Embolization-induced angiogenesis in cerebral arteriovenous malformations.

Endovascular occlusion of cerebral arteriovenous malformations (AVM) is often utilized as adjunctive therapy in combination with radiosurgery or microsurgery. Evidence supports that partial occlusion of AVM via endovascular embolization leads to increased angiogenesis. This phenomenon may be a contributing factor to the decreased efficacy of AVM radiosurgery following embolization. We review the literature for potential mechanisms of embolization-induced angiogenesis. A comprehensive literature search was performed using PubMed to identify studies that sought to elucidate the pathophysiology behind embolization-induced angiogenesis. The terms "arteriovenous malformation", "embolization", and "angiogenesis" were used to search for relevant publications individually and together. Three distinct mechanisms for embolization-induced angiogenesis were described in the literature: (1) hypoxia-mediated angiogenesis, (2) inflammatory-mediated angiogenesis, and (3) hemodynamic-mediated angiogenesis. Embolization-induced angiogenesis of cerebral AVM likely results from a combination of the three aforementioned mechanisms. However, future research is necessary to determine the relative contribution of each individual mechanism to overall post-embolization AVM neovascularization.

Mechanism of the reaction of radicals with peroxides and dimethyl sulfoxide in aqueous solution.

The reactions of methyl and methylperoxyl radicals derived from dimethyl sulfoxide (DMSO) with hydrogen peroxide, peroxymonocarbonate (HCO4 (-)), and persulfate were studied. The major reaction observed for the hydroperoxides was the abstraction of the hydrogen atom by the radicals. The radicals interact with a lone pair of electrons on the peroxide to produce methanol and formaldehyde. Furthermore, the results indicate that in RO2H and RO2R', electron-withdrawing groups cause a considerable increase in the reactivity of the peroxides towards the radicals and not only towards nucleophiles. The HO2 (.)/O2 (.-) and CO3 (.-) radicals react with DMSO to produce methyl radicals. Thus, the formation of the (.)CH3 radicals in the presence of DMSO is not proof of the formation of the (.)OH radicals in the system. These reactions must be considered when radical processes, such as in biological and catalytic systems, are studied. Especially, the plausible role of HCO4 (-) ions in biological systems as a source of oxidative stress cannot be overlooked.

Weak response of oceanic dimethylsulfide to upper mixing shoaling induced by global warming.

The solar radiation dose in the oceanic upper mixed layer (SRD) has recently been identified as the main climatic force driving global dimethylsulfide (DMS) dynamics and seasonality. Because DMS is suggested to exert a cooling effect on the earth radiative budget through its involvement in the formation and optical properties of tropospheric clouds over the ocean, a positive relationship between DMS and the SRD supports the occurrence of a negative feedback between the oceanic biosphere and climate, as postulated 20 years ago. Such a natural feedback might partly counteract anthropogenic global warming through a shoaling of the mixed layer depth (MLD) and a consequent increase of the SRD and DMS concentrations and emission. By applying two globally derived DMS diagnostic models to global fields of MLD and chlorophyll simulated with an Ocean General Circulation Model coupled to a biogeochemistry model for a 50% increase of atmospheric CO(2) and an unperturbed control run, we have estimated the response of the DMS-producing pelagic ocean to global warming. Our results show a net global increase in surface DMS concentrations, especially in summer. This increase, however, is so weak (globally 1.2%) that it can hardly be relevant as compared with the radiative forcing of the increase of greenhouse gases. This contrasts with the seasonal variability of DMS (1000-2000% summer-to-winter ratio). We suggest that the "plankton-DMS-clouds-earth albedo feedback" hypothesis is less strong a long-term thermostatic system than a seasonal mechanism that contributes to regulate the solar radiation doses reaching the earth's biosphere.

Degradation of DMSO by ozone-based advanced oxidation processes.

The present study investigates the oxidation of dimethyl sulfoxide (DMSO) by conventional ozonation and the advanced oxidation processes (AOPs). The major degradation products identified were methanesulfinate, methanesulfonate, formaldehyde, and formic acid in ozonation process. The subsequent degradation of intermediates shows that methanesulfonate is more resistance to ozonation, which reduces the mineralization rate of DMSO. The effect of t-butanol addition and ozone gas flow dosage on the degradation rate was evaluated. The rate constant of the reaction of ozone (k(D)) with DMSO was found to be 0.4162 M(-1)S(-1). In the second part of this study, DMSO degradation and TOC mineralization were investigated using O(3)/UV, O(3)/H(2)O(2) and UV/H(2)O(2) processes. In all theses processes the degradation of target organics is more pronounced than TOC removal. The efficiencies of these processes were evaluated and discussed. The formation of sulfate ion in all AOPs have been identified and compared with other processes. Overall it can be concluded that ozonation and ozone-based AOPs are promising processes for an efficient removal of DMSO in wastewater.

