170 insulin signaling & vldl overproduction
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1) The document discusses insulin signaling and VLDL overproduction in insulin resistance. It examines how fructose feeding impairs tyrosine phosphorylation of the insulin receptor, IRS-1, and IRS-2 in hepatocytes, reducing PI3-kinase activity and Akt phosphorylation while enhancing PTP-1B mass and activity. 2) It also finds that inhibition of cellular phosphatase activity with vanadate enhances insulin signaling and reduces ApoB secretion from hepatocytes by increasing insulin receptor phosphorylation, stabilizing cellular ApoB levels, and decreasing ApoB secretion. 3) The findings provide evidence that impaired insulin signaling and reduced PI3-kinase activity contribute to overproduction of VLDL in
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The document discusses research into producing recombinant forms of the Cynara cardunculus Cyprosins, which are aspartic proteinases with milk clotting activity found in cardoon flowers. Researchers constructed expression cassettes containing genes for the Cyprosins with different signal sequences and expressed them in Saccharomyces cerevisiae. Cyprosin A was produced intracellularly but was inactive. Cyprosin B was actively secreted when expressed with the MFα1 presequence and native prosequence. A site-directed mutagenesis was performed to change the active site sequence of Cyprosin B from Asp-Ser-Gly to Asp-Thr-Gly as in other aspartic proteinases, but
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127 arterial wall injury and temperature
This study explored temperature variations in the arterial wall following coronary wall injury using an animal model. Pigs underwent thermographic scans of a targeted coronary artery area before and after injury induced by a balloon. Temperature disruption was observed immediately after injury that correlated with macrophage concentration at the injury site. After 4 days, temperature increments remained correlated with macrophage levels, indicating local inflammation. The findings suggest wall injury promotes inflammation that could lead to hyperplasia or thrombosis, so minimizing trauma during coronary interventions is important.
147 vulnerable thrombogenic blood
This editorial discusses factors that influence whether a ruptured atherosclerotic plaque leads to a coronary thrombosis. It reports on a study that found increased levels of circulating tissue factor activity in poorly-controlled type 2 diabetics, smokers, and hyperlipidemic patients. This tissue factor increases blood thrombogenicity and correlates with an increased risk of atherothrombotic complications in these populations. The authors conclude that improved glycemic control in diabetics reduces tissue factor levels and thrombogenicity. Risk factors such as smoking and hyperlipidemia increase tissue factor and thrombogenicity levels.
081 carotid artery plaque
This document contains information about plaque imaging in arteries using MRI. It includes images and descriptions of plaque found in the left internal carotid artery, aortic plaque, and plaque in the left anterior descending coronary artery. The images demonstrate different plaque types and features visualized using MRI with resolutions between 450um and 4.5mm. Citations are provided for related studies on plaque imaging led by researchers at Mount Sinai School of Medicine.
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The document discusses research into producing recombinant forms of the Cynara cardunculus Cyprosins, which are aspartic proteinases with milk clotting activity found in cardoon flowers. Researchers constructed expression cassettes containing genes for the Cyprosins with different signal sequences and expressed them in Saccharomyces cerevisiae. Cyprosin A was produced intracellularly but was inactive. Cyprosin B was actively secreted when expressed with the MFα1 presequence and native prosequence. A site-directed mutagenesis was performed to change the active site sequence of Cyprosin B from Asp-Ser-Gly to Asp-Thr-Gly as in other aspartic proteinases, but
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143 plaque inflammation spio
This study investigated the use of superparamagnetic iron oxide (SPIO) nanoparticles to detect vulnerable atherosclerotic plaques via MRI. Histological analysis found higher SPIO uptake in inflamed plaques of WHHL rabbits compared to normal arterial walls. MRI of WHHL rabbits showed decreased aortic wall signal intensity after SPIO injection. Ex vivo MRI further revealed luminal irregularities and negative enhancement in WHHL aortas. The results suggest SPIO can detect plaque inflammation and vulnerability by MRI, with potential for targeted SPIO to precisely locate high-risk plaques.
140 mr imaging of fibrin
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127 arterial wall injury and temperature
This study explored temperature variations in the arterial wall following coronary wall injury using an animal model. Pigs underwent thermographic scans of a targeted coronary artery area before and after injury induced by a balloon. Temperature disruption was observed immediately after injury that correlated with macrophage concentration at the injury site. After 4 days, temperature increments remained correlated with macrophage levels, indicating local inflammation. The findings suggest wall injury promotes inflammation that could lead to hyperplasia or thrombosis, so minimizing trauma during coronary interventions is important.
147 vulnerable thrombogenic blood
This editorial discusses factors that influence whether a ruptured atherosclerotic plaque leads to a coronary thrombosis. It reports on a study that found increased levels of circulating tissue factor activity in poorly-controlled type 2 diabetics, smokers, and hyperlipidemic patients. This tissue factor increases blood thrombogenicity and correlates with an increased risk of atherothrombotic complications in these populations. The authors conclude that improved glycemic control in diabetics reduces tissue factor levels and thrombogenicity. Risk factors such as smoking and hyperlipidemia increase tissue factor and thrombogenicity levels.
