Search

Organophosphate (OP) pesticide residues have been found in rain, snow, fog and air samples collected in the Sierra Nevada mountains. The fate of these residues in this ecosystem is poorly understood. A major component of the Sierra Nevada ecosystem is the varied plant biomass. Interaction between chemicals vapors and plant material has been demonstrated for various semivolatile organic compounds. This research addresses the hypothesis that the extensive forests of the westem slopes of the Sierra Nevada mountains, which lie in the predominant downwind direction from the agricultural Central Valley of California, might serve as sinks for airborne OPs. The main paths of vapor-leaf interaction are cuticular and stomatal. More specifically, interactions may include sorption of residues to surface dust particles, or to the needle surface, solubilization in the cuticular wax of the needle, and penetration to the interior of the needle either by absorption through the stomata or migration through the cuticle. Analytical methods, which can separately assess surface, cuticle adsorbed, cuticle dissolved, and internal needle tissue residues, have been applied in two experimental situations. One involved measuring the vapor-needle distribution coefficient for several OPs exposed as vapors to pine branches in a laboratory chamber. A second, involving air and needle analyses for trees placed in, and downwind from a diazinon-treated orchard, provided outdoor distribution coefficients for comparison with chamber data. This paper addresses these two experimental situations, along with preliminary calculations of possible loading values for forests in the Sierra Nevadas. The results support the hypothesis that forests act as sinks for airborne pesticide vapors.

Hydroxocobalamin has been reported to interfere with the blood leak alarm on hemodialysis machines making it difficult to use this treatment modality after hydroxocobalamin infusion.The objective was to determine if this interference with hydroxocobalamin occurs across hemodialysis machines by different manufacturers. Additionally, we aimed to see if this represented a colorimetric interference alone or if it is the optical properties of hydroxocobalamin.Hydroxocobalamin was reconstituted per package insert. Food coloring was added to 0.9% saline to create the colors of the visual spectrum. Optical properties of absorbance and transmittance were measured. Hydroxocobalamin and the saline solutions were infused into the Fresenius 2008K™ and the Gambro Phoenix X36™ machines. Times were recorded from the start of the machine until the solution finished or the alarm triggered.When evaluating the Gambro Phoenix X36™ machine and dialysis circuit; the alarm did not trigger. In contrast, the blood leak alarm on the Fresenius 2008K™ machine was tripped by both the red solution and hydoxocobalamin infused per the package insert. The alarm stopped the machine between 128 and 132 seconds for the red solution and between 30 and 35 seconds with the hydroxocobalamin. Membranes of the circuits where the alarm tripped were examined and remained intact without blood. Results were validated on different machines with new circuits.Hydroxocobalamin infusion per package insert and the red saline solution prepared with Red Dye 40 both triggered the blood leak alarm and stopped the Fresenius 2008K™ machine. However, this was not true for the Gambro Phoenix X36™ machine as the alarm never triggered. The interference with the Fresenius 2008K™ appears colorimetric due to normal saline with Red Dye 40 triggering the alarm.We alert physicians to become familiar with the properties of individual dialysis machines prior to use of hydroxocobalamin. When facing difficulties with hemodialysis after the administration of hydroxocobalamin, consider attempting with a different manufactures machine or model if available or contact the manufacturer directly.

A method combining QuEChERS extraction, ultra-high pressure liquid chromatography and full scan high resolution mass spectrometry was evaluated for its use in screening for chemical residues and contaminants in animal-related food matrices. The method was evaluated by analysis of multiple replicates of whole milk, muscle tissue, liver tissue and corn silage. Analytes tested included plant alkaloids, carbamate and organophosphate pesticides, and several types of veterinary drugs. A database containing the chemical formula for each analyte was used to calculate accurate mass-to-charge ratios for expected pseudo-molecular ions. This information, as well as retention times, was used to identify analytes. Of 118 compounds chosen for analysis, 86 were detectable in all fortified replicates of at least one matrix at levels ranging from 1.0 to 5000 ng/g. Variability of response, as measured in % relative standard deviation of peak areas over seven replicate fortified sample analyses, was found to differ among the classes of analytes, ranging from10% to100%. Retention times were stable and analytes were routinely detected at measured mass-to-charge ratios within 2 ppm of their theoretical mass-to-charge ratios. These results indicate that the combination of generic extraction and chromatographic procedures with full scan high resolution mass spectrometry can serve as a useful method for screening complex matrices.

