Category Archives: Medicine and Health

Medicine and Health News

Fluorescent probes make nerves glow during surgery

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Claire Tree-Booker

Scientists at the San Diego School of Medicine, University of California have developed fluorescent protein fragments, also known as peptides, which specifically label nerves. It is hoped this new technology will help surgeons avoid damaging nerves during surgery.

Accidental damage to nerves during surgery can cause many problems including pain, numbness and even paralysis.

The scientists report, in the 6 February 2011 edition of Nature Biotechnology, that when the fluorescent peptides were injected into mice, nerves were labelled within two hours; this created a ten-fold contrast compared to other body tissues, allowing the nerves to be easily seen.

The fluorescent labelling was found to have no effect on the activity of the nerves or the animals’ behaviour.

Whilst surgeons can identify nerves by their appearance or by electrical stimulation, they can sometimes be missed if they are buried or have a different appearance.  Dr Quyen T. Nguyen, carrying out the study, said “if surgery is required in the setting of trauma or infection, the affected nerves might not look as they normally would, or their location may be distorted”.

 “We have yet to test the peptide in patients, but we have shown that the fluorescent probe also labels nerves in human tissue samples”, says Nguyen.

Damaged nerves were also fluorescently labelled, suggesting that this technique could be useful in nerve repair surgery in the future.

The paper can be found at http://www.nature.com/nbt/journal/vaop/ncurrent/full/nbt.1764.html

Social media: students go cold turkey

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Michaela Livingstone

200 students from the University of Maryland have kicked off a global study looking at young adult’s use of media, finding that the students actually experience symptoms akin to drug withdrawal.

The study, called Unplugged, which has also taken place at Bournemouth University, asked its students to go 24 hours without using any form of media: newspapers, televisions, iPods, phones, laptops, Facebook, Twitter or radio, and then blog about it afterwards.

As reported on the Unplugged website, many students reported feelings of loneliness, isolation and even physical symptoms like feeling fidgety.

“I noticed physically, that I began to fidget”, said one student, another reporting that instant messaging and texting their friends was comforting.

Students in the British contingent noted that making any plans was almost impossible without phones and Facebook, as things change within minutes, so making plans the day before was pointless.

The conclusion of the American study states that today’s youths’ use of media has not just changed the way they find and use information, but has also, “…caused them to make different and distinctive social, and arguably moral, decisions”. The study’s conclusions also draw light to the fact that the youth of today are “fickle” and do not care where their information comes from, rather it is the information itself that is coveted the most.

Although only a small and qualitative study that maybe cannot be considered to be truly representative of the teenage and young adult population of the US or the UK, it may well be seen as a worrying sign that our youth are just too dependent on media, and the potential harm this may be having.

The study did however find that the young were capable of developing coping skills during their media abstinence. So maybe it’s not all bad news.

Coffee and cake can be good for you!

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Maria Panagiotidi

Coffee and cake might be bad for your waistline but not for your brain! At least that is what a recent study published in the journal “Human Psychopharmacology: Clinical and Experimental” suggests.

Caffeine and glucose are part of our everyday life and are known to have stimulant effects. Previous studies have suggested that caffeine can have positive effects on cognitive function when consumed in moderation.  Other studies focused on the effects of glucose have found similar effects. However, only a few researchers so far had looked at the synergistic effect of those two substances on behaviour and cognitive function.

A group from the University of Barcelona have now done a novel study to investigate whether the consumption of caffeine and glucose, alone and combined, has any effect on cognitive performance. They tested their hypothesis by asking seventy-two healthy subjects to perform a variety of tasks after being administered either doses of water, water with caffeine, water with glucose, or water with both caffeine and glucose. The tests examined a number of functions like attention, memory, fine motor skills, and reaction time.

The most robust effects were observed in the group that consumed caffeine and glucose. More specifically, these participants performed better on tasks requiring attention, learning and verbal memory. The consumption of caffeine alone also lead to improvements in simple reaction time tasks. Similarly, glucose was associated with improved performance on reaction time and fine motor skills task.

 

Adan, A. and Serra-Grabulosa, J. M. (2010). Effects of caffeine and glucose, alone and combined, on cognitive performance. Hum. Psychopharmacol. Clin. Exp., 25(4):310-317. http://onlinelibrary.wiley.com/doi/10.1002/hup.1115/abstract

Asthma treatment to treat Alzheimer’s

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Kathryn Vaughan

New research into has raised the possibility of treating Alzheimer’s disease with drugs currently used by asthmatics.

