#Diabetes may raise risk for heart valve disease Rice university right Original Studyposted by Mike Williams-Rice on October 21 2014 There appears to be a link between high blood sugar and heart valve hardening.
and their activities says Peter Kamel a medical student at Baylor College of Medicine who completed the research as an undergraduate at Rice university.
That results in patients with diabetes having problems with vision and with their nerves and kidneys as well.
The results that high glucose concentration can also cause pathologic remodeling by the aortic-valve cells could suggest that diabetes is also directly a cause of aortic-valve disease he adds.
The work was based in the lab of Jane Grande-Allen of Rice s bioengineering department.
Her group studies the biomechanics of heart valves particularly their calcification or hardening a condition that lessens blood flow to the heart.
and cells drawn from the aortic heart valves of pigs. Most solutions also included a nutrientâ glucose pyruvate glutamine
We know that calcific aortic-valve disease is associated heavily with metabolic syndrome which can lead to type 2 diabetes.
It s not as common as the link between atherosclerosis and diabetes but it s definitely an appreciable strong subset.
To understand any heart valve-related disease we need to understand the mechanism of how the cells interact with excess lipids
and sugars and we re just starting to scratch the surface she says. So work like this is pretty fundamental.
Researchers from the University of California San diego and the University of Texas Medical school at Houston collaborated on the project.
The National institutes of health the Rice Century Scholars Program and a Hamill Innovation Award by the Rice university Institute of Biosciences and Bioengineering supported the research.
#Therapy cures hearing loss from loud noises University of Michigan rightoriginal Studyposted by Kara Gavin-U. Michigan on October 21 2014scientists restoredâ#hearing to mice that were deafened partly by noise.
The work reported in the journal elife suggests the protein might be a target for treating people who have suffered hearing loss due to noise or aging.
##It has become apparent that hearing loss due to damaged ribbon synapses is a very common and challenging problem
whether it s due to noise or normal aging##says Gabriel Corfas who led the team
and directs the University of Michigan Medical school s Kresge Hearing Research Institute.####We began this work 15 years ago to answer very basic questions about the inner ear
and now we have been able to restore hearing after partial deafening with noise a common problem for people.
Boosting NT3 production through gene therapy in humans could also be an option he says but a drug-based approach would be simpler
He also notes that the research may have implications for neurodegenerative diseases. Researcher from Harvard university collaborated on the project
which was funded by the National Institute on Deafness and Other Communication Disorders the Eunice Kennedy Shriver National Institute of Child Health and Human Development and the Hearing Health Foundation.
University of Michiganyou are free to share this article under the Creative Commons Attribution-Noderivs 3. 0 Unported license b
#Staph bacteria gang up to outsmart antibiotics Vanderbilt University rightoriginal Studyposted by Leigh Macmillan-Vanderbilt on October 20 2014 Relatively harmless bacteria can turn deadly
One way that Staphylococcus aureus and other pathogens can become resistant to antibiotics is to change the way they generate energy
and become small and weak colony variantssays Eric Skaar professor of pathology microbiology and immunology at Vanderbilt University.
and grow poorly in the laboratory cause such persistent infections in humans? Current studies support the notion that antibiotic-resistant staph bacteria including methicillin-resistant (MRSA) strains can exchange nutrients with each other
and even with other bacterial species including the normal microbes of the microbiome to increase their virulence during an infection.
& Microbe challenge infectious disease dogma Skaar says. The thinking has been that if an infection becomes resistant to antibiotics then the resistant organisms appeared clonally meaning they're all genetically the same.
Skaar and colleagues wondered if perhaps instead there are a bunch of organisms that became resistant in different ways
Next they tested the idea in a mouse model of the bone infection osteomyelitis. Antibiotic-resistant small colony variant S. aureus is the cause of chronic and difficult to treat osteomyelitis and also of lung infections in patients with cystic fibrosis (CF.
-or menaquinone-deficient) caused only minimal bone infection but mixed together they caused a fully virulent and bone-destroying infection.
