Preliminary studies of laser-induced breakdown spectrometry for the determination of Ba, Cd, Cr and Pb in toys

The performance of laser-induced breakdown spectrometry (LIBS) for the determination of Ba, Cd, Cr and Pb in toys has been evaluated by using a Nd:YAG laser operating at 1064 nm and an Echelle spectrometer with intensified charge-coupled device detector. Samples were purchased in different cities of Sao Paulo State market and analyzed directly without sample preparation. Laser-induced breakdown spectrometry experimental conditions (number of pulses, delay time. integration time gate and pulse energy) were optimized by using a Doehlert design. Laser-induced breakdown spectrometry signals correlated reasonably well with inductively coupled plasma optical emission spectrometry (ICP OES) concentrations after microwave-assisted acid digestion of selected samples. Thermal analysis was used for polymer identification and scanning electron microscopy to Visualize differences in crater geometry of different polymers employed for toy fabrication. Results indicate that laser-induced breakdown spectrometry can be proposed as a rapid screening method for investigation of potentially toxic elements in toys. The unique application of laser-induced breakdown spectrometry for identification of contaminants in successive layers of ink and polymer is also demonstrated. (C) 2009 Elsevier B.V. All rights reserved.

Right adolescent idiopathic thoracic curve (Lenke 1 A and B): does cost of instrumentation and implant density improve radiographic and cosmetic parameters?

In adolescent idiopathic scoliosis (AIS) there has been a shift towards increasing the number of implants and pedicle screws, which has not been proven to improve cosmetic correction. To evaluate if increasing cost of instrumentation correlates with cosmetic correction using clinical photographs. 58 Lenke 1A and B cases from a multicenter AIS database with at least 3 months follow-up of clinical photographs were used for analysis. Cosmetic parameters on PA and forward bending photographs included angular measurements of trunk shift, shoulder balance, rib hump, and ratio measurements of waist line asymmetry. Pre-op and follow-up X-rays were measured for coronal and sagittal deformity parameters. Cost density was calculated by dividing the total cost of instrumentation by the number of vertebrae being fused. Linear regression and spearman`s correlation were used to correlate cost density to X-ray and photo outcomes. Three independent observers verified radiographic and cosmetic parameters for inter/interobserver variability analysis. Average pre-op Cobb angle and instrumented correction were 54A degrees (SD 12.5) and 59% (SD 25) respectively. The average number of vertebrae fused was 10 (SD 1.9). The total cost of spinal instrumentation ranged from $6,769 to $21,274 (Mean $12,662, SD $3,858). There was a weak positive and statistically significant correlation between Cobb angle correction and cost density (r = 0.33, p = 0.01), and no correlation between Cobb angle correction of the uninstrumented lumbar spine and cost density (r = 0.15, p = 0.26). There was no significant correlation between all sagittal X-ray measurements or any of the photo parameters and cost density. There was good to excellent inter/intraobserver variability of all photographic parameters based on the intraclass correlation coefficient (ICC 0.74-0.98). Our method used to measure cosmesis had good to excellent inter/intraobserver variability, and may be an effective tool to objectively assess cosmesis from photographs. Since increasing cost density only improves mildly the Cobb angle correction of the main thoracic curve and not the correction of the uninstrumented spine or any of the cosmetic parameters, one should consider the cost of increasing implant density in Lenke 1A and B curves. In the area of rationalization of health care expenses, this study demonstrates that increasing the number of implants does not improve any relevant cosmetic or radiographic outcomes.

Increased endothelin-1 reactivity and endothelial dysfunction in carotid arteries from rats with hyperhomocysteinemia

