Experimental distribution of entanglement with separable carriers

The key requirement for quantum networking is the distribution of entanglement between nodes. Surprisingly, entanglement can be generated across a network without direct transfer-or communication-of entanglement. In contrast to information gain, which cannot exceed the communicated information, the entanglement gain is bounded by the communicated quantum discord, a more general measure of quantum correlation that includes but is not limited to entanglement. Here, we experimentally entangle two communicating parties sharing three initially separable photonic qubits by exchange of a carrier photon that is unentangled with either party at all times. We show that distributing entanglement with separable carriers is resilient to noise and in some cases becomes the only way of distributing entanglement through noisy environments

Optimal imaging of remote bodies using quantum detectors

We implement a general imaging method by measuring the complex degree of coherence using linear optics and photon number resolving detectors. In the absence of collective or entanglement-assisted measurements, our method is optimal over a large range of practically relevant values of the complex degree of coherence. We measure the size and position of a small distant source of pseudothermal light, and show that our method outperforms the traditional imaging method by an order of magnitude in precision. Finally, we show that a lack of photon-number resolution in the detectors has only a modest detrimental effect on measurement precision and simulate imaging using the new and traditional methods with an array of detectors, showing that the new method improves both image clarity and contrast

Optimal imaging of remote bodies using quantum detectors

We implement an optimal imaging method using number-resolving photon detectors. Measuring the complex degree of coherence, we obtain the size and position of a distant pseudothermal light source and show this method outperforms traditional imaging

Loss of Caveolin-1 Gene Expression Accelerates the Development of Dysplastic Mammary Lesions in Tumor-Prone Transgenic Mice

Caveolin-1 is the principal structural component of caveolae microdomains, which represent a subcompartment of the plasma membrane. Several independent lines of evidence support the notion that caveolin-1 functions as a suppressor of cell transformation. For example, the human CAV-1 gene maps to a suspected tumor suppressor locus (D7S522/7q31.1) that is frequently deleted in a number of carcinomas, including breast cancers. In addition, up to 16% of human breast cancers harbor a dominant-negative mutation, P132L, in the CAV-1 gene. Despite these genetic associations, the tumor suppressor role of caveolin-1 still remains controversial. To directly assess the in vivo transformation suppressor activity of the caveolin-1 gene, we interbred Cav-1 (−/−) null mice with tumor-prone transgenic mice (MMTV-PyMT) that normally develop multifocal dysplastic lesions throughout the entire mammary tree. Herein, we show that loss of caveolin-1 gene expression dramatically accelerates the development of these multifocal dysplastic mammary lesions. At 3 wk of age, loss of caveolin-1 resulted in an approximately twofold increase in the number of lesions (foci per gland; 3.3 ± 1.0 vs. 7.0 ± 1.2) and an approximately five- to sixfold increase in the total area occupied by these lesions. Similar results were obtained at 4 wk of age. However, complete loss of caveolin-1 was required to accelerate the appearance of these dysplastic mammary lesions, because Cav-1 (+/−) heterozygous mice did not show any increases in foci development. We also show that loss of caveolin-1 increases the extent and the histological grade of these mammary lesions and facilitates the development of papillary projections in the mammary ducts. Finally, we demonstrate that cyclin D1 expression levels are dramatically elevated in Cav-1 (−/−) null mammary lesions, consistent with the accelerated appearance and growth of these dysplastic foci. This is the first in vivo demonstration that caveolin-1 can function as a transformation suppressor gene