Archive for February, 2012

15-01-2012 17:08 Dr Elizabeth McDonald presents the latest research worldwide that may benefit people with MS (eg new treatments, stem cell therapies, genetics, etc.) and how Australian research is contributing to this.

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Latest research worldwide that may benefit people with MS presented by Dr Elizabeth McDonald - Video

Store-A-Tooth™, a service of Provia Labs, made its debut at the 2012 Yankee Dental Congress, held January 26-28 in Boston. Store-A-Tooth is partnering with dentists throughout New England to offer the highest quality in dental stem cell banking to their patients, enabling parents to preserve the stem cells from their children’s teeth for future therapies in regenerative medicine and dentistry.

Boston, MA (PRWEB) January 31, 2012

Store-A-Tooth™, a service of Provia Laboratories LLC, participated in last week’s 2012 Yankee Dental Congress in Boston. Dentists from across New England enrolled with Store-A-Tooth to offer the leading dental stem cell banking service to their patients, enabling families to preserve their own stem cells for future therapies in regenerative medicine and dentistry.

“One of the biggest advances in adult stem cell technology is the discovery of stem cells in dental pulp tissue by NIH researchers in 2000. Dental stem cells have the ability to differentiate into various cell types, such as osteoblasts, odontoblasts, adipocytes, neuronal, and cardiac cells. Stem cell based therapies are currently being studied around the world to treat multiple degenerative diseases. Awareness is rapidly building about this research and their potential to someday be used for a range of clinical applications,” says Dr. Nicholas Perrotta, DMD, a Store-A-Tooth provider who has been offering dental stem cell preservation services at his practice in Medford, MA for over five years.

Dental stem cells have the potential to be used in both dental and medical applications, and have already been used to regenerate alveolar jaw bone and to treat periodontal disease in human studies. Dental stem cells are being studied by scientists around the world to see how they could someday play a role in treating conditions such as diabetes, spinal cord injury, stroke, heart attack and neurological diseases like Parkinson’s and Alzheimer’s. In fact, new research has shown that dental stem cells can be transformed into islet-like cell aggregates which produce insulin in a glucose-dependent manner—a significant step toward eventually developing stem-cell therapies for type 1 (juvenile) diabetes.

Dr. Brian M. Smith, head of Oral and Maxillofacial Surgery at Cooper University Hospital with a practice in Sewell, NJ sees the potential for dental stem cells to bring innovation to the dental profession as well as new care options for patients. “I believe dental stem cell research could result in a broad range of medical and dental benefits, as discoveries in the laboratory lead to new therapies in everyday practice, making regenerative dentistry and medicine a standard of care. Our job as dental professionals is to help make this vision a reality.”

Provia Laboratories partners with dental practices to offer Store-A-Tooth to patients. The free program makes it easy for dental professionals to inform patients about dental stem cell preservation and includes patient education, training, free CE, professional discounts and instructions for tooth collection. Stem cells may be harvested from dental pulp from any healthy tooth: baby teeth, extracted molars/wisdom teeth, and teeth pulled for orthodontia.

During Yankee Dental, Provia announced a new Store-A-Tooth Territory Manager for New England – Terry Tesak. Based in Massachusetts, Terry brings 12 years of experience working with dental professionals to bring innovation to leading dental practices. Terry was part of the team at Align Technology Inc., the makers of Invisalign, and has also worked for Patterson Dental Supply and Dentsply.

For more information about Store-A-Tooth, call 1-877-857-5753 or visit our website to see recent news stories about dental stem cell banking, http://www.store-a-tooth.com/media/video-news-stories.

About Provia Laboratories, LLC                            

Provia Laboratories, LLC (http://www.provialabs.com) is a healthcare services company headquartered near Boston, Massachusetts which specializes in high quality biobanking (preservation of biological specimens). The company’s Store-A-Tooth™ service platform enables the collection, transport, processing, and storage of dental stem cells for potential use in future stem-cell therapies. The company advises industrial, academic, and governmental clients on matters related to the preservation of biological specimens for research and clinical use. In addition, Provia offers a variety of products for use in complex biobanking environments to improve sample logistics, security, and quality. Provia Labs is a member of ISBER, the International Society for Biological and Environmental Repositories. For more information on dental stem cells, call 1-877-867-5753, visit http://www.store-a-tooth.com or http://www.facebook.com/storeatooth, or follow us @StoreATooth.

###

Store-A-Tooth
Provia Laboratories, LLC
877-867-5753
Email Information

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Store-A-Tooth Dental Stem Cell Banking Featured at Yankee Dental Congress 2012

Updated: Tue Jan. 31 2012 19:10:38

ctvwinnipeg.ca

The federal health minister says the government would like to move away from "one size fits all" medicine.

An announcement was made in Ottawa on Tuesday that more than $67 million is being invested into cutting edge research to identify markers of disease.

The aim is to get doctors to understand a person's body through their genes, family background and environment, then tailor a treatment just for them.

"With these bio markers, doctors will be able to tailor treatments based on what we know about the patient being treated," said Leona Aglukkaq, Health Minister. "this holds the potential to make many medical treatments more effective."

Some Manitobans feel it's money well spent, like Carey Tarr who has type 1 diabetes. She says she already recieves some treatment personalized for her, but says more can be done for others.

"Someone living with type one diabetes or any type diabetes may also be living with other conditions, " explained Tarr, "So there's a lot of room to look at how their body makeup and different conditions they are living with are affecting others as well."

It's believed personalized approaches will be effective in many areas including cancer.

CancerCare Manitoba says this initiative is a small step in the right direction.

"This is an initiatve that will begin to improve the specificity of our care so we aren't using a shot gun approach as we are sometimes forced to because we have no other way," said Dr. Dhali Dhaliwal, of CancerCare Manitoba.

Dr Dhaliwal says it could take at least five years before patients will see the benifits of this research.

The government says the funding is a research competition supported by three research groups, who have to match the amount of money they receive.

It's not known at this time what diseases the groups will be conducting research on.

-- with a report from CTV's Ina Sidhu

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Personalized medicine could soon be reality

25-01-2012 18:17 Spinal cord injury treatment. http://www.projectwalk.org exists to provide an improved quality of life for people with spinal cord injuries through intense exercise-based recovery programs, education, support and encouragement.

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"Russ Bennett", "Project Walk Spinal Cord Injury Recovery" - Video

31-01-2012 13:32 James P. Watson, MD lecture sample from the 11th Clinical Applications for Age Management Medicine Conference, Fall 2011, Las Vegas, Nevada Pre-Conference Track 2: Regenerative and Cell Based Medicine This lecture focused on regenerative and cell-based medicine, Autologous Stem Cell Research. This field continues to grow in use by physicians across the world. From platelet rich plasma to culture expanded stem cells, the need for information about the applications of these therapies to treat patients has never been greater. This track will focus on the latest developments in cell-based medicine with speakers who are driving the research and using these technologies as part of their everyday practice of medicine. For more information about our upcoming conference visit our website http://www.agemed.org Or contact us at conference@agemed.org

Excerpt from:
An Overview of Data Trends in Autologous Stem Cell Research and Clinical Use - James P. Watson, MD - Video

NEW YORK, Feb. 1, 2012  /PRNewswire/ -- Reportlinker.com announces that a new market research report is available in its catalogue:

Cardiovascular Drug Delivery - technologies,markets and companies

http://www.reportlinker.com/p0203538/Cardiovascular-Drug-Delivery---technologiesmarkets-and-companies.html#utm_source=prnewswire&utm_medium=pr&utm_campaign=Drug_Delivery_Technology

Drug delivery to the cardiovascular system is different from delivery to other systems because of the anatomy and physiology of the vascular system; it supplies blood and nutrients to all organs of the body. Drugs can be introduced into the vascular system for systemic effects or targeted to an organ via the regional blood supply. In addition to the usual formulations of drugs such as controlled release, devices are used as well. This report starts with an introduction to molecular cardiology and discusses its relationship to biotechnology and drug delivery systems.

Drug delivery to the cardiovascular system is approached at three levels: (1) routes of drug delivery; (2) formulations; and finally (3) applications to various diseases. Formulations for drug delivery to the cardiovascular system range from controlled release preparations to delivery of proteins and peptides. Cell and gene therapies, including antisense and RNA interference, are described in full chapters as they are the most innovative methods of delivery of therapeutics. Various methods of improving systemic administration of drugs for cardiovascular disorders are described including use of nanotechnology.

Cell-selective targeted drug delivery has emerged as one of the most significant areas of biomedical engineering research, to optimize the therapeutic efficacy of a drug by strictly localizing its pharmacological activity to a pathophysiologically relevant tissue system. These concepts have been applied to targeted drug delivery to the cardiovascular system. Devices for drug delivery to the cardiovascular system are also described.

Role of drug delivery in various cardiovascular disorders such as myocardial ischemia, hypertension and hypercholesterolemia is discussed. Cardioprotection is also discussed. Some of the preparations and technologies are also applicable to peripheral arterial diseases. Controlled release systems are based on chronopharmacology, which deals with the effects of circadian biological rhythms on drug actions.A full chapter is devoted to drug-eluting stents as treatment for restenosis following stenting of coronary arteries.Fifteen companies are involved in drug-eluting stents.

