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Single Exposure (single + exposure)

Distribution by Scientific Domains

Medical Sciences	50%
Life Sciences	38%
Chemistry	7%

Selected Abstracts

Severe Hemorrhagic Complication Due to Acquired Factor V Inhibitor After Single Exposure to Bovine Thrombin Product

JOURNAL OF CARDIAC SURGERY, Issue 6 2000
Michio Kajitani M.D., Ph.D.
Our patient underwent emergency repair of acute aortic dissection and coronary artery bypass grafting. The patient developed leg wound infection at the saphenous vein harvest site, which was debrided and left open. Attempt to reclose the leg wound 1 month later was complicated by a life-threatening hemorrhage with markedly elevated activated partial thromboplatin time. There was no evidence of infection or disseminated intravascular coagulation, and further study identified low factor V level with positive factor V inhibitor. Treatment with plasmapheresis and steroid successfully reversed the coagulopathy. Detailed case review failed to reveal exposure to any thrombin products other than the one used for the aortic dissection repair. This case was unusual because only a single exposure to this product resulted in severe hemorrhagic complication 1 month after surgery. [source]

BRIEF REPORT: Single exposure to cocaine or ecstasy induces DNA damage in brain and other organs of mice

ADDICTION BIOLOGY, Issue 1 2010
Tathiana A. Alvarenga
ABSTRACT We evaluated the overall genetic damage induced by different doses of cocaine and MDMA (3,4-Methylenedioxymethamphetamine) in several organs. One hour after intraperitoneal drug administration, mice were euthanized; peripheral blood, liver and brain were collected, and the cellular suspensions were used for the single cell gel (comet) assay. We determined that all doses of cocaine and MDMA tested were able to induce DNA damage in blood cells. Extensive genotoxic damage was induced by cocaine or MDMA at the highest doses used in liver cells. Brain cells were affected by all doses administrated. These findings demonstrate that cocaine and MDMA are potent genotoxins. [source]

Intermittent exposure to low-concentration paraphenylenediamine can be equivalent to single, higher-dose exposure

CONTACT DERMATITIS, Issue 5 2007
Jonathan M. L. White
Hair dye allergy is an important and increasingly common cause of allergic contact dermatitis. The role of repeated exposure in elicitation of allergy has not previously been extensively studied. We have therefore compared elicitation between single and intermittent exposure to paraphenylenediamine (PPD). 23 subjects known to be allergic to PPD from positive patch tests were exposed to 0.3% and 0.03% PPD, both in petrolatum and water, for 5 min at the same site every day for up to 8 D. In the same subjects, single exposures were also performed at different sites, from 5 to 40 min. Other experiments exposed rat skin to radiolabelled PPD as one-off application or multiple exposures. There were 8 reactions in the cumulative exposure site using 0.3% PPD in aqueous solution. In 7 of these, there was an exact correlation with reaction to the cumulative time needed for repeat exposures to elicit a reaction and the time needed for a reaction to the single exposure. There were no reactions to 0.03% PPD in water or pet under either type of exposure condition. There was also a positive correlation between grade of original reaction in clinic (+++, ++, +) and appearance/intensity of elicitation reactions. In the animal study, cumulative time and single exposure time sites correlated with regards to retention of radiolabelled substance within the skin. This study therefore demonstrates for the first time that, over the time period tested, the allergenic component of PPD accumulates in the skin. Hence, intermittent exposure to lower concentrations of PPD may be equivalent to higher concentration, one-off exposure. [source]

Irritants in combination with a synergistic or additive effect on the skin response: an overview of tandem irritation studies

CONTACT DERMATITIS, Issue 6 2006
Francisca Kartono
Sodium lauryl sulfate (SLS) has often been chosen as a model for irritant contact dermatitis (ICD) to study the effect of irritants in combination (1,14). Recently ,tandem', or sequential, exposures with SLS have been performed to study the mechanism of skin barrier impairment in ICD (1,6, 15). The assessment of reactions have been documented with visual scoring, transepidermal water loss (TEWL), skin colour reflectance measurements, skin blood flow; among which TEWL has been noted as the most sensitive value (16). The matched control groups were treated with either a single exposure to a single irritant or in tandem with the same irritant repeatedly. Synergistic and additive effects have been reported for various tandem pairs of irritants, however, the mechanism for both remains unclear. The results of tandem irritation studies were evaluated to define and investigate the responses produced and deduce a possible mechanism of action. Clinical ramifications, albeit complex, are discussed. [source]

