Traditional strains of Klebsiella pneumoniae have largely affected hospitalised populations, who have weaker defence systems.

However, in the last ten-to-15 years, more virulent strains have been affecting healthy individuals in the community, Thomas Russo, MD, professor in the Department of Medicine at the UB School of Medicine and Biomedical Sciences, and head of its Infectious Disease Division, explained.

"This variant causes serious, life-threatening, invasive infections and is able to spread to other organs from the initial site of infection," he added.

The bacteria is so concerning as it has the ability to easily acquire mobile genetic units, called plasmids, containing multiple genes with high levels of antimicrobial resistance.

Dr Russo and his team are studying the microbiology of a new strain of Klebsiella pneumoniae  to determine what makes it so virulent and see if it can be stopped from spreading.

Currently, the bacterium is fatal in ten to 30 per cent of cases and is treated aggressively with antibiotics and drainage of abscesses.

"These hypervirulent strains are the next 'superbugs'–in-waiting. If they become resistant to antibiotics, they will become difficult, if not impossible to treat," he explained.

The strain is currently 'under-recognised' by both physicians and microbiology labs, despite spreading from where it was first recognised in the Pacific Rim to Europe, Canada, Israel, South Africa and several cities in North America.

Dr Russo said microbiology labs should be aware that when bacterial colonies grown on a solid surface in the laboratory are stretched by an inoculation loop, they form a 'string' greater than 5mm in length.

The European Centre for Disease Prevention and Control reported an increasing number of cases of antibiotic resistant Klebsiella Pneumonia.

Several member states reported between 15 and 50 per cent of cases have now developed a resistance to Carbapenems, the last line of defence class of antibiotics.

Ravi K Amaravadi, MD, an assistant professor of medicine at the Perelman School of Medicine, is among the scientists looking at the potential of combining hydroxychloroquine (HCQ) with cancer treatments including chemotherapy, targeted therapy, radiation, and immunotherapy.

Ongoing clinical trials and laboratory models of treatment-resistant tumours have identified that HCQ can boost the effectiveness of these therapies by blocking autophagy, a survival pathway which expresses increased activity in cancer cells.

Indeed, some believe cancer cells may be addicted to autophagy, as means of allowing the cancer to survive the nutrient limitation and lack of oxygen found within tumours.

Blocking this process is increasingly seen as a target for boosting the cancer-fighting power of therapies.

Dr Amaravadi explained: "Our assays performed on human blood and tissue samples indicate that high doses of HCQ are required to block autophagy in patients, and in some cases, such as in a brain tumour trial, these high doses, in combination with specific anticancer agents, can lead to toxicity for the tumour.

"As the first phase I trials of HCQ are being completed, it is clear that in most cases the high-dose HCQ, in combination with existing cancer therapy, is well tolerated."

Almost 30 phase I and Phase II trials involving HCQ have either been launched or are planned, and randomised controlled trials using HCQ combinations are planned to determine the effectiveness of the approach.

These focus on a number of different malignancies, including melanoma, multiple myeloma, renal cell carcinoma, colon cancer, prostate cancer, breast cancer.

Researchers at the University of Leeds in the UK are also assessing the potential for silver to be used as a cancer treatment.

Tests found that certain compounds within the silver are as toxic to cancer as Cisplatin. Silver is an attractive candidate for therapies as it is less toxic to humans than chemotherapy treatments.

A study carried out by experts in France, the UK and Japan, led by Professor Philippe Froguel from the School of Public Health at Imperial College London, showed that there is now a promising target for new drugs, which could help to target the health problems.

Published in the journal Nature, scientists revealed that those who had a certain mutation in the gene encoding the protein GPR120 were more likely to be obese.

"Being overweight is not always unhealthy if you can make more fat cells to store fat. Some people seem to be unable to do this, and instead they deposit fat around their internal organs, which is very unhealthy," said Professor Froguel.

Obesity is defined when a person has a body mass index of 30 or greater, with nearly a quarter of adults in the UK found to be in this position when the latest figures were released in 2008.