There are interactions between endothelin-1 (ET-1) and endothelial vascular injury in hyperhomocysteinemia (HHcy), but the underlying mechanisms are poorly understood. Here we evaluated the effects of HHcy on the endothelin system in rat carotid arteries. Vascular reactivity to ET-1 and ET(A) and ET(B) receptor antagonists was assessed in rings of carotid arteries from normal rats and those with HHcy. ET(A) and ET(B) receptor expression was assessed by mRNA (RT-PCR), immunohistochemistry and binding of [(125)I]-ET-1. HHcy enhanced ET-1-induced contractions of carotid rings with intact endothelium. Selective antagonism of ET(A) or ET(B) receptors produced concentration-dependent rightward displacements of ET-1 concentration response curves. Antagonism of ET(A) but not of ET(B) receptors abolished enhancement in HHcy tissues. ET(A) and ET(B) receptor gene expressions were not up-regulated. ET(A) receptor expression in the arterial media was higher in HHcy arteries. Contractions to big ET-1 served as indicators of endothelin-converting enzyme activity, which was decreased by HHcy, without reduction of ET-1 levels. ET-1-induced Rho-kinase activity, calcium release and influx were increased by HHcy. Pre-treatment with indomethacin reversed enhanced responses to ET-1 in HHcy tissues, which were reduced also by a thromboxane A(2) receptor antagonist. Induced relaxation was reduced by BQ788, absent in endothelium-denuded arteries and was decreased in HHcy due to reduced bioavailability of NO. Increased ET(A) receptor density plays a fundamental role in endothelial injury induced by HHcy. ET-1 activation of ET(A) receptors in HHcy changed the balance between endothelium-derived relaxing and contracting factors, favouring enhanced contractility. British Journal of Pharmacology (2009) 157, 568-580; doi:10.1111/j.1476-5381.2009.00165.x; published online 9 April 2009 This article is part of a themed section on Endothelium in Pharmacology. For a list of all articles in this section see the end of this paper, or visit: http://www3.interscience.wiley.com/journal/121548564/issueyear?year=2009.

beta 1 Integrin and VEGF expression in an experimental model of brain tissue heterotopia in the lung

Integrins and vascular endothelial growth factor (VEGF) are crucially involved in interaction, proliferation, migration, and survival of the cells. However, there is no report in the literature about beta 1 integrin and VEGF expression in heterotopic brain tissue. The aim of this study was to assess beta 1 integrin and VEGF expression in experimental brain tissue heterotopia in the lung during both fetal and neonatal periods. Twenty-four pregnant female Swiss mice were used to induce brain tissue heterotopia on the 15th gestational day. Briefly, the brain of one fetus of each dam was extracted, disaggregated, and injected into the right hemithorax of siblings. Six of these fetuses with pulmonary brain tissue implantation were collected on the 18th gestational day (group E18) and six other on the eighth postnatal day (group P8). Immunohistochemistry of the fetal trunks showed implantation of glial fibrillary acidic protein- and neuronal nuclei-positive heterotopic brain tissue, which were also positive for beta 1 integrin and VEGF in both groups E18 and P8. These results indicate that brain tissue heterotopia during fetal and postnatal period is able to complete integration with the lung tissue as well as to induce vascular proliferation which are the necessary steps for a successful implantation.

A double-blind, randomized study comparing pure chromated glycerin with chromated glycerin with 1% lidocaine and epinephrine for sclerotherapy of telangiectasias and reticular veins.

BACKGROUND Chromated glycerin (CG) is an effective, although painful, sclerosing agent for telangiectasias and reticular leg veins treatment. OBJECTIVE To determine pain level and relative efficacy of pure or one-third lidocaine-epinephrine 1% mixed chromated glycerin in a prospective randomized double-blind trial. METHOD Patients presenting with telangiectasias and reticular leg veins on the lateral aspect of the thigh (C(1A) or (S) E(P) A(S) P(N1) ) were randomized to receive pure CG or CG mixed with one-third lidocaine-epinephrine 1% (CGX) treatment. Lower limb photographs were taken before and after treatment and analyzed by blinded expert reviewers for efficacy assessment (visual vein disappearance). Patients' pain and satisfaction were assessed using visual analogue scales. RESULTS Data from 102 of 110 randomized patients could be evaluated. Patient pain scores were significantly higher when pure CG was used than with CGX (p<.001). Patient satisfaction with treatment outcome was similar in the two groups. Objective visual assessment of vessel disappearance revealed no significant difference between the two agents (p=.07). CONCLUSION Addition of lidocaine-epinephrine 1% to CG, in a ratio of one-third, significantly reduces sclerotherapy pain without affecting efficacy when treating telangiectasias and reticular leg veins. The authors have indicated no significant interest with commercial supporters.

TRAIL receptors 1 (DR4) and 2 (DR5) signal FADD-dependent apoptosis and activate NF-kappaB.

TRAIL induces apoptosis through two closely related receptors, TRAIL-R1 (DR4) and TRAIL-R2 (DR5). Here we show that TRAIL-R1 can associate with TRAIL-R2, suggesting that TRAIL may signal through heteroreceptor signaling complexes. Both TRAIL receptors bind the adaptor molecules FADD and TRADD, and both death signals are interrupted by a dominant negative form of FADD and by the FLICE-inhibitory protein FLIP. The recruitment of TRADD may explain the potent activation of NF-kappaB observed by TRAIL receptors. Thus, TRAIL receptors can signal both death and gene transcription, functions reminiscent of those of TNFR1 and TRAMP, two other members of the death receptor family.