081 carotid artery plaque
This document contains information about plaque imaging in arteries using MRI. It includes images and descriptions of plaque found in the left internal carotid artery, aortic plaque, and plaque in the left anterior descending coronary artery. The images demonstrate different plaque types and features visualized using MRI with resolutions between 450um and 4.5mm. Citations are provided for related studies on plaque imaging led by researchers at Mount Sinai School of Medicine.
131 the evolution of coronary atherosclerosis
The document discusses the natural progression of coronary atherosclerosis over time from normal artery to vulnerable plaque. It describes how snapshots can identify plaque vulnerability or likelihood to progress. Physiologic shear stress is protective for endothelium while low shear stress promotes atherosclerosis. 3D reconstruction of arterial segments can analyze plaque and shear stress. Regions of baseline low shear stress saw increased plaque and arterial enlargement over 6 months. Identification of minor obstructions likely to progress could allow preventive interventions to avert adverse events like heart attack.
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This document provides background on Jacques Barth, an expert in cardiovascular imaging and risk assessment. It discusses the evolution of ultrasound technology for measuring intima-media thickness (IMT) from 1986 to 2005. IMT is an early marker of atherosclerosis and cardiovascular risk. The document also addresses issues around vulnerable plaques, reporting IMT measurements, and assessing cardiovascular risk in children and adolescents.
123 coronary dialsysis
Atherosclerosis is a leading cause of death worldwide. It is a systemic inflammatory disease involving the buildup of plaque in artery walls. Inflammatory markers like C-reactive protein are associated with future coronary events. The authors describe a Cardiac Dialysis System designed to specifically target and remove inflammatory markers from the bloodstream to stabilize vulnerable plaques and prevent acute cardiac events like heart attack.
179 chlamydophila pneumoniae
C. pneumoniae infection of human aortic endothelial cells leads to increased expression of the cell adhesion molecule ICAM-1. The study found that C. pneumoniae activates the PKC and NF-κB signaling pathways in endothelial cells, resulting in increased transcription of the ICAM-1 gene. Inhibition of either PKC or NF-κB blocked the C. pneumoniae-induced upregulation of ICAM-1. The increased ICAM-1 expression contributes to the chronic inflammation associated with atherosclerosis by promoting adhesion and transmigration of monocytes into the arterial wall.
129 inflammation and culprit lesions
This document discusses inflammation in coronary arteries and culprit lesions. It finds that:
1. Inflammation is present in many non-culprit lesions, not just culprit lesions, based on a study of 74 coronary arteries.
2. Inflammation therefore has a very low positive predictive value (<3%) for identifying the actual culprit lesion responsible for a clinical event like a heart attack.
3. Inflammation appears to be a local arterial phenomenon, as cross-sectional sampling of inflammation in one part of an artery did not strongly correlate with levels in other parts or in paired left/right arteries.
187 athero reversa mice
The document describes a new mouse model called "AtheroReversa mice" that allows researchers to reverse hypercholesterolemia and atherosclerosis without drugs or diet changes. The mice lack the LDL receptor and ApoB genes but have a conditional Mttp gene that produces MTP. Injecting the mice with pI-pC activates Cre recombinase which inactivates Mttp in the liver, eliminating LDL cholesterol production and preventing atherosclerosis. This new model could help analyze regression of existing atherosclerotic plaques.
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The document discusses the role of lipoproteins, particularly LDL and HDL, in inflammation and atherosclerosis. LDL readily enters the artery wall where it can become modified, making it proinflammatory. Modified LDL stimulates expression of MCP-1, which recruits monocytes. Modified LDL also promotes differentiation of monocytes into macrophages. In contrast, HDL is potentially anti-inflammatory. Atherosclerosis is characterized as an inflammatory disease where lipoproteins influence multiple aspects of inflammation.
039 mr contrast agents for vulnerable plaque imaging
1. MS-325 is an albumin-targeted gadolinium contrast agent that highlights inflamed vessel walls and facilitates plaque imaging. It provides prolonged enhancement of the vessel wall and lumen, allowing for high resolution detection of plaque burden.
2. Studies show strong vessel wall enhancement with MS-325 due to increased capillary volume and binding to extravasated albumin in the vessel wall of patients with atherosclerosis. This may help identify stenosis and quantify plaque.
3. Experimental models demonstrate MS-325 can improve visualization of vulnerable plaque features like lipid cores and thin fibrous caps, as well as directly detect thrombus formation during plaque rupture.
243 b cell
I. The document summarizes several studies that investigated the role of the immune system, particularly B cells, in atherosclerosis using mouse models.
II. One study found that RAG-1 deficient mice, which lack functional B and T cells, exhibited increased neointimal formation following arterial injury compared to wild type mice. Transferring B cells from wild type mice to RAG-1 deficient mice reduced neointimal formation.
III. Overall, the studies suggest that B cells may play a protective role against atherosclerosis by reducing plaque formation and progression. The mechanism may involve antibodies that target oxidation-specific epitopes, but this requires further investigation.
190 virus infected monocyes
Virus-infected monocytes can initiate coagulation and promote inflammation. An in vitro study found that monocytes infected with cytomegalovirus, influenza A virus, or Chlamydia pneumoniae expressed tissue factor and reduced clotting time, indicating initiation of coagulation. The viruses also stimulated monocytes to produce inflammatory cytokines like IL-6 and IL-8. While all three viruses infected monocytes, influenza A most strongly induced cytokine production. This suggests virus-infected monocytes may contribute to both acute coronary events by promoting plaque instability and the chronic atherosclerosis process through sustained inflammation and coagulation.
