First Ebola boy likely infected by playing in bat tree

The Ebola victim who is believed to have triggered the current outbreak - a two-year-old boy called Emile Ouamouno from Guinea - may have been infected by playing in a hollow tree housing a colony of bats, say scientists.

They made the connection on an expedition to the boy's village, Meliandou.

They took samples and chatted to locals to find out more about Ebola's source.

The team's findings are published in EMBO Molecular Medicine.

Ebola trail

Meliandou is a small village surrounded by farmland and large trees

Meliandou is a small village of 31 houses.

It sits deep within the Guinean forest region, surrounded by towering reeds and oil palm cultivations - these are believed to have attracted the fruit bats carrying the virus passed on to Emile.

During their four-week field trip in April 2014, Dr Fabian Leendertz and colleagues found a large tree stump situated about 50m from Emile's home.

Villagers reported that children used to play frequently in the hollow tree.

Emile - who died of Ebola in December 2013 - used to play there, according to his friends.

The villagers said that the tree burned on March 24, 2014 and that once the tree caught fire, there issued a "rain of bats".

Children from the village used to play in and around the tree

A large number of these insectivorous free-tailed bats - Mops condylurus in Latin - were collected by the villagers for food, but disposed of the next day after a government-led ban on bushmeat consumption was announced.

While bushmeat is thought to be a possible source of Ebola, the scientists believe it didn't trigger the outbreak.

Instead, it was Emile's exposure to the bats and their droppings as he played with his friends in the hollowed tree.

Pest control

The scientists took and tested ash samples from the tree and found DNA traces that were a match for the animals.

While they were unable to test any of the bushmeat that the villagers had disposed of, they captured and tested any living bats they could find in and around Meliandou.

No Ebola could be detected in any of these hundred or so animals, however.

But previous tests show this species of bat can carry Ebola.

Dr Leendertz, from the Robert Koch Institute in Germany, and his colleagues say this must be a pretty rare occurrence though.

Dr Leendertz said: "That is also obvious when you think about how many tonnes of bat meat is consumed every year.

"If more bats carried the virus, we would see outbreaks all the time."

He says it is vital to find out more about the bats.

"They have moved into human settlements. They do not just live in the trees but also under the roofs of houses in the villages.

"The Ebola virus must jump through colonies from bat to bat, so we need to know more."

But culling the animals is not the answer.

"We need to find ways to live together with the wildlife. These bats catch insects and pests, such as mosquitoes. They can eat about a quarter of their body weight in insects a day.

"Killing them would not be a solution. You would have more malaria."

Most cancer types 'just bad luck'

Most types of cancer can be put down to bad luck rather than risk factors such as smoking, a study has suggested.

A US team were trying to explain why some tissues were millions of times more vulnerable to cancer than others.

The results, in the journal Science, showed two thirds of the cancer types analysed were caused just by chance mutations rather than lifestyle.

However some of the most common and deadly cancers are still heavily influenced by lifestyle.

And Cancer Research UK said a healthy lifestyle would still heavily stack the odds in a person's favour.

Time to throw caution to the wind?

So is it time to light-up, drink and eat what you want without a care in the world?

It won't come as a surprise that the answer is no.

All cancer has an element of chance - a roll of the dice that decides whether your DNA acquires a mutation that leads to cancer.

The study shows that two thirds of cancer types are simply chance.

But the remaining third are still heavily influenced by the choices we make.

Too much booze, time in the sun or being overweight mean we are playing with loaded dice and the odds are not in our favour.

Remember smoking accounts for a fifth of all cancers worldwide.

These findings are a reminder that cancer is often just bad luck and the only option is early detection.

But that's not an excuse to give up on those new year's resolutions already.

In the US, 6.9% of people develop lung cancer, 0.6% brain cancer and 0.00072% get tumours in their laryngeal (voice box) cartilage at some point in their lifetime.

Toxins from cigarette smoke could explain why lung cancer is more common.

But the digestive system is exposed to more environmental toxins than the brain, yet brain tumours are three times as common as those in the small intestine.

Root of cancer

The team at Johns Hopkins University School of Medicine and Bloomberg School of Public Health believe the way tissues regenerate is the answer.

Old tired cells in the body are constantly being replaced with new ones made by dividing stem cells.

