Think magazine Issue 12

Artificial Intelligence is here but it is not taking over. Prof. Georgios Yannakakis from the Institute of Digital Games brings a fresh view to how computers can be creative. He imagines a new social network of computers that can make new playable games on their own. Think as well how you might act like a computer. Yannakakis’s ideas have helped create games that help children with dyslexia, soldiers with PTSD, and many other problems, as published in the latest issue of Think Magazine available now.

Researchers at University are redesigning hip joints. A team of engineers and biomedicial scientists are testing new alloys that will make hip replacements safer and cheaper. In Malta during 2014, 145 people needed their hips replaced.

Prescription drugs are abused worldwide. Apart from illicit substances, legal drugs used off-prescription is a dangerous problem Europe-wide. In the US its use is second only to marijuana. The University of Malta is part of an EU-wide project studying the problem in order to tackle it.

The recent solar eclipse had everyone looking up to the skies. ISSA (Institute of Space Science & Astronomy) researcher Ian Fenech Conti writes about the Universe and how it was made. His work measures the most elusive matter in the universe.

Another elusive find was of black coral around the Maltese Islands by a team of marine researchers that includes Prof. Alan Deidun. They used underwater robots, ROVs, to map a new underwater forest just off the coast of Filfla. Fishing gear was found to have damaged this coral, in a different article JD Farrugia talks about overfishing and the need to change our fishing and eating habits to save our seas.

Alumni in Malta are finally getting the recognition they deserve. The University has just launched a new Outstanding Alumni Achievement award. If you know someone who has excelled after studying at the University of Malta then nominate them on:

The magazine is full of other stories from students and alumni on fish, lighter planes, hereditary disease, research funds, green chemistry, and robots. The fun section covers a range of reviews, with a comic strip by Gorg Mallia and a 100 word idea to change Malta—Think everyone.


Think, the University of Malta’s magazine, may be picked up for free in newsagents around Malta and Gozo and in Agenda bookstores, it is now available online at, available on Issuu, followed on Twitter @ThinkUoM  or liked on Facebook.



Cocaine, Heroin, Cannabis, Amphetamine, LSD, the contraceptive pill, The Doors and Rolling Stones are children of the 60s. Chemistry fuelled the rise of free love, drug use, and a new ever-resonant culture. But, this culture also has a dark side: sexually transmitted infections, lost potential, and lives.

The Poster

Interested? Professor Richard Muscat (University of Malta – Pro-Rector for Research) will be talking about ‘Sex, Drugs and Rock ‘n’ Roll’ on the 10th May at 7.15pm, Music Room, St. James Cavalier. The talk will be followed by an open discussion. Free entrance, no special science background is required, and all are welcome.

For over 20 years, Professor Richard Muscat has researched the effects of drugs of abuse on the brain. His research has focused on brain pleasure pathways and their relation to moods. In turn, how drugs affect the way people behave both in the short and long term. The brain chemical dopamine plays a critical role in influencing how people respond to pleasurable situations and unfortunately as a consequence relapse following repeated drug use. Another three important links are the predisposition to drug use, age of first drug use, and anxiety/depression.

The speaker Chairs the Research Platform of the Pompidou Group, Council of Europe, a group that combats drug abuse and illicit drug trafficking. Malta Cafe Scientifique is supported by The Malta Chamber of Scientists and the Malta Council for the Voluntary Sector, and aided by the University of Malta. Email or find us on Facebook for further information.

Administering neural progenitor cells (NPC) is one of the most promising ways to treat multiple sclerosis. Jingwu Zhang and co-workers1 now report in Cell how these cells release the cytokine leukaemia inhibitory factor (LIF) that reduces disease progression.

Multiple sclerosis is an autoimmune disease that attacks the central nervous system causing inflammation, loss of myelin sheets, and the eventual degeneration of neurons. These symptoms are linked to specialised cells of the immune system called helper T cells. A subset of helper T cells, T helper 17 (Th17), release interleukin-17 (IL-17), a key inflammatory factor in the development of multiple sclerosis.

Neural Progenitor Cells (NPC) help to reduce disease progression of MS. The researchers found that NPCs secrete a factor which inhibits specific cells in the immune system. The picture shows spinal cord sections, on the left untreated diseased tissue, on the right treatment with NPCs. © Cell.

The role of IL-17 in disease progression was cleared observed in several studies performed using mice with chemically induced multiple sclerosis (experimental autoimmune encephalomyelitis; EAE). Removal of IL-17 delayed disease onset and reduced its severity. On the other hand, the disease was worsened by the increased expression of IL-17 or a greater number of Th17 cells.

So, how do NPCs reduce multiple sclerosis? Currently, they are thought to migrate to damaged neurons and differentiate into myelin sheets that protect the neurons. However, only 5–10% of NPCs form myelin sheets. To discover any additional mechanisms, the researchers injected NPC cells into diseased mice. The cells migrated to the spleen and reduced symptoms by inhibiting Th17 cell formation, which suggested that the NPC cells must release a secreted factor. This was confirmed by treating the mice with irradiated NPC cells and an NPC cell supernatant, which also inhibited the disease.

To identify the factor responsible, the researchers tested several NPC secreted proteins on Th17 cell differentiation, identifying LIF. Recombinant LIF was then injected into diseased mice that suppressed disease progression. These mice had lower levels of Th17 cells, but normal levels of other immune cells. Conversely, inhibiting LIF with a neutralising antibody reserved this recovery.

Further studies showed that LIF works by binding to CD4+ T cells and preventing their differentiation into Th17 cells. Upon binding to the LIF receptor, LIF triggers the extracellular signal-regulated MAP kinase (ERK) signalling pathway that increases the level of suppressor of cytokine signaling 3 (SOCS3). SOCS3 prevents the phosphorylation of Janus kinase-2 (JAK-2) and signal transducer and activator of transcription 3 (STAT3) inhibiting differentiation of the Th17 cells.

Finally, the researchers tested whether LIF has the same role in humans. They first purified healthy CD4+ T cells and then added either recombinant human LIF or NPC supernatant. Similarly to the mouse, these treatments prevented Th17 cell differentiation, which was negated by adding a LIF-neutralising antibody. These results were repeated in cells from 18 subjects with multiple sclerosis, confirming their relevance to human disease.

This important work shows how LIF inhibits Th17 differentiation in both mice and human models. The advantage of LIF is its selectivity — it specifically inhibits Th17 cells and does not affect other immune cells. Other studies specify how LIF can stimulate a neural repair mechanism, which also improves neuronal survival. The researchers suggest that this dual action makes LIF a strong candidate to develop a better therapy to treat multiple sclerosis.

Cao, W. et al. Leukemia inhibitory factor inhibits T helper 17 cell differentiation and confers treatment effects of neural progenitor cell therapy in autoimmune disease. Immunity 35, 273–284 (2011).

doi: 10.1016/j.immuni.2011.06.011

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