Plug-In Hybrid Vehicle Has Wings.


Maybe I’ve just watched “Back to the Future” too many times but the latest design from Ma.-based Terrafugia, the maker of flying aircrafts that also work as cars, looks like all that’s missing is Doc and some plutonium. The next-gen TF-X will be a street legal plug-in hybrid car that has collapsible wings, retractable propellers, and is capable of driving and flying on its own in the event of an emergency.

Flying Car Gets FAA Approval

When I talked to Terrafugia co-founder and CEO Carl Dietrich about the highly anticipated Transition, Terrafugia first street legal plane, four years ago, Dietrich said the fuel-efficient vehicle promised to both revitalize under-utilized regional airports and alleviate traffic congestion .

Just getting on a commercial airplane is tough enough these days, so it’s no surprise that Terrafugia has taken so long to navigate regulatory hurdles. Earlier this year, it cleared a major one when the FAA classified the Transition as a Light-Sport Aircraft, which means drivers don’t need a pilot’s license, just FAA certification in this category. While the company has been working on getting the Transition in the air, Terrafugia hasn’t stopped designing.

That’s where the TF-X plan comes in. Unlike the two-seater Transition, this new street-legal aircraft will seat four and run on electricity. That means the engine will recharge the batteries in the air or it could be plugged into a charging station on the ground. According to Terrafugia, the vehicle will also have electric ground drive and electric power assist for takeoff and landing.

Other cool features include retractable wings and the propellers that open from two motor pods. Initially the propellers point up for takeoff, then the motor pods tilt forward until the vehicle cruises and after that the propellers can fold in. The TF-X will have a non-stop flight range of at least 500 miles, and is expected to be able to automatically avoid other air traffic, bad weather, and restricted and tower-controlled airspace, according to the website, as well as implement an emergency auto-land at the nearest airport, if the operator became unresponsive.

The vehicle will also have extensive safety features such as a parachute system to prevent it from crashing horribly should something go seriously wrong. Terrafugia indicated that learning how to safely operate the TF-X will take the average person five hours; a light-sport aircraft certification takes an additional 20 hours.

Dutch ‘Flying Car’ Takes to the Skies

Before you get your hopes up, the TF-X will likely be in development for eight to 12 years and cost way, way more than a new car. According to the company, Transition owners will have the first shot at purchasing these vehicles when they do get produced. Nevertheless, I look forward to the day when we hear drivers turn to their passengers and say, “Roads? Where we’re going, we don’t need roads.”

See the video on youtube. URL : http://www.youtube.com/watch?v=KPh4r8rDcts

 

 

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Swimming with asthma.


bikeriderlondon_swimming_Shutterstock

New research by medical students working in the Breathe Well Centre of Research Excellence at the UTAS School of Medicine has revealed swimming has health benefits for young people with asthma, with no adverse effects on asthma control or exacerbations.

Asthma is a common condition among children and adolescents causing intermittent wheezing, coughing and chest tightness and is the main reason why Tasmanian children present at emergency departments or are hospitalised.

Director of Paediatric Education at the Royal Hobart Hospital Dr Sean Beggs, who assisted in the research, said concerns that physical exercise such as swimming could worsen asthma, had the potential to reduce participation, resulting in reduced physical fitness.

“The review aimed to determine the effectiveness and safety of swimming training in children and adolescents with asthma aged 18 years and under,” Dr Beggs said.

“Our research found swimming training is well-tolerated in children and adolescents with stable asthma, and increases physical and cardio-pulmonary fitness as well as lung function.”

In 2011, the Asthma Foundation of Tasmania (AFT) provided funding to jointly support students Yi Chao Foong, Hong C Le and Danial Noor, undertaking their first health professional degree, to conduct the asthma review. The review was co-supervised by UTAS’ Dr Julia Walters who heads the health services theme within the Centre of Research Excellence.

AFT Chief Executive Officer Cathy Beswick said the outcome of the project would ensure swimmers with respiratory problems achieved the best outcomes when trying to improve their health.

“Anecdotally it is understood swimming is an outstanding form of exercise for children and adults with asthma, but there have been concerns that it might have an impact on asthma control or even induce exacerbations,” Ms Beswick said.

“This research provides a strong scientific foundation for deciding who to recommend this form of exercise to and the type of exercise they should undertake.”

Ms Beswick said the student scholarship was awarded following an agreement with the UTAS School of Medicine, continuing the Australian Satellite of the Cochrane Airways Group’s scholarship scheme.

“The Australian Satellite of the Cochrane Airways Group’s scholarship scheme facilitates the activities of the Cochrane Collaboration, which encourages individuals to work together to provide the best evidence for health care,” Ms Beswick said.

“Our funding has ensured a future for the scholarship scheme in Tasmania, meaning greater knowledge and insight into asthma and other respiratory diseases in our population.”

The Tasmanian asthma research reviewed evidence from eight studies involving 262 participants and combined the results to see if swimming was a safe and beneficial activity for young people.

The review titled “Swimming training for asthma in children and adolescents aged 18 years and under” has been published online together with a podcast of the findings in the Cochrane Library.

The NHMRC-funded “Breathe Well” Centre of Research Excellence (CRE) focuses on preserving respiratory health in the community from youth to old age, and optimising respiratory health through innovative approaches to detection and therapy. The CRE houses the official Australian Satellite of the Cochrane Airways Group based in London.

Source: http://www.sciencealert.com.au

Animals in research: zebrafish .


HealthLab_zebrafish_TheConversation

Zebrafish are probably not the first creatures that come to mind when it comes to animals that are valuable for medical research.

