aThe presence of water in lubricating oil affects the performance of lubricated rolling contacts. This work particularly focuses on the role of water in altering the evolution of zinc dialkyldithiophosphate (ZDDP)-derived reaction layers. A series of tribological tests were carried out using a rolling four-ball machine. Different initial water amounts were added to 2 wt% ZDDP in poly-alpha-olefin (PAO). The reaction layer evolution and its chemical properties were studied using XPS and SEM. SEM analyses show that water seems to inhibit the growth of the ZDDP-derived reaction layer. XPS analyses reveal that the reaction layer undergoes a depolymerisation of the polyphosphate chain when water is present in lubricated contacts. Surface distress was observed in 2 wt% ZDDP in poly-alpha-olefin, whereas when water was mixed with pure base oil, the surface distress increased. Different mechanisms of the influence of water on the ZDDP-derived reaction layer evolution are discussed.

BackgroundHuman Herpesvirus 8 (HHV8), the causative agent of Kaposi’s sarcoma, induces an intense modification of lipid metabolism and enhances the angiogenic process in endothelial cells. In the present study, neutral lipid (NL) metabolism and angiogenesis were investigated in HHV8-infected HUVEC cells. The viral replication phases were verified by rtPCR and also by K8.1 and LANA immunostaining.ResultsLipid droplets (Nile Red) were higher in all phases and NL staining (LipidTOX) combined with viral-antigen detection (immunofluorescence) demonstrated a NL content increase in infected cells. In particular, triglyceride synthesis increases in the lytic phase, whereas cholesteryl ester synthesis rises in the latent one. Moreover, the inhibition of cholesterol esterification reduces neo-tubule formation mainly in latently infected cells.ConclusionsWe suggest that a reprogramming of cholesteryl ester metabolism is involved in regulating neo-angiogenesis in HHV8-infected cells and plays a likely role in the high metastatic potential of derived-tumours.

Modelling of surface roughness evolution in time, as a function of the lubrication condition and other operating parameters (i.e. load, sliding/rolling ratio, and initial roughness of both contacting surfaces), is important for the understanding and prediction of various surface damage modes, such as surface distress, wear, and scuffing. Moreover, it is one of the key aspects in understanding friction and running-in phenomena. In the present study, a previously developed model for partial micro-elastohydrodynamic lubrication conditions is combined with a local Archard-type wear model to describe the surface topography evolution during the operation of a rolling/sliding lubricated contact. The model has been compared with a series of experimental results showing similar trends.

11A modelling framework has recently been developed which considers tribochemistry in 12 deterministic contact mechanics simulations in boundary lubrication. One of the capabilities of 13 the model is predicting the evolution of surface roughness with respect to the effect of

The prevalence of Human Herpesvirus 8 (HHV8) DNA and antiviral antibodies in Diabetes type 2 (DM2) and control subjects was studied, in order to confirm a possible link between DM2 and HHV8 infection. The HHV8-DNA from diabetic patients was typed for detecting possible genomic differences with known HHV8 reference viruses.DM2 patients and healthy controls were examined for the presence of HHV8 DNA into the peripheral blood lymphocytes. Both anti-lytic and latent phase antibodies were detected in HHV8 positive and negative diabetic patients, as well in a number of controls. The HHV8 ORF K1 and ORF 26 genes from DM2 patients were typed and matched to reference strains.A significant prevalence of HHV8 DNA in DM2 subjects versus healthy controls was detected (about 58 % against 27 %). Anti-lytic phase, but not anti-latent phase antibodies, were significantly increased in DM2 patients versus controls. In addition, about 30 % of HHV8 strains isolated from DM2 lymphocytes showed consistent differences in the ORF 26 gene sequence, so that a new HHV8 subtype was proposed. These findings give additional support to the hypothesis that HHV8 could be considered an additional risk factor for DM2 onset.

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Kaposi Sarcoma Herpesvirus (KSHV), also known as Human Herpesvirus 8, is the causative agent of Kaposi sarcoma; this malignant angiosarcoma is usually treated with conventional anti-tumor agents, which can control disease evolution, but do not clear the latent KSHV episome that binds to cellular DNA. Some commercial antibacterial sulfonamides were tested for the ability to suppress latent KSHV. qPCR and cytofluorometry assays were used for detecting both viral DNA and the latency factor LANA in BC3 cells, respectively. The capacity of sulfonamides to impair MDM2-p53 complex formation was detected by an ELISA method. The analysis of variance was performed according to one-way ANOVA with Fisher as a post-hoc test. Here we show that sulfonamide antibiotics are able to suppress the KSHV latent state in permanently-infected BC3 lymphoma-cells and interfere with the formation of the MDM2-p53 complex, which KSHV seemingly needs to support latency and to trigger tumor cell transformation. These findings detected a new molecular target for the activity of sulfonamides and offer a new potential perspective for treating KSHV-induced lymphoproliferative diseases.

Introduction: Human Herpesvirus 8 (HHV8) is known to be the cause of the malignant tumour named Kaposi's sarcoma. It is believed to induce an intense modification of cell metabolism in endothelial cells. In this work we analysed the role of anti-HHV8 antibodies in both the insulin and glucose uptake of HHV8-infected primary human endothelial cells (HUVEC). Methodology: Western blotting, immunofluorescence and radiolabelled glucose were employed to assess the pPI3K expression, insulin binding and glucose-uptake by HUVEC cells, respectively. Results: We confirmed that HHV8-infection is able to enhance both insulin binding and glucose-uptake in HHV8-infected primary endothelial cells; in addition, we found that anti-HHV8 specific antibodies are able to further increase both insulin and glucose uptake during the late latent phase of HHV8-infection in vitro. Conclusions: These findings suggest that a specific immune response to HHV8-infection may cooperate in boosting the cell metabolism, further enhancing the already increased insulin binding and glucose-uptake in HHV8-infected cells, which is a peculiar property of several oncogenic viruses.