Optical effects of exposing intact human lenses to ultraviolet radiation and visible light

<p>Abstract</p> <p>Background</p> <p>The human lens is continuously exposed to high levels of light. Ultraviolet radiation is believed to play a causative role in the development of cataract. In vivo, however, the lens is mainly exposed to visible light and the ageing lens absorbs a great part of the short wavelength region of incoming visible light. The aim of the present study was to examine the optical effects on human lenses of short wavelength visible light and ultraviolet radiation.</p> <p>Methods</p> <p>Naturally aged human donor lenses were irradiated with UVA (355 nm), violet (400 and 405 nm) and green (532 nm) lasers. The effect of irradiation was evaluated qualitatively by photography and quantitatively by measuring the direct transmission before and after irradiation. Furthermore, the effect of pulsed and continuous laser systems was compared as was the effect of short, intermediate and prolonged exposures.</p> <p>Results</p> <p>Irradiation with high intensity lasers caused scattering lesions in the human lenses. These effects were more likely to be seen when using pulsed lasers because of the high pulse intensity. Prolonged irradiation with UVA led to photodarkening whereas no detrimental effects were observed after irradiation with visible light.</p> <p>Conclusions</p> <p>Irradiation with visible light does not seem to be harmful to the human lens except if the lens is exposed to laser irradiances that are high enough to warrant thermal protein denaturation that is more readily seen using pulsed laser systems.</p

Differential Role of Human Choline Kinase α and β Enzymes in Lipid Metabolism: Implications in Cancer Onset and Treatment

11 pages, 6 figures, 1 table.Background The Kennedy pathway generates phosphocoline and phosphoethanolamine through its two branches. Choline Kinase (ChoK) is the first enzyme of the Kennedy branch of synthesis of 1phosphocholine, the major component of the plasma membrane. ChoK family of proteins is composed by ChoKα and ChoKβ isoforms, the first one with two different variants of splicing. Recently ChoKα has been implicated in the carcinogenic process, since it is over-expressed in a variety of human cancers. However, no evidence for a role of ChoKβ in carcinogenesis has been reported. Methodology/Principal Findings Here we compare the in vitro and in vivo properties of ChoKα1 and ChoKβ in lipid metabolism, and their potential role in carcinogenesis. Both ChoKα1 and ChoKβ showed choline and ethanolamine kinase activities when assayed in cell extracts, though with different affinity for their substrates. However, they behave differentially when overexpressed in whole cells. Whereas ChoKβ display an ethanolamine kinase role, ChoKα1 present a dual choline/ethanolamine kinase role, suggesting the involvement of each ChoK isoform in distinct biochemical pathways under in vivo conditions. In addition, while overexpression of ChoKα1 is oncogenic when overexpressed in HEK293T or MDCK cells, ChoKβ overexpression is not sufficient to induce in vitro cell transformation nor in vivo tumor growth. Furthermore, a significant upregulation of ChoKα1 mRNA levels in a panel of breast and lung cancer cell lines was found, but no changes in ChoKβ mRNA levels were observed. Finally, MN58b, a previously described potent inhibitor of ChoK with in vivo antitumoral activity, shows more than 20-fold higher efficiency towards ChoKα1 than ChoKβ. Conclusion/Significance This study represents the first evidence of the distinct metabolic role of ChoKα and ChoKβ isoforms, suggesting different physiological roles and implications in human carcinogenesis. These findings constitute a step forward in the design of an antitumoral strategy based on ChoK inhibition.This work has been supported by grants to JCL from Comunidad de Madrid (GR-SAL-0821-2004), Ministerio de Ciencia e Innovación (SAF2008-03750, RD06/0020/0016), Fundación Mutua Madrileña, and by a grant to ARM from Fundación Mutua Madrileña.Peer reviewe

Proteomic Analysis of the Cyst Stage of Entamoeba histolytica

We used tandem mass spectrometry to identify E. histolytica cyst proteins in 5 cyst positive stool samples. We report the identification of 417 non-redundant E. histolytica proteins including 195 proteins that were not identified in existing trophozoite derived proteome or EST datasets, consistent with cyst specificity. Because the cysts were derived directly from patient samples with incomplete purification, a limited number of proteins were identified (N = 417) that probably represent only a partial proteome. Nevertheless, the study succeeded in identifying proteins that are likely to be abundant in the cyst stage of the parasite. Several of these proteins may play roles in E. histolytica stage conversion or cyst function. Proteins identified in this study may be useful markers for diagnostic detection of E. histolytica cysts. Overall, the data generated in this study promises to aid the understanding of the cyst stage of the parasite which is vital for disease transmission and pathogenesis in E. histolytica

