Thursday, September 10, 2009

“Vitamin C can help protect DNA damage of skin cells - Newstrack India” plus 4 more

“Vitamin C can help protect DNA damage of skin cells - Newstrack India” plus 4 more

Vitamin C can help protect DNA damage of skin cells - Newstrack India

Posted: 10 Sep 2009 03:39 AM PDT

Washington, Sept 10 (ANI): Researchers at the University of Leicester and Institute for Molecular and Cellular Biology in Portugal have found that vitamin C can help protect DNA damage of skin cells and lead to better skin regeneration.

 

Previous research has shown that DNA repair is upregulated in people consuming vitamin C supplements.

 

 

In the new study, the researchers have provided some mechanistic evidence.

 

The researchers used affymetrix microarray, for looking at gene expression, and the 'Comet' assay to study DNA damage

 

"The exposure to solar ultraviolet radiation increases in summer, often resulting in a higher incidence of skin lesions. Ultraviolet radiation is also a genotoxic agent responsible for skin cancer, through the formation of free radicals and DNA damage," said lead researcher Tiago Duarte, formerly of the University of Leicester, and now at the Institute for Molecular and Cellular Biology in Portugal.

 

"Our study analysed the effect of sustained exposure to a vitamin C derivative, ascorbic acid 2-phosphate (AA2P), in human dermal fibroblasts.

 

"We investigated which genes are activated by vitamin C in these cells, which are responsible for skin regeneration.

 

"The results demonstrated that vitamin C may improve wound healing by stimulating quiescent fibroblasts to divide and by promoting their migration into the wounded area. Vitamin C could also protect the skin by increasing the capacity of fibroblasts to repair potentially mutagenic DNA lesions," Duarte added.

 

The researchers hope that the results will be of great relevance to the cosmetics industry.

 

"The study indicates a mechanism by which vitamin C could contribute to the maintenance of a healthy skin by promoting wound healing and by protecting cellular DNA against damage caused by oxidation," said Dr Marcus S. Cooke from the Department of Cancer Studies and Molecular Medicine and Department of Genetics, at the University of Leicester.

 

"These findings are particular importance to our photobiology interests, and we will certainly be looking into this further," Cooke added.

 

The findings have been published in the journal Free Radical Biology and Medicine. (ANI)

 

Plants On Steroids: Key Missing Link Discovered Could Improve ... - Science Daily

Posted: 09 Sep 2009 11:04 AM PDT

ScienceDaily (Sep. 9, 2009) — Researchers at the Carnegie Institution's Department of Plant Biology have discovered a key missing link in the so-called signaling pathway for plant steroid hormones (brassinosteroids). Many important signaling pathways are relays of molecules that start at the cell surface and cascade to the nucleus to regulate genes. This discovery marks the first such pathway in plants for which all the steps of the relay have been identified.

Since this pathway shares many similarities with pathways in humans, the discovery not only could lead to the genetic engineering of crops with higher yields, but also could be a key to understanding major human diseases such as cancer, diabetes, and Alzheimer's.

Steroids are important hormones in both animals and plants. Brassinosteroids regulate many aspects of growth and development in plants. Mutants deficient in brassinosteroids are often stunted and infertile. Brassinosteroids are similar in many respects to animal steroids, but appear to function very differently at the cellular level. Animal cells usually respond to steroids using internal receptor molecules within the cell nucleus, whereas in plants the receptors, called receptor-like kinases, are anchored to the outside surface of the cell membranes. For over a decade, scientists have tried to understand how the signal is passed from the cell surface to the nucleus to regulate gene expression. The final gaps were bridged in the study published in the advanced on-line issue of Nature Cell Biology September 6, 2009.

The research team unraveled the pathway in cells of Arabidopsis thaliana, a small flowering plant related to cabbage and mustard often used as a model organism in plant molecular biology.