DNA adduct kinetics in reproductive tissues of DNA repair proficient and deficient male mice after oral exposure to benzo(a)pyrene

ENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 2 2010
Nicole Verhofstad
Abstract Benzo(a)pyrene (B[a]P) can induce somatic mutations, whereas its potential to induce germ cell mutations is unclear. There is circumstantial evidence that paternal exposure to B[a]P can result in germ cell mutations. Since DNA adducts are thought to be a prerequisite for B[a]P induced mutations, we studied DNA adduct kinetics by 32P-postlabeling in sperm, testes and lung tissues of male mice after a single exposure to B[a]P (13 mg/kg bw, by gavage). To investigate DNA adduct formation at different stages of spermatogenesis, mice were sacrificed at Day 1, 4, 7, 10, 14, 21, 32, and 42 after exposure. In addition, DNA repair deficient (Xpc,/,) mice were used to study the contribution of nucleotide excision repair in DNA damage removal. DNA adducts were detectable with highest levels in lung followed by sperm and testis. Maximum adduct levels in the lung and testis were observed at Day 1 after exposure, while adduct levels in sperm reached maximum levels at ,1 week after exposure. Lung tissue and testis of Xpc,/, mice contained significantly higher DNA adduct levels compared to wild type (Wt) mice over the entire 42 day observation period (P < 0.05). Differences in adduct half-life between Xpc,/, and Wt mice were only observed in testis. In sperm, DNA adduct levels were significantly higher in Xpc,/, mice than in Wt mice only at Day 42 after exposure (P = 0.01). These results indicate that spermatogonia and testes are susceptible for the induction of DNA damage and rely on nucleotide excision repair for maintaining their genetic integrity. Environ. Mol. Mutagen. 2010. © 2009 Wiley-Liss, Inc. [source]

Effects of carbaryl on green frog (Rana clamitans) tadpoles: Timing of exposure versus multiple exposures

ENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 11 2003
Michelle D. Boone
Abstract The majority of studies on pesticide impacts have evaluated the effects of single exposures. However, multiple exposures to a pesticide may be more prevalent. The objective of our study was to determine how multiple exposures versus single exposure at different times during development affected survival to metamorphosis, tadpole survival, tadpole mass, and tadpole developmental stage of green frog (Rana clamitans) tadpoles reared at low and high density in outdoor cattle tank ponds. Tadpoles were exposed to carbaryl zero, one, two, or three times at 14-d intervals. We applied single doses of carbaryl at one of three times, specifically during early, mid, or late development. Overall, we found that multiple exposures had a greater impact than single exposures during development. More individuals reached metamorphosis in ponds exposed to multiple doses of carbaryl compared with controls, indicating that the presence of carbaryl stimulated metamorphosis. The presence of carbaryl in the aquatic environment also resulted in more developed tadpoles compared with controls. Tadpoles in control ponds did not reach metamorphosis and were less developed than individuals exposed to carbaryl; this effect indicates that, under ideal conditions, green frogs could overwinter in ponds so that greater size could be attained before metamorphosis in the following spring or summer. Our study demonstrated the importance of including realistic application procedures when evaluating the effects of a pesticide and that multiple exposures to a short-lived pesticide are more likely to affect an amphibian population. [source]

Activation of afferents to the ventral tegmental area in response to acute amphetamine: a double-labelling study

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 4 2007
Joyce Colussi-Mas
Abstract The ventral tegmental area (VTA), primary source of the mesocorticolimbic dopaminergic system, is regarded as a critical site for initiation of behavioural sensitization to psychostimulants. The present study was undertaken to identify the neural pathways converging on the VTA that are potentially implicated in this process. Rats were sensitized by a single exposure to amphetamine (5 mg/kg, s.c.). The distribution of VTA-projecting neurons activated by amphetamine was examined by combining retrograde transport of the cholera toxin , subunit (CTb), injected into the VTA, with immunodetection of Fos. The quantitative analysis of CTb,Fos double labelling demonstrates that amphetamine induced a rapid activation of Fos in a large number of brain areas projecting to the VTA. More than half of the CTb,Fos double-labelled neurons were located in the prefrontal cortex, lateral preoptic area,lateral hypothalamus, pontomesencephalic tegmentum, dorsal raphe nucleus, ventral pallidum and nucleus accumbens. In addition, scattered CTb,Fos double-labelled cells were observed in many other VTA afferent structures, such as claustrum, lateral septum, diagonal band,magnocellular preoptic nucleus, deep mesencephalic nucleus, oral part of pontine reticular nucleus and dorsomedial tegmental area. This suggests that systemic amphetamine activates a wide population of neurons projecting to the VTA that may be important for the modulation of neurobehavioural plasticity produced by this psychostimulant. [source]

