Norske Skog eyes “poor man’s M&A” in European paper

June 8, 2010 By Leave a Comment

(Reuters) – Norwegian papermaker Norske Skog

Deals

repeated its calls for more consolidation to combat overcapacity in Europe and said the cash-poor sector was likely to favor deals such as asset swaps.

“You will probably see some kind of a poor man’s M&A solution — (for instance) joint ventures, asset swapping,” Ombudstvedt said. “I don’t think that you will see many straight acquisitions,” Norske Skog Chief Executive Sven Ombudstvedt told journalists on Monday.

The global paper industry has been mired in a slump caused by soft demand and overcapacity, exacerbated by the global recession. Norske Skog’s newsprint business has additionally been hammered by a slump advertising spending and subscriptions.

“One reason to have consolidation is to foster a more healthy supply-demand balance,” the CEO said.

Europe is still much more fragmented than North America, were several companies have been through debt restructuring. In Europe, many players “wouldn’t take the pain” of closing down old paper mills, Ombudstvedt said.

“People are beating each other to death within the same segment … so consolidation will foster a clearer leadership within the paper grades,” he said.

The global financial crisis compounded years of struggle by Norske Skog and much of the paper industry with soft demand and overproduction so companies do not have a lot of cash for deals.

Ombudstvedt said Norske Skog’s ability to acquire others was for the most part limited by its own balance sheet, as credit for making deals was probably still available despite markets risk premiums having surged with recent European debt woes.

Norske Skog is currently talking to its creditors about its maturity profile, which calls for big repayments in 2012. It’s also looking to divest up to 1 billion crowns ($150.5 million) worth of non-core assets to reduce the debt load.

Ombudtsvedt said the timing was not right for a complete debt restructuring.

“You probably pay twice the funding cost we have on the debt today … it wouldn’t really be prudent management,” he said.

Instead, Norske Skog has put up for sale the real estate for its old Union paper mill in Norway, some other property and forest land, as well as surplus electricity contracts in Norway, Brazil and New Zealand, he said.

($1=6.644 Norwegian Crown)

(Editing by Jon Loades-Carter)

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Swine flu more dangerous for young adults with strong immune systems

May 6, 2009 By Leave a Comment

Washington, May 6 (ANI): Scientists are suggesting that the swine flu virus may be more dangerous for healthy young adults because it likely kills its victims by inducing a “cytokine storm”, in which a patient’s hyper-activated immune system causes potentially fatal damage to the lungs.

Cytokines are signalling chemicals that help mobilize immune cells capable of removing infectious agents from the body.

Research studies and review articles published in the journal Viral Immunology reveal that a cytokine storm occurs when the body’s immune system over-reacts to an intruder, such as a virus, by producing high levels of cytokines.

The reports further suggest that too much production of cytokines can stimulate an inflammatory response in which the accumulation of immune cells and fluid at the site of infection may prevent affected organs, such as the lung, from functioning properly, and may even cause death.

The researchers behind these articles say that the swine flu contains genetic components of the H5N1 avian influenza virus, which tend to cause an unusually high proportion of deaths among healthy young adults, most likely due to the overproduction of cytokines.

Dr. David L. Woodland, Editor-in Chief of Viral Immunology, emphasizes that much is still not known about the current influenza outbreak and the human/avian combination virus causing it.

“We do not know how long ago this virus emerged, how deadly it is, whether it has pandemic potential, how the severity of infection relates to patient age, and why some infected patients die-whether a cytokine storm is responsible for these deaths,” he says.

He further says what scientists know is that some H1N1 viruses have pandemic potential, and that historical evidence supports the possibility that young healthy adults may be especially susceptible to more severe infection and poor outcomes due to the ability of a strong immune system to initiate a cytokine storm. (ANI)

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Computational model to examine Alzheimer’s pathways in young adults created

April 19, 2009 By Leave a Comment

Washington, Apr 19 (ANI): Scientists at University of Virginia have developed a computational model to examine the role of certain proteins in the development of Familial Alzheimer’s disease (FAD), which affects people as young as 30.

