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Techniques for Improving Positron Emission Tomography Image Quality and Tracking Real-Time Biological Processes

Researchers at the University of California, Davis have developed methodologies that perform dynamic PET imaging and provide opportunities for tracing blood flow and other biological systems in real-time.

Novel Adjustable Caliber Catheter System

UCLA researchers in the Department of Radiological Sciences have designed a new adjustable catheter system for use in embolectomy or thrombectomy procedures.

Adenylyl Cyclase Catalytic Domain Gene Transfer for Heart Failure

Heart failure (HF) is a disease of epidemic portions in the United States affecting over 6 million patients with heart failure in the US, with 400,000 new cases per year. It is the most common cause of non-elective admission to the hospital in subjects 65 yrs and older. The introduction of new drugs over the last 30 years that target pathways critical to progression of HF, along with implantable cardiac defibrillators and resynchronization devices have shown some successes, however, both the morbidity and mortality associated with heart failure remains at unacceptable levels, with as many as 30-40% of affected individuals dying within 5 years of diagnosis. Recently, preclinical and clinical trials have tested gene transfer to increase left ventricular (LV) function, especially in heart failure with reduced ejection fraction.

Heart Assist Device for Patients

Researchers at UCI have developed a cardiac assist device for patients with failing heart functions. The device contracts and expands the heart with the help of a pacemaker to help restore natural heart pace and blood flow.

Noninvasive Method and Apparatus for Peripheral Assessment of Vascular Health

UCI researchers introduce a medical device which noninvasively and accurately monitors vascular health metrics such as endothelial function, arterial stiffness, and blood pressure.

All-In-One Arterial Access and Closure System (ACS)

Arterial access-site complications are a leading cause of morbidity following a catheterization procedure. There lacks a reliable, fail safe method for arterial closure. At the same time, the arterial access and closure procedures are independent of each other. A UCI surgeon presents an alternative with an all-in-one arterial access and closure port system (ACS) to provide fail-safe percutaneous entry and exit into any artery.ACS opens the door for using high flow, high pressure arteries such as the carotid artery, an important access point.

New Indications For ENPP1 Inhibitors, Part Two

UCLA researchers in the Department of Medicine have developed small molecule ENPP1 inhibitors and monoclonal antibodies for treating myocardial infarction and ocular calcification.

New Indications For ENPP1 Inhibitors

UCLA researchers in the Department of Medicine have developed small molecule ENPP1 inhibitors and monoclonal antibodies for treating myocardial infarction and ocular calcification.

Neural Modulation Of Autonomic Nervous System To Alter Memory And Plasticity Of The Autonomic Network

Researchers at UCLA from the Departments of Medicine and Bioengineering have created a device that modulates the autonomic nervous system to treat heart conditions like arrhythmias.

TRM: Dishevelled Segment Polarity Protein 3 (Dvl3) Mutant Mice

Dishevelled (Dvl) proteins are important signaling components of both the canonical β-catenin/Wnt pathway, which controls cell proliferation and patterning, migration, differentiation, stem cell renewal and the planar cell polarity (PCP) pathway. Mammals share three Dishevelled (Dvl) family members and while the roles of Dvl1 and Dvl2 have been described previously, the functions of Dvl3 have remained an area of active research. The lack of Dvl3 in mice affects the formation of the heart, neural tube, and inner ear and that the defects in these tissues are much more severe when the mice are deficient in more than one Dvl family member, indicating redundant functions for these genes. Congenital heart disease affects approximately 75 in every 1,000 live human births, and approximately 30% of these diseases are due to disruptions in the outflow tract, the region affected in mice lacking Dvl genes.

