Carbon Modified with Vanadium Nanoparticles for Hydrogen Peroxide Electrogeneration

This paper compares the results of two preparation routes for the production of carbon (Vulcan XC 72R) modified with vanadium nanostructured electrocatalysts for hydrogen peroxide (H2O2) electrogeneration using the following mass proportions of vanadium on carbon (V/C): 1, 3, 5, 7, 10, and 13%. Best results for H2O2 electrogeneration were obtained using a V/C sol-gel method (SGM) with 3%, highest ring currents. For oxygen reduction reaction (ORR), using the V/C SGM with 3% and V/C polymeric precursor method (PPM) with 7%, the results of ring currents measured are very high when compared to Vulcan XC 72R. X-ray diffraction (XRD) analysis mainly showed the V2O5 phase. X-ray photoelectron spectroscopy (XPS) results of the V/C PPM 7% and V/C SGM 3% samples highlight the predominance of the V2O5 phase and, for the latter catalyst, a more oxidized carbon surface. For the most promising electrocatalysts, the contact angle was evaluated, showing that the anchoring of the metal in the carbon surface increases the hydrophilicity of the materials. The prepared materials are promising for peroxide electrogeneration mainly due to the synergetic effect of vanadium oxide nanoparticles and acid oxygen species of the carbon, contributing to enhancing catalyst hydrophilicity

PTRF/cavin-1 neutralizes non-caveolar caveolin-1 microdomains in prostate cancer

Caveolin-1 has a complex role in prostate cancer and has been suggested to be a potential biomarker and therapeutic target. As mature caveolin-1 resides in caveolae, invaginated lipid raft domains at the plasma membrane, caveolae have been suggested as a tumor-promoting signaling platform in prostate cancer. However, caveola formation requires both caveolin-1 and cavin-1 (also known as PTRF; polymerase I and transcript release factor). Here, we examined the expression of cavin-1 in prostate epithelia and stroma using tissue microarray including normal, non-malignant and malignant prostate tissues. We found that caveolin-1 was induced without the presence of cavin-1 in advanced prostate carcinoma, an expression pattern mirrored in the PC-3 cell line. In contrast, normal prostate epithelia expressed neither caveolin-1 nor cavin-1, while prostate stroma highly expressed both caveolin-1 and cavin-1. Utilizing PC-3 cells as a suitable model for caveolin-1-positive advanced prostate cancer, we found that cavin-1 expression in PC-3 cells inhibits anchorage-independent growth, and reduces in vivo tumor growth and metastasis in an orthotopic prostate cancer xenograft mouse model. The expression of α-smooth muscle actin in stroma along with interleukin-6 (IL-6) in cancer cells was also decreased in tumors of mice bearing PC-3-cavin-1 tumor cells. To determine whether cavin-1 acts by neutralizing caveolin-1, we expressed cavin-1 in caveolin-1-negative prostate cancer LNCaP and 22Rv1 cells. Caveolin-1 but not cavin-1 expression increased anchorage-independent growth in LNCaP and 22Rv1 cells. Cavin-1 co-expression reversed caveolin-1 effects in caveolin-1-positive LNCaP cells. Taken together, these results suggest that caveolin-1 in advanced prostate cancer is present outside of caveolae, because of the lack of cavin-1 expression. Cavin-1 expression attenuates the effects of non-caveolar caveolin-1 microdomains partly via reduced IL-6 microenvironmental function. With circulating caveolin-1 as a potential biomarker for advanced prostate cancer, identification of the molecular pathways affected by cavin-1 could provide novel therapeutic targets

Oxidative stress and the ageing endocrine system

Ageing is a process characterized by a progressive decline in cellular function, organismal fitness and increased risk of age-related diseases and death. Several hundred theories have attempted to explain this phenomenon. One of the most popular is the 'oxidative stress theory', originally termed the 'free radical theory'. The endocrine system seems to have a role in the modulation of oxidative stress; however, much less is known about the role that oxidative stress might have in the ageing of the endocrine system and the induction of age-related endocrine diseases. This Review outlines the interactions between hormones and oxidative metabolism and the potential effects of oxidative stress on ageing of endocrine organs. Many different mechanisms that link oxidative stress and ageing are discussed, all of which converge on the induction or regulation of inflammation. All these mechanisms, including cell senescence, mitochondrial dysfunction and microRNA dysregulation, as well as inflammation itself, could be targets of future studies aimed at clarifying the effects of oxidative stress on ageing of endocrine glands