Paper is known for its ability to absorb liquids, making it ideal for products such as paper towels. But by modifying the underlying network of cellulose fibres, etching off surface ‘fluff’ and applying a thin chemical coating, researchers have created a new type of paper that repels a wide variety of liquids – including water and oil.
The paper takes advantage of the so-called ‘lotus effect’ – used by leaves of the lotus plant – to repel liquids through the creation of surface patterns at two different size scales and the application of a chemical coating. The material, developed at the Georgia Institute of Technology, uses nanometer- and micron-scale structures, plus a surface fluorocarbon, to turn old-fashioned paper into an advanced material.
The modified paper could be used as the foundation for a new generation of inexpensive biomedical diagnostics in which liquid samples would flow along patterns printed on the paper using special hydrophobic ink and an ordinary desktop printer. This paper could also provide an improved packaging material that would be less expensive than other oil- and water-repelling materials, while being both recyclable and sustainable.
‘Paper is a very heterogeneous material composed of fibres with different sizes, different lengths and a non-circular cross-section,’ said Dennis Hess, a professor in the Georgia Tech School of Chemical and Biomolecular Engineering. ‘We believe this is the first time that a superamphiphobic surface – one that repels all fluids – has been created on a flexible, traditional and heterogeneous material like paper.’
The new paper, which is both superhydrophobic (water-repelling) and super oleophobic (oil-repelling), can be made from standard softwood and hardwood fibres using a modified paper process. In addition to Hess, the research team included Lester Li, a graduate research assistant, and Victor Breedveld, an associate professor in the School of Chemical and Biomolecular Engineering
Producing the new paper begins with breaking up cellulose fibres into smaller structures using a mechanical grinding process. As in traditional paper processing, the fibres are then pressed in the presence of water – but then the water is removed and additional processing is done with the chemical butanol. Use of butanol inhibits the hydrogen bonding that normally takes place between cellulose fibres, allowing better control of their spacing.
‘The desirable properties we are seeking are mainly controlled by the geometry of the fibres,’ Hess explained.
The second step involves using an oxygen plasma etching process – a technique commonly used in the microelectronics industry – to remove the layer of amorphous ‘fluffy’ cellulose surface material, exposing the crystalline cellulose nanofibrils. The process thereby uncovers smaller cellulose structures and provides a second level of ‘roughness’ with the proper geometry needed to repel liquids.
Finally, a thin coating of a fluoropolymer is applied over the network of cellulose fibers. In testing, the paper was able to repel water, motor oil, ethylene glycol and n-hexadecane solvent.
The researchers have printed patterns onto their paper using a hydrophobic ink and a desktop printer. Droplets applied to the pattern remain on the ink pattern, repelled by the adjacent superamphiphobic surface.
That capability could facilitate development of inexpensive biomedical diagnostic tests in which a droplet containing antigens could be rolled along a printed surface where it would encounter diagnostic chemicals. If appropriate reagents are used, the specific colour or colour intensity of the patterns could indicate the presence of a disease. Because the droplets adhere tightly to the printed lines or dots, the samples can be sent to a laboratory for additional testing.
‘We have shown that we can do the operations necessary for a microfluidic device,’ Hess said. ‘We can move the droplet along a pattern, split the droplet and transfer the droplet from one piece of paper to another. We can do all of these operations on a two-dimensional surface.’
For Hess, Li and Breedveld, creating a superhydrophobic suface was relatively straightforward because water has a high surface tension. For oils, which have a low surface tension, the key to creating the repellent surface is to create re-entrant – or undercut – angles between the droplets and the surface.
Previous examples of superamphiphobic surfaces have been made on rigid surfaces through lithographic techniques. Such processes tend to produce fragile surfaces that are prone to damage, Hess said.
The principal challenge has been to create high-performance in a material that is anything but geometrically regular and consistent.
‘Working with heterogeneous materials is fascinating, but it’s very difficult not just to control them, because there is no inherent consistent structure, but also to change the processing conditions so you can get something that, on average, is what you need,’ he said. ‘It’s been a real learning experience for us.’