Neurochemical profile of the developing mouse cortex determined by in vivo 1H NMR spectroscopy at 14.1 T and the effect of recurrent anaesthesia.

The neurochemical profile of the cortex develops in a region and time specific manner, which can be distorted by psychiatric and other neurological pathologies. Pre-clinical studies often involve experimental mouse models. In this study, we determined the neurochemical profile of C57BL/6 mice in a longitudinal study design to provide a reference frame for the normal developing mouse cortex. Using in vivo proton NMR spectroscopy at 14 T, we measured the concentrations of 18 metabolites in the anterior and posterior cortex on postnatal days (P) 10, 20, 30, 60 and 90. Cortical development was marked by alterations of highly concentrated metabolites, such as N-acetylaspartate, glutamate, taurine and creatine. Regional specificity was represented by early variations in the concentration of glutamine, aspartate and choline. In adult animals, regional concentration differences were found for N-acetylaspartate, creatine and myo-inositol. In this study, animals were exposed to recurrent isoflurane anaesthesia. Additional experiments showed that the latter was devoid of major effects on behaviour or cortical neurochemical profile. In conclusion, the high sensitivity and reproducibility of the measurements achieved at 14 T allowed us to identify developmental variations of cortical areas within the mouse cortex.

In vitro attachment of glycosyl-inositolphospholipid anchor structures to mouse Thy-1 antigen and human decay-accelerating factor.

Glycosyl-inositolphospholipid (GPL) anchoring structures are incorporated into GPL-anchored proteins immediately posttranslationally in the rough endoplasmic reticulum, but the biochemical and cellular constituents involved in this "glypiation" process are unknown. To establish whether glypiation could be achieved in vitro, mRNAs generated by transcription of cDNAs encoding two GPL-anchored proteins, murine Thy-1 antigen and human decay-accelerating factor (DAF), and a conventionally anchored control protein, polymeric-immunoglobulin receptor (IgR), were translated in a rabbit reticulocyte lysate. Upon addition of dog pancreatic rough microsomes, nascent polypeptides generated from the three mRNAs translocated into vesicles. Dispersal of the vesicles with Triton X-114 detergent and incubation of the hydrophobic phase with phosphatidylinositol-specific phospholipases C and D, enzymes specific for GPL-anchor structures, released Thy-1 and DAF but not IgR protein into the aqueous phase. The selective incorporation of phospholipase-sensitive anchoring moieties into Thy-1 and DAF but not IgR translation products during in vitro translocation indicates that rough microsomes are able to support and regulate glypiation.

MRI visualized neo-intimal dissection and co-localization of novel apoptotic markers apolipoprotein C-1, ceramide and caspase-3 in a Watanabe hyperlipidemic rabbit model

PURPOSE: Apoptotic arterial wall vascular smooth muscle cell death is known to contribute to plaque vulnerability and rupture. Novel apoptotic markers like apolipoprotein C-I have been implicated in apoptotic human vascular smooth muscle cell death via recruiting a neutral sphingomyelinase (N-SMase)-ceramide pathway. In vivo relevance of these observations in an animal model of plaque rupture has not been shown. METHODS AND RESULTS: Using Watanabe rabbits, we investigated three different groups (group 1, three normal Watanabe rabbits; group 2, six Watanabe rabbits fed with high cholesterol diet for 3 months; group 3, five Watanabe rabbits with similar diet but additional endothelial denudation). We followed progression of atherosclerosis to pharmacologically induced plaque rupture non-invasively using novel 3D magnetic resonance Fast-Field-Echo angiography (TR=7.2, TE=3.6 ms, matrix=512 x 512) and Fast-Spin-Echo vessel wall imaging methods (TR=3 heart beats, TE=10.5 ms, matrix=304 x 304) on 1.5 T MRI. MRI provided excellent image quality with good MRI versus histology vessel wall thickness correlation (r=0.8). In six animals of group 2/3 MRI detected neo-intimal dissection in the abdominal aorta which was accompanied by immuno-histochemical demonstration of concomitant aforementioned novel apoptotic markers, previously implicated in the apoptotic smooth muscle cell death in vitro. CONCLUSIONS: Our studies suggest a potential role for the signal transduction pathway involving apolipoprotein C-I for in vivo apoptosis and atherosclerotic plaque rupture visualized by MRI.

