all biomedical engineering stories

Panel investigates media reporting on science and politics of stem cells

jake — Mon, 29 Oct 2007 11:21:33 -0400

Stem cells, politics, "fairness," and what one participant termed "the disintegration of traditional journalism," were all on the bill at Thursday night’s (Oct. 18) public forum titled "Stem Cells and the Media," hosted by the Harvard Stem Cell Institute.

A panel of four science journalists who have extensively covered the stem cell "story" gathered in the Radcliffe Gym to discuss and debate the challenges and complexities of stem cell research coverage by the mainstream media.

"This is the most political issue in science," said William Saletan, a national correspondent for Slate magazine.

Man-made medical mystery gets second solution

50443248 — Mon, 01 Oct 2007 17:04:10 -0400

Researchers have created a new material that they believe improves on an eight-year-old solution to a decades-long medical mystery over the cause of widespread artificial joint failure.

The new material, developed at Harvard-affiliated Massachusetts General Hospital (MGH) and implanted for the first time July 19, could help fill the demand for higher-performance joints from a new generation of patients.

Manipulating genetic switch in mice eases MD symptoms

Tue, 10 Jul 2007 15:57:40 -0400

Scientists at Dana-Farber Cancer Institute have shown in a laboratory study that revving up a crucial set of muscle genes counteracts the damage caused by a form of muscular dystrophy.

Reporting in the April 1 issue of Genes and Development, the researchers demonstrated that manipulating a genetic molecular switch increased the genes’ activity in the muscles of mice with Duchenne muscular dystrophy, slowing the disease-associated muscle wasting. The authors caution that they have not yet found a way to tweak the switch, known as PGC-1alpha, in humans.

Genome-wide map will help fight diabetes

Wed, 11 Jul 2007 10:57:51 -0400

The Broad Institute of MIT and Harvard, Lund University, and Novartis have announced the completion of a genome-wide map of genetic differences in humans and their relationship to type 2 diabetes and other metabolic disorders. All results of the analysis are being made accessible, free of charge, on the Internet to scientists around the world.

The work is the result of a pioneering public-private collaboration known as the Diabetes Genetics Initiative (DGI), which was formed in 2004 and is aimed at deciphering the genetic causes of type 2 diabetes. The collaboration brings together diverse expertise in diabetes and metabolic disease, human genetics, genomics, statistical analysis, and drug development.

"These discoveries are but a first step. To translate this study's provocative identification of diabetes-related genes into the invention of new medicines will require a global effort. We hope many will race to do so," said Mark Fishman, president of the Novartis Institutes for BioMedical Research. "We hope as well that others adopt this novel and effective mode of open collaboration between scientists and physicians, in business and academia, and dedicate work to our patients by making the data quickly and freely available to all."

Type 2 diabetes and related cardiovascular risk factors, including obesity, high blood pressure, and high cholesterol, are among the most common and significant public health challenges in the industrialized world. Their incidence continues to climb despite advances in biomedicine, highlighting the need for new insights into the disorders' root causes and novel strategies for prevention and treatment. Although type 2 diabetes clearly runs in families, suggesting the importance of inherited factors, its genetic origins remain largely unclear.

DGI is an international collaboration of the Broad Institute of MIT and Harvard, Lund University, and Novartis. Collaborators include scientists from the Jackson Heart Study and the University of Southern California. The Broad Institute team includes scientists from its partner institutions, which include Harvard Medical School, Massachusetts General Hospital, and Children's Hospital Boston.

Muscle cells grown into working heart cells

Fri, 13 Jul 2007 09:32:26 -0400

Muscle cells have been used successfully to restore life-sustaining rhythms to ailing hearts, a first step toward developing natural pacemakers. Placed in a tiny raft of collagen implanted into the hearts of rats, these cells survived for the entire lifespan of the animals.

"Our experiments provide proof that engineered tissue can function as an electric conduit in the heart and, ultimately, may offer a substitute for artificial (electronic) devices," says Douglas Cowan. He is an assistant professor of anesthesiology at Harvard Medical School who led a team of biologists, cardiologists, and surgeons at Children's Hospital Boston to create a biological substitute for the tissue that keeps the heart beating regularly.