You might struggle to imagine you have much in common with this small tropical freshwater fish, though you may be inclined to keep a few “zebra danios” in your home aquarium, given they are hardy, undemanding animals that cost only a few dollars each.

Yet each year more and more scientists are turning to zebrafish to unravel the mechanisms underlying their favourite genetic or infectious disease, be it muscular dystrophy, schizophrenia, tuberculosis or cancer.

My (conservative) estimate is that zebrafish research is now carried out in at least 600 labs worldwide, including 20 in Australia.

So what is it about zebrafish that has taken them from the freshwater rivers and streams of Southeast Asia, beyond the pet shops and into universities and research institutes the world over?

A short history of zebrafish

A scientist called George Streisinger, working at the University of Oregon in Eugene, USA in the 1970s and 80s, recognised the vast potential of this organism for developmental biology and genetics research.

In contrast to fruit flies and worms, the other simple model organisms established at the time, zebrafish are vertebrates.

They have a backbone, brain and spinal cord as well as several other organs, including a heart, liver and pancreas, kidneys, bones and cartilage, which makes them much more similar to humans than you may have otherwise thought.

But as a vertebrate model, could they be as useful as mice?

Several things captured Streisinger’s imagination.

Most famously, zebrafish embryos, unlike mouse embryos, develop outside the mother’s body and are transparent throughout the first few days of life.

This provides unparallelled opportunities for researchers to scrutinise the fine details of embryonic vertebrate development without first having to resort to invasive procedures or killing the mother.

But this advantage is enhanced by the fact zebrafish reproduce profusely (each pair can produce 200-300 fertilised eggs every week); an ideal attribute for genetic studies. Again, the large, external embryos are a critical part of this success.

When just one or two cells old, zebrafish embryos can be easily microinjected with mRNA or DNA corresponding to genes of interest; undeterred, they then they go on to grow and reproduce, handing down the injected gene to the next generation.

From zebrafish to humans

A paper published in Nature unveiled the long-awaited sequence of the zebrafish genome, revealing that zebrafish, mice and human have 12,719 genes in common.

Put another way, 70% of human genes are found in zebrafish.

But even more notable is the finding that 84% of human disease-causing genes are found in zebrafish.

Perhaps not surprisingly then, when these genes are injected into zebrafish embryos, the growing animals are doomed to acquire the same diseases.

And while zebrafish are still used widely to answer fundamental questions of developmental biology, much current research is directed towards combining their many attributes in studies that are designed to improve human health.

This is especially true for cancer research where the expression of cancer-causing genes (oncogenes) can be directed to specific organs, virtually at will.

This process, known as transgenesis, is very straightforward in zebrafish and has allowed researchers to produce zebrafish models of liver, pancreatic, skeletal muscle, blood and skin cancers, to name but a few.

And when the genomic make-up of these zebrafish tumours is deciphered using the latest DNA sequencing technology, the patterns of mutations, or “gene signatures”, are found to overlap substantially with those in the corresponding human tumours.

Trialling cancer drugs

These parallels have encouraged researchers to exploit zebrafish in drug development – in particular for high throughput approaches such as chemical/small molecule screens.

Here, the ability to generate tens of thousands of zebrafish embryos harbouring the same disease-causing mutations is crucial.

Then, as the tumours grow in the synchronously developing larvae, the fish are transferred to small volumes of water containing chemicals that may stop the growth, or better still, kill the cancer cells.

Large collections of drugs can be screened relatively quickly for anti-cancer efficacy in this way.

One drug, Leflunomide, identified in such a screen is now in early phase clinical trials to kill melanoma cells.

The only other drug from a zebrafish chemical screen currently in clinical trials is dimethyl-prostaglandin E2 (dmPGE2).

There, the intent is not to kill cancer cells but rather to make mainstream leukaemia treatment more effective.

Studies of dmPGE2 increased the number of blood stem cells in zebrafish embryos and it is being trialled now as a way to expand the number of stem cells in human cord blood samples.

Human cord blood samples are a valuable commodity to restore bone marrow in leukaemia patients after high dose chemotherapy when a matched bone marrow transplant is unavailable.

But the success of this approach is currently limited by the scant number of stem cells in individual cord blood samples, requiring the use of two precious samples for each patient.

Tumour growth

As well as the transgenic zebrafish models of cancer described above, researchers are alsotransplanting cells derived from human tumours into zebrafish embryos and watching them grow and spread.

The creation of a transparent (non-striped) version of adult zebrafish (called casper, after thecartoon ghost) means the behaviour of tumour cells inside these living organisms can be followed for days at a time.

Coupled with the advent of high resolution live-imaging techniques, the birth, growth and spread of tumours can be scrutinised in movies that can be played over and over again.

These experiments are usually conducted in zebrafish that have been genetically modified to express genes that glow in specific body compartments, giving researchers the ability to pinpoint potentially critical connections between “host” cells and tumour cells that may determine whether the latter survive or die.

This type of experiment is revealing a complex interplay of potentially beneficial and detrimental components.

While the proximity of immune cells may instigate mechanisms capable of destroying the tumour, the stimulation of new blood and lymphatic vessel growth towards the tumour is more insidious, since it delivers the tumour with both the nutrients it needs to survive and a network to spread throughout the body.

These processes, once properly understood, are likely to provide opportunities for therapeutic intervention in the future.

The future of zebrafish

Cancer research is just one part of the zebrafish story. In Australia alone, investigators are also using zebrafish to study metabolic disorders such as diabetes, muscle diseases, includingmuscular dystrophyneurodegenerative disease, and the response of the host innate immune system to bacterial and fungal infections

Excitingly, research is also underway in this country to unravel the genetic mechanisms controlling heart, skeletal muscle and nervous tissue regeneration in zebrafish, in the hope that these processes can be one day recapitulated in humans to address the burgeoning socioeconomic problem of tissue degeneration in our ageing population.

