Professor of Medicine, Division of Cardiovascular Medicine, University of Wisconsin-Madison
Cardiology
Dr. Craig T. January, MD
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Craig January is an expert in the field of Cardiology. He attended University of Iowa Carver College of Medicine. University of Iowa Carver College of Medicine is ranked 29 in research and 16 in primary care medicine He has 2 awards "Meaningful Use Stage 1 Certification" and "Fellow (FACC)". Craig January has written publications. He has 101 publications published with PubMed. The lastest paper is: 'Temperature dependence of early and late currents in human cardiac wild-type and long Q-T DeltaKPQ Na+ channels.' He accepts Medicare payments and is registered with Medicare.gov.
Publications
- In memoriam: harry a. Fozzard, MD, april 22, 1931-december 9, 2014.
- Harry A. Fozzard, MD: 1931–2014.
- Mouse ERG K(+) channel clones reveal differences in protein trafficking and function.
- Calcium Transients Closely Reflect Prolonged Action Potentials in iPSC Models of Inherited Cardiac Arrhythmia.
- KCNJ2 Mutation Causes an Adrenergic-Dependent Rectification Abnormality with Calcium Sensitivity and Ventricular Arrhythmia.
- Pharmacological Correction of Long QT-linked Mutations in KCHN2 (hERG) Increases the Trafficking of Kv11.1 Channels Stored in the Transitional ER.
- Effect of microculture on cell metabolism and biochemistry: do cells get stressed in microchannels?
- Mechanism of Loss of Kv11.1 K+ Current in Mutant T421M-Kv11.1 Expressing Rat Ventricular Myocytes: Interaction of Trafficking and Gating.
- High Purity Human Induced Pluripotent Stem Cell (hiPSC) Derived Cardiomyocytes: Electrophysiological Properties of Action Potentials and Ionic Currents.
- Trafficking-deficient hERG K+ channels linked to long QT Syndrome are regulated by a microtubule-dependent quality control compartment in the ER.
- The common African American polymorphism SCN5A-S1103Y interacts with mutation SCN5A-R680H to increase late Na current.
- Small GTPase Rab11b regulates degradation of surface membrane L-type Cav1.2 channels.
- 2011 ACCF/AHA/HRS focused update on the management of patients with Atrial fibrillation (update on dabigatran): a report of the American College of Cardiology Foundati...
- 2011 ACCF/AHA/HRS focused update on the management of patients with Atrial fibrillation (update on dabigatran). A report of the American College of Cardiology Foundati...
- Novel chemical suppressors of long QT Syndrome identified by an in vivo functional screen.
- R231C mutation in KCNQ1 causes long QT Syndrome type 1 and familial atrial fibrillation.
- Microfluidic cell culture and its application in high-throughput drug screening: cardiotoxicity assay for hERG channels.
- Rescue of mutated cardiac ion channels in inherited arrhythmia Syndromes.
- Properties of WT and mutant hERG K(+) channels expressed in neonatal mouse cardiomyocytes.
- Alpha1-syntrophin mutations identified in sudden infant death Syndrome cause an increase in late cardiac sodium current.
- Genotype-phenotype aspects of type 2 long QT Syndrome.
- Reduction of repolarization reserve unmasks the proarrhythmic role of endogenous late Na(+) current in the Heart.
- Small GTPase determinants for the Golgi processing and plasmalemmal expression of human ether-a-go-go related (hERG) K+ channels.
- Fever-induced QTc prolongation and ventricular arrhythmias in individuals with type 2 congenital long QT Syndrome.
- Is ranolazine an antiarrhythmic drug?
- Inherited arrhythmias: a National Heart, Lung, and Blood Institute and Office of Rare Diseases workshop consensus report about the diagnosis, phenotyping, molecular me...
- Kv11.1 (ERG1) K+ channels localize in cholesterol and sphingolipid enriched membranes and are modulated by membrane cholesterol.
- Specific serine proteases selectively damage KCNH2 (hERG1) potassium channels and I(Kr).
- Most LQT2 mutations reduce Kv11.1 (hERG) current by a class 2 (trafficking-deficient) mechanism.
- Intragenic suppression of trafficking-defective KCNH2 channels associated with long QT Syndrome.
- An intronic mutation causes long QT Syndrome.
- Pharmacological rescue of trafficking Defective HERG channels formed by coassembly of wild-type and long QT mutant N470D subunits.
- Biology of cardiac Arrhythmias: ion channel protein trafficking.