But with each division comes the risk of a dangerous mutation that moves the stem cell one step closer to being cancerous.

The pace of turnover varies throughout the body with rapid turnover in the lining of the gut and a slower pace in the brain.

Bone cancer in the right leg

The researchers compared how often stem cells divided in 31 tissues in the body over a lifetime with the odds of a cancer in those tissues.

They concluded that two thirds of cancer types were "due to bad luck" from dividing stem cells picking up mutations that could not be prevented.

These cancer types included Glioblastoma (brain cancers), small intestine cancers and pancreatic cancers.

Cristian Tomasetti, an assistant professor of oncology and one of the researchers, said a focus on prevention would not prevent such cancers.

"If two thirds of cancer incidence across tissues is explained by random DNA mutations that occur when stem cells divide, then changing our lifestyle and habits will be a huge help in preventing certain cancers, but this may not be as effective for a variety of others.

"We should focus more resources on finding ways to detect such cancers at early, curable stages."

Poor lifestyle

The remaining third of cancer types, which are affected by lifestyle factors, viruses or a heightened family risk, include some of the most common:

• Basal cell carcinoma - a type of skin cancer made more common by too much UV exposure
• Lung cancer - strongly linked to smoking
• Colon cancer - increased by poor diet and family risk genes

Two common types of cancer - breast and prostate - were not analysed as the researchers could not find a consistent rate of stem cell division in those tissues.

Separate research by Cancer Research UK shows more than four in 10 of the total number of cancers were down to lifestyle.

Dr Emma Smith, senior science information officer at the charity, told the BBC: "We estimate that more than four in 10 cancers could be prevented by lifestyle changes, like not smoking, keeping a healthy weight, eating a healthy diet and cutting back on alcohol.

"Making these changes is not a guarantee against cancer, but it stacks the odds in our favour.

"It's vital that we continue making progress to detect cancer earlier and improve treatments, but helping people understand how they can reduce their risk of developing cancer in the first place remains crucial in tackling cancer."

Ability to culture 'organoids' set to transform pancreatic cancer research

new 3D "organoid" culture system for growing both normal and cancerous pancreatic cells in the lab promises to transform research on pancreatic cancer and the development of new personalized treatments.

The ability to grow organoids - 3D cultures of pancreatic tissue - in the lab promises to transform pancreatic cancer research and pave the way for new personalized treatments.

The researchers report how they used the new organoid technique to grow pancreatic tissue from cells isolated from lab mice and human patients in the journal Cell.

There is a desperate need for radical new approaches in the fight against pancreatic cancer - a deadly disease where only 6% of patients live more than 5 years after diagnosis. It is notoriously difficult to spot pancreatic cancer in the early stages and most cases are only diagnosed after it has started to spread.

Estimates from the National Cancer Institute for the US suggest in 2014 there were over 46,400 new cases of pancreatic cancer, and over 39,500 deaths to the disease.

The new study is a significant step forward, as David Tuveson, co-leader of the study and professor at Cold Spring Harbor Laboratory (CSHL), NY, and Director of Research for The Lustgarten Foundation, NY, notes:

"With this development, we are now able to culture both mouse and human organoids, providing a very powerful tool in our fight against pancreatic cancer."

Researchers will be able to examine molecular pathways of pancreatic cancer

The new organoid technique means researchers will be able to examine what happens at the molecular level to drive the disease and look for new drug targets.

To study a disease like cancer - which develops when cells malfunction and spread - you need a steady supply of normal and cancerous cells that can be grown in the lab.

But normal and cancerous pancreatic cells are extremely difficult to grow in the lab. This is further complicated by the fact the cancer arises in pancreatic ductal cells - which account for only around 10% of the cells in the organ - making it hard to track the small, cell-level changes that accompany tumor progression.

Because of these difficulties, researchers tend to use genetically engineered mice rather than tissue cultures to study pancreatic cancer in the lab. But it can take up to a year to breed the number and type of mice required for a particular investigation.

Organoids will allow labs to grow 3D pancreatic tissue entirely of ductal cells

The potential to use organoids is a game changer for pancreatic cancer research. It means researchers can grow 3D tissue made entirely of ductal cells, uncontaminated by the other types of cell that normally accompany them when retrieved from samples.

The organoids grow as 3D hollow spheres in a gel-like complex filled with growth-inducing factors and connecting fibers. When the organoids are big enough, they can be transplanted into mice, where they develop fully into pancreatic cancer.

