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Solazyme and Bunge Plan Factory to Make Oil From Algae

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Solazyme and Bunge Plan Factory to Make Oil From Algae

The promise of using algae to make biofuels - a dream scientists have chased for decades - might seem particularly welcome in a time of stubbornly high gasoline prices.


But the path to commercial-scale production has been circuitous.

Young companies have attracted investors and interest, but as they struggle to make large quantities of ethanol and biodiesel at a competitive cost, some have branched out into making oils for products with higher profit margins, like cosmetics, food and soap.

Now, one of these companies, Solazyme, is about to take a step toward large-scale fuel production. On Tuesday, it will announce an agreement with Bunge Global Innovation to build a factory in Brazil that would make triglyceride oils for both chemical and fuel products.

Under the joint venture, whose financial terms were not disclosed, the factory would rise next to Bunge’s Moema sugar cane mill and have an annual capacity of 100,000 metric tons, or about 110,250 short tons, of oil. It would start production in the second half of next year, making oils for fuel as well as additives for soaps, detergents and plastics.

Ben Pearcy, a managing director of Bunge Ltd., a global agribusiness and food company, said in a prepared statement that the partnership would “enable us to link our sugar and vegetable oil value chains,” and expand the company’s reach in fuels and chemicals. For Solazyme, which has skin care and nutritional supplement lines, the arrangement provides a boost in production capacity “to meet the strong demand we’re seeing in our initial target markets,” said Jonathan Wolfson, the company’s chief executive.

So far, the company has produced only limited quantities of biofuels, including several hundred thousand liters to the United States military, which is seeking to promote alternatives to conventional fuels.

Solazyme, which is based in South San Francisco, Calif., bioengineers its algae so that it can convert sugars directly into oils without photosynthesis. This allows the organisms to be grown in fermentation tanks, which reduces the costs of a still-expensive process.

A competitor, Sapphire Energy, announced on Monday that it had secured $144 million from investors for its demonstration plant in New Mexico. Sapphire, which does use photosynthesis in its production process, has also received a $50 million grant from the Energy Department and a $54.4 million loan guarantee from the Agriculture Department, according to the company.

Increasing height and body mass index are risk factors for ovarian cancer

Study suggests increasing height and increased body mass index are risk factors for developing ovarian cancer.

A study in this week's PLoS Medicine suggests that increasing height and, among women who have never taken menopausal hormone therapy, increased body mass index are risk factors for developing ovarian cancer.

These findings are important as in high income countries, the average height and average body mass index of women have increased by about 1 cm and 1 kg/m2 respectively per decade. These findings suggest that if all other factors that affect ovarian cancer risk had remained constant, the increases in height and weight among women would have resulted in ovarian cancer incidence increasing by 3% per decade.

The Collaborative Group on Epidemiological Studies of Ovarian Cancer, based in the University of Oxford and involving over 100 researchers internationally, reached these conclusions by analyzing individual-patient data from 47 epidemiological studies from 14 countries which comprised a total of 25,157 women with ovarian cancer and 81,311 women without ovarian cancer – virtually all the relevant data on the topic worldwide.

The researchers found a significant increase in the risk of developing ovarian cancer for every 5cm increase in height which did not vary when other factors such as age, menopausal status, smoking, alcohol consumption, having first degree relatives with ovarian or breast cancer, use of oral contraceptives, or use of menopausal hormone therapy, were taken into account. However, for body mass index, the risks depended on whether women had ever taken menopausal hormone therapy but not on 11 other factors examined.

The collaborators say: "This collaboration has brought together and re-analysed individual data from 47 studies on ovarian cancer risk associated with adult height, weight, and body mass index, that is, most of the available epidemiological information worldwide. Collectively, the findings show a highly significant increase in the risk of ovarian cancer with increasing values for each of the anthropometric variables examined."

They continue: "The increase in ovarian cancer risk with increasing height and with increasing body mass index did not vary materially by women's age, year of birth, ethnicity, education, age at menarche, parity, family history of ovarian or breast cancer, use of oral contraceptives, menopausal status, hysterectomy, or consumption of alcohol and tobacco. However use of hormone therapy for the menopause attenuated the relationship with body mass index, since an increase in ovarian cancer risk with increasing adiposity was found only in never-users of such therapy."

They add: "An advantage of seeking to review all epidemiological studies of ovarian cancer with relevant information on body size, published and unpublished, is that this helps avoid unduly selective emphasis on published results or just on some studies."

Funding: Funding for this collaborative reanalyis of original data was provided by Cancer Research UK. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing Interests: The authors have declared that no competing interests exist.

