Obstructive Coronary Artery Disease diagnosed by RNA levels of 23 genes – CardioDx, a Pioneer in the Field of Cardiovascular Genomic Diagnostics
Curator: Aviva Lev-Ari, PhD, RN
UPDATED on 11/15/2013
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SOURCE
http://www.devicespace.com/news_story.aspx?NewsEntityId=315972&type=email&source=DS_111513
CardioDx had planned to use some of the funds to expand its commercial efforts, including its sales and marketing workforce; to fund operations as the company pursues more insurance coverage and reimbursement; to “conduct additional clinical and marketing activities” for the company’s Corus CAD blood-based gene expression test; to fund R&D activity; and for “general corporate purposes.” CardioDx will later specify just the how much it plans to put toward each of those activities.
Investors in the company include V-Sciences Investments, Longitude Venture Partners, Artiman Ventures, Kleiner Perkins Caufield & Byers, JP Morgan and Mohr Davidow Ventures.
SOURCE
http://www.massdevice.com/news/cardiodx-spikes-ipo
CardioDX pulls IPO, citing poor market conditions
CardioDX, led by David Levison, was one of three medical technology companies to postpone their IPOs on Thursday due to poor market conditions.
- Cromwell Schubarth
- Senior Technology Reporter-Silicon Valley Business Journal
- CardioDX postponed an IPO on Thursday after deciding that the market is unfavorable at this time.
The Palo Alto company led by CEO David Levison was one of three planned medical tech companies that postponed going public on Thursday. San Diego-basedCelladon and Monrovia-based Xencor also decided to hold off due to poor market conditions.
Redwood City pharmaceutical developer Relypsa, meanwhile, went ahead with a drastically reduced IPO that raised about half of what it had been projected for it.
CardioDX, which sells diagnostic tests for cardiovascular disease, reported total revenue in in 2012 of $2.5 million and a net loss of $25.6 million. The company expects to continue to show losses for the next several years and has an accumulated deficit through June totaling $165.9 million. As of June 30, it had $46.8 million in cash, equivalents and investments.
The company’s biggest existing stakeholder is V-Sciences Investments, a wholly owned subsidiary of Temasek Life Sciences Private Ltd., which holds 19.9 percent of outstanding shares.
Other big stakeholders are Longitude Venture Partners, with a 17.9 percent stake; Artiman Ventures, 13.9 percent; Kleiner Perkins Caufield & Byers, 9.5 percent; JP Morgan, 6.4 percent; and Mohr Davidow Ventures, 5.8 percent.
SOURCE
http://www.bizjournals.com/sanjose/news/2013/11/15/cardiodx-pulls-ipo-citing-poor-market.html
Cardiovascular MDx Firm CardioDx Files to Go Public
UPDATED on 10/14/2013
NEW YORK (GenomeWeb News) – Cardiovascular molecular diagnostics firm CardioDx has filed with the US Securities and Exchange Commission to go public with an intended offering of up to $86.3 million of common stock.
The Palo Alto, Calif.-based firm has not priced its offering yet or said how many shares it plans on offering. Bank of America Merrill Lynch and Jefferies are listed as joint book-running managers on the offering, while Piper Jaffray and William Blair are co-managers.
The company plans on listing on the Nasdaq Global Market under ticker symbol “CDX.”
In its Form S-1, CardioDx said that its tests provide healthcare professionals with “critical, actionable information to improve patient care and management,” with an initial focus on coronary artery diseases (CAD), arrhythmia, and heart failure.
Its flagship product is the Corus CAD, a gene expression-based test for assessing non-diabetic patients who display symptoms suggestive of obstructive CAD. The test was launched in 2009 and through June 30, CardioDx delivered results for more than 40,000 tests, it said.
Corus CAD received Medicare Part B coverage in August 2012, making it a covered benefit for about 48 million Medicare beneficiaries, the company added.
In 2012, CardioDx posted $2.5 million in revenues with a net loss of $25.6 million. Through the first six months of 2013, the firm had revenues $2.9 million and a net loss of $18.4 million.
It had $46.8 million in cash, cash equivalents, and investments as of June 30, it said.
