Google Finally Revealed Android N’s Name Officially!       

Hey everyone, it’s that time of year again. As you all know, Google likes to follow a very specific pattern for its Android releases. We’ve had Alpha, Beta, Cupcake, Donuts, Éclair, Froyo, Gingerbreak, Honeycomb, Ice cream sandwich, Jelly Bean, Kit Kat, Lollipop and Marshmallow.

As you can see, they have followed alphabetical order and aside from the Alpha and Beta versions, they all have deserts name. Every year, the reveal of the name has become a tradition and people like to try and guess in advance what the name could be. This year, Google even put up a website to get suggestions from users.

Today, we got the big news, finally! Google Android N will be called Android Nougat. Now, I have been waiting since Android K to get to N. Why? Because Android K was Kit Kat and it showed us that Google was perfectly capable of striking a deal to use a brand name. That is why I couldn’t wait to get to Android N! What is the most delicious, popular, recognizable brand that starts with an N? NUTELLA! We had one chance and Google blew it. And to prove how much they blew it, they even had to release a video to explain how to pronounce Nougat since they picked such a random, unmarketable term, that no one says it the same way.

The other issue I have is the statue. Back in the days, Android’s mascot literally became a Kit Kat bar, an ice cream sandwich or a jelly bean distributor… hell… Even the Lollipop mascot was only holding the candy treat but with some sort or angle and giving the peace sign. Since Marshmallow last year and now Nougat, the mascot is just standing there holding a Marshmallow and standing on Nougat. Really unoriginal.
Even if I feel like google is losing their spark and slacking off on the creativity side, and even if I will never forgive them for not choosing Nutella when it was their only chance, I am still excited by the new Android… Even if it’s called Nougat.

New techniques to assess the fate of stem cells in vivo

This is a picture of blanpain.

Credit: ULB C. Blanpain

Stem cells ensure the development of tissues, their daily maintenance and their repair following injuries. One of the key questions in the field of stem cell biology is to define the different cell lineages in which stem cells can differentiate into. Stem cells can be multipotent, meaning they present the ability to give rise to more than one lineage, or unipotent, meaning they can only differentiate into one cell lineage. Lineage tracing experiments are routinely used in the fields of developmental and stem cell biology to assess the fate of stem cells in vivo. However, no rigorous method has yet been established to interpret with great precision and statistical confidence the issue of multipotency versus unipotency in lineage tracing experiments.

In a study that makes the cover of the current issue of Genes & Development, researchers from the ULB Cancer Research Center, U-CRC, led by Cédric Blanpain, MD/PhD, WELBIO investigator and Professor at the Faculty of Medicine, Université libre de Bruxelles, Belgium, developed new methods to assess with great precision the multipotent or unipotent fate of mammary gland and prostate stem cells.

Aline Wuidart and colleagues developed two novel methods to determine whether stem cells in the mammary gland and in the prostate are multipotent or unipotent during development and adult maintenance. In collaboration with physicists of the University of Cambridge, they developed a novel bio-statistical framework to define multipotency with high confidence in multicolor lineage tracing experiments. They developed another method called lineage tracing at saturation to assess the fate of all stem cells in a given tissue and the flux of cells between different lineages. "It was really important to sort out the issue of multipotency of mammary and prostate stem cells in a definitive manner. These novel and powerful tools combining multicolor lineage tracing, bio-statistical analysis and lineage tracing at saturation will allow to interpret the lineage experiments with much greater confidence," comments Aline Wuidart, the first author of this study.

These new findings unambiguously demonstrate that, while the prostate develops from multipotent stem cells, only unipotent stem cells mediate mammary gland development and adult tissue remodeling. "These methods offer a rigorous framework to assess the lineage relationship and stem cell fate in different organs and tissues. These techniques will become the new standard to decipher the lineage relationship in many other organs or tissues during development, tissue repair and tumor initiation." comments Cédric Blanpain, the senior author of the Genes & Development paper.