First edition of HapMap released

70652986 — Mon, 26 Mar 2007 05:41:20 -0400

A flurry of high-profile scientific manuscripts published in October 2005 describe both the content and uses of HapMap, a catalog that maps human genetic variation and relates it both to disease and to human evolutionary history. HapMap gives scientists worldwide a first good look at the "order in variety" that is the human genome.

All these studies are grounded in data presented in a significant paper published in the Oct. 27, 2005 issue of the journal Nature by an international consortium of more than 200 researchers from Canada, China, Japan, Nigeria, the United Kingdom and the United States. In this paper, the authors describe the patterns of genetic variation in hundreds of human DNA samples collected from four sites around the world.

Perhaps the most striking finding in this mountain of data is the overwhelming evidence for previous work that suggested that human genetic variants located physically close to each other in the genome are collectively inherited as groups, or "haplotypes." The comprehensive catalog of human genetic variation, now known as the "HapMap", is publicly available to the biomedical research community. The implications - and potential value - of the genome's haplotype structure for medicine has only begun to be realized.

"Built upon the foundation laid by the human genome sequence, the HapMap is a powerful new tool for exploring the root causes of common diseases. We absolutely require such a resource so that we can develop new and much-needed approaches to understand these diseases, such as diabetes, bipolar disorder, cancer and many others, " said David Altshuler, director of the program in Medical and Population Genetics of the Broad Institute of Harvard and MIT and associate professor of genetics and of medicine at Massachusetts General Hospital and Harvard Medical School. Altshuler and Peter Donnelly, of the University of Oxford in England, are the corresponding authors of the Nature paper.

Adult cells transformed into stem cells

70652986 — Mon, 26 Mar 2007 06:22:02 -0400

Harvard researchers fused adult skin cells with embryonic stem cells in such a way that the genes of the embryonic cells reset the genetic clock of the adult cells, turning them back to their embryonic form.

Such adult-cum-embryo cells, taken from people with juvenile diabetes, Parkinson's, Alzheimer's, and other genetic diseases, could reveal how such diseases develop and provide novel treatments for them. For example, normal cells might be made to replace abnormal ones that cause juvenile diabetes and Alzheimer's disease. It should be possible to coax these newly created embryonic cells "into replacement cells and even organs," says biologist Chad Cowan who participated in the experiments. "But it would definitely not be possible to clone the person from which the adult cell came."

Cowan is the lead author of a report of the research published in the Aug. 26 issue of Science. The other authors are Kevin Eggan, Douglas Melton, and Jocelyn Atienza of the Harvard Stem Cell Institute.

Protein reverses engineering of chromosome structure

70652986 — Mon, 26 Mar 2007 05:36:35 -0400

An enzyme, a histone demethylase, removes methyl groups appended to histones, nuclear proteins that organize DNA and regulate gene activity. Methyl groups and other chemical tags on histones regulate how the DNA wraps around the proteins to form a chromatin structure that either promotes gene activity or represses it. Chromatin, which contains DNA, RNA, and various proteins, is the substance that constitutes chromosomes. Professor Yang Shi and his colleagues discovered the demethylase during functional studies of novel gene repressor proteins. The enzyme, dubbed LSD1 for lysine specific demethylase 1, turns off gene activity by removing one particular methyl tag that normally functions as a green light for gene activity. Cells engineered to lack LSD1 accumulated methylated histones and turned on genes that were previously silent. In some tumors, addition of methyl groups at LSD1's target lysine seems to play a role in aberrant activation of genes that drive cell growth, suggesting that LSD1 might be useful to counteract this progrowth signal. "Previously, people thought that histone methylation was stable and irreversible," said Shi. "The fact that we've identified a demethylase suggests a more dynamic process of gene regulation via methylation of histones. The idea of yin and yang is universal in biology; our results show that histone methylation is no different."

War stories of a soldier/scientist

705287540 — Tue, 06 Nov 2007 11:08:57 -0500

Kit Parker's 9 mm pistol lay on the table next to the laptop as he typed. He was stripped to the waist in the 130-degree heat, sweating and writing while he waited for a flight home from Afghanistan.

After 10 months on patrol for the U.S. Army south of Kandahar, Parker's other life was demanding attention. He had a grant proposal due Aug. 22.

"It was miserable," Parker said of the heat, the stress of making the deadline, and the need to get cracking at a time when most soldiers would be thinking of finally relaxing. "But I dig my science."