Substance induced plasticity in noradrenergic innervation of the paraventricular hypothalamic nucleus

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 2 2003
Arthur S. P. Jansen
Abstract Single administration of the cytokine interleukin-1, (IL-1), or the psychostimulant amphetamine, enhanced adrenocorticotropin hormone and corticosterone responses to a stress challenge weeks later. This long-lasting hypothalamic-pituitary-adrenal (HPA)-sensitization is paralleled by an increase in electrically evoked release of noradrenaline in the paraventricular hypothalamic nucleus (PVN). We hypothesized that these functional changes may be associated with morphological plasticity of noradrenergic projections to the PVN, a parameter that shows high reproducibility. Specific alterations in relative (nor)adrenergic innervation density were studied by using dopamine-,-hydroxylase (DBH) as a marker. An image analysis system was used to detect changes in the relative DBH innervation density of the PVN. Groups of adult male rats were given IL-1 (10 µg/kg i.p.), amphetamine (5 mg/kg i.p.), or saline. Three weeks later, IL-1 and amphetamine primed rats showed enhanced adrenocorticotropin hormone and corticosterone responses to an amphetamine challenge. In another set of experiments, the relative DBH innervation density was measured in different PVN subnuclei at four rostro-caudal levels. Single administration of either IL-1 or amphetamine causes three weeks later a selective decrease in relative DBH innervation density in those subnuclei of the PVN that contain high numbers of corticotrophin-releasing hormone (CRH) producing neurons: the dorsal parvocellular and medial parvocellular PVN. We conclude that (1) long-lasting sensitization induced by single exposure to IL-1 and amphetamine induces specific pattern of neuroplastic changes in (nor)adrenergic innervation in the PVN and (2) reduction of relative DBH innervation density in CRH-rich areas is associated with paradoxical increase of electrically evoked release of (nor)adrenaline. [source]

Solar-simulating irradiation of the skin of human subjects in vivo produces Langerhans cell responses distinct from irradiation ex vivo and in vitro

EXPERIMENTAL DERMATOLOGY, Issue 4 2000
J. K. Laihia
Abstract: It has been postulated that Langerhans cells (LC) provide tolerogenic signals in the local impairment of cutaneous immune functions and antigen-specific tolerance induced by UV radiation. Studies in vitro and ex vivo have indicated that UV radiation may down-regulate the expression of costimulatory molecules on LC, leading to reduced antigen-presenting function. In contrast, we recently observed an up-regulatory stage in the number of human epidermal LC with induced expression of B7 costimulatory molecules 12,24 h after solar-simulating UV radiation (SSR) in vivo. To examine the apparent discrepancy between the observed human LC responses in vitro, ex vivo and in vivo, we compared the three protocols in a parallel fashion. The intact skin as well as skin explants and epidermal cell suspensions from the same individuals were irradiated with a single erythematogenic dose of SSR. The expression of cell surface markers in the epidermal cells was analysed with flow cytometry 24 h later. The number of CD1a+/HLA-DR+ LC increased post-SSR in vivo by a factor of 2.8±0.4, whereas in irradiated skin explants ex vivo or in cell suspensions in vitro, reduced numbers were seen. HLA-DR expression intensities were found to have increased on DR+ and CD1a+/DR+ cells in vivo. Similarly, SSR induced B7-2 (CD86) expression in CD1a+ cells significantly in vivo (P=0.031) but reduced the expression ex vivo or in vitro. We conclude that the early up-regulatory stage of human LC number and membrane markers, recorded at 24 h after a single exposure to SSR, is exclusively an in vivo phenomenon. [source]

