High Throughput, Direct Determination of 226Ra in Water and Digested Geological Samples.

A method was developed for direct measurements of 226Ra in water samples with triple quadrupole inductively coupled plasma mass spectrometry (ICP-QQQ). The limit of detection was 0.42 pg L-1 226Ra (15 mBq L-1, 0.42 pCi L-1), which is compliant with the specifications for methods used for routine analysis of drinking water quality according to European and U.S. regulations. The use of N2O as reaction gas ensured that no separation before analysis was necessary. Water samples with high total dissolved solids (conductivity >100 mS cm-1) were also successfully analyzed after a simple dilution, yet the associated detection limit was higher (17 pg L-1, 0.61 Bq L-1, 16 pCi L-1). 226Ra content in soil and rock samples was determined with the same method after acid (HNO3 + H3PO4) digestion and dilution, resulting in a limit of detection of 0.75 ng kg-1 (27 Bq kg-1, 0.74 nCi L-1). Analysis of water samples was achieved within 2 min on a running instrument, while the preparation and analysis of 15 geological samples can be completed in 3 h. The key advantages of this direct analysis method are short preparation time, low labor intensity, low sample input (2 mL for water samples, 0.2 g for geological material), high sample throughput (2 min sample to sample, >150 samples measured in 8 h), and use of standard ICP-QQQ hardware. Overall, the proposed method offers a new opportunity for measuring a large number of samples with minimal effort and, in turn, for improving emergency preparedness, environmental monitoring, and data collection for environmental modeling.

Toxicity of pristine and paint-embedded TiO2 nanomaterials.

Little is known on the toxicity of nanomaterials in the user phase. Inclusion of nanomaterials in paints is a common nanotechnology application. This study focuses on the toxicity of dusts from sanding of paints containing nanomaterials. We compared the toxicity of titanium dioxide nanomaterials (TiO2NMs) and dusts generated by sanding boards coated with paints with different amounts of two different types of uncoated TiO2NMs (diameters:10.5 nm and 38 nm). Mice were intratracheally instilled with a single dose of 18, 54 and 162 µg of TiO2NMs or 54, 162 and 486 µg of sanding dusts. At 1, 3 and 28 days post-instillation, we evaluated pulmonary inflammation, liver histology and DNA damage in lung and liver. Pulmonary exposure to both pristine TiO2NMs and sanding dusts with different types of TiO2NMs resulted in dose-dependently increased influx of neutrophils into the lung lumen. There was no difference between the sanding dusts from the two paints. For all exposures but not in vehicle controls, mild histological lesions were observed in the liver. Pulmonary exposure to pristine TiO2NMs and paint dusts with TiO2NMs caused similar type of histological lesions in the liver.

Testing the near field/far field model performance for prediction of particulate matter emissions in a paint factory.

A Near Field/Far Field (NF/FF) model is a well-accepted tool for precautionary exposure assessment but its capability to estimate particulate matter (PM) concentrations is not well studied. The main concern is related to emission source characterization which is not as well defined for PM emitters compared to e.g. for solvents. One way to characterize PM emission source strength is by using the material dustiness index which is scaled to correspond to industrial use by using modifying factors, such as handling energy factors. In this study we investigate how well the NF/FF model predicts PM concentration levels in a paint factory. PM concentration levels were measured during big bag and small bag powder pouring. Rotating drum dustiness indices were determined for the specific powders used and applied in the NF/FF model to predict mass concentrations. Modeled process specific concentration levels were adjusted to be similar to the measured concentration levels by adjusting the handling energy factor. The handling energy factors were found to vary considerably depending on the material and process even-though they have the same values as modifying factors in the exposure models. This suggests that the PM source characteristics and process-specific handling energies should be studied in more detail to improve the model-based exposure assessment.

Peroxyl radicals are potential agents of lignin biodegradation.