So next time you peer into someone’s home aquarium, imagine the biomedical possibilities inherent in this lively and amiable little fish!

Source: http://www.sciencealert.com.au

Research reveals cancer-suppressing protein ʻmultitasksʼ.


The understanding of how a powerful protein called p53 protects against cancer development has been upended by a discovery by Walter and Eliza Hall Institute researchers.

More than half of human cancers carry defects in the gene for p53, and almost all other cancers, with a normal p53 gene, carry other defects that somehow impair the function of the p53 protein. Inherited mutations in the p53 gene put people at a very high risk of developing a range of cancers.

The p53 protein’s functions are normally stimulated by potentially cancer-causing events, such as DNA damage from ultraviolet radiation (a cause of skin cancer), or the over-activity of cancer-causing genes.

Ms Liz Valente, Dr Ana Janic and Professor Andreas Strasser from the Molecular Genetics of Cancer division at the Walter and Eliza Hall Institute have been dissecting the processes that are controlled by p53, to discover how this protein can suppress cancer development. Their surprising results are published online today in the journal Cell Reports.

Dr Janic said many scientists believed that the most important processes activated by p53 to prevent cancer formation were stopping cells with DNA damage from dividing until the DNA could be repaired, and making cells die if they had sustained irreparable genetic damage.

“Changes that make damaged cells become long-lived and divide uncontrollably are key features of cancer formation,” Dr Janic said. “Because p53 can control cell survival and cell division, it was assumed that these two processes constituted the critical functions that p53 used to prevent cancer. The purpose of our research was to examine whether this assumption was correct.”

Ms Valente said the team compared cells that lacked p53 with cells in which p53 could not regulate cell survival and cell division. “In the past 20 years it has become clear which proteins are activated by p53 to block cell division and promote cell death,” Ms Valente said. “We were able to remove all of these proteins (called p21, Puma and Noxa) from cells, to completely disable the ability of p53 to stop cell division and trigger cell death. To our surprise, p53 could still prevent cancer formation, even without being able to make cells die or stop dividing after DNA damage.”

Professor Strasser said the team’s discovery had upended the understanding of how p53 functions. “When p53’s cancer-suppressing function was first discovered, it was important to understand how this protein functioned,” he said. “Many scientists had concluded that regulation of cell death and division were the key roles of p53,” he said.

“Our findings have re-opened the question of how p53 functions. My suspicion is that it is not one protein but several with very many critical functions that work together to prevent cancer formation by coordinating the proper repair of damaged DNA, rather than stopping cells from dividing or killing them. Further research to decipher how these processes are integrated will be an important step towards understanding the tumour-suppressing function of p53 function. This knowledge, in turn, may then be exploited to develop improved cancer therapies,” Professor Strasser said.

Source: http://www.sciencealert.com.au

Blood hormone restores youthful hearts to old mice.


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Protein relieves age-related stiffening and thickening of cardiac muscle.

Researchers have identified a blood hormone that makes ageing hearts in mice look young again. The authors of the study say their finding offers therapeutic potential for the treatment of age-related heart disease, an increasingly common cause of heart failure.

The protein, known as growth differentiation factor 11 (GDF11), circulates at high levels in the blood of young mice but declines with age. In a study published this week in Cell1, the researchers report that elderly mice treated with the protein experience a reversal of tissue ageing in the heart.

“I think it’s a stunning result that, for the first time, points at a secreted protein that maintains the heart in a young state,” says cardiologist Deepak Srivastava, director of the Gladstone Institute of Cardiovascular Disease in San Francisco, California, who was not involved with the research. “That’s pretty remarkable.”

With age and after some forms of stress, such as longstanding high blood pressure, the heart muscle becomes stiff and fails to properly relax between beats. Its wall also thickens — a condition known as ‘hypertrophy’. When the heart gets thicker and stiffer, it can’t fill properly and fluid backs up into the lungs. Patients feel short of breath as a result. There are few, if any, viable treatments for this form of cardiac failure that is most common in the elderly.

Young blood

The researchers, based in Massachusetts, were using a surgical technique that merges the circulatory systems of young and old mice. When older mice were exposed to the circulating blood of young mice for 4 weeks, the older hearts became noticeably smaller and more similar in appearance to those of younger mice, suggesting that the tissue had become more youthful.

“Even at the gross anatomy level, the hearts were clearly responding to a factor in the blood of the young mice,” says Amy Wagers, a stem-cell biologist with the Howard Hughes Medical Institute who works at Harvard University in Cambridge, Massachusetts, and is a lead author of the study. “We knew we needed to go after a substance in the blood, so then it became this long process of trying to identify what that substance might be.”

Using a protein screening technique in collaboration with the biotechnology company SomaLogic in Boulder, Colorado, the team identified GDF11 as a protein that declines in ageing mice. GDF11 is in a family of proteins that has been implicated in various healing and developmental processes, says Wagers. When the researchers injected GDF11 into old mice, restoring the protein to levels similar to those of young mice, the older mice experienced a reversal in the thickening of heart muscle tissue. Heart muscle cells in the ageing mice also shrank in size.

“We did this pretty much as a long-shot experiment to see if there was some pathway that would give us insight into the heart-ageing process,” says Richard T. Lee, a cardiologist at Brigham and Women’s Hospital in Boston, Massachusetts and the Harvard Stem Cell Institute in Cambridge, who is also a lead author of the study. “We were just totally stunned when it worked.”