Kinetics and mechanisms of DMSO (dimethylsulfoxide) degradation by UV/H(2)O(2) process.

The objective of this study was to elucidate the degradation pathways of dimethylsulfoxide (DMSO) during its mineralization caused by UV/H(2)O(2) treatment. In order to accomplish this, we measured the concentration time-profiles of DMSO and its degradation intermediates during the UV/H(2)O(2) treatment. In addition, we proposed a kinetic model that could account for the degradation pathways of DMSO during its UV/H(2)O(2) treatment. The results show that the degradation of DMSO by the UV/H(2)O(2) treatment can be classified into two major pathways, and this is supported by both the analysis of the intermediates and total organic carbon (TOC) measurements. Firstly, DMSO was degraded into sulfate (SO(4)(2-)) through the formation of methansulfinate (CH(3)SO(2)(-)) and methansulfonate (CH(3)SO(3)(-)) as sulfur-containing intermediates. One of the two carbon constituents of DMSO was highly resistant to mineralization, due to the formation of methansulfonate, which reacted very slowly with (.-)OH k = 0.8 x 10(7) M(-1)s(-1)). Secondly, the other carbon constituent of DMSO was relatively easily mineralized through the formation of formaldehyde (HCHO) and formate (HCO(2)(-)) as non-sulfur-containing intermediates. The kinetic model proposed in this study for the degradation of DMSO by (.-)OH in the UV/H(2)O(2) process was able to successfully predict the patterns of concentration time-profiles of all components during the UV/H(2)O(2) treatment of DMSO.

Electromagnetic re-warming of cryopreserved tissues: effect of choice of cryoprotectant and sample shape on uniformity of heating.

A method that has been proposed for the cryopreservation of tissues and organs is to add a cryoprotective agent (CPA) in sufficient concentration to allow vitrification, and to use rapid electromagnetic heating to prevent the formation of ice crystals during the re-warming. We have compared the physical and biological properties of four CPAs, measuring the speed and uniformity of heating in a 36 mm sphere placed in a 434 MHz applicator, and the toxicity to ECV304 endothelial cells. Ethanediol and dimethyl sulfoxide were found to be suitable for rapid, uniform heating but toxic to the endothelial cells at vitrifying concentrations. Butane-2,3-diol was less toxic, but the heating patterns were unacceptably non-uniform. Propane-1,2-diol was not significantly more toxic than butane-2,3-diol, and did allow uniform heating. It is therefore the best choice of CPA for the vitrification of tissues. We have shown that the uniformity of heating correlates with the dielectric properties of the perfusate. Furthermore, we have shown that uniform heating is feasible in non-spherical samples provided they are approximately ellipsoidal.

Cell attachment to extracellular matrices is modulated by pulsed radiation at 820 nm and chemicals that modify the activity of enzymes in the plasma membrane.

BACKGROUND AND OBJECTIVES: Adhesive interactions between cells and extracellular matrices play a regulative role in wound repair processes. The objective of this investigation is to study action mechanisms of pulsed radiation at 820 nm on cellular adhesion in vitro. Light emitting diodes (LED) at 820 nm are widely used for treatment of wounds of various etiology. STUDY DESIGN/MATERIALS AND METHODS: The LED (820 +/- 10 nm, 10 Hz, 16-120 J/m(2)) is used for the irradiation of HeLa cell suspension. In parallel experiments, amiloride (5 x 10(-4) M), ouabain (7 x 10(-5) M, 7 x 10(-4) M), quinacrine (6 x 10(-4) M), arachidonic acid (1 x 10(-5) M), glucose (2 x 10(-4) M), and ATP (5 x 10(-5) M) are added to the cell suspension before or after the irradiation procedure. The cell-glass adhesion is studied using the adhesion assay technique described in Lasers Surg Med 1996; 18:171. RESULTS: Cell-glass adhesion increases in a dose-dependent manner following the irradiation. Preirradiation eliminates the inhibition of cell attachment caused by ouabain, arachidonic acid, and ATP. The inhibitive effect of quinacrine on the cell attachment is eliminated by the irradiation performed after the treatment with the chemical. Irradiation and amiloride have a synergetic stimulative effect on the cell attachment. The threshold dose for the cell attachment stimulation by the irradiation is decreased by the treatment of the cell suspension with amiloride or ouabain. CONCLUSIONS: The results obtained indicate that pulsed IR radiation at 820 nm increases the cell-matrix attachment. It is the modulation of the monovalent ion fluxes through the plasma membrane and not the release of arachidonic acid that is involved in the cellular signaling pathways activated by irradiation at 820 nm. Preirradiation has a protective effect against the inhibitive action of ouabain, arachidonic acid, ATP, and quinacrine on cell attachment process. It is supposed that irradiation activates those signaling pathways in cells which attenuate the inhibitive action of these chemicals.