The new paper has so far been made in samples about four inches on a side, but Hess sees no reason why the process couldn’t be scaled up. Though long-term testing of the new paper hasn’t been done, Hess is encouraged by what he’s seen so far. Georgia Institute of Technology

A multi-institutional team of researchers have pinpointed the genetic traits of the cells that give rise to gliomas – the most common form of malignant brain cancer. The findings provide scientists with rich new potential set of targets to treat the disease.
‘This study identifies a core set of genes and pathways that are dysregulated during both the early and late stages of tumour progression,’ said University of Rochester Medical Center (URMC) neurologist Steven Goldman, M.D., Ph.D., the senior author of the study and co-director of the Center for Translational Neuromedicine. ‘By virtue of their marked difference from normal cells, these genes appear to comprise a promising set of targets for therapeutic intervention.’
As its name implies, gliomas arise from a cell type found in the central nervous system called the glial cell. Gliomas progress in severity over time and ultimately become highly invasive tumours known as glioblastomas, which are difficult to treat and almost invariably fatal. Current treatments, which include surgery, radiation therapy, and chemotherapy, can delay disease progression, but ultimately prove ineffective.
Cancer research has been transformed over the past several years by new concepts arising from stem cell biology. Scientists now appreciate that many cancers are the result of rogue stem cells or their offspring, known as progenitor cells. Traditional cancer therapies often do not prevent a recurrence of the disease since they may not effectively target and destroy the cancer-causing stem cells that lie at the heart of the tumours.
Gliomas are one such example. The source of the cancer is a cell found in the brain called the glial progenitor cell. The cells, which arise from and maintain characteristics of stem cells, comprise about three percent of the cell population of the human brain. When these cells become cancerous they are transformed into glioma stem cells, essentially glial progenitor cells whose molecular machinery has gone awry, resulting in uncontrolled cell division.
Goldman and his team have long studied normal glial progenitor cells. These cells produce glia, a category that includes both astrocytes – cells that support the function of neurons – and oligodendrocytes – cells that produces myelin, the fatty insulation that allows the long-distance conduction of neural impulses.
While Goldman’s group’s work has primarily focused on ways to use glial progenitor cells to treat neurological disorders such as multiple sclerosis, their understanding of the biology of these cells and mastery of the techniques required to sort, identify, and isolate these cells has also enabled them to explore the molecular and genetic changes that transform these cells into cancers.
Using human tissue samples representing the three principal stages of the cancer, the researchers were able to identify and isolate the cancer-inducing stem cells. Working with Goldman, lead authors Romane Auvergne, Ph.D. and Fraser Sim, Ph.D. then compared the gene expression profiles of these cancer stem cells to those of normal glial progenitor cells. The objective was to both pinpoint the earliest genetic changes associated with cancer formation and identify those genes that were unique to the cancer stem cells and were expressed at every stage of disease progression.
Out of a pool over 44,000 tested genes and sequences, the scientists identified a small set of genes in the cancerous glioma progenitor cells that were over-expressed at all stages of malignancy. These genes formed a unique ‘signature’ that identified the tumour progenitor cells and enabled the scientists to define a corresponding set of potential therapeutic targets present throughout all stages of the cancer.
‘One of the key things you are looking for in drug development in cancer is a protein or gene that is over-expressed, so that you can attempt to achieve therapeutic benefit by inhibiting it,’ said Goldman.
The researchers chose to test this hypothesis by targeting one such gene, called SIX1, which was highly over-expressed in the glioma progenitor cells. While this particular gene is active in the early development of the nervous system, it had not been observed in the adult brain before. However, SIX1 signalling has been associated with breast and ovarian cancer, raising the possibility of its contribution to brain cancer as well. This turned out to indeed be the case. When the researchers blocked – or knocked down – the expression of this gene, the tumour cells ceased growing, and implanted tumours shrank.
