Scotin, a novel p53-inducible proapoptotic protein located in the ER and the nuclear membrane

p53 is a transcription factor that induces growth arrest or apoptosis in response to cellular stress. To identify new p53-inducible proapoptotic genes, we compared, by differential display, the expression of genes in spleen or thymus of normal and p53 nullizygote mice after γ-irradiation of whole animals. We report the identification and characterization of human and mouse Scotin homologues, a novel gene directly transactivated by p53. The Scotin protein is localized to the ER and the nuclear membrane. Scotin can induce apoptosis in a caspase-dependent manner. Inhibition of endogenous Scotin expression increases resistance to p53-dependent apoptosis induced by DNA damage, suggesting that Scotin plays a role in p53-dependent apoptosis. The discovery of Scotin brings to light a role of the ER in p53-dependent apoptosis

Overcoming a limitation of deterministic dense coding with a non-maximally entangled initial state

Under two-party deterministic dense-coding, Alice communicates (perfectly distinguishable) messages to Bob via a qudit from a pair of entangled qudits in pure state |Psi>. If |Psi> represents a maximally entangled state (i.e., each of its Schmidt coefficients is sqrt(1/d)), then Alice can convey to Bob one of d^2 distinct messages. If |Psi> is not maximally entangled, then Ji et al. [Phys. Rev. A 73, 034307 (2006)] have shown that under the original deterministic dense-coding protocol, in which messages are encoded by unitary operations performed on Alice's qudit, it is impossible to encode d^2-1 messages. Encoding d^2-2 is possible; see, e.g., the numerical studies by Mozes et al. [Phys. Rev. A 71, 012311 (2005)]. Answering a question raised by Wu et al. [Phys. Rev. A 73, 042311 (2006)], we show that when |Psi> is not maximally entangled, the communications limit of d^2-2 messages persists even when the requirement that Alice encode by unitary operations on her qudit is weakened to allow encoding by more general quantum operators. We then describe a dense-coding protocol that can overcome this limitation with high probability, assuming the largest Schmidt coefficient of |Psi> is sufficiently close to sqrt(1/d). In this protocol, d^2-2 of the messages are encoded via unitary operations on Alice's qudit, and the final (d^2-1)-th message is encoded via a (non-trace-preserving) quantum operation.Comment: 18 pages, published versio

Deterministic dense coding and entanglement entropy

We present an analytical study of the standard two-party deterministic dense-coding protocol, under which communication of perfectly distinguishable messages takes place via a qudit from a pair of non-maximally entangled qudits in pure state |S>. Our results include the following: (i) We prove that it is possible for a state |S> with lower entanglement entropy to support the sending of a greater number of perfectly distinguishable messages than one with higher entanglement entropy, confirming a result suggested via numerical analysis in Mozes et al. [Phys. Rev. A 71 012311 (2005)]. (ii) By explicit construction of families of local unitary operators, we verify, for dimensions d = 3 and d=4, a conjecture of Mozes et al. about the minimum entanglement entropy that supports the sending of d + j messages, j = 2, ..., d-1; moreover, we show that the j=2 and j= d-1 cases of the conjecture are valid in all dimensions. (iii) Given that |S> allows the sending of K messages and has the square roof of c as its largest Schmidt coefficient, we show that the inequality c <= d/K, established by Wu et al. [ Phys. Rev. A 73, 042311 (2006)], must actually take the form c < d/K if K = d+1, while our constructions of local unitaries show that equality can be realized if K = d+2 or K = 2d-1.Comment: 19 pages, 2 figures. Published versio

Unital quantum operators on the Bloch ball and Bloch region

For one qubit systems, we present a short, elementary argument characterizing unital quantum operators in terms of their action on Bloch vectors. We then show how our approach generalizes to multi-qubit systems, obtaining inequalities that govern when a ``diagonal'' superoperator on the Bloch region is a quantum operator. These inequalities are the n-qubit analogue of the Algoet-Fujiwara conditions. Our work is facilitated by an analysis of operator-sum decompositions in which negative summands are allowed.Comment: Revised and corrected, to appear in Physical Review

Deciphering metal-induced oxidative damages on glycated albumin structure and function

Background: Metal ions such as copper or zinc are involved in the development of neurodegenerative pathologies and metabolic diseases such as diabetes mellitus. Albumin structure and functions are impaired following metal- and glucose-mediated oxidative alterations. The aim of this study was to elucidate effects of Cu(II) and Zn(II) ions on glucose-induced modifications in albumin by focusing on glycation, aggregation, oxidation and functional aspects. Methods: Aggregation and conformational changes in albumin were monitored by spectroscopy, fluorescence and microscopy techniques. Biochemical assays such as carbonyl, thiol groups, albumin-bound Cu, fructosamine and amine group measurements were used. Cellular assays were used to gain functional information concerning antioxidant activity of oxidized albumins. Results: Both metals promoted inhibition of albumin glycation associated with an enhanced aggregation and oxidation process. Metal ions gave rise to the formation of β-amyloid type aggregates in albumin exhibiting impaired antioxidant properties and toxic activity to murine microglia cells (BV2). The differential efficiency of both metal ions to inhibit albumin glycation, to promote aggregation and to affect cellular physiology is compared. Conclusions and general significance: Considering the key role of oxidized protein in pathology complications, glycation-mediated and metal ion-induced impairment of albumin properties might be important parameters to be followed and fought. © 2013 Elsevier B.V

Physical and chemical processes and the morphofunctional characteristics of human erythrocytes in hyperglycaemia

Background: This study examines the effect of graduated hyperglycaemia on the state and oxygen-binding ability of hemoglobin, the correlation of phospholipid fractions and their metabolites in the membrane, the activity of proteolytic enzymes and the morphofunctional state of erythrocytes. Methods: Conformational changes in the molecule of hemoglobin were determined by Raman spectroscopy. The structure of the erythrocytes was analyzed using laser interference microscopy (LIM). To determine the activity of NADN-methemoglobinreductase, we used the P.G. Board method. The degree of glycosylation of the erythrocyte membranes was determined using a method previously described by Felkoren et al. Lipid extraction was performed using the Bligh and Dyer method. Detection of the phospholipids was performed using V. E. Vaskovsky method. Results: Conditions of hyperglycaemia are characterized by a low affinity of hemoglobin to oxygen, which is manifested as a parallel decrease in the content of hemoglobin oxyform and the growth of deoxyform, methemoglobin and membrane-bound hemoglobin. The degree of glycosylation of membrane proteins and hemoglobin is high. For example, in the case of hyperglycaemia, erythrocytic membranes reduce the content of all phospholipid fractions with a simultaneous increase in lysoforms, free fatty acids and the diacylglycerol (DAG). Step wise hyperglycaemia in incubation medium and human erythrocytes results in an increased content of peptide components and general trypsin-like activity in the cytosol, with a simultaneous decreased activity of µ-calpain and caspase 3. Conclusions: Metabolic disorders and damage of cell membranes during hyperglycaemia cause an increase in the population of echinocytes and spherocytes. The resulting disorders are accompanied with a high probability of intravascular haemolysis.</p

A hypercyclic finite rank perturbation of a unitary operator

A unitary operator $V$ and a rank $2$ operator $R$ acting on a Hilbert space \H are constructed such that $V+R$ is hypercyclic. This answers affirmatively a question of Salas whether a finite rank perturbation of a hyponormal operator can be supercyclic.Comment: published in Mathematische Annale