The finding suggests that GDF11 is a circulating factor that “essentially prevents the heart from turning into this old phenotype”, Lee says. “Then, when the mouse ages, we believe that this hormonal system fails.”

Jonathan Epstein, a cardiologist and developmental biologist at the University of Pennsylvania in Philadelphia, says that the study is “provocative” and could offer an important insight into age-related heart failure. But he cautions that the research does not yet show that the ‘more youthful’ appearance of the heart in ageing mice produced by GDF11 means that heart function or survival is improved. Lee says his team is initiating studies to test whether the protein actually has functional benefits.

Wagers, Lee and their team also plan to study whether GDF11 has similar effects in humans. They are also examining whether the protein could mediate ageing processes in other tissues in mice. “We’re working feverishly on different systems,” says Lee, “and we’re very hopeful that this is not just a cardiac story.”

Source: nature

 

A protein protects against the big C


RAGMA_IMAGES_cancer_shutterstock

The understanding of how a powerful protein called p53 protects against cancer development has been upended by a discovery by Walter and Eliza Hall Institute researchers. More than half of human cancers carry defects in the gene for p53, and almost all other cancers, with a normal p53 gene, carry other defects that somehow impair the function of the p53 protein. Inherited mutations in the p53 gene put people at a very high risk of developing a range of cancers. The p53 protein’s functions are normally stimulated by potentially cancer-causing events, such as DNA damage from ultraviolet radiation (a cause of skin cancer), or the over-activity of cancer-causing genes. Ms Liz Valente, Dr Ana Janic and Professor Andreas Strasser from the Molecular Genetics of Cancer division at the Walter and Eliza Hall Institute have been dissecting the processes that are controlled by p53, to discover how this protein can suppress cancer development. Their surprising results are published online in the journal Cell Reports. Dr Janic said many scientists believed that the most important processes activated by p53 to prevent cancer formation were stopping cells with DNA damage from dividing until the DNA could be repaired, and making cells die if they had sustained irreparable genetic damage. “Changes that make damaged cells become long-lived and divide uncontrollably are key features of cancer formation,” Dr Janic said. “Because p53 can control cell survival and cell division, it was assumed that these two processes constituted the critical functions that p53 used to prevent cancer. The purpose of our research was to examine whether this assumption was correct.” Ms Valente said the team compared cells that lacked p53 with cells in which p53 could not regulate cell survival and cell division. “In the past 20 years it has become clear which proteins are activated by p53 to block cell division and promote cell death,” Ms Valente said. “We were able to remove all of these proteins (called p21, Puma and Noxa) from cells, to completely disable the ability of p53 to stop cell division and trigger cell death. To our surprise, p53 could still prevent cancer formation, even without being able to make cells die or stop dividing after DNA damage.” Professor Strasser said the team’s discovery had upended the understanding of how p53 functions. “When p53’s cancer-suppressing function was first discovered, it was important to understand how this protein functioned,” he said. “Many scientists had concluded that regulation of cell death and division were the key roles of p53,” he said. “Our findings have re-opened the question of how p53 functions. My suspicion is that it is not one protein but several with very many critical functions that work together to prevent cancer formation by coordinating the proper repair of damaged DNA, rather than stopping cells from dividing or killing them. Further research to decipher how these processes are integrated will be an important step towards understanding the tumour-suppressing function of p53 function. This knowledge, in turn, may then be exploited to develop improved cancer therapies,” Professor Strasser said. The research was supported by the Australian National Health and Medical Research Council, the Leukemia and Lymphoma Society (US), Cancer Council Victoria, the Lady Tata Memorial Trust, the Beatriu de Pinós Fellowship (European Union/Spain), and the Victorian Government.   Source: http://www.sciencealert.com.au

Statin Nation: The Great Cholesterol Cover-Up


There’s serious confusion about cholesterol; whether high cholesterol levels are responsible for heart disease, and whether statins — which are cholesterol drugs— are really the appropriate solution to reduce heart disease risk.

The documentary above, Statin Nation — The Great Cholesterol Cover-Up, sheds much needed light on this topic. The film is available for free viewing for only seven days, so please share it widely as soon as possible.

As noted in the film, heart disease is the leading cause of death worldwide, the most common form of which is coronary heart disease (CHD). CHD affects the blood vessels supplying blood to your heart, causing them to narrow, thereby restricting the amount of oxygen supplied to your heart.

The conventional view is that high cholesterol is a major risk factor for this condition — even children “know” that cholesterol forms plaque and is bad for your heart.

The focus on cholesterol has created an enormous market for statins; drugs that act by blocking the enzyme in your liver that is responsible for making cholesterol.

Statins are now among the most widely prescribed drugs on the market, and are the number one profit-maker for the pharmaceutical industry, largely due to relentless and highly successful direct-to-consumer advertising campaigns.

Meanwhile, as of 2010, there were no less than 900 studies proving their adverse effects, which run the gamut from muscle problems to increased cancer risk! Besides the fact that statins are dangerous to your health, they also do not reduce your risk for heart disease, because high cholesterol does NOT increase heart disease risk…

Where Did the High Cholesterol-Heart Disease Myth Originate?

The idea that high cholesterol causes heart disease can be traced back to Rudolph Virchow (1821-1902), a German pathologist who found thickening in the arteries in people he autopsied, which he ascribed to a collection of cholesterol.

Later, Ancel Keys (1904-2004), a well-known physiologist, published his seminal paper known as the “Seven Countries Study1,” which served as the basis for nearly all of the initial scientific support for the Cholesterol Theory.

The study linked the consumption of saturated fat to coronary heart disease. However, what many don’t know is that Keys selectively analyzed information from only seven countries to prove his correlation, rather than comparing all the data available at the time — from 22 countries.