Neuroendocrine Function and Chronic Inflammatory Stress

EXPERIMENTAL PHYSIOLOGY, Issue 5 2002
Michael Harbuz
The factors regulating susceptibility and severity of autoimmune diseases are poorly understood. That neuroendocrine factors are critical modulators in this regard is self-evident. For example, there are major gender differences in susceptibility with women at greater risk than men of, for example, rheumatoid arthritis (RA) and multiple sclerosis (MS). The hypothalamo-pituitary-adrenal (HPA) axis has rightly attracted a considerable amount of attention. Of particular interest has been the hypothesis that susceptibility to autoimmune disease may be related to an impaired responsiveness of the HPA axis; that is, an inability to mount an appropriate cortisol response with which to down-regulate the immune system might allow the immune system to rampage unchecked and attack self. This hypothesis links regulation of the release from the adrenal gland of the potent anti-inflammatory glucocorticoids to the disease process. Endogenous glucocorticoids are crucial for the regulation of the severity of the disease process. The hypothesis proposing a link between a hyporesponsive HPA axis and susceptibility to disease is compelling. However, evidence from a number of sources has suggested that this may not be the entire story and alterations in the activity of the HPA axis have not been consistently observed in patients with RA. This review will concentrate on recent findings concerning the HPA axis in determining susceptibility to, and in regulating the severity of, inflammatory processes in autoimmune disease. These studies have revealed that a single exposure to endotoxin can confer protection to subsequent development of inflammation in an arthritis model in both neonatal and adult rats. Behavioural differences within a single population of rats are associated with differences in the plasma corticosterone responses to stress. However, relative hyporesponsiveness is not reflected by an increase in the severity of inflammation. In humans with RA the dexamethasone-corticotrophin-releasing factor (CRF) test has revealed two distinct sub-populations of patients. Studies in patients with MS have shown that this is not related to depression but rather to the severity of the disease. A better understanding of these complex neuroendocrine interactions may lead to novel clinical interventions. [source]

Memory retrieval after contextual fear conditioning induces c-Fos and JunB expression in CA1 hippocampus

GENES, BRAIN AND BEHAVIOR, Issue 1 2003
T. Strekalova
Using specific polyclonal antisera against c-Fos, JunB, c-Jun and JunD, we tried to identify the candidate transcription factors of the immediate early gene family which may contribute to the molecular processes during contextual memory reconsolidation. For that purpose we analyzed the expression of these proteins in the hippocampus after contextual memory retrieval in a mouse model of fear conditioning. A single exposure to a foot shock of 0.8 mA was sufficient to induce robust contextual fear conditioning in C57Bl/6N mice. In these mice context dependent memory retrieval evoked a marked induction of c-Fos and JunB, but not of c-Jun and JunD, in pyramidal CA1 neurons of the dorsal hippocampus. In contrast, mice exposed and re-exposed only to the context, without foot shock, did not show behavioral signs of contextual fear conditioning and exhibited significantly less expression of c-Fos and JunB in CA1 neurons. Mice which received a foot shock but were not re-exposed to the context revealed no immediate early gene induction. These results demonstrate that contextual memory retrieval is associated with de novo synthesis of specific members of the Fos/Jun transcription factor family. Therefore we suggest that these genes may contribute to plasticity and reconsolidation accompanying the retrieval process. The specific activation of CA1 neurons during the retrieval of contextual fear associations supports the postulated concept of a mnemonic role of this hippocampal subsector during the retrieval of contextual informations. [source]

Altered expression of transcripts for ,-tubulin and an unidentified gene in the spinal cord of phenyl saligenin phosphate treated hens (Gallus gallus)

JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY, Issue 5 2003
Jonathan H. Fox
Abstract Phenyl saligenin phosphate (PSP) induces a central-peripheral distal axonopathy in domestic fowl that develops 7,21 days after a single exposure. Neurotoxic esterase (NTE) is the initial molecular target for this neurotoxicity. PSP has to covalently bind to NTE and chemically "age" for induction of axonopathy. It was hypothesized that exposure to PSP results in early changes in spinal cord gene expression that do not occur with phenylmethylsulfonyl fluoride, a non-neuropathic compound that also inhibits NTE, or DMSO controls. Targeted display was used to screen ,15,000 gel bands. Three candidate genes were identified, but only the transcript designated P1 showed decreased expression following PSP exposure (2 mg/kg i.m.) in subsequent Northern blot and in situ hybridization experiments in samples taken <48 h after exposure. Additional experiments revealed that a ,2.5 kb ,-tubulin transcript had decreased expression at 12,48 h after PSP exposure, with maximum change at 48 h (33%, p = 0.0479). A ,4.5 kb ,-tubulin transcript had increased expression at 12 h (38%, p = 0.0125) and decreased expression at 48 h (28%, p = 0.0576). In situ hybridization on spinal cord revealed neuronal expression of P1 and ,-tubulin transcripts. Decreased expression of transcripts for P1 and ,-tubulin was present at 12 and 48 h, respectively. This decrease occurred in all neurons, not just those whose axons degenerate. Results suggest that (1) in PSP-induced OPIDN (organophosphorus-induced delayed neurotoxicity) some gene transcript expression changes are associated with initiation of axonopathy, and (2) PSP modulates spinal cord gene expression in neuronal types that do not undergo axonal degeneration. © 2003 Wiley Periodicals, Inc. J Biochem Mol Toxicol 17:263,271, 2003; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.10088 [source]

Different apoptosis ratios and gene expressions in two human cell lines after sevoflurane anaesthesia

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 9 2009
S. KVOLIK
Background: The aim of this study was to determine the effect of a single exposure of carcinoma cells (Caco-2 and HEp-2) to an anaesthetic gas mixture containing sevoflurane 3%, applied for a period of either 1 or 2 h, on the induction of apoptosis, propapototic gene expression and sphingomyelinase activity. Methods: Apoptosis was determined by flow cytometry. p53, caspase 3 and CYP2E1 gene expression was determined using reverse transcriptase polymerase chain reaction. Activities of acid (aSMase) and neutral sphingomyelinases (nSMase) were measured using methyl- 14C sphingomyeline, and for de novo ceramide and lipid synthesis [3H] palmitic acid was used. All results were compared with controls and analysed by Mann,Whitney and Kruskal,Wallis tests. Results: In the treated Caco-2 cells, the apoptotic ratio increased 24 h after anaesthesia (16.9%; P=0.04). The expression of both p53 and caspase-3 genes increased in Caco-2 and decreased in HEp-2 cells. The CYP2E1 gene expression was observed only in the Caco-2 cells. In control cells, the catalytic activity of aSMase was 2.3 times higher than that of nSMase activity. Decreased aSMase and nSMase activities were observed in Caco-2 cells 24 h after exposition. aSMase activity was halved (54.2%; P=0.06) in HEp-2 cells 24 h after anaesthesia. De novo ceramide synthesis correlated with SMase activity in Caco-2 cells. Conclusion: Sevoflurane anaesthesia induces late apoptosis in the colonic and laryngeal cancer cells investigated. Although the results obtained may indicate that an anaesthetic gas mixture containing sevoflurane induces p53-dependent apoptosis in the Caco-2 cells, the mechanism of apoptosis induction is unclear and remains to be elucidated. [source]

Severe Hemorrhagic Complication Due to Acquired Factor V Inhibitor After Single Exposure to Bovine Thrombin Product

Chronic passive exposure to aggression escalates aggressiveness of rat observers

AGGRESSIVE BEHAVIOR, Issue 1 2010
Hideo Suzuki
Abstract Previous studies have documented that exposure to aggression increases aggressiveness of human witnesses. However, the question of whether passive exposure to aggression can exclusively cause a risk of aggressive inclination for observers through a learning process, rather than mimicry effect, has not been readily addressed in the clinical literature. This study aimed to investigate this question by using a simple animal model to test the behavioral effect of chronic passive exposure to aggression. Our results indicate that observer rats that had been passively exposed to aggression for 10,min per day for 23 consecutive days exhibited more aggressive behavior than controls or those groups undergoing a single exposure to passive aggression. Furthermore, aggression levels in the group of 23-day chronic exposure to aggression lasted 16 days after the recovery from exposure to aggression. These data suggest that the development of aggression in this model occurred through a learning process because only chronic exposure to aggression resulted in this behavioral outcome in the long run. Aggr. Behav. 36:54,66, 2010. © 2009 Wiley-Liss, Inc. [source]