New cell-based therapeutic strategies are being developed in response to the shortcomings of available treatments for heart disease. Potential repair by cell grafting or mobilizing endogenous cells holds particular attraction in heart disease, where the meager capacity for cardiomyocyte proliferation likely contributes to the irreversibility of heart failure. Cell therapy approaches include attempts to reinitiate cardiomyocyte proliferation in the adult, conversion of fibroblasts to contractile myocytes, conversion of bone marrow stem cells into cardiomyocytes, and transplantation of myocytes or other cells into injured myocardium.

Advances in molecular pathophysiology of cardiovascular diseases have brought gene therapy within the realm of possibility as a novel approach to treatment of these diseases. It is hoped that gene therapy will be less expensive and affordable because the techniques involved are simpler than those involved in cardiac bypass surgery, heart transplantation and stent implantation. Gene therapy would be a more physiologic approach to deliver vasoprotective molecules to the site of vascular lesion. Gene therapy is not only a sophisticated method of drug delivery; it may at time need drug delivery devices such as catheters for transfer of genes to various parts of the cardiovascular system.

The cardiovascular drug delivery markets are estimated for the years 2011 to 2021 on the basis of epidemiology and total markets for cardiovascular therapeutics. The estimates take into consideration the anticipated advances and availability of various technologies, particularly drug delivery devices in the future. Markets for drug-eluting stents are calculated separately. Role of drug delivery in developing cardiovascular markets is defined and unmet needs in cardiovascular drug delivery technologies are identified.

Selected 80 companies that either develop technologies for drug delivery to the cardiovascular system or products using these technologies are profiled and 74 collaborations between companies are tabulated. The bibliography includes 200 selected references from recent literature on this topic. The report is supplemented with 27 tables and 7 figures

TABLE OF CONTENTS

0. Executive Summary 11

1. Cardiovascular Diseases 13

Introduction 13

History of cardiovascular drug delivery 13

Overview of cardiovascular disease 14

Coronary artery disease 14

Angina pectoris 14

Limitations of current therapies for myocardial ischemic disease 14

Cardiomyopathies 14

Cardiac arrhythmias 15

Congestive heart failure 15

Peripheral arterial disease 15

Current management 16

Atherosclerosis 16

The endothelium as a target for cardiovascular therapeutics 16

Molecular cardiology 17

Cardiogenomics 17

Cardioproteomics 17

Personalized cardiology 18

Pharmacogenomics of cardiovascular disorders 18

Modifying the genetic risk for myocardial infarction 19

Management of heart failure 19

Management of hypertension 20

Pharmacogenomics of diuretic drugs 20

Pharmacogenomics of ACE inhibitors 20

Management of hypertension by personalized approach 21

Pharmacogenetics of lipid-lowering therapies 21

Polymorphisms in genes involved in cholesterol metabolism 21

Role of eNOS gene polymorphisms 22

Important advances in cardiovascular therapeutics 22

Drug delivery, biotechnology and the cardiovascular system 23

Role of cardiovascular imaging in cardiovascular therapeutics 23

Chronopharmacotherapy of cardiovascular diseases 23

2. Methods for Drug Delivery to the Cardiovascular System 25

Introduction 25

Routes of drug delivery to the cardiovascular system 25

Local administration of drugs to the cardiovascular system 25

Intramyocardial drug delivery 25

Drug delivery via coronary venous system 26

Intrapericardial drug delivery 26

Formulations for drug delivery to the cardiovascular system 27

Sustained and controlled release 27

Programming the release at a defined time 28

Dosage formulation of calcium channel blockers 28

Sustained and controlled release verapamil 28

Methods of administration of proteins and peptides 28

Delivery of peptides by subcutaneous injection 29

Depot formulations and implants 29

Poly(ethylene glycol) technology 29

Liposomes for cardiovascular drug delivery 30

Microencapsulation for protein delivery 30

Localized delivery of biomaterials for tissue engineering 30

Oral delivery of proteins and peptides 30

DDS to improve systemic delivery of cardiovascular drugs 32

Nanotechnology-based drug delivery 32

Controlled delivery of nanoparticles to injured vasculature 33

Nanoparticles for cardiovascular imaging and targeted drug delivery 34

Nanofiber-based scaffolds with drug-release properties 34

Targeted drug delivery to the cardiovascular system 35

Immunotargeting of liposomes to activated vascular endothelial cells 35

PEGylated biodegradable particles targeted to inflamed endothelium 36

Devices for cardiovascular drug delivery 36

Local drug delivery by catheters 37

Microneedle for periarterial injection 38

Nanotechnology-based devices for the cardiovascular system 39

Liposomal nanodevices for targeted cardiovascular drug delivery 39

Nanotechnology approach to the problem of "vulnerable plaque" 40

Drug delivery in the management of cardiovascular disease 40

Drug delivery in the management of hypertension 40

Transnasal drug delivery for hypertension 41

Transdermal drug delivery for hypertension 41

Oral extended and controlled release preparations for hypertension 42

Long-acting hypertensives for 24 h blood pressure control 43

Drug delivery to control early morning blood pressure peak 43

Role of drug delivery in improving compliance with antihypertensive therapy 44

Drug delivery for congestive heart failure 44

Oral human brain-type natriuretic peptide 44

Nitric oxide-based therapies for congestive heart failure 44

Automated drug delivery system for cardiac failure 45

DDS in the management of ischemic heart disease 45

Intravenous emulsified formulations of halogenated anesthetics 46

Injectable peptide nanofibers for myocardial ischemia 46

Delivery of angiogenesis-inducing agents for myocardial ischemia 47

Drug delivery for cardioprotection 47

Drug delivery for cardiac rhythm disorders 48

Drug delivery in the treatment of angina pectoris 49

Sustained and controlled-release nitrate for angina pectoris 49

Transdermal nitrate therapy 49

Controlled release calcium blockers for angina pectoris 51

Vaccines for hypertension 51

Drug delivery in the management of pulmonary hypertension 51

Prostacyclin by inhalation 52

Endothelin receptor antagonist treatment of PAH 52

Anticoagulation in cardiovascular disease 52

Oral heparin 52

Low molecular weight heparin-loaded polymeric nanoparticles 53

Transdermal anticoagulants 53

Thrombolysis for cardiovascular disorders 53

Use of ultrasound to facilitate thrombolysis 54

Delivery of alteplase through the AngioJet rheolytic catheter 54

Drug delivery for peripheral arterial disease 54

Delivery of thrombolytic agent to the clot through a catheter 55

Delivery of growth factors to promote angiogenesis in ischemic limbs 55

Immune modulation therapy for PAD 55

NO-based therapies for peripheral arterial disease 55

Drug delivery in the management of hypercholesterolemia 56

Controlled/sustained release formulations of statins 56

Combinations of statins with other drugs to increase efficacy 56

Controlled release fenofibrate 57

Extended release nicotinic acid 58

Intravenous infusion of lipoprotein preparations to raise HDL 59

Innovative approaches to hypercholesterolemia 59

Single dose therapy for more than one cardiovascular disorder 59

3. Cell Therapy for Cardiovascular Disorders 61

Introduction 61

Inducing the proliferation of cardiomyocytes 61

Role of stem cells in repair of the heart 61

Cell-mediated immune modulation for chronic heart disease 61

Cell therapy for atherosclerotic coronary artery disease 62

Transplantation of myoblasts for myocardial infarction 62

MyoCell™ (Bioheart) 63

Transplantation of cardiac progenitor cells for revascularization of myocardium 64

