An analysis of monkeys living

An analysis of monkeys living in Tanzania's Udzungwa Mountains suggests that the impact of external factors, such as human activity, on species numbers is felt in forests as large as 40 square kilometres.

Researchers also found that the health of monkey populations is closely related to the type of habitat found between forest fragments, rather than the distance that separates them.

The findings have broader implications for conservationists as the number of monkeys and the variety of species is a visible indicator of the underlying health of their habitat.

The research was conducted by Dr Andrew Marshall, from the Environment Department at the University of York and Director of Conservation at Flamingo Land Theme Park and Zoo, in collaboration with colleagues from the University of York, the University of Copenhagen, the Tremto Museum of Natural History (Italy) and the Udzungwa Ecological Monitoring Centre (Tanzania).

Dr Marshall said: "This study suggests that while small forest fragments need protecting we should intervene at an earlier stage to protect larger forest areas that are under threat.

"It also supports the case for working with local communities on practical steps that will help forest species. These could include reducing dependence on bush meat and encouraging the planting of habitat that can form corridors between forest fragments."

The research investigated the distribution of seven species living in an area covering 10,000 km² and has led to a wider conservation and education project in the area led by Dr Marshall, through Flamingo Land Theme Park and Zoo. The discovery of a new species of chameleon in this area was announced last year.

Cigarette smoking

For people who carry common gene variants, cigarette smoking greatly increases the risk that a blood vessel in the brain will weaken and balloon out – called an aneurysm – which could be life-threatening if it ruptures, according to research presented at the American Stroke Association's International Stroke Conference 2010. Researchers reported on two new studies from the Familial Intracranial Aneurysm (FIA) project, a multinational collaboration funded by the National Institutes of Neurological Disorders and Stroke to study genetic and other risk factors in families with at least two members affected by intracranial aneurysm.

In one study (Broderick, abstract 156), researchers found that the chance of an intracranial aneurysm increased between 37 percent and 48 percent for people who carried one copy of an identified risky gene variation. However, when the gene variant was combined with smoking the equivalent of one pack a day for 20 years, the risk increased more than five-fold. People with two copies of the gene variant were at even higher risk.

"Like putting a match to kindling, smoking greatly increases the likelihood of a ruptured aneurysm in people with a genetic susceptibility," said Joseph P. Broderick, M.D., study author and professor and chair of the neurology department at the University of Cincinnati Neuroscience Institute.

Cigarette smoking is the leading environmental cause of intracranial aneurysm. An estimated 70 percent to 80 percent of people who experience aneurysms are current or former smokers, he said. In the study, 82.5 percent of participants were smokers at some point. Intracranial aneurysms also occur in multiple members of certain susceptible families.

A ruptured intracranial aneurysm can create a subarachnoid hemorrhage. When that occurs, 40 percent of patients die, and most others experience major disability from the brain injury caused by the rapid bleeding.

By comparing the frequency in 406 patients from the FIA families with that of 392 control subjects without aneurysm in the Cincinnati area, researchers confirmed that certain gene variants on chromosomes 8 and 9 raise the risk of intracranial aneurysm. Other variants on chromosome 2, suggested as genetic risks in a prior study on other populations, were not found to be risk factors in this study.

In the study about 22 percent of controls had a least one copy of the gene variant on chromosome 8 and 73 percent had at least one copy of the variant for chromosome 9. Broderick noted that this percentage is about what is expected in the general population – at least among whites in this region.

"These results tell us the approximate location of the risk-inducing gene on the chromosomes but does not identify the exact gene or how its functioning contributes to the risk of aneurysm," said Broderick, principal investigator of the FIA project.

"This is a powerful message to family members of people who have had ruptured aneurysms. Even if you have the gene, you can dramatically affect your risk by not smoking. If you smoke, you are multiplying the effect of the gene," he said.

Broderick noted that since it is too early to recommend genetic testing, all family members of people who have had an intracranial aneurysm should stop smoking.

In a second presentation from the FIA study, (Sauerbeck, abstract 156), researchers reported that the primary causes of death in FIA families are cancer and cardiac problems other than aneurysm. In an average 3.27 years follow-up of 1,073 people with a diagnosis of intracranial aneurysm and 1,721 family members undiagnosed with an intracranial aneurysm at enrollment in the study, none of those without aneurysm at study onset died from a ruptured intracranial aneurysm. In addition, most deaths in those with aneurysm were unrelated to their aneurysms.

"Especially for those diagnosed with an unruptured aneurysm, if the condition is treated or medically monitored to make sure it's not growing, you can modify your risk factors — by not smoking and keeping blood pressure under control — and not worry as much about the risk of rupture," said Laura