In August 2012, CardioDx raised $58 million in private financing. Before that, it raised $60 million in a financing round. In 2010, GE Healthcare invested $5 million in the company as part of a Series D financing round.
David Levison heads the firm as President and CEO. Other members of the management team include CFO Andrew Guggenhime; Chief Scientific Officer Steven Rosenberg; Chief Medical Officer Mark Monane; and Chief Commercial Officer Deborah Kilpatrick.
CardioDx is the latest in a recent string of omics-related companies who have gone public or have filed to go public in the US. Cancer Genetics, NanoString Technologies, and Foundation Medicine launched their IPOs earlier this year. Meanwhile, Veracyte, Biocept, and Evogene have filed to float.
Related Stories
- CAP Accredits CardioDx’s Laboratory
May 9, 2013 / GenomeWeb Daily News
- CardioDx Raises $58M in Private Financing
August 27, 2012 / GenomeWeb Daily News
- CardioDx Gets Medicare Coverage for Coronary Artery Disease Test
August 8, 2012 / GenomeWeb Daily News
- GE Healthcare Takes Stake in CardioDx; Forms MDx Alliance
May 13, 2010 / GenomeWeb Daily News
- CTC Dx Firm Biocept Files for IPO
September 24, 2013 / GenomeWeb Daily News
UPDATED on 2/25/2013
CardioDx Announces Publication of COMPASS Study Demonstrating the Corus CAD Test Outperforms Myocardial Perfusion Imaging in Overall Diagnostic Accuracy for Obstructive Coronary Artery Disease
Tue Feb 19, 2013 8:30am EST
– Study Highlights the Validity of Corus CAD as a First-Line Test to Help Clinicians Exclude Obstructive CAD as a Cause of the Patient’s Symptoms – PALO ALTO, Calif., Feb. 19, 2013
/PRNewswire/ — CardioDx, Inc., a pioneer in the field of cardiovascular genomic diagnostics, today announced the publication of the COMPASS (Coronary Obstruction Detection by Molecular
Personalized Gene Expression) study in Circulation: Cardiovascular Genetics, a journal of the American Heart Association.
Results of the prospective, multi-center U.S. study showed that Corus® CAD, a blood-based gene expression test, demonstrated high accuracy with both a high negative predictive value (96 percent) and high sensitivity (89 percent) for assessing obstructive coronary artery disease (CAD) in a population of patients referred for stress testing with myocardial perfusion imaging (MPI). The study’s authors conclude that using Corus CAD earlier in the diagnostic algorithm could reduce the number of invasive cardiac tests by more accurately evaluating the presence of obstructive coronary artery disease compared to the traditional algorithm of stress myocardial perfusion imaging (MPI) in these patients.
COMPASS enrolled stable patients with symptoms suggestive of CAD who had been referred for MPI at 19 U.S. sites. A blood sample was obtained in all 431 patients prior to MPI and Corus CAD gene expression testing was performed with study investigators blinded to Corus CAD test results. Following MPI, patients underwent either invasive coronary angiography or coronary CT angiography, gold-standard anatomical tests for the diagnosis of coronary artery disease.
The study was designed to provide additional independent validation of the Corus CAD test in a real-world intended use patient population of patients presenting for MPI, a common noninvasive test for CAD, and builds on the results of the previous PREDICT validation study. Corus CAD requires only a simple blood draw for testing, making it safe, convenient, and easy to administer. The study evaluated results in stable non-diabetic patients with typical or atypical symptoms suggestive of CAD and found that Corus CAD surpassed the accuracy of MPI, a test that was administered more 10 million times in the U.S. in 2010.[1]
“The evaluation of stable patients with chest pain and other symptoms suggestive of CAD is a common challenge for clinicians, accounting for as many as 10,000 outpatient visits each day,” said the publication’s lead author, Gregory S. Thomas, M.D., M.P.H., Medical Director of the MemorialCare Heart & Vascular Institute at Long Beach Memorial Medical Center and Clinical Professor of Medicine and Director of Nuclear Cardiology Education at the University of California-Irvine School of Medicine. “In the U.S., MPI testing is often performed in these patients and is followed by referral to invasive coronary angiography. Based on the results of this study of the Corus CAD gene expression test, we now have a reliable diagnostic approach for evaluating patients with symptoms of obstructive CAD. With its high sensitivity and negative predictive value, Corus CAD may help clinicians accurately and efficiently exclude the diagnosis of obstructive CAD early in the diagnostic pathway, so they can assess for other causes of their patients’ symptoms.”