Methods of delivery of cells to the heart 64

Cellular cardiomyoplasty 64

IGF-1 delivery by nanofibers to improve cell therapy for MI 65

Intracoronary infusion of bone marrow-derived cells for AMI 65

Non-invasive delivery of cells to the heart by Morph®guide catheter 65

Transplantation of stem cells for myocardial infarction 66

Transplantation of embryonic stem cells 66

Transplantation of hematopoietic stem cells 66

Transplantation of cord blood stem cells for myocardial infarction 66

Intracoronary infusion of mobilized peripheral blood stem cells 67

Human mesenchymal stem cells for cardiac regeneration 67

Cytokine preconditioning of human fetal liver CD133+ SCs 68

Transplantation of expanded adult SCs derived from the heart 68

Transplantation of endothelial cells 68

Transplantation of genetically modified cells 69

Transplantation of cells secreting vascular endothelial growth factor 69

Transplantation of genetically modified bone marrow stem cells 69

Cell transplantation for congestive heart failure 69

Injection of adult stem cells for congestive heart failure 69

Intracoronary infusion of cardiac stem cells 70

Myoblasts for treatment of congestive heart failure 70

Role of cell therapy in cardiac arrhythmias 70

Atrioventricular conduction block 71

Ventricular tachycardia 71

ESCs for correction of congenital heart defects 72

Cardiac progenitors cells for treatment of heart disease in children 72

Stem cell therapy for peripheral arterial disease 73

Targeted delivery of endothelial progenitor cells labeled with nanoparticles 73

Clinical trials of cell therapy in cardiovascular disease 73

A critical evaluation of cell therapy for heart disease 75

Publications of clinical trials of cell therapy for CVD 76

Future directions for cell therapy of CVD 76

4. Gene Therapy for Cardiovascular Disorders 79

Introduction 79

Techniques of gene transfer to the cardiovascular system 80

Direct plasmid injection into the myocardium 80

Catheter-based systems for vector delivery 80

Ultrasound microbubbles for cardiovascular gene delivery 81

Vectors for cardiovascular gene therapy 81

Adenoviral vectors for cardiovascular diseases 81

Intravenous rAAV vectors for targeted delivery to the heart 82

Plasmid DNA-based delivery in cardiovascular disorders 82

Hypoxia-regulated gene therapy for myocardial ischemia 82

Angiogenesis and gene therapy of ischemic disorders 83

Therapeutic angiogenesis vs. vascular growth factor therapy 83

Gene painting for delivery of targeted gene therapy to the heart 84

Gene delivery to vascular endothelium 84

Targeted plasmid DNA delivery to the cardiovascular system with nanoparticles 84

Gene delivery by vascular stents 85

Gene therapy for genetic cardiovascular disorders 85

Genetic disorders predisposing to atherosclerosis 85

Familial hypercholesterolemia 86

Apolipoprotein E deficiency 87

Hypertension 87

Genetic factors for myocardial infarction 88

Acquired cardiovascular diseases 88

Coronary artery disease with angina pectoris 88

Ad5FGF-4 88

Ischemic heart disease with myocardial infarction 89

Angiogenesis for cardiovascular disease 89

Myocardial repair with IGF-1 therapy 90

miRNA gene therapy for ischemic heart disease 91

Congestive heart failure 91

Rationale of gene therapy in CHF 91

?-ARKct gene therapy 91

Intracoronary adenovirus-mediated gene therapy for CHF 92

AAV-mediated gene transfer for CHF 92

AngioCell gene therapy for CHF 93

nNOS gene transfer in CHF 93

Gene therapy for cardiac arrhythmias 93

Gene transfer for biological pacemakers 94

Management of arrhythmias due to myoblast transplantation 95

Genetically engineered cells as biological pacemakers 95

Gene therapy and heart transplantation 95

Gene therapy for peripheral arterial disease 96

Angiogenesis by gene therapy 96

HIF-1? gene therapy for peripheral arterial disease 96

HGF gene therapy for peripheral arterial disease 97

Ischemic neuropathy secondary to peripheral arterial disease 97

Maintaining vascular patency after surgery 97

Antisense therapy for cardiovascular disorders 98

Antisense therapy for hypertension 99

Antisense therapy for hypercholesterolemia 99

RNAi for cardiovascular disorders 100

RNAi for hypercholesterolemia 100

microRNA and the cardiovascular system 101

Role of miRNAs in angiogenesis 101

Role of miRNAs in cardiac hypertrophy and failure 101

Role of miRNAs in conduction and rhythm disorders of the heart 102

miRNA-based approach for reduction of hypercholesterolemia 102

miRNAs as therapeutic targets for cardiovascular diseases 103

Future prospects of miRNA in the cardiovascular therapeutics 103

Future prospects of gene therapy of cardiovascular disorders 103

Companies involved in gene therapy of cardiovascular disorders 104

5. Drug-Eluting Stents 107

Introduction 107

Percutaneous transluminal coronary angioplasty 107

Stents 107

Restenosis 107

Pathomechanism 108

Treatment 108

Nitric oxide-based therapies for restenosis 109

Carbon monoxide inhalation for preventing restenosis 109

Antisense approaches for prevention of restenosis after angioplasty 110

miRNA-based approach for restenosis following angioplasty 111

Gene therapy to prevent restenosis after angioplasty 111

Techniques of gene therapy for restenosis 112

NOS gene therapy for restenosis 113

Nonviral gene therapy to prevent intimal hyperplasia 113

HSV-1 gene therapy to prevent intimal hyperplasia 114

Drug delivery devices for restenosis 114

Local drug delivery by catheter 114

Stenosis associated with stents 115

Absorbable metal stents 115

Drug-eluting stents 115

Various types of DES 116

CYPHER® sirolimus-eluting coronary stent 116

Dexamethasone-eluting stents 116

NO-generating stents 117

Paclitaxel-eluting stents 117

Sirolimus-eluting vs paclitaxel-eluting stents 118

Novel technologies for DES 118

Absorbable DES 118

Bio-absorbable low-dose DES 119

Drug-eluting stents coated with polymer surfaces 119

Endeavour DES 119

Stents for delivery of gene therapy 120

Stem cell-based stents 121

VAN 10-4 DES 121

Nanotechnology-based stents 122

Drugs encapsulated in biodegradable nanoparticles 122

Magnetic nanoparticle-coated DES 122

Magnetic nanoparticles encapsulating paclitaxel targeted to stents 123

Nanocoated DES 123

Nanopores to enhance compatibility of DES 124

Paclitaxel-encapsulated targeted lipid-polymeric nanoparticles 124

The ideal DES 124

Companies developing drug-eluting stents 125

Clinical trials of drug-eluting stents 126

Measurements used in clinical trials of DES 126

TAXUS paclitaxel-eluting stents 126

XIENCE™ V everolimus-eluting coronary stent 127

COSTAR II clinical trial 128

Endeavor RESOLUTE zotarolimus-eluting stent system 128

CUSTOM I clinical trial 129

NOBORI CORE Trial 129

LEADERS trial 130

Comparison of DES in clinical trials 130

Comparison of DES with competing technologies 131

DES versus coronary artery bypass graft 131

DES versus bare metal stents 131

Multi-Link Vision bare metal stent vs DES 134

Guidelines for DES vs BMS 134

DES vs BMS for off-label indications 134

Role of DES in cases of bare-metal in-stent restenosis 135

DES versus balloon catheter coated with paclitaxel 135

DES versus intracoronary radiation therapy for recurrent stenosis 135

Cost-effectiveness of DES 136

Safety issues of DES 137

Adverse reactions to DES 137

Endothelial vascular dysfunction due to sirolismus 137

Risk of clotting with DES 137

Clopidogrel use and long-term outcomes of patients receiving DES 139

Prasugrel as antiplatelet agent 139

Effect of blood clot on release of drug from DES 140

Use of magnetized cell lining to prevent clotting of DES 140

Long-term safety studies of DES 140

Regulatory issues of DES 141

Future prospects for treatment of restenosis by DES 143

Future role of DES in management of cardiovascular diseases 143

Stent cost and marketing strategies 144

Improvements in stent technology 144

Bioabsorbale stent 144

DES vs drug-eluting balloons 145

6. Markets for Cardiovascular Drug Delivery 147

Introduction 147

Epidemiology of cardiovascular disease 147

Cost of care of cardiovascular disorders 148

Cardiovascular markets according to important diseases 149

Antithrombotics 149

Anticholesterol agents 149

Antihypertensive agents 150

Drugs for congestive heart failure 150

Markets for innovative technologies for cardiovascular disorders 150

Markets for cell therapy of cardiovascular disorders 150

Markets for gene therapy of cardiovascular disorders 151

Markets for drug-eluting stents 151

Major players in DES market 151

Impact of safety issues on future markets for DES 151

DES market in Asia 152

Patenting and legal issues of DES 153

The financial impact of DES on cardiovascular markets 153

Unmet needs for cardiovascular drug delivery 154

Role of DDS in developing cardiovascular markets 155

Markets for cardiovascular devices 155

Marketing of innovative cardiovascular drug delivery devices 155

Direct to consumer advertising of DES 156

Future trends in the integration of drug delivery with therapeutics 156

Future prospects of cardiovascular drug delivery 156

7. Companies involved in Cardiovascular Drug Delivery 157

Profiles of companies 157

Collaborations 243

8. References 247

List of Tables

Table 1 1: Landmarks in the historical evolution of cardiovascular drug delivery 13Table 1 2: Gene polymorphisms that alter cardiovascular response to drugs 18Table 2 1: Routes of drug delivery used for treatment of cardiovascular disorders 25Table 2 2: Formulations for drug delivery to the cardiovascular system 27Table 2 3: Improved methods of systemic drug delivery of cardiovascular drugs 32Table 2 4: Targeted delivery of therapeutic substances to the cardiovascular system 35Table 2 5: Classification of devices for drug delivery to the cardiovascular system 36Table 2 6: Various methods of delivery of therapeutic agents for hypertension 41Table 2 7: Marketed controlled/ extended release preparation for hypertension 43Table 2 8: Drug delivery in ischemic heart disease 45Table 2 9: Methods of delivery of nitrate therapy in angina pectoris 49Table 2 10: Drug delivery for peripheral arterial disorders 54Table 3 1: Clinical trials of cell therapy in cardiovascular disease 73Table 4 1: Cardiovascular disorders for which gene therapy is being considered. 79Table 4 2: Catheter-based systems for vector delivery to the cardiovascular system 80Table 4 3: Potential applications of antisense in cardiovascular disorders 99Table 4 4: Companies involved in gene therapy of cardiovascular diseases 104Table 5 1: Treatment of restenosis 108Table 5 2: Devices used for drug delivery in restenosis 114Table 5 3: Companies involved in drug-eluting stents 125Table 6 1: Prevalence of cardiovascular disorders in major markets: US 2011-2021 148Table 6 2: Prevalence of cardiovascular disorders in major markets: Europe 2011-2021 148Table 6 3: Prevalence of cardiovascular disorders in major markets: Japan 2011-2021 148Table 6 4: Values of cardiovascular DDS in major markets 2011-2021 149Table 6 5: Markets for innovative technologies for cardiovascular disorders 2011-2021 150Table 7 1: Top 5 companies in cardiovascular drug delivery 157Table 7 2: Collaborations in cardiovascular drug delivery 243

List of Figures

Figure 1 1: Drug delivery, biotechnology and cardiovascular diseases 23

Figure 2 1: MicroSyringe for periarterial injection 39

Figure 5 1: Vicious circle of vascular occlusion following angioplasty and stenting 109

Figure 5 2: Measurement of in-stent stenosis 115

Figure 5 3: Medtronic's Endeavour drug-eluting stent 120

Figure 5 4: Magnetic nanoparticle-coated stent 123

Figure 6 1: Unmet needs for cardiovascular drug delivery 154

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Original post:
Cardiovascular Drug Delivery - technologies,markets and companies

Washington, Feb 1 (IANS) Scientists have successfully converted mouse skin cells directly into cells that become the three main parts of the nervous system, bypassing the stem cell stage, throwing up many new possibilities in the medical world.

