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1.
Various indicators of pesticide environmental risk have been proposed, and one of the most widely known and used is the environmental impact quotient (EIQ). The EIQ has been criticized by others in the past, but it continues to be used regularly in the weed science literature. The EIQ is typically considered an improvement over simply comparing the amount of herbicides applied by weight. Herbicides are treated differently compared to other pesticide groups when calculating the EIQ, and therefore, it is important to understand how different risk factors affect the EIQ for herbicides. The purpose of this work was to evaluate the suitability of the EIQ as an environmental indicator for herbicides. Simulation analysis was conducted to quantify relative sensitivity of the EIQ to changes in risk factors, and actual herbicide EIQ values were used to quantify the impact of herbicide application rate on the EIQ Field Use Rating. Herbicide use rate was highly correlated with the EIQ Field Use Rating (Spearman’s rho >0.96, P-value <0.001) for two herbicide datasets. Two important risk factors for herbicides, leaching and surface runoff potential, are included in the EIQ calculation but explain less than 1% of total variation in the EIQ. Plant surface half-life was the risk factor with the greatest relative influence on herbicide EIQ, explaining 26 to 28% of the total variation in EIQ for actual and simulated EIQ values, respectively. For herbicides, the plant surface half-life risk factor is assigned values without any supporting quantitative data, and can result in EIQ estimates that are contrary to quantitative risk estimates for some herbicides. In its current form, the EIQ is a poor measure of herbicide environmental impact. 相似文献
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Metabolic acidosis produces a phosphaturia which is independent of parathyroid hormone or dietary phosphorus intake. To study the underlying mechanism, inorganic phosphate (Pi) and glucose transport were studied in brush-border membrane vesicles prepared from the renal cortex of parathyroidectomized rats gavaged for three days with either 7.5 ml of 1.6% NaCl (control) or 1.5% NH4Cl (acidosis). At killing, blood pH and plasma bicarbonate were and , respectively, in control and () and () in acidotic rats. Serum Pi was similar in both groups, while 24 h urine Pi excretion was higher in the acidotic group (). Peak sodium-dependent uptake of Pi, measured after 1.5 min of incubation, was higher in controls than acidotic rats ( vs. protein, ), whereas peak glucose uptake at 1.5 min was not significantly different between the groups. Equilibrium values for Pi and glucose uptake were similar in the two groups. for Pi uptake in the control and acidotic animals were not different, 0.036 and 0.040 mM, respectively. By contrast, was higher in controls than in the acidotic group, 3.13 vs. 1.15 nmol/mg protein per 15 s. These results suggest that metabolic acidosis directly inhibits Pi uptake by the brush border of the proximal tubule by decreasing the availability of Pi carriers of the renal brush-border membrane. 相似文献
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Charles R. Kleeman Jack W. Coburn Arnold S. Brickman David B. N. Lee Robert G. Narins Richard M. Ehrlich 《The Western journal of medicine》1980,132(4):313-332
The prevalence of kidney stones has steadily risen during this century; passage of a calculus and a positive family history increase the probability of recurrence. Findings from recent studies on the cause of renal calculi have stressed crystallization and crystal aggregation of stone minerals from supersaturated urine, rather than excessive organic matrix. Absence of normal urine inhibitors of calcium salts is also stressed. Formation of calcium oxalate stones is the major problem. Therapy with decreased calcium and oxalate intake, thiazides, phosphate salts and allopurinol in various combinations has substantially decreased the prevalence of recurrent stones. The rationale for the use of allopurinol is that uric acid salts enhance the tendency for calcium oxalate to crystallize from supersaturated urine. The hypercalciuria seen in 30 percent to 40 percent of patients with oxalate stones is usually caused by intestinal hyperabsorption of calcium. Although patients with uric acid calculi constitute only a small fraction of those in whom stones form, they represent a group in whom good medical therapy, based on sound physiologic principles, has proved extremely successful. Renal tubular syndromes lead to nephrocalcinosis and lithiasis through hypercalciuria, alkaline urine and hypocitraturia, the latter an inhibitor of calcium salt precipitation. Recent advances in surgical techniques are discussed, including the rationale for removing staghorn calculi. The ileal ureter and coagulum pyelolithotomy deserve special emphasis. 相似文献
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Neuroprotective effects of Argon are mediated via an ERK‐1/2 dependent regulation of heme‐oxygenase‐1 in retinal ganglion cells 下载免费PDF全文
Felix Ulbrich Kai B. Kaufmann Mark Coburn Wolf Alexander Lagrèze Martin Roesslein Julia Biermann Hartmut Buerkle Torsten Loop Ulrich Goebel 《Journal of neurochemistry》2015,134(4):717-727
Retinal ischemia and reperfusion injuries (R‐IRI) damage neuronal tissue permanently. Recently, we demonstrated that Argon exerts anti‐apoptotic and protective properties. The molecular mechanism remains unclear. We hypothesized that Argon inhalation exert neuroprotective effects in rats retinal ganglion cells (RGC) via an ERK‐1/2 dependent regulation of heat‐shock proteins. Inhalation of Argon (75 Vol%) was performed after R‐IRI on the rats′ left eyes for 1 h immediately or with delay. Retinal tissue was harvested after 24 h to analyze mRNA and protein expression of heat‐shock proteins ?70, ?90 and heme‐oxygenase‐1, mitogen‐activated protein kinases (p38, JNK, ERK‐1/2) and histological changes. To analyze ERK dependent effects, the ERK inhibitor PD98059 was applicated prior to Argon inhalation. RGC count was analyzed 7 days after injury. Statistics were performed using anova . Argon significantly reduced the R‐IRI‐affected heat‐shock protein expression (p < 0.05). While Argon significantly induced ERK‐1/2 expression (p < 0.001), inhibition of ERK‐1/2 before Argon inhalation resulted in significantly lower vital RGCs (p < 0.01) and increase in heme‐oxygenase‐1 (p < 0.05). R‐IRI‐induced RGC loss was reduced by Argon inhalation (p < 0.001). Immunohistochemistry suggested ERK‐1/2 activation in Müller cells. We conclude, that Argon treatment protects R‐IRI‐induced apoptotic loss of RGC via an ERK‐1/2 dependent regulation of heme‐oxygenase‐1.