The pre-specified primary endpoint of the COMPASS study was the receiver-operator characteristics (ROC) analysis to evaluate the ability of Corus CAD to identify coronary arterial blockages of 50 percent or greater by quantitative coronary angiography. Corus CAD outperformed MPI in overall diagnostic accuracy for assessing obstructive CAD, with an area under the curve (AUC) of 0.79 for the Corus CAD test compared to MPI site and core-lab read AUCs of 0.59 and 0.63 respectively (p<0.001). In addition, Corus CAD performed better than MPI in sensitivity (89 percent vs. 27 percent, p<0.001) and negative predictive value (96 percent vs. 88 percent, p<0.001) parameters, thus demonstrating excellent performance for excluding obstructive CAD as the cause of a patient’s symptoms. The COMPASS results corroborated earlier findings from the PREDICT multicenter U.S. validation study[2] demonstrating that the Corus CAD score is proportional to coronary artery stenosis severity.
“Corus CAD can help solve an enormous unmet need in healthcare by providing clinicians with a safe, convenient and reliable tool to help evaluate common patient symptoms and triage them more appropriately for subsequent therapy or additional testing,” said David Levison, President and CEO of CardioDx. “In addition to its higher diagnostic accuracy, Corus CAD holds potential to reduce a major healthcare expense category – unnecessary noninvasive imaging and/or invasive coronary angiography procedures and their associated risks and side effects. We have worked closely with leading clinicians to build a solid clinical and economic foundation for Corus CAD, leading to its growing acceptance in the medical and payer communities as evidenced by the more than 35,000 tests performed to date and Medicare’s decision to cover the test.”
SOURCE:
CardioDx is promoting yet another post-marketing study whose data may help the company’s gene expression test for obstructive coronary artery disease reach more patients, better compete with the standard of care and also build vital market share.
Executives at the California-based 2012 Fierce 15 company say they wanted more data on Corus CAD‘s real-world use, building on its previous PREDICT validation trial as a result. The test has been on sale commercially since 2009 and won crucial Medicare reimbursement last fall. Chief Scientific Officer Steven Rosenberg told FierceMedicalDevices via email that the results from the latest study pointed in a number of positive directions.
“It demonstrates performance at least as good as that seen in the PREDICT study, but in the population the Corus CAD is indicated for,” Rosenberg said, “It shows significantly higher performance for obstructive CAD than MPI, which is the most common non-invasive imaging test used in this regard.”
A 431-patient clinical study of the blood diagnostic rated the test with a 96% negative predictive value and 89% high sensitivity, in assessing the condition in patients who were referred for stress testing with myocardial perfusion imaging (MPI). (Last November, CardioDx heralded similar results from another study using Corus CAD on 98 geriatric patients.) Details are published in the journal Circulation: Cardiovascular Genetics.
The blood test, conducted at 19 U.S. sites through multiple academic institutions, determined that using Corus CAD earlier in the diagnostic process better assessed the presence of coronary artery disease versus MPI. This might encourage doctors to cut back on invasive, more expensive cardiac tests by ruling out obstructive CAD sooner. In other words, determining a patient doesn’t have obstructive CAD eliminates the need for diagnostic procedures such as coronary angiography or coronary CT angiography, the company explains.
Post-marketing studies are increasingly important in today’s health care market, with the need to demonstrate the utility of a device or diagnostic in as most detailed a way possible. And it’s not just boosting the standard of care; the Affordable Care Act means value matters, too, more than ever before. Success with this mission can help broaden market share and also increase the chance of private as well as government insurance coverage. Additionally, new post-marketing trials can also set the stage for expanded indications down the line.