This new study is a substantial advance over the previous paper in that it transforms the skin cells into neural precursor cells, as opposed to neurons.

While neural precursor cells can differentiate into neurons, they can also become the two other main cell types in the nervous system: astrocytes and oligodendrocytes.

The finding is an extension of a previous study by the same group from the Stanford University School of Medicine, showing that mouse and human skin cells can be turned into functional neurons or brain cells.

The multiple successes of the direct conversion method overrides the idea that pluripotency (the ability of stem cells to become nearly any cell) is necessary for a cell to transform from one type to another, the journal Proceedings of the National Academy of Sciences reports.

"We are thrilled about the prospects for potential medical use of these cells," said Marius Wernig, study co-author and assistant professor of pathology and member, Stanford's Institute for Stem Cell Biology and Regenerative Medicine, according to a Stanford statement.

Beside their greater versatility, the newly derived neural precursor cells offer another advantage over neurons because they can be cultivated in large numbers in the lab, a feature critical for their long-term usefulness in transplantation or drug screening.

"We've shown the cells can integrate into a mouse brain and produce a missing protein important for the conduction of electrical signal by the neurons," said Wernig, who co-authored the study with graduate student Ernesto Lujan.

-Indo-Asian News Service

st/pg/vm

Read more from the original source:
Some nerve! Now bypass stem cells

24-01-2012 18:39 Four minute excerpt from the Spotlight on Genomics seminar presentation during the January 17th 2012 California Institute for Regnerative Medicine governing board meeting. The video features a conversation between Catriona Jamieson, director for stem cell research at UCSD Moores Cancer Center, and one of her patients who is participating in a clinical trial for the treatment of myelofibrosis, a life-threatening blood disorder.

Read more:
Clinical Trial for Myelofibrosis that Targets Cancer Stem Cells | CIRM Spotlight on Genomics - Video

31-01-2012 13:21 Ronald W. Hanson, Jr., MD lectures at the 11th Clinical Applications for Age Management Medicine in November 2011, in Las Vegas, Nevada This focused conference track cocentrated on regenerative and cell-based medicine continue to grow in use by physicians across the world. From platelet rich plasma to culture expanded stem cells, the need for information about the applications of these therapies to treat patients has never been greater. This track will focus on the latest developments in cell-based medicine with speakers who are driving the research and using these technologies as part of their everyday practice of medicine. For more information contact conference@agemed.org Visit our website at agemed.org

More here:
The Use of Guided Bone Marrow Nucleated Cell Fraction Injections - Ronald W. Hanson, Jr., MD - Video

The federal government is pledging up to $67.5 million for research into "personalized medicine," which tailors treatment to a patient's genetics and environment.

The funds will flow through Genome Canada, the Cancer Stem Cell Consortium and the Canadian Institutes of Health Research, the federal government's health research agency.

Federal Health Minister Leona Aglukkaq and Minister of State for Science Gary Goodyear made the announcement at the University of Ottawa's health campus Tuesday.

The field of personalized medicine is touted as having the potential to transform the way patients are treated. It looks at the genetic makeup of a person, the patient's environment and the exact course of a particular disease so that an appropriate and effective treatment can be tailored for that individual.

The idea is to move from a one-size-fits-all approach to one that is designed for a specific person and relies on the genetic signatures, or biomarkers, of both the patient and the disease.

Proponents of personalized medicine say it is likely to change the way drugs are developed, how medicines are prescribed and generally how illnesses are managed. They say it will shift the focus in health care from reaction to prevention, improve health outcomes, make drugs safer and mean fewer adverse drug reactions, and reduce costs to health-care systems.

"The potential to understand a person's genetic makeup and the specific character of their illness in order to best determine their treatment will significantly improve the quality of life for patients and their families and may show us the way to an improved health-care system and even save costs in certain circumstances," Aglukkaq said in a news release.

Research projects could last four years

The sequencing of the human genome paved the way for personalized medicine and there have been calls for more research funding so that the discoveries in laboratories can be translated further into the medical field so they will benefit patients more.

Identifying a person's genetic profile, for example, could then indicate a susceptibility to a certain disease, if the biomarkers of that disease have also been discovered. If people know they are genetically at risk of an illness they can take actions to prevent it, and their health-care providers can monitor for it.

Cancer patients could be pre-screened to determine if chemotherapy would work for them, which could not only save a lot of money on expensive treatments but also prevent pain and suffering for patients.

Genome Canada is leading the research initiative, in collaboration with Cancer Stem Cell Consortium and CIHR which on Tuesday launched its Personalized Medicine Signature Initiative. CIHR is committing up to $22.5 million to the large-scale initiative with the other two partners, but it will be providing more funding for other projects under its personalized medicine program.

The research projects are aiming to bring together biomedical, clinical, population health, health economics, ethics and policy researchers to identify areas that are best suited to personalized medicine.

Oncology, cardiovascular diseases, neurodegenerative diseases, psychiatric disorders, diabetes and obesity, arthritis, pain, and Alzheimer’s disease are all considered to be areas that hold promise for personalized medicine.

Funding will also go to projects that are aimed at developing more evidence-based and cost-effective approaches to health care.

Researchers can get up to four years of funding, but 50 per cent of their requested funding must be matched from another source, such as a provincial government or from the academic or private sectors.

Genome Canada, CIHR and the cancer consortium will invest a maximum of $5 million in each individual project.

The successful applicants for the $67.5 million worth of funding won't be announced until December.

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'Personalized medicine' gets $67.5M research boost

HOUSTON--(BUSINESS WIRE)-- Officials at the Texas Heart Institute (THI) at St. Luke’s Episcopal Hospital (St. Luke’s) announced today that Doris Taylor, PhD, FAHA, FACC, one of the world’s leading cell therapy and cardiac regeneration scientists, will join THI beginning March 1, 2012.

Dr. Taylor’s research includes: Cell and gene therapy for treatment of cardiovascular disease; tissue engineering of bioartificial organs and vasculature; cell-based prevention of disease; stem cells and cancer; and holistic approaches to using cell therapy for treating chronic disease.

Most recently, Dr. Taylor and her team garnered international recognition for work involving “whole organ decellularization” by showing they were able to remove existing cells from hearts of laboratory animals and even humans leaving a framework to build new organs. They repopulated the framework with other adult stem cells then provided a blood supply, and the heart regenerated with the characteristics and functions of a revitalized beating heart.

The hope is that this research is an early step toward being able to grow a fully functional human heart in the laboratory. Dr. Taylor has demonstrated that the process works for other organs as well – opening a door in the field of organ transplantation.

It is significant in that the need for transplants continues to grow, while the supply of donor organs remains critically low.

“Dr. Taylor is certainly one of the stars in the adult human stem cell field, and we feel extremely fortunate to have her join our team,” said Dr. James T. Willerson, THI’s President and Medical Director. “Her work fits very well with our mission and goals, and she certainly helps to solidify THI as a leader in cell therapy, which is one of the most promising hopes for treating cardiovascular disease.”

“The chance to work with Dr. Willerson and the THI team as colleagues is very exhilarating. From molecules, to cells, to organs and tissues, we want to create solutions for people with disease,” said Dr. Taylor. “I am confident that I am joining a regenerative medicine program that is unparalleled. And, given the breadth of innovation and science in Houston, I have every confidence that building solutions for heart diseases not only has a long history, but a bright future.”

The move to Houston will also bring her closer to her family, notes Dr. Taylor.

Dr. Taylor has been serving as director of the Center for Cardiovascular Repair and Medtronic Bakken Chair in Integrative Biology and Physiology at the University of Minnesota. Prior to that she was on the faculty as Associate Professor in Cardiology at Duke University Medical Center.

A native of Mississippi, Dr. Taylor holds a B.S. in biology from Mississippi University for Women and a Doctorate in pharmacology from the University of Texas Southwestern Medical School in Dallas.

About the Texas Heart® Institute

The Texas Heart Institute (www.texasheart.org), founded by world-renowned cardiovascular surgeon Dr. Denton A. Cooley in 1962, is a nonprofit organization dedicated to reducing the devastating toll of cardiovascular disease through innovative and progressive programs in research, education and improved patient care. Together with its clinical partner, St. Luke’s Episcopal Hospital, it has been ranked among the top 10 cardiovascular centers in the United States by U.S. News & World Report’s annual guide to “America’s Best Hospitals” for the past 21 years. The Texas Heart Institute is also affiliated with the University of Texas (UT) System, which promotes collaboration in cardiovascular research and education among UT and THI faculty at the Texas Heart Institute and other UT components.

