Pulmonary edema (UK/Ireland: oedema) is fluid accumulation in the lungs. This fluid collects in air sacs in the lungs, making it difficult to breathe. It leads to impaired gas exchange and may cause respiratory failure.
According to Medilexicon's medical dictionary, pulmonary edema is: "edema of lungs usually resulting from mitral stenosis or left ventricular failure."
In most cases, heart problems cause pulmonary edema. But fluid can accumulate for other reasons, including pneumonia, exposure to certain toxins and medications, and exercising or living at high elevations.
Treatment depends on the cause, but it focuses on maximizing respiratory function and removing the source of the problem. It generally includes supplemental oxygen and medications.
When pulmonary edema develops suddenly, it is a medical emergency requiring immediate care. Pulmonary edema can sometimes be fatal. The outlook depends on the rapidity in receiving treatment along with treatment for the underlying problem.
Script taken from the link below
http://www.medicalnewstoday.com/articles/167533.php
Sunday, October 18, 2009
Stem & Lineage Cell Markers
Flow cytometric analysis of Stem and Lineage Cell Markers
Research on stem cells is the subject of intense investigation, both from a basic science point of view, as well as a basis for cell-based therapies to treat disease. The ability to study and characterize stem cells has been aided by the identification of specific markers which allow researchers to characterize and enrich these cells. The use of immunophenotyping is an important technique to distinguish one population of cells from another. eBioscience is dedicated to providing you with a choice of innovative primary antibody reagents and flurochromes to accelerate your stem cell research using multicolor flow cytometry. Listed below are some of our newest lineage and stem cell markers.
Human Stem Cell Markers
- CD34 (clone 4H11)
- CD90 (clone 5E10)
- CD96 (clone NK92.39 )
- CD133 (clone TMP4)
- CD133 (clone EMK08)
- CD325 (N-Cadherin) (clone 8C11)
- Oct 3/4 (clone EM92)
- FITC Hematopoietic Lineage Flow Cocktail
Mouse Stem Cell Markers
- CD9 (clone eBioKMC8)
- CD201 (clone eBio1560)
- Delta-Like 1
- Endomucin (clone V.7C7)
- Nanog (clone MLC-51)
- Notch1
- Notch3
- Notch4
- Oct 3/4 (clone EM92)
- Pacific Blue® Hematopoietic Lineage Flow Cocktail
link copied from the given website
http://www.ebioscience.com
For more detail about the system please concern this link
http://www.ebioscience.com/ebioscience/whatsnew/stemcells.htm?gclid=CPDe5_u4x50CFQkwpAodRSvDqw
Immune Cell Entry Into The Pancreatic Islets Key To Understanding Type 1 Diabetes Origins
St. Jude Children's Research Hospital investigators have discovered how destructive immune cells gain access to insulin-producing cells and help cause diabetes.
The finding points to possible new strategies to halt or prevent type I diabetes.
Working in mice, researchers demonstrated that to enter key areas of the pancreas known as the islets of Langerhans, immune cells known as T cells must recognize a marker on the surface of insulin-producing cells housed there. T cells play a key role in regulating immune response. Once inside the islets, T cells trigger the inflammation that can lead to destruction of the insulin-producing beta cells. The result is type I diabetes.
The report answers a fundamental question about the role of T cell entry and accumulation in the islets in development of type I disease, a disease that affects as many as 3 million Americans. The research appears in the October 16 edition of the journal Immunity. Dario Vignali, Ph.D., is the paper's senior author and vice chair of the St. Jude Immunology department.
The St. Jude results contradict a widely held theory that only a small percentage of T cells that infiltrate the islets were actively involved in causing type I diabetes. The old scenario held that most of the T cells found in the islets were recruited to the site by a small number of specialized T cells. Those recruited or bystander T cells were thought to play no role in causing diabetes. Furthermore, it was thought that any T cell could gain access to the islets.