Cannabis-induced propriospinal myoclonus

MOVEMENT DISORDERS, Issue 6 2004
Dora A. Lozsadi D.Phil
Abstract We report on a case of a 25-year-old woman with clusters of myoclonus induced by a single exposure to inhaled cannabis. Investigations excluded a structural abnormality of the spine. Multi-channel surface EMG with parallel frontal EEG recording confirmed the diagnosis of propriospinal myoclonus. © 2004 Movement Disorder Society [source]

Feasibility of one-shot-per-crystal structure determination using Laue diffraction

ACTA CRYSTALLOGRAPHICA SECTION D, Issue 1 2010
Sterling Cornaby
Crystal size is an important factor in determining the number of diffraction patterns which may be obtained from a protein crystal before severe radiation damage sets in. As crystal dimensions decrease this number is reduced, eventually falling to one, at which point a complete data set must be assembled using data from multiple crystals. When only a single exposure is to be collected from each crystal, the polychromatic Laue technique may be preferable to monochromatic methods owing to its simultaneous recording of a large number of fully recorded reflections per image. To assess the feasibility of solving structures using single Laue images from multiple crystals, data were collected using a `pink' beam at the CHESS D1 station from groups of lysozyme crystals with dimensions of the order of 20,30,µm mounted on MicroMesh grids. Single-shot Laue data were used for structure determination by molecular replacement and correct solutions were obtained even when as few as five crystals were used. [source]

Accumulation of apoptotic cells in the epidermis of patients with cutaneous lupus erythematosus after ultraviolet irradiation

ARTHRITIS & RHEUMATISM, Issue 3 2006
Annegret Kuhn
Objective To examine whether apoptosis contributes to the pathogenesis of skin lesions in patients with cutaneous lupus erythematosus (CLE) after ultraviolet (UV) irradiation. Methods In situ nick translation and TUNEL were performed to detect apoptosis in 85 skin biopsy specimens from patients with various subtypes of CLE. Specimens from normal healthy donors and patients with polymorphous light eruption were used as controls. In addition to assessment of primary lesions, provocative phototesting was carried out to investigate events occurring secondary to UV irradiation during a very early stage of lesion formation. Results A significant increase in apoptotic nuclei was found in the upper epidermal layer of primary and UV light,induced skin lesions of CLE patients compared with controls. In tissue sections obtained from control subjects at 24 hours after a single exposure to UV light, a slight increase in the count of epidermal apoptotic nuclei was present as compared with skin tissue from CLE patients obtained under the same conditions before lesion formation. In sections obtained from controls at 72 hours after irradiation, a significant decrease in the apoptotic nuclei count was observed, consistent with a proper clearance of apoptotic cells in the period between 24 and 72 hours after irradiation. In striking contrast, the number of apoptotic nuclei increased significantly within this period in tissue sections from patients with CLE. Conclusion These data support the hypothesis that apoptotic cells accumulate in the skin of patients with CLE after UV irradiation, as a result of impaired or delayed clearance. The nonengulfed cells may undergo secondary necrosis and release proinflammatory compounds and potential autoantigens, which may contribute to the inflammatory micromilieu that leads to formation of skin lesions in this disease. [source]

A clinical trial and molecular study of photoadaptation in vitiligo

BRITISH JOURNAL OF DERMATOLOGY, Issue 3 2009
C.L. Hexsel
Summary Background, Photoadaptation to ultraviolet (UV) B phototherapy is due to both pigmentary and nonpigmentary influences. Objectives, To measure photoadaptation in vitiliginous skin and to compare it with normal pigmented skin. Methods, Seventeen patients with Fitzpatrick skin phototypes III,VI with vitiligo received six to nine UVB treatments, two to three times weekly. Minimal erythema dose (MED) testing was done at baseline and after all treatments; the percentage change in MED was analysed as a measure of photoadaptation. The percentage decrease in cyclobutane pyrimidine dimers (CPDs) over 24 h after a single exposure of 1 MED was analysed on vitiliginous and normal skin. Results, The mean ± SD percentage change in MED from before to after treatments was: treated vitiliginous skin 28·5 ± 39·9% (P = 0·015), treated normal skin 35·9 ± 49·9% (P = 0·015), untreated vitiliginous skin 11·9 ± 22·6% (P =0·070), untreated normal skin 25·1 ± 41·3% (P = 0·041). Of these patients, two-thirds had a positive percentage change in MED (photoadaptation). The mean amount of CPDs induced per megabase of DNA immediately after exposure was significantly higher in vitiliginous skin. The mean ± SD percentage decrease in CPDs (rate of repair) in 24 h was 35·7 ± 26·8% in vitiliginous skin (P = 0·027) and 46·2 ± 19·5% in normally pigmented skin (P = 0·001); no difference was noted in the repair in vitiliginous skin compared with normal skin (P = 0·4). Conclusions, Photoadaptation in vitiliginous and normal skin was observed in two-thirds of patients. Vitiliginous skin had significantly more CPDs following UVB exposure; the rate of repair of UVB-induced DNA damage was equivalent to that in normal skin. [source]

