Seroprevalence of Human Malawi Polyomavirus

The seroprevalence of the recently discovered human Malawi polyomavirus (MWPyV) was determined by virus-like particle-based enzyme-linked immunosorbent assay (ELISA) in age-stratified Italian subjects. The findings indicated that MWPyV infection occurs early in life, and seroprevalence was shown to reach 42% in adulthood.     

Are all forms of feature binding disturbed in schizophrenia? Evidence from a central vs. peripheral distinction in working memory

In this study we investigated central and peripheral feature binding in a group of 24 high pre-morbid IQ patients with schizophrenia and 24 healthy controls. In particular, participants were asked to remember specific single (e.g., word, colour) or multiple features (e.g., coloured words) of experimental items with central (coloured word) vs. peripheral (a coloured frame) attributes in a working memory binding task. Performance of the patients was significantly inferior to that of controls, especially when required to remember the peripheral combination of multiple features. Results suggest that patients with schizophrenia may have difficulties in unitizing peripheral features in working memory.     

European Rabbits as Reservoir for Coxiella burnetii

We studied the role of European rabbits (Oryctolagus cuniculus) as a reservoir for Coxiella burnetii in the Iberian region. High individual and population seroprevalences observed in wild and farmed rabbits, evidence of systemic infections, and vaginal shedding support the reservoir role of the European rabbit for C. burnetii.     

Microenvironment and tumor cell plasticity: An easy way out

Cancer cells undergo genetic changes allowing their adaptation to environmental changes, thereby obtaining an advantage during the long metastatic route, disseminated of several changes in the surrounding environment. In particular, plasticity in cell motility, mainly due to epigenetic regulation of cancer cells by environmental insults, engage adaptive strategies aimed essentially to survive in hostile milieu, thereby escaping adverse sites. This review is focused on tumor microenvironment as a collection of structural and cellular elements promoting plasticity and adaptive programs. We analyze the role of extracellular matrix stiffness, hypoxia, nutrient deprivation, acidity, as well as different cell populations of tumor microenvironment.     

Impact of treatment‐related liver toxicity on the outcome of HCV‐positive non‐Hodgkin's lymphomas

We studied 160 Hepatitis C virus (HCV)‐positive patients with NHL (59 indolent NHL, 101 aggressive). Median age was 67 years. HCV‐RNA was present in 146. HBsAg was positive in seven patients. At diagnosis, ALT value was above UNL in 67 patients. One hundred and twenty patients received an anthracycline‐based therapy, alkylators, 28 received chemotherapy plus rituximab. Cytotoxic drugs dose was reduced in 63 patients. Among 93 patients with normal ALT at presentation, 16 patients developed WHO grade II–III liver toxicity. Among 67 patients with abnormal ALT, eight patients had a 3.5 times elevation during treatment. Among 28 patients treated with rituximab and chemotherapy, five patients (18%) developed liver toxicity. Thirty four patients (21%) did not complete treatment (eight for liver toxicity). Median progression‐free survival (PFS) for patients who experienced liver toxicity is significantly shorter than median PFS of patients without toxicity (respectively, 2 years and 3.7 years, P = 0.03). After a median F‐UP of 2 years, 32 patients died (three for hepatic failure). A significant proportion of patients with HCV+ NHL develop liver toxicity often leading to interruption of treatment. This could be a limit to the application of immunochemotherapy programs. HCV+ lymphomas represent a distinct clinical subset of NHL that deserves specific clinical approach to limit liver toxicity and ameliorate survival. Am. J. Hematol., 2010. © 2009 Wiley‐Liss, Inc.     

Insight into the mechanisms underlying tumor response to boron neutron capture therapy in the hamster cheek pouch oral cancer model

Objective: The therapeutic success of different boron neutron capture therapy (BNCT) protocols employing the hamster cheek pouch oral cancer model has been previously reported by our laboratory. The aim of this study was to explore potential mechanisms of BNCT‐induced damage to tumor in terms of potential inhibition in DNA synthesis and induction of apoptosis in the tumors that underwent partial remission following application of the different BNCT protocols in this model. Materials and methods: We evaluated DNA synthesis employing incorporation of 5‐bromo‐2′‐deoxyuridine as an end‐point. Apoptosis was evaluated by immunohistochemistry employing the deoxynucleotidyl transferase‐mediated deoxyuridine triphosphate‐biotin nick end‐labeling technique and Bax and Bcl‐2 labeling. These studies were performed in tumors that underwent partial remission 1–30 days post‐BNCT mediated by boronophenylalanine (BPA), GB‐10 (Na₂¹⁰B₁₀H₁₀) or (BPA + GB‐10). Results: BNCT exerted a marked inhibitory effect on DNA synthesis in tumors for all the protocols under study. The inhibitory effect of BPA‐BNCT occurred as soon as 1 day post‐treatment (P < 0.001). Conversely, the effect of GB‐10‐BNCT became apparent 7–14 days after therapy (P < 0.001) and was sustained until killed at 30 days post‐treatment (P < 0.001). (GB‐10 + BPA)‐BNCT exerted a rapid and persistent effect, conceivably because of the combined effect of BNCT mediated by both boron compounds. The apoptosis studies did not show differences between the pre‐treatment group and any of the BNCT groups. Conclusions: One of the mechanisms involved in BNCT‐induced tumor control in our model would be an inhibitory effect on DNA synthesis. Apoptosis does not seem to have a significant role in BNCT‐induced tumor control in our model.     

Vasculogenesis in infantile hemangioma

Infantile hemangioma is a vascular tumor that occurs in 5–10% of infants of European descent. A defining feature of infantile hemangioma is the dramatic growth and development into a disorganized mass of blood vessels. Subsequently, a slow spontaneous involution begins around 1 year of age and continues for 4–6 years. The growth and involution of infantile hemangioma is very different from other vascular tumors and vascular malformations, which do not regress and can occur at any time during childhood or adult life. Much has been learned from careful study of the tissue morphology and gene expression patterns during the life-cycle of hemangioma. Tissue explants and tumor-derived cell populations have provided further insight to unravel the cellular and molecular basis of infantile hemangioma. A multipotent progenitor cell capable of de novo blood vessel formation has been isolated from infantile hemangioma, which suggests that this common tumor of infancy, long considered to be a model for pathologic angiogenesis, may also represent pathologic vasculogenesis. Whether viewed as angiogenesis or vasculogenesis, infantile hemangioma represents a vascular perturbation during a critical period of post-natal growth, and as such provides a unique opportunity to decipher mechanisms of human vascular development.