The 1st Poster Evening Event by The Postgraduate Committee at the Institute of Cellular Medicine, Newcastle University

Before talking about the 1st Poster Evening, I want to introduce the organizers of this successful event; PrICM is the postgraduate committee at the Institute of Cellular Medicine within the Faculty of medical Sciences, Newcastle University. PrICM is the one-stop space to meet, share and communicate with the diverse research community within the ICM. The three leaders of prICM are PhD students from different departments of the institute and they are Rihab Gam, Kile Green and Marco Silipo. Their aim is to promote social interaction and networking between postgraduate students, through the organization of social events and also outside the ICM. Amongst their socials we find very popular coffee mornings, scientific seminars, sponsored workshops, guided outdoors, charity pub quizzes and also surfing classes. Although prICM is a very young community (2 years old), it has gained high popularity within the Faculty of Medical Sciences in such short time thank to the efforts of its reps.

The 1st Poster Evening is the most recent amongst the several prICM events. It was a student-led session featuring scientific poster presentations from staff and students within the different institutes of the faculty. Posters were approved for presentation by staff as well as PhD, Mres and undergraduate students, whose intention is to continue with research in academia. The opening of the event was led by Dr. Richy Hetherington who invited 6 students, selected by the prestigious Insights Public Lecture competition of the Faculty of Medical Science, to present their work.

Afterwards, prICM opened the poster session acknowledging the sponsors of the event. In fact, although the community has received no funding from the University, Poster Evening was supported by the companies QIAGEN© (guest of the event) and VWR©, and the Marie Curie Initial Training Network organisation working under the 7th Framework Program “PEOPLE”, CellEurope. These bodies hugely contributed for making this event very special.

More than 50 members of academia including students, Post-Docs and PIs attended the event.  23 students in total presented their poster: 11 PhD, 8 Masters and 3 undergraduates.

Posters were judged by Prof Xiao Nong Wang, assisted by the prICM committee, on the base of content of the research, clarity in presenting and also poster layout. Six prizes were provided for the best poster from the different categories. 2 posters were selected on each category.

Because of the successful 1st edition, the Faculty of Medical Sciences wants to make Poster Evening an annual event in order to give the opportunity to all academics to present and discuss their own research, to promote networking between researchers, and share ideas and extend knowledge. And also the next years, the Faculty can always rely on prICM.

Written by ESR1 Rihab Gam

When passionate young scientists use the right way to communicate science!

We are glad to say that our blog has been “tweeted” about by EngageNU emphasizing the important role played by the CELLEUROPE Project to involve young researchers in communicating sience to others.

EngageNU is all about Newcastle University and Communities
working together

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Engagement is central to Newcastle University’s mission to be a leading civic university with a global reputation for excellence, and is integral to ensuring that our research, teaching and professional activities have genuine economic, cultural and social benefits and impact. Our work today continues to build on the successes and learning developed as a Beacon for Public Engagement. The UK Beacon initiative ran from 2007 to 2011, and was designed to create a culture change across the higher education sector, seeking to support, recognise, reward and build capacity for public engagement

Check out @EngageNCL’s Tweet: https://twitter.com/EngageNCL/status/531568720540610562?s=09
Written by: Rihab Gam, Early Stage Marie Curie Researcher #1 based at Newcastle University, UK.

Experience of Immunohistochemistry Workshop at Newcastle University!

CELLEUROPE Immunohistochemistry Workshop: 20th – 22nd October, 2014

Some of our workshop group during the first practical session, Haematological Sciences Laboratory- Day 2. From L-R Marsela Qesari (Celleurope ER); Margherita Boirei (Celleurope ESR); Moyassar Al-Shaibani (PhD Newcastle); Monica Reis (Celleurope ESR); Rihab Gam(Celleurope ESR);, Shaheda Ahmed (Alcyomics Ltd)
Some of our workshop group during the first practical session, Haematological Sciences Laboratory- Day 2.
From L-R Marsela Qesari (Celleurope ER); Margherita Boirei (Celleurope ESR); Moyassar Al-Shaibani (PhD Newcastle); Monica Reis (Celleurope ESR); Rihab Gam(Celleurope ESR);, Shaheda Ahmed (Alcyomics Ltd)

The workshop took place within Newcastle University, Institute of Cellular Medicine and it was very valuable in bringing different organisations together to establish basic knowledge about immunohistochemistry. The workshop was held over two days and incorporated both theory and practical sessions. Our group was made of up Celleurope Marie Curie fellows and PhD students from the Haematological Sciences department.

