ED medication, such as Viagra, to improve their erectile ability, which works for a time in most cases. However, as men get older, the gap between desire and arousal widens and many men become deeply disappointed when Viagra doesn't give them the desire to have sex. That's because Viagra doesn't boost testosterone levels.

The first issue for men, and their partners, is to accept the very concept of male menopause, talk about it as a couple, and, if they’re concerned, make an appointment with an endocrinologist to check hormone levels. But beyond medical therapies, it's also about knowing, understanding and accepting that sex evolves with the passage of life.

For guys who can embrace a deeper intimacy and open themselves up to a different experience of sex, the passage of time brings many rewards. Unfortunately, many men have a limited idea of sex, and they feel that if they're not having sex the way they were at age 20 or 30, then something must be wrong. It's too bad more men aren't open to sharing their experiences with each other, since changes in sexual function are so common. Fortunately, if women know what's going on and realize that hormonal decline can affect their partners, too, then they can take a proactive lead in starting a dialogue.

For more on this subject, consider reading Jed Diamond's "Surviving Male Menopause: A Guide for Women and Men."

Cigarette packs patch up hole in chest - if you take if out you can see the heart beating

Rao Jiacang, the man with cigarettes on his chest

Never mind nicotine patches - a DIY patient is using cigarette packets to cover up a gaping hole in his chest.

Rao Jiacang plastered the packets over himself after running out of money for crucial heart surgery.

Somehow he has survived for ten years, despite his beating heart being gruesomely visible through the paper folds.

 

Rao Jiacang measures up

But he is now desperate for a donor to come forward to pay for proper treatment to cover over the wound measuring seven by three inches.

Part of his ribs and skin were hacked away by surgeons in 1998, hoping to remove part of his infected lungs.

But the 51-year-old, from Taining in China's Guangdong province, says he was unable to afford the rest of the treatment after stitches were taken out.

He said: "I had the operation in 1998. I was then laid up for almost five years but gradually got used to the wound, and since 2003 I have been back on my feet.

"But no-one would give me a job and people were scared of me with the big hole in my chest.

"Because of that, I haven't dared to go outside, in case people get frightened."

He says he keeps the plaster coverings sterile, and changes the cigarette boxes several times each day.

Local doctor Wan Fi said: "It's a miracle that Rao could have lived so many years with such a massive opening in his chest."

His friend Xi Lin, 35, who was present when the plaster was changed, said: "I did not know what to expect but then I saw a heart through the hole in his chest, and it was actively beating."

An estimated one in 8,000 people are dextrocardiac - that is, their heart is not on the left hand side of their body, but slightly to the right.

Researchers uncover details about how dietary restriction slows down aging

University of Washington scientists have uncovered details about the mechanisms through which dietary restriction slows the aging process. Working in yeast cells, the researchers have linked ribosomes, the protein-making factories in living cells, and Gcn4, a specialized protein that aids in the expression of genetic information, to the pathways related to dietary response and aging. The study, which was led by UW faculty members Brian Kennedy and Matt Kaeberlein, appears in the April 18 issue of the journal Cell.

Previous research has shown that the lifespan-extending properties of dietary restriction are mediated in part by reduced signaling through TOR, an enzyme involved in many vital operations in a cell. When an organism has less TOR signaling in response to dietary restriction, one side effect is that the organism also decreases the rate at which it makes new proteins, a process called translation.

In this project, the UW researchers studied many different strains of yeast cells that had lower protein production. They found that mutations to the ribosome, the cell's protein factory, sometimes led to increased life span. Ribosomes are made up of two parts -- the large and small subunits -- and the researchers tried to isolate the life-span-related mutation to one of those parts.

“What we noticed right away was that the long-lived strains always had mutations in the large ribosomal subunit and never in the small subunit,” said the study's lead author, Kristan Steffen, a graduate student in the UW Department of Biochemistry.

The researchers also tested a drug called diazaborine, which specifically interferes with synthesis of the ribosomes' large subunits, but not small subunits, and found that treating cells with the drug made them live about 50 percent longer than untreated cells. Using a series of genetic tests, the scientists then showed that depletion of the ribosomes' large subunits was likely to be increasing life span by a mechanism related to dietary restriction -- the TOR signaling pathway.