"This is the first completely connected signaling pathway from a plant receptor-like kinase, which is one of the biggest gene families in plants," says Carnegie's Zhi-Yong Wang, leader of the research team. "The Arabidopsis genome encodes over 400 receptor-like kinases and in rice there are nearly 1,000. We know the functions of about a dozen or so. The completely connected brassinosteroid pathway uses at least six proteins to pass the signal from the receptor all the way to the nuclear genes expressed. This will be a new paradigm for understanding the functional mechanism of other receptor-like kinases."

Understanding the molecular mechanism of brassinosteroid signaling could help researchers develop strategies and molecular tools for genetic engineering of plants with modified sensitivity to hormones, either produced by the plant or sprayed on crops during cultivation, resulting in higher yield or improved traits. "We perhaps could engineer plants with altered sensitivity in different portions of the plant," says Wang. "For example, we could manipulate the signal pathway to increase the biomass accumulation in organs such as fruits that are important as agricultural products, an area highly relevant for food and biofuel production."

Another of the study's findings has potentially far-reaching consequences for human health. The newly identified brassinosteroid signaling pathway component shares evolutionarily conserved domains with the glycogen synthase kinase 3 (GSK3). "GSK3 is found in a wide range of organisms, including mammals," says Wang. "Our study identified a distinct mechanism for regulating GSK3 activity, different from what had been identified in earlier work. GSK3 is known to be critical in the development of health issues such as neural degeneration, cancer, and diabetes, so our finding could open up new avenues for research to understand and treat these diseases."

The research was supported by grants from the National Institutes of Health (R01GM066258), National Science Foundation (0724688), U.S. Department of Energy (DE-FG02-08ER15973), and the Herman Frasch Foundation.

New U. South Florida grade policy weeds out 'struggling' students - U-Wire.com

Posted: 10 Sep 2009 07:35 AM PDT

 

Under a new policy, University of South Florida students who are failing will be forced to switch majors if they receive three D and/or F grades in any courses needed for biomedical sciences, biology, microbiology, chemistry or medical technology majors.

The policy, which was implemented this semester, also includes pre-medical sciences students who have not declared a major.

"The new policy arose from our concern for students who are not progressing in their major," said Katharine Cole, assistant dean of Undergraduate Studies in the College of Arts and Sciences. "We want to identify struggling students and help them find a new path for success."

Patricia Muisener, assistant chair and instructor in the Department of Chemistry, said the policy opens up more seats for successful students.

"There are many high-demand courses in the sciences, and now seats won't be filled by students who are retaking a course multiple times," Muisener said.

Students who enter USF this semester and later subsequently earn three D's and/or F's in their major courses or courses supporting their major will be required to switch.

Continuing students with no D's or F's can earn up to three D or F grades before they are required to find a new major, while students who already have one or more D or F grades are only allowed two more.

Students forced to switch must choose a major outside the Department of Chemistry, Department of Integrative Biology and Department of Cell Biology, Microbiology and Molecular Biology.

Cole said students can't use grade forgiveness, which allows them to retake a course to replace a failing grade, to avoid changing majors.

"If a student fails and retakes a class multiple times, their chances of being successful are still small, because science builds on itself," she said.

Cole said very few science majors who fail general biology and chemistry classes go on to graduate.

"I've seen students who have failed general biology seven times and biology II eight times," Cole said.

Diane Te Strake, a professor in the Department of Cell Biology, Microbiology and Molecular Biology, said the new policy benefits everyone.

"I think it will help struggling students get going in the proper direction instead of doing the same thing and expecting different results," she said.

Students, who were notified of the new policy via e-mail and Blackboard, have mixed feelings about the change.

"I think it's a good policy, because it will help people re-evaluate," said Samantha Dedrick, a senior majoring in biomedical sciences. "I know people who did bad in classes and kept taking them and doing bad in them."

Kendra Broomfield, a senior majoring in biomedical sciences, said she isn't worried about the policy but thinks it is unnecessary.

"Some students might just be having trouble, and they may be forced to pursue something they have no interest in," Broomfield said.