SOURCE:
A Blood Based Gene Expression Test for Obstructive Coronary Artery Disease Tested in Symptomatic Non-Diabetic Patients Referred for Myocardial Perfusion Imaging: The COMPASS Study
- Gregory S. Thomas1*,
- Szilard Voros2,
- John A. McPherson3,
- Alexandra J. Lansky4,
- Mary E. Winn5,
- Timothy M. Bateman6,
- Michael R. Elashoff7,
- Hsiao D. Lieu7,
- Andrea M. Johnson7,
- Susan E. Daniels7,
- Joseph A. Ladapo8,
- Charles E. Phelps9,
- Pamela S. Douglas10 and
- Steven Rosenberg7
+Author Affiliations
1Long Beach Memorial Medical Center, Long Beach & University of California, Irvine, CA
2Stony Brook University Medical Center, Stony Brook, NY
3Vanderbilt University, Nashville, TN
4Yale University School of Medicine, New Haven, CN
5Scripps Translational Science Institute, La Jolla, CA
6University of Missouri, Kansas City, MO
7CardioDx, Inc., Palo Alto, CA
8New York University School of Medicine, New York, NY
9University of Rochester, Rochester, NY
10Duke Clinical Research Institute, Duke University, Durham, NC
- ↵* MemorialCare Heart and Vascular Institute, Long Beach Memorial Medical Center, 2801 Atlantic Avenue, Long Beach, CA 90806 gthomas@mimg.com
Abstract
Background—Obstructive coronary artery disease (CAD) diagnosis in symptomatic patients often involves non-invasive testing before invasive coronary angiography (ICA). A blood-based gene expression score (GES) was previously validated in non-diabetic patients referred for ICA but not in symptomatic patients referred for myocardial perfusion imaging (MPI).
Methods and Results—This prospective multi-center study obtained peripheral blood samples for GES before MPI in 537 consecutive patients. Patients with abnormal MPI usually underwent ICA; all others had research coronary CT-angiography (CTA), with core laboratories defining coronary anatomy. A total of 431 patients completed GES, coronary imaging (ICA or CTA), and MPI. Mean age was 56±10 (48% women). The pre-specified primary endpoint was GES receiver-operator characteristics (ROC) analysis to discriminate ≥50% stenosis (15% prevalence by core laboratory analysis). ROC curve area (AUC) for GES was 0.79 (95% CI 0.73-0.84, p<.001), with sensitivity, specificity, and negative predictive value (NPV) of 89%, 52%, and 96%, respectively, at a pre-specified threshold of ≤15 with 46% of patients below this score. The GES outperformed clinical factors by ROC and reclassification analysis and also showed significant correlation with maximum percent stenosis. Six-month follow-up on 97% of patients showed that 27/28 patients with adverse cardiovascular events or revascularization had GES >15. Site and core-lab MPI had AUCs of 0.59 and 0.63, respectively, significantly less than GES.
Conclusions—A GES has high sensitivity and NPV for obstructive CAD. In this population clinically referred for MPI, the GES outperformed clinical factors and MPI.
Clinical Trial Registration Information—www.clinicaltrials.gov; Identifier: NCT01117506.
- Received June 6, 2012.
- Revision received January 15, 2013.
- Accepted February 5, 2013.
- Copyright © 2013, Circulation: Cardiovascular Genetics
CardioDx heart disease test wins Medicare coverage
San Francisco Business Times by Ron Leuty, Reporter
Date: Wednesday, August 8, 2012, 4:00am PDT
CardioDx’s test for obstructive heart disease will be covered by Medicare retroactive to Jan. 1.
- Ron Leuty
- Reporter- San Francisco Business Times
A key national Medicare contractor will cover the cost of a coronary artery disease test developed by CardioDx Inc.
The move is important for Palo Alto-based CardioDx because private insurers tend to follow the federal government’s Medicare health insurance program. The company has had to seek reimbursement on a case-by-case basis with those private insurers since its Corus CAD gene expression test hit the market in June 2009.
The decision disclosed Tuesday by Palmetto GBA, a national contractor that administers Medicare benefits in Columbia, S.C., means that Medicare will cover the test for as many as 40 million enrollees. Coverage is retroactive to Jan. 1.