159 spio uptake by macrophages
This document describes a study comparing four types of superparamagnetic iron oxide (SPIO) nanoparticles and their ability to be taken up by macrophages and detect plaque inflammation via MRI. The study finds that lipid-coated SPIO-2 is taken up strongly by macrophages, induces less oxidative stress than dextran-coated SPIO, and is not inhibited by a mannose receptor inhibitor. SPIO-2 therefore shows potential as a contrast agent for noninvasive MR imaging of vulnerable atherosclerotic plaques containing macrophage inflammation. Such detection could help identify high-risk patients and reduce deaths from heart attacks and strokes.
511 first steps towards understanding
This study investigated genetic differences in vascular remodeling and shear stress regulation in response to altered blood flow in four inbred rat strains. The results showed significant differences among strains in their ability to maintain normal endothelial shear stress levels through outward arterial remodeling when flow was increased or decreased. Specifically, the GH strain was better able to regulate shear stress through remodeling compared to the SHR-SP strain. These genetic differences in vascular responses to changes in blood flow have important implications for understanding the variable manifestations of atherosclerosis and susceptibility to cardiovascular disease in individuals and populations. Future studies are needed to investigate whether similar genetic differences exist in humans and their role in clinical outcomes.
061 a nano mega initiative
The document summarizes a meeting on vulnerable plaque research between UT-THI and Rice Coalition. It provides background on vulnerable plaque, describing it as dangerous forms of fat buildup in the arterial wall that can rupture or induce thrombosis. It reviews the history of research in this area dating back to the 19th century, and profiles the many contributors to the field. Emerging techniques for detecting vulnerable plaque non-invasively or invasively are also summarized, such as various imaging modalities, blood tests, and endothelial function tests.
209 trans blood vision™
Trans-Blood Vision is a patented infrared technique that uses short-wave infrared wavelengths to see directly through blood. It has the potential to find vulnerable plaque lesions without first entering them, determine their size and surface characteristics in high resolution, and look at their material constituents both on and below the surface. While it cannot provide direct visual guidance for therapy or penetrate as deeply as ultrasound, combining it with augmentative technologies could allow for real-time multi-mode detection, analysis, and therapy guidance of vulnerable plaque lesions. The document concludes that Trans-Blood Vision warrants significant investigation, possibly in combination with other emerging technologies.
503 troponin t and quantitative st segment depression
Troponin T and ST-segment depression provide complementary prognostic information for risk stratification of acute coronary syndrome patients. Both are associated with increased risk of death or myocardial infarction at 6 months, with troponin T showing stronger associations. While both are effective risk markers, troponin T may be superior to ST-segment depression in guiding treatment decisions. The combination of troponin T levels and ST-segment depression can better assess patient risk compared to either marker alone.
501 autoimmune disease
1. Autoimmune reactions against heat shock proteins (HSPs), particularly HSP60, may play an important role in the early development of atherosclerosis.
2. HSPs released from necrotic cells in advanced atherosclerotic plaques can stimulate the innate immune response and promote inflammation, attracting more inflammatory cells. This may link HSPs to complications like plaque rupture and thrombosis.
3. Both humoral and cellular immune reactions against HSP60 work together with classical cardiovascular risk factors to promote atherosclerosis and its complications.
076 cardiac magnetic resonance imaging
MRI can effectively evaluate patients presenting to the emergency department with possible acute coronary syndrome. In a study of 161 such patients, MRI had higher sensitivity and specificity than electrocardiography, troponin levels, or clinical risk scores for detecting acute coronary syndrome, non-ST elevation myocardial infarction, and ischemic heart disease. Regional wall motion abnormalities detected by MRI had 89% sensitivity and 99% specificity for detecting ischemic heart disease compared to 67% sensitivity and 99% specificity for detecting ischemic heart disease using delayed hyperenhancement. MRI provides accurate information to guide patient management in the emergency department.
070 visualization of atherosclerotic vulnerable plaque
This document discusses the use of super paramagnetic iron oxide (SPIO) as a contrast agent for MRI to visualize vulnerable atherosclerotic plaques. SPIO can accumulate in macrophages and allow detection of inflammation in plaques. The hypotheses are that SPIO injection followed by MRI could identify active macrophages in inflamed vulnerable plaques through changes in T1 and T2 relaxation times, and correlate MRI findings with plaque vulnerability. A study is proposed using SPIO injection in rabbits followed by MRI and pathology evaluation to investigate visualization of plaque inflammation. Preliminary studies in mice showed SPIO particles trapped by RES and some pulmonary and lymphatic macrophages.
180 aortic thermography catheter
The document discusses a study conducted by the Department of Cardiology at Athens Medical School in 2001 that used a new aortic thermography catheter to measure temperatures in the aorta and coronary sinus of patients. The study involved 18 patients with documented coronary artery disease and 12 patients with normal coronary arteries, as determined by angiography. The purpose was to investigate if there are temperature differences in blood between the coronary sinus and right atrium in patients with left coronary artery lesions compared to those without.