Citation: Collaborative Group on Epidemiological Studies of Ovarian Cancer (2012) Ovarian Cancer and Body Size: Individual Participant Meta-Analysis Including 25,157 Women with Ovarian Cancer from 47 Epidemiological Studies. PLoS Med 9(4): e1001200. doi:10.1371/journal.pmed.1001200

Harmless human virus may be able to boost the effects of chemotherapy

Trials show promise of human virus to treat head and neck cancer patients

A naturally-occurring harmless human virus may be able to boost the effects of two standard chemotherapy drugs in some cancer patients, according to early stage trial data published in Clinical Cancer Research.

The paper titled: Phase I/II trial of carboplatin and paclitaxel chemotherapy in combination with intravenous oncolytic reovirus in patients with advanced malignancies with first author Eleni M. Karapanagiotou from the ICR and The Royal Marsden was published in the print edition of Clinical Cancer Research on April 1.

RT3D, trade name Reolysin, is a new drug developed by Oncolytics Biotech Inc with preclinical and clinical studies conducted at The Institute of Cancer Research (ICR) and The Royal Marsden Hospital. It is based on a virus (reovirus type 3 Dearing) that is found in almost all adults' respiratory and gastrointestinal tracts without causing any symptoms.

RT3D has the ability to grow in and kill certain types of cancer cells, but does not grow in normal cells.

Previous trials injecting patients with the virus on its own showed limited effectiveness, but the team found that RT3D appeared to magnify the effects of platin and taxane-based chemotherapy on tumour cells.

Dr Kevin Harrington and colleagues in Leeds therefore started a clinical trial testing intravenous RT3D in combination with chemotherapeutics carboplatin and paclitaxel in 31 patients with advanced cancers who had stopped responding to standard treatments.

An initial Phase I study was carried out in patients with a range of advanced cancers, which showed the drug combination was safe. Side-effects were found to be generally mild, and consistent with chemotherapy alone.

Patients with head and neck cancers were found to have the best responses, so a Phase II expansion study at The Royal Marsden Hospital, London, and St James's Hospital, Leeds, was therefore targeted to patients with these types of cancers.

Cancers shrank for about one third of the patients who could be evaluated, and disease stabilised for a further third. For one patient, all signs of their cancer disappeared.

"We saw really very impressive response rates in these patients. These are patients whose cancers had grown despite a great deal of previous treatment, including platinum-based chemotherapy for many," Dr Harrington, Leader of the ICR's Targeted Therapy Team and Consultant Oncologist at The Royal Marsden, said. "Under those circumstances, we'd expect that the average response rate to chemotherapy alone might be as low as single digits figures and the average survival would be somewhere between three to four months. In our Phase I/II study we show this had been prolonged to an average of seven months, albeit not in a randomised trial."

"Based on the results of this study we've now started recruiting patients with advanced head and neck cancer to a randomised Phase III trial, in which all patients will receive chemotherapy and half will receive Reolysin as well. We are extremely excited about this progress."

The study also found the virus was not shed after treatment. This means people could be given the drug as outpatients as no risk was found that they could transmit the virus to others.

Stopping the spread of a deadly childhood bone cancer

Many children with the bone cancer, osteosarcoma, die after the tumor spreads to their lungs

CHICAGO -. In a critical step toward finding a way to stop metastasis, researchers at Georgetown Lombardi Comprehensive Cancer Center say they have discovered an agent that prevents this type of cancer from spreading to the lungs in mice with the disease.

The new agent stops or inhibits "ezrin," a protein vital to the spread of osteosarcoma, say the researchers who presented their findings today at the American Association for Cancer Research (AACR) Annual Meeting 2012. If proven effective in human studies, their ezrin inhibitor might potentially treat adults whose cancers are fueled by over-expression of this protein, and could be a life-saver for children with bone tumors.

"If we can prevent metastatic disease in osteosarcoma, we will significantly improve survival and quality of life for these patients," says the study's senior investigator, Aykut Üren, M.D., an associate professor of oncology, and of biochemistry and molecular & cellular biology at Georgetown Lombardi Comprehensive Cancer Center.

The molecule they discovered represents the first-in-class ezrin inhibitor, he says. "In addition to its potential clinical application, an ezrin inhibitor will be an extremely valuable tool in the laboratory as we work to better understand how ezrin works."

Ezrin is present in many types of cells in the body including cancer cells. It controls how the cell interacts with its environment, how the cell moves and how it survives in new locations.

In osteosarcoma, the tumor cells that produce high levels of ezrin are more aggressively invasive, Üren says. "Ezrin also helps cancer cells survive when they reach the lungs. If an osteosarcoma cell with no ezrin spreads to the lung, it can't grow there. Having too much ezrin makes it easier for cancer cells to move to the lungs and, once there, it gives these cells a growth advantage."