In bone these bacteria are trading molecules Skaar says. Researchers then isolated samples of staph small colony variants and normal bacteria from the lungs of CF patients.
The microbiome of a cystic fibrosis patient s lungs can provide nutrients to these small colony variants
Our findings show that these antibiotic-resistant infections are not what we thought they were they're not a single strain of bacteria with a single lesion leading to the small colony variant phenotype.
Instead they re a mixed population of organisms that are sharing nutrients. They act like a big group of bullies until you hit them with drugs then they stop sharing resources
We're now a little bit smarter about how these organisms are behaving in an infection which
Preventing the nutrient exchange for example may offer a new therapeutic strategy against these antibiotic-resistant organisms The National institutes of health supported the research.
#Drug flips cells to limit damage after heart attack University of North carolina at Chapel hill rightoriginal Studyposted by Mark Derewicz-UNC on October 16 2014a new way to generate more blood vessels after a heart attack can reduce damage
This switch is driven by p53 the well-documented tumor-suppressing protein. Researchers showed that increasing the level of p53 in scar-forming cells significantly reduced scarring
and improved heart function after heart attack. The finding published in the journal Nature shows that it is possible to limit the damage wrought by heart attacks which strike nearly one million people in the United states each year.
Heart disease accounts for one in four deaths every year.####Scientists have thought that fibroblasts are differentiated terminally meaning they can t adopt the fate of other kinds of cells;
but our study suggests this may not be entirely true##says Eric Ubil a postdoctoral fellow at the University of North carolina at Chapel hill and first author of the study.##
##It appears that injury itself can induce fibroblasts to change into endothelial cells so the heart heals better.
We found a drug that could push this process forward making even more endothelial cells that help form blood vessels.##
##After a heart attack fibroblasts replace damaged heart muscle with scar tissue. This scarring can harden the walls of the heart
and lessen its ability to pump blood throughout the body. Meanwhile endothelial cells create new blood vessels to improve circulation to the damaged area.
To explore this idea they induced heart attacks in mice and then studied the fibroblasts to see if the cells expressed markers characteristic of endothelial cells.
To their surprise almost a third of the fibroblasts in the area of the cardiac injury expressed these endothelial markers.
Because a heart attack is such a stressful event Ubil created a list of genes that were known to be involved in cellular responses to stress.
Topping the list was p53 a protein often called the##guardian of the genome ##because it causes damaged out of control cells to commit suicide
or apoptosis which reduces the likelihood that they will go on to form tumors.####As luck would have it that was the first gene
I tried##says Ubil who conducted the research as a graduate student in the laboratory of former UNC faculty member
##or overexpressed in the fibroblasts after heart injury and this seemed to regulate fibroblasts becoming endothelial cells.
and used it to treat mice for a few days after cardiac injury. The drug had dramatic results doubling the number of fibroblasts that turned into endothelial cells.
They had more blood vessels at the site of injury and their heart function was better.##
##By increasing the number of blood vessels in the injury region we were able to greatly reduce the effects of the heart attack.##
##Ubil says his study shows that this could be a novel strategy for treating heart attacks.
##But our work shows it s possible to change the fate of scar-forming cells in the heart
and this could potentially benefit people who have heart attacks.####Deb adds:####We are also currently investigating
whether such an approach could be applied for treating scarring in other organs after injury.####The American Heart Association and the National institutes of health funded the work.
Source: UNC-Chapel Hillyou are free to share this article under the Creative Commons Attribution-Noderivs 3. 0 Unported license h
Researchers would like to place very small implants deep inside our bodies to monitor health or treat pain.
But providing electric power to implants without wires or batteries has been a big obstacle. Now engineers are developing a way to send power safely
and wirelessly to smart chips programmed to perform medical tasks and report back the results.
The approach involves beaming ultrasound at a tiny device inside the body designed to do three things:
convert the incoming sound waves into electricity process and execute medical commands and report the completed activity via a tiny built-in radio antenna."