Mrs Edith Fick (Senior Engineer, department of Clinical Medicine at the University of Bergen, Norway) gave an introduction to the basics of immunohistochemistry (IHC), explaining the different steps ranging from the processing of tissue, the selection of appropriate reagents until the interpretation of the stained tissue sections. We practiced this during the laboratory session with Dr Shaheda Ahmed (Alcyomics Ltd) who successfully lead to the session, showing us how to apply the IHC protocol on skin slides and learn the difference between the manually applied protocol and the automated system used within Haematological sciences, Newcastle University.

Professor Anne Dickinson (Professor of Marrow Transplant Biology, Newcastle University, UK and Director, Alcyomics Ltd) gave an excellent talk about the Skin Explant Assay development for predicting and investigating Graft versus Host Disease (GvHD) and presented the use and application of this model along with some of the recent achievements that Alcyomics Ltd, in collaboration with Newcastle University, reached in the field of GvHD. Mrs Jean Norden (Senior Biomedical Scientist, Haematological Sciences, Newcastle University, UK), an expert in the field of Molecular biology, detailed the different applications of the Skin Explant Assay showing promising results of the use of this model in the field of GvHD.

Professor Lisbet Sviland (Adjunct Professor, University of Bergen, Norway) presented the pathology of acute graft versus host disease and showed images of the histology of GvHD in different tissue types and their related diagnosis. I really enjoyed the cell imaging session led by Prof Sviland during which we were given the opportunity to read our slides stained during the practical session and also to grade different clinical slides for GvHD. We would like to believe that we are now ‘experts’ in grading skin GvHD!

To focus on the Newcastle experience, Dr Xiao Nong Wang (Senior Lecturer, Haematological Sciences, Newcastle University, UK) gave a presentation about the impact of IHC and IF (immunofluorescence) on GvHD research. In the first part of her talk, Dr Wang explained the use of a skin explant model and IHC staining to study the mechanism of T regulatory cells mediated GVHD protection and in a second part, detailed the use of immunofluorescence whole mount staining to study human cutaneous GVHD. Dr Wang also presented some of the many impressive IF images that she likes to take, both for the sake of research and as a hobby also!

Dr Rachel Crossland (Research Associate, Haematological Sciences, Newcastle University, UK) focused on the molecular biology related to the formalin-fixed, paraffin-embedded (FFPE) tissues broadening our ideas about how to unlock our FFPE archives and exploit the samples to a maximum level.

In my opinion, the workshop was excellent. There was a wide range of presentations and all the attendees were given the opportunity for hands on learning and practical application of theoretical content.

Written by: Early Stage Marie Curie Researcher #1 – Rihab Gam- based at Newcastle University, UK.

www.celleurope.eu
@CELLEurope

Hunger games: How the brain ‘browns’ fat to aid weight loss

"Our studies reveal white fat "browning" as a highly dynamic physiological process that the brain controls," said Yang. "This work indicates that behavioral modifications promoted by the brain could influence how the amount of food we eat and store in fat is burned." Credit: Illustration by Michael S. Helfenbein
“Our studies reveal white fat “browning” as a highly dynamic physiological process that the brain controls,” said Yang. “This work indicates that behavioral modifications promoted by the brain could influence how the amount of food we eat and store in fat is burned.”
Credit: Illustration by Michael S. Helfenbein

A molecular process in the brain known to control eating that transforms white fat into brown fat has been uncovered by researchers. This process impacts how much energy we burn and how much weight we can lose, they report.