Osteosarcoma most commonly develops around knee and shoulder joints in children and is "relatively easy to treat the tumor on the limbs, but when the lungs are involved, patients usually die due to pulmonary insufficiency," he says.

If successfully developed, an ezrin inhibitor may be useful in preventing the spread of other tumors, too. Breast cancers, colon cancers, melanoma, ovarian carcinoma, brain tumors, and soft tissue sarcomas all show evidence that too much ezrin may mean poor survival outcomes for the patient, says Üren.

Üren and his research team are currently testing several novel compounds in other disease models, including rhabdomyorsarcoma (tumors of the skeletal muscles). They also are making derivatives of several compounds to further increase effectiveness. Some of these new derivatives are also presented the same annual meeting of the AACR today.

"Although we feel we have made a great discovery towards establishing a novel targeted therapy, we are far from our ultimate goal of using this in humans," Üren says.

Other investigators on this work include Jared T. Murdoch, Sung-Hyeok Hong, Gulay Bulut, George W. Kosturko, Lauren E. Drebing, and Jeffrey A. Toretsky, all of Georgetown Lombardi. The authors also wish to thank Milton Brown and Mikell A. Paige for their contributions.

The study has been funded by a peer reviewed grant support from The Children's Cancer Foundation® of Baltimore, Md. and the Department of Defense.

Üren, Bulut, Kosturko, Toretsky, Brown and Paige are named as co- inventors on a patent application that has been filed by Georgetown University related to technology described in this abstract.

Uganda's nodding disease: 'I've lost hope'

In the north of Uganda, thousands of children have fallen ill with a fatal, incurable disease known as nodding disease.

Communities are starting to panic and some people are losing hope as the medical community struggles to either find a cause or a cure, as the BBC's Will Ross reports.

Driving through villages of Uganda's northern Kitgum district it is staggering how many families have been affected by the debilitating nodding syndrome. In Tumangu village it is like a plague.

Francis Anywar sits in front of the grass thatched home. The 15-year-old is naked and appears to be in another world - never speaking. The scars on his head point to the violent seizures that strike several times a day. Francis's health started deteriorating eight years ago and both his physical and mental development have steadily been eroded.

Tied to a tree

A few hundred metres further down the dirt road a mother tells me something I will never forget.

"I've lost hope. I'm just taking care of Sarah and Moses like flowers in the home knowing they are of no use in the future," Betty Olana says. Because of the neurological syndrome, her 14-year-old daughter and 12-year-old son look much younger and need round-the-clock care. They cannot wash themselves or get dressed without help. "When I go off to farm I tie them to the tree so they don't get injured.

"If they walk off they don't know where they are going they just keep walking and get lost."

One nurse told me that when the children develop psychosis and wander off into the bush they often do not return home. She said hunger can then kill them and mentioned incidents of dogs carrying the bodies of dead children back to a village.

When Ms Olana brings out a tray of millet porridge and stew, Sarah and Moses wash their hands and tuck in. But within minutes Moses's head starts to drop, his eyes close and as if in a trance he appears to be drifting off into another world. Food, heat and cold weather are the triggers.

There are more than 3,000 reported cases in northern Uganda and the government has now set up nodding syndrome screening centres at health centres. However, due to deep poverty, many families cannot afford to pay for the transport. Others like Ms Olana have simply given up on their children.

Ojok Samuel sits at the clinic staring into space. He is nine but looks three or four. "He started nodding his head at the age of two whenever we gave him food," his father John Oboda says, adding that the stress on the family has affected his own health. Unable to farm, because he always has to care for the children, the family is slipping deeper and deeper into poverty.


The cause of nodding disease, which causes wastage of the brain tissue, abnormal brain waves and seizures, remains unknown.

One theory is that it is connected to infection with a parasitic worm carried by the black fly - already known to cause river blindness.

In an outbreak in 2004, more than nine out of 10 children who showed symptoms were found to be harbouring the parasite.

It is possible that infection with the parasite triggers the immune system to over-react, and to inflict damage on the brain and nervous system.

However, scientists have been unable to explain why Nodding disease does not occur in some areas where the worm is common.

Other theories have linked the condition to exposure to toxic chemicals, contaminated meat, a lack of a form of vitamin B and psychiatric problems.


He has also brought his 10-year-old daughter Jaqueline Amony who now suffers regular seizures, which have affected her mental ability. Neither of these children are going to school and most worrying for Ojok is that they have not shown any sign of improvement since beginning medication to control seizures a year ago.

There is also stigma. "Neighbours don't allow their children to interact with Samuel and Jaqueline. Our family is now isolated." I am told some motorbike taxis have been refusing to carry affected children.

Cases were seen in Tanzania back in the 1960s and in recent years in South Sudan. Despite its devastating impact, health officials have been left baffled as they try to find the cause and the cure.