Kinetic modeling of ethanol pyrolysis and combustion

This article reports new kinetic modeling results concerning ethanol pyrolysis and oxidation. We propose a comprehensive kinetic reaction mechanism for ethanol pyrolysis and oxidation issued from detailed modeling of today’s available data including species concentration profiles measured in flow reactors during the pyrolysis and oxidation of ethanol, ignition delays measured in shock tube and ethanol-air flame speeds. The same mechanism is able to reproduce available combustion data concerning hydrogen, methane, ethylene, ethane, propene, and propane in similar conditions (1-10 atm, 800-2000K). The agreement between the data and the computed results is generally good and confirms the comprehensiveness of our C1-C3 detailed reaction mechanism

Kinetic modeling of n-butane oxidation using detailed mechanisms

A chemical kinetic reaction mechanism has been developed previously to reproduce the experimental data of an analytical study of n-butane oxidation in a jet-stirred flow reactor, in the temperature range 900-1200 K at pressures extending from 1 to 10 atm for a wide range of fuel-oxygen equivalence ratios (0.15 to 4.0).This large mechanism consisting of 344 reversible reactions among 51 species is reduced to 46 species and 133 reactions. The agreement between computed and measured concentrations of major chemical species remains correct in the entire experimental area.Experimental ignition delays of n-butane measured behind reflected shock waves up to 1400K by other authors are also reproduced by the same mechanism. In addition the mechanism can be further reduced to 76 reactions among 40 species for the prediction of the ignition delay times

Pyrolysis, oxidation and ignition of C

The kinetics of the oxidation of natural gas blends (CH4/C2H6) and of ethylene and ethane has been studied in a jet stirred reactor (850 ≤ T/K ≤ 1240, 1 ≤ P/atm ≤ 10, 0.02 ≤ equivalence ratio ≤ 2.0) for the first time. The concentration profiles of reactants, intermediates and products measured in a JSR have been used to validate a detailed kinetic reaction mechanism. Literature ignition delay times of CH4/C2H6 mixtures measured in shock tube have also been modeled as well as shock tube pyrolysis of ethylene. A general good agreement between the data and the model is found. The same mechanism has also been used to successfully represent the oxidation of methane, ethyne, ethene, ethane, propene, and propane in various conditions including JSR, shock tube and flame. The present study clearly shows the importance of traces of ethane on the oxidation of methane. The computations indicate that the oxidation of methane is initiated by its reaction with O2 and by thermal dissociation when no other hydrocarbon is present. However, in the studied CH4/C2H6 mixtures, ethane reacts before methane leading to the formation of OH, H and O radicals which initiate methane oxidation. The major importance of ethyl radical reactions is demonstrated by the computations

Kinetic modeling of pressure and equivalence ratio effects on methane oxidation

The kinetics of methane oxidation in a jet-stirred reactor was modeled using a comprehensive kinetic reaction mechanism including the most recent findings concerning the kinetics of the reactions involved in the oxidation of C1-C4 hydrocarbons. The computed results are discussed in terms of pressure and equivalence ratio (ø) effects on methane oxidation. The previously validated mechanism is able to reproduce experimental data obtained in our high-pressure jet stirred reactor (concentration profiles for CH4, CO, CO2, H2, C2H4, C2H6, et C2H2 ; 900 ≤ T/K ≤ 1300 ; 1 ≤ P/atm ≤ 10 ; 0.1 ≤ ø ≤ 2) and methane ignition delay times measured in shock tube (800 ≤ T/K ≤ 2000 ; 1 ≤ P/atm ≤ 13 ; 0.1 ≤ ø ≤ 2). It is also able to reproduce H and O atoms concentrations measured in shock tube at ≈ 2 atm. Burning velocities of methane in air between 1 and 3 atm and methane-air flame structures were also modeled. The same detailed kinetic mechanism can also be used to model the oxidation of ethane, ethylene, propene, and propane in similar conditions

Allene oxidation in jet-stirred reactor : a kinetic modeling study

Allene oxidation was modeled using a comprehensive kinetic reaction mechanism including the most recent findings concerning the kinetics of the reactions involved in the oxidation of allene. The proposed mechanism is able to reproduce experimental data (molecular species concentration profiles) obtained in our jet stirred reactor at 1 atm, for temperatures extending from 1030 to 1070K and equivalence ratios of 0.2 to 2. The proposed oxidation mechanism is also able to correctly reproduce ignition delay times measured in shock tube and molecular species concentrations measured in our jet stirred reactor for the oxidation of propyne

Derivation of a global chemical kinetic mechanism for methane ignition and combustion

A new method for the reduction of chemical kinetic detailed mechanisms is presented. It is based on atomic fluxes calculations and reaction pathways analyses. The method was applied to a CH4/O2/Nx2 comprehensive combustion mechanism, including NOx reactions, previously validated for several types of experiments (flow reactors, shock tubes, laminar flames). A global mechanism for methane combustion and NO formation has been elaborated involving 6 chemical reactions among 10 species. This mechanism is able to reproduce accurately the ignition delays, temperature profiles and concentration profiles of major species and NO over a wide range of experimental conditions (P = 1 atm, 60% ≤ N2 ≤ 80%, 0.2 ≤ ϕ ≤ 2.2 and 900 K ≤ Tinitial ≤ 1500 K)