As you might suspect, the studies he excluded were those that did not fit with his hypothesis, namely those that showed a low percentage fat in their diet and a high incidence of death from CHD as well as those with a high-fat diet and low incidence of CHD. When all 22 countries are analyzed, no correlation at all can be found.

And that is what mounting research now confirms. There really is NO correlation between high cholesterol and plaque formation that leads to heart disease.

Why Do You Need Cholesterol?

Missing from the cholesterol-CHD hypothesis is the holistic understanding of how cholesterol operates inside your body, and why arterial plaques form in the first place, which is clearly described in the film. Cholesterol is actually a critical part of your body’s foundational building materials and is absolutely essential for optimal health. It’s so important that your body produces it both in your liver and in your brain.

There’s no doubt that your body needs cholesterol. In fact, we now have evidence showing that cholesterol deficiency has a detrimental impact on virtually every aspect of your health. One of the primary reasons is because cholesterol plays a critical role within your cell membranes.

Your body is composed of trillions of cells that need to interact with each other and cholesterol is one of the molecules that allow for these interactions to take place. For example, cholesterol is the precursor to bile acids, so without sufficient amounts of cholesterol, your digestive system can be adversely affected.

Cholesterol also plays an essential role in your brain, which contains about 25 percent of the cholesterol in your body. It is critical for synapse formation, i.e. the connections between your neurons, which allow you to think, learn new things, and form memories. In fact, there’s reason to believe that low-fat diets and/or cholesterol-lowering drugs may cause or contribute to Alzheimer’s disease. Low cholesterol levels have also been linked to violent behavior, due to adverse changes in brain chemistry.

Furthermore, you need cholesterol to produce steroid hormones, including your sex hormones. Vitamin D is also synthesized from a close relative of cholesterol: 7-dehydrocholesterol.

To further reinforce the importance of cholesterol, I want to remind you of the work of Dr. Stephanie Seneff, who works with the Weston A. Price Foundation. One of her theories is that cholesterol combines with sulfur to form cholesterol sulfate, and that this cholesterol sulfate helps thin your blood by serving as a reservoir for the electron donations you receive when walking barefoot on the earth (also called grounding). She believes that, via this blood-thinning mechanism, cholesterol sulfate may provide natural protection against heart disease. In fact, she goes so far as to hypothesize that heart disease is likely the result of cholesterol deficiency — which of course is the complete opposite of the conventional view.

Identifying Risk Factors for Heart Disease

As mentioned in the film, if you want to understand what causes heart disease, you have to look at what causes damage to your artery walls, interferes in disease processes, and causes blood clotting. When the endothelial wall is damaged, repair mechanisms are set into motion, creating a “scab.” To prevent this scab from dislodging, the endothelial wall grows over it, causing the area to become thickened. This is what is called atherosclerosis. There’s no fat (cholesterol) “clogging the pipe” at all; rather the arterial wall is thickened as a result of your body’s natural repair process. So what causes damage to your arteries?

One of the primary culprits is sugar and fructose in particular. So eating a high sugar diet is a sure-fire way to put heart disease on your list of potential health problems. Meanwhile, total cholesterol will tell you virtually nothing about your disease risk, unless it’s exceptionally elevated (above 330 or so, which would be suggestive of familial hypercholesterolemia, which, in my view, would be about the only time a cholesterol-reducing drug would be appropriate).

Two ratios that are far better indicators of heart disease risk are:

  • Your HDL/total cholesterol ratio: HDL percentage is a very potent heart disease risk factor. Just divide your HDL level by your total cholesterol. This percentage should ideally be above 24 percent. Below 10 percent, it’s a significant indicator of risk for heart disease
  • Your triglyceride/HDL ratios: This ratio should ideally be below 2

Additional risk factors for heart disease include:

  • Your fasting insulin level: Any meal or snack high in carbohydrates like fructose and refined grains generates a rapid rise in blood glucose and then insulin to compensate for the rise in blood sugar. The insulin released from eating too many carbs promotes fat and makes it more difficult for your body to shed excess weight, and excess fat, particularly around your belly, is one of the major contributors to heart disease
  • Your fasting blood sugar level: Studies have shown that people with a fasting blood sugar level of 100-125 mg/dl had a nearly 300 percent increase higher risk of having coronary heart disease than people with a level below 79 mg/dl
  • Your iron level: Iron can be a very potent oxidative stress, so if you have excess iron levels you can damage your blood vessels and increase your risk of heart disease. Ideally, you should monitor your ferritin levels and make sure they are not much above 80 ng/ml. The simplest way to lower them if they are elevated is to donate your blood. If that is not possible you can have a therapeutic phlebotomy and that will effectively eliminate the excess iron from your body

Statin Drugs Place Millions of Americans at Risk of Serious Health Problems

It’s important to note that statins are classified as a “pregnancy Category X medication” meaning, it causes serious birth defects, and should NEVER be used by a woman who is pregnant or planning a pregnancy. If it is prescribed it is simply gross negligence and malpractice as many doctors are ignorant of this important piece of information as it is relatively recently identified.

Statins have also been shown to increase your risk of diabetes, via a number of different mechanisms. The most important one is that they increase insulin resistance, which can be extremely harmful to your health. Increased insulin resistance contributes to chronic inflammation in your body, and inflammation is the hallmark of most diseases. In fact, increased insulin resistance can lead to heart disease, which, ironically, is the primary reason for taking a cholesterol-reducing drug in the first place. It can also promote belly fat, high blood pressure, heart attacks, chronic fatigue, thyroid disruption, and diseases like Parkinson’s, Alzheimer’s, and cancer.

