Investigation of thermal and fluid characteristics in Automotive headlights

Headlights manufactures in the automotive industry make a large usage of polymers and plastic materials addressing important issues such as thermal stress control and water condensation on the inner surfaces of the headlamp as important factors for headlight design. In this paper, an innovative simulation methodology to calculate thermal distribution in automotive headlights is illustrated. With this method radiation is accurately calculated by means of a dedicated software whereas conductive and convective heat transfer is calculated by means of a general CFD code. A condensation model has also been developed and utilized with the CFD code to investigate the effect of forced convection flow through the headlight vents on water film evaporation. CFD results have been validated against measured headlight wall temperatures and flow velocities showing an encouraging degree of agreement

Prediction of Non-premixed Combustion and Soot Formation using an Interactive Flamelet Approach

n this work, a multiple Representative Interactive Flamelet (RIF) approach for Diesel engine Compu- tational Fluid Dynamic (CFD) combustion modelling is presented. The CFD solver is responsible for the calcula- tion of the flow field, spray formation, turbulence and additional transport equations and provides boundary con- ditions to the flamelet model for one or more ‘representative’ flamelets. The interactive flamelet software package, in turn, solves the non-stationary laminar flamelet equations for chemical species, soot moments and enthalpy under the assumption of unity for the Lewis number. Thus, prediction of processes such as low tem- perature auto-ignition, high temperature energy release and emissions formation are calculated by means of a de- tailed chemical mechanism for a wide range of air/fuel (A/F) ratios and mixing scales. In this work, a detailed kinetic mechanism for n-heptane based on 209 species and 2115 reactions covering the kinetics for low/high temperature oxidation and emission formation has been applied. However, the current implementation allows also user-defined types of pure fuels and fuel blends as well as oxidiser being defined as a mixture of air and products. Moreover, in order to take into account the influence of flamelet-flamelet interactions in case of multi- ple injections, a simplified flamelet interaction model was implemented and applied to a double injection test- case. Soot modelling is approached by using the method of moments to mathematically describe the particle size distribution function (PSDF). The approach has been validated against Diesel engine experiments with single and multiple injection strategies. The numerical results show a good correlation to standard Diesel engine meas- urements as to time resolved experimental soot maps obtained through a 3D-2Color Method. Application of the multiple RIF model provides an improved prediction of pollutants and allows new insight into the soot formation process

Acute administration of 3,4-methylenedioxymethamphetamine (MDMA) induces oxidative stress, lipoperoxidation and TNFα-mediated apoptosis in rat liver

Liver toxicity is one of the consequences of ecstasy (3,4- methylenedioxymethamphetamine MDMA) abuse and hepatocellular damage is reported after MDMA consumption. Various factors probably play a role in ecstasy-induced hepatotoxicity, namely its metabolism, the increased efflux of neurotransmitters, the oxidation of biogenic amines, and hyperthermia. MDMA undergoes extensive hepatic metabolism that involves the production of reactive metabolites which form adducts with intracellular nucleophilic sites. MDMA-induced-TNF-α can promote multiple mechanisms to initiate apoptosis in hepatocytes, activation of pro-apoptotic (BID, SMAC/DIABLO) and inhibition of anti-apoptotic (NF-κB, Bcl-2) proteins. The aim of the present study was to obtain evidence for the oxidative stress mechanism and apoptosis involved in ecstasy-induced hepatotoxicity in rat liver after a single 20 mg/kg, i.p. MDMA administration. Reduced and oxidized glutathione (GSH and GSSG), ascorbic acid (AA), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR) and malondialdehyde (MDA), an indicator of lipid peroxidation, were determined in rat liver after 3 and 6 h after MDMA treatment. The effect of a single MDMA treatment included decrease of GR and GPx activities (29% and 25%, respectively) and GSH/GSSG ratio (32%) with an increase of MDA (119%) after 3 h from ecstasy administration compared to control rats. Liver cytosolic level of AA was increased (32%) after 6 h MDMA treatment. Our results demonstrate a strong positive reaction for TNFα (p < 0.001) in hepatocytes and a diffuse apoptotic process in the liver specimens (p < 0.001). There was correlation between immunohistochemical results and Western blotting which were quantitatively measured by densitometry, confirming the strong positivity for TNF-α (p < 0.001) and NF-κB (p < 0.001); weak and intense positivity reactions was confirmed for Bcl-2, SMAC/DIABLO (p < 0.001) and BID reactions (p < 0.001). The results obtained in the present study suggest that MDMA induces loss of GSH homeostasis, decreases antioxidant enzyme activities, and lipoperoxidation that causes an oxidative stress that accompaines the MDMA-induced apoptosis in liver cells. © 2011 Elsevier Ltd