Corus CAD is a shoebox-size kit that uses a simple blood draw to measure the RNA levels of 23 genes. Using an algorithm, it then creates a score that determines the likelihood that a patient has obstructive coronary artery disease.
“By providing Medicare beneficiaries access to Corus CAD, this coverage decision enables patients to avoid unnecessary procedures and risks associated with cardiac imaging and elective invasive angiography, while helping payers address an area of significant healthcare spending,” CardioDx President and CEO David Levison said in a press release.
The decision represents the latest Medicare-coverage win for Bay Area diagnostic test makers. Palmetto earlier this year opted to cover the Afirma gene expression test from South San Francisco’s Veracyte Inc. to diagnosis thyroid nodules, and last summer Palmetto said it would cover Redwood City-based Genomic Health Inc.’s (NASDAQ: GHDX)colon cancer recurrence test.
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This is a remarkable victory for the development of genomics testing, and the justification for reimbursement is just the right way to go about it. You see it required a combinatorial analysis on 23 predictive RNAs. If each test is scaled 0 or 1 (which may not be the case because of the weight of information), just to keep it simple – there would be a minimum of 529 combinatorial classes by a Bernoulli test if there was no information in the data. Of course the research looked at RNAs that were unimportant for the classification and were rejected. I don’t know how many patients that they had to look at just to extract the information, but it would have to follow the principles that Jay Magidson is writing about with respect to sample size, probably a bootstrap or randomization, validation and cross validation. In reality you end up with a truth table that has combinatorial classes with a small frequency and others with very large frequencies. What is remarkable is that this may be a really good identification of genomics tied to a metabolic disease (with eNOS, the ratio of w-3/w-6 PUFAs, HDL cholesterol, some tie in with abdominal or truncal adiposity and adipokines, none of which is expressed in the diagnostic prediction. I would imagine that they calculate a probability estimation. It could be that the cost of imaging methods will take time before the physicians have complete confidence. The other factor that Anderson has made is that for this to get really big, it will have to get to a production level of the hemogram, but his statement didn’t refer to genomics, but to proteomics.
Dr. Larry
Thank you for the outstanding comment on my Post above.
I am to look for now for a Category Owner for Genomic Testing Methodologies.
You are welcome, in the near future, to consider Authoring a post on identification of genomics ties to metabolic diseases “(with eNOS, the ratio of w-3/w-6 PUFAs, HDL cholesterol, some tie in with abdominal or truncal adiposity and adipokines)” none of which is expressed in the diagnostic prediction at present time. Thus, omission due to the scientific Unkown !!
I have something to post that is closely related. I just have to continue the completion of my links. There is a really interesting work that leads in that direction.
Links conversion to LIVE links is a MUST before a Publish, for future reference.
Connecting EACH post with all Your Groups of RELEVANCE to the post is a MUST after Publishing, for future reference.
I am happy you are to Connect each post to our FAceBook Page and to Tweet about it via LinkedIn Screen or as a stand alone tweet.
The Business aspect of the Blog is in the HITS !!
PUT IT IN CONTEXT OF CANCER CELL MOVEMENT
The contraction of skeletal muscle is triggered by nerve impulses, which stimulate the release of Ca2+ from the sarcoplasmic reticuluma specialized network of internal membranes, similar to the endoplasmic reticulum, that stores high concentrations of Ca2+ ions. The release of Ca2+ from the sarcoplasmic reticulum increases the concentration of Ca2+ in the cytosol from approximately 10-7 to 10-5 M. The increased Ca2+ concentration signals muscle contraction via the action of two accessory proteins bound to the actin filaments: tropomyosin and troponin (Figure 11.25). Tropomyosin is a fibrous protein that binds lengthwise along the groove of actin filaments. In striated muscle, each tropomyosin molecule is bound to troponin, which is a complex of three polypeptides: troponin C (Ca2+-binding), troponin I (inhibitory), and troponin T (tropomyosin-binding). When the concentration of Ca2+ is low, the complex of the troponins with tropomyosin blocks the interaction of actin and myosin, so the muscle does not contract. At high concentrations, Ca2+ binding to troponin C shifts the position of the complex, relieving this inhibition and allowing contraction to proceed.