059 can oct catheter see plaque macrophages
- Optical coherence tomography (OCT) is a high-resolution imaging technique analogous to ultrasound that uses near-infrared light instead of sound waves. OCT was originally developed for eye imaging and can now be delivered via intravascular catheters.
- Studies have shown that OCT, with its 10-20 micron resolution, can identify thin fibrous caps and characterize atherosclerotic plaque components like lipid pools. Ex vivo studies also demonstrated OCT's ability to quantify macrophage content in plaque caps.
- In vivo studies confirmed OCT's feasibility for human coronary artery imaging and identification of plaque structures with higher resolution than IVUS. This suggests OCT may replace IVUS and provide important clinical information for cardiovascular evaluations.
Adeli 9 20
1) The document discusses mechanisms of VLDL overproduction in insulin resistance using a fructose-fed hamster model.
2) Hamsters fed a high fructose diet develop insulin resistance, hypertriglyceridemia, and increased hepatic VLDL production.
3) Studies show that insulin resistance in hamster liver leads to overexpression of MTP and overproduction of VLDL, possibly due to disruption of insulin signaling pathways involving IRS-1 and PI3-kinase.
195 hepatic synthesis and secretion of vldl
1) The document discusses mechanisms of VLDL overproduction in insulin resistance using a fructose-fed hamster model.
2) Hamsters fed a high fructose diet develop insulin resistance, hypertriglyceridemia, and increased hepatic VLDL production.
3) Studies show that insulin resistance in hamster liver leads to overexpression of MTP and overproduction of VLDL, possibly due to disruption of insulin signaling pathways involving IRS-1 and PI3-kinase.
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131 the evolution of coronary atherosclerosis
The document discusses the natural progression of coronary atherosclerosis over time from normal artery to vulnerable plaque. It describes how snapshots can identify plaque vulnerability or likelihood to progress. Physiologic shear stress is protective for endothelium while low shear stress promotes atherosclerosis. 3D reconstruction of arterial segments can analyze plaque and shear stress. Regions of baseline low shear stress saw increased plaque and arterial enlargement over 6 months. Identification of minor obstructions likely to progress could allow preventive interventions to avert adverse events like heart attack.
Barth imt
This document provides background on Jacques Barth, an expert in cardiovascular imaging and risk assessment. It discusses the evolution of ultrasound technology for measuring intima-media thickness (IMT) from 1986 to 2005. IMT is an early marker of atherosclerosis and cardiovascular risk. The document also addresses issues around vulnerable plaques, reporting IMT measurements, and assessing cardiovascular risk in children and adolescents.
123 coronary dialsysis
Atherosclerosis is a leading cause of death worldwide. It is a systemic inflammatory disease involving the buildup of plaque in artery walls. Inflammatory markers like C-reactive protein are associated with future coronary events. The authors describe a Cardiac Dialysis System designed to specifically target and remove inflammatory markers from the bloodstream to stabilize vulnerable plaques and prevent acute cardiac events like heart attack.
179 chlamydophila pneumoniae
C. pneumoniae infection of human aortic endothelial cells leads to increased expression of the cell adhesion molecule ICAM-1. The study found that C. pneumoniae activates the PKC and NF-κB signaling pathways in endothelial cells, resulting in increased transcription of the ICAM-1 gene. Inhibition of either PKC or NF-κB blocked the C. pneumoniae-induced upregulation of ICAM-1. The increased ICAM-1 expression contributes to the chronic inflammation associated with atherosclerosis by promoting adhesion and transmigration of monocytes into the arterial wall.
129 inflammation and culprit lesions
This document discusses inflammation in coronary arteries and culprit lesions. It finds that:
1. Inflammation is present in many non-culprit lesions, not just culprit lesions, based on a study of 74 coronary arteries.
2. Inflammation therefore has a very low positive predictive value (<3%) for identifying the actual culprit lesion responsible for a clinical event like a heart attack.
3. Inflammation appears to be a local arterial phenomenon, as cross-sectional sampling of inflammation in one part of an artery did not strongly correlate with levels in other parts or in paired left/right arteries.
187 athero reversa mice
The document describes a new mouse model called "AtheroReversa mice" that allows researchers to reverse hypercholesterolemia and atherosclerosis without drugs or diet changes. The mice lack the LDL receptor and ApoB genes but have a conditional Mttp gene that produces MTP. Injecting the mice with pI-pC activates Cre recombinase which inactivates Mttp in the liver, eliminating LDL cholesterol production and preventing atherosclerosis. This new model could help analyze regression of existing atherosclerotic plaques.
1031 talk2
The document discusses the role of lipoproteins, particularly LDL and HDL, in inflammation and atherosclerosis. LDL readily enters the artery wall where it can become modified, making it proinflammatory. Modified LDL stimulates expression of MCP-1, which recruits monocytes. Modified LDL also promotes differentiation of monocytes into macrophages. In contrast, HDL is potentially anti-inflammatory. Atherosclerosis is characterized as an inflammatory disease where lipoproteins influence multiple aspects of inflammation.
039 mr contrast agents for vulnerable plaque imaging
1. MS-325 is an albumin-targeted gadolinium contrast agent that highlights inflamed vessel walls and facilitates plaque imaging. It provides prolonged enhancement of the vessel wall and lumen, allowing for high resolution detection of plaque burden.