The findings were published in the journal Cell, and they showed that the TAK1 protein was key to the growth of KRAS-dependant cancer cells.

However, by blocking the protein's activity it was possible to kill these cells, and the process triggered a suicide which is known as apoptosis.

"This study shows that if you understand the interrelationships between all the signalling pathways in a particular type of tumour, you may uncover a vulnerability," said co-author of the study Dr Daniel Haber.

According to the NHS, bowel cancer is the third most common form of the disease in the UK, with nearly 40,000 cases registered in 2008.

It is most common in those over the age of 60, with 80 per cent of instances developing in pensioners.

Previously, it has been found that a diet high in red or processed meats and a high intake of alcohol and smoking can increase the chances of getting bowel cancer.

Professor Owen Sansom, a cell signalling expert from Cancer Research UK's Beatson Institute, said that the discovery could lead to new treatments being developed to combat aggressive bowel cancer.

"The TAK1 protein has previously been linked to inflammation, but this is the first time it has been shown to play a key role in cancer. People whose bowel cancer is driven by a mutant KRAS gene tend to have the least favourable outlook, and new-generation targeted therapies like cetuximab aren't generally effective," he added.

Professor Sansom went on to say that the results from Massachusetts General Hospital Cancer Center suggest that, in theory, drugs that block TAK1 could be helpful for at least a proportion of these patients.

Experts from Brown University managed to create a glioma with a network of blood vessels surrounding it.

The tumour model was then used in a number of experiments, which included showing how iron-oxide nanoparticles carrying tumstatin were able to break into the vessels which keep the tumour going with oxygen and other nutrients.

The research paper was published in the journal Theranostics, with Don Ho, lead author of the study, stating that the model "offers a facile process to test diffusion and penetration into a glioma that is covered by a blood vessel-like coating of endothelial cells".

"This assay would save time and money, while reducing tests in living organisms, to examine an agent's 3D characteristics such as the ability for targeting and diffusion," he added.

Mr Ho, a graduate student in the lab of chemistry professor Shouheng Sun, went on to say that the benefit of a 3D model over 2D is that it is possible to see nanoparticles diffusing through the endothelial cells.

The new model is also preferred to previous 3D tissue models as it allows the glioma and endothelial cells to assemble just as they would in real life.

The researchers hope that in the future the model will have "significant potential" to help test and optimise the design of therapeutic and diagnostic nanocarriers and then determine their capabilities.

In the UK, around 4,500 new cases of primary brain tumours are discovered every year, according to the NHS, with the exact cause being unknown.

The organisation advises that treatment should be sought as soon as possible as this could prevent it from spreading to other parts of the brain and into the spinal cord.

Research carried out by researchers at the University of Copenhagen backed up previous speculation on the subject while also providing physicians with a theory of testing the cellular health of a person.

Using around 20,000 Danes for the research, experts isolated each person's DNA to examine their specific telomere length, which highlights cellular ageing.

Telomeres shorten over the duration of a person's life, while they can also be affected by lifestyle choices like obesity and smoking.

Borge Nordestgaard, clinical professor of genetic epidemiology at the Faculty of Health and Medical Sciences at the institute, explained that the risk of having a heart attack or early death is increased when telomeres are found to be shortened.

"That smoking and obesity increases the risk of heart disease has been known for a while. We have now shown, as has been speculated, that the increased risk is directly related to the shortening of the protective telomeres – so you can say that smoking and obesity ages the body on a cellular level, just as surely as the passing of time," he added.

Mr Nordestgaard went on to say that any future studies will be able to reveal the actual molecular mechanism which will show why short telomere length causes heart attacks.

According to the NHS, around 111,000 people have a heart attack every year in England, with many of those that lead to death being preventable.

It added that some of the risk factors of a heart attack are smoking, enjoying a high-fat diet and being obese.

The research, which is titled 'Short telomere length, myocardial infarction, ischemic heart disease, and early death' will be published in next month's issue of the journal Arteriosclerosis, Thrombosis and Vascular Biology.