Co-lead author Dr. Chang-Il Hwang, who works in Prof. Tuveson's group at CSHL, says, "We now have a model for each stage in the progression of the disease."

Another advantage the new technique brings is to broaden the scope of patients from whom pancreatic tissue can be obtained.

Currently, researchers have limited access to patient samples, which can only be obtained during surgery or autopsy. However, only around 15% of pancreatic cancer patients are eligible for surgery by the time they are diagnosed - either because the disease is too advanced, or because the tumor is entwined in critical blood vessels.

But the new technique the study describes allows scientists to grow organoids from material obtained in biopsies which are used to diagnose pancreatic cancer.

Thus the study shows there is a way to grow 3D tissue in the form of organoids relatively quickly from any pancreatic cancer patient, offering the potential to study the disease in a much wider population.

The team is now working with the National Cancer Institute to build a repository of pancreatic tumor samples that they hope to make available to all pancreatic cancer researchers.

In October 2014, Medical News Today reported another study where researchers grew fully functional organoids of human intestines and successfully transplanted them into mice. The team in that study - from Cincinnati Children's Hospital Medical Center - also hopes the technique means we will eventually be able to grow personalized human tissue, in their case for the treatment of gastrointestinal diseases.

High intelligence linked to reduced risk of schizophrenia

people with high intelligence may be less likely to develop schizophrenia, particularly those who have a genetic susceptibility to the condition. This is according to a new study published in The American Journal of Psychiatry.

People with a high IQ may be less likely to develop schizophrenia than those with a low IQ.

The researchers, including first author Dr. Kenneth S. Kendler of the Virginia Commonwealth University, say their findings challenge past studies indicating that people who are intelligent are more likely to be mentally ill.

"If you're really smart, your genes for schizophrenia don't have much of a chance of acting," says Dr. Kendler.

Schizophrenia is a disabling brain disorder that affects around 2.4 million adults in the US. Onset of the condition usually occurs in early adolescence, and it is characterized by hallucinations, delusions, abnormal thoughts and agitated body movements.

The exact causes of schizophrenia are unclear, but scientists have established that the disorder is familial; around 1% of the general population have schizophrenia, but it occurs in around 10% of people who have have a first-degree relative - such as a parent, brother or sister - with the condition.

In this study, Dr. Kendler and colleagues set out to assess the association between IQ and subsequent schizophrenia risk among the general population and those have a genetic predisposition for the disorder.

Not achieving predicted IQ 'most strongly predisposes for schizophrenia'

The team assessed the IQ at ages 18-20 years of 1,204,983 Swedish males who were born between 1951 and 1975.

The researchers used Cox proportional hazard models to calculate how IQ influences schizophrenia risk among the general population and among cousin, half-sibling and full-sibling pairs, some of which had a relative with the condition.

Up until 2010, the team monitored any schizophrenia-related hospital admissions among the participants.

The results of the analysis revealed that individuals with a low IQ were more likely to develop schizophrenia than those with a high IQ. This relationship was strongest among participants with a family history of the disorder; among cousin, half-sibling and full-sibling pairs, the individual with the lowest IQ was at highest risk for schizophrenia.

Commenting on the team's findings, Dr. Kendler says:

"What really predicted risk for schizophrenia is how much you deviate from the predicted IQ that we get from your relatives.

If you're quite a bit lower, that carries a high risk for schizophrenia. Not achieving the IQ that you should have based on your genetic constitution and family background seems to most strongly predispose for schizophrenia."

He adds that high risk of schizophrenia associated with low IQ may be influenced by environmental factors that lower intelligence, such as early drug use or childhood trauma.

Dr. Kendler stresses, however, that their findings do not suggest that people with high intelligence are unable to develop schizophrenia. He uses the example of American mathematician John Nash. As portrayed in the 2001 movie A Beautiful Mind by actor Russell Crowe, Nash won a Nobel Memorial Prize in Economic Sciences despite having schizophrenia.

"The question is," Dr. Kendler adds, "might we see some upward bump at that high level of intelligence where really brilliant people have increased risk for the disease and we show no such trend?"

In October last year, Medical News Today reported on a study claiming a child's later-life intelligence is not influenced by parenting and is more dependent on genetics.