Titlebook: Imaging Coronary Atherosclerosis; Stephen J. Nicholls,Tim Crowe Book 2014 Springer Science+Business Media New York 2014

摻和

jarring

glucagon

deactivate

Molecular Imaging of Coronary Atherosclerosis,lecular imaging of atherosclerosis. For human coronary artery imaging, however, tissue penetration severely limits external optical imaging. Thus, for coronary arterial applications, NIRF will require intra-arterial approaches. Imaging targets identified by basic research include endothelial activat

星星

Rishi Puri MBBS, FRACP,Stephen J. Nicholls MBBS, PhD, FRACP, FACC, FESC, FAHA, FCSANZt these algorithms have to offer. The book is ideally suited as a graduate-level textbook, whereby students may be tasked with the study of the rich variants of BSO algorithms that involves a hands-on implement978-3-030-15072-3978-3-030-15070-9Series ISSN 1867-4534 Series E-ISSN 1867-4542

儲(chǔ)備

小蟲

hysiological correlates of functional brain activation in more detail than noninvasive recordings. The proximity of ECoG electrodes to EEG sources enhances their spatial resolution, as well as their sensitivity and signal-to-noise ratio, particularly for high frequency EEG activity. ECoG recordings

一回合

Yu Kataoka MD,Stephen J. Nicholls MBBS, PhD, FRACP, FACC, FESC, FAHA, FCSANZays for studying drug-receptor interactions, rapid advances have been made in the biochemical investigation of drug and transmitter mechanisms. Our knowledge of the physiological actions of neuroactive drugs has also progressed in recent years, due in large part to the extensive use of the iontophor

自傳

Femi Philip MD,Samir R. Kapadia MDays for studying drug-receptor interactions, rapid advances have been made in the biochemical investigation of drug and transmitter mechanisms. Our knowledge of the physiological actions of neuroactive drugs has also progressed in recent years, due in large part to the extensive use of the iontophor

Dissonance

Sorin J. Brener MD leading to hyperinsulinemia, hyperglycemia, and enlarged fatty liver. Our laboratory have developed a mouse model that mimics these features of generalized lipodystrophy: the syndrome occurs in transgenic mice expressing a truncated version of a nuclear protein known as nSREBP-1c (sterol-regulatory