Bold personality makes domestic dogs entering a shelter less vulnerable to diseases.

It is widely recognised that for vertebrate species, personalities vary along an axis with extremes represented by 'proactive' and 'reactive' individuals. The aim of this study was to verify whether there is a relationship between personality and disease vulnerability in domestic dogs (Canis familiaris) exposed to an intensely stressful situation such as entering a shelter. Twenty-eight shelter dogs participated in the study.

Ketoprofen, peginterferon 2a and ribavirin for genotype 1 chronic hepatitis C: a phase II study.

Aim: To evaluate the safety of adding ketoprofen to pegylated-interferon (PEG-IFN) with or without ribavirin and the effect on viral kinetics, STAT1 activity and expression of 2'-5'-oligoadenylate synthetase (2'-5'OAS) in genotype 1 chronic hepatitis C in a phase II study.

Methods: Forty-five patients were studied: fifteen were randomized to PEG-IFN plus ribavirin (PR), 16 to PEG-IFN plus ketoprofen and 14 to PR and ketoprofen. The molecular study of IFN-dependent signal transduction was conducted in 9 patients from each group.

A study of the prevalence and genotypes of Giardia duodenalis infecting kennelled dogs.

Giardia duodenalis is a protozoan parasite of animals that is zoonotic. Given the capacity of this organism to spread via the faecal-oral route, animals held in overcrowded and unhygienic conditions are at high risk of infection. Faecal samples from dogs in three kennels in Rome were examined by microscopy and PCR for G.

Involvement of PI3K in HCV-related lymphoproliferative disorders.

Hepatitis C virus (HCV) core protein has been shown to deregulate cell growth and programmed cell death in hepatoma cells, but only minimal informations are available about its possible role on B-lymphoproliferative disorders (LPDs). The aim of our work was to analyze the biological activity of HCV core protein on B-cell proliferation. We established Wil2-ns and Ramos B-cell lines that stably expressed the HCV core protein.

Role of p38 MAPK and RNA-dependent protein kinase (PKR) in hepatitis C virus core-dependent nuclear delocalization of cyclin B1.

Some hepatitis C virus (HCV) proteins, including core protein, deregulate the cell cycle of infected cells, thereby playing an important role in the viral pathogenesis of HCC. Thus far, there are only few studies that have deeply investigated in depth the effects of the HCV core protein expression on the progression through the G1/S and G2/M phases of the cell cycle. To shed light on the molecular mechanisms by which the HCV core protein modulates cell proliferation, we have examined its effects on cell cycle in hepatocarcinoma cells.

Physical and functional interaction between HCV core protein and the different p73 isoforms.

Hepatitis C virus (HCV) core protein is a structural viral protein that packages the viral genomic RNA. In addition to this function, HCV core also modulates a number of cellular regulatory functions. In fact, HCV core protein has been found to modulate the expression of the cyclin-dependent inhibitor p21(WAF1/CIP1) and to promote both apoptosis and cell proliferation through its physical interaction with p53.