2. Studies show strong vessel wall enhancement with MS-325 due to increased capillary volume and binding to extravasated albumin in the vessel wall of patients with atherosclerosis. This may help identify stenosis and quantify plaque.
3. Experimental models demonstrate MS-325 can improve visualization of vulnerable plaque features like lipid cores and thin fibrous caps, as well as directly detect thrombus formation during plaque rupture.
243 b cell
I. The document summarizes several studies that investigated the role of the immune system, particularly B cells, in atherosclerosis using mouse models.
II. One study found that RAG-1 deficient mice, which lack functional B and T cells, exhibited increased neointimal formation following arterial injury compared to wild type mice. Transferring B cells from wild type mice to RAG-1 deficient mice reduced neointimal formation.
III. Overall, the studies suggest that B cells may play a protective role against atherosclerosis by reducing plaque formation and progression. The mechanism may involve antibodies that target oxidation-specific epitopes, but this requires further investigation.
190 virus infected monocyes
Virus-infected monocytes can initiate coagulation and promote inflammation. An in vitro study found that monocytes infected with cytomegalovirus, influenza A virus, or Chlamydia pneumoniae expressed tissue factor and reduced clotting time, indicating initiation of coagulation. The viruses also stimulated monocytes to produce inflammatory cytokines like IL-6 and IL-8. While all three viruses infected monocytes, influenza A most strongly induced cytokine production. This suggests virus-infected monocytes may contribute to both acute coronary events by promoting plaque instability and the chronic atherosclerosis process through sustained inflammation and coagulation.
159 spio uptake by macrophages
This document describes a study comparing four types of superparamagnetic iron oxide (SPIO) nanoparticles and their ability to be taken up by macrophages and detect plaque inflammation via MRI. The study finds that lipid-coated SPIO-2 is taken up strongly by macrophages, induces less oxidative stress than dextran-coated SPIO, and is not inhibited by a mannose receptor inhibitor. SPIO-2 therefore shows potential as a contrast agent for noninvasive MR imaging of vulnerable atherosclerotic plaques containing macrophage inflammation. Such detection could help identify high-risk patients and reduce deaths from heart attacks and strokes.
511 first steps towards understanding
This study investigated genetic differences in vascular remodeling and shear stress regulation in response to altered blood flow in four inbred rat strains. The results showed significant differences among strains in their ability to maintain normal endothelial shear stress levels through outward arterial remodeling when flow was increased or decreased. Specifically, the GH strain was better able to regulate shear stress through remodeling compared to the SHR-SP strain. These genetic differences in vascular responses to changes in blood flow have important implications for understanding the variable manifestations of atherosclerosis and susceptibility to cardiovascular disease in individuals and populations. Future studies are needed to investigate whether similar genetic differences exist in humans and their role in clinical outcomes.
061 a nano mega initiative
The document summarizes a meeting on vulnerable plaque research between UT-THI and Rice Coalition. It provides background on vulnerable plaque, describing it as dangerous forms of fat buildup in the arterial wall that can rupture or induce thrombosis. It reviews the history of research in this area dating back to the 19th century, and profiles the many contributors to the field. Emerging techniques for detecting vulnerable plaque non-invasively or invasively are also summarized, such as various imaging modalities, blood tests, and endothelial function tests.
209 trans blood vision™
Trans-Blood Vision is a patented infrared technique that uses short-wave infrared wavelengths to see directly through blood. It has the potential to find vulnerable plaque lesions without first entering them, determine their size and surface characteristics in high resolution, and look at their material constituents both on and below the surface. While it cannot provide direct visual guidance for therapy or penetrate as deeply as ultrasound, combining it with augmentative technologies could allow for real-time multi-mode detection, analysis, and therapy guidance of vulnerable plaque lesions. The document concludes that Trans-Blood Vision warrants significant investigation, possibly in combination with other emerging technologies.
503 troponin t and quantitative st segment depression
Troponin T and ST-segment depression provide complementary prognostic information for risk stratification of acute coronary syndrome patients. Both are associated with increased risk of death or myocardial infarction at 6 months, with troponin T showing stronger associations. While both are effective risk markers, troponin T may be superior to ST-segment depression in guiding treatment decisions. The combination of troponin T levels and ST-segment depression can better assess patient risk compared to either marker alone.
501 autoimmune disease
1. Autoimmune reactions against heat shock proteins (HSPs), particularly HSP60, may play an important role in the early development of atherosclerosis.
2. HSPs released from necrotic cells in advanced atherosclerotic plaques can stimulate the innate immune response and promote inflammation, attracting more inflammatory cells. This may link HSPs to complications like plaque rupture and thrombosis.
3. Both humoral and cellular immune reactions against HSP60 work together with classical cardiovascular risk factors to promote atherosclerosis and its complications.
076 cardiac magnetic resonance imaging
MRI can effectively evaluate patients presenting to the emergency department with possible acute coronary syndrome. In a study of 161 such patients, MRI had higher sensitivity and specificity than electrocardiography, troponin levels, or clinical risk scores for detecting acute coronary syndrome, non-ST elevation myocardial infarction, and ischemic heart disease. Regional wall motion abnormalities detected by MRI had 89% sensitivity and 99% specificity for detecting ischemic heart disease compared to 67% sensitivity and 99% specificity for detecting ischemic heart disease using delayed hyperenhancement. MRI provides accurate information to guide patient management in the emergency department.