About St. Luke’s Episcopal Health System

St. Luke’s Episcopal Health System (StLukesTexas.com) includes St. Luke’s Episcopal Hospital in the Texas Medical Center, founded in 1954 by the Episcopal Diocese of Texas; St. Luke’s The Woodlands Hospital; St. Luke’s Sugar Land Hospital; St. Luke’s Lakeside Hospital; St. Luke’s Patients Medical Center; St. Luke’s Hospital at The Vintage; and St. Luke’s Episcopal Health Charities, a charity devoted to assessing and enhancing community health, especially among the underserved. St. Luke’s Episcopal Hospital is home to the Texas Heart®Institute, which was founded in 1962 by Denton A. Cooley, MD, and is consistently ranked among the top 10 cardiology and heart surgery centers in the country by U.S. News & World Report. Affiliated with several nursing schools and three medical schools, St. Luke’s Episcopal Hospital was the first hospital in Texas named a Magnet hospital for nursing excellence, receiving the award three times.

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World-Renowned Cell-Therapy Researcher, Doris Taylor, PhD, Joins Texas Heart Institute at St. Luke’s Episcopal Hospital

Bypassing stem cells, mouse skin cells have been converted directly into cells that become the three main parts of the animal's nervous system, according to new research at the Stanford University School of Medicine.

The startling success of this method seems to refute the idea that "pluripotency" -- the ability of stem cells to become nearly any cell in the body -- is necessary for a cell to transform from one cell type to another.

It raises the possibility that embryonic stem cell research, as well as a related technique called "induced pluripotency," could be supplanted by a more direct way of generating cells for therapy or research.

"Not only do these cells appear functional in the laboratory, they also seem to be able to integrate ... in an animal model," said lead author and graduate student Ernesto Lujan.

The study was published online Jan. 30 in the Proceedings of the National Academy of Sciences.

The finding implies that it may one day be possible to generate a variety of neural-system cells for transplantation that would perfectly match a human patient.

While much research has been devoted to harnessing the potential of embryonic stem cells, taking those cells from an embryo and then implanting them in a patient could prove difficult because they would not match genetically.

The Stanford team is working to replicate the work with skin cells from adult mice and humans.

But Lujan emphasized that

much more research is needed before any human transplantation experiments could be conducted.

In the meantime, however, the ability to quickly and efficiently generate cells -- grown in mass quantities in the laboratory, and maintained over time -- will be valuable in disease and drug-targeting studies.

Contact Lisa M. Krieger at 408-920-5565.

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Stanford scientists bypass stem cells to create nervous system cells

ScienceDaily (Jan. 30, 2012) — Mouse skin cells can be converted directly into cells that become the three main parts of the nervous system, according to researchers at the Stanford University School of Medicine. The finding is an extension of a previous study by the same group showing that mouse and human skin cells can be directly converted into functional neurons.

The multiple successes of the direct conversion method could refute the idea that pluripotency (a term that describes the ability of stem cells to become nearly any cell in the body) is necessary for a cell to transform from one cell type to another. Together, the results raise the possibility that embryonic stem cell research and another technique called "induced pluripotency" could be supplanted by a more direct way of generating specific types of cells for therapy or research.

This new study, published online Jan. 30 in the Proceedings of the National Academy of Sciences, is a substantial advance over the previous paper in that it transforms the skin cells into neural precursor cells, as opposed to neurons. While neural precursor cells can differentiate into neurons, they can also become the two other main cell types in the nervous system: astrocytes and oligodendrocytes. In addition to their greater versatility, the newly derived neural precursor cells offer another advantage over neurons because they can be cultivated to large numbers in the laboratory -- a feature critical for their long-term usefulness in transplantation or drug screening.

In the study, the switch from skin to neural precursor cells occurred with high efficiency over a period of about three weeks after the addition of just three transcription factors. (In the previous study, a different combination of three transcription factors was used to generate mature neurons.) The finding implies that it may one day be possible to generate a variety of neural-system cells for transplantation that would perfectly match a human patient.

"We are thrilled about the prospects for potential medical use of these cells," said Marius Wernig, MD, assistant professor of pathology and a member of Stanford's Institute for Stem Cell Biology and Regenerative Medicine. "We've shown the cells can integrate into a mouse brain and produce a missing protein important for the conduction of electrical signal by the neurons. This is important because the mouse model we used mimics that of a human genetic brain disease. However, more work needs to be done to generate similar cells from human skin cells and assess their safety and efficacy."

Wernig is the senior author of the research. Graduate student Ernesto Lujan is the first author.

While much research has been devoted to harnessing the pluripotency of embryonic stem cells, taking those cells from an embryo and then implanting them in a patient could prove difficult because they would not match genetically. An alternative technique involves a concept called induced pluripotency, first described in 2006. In this approach, transcription factors are added to specialized cells like those found in skin to first drive them back along the developmental timeline to an undifferentiated stem-cell-like state. These "iPS cells" are then grown under a variety of conditions to induce them to re-specialize into many different cell types.

Scientists had thought that it was necessary for a cell to first enter an induced pluripotent state or for researchers to start with an embryonic stem cell, which is pluripotent by nature, before it could go on to become a new cell type. However, research from Wernig's laboratory in early 2010 showed that it was possible to directly convert one "adult" cell type to another with the application of specialized transcription factors, a process known as transdifferentiation.

Wernig and his colleagues first converted skin cells from an adult mouse to functional neurons (which they termed induced neuronal, or iN, cells), and then replicated the feat with human cells. In 2011 they showed that they could also directly convert liver cells into iN cells.

"Dr. Wernig's demonstration that fibroblasts can be converted into functional nerve cells opens the door to consider new ways to regenerate damaged neurons using cells surrounding the area of injury," said pediatric cardiologist Deepak Srivastava, MD, who was not involved in these studies. "It also suggests that we may be able to transdifferentiate cells into other cell types." Srivastava is the director of cardiovascular research at the Gladstone Institutes at the University of California-San Francisco. In 2010, Srivastava transdifferentiated mouse heart fibroblasts into beating heart muscle cells.

"Direct conversion has a number of advantages," said Lujan. "It occurs with relatively high efficiency and it generates a fairly homogenous population of cells. In contrast, cells derived from iPS cells must be carefully screened to eliminate any remaining pluripotent cells or cells that can differentiate into different lineages." Pluripotent cells can cause cancers when transplanted into animals or humans.

The lab's previous success converting skin cells into neurons spurred Wernig and Lujan to see if they could also generate the more-versatile neural precursor cells, or NPCs. To do so, they infected embryonic mouse skin cells -- a commonly used laboratory cell line -- with a virus encoding 11 transcription factors known to be expressed at high levels in NPCs. A little more than three weeks later, they saw that about 10 percent of the cells had begun to look and act like NPCs.

Repeated experiments allowed them to winnow the original panel of 11 transcription factors to just three: Brn2, Sox2 and FoxG1. (In contrast, the conversion of skin cells directly to functional neurons requires the transcription factors Brn2, Ascl1 and Myt1l.) Skin cells expressing these three transcription factors became neural precursor cells that were able to differentiate into not just neurons and astrocytes, but also oligodendrocytes, which make the myelin that insulates nerve fibers and allows them to transmit signals. The scientists dubbed the newly converted population "induced neural precursor cells," or iNPCs.

In addition to confirming that the astrocytes, neurons and oligodendrocytes were expressing the appropriate genes and that they resembled their naturally derived peers in both shape and function when grown in the laboratory, the researchers wanted to know how the iNPCs would react when transplanted into an animal. They injected them into the brains of newborn laboratory mice bred to lack the ability to myelinate neurons. After 10 weeks, Lujan found that the cells had differentiated into oligodendroytes and had begun to coat the animals' neurons with myelin.

"Not only do these cells appear functional in the laboratory, they also seem to be able to integrate appropriately in an in vivo animal model," said Lujan.

The scientists are now working to replicate the work with skin cells from adult mice and humans, but Lujan emphasized that much more research is needed before any human transplantation experiments could be conducted. In the meantime, however, the ability to quickly and efficiently generate neural precursor cells that can be grown in the laboratory to mass quantities and maintained over time will be valuable in disease and drug-targeting studies.

"In addition to direct therapeutic application, these cells may be very useful to study human diseases in a laboratory dish or even following transplantation into a developing rodent brain," said Wernig.

In addition to Wernig and Lujan, other Stanford researchers involved in the study include postdoctoral scholars Soham Chanda, PhD, and Henrik Ahlenius, PhD; and professor of molecular and cellular physiology Thomas Sudhof, MD.

The research was supported by the California Institute for Regenerative Medicine, the New York Stem Cell Foundation, the Ellison Medical Foundation, the Stinehart-Reed Foundation and the National Institutes of Health.

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The above story is reprinted from materials provided by Stanford University Medical Center. The original article was written by Krista Conger.

