Crosstalk between EET and HO-1 downregulates Bach1 and adipogenic marker expression in mesenchymal stem cell derived adipocytes

Epoxygenase activity and synthesis of epoxyeicosatrienoic acids (EETs) have emerged as important modulators of obesity and diabetes. We examined the effect of the EET-agonist 12-(3-hexylureido)dodec-8(2) enoic acid on mesenchymal stem cell (MSC) derived adipocytes proliferation and differentiation. MSCs expressed substantial levels of EETs and inhibition of soluble epoxide hydrolase (sEH) increased the level of EETs and decreased adipogenesis. EET agonist treatment increased HO-1 expression by inhibiting a negative regulator of HO-1 expression, Bach-1. EET treatment also increased βcatenin and pACC levels while decreasing PPARγ C/EBPα and fatty acid synthase levels. These changes were manifested by a decrease in the number of large inflammatory adipocytes, TNFα, IFNγ and IL-1α, but an increase in small adipocytes and in adiponectin levels. In summary, EET agonist treatment inhibits adipogenesis and decreases the levels of inflammatory cytokines suggesting the potential action of EETs as intracellular lipid signaling modulators of adipogenesis and adiponectin.     

Nail lengthening and fingertip amputations

Fingertip injuries can be treated in different ways, including shortening with primary closure, skin grafts, and local or distant flaps. Nail bed involvement complicates fingertip reconstruction and may influence the choice of treatment. Local flaps can usually replace the pulp and provide a satisfactory functional and aesthetic result, whereas reconstruction of the fingernail apparatus is more difficult. In the period between 1998 and 2001, 12 fingertip injuries with nail bed involvement were treated with a combination of local flaps (Tranquilli-Leali and Venkataswami flaps) and the eponychial flap. The eponychial flap described by Bakhach is a backward cutaneous translation flap that lengthens the nail plate and restores a good appearance of the nail apparatus. This technique is simple to use and can be used with different flaps for pulp reconstruction.     

Carvedilol inhibits mitochondrial complex I and induces resistance to H2O2 -mediated oxidative insult in H9C2 myocardial cells

Carvedilol, a beta-adrenoreceptor antagonist with strong antioxidant activity, produces a high degree of cardioprotection in a variety of experimental models of ischemic cardiac injury. Although growing evidences suggest specific effects on mitochondrial metabolism, how carvedilol would exert its overall activity has not been completely disclosed. In the present work we have investigated the impact of carvedilol-treatment on mitochondrial bioenergetic functions and ROS metabolism in H9C2 cells. This analysis has revealed a dose-dependent decrease in respiratory fluxes by NAD-dependent substrates associated with a consistent decline of mitochondrial complex I activity. These changes were associated with an increase in mitochondrial H(2)O(2) production, total glutathione and protein thiols content. To evaluate the antioxidant activity of carvedilol, the effect of the exposure of control and carvedilol-pretreated H9C2 cells to H(2)O(2) were investigated. The H(2)O(2)-mediated oxidative insult resulted in a significant decrease of mitochondrial respiration, glutathione and protein thiol content and in an increased level of GSSG. These changes were prevented by carvedilol-pretreatment. A similar protective effect on mitochondrial respiration could be obtained by pre-treatment of the cells with a sub-saturating amount of rotenone, a complex I inhibitor. We therefore suggest that carvedilol exerts its protective antioxidant action both by a direct antioxidant effect and by a preconditioning-like mechanism, via inhibition of mitochondrial complex I.     

A Structure Comparison of two Approaches to LCA Inventory Data, Based on the MIET and ETH Databases (10 pp)

Goal and Scope This study compared two different approaches to general inventory data in LCA, one involving the process-based ETH 96 database and the other an environmentally extended Input-Output table for the US, referring to MIET (Missing Inventory Estimation Tool) 2.0. The purpose of the present paper is to highlight and explain some of the differences between the two approaches, in order to give LCA practitioners a clearer idea of the advantages and limitations of using Input-Output analysis combined with process LCA. Methods The comparison was made despite substantial differences between the two approaches, through a reduction and reclassification of the ETH process technology matrix to fit the Input-Output classification scheme and by concentrating on the structure of the processes rather than their absolute values. The structure is described in terms of the percentage of the CO2 contribution to the total emission by all processes involved in the supply chain. An input and output structure comparison was carried out between ETH 96 and MIET 2.0, to extract information about their structures. Results and Discussion The results of the study show that, despite their methodological differences, MIET 2.0 and ETH 96 show substantial similarities in their overall structures. There are also differences in the structure of the two databases, and most of them have occurred randomly, while, for certain particular sectors, the differences are rather persistent. Especially the contributions by capital goods are constantly lower in ETH 96 database and vice versa. The results imply possible systematic truncation in process LCA databases, especially for a few sectors such as capital goods. Recommendation and Perspective Hybrid analysis can overcome the problem of incompleteness in process LCA, while avoiding such disadvantages of IOA as aggregation problem.