"The new research argues that every T cell in the islet is important. What these T cells recognize that allowed them to gain access to the islets may provide us with clues as to what might be needed to prevent diabetes," Vignali said. "Understanding the molecular differences between the T cells in the islets and the T cells in the periphery might also start to tell us a lot about what it takes to make a T cell attack the beta cells and cause diabetes."
Without insulin to turn food into fuel for cells, patients develop type I diabetes and are left dependent on insulin injections, an insulin pump or in rare cases a pancreas transplant. Unlike the more common form of the disease, known as type II diabetes, type I diabetes usually affects children and is sometimes called juvenile diabetes. About 15,000 new cases are diagnosed annually in the United States. Even with treatment, patients with type I diabetes are at risk for blindness, kidney failure and other complications.
"This paper also presents a new clinical intervention strategy--blocking T cells from even getting into the islet cells in the first place," Vignali added.
If any T cell could enter the islets, then it would be less likely that there were any "special rules" for entering islets and thus nothing unique about entry into the islets that might be targeted by treatment, he explained.
Understanding how T cell access to islets is controlled also raises hopes for developing a therapy to re-educate the immune system to tolerate rather than attack the beta cells. The St. Jude research points to a new route into islet cells.
For this study, scientists used a technique Vignali's laboratory developed in 2006. The technique allows researchers to quickly modify T cell production in mice. Normally mice make millions of T cells that can recognize many different cells and microorganisms. Each T cell carries on its surface a receptor that recognizes and binds to just one specific antigen, or marker, on the surface of the T cell's intended target.
The modification technique allowed researchers to create strains of mice with only two types of T cells, each with different receptors. One population carried a receptor that recognized the insulin-producing beta cells and could cause diabetes. The other group was programmed to recognize a different antigen. Researchers reported they could not induce the latter group of T cells to enter the islets.
Then investigators created and tracked T cells with three types of receptors--receptors from T cells with a proven ability to enter islet cells and cause diabetes, those able to enter islets and cause inflammation, but not diabetes, and a third group of receptors with no connection to type 1 diabetes or islet cells. The scientists reported that none of the T cells, even those with a demonstrated ability to cause diabetes in mice, could induce bystander T cells to enter the islet cells.
Finally, investigators tracked T cells carrying receptors from mice that naturally developed type I diabetes. They created mice with 17 new T cell receptors, five from the spleen of diabetic mice and 12 from T cells isolated in the islets of those diabetic mice. If the islets control T cells entry, then islets in the new mouse strains would be infiltrated by T cells with islet-derived, but not spleen-derived, receptors.
That is what happened. "About 70 percent of the receptors that came from the islets could mediate T cell migration back into the islets, while none of the receptors that came from the spleen could do likewise," Vignali said. The islet-derived receptors were also linked to rapid development of diabetes, with one-third causing diabetes during the 10-week study.
Script taken from the link below
http://www.medicalnewstoday.com/articles/166818.php
The finding points to possible new strategies to halt or prevent type I diabetes.
Working in mice, researchers demonstrated that to enter key areas of the pancreas known as the islets of Langerhans, immune cells known as T cells must recognize a marker on the surface of insulin-producing cells housed there. T cells play a key role in regulating immune response. Once inside the islets, T cells trigger the inflammation that can lead to destruction of the insulin-producing beta cells. The result is type I diabetes.
The report answers a fundamental question about the role of T cell entry and accumulation in the islets in development of type I disease, a disease that affects as many as 3 million Americans. The research appears in the October 16 edition of the journal Immunity. Dario Vignali, Ph.D., is the paper's senior author and vice chair of the St. Jude Immunology department.
The St. Jude results contradict a widely held theory that only a small percentage of T cells that infiltrate the islets were actively involved in causing type I diabetes. The old scenario held that most of the T cells found in the islets were recruited to the site by a small number of specialized T cells. Those recruited or bystander T cells were thought to play no role in causing diabetes. Furthermore, it was thought that any T cell could gain access to the islets.
