Follow along with the video below to see how to install our site as a web app on your home screen.
Note: This feature currently requires accessing the site using the built-in Safari browser.
A new type of antibiotic can effectively treat an antibiotic-resistant infection by disarming instead of killing the bacteria that cause it. Researchers report their findings in the October 2 issue of mBio, the online open-access journal of the American Society for Microbiology.
"Traditionally, people have tried to find antibiotics that rapidly kill bacteria. But we found a new class of antibiotics which has no ability to kill Acinetobacter that can still protect, not by killing the bug, but by completely preventing it from turning on host inflammation," says Brad Spellberg of the UCLA Medical Center and David Geffen School of Medicine, a researcher on the study. New drugs are badly needed for treating infections with the bacterium Acinetobacter baumannii, a pathogen that most often strikes hospital patients and immune- compromised individuals through open wounds, breathing tubes, or catheters.
The bacterium can cause potentially lethal bloodstream infections. Strains of A. baumannii have acquired resistance to a wide range of antibiotics, and some are resistant to every FDA-approved antibiotic, making them untreatable. Spelling and his colleagues found that in laboratory mice it was possible to mitigate the potentially lethal effects of the bacterium by blocking one of its toxic products rather than killing it. "We found that strains that caused the rapidly lethal infections shed lipopolysaccharide [also called LPS or endotoxin] while growing. The more endotoxin shed, the more virulent the strain was," says Spellberg. This pinpointed a new therapy target for the researchers: the endotoxin these bacteria shed in the body.
An international team of scientists have identified for the first time a key factor responsible for declining muscle repair during aging, and discovered how to halt the process in mice with a common drug
An international team of scientists have identified for the first time a key factor responsible for declining muscle repair during ageing, and discovered how to halt the process in mice with a common drug. Although an early study, the findings provide clues as to how muscles lose mass with age, which can result in weakness that affects mobility and may cause falls.
The study, to be published in the journal Nature, involved researchers from King's College London, Harvard University and Massachusetts General Hospital.
The study looked at stem cells found inside muscle – which are responsible for repairing injury – to find out why the ability of muscles to regenerate declines with age. A dormant reservoir of stem cells is present inside every muscle, ready to be activated by exercise and injury to repair any damage. When needed, these cells divide into hundreds of new muscle fibres that repair the muscle. At the end of the repairing process some of these cells also replenish the pool of dormant stem cells so that the muscle retains the ability to repair itself again and again.
The researchers carried out a study on old mice and found the number of dormant stem cells present in the pool reduces with age, which could explain the decline in the muscle's ability to repair and regenerate as it gets older. When these old muscles were screened the team found high levels of FGF2, a protein that has the ability to stimulate cells to divide. While encouraging stem cells to divide and repair muscle is a normal and crucial process, they found that FGF2 could also awaken the dormant pool of stem cells even when they were not needed. The continued activation of dormant stem cells meant the pool was depleted over time, so when the muscle really needed stem cells to repair itself the muscle was unable to respond properly.
Following this finding, the researchers attempted to inhibit FGF2 in old muscles to prevent the stem cell pool from being kick-started into action unnecessarily. By administering a common FGF2 inhibitor drug they were able to inhibit the decline in the number of muscle stem cells in the mice.
Dr Albert Basson, Senior Lecturer at the King's College London Dental Institute, said: 'Preventing or reversing muscle wasting in old age in humans is still a way off, but this study has for the first time revealed a process which could be responsible for age-related muscle wasting, which is extremely exciting.
'The finding opens up the possibility that one day we could develop treatments to make old muscles young again. If we could do this, we may be able to enable people to live more mobile, independent lives as they age.'
Dr Andrew Brack, senior and corresponding author of the study from Harvard University, said: 'Analogous to the importance of recovery for athletes training for a sporting event, we now know that it is essential for adult stem cells to rest between bouts of expenditure. Preventing stem cell recuperation leads to their eventual demise.'
Kieran Jones, co-author of the study from King's, added: 'We do not yet know how or why levels of the protein FGF2 increase with age, triggering stem cells to be activated when they are not needed. This is something that needs to be explored.
'The next step is to analyse old muscle in humans to see if the same mechanism could be responsible for stem cell depletion in human muscle fibres, leading to loss of mass and wastage.'
A team of researchers from the Spanish National Cancer Research Centre (CNIO), headed by CNIO Director María Blasco, has demonstrated in a pioneering study on mammals that longevity is defined at a molecular level by the length of telomeres. The work -- which is published September 27 in the online edition of the journal Cell Reports -- opens the door to further study of these cellular components in order to calculate the rate at which cells age and thus be able to determine life expectancy for a particular organism.