Researchers at Yale School of Medicine have uncovered a molecular process in the brain known to control eating that transforms white fat into brown fat. This process impacts how much energy we burn and how much weight we can lose. The results are published in the Oct. 9 issue of the journal Cell.
Obesity is a rising global epidemic. Excess fatty tissue is a major risk factor for type 2 diabetes, cardiovascular disease, hypertension, neurological disorders, and cancer. People become overweight and obese when energy intake exceeds energy expenditure, and excess calories are stored in the adipose tissues, which are made up of both white and brown fat. While white fat primarily stores energy as triglycerides, brown fat dissipates chemical energy as heat. The more brown fat you have, the more weight you can lose.
It has previously been shown that energy-storing white fat has the capacity to transform into energy-burning “brown-like” fat. In this new study, researchers from the Yale Program in Integrative Cell Signaling and Neurobiology of Metabolism, demonstrate that neurons controlling hunger and appetite in the brain control the “browning” of white fat.
Lead author Xiaoyong Yang, associate professor of comparative medicine and physiology at Yale School of Medicine, conducted the study with Tamas Horvath, professor and chair of comparative medicine, and professor of neurobiology and Obstetrics/gynecology at Yale School of Medicine, and their co-authors.
The team stimulated this browning process from the brain in mice and found that it protected the animals from becoming obese on a high-fat diet. The team then studied the molecular changes in hunger-promoting neurons in the hypothalamus and found that the attachment of a unique sugar called “O-GlcNAc” to potassium ion channels acts as a switch to control brain activity to burn fat.
“Our studies reveal white fat “browning” as a highly dynamic physiological process that the brain controls,” said Yang. “This work indicates that behavioral modifications promoted by the brain could influence how the amount of food we eat and store in fat is burned.”
Yang said hunger and cold exposure are two life-history variables during the development and evolution of mammals. “We observed that food deprivation dominates over cold exposure in neural control of white fat browning. This regulatory system may be evolutionarily important as it can reduce heat production to maintain energy balance when we are hungry. Modulating this brain-to-fat connection represents a potential novel strategy to combat obesity and associated illnesses.”
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The above story is based on materials provided by Yale University. The original article was written by Karen N. Peart. Note: Materials may be edited for content and length.

Lung cancer can stay hidden for over 20 years

Doctor examining a lung radiography (stock image). Credit: © Minerva Studio / Fotolia
Doctor examining a lung radiography (stock image).
Credit: © Minerva Studio / Fotolia

Scientists have discovered that lung cancers can lie dormant for over 20 years before suddenly turning into an aggressive form of the disease.

UK scientists have discovered that lung cancers can lie dormant for over 20 years before suddenly turning into an aggressive form of the disease, according to a study published in Science* on the 9th of october 2014.
The team studied lung cancers from seven patients — including smokers, ex-smokers and never smokers. They found that after the first genetic mistakes that cause the cancer, it can exist undetected for many years until new, additional, faults trigger rapid growth of the disease.
During this expansion there is a surge of different genetic faults appearing in separate areas of the tumour. Each distinct section evolves down different paths — meaning that every part of the tumour is genetically unique.
This research — jointly funded by Cancer Research UK and the Rosetrees Trust — highlights the need for better ways to detect the disease earlier. Two-thirds of patients are diagnosed with advanced forms of the disease when treatments are less likely to be successful.
By revealing that lung cancers can lie dormant for many years the researchers hope this study will help improve early detection of the disease.
Study author Professor Charles Swanton, at Cancer Research UK’s London Research Institute and the UCL Cancer Institute, said: “Survival from lung cancer remains devastatingly low with many new targeted treatments making a limited impact on the disease. By understanding how it develops we’ve opened up the disease’s evolutionary rule book in the hope that we can start to predict its next steps.”
The study also highlighted the role of smoking in the development of lung cancer. Many of the early genetic faults are caused by smoking. But as the disease evolved these became less important with the majority of faults now caused by a new process generating mutations within the tumour controlled by a protein called APOBEC.
The wide variety of faults found within lung cancers explains why targeted treatments have had limited success. Attacking a particular genetic mistake identified by a biopsy in lung cancer will only be effective against those parts of the tumour with that fault, leaving other areas to thrive and take over.
Over 40,000 people are diagnosed with lung cancer each year and, despite some positive steps being made against the disease it remains one of the biggest challenges in cancer research, with fewer than 10 per cent surviving for at least five years after diagnosis.
Building on this research will be a key priority for the recently established Cancer Research UK Lung Cancer Centre of Excellence at Manchester and UCL. The Centre — where Professor Swanton is joint centre lead — is a key part of Cancer Research UK’s renewed focus to beat lung cancer; bringing together a unique range of internationally renowned scientists and clinicians to create an environment that catalyses imaginative and innovative lung cancer research.
Professor Nic Jones, Cancer Research UK’s chief scientist, said: “This fascinating research highlights the need to find better ways to detect lung cancer earlier when it’s still following just one evolutionary path. If we can nip the disease in the bud and treat it before it has started travelling down different evolutionary routes we could make a real difference in helping more people survive the disease.
“Building on this work Cancer Research UK is funding a study called TRACERx which is studying 100s of patient’s lung cancers as they evolve over time to find out exactly how lung cancers mutate, adapt and become resistant to treatments ”
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The above story is based on materials provided by Cancer Research UK. Note: Materials may be edited for content and length.