‘This study gives us a blueprint to develop new therapies,’ said Goldman. ‘We can now devise a strategy to systematically and rationally analyse – and eliminate – glioma stem and progenitor cells using compounds that may selectively target these cells, relative to the normal glial progenitors from which they derive. By targeting genes like SIX1 that are expressed at all stages of glioma progression, we hope to be able to effectively treat gliomas regardless of their stage of malignancy. And by targeting the glioma-initiating cells in particular, we hope to lessen the likelihood of recurrence of these tumours, regardless of the stage at which we initiate treatment.’ University of Rochester Medical Center

A gene linked to autism spectrum disorders that was manipulated in two lines of transgenic mice produced mature adults with irreversible deficits affecting either learning or social interaction.
The findings have implications for potential gene therapies but they also suggest that there may be narrow windows of opportunity to be effective, says principal investigator Philip Washbourne, a professor of biology and member of the University of Oregon’s Institute of Neuroscience.
The research, reported by an 11-member team from three universities, targeted the impacts of alterations in the gene neuroligin 1 — one of many genes implicated in human autism spectrum disorders — to neuronal synapses in the altered mice during postnatal development and as they entered adulthood. One group over-expressed the normal gene, the other a mutated version.
Mice with higher-than-normal levels of the normal gene after a month had skewed synapses at maturity. Many were larger, appearing more mature, than normal. In these mice, Washbourne said, there were clear cognitive problems. ‘Behaviour was just not normal. They didn’t learn very well, and they were slower to learn, but their social behaviour was not impacted.’
Mice over-producing a mutated version of the gene reached adulthood with structurally immature synapses. ‘They were held back in development and behaviour — the way they behave in terms of learning and memory, in terms of social interaction,’ he said. ‘These were adult mice, three months old, but they behaved like normal mice at four weeks old. We saw arrested development. Learning is a little bit better, they are more flexible just like young mice, they learn faster, but their social interaction is off. To us, this looked more like Asperger’s syndrome.
‘So with the same gene, doing two different manipulations — over-expressing the normal form or over-expressing a mutated form — we’ve gone to two different ends of the autism spectrum,’ said Washbourne, whose lab focuses on basic synapse formation and what goes wrong in relationship to autism. Work has been done in both mice and zebra fish.
‘We made these mice so that we can turn the genes on and off as we want,’ Washbourne said. ‘Using an antibiotic, doxycycline, it turns off these altered genes that we inserted into their chromosomes. While on doxycycline, the mice are absolutely normal.’
However, if the inserted gene was turned off after the completion of development, mice still showed altered synapses and behaviour. This result suggests that any kind of gene therapy may have to be applied to individuals with autism early on.
Effects seen in the social behaviour of mice with the mutated gene, he said, are not unlike observations reported by parents of many autistic children. While normal mice prefer to engage with new mice entering their world rather than familiar others, or even a new inanimate object, these mice split their time equally. ‘It’s not a deficit in memory regarding which mouse is which, it’s more a weighting of their interaction. Does that mean they are autistic? I don’t know, but if you talk to parents of autistic children, one of the frustrating things they report is that their children treat complete strangers in exactly the same way that they treat them.’
While the findings provide new insights, Washbourne said, any translation into treatment could be decades away. ‘A problem with autism is there are many different genes potentially involved. It could be that some day, if you are diagnosed with autism, a mouth swab might allow for the identification of the exact gene that is mutated and allow for targeted therapy,’ he said. ‘Genome sequencing already has turned up subtle mutations in lots of genes. Autism might be like cancer, with hundreds of potential combinations of faulty genes.’ University of Oregon

Women at a particular stage in their monthly menstrual cycle may be more vulnerable to some of the psychological side-effects associated with stressful experiences, according to a study from UCL.
The results suggest a monthly window of opportunity that could potentially be targeted in efforts to prevent common mental health problems developing in women. The research is the first to show a potential link between psychological vulnerability and the timing of a biological cycle, in this case ovulation.