Figure 11.25
Association of tropomyosin and troponins with actin filaments. (A) Tropomyosin binds lengthwise along actin filaments and, in striated muscle, is associated with a complex of three troponins: troponin I (TnI), troponin C (TnC), and troponin T (TnT). In (more ) Contractile Assemblies of Actin and Myosin in Nonmuscle Cells
Contractile assemblies of actin and myosin, resembling small-scale versions of muscle fibers, are present also in nonmuscle cells. As in muscle, the actin filaments in these contractile assemblies are interdigitated with bipolar filaments of myosin II, consisting of 15 to 20 myosin II molecules, which produce contraction by sliding the actin filaments relative to one another (Figure 11.26). The actin filaments in contractile bundles in nonmuscle cells are also associated with tropomyosin, which facilitates their interaction with myosin II, probably by competing with filamin for binding sites on actin.
Figure 11.26
Contractile assemblies in nonmuscle cells. Bipolar filaments of myosin II produce contraction by sliding actin filaments in opposite directions. Two examples of contractile assemblies in nonmuscle cells, stress fibers and adhesion belts, were discussed earlier with respect to attachment of the actin cytoskeleton to regions of cell-substrate and cell-cell contacts (see Figures 11.13 and 11.14). The contraction of stress fibers produces tension across the cell, allowing the cell to pull on a substrate (e.g., the extracellular matrix) to which it is anchored. The contraction of adhesion belts alters the shape of epithelial cell sheets: a process that is particularly important during embryonic development, when sheets of epithelial cells fold into structures such as tubes.
The most dramatic example of actin-myosin contraction in nonmuscle cells, however, is provided by cytokinesisthe division of a cell into two following mitosis (Figure 11.27). Toward the end of mitosis in animal cells, a contractile ring consisting of actin filaments and myosin II assembles just underneath the plasma membrane. Its contraction pulls the plasma membrane progressively inward, constricting the center of the cell and pinching it in two. Interestingly, the thickness of the contractile ring remains constant as it contracts, implying that actin filaments disassemble as contraction proceeds. The ring then disperses completely following cell division.
Figure 11.27
Cytokinesis. Following completion of mitosis (nuclear division), a contractile ring consisting of actin filaments and myosin II divides the cell in two.
http://www.ncbi.nlm.nih.gov/books/NBK9961/
This is good. I don’t recall seeing it in the original comment. I am very aware of the actin myosin troponin connection in heart and in skeletal muscle, and I did know about the nonmuscle work. I won’t deal with it now, and I have been working with Aviral now online for 2 hours.
I have had a considerable background from way back in atomic orbital theory, physical chemistry, organic chemistry, and the equilibrium necessary for cations and anions. Despite the calcium role in contraction, I would not discount hypomagnesemia in having a disease role because of the intracellular-extracellular connection. The description you pasted reminds me also of a lecture given a few years ago by the Nobel Laureate that year on the mechanism of cell division.
PUT IT IN CONTEXT OF CANCER CELL MOVEMENT
The contraction of skeletal muscle is triggered by nerve impulses, which stimulate the release of Ca2+ from the sarcoplasmic reticuluma specialized network of internal membranes, similar to the endoplasmic reticulum, that stores high concentrations of Ca2+ ions. The release of Ca2+ from the sarcoplasmic reticulum increases the concentration of Ca2+ in the cytosol from approximately 10-7 to 10-5 M. The increased Ca2+ concentration signals muscle contraction via the action of two accessory proteins bound to the actin filaments: tropomyosin and troponin (Figure 11.25). Tropomyosin is a fibrous protein that binds lengthwise along the groove of actin filaments. In striated muscle, each tropomyosin molecule is bound to troponin, which is a complex of three polypeptides: troponin C (Ca2+-binding), troponin I (inhibitory), and troponin T (tropomyosin-binding). When the concentration of Ca2+ is low, the complex of the troponins with tropomyosin blocks the interaction of actin and myosin, so the muscle does not contract. At high concentrations, Ca2+ binding to troponin C shifts the position of the complex, relieving this inhibition and allowing contraction to proceed.