Biomedical engineers Lydia S. Glaw and Thomas C. Skalak, Ph.D., of the Department of Biomedical Engineering, University of Virginia, Charlottesville, constructed the model to measure plaques and tangles and their influence in causing FAD.

The model tested the hypothesis that certain variables-genetic mutations in proteins and “tau” tangles-might be predicative of the development of the disease.

The model is a first-of-its-kind approach to modelling, understanding and predicting Alzheimer’s pathways.

One of the biggest hypotheses tested by the model was the idea that GSK3 is a link between amyloid beta buildup and tau tangle development.

The researchers studied the proteins presenilin-1 (PS1) (a mutated gene found in familial AD) and glycogen synthase kinase (GSK-3) and amyloid beta (Aá) plaque, to quantitatively examine their roles in the development of Alzheimer’s pathology.

The elements were applied to the model, which was constructed of kinetic equations developed from literature searches, and analysed the interactions of the proteins and complexes under various scenarios.

The researchers found that GSK3 had a large effect on tangle formation, but very little on the plaques.

Also, activating GSK3 was not found to be sufficient to cause changes in the brain to the extent seen in Alzheimer’s patients.

However, overproduction of GSK3 as opposed to activation could lead to those changes.

Besides there was no link found between amyloid beta plaque and tau tangles.

They concluded that no single change to the system could cause Alzheimer’s disease; instead it was caused by multiple changes, such as a PS1 mutation combined with GSK3 over-activation.

They suggested that a multi-pronged approach to treating the disease may be best.

The findings will be presented at the 122nd Annual Meeting of the American Physiological Society. (ANI)

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Potential therapeutic target for Down’s syndrome identified

March 14, 2009 By Leave a Comment

Washington, Mar 14 (ANI): Researchers from Salk Institute for Biological Studies have identified a molecular pathway that can be a potential therapeutic target for Down’s syndrome, the most frequent cause of mental retardation.

The study showed that synaptojanin-1, a central component of the pathway, is essential to production of glia, brain cells that act as neurons’ personal assistants.

Down’s syndrome, spinal cord injury, Alzheimer’s disease, and stroke all are linked by an overproduction of glia.

“The discovery of this molecular signalling pathway promises to completely change the way we think about central nervous system maladies, allowing the development of drugs that inhibit glial proliferation and improve the prognosis of patients with a host of devastating conditions,” said Salk professor David Schubert, who heads the Cellular Neurobiology Laboratory.

With the help of new mass spectrometry technique and stem cells that can be made to produce either neurons or glia, the researchers led by Federico Herrera, Ph.D., a senior scientist in the Cellular Neurobiology Laboratory, identified a molecular signalling pathway that is required for the production of glial cells.

They later studied the pathway in Down’s syndrome patients and a mouse model of the condition.

The findings revealed that the level of a protein called synaptojanin-1, which is encoded in chromosome 21, is much higher in both and is strongly correlated with a greater number of glial cells.

“Given the required balance between the numbers of neurons and glia in a normal brain, an excess of glia may contribute to the cognitive deficits that characterize Down’s syndrome,” said Herrera.

Moreover, a particular part of the Synaptojanin-1 molecule was responsible for generating glia.

“This is a critical first step to identifying drugs that specifically block the excess proliferation of glial cells associated with Down’s syndrome and perhaps promote the production of more neurons,” Herrera added.

The newly identified molecular pathway may also have implications for the onset of glioblastoma, the most common and malignant type of brain tumour.

The findings are published Cell Death and Differentiation. (ANI)

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Compound used in BP drugs may benefit brain tumour patients

February 19, 2009 By Leave a Comment

Washington, Feb 19 (ANI): Researchers from at Wake Forest University Baptist Medical Centre have found that a compound used in blood pressure medication may help prevent cognitive loss after radiation therapy in brain tumour patients.

