Here is an example of actual student work from last year. This article analysis received a grade of 25/30. The student needed to be more overt in their identification of the parts of the process—“Observations were”. “The procedure was…”. “The authors concluded…”.. Also she could have provided more background and extension for extra credit. Look at the rubric. There are lots of opportunity for EC on this assignment.
For the first Article Analysis, I went on Science Daily and looked at current events. I immediately went to the biology section so I could find an article that I would be easily interested in. The article I chose was “Study Offers Clues as to Why Some Patients Get Infections from Cardiac Implants”. Right away this article was extremely interesting to me. The article starts off by talking about the problem at hand. The problem is that some patients receiving implanted devices such as pacemakers, defibrillators, and prosthetic cardiac valves are becoming sick with infections on these devices. Scientist determined that biofilms, or layers of bacterial bugs form on these devices cause the patients to become sick with an infection. For treatment scientist discovered that taking out the device with the infections and replacing them was the quickest way to get rid of the infection. A common bacterium, Staphylococcus aureus may contain variants that let the biofilms produce and grow. I found this interesting for many reasons; one is that I didn’t think if bacteria formed on these devices it would cause such harm to the person whom contains the device. After reading the article I know think that if these bacteria were to form a biofilm on a pacemaker and be untreated just for an example, it would pose a great threat because it could directly attack the heart and enter the main blood stream. Scientist decided to collect Staph cells from patients with cardiac devices, to try to figure out how the biofilms are created, and how the bonds of the cells in the body form these films. They concluded that the bonds form when a protein on the cell surface connects with a common blood protein that eventually coats the device. A major question scientist have is why do some types of Staph cells form these biofilms? Staph cells are present in half of American’s nose. So why do only some of them form this infectious biofilms? To find an answer to these questions scientist much first start with a much simpler question, one being, how do these bacteria form and connect to the cells and surface of these devices. Starting out with such a simple question and finding the answer to that is going to let the scientist understand a lot more about what happens to these devices and why they contract these biofilms. During a study 80 Staph samples were taken from 3 different groups of people; patients with a blood infection and infection on their cardiac devices, patients with a blood infection but an uninfected cardiac devices, and the third group was Staph cells from the noses of healthy people living in the same area of those people in the other two groups. By taking these samples, conclusions can be made on how the infection forms, and what the infection infects, the blood stream, the device or both. Nadia Casillas-Ituarte performed experiments that involved connecting Staph bacteria to a protein-coated device. After connecting the two she would break the bond that she had formed. She did this to measure the power to break the bonds, and the strength of the bonds. She was quoted saying “The first step in all of this is to determine how bacterium feels a surface. You can’t stop the process until you first understand how it happens.” I agree with her, like I said before, being able to answer a smaller question can help lead to being able to answer bigger questions and hopefully it could help to finding a cure or prevention for getting an infection on these devices.
After the article talked about experiments it connected a little bit to physics. Steven Lower, an associate working at Ohio State said, “Most physicists would tell you there are certain laws of physics that dictate what happens and when it happens…” I think that this is really important given the situation with the bacteria and these devices. I think this because if people try to force a biofilm to disconnect itself to the device it could cause more harm to the human containing the device. Even with some experimental research already done, its going to take time for these scientist to discover why these infections occur and how to make them go away, with out having to completely take the device out and put a new one in.
After reading the entire article and discussing it I think that the steps already taken to understand information about the biofilms and infections are heading in the right direction. I believe by just from the article the questions the scientist brought up seemed to be very important in the early process of the research to this problem.
Article:
New research suggests that some patients develop a potentially deadly blood infection from their implanted cardiac devices because bacterial cells in their bodies have gene mutations that allow them to stick to the devices.
Patients with implants can develop infections because of a biofilm of persistent bacterial bugs on the surfaces of their devices. Researchers found that some strains of the bacteria,Staphylococcus aureus, have just a few genetic variants in the proteins on their surfaces that make them more likely to form these biofilms.
The research seeks to get to the heart of a medical paradox: Devices such as pacemakers, defibrillators and prosthetic cardiac valves save lives, but they cause infections in about 4 percent of the estimated 1 million patients receiving implants each year in the United States. Because biofilms resist antibiotics, the only treatment is surgery to remove the contaminated device and implant a new one. This adds up to thousands of surgeries and more than $1 billion in health care costs every year.
A team led by scientists at Ohio State University and Duke University Medical Center used atomic-force microscopy and powerful computer simulations to determine howStaphbacteria bond to the devices in the process of forming these biofilms. The findings offer clues about potential techniques that could be employed to prevent infections in patients who need these devices to stay alive.
"We're probing the initial step to that biofilm formation. Can you shut that down somehow? If that bacterium never sticks, there's no biofilm. It's that simple. But it's not quite that simple in practice," said Steven Lower, associate professor in the School of Earth Sciences at Ohio State and co-lead author of the study.
The research is published online this week in the early edition of theProceedings of the National Academy of Sciences.
UsingStaphcells collected from patients -- some with cardiac device-related infections -- the researchers examined how these bacteria adhere to implants to create a biofilm. The bond forms when a protein on the bacterial cell surface connects with a common human blood protein coating an implanted device.