"The new research argues that every T cell in the islet is important. What these T cells recognize that allowed them to gain access to the islets may provide us with clues as to what might be needed to prevent diabetes," Vignali said. "Understanding the molecular differences between the T cells in the islets and the T cells in the periphery might also start to tell us a lot about what it takes to make a T cell attack the beta cells and cause diabetes."
Without insulin to turn food into fuel for cells, patients develop type I diabetes and are left dependent on insulin injections, an insulin pump or in rare cases a pancreas transplant. Unlike the more common form of the disease, known as type II diabetes, type I diabetes usually affects children and is sometimes called juvenile diabetes. About 15,000 new cases are diagnosed annually in the United States. Even with treatment, patients with type I diabetes are at risk for blindness, kidney failure and other complications.
"This paper also presents a new clinical intervention strategy--blocking T cells from even getting into the islet cells in the first place," Vignali added.
If any T cell could enter the islets, then it would be less likely that there were any "special rules" for entering islets and thus nothing unique about entry into the islets that might be targeted by treatment, he explained.
Understanding how T cell access to islets is controlled also raises hopes for developing a therapy to re-educate the immune system to tolerate rather than attack the beta cells. The St. Jude research points to a new route into islet cells.
For this study, scientists used a technique Vignali's laboratory developed in 2006. The technique allows researchers to quickly modify T cell production in mice. Normally mice make millions of T cells that can recognize many different cells and microorganisms. Each T cell carries on its surface a receptor that recognizes and binds to just one specific antigen, or marker, on the surface of the T cell's intended target.
The modification technique allowed researchers to create strains of mice with only two types of T cells, each with different receptors. One population carried a receptor that recognized the insulin-producing beta cells and could cause diabetes. The other group was programmed to recognize a different antigen. Researchers reported they could not induce the latter group of T cells to enter the islets.
Then investigators created and tracked T cells with three types of receptors--receptors from T cells with a proven ability to enter islet cells and cause diabetes, those able to enter islets and cause inflammation, but not diabetes, and a third group of receptors with no connection to type 1 diabetes or islet cells. The scientists reported that none of the T cells, even those with a demonstrated ability to cause diabetes in mice, could induce bystander T cells to enter the islet cells.
Finally, investigators tracked T cells carrying receptors from mice that naturally developed type I diabetes. They created mice with 17 new T cell receptors, five from the spleen of diabetic mice and 12 from T cells isolated in the islets of those diabetic mice. If the islets control T cells entry, then islets in the new mouse strains would be infiltrated by T cells with islet-derived, but not spleen-derived, receptors.
That is what happened. "About 70 percent of the receptors that came from the islets could mediate T cell migration back into the islets, while none of the receptors that came from the spleen could do likewise," Vignali said. The islet-derived receptors were also linked to rapid development of diabetes, with one-third causing diabetes during the 10-week study.
Script taken from the link below
http://www.medicalnewstoday.com/articles/166818.php
BRCA1 does not paint the inactive X to localize XIST RNA
The BRCA1 tumor suppressor involved in breast and ovarian cancer is linked to several fundamental cell regulatory processes. Recently, it was reported that BRCA1 supports localization of XIST RNA to the inactive X chromosome (Xi) in women. The apparent cytological overlap between BRCA1 and XIST RNA across the Xi raised the possibility a direct role of BRCA1 in localizing XIST. We report here that BRCA1 does not paint the Xi or XIST territory, as do markers of Xi facultative heterochromatin. A smaller BRCA1 accumulation abuts Xi, although this is not exclusive to Xi. In BRCA1 depleted normal and tumor cells, or BRCA1 reconstituted cells, BRCA1 status does not closely correlate with XIST localization, however in a BRCA1 inducible system over-expression correlated strongly with enhanced XIST expression. We confirm frequent loss of an Xi in tumor cells. In addition to mitotic loss of Xi, we find XIST RNA expression or localization frequently become compromised in cultured breast cancer cells, suggesting Xi heterochromatin may not be fully maintained. We demonstrate that complex epigenetic differences between tumor cell subpopulations can have striking effects on XIST transcription, accumulation, and localization, but this does not strictly correlate with BRCA1. Although BRCA1 can have indirect effects that impact XIST, our results do not indicate a direct and specific role in XIST RNA regulation. Rather, regulatory factors such as BRCA1 that have broad effects on chromatin or gene regulation can impact XIST RNA and the Xi. We provide preliminary evidence that this may occur as part of a wider failure of heterochromatin maintenance in some cancers.