"We think this will enable researchers to develop a new generation of tiny implants designed for a wide array of medical applications"says Amin Arbabian assistant professor of electrical engineering at Stanford university.
Arbabian's team recently presented a working prototype of this wireless medical implant system at the IEEE Custom Integrated circuits Conference in San jose California.
The researchers chose ultrasound to deliver wireless power to their medical implants because it has been used safely in many applications such as fetal imaging
and can provide sufficient power to implants a millimeter or less in size. Now Arbabian and his colleagues are collaborating with other researchers to develop sound-powered implants for a variety of medical applications including studying the nervous system
and treating the symptoms of Parkinson's disease.""Tiny wireless nodes such as these have the potential to become a key tool for addressing neurological disorders"says Florian Solzbacher professor of electrical and computer engineering at University of Utah and director of its Center for Engineering Innovation.
The implant chip is powered by piezoelectricity which is caused electricity by pressure. In a piezoelectric material pressure compresses its molecular structure much like a child jumping on a bed compresses the mattress.
When the pressure abates the piezoelectric material's molecular structure like the mattress springs back into shape.
Every time a piezoelectric structure is compressed and decompressed a small electrical charge is created. Researchers created pressure by aiming ultrasound waves at a tiny piece of piezoelectric material mounted on the device."
"The implant is like an electrical spring that compresses and decompresses a million times a second providing electrical charge to the chip"says Marcus Weber who worked on the team with fellow graduate students Jayant Charthad and Ting Chia Chang.
The piezoelectric effect is the power delivery mechanism. In the future the team plans to extend the capabilities of the implant chip to perform medical tasks such as running sensors
or delivering therapeutic jolts of electricity right where a patient feels pain. Finally the"smart chip"contains a radio antenna to beam back sensor readings or signal the completion of its therapeutic task.
The current prototype is the size of the head of a ballpoint pen. Researchers hope to design a next-generation implant one-tenth that size.
The goal is to produce smaller devices that could be used to create a network of electrodes to study the brains of experimental animals in ways not currently possible."
"US and European brain initiatives are pushing for a more complete understanding of the central nervous system"Solzbacher says."
"This requires being able to interface with cells using arrays of micro implants across the entire 3d structure of the brain."
"Arbabian's team wants to test many other applications using this basic technology to wirelessly power small implants deep inside the body."
"Many biosensing and stimulation applications require small deep medical implants"he says.""We believe our platform provides the recipe for building small devices that can be powered wirelessly
and programmed to perform a wide array of tasks.""Source: Stanford Universityyou are free to share this article under the Creative Commons Attribution-Noderivs 3. 0 Unported license e
#Brain surgery robot would go through the cheek Vanderbilt University Posted by David Salisbury-VU on October 16 2014for people with severe epilepsy treatment can mean drilling through the skull deep into the brain
to destroy the small area where the seizures originateâ##invasive dangerous and comes with a long recovery.
Five years ago a team of engineers at Vanderbilt University wondered if it was possible to address epileptic seizures in a less invasive way?
They decided it would be possible. Because the area of the brain involved is the hippocampus
which is located at the bottom of the brain they could develop a robotic device that pokes through the cheek
and enters the brain from underneath. This strategy avoids having to drill through the skull
and is much closer to the target area. To do so however meant developing a shape-memory alloy needle that can be steered precisely along a curving path
and a robotic platform that can operate inside the powerful magnetic field created by an MRI SCANNER.
The engineers have developed a working prototype which was unveiled in a live demonstration this week at the Fluid Power Innovation
and Research Conference in Nashville by David Comber the graduate student in mechanical engineering who did much of the design work.
The business end of the device is a 1. 14 mm nickel-titanium needle that operates like a mechanical pencil with concentric tubes some
Unlike many common metals nickel-titanium is compatible with MRIS. Using compressed air a robotic platform controllably steers
In addition the needle is inserted in tiny millimeter steps so the surgeon can track its position by taking successive MRI scans.