Protection against radiation-induced degradation of DNA bases by polyamines.

Polyamines have been reported to protect DNA against the formation of radiation-induced strand breaks and crosslinks to proteins. The present study was aimed at investigating the protective effect of spermine, spermidine and putrescine against the degradation of DNA bases upon exposure to gamma rays in aerated aqueous solution. The yield of 8-oxo-7,8-dihydroguanine and 5-hydroxycytosine was found to decrease for concentrations of spermine and spermidine greater than 0.1 mM. A protection factor of 10 was observed for a concentration of 1 mM of the latter two polyamines. Putrescine afforded a lower protection. In addition, the formation yield of a series of radiation-induced degradation products of the purine and pyrimidine bases was determined within DNA in the presence or absence of spermine. The protection factor was within the same range for all the lesions measured. The latter observation ruled out the possibility of degradation of DNA by radiation-induced polyamine peroxyl radicals. This was confirmed by studies involving radiolysis of DMSO and decomposition of 2,2'-azobis(2-methyl-propionamidine) as sources of alkylperoxyl radicals. Therefore, it is likely that the polyamine-mediated protection against the radiation-induced degradation of DNA bases is due to the compaction of the DNA structure and the reduction in the accessibility of DNA to .OH rather than by scavenging .OH in the bulk solution or in the vicinity of the DNA.

Development of assays for the detection of photomutagenicity of chemicals during exposure to UV light--I. Assay development.

Two complementary assay systems have been adapted for the detection of compounds which may form mutagenic photoproducts during exposure to UV light from an Osram Ultra-Vitalux sunlamp as used in the evaluation of the effectiveness of sun filters. The effects of UVA and of UVB were evaluated. A bacterial plate test using Escherichia coli strain WP2 allowed the bacteria, co-plated with test chemical in soft agar, to be irradiated with various doses of UV light. Mutagenesis was assessed by scoring numbers of tryptophan-independent colonies. The chosen reference compound was 8-methoxypsoralen (8-MOP) which was non-mutagenic alone at the highest dose tested (1000 micrograms/plate). Following simultaneous exposure of bacteria to 8-MOP and doses of UV light which alone had little effect, large numbers of revertants were scored. Numbers of mutants were dependent upon the doses of both 8-MOP and of UV light. The second test system involved the exposure of Chinese hamster ovary cells to UV light in the presence of test chemical to determine the clastogenic effects of photoproducts. Treatment with 8-MOP alone up to 50 micrograms/ml was not clastogenic but concomitant exposure to non-damaging doses of UV light caused large increases in the incidence of chromosome aberrations of all types. Damage was again dependent on the doses of both components. Two additional photoactive compounds, para-aminobenzoic acid and chlorpromazine both show photoclastogenic but not photomutagenic properties. These two complementary assay systems take advantage of using no-effect levels of UV light as a baseline against which photomutagenicity readily can be compared.(ABSTRACT TRUNCATED AT 250 WORDS)

[Are there pseudophototropic reactions in biology? Part 2: Pseudophototropy and the course of cancer (author's transl)]. / Gibt es pseudophototrope Reaktionen in der Biologie? Teil 2: Pseudophototropie und Krebsverlauf

The phenomenon of pseudophototropy is compared with well-known theories of the origin and treatment of cancer, by means of practical medical experiments. The reaction cycles or life processes of both systems are comparable, in spite of considerable differences between them, and suggest, at least as a hypothesis, that there is a general mechanism for the formation of double-bond sequences liable to reaction.

[Are there pseudophototropic reactions in biology? Part 1: Some considerations on molecular repair (author's transl)]. / Gibt es pseudophototrope Reaktionen in der Biologie? Teil 1: Gedanken über das Molekülrepair

The phenomenon of repair in light and darkness in biological systems is compared with the reactions of the pseudophototropy of synthetic macromolecules. The reactions of the pseudophototropy, that is the formation of terminal double bond sequences and their reactions which are effected through ultraviolet irradiation or oxidation, seem to be identical to the mechanism of DNA repair.