- Molecular and functional characterization of common polymorphisms in HERG (KCNH2) potassium channels.
- Molecular heterogeneity of calcium channel beta-subunits in canine and human Heart: evidence for differential subcellular localization.
- Potassium and long QT Syndrome: a new look at an old therapy.
- Thapsigargin selectively rescues the trafficking Defective LQT2 channels G601S and F805C.
- Interaction with GM130 during HERG ion channel trafficking. Disruption by type 2 congenital long QT Syndrome mutations. Human Ether-Ã -go-go-Related Gene.
- Genetic basis for the origin of cardiac Arrhythmias: implications for therapy.
- Role of glycosylation in cell surface expression and stability of HERG potassium channels.
- Pharmacological rescue of human K(+) channel long-QT2 mutations: human ether-a-go-go-related gene rescue without block.
- Large-scale mutational analysis of Kv11.1 reveals molecular insights into type 2 long QT Syndrome.
- International Life Sciences Institute (Health and Environmental Sciences Institute, HESI) initiative on moving towards better predictors of drug-induced torsades de po...
- [Asymmetrical changes in electrical activity of Purkinje fibers and muscle cells after administration of BAY K 8644. A new model of cardiac arrhythmia].
- Manpower challenges in the future of cardiology.
- Internet resources for exploring gene family diversity.
- Enhancement of delayed afterdepolarizations and triggered activity by class III antiarrhythmic drugs: multiple effects of E-4031 and dofetilide.
- Droperidol lengthens cardiac repolarization due to block of the rapid component of the delayed rectifier potassium current.
- Preferential block of late sodium current in the LQT3 DeltaKPQ mutant by the class I(C) antiarrhythmic flecainide.
- Correction of defective protein trafficking of a mutant HERG potassium channel in human long QT Syndrome. Pharmacological and temperature effects.
- Block of HERG potassium channels by the antihistamine astemizole and its metabolites desmethylastemizole and norastemizole.
- Effect of acetylstrophanthidin on action potential duration and relation with extracellular potassium in sheep isolated Purkinje fibers.
- Mechanism of block and identification of the verapamil binding domain to HERG potassium channels.
- Novel mechanism associated with an inherited cardiac arrhythmia: Defective protein trafficking by the mutant HERG (G601S) potassium channel.
- Temperature dependence of early and late currents in human cardiac wild-type and long Q-T DeltaKPQ Na+ channels.
- HERG channel dysfunction in human long QT Syndrome. Intracellular transport and functional defects.
- Molecular basis for the lack of HERG K+ channel block-related cardiotoxicity by the H1 receptor blocker cetirizine compared with other second-generation antihistamines.
- Both T- and L-type Ca2+ channels can contribute to excitation-contraction coupling in cardiac Purkinje cells.
- Properties of HERG channels stably expressed in HEK 293 cells studied at physiological temperature.
- Blockage of the HERG human cardiac K+ channel by the gastrointestinal prokinetic agent cisapride.
- Adverse effects of low dose amiodarone: a meta-analysis.
- Torsade de pointes with an antihistamine metabolite: potassium channel blockade with desmethylastemizole.
- The monophasic action potential technique and its application in cardiac electropharmacology.
- Induction of delayed afterdepolarizations and triggered Arrhythmias in isolated Purkinje fibers: comparison of resibufogenin and acetylstrophanthidin.
- Digoxin-induced delayed afterdepolarizations: biphasic effects of digoxin on action potential duration and the Q-T interval in cardiac Purkinje fibers.
- ECG changes in pneumothorax. A unique finding and proposed mechanism.
- Isolation and characterization of single canine cardiac purkinje cells.
- The effects of membrane potential, extracellular potassium, and tetrodotoxin on the intracellular sodium ion activity of sheep cardiac muscle.
- Electrophysiologic and inotropic actions of prostaglandin F2alpha in rat myocardium.
- Excitability and oscillatory afterpotentials in isolated sheep cardiac Purkinje fibers.
- Effects of Ca2+/Mg2+ removal on aiNa, aiK, and tension in cardiac Purkinje fibers.
- Sodium current in voltage clamped internally perfused canine cardiac Purkinje cells.
- Delayed afterdepolarizations in Heart muscle: mechanisms and relevance.
- New studies of the excitatory sodium currents in Heart muscle.
- Inactivation properties of T-type calcium current in canine cardiac Purkinje cells.