Secondly, statins increase your diabetes risk by actually raising your blood sugar. When you eat a meal that contains starches and sugar, some of the excess sugar goes to your liver, which then stores it away as cholesterol and triglycerides. Statins work by preventing your liver from making cholesterol. As a result, your liver returns the sugar to your bloodstream, which raises your blood sugar levels.

Drug-induced diabetes and genuine type 2 diabetes are not necessarily identical. If you’re on a statin drug and find that your blood glucose is elevated, it’s possible that what you have is just hyperglycemia — a side effect, and the result of your medication. Unfortunately, many doctors will at that point mistakenly diagnose you with “type 2 diabetes,” and possibly prescribeanother drug, when all you may need to do is simply discontinue the statin in order for your blood glucose levels to revert back to normal.

Statin drugs also interfere with other biological functions. Of utmost importance, statins deplete your body of CoQ10, which accounts for many of its devastating results. Therefore, if you take a statin, you MUST take supplemental CoQ10, or better, the reduced form called ubiquinol.  A recent study in the European Journal of Pharmacology2showed that ubiquinol effectively rescued cells from the damage caused by the statin drug simvastatin, thereby protecting muscle cells from myopathies. Another study3 evaluated the benefits of CoQ10 and selenium supplementation for patients with statin-associated myopathy. Compared to those given a placebo, the treatment group experienced significantly less pain, decreased muscle weakness and cramps, and less fatigue.

Statins also interfere with the mevalonate pathway, which is the central pathway for the steroid management in your body.

How to Optimize Your Cholesterol Levels Naturally

The most effective way to optimize your cholesterol profile and prevent heart disease is via diet and exercise. Remember that 75 percent of your cholesterol is produced by your liver, which is influenced by your insulin levels. Therefore, if you optimize your insulin level, you will automatically optimize your cholesterol and reduce your risk of both diabetes and heart disease.

There is NO drug to cure heart disease, as the underlying cause is insulin resistance and arterial wall damage — both of which are caused by eating too many sugars, grains, and especially fructose. So, my primary recommendations for safely regulating your cholesterol and reducing your risk of heart disease include:

  • Reduce, with the plan of eliminating grains and fructose from your diet. This is one of the best ways to optimize your insulin levels, which will have a positive effect on not just your cholesterol, but also reduces your risk of diabetes and heart disease, and most other chronic diseases. Use my Nutrition Plan to help you determine the ideal diet for you, and consume a good portion of your food raw.
  • Get plenty of high-quality, animal-based omega 3 fats, such as krill oil, and reduce your consumption of damaged omega-6 fats (trans fats, vegetable oils) to balance out your omega-3 to omega-6 ratio.
  • Include heart-healthy foods in your diet, such as olive oil, coconut and coconut oil, organic raw dairy products and eggs, avocados, raw nuts and seeds, and organic grass-fed meats.
  • Optimize your vitamin D levels by getting proper sun exposure or using a safe tanning bed.
  • Optimize your gut flora, as recent research suggests the bacterial balance in your intestines may play a role in your susceptibility to heart disease as well
  • Exercise daily. Make sure you incorporate Peak Fitness exercises, which also optimizes your human growth hormone (HGH) production.
  • Walk barefoot to ground yourself to the earth. Lack of grounding has a lot to do with the rise of modern diseases as it affects inflammatory processes in your body. Grounding thins your blood, making it less viscous. Virtually every aspect of cardiovascular disease has been correlated with elevated blood viscosity. When you ground to the earth, your zeta potential quickly rises, which means your red blood cells have more charge on their surface, which forces them apart from each other. This action causes your blood to thin and flow easier. By repelling each other, your red blood cells are also less inclined to stick together and form a clot.
  • Avoid smoking or drinking alcohol excessively.
  • Be sure to get plenty of good, restorative sleep.

Ninety-Nine Out of 100 People Do Not Need Statin Drugs

The odds are very high — greater than 100 to 1 — that if you’re taking a statin, you don’t really need it. From my review, the ONLY subgroup that might benefit are those born with a genetic defect called familial hypercholesterolemia, as this makes them resistant to traditional measures of normalizing cholesterol.

Remember, your body NEEDS cholesterol for the production of cell membranes, hormones, vitamin D and bile acids that help you to digest fat. Cholesterol also helps your brain form memories and is vital to your neurological function. There is also strong evidence that having too little cholesterol INCREASES your risk for cancer, memory loss, Parkinson’s disease, hormonal imbalances, stroke, depression, suicide, and violent behavior.

Statins really have nothing to do with reducing your heart disease risk. In fact, this class of drugs can increase your heart disease risk — especially if you do not take Ubiquinol (CoQ10) along with it to mitigate the depletion of CoQ10 caused by the drug.

Knowing that high cholesterol is NOT the cause of heart disease finally frees you to take a serious look at what does cause this potentially lethal condition. And as described above, poor lifestyle choices are primarily to blame, such as too much sugar, too little exercise, lack of sun exposure and never grounding to the earth. These are all things that are within your control, and don’t cost much (if any) money to address.

Early Capsule Endoscopy for Overt Obscure Gastrointestinal Bleeding.


Procedures performed within 3 days of hospital admission were associated with higher diagnostic yield, more therapeutic interventions, and shorter stays.

 

Early endoscopy for bleeding peptic ulcers is known to be effective in identifying bleeding sites, allowing directed therapy, and predicting rebleeding. Early capsule endoscopy (CE) may also be effective in identifying the site of overt obscure gastrointestinal bleeding (OOGIB; World J Gastroenterol 2011; 17:774).