Past work has shown that the extracellular manganese-dependent peroxidases (MnPs) of ligninolytic fungi degrade the principal non-phenolic structures of lignin when they peroxidize unsaturated fatty acids. This reaction is likely to be relevant to ligninolysis in sound wood, where enzymes cannot penetrate, only if it employs a small, diffusible lipid radical as the proximal oxidant of lignin. Here we show that a non-phenolic beta-O-4-linked lignin model dimer was oxidized to products indicative of hydrogen abstraction and electron transfer by three different peroxyl radical-generating systems: (a) MnP/Mn(II)/linoleic acid, (b) arachidonic acid in which peroxidation was initiated by a small amount of H(2)O(2)/Fe(II), and (c) the thermolysis in air of either 4,4'-azobis(4-cyanovaleric acid) or 2,2'-azobis(2-methylpropionamidine) dihydrochloride. Some quantitative differences in the product distributions were found, but these were attributable to the presence of electron-withdrawing substituents on the peroxyl radicals derived from azo precursors. Our results introduce a new hypothesis: that biogenic peroxyl radicals may be agents of lignin biodegradation.

Oxidative degradation of non-phenolic lignin during lipid peroxidation by fungal manganese peroxidase.

A non-phenolic lignin model dimer, 1-(4-ethoxy-3-methoxyphenyl)-2-phenoxypropane-1,3-diol, was oxidized by a lipid peroxidation system that consisted of a fungal manganese peroxidase, Mn(II), and unsaturated fatty acid esters. The reaction products included 1-(4-ethoxy-3-methoxyphenyl)-1-oxo-2-phenoxy-3-hydroxypropane and 1-(4-ethoxy-3-methoxyphenyl)-1-oxo-3-hydroxypropane, indicating that substrate oxidation occurred via benzylic hydrogen abstraction. The peroxidation system depolymerized both exhaustively methylated (non-phenolic) and unmethylated (phenolic) synthetic lignins efficiently. It may therefore enable white-rot fungi to accomplish the initial delignification of wood.

ICP during anaesthesia with sevoflurane: a dose-response study. Effect of hypocapnia.

In patients with a supratentorial cerebral tumor, an increase in sevoflurane concentration from 1.5% (0.7 MAC) to 2.5% (1.3 MAC) did not change the intracranial pressure (ICP) significantly (12 to 14 mm Hg (medians)). However, a significant increase in cerebral blood flow (CBF) from 29 to 39 ml/100 g/min (medians) was disclosed. During administration of sevoflurane 1.5% and 2.5%, a significant decrease in ICP (3.5 and 3.0 mm Hg (median) respectively) was found when PaCO2 was decreased by 0.8 kPa.

[Cerebral blood flow and indomethacin. The effect of different doses administered as continuous intravenous infusions or as suppositories in healthy adults]. / Hjernens gennemblødning og indomethacin. Effekten af forskellige doser givet som kontinuerlig intravenøs infusion eller som suppositorier hos raske forsøgspersoner.

Administration of indomethacin may aid treatment of intracranial hypertension, and the present study was conducted to determine the optimal dose. In healthy volunteers, cerebral blood flow (CBF) has been shown to decrease considerably after a bolus dose of indomethacin, 0.4 mg/kg, followed by continuous infusion, 0.4 mg/kg/h. This decrease was sustained for 6 h without any evidence of adaptation. In a randomized study in healthy volunteers, indomethacin, 0.1, 0.2 and 0.3 mg/kg, was given as bolus, followed by continuous infusion of 0.1, 0.2 and 0.3 mg/kg/h. CBF decreased from normal levels (52-74 ml/100 mg/min) to 38-51 ml/100 g/min. There were no differences among the three groups in CBF reduction, and the reduction was sustained during the 6-h infusion period. Rectal application of 100 mg indomethacin was found to reduce CBF from normal levels (54-74 ml/100 mg/min) to 33-48 ml/100 mg/min. These low levels were only sustained for 2 h, and values returned to normal over the next 6 h. We observed no rebound phenomenon 2 h after stopping the infusion and no rebound after 100 mg of rectally applied indomethacin. Since a dose as low as 0.1 mg/kg/h is effective, it is possible to treat most patient in a 24-h schedule without going over maximum recommended doses.

[Effect of indomethacin on the intracranial pressure]. / Indomethacins virkning på det intrakranielle tryk.