Junior biomedical science major Sabair Pradhan said he was a little worried about the new policy, but it will motivate him to stay focused on his coursework.

"It's good for a science major, because it's hard to get into medical school with D's or F's anyway," Pradhan said.

Harvard biologists recount their shared pasts, discuss future ... - U-Wire.com

Posted: 10 Sep 2009 05:27 AM PDT

 

Nobel Prize-winning biologist James D. Watson and Pulitzer Prize-winning Biology Professor Edward O. Wilson spoke in front of a nearly 1,000-person audience in Harvard University's Sanders Theater yesterday, marking the 150th Anniversary of the publication of Charles Darwin's Origin of Species.

The two modern-day scientific luminaries discussed their storied careers—including a once-intense professional rivalry—and reflected on the future of the biological sciences.

Watson, best known for his groundbreaking discovery of the structure of DNA, began his career as a student of zoology, but later switched to the budding field of genetic biology in the early 1950s, after finding ecology "not very intellectually demanding."

Meanwhile, Wilson joined the Harvard faculty a year before Watson in 1955 in the Biology Department, and has since continued as a pioneer in the discipline, discovering scores of insect species over the course of his 60-year career.

The two famously butted heads during their concurrent 20-year tenures on the Harvard Faculty between 1956 and 1976.

Event moderator and NPR journalist Robert Krulwich did not shy away from the long-time rivalry between the two luminaries.

"They rarely spoke, and when they did it wasn't exactly lovely. These two men not only challenged each other. Together, they have challenged the way we think about biology, and the way we think about living things," Krulwich said. "Their once rather fierce rivalry has become a trusting friendship."

Watson and Wilson had once exemplified the two polarized factions of the biological sciences. Watson focused much of his career on the molecular basis of life and Wilson studied the evolution and social behavior of 'critters.'

The rivalry has lessened of late, both agreed, due in large part to the recent convergence of the two fields.

"Molecular biology had a 'bacterial' explosion...and it produced a bunch of methods and ideas that [ecologists] started grabbing hold of," Wilson said. "Meanwhile, MCB is starting to go evolutionary."

Though now reformed rivals, Watson and Wilson did attest to the critical role of ambition and competition in making scientific advances. "You have to have an enemy," Watson said.

Wilson admitted that he enjoys the thrill of the attack. During a controversial lecture on the biological basis for human nature in 1978 an audience member emptied a pitcher of water on Wilson's head.

"I was the only scientist in modern times to be physically attacked for an idea." Wilson said. "Take that Jim," he added.

As the discussion closed, Wilson addressed the complex challenges of the coming century, such as climate change and the loss of biodiversity.

"We have Paleolithic emotions, Middle Age institutions, and god-like technologies and we will be facing a point of crisis in the coming decades," Wilson said. "We have to answer huge questions of philosophy that philosophers abandoned decades ago—of who we are and where we come from rationally...or we are running a dangerous course."


Individual Cells Isolated From Biological Clock Can Keep Daily Time - Redorbit.com

Posted: 10 Sep 2009 05:41 AM PDT

Posted on: Thursday, 10 September 2009, 07:48 CDT

Alexis Webb enters a small room at Washington University in St. Louis with walls, floor and ceiling painted dark green, shuts the door, turns off the lights and bends over a microscope in a black box draped with black cloth. Through the microscope, she can see a single nerve cell on a glass cover slip glowing dimly.

The glow tells her the isolated nerve cell is busy keeping time.

Webb, a graduate fellow in the Neuroscience Ph.D. Program, working with Erik Herzog, Ph.D., associate professor of biology in Arts & Sciences; Nikhil Angelo, an undergraduate biology major; and James Huettner, Ph.D., associate professor of cell biology and physiology in the School of Medicine, has demonstrated that individual cells isolated from the biological clock can keep daily time all by themselves.

However, by themselves, they are unreliable. The neurons get out of synch and capriciously quit or start oscillating again.