To further evaluate such benefits of early CE, investigators retrospectively reviewed outcomes of 144 inpatients and 116 outpatients who underwent CE for OOGIB (defined by visible bleeding with negative upper and lower endoscopic evaluations) during a 2-year period. Inpatients were classified as those who had early CE (within 3 days of admission) or late CE (after 3 days). Results were as follows:

  • Lesions (including red spots) were found in slightly more inpatients than outpatients (65.9% vs. 53.4%; P=0.054).
  • Active bleeding or angioectasias (excluding red spots) were found in 25.8% of outpatients and in significantly more inpatients who had early versus late CE (44.4% vs. 27.8%; P=0.046).
  • Therapeutic procedures were performed in 10.3% of outpatients and in significantly more inpatients who had early versus late CE (18.9% vs. 7.6%; P=0.046).
  • Diagnostic yield and therapeutic intervention rates were similar for outpatients and inpatients who had late CE.
  • Hospital stays were shorter for inpatients who had early versus late CE (6.1 vs. 10.3 days, P<0.0001).

The authors conclude that early CE for inpatients with OOGIB results in a higher diagnostic yield, more therapeutic interventions, and shorter hospital stays compared with late CE. They speculate that the lack of a significant difference in diagnostic yield between the inpatient and outpatient groups is due to the dilution of the inpatient sample by those receiving late CE.

Comment: This study demonstrates that, as in peptic-ulcer bleeding, early endoscopy in overt obscure gastrointestinal bleeding increases diagnostic yield and leads to potential therapy. Early capsule endoscopy identifies lesions that are still bleeding or have stigmata of bleeding. The data also showed that active bleeding decreased with each day after presentation. The results suggest that patients who present with OOGIB should undergo early CE after negative bidirectional endoscopy if the technology is available.

 

Source: Journal Watch Gastroenterology

 

 

 

Meeting aliens will be nothing like Star Trek.


 

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The latest Star trek movie raises an eternal question: why are the Klingons (or Cylons orDaleks) always at roughly our technological level?

For any sense of drama, interplanetary protagonists have to be evenly matched. Usually, the aliens have technology that is sufficiently superior to humans to promise them victory – yet not infinitely superior, thus permitting nail-biting battle scenes and humanity’s eventual triumph against (almost) insurmountable odds.

But the technological progress of life on Earth – as deduced from palaeontology, archaeology and modern history – indicates this cliché makes no sense.

Should we meet aliens, they will almost certainly either be at the bacterial level, or so advanced that they would see us as bacteria. Either way, it would not be a very exciting encounter, at least by Hollywood standards.

The fossil and archaeological record emphasises the jerkiness of technological progress on Earth. Life has existed on earth for more than 3.5 billion (3500 million) years, but was at the microbial level for 85% of this time.

Tools were only invented in the past couple of million years, by a select few species (such as humans, chimps and Caledonian crows).

Technology – complex tools – is unique to humans and only appeared in the past few thousand years. But when technology finally appeared after aeons, innovation accelerated exponentially.

I quantified this exponential growth by consulting a detailed timeline of modern inventions: a list of game-changing technological breakthroughs that transformed society, such as the printing press, antibiotics, the car, the aeroplane, TV and the internet (any such list has inherent subjectivity, so you might want to find your own).

I plotted the cumulative amount of technology available to humanity through time based on this list: so, for instance, the earliest piece of technology on the list (the abacus) appeared around 2400BC, so humanity’s (and Earth’s) technological “score” finally moves up to 1 at that time, after being stuck at 0 since the origin of life.

The resultant graph of technological progress shows innovation proceeds rather slowly until about 1400AD, and then really takes off.

Between 1400 and 1600, there were 12 revolutionary innovations, which exceeded the number of such innovations in the entirety of human existence (and thus Earth’s existence) up to that point.

Between 1600 and 1800, there were 21 such inventions; and between 1800 and 2000 there were 75.

Technology is growing exponentially, and since 1400 has doubled every 200 years (analogous to a computing phenomenon known as Moore’s law, applied across all technology).

The next double-century (2000-2200) therefore promises no fewer than 150 breakthrough innovations on par with the steam engine, antibiotics and the aeroplane. No wonder technophobes moan “stop the world, I want go get off”.

This exponential growth is no surprise. Innovation is a positive feedback process. Every invention sets in train further innovations, which can further drive elaboration of the original invention.

Think of inventions that improve communication (eg writing, print, telephone, radio, TV, internet). Better communication means ideas circulate much more rapidly, interact and synergise, resulting in further innovation, which in turn quickly yields even further improvements to communication.

Every invention relies on, and sets the groundwork for, other innovations, though some links are not immediately obvious.

The technology to build tall buildings has existed for many thousands of years, as evidenced by the massive temples and columns of the ancient world. Yet the first skyscraper – the first inhabited tall building – only appeared Chicago as late as the 1880s.

It was built shortly after the invention of the lift and the powered industrial water pump.

This is logical: a skyscraper would not be very popular if there were no lifts, and the toilets are were on the ground floor. So an efficient water pump, as much as the lift, made possible the skyscraper. And of course, as those buildings got ever taller, the pressure to improve pumps increased.

Once life on any planet – such as Earth – hits upon technology, the rate of change will rapidly and continuously accelerate, and society will spend less and less time at any particular technological level.

Humans spent more than two million years at roughly the same stone-age level: transplant a palaeolithic caveman 100,000 years into his past or future, and he probably wouldn’t notice any change.

But imagine the angst that would result if you put a teenager 50 years into her past, or yourself 50 years into the future. Things are now changing faster than ever, and the pace of progress will only increase.

Our current technological level will probably span about 100 years, from 1950 to 2050: daily life before and after this period will be qualitatively different.

