Cytotoxicity of mercury compounds in LLC-PK1, MDCK and human proximal tubular cells. Six mercury compounds HgCl2 (MC), Hg(CH3COO)2 (MA), Hg(NO3)2 (MN), C2H5HgSC6H4COONa (EMT), C6H5HgOCOCH3 (PMA) and ...CH3CIHg (MMC) were studied using two kidney cell lines (MDCK and LLC-PK1), primary cultures of human proximal tubular cells (hPTC) and nonrenal cell lines (SAOS and Hep G2). Cell damage was measured with four different tests: neutral red uptake, mitochondrial dehydrogenase activity (MTT conversion), thymidine incorporation and protein content. Relative toxicity was established by the determination of the concentration of test compound inducing a 50% reduction of the parameter considered (EC50 value). Two groups could be distinguished: PMA, EMT and MMC are one order of magnitude more toxic than MC, MN and MA. Cellular uptake was measured by the HPLC-hybrid generation AAS after 24 hours treatment with 1.5 µM MC, MMC, PMA or EMT in MDCK cells, revealing Hg concentrations of 42.8 ± 2.5 ng/mg protein for MC, 596.9 ± 87.8 ng/mg protein for MMC, 269.8 ± 75.7 ng/mg protein for PMA and of 115.9 ± 25.2 ng/mg protein for EMT. Cytotoxicity was positively correlated with cellular uptake. The effect of the cellular GSH content on the toxicity of mercury was studied using the GSH synthesis inhibitor L-buthionine sulfoximine (BSO). In all cases an enhanced cytotoxicity was observed after BSO treatment. 2-Oxo-4-thiazolidine carboxylic acid (OTC) was used as a substrate for the GSH synthesis. Although OTC did not enhance the GSH content, the cytotoxicity of MC, MN and MA decreased significantly, no changes were observed for the other mercurials. HPLC-hydrid generation AAS revealed that OTC is complexed in the growth medium with MC, but not with EMT, whereas no interactions were observed between BSO and the mercury compounds. From a toxicological point of view two groups can be considered: MMC, EMT and PMA are one order of magnitude more toxic than MC, MA and MN in all cell lines studied. This difference in toxicity was proportional with the uptake of those compounds. Extracellular complexation of mercury with OTC is correlated with decreasing cytotoxicity in the absence of enhanced GSH. GSH inhibition by BSO resulted in a higher toxicity, within comparable cellular uptake, confirming the function of GSH in the detoxification of mercury.
To simulate the bow of wafers with integrated capacitors in the form of pit arrays, various approaches were pursued. After unfruitful attempts to reliably obtain the wafer bow directly from ...simulating part of the wafer, a multi-scale approach was used. In this approach, the layer with the integrated capacitors was replaced by a homogeneous material having the same properties. Small-scale simulations of representative parts of the layer were performed to determine its effective stiffness tensor. Inclusion of the intrinsic strains of the grown and deposited dielectric and conductive layers enabled the volume change to be calculated of the layer with the integrated capacitors upon fabrication. Finally, the structure obtained was used in a full-wafer-scale model to simulate the bow of the wafers. Even for uncalibrated values for the coefficients of thermal expansion, most simulations agreed well with measurements.
Monitoring of the complex cold atmospheric plasma spraying process currently relies on technologically advanced systems, that often measure only a single parameter. This research introduces a more ...integrated approach, that uses a comprehensive set of parameters, consolidated in the characteristics of the plasma flame, is used to accurately classify particle temperature and coating materials. A simple optical camera system and image analysis based on a transfer learning model predicts with an 85% success rate. This approach simplifies and complements the monitoring process. Accuracy could be increased by using additional machine data already recorded, which could allow a complete replacement of additional the plasma flame monitoring.
Hereditary hemorrhagic telangiectasia is associated with a wide range of neurovascular abnormalities. The aim of this study was to characterize the spectrum of cerebrovascular lesions, including ...brain arteriovenous malformations, in patients with hereditary hemorrhagic telangiectasia and to study associations between brain arteriovenous malformations and demographic variables, genetic mutations, and the presence of AVMs in other organs.
Consecutive patients with definite hereditary hemorrhagic telangiectasia who underwent brain MR imaging/MRA, CTA, or DSA at our institution from 2001 to 2015 were included. All studies were re-evaluated by 2 senior neuroradiologists for the presence, characteristics, location, and number of brain arteriovenous malformations, intracranial aneurysms, and nonshunting lesions. Brain arteriovenous malformations were categorized as high-flow pial fistulas, nidus-type brain AVMs, and capillary vascular malformations and were assigned a Spetzler-Martin score. We examined the association between baseline clinical and genetic mutational status and the presence/multiplicity of brain arteriovenous malformations.
Three hundred seventy-six patients with definite hereditary hemorrhagic telangiectasia were included. One hundred ten brain arteriovenous malformations were noted in 48 patients (12.8%), with multiple brain arteriovenous malformations in 26 patients. These included 51 nidal brain arteriovenous malformations (46.4%), 58 capillary vascular malformations (52.7%), and 1 pial arteriovenous fistula (0.9%). Five patients (10.4%) with single nidal brain arteriovenous malformation presented with hemorrhage. Of brain arteriovenous malformations, 88.9% (88/99) had a Spetzler-Martin score of ≤2. Patients with brain arteriovenous malformations were more likely to be female (75.0% versus 57.6%, P = .01) and have a family history of hereditary hemorrhagic telangiectasia (95.8% versus 84.8%, P = .04). The prevalence of brain arteriovenous malformation was 19.7% in endoglin (ENG) mutations and 12.5% in activin receptor-like kinase (1ACVRL1) mutations.
Our study of 376 patients with hereditary hemorrhagic telangiectasia demonstrated a high prevalence of brain arteriovenous malformations. Nidal brain arteriovenous malformations and capillary vascular malformations occurred in roughly equal numbers.
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