Retinal vessel oximetry using sequential and 'snapshot' hyperspectral imaging

ACTA OPHTHALMOLOGICA, Issue 2009
A MCNAUGHT
Purpose Use of sequential, and 'snapshot' hyperspectral imagers to measure oxygen saturation in retinal vessels in normals, and examples of eye disease, eg glaucoma, and retinovascular diseases. Validation of estimated oximetry values using a model eye. Methods A sequential hyperspectral imager was constructed using a fundus camera with built-in liquid-crystal tuneable filter. Images of normals,and ocular disease are presented. A novel 'snapshot' hyperspectral imager is also described: this produces images in a single exposure. Validation of both devices using an artificial eye with capillary tubes containing human blood of known oxygen saturation, placed in front of an 'artificial retina' is described. The image analysis used to detect retinal vessels, and generate oximetric values is detailed. Results Both the sequential, and 'snapshot' retinal imagers produced accurate estimations of retinal vessel oxygen saturation, when compared with the model eye. Imaging of a small group of glaucoma eyes showed abnormally elevated venous oxygen saturation. In proliferative diabetic retinopathy, abnormally elevated venular saturation was found in areas of capillary loss on FFA. In vein occlusion, elevated venous saturation was found in eyes with ischaemic FFAs. Conclusion Both the sequential and 'snapshot' hyperspectral imagers deliver useful oximetric maps of the retina. The 'snapshot' device allows more rapid imaging. The elevated venular oxygen saturation seen in both glaucoma, and retinovascular disease, is perhaps evidence of reduced oxygen consumption in damaged inner retina in glaucoma, and/or vascular 'shunting' in retinovascular disease. [source]

Preconditioning protects the retinal pigment epithelium cells from oxidative stress-induced cell death

ACTA OPHTHALMOLOGICA, Issue 1 2009
Rajesh K. Sharma
Abstract. Purpose:, The cytotoxic effects of oxidative stress, which play an important role in ocular diseases, are well known. In this study, we investigated the effect of non-lethal doses of oxidative stress on various cell functions, namely cell viability, cell attachment and cell migration in a widely used retinal pigment epithelium (RPE) cell line (ARPE-19). Methods:, A single exposure to various concentrations of hydrogen peroxide (H2O2) was used to establish a dose response for H2O2 -induced cell death. Other cellular responses, such as changes in cell attachment and migration, were monitored after exposure to increasing doses. Finally, the effects of preconditioning cells with increasing non-lethal doses of H2O2, with and without a subsequent exposure to lethal doses of H2O2, were determined. Results:, The optimum dose for inducing cell death in ARPE-19 cells was between 900 and 1000 ,m H2O2. Preconditioning the cells with 1, 10 and 50 ,m of H2O2 provided a dose-dependent protection against cell death induced by a lethal dose (900,1000 ,m) of H2O2. Preconditioning with higher doses caused cells to become more susceptible to the cytotoxic effects of the lethal dose. Although H2O2 increased cell attachment in lower doses, it induced a dose-dependent inhibition of cell attachment to the substrate in higher doses. H2O2 did not affect cell migration in sub-lethal doses. Conclusion:, Preconditioning RPE cells with limited exposure to non-lethal oxidative stress confers significant protection against subsequent H2O2 -induced cell death. It also affects cell attachment in a dose-specific manner. This finding may help in understanding the pathogenesis of diseases in which oxidative stress plays an important role and in determining the suitability of certain treatment strategies, in particular RPE transplantation in the treatment of age-related macular degeneration. [source]

Intermittent exposure to low-concentration paraphenylenediamine can be equivalent to single, higher-dose exposure

Effects of carbaryl on green frog (Rana clamitans) tadpoles: Timing of exposure versus multiple exposures