In the study conducted using a rat model, the researchers assumed that that a compound similar to the anti-hypertensive drug losartan can prevent the cognition loss that has been closely-associated with radiation therapy for brain tumour treatment.

The researchers hope that the same theory could easily be applied in a human clinical trial setting because the drug used has a long-established safety profile in patients who have taken it to treat high blood pressure.

“We need to kill cancer cells but also prevent or reduce treatment-related side effects,” said Mike E. Robbins, Ph.D., a professor in the department of radiation oncology at the Brain Tumour Centre of Excellence, part of Wake Forest University School of Medicine.

“One very interesting feature of this compound is that it has never shown any pro-tumor effects. If anything, it appears to have anti-tumor properties.

“We’re very close to having a compound that will protect the normal brain from cognitive injury as a result of radiation and, at the same time, we may very well increase the likelihood of one day curing brain cancer patients of their tumours,” he added.

Previous studies had shown that radiation may lead to the overproduction of angiotensin II (Ang II), a peptide that has been associated with decline of brain function.

Blocking the binding of Ang II to the Ang type I receptor in patients receiving radiation, researchers suggest that they could prevent or hinder cognitive decline.

In the study involving 80 rats, each group was divided in half to either receive radiation or no treatment.

Then, each of those halves was divided into two more groups: one that received L-158,809, the compound similar to losartan, in its drinking water, and one group that received plain drinking water. The rats that received the drug received it before, during and for different time intervals – 14, 28 or 54 weeks – post-radiation.

In addition, a small group of rats continued to receive the drug for only five weeks after radiation.

They found that administering L-158,809 before, during and for as little as five weeks after radiation either prevents or lessens the severity of radiation-induced cognitive impairment.

“This study provides hope that we may be able to take a drug that has been prescribed to millions of individuals with essentially very little morbidity and give it to cancer patients and stop them from experiencing cognitive impairment as a result of brain radiation,” said Robbins.

The findings appear in the International Journal of Radiation, Biology, Physics. (ANI)

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Identification of protein that amplifies cell death may revolutionise cancer treatment

January 15, 2009 By Leave a Comment

Washington, January 15 (ANI): Scientists at Albert Einstein College of Medicine of Yeshiva University have found out a protein that helps cells commit suicide, offering a potentially new way to cure cancer.

Revealing their discovery in the Journal of Biological Chemistry, the researchers said that it could lead to drugs for combating cancer and other diseases characterized by overproduction of cells.

Late Dr. Dennis Shields, a professor in Einstein’s Department of Developmental and Molecular Biology for 30 years who died unexpectedly in December, was the one who had initiated the current study.

The programmed suicide among cells is scientifically known as apoptosis. Cancer cells often become immortal and dangerous by developing the ability to suppress apoptosis.

While apoptosis had been thought to be directed solely by the nucleus and mitochondria of cells for about a decade, Dr. Shields’ laboratory showed it for the first time that a cellular organelle called the Golgi apparatus also plays a role in apoptosis.

The Einstein researchers have revealed that the Golgi package proteins and other substances made by cells, and direct them to their destination within the cell.

According to them, a protein called p115 is vital for maintaining the structure of the Golgi.

A past study led by Dr. Shields had shown that the Golgi’s p115 protein splits into two pieces early in apoptosis, and that the smaller of the protein fragments-205 amino acids in length-helps to maintain the cell-suicide process.

The current study has led to the identification of the smallest region of this p115 protein fragment that is required for apoptosis: a peptide of just 26 amino acids in length that exerts its apoptotic action by traveling to the nucleus.

“Dennis Shields was one of our most outstanding scientists. His efforts to uncover fundamental mechanisms governing how cells work has led to new ways of thinking about apoptosis, in particular, how the Golgi regulates this process,” says Dr. E. Richard Stanley, chairman of developmental and molecular biology at Einstein. (ANI)

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