070 visualization of atherosclerotic vulnerable plaque
This document discusses the use of super paramagnetic iron oxide (SPIO) as a contrast agent for MRI to visualize vulnerable atherosclerotic plaques. SPIO can accumulate in macrophages and allow detection of inflammation in plaques. The hypotheses are that SPIO injection followed by MRI could identify active macrophages in inflamed vulnerable plaques through changes in T1 and T2 relaxation times, and correlate MRI findings with plaque vulnerability. A study is proposed using SPIO injection in rabbits followed by MRI and pathology evaluation to investigate visualization of plaque inflammation. Preliminary studies in mice showed SPIO particles trapped by RES and some pulmonary and lymphatic macrophages.
180 aortic thermography catheter
The document discusses a study conducted by the Department of Cardiology at Athens Medical School in 2001 that used a new aortic thermography catheter to measure temperatures in the aorta and coronary sinus of patients. The study involved 18 patients with documented coronary artery disease and 12 patients with normal coronary arteries, as determined by angiography. The purpose was to investigate if there are temperature differences in blood between the coronary sinus and right atrium in patients with left coronary artery lesions compared to those without.
059 can oct catheter see plaque macrophages
- Optical coherence tomography (OCT) is a high-resolution imaging technique analogous to ultrasound that uses near-infrared light instead of sound waves. OCT was originally developed for eye imaging and can now be delivered via intravascular catheters.
- Studies have shown that OCT, with its 10-20 micron resolution, can identify thin fibrous caps and characterize atherosclerotic plaque components like lipid pools. Ex vivo studies also demonstrated OCT's ability to quantify macrophage content in plaque caps.
- In vivo studies confirmed OCT's feasibility for human coronary artery imaging and identification of plaque structures with higher resolution than IVUS. This suggests OCT may replace IVUS and provide important clinical information for cardiovascular evaluations.
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039 mr contrast agents for vulnerable plaque imaging
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1) The document discusses mechanisms of VLDL overproduction in insulin resistance using a fructose-fed hamster model.
2) Hamsters fed a high fructose diet develop insulin resistance, hypertriglyceridemia, and increased hepatic VLDL production.
3) Studies show that insulin resistance in hamster liver leads to overexpression of MTP and overproduction of VLDL, possibly due to disruption of insulin signaling pathways involving IRS-1 and PI3-kinase.
195 hepatic synthesis and secretion of vldl
1) The document discusses mechanisms of VLDL overproduction in insulin resistance using a fructose-fed hamster model.
2) Hamsters fed a high fructose diet develop insulin resistance, hypertriglyceridemia, and increased hepatic VLDL production.
3) Studies show that insulin resistance in hamster liver leads to overexpression of MTP and overproduction of VLDL, possibly due to disruption of insulin signaling pathways involving IRS-1 and PI3-kinase.
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1) The document discusses mechanisms of VLDL overproduction in insulin resistance, using a fructose-fed hamster model.
2) Hamsters fed a high fructose diet develop insulin resistance, hypertriglyceridemia, and increased hepatic VLDL production.
3) Studies show that insulin resistance in hamster hepatocytes leads to overexpression of MTP and overproduction of VLDL, possibly due to disruption of insulin signaling pathways involved in lipid metabolism.
195 hepatic synthesis and secretion of vldl
1) The document discusses mechanisms of VLDL overproduction in insulin resistance using a fructose-fed hamster model.
2) Hamsters fed a high fructose diet develop insulin resistance, hypertriglyceridemia, and increased hepatic VLDL production.
3) Studies show that insulin resistance in hamster liver leads to overexpression of MTP and overproduction of VLDL, possibly due to disruption of insulin signaling pathways involving IRS-1 and PI3-kinase.
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1) The document discusses mechanisms of VLDL overproduction in insulin resistance using a fructose-fed hamster model.
2) Hamsters fed a high fructose diet develop insulin resistance, hypertriglyceridemia, and increased hepatic VLDL production.
3) Studies show enhanced MTP expression and VLDL secretion in hepatocytes from fructose-fed hamsters, suggesting insulin resistance leads to overproduction of VLDL particles in the liver.