Wine molecule slows aging process

70652986 — Mon, 26 Mar 2007 05:30:12 -0400

Called resveratrol, a wonder substance discovered by Harvard researchers seems to work in the same way as does drastic calorie cutting. Dramatic reduction of calories has been shown to increase the life span of mice, rats, and monkeys. Such diets are being tried in humans but results are not yet in. Severe dieting also cuts the risk of dying from cancer, heart problems, and other age-related diseases in monkeys. If resveratrol and related molecules are found to work as well in humans, we could gain extra years of healthy life without starving for them. We could have our cake and eat it, too. "The discovery brings closer a time when a drug that extends life and prevents many diseases of aging becomes a reality," says David Sinclair, who leads the research at Harvard Medical School. "I'm not a doctor so I can't speculate on how much wine to drink, but I've increased my consumption since we made the discovery." Physicians recommend a glass or two of red wine a day as part of a heart-healthy diet. No one would advise nondrinkers to starting gulping red wine until better information about its anti-aging effect becomes available.

Students develop system to fight TB

70652986 — Mon, 26 Mar 2007 05:23:46 -0400

A new system developed by Harvard undergraduates delivers anti-tuberculosis drugs through an inhaler, increasing the likelihood that patients will take them over longer periods, and reducing the side effects of pills and injections. To test and market the system, the group has formed a nonprofit corporation called MEND (MEdicine in NeeD). "It's the beginning of an effort to bring new technology from the labs and classrooms of Harvard to patients by the quickest means possible," according to David Darst, a 21-year-old junior.

Researchers isolate key part of cells' 'death' signals

70652986 — Mon, 26 Mar 2007 05:24:58 -0400

In the cover article of the September 2002 issue of the journal Cancer Cell, researchers from Dana-Farber Cancer Institute reported that peptide subunits of cell-signaling "BH3" proteins could out-maneuver opposing "anti-death" proteins and trigger the suicide process. Cell suicide or "apoptosis" prevents wayward cells from growing out of control and becoming cancerous. "Many cancer cells may stay alive due to the overexpression of anti-death proteins," said Dana-Farber's Anthony Letai, lead author of the paper and an instructor in medicine at Harvard Medical School.

New way to 'see' DNA

70652986 — Mon, 26 Mar 2007 05:14:23 -0400

Research by Harvard scientists was driven by the need to make extremely small holes that mimic the pores in human cells through which different molecules must pass to keep the cells alive and healthy. "My colleagues and I first had the idea of sequencing genes by forcing DNA molecules through minute openings," explains David Branton, Higgins Research Professor of Biology. Branton teamed up with Jene Golovchenko, professor of physics and applied physics at Harvard, who came up with the idea of making the holes in solid materials. "We have discovered how to move atoms across a surface with such high precision and control that we can make structures to detect and analyze particles as small as a single molecule of DNA," says Golovchenko.

Potent cancer drugs made from sea squirts

70652986 — Mon, 26 Mar 2007 05:08:17 -0400

In May 2000, researchers at Harvard University announced that they had succeeded in synthesizing a complex anti-tumor drug that is more powerful than any other known drug. The drug, ecteinascidin, is so potent that a mere 11 pounds of it should be enough to satisfy the present world demand for an entire year, Elias J. Corey estimated. "I believe it's the most complicated molecule ever made on a commercial scale," said Corey, winner of the 1990 Nobel Prize in chemistry, in whose laboratory the compound was first fashioned. Ecteinascidin (ek-TIN-aside-in) is being tested on terminally ill patients suffering with cancers of the blood vessels, tendons, muscles, and other soft tissues. "That's the most striking result so far," adds Corey.

Researchers switch cancer off and on in mice

70652986 — Mon, 26 Mar 2007 05:08:53 -0400

An antibiotic added to the drinking water of mice stops the progress of leukemia. Harvard researcher Claudia Huettner cannot do the same thing in humans, unfortunately, but through such experiments Huettner and her colleagues are gaining an understanding of how human leukemias arise. The new knowledge they have gained is providing them with a means to easily test new treatments for cancer. For example, new drugs are being developed to prolong the lives of people with acute lymphoblastic leukemia (ALL), the most common bone marrow cancer in children. Experiments with mice that get an equivalent disease in the same way as children with ALL do – by genetic mutation – could speed up testing of these and other therapies designed to prolong the lives of ALL patients.