Today’s artificial hearts contain pumps whose spinning rotors can damage blood cells, causing clotting that can lead to strokes. A new pump design could prevent that damage by mimicking the natural movement of human tissue.
Christopher Suprock, founder of product-design firm Suprock Technologies, made the demonstration pump using flexible membranes and a ferrofluid, or magnetic liquid. Suprock injected the ferrofluid between two 0.005-inch-thick elastic membranes and placed an electromagnet less than an inch away. When the electromagnet is turned on, it attracts the ferrofluid, stretching the membrane toward the magnet. When the electromagnet is off, the membrane springs back to its original position. Suprock says his next step is to team up with a medical-device maker, refine the design, and test it in a living animal.
Fifty hours. That’s how long it now takes to decode and interpret a newborn baby’s genome — an undertaking that used to take weeks, or even months. And those two days can mean the difference between life and death for a critically ill infant.
In a paper published in the journal Science Translational Medicine, researchers led by Stephen Kingsmore, director of the Center for Pediatric Genomic Medicine at Children’s Mercy Hospital, describe a new genetic test that can rapidly screen the DNA of babies in the neonatal intensive care unit (NICU) for about 3,500 diseases known to be linked to single-gene mutations. Of these, doctors can treat about 500.
Up to a third of babies admitted to the NICU have a genetic disease. But many newborns are not diagnosed properly and may therefore miss the opportunity for a potentially life-saving therapy. Many of the symptoms of such genetic diseases are both general and shared by many different conditions, which makes them difficult to diagnose; what’s more, many of the genetic conditions in question are rare, so most physicians, even NICU specialists, may not be familiar them or unable to recognize their symptoms. Currently used genetic tests are also too expensive and time-consuming to be clinically useful; because the tests can take weeks, or sometimes months, most NICU babies will have either gone home or died by the time the results are ready.
Published on October 4, 2012 at 5:29 AM
Nanoparticles Selectively Release Drugs in Aged Human Cells
A team of Spanish scientists has developed an intelligent nanodevice that lays the foundations for the future development of new therapies against aging. The device consists of nanoparticles that can selectively release drugs in aged human cells. Its potential future use ranges from the treatment of diseases involving tissue or cellular degeneration such as cancer, Alzheimer's or Parkinson's, among others, to accelerated aging disorders (progeria).
Internalization and controlled release of the fluorescent molecule rhodamine in senescent fibroblasts of patients with dyskeratosis congenita, by MSN-S1 nanodevice
This research has been carried out by the Centro de Reconocimiento Molecular y Desarrollo Tecnológico (IDM), Mixed Unit Universitat Politècnica de València - Universitat de València; the Instituto de Biología Molecular y Celular de Plantas (UPV-CSIC), the Instituto de Investigaciones Biomédicas (CSIC/UAM), the CIBER of Rare Diseases (CIBERER) and CIBER on Bioengineering, Biomaterials and Nanomedicine (CIBER-BBN). The work has been published in the prestigious journal Angewandte Chemie.
"The nanodevice that we have developed consists of mesoporous nanoparticles with a galactooligosaccharide outer surface that prevents the release of the load and that only selectively opens in degenerative phase cells or senescent cells. The proof of concept demonstrates for the first time that selected chemicals can be released in these cells and not in others," says Ramón Martínez Máñez, researcher at the IDN Centre - Universitat Politècnica de València and CIBER-BBN member.
Read more at: Researchers use magnets to cause programmed cancer cell deathsA major problem with treating cancer is how to effectively and efficiently apply a therapy, one that discriminates between cancer and healthy cells: killing the bad while retaining the good. Numerous methods have been tried over the years with varying degrees of success. In this new research, the team has been experimenting with the introduction of iron oxide nanoparticles, which attach to antibodies, into the system. The antibodies, in turn, bind to tumor cell receptors. When a magnetic field is introduced, the nanoparticles bunch up or cluster, which triggers a natural response called a death signal. When that happens, apoptosis (aka, programmed cell death) occurs, causing destruction of the tumor. The work is based on apoptosis, a process that continually occurs in living organisms.
This process is marked by biochemical events that lead to changes in cells causing their death; it is referred to as a programmed death because it controls the way cells grow in multi-cellular organisms. One clear example is the way cells between the fingers are allowed to die, while digits grow as individual members.
