Studies in mice have shown that there is little genetic overlap between male and female fat cell genes.

Human men are more likely to carry extra weight around their guts, while pre-menopausal women store it in their bottoms, hips and thighs, say researchers at UT Southwestern Medical Centre, Dallas. Their studies in mice have shown that out of around 40,000 genes that code for fat in mice, only 138 are found in both male and female fat cells.

A fat and a normal mouse

Even though the studies were only carried out in mice, human and mice species both differ in the way that males and females distribute their fat. So the researchers used the mice to model humans.

“Given the difference in gene expression profiles, a female fat tissue won’t behave anything like a male fat tissue and vice versa,” says Dr. Deborah Clegg, assistant professor of internal medicine said. “The notion that fat cells between males and females are alike is inconsistent with our findings.”

Belly fat is associated with obesity-related conditions like diabetes and heart disease, so men are at a higher risk of these. But when women hit the menopause their ovarian hormone levels drop and their fat storage changes towards their waists.

Dr Clegg says that her ultimate goal is to “determine how fat tissue is affected by sex hormones and whether it would be possible to develop a ‘designer’ hormone replacement therapy that protected post-menopausal women from belly fat and related diseases such as metabolic syndrome.”

Climate change and the environment did not feature highly in the General Election, with the economy taking centre stage. But at least some of the public must feel concerned about the environment, having voted in the first green MP in British Political history, leader of the Green Party, Caroline Lucas.

Simon and Ed did not agree on a few things.

So what are the three main party’s views on the big issues of the environment and climate change today? Laura Husband and Charlotte King went to the Climate Change debate hosted by the Guardian a week before the General Election to find out: In order of appearance in the first piece of audio, here’s what Greg Clark from the Conservatives, Ed Miliband from the Labour Party and Simon Hughes from the Liberal Democrats had to say on some major climate change issues.

Expanding Heathrow

Expanding London’s Heathrow airport has been a hotly-contested issue. Labour’s general consensus has been ‘for’ the airport, the Liberal Democrats ‘against’ the airport and the Conservatives against but in favour of an airport elsewhere.

Will the Tory-Lib Dem alliance increase air travel to and from the UK? Picture credit: Axwel on Flickr

Climate Skeptics

A number of climate skeptics have spoken out against the existence of man made climate change following the controversial emails sent by a climate scientist from the University of East Anglia stating that some of the tree data was a ‘trick.’ There are also members of the three main parties who admit to being skeptical about climate change. So how do the three main parties deal with climate change skeptism?

Greg had to defend the Tories

Present climate change policy

Prior to the general election, Labour’s carbon emissions policy was to reach a 34 per cent reduction against 1990 levels by 2020. But did the other main parties think this was realistic or indeed enough?

Peak Oil

Peak oil is the point in time when there is no more petroleum in the ground to be extracted. There is uncertainty about when peak oil will be reached, what to do in the mean time and what to do when it is finally happens among the major parties.

Have we reached peak oil or is it yet to come? Image credit: Chad Teer

Commentator at the Guardian George Monbiot asks how we will reduce fossil fuel consumption, in particular oil.

Whether to use the UK’s entire quota of oil before it runs out or whether to save some of it is a dividing question among the major parties.

George Monbiot wrote the book 'Heat'. Image credit: JK the Unwise

Climate modeling

There is debate among scientists about how to measure climate change, and different models produce varying degrees of environmental change. A physicist questioned the model the politicians have been working with and suggests they should be using an alternative, which would be more accurate.

The healing of bone fractures could be improved using tiny sensors that are strapped on the metal healing plate to measure the change in weight on the sensor as the bone heals.

Bad fracture healing

Currently it is very difficult for doctors to monitor the healing of fractures. A lot of it is done by guesswork and, as such, around one in 10 do not properly heal due to wrong guesses. Without re-opening the wound every time it is impossible to tell whether a break is healing correctly.

The model here shows the wood bending as bone does if it is fractured

Biosensors

So scientists at Bilkent University in Ankara, Turkey, are working on many nanotechnology projects, including tiny wireless sensors that will get placed across a fracture to monitor how a fracture is healing.