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Journal Reference:

E. Lujan, S. Chanda, H. Ahlenius, T. C. Sudhof, M. Wernig. Direct conversion of mouse fibroblasts to self-renewing, tripotent neural precursor cells. Proceedings of the National Academy of Sciences, 2012; DOI: 10.1073/pnas.1121003109

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

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Skin cells turned into neural precusors, bypassing stem-cell stage

Public release date: 31-Jan-2012
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Contact: Phil Sahm
phil.sahm@hsc.utah.edu
801-581-2517
University of Utah Health Sciences

SALT LAKE CITY -- A team of scientists from the University of Utah and the University of California at San Francisco has discovered that the mutation of a gene encoding a ketone body transporter triggers accumulation of fat and other lipids in the livers of zebrafish. This discovery, published in the Feb. 1, 2012, issue of Genes & Development, reveals that transport of ketone bodies out of the liver is a critical step in energy metabolism during fasting. It also provides a new approach for studying the development of fatty liver disease in humans.

Nonalcoholic fatty liver disease (NAFLD), or abnormally high accumulation of lipids in the liver, is the most common cause of chronic liver disease worldwide. Lipids are a broad group of molecules that include fats, triglycerides, and cholesterol. In some people, NAFLD causes no complications, but in others, excess fat in the liver can lead to inflammation or development of scar tissue, resulting in permanent liver damage or even liver failure. NAFLD may also increase the risk of heart disease in people who are overweight or obese. The increasing prevalence of NAFLD in the United States is due, in large part, to the obesity epidemic and it is estimated that more than 6 million U.S. children already have fatty liver disease.

"Currently, there are a limited number of treatment options for decreasing excess fat in the liver and there are no methods for reversing damage to liver tissue due to NAFLD," says Amnon Schlegel, M.D., Ph.D., investigator in the University of Utah Molecular Medicine program, assistant professor of internal medicine at the University of Utah School of Medicine, and senior author on the study. "By identifying and characterizing novel genes that regulate accumulation of lipids in the liver, we may be able to gain new insight into the physiological processes that lead to NAFLD."

Previous research has shown that many of the proteins known to control lipid metabolism in humans are also present in zebrafish. Schlegel and his colleagues began by identifying a zebrafish mutant known as red moon (rmn), which developed abnormal lipid accumulation in liver cells, without evidence of associated liver inflammation or liver damage, when exposed to fasting conditions. Schlegel and his colleagues then used a molecular genetic technique called positional cloning to isolate the gene disrupted by the rmn mutation. They found that the rmn mutation inactivated slc16a6a, a gene thought to encode a protein required in the transport of nutrients during fasting.

"Until now, the activity of the Slc16a6a protein has not been functionally characterized in any organism," says Schlegel, who's also an adjunct assistant professor of biochemistry at the U medical school. "Our studies indicate that Slc16a6a is a protein involved in the transport of ?-hydroxybutyrate."

?-hydroxybutyrate is a ketone body, a compound that is produced in the liver when blood glucose is low and fatty acids are broken down for energy. During periods of fasting, most body tissues can use fatty acids as an energy source, but the brain relies on ?-hydroxybutyrate and other ketone bodies for fuel. Schlegel and his colleagues discovered that, in rmn mutants deprived of nutrition, loss of Slc16a6a function disabled secretion of ketone bodies from liver cells and increased lipid accumulation in the liver. They also found that introducing the human form of the SLC16A6 protein into rmn mutant livers restored ketone body secretion.

"Our research has uncovered a previously unrecognized, but critical step, in the complicated physiology of fasting," says Schlegel. "We still don't know whether altered fasting liver metabolism influences the development of NAFLD, but knowing that Slc16a6a is required for secretion of ketone bodies from liver cells during fasting may have implications for our understanding and treatment of other medical conditions where ketone bodies play a role. These include uncontrolled type 1 diabetes, obesity, and childhood metabolic disorders caused by defects in fatty acid metabolism."

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Gene mutation is linked to accumulation of fat, other lipids in liver

Experts who made an unprecedented recommendation that bird-flu researchers hold back some details of their work justified the controversial decision on Tuesday, saying that the experiments were akin to the 1940s work on nuclear weapons or the first attempts at genetic engineering in the 1970s.

Members of the National Science Advisory Board for Biosecurity said that bioterrorists or rogue governments could use details of the experiments to make a global weapon of catastrophic potential.

“We found the potential risk of public harm to be of unusually high magnitude,” they wrote in a statement published jointly in the rival journals Science and Nature.

The decision, they said, is too big for the scientific community to make on its own. “Physicists faced a similar situation in the 1940s with nuclear-weapons research, and it is inevitable that other scientific disciplines will also do so.”

Since it started spreading in 2003, H5N1 bird flu has killed 344 of the 583 people it is known to have infected--a mortality rate of 59 percent. This compares to a 2.5 percent fatality rate for the 1918 flu, which killed tens of millions of people, or 30 percent for smallpox before it was eliminated in 1979. Luckily, H5N1 doesn’t infect people easily, but it spreads rapidly through flocks of chickens, infects ducks with barely a symptom, and appears to be carried by migrating wild birds. All flu viruses mutate, and most flu experts fear it is only a matter of time before H5N1 either evolves or mixes up with another flu virus to make a form that can easily infect people.

“A pandemic, or the deliberate release of a transmissible highly pathogenic influenza A/H5N1 virus, would be an unimaginable catastrophe for which the world is currently inadequately prepared,” the NSABB wrote.

Usually, when viruses acquire the ability to infect easily, they also become less lethal. So scientists are keen to find out what an H5N1 virus that could easily infect people might look like. If it transmits easily from one person to another, does it give up some of its killing power?

Two labs took a big step toward this goal last year, one in the Netherlands and one at the University of Wisconsin. They engineered forms of H5N1 that ferrets could easily pass to one another--ferrets being the closest thing in the animal world to humans when it comes to getting flu. The good news was that vaccines and drugs both worked against the new strain.

One team sent its findings to Science to be published, while the other submitted its results to Nature. The usual process would have been for the journals to ask other flu and genetics experts to critique the papers, and then they would publish them so other researchers could try to replicate the findings, adding to the world’s knowledge about H5N1, how to watch for dangerous changes, and how to make drugs and vaccines to protect people.

The flu community was atwitter about the pending news, and the potential consequences alarmed the NSABB, which was set up after the 2001 anthrax attacks and which includes heavyweight experts on bioterrorism such as Paul Keim of Northern Arizona University and Mike Osterholm of the University of Minnesota, as well as genetics experts like Claire Fraser-Liggett of the University of Maryland. They asked the two labs to hold off last year until the scientific community could agree on a way to make sure the information got into the right hands--and not into the wrong hands. The experts and the journals have agreed to wait for the time being, and the World Health Organization has set up a meeting in February in Geneva that includes experts from the two teams.

To say the decision frightened and irritated the scientific community would be an understatement. Almost everybody who is anybody in the world of viral research, bioterrorism, and scientific freedom has weighed in--most recently in eight letters to The New York Times.

Keim wrote a separate explanation for the online journal mBio, published by the American Society for Microbiology. “I carefully considered how restricting the information would compromise scientific research progress and even how it would hinder public health efforts to prevent such a horrific pandemic,” Keim wrote. “The short-term negative consequences of restricting experimental details seemed small in contrast to the large consequences of facilitating the replication of these experiments by someone with nefarious intent…. Publishing a detailed experimental protocol on how to produce a highly transmissible H5N1 virus in a highly regarded scientific journal is a very bad idea.”

Dr. Robert Webster of St. Jude Children’s Research Hospital in Memphis, Tenn., a pioneer in influenza research who doesn’t serve on the NSABB, agreed.  “It has been argued that suppression of information serves no purpose, as the information will inevitably be ‘leaked.’ Although this viewpoint is likely correct, I do not believe we should publish the detailed methods of preparing transmissible H5N1,” Webster wrote in a separate commentary in mBio. But he said that the research itself must continue. “While bioterrorism is of real concern, nature has the potential to do much greater damage,” Webster pointed out.

Vincent Racaniello, a microbiologist at Columbia University College of Physicians and Surgeons, disagreed. “Bioterrorists do not want to carry out an experiment; they want to instill terror,” he wrote in mBio. “Science has always worked best when information is freely accessible. Fear has clouded the NSABB’s vision. We cannot allow fear to limit our ability to address medical problems.”

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ScienceDaily (Jan. 31, 2012) — A report from investigators at the Massachusetts General Hospital (MGH) Cancer Center has defined the role of a recently identified gene abnormality in a deadly form of lung cancer. Tumors driven by rearrangements in the ROS1 gene represent 1 to 2 percent of non-small-cell lung cancers (NSCLC), the leading cause of cancer death in the U.S. The researchers show that ROS1-driven tumors can be treated with crizotinib, which also inhibits the growth of tumors driven by an oncogene called ALK, and describe the remarkable response of one patient to crizotinib treatment.

"ROS1 encodes a protein that is important for cell growth and survival, and deregulation of ROS1 through chromosomal rearrangement drives the growth of tumors," says Alice Shaw, MD, PhD, of the MGH Cancer Center -- co-lead author of the paper which has been published online in the Journal of Clinical Oncology. "This finding is important because we have drugs that inhibit ROS1 and could lead to the sort of dramatic clinical response we describe in this paper."