Script was taken from the given link
http://www.ncbi.nlm.nih.gov
Script was taken from the given link
http://www.ncbi.nlm.nih.gov
Loss of the inactive X chromosome and replication of the active X in BRCA1-defective and wild-type breast cancer cells
In females, X chromosome inactivation (XCI) begins with the expression of the XIST gene from the X chromosome destined to be inactivated (Xi) and the coating of XIST RNA in cis. It has recently been reported that this process is supported by the product of the BRCA1 tumor suppressor gene and that BRCA1-/- cancers show Xi chromatin structure defects, thus suggesting a role of XCI perturbation in BRCA1-mediated tumorigenesis. Using a combined genetic and epigenetic approach, we verified the occurrence of XCI in BRCA1-/- and BRCA1wt breast cancer cell lines. It was ascertained that the Xi was lost in all cancer cell lines, irrespective of the BRCA1 status and that more than one active X (Xa) was present. In addition, no epigenetic silencing of genes normally subjected to XCI was observed. We also evaluated XIST expression and found that XIST may be occasionally transcribed also from Xa. Moreover, in one of the BRCA1wt cell line the restoring of XIST expression using a histone deacetylase inhibitor, did not lead to XCI. To verify these findings in primary tumors, chromosome X behavior was investigated in a few BRCA1-associated and BRCA1-not associated primary noncultured breast carcinomas and the results mirrored those obtained in cancer cell lines. Our findings indicate that the lack of XCI may be a frequent phenomenon in breast tumorigenesis, which occurs independently of BRCA1 status and XIST expression and is due to the loss of Xi and replication of Xa and not to the reactivation of the native Xi.
Script taken from the given link
http://www.ncbi.nlm.nih.gov
Script taken from the given link
http://www.ncbi.nlm.nih.gov
chromosomal abnormalities in basal-like human breast cancer.
Sporadic basal-like cancers (BLC) are a distinct class of human breast cancers that are phenotypically similar to BRCA1-associated cancers. Like BRCA1-deficient tumors, most BLC lack markers of a normal inactive X chromosome (Xi). Duplication of the active X chromosome and loss of Xi characterized almost half of BLC cases tested. Others contained biparental but nonheterochromatinized X chromosomes or gains of X chromosomal DNA. These abnormalities did not lead to a global increase in X chromosome transcription but were associated with overexpression of a small subset of X chromosomal genes. Other, equally aneuploid, but non-BLC rarely displayed these X chromosome abnormalities. These results suggest that X chromosome abnormalities contribute to the pathogenesis of BLC, both inherited and sporadic.
Script taken from the given link,
http://www.ncbi.nlm.nih.gov/pubmed/16473279
Script taken from the given link,
http://www.ncbi.nlm.nih.gov/pubmed/16473279
Cell Culture Reagents
Extracellular Matrices
From reconstituted basement membranes to completely synthetic 3D culture, BD extracellular matrix products can help you from cellular maintenance through differentiation.- Cell Recovery Solution
- BD Cell-Tak™ Cell and Tissue Adhesive
- Collagen I
- Collagen II
- Collagen III
- Collagen IV
- Collagen V
- Collagen VI
- Dispase
- Fibronectin
- Human Extracellular Matrix
- Laminin
- BD Matrigel™ Basement Membrane Matrix
- Osteopontin
- Poly-D-Lysine
- BD PuraMatrix™ Peptide Hydrogel
- Three-Dimensional Scaffolds
- Vitronectin
Cytokines, Growth Factors, and Media Additives
BD Biosciences offers a comprehensive line of high-quality cytokines and media additives to meet your individual needs for culturing animal or human cells in vitro.