The sensors could, in future, be planted on the metal plate placed on the bone where the fracture is. It would monitor the change in stress on the break from the body weight above. The sensors currently in development use low frequency waves that pass through them to a monitor near to the sensor, to survey the stress on the plate.

As the bone heals, the stress on the plate decreases, so decreasing stress over time means healing over time. If there is no decrease, the bone is not healing. So this could be a non-obtrusive way to monitor the healing of bones.

Emre ünal, who is working on the biosensor project at Bilkent says “the motivation for this project was that there is no such wireless bio-implant, chip-scale device. You can look at the resonance frequency to monitor strain changes on the chip. Doctors currently have to guess if a fracture has healed or not”.

Sheep

Bilkent’s colleagues at the National Institute of Health, USA, have tested the latest model of the biosensors on real sheep metatarsal and have demonstrated proof of concept.

The next stage will be to try the sensor on a live sheep which should show real healing over time.

Ten years ago the first working draft of the full sequence of the human genome was completed. The international Human Genome Project was started in order to map the location of all genes in human DNA.

Our DNA

A human has 23 pairs of chromosomes that contain all our genes: one in each pair came from the mother and the other from the father. Genes are the code for the structures in the body as well as providing maintenance throughout life. But because there are around 3 billion DNA bases within these chromosomes it was not an easy task to sequence them all.

The Project

A human male complement of chromosomes

The Human Genome Project was started in 1990 by James Watson, who was one of the original discoverers of the helical structure of DNA along with Rosalind Franklin and Francis Crick. The final sequence was composed of a combination of DNA from four men.

The original genome sequencing method, Sanger Sequencing, was pioneered in the 1970s and was the main method used to sequence DNA for 30 years. But new methods have started to emerge and with these new technologies, centres will be able to generate thousands of millions of DNA letters per day, rather than the current 100 million per day. It costs $10,000 a day (£6,505) to have one’s genome sequenced.

The genomes of any two people are always more than 99 per cent the same. This means the sequence of two people’s genomes will be similar, although not identical. The project has involved sequencing different variations (alleles) of the same gene that are located in the same place along the DNA. An example would be different alleles of genes that cause different eye colours.

Pros and cons of DNA sequencing

Once an allele is linked to a disease, it can potentially be tested for in a person’s DNA sample, so a person may discover they are likely to get a disease. Scientists can share what they have found out about genes.
But in the future if it ever becomes standard to have a genome sequenced and checked for diseases, there are many ethical issues. What if one’s genes reveals that they are likely to get 10 diseases – does this mean you should be treated for all of them ‘just in case’?

There are also issues about where information is shared and stored: should your employer and insurance company know, and will this lead to discrimination? What if the information was not securely stored and got into the wrong hands? There are still many questions to answer.

The reality is that we are still in the early stages of interpreting the results from the human genome sequence. Despite the fact the genome was declared to be sequenced already, not all of it is currently sequencable and there is much left to be done in understanding the complete genetic nature of humans – likely never.

The ‘Food in the City’ project based at City University, Islington, plans to grow food on a derelict site in the centre of London by Summer 2010.

Laura Husband and Charlotte King speak to one of the project’s organisers, Imogen Riley to find out how it’s going to work.

But will it be safe to eat fruit and vegetables grown in a polluted city?

Professor of environmental pollution, Nigel Bell from Imperial College London gives his expert opinion on how pollution will affect the food and whether he’d personally choose to eat it.

According to Cancer Research UK, 22 per cent of all cancer deaths are from lung cancer. But it is not just smokers who have a risk of getting the disease.

Underperforming gene in 30 per cent of non-smokers

New research shows putting a fag out does not necessarily protect against lung cancer. Image source: Wikimedia Commons

Researchers at the Mayo Clinic, Arizona, have found that about 30 per cent of patients who have never smoked but developed lung cancer had the same uncommon variant residing in a gene known as GPC5. The variant means the gene is ‘underperforming’.

Little is known about this GPC5 gene, except that it can be over-expressed in multiple sclerosis, and alterations in the part of the genome where GPC5 is located are common in a wide variety of human tumours. The researchers think the gene variation is a cancer-trigger in the 1/3 of never-smokers with lung cancer, but something else is causing the lung cancer in the other 2/3.