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This document discusses several potential mechanisms of insulin resistance including increased levels and activity of PTP-1B, impaired phosphorylation of the insulin receptor and IRS-1, reduced PI-3 kinase activity, and attenuated insulin signaling. This leads to reduced phosphorylation of ApoB or its chaperone, enhanced stability and accelerated assembly of ApoB, and overproduction of VLDL. The document also discusses the contribution of intestinal lipoproteins to metabolic dyslipidemia in insulin resistance, including a hypothesis that fasting and postprandial hyperlipidemia may be attributable to intestinal oversecretion of apoB-48 containing lipoproteins. An experimental approach is described to test this using a high fructose fed hamster
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This document discusses several potential mechanisms of insulin resistance including increased levels and activity of PTP-1B, impaired phosphorylation of the insulin receptor and IRS-1, reduced PI-3 kinase activity, and attenuated insulin signaling. This leads to reduced phosphorylation of ApoB or its chaperone, enhanced stability and accelerated assembly of ApoB, and overproduction of VLDL. The document also discusses the contribution of intestinal lipoproteins to metabolic dyslipidemia in insulin resistance, including a hypothesis that fasting and postprandial hyperlipidemia may be attributable to intestinal oversecretion of apoB-48 containing lipoproteins. An experimental approach is described to test this using a high fructose fed hamster
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This document discusses several potential mechanisms of insulin resistance including increased levels and activity of PTP-1B, impaired phosphorylation of the insulin receptor and IRS-1, reduced PI-3 kinase activity, and attenuated insulin signaling. This leads to reduced phosphorylation of ApoB or its chaperone, enhanced stability and accelerated assembly of ApoB, and overproduction of VLDL. The document also discusses the contribution of intestinal lipoproteins to metabolic dyslipidemia in insulin resistance, including a hypothesis that fasting and postprandial hyperlipidemia may be attributable to intestinal oversecretion of apoB-48 containing lipoproteins. An experimental approach is described to test this using a high fructose fed hamster
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This document discusses several potential mechanisms of insulin resistance including increased levels and activity of PTP-1B, impaired phosphorylation of the insulin receptor and IRS-1, reduced PI-3 kinase activity, and attenuated insulin signaling. This leads to reduced phosphorylation of ApoB or its chaperone, enhanced stability and accelerated assembly of ApoB, and overproduction of VLDL. The document also discusses the contribution of intestinal lipoproteins to metabolic dyslipidemia in insulin resistance, and a hypothesis that fasting and postprandial hyperlipidemia in insulin resistant states may be attributable in part to intestinal oversecretion of apoB-48 containing lipoproteins.
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The document describes TAPBOOST, a breakthrough protein production platform that enhances protein folding and secretion. It works by controlling the protein folding system and cellular quality control mechanisms in the host cell. The platform can increase yields of various target proteins including antibodies, enzymes, and difficult-to-express proteins. It has been shown to boost production levels by over 2000% for some proteins while also reducing aggregation. The platform works in mammalian, bacterial, and yeast expression systems and provides advantages such as increased productivity for any target protein and easy implementation into existing bioprocesses.
Discriminating Facts from Artefacts in the Secreted Ly-6 Protein Family
The document discusses several issues related to accurately characterizing the secreted Ly-6 protein family based on bioinformatic analysis. It describes the discovery of novel rat Ly-6 proteins from urine samples and EST data, but also finds chimeric mRNA sequences that combined portions of unrelated genes with Ly-6 sequences, complicating the analysis. Genome mapping showed the chimeras did not represent real gene fusions but likely arose from artifacts. While many rat and mouse homologs were identified, clear orthologs between species were difficult to determine due to high sequence divergence over time.
Animal biotech
This document summarizes a study that used CRISPR/Cas9 to knockout the elovl2 gene in Atlantic salmon in order to increase their omega-3 fatty acid content. The researchers found that elovl2 knockout inhibited the elongation of polyunsaturated fatty acids like EPA and DHA, leading to higher levels of shorter chain omega-3s. This inhibition also induced the expression of hepatic genes related to lipogenesis. The study demonstrates the key role of elovl2 in salmon fatty acid biosynthesis and suggests its potential as a selective breeding marker to increase the conversion of plant oils to EPA/DHA for aquaculture and human nutrition.
Pathways of intracellular signal transduction
This document summarizes various cellular signaling pathways. It discusses how receptors can be linked to enzymatic activities like protein kinases and guanylyl cyclases. It then describes several key intracellular signaling pathways, including the cyclic AMP pathway, cyclic GMP pathway, phospholipid and calcium signaling, PI3 kinase/Akt pathway, and MAP kinase pathway. Each of these pathways transmit signals from cell surface receptors to intracellular targets and regulate processes like gene expression, metabolism, cell growth and differentiation.
CDD 2016
Oncogenic Ras promotes the survival of cancer cells detached from the extracellular matrix (ECM) through distinct downstream pathways. Ras activates phosphatidylinositol 3-kinase (PI3K) signaling to regulate metabolism in detached cells, but surprisingly does not do so through Akt. Instead, Ras utilizes serum and glucocorticoid-regulated kinase 1 (SGK1) to promote ATP generation. Additionally, Ras blocks anoikis or detachment-induced apoptosis by reducing expression of the phosphatase PHLPP1, which activates p38 MAPK to induce anoikis. Thus, Ras facilitates survival of detached cancer cells through divergent effectors to regulate metabolism and anoikis.
Similar to 170 insulin signaling & vldl overproduction (16)
6 RTK signaling MAPK Akt.pdfCell signaling presentation
6 RTK signaling MAPK Akt.pdfCell signaling presentation
Discriminating Facts from Artefacts in the Secreted Ly-6 Protein Family
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This document describes a study that uses intravascular ultrasound (IVUS), biplane coronary angiography, and blood flow measurements to characterize endothelial shear stress (ESS) in coronary arteries. It found that over 6 months, areas of low ESS demonstrated plaque progression, areas of normal ESS remained stable, and areas of high ESS developed outward remodeling. The technology allows in vivo determination of intracoronary flow velocity and ESS, which has not previously been possible. This provides a method to predict progression of atherosclerosis and vascular remodeling. A pilot study applied this technique in 8 patients at baseline and 6 months to analyze changes in native coronary artery disease and in-stent restenosis while taking candesartan vs fel
101205 shape aha 2005 f
Zahi A. Fayad is an Associate Professor who studies molecular imaging of atherosclerosis using MRI. His research focuses on developing targeted contrast agents to noninvasively detect unstable plaque. Some agents under investigation include annexin A5 labeled with a radioisotope to detect apoptosis, FDG-PET to assess plaque activity, and fibrin-targeted and MMP-targeting Gd-based contrasts. Additional work involves lipid-based particulate agents using reconstituted HDL or iron oxide nanoparticles. The goal is to improve MRI detection sensitivity and specificity for high-risk plaque characterization.