New Treatment For Aortic Aneurysms

Aortic aneurysms account for 1-2% of deaths in Western countries, and despite improvements in surgical repair, morbidity and mortality remain high, especially with thoracic aortic aneurysms and dissections (TAAD). Degeneration of the medial layer of the aorta leads to aortic dilation and/or rupture; pathological changes in the media include progressive elastin fiber fragmentation, loss of smooth muscle cells, and proteoglycan accumulation. Mutations causing hereditary TAAD affect proteins regulating transforming growth factor-β signaling (e.g., Loeys-Dietz syndrome and Marfan syndrome), or components of the smooth muscle cell contractile apparatus. Aortic pathology has been attributed to smooth muscle cell phenotypic alterations and activation of stress pathways, leading to increased production of tissue-destructive matrix metalloproteinases and increased oxidative stress. Abdominal aortic aneurysms (AAAs) may share with TAAD some of these pathogenic mechanisms. While blood pressure control with β-adrenergic or angiotensin receptor blockers modestly improve the prognosis of patients with TAAD, there is no treatment to prevent the pathologic changes in the aorta.          

At Home Fetal Electrocardiogram/Heartrate Monitor for Congenital Heart Defect Diagnosis

Congenital heart defects affect >1% of babies born in the United States. These defects originate early on in fetal development. Inventors at UC Irvine have developed a flexible medical device that allows at home fetal electrocardiogram (ECG) monitoring to diagnosis congenital heart defects during development.

Atrial Cage For Placement, Securing And Anchoring Of Atrioventricular Valves

A collapsible heart valve supporting structure that securely anchors and prevents unwanted valvular dislodgment post implantation.

Automated Selection of Myocardial Inversion Time with a Convolutional Neural Network

Magnetic resonance imaging (MRI) has been noted for its excellent soft tissue imaging capability with zero radiation dose. It has repeatedly been touted as the imaging modality of the future, but due to its complexity, long exam times and high cost, its growth has been severely limited. This especially has been the case for cardiac MRI, which only accounts for about I percent of all MRI exams in the United States. Delayed enhancement (DE) imaging is an essential component of cardiac MRI, widely used for the evaluation of myocardial scar and viability. The selection of an optimal inversion time (TI), known as the myocardial null point (TINP), to suppress the background myocardial signal is required to optimize image contrast in myocardial delayed enhancement (MDE) acquisitions. Incorrect selection of TINP can impair diagnostic quality. In certain diffuse myocardial diseases such as amyloidosis, it may be difficult to identify a single optimal null point. Further, it is known that TINP varies after intravenous contrast administration, and is therefore time-sensitive. In practice, selection of myocardial inversion time is generally performed through visual inspection and selection of TINP from an inversion recovery scout acquisition. This is dependent on the skill of a technologist or physician to select the optimal inversion time, which may not be readily available outside of specialized centers. However, such methods still rely on visual inspection of an image series by a trained human observer to select an optimal myocardial inversion time. A way to overcome these deficiencies is to embrace Deep learning approaches, including convolutional neural networks (CNNs),     which have the potential to automate selection of inversion time, and are the current state-of-the-art technology for image classification, segmentation, localization, and Spatial Temporal Ensemble Myocardium Inversion NETwork (STEMI-NET) prediction. However, these static CNN models have some drawbacks which could be overcome via the use of dynamic temporal activities for object recognition.

Covalent Activators Of K2p Channels

Researchers at UCSF have developed a series of small-molecules that selectively label the TREK1 (KCNK2) potassium ion channel. These compounds are the first covalent activator of any member of the K2P family of potassium ion channels.

Preventative Trackable Anticoagulants for Atrial Fibrillation Treatment

Researchers at the University of California, Davis have developed a process to localize anticoagulation drugs for treatment of inflammation and atrial fibrillations.

Development of a New Biomarker for Diagnosis of Cardiovascular Disease: Monoclonal Antibody to Oxidized Cholesteryl Esters

Cardiovascular disease (CVD) is the leading cause of death and disability worldwide. The primary prevention of CVD is dependent upon the ability to identify high-risk individuals long before the development of overt events. This highlights the need for accurate risk stratification. An increasing number of novel biomarkers have been identified to predict cardiovascular events. Biomarkers play a critical role in the definition, prognostication, and decision-making regarding the management of cardiovascular events. There are several promising biomarkers that might provide diagnostic and prognostic information. The myocardial tissue-specific biomarker cardiac troponin, high-sensitivity assays for cardiac troponin, and heart-type fatty acid binding potential help diagnose myocardial infarction (MI) in the early hours following symptoms. Inflammatory markers such as growth differentiation factor-15, high-sensitivity C-reactive protein, fibrinogen, and uric acid predict MI and death and many others. However, there is a high unmet medical need for the more specific biomarkers that reflect different aspects of the development of atherosclerosis. 