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High levels of vitamin D is suspected of increasing mortality

It can be disadvantageous to have too much vitamin D.

Credit: © Le Do / Fotolia

The level of vitamin D in our blood should neither be too high nor to low. Scientists from the University of Copenhagen are the first in the world to show that there is a connection between high levels of vitamin D and cardiovascular deaths.

In terms of public health, a lack of vitamin D has long been a focal point. Several studies have shown that too low levels can prove detrimental to our health. However, new research from the University of Copenhagen reveals, for the first time, that also too high levels of vitamin D in our blood is connected to an increased risk of dying from a stroke or a coronary.

The results have just been published in the Journal of Endocrinology and Metabolism.

"We have studied the level of vitamin D in 247,574 Danes, and so far, it constitutes the world's largest basis for this type of study. We have also analysed their mortality rate over a seven-year period after taking the initial blood sample, and in that time 16,645 patients had died. Furthermore, we have looked at the connection between their deaths and their levels of vitamin D," Professor at the Department of Clinical Medicine, Peter Schwarz explains.

The conclusion is clear: the study confirms that there is indeed a correlation between mortality rates and too low levels of vitamin D, but the new thing is that the level of vitamin D can also be too high.

"If your vitamin D level is below 50 or over 100 nanomol per litre, there is an greater connection to deaths. We have looked at what caused the death of patients, and when numbers are above 100, it appears that there is an increased risk of dying from a stroke or a coronary. In other words, levels of vitamin D should not be too low, but neither should they be too high. Levels should be somewhere in between 50 and 100 nanomol per litre, and our study indicates that 70 is the most preferable level," Peter Schwartz states.

That having too much vitamin D in our blood can be bad for our health has never been proven before, and it may have great influence on our future intake of nutritional supplements.

"These are very important results, because there is such great focus on eating vitamin D. We should use this information to ask ourselves whether or not we should continue to eat vitamins and nutritional supplements as if they were sweets. You shouldn't simply up the dose to feel better. We should only consume such vitamins in close coordination with our GP," Peter Schwartz concludes.

Immune system link to kidney disease risk, research finds

A gene which forms part of our body's first line of defence against infection may be associated with an increased risk with a type of kidney disease, research involving academics at The University of Nottingham has discovered.

The work, which is published in the academic journal Science Translational Medicine, found that the difference in the number of copies of the alpha-defensin genes was a major genetic factor in developing the condition IgA nephropathy.

Professor John Armour, Professor of Human Genetics in the University's School of Life Sciences, said: "The observation that variation in the gene numbers for these alpha-defensin genes is strongly correlated with risk of IgA nephropathy creates an interesting puzzle.

"The data overwhelmingly support the association, but we still don't understand what the connection might be between alpha-defensins and molecular events that cause the kidney problems."

IgA nephropathy, also known as Berger's Disease, is a condition in which Immunoglobulin A, one of the types of antibody the body produces to fight infection, settles in the kidney causing scarring and inflammation. The condition can lead to high blood pressure, swollen ankles and high levels of cholesterol in the blood and, in the most serious cases, can lead to kidney failure.

It is a relatively rare condition in Europe, but is much more common in China and East Asia, where it is the leading cause of patients needing dialysis because of kidney failure.

Previous studies have demonstrated that there are genetic factors involved in predisposition to the disease and scientists have been working to map these factors more precisely.

In this latest study, Professor Armour and colleagues at Nottingham have worked in collaboration with teams at the University of Leicester, Sun Yat-sen University in Guangzhou, China, and the Genome Institute of Singapore.

They came to the unexpected conclusion that the strongest genetic factor is the variation in numbers of genes for defence proteins.

People have two copies of most genes in the human genome, one from each parent, but some genes are present in different numbers in different people.

The team looked at genetic variation in more than 1,000 patients with IgA nephropathy, compared with more than 1,000 people without the condition, and found a significant difference in the numbers of alpha-defensin genes between the two groups.