Some of the symptoms are similar to epilepsy and health workers prescribe the anti-convulsant medicine carbamazepine, which is used to manage epileptic seizures.

In northern Uganda they have just started trying out a new drug, sodium valproate, which is also used to treat epilepsy. The medical staff point out that when brought to hospital and given the medication some children improve and suffer less frequent seizures. But, sadly, by this stage the damage to the child's development has already been done and cannot be reversed.

In November 2009, the Ugandan government requested help from the US-based Centers For Disease Control and Prevention. CDC experts have visited the affected area and taken away samples to test but they are struggling to find the underlying cause.

"The CDC teams documented for the first time that Nodding Syndrome is a novel complex epilepsy syndrome, and that the head nodding was a direct manifestation of seizures that cause a brief lapse in muscle tone due to alterations in brain function," the public health organisation says.

"Children living under the poorest conditions where there is not enough food, pure water, or decent housing seem most susceptible to this condition."

The last time I was in Kitgum hospital in 2004 it was a nightly refuge for thousands of children who could not sleep at home for fear of abduction by the Lord's Resistance Army rebels. Northern Uganda is now peaceful but the families and health workers tell me that they feel like they are fighting a new war.

"We are getting stressed dealing with this traumatic situation. You see new cases every day - children having fits, others falling down. As a human being you feel the pain," says Adong Josephine, a psychiatric nurse in Kitgum hospital. "Even me I have started to develop stress on seeing these patients. You don't know what really causes the problem," Ms Josephine says.

"You put yourself into the shoes of these parents. Supposing these were my children; what if the problem comes to my family; where will I be? Where will I go?"

"So many have died and others are still at the critical stages of dying because when you look at them - some are too wasted unable to eat unable to walk. If they are not brought to the hospital they are most likely to die in some days to come," she adds.

On the ward are two badly burnt children. The cooking fire at home is a death trap for the affected children because when a seizure strikes they are unable to move away from the flames.

Outside at the screening centre 13-year-old Augustin Oola goes into spasms as a nurse tries to get him to stand up. He only appears moderately comfortable when he is allowed to flop on the floor where he sits silently.

With no known cause or cure speculation is rife. "It could be an effect of the war. There were many deaths around this area - many people were killed. So maybe it is their spirit which is making these children sick," suggests Ms Olana, whose home is in an area the LRA rebels used as a base. "We see many people coming now to try to investigate. So we have a little bit of hope. We are praying that these children will be cured."

Are DNA Patents Doomed?

DNA is special. Unlike other body parts, it holds information. Even discarding a blood spot or saliva sample doesn’t necessarily prevent the telltale DNA sequences from living on in a database.

By Ricki Lewis | April 3, 2012

We guard our DNA data in a way that we don’t other test results, such as cholesterol levels. “Genes are uniquely ‘ours.’ They say something about us at some fundamental level, more than a mammogram or a Pap smear or an x-ray,” said James Evans, MD PhD, professor of genetics at the University of North Carolina, Chapel Hill, at a symposium on DNA patenting at the International Congress of Human Genetics in Montreal in October 2011.

Our emotional attachment to our genomes may be part of why the patentability of the breast and ovarian cancer susceptibility genes BRCA1 and BRCA2 has been pinging from court to court for years. The latest chapter: on March 26, the U.S. Supreme Court asked the U.S. Court of Appeals for the Federal Circuit, which had upheld the Myriad Genetics and University of Utah’s patents on the two genes, to reconsider.

This move, many think, stemmed from the March 20 invalidation of Prometheus Laboratories patents on measuring levels of a metabolite to assess whether a dosage of 6-mercaptopurine to treat inflammatory bowel disease is too low to work or high enough to cause adverse effects, procedures that the court found “add nothing specific to the laws of nature other than what is well-understood, routine, conventional activity.” Patents for cancer genes useful as a diagnostic may seem to have little to do with measuring a metabolite to adjust a dosage, but, at the risk of evoking a double negative, they share a lack of “non-obviousness,” one of the key requirements of a patentable invention.

Cervixes and Spleens Led the Way

The two most famous cases of body parts exploited for profit – Henrietta Lacks’s wild cancer cells and John Moore’s celebrated spleen – can’t match the power in the 3-billion-bit identifier that is a human genome.

HeLa cells originated in the cervix of a poor, uneducated African-American woman. In 1951 Henrietta Lacks’s unusually prolific cells were sampled, cultured, and sent to labs all over the world, without her or her family’s knowledge.

John Moore gave up his swollen spleen in 1976 to treat his leukemia, unaware that his physician, hospital, and a biotech company would patent the cells and sell an unusual protein that they produced. Moore sued, but the California Supreme Court ruled against him, finding that removed cells are not the equivalent nor the product of a person.

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