“We knew that dietary restriction decreased TOR signaling, and that decreased TOR signaling reduced translation or protein production, but this was the first direct evidence that all three were acting in the same genetic pathway,” said Kennedy, an associate professor of biochemistry.

"The big question then became what’s happening in these translation-deficient cells to slow aging," added Kaeberlein, an assistant professor of pathology. "That’s when Vivian MacKay, a co-author on the study, had the idea to look at Gcn4."

Gcn4 is a specialized protein called a transcription factor, which helps transfer genetic information during cell growth. The protein is activated when a cell is starving for amino acids. What made Gcn4 interesting to the UW team was its unique mode of regulation.

"When ribosomes aren’t working at 100 percent capacity, most proteins are made less efficiently, but Gcn4 is different," explained Dr. MacKay, a research professor of biochemistry. "Sometimes, you actually get more Gcn4 produced even when everything else is going down. That's precisely what we found in the longer-lived yeast strains with mutations in the large subunit of the ribosome."

To make the link between Gcn4 and longevity, the scientists then asked whether preventing the increase of Gcn4 would block life span extension. In every case, cells lacking Gcn4 did not respond as strongly as Gcn4-positive cells.

"The increased production of Gcn4 in long-lived yeast strains, combined with the requirement of Gcn4 for full life-span extension, makes a compelling case for Gcn4 as an important downstream factor in this longevity pathway," Kaeberlein said.

Although scientists don’t yet know whether Gcn4 plays a similar role in organisms other than yeast, Kennedy points out that worms, flies, mice and humans all have Gcn4-like proteins that appear to be regulated in a similar way.

"The role of TOR and translation in aging is known to be conserved across many different species, so it’s plausible that this function of Gcn4 is conserved as well," Kennedy said. Future research will be aimed at testing this hypothesis.

"Clearly TOR signaling is one component, and perhaps the major component, of the beneficial health effects associated with dietary restriction," said Kaeberlein. "The difficulty with TOR as a therapeutic target, however, is the potential for negative side effects. As we learn more of the mechanistic details behind how TOR regulates aging, we will hopefully be able to identify even better targets for treating age-associated diseases in people."

We can now remove your appendix through your mouth - and yes - it taste like chicken

New treatment for appendicitis

The ground-breaking procedure ensured the man, who was acutely ill with appendicitis, had no visible scar.

Jeff Scholz, 40, also recovered faster than he would have done with the current keyhole technique.

Mr Scholz told Sky News: "I was eating pizza and doing sit-ups three days later.

"You'd think the way it was done, you know going through the stomach wall, I'd have all kind of stomach pains, but there was nothing."

Surgeons at the University of California San Diego Medical Centre threaded miniaturised instruments attached to long control wires down the throat of the former US marine.

Once they had emptied his stomach of its contents they made a small incision in the lining to reach inside the body cavity.

The inflamed appendix was cut away, bagged up, pulled back into the stomach and out of Mr Scholz's mouth.

He was discharged from hospital after just 17 hours and back at work a day later.

The University has pioneered so-called trans-gastric procedures at its Centre for Future Surgery.

Director Professor Santiago Horgan said operating through the stomach reduces the risk of infections. Bacteria such as MRSA, that commonly cause post-surgical complications, cannot survive in the acidic environment of the stomach.

Treatment is faster than surgery

The technique also allows much quicker recovery.

Professor Santiago said: "My dad was a surgeon and in his time, the larger the incision, the better the surgeon. Today we are moving away from that and trying to minimise trauma.

"If we don't make any incisions in the abdomen, we can improve pain, we can improve post operative complications from incisions, infections, hernias and again pain."

Trans-gastric surgery is still experimental.

Surgeons need to be sure that there is no risk of stomach contents contaminating the body cavity.

A team of surgeons in India also claim to have removed a patient's appendix through their mouth. But they haven't demonstrated their technique to the outside world.

Other natural orifices can also be used to access internal organs.

Tree man: 'I want to get married' (you have to see this amazing pic)

Tree man: 'I want to get married'

Dede Koswara says he hopes to get married again

A man dubbed 'iTree Man of Java' is planning to get married after 4lb of bark were cut away.

Dede Koswara, 37, says he plans to get hitched now that he can use his hands and walk without pain.