Evidence for a cost of immunity when the crustacean Daphnia magna is exposed to the bacterial pathogen Pasteuria ramosa

JOURNAL OF ANIMAL ECOLOGY, Issue 6 2007
TOM J. LITTLE
Summary 1The deployment of the immune system has the obvious potential to ameliorate infection outcomes, but immune responses can also harm hosts by either damaging host tissues or monopolizing resources, leading to enhanced mortality. To gain insight into such a ,cost of immunity' when the crustacean Daphnia magna is challenged with the bacterium Pasteuria ramosa, we measured survivorship among hosts that resisted infection following exposure to various strains and doses of the parasite. 2In the first of two experiments, these exposures were: single exposures with relatively non-aggressive strains, double exposures with non-aggressive strains, and exposure to aggressive strains. Mortality increased across this gradient of exposure. In a second experiment, we varied the dose of the most aggressive P. ramosa strain and found that resisting infection when a large dose was applied resulted in greater mortality than when a medium or low dose was applied. 3Assuming that resistance is accomplished with an immune response, and that more aggressive parasites and/or larger doses of parasites are more immunostimulatory, these data are compatible with a cost of immunity. Indeed, in terms of survival, resisting parasites can be more harmful than infection. [source]

Renal, vascular and cardiac fibrosis in rats exposed to passive smoking and industrial dust fibre amosite

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 11-12 2009
Peter Boor
Abstract Passive smoking is an independent risk factor for cardiovascular diseases. Industrial fibrous dust, e.g. the asbestos group member, amosite, causes lung cancer and fibrosis. No data are available on renal involvement after inhalational exposure to these environmental pollutants or of their combination, or on cardiovascular and renal toxicity after exposure to amosite. Male Wistar rats were randomized into four groups (n= 6): control and amosite group received initially two intratracheal instillations of saline and amosite solution, respectively. Smoking group was subjected to standardized daily exposure to tobacco smoke for 2 hrs in a concentration resembling human passive smoking. Combined group was exposed to both amosite and cigarette smoke. All rats were killed after 6 months. Rats exposed to either amosite or passive smoking developed significant glomerulosclerosis and tubulointerstitial fibrosis. Combination of both exposures had additive effects. Histomorphological changes preceded the clinical manifestation of kidney damage. In both groups with single exposures, marked perivascular and interstitial cardiac fibrosis was detected. The additive effect in the heart was less pronounced than in the kidney, apparent particularly in changes of vascular structure. Advanced oxidation protein products, the plasma marker of the myeloperoxidase reaction in activated monocytes/macrophages, were increased in all exposed groups, whereas the inflammatory cytokines did not differ between the groups. In rats, passive smoking or amosite instillation leads to renal, vascular and cardiac fibrosis potentially mediated via increased myeloperoxidase reaction. Combination of both pollutants shows additive effects. Our data should be confirmed in subjects exposed to these environmental pollutants, in particular if combined. [source]

Impairment of Eye Lens Cell Physiology and Optics by Broadband Ultraviolet A,Ultraviolet B Radiation,

PHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 3 2002
O. M. Oriowo
ABSTRACT The phototoxicity of ultraviolet A (UVA) alone and UVA plus ultraviolet B (UVB) combined on cultured porcine lenses was investigated by analyzing cellular function as measured with a fluorescence bioassay approach and optical integrity, in terms of sharpness of the lens focus as measured with a scanning laser system. The bioassay consisted of carboxyfluorescein diacetate-acetoxymethyl ester and alamarBlue fluorescent dyes. Aseptically dissected porcine lenses were maintained in modified medium 199 without phenol red supplemented with 1% penicillin,streptomycin and 4% porcine serum. At 1 week of preincubation, baseline measurements were obtained. Then the lenses were treated with single exposures of different UVA and UVB energy levels. The lenses treated with 86 J/cm2 UVA alone showed a significant (P < 0.05) decrease in cellular and optical integrity at 48 h after exposure, whereas those treated with 43 J/cm2 UVA alone did not show significant phototoxic effect. Lenses treated with 15.63 J/cm2 UVA plus 0.019 J/cm2 UVB combined showed significant adverse effects beginning from 48 h after exposure. Also, there was no recovery. These findings show that a high UVA dose alone and relatively low UVA in combination with low UVB radiant exposure can impair lens cellular and optical functions, respectively. [source]