Specialty Research Media
- Cell MAb Media
- Endothelial Cell Culture Medium
- Enterocyte Differentiation Medium
- Enterocyte Seeding Medium
- Hepatocyte Culture Medium
- Intestinal Differentiation Media Pack
- Smooth Muscle Cell Differentiation Medium
- Smooth Muscle Cell Proliferation Medium
Script taken from the given link,
http://www.bdbiosciences.com/cellculture/
Development of Novel Advanced Cell Culture Surfaces
Cell-based assays are an essential component of basic research, drug discovery as well as regenerative medicine. Throughout these areas of research, there is an increasing need to culture cells reproducibly in better defined conditions. BD PureCoat™ surfaces are chemically defined, animal-free enhanced cell culture surfaces. This presentation will focus on applications demonstrating the use of BD PureCoat surfaces. More specifi cally, we show that these surfaces provide better post-thaw recovery of cryopreserved cells, and provide enhanced cell attachment and growth of primary, transformed, transfected, and fastidious cell lines when compared to standard TC vessels. Furthermore, we demonstrate that BD PureCoat surfaces continue to provide robust cell attachment in reduced serum and serum-free media conditions. These surfaces also maintain the integrity of cell monolayers and offer superior consistency during vigorous liquid handling procedures used in cell-based assays. BD PureCoat surfaces provide an alternative to biological coatings, without compromising cell attachment and function
This script is not from us and has taken from the link below
http://www.bdbiosciences.com/hotlines/webinars/index.jsp
This script is not from us and has taken from the link below
http://www.bdbiosciences.com/hotlines/webinars/index.jsp
Multicolor Flow Cytometry
Multicolor flow cytometry is a powerful tool for analyzing multiple cellular parameters simultaneously. Recent innovations have dramatically improved the capabilities of instruments to detect and monitor more than four targets at the same time. Using the power of multicolor flow cytometry, researchers have advanced many areas of cellular immunology, including detection of rare cell population subsets using assays with 8, 10, or even up to 17 colors. This Webinar will include examples of multicolor antibody panels and focus on the principles of multicolor panel design such as optimal matching of antigens to labeled fluorochromes, proper use of tandem dyes, and appropriate use of controls.
Script taken from the link below.
www.bdbiosciences.com
for more detail hit this link,
http://www.bdbiosciences.com/hotlines/webinars/index.jsp
Script taken from the link below.
www.bdbiosciences.com
for more detail hit this link,
http://www.bdbiosciences.com/hotlines/webinars/index.jsp
Saturday, October 17, 2009
Jumping On Genetic Testing—The War of the SNPs
How many SNPs does it take to provide a definitive disease risk profile? Quite a few, apparently, as companies continue to pile them higher and deeper into genetic tests. Firms have bet that these tests will be widely adopted by physicians and the public to predict everything from risk of lung cancer among smokers, to prostate cancer, to Alzheimer’s disease, to baldness.
All told, about three dozen companies claim that they can provide genetic testing that predicts an individual’s risk of developing almost everything. “There is a bit of a wild wild west going on in terms of some of the DNA testing that’s out there,” said Francis S. Collins, M.D., Ph.D., the newly appointed NIH head, in an interview with CBS News in September 2008 with regard to a new offering from Smart Genetics purporting to predict susceptibility to Alzheimer’s disease (AD).
“Some of it is done by reputable companies, but there are some that are even unscrupulous who will offer you tests or DNA variations that, frankly, you’re not sure what they mean at all.” Smart Genetics stopped offering its controversial Alzheimer’s Mirror genetic test just eight months after introducing it, and the company subsequently shut its doors.
The Ones Doing the Testing
Major players include deCODE genetics, Navigenics, 23andMe, and Proactive Genomics. In January Proactive Genomics made available a $300 prostate cancer genetic test based on five SNPs, called Focus5. deCODE’s $500 PrCa test was announced less than a month later, for analyzying eight SNPs. Navigenics offers a personalized DNA profile, explained by a genetic counselor, for $2,500. 23andMe and deCODE also advertise their own versions of such profiles.
