Chips on the left are from potatoes infected with the zebra chip disease, which alters the sugar levels and causes the sugar to carmelize and give a burned appearance, according to Dr. Don Henne, Texas AgriLife Research assistant research scientist.

Credit: (Texas AgriLife Research photo by Kay Ledbetter)
Dr. Don Henne isn't wasting his degree when he's standing by the deep fryer waiting for potato slices to turn brown. He's conducting research that will help the potato industry and consumers.

Henne, an assistant research scientist in the Texas AgriLife Research plant pathology program in Amarillo, is one of a number of who are trying to find answers about zebra chip. Zebra chip is the latest disease to plague the potato industry, particularly those in the chipping business.

Dr. Charlie Rush, AgriLife Research plant pathologist and leader of the program, began working on the project at the request of local producers in early 2007. His work later became a part of the Zebra Chip State Initiative through the Texas Department of Agriculture.

The initiative brought together scientists from throughout the state and country to try to find answers for zebra chip, Rush said.

"When we first began working on it, the pathogen and vector were unknown," he said. "Only recently have scientists began pinning those down".

Rush said Henne was brought into the program in May because of his experience and background. His primary responsibility is to help understand the factors that impact disease onset and spread. Zebra chip is a disease that alters the sugar levels in the potato, Henne said. The sugar caramelizes and turns the chip brown when it is fried, giving it an off taste and burnt appearance. While it is not harmful, it is a cosmetic and taste concern for consumers.

Potato growers have had to abandon entire infected fields, costing as much as $2 million a year in damage, he said.

Henne, who has a degree in entomology, is trying to chase the potato psyllid, the insect that likely carries the pathogens which cause the disease. He is trying to find out what makes it move through a field, as well as when it moves and how fast.

He has visited grower fields from Weslaco to Pearsall and Olton to Dalhart already this year, as well as made contact with other zebra chip scientists around the nation to familiarize himself with this new chipping potato disease.

Zebra chip first appeared in Mexico and Guatemala in the early 2000s. It has been found in potato fields through South Texas and the Rio Grande Valley and now up into the South Plains and Panhandle regions.

The disease presents itself as curled leaves and stunted growth in the plant itself, and then the tubers exhibit a brown striped or mottled pattern when sliced, Henne said.

AgriLife Research and other researchers around the country have studied the vector or insect that transmits the pathogen, he said. Others are trying to identify the pathogen or bacteria that actually causes disease in the plant when the psyllid feeds on it.

Henne and other Amarillo-based scientists are working with commercial growers to monitor the movement of the insect and disease appearance. At the same time, they have established potato plots at the Texas AgriLife Research Station at Bushland and are doing some greenhouse work.

"We're focusing on the epidemiological aspects of the disease," Henne said. "We are trying to understand how the disease progresses in a potato field over time. We are looking at canopy structure, edge effect and how the insects are landing in fields and distributing the disease".

Henne and Dr. Fekede Workneh, an AgriLife Research quantitative plant disease epidemiologist, have planted six acres of potatoes at the Bushland station where they are looking at planting dates, canopy structure and insect dispersal.

Potatoes are planted in late March to early June in the Panhandle, so they are experimenting with planting dates May 2, May 28 and June 16 at Bushland to see if there is a relation between insect movement and disease severity.

"We are also working in the lab to graft diseased portions onto healthy plants to understand the movement of the disease through the plant," Henne said.

"We want to understand how the disease progresses so we can focus management practices on specific areas," he said. "Do the insects move up the plant, down or out from the stem? Some varieties have more canopy than others and is that acting as a natural bridge for insect movement?".

There is no adequate control for the insect or the disease at this time, he said.

Because there are other diseases that have similar symptoms as zebra chip, Henne said, one of the challenges they face is being able to correctly identify diseased plants in the field.

"When we find plants that appear to be infected, we bring the tubers back to the lab where they are sliced and fried to make the final determination," he said.

Henne said they hoped to have some management suggestions on how to help alleviate the problem for growers by the end of this year.


Posted by: Evelyn    Source

Scientists at the University of Minnesota have discovered a gene that may provide a clue as to why obesity rates increase with age. The research was published recently in the Proceedings of the National Academy of Sciences
Scientists in the lab of Kevin Wickman, Ph.D., associate professor of pharmacology at the University of Minnesota Medical School, removed a single gene from mice as part of a research study that's ongoing to understand how the brain controls heart function. While some cardiac deficiencies were detected in these mice, the scientists unexpectedly observed that these mice exhibited a predisposition to adult-onset obesity.

"This was not an outcome we expected, but now we have an animal model that may provide new insight into human obesity," said Wickman, co-author of the article.

By examining closely where this gene, termed Girk4, is expressed in the body, the scientists found especially high levels in the hypothalamus, a brain region involved in regulating food intake and energy expenditure. Wickman speculated that disruption of normal function in the hypothalamus may underlie the obesity seen in the mutant mice, but he acknowledges that more studies are needed to understand where and how this gene works, and consequently, why mice missing this gene develop obesity.

The age-dependence of the obesity seen in this mouse model mimics human obesity patterns, scientists said. Indeed, the likelihood of people developing obesity more than doubles between the ages of 20 and 60.