The biological clock, a one-square millimeter area of the brain called the suprachiasmic nucleus, or SCN, just above the roof of the mouth and atop the crossing of the optic nerves, comprises about 20,000 neurons.

These cells, remarkably, contain the machinery to generate daily, or circadian, rhythms in gene expression and electrical activity. But the individual cells are sloppy and must communicate with one another to establish a coherent 24-hour rhythm, says Herzog.

These features make the SCN a flexible clock that can reset to stay in synch in an ever-changing environment. The underlying sloppiness is probably what allows us to adjust to local time when we cross time zones and to vary our sleep cycles with the season, say the WUSTL researchers.

The research was published the week of Sept. 7 in the online Early Edition of the Proceedings of the National Academy of Sciences.

"We've known for more than 15 years that unicellular organisms like cyanobacteria can keep 24-hour time, and isolated cells from the marine snail eye can as well," says Herzog. "But nobody was sure whether individual cells in vertebrates are circadian pacemakers."

The SCN includes many kinds of neurons that make different neurochemicals and connections within the SCN and to other parts of the brain.

"Some scientists felt that all of the cells in the SCN would be intrinsically rhythmic and that there was nothing special about any of them," says Herzog. "Some thought that none of the cells would be rhythmic and that the rhythm arose instead from their network interactions, and a third group thought specialized SCN neurons would be rhythmic and the others wouldn't be at all capable. Our experiments proved all three hypotheses wrong."

Capturing the rhythm

Webb digested slices of mouse SCN with enzymes to isolate individual neurons and then plated the cells sparsely on a dish. "The neurons will actually attach to the glass and grow," says Webb, who is in the Division of Biology and Biomedical Sciences. "And as long as you give them all of the nutrients they need, they'll live for months."

The cells had been genetically engineered to glow whenever they expressed the time-keeping gene Period 2. (The cells came from transgenic mice where the Period 2 gene had been linked to one found in firefly tails.)

The rhythmically waxing and waning glow was detected by a camera designed to capture the light from distant stars and so sensitive that it will register the passage of even a single cosmic ray.

The recordings showed that all cells seem to be able to keep a 24-hour rhythm — there are no special pacemaker cells — but they don't seem to do it all the time. Neurons that make different neurochemicals show circadian rhythms in gene expression, and none was more dependable than the others.

"Single cells sometimes will be very robust and rhythmic, but most of the time they quit or lose the rhythm," says Webb. "It appears that the network structure of the SCN is important for stabilizing these sloppy intrinsic rhythms."

To show that different kinds of SCN neurons did not have rigidly defined roles, Webb exposed SCN to the drug TTX, a pufferfish toxin that shuts down cell-to-cell communication. "In a sense we just isolated the nerve cells again," she says, "but chemically rather than physically and in a reversible way."

She washed off the TTX, and then added it again, to see if the second time the cells were exposed to the toxin, they would behave the same way.

"We found cells that changed their behavior," she says. "So the first time they were isolated, or uncoupled, with TTX, they continued to oscillate, but the second time they stopped oscillating. But we also saw the reverse: cells that were non-oscillatory becoming oscillatory."

Paradoxically the sloppiness of the clock is what makes it so precise.

"The SCN is the master clock that synchronizes other biological clocks, like your liver or your lung. Those peripheral clocks can keep 24-hour time, but not for very long," says Herzog. "Because the SCN is built differently, it can self-sustain — it can keep on ticking like a good Timex."

The researchers are now focusing on the connections that help synchronize and stabilize these biological oscillators.

By Diana Lutz, Washington University in St. Louis

---

Image Caption: Researchers at Washington University in St. Louis have shown that isolated nerve cells like this one from the biological clock are capable of keeping time, but they do a better job when there are some 20,000 other neurons around. (Washington University in St. Louis)

---

On the Net:

More News in this Category
Posted by at

0 comments:

Post a Comment

Subscribe to: Post Comments (Atom)