Alzheimer’s disease (AD) is a neurodegenerative disorder and the most common cause of dementia. Often diagnosed in people over 65 years of age, symptoms include inability to recall recent events, confusion, aggression, long-term memory loss and irritability. As the disease progresses bodily functions also deteriorate, ultimately leading to death.

The cause(s) of AD is not well understood and as such there are no treatments available to cure or delay the progression of the disease. Research characterises the disease by the development of plaques and the deposition and aggregation of proteins within neurons of the brain, leading to neurone degradation. These are thought to arise by both genetic and environmental factors. Amyloid, a fibrous protein, has been identified as a major component in these deposits, and is formed by the processing of a precursor protein by secretase enzymes. The secretase is composed of 4 membrane proteins, which are transcribed upon the activation and nuclear translocation of CREB (cAMP Response Element Binding).

A recent study from Temple University, School of Medicine, Philadelphia, has implicated the enzyme 5-lipoxygenase (5-LO) in AD. This enzyme catalyses the conversion of arachidonic acid to 5-hydroxy-peroxy-eicosatetraenoic acid (5-HPETE), and subsequently to 5-hydroxy-eicosatetraenoic acid (5-HETE).  The eicosanoid 5-HETE is an intermediate for leukotriene synthesis, where leukotrienes are lipid mediators that are important in the inflammatory response.

The research group, led by Dr Domenico Praticó, used both pharmacological and genetic approaches to show that 5-LO may provide better understanding of the processes leading to AD. They found that the expression of 5-LO is greater in AD patient brains compared to healthy controls and that knocking-out the 5-LO gene in a mouse model of amyloidosis (accumulation of insoluble amyloid protein) significantly reduced the levels of amyloid and secretase, without drastically affecting other biological processes.

This potentially establishes a novel role for 5-LO in regulating amyloid levels. If you can control the levels of secretase, the only source of amyloid in the brain, then you can control amyloid levels and hence AD. Thus 5-LO may provide a potential target for the treatment of AD by use of 5-LO inhibitors that are currently used for the treatment of asthma.

Chu and Praticó (2010) 5-Lipoxygenase as an endogenous modulator o amyloid beta formation in vivo. Annals of Neurology

Scientists discover how to regenerate damaged heart muscle cells

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Claire Tree-Booker

Scientists have uncovered how to turn common heart cells into beating muscle cells.

Around 68 000 people suffer from heart failure annually in the UK, because the heart is unable to repair itself after an attack.

The muscle cells that cause the heart to beat, called cardiac myocytes, die during a heart attack and are replaced by non-beating connective tissue cells, called fibroblasts. This loss of beating muscle cells means that the heart is no longer able to pump as effectively.

Researchers Deepak Srivastava and Masaki Ieda from the Gladstone Institute of Cardiovascular Disease in California investigated whether they could turn fibroblasts into beating cardiac myocytes.

The scientists put several genes known to be important in heart development into mouse cardiac fibroblasts, to see whether they would change into myocytes.

The technique, known as cellular reprogramming, worked successfully and three genes were identified that altered the cells.

After one month of treatment with extra copies of the three genes, known as Gata4, Mef2c and Tbx5, around 20% of the fibroblasts had the characteristics of myocytes, and began to contract like beating heart cells.

In the 6th August issue of Cell, the scientists showed that the reprogrammed cells had proteins on their surface that are normally found in cardiac myocytes, and they expressed similar genes.

The researchers’ next step is to test whether the same genes can be used in human hearts; “I envision such factors being loaded onto a stent that is placed in the coronary artery”, says Professor Srivastava. He believes it is “not unreasonable to imagine being ready for a clinical trial in the next five years”.

Bacterial enzyme reveals novel mechanism of DNA repair

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Arran-Leigh Roberts

Our DNA comes under attack daily from a variety of things in our environment; cigarette smoke, industrial waste and UV radiation from the sun to name a few. This is in addition to natural damage that occurs in our cells from chemical conditions and errors in DNA replication. All this amounts to that in a given cell, up to 1 million bases of DNA are damaged per day. Fortunately, our cells contain a number of molecular repair mechanisms which deal with this damage by restoring the correct DNA sequence.

Researchers at Vanderbilt University, Pennsylvania State University and the University of Pittsburgh have now uncovered a new mechanism by which DNA is repaired when it has undergone damage by a process called alkylation. Alkylation is a common type of DNA damage which is caused by certain industrial toxins, some components of cigarette smoke and even some chemotherapy drugs. These alkylating agents transfer methyl or other alkyl groups onto guanine bases in the DNA – where they do not belong. This causes an alteration in the shape of the DNA molecule itself and stops replication occurring successfully, especially if the damage occurs within a gene-containing region.