The current findings add ROS1 to the list of genes known to drive NSCLC growth when altered -- a list that includes KRAS, mutations of which account for about 25 percent of cases; EGFR, accounting for 10 to 15 percent; and ALK, rearranged in about 4 percent. Altogether, known cancer-causing genetic changes have been found in a little more than half of NSCLC tumors. Originally identified in brain tumors, ROS1 rearrangement previously had been identified in one NSCLC patient and one NSCLC cell line. The current study was designed to determine the frequency of ROS1 rearrangement in NSCLC and to define the characteristics of patients with ROS1-rearranged tumors.

The investigators screened tumor samples from more than 1,000 NSCLC patients treated at the MGH, Vanderbilt University, the University of California at Irvine, and Fudan University in Shanghai, China. ROS1 rearrangement was identified in 18 tumor samples, for a prevalence of 1.7 percent; ALK rearrangements were identified in 31 samples, with no samples showing alterations in both genes. Patients with ROS1-positive tumors tended to be younger, never to have smoked and to have a type of lung cancer called adenocarcinoma -- characteristics very similar to those of ALK-positive patients.

An earlier MGH study of an experimental ALK inhibitor had found the drug suppressed the growth of a ROS1-positive cell line in addition to ALK-positive cell lines, suggesting that ROS1-positive tumors might be sensitive to the ALK-inhibitor crizotinib. This observation led corresponding author John Iafrate, MD, PhD, and his team to develop a diagnostic test that could identify ROS1-positive tumors. Around the time that test became clinically available, a lung cancer patient whose tumor had not responded to drugs targeting EGFR mutations was referred to the MGH Cancer Center for genetic testing. His tumor was negative for ALK but later proved to harbor a ROS1 rearrangement, and he was enrolled in an extension of the crizotinib clinical trial first reported in the October 28, 2010, New England Journal of Medicine.

"When he enrolled in the trial last April, this patient was extremely sick -- with significant weight loss and very low oxygen levels -- and was barely able to walk," says Shaw. "Within a few days of starting crizotinib, he felt better; and by the time we scanned his chest at seven weeks, the tumors had essentially disappeared from his lungs." Nine months after starting crizotinib therapy, this patient continues to do well. Additional ROS1-positive patients have been enrolled in this trial at MGH, at UC Irvine and at the University of Colorado.

Shaw is an assistant professor of Medicine and Iafrate is an associate professor of Pathology at Harvard Medical School. Co-lead authors are Kristin Bergethon, MGH Pathology, and Sai-Hong Ignatius Ou, MD, PhD, University of California at Irvine. The study was supported by grants from the National Institutes of Health and from Pfizer, which received FDA approval for crizotinib in August 2011.

Additional co-authors are Ryohei Katayama, Eugene Mark, Julie Batten, Eunice Kwak, Jeffrey Clark, Jeffrey Engelman, and Mari Mino Kenudson, MGH Cancer Center; Christina Siwak-Tapp, University of California at Irvine; Keith D. Wilner, Pfizer; Christine Lovly, Nerina McDonald, Pierre Massion, Adriana Gonzalez, David Carbone, and William Pao, Vanderbilt University Medical Center; Pierre Massion, Nashville Veterans Affairs Medical Center; Rong Fang and Hongbin Ji, Shanghai Institutes for Biological Sciences; and Haiquan Chen, Shanghai Medical College, Fudan University.

Massachusetts General Hospital, founded in 1811, is the original and largest teaching hospital of Harvard Medical School. The MGH conducts the largest hospital-based research program in the United States, with an annual research budget of more than $750 million and major research centers in AIDS, cardiovascular research, cancer, computational and integrative biology, cutaneous biology, human genetics, medical imaging, neurodegenerative disorders, regenerative medicine, reproductive biology, systems biology, transplantation biology and photomedicine.

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Journal Reference:

K. Bergethon, A. T. Shaw, S.-H. Ignatius Ou, R. Katayama, C. M. Lovly, N. T. McDonald, P. P. Massion, C. Siwak-Tapp, A. Gonzalez, R. Fang, E. J. Mark, J. M. Batten, H. Chen, K. D. Wilner, E. L. Kwak, J. W. Clark, D. P. Carbone, H. Ji, J. A. Engelman, M. Mino-Kenudson, W. Pao, A. J. Iafrate. ROS1 Rearrangements Define a Unique Molecular Class of Lung Cancers. Journal of Clinical Oncology, 2012; DOI: 10.1200/JCO.2011.35.6345

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New genetic subtype of lung cancer defined

SALT LAKE CITY, Jan. 31, 2012 (GLOBE NEWSWIRE) -- Myriad Genetics, Inc. (Nasdaq:MYGN - News) today announced results for its second fiscal quarter and six months ending December 31, 2011. Revenue for the second fiscal quarter was $122.8 million, an increase of 22 percent over the $100.4 million reported in the second fiscal quarter of 2011. Earnings per diluted share were $0.33, an increase of 27 percent over the same period of the prior year.

"These results represent the second quarter in a row of 20 percent or greater year-over-year revenue growth," said Peter D. Meldrum, President and Chief Executive Officer of Myriad Genetics, Inc. "As a result, I'm pleased to announce increased guidance for fiscal 2012. We remain focused on delivering strong top-line growth and implementing our broader strategic plan to diversify revenue across multiple disease indications and geographies."

Analysis of Second Fiscal Quarter 2012

Molecular diagnostic testing revenue in the second fiscal quarter equaled $117.6 million, an increase of 17 percent compared to the prior year period. This increase was driven by strong growth across all segments and products. Oncology revenue equaled $79.8 million, an increase of 15 percent over the second quarter of 2011. Women's Health revenue totaled $37.9 million, an increase of 22 percent over the same period in the prior year. Revenue from the BRACAnalysis(R) test, which represented 82.6 percent of total revenue in the second quarter, was $101.4 million, a 14 percent increase over the same period of the prior year. Revenue from the COLARIS(R) and COLARIS AP(R) tests, which represented 8.9 percent of total revenue during the quarter, was $10.9 million, an increase of 56 percent compared to the same fiscal quarter of the prior year. Myriad's remaining molecular diagnostic tests contributed $5.3 million to second quarter revenue, an increase of 24 percent over the same period in the prior year, and accounted for 4.3 percent of total revenue. Companion diagnostic service revenue in the second fiscal quarter equaled $5.2 million and represented 4.2 percent of total company revenue. There is no prior year revenue, as the Company acquired this business in May 2011. Operating income was $45.5 million, an increase of 18 percent from the prior year period. This record level of operating income included the impact of a 68 percent increase in R&D investment to support the Company's existing molecular diagnostic tests and future product opportunities. Net income for the second fiscal quarter was $28.3 million, an increase of 17 percent over the $24.2 million reported in same period of the prior year. The Company repurchased 927,709 shares of its common stock during the quarter under its previously announced stock repurchase program. Diluted weighted average shares outstanding were 86.2 million in the second fiscal quarter as compared to 93.6 million in the same period of the prior year. The Company ended the quarter with $428.3 million in cash, cash equivalents and marketable investment securities. Days sales outstanding for Myriad's accounts receivable improved to 32 days, compared with 37 days in the same period of the prior year. Bad debt expense in the second fiscal quarter equaled 5.2 percent of revenue, compared with 4.2 percent in the same period of the prior year.

Year-to-Date Performance

Total revenue for the first half of fiscal 2012 was $233.3 million, an increase of 21 percent over $192.3 million reported for the half of fiscal 2011. Operating income for the first half of fiscal 2012 was $86.9 million, an increase of 17 percent year-over-year. Net income for the first half of fiscal 2012 equaled $53.4 million, compared to $46.7 million for the first half of the prior year, an increase of 14 percent. In the first half of fiscal 2012, diluted earnings per share increased 24 percent to $0.62 from $0.50 for the same period of the prior year.

Fiscal Year 2012 Outlook

The Company has increased its expectations for fiscal year 2012 financial performance. Total revenue is now expected to be $465 million to $475 million, an increase from the $445 million to $465 million previously announced. This level of revenue is expected to result in fully diluted earnings per share of $1.24 to $1.28, up from the original guidance of $1.20 to $1.25. Molecular diagnostic revenue is now expected to range between $440 million and $450 million and companion diagnostic service revenue continues to be expected to range between $24 million and $26 million. These projections are forward looking statements and are subject to the risks summarized in the safe harbor statement at the end of this press release. The Company will provide further detail on its business outlook during the conference call it is holding today to discuss its fiscal results for the second fiscal quarter and first half of fiscal 2012.

Conference Call and Webcast

A conference call will be held on Tuesday, January 31, 2012, at 4:30 p.m. Eastern time to discuss Myriad's second fiscal quarter and first half 2012 financial results and fiscal year 2012 outlook. The dial-in number for domestic callers is (888) 225-2734. International callers may dial (303) 223-2685. All callers will be asked to reference reservation number 21566441. An archived replay of the call will be available for seven days by dialing (800) 633-8284 and entering the reservation number above. The conference call will also be available through a live Webcast at http://www.myriad.com.

About Myriad Genetics

Myriad Genetics, Inc. (Nasdaq:MYGN - News) is a leading molecular diagnostic company dedicated to developing and marketing transformative tests to assess a person's risk of developing disease, guide treatment decisions and assess a patient's risk of disease progression and disease recurrence. Myriad's portfolio of nine molecular diagnostic tests are based on an understanding of the role genes play in human disease and were developed with a focus on improving an individual's decision making process for monitoring and treating disease. With fiscal year 2011 annual revenue of over $400 million and more than 1,000 employees, Myriad is working on strategic directives, including new product introductions, companion diagnostics, and international expansion, to take advantage of significant growth opportunities. For more information on how Myriad is making a difference, please visit the Company's website: http://www.myriad.com.