Twenty patients subjected to craniotomy for supratentorial cerebral tumours were anaesthetized with thiopental, fentanyl, nitrous oxide, and isoflurane. A PaCO2 level averaging 4.8 kPa was achieved. The patients were randomized to intravenous indomethacin 50 mg or placebo administrated after exposure of the dura. A significant decrease in intracranial pressure from 6.5 to 1.5 mmHg (medians) was found after indomethacin administration. This decrease was caused by a significant decrease in cerebral blood flow associated with a significant increase in the arterio-venous oxygen difference. Indomethacin did not affect cerebral oxygen uptake, arteriovenous difference in lactate or the lactate/oxygen index, suggesting that indomethacin did not provoke global cerebral ischaemia. In the indomethacin group, dura was sufficiently relaxed in eight of nine patients, and dura was opened without the occurrence of cerebral swelling. In the placebo group, mannitol supplemented with hypocapnia was applied in five patients. These findings suggest that perioperative treatment with indomethacin is an excellent treatment of intracranial hypertension during normocapnic isoflurane anaesthesia for craniotomy.

[CO2 and indomethacin vasoreactivity in patients with cranial trauma]. / CO2-og indometacinvasoreaktivitet hos patienter med kranietraume.

The purpose of this study was to compare the effect of hyperventilation and indomethacin on cerebral circulation, metabolism and systemic and intracerebral pressures in patients with severe head injury. Fourteen moderately (PaCO2 = 4.05 kPa) hyperventilated patients with median [CP = 14.8 mmHg entered the study. Cerebral blood flow (CBF), intracranial pressure (ICP), arteriovenous difference of oxygen (AVDO2) and lactate (AVdL) and oxygen saturation in the jugular bulb (SvjO2) were measured before and after hyperventilation and after a bolus dose of indomethacin (30 mg). During hyperventilation CBF decreased by 11.8%/kPa and ICP decreased by 3.8 mmHg. AVDO2 increased by 34.0%/kPa. After indomethacin CBF decreased by 14.7% and ICP decreased by 4.3 mmHg. AVDO2 increased with 27.8%. No changes in median SvjO2 and AVdL were observed after the two treatments. The risk of cerebral ischaemia seems identical after the two treatments. No correlations between the effects of the two treatments on CBF, ICP and AVDO2 were found. These results suggest that indomethacin and hyperventilation might act independently or in a complementary fashion in the treatment of patients with severe head injury.

Double blind placebo controlled exposure to molds: exposure system and clinical results.

UNLABELLED: The objective was to develop an experimental setup for human exposure to mold spores, and to study the clinical effect of this exposure in sensitive subjects who had previously experienced potentially building-related symptoms (BRS) at work. From three water-damaged schools eight employees with a positive histamine release test to Penicillium chrysogenum were exposed double- blinded to either placebo, approximately 600,000 spores/m3 air of P. chrysogenum or approximately 350,000 spores/m3 of Trichoderma harzianum for 6 min on three separate days. A statistically significant rise in symptoms from mucous membranes appeared from the 9-graded symptom scale after exposure to T. harzianum or placebo. Dichotomizing the data, whether the participants experienced at least a two-step rise on the symptom scale or not, gave borderline increase in mucous membrane symptoms after exposure to P. chrysogenum. In conclusion this is, to our knowledge, the first study to successfully conduct a human exposure to a highly controlled dose of fungal material aerosolized directly from wet building materials. This short-term exposure to high concentrations of two different molds induced no more reactions than exposure to placebo in eight sensitive school employees. However, a statistical type II error cannot be excluded because of the small sample size. PRACTICAL IMPLICATIONS: In this double blind, placebo controlled study of mold exposure changes in symptoms, objective measurements and blood samples were small and mostly non-significant, and at the same level as after placebo exposure. The developed exposure system based on the Particle-Field and Laboratory Emission Cell (P-FLEC) makes it possible to deliver a precise and highly controlled dose of mold spores from water-damaged building materials, imitating realistic field exposure conditions. The present experiment is too small to rule out an effect of mold exposure; long-term experimental exposure studies on larger number of subjects are needed.

DNA repair within nucleosome cores of UV-irradiated human cells.