Whilst humans only have one enzyme to repair different types of alkylation, namely a glycosylase called AAG, bacteria have several of these, with each targeting specific types of damage. Whilst studying bacterial glycosylases, the researchers discovered the enzyme AlkD, which functions in a novel manner. The enzyme essentially causes the base pair damaged by alkylation to rotate out of the DNA helix. Once outside the helix, it is able to spontaneously detach and AlkD helps to accelerate this process.

Although this research highlights the function of just a single bacterial enzyme, it provides invaluable insight into the process by which enzymes may recognise and deal with DNA damage. This has been previously impossible to pin down with the help of the human enzyme, AAG.

This finding may be particularly relevant to the production of new chemotherapy drugs for cancer treatment. These drugs specifically aim to cause lethal alkylation of the DNA contained in tumour cells. The trouble with current chemotherapy drugs is that they can potentially cause harmful mutations in the DNA of healthy cells. It is hoped that by better understanding the mechanisms of DNA repair, novel chemotherapy drugs can be produced that are able to target their toxic effects to tumour cells only.

Inflammation and Diabetes – a Fishy Tale

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Kathryn Vaughan

Researchers investigating the function of a particular G-protein coupled receptor, GPR120, have found potent anti-inflammatory effects to be mediated when stimulated with ingredients of fish oil.

Docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) are omega-3 fatty acids found in fish oil. These fatty acids have already been shown to have health benefits, e.g. DHA reduces blood triglycerides to decrease the risk of atherosclerosis and heart disease.

Chronic inflammation, mediated by macrophages (white blood cells that enter diseased tissues and mediate an inflammatory response), is linked to decreased sensitivity to insulin in obesity, thus the anti-inflammatory effects mediated upon GPR120 activation may promote insulin sensitisation.

Adipose (fat) tissue and pro-inflammatory tissue macrophages were found to express GPR120, and, in particular, the receptor was highly induced in the obese murine model. Further investigation by the research team found that DHA activation of GPR120 increased the translocation of GLUT4 (Glucose Transporter 4) to the cellular surface and hence transportation of glucose into the cells.

Monocytic cell lines and murine primary intraperitoneal macrophages both containing and lacking the GPR120 receptor were also used in the research. A high-fat diet with or without omega-3 fatty acid supplementation was fed to the mice, and in ordinary mice DHA and EPA mediated anti-inflammatory effects by inhibition of both the TLR (Toll-like Receptor) and TNF (Tumour Necrosis Factor) inflammatory pathways. In the GPR120 knockout mice DHA and EPA had no effect.

The research was led by Jerrold Olefsky, Associate Dean for Scientific Affairs and Professor of Medicine at University of California, San Diego School of Medicine. Speaking in video clips posted on the University of California’s website Prof. Olefsky said that potentially the effects seen in mice may be mediated in humans to treat insulin resistance. However, in experiments they had to give the mice relatively high doses of fatty acids, which would be non-beneficial to humans. Therefore it may be more reasonable to target GPR120 for therapeutic treatment. If they could find a small molecule that mimics the effects of the fatty acids then a reasonable dose may be consumed to mediate anti-inflammatory and anti-insulin resistance effects.

The researchers conclude that GPR120 may be an important signalling molecule in anti-inflammatory and insulin-sensitising responses thus may provide a new approach for the treatment of insulin resistant diseases.

 

Oh et al (2010) GPR120 is an omega-3 fatty acid receptor mediating potent anti-inflammatory and insulin-sensitizing effects. Cell, 142, 687-698.

The paper can be found at:

http://www.cell.com/fulltext/S0092-8674%2810%2900888-3

A step closer to HIV vaccine

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Helen Phillips

 

An antibody has been discovered which can neutralise the Human Immunodeficiency Virus, the pathogen that causes AIDS. The antibody can fight 90% of HIV-1 strains, the most common form of the virus. Researchers at the NIAID Vaccine Research Center have even been able to establish how the antibody works.

A vaccine to HIV has been difficult to develop as the surface of the virus constantly changes. This antibody is interesting because it attaches to a part of the virus which hardly changes. This is possibly the reason why the antibody has such a broad effect across strains.

The antibody is naturally occurring and has been extracted from an infected patient’s blood. However, not everyone carries these antibodies.  The next important step will be finding a way to stimulate the production of these antibodies in other people.

These findings have recently been published in the journal Science; the discovery of these broadly neutralising antibodies is one of the most significant steps in the quest to find a vaccine.

 

Articles: 

Wu X et al. Rational design of envelope surface identifies broadly neutralizing human monoclonal antibodies to HIV-1. Science. 2010.