Acute administration of 3,4-methylenedioxymethamphetamine (MDMA) induces oxidative stress, lipoperoxidation and TNFa-mediated apoptosis in rat liver

Liver toxicity is one of the consequences of ecstasy (3,4-methylenedioxymethamphetamine MDMA) abuse and hepatocellular damage is reported after MDMA consumption. Various factors probably play a role in ecstasy-induced hepatotoxicity, namely its metabolism, the increased efflux of neurotransmitters, the oxidation of biogenic amines, and hyperthermia. MDMA undergoes extensive hepatic metabolism that involves the production of reactive metabolites which form adducts with intracellular nucleophilic sites. MDMA-induced-TNF-α can promote multiple mechanisms to initiate apoptosis in hepatocytes, activation of pro-apoptotic (BID, SMAC/DIABLO) and inhibition of anti-apoptotic (NF-κB, Bcl-2) proteins. The aim of the present study was to obtain evidence for the oxidative stress mechanism and apoptosis involved in ecstasy-induced hepatotoxicity in rat liver after a single 20 mg/kg, i.p. MDMA administration. Reduced and oxidized glutathione (GSH and GSSG), ascorbic acid (AA), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR) and malondialdehyde (MDA), an indicator of lipid peroxidation, were determined in rat liver after 3 and 6h after MDMA treatment. The effect of a single MDMA treatment included decrease of GR and GPx activities (29% and 25%, respectively) and GSH/GSSG ratio (32%) with an increase of MDA (119%) after 3h from ecstasy administration compared to control rats. Liver cytosolic level of AA was increased (32%) after 6 h MDMA treatment. Our results demonstrate a strong positive reaction for TNFα (p<0.001) in hepatocytes and a diffuse apoptotic process in the liver specimens (p<0.001). There was correlation between immunohistochemical results and Western blotting which were quantitatively measured by densitometry, confirming the strong positivity for TNF-α (p<0.001) and NF-κB (p<0.001); weak and intense positivity reactions was confirmed for Bcl-2, SMAC/DIABLO (p<0.001) and BID reactions (p<0.001). The results obtained in the present study suggest that MDMA induces loss of GSH homeostasis, decreases antioxidant enzyme activities, and lipoperoxidation that causes an oxidative stress that accompaines the MDMA-induced apoptosis in liver cells

Effect of low-dose tamoxifen after surgical excision of ductal intraepithelial neoplasia: results of a large retrospective monoinstitutional cohort study

Standard doses of tamoxifen has not reached a consensus yet. Given positive results of low-dose tamoxifen on breast cancer biomarkers modulation, we analyzed a large cohort of DIN patients treated with low-dose tamoxifen or no treatment as per institutional guidelines. BACKGROUND: Postsurgical treatment of ductal intraepithelial neoplasia (DIN) with standard doses of tamoxifen has not reached a consensus yet. Given positive results of low-dose tamoxifen on breast cancer biomarkers modulation, we analyzed a large cohort of DIN patients treated with low-dose tamoxifen or no treatment as per institutional guidelines. PATIENTS AND METHODS: All consecutive women operated on at the European Institute of Oncology for estrogen receptor (ER)-positive DIN (474 treated with low-dose tamoxifen and 509 untreated patients) were followed up for a median of 7 years. RESULTS: Compared with untreated patients, a significant 30% reduction in breast cancer risk was observed on low-dose tamoxifen with an adjusted hazard ratio (HR) = 0.70 [95% confidence interval (CI) 0.51-0.94], with a greater benefit in postmenopausal (HR = 0.57; 95% CI 0.34-0.94) than in premenopausal women (HR = 0.79; 95% CI 0.54-1.17). Treated patients with ER and progesterone receptor (PgR) >50% DIN had a lower incidence of breast events than untreated ones (HR = 0.61; 95% CI 0.40-0.94), whereas no protective effect has been observed in patients with ER or PgR <50% DIN. Drug discontinuation resulted in a doubled risk of recurrence in premenopausal women only (HR = 1.95; 95% CI 0.98-3.89). No excess of endometrial cancer occurred. CONCLUSIONS: Low-dose tamoxifen is a promising and safe strategy for highly endocrine responsive DIN. Treatment adherence is crucial in premenopausal women. A definitive trial is ongoing