Topological insulators are a new class of materials, that exhibit robust gapless surface states protected by time-reversal symmetry. The interplay between such symmetry-protected topological surface ...states and symmetry-broken states (e.g. superconductivity) provides a platform for exploring novel quantum phenomena and new functionalities, such as 1D chiral or helical gapless Majorana fermions, and Majorana zero modes which may find application in fault-tolerant quantum computation. Inducing superconductivity on topological surface states is a prerequisite for their experimental realization. Here by growing high quality topological insulator Bi\(_2\)Se\(_3\) films on a d-wave superconductor Bi\(_2\)Sr\(_2\)CaCu\(_2\)O\(_{8+\delta}\) using molecular beam epitaxy, we are able to induce high temperature superconductivity on the surface states of Bi\(_2\)Se\(_3\) films with a large pairing gap up to 15 meV. Interestingly, distinct from the d-wave pairing of Bi\(_2\)Sr\(_2\)CaCu\(_2\)O\(_{8+\delta}\), the proximity-induced gap on the surface states is nearly isotropic and consistent with predominant s-wave pairing as revealed by angle-resolved photoemission spectroscopy. Our work could provide a critical step toward the realization of the long sought-after Majorana zero modes.
Lipid-lowering therapy, as assessed by angiography, clearly benefits the arterial disease process. For example, among intensively treated patients in FATS the frequency of definite progression per ...lesion at risk was reduced by 75% among mild and moderate lesions, which form the great preponderance of the lesion population. Regression frequency per lesion was more than doubled by intensive therapy in mild and moderate subgroups and quadrupled in the subgroup with severe lesions. Clinical events were reduced by 73%. This was clearly due to a 15-fold reduction in the likelihood that a mildly or moderately diseased arterial segment would undergo abrupt and substantial progression to a severe lesion at the time of the clinical event. It has been shown that the process of plaque fissuring, leading to plaque disruption, thrombosis, and clinical coronary events, is predicted by the size of the plaque core lipid pool and the abundance of lipid-laden macrophages in its fibrous cap. Experimentally, lipid lowering therapy decreases the number of lipid-laden intimal macrophages and more slowly depletes core cholesteryl ester deposits. Thus the composite of new and previously published data presented here supports the idea that lipid-lowering therapy selectively lipid-depletes (causes regression of) those fatty lesions containing a large lipid core and abundant intimal foam cells. By doing so, these lesions, which are most vulnerable to fissuring, are rendered much more stable and the clinical event rate is accordingly decreased.
