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Biomedical engineers have successfully grown living skeletal muscle that has many properties of ordinary muscle tissue and, for the first time, demonstrates its ability to heal itself in the laboratory and in animals.

Researchers at Duke University tested the bioengineered muscle by watching it through a window on the back of a living mouse. This allowed them to monitor the muscle's integration and maturation inside a living, walking animal.

Nenad Bursac, associate professor of biomedical engineering at Duke, said: "The muscle we have made represents an important advance for the field. It's the first time engineered muscle has been created that contracts as strongly as native neonatal skeletal muscle."

Throughout years of honing their research methods, a team led by Prof Bursac and graduate student Mark Juhas found two things are necessary for preparing better muscle: well-developed contractile muscle fibres and a pool of muscle stem cells, known as satellite cells.

Satellite cells are available to every muscle, ready to activate upon injury and begin the regeneration process. The key to the team's success lay in creating the microenvironments – called niches – where these stem cells await their 'call to duty'.

The researchers subjected the muscle to a number of laboratory trials. They measured its contractile strength by stimulating it with electrical pulses and showed it was more than ten times stronger than any previously engineered muscles. 

A toxin found in snake venom was used to prove the satellite cells could activate, multiply and successfully heal the injured muscle fibers.

The muscle was then inserted into a small chamber on the backs of mice which was covered by a glass panel. They checked on its progress every two days for two weeks.

Muscle fibres had been genetically modified to produce fluorescent flashes during calcium spikes – which cause muscle to contract – and researchers were able to watch the flashes grow brighter as it strengthened. 

"We could see and measure in real time how blood vessels grew into the implanted muscle fibres, maturing toward equalling the strength of its native counterpart," Mr Juhas commented.

The team are now beginning to undertake work to see whether their bioengineered muscle can be used to repair actual injuries and treat disease.

New research suggests that brain irregularities in autistic children could be traced back to prenatal development.

The study, published in the New England Journal of Medicine, shows that the origins of the architecture of the autistic brain, which contains patches of abnormal neurons, may lie in this stage of development.

"While autism is generally considered a developmental brain disorder, research has not identified a consistent or causative lesion," said Thomas Insel, director of the National Institute of Mental Health. 

"If this new report of disorganised architecture in the brains of some children with autism is replicated, we can presume this reflects a process occurring long before birth. This reinforces the importance of early identification and intervention."

Researchers from the University of California, San Diego, and the Allen Institute for Brain Science joined forces to investigate the structure of the brain's outermost layer, the cortex, in children with autism.

They analysed gene expression in postmortem brain tissue from children with and without autism, all between two and 15 years of age.

As the prenatal brain develops, neurons in the cortex differentiate into six layers, with each layer composed of different types of brain cells with specific patterns of connections.

In addition to genes associated with autism, the research team focused on genes that serve as cellular markers for each of the cortical layers.

Some 91 per cent of autistic samples lacked the markers for several layers of the cortex. For control samples, the figure was nine per cent.

Signs of disorganisation were localised in focal patches that were 5-7 mm in length and encompassed multiple cortical layers.

These signs were located in the frontal and temporal lobes of the cortex – regions that mediate social, emotional, communication and language functions. 

As disturbances in these types of behaviour are hallmarks of autism, the researchers concluded that the specific locations of the patches may be linked to the expression and severity of various symptoms in a child with the disorder.

Early treatments for children with autism may be successful because of the patchy nature of these defects – the developing brain may be able to rewire its connections by enlisting the aid of cells from neighbouring regions to bypass the pathological areas.

Mathematicians and scientists from two UK universities have collaborated to shed new light on the process of viral replication during an infection.

Experimentalists from the University of Leeds and mathematicians from the University of York devised a mathematical model that gives new insights into the molecular mechanisms behind virus assembly, helping to explain the efficiency of their operation.

Researchers from the Departments of Mathematics and Biology at the University of York have developed a theoretical basis for the speed and efficiency with which viruses assemble the protective proteins for their genetic information – in this case an RNA molecule – during an infection.

The team incorporated multiple specific contacts between the genomic RNA and the proteins in the containers, along with other details of real virus infections, into a mathematical model that demonstrates how these contacts act collectively to reduce the complexity of virus formation.

They thus solved a longstanding puzzle about virus assembly – a form of Levinthal's paradox.

The process also ensures efficient and selective packaging of the viral genome and has evolved because it provides significant selective advantages to viruses that function in this way.

As a result of the research, new antiviral therapies could be developed. The team's findings could help to treat a range of diseases from HIV and Hepatitis B and C to the "winter vomiting bug" norovirus and the common cold.