New Method for the Detection of Vulnerable Plaques in Coronary Artery Atherosclerotic Disease (CAD)

Heart disease is a major leading cause of morbidity and mortality in the U.S. largely due to coronary artery atherosclerotic disease (CAD), which affects millions and costs billions annually. The concept of plaque vulnerability, based on likelihood of fibroatheroma rupture, has prompted many pursuits to identify high risk lesions, costing $150 million per year. However, identifying vulnerable plaques based on structure, via coronary angiograms or CT/MRI scans, has not translated to improved clinical outcome. Thus, the failure to identify and predict plaques at high risk of rupture, which may lead to myocardial infarction, heart failure and/or sudden cardiac death, is likely because structure may not optimally discern plaque vulnerability. Molecular imaging, in contrast, offers an innovative approach for discriminating the vulnerable plaque in that it not only visualizes structure, but also interrogates underlying molecular function. Based on the current methods to detect plaques, there is a need for a better method for measuring plaque rupture vulnerability.

Intravascular Ultrasound-guided Electrochemical Impedance Spectroscopy (IVUS-EIS) to Assess Lipid-Laden Plaques

UCLA researchers in the Department of Medicine have developed a novel intravascular ultrasound-guided electrochemical impedance spectroscopy (IVUS-EIS) system for the detection of oxLDL-laden plaques in arteries.

A Method To Determine Cause Of A Cardiac Arrest And Provide Cause-Specific Decision Support In Real-Time Using Continuous Electrocardiography

Researchers led by Duc Hong Do from the Department of Cardiology at UCLA have developed an algorithm to detect the cause of cardiac arrest in a hospital setting.

Flexible Balloon-Inflatable Electrochemical Impedance Spectroscopy To Assess Endoluminal Lipid-Rich Lesions

UCLA researchers have developed a novel flexible balloon-inflatable electrochemical impedance spectroscopy to facilitate the diagnosis of metabolically active atherosclerotic lesions.

New Method for Generation of Human Pacemaker Cardiomyocytes

The heart consists of a multitude of diverse cardiomyocyte cell types, including atrial, ventricular and pacemaker cells, which cooperate to ensure proper cardiac function and circulation throughout the body. The rhythm of the heart beat is regulated by the sinoatrial node (SAN), functionally known as the cardiac pacemaker. Loss or dysfunction of these pacemaker cardiomyocytes leads to severe cardiac arrhythmias, syncope and/or even death. Although artificial pacemakers exist to help overcome these issues, several serious limitations and problems have emerged with this approach over the past several decades including electrode fracture or damage to insulation, infection, re-operations for battery exchange, and venous thrombosis. Moreover, size mismatch and the fact that pacemaker leads do not grow with children are a concerning problem. Thus, replacing artificial pacemakers with biological pacemakers potentially overcomes these artificial pacemaker issues including the expense and complications associated with device replacement, device or lead failure, and infection. To achieve these goals, understanding how pacemaker cardiomyocytes are generated is necessary to develop a human biological pacemaker for cardiac cellular therapies.

A Novel Method To Enhance Tg6f Amelioration Of Dyslipidemia

UCLA researchers in the Department of Medicine have developed a novel protocol that enhances the effects of Tg6F in treating dyslipidemia.

A New Mechanism For Hypertriglyceridemia In Humans

UCLA researchers in the Department of Medicine have identified autoantibodies against GPIHBP1, a GPI anchored protein of capillary endothelial cells, which may provide a novel therapeutic strategy for patients with hypertriglyceridemia.

Inhibition of the Aggregation of Transthyretin by Specific Binding of Peptides to Aggregation-Driving Segments

UCLA researchers from the Department of Chemistry and Biochemistry have developed a novel process to inhibit amyloid aggregation of Transthyretin, which is associated with three debilitating disorders including senile systemic amyloidosis (SSA), Familial Amyloidotic Polyneuropathies (FAP), and Familial Amyloidotic Cardiomyopathies (FAC).

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