As recent as January, deCODEme, a division of deCODE genetics, launched two new services, one designed to detect genetic variations associated with cardiovascular diseases and a screen to detect genetic variations linked to the risk of developing various cancers. At $195 and $225, respectively, the new tests cost less than the company’s genome-wide screen, which for $985 assesses genetic risk for 34 diseases and traits ranging from diabetes to male-pattern baldness. deCODE president and founder, Kari Stefansson, M.D., said that the company wanted to give people an opportunity to buy tests that would address their specific needs.
On September 17, the company received a notice from Nasdaq stating that it was not in compliance with the Minimum Bid Price Rule. deCODE got a slight bump on September 20 after reporting that it and multinational collaborators had discovered four novel SNPs conferring increased risk of prostate cancer.
This marked the sixth set of prostate cancer risk factors the company has found. “Using our ability to put these SNPs in a population-wide context, we show that it is now possible to identify those who are at more than a 30% increased lifetime risk, independent of other standard risk factors such as age and family history,” Dr. Steffanson noted.
On September 30, however, deCODE decided to closed its Illinois facility, cutting 60 positions and estimates savings to be about $1.5 million.
Material is taken from the link below.For more detail just click the link below.
www.genengnews.com
http://www.genengnews.com/specialreports/sritem.aspx?oid=65516124
All told, about three dozen companies claim that they can provide genetic testing that predicts an individual’s risk of developing almost everything. “There is a bit of a wild wild west going on in terms of some of the DNA testing that’s out there,” said Francis S. Collins, M.D., Ph.D., the newly appointed NIH head, in an interview with CBS News in September 2008 with regard to a new offering from Smart Genetics purporting to predict susceptibility to Alzheimer’s disease (AD).
“Some of it is done by reputable companies, but there are some that are even unscrupulous who will offer you tests or DNA variations that, frankly, you’re not sure what they mean at all.” Smart Genetics stopped offering its controversial Alzheimer’s Mirror genetic test just eight months after introducing it, and the company subsequently shut its doors.
The Ones Doing the Testing
Major players include deCODE genetics, Navigenics, 23andMe, and Proactive Genomics. In January Proactive Genomics made available a $300 prostate cancer genetic test based on five SNPs, called Focus5. deCODE’s $500 PrCa test was announced less than a month later, for analyzying eight SNPs. Navigenics offers a personalized DNA profile, explained by a genetic counselor, for $2,500. 23andMe and deCODE also advertise their own versions of such profiles.
As recent as January, deCODEme, a division of deCODE genetics, launched two new services, one designed to detect genetic variations associated with cardiovascular diseases and a screen to detect genetic variations linked to the risk of developing various cancers. At $195 and $225, respectively, the new tests cost less than the company’s genome-wide screen, which for $985 assesses genetic risk for 34 diseases and traits ranging from diabetes to male-pattern baldness. deCODE president and founder, Kari Stefansson, M.D., said that the company wanted to give people an opportunity to buy tests that would address their specific needs.
On September 17, the company received a notice from Nasdaq stating that it was not in compliance with the Minimum Bid Price Rule. deCODE got a slight bump on September 20 after reporting that it and multinational collaborators had discovered four novel SNPs conferring increased risk of prostate cancer.
This marked the sixth set of prostate cancer risk factors the company has found. “Using our ability to put these SNPs in a population-wide context, we show that it is now possible to identify those who are at more than a 30% increased lifetime risk, independent of other standard risk factors such as age and family history,” Dr. Steffanson noted.
On September 30, however, deCODE decided to closed its Illinois facility, cutting 60 positions and estimates savings to be about $1.5 million.