HIV-1 immune activation induces Siglec-1 expression and enhances viral trans-infection in blood and tissue myeloid cells.

BACKGROUND: Myeloid cells are key players in the recognition and response of the host against invading viruses. Paradoxically, upon HIV-1 infection, myeloid cells might also promote viral pathogenesis through trans-infection, a mechanism that promotes HIV-1 transmission to target cells via viral capture and storage. The receptor Siglec-1 (CD169) potently enhances HIV-1 trans-infection and is regulated by immune activating signals present throughout the course of HIV-1 infection, such as interferon α (IFNα). RESULTS: Here we show that IFNα-activated dendritic cells, monocytes and macrophages have an enhanced ability to capture and trans-infect HIV-1 via Siglec-1 recognition of viral membrane gangliosides. Monocytes from untreated HIV-1-infected individuals trans-infect HIV-1 via Siglec-1, but this capacity diminishes after effective antiretroviral treatment. Furthermore, Siglec-1 is expressed on myeloid cells residing in lymphoid tissues, where it can mediate viral trans-infection. CONCLUSIONS: Siglec-1 on myeloid cells could fuel novel CD4(+) T-cell infections and contribute to HIV-1 dissemination in vivo.

Evolution of dosage compensation under sexual selection differs between X and Z chromosomes.

Complete sex chromosome dosage compensation has more often been observed in XY than ZW species. In this study, using a population genetic model and the chicken transcriptome, we assess whether sexual conflict can account for this difference. Sexual conflict over expression is inevitable when mutation effects are correlated across the sexes, as compensatory mutations in the heterogametic sex lead to hyperexpression in the homogametic sex. Coupled with stronger selection and greater reproductive variance in males, this results in slower and less complete evolution of Z compared with X dosage compensation. Using expression variance as a measure of selection strength, we find that, as predicted by the model, dosage compensation in the chicken is most pronounced in genes that are under strong selection biased towards females. Our study explains the pattern of weak dosage compensation in ZW systems, and suggests that sexual selection plays a major role in shaping sex chromosome dosage compensation.

Pressure dependence of spin fluctuations in metallic glasses Zrâ â Niâ â ,Zrâ â (Nix/Feâ â â -x)â â and /Zrx/feâ â â -x

The superconducting transition temperature Tc of metallic glasses ZrxFelOO-x (x=80, 75), Zr75(NixFelOO-x)25 (x=75, 50, 25), and CU2SZr75 were measured under quasi-hydrostatic pressure up to 8 OPa (80kbar). The volume (pressure) dependence of the electron-phonon coupling parameters Aep for CU25Zr75 was calculated using the McMillan equatio11. Using this volume dependence of Aep and the modified McMillan equation which incorporates spin-fluctuations, the volume dependence of the spin fluctuation parameter, Asf, was determined in Zr75Ni25, ZrxFelOO-x , a11d Zr75(NixFelOO-x)25. It was found that with increasing pressure, spinfluctuations are suppressed at a faster rate in ZrxFe lOO-x and Zr75(NixFelOO-x)25, as Fe concentration is increased. The rate of suppression of spin-fluctuations with pressure was also found to be higher in Fe-Zr glasses than in Ni-Zr glasses of similar composition.

Effect of polymer architecture on Curcumin 1 encapsulation and release from PEGylated polymer nanoparticles: toward a drug delivery nano-platform to the CNS

We developed a nanoparticles (NPs) library from poly(ethylene glycol)–poly lactic acid comb-like polymers with variable amount of PEG. Curcumin was encapsulated in the NPs with a view to develop a delivery platform to treat diseases involving oxidative stress affecting the CNS. We observed a sharp decrease in size between 15 and 20% w/w of PEG which corresponds to a transition from a large solid particle structure to a “micelle-like” or “polymer nano-aggregate” structure. Drug loading, loading efficacy and release kinetics were determined. The diffusion coefficients of curcumin in NPs were determined using a mathematical modeling. The higher diffusion was observed for solid particles compared to “polymer nano-aggregate” particles. NPs did not present any significant toxicity when tested in vitro on a neuronal cell line. Moreover, the ability of NPs carrying curcumin to prevent oxidative stress was evidenced and linked to polymer architecture and NPs organization. Our study showed the intimate relationship between the polymer architecture and the biophysical properties of the resulting NPs and sheds light on new approaches to design efficient NP-based drug carriers.