Therefore, apoptosis is considered a healthy process as opposed to necrosis, where cells die due to trauma. Normally the process occurs when old or faulty cells are detected, such as when skin cells are damaged from exposure to the elements. When such cells are detected, chemicals are delivered which cause the cells to break apart, effectively killing them. In the present study, researchers took advantage of this process by causing such chemicals to be sent to tumor cells. The researchers applied zinc-doped iron oxide nanoparticles to colon cancer cells, which naturally bind to antibodies. Those antibodies then bind very strongly to what is known as the death receptor 4(DR4) which exists on DLD-1 colon cancer cells. When a magnetic field is applied, the death receptor sends out a signal telling the system to attack the cell. Chemicals are then sent, killing the tumor.
A nanotech material containing an extract from liquorice can be used to sterilize and protect medical devices and implants which include biological components, and protects these functional bio-components during the sterilization process.
Publishing their findings in the latest issue of Materials Today, a team of researchers from Germany and Austria explain how conventional sterilization techniques based on a blast of radiation, or exposure to toxic gas can damage the functional biological components of the device. The coating, containing a component found in liquorice and developed by German biotech company LEUKOCARE AG, protects these sensitive components.
Joachim Koch of the Georg-Speyer Haus, Institute for Biomedical Research in Frankfurt am Main in Germany and colleagues explain how medical devices and implants are increasingly functionalized using pharmacologically active proteins, antibodies and other biomolecules. Harsh sterilization procedures, including beta and gamma irradiation or exposure to toxic ethylene oxide can damage these sensitive molecules and render the device useless. However, without sterilization the patient is at risk of infection when the device is used or implanted.
A laser device for less painful injections has been developed by South Korean scientists.
The system could replace traditional needles, with a jab as painless as being hit with a puff of air.
The laser is already used in aesthetic skin treatments. The aim now is to make low-cost injectors for clinical use.
A team from Seoul National University in South Korea describe the process in the Optical Society's journal Optics Letters.
The researchers write that the laser, called erbium-doped yttrium aluminium garnet, or Er:YAG, propels a stream of medicine with the right force to almost painlessly enter the skin.
The jet is slightly larger than the width of a human hair and can reach the speed of 30m (100ft) per second.
"The impacting jet pressure is higher than the skin tensile strength and thus causes the jet to smoothly penetrate into the targeted depth underneath the skin, without any splashback of the drug," said Prof Jack Yoh of Seoul National University, who led the study.
A new Alzheimer’s drug could dramatically slow the pace of memory loss in those with the disease, it was revealed on Monday.
The drug, solanezumab, is the first to show that targeted the build up of brain proteins, called amyloid plaques, can slow Alzheimer's. Photo: Getty Images/Peter Macdiarmid
By Stephen Adams, Medical Correspondent
8:28PM BST 08 Oct 2012
Combined results from two trials shows the drug, called solanezumab, slows the speed of mental decline by a third in those with mild-to-moderate disease.
Alzheimer’s disease is the most common form of dementia, with about 500,000 people in Britain suffering from it.
Despite enormous investment in experimental treatments, only a handful of drugs to tackle the degenerative brain disease have been approved. These drugs are effective at alleviating some of the symptoms but they do not tackle the underlying cause of disease.
Now Eli Lilly, a pharmaceutical firm, has announced results for its new drug, which works to help clear the protein ‘plaques’ thought to cause Alzheimer’s.
Combined results from two trials showed that it slowed the pace of cognitive decline by 34 per cent, over an 18-month period, compared to those given a placebo.
do we really want people to live forever? talk about overpopulation?
there is a sc fi on ...suddenly there is no death....only living and suffering....it did not go well
in Neuroscience A team of Canadian scientists and clinicians, led by Dr. Michael Hill of the Calgary Stroke Program at Foothills Medical Centre and University of Calgary's Hotchkiss Brain Institute (HBI), have demonstrated that a neuroprotectant drug, developed by Dr. Michael Tymianski at the Krembil Neuroscience Centre, located at the Toronto Western Hospital, protects the human brain against the damaging effects of stroke.
The study, "Safety and efficacy of NA-1 for neuroprotection in iatrogenic stroke after endovascular aneurysm repair: a randomized controlled trial," published online today in The Lancet Neurology, was conducted concurrently with a laboratory study published in Science Translational Medicine, that predicted the benefits of the stroke drug. This landmark clinical trial was a randomized, double blinded, multi-centre trial that was conducted in Canada and the USA. The study evaluated the effectiveness of NA-1[Tat-NR2B9c] when it was administered after the onset of small strokes that are incurred by patients who undergo neurointerventional procedures to repair brain aneurysms. This type of small ischemic stroke occurs in over 90% of aneurysm patients after such a procedure, but usually does not cause overt neurological disability.
(Reuters) - Two American scientists won the 2012 Nobel Prize for chemistry for showing how cells in the body respond to stimuli such as a rush of adrenalin, work that is helping the development of more effective drugs, the prize committee said on Wednesday.