Archaeologists of the future, and palaeontologists from the very distant future, will look upon this period as a unique period in human (and Earth) history, and perhaps label it the “palaeodigital age”: the age when life first made crude digital tools (such as plastic watches, Pac-Man machines and iPads).

If evolution on alien worlds proceeds even vaguely like that on Earth, then extraterrestrial life, too, will be stuck at zero technology for aeons.

When technology finally appears, it will hurtle forwards with increasing momentum so that life spends short (and increasingly shorter) intervals at any particular technological level.

Even a slight time displacement on this steep learning curve translates to monumental differences in technological capability. For intance, the end of the age of sail was separated from the beginning of the space age by less than a century.

And human societies, which all shared similar tools until some left Africa perhaps 60,000 years ago, diverged sharply in technological advancement very rapidly, resulting in grossly unequal encounters during the Age of Exploration.

There is therefore effectively zero chance of meeting an alien society at the fleeting moment that it happens to occupy a similar point on the technological learning curve as humanity.

Rather, any inhabited alien world we encounter will either be filled with bacteria – or brimming with technology advanced far beyond our comprehension.

And, of course, neither scenario would make for a very exciting movie.

Source: http://www.sciencealert.com.au

Campaign to nominate African midwife for Nobel Peace Prize.


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  Dressed in a pink uniform, midwife Esther Madudu 130509105951-highest-infant-mortality-ssa-chart-entertain-features

shuffle past rows of beds to check on the five babies she delivered the night before inside a small health center in rural eastern Uganda.

Lying underneath a sky blue mosquito net, a newborn girl wrapped in a white sheet tries to stretch her tiny body as Madudu slowly approaches.

“Esther is there,” says the midwife, pointing to the baby girl resting next to her mother. “Esther Madudu — they gave the baby my names, all my names, because yesterday it was born on my birthday,” she continues, with a smile on her face.

“The mother was too excited because she never expected the baby to be alive so she said: ‘these are all your names.’ The pain was too much; she walked for a long distance and she thought the baby was dying.”

Midwife stands up for Africaers

Uganddwife: We lack resources

How midwife lost her own baby

Pain medication is a rare luxury in the small village of Atitiri so Madudu had to rely on one special treatment to help the woman bring her baby to life.

“I gave her ‘verbocain,'” says Madudu. “You know ‘verbocain’ is the only drug we can give them in Africa,” she explains ironically. “‘Verbocain’ — you verbally talk to the mother; giving her just consoling words and patting her, rubbing her back, until she gave birth.”

‘Stand Up For Mothers’

Madudu is well known here as a midwife who has a very good record of saving both mothers and babies during difficult deliveries.

But her reputation extends far beyond eastern Uganda. Since 2011, Madudu has become the poster girl for all of Africa’s midwives, fronting an international campaign to highlight the plights of mothers and babies on the continent.

Called “Stand Up For African Mothers,” the initiative by the African Medical and Research Foundation (AMREF) aims to ensure that all pregnant women throughout Africa have access to trained midwives to ensure a reduction in high maternal mortality rates.

In sub-Saharan Africa, AMREF says 200,000 women die every year from complications during pregnancy or childbirth — that’s 60% of the global total.

In Africa, maternal mortality death is really unacceptably high,” says Abenet Berhanu, AMREF country director for Uganda.

The group, one of Africa’s top health and development research organizations, works together with local authorities to improve education and facilitation of care.

It also aims to train 15,000 midwives by 2015 to equip them with the necessary skills to maintain good health and has launched an online petition to symbolically nominate Madudu as a candidate for the 2015 Nobel Peace Prize.

We hope to create a future where no baby is left alone, where no mother dies while giving birth.
Esther Madudu, Ugandan midwife

 

“She really has a passion for her work,” says Berhanu of Madudu. “She has been working extra hours; she is passionate in handling mothers,” he adds. “This [the nomination] is in recognition for all midwives who have been working under challenging circumstances.”

To support the “Stand Up For African Mothers” campaign, Madudu has visited different countries giving several speeches to draw attention to the issue of maternal mortality in Africa.

“This campaign is not a political campaign,” explains Madudu. “It is just a campaign which is creating awareness that there is death, maternal mortality rate which is high in Africa; mothers are dying; babies are dying. The solution should be, we train midwives,” she says.

Devotion

Like many maternity clinics in rural parts of Africa, the health center in Atitiri is lacking several necessary resources — shortage of running water, electricity challenges, broken beds and scarcity of medicines all make Madudu’s job very difficult.

But despite the challenges, the midwife extraordinaire remains devoted to her patients.

A mother of two, Madudu has chosen to live hours away from her family to be able to cater to the women that need her.

“I opted to give my children to my mother, not because I don’t love them,” she says. “I love my children but because I could not have time for them, to cook for them, take care of them, because of my tight schedule of duties.”

Madudu can completely identify with the fears of the mothers she helps. Soon after becoming a midwife, she suffered herself the cruel experience of losing a child.

“I am a victim of mortality because I lost my baby during child birth,” recalls Madudu. “It was a terrible condition for me; it was psychological torture, because a midwife losing a baby? And yet I’m the one saving other babies,” she adds.

“It was terrible and I said ‘no mother should lose a baby; I’ll try my level best, I will improvise, whatever I can, so long as I have the knowledge to save that woman and her baby.'”

And that’s what she’s been doing ever since, working tirelessly to ensure that mothers get the right treatment during pregnancy and child birth.

She is optimistic that the “Stand Up For Afican Mothers” campaign will create much needed awareness of the plights of the people she’s helping.

“We hope to create a future where no baby is left alone, where no mother dies while giving birth,” she says. “That is my hope.”

Source:CNN