Alpha-defensins are proteins that kill bacteria as part of the innate immune system, our first line of defence against infection.

Although the findings do not immediately suggest new therapies for the disorder, they will improve our chances of identifying those who are most at risk and offer a new line of investigation to understand exactly how the defensin gene copy number variants lead to kidney disease. The team is already undertaking the next stage of research to further develop our knowledge.

High nitrate levels in some WA water supplies could cause kidney disease, doctor warns

PHOTO: The Western Desert Kidney Health Project clinic truck travelled to 10 towns and communities over three years. 

A West Australian regional doctor says there could be a link between elevated levels of nitrates in the drinking water of some towns and health issues such as kidney disease.

Dr Christine Jeffries-Stokes was a chief investigator for the Western Desert Kidney Health Project which looked at five Indigenous communities and five towns in WA's Goldfields and Western Desert regions.

The study of more than 1,000 people over three years aimed to determine the prevalence of type 2 diabetes and end-stage renal disease.

Just over one third of Aboriginal participants and a quarter of non-Aboriginal residents tested had an elevated albumin-creatinine ratio in their urine which indicated kidney damage.

Dr Jeffries-Stokes said the results were surprising.

"We found that the risk factors for kidney disease and diabetes, that is protein leaking in your urine, blood in your urine, blood pressure problems and the early signs of diabetes, were actually a problem for everybody, much more common in the non-Aboriginal community than we expected," she said.

"Which suggested that environmental factors or exposures probably were more significant than we had thought.

PHOTO: A girl has her blood pressure taken in Menzies as part of the Western Desert Kidney Health Project. (ABC News: Roman Kutzowitz)

"So then we went looking for what those factors might be and obviously lack of access to fresh food is a problem for everyone and exercise opportunities are a problem for everyone, but we also found that the water quality probably is a significant factor as well."

An auditor-general's report released in May last year showed more than a dozen WA communities had enough nitrate in their water supply to cause the potentially fatal condition blue baby syndrome.

Nitrates above safe levels

The Australian Drinking Water Guidelines specify a health guideline of 11.3mg/L of nitrogen for infants less than three months old and 22.6mg/L for adults and children.

Two of the communities included in the Western Desert Kidney Health Project study, Tjuntjuntjarra and Mulga Queen, showed more than 50mg/L of nitrate in their drinking water.

The town of Menzies had nitrate levels as high as 12mg/L, so bottled water was supplied to parents with infants.

Other towns included in the study were within safe drinking guidelines for adults and infants.

But Dr Jeffries-Stokes claimed chronic low-grade exposure to nitrate could also be a problem.

PHOTO: Dr Christine Jefferies-Stokes and Annette Stokes with the Western Desert Kidney Health Project clinic truck. (ABC News: Emma Wynne)

"The World Health Organisationlast year came out and talked about how nitrates, which are used in some foods as a preservative, are a class 1 carcinogen and the nitrates in the water are the same as the nitrates in those foods," Dr Jeffries-Stokes said.

"There is also ongoing research that the nitrates forming the nitrosamines can contribute to the development of type 2 diabetes and kidney disease.

Dr Jeffries-Stokes said people in rural and remote areas were at higher risk of most diseases, particularly diabetes and kidney disease.

"Now we know that the nitrates might be a significant factor," she said.

More research needed

Kidney Health Australia Medical Advisor Alan Cass said he welcomed research into kidney-health-related issues.

"There are many health issues contributing to the high prevalence of chronic kidney disease amongst Indigenous communities and these include low birth weight, high blood pressure and diabetes," Professor Cass said.

"To date there has been uncertainty regarding the long-term effects of drinking water with elevated nitrate levels.

"Kidney Health Australia strongly supports an independent rigorous appraisal of current evidence regarding the effects of the environment on kidney health."