Speaking from an Indonesian hospital, he told the Daily Telegraph website: "What I really want first is to get better and find a job. But then, one day, who knows? I might meet a girl and get married."

 

Dede's first wife left him and he lost his job because of his bizarre affliction.

At one point to feed his two children he joined a freak show with other victims of peculiar diseases.

But now, following a series of operations to cut away the tree-like growths, he can see the outline of his toes for the first time.

He has also become a sudoko addict now he can hold a pen.

He said he hopes that he will resume a normal life after two more operations to graft undamaged skin onto his hands, feet and face.

Since Dede cut his knee as a teenager, strange roots have been growing out of him.

A small wart developed on his lower leg and spread uncontrollably.

But last year US dermatology expert Dr Anthony Gaspari took up his case.

He concluded Dede's odd affliction was caused by the Human Papilloma Virus (HPV), a fairly common infection usually causing only small warts.

But in Dede's case he had an extremely rare immune system deficiency, leaving his body unable to contain the warts.

Drug experiment blocks radiation damage

WASHINGTON - Scientists mimicked one of cancer's sneaky tricks to create a drug that promises to prevent a serious side effect of cancer treatment — radiation damage — or offer an antidote during a nuclear emergency.

A single dose of the experimental drug protected both mice and monkeys from what should have been lethal doses of radiation, researchers report in Friday's edition of the journal Science. A study to see if the compound is safe in people could begin as early as this summer.

It's still early-stage research, and other efforts to create radiation protectants haven't yet panned out. But specialists are closely watching the work — and the government is helping to fund it — because it's a new approach to protecting the body's most radiation-sensitive tissues from being blasted.

"It has important implications for radiation exposure," said Dr. David Kirsch, a Duke University radiation oncologist who wasn't involved in the drug research.

Radiation is a powerful tool to destroy cancer cells. But certain healthy tissues are especially sensitive to it, too, particularly the bone marrow and gastrointestinal tract. That vulnerability can limit how much radiation physicians are able to give cancer patients.

And when it comes to radiation emergencies, such as the Chernobyl accident, full-body exposure to high doses can cause an extremely lethal "GI syndrome" that has no treatment.

It turns out that radiation doesn't kill healthy cells in the same way that it kills cancer cells. Instead, bone marrow and GI cells overreact to what should be reparable damage and commit suicide, through a well-known process called apoptosis, explained Andrei Gudkov of the Roswell Park Cancer Institute, who led development of the drug code-named CBLB502.

Learning that was the "eureka" moment, Gudkov said. Apoptosis is the body's way of stopping defective cells, with damaged genes, from spreading. Tumors grow because cancer cells block apoptosis in various ways, including by activating a normally dormant cell-signaling pathway called "nuclear factor-KappaB" or NFKB.

Gudkov's team decided to try activating that same pathway in healthy tissue, to see if it could keep radiation-blasted cells from triggering their suicide program.

"We imitated a tumor trick," is how Gudkov puts it.

The team knew that flagellin, a protein from normal gut bacteria, can wake up NFKB. So they created a drug based on that natural protein.

In a series of experiments, they injected the drug into mice and rhesus monkeys anywhere from 15 minutes to an hour before exposing the animals to lethal doses of full-body radiation. The drug dramatically improved the animals' survival, protecting against both bone marrow and GI destruction, with no obvious side effects.

The drug also improved survival when given to mice an hour after fairly high radiation doses, although not the very highest.

A final experiment showed the drug didn't block radiation from treating the tumors of the mice even as it protected their healthy tissue.

Gudkov founded a company called Cleveland Biolabs Inc. that is working to bring the drug to market — both for use in cancer radiotherapy and for biodefense. The Defense Department and other government agencies are helping to fund the research.

"For many years, the radiation oncology community has tried to develop radioprotectants" based on different biology, said Dr. Richard Kolesnick of Memorial Sloan-Kettering Cancer Center, who has long researched radiation's effects. "This new information on the mechanisms of tissue damage to the GI tract has resulted in a potentially important new drug to prevent this lethal GI syndrome after a radiation accident or potential terrorist attack."