According to project leader Eric Barth associate professor of mechanical engineering the next stage in the surgical robot s development is testing it with cadavers.
##I ve done a lot of work in my career on the control of pneumatic systems##Barth says.##
##We knew we had this ability to have a robot in the MRI SCANNER doing something in a way that other robots could not.
'##At the same time Robert Webster associate professor of mechanical engineering had developed a system of steerable surgical needles.####The idea for this came about when Eric and
I were talking in the hallway one day and we figured that his expertise in pneumatics was perfect for the MRI environment
and could be combined with the steerable needles I d been working on##says Webster. The engineers identified epilepsy surgery as an ideal high-impact application through discussions with Joseph Neimat associate professor of neurological surgery.
They learned that neuroscientists currently use the through-the-cheek approach to implant electrodes in the brain to track brain activity
and identify the location where the epileptic fits originate. But the straight needles they use can t reach the source region
so they must drill through the skull and insert the needle used to destroy the misbehaving neurons through the top of the head.
Comber and Barth shadowed Neimat through brain surgeries to understand how their device would work in practice.##
and unlimited access would make surgeries minimally invasive. We could do a dramatic surgery with nothing more than a needle stick to the cheek.##
##The engineers have designed the system so that much of it can be made using 3d printing in order to keep the price low.
This was achieved by collaborating with Jonathon Slightam and Vito Gervasi at the Milwaukee School of engineering. Current funding comes the Center for Compact and Efficient Fluid Power a National Science Foundation Engineering Research center that supports advances in fluid power and past funding from Martin Ventures.
Source: Vanderbilt Universityyou are free to share this article under the Creative Commons Attribution-Noderivs 3. 0 Unported license e
#Can mom s age help predict mitochondrial disease? The discovery of a aternal age effectfor mitochondrial diseases could be a valuable tool for genetic counseling, report researchers.
Their findings could be used to predict the accumulation of MITOCHONDRIAL DNA mutations in maternal egg cells, as well as the transmission of these mutations to children.
These mutations cause more than 200 diseases and contribute to others such as diabetes, cancer, Parkinson disease,
and Alzheimer disease. The study found greater rates of the MITOCHONDRIAL DNA variants in children born to older mothers,
as well as in the mothers themselves. Mitochondria are structures within cells that produce energy and that contain their own DNA. any mitochondrial diseases affect more than one system in the human body,
says Kateryna Makova, professor of biology at Penn State and one of the study primary investigators. hey affect organs that require a lot of energy,
including the heart, skeletal muscle, and brain. They are devastating diseases and there is no cure, so our findings about their transmission are very important.
BLOOD AND CHEEK CELLS The research team set out to learn whether maternal age is important in the accumulation of MITOCHONDRIAL DNA (mtdna) mutations, both in the mother and in the child as a result of transmission.
Collaborating with Ian Paul, a pediatrician at the Penn State Milton S. Hershey Medical center they took samples of blood and of cells inside the cheek from 39 healthy mother-child pairs.
Because mtdna is inherited only maternally, paternal mtdna was not a factor in the study. Studying healthy individuals gave the researchers a baseline for future studies of disease-causing mutations.
Through DNA sequencing, they found more mutations in blood and cheek cells in the older mothers in the study.
Maternal age of study participants ranged from 25 to 59. his finding is not surprising,
Makova says, ecause as we age, cells keep dividing, and therefore we will have more mutant genes.
But finding greater rates of mutations in children born to the older mothers did come as a surprise.
The researchers believe a similar mutation process is occurring both in the cells of the mothersbodies and in their germ lines.
OTTLENECKPREDICTIONS The study led to another important discovery about egg-cell development. Although it was known that developing egg cells go through a ottleneckperiod that decreases the number of mtdna molecules,
scientists didn know how small or large this bottleneck is. f the bottleneck is large, the genetic makeup of the mother mitochondria will be passed to her children,
Makova explains. owever, if it is tinyf there is a severe decrease in mitochondrial molecules during the egg-cell developmenthen the genetic makeup of the child might differ dramatically from that of the mother.
