Low-dose apixaban or rivaroxaban as secondary prophylaxis of upper extremity deep vein thrombosis.

Upper extremity deep vein thrombosis (UEDVT) may occur without inciting factor or may be secondary to malignancy, surgery, trauma, central venous catheter or related to thoracic outlet syndrome (TOS). International guidelines recommend anticoagulant treatment for at least three months, in particular the use of vitamin K antagonists (VKAs) and direct oral anticoagulants (DOACs). No data on extended anticoagulant therapy and reduced dose of DOACs have been reported in patients affected by UEDVT with persistent thrombotic risk (active cancer, major congenital thrombophilia) or without affected vein recanalization. In our retrospective observational study, including 43 patients, we treated secondary UEDVT with DOACs. In the acute phase of thrombosis (median time of 4 months), we used therapeutic dose of DOACs; the 32 patients with permanent thrombotic risk factors or without recanalization of the UEDVT were shifted to low-dose DOACs (apixaban 2.5 mg twice daily or rivaroxaban 10 mg daily). During therapy with full-dose DOACs, 1 patient presented recurrence of thrombosis; no thromboembolic events were observed during treatment with low-dose DOACs. During full-dose treatment, 3 patients presented minor hemorrhagic complications; no hemorrhagic events were observed during DOACs at low dose. We think our preliminary data could support the indication to extend the anticoagulation with dose reduction of DOACs in patients affected by UEDVT and no-transient thrombotic risk. These data should be confirmed in randomized controlled prospective study.

Complexation of the mycotoxin zearalenone with ß-cyclodextrin: Study of the interaction and first promising applications.

This work reports the study of the interactions between native and substituted ß-cyclodextrins and zearalenone and its derivatives α- and ß-zearelonol. The data obtained by fluorescence and NMR experiments suggested that zearalenone, α- and ß-zearalenol and cyclodextrins give rise to host-guest complexation, with the inclusion of the phenolic moiety inside the cyclodextrin cavity. The high stability of these complexes induces a high fluorescence enhancement upon complexation. These results have been successfully applied to the spectrofluorimetric determination of zearalenone in maize raw samples, without any chromatographic separation.

Binding of bovine papillomavirus type 4 E8 to ductin (16K proteolipid), down-regulation of gap junction intercellular communication and full cell transformation are independent events.

The E8 open reading frame of bovine papillomavirus type 4 encodes a small hydrophobic polypeptide that contributes to primary cell transformation by conferring to cells the ability to form foci and to grow in low serum and in suspension. Wild-type E8 binds in vitro to ductin, a component of gap junctions, and this binding is accompanied by a loss of gap junction intercellular communication in transformed bovine fibroblasts. However, through the analysis of a panel of E8 mutants, we show here that binding of E8 to ductin is not sufficient for down-regulation of gap junction communication and that there is no absolute correlation between down-regulation of gap junction communication and the transformed phenotype.

The bovine papillomavirus type 4 E8 protein binds to ductin and causes loss of gap junctional intercellular communication in primary fibroblasts.

The E8 open reading frame of bovine papillomavirus type 4 encodes a small hydrophobic polypeptide which contributes to cell transformation by conferring anchorage-independent growth. Using an in vitro translation system, we show that the E8 polypeptide binds to ductin, the 16-kDa proteolipid that forms transmembrane channels in both gap junctions and vacuolar H+-ATPase. This association is not due to nonspecific hydrophobic interactions. PPA1, a Saccharomyces cerevisiae polypeptide homologous (with 25% identity) to ductin, does not complex with E8. Furthermore, E5B, structurally similar to E8 but with no transforming activity, does not form a complex with ductin. Primary bovine fibroblasts expressing E8 show a loss of gap junctional intercellular communication, and it is suggested that this results from the interaction between E8 and ductin.

An ultrastructural evaluation of cell heterogeneity in invasive ductal carcinomas of the human breast. I. An in vivo study.

The present ultrastructural study has been undertaken in order to contribute to the problem of morphological heterogeneity in the ductal infiltrating carcinoma of the human breast. In spite of the well known topographical variability of scirrhous breast cancers, the comparative analysis of 12 primary tumours has brought to light some basic phenotypical expressions of the neoplastic cell population. The major observation is the occurrence of two main categories of cells, which are interpretable as the transformed counterparts of the dark and light lumenal cells of the normal mammary epithelium. The phenotypical identity of the two categories has been assessed by in vitro cultivation (parallel paper). Many aberrant morphological variants, attributable to the two cell types, were observed at the tumour-stroma interface. We have therefore suggested that the high level of morphological heterogeneity may, at least in part, be the result of stromal influences on the gene expression of the transformed cells.

An ultrastructural evaluation of cell heterogeneity in invasive ductal carcinomas of the human breast. II. An in vitro study.

The ultrastructural characterization of the present continuous cell line, derived from a primary ductal infiltrating carcinoma (d.i.c.) of the human breast, has brought to light a remarkable morphological similarity with the original neoplastic cell population. A major parallelism is the permanent presence in culture of two categories of cells, exhibiting a strong isomorphism with the in vivo counterparts. The presence of well defined ultrastructural features, as duct-like structures, microvillous projections, junctional complexes and intracytoplasmic crypts, is a further confirmation of the breast cancer origin of this line. The significance and perspective of these findings are discussed.