Duke's Kirsch agreed that the animal experiments suggest the drug has potential for radiation emergencies. But he stressed that a cancer role is less clear, because cancer patients' biggest trouble comes with late-stage radiation effects, the cumulative buildup of damage. "That's what's dose-limiting," he said.

Viper venom examined to save stroke sufferers

The whole episode remains a blur to Kenneth Transeau of Katy, Texas, as he was transported by an air ambulance to a stroke center in Houston. But sometime after the noisy helicopter ride and the hurried hospital brain scans, Transeau went from being a stroke victim to a test subject.

Researchers began dripping an experimental drug made from viper snake venom into the veins of the 69-year-old husband, father and grandfather.

The pet supply salesman doesn't recall anybody mentioning risks. "They may have," he says. "I just knew I wanted to take it. I knew they wouldn't be testing it if it wasn't safe."

But the safety of the drug Viprinex is anything but certain.

 

Similar human studies were "an abysmal failure in Europe," says Paul Freiman, president and CEO of Neurobiological Technologies, a U.S. company testing the drug.

For the record, Transeau was told of the risks, the hospital says.

His wife Irene signed the consent form, which detailed the bleeding and deaths seen in previous studies, to enroll her husband in the worldwide trial that hopes to study 650 patients.

"We're taking this (failed experiment) and transforming it" by changing the way it is administered to patients, Freiman says.

The study, launched in November 2005, is designed to determine whether infusing select parts of Malaysian viper venom into some patients can halt a stroke and prevent more brain damage.

For years, the concept has tempted scientists, who believe the way the snake's venom kills also should help doctors put the brakes on a stroke.

When a blood clot forms in the brain, doctors try to dissolve it while getting blood to flow more freely around the blockage and in smaller blood vessels nearby so that surrounding neurons can be nourished and survive.

The viper's venom causes its prey's blood to thin, a transformation that is exactly what doctors want to happen when trying to reverse a stroke caused by a clot, only on a much smaller scale.

"The snakes cause their victims to bleed to death internally," Freiman says. "It would be nice if you could thin blood out like this for stroke victims."

Transeau's case shows the typical race against time doctors face when they encounter a patient suffering a stroke. A stroke occurs when blood flow is cut off to part of the brain, either because of a blood clot or because of bleeding in the brain, causing the brain tissue to die. More than 700,000 strokes occur in the United States each year, making it the leading cause of disability and the third leading cause of death.

"In an average stroke, 2 million neurons die per minute in the first few hours so we are racing against the clock," says Transeau's doctor, David Chiu, director of the Eddy Scurlock Stroke Center at Methodist Neurological Institute in Houston. "The earlier we treat, the better the benefit."

The best drug Chiu has is the clot-busting drug known as tPA, tissue plasminogen activator, which must be given within three hours. The study of Viprinex is trying to determine whether the snake venom can give doctors twice as much time — six hours — to treat stroke.

Extra time is key because people often respond too slowly to signs of a stroke, experts say.

Viprinex is a new class of drug, says Warren Wasiewski, vice president and chief medical officer for Neurobiological Technologies. It makes blood flow more freely, and it may break up clots.

By reviewing what worked and what didn't work in 2,000 patients previously given the drug, researchers suspect that too much of the drug was given. The current trial reduces the amount.

Chui, who is an investigator in the study but who has no other financial ties to the company, says Viprinex "could be a major advance in the treatment of stroke" if it works. He says the trial is a reminder that even failed clinical studies can lead to advances.

"We have learned some valuable lessons from the failed trials," he says. "We have to be smarter at selecting patients who stand to benefit from treatment."

Transeau is convinced the speedy recovery that has allowed him to return to work is due to the drug. He talks fine and regained his strength and motor skills through physical therapy.

"I think if I had the placebo and not the actual pit viper venom, I don't think I would be as far along as I am today," Transeau says. "I started speaking the next day, and my writing became more legible as each day went along."

But neither he nor Chui knows whether he got the drug because it is being used in a double-blind study against a placebo. No one knows who is receiving what.

The method is considered the gold standard in clinical trials because it is thought to produce objective results.

The study might show Transeau benefited only from the speedy help. He and his family recognized the stroke from his impaired speech during a cellphone conversation. Paramedics found him on the side of the road in about 15 minutes, he says, and they called for a helicopter to take him directly to the specialty hospital where Chiu's team has experience moving swiftly against strokes.