A common symptom of mood and anxiety problems is the tendency to experience repetitive and unwanted thoughts. These ‘intrusive thoughts’ often occur in the days and weeks after a stressful experience.
In this study, the researchers examined whether the effects of a stressful event are linked to different stages of the menstrual cycle. The participants were 41 women aged between 18 and 35 who had regular menstrual cycles and were not using the pill as a form of contraception. Each woman watched a 14-minute stressful film containing death or injury and provided a saliva sample so that hormone levels could be assessed. They were then asked to record instances of unwanted thoughts about the video over the following days.
There is actually a fairly narrow window within the menstrual cycle when women may be particularly vulnerable to experiencing distressing symptoms after a stressful event.
‘We found that women in the ‘early luteal’ phase, which falls roughly 16 to 20 days after the start of their period, had more than three times as many intrusive thoughts as those who watched the video in other phases of their menstrual cycle,’ explains author Dr Sunjeev Kamboj, Lecturer in UCL’s Department of Clinical, Educational and Health Psychology.
‘This indicates that there is actually a fairly narrow window within the menstrual cycle when women may be particularly vulnerable to experiencing distressing symptoms after a stressful event.’
The findings could have important implications for mental health problems and their treatment in women who have suffered trauma.
‘Asking women who have experienced a traumatic event about the time since their last period might help identify those at greatest risk of developing recurring symptoms similar to those seen in psychological disorders such as depression and post-traumatic stress disorder (PTSD),’ said Dr Kamboj.

‘This work might have identified a useful line of enquiry for doctors, helping them to identify potentially vulnerable women who could be offered preventative therapies,’ continued Dr Kamboj. University College London

Researchers have identified a set of genes that allow melanoma cells, a type of cancer cell, to change rapidly between two shapes to escape from the skin and spread around the body. This new research – funded by the Wellcome Trust, Cancer Research UK and the US National Institutes of Health – could pave the way for scientists to develop desperately needed drugs for malignant melanoma, the deadliest form of skin cancer, which kills more than 2200 people every year.
The most dangerous aspect of melanoma is its ability to spread, or become malignant, to other parts of the body in the later stages of disease. This most often includes the liver, lungs and brain.
Dr Chris Bakal, a Wellcome Trust research fellow at the Institute of Cancer Research, London, explains: ‘We already knew that metastatic melanoma cells, or cells that are able to spread through the body, have to be able to adopt different shapes so that they can squeeze their way between healthy cells and move around the body.
‘The cells have to become rounded to travel through the bloodstream or invade soft tissues such as the brain, but they take on an elongated shape to travel through harder tissues like bone. But until now, we knew hardly anything about how the cells assume either of these shapes and how they switch between the two.’
To investigate this, researchers at the Institute of Cancer Research, London, and Weill Cornell Medical College in Houston started out by looking at fruit fly cells. They found that under normal conditions, the fruit fly cells grew in five different shapes. By switching off specific genes, they were able to change the mix of shapes among the fruit fly cells and identify several different genes that control a cell’s shape-shifting ability.
When they looked in human melanoma cells, they found that the human versions of these genes had a similar effect. In particular, they noted that switching off a gene called PTEN increased the proportion of cells that were elongated rather than rounded.
PTEN is a gene that is also involved in stopping healthy cells from becoming cancer cells, a so-called ‘tumour suppressor’ gene. This particular gene is switched off in around 1 in 8 melanoma patients and in almost half of melanoma patients who carry a mutation in another cancer gene called BRAF.
‘We think that metastatic melanoma cells lose their PTEN function so that they can increase their shape-shifting ability, which in turn enables them to move to many different tissues within the body. It’s early days, but taken together our findings offer new opportunities to develop drugs to try and stop the spread of melanoma,’ Dr Bakal added.
Dr Julie Sharp, Senior Science Communications Manager at Cancer Research UK, said: ‘This is still early research, but it gives us a better grasp of the way cancer cells behave in the body. By mimicking these conditions, our researchers are learning more about melanoma and bringing us closer to beating it. Wellcome Trust