Multiple neurodevelopmental disorders have a common molecular cause

A large fraction of neurodevelopmental disorders are associated with variation in specific genes, but the genetic factors responsible for these diseases are very complex. Credit: © agsandrew / Fotolia
A large fraction of neurodevelopmental disorders are associated with variation in specific genes, but the genetic factors responsible for these diseases are very complex.
Credit: © agsandrew / Fotolia

Neurodevelopmental disorders such as Down syndrome and autism-spectrum disorder can have profound, lifelong effects on learning and memory, but relatively little is known about the molecular pathways affected by these diseases. A study shows that neurodevelopmental disorders caused by distinct genetic mutations produce similar molecular effects in cells, suggesting that a one-size-fits-all therapeutic approach could be effective for conditions ranging from seizures to attention-deficit hyperactivity disorder.

Neurodevelopmental disorders such as Down syndrome and autism-spectrum disorder can have profound, lifelong effects on learning and memory, but relatively little is known about the molecular pathways affected by these diseases. A study published by Cell Press October 9th in the American Journal of Human Genetics shows that neurodevelopmental disorders caused by distinct genetic mutations produce similar molecular effects in cells, suggesting that a one-size-fits-all therapeutic approach could be effective for conditions ranging from seizures to attention-deficit hyperactivity disorder.
“Neurodevelopmental disorders are rare, meaning trying to treat them is not efficient,” says senior study author Carl Ernst of McGill University. “Once we fully define the major common pathways involved, targeting these pathways for treatment becomes a viable option that can affect the largest number of people.”
A large fraction of neurodevelopmental disorders are associated with variation in specific genes, but the genetic factors responsible for these diseases are very complex. For example, whereas common variants in the same gene have been associated with two or more different disorders, mutations in many different genes can lead to similar diseases. As a result, it has not been clear whether genetic mutations that cause neurodevelopmental disorders affect distinct molecular pathways or converge on similar cellular functions.
To address this question, Ernst and his team used human fetal brain cells to study the molecular effects of reducing the activity of genes that are mutated in two distinct autism-spectrum disorders. Changes in transcription factor 4 (TCF4) cause 18q21 deletion syndrome, which is characterized by intellectual disability and psychiatric problems, and mutations in euchromatic histone methyltransferase 1 (EHMT1) cause similar symptoms in a disease known as 9q34 deletion syndrome.
Interfering with the activity of TCF4 or EHMT1 produced similar molecular effects in the cells. Strikingly, both of these genetic modifications resulted in molecular patterns that resemble those of cells that are differentiating, or converting from immature cells to more specialized cells. “Our study suggests that one fundamental cause of disease is that neural stem cells choose to become full brain cells too early,” Ernst says. “This could affect how they incorporate into cellular networks, for example, leading to the clinical symptoms that we see in kids with these diseases.”
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The above story is based on materials provided by Cell Press. Note: Materials may be edited for content and length.