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Jeannine M. Coburn Nicholas Bernstein Rahul Bhattacharya Udayanath Aich Kevin J. Yarema Jennifer H. Elisseeff 《PloS one》2013,8(3)
Articular cartilage has a limited ability to self-repair because of its avascular nature and the low mitotic activity of the residing chondrocytes. There remains a significant need to develop therapeutic strategies to increase the regenerative capacity of cells that could repair cartilage. Multiple cell types, including chondrocytes and mesenchymal stem cells, have roles in articular cartilage regeneration. In this study, we evaluated a platform technology of multiple functionalized hexosamines, namely 3,4,6-O-tributanoylated-N-acetylgalactosamine (3,4,6-O-Bu3GalNAc), 3,4,6-O-tributanoylated-N-acetylmannosamine (3,4,6-O-Bu3ManNAc) and 3,4,6-O-Bu3GlcNAc, with the potential ability to reduce NFκB activity. Exposure of IL-1β-stimulated chondrocytes to the hexosamine analogs resulted in increased expression of ECM molecules and a corresponding improvement in cartilage-specific ECM accumulation. The greatest ECM accumulation was observed with 3,4,6-O-Bu3GalNAc. In contrast, mesenchymal stem cells (MSCs) exposed to 3,4,6-O-Bu3GalNAc exhibited a dose dependent decrease in chondrogenic differentation as indicated by decreased ECM accumulation. These studies established the disease modification potential of a hexosamine analog platform on IL-1β-stimulated chondrocytes. We determined that the modified hexosamine with the greatest potential for disease modification is 3,4,6-O-Bu3GalNAc. This effect was distinctly different with 3,4,6-O-Bu3GalNAc exposure to chondrogenic-induced MSCs, where a decrease in ECM accumulation and differentiation was observed. Furthermore, these studies suggest that NFκB pathway plays a complex role cartilage repair. 相似文献
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Astrid V. Fahlenkamp Christian Stoppe Jan Cremer Ingeborg A. Biener Dirk Peters Ricarda Leuchter Albrecht Eisert Christian C. Apfel Rolf Rossaint Mark Coburn 《PloS one》2016,11(4)
ObjectiveLike other inhalational anesthetics xenon seems to be associated with post-operative nausea and vomiting (PONV). We assessed nausea incidence following balanced xenon anesthesia compared to sevoflurane, and dexamethasone for its prophylaxis in a randomized controlled trial with post-hoc explorative analysis.Methods220 subjects with elevated PONV risk (Apfel score ≥2) undergoing elective abdominal surgery were randomized to receive xenon or sevoflurane anesthesia and dexamethasone or placebo after written informed consent. 93 subjects in the xenon group and 94 subjects in the sevoflurane group completed the trial. General anesthesia was maintained with 60% xenon or 2.0% sevoflurane. Dexamethasone 4mg or placebo was administered in the first hour. Subjects were analyzed for nausea and vomiting in predefined intervals during a 24h post-anesthesia follow-up.ResultsLogistic regression, controlled for dexamethasone and anesthesia/dexamethasone interaction, showed a significant risk to develop nausea following xenon anesthesia (OR 2.30, 95% CI 1.02–5.19, p = 0.044). Early-onset nausea incidence was 46% after xenon and 35% after sevoflurane anesthesia (p = 0.138). After xenon, nausea occurred significantly earlier (p = 0.014), was more frequent and rated worse in the beginning. Dexamethasone did not markedly reduce nausea occurrence in both groups. Late-onset nausea showed no considerable difference between the groups.ConclusionIn our study setting, xenon anesthesia was associated with an elevated risk to develop nausea in sensitive subjects. Dexamethasone 4mg was not effective preventing nausea in our study. Group size or dosage might have been too small, and change of statistical analysis parameters in the post-hoc evaluation might have further contributed to a limitation of our results. Further trials will be needed to address prophylaxis of xenon-induced nausea.