This finding is especially important for mothers who have a mitochondrial disease. For many mitochondrial diseases, 70 to 80 percent of molecules need to have the disease-causing variant for the disease to manifest itself.
But for others, only 10 percent of the mtdna molecules with the variant are needed to cause disease. f the bottleneck is very small,
as wee found in our study, these percentages can change dramatically, Makova says. nowing the size of the bottleneck allows us to predict, within a range,
the percentage of disease-carrying molecules that will be passed on to the child. Knowledge about both the maternal age effect and the bottleneck size is useful in family planning. e have some predictive power now
and can assist genetic counselors in advising couples about the chances of mitochondrial diseases being passed to the next generation,
Makova says. veryone is concerned about Down syndrome because that is a common genetic problem. We have added now another set of genetic disorders that also might be affected by the age of the mother.
It is good for couples to have this knowledge as they make family-planning decisions. The research appears in the early online edition of the Proceedings of the National Academy of Sciences.
In addition to researchers from Penn State, coauthors contributed from Nottingham Trent University in the United kingdom and the University of California
Berkeley. Penn State Huck Institutes of Life sciences, the Pennsylvania Department of health, Battelle Memorial Institute, and Penn State Clinical and Translational Sciences Institute funded the work e
#Why cancer researchers are excited about this amoeba A type of amoeba that lives in soil has a gene that is very similar to a tumor-fighting gene found in humans.
The human gene is called PTEN. When it s healthy it stops tumors from growing. But the gene is prone to mutations
and those mutations are linked to lots of cancersin fact when researchers from the University of Iowa conducted a literature review they found that PTEN mutations show up in 40 percent of breast cancer cases up to 70 percent of prostate cancer cases and nearly half of all leukemia cases.
If you look at tumors across the boardâ and that doesn t mean just breast cancer or prostate cancerâ you find that PTEN is the most generally mutated gene.
And when you mutate PTEN in mice you cause tumors says David Soll biology professor
and corresponding author on the study published in the journal PLOS ONE. While it s unknown how to prevent PTEN mutations Soll
and colleagues became interested in finding out whether other human genes may substitute for PTEN like a player coming off the bench
when the star has been injured. After some searching the team found that an amoeba Dictyostelium discoideum has the gene ptena
which mutates similarly to the human PTEN gene and causes behavioral defects in the cell.
They also found a close relative of ptena in the amoeba which they called lpten that performs the same functions of ptena but to a lesser degreeâ a possible bench player in the amoeba s genome.
If the hypothesis holds true for human cells it could lead to a new way to treat cancer.
Once a patient is diagnosed with cancer caused by a PTEN mutation the patient could take the drug over-express the PTEN bench player gene
and potentially stop cancer in its tracks Soll says. That could save many cancer patients from undergoing chemotherapy and radiation treatment for breast and other common cancers.
The finding has led the team to study other human genes that may be able to step in for the mutated PTEN gene
and perform the same tumor-suppressing role. There are at least two close relatives of PTEN the researchers are currently studying.
Somewhere there may be a backup system what we call redundancy that might be the basis for better identifying tumors
and possibly creating cancer-fighting drugs. You have another gene which might be able to step in for the broken gene to keep things normal and that s
The Developmental Studies Hybridoma Bank a national resource created by the National institutes of health and housed at the University of Iowa supported the study.
Source: University of Iow
#Topical antibiotics may raise pneumonia risk University of Melbourne rightoriginal Studyposted by David Scott-Melbourne on October 13 2014patients in hospital intensive care units have a higher risk of developing pneumonia
when they are treated with topical antibiotics. The findings contradict previously published research that topical antibioticsâ##medication applied to the patient s airwayâ##would decrease pneumonia rates.
Ventilator-associated pneumonia develops in approximately 20 percent of patients in intensive care units (ICUS) who are receiving prolonged medical ventilation.