The Royal Swedish Academy of Sciences said the 8 million crown ($1.2 million) prize went to Robert Lefkowitz and Brian Kobilka for discovering the inner workings of G-protein-coupled receptors, gateways to cells that react to chemical messages.
"Around half of all medications act through these receptors, among them beta blockers, antihistamines and various kinds of psychiatric medications," the committee said.
Working out better ways to target the receptors, known as GPCRs, is an area of keen focus for pharmaceutical and biotechnology companies.
Lefkowitz told a news conference by telephone that he was asleep when the phone call came from Sweden.
"I did not hear it - I must share with you that I wear earplugs to sleep. So my wife gave me an elbow. So there it was, a total shock and surprise," he said.
Sven Lidin, Professor of Inorganic Chemistry at Lund University and chairman of the committee, told a news conference the discovery had been key in medical research.
"Knowing what they (the receptors) look like and how they function will provide us with the tools to make better drugs with fewer side effects," he added.
Chemistry was the third of this year's Nobel prizes. Prizes for achievements in science, literature and peace were first awarded in 1901 in accordance with the will of dynamite inventor and businessman Alfred Nobel.
Washington State University researchers have developed a new drug candidate that dramatically improves the cognitive function of rats with Alzheimer's-like mental impairment.
Their compound, which is intended to repair brain damage that has already occurred, is a significant departure from current Alzheimer's treatments, which either slow the process of cell death or inhibit cholinesterase, an enzyme believed to break down a key neurotransmitter involved in learning and memory development. Such drugs, says Joe Harding, a professor in WSU's College of Veterinary Medicine, are not designed to restore lost brain function, which can be done by rebuilding connections between nerve cells.
"This is about recovering function," he says. "That's what makes these things totally unique. They're not designed necessarily to stop anything. They're designed to fix what's broken. As far as we can see, they work."
Could this mean "Goodbye Glasses" in curing myopia?
Biomedical scientists led by David Troilo at the State University of New York (SUNY) College of Optometry are working on a potential cure for myopia by using specialty contact lenses.
Such special lenses can coax the eye to grow in a way that can correct myopia or nearsighted vision while reducing myopia progression, reported science site Phys.org.
"Troilo has shown that specially designed contact lenses that alter how light is focused in the peripheral retina can induce changes in growth that help reshape the eye in the desired way. The experimental lenses use different focal powers within a single lens: either alternating focal powers across the lens, or confined to the outer edge," Phys.org said.
Troilo will describe his findings at the Optical Society's (OSA) Annual Meeting, Frontiers in Optics (FiO) 2012, on Oct. 14 in Rochester, New York.
He also said several contact lens designs may soon be available to help eye doctors manage the progression of myopia in children.
Myopia develops when the eye is too long, making it difficult to focus light from distant objects on the retina.
He said that while glasses or ordinary contact lenses can correct the defocus on the main visual axis, they can create slight farsightedness in the peripheral retina.
Such peripheral farsightedness may worsen myopia because, as children grow, the eye grows to move the retina to where the light is focused, thus naturally lengthening the eye further.
Nearsightedness or myopia affects up to 90 percent of children in some areas in Asia, and more than 40 percent of people in the United States, Phys.org said.
It usually begins in childhood and often progresses with age, it added.
While standard prescription lenses can correct the defocus, they do not cure nearsightedness. Neither do they slow progression rates as children grow.
New lenses
Phys.org said the new lenses changed eye growth and refractive state, or focus, in a predictable way.
The lenses also successfully reduced the elongation of the eye that causes myopia progression.
Goodbye to glasses
A separate report on TechCrunch said the lenses may have other benefits: unlike glasses, they are less likely to get a child bullied, they’re not too expensive, and they can be used in sports.
A study by UT Southwestern Medical Center researchers finds that a starvation hormone markedly extends life span in mice without the need for calorie restriction.
"Restricting food intake has been shown to extend lifespan in several different kinds of animals. In our study, we found transgenic mice that produced more of the hormone fibroblast growth factor-21 (FGF21) got the benefits of dieting without having to limit their food intake. Male mice that overproduced the hormone had about a 30 percent increase in average life span and female mice had about a 40 percent increase in average life span," said senior author Dr. Steven Kliewer, professor of molecular biology and pharmacology.
The study published online in eLife -- a new peer-reviewed, open access journal -- defined average life span as the point at which half the members of a given test group remained alive. A study to determine differences in maximum life span is ongoing: While none of the untreated mice lived longer than about 3 years, some of the female mice that overproduced FGF21 were still alive at nearly 4 years, the researchers report.