Zhou T et al. Structural basis for broad and potent neutralization of HIV-1 by antibody VRC01. Science. 2010.

Alcohol to Treat Rheumatoid Arthritis?

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Kathryn Vaughan

A team of researchers, led by Professor Gerry Wilson, from the University of Sheffield, have found that consuming alcohol reduces the risk and severity of rheumatoid arthritis.

Rheumatoid arthritis (RA) is an autoimmune disorder that causes systemic inflammation and affects approximately one percent of the world’s population. RA typically causes inflammation around the joints, causing the joints to become swollen, painful and stiff, as well as affecting other organs. This can become debilitating for the patient as the disease progresses, for example, fingers can lose their shape and alignment causing loss of movement.

Human volunteers were used in the study involving 873 white Caucasian RA patients and 1004 controls (people without RA). Volunteers were asked in fill in a questionnaire relating to their alcohol intake, indicating the number of days on which they had at least one alcoholic drink over the past month. The risk and severity of RA was then assessed after adjusting for age, gender and smoking habits.

Data show that the risk of RA decreased in relation to the frequency of alcohol consumption, i.e. compared to non-drinkers volunteers that drank on more than ten days per month had a highly significant reduced risk of developing RA.

The severity of RA was assessed by the CRP (C-Reactive Protein) test and measuring anti-CPP antibody levels. Both of these protein concentrations in the blood rise during inflammatory episodes and are associated with RA. The DAS (Disease Activity Score) assessment was also used, whereby joints are scored according to their tenderness and swelling, as well as the volunteer scoring their pain on a visual scale, and x-rays taken to assess inflammation. All these measures for severity of RA were inversely related to the increased frequency of alcohol consumption.

Speaking on BBC Radio Sheffield, first author Dr James Maxwell, consultant rheumatologist at the Rotherham Foundation NHS Trust and senior clinical lecturer at the University of Sheffield, explained that studies in animals had shown alcohol to suppress the immune system. Thus the anti-inflammatory properties of alcohol may influence pathways through which RA develops. However, Dr Maxwell was quick to iterate that he would not recommend patients to specifically drink alcohol to treat their joints, despite the study concluding “alcohol consumption has an inverse and dose-related association with both risk and severity of RA”.

Maxwell et al (2010) Alcohol consumption is inversely associated with risk and severity of rheumatoid arthritis. Rheumatology (Oxford), ahead of print.
The paper can be found at: http://rheumatology.oxfordjournals.org/cgi/content/full/keq202v1?view=long&pmid=20667949

Crohn’s disease: the result of a gene plus a virus?

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Claire Tree-Booker

Many of us are carrying genes for lots of different diseases that we’ll never actually get.  Crohn’s disease, for example, is an inflammatory disease of the intestinal tract affecting less than 1% of the population, but over half of us are carrying at least one gene linked to it. 

Environmental triggers can help account for this inconsistency, but scientists have been unable to explain exactly how.

However, a recent study published in Cell has shown that when mice with a particular Crohn’s disease gene are exposed to a norovirus infection, they develop similar symptoms to people with the disease.

The finding was a chance discovery; Professor Thaddeus Stappenbeck from Washington School of Medicine was working with mice carrying a Crohn’s disease susceptibility gene, Atg16L1m. He moved the mice to cleaner housing, to keep them away from viruses that can affect lab mice, and found that when they were in the cleaner facility they no longer showed symptoms of Crohn’s disease.

The researchers investigated whether murine norovirus, which was absent from the clean facility, was responsible for the development of Crohn’s disease in the mice carrying the Atg16L1m susceptibility gene.

The investigators infected the susceptible Atg16L1m mice with a particular strain of murine norovirus (MNV CR6), which caused them to develop inflammation in cells of the intestine called Paneth cells. This is the same abnormality the mice had when kept in less clean conditions, and patients with Crohn’s disease have similar inflammation in Paneth cells. Mice not carrying the Crohn’s disease susceptibility gene did not develop any symptoms, and susceptible mice infected with a different strain of norovirus (MNV CW3) remained healthy.

Noroviruses are common in humans, causing gastrointestinal upset; doctors had previously noted that many patients with newly diagnosed Crohn’s disease had recently been ill with a stomach virus.

In response to this work, R.Balfour Sartor, chief medical adviser to the Crohn’s and Colitis Foundation of America,  says that  the research could explain why many people who have genes for Crohn’s disease don’t develop any symptoms. Sartor says that many factors are necessary to cause Chron’s disease, and that more work must be done to see whether these findings also apply to people. 

The researchers’ future plans include investigating which particular viruses people with Crohn’s disease have been exposed to.