But an estimated half of all Americans haveStaphbacteria living in their noses, and not every cardiac implant patient develops an infection. So why do some strains of these bacteria cause infection while others remain dormant?
The researchers discovered thatStaphsurface proteins containing three genetic variants, or single-nucleotide polymorphisms, formed stronger bonds with the human proteins than didStaphproteins without those variants. The presence of these genetic variants was associated with the strains of bacteria that had infected implanted cardiac devices.
The finding is a first step toward preventing the bacteria from bonding to the devices. Though many scientists are trying to develop materials that repel bacteria, these researchers wonder if there might be another way to work around the bacteria's manipulative behavior.
"It will be useful to explore this in more detail and see if we can understand the basic science behind how these bonds form, and why they form. Perhaps then we can exploit some fundamental force law," said Lower, who also has a faculty appointment in the School of Environment and Natural Resources.
Lower, a scientist with a background in geology, physics and biology, has collaborated for a decade with Vance Fowler, an associate professor of medicine at Duke's Medical Center and the study's co-lead author. Fowler, who specializes in infectious diseases, has assembled a rare library of hundreds ofStaphylococcus aureusisolates collected from patients. Lower specializes in atomic-force microscopy and molecular dynamics simulations to explore molecular-level relationships between inanimate surfaces and living microorganisms.
Fowler hopes his samples might help answer a broader question related to varied patient responses to the blood infection bacteremia.
"Staphylococcus aureusinfections of prosthetic devices are devastating to patients and expensive to health-care systems. For this reason, the best way to treat these infections is to prevent them in the first place. I believe that our research is a critical first step towards understanding, and eventually preventing, cardiac device infections caused byStaphylococcus aureus," Fowler said.
For this study, the researchers used 80Staphisolates from three different groups: patients with a blood infection and a confirmed cardiac device infection, patients with a blood infection and an uninfected cardiac device, andStaphfrom the noses of healthy people living in the same area.
Single-cell studies of bacteria are complicated by their tiny size, one millionth of a meter, so an atomic-force microscope is required to visualize their behavior. Co-author and Ohio State postdoctoral researcher Nadia Casillas-Ituarte performed these experiments, connecting singleStaphbacteria to a protein-coated probe to allow bonds to form, and then rupturing the bonds to measure the strength of each connection.
Casillas-Ituarte simulated the human heartbeat, allowing bonds to form over the course of a second and then pulling the probe away. By doing this at least 100 times on each cell and verifying the work on hundreds of additional cells, she generated over a quarter-million force curve measurements for the analysis.
"The first step in all of this is to determine how a bacterium feels a surface," she said. "You can't stop that process until you first understand how it happens."
The researchers coated the probe with fibronectin, a common human blood protein found on the surface of implanted devices.Staphbacteria can create a biofilm by forming bonds with this protein through a protein on their own surface called fibronectin-binding protein A. To learn more about the bacterial protein, the scientists then sequenced the amino acids that make up fibronectin-binding protein A in each isolate they studied.
And this is where they found the single-nucleotide polymorphisms (or SNPs, pronounced "snips"), which were more common in the isolates collected from patients with infections related to their heart implants.
To further test the effects of these SNPs, the team used a supercomputer to simulate the formation of the bond between the bacterial and human proteins. When they plugged standard amino acid sequences from each protein into the supercomputer, the molecules maintained a distance from each other. When they altered the sequence of three amino acids in the bacterial surface protein and entered that data, hydrogen bonds formed between the bacterial and human proteins.
"We changed the amino acids to resemble the SNPs found in theStaphthat came from cardiac device-infected patients," Lower said. "So the SNPs seem to have a relationship to whether a bond forms or not."
Fibronectin-binding protein A is just one of about 10 of these types of molecules on theStaphsurface that can form bonds with proteins on host cells, Lower noted. And it's also possible that fibronectin, the human protein on the other side of the bond studied so far, might contain genetic variants that contribute to the problem as well.
What the scientists do know is that bacteria will do all they can to survive, so it won't be easy to outsmart them.
"Bacteria obey Charles Darwin's law of natural selection and can evolve genetic capabilities to allow them to live in the presence of antibiotics," Lower said. "Most physicists would tell you there are certain laws of physics that dictate what happens and when it happens, and you can't evade or evolve ways around those. If you understand the basic physics of it, can you exploit a fundamental force law that bacteria can't evade or evolve a mechanism around?"
This work was supported by grants from the National Institutes of Health, the National Science Foundation, the Brazilian National Council for Scientific and Technological Development/Brazilian National Science and Technology Institute, and the Swiss National Science Foundation/Swiss Medical Association.
Additional co-authors include Supaporn Lamlertthon and L. Barth Reller of Duke; Roberto Lins of the Universidade Federal de Pernambuco in Brazil; Ruchirej Yongsunthon, Eric Taylor, Alex DiBartola and Brian Lower of Ohio State; Catherine Edmonson and Lauren McIntyre of the University of Florida; Yok-Ai Que of the University of Lausanne in Switzerland; and Robert Ros of Arizona State University.