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#1 killer of human beings in the 21st century
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This progress report discusses ongoing near-infrared (NIR) spectroscopy studies. It notes that a new probe design is being developed to improve signal detection in the NIR range. Characterization of a new light source and additional tissue phantom studies are needed. The report identifies ongoing difficulties with depth penetration studies and experimental setup issues. Priorities include analyzing existing data to inform probe redesign, characterizing the new light source, conducting depth penetration and tissue phantom studies, and addressing experimental setup challenges.
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170 insulin signaling & vldl overproduction
- 1. CytosolCytosol HepatocyteHepatocyte ApoB DegradationDegradation 5' 3' ApoB mRNAApoB mRNA TranslationTranslation ERMembraneERMembrane Insulin IRS1/IRS2 IR InsulinSignalingPathway InsulinSignalingPathway Plasm a Plasm a VLDLVLDL Insulin Signaling & VLDL OverproductionInsulin Signaling & VLDL Overproduction in Insulin Resistancein Insulin Resistance PI3-Kinase VLDL AssemblyVLDL Assembly PIP3/Phosphorylation CascadePIP3/Phosphorylation Cascade Akt/PKBAkt/PKB PTP-1BPTP-1B 3'
- 2. D InsulinReceptorproteinMass (scanningunits/mgproteinx10-3 ) Control Fructose-fed Control Fructose-fed 0 50 100 150 200 250 IRS-1ProteinMass (scanningunits/mgproteinx10-3 ) Control Fructose-fed Control Fructose-fed 0 40 80 120 E F Control Fructose-fed 0 20 40 60 80 100 120 Control Fructose-fed IRS-2Mass(percentofcontrol) C PhosphorylatedIRS-2 (relativetobasallevelofcontrol) 0 20 40 60 80 100 120 140 160 180 _ + _ + Insulin + + + +Insulin _ _ _ _ Control Fructose-fed Control Fructose-fed Impaired Hepatic Tyrosine Phosphorylation of Insulin Receptor, IRS-1, and IRS-2 in Fructose-Fed Hamsters A PhosphorylatedInsulinReceptorMass (scanningunits/mgproteinx10-3 ) Control Fructose-fed 0 100 200 300 400 500 600 _ + _ + Insulin + + + +Insulin _ _ _ _ * B _ + _ + Insulin PhosphorylatedIRS-1 (scanningunits/mgproteinx10-3 ) Control Fructose-fed 0 20 40 60 80 100 120 Control Fructose-fed + + + +Insulin _ _ _ _ P= 0.04 P= 0.009 P= 0.02 P= 0.03 P= 0.029 * *
- 3. B 0 50 100 150 200 PTP-1BMass (percentofcontrol) Control Fructose-fed Control Fructose-fed C 0 100 200 300 PTP-1BActivity (percentofcontrol) Control Fructose-fed A 0 20 40 60 80 100 120 PI3-KinaseActivity (percentofcontrol) Control Fructose-fed * ** *** D + + + +Insulin 0 20 40 60 80 100 120 140 Insulin-InducedAktSerine Phosphorylation(%ofcontrol) Control Fructose-fed Insulin _ + _ + E Insulin Insulin-InducedAktThreonine Phosphorylation(%ofcontrol) Control Fructose-fed 0 20 40 60 80 100 120 _ + _ + + + + + Insulin F Control Fructose-fed 20 40 60 80 100 120 140 160 AktProteinMass (percentofcontrol) 0 Control Fructose-fed **** *** * Evidence for Reduced PI-3 Kinase Activity, Reduced Akt Phosphorylation, & Enhanced PTP-1B Mass & Activity
- 4. 0 20 40 60 80 100 120 0 20 40 60 80 Vanadate (µM) RecoveredCellularApoB (relativetountreated) B 0 20 40 60 80 100 120 0 20 40 60 80 Vanadate (µM) RecoveredLabeledMediaApoB (relativetountreated) C Vanadate (µM) RecoveredTotalApoB (relativetountreated) 0 20 40 60 80 100 120 0 20 40 60 80 D Vanadate (µM) 0 10 40 80 IR-pY 0 100 200 300 400 500 600 0 20 40 60 80 Vanadate (µM) InsulinReceptorPhosphorylation (relativetountreated) A 0 10 20 40 80Vanadate (µM) Cellular ApoB Secreted ApoB E Inhibition of Cellular Phosphatase Activity with Vanadate Enhances Insulin Signaling and Reduces ApoB Secretion IR-IR-ppYY Cellular ApoBCellular ApoB ApoB StabilityApoB Stability ApoB SecretionApoB Secretion