Chui says the most immediate way to help stroke victims is for family members and friends to be more aware of signs and symptoms and for them to act fast to get patients to specialty hospitals.

"We need to do better in the community," he says. "It's not something you can afford to delay treatment for."

First cancer vaccine

First cancer vaccine

   

Russian regulators have approved the world's first cancer vaccine, validating an unusual strategy by its maker to introduce the product even though it failed a late-stage clinical trial.

Shares of Antigenics Inc, the tiny New York-based biotechnology company which has been developing the vaccine for 11 years, rose as much as 58 percent on the news.

It is the first time the Russian government has approved a drug that was not first cleared in its country of origin, according to Antigenics, and clears the way for the company to start generating revenue from Oncophage later this year.

The company plans to file for approval of the vaccine in Europe by the end of the year, based on a relatively new set of guidelines in that jurisdiction.

Regulators in Russia approved Oncophage based on a subset of data from a late-stage clinical trial that in 2006 failed to show the vaccine delayed the recurrence of kidney cancer.

In the subset of patients -- those whose cancer was least likely to recur following surgery -- Oncophage lengthened the period before which the disease recurred by 45 percent, or an average of 1.8 years, versus those in the control group.

The U.S. Food and Drug Administration does not consider subset analysis a valid measure of success or failure since all manner of sub-populations can be carved out retrospectively. Therefore the vaccine stands little chance of approval in the United States.

"What this company needs to do now is a trial based on their findings with the good prognosis patients," said Dr. Otis Brawley, Chief Medical Officer at the American Cancer Society. "If they have a positive finding at that point then I'm going to be excited, and then I believe it would go before the FDA very quickly."

Conducting such trials, however, could take up to 10 years and vast sums of money, and would take the product's development cycle to 20 years.

"No one in their right mind would authorize that," said Garo Armen, the company's chief executive, in an interview. "Even if we had the money it wouldn't be practical."

SEEKING BROAD APPROVAL

Unlike their U.S. counterparts, Russian regulators have accepted the validity of the subset -- in part because roughly a third of the 604 patients enrolled in the late-stage trial were tested in Russia, and about 70 percent of those fell into the subset of patients whose prognosis following surgery was better than that of the total population.

Antigenics thinks it will be able to win approval elsewhere in the world too.

European regulators can now approve drugs on a conditional basis, meaning companies can market their products while simultaneously conducting additional follow-up of patients or further clinical studies.

If at the end of the trial period the regulatory agency were not satisfied, it could pull the drug from the market.

"Filing in Europe won't be a slam dunk, and will probably be more difficult than in Russia," said Armen, who added that the European review process would likely take 12 to 18 months.

The Russian approval caps years of dogged determination to bring the vaccine to the market despite multiple setbacks and investor skepticism of cancer vaccines in general.

Oncophage is designed to reprogram a patient's immune system to target cancer cells from a specific tumor.

The company takes tissue from a tumor following surgery, extracts proteins it says activate the immune system and then injects the enriched proteins back into the body through the skin.

Unlike a vaccine such as Merck & Co's Gardasil, which is designed to ward off a virus that is believed to cause some 70 percent of cervical cancer cases, Oncophage is designed to target the cancer directly and delay or prevent it from spreading once it has developed.

There are about 16,000 new cases of kidney cancer a year in Russia, according to Armen, of which about a quarter fit the profile of patients most likely to benefit from Oncophage -- a market theoretically worth about $200 million to Antigenics.

The Russian pharmaceuticals market is one of the fastest growing in the world. It will grow by nearly 60 percent to $19.4 billion in 2009 from about $12.3 billion in 2006, the research group DSM estimates.

Armen said he expects the initial sales growth for Oncophage to be "modest."

"We would have to price this probably at the low- to mid-range of other new-generation cancer drugs," Armen said.

Such drugs can cost as much as $60,000 per patient per year, he said.

"How much of that market we achieve depends on how well we iron out reimbursement issues and how effectively we can reach every single patient," Armen said.

Shares of Antigenics were up 62 cents or 25 percent to $3.09 in late afternoon trading on Nasdaq after touching $3.90 earlier in the day, an increase of about 58 percent.