Mechanism that repairs brain after stroke discovered

A stroke is caused by a blood clot blocking a blood vessel in the brain, which leads to an interruption of blood flow and therefore a shortage of oxygen. Many nerve cells die, resulting in motor, sensory and cognitive problems. Credit: Image courtesy of Lund University
A stroke is caused by a blood clot blocking a blood vessel in the brain, which leads to an interruption of blood flow and therefore a shortage of oxygen. Many nerve cells die, resulting in motor, sensory and cognitive problems.
Credit: Image courtesy of Lund University

A previously unknown mechanism through which the brain produces new nerve cells after a stroke has been discovered by researchers. A stroke is caused by a blood clot blocking a blood vessel in the brain, which leads to an interruption of blood flow and therefore a shortage of oxygen. Many nerve cells die, resulting in motor, sensory and cognitive problems. The researchers have shown that following an induced stroke in mice, support cells, so-called astrocytes, start to form nerve cells in the injured part of the brain.

A previously unknown mechanism through which the brain produces new nerve cells after a stroke has been discovered at Lund University and Karolinska Institutet in Sweden. The findings have been published in the journal Science.
A stroke is caused by a blood clot blocking a blood vessel in the brain, which leads to an interruption of blood flow and therefore a shortage of oxygen. Many nerve cells die, resulting in motor, sensory and cognitive problems.
The researchers have shown that following an induced stroke in mice, support cells, so-called astrocytes, start to form nerve cells in the injured part of the brain. Using genetic methods to map the fate of the cells, the scientists could demonstrate that astrocytes in this area formed immature nerve cells, which then developed into mature nerve cells.
“This is the first time that astrocytes have been shown to have the capacity to start a process that leads to the generation of new nerve cells after a stroke,” says Zaal Kokaia, Professor of Experimental Medical Research at Lund University.
The scientists could also identify the signalling mechanism that regulates the conversion of the astrocytes to nerve cells. In a healthy brain, this signalling mechanism is active and inhibits the conversion, and, consequently, the astrocytes do not generate nerve cells. Following a stroke, the signalling mechanism is suppressed and astrocytes can start the process of generating new cells.
“Interestingly, even when we blocked the signalling mechanism in mice not subjected to a stroke, the astrocytes formed new nerve cells,” says Zaal Kokaia.
“This indicates that it is not only a stroke that can activate the latent process in astrocytes. Therefore, the mechanism is a potentially useful target for the production of new nerve cells, when replacing dead cells following other brain diseases or damage.”
The new nerve cells were found to form specialized contacts with other cells. It remains to be shown whether the nerve cells are functional and to what extent they contribute to the spontaneous recovery that is observed in a majority of experimental animals and patients after a stroke.
A decade ago, Kokaia’s and Lindvall’s research group was the first to show that stroke leads to the formation of new nerve cells from the adult brain’s own neural stem cells. The new findings further underscore that when the adult brain suffers a major blow such as a stroke, it makes a strong effort to repair itself using a variety of mechanisms.
The major advancement with the new study is that it demonstrates for the first time that self-repair in the adult brain involves astrocytes entering a process by which they change their identity to nerve cells.
“One of the major tasks now is to explore whether astrocytes are also converted to neurons in the human brain following damage or disease. Interestingly, it is known that in the healthy human brain, new nerve cells are formed in the striatum. The new data raise the possibility that some of these nerve cells derive from local astrocytes. If the new mechanism also operates in the human brain and can be potentiated, this could become of clinical importance not only for stroke patients, but also for replacing neurons which have died, thus restoring function in patients with other disorders such as Parkinson’s disease and Huntington’s disease,” says Olle Lindvall, Senior Professor of Neurology.
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The above story is based on materials provided by Lund University. Note: Materials may be edited for content and length.