Professor Reidun Twarock, a member of the York Centre for Complex Systems Analysis, said: "This truly interdisciplinary effort has provided surprising insights into a fundamental mechanism in virology. 

"Existing experimental techniques for studying viral assembly are unable to identify the cooperative roles played by all the important components, highlighting the need and power of mathematical modelling. 

"This model is a paradigm shift in the field of viral assembly."

He went on to say that the study helps elucidate the process of virus assembly and could help to develop antiviral therapies.

The findings of the research are published in the Proceedings of the National Academy of Sciences.

Researchers from Chicago and Beijing have identified a major mechanism behind the progression of kidney cancer and their findings could lead to new treatments for the disease. 

Their research, published in the March 20th edition of the journal Cancer Cell, shows how a shortage of oxygen, or hypoxia, created when rapidly multiplying kidney cancer cells outgrow their local blood supply, can accelerate tumor growth.

It does this by causing a nuclear cell protein known as SPOP (speckle-type POZ protein) – which normally suppresses tumour growth – to move into the cytoplasm, where it has the opposite effect.

In the cytoplasm, SPOP closes down the protective pathways that should restrict tumour growth. The team notes that the cytoplasmic overaccumulation of SPOP "is sufficient to convey tumourigenic properties onto otherwise non-tumourigenic cells."

"It becomes a vicious cycle," said the study's senior author Kevin White, professor of human genetics, and ecology and evolution, and director of the Institute for Genomics and Systems Biology at the University of Chicago.

"In people with clear-cell renal cell carcinoma, hypoxia-inducible factors enter the nucleus and target the SPOP gene. 

"SPOP gets overexpressed and misdirected to the cytoplasm, where it interferes with multiple systems designed to suppress tumor growth. This encourages tumor growth, leading to more hypoxia."

A role for SPOP as a biomarker for kidney cancer was identified by Professor White and colleagues in 2009.

They found that 99 per cent of clear cell renal cell cancers (ccRCC, the most common type of kidney cancer) had elevated SPOP levels.

The researchers hope that understanding how misplaced but not mutated SPOP contributes to cancer growth could help them identify new ways to intervene.

Work conducted on fruit flies showed that SPOP acts as a regulatory hub, influencing several cancer-related pathways.

In humans, SPOP has a profound effect, degrading multiple regulatory proteins in the cytoplasm that ordinarily serve to suppress tumour growth.

The most important was PTEN, a gene that is damaged or lost in several types of cancer. Several other tumour-suppressing proteins could be degraded by SPOP, removing additional barriers to rapid tumour growth.

SPOP may therefore turn out to be a good drug target, Professor White noted.

Scientists have successfully used stem cells derived from human muscle tissue to repair nerve damage and restore function in an animal model. 

Their findings raise hopes that cell therapy of certain nerve diseases, such as multiple sclerosis, might one day be available.

Treatments for damage to peripheral nerves – those outside the brain and spinal cord – have hitherto had limited success, often leaving patients with impaired muscle control and sensation, pain and decreased function.

Researchers at the University of Pittsburgh school of medicine cultured human muscle-derived stem/progenitor cells in a growth medium suitable for nerve cells.

When prompted using specific nerve growth factors, the stem cells differentiated into neurons and glial support cells, including Schwann cells that form the myelin sheath around the axons of neurons to improve conduction of nerve impulses.

In mouse models, the researchers surgically created a quarter-inch defect in the right sciatic nerve, which controls right leg movement. They then injected the human-derived stem or progenitor cells into the defect.

After six weeks, the nerve had fully regenerated in stem-cell treated mice, while the untreated group had limited nerve regrowth and functionality.

Twelve weeks later, treated mice were able to keep their treated and untreated legs balanced at the same level while being held vertically by their tails. 

When the treated mice ran through a maze, analysis conducted on their paw prints showed an eventual restoration of gait. 

Both sets of mice experienced muscle atrophy following nerve injury but only those treated with stem cells had regained normal muscle mass by 72 weeks post-surgery.

"Even 12 weeks after the injury, the regenerated sciatic nerve looked and behaved like a normal nerve," Dr Mitra Lavasani, first author and assistant professor of orthopaedic surgery at the Pitt School of Medicine, commented. 

"This approach has great potential for not only acute nerve injury, but also conditions of chronic damage, such as diabetic neuropathy and multiple sclerosis."

The team are now trying to understand how the human-derived stem cells triggered repair of the injury and are working on delivery systems, such as gels, that could hold the cells in place at larger injury sites.