Electronic structure and carrier transfer in B-DNA monomer polymers and dimer polymers: Stationary and time-dependent aspects of wire model vs. extended ladder model

We employ two Tight-Binding (TB) approaches to study the electronic structure and hole or electron transfer in B-DNA monomer polymers and dimer polymers made up of $N$ monomers (base pairs): (I) at the base-pair level, using the on-site energies of base pairs and the hopping integrals between successive base pairs, i.e., a wire model and (II) at the single-base level, using the on-site energies of the bases and the hopping integrals between neighboring bases, i.e., an \textit{extended} ladder model since we also include diagonal hoppings. We solve a system of $MD$ ("matrix dimension") coupled equations [(I) $MD$ = $N$, (II) $MD$ = $2N$] for the time-independent problem, and a system of $MD$ coupled $1^\text{st}$ order differential equations for the time-dependent problem. We study the HOMO and the LUMO eigenspectra, the occupation probabilities, the Density of States (DOS) and the HOMO-LUMO gap as well as the mean over time probabilities to find the carrier at each site [(I) base pair or (II) base)], the Fourier spectra, which reflect the frequency content of charge transfer (CT) and the pure mean transfer rates from a certain site to another. The two TB approaches give coherent, complementary aspects of electronic properties and charge transfer in B-DNA monomer polymers and dimer polymers.Comment: 20 pages, 23 figure

bcl-2 in normal human breast and carcinoma, association with oestrogen receptor-positive, epidermal growth factor receptor-negative tumours and in situ cancer.

The role of bcl-2 expression in solid tumours is as yet undefined. It was, therefore, the purpose of this study to investigate expression of bcl-2 protein in 111 human breast carcinomas using immunohistochemistry and the monoclonal antibody bcl-2 124. Expression was then compared with the established indicators of prognosis and biological behaviour in malignant breast disease. No relationship could be observed between bcl-2 and node status, tumour size, differentiation, type or age at excision. However, a strong positive relationship was seen between bcl-2 and oestrogen receptor (ER), with 70 of 88 (80%) bcl-2-positive tumours being ER positive also, compared with seven of 23 (30%) bcl-2-negative tumours being ER positive (P < 0.0001). The converse was found when bcl-2 was compared with epidermal growth factor receptor (EGFR). A strong negative relationship was observed, with 26 of 88 (30%) bcl-2-positive tumours being EGFR positive, compared with 16 of 23 (70%) bcl-2-negative tumours being EGFR positive (P = 0.001), raising the possibility that bcl-2 is an ER-regulated gene. An inverse relationship was also found between bcl-2 and the oncogenes c-erbB-2 and p53. Thus, loss of bcl-2 expression in breast cancer is associated with a range of molecular markers of poor prognosis and may define part of an ER-negative, EGFR-positive phenotype

Loss of antigen-presenting molecules (MHC class I and TAP-1) in lung cancer.

Presentation of endogenous antigenic peptides to cytotoxic T lymphocytes is mediated by the major histocompatibility complex (MHC) class I molecules. For the stable assembly of MHC class I complex it is necessary that the antigenic peptide is transported by the MHC-encoded transporters TAP-1 and TAP-2 into a pre-Golgi region. T-cell-mediated host-vs-tumour response might therefore depend on the presence of these molecules on tumour cells. The presence of MHC class I antigens and TAP-1 was studied in a series of 93 resection specimens of non-small-cell lung carcinomas (NSCLCs) by immunohistochemical methods using antibodies against the assembled class I molecule, beta 2-microglobulin (beta 2-m), heavy-chain A locus, A2 allele and TAP-1 protein. Eighty-six patients were included in the survival analysis. Total loss of class I molecule was observed in 38% of the cases and was usually accompanied by loss of beta 2-m and of heavy chain A locus. Selective loss of A locus was seen in 8.3% and of A2 allele in 27% of the cases. TAP-1 loss was always combined with beta 2-m and/or heavy chain A locus loss. No correlation was found between the expressional status of any of the above molecules, including the selective A2 allelic loss and histological type, degree of differentiation, tumoral stage, nodal stage and survival. Our findings suggest that loss of antigen-presenting molecules (including both MHC class I alleles and TAP-1) is a frequent event in lung cancer. However, the immunophenotypic profile of MHC class I and TAP-1 seems to be unrelated in vivo to the phenotype, growth or survival of NSCLC

Large asymptomatic Left Atrial Myxoma with ossification: case report

<p>Abstract</p> <p>Background</p> <p>Atrial myxomas are the most common primary cardiac tumors. They are usually small or moderate in size by the time of the diagnosis, exhibiting non specific cardiac or systemic symptoms, and are most frequently soft and friable without microscopic signs of ossification. We describe herein an extremely rare case of an asymptomatic giant left atrial myxoma with angiographic neovascularization and ossification.</p> <p>Case presentation</p> <p>An asymptomatic 58-year-old male with a giant left atrial tumor, was transferred to our Unit for surgical treatment. The tumor was an incidental finding during a work-up for hemoptysis due to bronchectasis. The coronary angiogram showed tumor vessels originating from the RCA. The tumor macroscopically did not resemble a myxoma, considering its dimensions (12 × 10 cm) and its solid substance. The mass was excised together with the interatrial septum and the right lateral LA wall close to the right pulmonary veins orifices. The defect was closed with Dacron patches in order to prevent malformation of both atria. The pathology study revealed a benign myxoma with excessive osteoid (mature bone) content.</p> <p>Conclusion</p> <p>We consider our case as extremely rare because of the asymptomatic course despite the large size of the tumor, the blood supply from the right coronary artery and the bone formation.</p