- Characteristics of L- and T-type Ca2+ currents in canine cardiac Purkinje cells.
- Early afterdepolarizations: mechanism of induction and block. A role for L-type Ca2+ current.
- A model for early afterdepolarizations: induction with the Ca2+ channel agonist Bay K 8644.
- Sodium currents in single cardiac Purkinje cells.
- Triggered activity in the Heart: cellular mechanisms of early after-depolarizations.
- Cellular mechanisms of early afterdepolarizations.
- Direct measurement of L-type Ca2+ window current in Heart cells.
- L- and T-type Ca2+ channels in canine cardiac Purkinje cells. Single-channel demonstration of L-type Ca2+ window current.
- Potentials in mammalian skeletal muscle from collagenase-treated tissue.
- Rate-dependent QT shortening mechanism for the LQT3 deltaKPQ mutant.
- [3H]dofetilide binding to HERG transfected membranes: a potential high throughput preclinical screen.
- Cocaine blocks HERG, but not KvLQT1+minK, potassium channels.
- Long QT Syndrome: cellular basis and arrhythmia mechanism in LQT2.
- Differences in action potential and early afterdepolarization properties in LQT2 and LQT3 models of long QT Syndrome.
- The anti-malarial drug halofantrine and its metabolite N-desbutylhalofantrine block HERG potassium channels.
- Blockade of HERG cardiac K+ current by antifungal drug miconazole.
- Blockade of HERG channels by HIV protease inhibitors.
- Protein trafficking abnormalities: a new mechanism in drug-induced long QT Syndrome.
- Purulent pericarditis induced by endobronchial needle injection of adenoviral-mediated gene therapy.
- Comparison of HERG channel blocking effects of various beta-blockers-- implication for clinical strategy.
- Coexistence of hERG current block and disruption of protein trafficking in ketoconazole-induced long QT Syndrome.
- Drug-induced long QT Syndrome: hERG K+ channel block and disruption of protein trafficking by fluoxetine and norfluoxetine.
- HERG trafficking and pharmacological rescue of LQTS-2 mutant channels.
- Different times of development of tremor to harmaline and oxotremorine in neonatal rats.
- Fever-triggered ventricular arrhythmias in Brugada Syndrome and type 2 long-QT Syndrome.
Schools
University of Ia Roy J amp L Carver Com
Procedures Preformed
- Cardiac Catheterization (incl. Coronary Angiography)
- Cardiac Imaging
- Cardiac MRI (Magnetic Resonance Imaging) of Heart or Chest
- Cardiac Myocardial Perfusion Imaging
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Conditions Treated
- Aneurysm and Dissection of Heart
- Angina and Acute Coronary Syndrome
- Aortic Aneurysm
- Aortic Dissection
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Doctors Specialties
- Cardiology
Accepted Insurances
- Choice Plus POS II
- American Enterprise Group
- American Republic
- Anthem Blue Cross Blue Shield HMO
- Anthem Blue Cross Blue Shield PPO
- Blue Preferred Plus POS
- Assurant Health
- Blue Card PPO
- Blue Cross Blue Shield of Illinois PPO
- Cigna PPO
- Great West Healthcare-Cigna PPO
- Open Access Plus
- Commercial Insurance Company
- First Health (Coventry Health Care) PPO
- Golden Rule
- GEHA
- Group Health Cooperative
- Choice Care PPO
- Medicare MCR
- Meritain Health
- MultiPlan
- National Elevator
- Pekin Insurance
- Pipefitters
- Principal Life
- Thrivent Financial
- United Healthcare
- Universal American
Awards
- Meaningful Use Stage 1 Certification
- Fellow (FACC)
Education
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University of Chicago -
University of Iowa Carver College of Medicine
Hospital
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University of Wisconsin Hospital and Clinics -
William S. Middleton Memorial Veterans Hospital
Drug Facts
| NPI NUMBER | 1801862818 | |
| NPPES Provider LastName | JANUARY | |
| NPPES Provider FirstName | CRAIG | |
| NPPES Provider ZIPCode | 53792 | |
| NPPES Provider State | WI | |
| Specialty Description | Cardiac Electrophysiology | |
| Total Claim Count | 479.0 | |
| Distinct Opioid Count | 0.0 | |
| Opioid Claim Count | 0.0 | |
| Percent Opioid Claims | 0.0 |
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1801862818 |
| Last Name Of The Provider | JANUARY |
| First Name Of The Provider | CRAIG |
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