Material is taken from the link below.For more detail just click the link below.
www.genengnews.com
http://www.genengnews.com/specialreports/sritem.aspx?oid=65516124
Monday, October 12, 2009
Heat shock protein
Heat shock proteins (HSP) are a class of functionally related proteins whose expression is increased when cells are exposed to elevated temperatures or other stress.This increase in expression istranscriptionally regulated. The dramatic upregulation of the heat shock proteins is a key part of the heat shock response and is induced primarily by heat shock factor (HSF).HSPs are found in virtually all living organisms, from bacteria to humans.
Heat-shock proteins are named according to their molecular weight. For example, Hsp60, Hsp70 and Hsp90 (the most widely-studied HSPs) refer to families of heat shock proteins on the order of 60, 70 and 90 kilodaltons in size, respectively. The small 8 kilodalton protein ubiquitin, which marks proteins for degradation, also has features of a heat shock protein
Discovery:
It is known that rapid heat hardening can be elicited by a brief exposure of cells to sub-lethal high temperature, which in turn provides protection from subsequent and more severe temperature. In 1962, Ritossa reported that heat and the metabolic inhibitor dinitrophenol induced a characteristic pattern of puffing in the chromosomes of Drosophila. This discovery eventually led to the identification of the heat-shock proteins (HSP) or stress proteins whose expression these puffs represented. Increased synthesis of selected proteins in Drosophila cells following stresses such as heat shock was first reported in 1974.
Beginning in the mid-1980s, investigators recognized that many HSPs function as molecular chaperones and thus play a critical role in protein folding, intracellular trafficking of proteins, and coping with proteins denatured by heat and other stresses. Accordingly, the study of stress proteins has undergone explosive growth.
for more detail you can see this link below.These are an open source files that are taken from other links
Heart-to-Heart Tool
We all know the statistics: millions suffer from heart disease, and many suffer heart attacks. Even more alarming is the fact that by some estimates more than 350,000 people die from so-called "sudden death" after a heart attack. Researchers have been baffled by the exact nature and cause of these deaths. Last week, scientists at the University of North Carolina Chapel Hill unveiled a promising new modeling procedure which may shed some light on the mechanisms associated with heart attacks and sudden death.
This new system involved cultured heart cells. In a heart attack, some cells become deprived of oxygen while others continue to receive sufficient oxygen. The region between these two types of cells, called the border zone, is simulated in the cultured model. Since the culture focuses on the interactions in the border zone, it could be very helpful in studying arrhythmias. Arrhythmias are irregularities in the heartbeat usually associated with decreased blood flow in the coronary arteries.
The complex interactions within a particular organism and the size of the actual zone have made animal models particularly difficult in studying the border zone. Likewise, single cells don't display the border irregularities. By using a culture of cells, the research team was able to overcome both limitations. The border zone can be produced and the interactions are essentially isolated for practical purposes.
The cultures appear to be stable for a couple of hours, thus allowing the team to do basic time-based studies.
Since the causes and mechanisms associated with sudden death are so poorly understood, researchers are optimistic that this new modeling system will shed some light on sudden death. By focusing on the internal changes associated with cells and the resulting interactions, the team believes that the culture model will be successful.
script taken from the link below
http://biology.about.com
This new system involved cultured heart cells. In a heart attack, some cells become deprived of oxygen while others continue to receive sufficient oxygen. The region between these two types of cells, called the border zone, is simulated in the cultured model. Since the culture focuses on the interactions in the border zone, it could be very helpful in studying arrhythmias. Arrhythmias are irregularities in the heartbeat usually associated with decreased blood flow in the coronary arteries.
The complex interactions within a particular organism and the size of the actual zone have made animal models particularly difficult in studying the border zone. Likewise, single cells don't display the border irregularities. By using a culture of cells, the research team was able to overcome both limitations. The border zone can be produced and the interactions are essentially isolated for practical purposes.
The cultures appear to be stable for a couple of hours, thus allowing the team to do basic time-based studies.
Since the causes and mechanisms associated with sudden death are so poorly understood, researchers are optimistic that this new modeling system will shed some light on sudden death. By focusing on the internal changes associated with cells and the resulting interactions, the team believes that the culture model will be successful.
script taken from the link below
http://biology.about.com
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