Entropy Bounds for Device-Independent Quantum Key Distribution with Local Bell Test.

One of the main challenges in device-independent quantum key distribution (DIQKD) is achieving the required Bell violation over long distances, as the channel losses result in low overall detection efficiencies. Recent works have explored the concept of certifying nonlocal correlations over extended distances through the use of a local Bell test. Here, an additional quantum device is placed in close proximity to one party, using short-distance correlations to verify nonlocal behavior at long distances.

Device-independent quantum key distribution with random key basis.

Device-independent quantum key distribution (DIQKD) is the art of using untrusted devices to distribute secret keys in an insecure network. It thus represents the ultimate form of cryptography, offering not only information-theoretic security against channel attacks, but also against attacks exploiting implementation loopholes. In recent years, much progress has been made towards realising the first DIQKD experiments, but current proposals are just out of reach of today's loophole-free Bell experiments.

Advantage Distillation for Device-Independent Quantum Key Distribution.

Device-independent quantum key distribution (DIQKD) offers the prospect of distributing secret keys with only minimal security assumptions, by making use of a Bell violation. However, existing DIQKD security proofs have low noise tolerances, making a proof-of-principle demonstration currently infeasible. We investigate whether the noise tolerance can be improved by using advantage distillation, which refers to using two-way communication instead of the one-way error correction currently used in DIQKD security proofs.

Insulin receptor substrate-2 regulates aerobic glycolysis in mouse mammary tumor cells via glucose transporter 1.

The insulin receptor substrate (IRS) proteins are cytoplasmic adaptor molecules that function as signaling intermediates downstream of activated cell surface receptors. Based on data implicating IRS-2 but not IRS-1 in breast cancer invasion, survival, and metastasis, we assessed the contribution of IRS-1 and IRS-2 to aerobic glycolysis, which is known to impact tumor growth and progression. For this purpose, we used tumor cell lines derived from transgenic mice that express the polyoma virus middle T antigen (PyV-MT) in the mammary gland and that are wild-type (WT) or null for either Irs-1 (Irs-1-/-) or Irs-2 (Irs-2-/-).

Adenosine upregulates CXCR4 and enhances the proliferative and migratory responses of human carcinoma cells to CXCL12/SDF-1alpha.

The level of expression of the chemokine receptor CXCR4 has been shown to play a crucial role in determining the ability of cancer cells to metastasize from the primary tumor and become established in tissue sites that are rich in the CXCR4 ligand CXCL12/SDF-1alpha. High CXCR4 expression on cancer cells is associated with an increased risk of recurrence and poorer overall survival. We propose that local tissue mediators within the primary tumor or at secondary sites may modulate the level of CXCR4 expression and, therefore, potentially affect the ability of the cancer cells to metastasize.

Adenosine downregulates DPPIV on HT-29 colon cancer cells by stimulating protein tyrosine phosphatase(s) and reducing ERK1/2 activity via a novel pathway.

The multifunctional cell-surface protein dipeptidyl peptidase IV (DPPIV/CD26) is aberrantly expressed in many cancers and plays a key role in tumorigenesis and metastasis. Its diverse cellular roles include modulation of chemokine activity by cleaving dipeptides from the chemokine NH(2)-terminus, perturbation of extracellular nucleoside metabolism by binding the ecto-enzyme adenosine deaminase, and interaction with the extracellular matrix by binding proteins such as collagen and fibronectin. We have recently shown that DPPIV can be downregulated from the cell surface of HT-29 colorectal carcinoma cells by adenosine, which is a metabolite that becomes concentrated in the extracellular fluid of hypoxic solid tumors.

Adenosine down-regulates the surface expression of dipeptidyl peptidase IV on HT-29 human colorectal carcinoma cells: implications for cancer cell behavior.

Dipeptidyl peptidase IV (DPPIV) is a multifunctional cell-surface protein that, as well as having dipeptidase activity, is the major binding protein for adenosine deaminase (ADA) and also binds extracellular matrix proteins such as fibronectin and collagen. It typically reduces the activity of chemokines and other peptide mediators as a result of its enzymatic activity. DPPIV is aberrantly expressed in many cancers, and decreased expression has been linked to increases in invasion and metastasis.