AIMS: To assess the feasibility of training nurse practitioners to perform bone marrow aspiration and trephine biopsy, and to compare the quality of these samples with those obtained by medical staff. METHODS: A retrospective audit was undertaken of nurse practitioner and medical staff performance in bone marrow procedures in a busy haematology day unit. RESULTS: Nurse practitioners fared favourably in comparison with medical staff in performing bone marrow trephine biopsies, with mean biopsy lengths of 11 mm and 10.7 mm respectively. However, only 78% of the smears obtained by the nurses were judged technically satisfactory, compared with 91% prepared by doctors. This discrepancy was thought to be due largely to the quality of slide spreading. CONCLUSIONS: With motivated staff and a structured educational and training programme it is possible for nurse practitioners to perform the techniques of bone marrow aspiration and biopsy, and obtain specimens of satisfactory quality, thus improving efficiency of the haematology day unit and increasing quality of patient care.

In Wilson's disease and Indian childhood cirrhosis (ICC) copper accumulates in the liver resulting in poor hepatocyte regeneration and fibrosis. An inhibition of hepatocyte proliferation and an increase in cell death could account for these outcomes. To establish how the toxicity of this metal ion impacts upon the proliferation and viability ofthe HepG2 cells they were cultured in 4-32 jiM copper(II) sulphate (CuS04)). These levels were comparable to the circulatory and tissue concentrations of copper recorded for these two diseases. Specific uptake comparable to levels of copper recorded in the livers of patients with Wilson's disease and ICC was measured in the HepG2 cells. After 48 h acid vesicle function increased from 4 to 32 jiM Cu2 + but significantly declined at 64 MM compared to the controls. Lysosomal acid phosphatase showed a concen-tration dependent decline in activity at 72 h. Introduction Copper is a potent catalyst of processes generating reactive oxygen intermediates and its cellular up-take, transport and excretion are therefore tightly controlled. Elevated hepatic copper concentrations are associated with liver damage in Wilson's disease2, in Indian childhood cirrhosis3 (ICC), and in other copper-related cirrhoses of infancy. Nevertheless, the cellular consequences of copper toxicity remain to be understood in the context of the disease pathology. In Wilson's disease, biliary excretion of copper is impaired by mutations in a trans-Golgi P-type ATPase4 resulting in intracellular hepatic copper accumulation5 with progressive dysfunction, fibrosis, and liver failure. However, clinical variability of Wilson's disease and the lack of a clear genotype/ Cellls exposed to 64 MM Cu2 + had a potential doubling time (Tpot) 21 h longer than the control cells due to a prolonged DNA synthesis phase. At 64 jiM Cu2 +, increases of necrosis up to 18% were seen whereas comparable levels ofapoptotic and necrotic cells (< 5%) were seen below this concentration. Chronic exposure over 8 weeks impaired colony-forming effi-ciency at concentrations of 16 MM Cu2 + and above. This study suggests that when liver cells sequester large amounts of copper, the toxic effects include delayed cell-cycle progression, a gradual loss of replicative capacity, and an increased incidence of cell death.

Currently, no vaccine exists for hepatitis C virus (HCV), a major pathogen thought to infect 170 million people globally. Many studies suggest that host T cell responses are critical for spontaneous resolution of disease, and preclinical studies have indicated a requirement for T cells in protection against challenge. We aimed to elicit HCV-specific T cells with the potential for protection using a recombinant adenoviral vector strategy in a phase 1 study of healthy human volunteers. Two adenoviral vectors expressing NS proteins from HCV genotype 1B were constructed based on rare serotypes [human adenovirus 6 (Ad6) and chimpanzee adenovirus 3 (ChAd3)]. Both vectors primed T cell responses against HCV proteins; these T cell responses targeted multiple proteins and were capable of recognizing heterologous strains (genotypes 1A and 3A). HCV-specific T cells consisted of both CD4(+) and CD8(+) T cell subsets; secreted interleukin-2, interferon-gamma, and tumor necrosis factor-alpha; and could be sustained for at least a year after boosting with the heterologous adenoviral vector. Studies using major histocompatibility complex peptide tetramers revealed long-lived central and effector memory pools that retained polyfunctionality and proliferative capacity. These data indicate that an adenoviral vector strategy can induce sustained T cell responses of a magnitude and quality associated with protective immunity and open the way for studies of prophylactic and therapeutic vaccines for HCV.