A report published in the British Journal of Cancer, on the back of a study carried out by experts at The Institute of Cancer Research, revealed that of around 300 women with TN breast cancer, BRCA1 mutations were present in around 20 per cent of those under 50.

Professor Nazneen Rahman, lead author, said that the findings show that using a simple age criteria for testing will provide a "clear and understandable guide for doctors and women to follow".

The expert added that this should therefore result in more women benefitting from optimised care which is possible through the study of genetic information.

TN breast cancer is diagnosed when a pathology report shows that cells tested negative for estrogen receptors, HER2 and progesterone receptors, with between ten and 20 per cent of cases of disease being in this form.

Currently, the test for the BRCA1 mutation is only given where there is a greater than 20 per cent chance of successful detection because of the costs involved, according to NICE guidance.

The researchers revealed that if the guidelines are changed then this could enable an extra 1,200 tests to be carried out on an annual basis, although the challenge of coping with this extra burden will need to be met.

"There are hurdles to overcome so that NHS testing services can cope with more BRCA1 testing, but we’re moving towards an era of faster and cheaper genetic testing, so it will soon be possible," Professor Rahman added.

Professor Peter Johnson, a chief clinician at Cancer Research UK, said that identifying women and their families with the BRCA1 mutations could help doctors provide targeted screening and tailored treatments to these patients.

The method could eventually help to create drugs which can target rogue DNA, according to results published in Nature Chemistry.

Researchers based at the University of Texas at Austin said that this breakthrough might help in the treatment of genetic diseases, cancer or retroviruses including HIV.

Professor of chemistry and chair of the department of chemistry and biochemistry at the institute Brent Iverson said: "If you think of DNA as a spiral staircase, imagine sliding something between the steps. That's what our molecule does. It can be visualised as binding to DNA in the same way a snake might climb a ladder."

DNA is found in all humans and most other organisms and contains around three million bases, with the sequence of these determining the information for how an organism is built and maintained.

The institute is based at the University of Gothenburg, Sweden, and Mattias Lorentzon and his colleagues found that those who undertook physical activity between the age of 19 and 24 were able to increase their bone density in their hips, arms, lower legs and lumbar spine.

It was previously known that the strength of bones is developed early in life, with exercising before and after puberty being important for this.

Osteoporosis causes bones to become weak and therefore more likely to break, with many fractures being caused when elderly people fall or bump into objects.

According to the NHS, around three million people in the UK have osteoporosis, and this condition is to blame for up to 230,000 fractures each year.

The study in Sweden of 833 men showed that those who did not undertake increased levels of physical exercise in their early 20s were found to have significantly more brittle bones, say the researchers.

"The men who increased or maintained high levels of physical activity also developed larger and thicker bones in their lower arms and legs. These findings suggest that maintaining or, ideally, increasing physical activity can improve bone growth in our youth, which probably reduces the risk of fractures later on," added Dr Lorentzon.

This study was published in the Journal of Bone and Mineral Research under the title Increased physical activity is associated with enhanced development of peak bone mass in men: A five-year longitudinal study.

Sweden is thought to be one of the highest-risk countries in the world for osteoporosis, with figures revealing that one in two women and one in four men will suffer a fracture because of this condition during their lifetime.

Experts at NYU Langone Medical Center carried out tests on a protein called SAMHD1, which was recently found to be resistant to infection by HIV.

It is now hoped that this mechanism could provide a stimulus for therapeutic research which will slow down the virus' progression into AIDS.

The research was published in Nature Immunology and explains how Dr Nathaniel Landau and his team discovered that SAMHD1 protects a cell from a virus by destroying the pool of dNTPs, which then left it without any building blocks for its genetic information.

"SAMHD1 essentially starves the virus. The virus enters thecell and then nothing happens. It has nothing to build and replicate with, so no DNA is made," he said.

Around 90,000 people in the UK are living with HIV, while around a quarter of people with the infection are undiagnosed.