A bad gene

So it does not seem to be a good gene: “This is the first gene that has been found that is specifically associated with lung cancer in people who have never smoked,” says the study’s lead investigator, Dr Ping Yang, a genetic epidemiologist.

Genetic test in future

Yang also said it is highly likely there could be a standard genetic test in future to look for the variant of the GPC5 gene to monitor for lung cancer more carefully if a person has the dodgy variant.

The researchers’ next steps will be to identify any functional changes, such as in the lung, caused by the DNA variations, and define the way to intervene or develop drug targets. Also further studies are needed to confirm or refute whether the gene is linked to the prevalence of other diseases.

New insights into the neurones that influence milk production, obesity and sex drive, may help develop more targeted treatments with fewer side effects for conditions affecting these processes.

The hormone prolactin, normally associated with triggering breast milk production, is regulated due to “rhythmic oscillations” in a group of brain cells according to researchers at the Karolinska Institute in Sweden.

La monstrua de nuda

Prolactin is normally suppressed in males and in non-pregnant females by another hormone, dopamine, which is released every 20 seconds by a group of brain cells called the TIDAs. The team at the Institute studied the electrical activity in this group of brain cells in rats and found a robust 0.05Hz oscillation. The release of dopamine means that normally people do not produce breast milk and have a regular metabolism and libido. So abnormal firing of the TIDAs could potentially cause abnormal prolactin levels.

According to David Lyons who worked on the research at the Karolinska Institute, there are “all manner of reasons” why there might be an increase in prolactin, as the brain is a complex network of feedback loops and “disturbed modulation of the group of neurones can cause problems”. These reasons could include brain adenomas which are normally benign tumours that can eventually turn malignant.

Also certain drugs, notably those for psychological conditions such as schizophrenia and bipolar disorder, affect the production of prolactin by blocking the dopamine receptors. As dopamine normally inhibits prolactin, prolactin is released abnormally, meaning psychiatric patients using these drugs could now also be lactating.

Currently the drug bromocriptine is used to regulate prolactin. It mimics dopamine, so adding it decreases the release of prolactin. But, according to Dr Lyons, because the drug is not delivered in a targeted way to the prolactin pathway, there are side effects, one of which affects the reward and addiction pathways in the brain.

The more scientists understand about the neurones that regulate prolactin, the more potential there is to treat conditions caused by its abnormal levels, with fewer side effects for patients.

David Lyons says that “by understanding how the oscillation of these TIDA neurones works, and whether other prolactin inhibitory or release factors modulate the rhythms, we have a greater chance of producing therapies that can target these neurones specifically.”

Jonathan Fry who works on hormones and the nervous system at University College London agrees. “The findings open up new possibilities for manipulating the release of prolactin. However, before taking this idea much further, the investigation must be extended to mature animals.”

Our normal DNA sequence and the way it is read to make proteins can be altered thanks to research by Dr Jason Chin and his team.

Chin, a Cambridge University fellow, received the Francis Crick prize for his revolutionary work on the manipulation of DNA, at the Royal Society late last year.

The way that DNA is read to make proteins is crucial to life, growth and repair but what happens if the natural way of reading the code is changed to make unnatural proteins?

Normal DNA is read in a process involving large proteins within each cell, which form the proteins in the body, such as those in skin and new tissue for growth. But Chin and colleagues manipulated the genetic code and the tools that read it in order to make unnatural proteins.

They wrote a new DNA sequence and created new enzymes and machinery to direct the reading of the new sequence so that these new proteins were made.

There are many potential uses for these proteins. The main one is labeling them to study interactions within cells, to discover why certain diseases happen so new drugs can be made. There are no specific diseases in mind at present, but Chin says these are “techniques for better understanding of disease processes” and to find new drug targets, such as “growth hormones”.

The prize Chin won is in honour of Francis Crick, who was one of the co-discoverers of the structure of DNA. It goes to a scientist who has made developments in areas that are relevant to Crick’s area of work (molecular biology, physics and neuroscience) up until he died in 2004. The lecture delivered by Chin in November 2009 can be viewed online.

Chin’s research papers can also be viewed online.