"This is a novel finding that may provide important new insight to the underlying cellular mechanisms that influence obesity," said Catherine Kotz, Ph.D., co-author of the article, scientist at the Minneapolis VA Medical Center and adjunct professor in the Department of Food Science and Nutrition at the University of Minnesota.


Posted by: Evelyn    Source

HOUSTON -- (July 16, 2008) -- The burial service for Dr. Michael E. DeBakey will be at 10 a.m. Friday, July 18, at Arlington National Cemetery.

The memorial service is today, July 16, at 1 p.m. at Co-Cathedral of the Sacred Heart, 1111 St. Joseph's Parkway. The service is open to the public.

HOUSTON -- (July 15, 2008) -- Overweight mothers give birth to offspring who become even heavier, resulting in amplification of obesity across generations, said Baylor College of Medicine researchers in Houston who found that chemical changes in the ways genes are expressed – a phenomenon called epigenetics -- could affect successive generations of mice.

"There is an obesity epidemic in the United States and it's increasingly recognized as a worldwide phenomenon," said Dr. Robert A. Waterland, assistant professor of pediatrics – nutrition at BCM and lead author of the study that appears in the International Journal of Obesity. "Why is everyone getting heavier and heavier? One hypothesis is that maternal obesity before and during pregnancy affects the establishment of body weight regulatory mechanisms in her baby. Maternal obesity could promote obesity in the next generation."

Waterland and his colleagues studied the effect of maternal obesity in three generations of genetically identical mice, all with the same genetic tendency to overeat. One group of mice received a standard diet; the other a diet supplemented with the nutrients folic acid, vitamin B12, betaine and choline. The special 'methyl supplemented' diet enhances DNA methylation, a chemical reaction that silences genes.

"We wanted to know if, even among genetically identical mice, maternal obesity would promote obesity in her offspring, and if the methyl supplemented diet would affect this process," said Waterland. "Indeed, those on the regular diet got fatter and fatter with each generation. Those in the supplemented group, however, did not."

"We think DNA methylation may play an important role in the development of the hypothalamus (the region of the brain that regulates appetite)," said Waterland.

"Twenty years ago, it was proposed that just as genetic mutations can cause cancer, so too might aberrant epigenetic marks – so called 'epimutations.' That idea is now largely accepted and the field of cancer epigenetics is very active. I would make the same statement for obesity. We are on the cusp of understanding that," he said.

Waterland is also a researcher at the USDA/ARS Children's Nutrition Research Center at BCM and Texas Children's Hospital. Others who contributed to this research include Kajal Tahiliani, Marie-Therese Rached and Sherin Mirza of Baylor College of Medicine and the USDA/ARS Children's Nutrition Research Center in Houston and Michael Travisano of the University of Minnesota in St. Paul.

Funding for this work came from the National Institutes of Health, the March of Dimes Birth Defects Foundation and the U.S. Department of Agriculture.

The report is available at http://www.nature.com/ijo/index.html.

For more information on basic science research at Baylor College of Medicine, please go to http://www.bcm.edu/fromthelab/.

HOUSTON -- (July 11, 2008) -- On behalf of the entire Baylor College of Medicine and The Methodist Hospital families, it is with profound sadness that we announce the death of pioneering heart surgeon Dr. Michael E. DeBakey. The college, the hospital, and indeed the entire world, have lost a great man today.

Dr. DeBakey died at 9:38 p.m. Friday, July 11 from natural causes at The Methodist Hospital in Houston.

In a career spanning more than 70 years, Dr. DeBakey performed more than 60,000 heart surgeries. Other surgeons have used his innovations in cardiovascular surgery worldwide to save the lives of countless millions.

"Dr. DeBakey's reputation brought many people into this institution, and he treated them all: heads of state, entertainers, businessmen and presidents, as well as people with no titles and no means," said Ron Girotto, president of The Methodist Hospital System. "He always said that Methodist is a hospital with a soul ... and for more than 50 years, Dr. DeBakey has been the heart and soul of Methodist."

"He has improved the human condition and touched the lives of generations to come," continued Girotto. "We will greatly miss him."

"With each passing year, Dr. DeBakey continued to provide great wisdom to those who sought his counsel," said Dr. Peter G. Traber, BCM president. "As Baylor College of Medicine's first President, he set a standard for preeminence and never let anyone here forget the importance of leadership in academic medicine. We have lost a man who was a great physician, educator, leader and above all, a great friend."

"We will miss him, but we will honor his memory by continuing to excel in those things he taught us," Traber said.

"Dr. DeBakey singlehandedly raised the standard of medical care, teaching and research around the world," said Dr. George Noon, a cardiovascular surgeon and longtime partner of DeBakey's. "He was the greatest surgeon of the 20th century, and physicians everywhere are indebted to him for his contributions to medicine."

"Dr. DeBakey was an incredible man and his contributions to medicine are unmatched," said Dr. Bobby R. Alford, Chancellor of Baylor College of Medicine and Chairman of the Department of Otolaryngology at Baylor and The Methodist Hospital. "He was a dear friend and colleague for more than 40 years. He will be missed dearly."

For more information on the legacy of Dr. Michael DeBakey, visit www.bcm.edu and www.methodisthealth.com. Photographs and video are available on the websites, and by contacting Lori Williams at 713-775-6912 or 713-798-4710 or Denny Angelle at 832-667-5807 or 832-667-5807.