Dr Jeffries-Stokes said all towns and communities should have water filtration systems.

"I understand the cost of installing a water system is about the same as providing renal dialysis for one patient for one year," she said.

Parkinson's linked with 2 dangerous proteins c Abl and synuclein

Parkinson's disease: New protein discovery could fuel new treatments

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New treatments for Parkinson's disease could be in sight, after researchers reveal how inhibiting the activity of a specific protein in the brain could stop or slow development of the disease. What is more, there is already a drug approved for the treatment of leukemia that can block the protein in question.

Researchers suggest blocking a protein in the brain called c-Abl could prevent or slow the development of Parkinson's disease.

Study co-author Dr. Ted Dawson, of Johns Hopkins University School of Medicine in Baltimore, MD, and colleagues publish their findings in The Journal of Clinical Investigation.

Parkinson's disease(PD) is a chronic, progressive neurological disorder characterized by movement problems. 

Symptoms of PD include tremors in the hands, arms, legs, jaw, and face, problems with balance and coordination, stiffness of the limbs and trunk, and slowed movement. These symptoms worsen as the disease progresses.

According to the Parkinson's Disease Foundation, up to 1 million people in the United States are living with PD, and each year, around 60,000 new cases are diagnosed.

While the exact cause of PD remains unclear, researchers have suggested that a protein called c-Abl might play a role in development of the disease, after studies have identified increased activity of this enzyme in PD patients.

Furthermore, previous studies in mice have suggested that blocking c-Abl could halt or slow PD. 

However, study co-author Han Seok Ko, Ph.D., assistant professor of neurology at Johns Hopkins, notes that the drugs used to block c-Abl in these studies were also blocking similar proteins, making it hard to determine whether the beneficial results were solely down to c-Abl inhibition.

Increased c-Abl levels lead to PD development

To find out whether this is the case, the team conducted experiments on mice that were genetically engineered to develop PD.

On eliminating the gene that codes for c-Abl in the mice, the researchers found that their symptoms of PD worsened and disease progression accelerated. Furthermore, the team found that increasing c-Abl production in normal mice led them to develop PD.

Fast facts about PD

• Worldwide, there are around 10 million people living with PD
• The condition is around 1 ½ times more common among men than women
• PD is estimated to cost the U.S. around $25 billion each year.

Learn more about PD

Next, the researchers set out to identify the underlying mechanisms by which c-Abl appears to cause PD development.

They found that c-Abl works with another protein called α-synuclein, which is known to accumulate in the brains of people with PD, forming clumps known as Lewy bodies. Previous research has suggested that a buildup of α-synuclein results in the death of brain cells related to motor control.

In detail, the researchers found that c-Abl guides another molecule called "phosphate group" to a certain region of α-synuclein, which may increase the formation of α-synuclein clumps; the higher the c-Abl levels, the more α-synuclein clumping that occurred.

These findings, say the authors, indicate that blocking c-Abl activity could prevent or slow the development of PD. 

Dr. Dawson notes that there is already a c-Abl-inhibiting drug that has been approved by the U.S. Food and Drug Administration (FDA) for the treatment of leukemia. The team now plans to investigate whether this drug might show promise for the prevention of PD, or whether it could lead them to other possible treatments.

The researchers also want to determine whether the newly identified c-Abl-phosphate group interaction with α-synuclein could be a useful biochemical marker of PD severity. At present, no such marker exists, which the team says is holding back research into new PD treatments.

Dementia cannot be caught through blood transfusions, say scientists 

Fears that dementia could be caught through blood transfusions are unfounded, say researchers  

Dementia cannot be caught through blood transfusions, a new study has shown.

Last year researchers at University College London warned that some patients who had contracted Creuzfeldt Jakob Disease (CJD) through medical accidents also had Alzheimer’s disease, suggesting that the diseases were transmitted at the same time.

They warned that ‘theoretically’ the seeds of dementia could be accidentally passed on through a blood transfusion.