Figure 11.25
Association of tropomyosin and troponins with actin filaments. (A) Tropomyosin binds lengthwise along actin filaments and, in striated muscle, is associated with a complex of three troponins: troponin I (TnI), troponin C (TnC), and troponin T (TnT). In (more ) Contractile Assemblies of Actin and Myosin in Nonmuscle Cells
Contractile assemblies of actin and myosin, resembling small-scale versions of muscle fibers, are present also in nonmuscle cells. As in muscle, the actin filaments in these contractile assemblies are interdigitated with bipolar filaments of myosin II, consisting of 15 to 20 myosin II molecules, which produce contraction by sliding the actin filaments relative to one another (Figure 11.26). The actin filaments in contractile bundles in nonmuscle cells are also associated with tropomyosin, which facilitates their interaction with myosin II, probably by competing with filamin for binding sites on actin.
Figure 11.26
Contractile assemblies in nonmuscle cells. Bipolar filaments of myosin II produce contraction by sliding actin filaments in opposite directions. Two examples of contractile assemblies in nonmuscle cells, stress fibers and adhesion belts, were discussed earlier with respect to attachment of the actin cytoskeleton to regions of cell-substrate and cell-cell contacts (see Figures 11.13 and 11.14). The contraction of stress fibers produces tension across the cell, allowing the cell to pull on a substrate (e.g., the extracellular matrix) to which it is anchored. The contraction of adhesion belts alters the shape of epithelial cell sheets: a process that is particularly important during embryonic development, when sheets of epithelial cells fold into structures such as tubes.
The most dramatic example of actin-myosin contraction in nonmuscle cells, however, is provided by cytokinesisthe division of a cell into two following mitosis (Figure 11.27). Toward the end of mitosis in animal cells, a contractile ring consisting of actin filaments and myosin II assembles just underneath the plasma membrane. Its contraction pulls the plasma membrane progressively inward, constricting the center of the cell and pinching it in two. Interestingly, the thickness of the contractile ring remains constant as it contracts, implying that actin filaments disassemble as contraction proceeds. The ring then disperses completely following cell division.
Figure 11.27
Cytokinesis. Following completion of mitosis (nuclear division), a contractile ring consisting of actin filaments and myosin II divides the cell in two.
http://www.ncbi.nlm.nih.gov/books/NBK9961/
This is good. I don’t recall seeing it in the original comment. I am very aware of the actin myosin troponin connection in heart and in skeletal muscle, and I did know about the nonmuscle work. I won’t deal with it now, and I have been working with Aviral now online for 2 hours.
I have had a considerable background from way back in atomic orbital theory, physical chemistry, organic chemistry, and the equilibrium necessary for cations and anions. Despite the calcium role in contraction, I would not discount hypomagnesemia in having a disease role because of the intracellular-extracellular connection. The description you pasted reminds me also of a lecture given a few years ago by the Nobel Laureate that year on the mechanism of cell division.
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Open Journals vs. Subscription-based « Pharmaceutical Intelligenceâ, very compelling plus the blog post ended up being a good read.
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I actually consider this amazing blog , âSAME SCIENTIFIC IMPACT: Scientific Publishing –
Open Journals vs. Subscription-based « Pharmaceutical Intelligenceâ, very compelling plus the blog post ended up being a good read.
Many thanks,Annette
I actually consider this amazing blog , âSAME SCIENTIFIC IMPACT: Scientific Publishing –
Open Journals vs. Subscription-based « Pharmaceutical Intelligenceâ, very compelling plus the blog post ended up being a good read.
Many thanks,Annette
I actually consider this amazing blog , âSAME SCIENTIFIC IMPACT: Scientific Publishing –
Open Journals vs. Subscription-based « Pharmaceutical Intelligenceâ, very compelling plus the blog post ended up being a good read.
Many thanks,Annette
I actually consider this amazing blog , âSAME SCIENTIFIC IMPACT: Scientific Publishing –
Open Journals vs. Subscription-based « Pharmaceutical Intelligenceâ, very compelling plus the blog post ended up being a good read.
Many thanks,Annette