Myriad, the Myriad logo, BRACAnalysis, Colaris, Colaris AP, Melaris, TheraGuide, Prezeon, OnDose, Panexia and Prolaris are trademarks or registered trademarks of Myriad Genetics, Inc. in the United States and foreign countries. MYGN-F, MYGN-G

Safe Harbor Statement

This press release contains "forward-looking statements" within the meaning of the Private Securities Litigation Reform Act of 1995, including statements relating to the Company's focus on delivering strong top-line growth and implementing its broader strategic plan to diversify revenue across multiple disease indications and geographies; the Company's investment in R&D to support its existing molecular diagnostic tests and future product opportunities; the Company's increased guidance for fiscal year 2012 under the caption "Fiscal Year 2012 Outlook;"and the Company's strategic directives under the caption "About Myriad Genetics". These "forward-looking statements" are based on management's current expectations of future events and are subject to a number of risks and uncertainties that could cause actual results to differ materially and adversely from those set forth in or implied by forward-looking statements. These risks and uncertainties include, but are not limited to: the risk that sales and profit margins of our existing molecular diagnostic tests and companion diagnostic services may decline or will not continue to increase at historical rates; the risk that we may be unable to expand into new markets outside of the United States; the risk that we may be unable to develop or achieve commercial success for additional molecular diagnostic tests and companion diagnostic services in a timely manner, or at all; the risk that we may not successfully develop new markets for our molecular diagnostic tests and companion diagnostic services, including our ability to successfully generate revenue outside the United States; the risk that licenses to the technology underlying our molecular diagnostic tests and companion diagnostic services and any future products are terminated or cannot be maintained on satisfactory terms; risks related to delays or other problems with manufacturing our products or operating our laboratory testing facilities; risks related to public concern over genetic testing in general or our tests in particular; risks related to regulatory requirements or enforcement in the United States and foreign countries and changes in the structure of healthcare payment systems; risks related to our ability to obtain new corporate collaborations and acquire new technologies or businesses on satisfactory terms, if at all; risks related to our ability to successfully integrate and derive benefits from any technologies or businesses that we acquire; the development of competing tests and services; the risk that we or our licensors may be unable to protect the proprietary technologies underlying our tests; the risk of patent-infringement and invalidity claims or challenges of our patents; risks of new, changing and competitive technologies and regulations in the United States and internationally; and other factors discussed under the heading "Risk Factors" contained in Item 1A in our most recent Annual Report on Form 10-K filed with the Securities and Exchange Commission, as well as any updates to those risk factors filed from time to time in our Quarterly Reports on Form 10-Q or Current Reports on Form 8-K. All information in this press release is as of the date of the release, and Myriad undertakes no duty to update this information unless required by law.

MYRIAD GENETICS, INC. AND SUBSIDIARIES CONDENSED CONSOLIDATED INCOME STATEMENTS (Unaudited)

(in thousands, except per share amounts) Three Months Ended Six Months Ended
Dec. 31, 2011 Dec. 31, 2010 Dec. 31, 2011 Dec. 31, 2010

Molecular diagnostic testing $117,610 $100,440 $221,579 $192,298 Companion diagnostic services 5,201 -- 11,684 -- Total revenue 122,811 100,440 233,263 192,298

Costs and expenses:

Cost of molecular diagnostic testing 12,815 12,046 24,115 23,058 Cost of companion diagnostic services 3,302 -- 6,364 -- Research and development expense 10,243 6,092 18,748 11,853 Selling, general, and administrative expense 50,986 43,716 97,100 83,210 Total costs and expenses 77,346 61,854 146,327 118,121

Operating income 45,465 38,586 86,936 74,177

Other income (expense):

Interest income 1,382 548 1,856 1,269 Other (64) (80) (205) (214) Total other income 1,318 468 1,651 1,055

Income before income taxes 46,783 39,054 88,587 75,232

Income tax provision (benefit) 18,487 14,863 35,193 28,503

Net income $28,296 $24,191 $53,394 $46,729

Earnings per share:

Basic $0.33 $0.26 $0.63 $0.51 Diluted $0.33 $0.26 $0.62 $0.50

Weighted average shares outstanding

Basic 84,498 91,528 84,870 92,395 Diluted 86,231 93,647 86,602 94,178

Condensed Consolidated Balance Sheets
Dec. 31, 2011 Jun. 30, 2011

(In thousands)

Cash, cash equivalents, and marketable investment securities $428,259 $417,314

Trade receivables, net 42,988 50,272

Other receivables 1,083 575

Prepaid taxes 16,569 --

Inventory, net 10,294 8,218

Prepaid expenses 3,087 2,949

Equipment and leasehold improvements, net 24,329 23,080

Note receivable 17,667 --

Other assets 8,000 --

Intangibles, net 16,265 16,715

Goodwill 56,850 56,051

Deferred tax assets 35,867 35,653

Total assets $661,258 $610,827

Accounts payable and accrued liabilities $32,612 $33,040

Deferred revenue 2,434 1,347

Uncertain tax benefits 9,448 9,648

Stockholders' equity 616,764 566,792

Total liabilities and stockholders' equity $661,258 $610,827

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Myriad Genetics Reports Second Quarter Fiscal Year 2012 Results

Arthur Chovnick, a professor at the University of Connecticut, was a pioneer in the field of genetics whose influence was felt across the field of molecular genetics and biology.

"Arthur did something that has effectively jump-started enormous strides in the genetics of higher organisms," said Hal Krider, a former professor of genetics at UConn. "He was probably the most recognized, under-honored geneticist, but people with Nobel prizes would call and ask him for advice."

Chovnick, 84, of Chaplin, died Sept. 5.

One anecdote from his life reflected Chovnick's stature in the world of genetics. When his daughter Lisa was taking a biology course, she learned about Watson and Crick, who discovered the structure of DNA, but when the home phone rang one day and a caller identified himself as Francis Crick, Lisa hung up on him. "Quit joking," she told the Nobel Prize winner the next time he called.

Later that night, Arthur Chovnick picked up the phone himself. "Hello, Francis," he said.

"People of that stature were available to Arthur all the time," said Krider. "Everybody knew him. He was very, very well known and inordinately highly regarded."

Chovnick conducted experiments on drosophila melanogaster, a relative of the humble fruit fly that, rather than being a laboratory pest, is a valuable scientific specimen used for years in genetics research. First used to study heredity, the fly is now used in the study of disease as scientists search for the genes responsible for Alzheimer's or Parkinson's or Huntington's.

Drosophila genes are nearly identical to human genes. They also reproduce very quickly, meaning mutations may be studied in weeks rather than months or years. They have only four chromosomes. Even better, no groups picket against drosophila experimentation as they do against higher-order species.

"It is easy to grow and manipulate, and they have genes like us," said Christine Rushlow, a Chovnick-trained geneticist who is a professor at New York University. "We use them as a model system to see how genes work. We share so many genes."

Chovnick, known for pioneering work in gene organization and in demonstrating the way traits cross over within a gene, could look at events that were rare and re-create them.

Chovnick, born in Brooklyn, N.Y., on Aug. 2, 1927, grew up in Queens, where he graduated from Jackson High School in 1944. He was the oldest of four children born to Fannie and Herman Chovnick, who had both emigrated from Russia. He attended Indiana University for a year before joining the U.S. Navy, where he served on a hospital ship. After he was discharged, he returned to Indiana and obtained his undergraduate degree in 1949 and his master's in 1951. He got a doctorate in genetics from Ohio State University two years later, and obtained a grant from the National Institutes of Health that continued until 1995, one of the longest continuous NIH grants.

He spent two years at the University of Connecticut doing research and teaching before going to the Cold Spring Harbor Laboratory in Long Island, first as assistant director, then as director. In 1962, he returned to UConn as a professor, where he remained until he retired in 1994. He was a fellow of the American Association for the Advancement of Science and a founding member of the Connecticut Academy of Science and Engineering.

Chovnick was revered as a mentor as well as a teacher, his colleagues said.

"He left you alone, except he would always teach or help you," Rushlow said. "He was a great analytical thinker, which he could do in his head because he was so experienced."

He helped his students design experiments that would create a certain type of drosophila — with pink eyes for example, or missing a wing — to help them create their own mutations. "You see the consequences to the fly, and what it is doing to the fly," Rushlow said.

Chovnick also did early work on cloning, providing a fly with unusual chromosomes for other scientists to study. He studied how to regulate the activity of genes.

"When things go wrong because genes are out of control, you get disease," Rowlson said. "He was at the forefront, a leader in the genetics field, and famous for the work he had done." He also understood how genes recombine and how a new DNA sequence is created with potentially new effects.

Today, as scientists intensify their search for the genetic cause of disease, Chovnick's work is significant.

"He was a seminal character in the transition from classical genetics to modern genetic cloning and gene manipulation," said Krider, his former colleague.

"He was a very careful and highly creative thinker with a keenly analytical mind," said Arthur Hilliker, a professor at York University in Toronto, who studied under and later collaborated with Chovnick.

Originally posted here:
Genetics Pioneer Was UConn Professor, Mentor