We have compared the distributions of repair synthesis and pyrimidine dimers (PD) in nucleosome core DNA during the early (fast) repair phase and the late (slow) repair phase of UV-irradiated human fibroblasts. As shown previously [Lan, S. Y., & Smerdon, M. J. (1985) Biochemistry 24, 7771-7783], repair synthesis is nonuniform in nucleosome core particles during the fast repair phase, and the distribution curve can be approximated by a model where repair synthesis occurs preferentially in the 5' and 3' end regions. In this report, we show that, during the slow repair phase, [3H]dThd-labeled repair patches are much more uniformly distributed in core DNA, although they appear to be preferentially located in sequences degraded slowly by exonuclease III. This change in distribution cannot be explained by an increase in patch size during slow repair, since the size of these patches actually decreases to about half the size measured during the fast repair phase. Furthermore, PD mapping within core DNA at the single-nucleotide level demonstrated that, at least within the 30-130-base region from the 5' end, there is little (or no) selective removal of PD during the fast repair phase. However, the nonuniform distribution of repair synthesis obtained during fast repair throughout most of the core DNA region (approximately 40-146 bases) is accounted for by the nonuniform distribution of PD in core DNA. The near-uniform distribution of repair synthesis observed during slow repair may result from more extensive nucleosome rearrangement and/or nucleosome modification during this phase.

Abnormal gamma globulin binding of thyroid hormones.

Thyroid hormone levels were studied in a thyrotoxic patient, who was treated with propylthiouracil. He had heavily increased triiodothyronine concentrations, measured by radioimmunoassay, in spite of only mild clinical symptoms of thyrotoxicosis. A moderately increased serum triiodothyronine concentration was observed in another patient, who was euthyroid and who had recently recovered from subacute thyroiditis. By gel electrophoresis and precipitation tests with human anti-IgG and anti-IgA, a binding to the gamma globulins of both triiodothyronine and thyroxine was detected in patient 1, and of triiodothyronine in patient 2. Such abnormal binding may result in serious errors in the determination of thyroid hormone concentration by radioimmunoassay.

The effect of phenobarbital on cerebral blood flow in newborn infants with foetal distress.

The effect of phenobarbital on cerebral blood flow (CBF) was investigated by the intravenous Xenon133 clearance technique in seven term newborn infants with signs of mild to moderate hypoxic ischaemic encephalopathy, all on sustained spontaneous ventilation. Phenobarbital treatment had no significant effect on CBF 60 min after loading dosage (20 mg/kg i.v.). Likewise, no significant change in mean arterial blood pressure, heart rate or transcutaneous gas tensions was observed. Though slight changes in CBF of short duration cannot be excluded, conventional dosage of phenobarbital to term newborn infants with foetal distress apparently imposes no risk of cerebrovascular damage.

Indomethacin in the management of postoperative pain.

We have examined the analgesic effects of indomethacin in a double-blind study of 56 patients undergoing surgery for lumbar disc prolapse. The patients were allocated randomly to receive either indomethacin 100 mg i.v. before surgery, followed by 100 mg rectally 6 and 12 h after surgery and at 08:00, 16:00 and 23:00 on the next day, or placebo. Postoperative pain was assessed using a 10-cm visual analogue scale at fixed times. Side effects and consumption of supplementary analgesics were recorded. Patients receiving placebo had significantly greater pain scores and significantly more patients in the placebo group required supplementary analgesics.

Fungal degradation of recalcitrant nonphenolic lignin structures without lignin peroxidase.

Lignin peroxidases (LiPs) are likely catalysts of ligninolysis in many white-rot fungi, because they have the unusual ability to depolymerize the major, recalcitrant, non-phenolic structures of lignin. Some white-rot fungi have been reported to lack LiP when grown on defined medium, but it is not clear whether they exhibit full ligninolytic competence under these conditions. To address this problem, we compared the abilities of a known LiP producer, Phanerochaete chrysosporium, with those of a reported nonproducer, Ceriporiopsis subvermispora, to degrade a synthetic lignin with normal phenolic content, a lignin with all phenolic units blocked, and a dimer, 1-(4-ethoxy-3-methoxyphenyl)-2-(2-methoxyphenoxy)propane-1,3-diol, that represents the major nonphenolic structure in lignin. P. chrysosporium mineralized all three models rapidly in defined medium, but C. subvermispora showed appreciable activity only toward the more labile phenolic compound under these conditions. However, in wood, its natural environment, C. subvermispora mineralized all of the models as rapidly as P. chrysosporium did. Defined media therefore fail to elicit a key component of the ligninolytic system in C. subvermispora. A double-labeling experiment with the dimeric model showed that a LiP-dependent pathway was responsible for at least half of dimer mineralization in wood by P. chrysosporium but was responsible for no more than 6-7% of mineralization by C. subvermispora in wood. Therefore, C. subvermispora has mechanisms for degradation of nonphenolic lignin that are as efficient as those in P. chrysosporium but that do not depend on LiP.