However in the control groups of these published clinical trials of topical antibiotics in this patient group the pneumonia rates were as high as 40 percent.
For a new study published in the journal CHEST researchers analyzed 206 international publications evaluating pneumonia prevention methods in ICUÂ##s from the last 30 years.
The new findings will help improve understanding of how to evaluate pneumonia prevention methods in the ICU says associate professor James Hurley from the University of Melbourne.
Use of topical antibiotics increases the pneumonia risk in ICU patients by disrupting the balance of bacteria
not only in patients that received these antibiotics but also in control group patients also staying in the ICU.##
##This changed flora is spread around the ICU environment to other patients through cross-infection##Hurley says.##
##This surprising finding is not apparent in any one study examined in isolationâ##it requires a meta-analysis of the control group pneumonia rates in all 206 studies to demonstrate these findings.
Pneumonia is acquired commonly by ICU patients leads to longer stays in intensive care and can also increase mortality risk.##
###Therefore it appears topical antibiotics used in an effort to prevent pneumonia in the ICU are a hazard
and the method is unsafe.####Source: University of Melbourneyou are free to share this article under the Creative Commons Attribution-Noderivs 3. 0 Unported license o
#Health insurance for India s poor cuts death rate Stanford university University of California Berkeley University of Southern California rightoriginal Studyposted by Robert Perkins-USC on October 8 2014a
government program that provides health insurance for catastrophic illness lowered both mortality rates and out-of-pocket expenses for people in households below the poverty line in Karnataka India.
Researchers studied roughlyâ#80000 households from 600 villages and found a 64 percent drop in mortality from diseases covered by insurance.
The program the Vajpayee Arogyashree Scheme (VAS) is implemented by the Karnataka government with support from the World bank Group.
Among the findings the research shows:####This World bank study clearly shows how this program benefits the health of the poor in Karnataka##says U. T. Khader the stateâ##s Minister of Health and Family Welfare.##
##It provides hospital care that the poor would have difficulty receiving without the help of the scheme.##
##The free insurance covered specific high-impact medical conditionsâ##such as heart disease and cancerâ ##which poor residents often die from
because they are unable to pay for the necessary expensive treatments. Some of the unique features of the VAS program includes free tertiary care at both private
and public hospitals empaneled by VAS for below-the-poverty-line (BPL) families with little or no access to tertiary care;
automatic enrollment of all BPL families with no annual premiums user fees or copayments; and health camps in rural areas by empanelled hospitals
which helped screen patients for tertiary care and transport them to hospitals in urban centers.####The results of this study are important to India as it makes choices on how to make progress towards universal health coverage##says Onno Ruhl World bank Group Country Director for India.##
##The program shows how purchasing health services for the poorest can both improve health and provide protection from impoverishment due to out-of-pocket payments for health care.##
##The study published in the journalâ#BMJ included more than 82000 households. Since the program was phased covering poor households in the northern part of Karnataka in the first phase before expanding to the rest of the state the study compared the health outcomes of roughly 45000 households from villages that were covered by the insurance to roughly 37000 households
from villages that were covered not by the program.####The study shows that public policy can play a strong role in reducing disparities in health due to socioeconomic status. In villages without insurance the poor had much higher mortality than the rich
but such disparities were eliminated completely in villages with insurance coverage##says Neeraj Sood professor and director of research at the Schaeffer Center for Health policy and Economics at University of Southern California.##
##Rates of early death and illness from chronic conditionsâ##such as heart disease and cancerâ##have increased dramatically in India in the past few decades putting the poor at high risk of not having access to services they need
and incurring payments for health care that push them deeper into poverty##says Patrick Mullen a World bank Group senior health specialist and the manager of the evaluation.
Theâ#World bank Groupâ##s Health Results Innovation Trust fund funded the study. Researchers from Stanford university; University of California Berkeley;
the Indian Institute of Management in Bangalore; and the World bank Group are coauthors. Source: USCYOU are free to share this article under the Creative Commons Attribution-Noderivs 3. 0 Unported license
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