But now a large study by the Karolinska Institute in Sweden has found that there is no risk of transference.

Researchers looked at 2.1 million people who had received blood transfusions from 1.7 million donors over a 40 year period.

They found there was no difference in the rates of neurological disease between those given transfusions from dementia sufferers or the dementia-free.

“The results are unusually clear for such a complicated subject as this,” says principal investigator Gustaf Edgren, docent at the Department of Medical Epidemiology and Biostatistics at the Karolinska Institute.

“We’ve been working with this 

question for a long time now and have found no indication that these diseases can be transmitted via transfusions.

“Blood transfusions are extremely safe in the Western world today, but even so we are working continuously and proactively on identifying any overlooked risks.”

There were fears that dementia caught through medical accidents would not emerge for 40 years  CREDIT: ALAMY 

Between 1958 and 1985 nearly 2,000 people of short stature in Britain were given pituitary growth hormone taken from dead donors in the belief if would help them grow.

But unknowingly the hormones were infected with CJD and nearly 80 people have since died because of medical error.

Last year British scientists who were studying the brains of patients who had died from CJD, found large quantities of amyloid beta protein - a sticky deposit which forms among brain cells and stops them communicating with each other properly in Alzheimer's patients.Mm

They found there was no difference in the rates of neurological disease between those given transfusions from dementia sufferers or the dementia-free.

“The results are unusually clear for such a complicated subject as this,” says principal investigator Gustaf Edgren, docent at the Department of Medical Epidemiology and Biostatistics at the Karolinska Institute.

“We’ve been working with this question for a long time now and have found no indication that these diseases can be transmitted via transfusions.

“Blood transfusions are extremely safe in the Western world today, but even so we are working continuously and proactively on identifying any overlooked risks.”

There were fears that dementia caught through medical accidents would not emerge for 40 years  CREDIT: ALAMY 

Between 1958 and 1985 nearly 2,000 people of short stature in Britain were given pituitary growth hormone taken from dead donors in the belief if would help them grow.

But unknowingly the hormones were infected with CJD and nearly 80 people have since died because of medical error.

Last year British scientists who were studying the brains of patients who had died from CJD, found large quantities of amyloid beta protein - a sticky deposit which forms among brain cells and stops them communicating with each other properly in Alzheimer's patients.

The researchers suggested that dementia was ‘seeded’ in the brains of the patients at the same times as CJD.

The also warned that because the incubation period can be up to 40 years, people could be unaware that they had been contaminated in medical procedures.

However the government's Chief Medical Officer, Dame Sally Davies, said the Department of Health was monitoring the situation and reassured the public that there was little risk.

The new research was published in the Annals of Internal Medicine. 

What is dementia? In 60 secondsPlay!01:05

A daily handful of walnuts may lower fatal heart attack risk

A serving of fatty fish twice a week or gobbling down a handful of walnuts every day might save your life, a new study suggests.

Kerdkanno / Shutterstock

Good sources of omega 3 and unsaturated fats include fish and walnuts.

An international team of researchers found that people with higher levels of omega-3 fatty acids in their bodies have a lower risk of dying from a heart attack, according to the report published in JAMA Internal Medicine.

The new research measured the various types of omega-3 fatty acids in blood and tissue of 45,637 people from 16 countries.

During an average of 10 years follow-up there were 2,781 fatal and 7,157 non-fatal heart attacks. When the researchers analyzed people's omega-3 levels and heart health, they found moderate levels of the nutrient were associated with a 10 percent lower risk of death from heart attacks.

RELATED: Why kids' diets put them on the road to heart disease 

The news is even better if you consume more foods with omega-3 fatty acids, said the study's lead author Liana Del Gobbo, a researcher at the Stanford University School of Medicine.

"If you went from eating almost no fish to eating a lot, it's more like a 23 or 24 percent lower risk of dying from a heart attack," Del Gobbo said.