A broad-scale spatial analysis of the environmental benefits of fertiliser closed periods implemented under the Nitrates Directive in Europe.

Nutrient pollution from agriculture has been an ongoing challenge for decades, contributing to numerous negative environmental impacts. In the European Union policies have been developed to address nutrient pollution, including Nitrate Action Programmes under Council Directive 91/676/EEC. Although Member States report on progress on implementation, there have been few studies that explore how measures have been implemented; the environmental implications of any differences; and how they vary spatially on a European scale. This study aims to address this gap with respect to fertiliser closed periods (1155 different closed periods across 69 Nitrate Action Programmes). This included the development of an approach that can be applied using readily available spatial data. Each closed period was scored for its coverage of risk periods for losses of nitrate; organic material; nitrous oxide and ammonia. Closed periods were then matched to relevant combinations of spatial data for each environmental zone and fertiliser type. The scores for each combination were used to create maps and calculate spatial statistics. The results show that in addition to nitrate, closed periods also reduce the risk of organic material run-off, emissions of nitrous oxide and to a lesser extent ammonia. However, risk reduction is spatially variable across all the impacts and the scope for synergy is also variable (e.g. nitrate loss does not always correlate with nitrous oxide or ammonia risk reduction). Regions in the Atlantic, Lustanian and some areas within the Mediterranean zones appear to provide the greatest combined risk reduction, with other zones, especially in eastern Europe, having a lower combined risk reduction (due to a combination of different risk periods coupled with lower coverage of individual risks). The spatial analysis within this study is relatively simple; is based on a snapshot of closed periods during 2019-2020; and only explores one measure. However, it does provide some useful data and insights that could support policy development in the future. This includes scope for Member States and regions to learn from others where greater coverage of risk periods has been achieved; and highlighting how a more holistic perspective can be taken to the environmental management of nutrients. As we strive towards developing sustainable production systems, farmers and policy makers need to take a more integrated approach to incorporate additional environmental objectives; which increases the complexity of the challenge. Consequently, the demand for pragmatic approaches that take a more holistic approach is likely to increase in the future.

Acute renal failure after large doses of intravenous immune globulin.

OBJECTIVE: To describe a case of acute renal failure after high-dose intravenous immune globulin (IVIG) therapy and the measures undertaken to prevent this complication during subsequent administration. CASE SUMMARY: A 54-year-old white man with valvular cardiomyopathy was receiving large doses (2 g/kg/mo) of IVIG in order to attenuate his immune system in preparation for a heart transplant. After his first infusion, he had to be rehospitalized for nausea, vomiting, fever, chills, and acute renal failure (serum creatinine [Scr] peak 8.4 mg/dL, baseline 1.0 mg/dL). His second infusion produced similar complications. Sandoglobulin 100 mL/h (172 g; 10% solution prepared with sterile water) was used on both occasions, and the large sucrose load (1.67 g sucrose/g protein) was suspected to be the causative agent. Upon switching to Polygam (170 g; 10% solution prepared with sterile water), a glucose-containing product which only has 0.4 g glucose/g protein, and infusing it at half of the Sandoglobulin rate (50 mL/h), the patient was able to tolerate the infusion without complications (Scr and blood urea nitrogen unchanged). DISCUSSION: Stabilizing agents such as sucrose, maltose, and glucose are added to IVIG preparations to help reduce immunoglobulin aggregation. These aggregates are associated with some of the more serious adverse effects of IVIG administration. When large doses of IVIG are used, the stabilizing agents can induce an osmotic nephrosis due to the large solute load. A review of the previous literature on IVIG-induced renal failure is provided, as well as the differences in the various IVIG formulations. Also, general guidelines are offered to prevent this complication. CONCLUSIONS: Large doses of Sandoglobulin (400-2000 mg/kg) have been associated with acute renal failure due to the large sucrose load. By taking certain precautions, especially in high-risk patients, this uncommon, but serious, adverse effect can be avoided.

A clinical comparison of two pressure-reducing surfaces in the management of pressure ulcers.

The purpose of this study was to compare the clinical outcomes of pressure ulcers treated on a low-air loss bed and a foam mattress with loose-fitting top cover. The two-group, non-randomized study design consisted of a convenience sample of 20 subjects: 10 subjects treated on the low-air loss bed and 10 subjects treated on the foam mattress with loose-fitting top cover. Subjects were selected from among patients located in the medical/surgical, critical care, and the skilled nursing units of a metropolitan public teaching hospital. Descriptive data, laboratory data, pressure ulcer transparency drawing, and pressure ulcer photographs were obtained on each subject every seven days from two to four weeks. A one-way analysis of variance indicated that there was no statistically significant difference in the pressure ulcer outcomes of subjects treated on the low-air loss bed (Mediscus) compared to the pressure ulcer outcomes of subjects treated on the foam mattress with loose-fitting top cover (Comfortex). Analysis of covariance further indicated no statistically significant difference in the pressure ulcer outcome of subjects treated on either pressure-relieving surface according to the subjects': a) age, percent ideal body weight, presence of pressure ulcer infection; b) leukocyte count, total lymphocyte count, and albumin level; and c) level of sensory perception, moisture, activity, mobility, nutrition, friction, and shear. Results from this study indicate that the low-air loss bed and foam mattress with loose-fitting top cover provide comparable pressure ulcer outcomes. Implications for nursing and recommendations for further study are included in the text.

Effects of systemic complement activation and neutrophil-mediated pulmonary injury on the retention and metastasis of circulating cancer cells in mouse lungs.

Vascular pathways are major transit routes for the dissemination of malignant neoplasms and are also regulators of cancer metastasis, in part because the endothelium and vascular basement membrane are barriers to the entry and exit of tumor cells. In this study, we have examined the hypothesis that host cell-mediated damage to the pulmonary microvasculature facilitates the experimental metastasis of a syngeneic fibrosarcoma in the C57BL/6J mouse. Intravenous injection of purified cobra venom factor was followed in 30 minutes by complement activation, neutropenia with sequestration of neutrophils in the lung, and increased pulmonary vasopermeability. When syngeneic fibrosarcoma cells were injected simultaneously with cobra venom factor, there was a 3 fold increase in cancer cell retention in the lungs after 24 hours and a 3- to 20-fold increase in metastatic tumor burden after 14 days. Enhanced cancer cell retention after cobra venom factor was not seen in mice deficient in complement component C5 and was diminished by pretreatment of animals with antineutrophil antibodies, catalase, inhibitors of lipoxygenase, thromboxane synthetase, and lipid peroxidation (oxygen radical scavenger). We conclude that neutrophil-mediated microvascular injury can promote the organ localization and metastasis of circulating cancer cells.

Enhanced cancer metastasis after monocrotaline-induced lung injury.

The lung is a target in several models of environmentally induced injury and is also a common site for the growth of metastases from circulating cancer cells. In these experiments, we have tested the hypothesis that pulmonary damage can facilitate the metastasis of cancer to the lung. We have studied the effect of monocrotaline-induced lung injury on the retention and metastasis of intravenously injected Walker carcinosarcoma 256 cells in the lung and the effect of this injury on spontaneous metastasis in animals with intramuscular tumor transplants. Female Wistar rats were given a single subcutaneous injection of monocrotaline (60 mg/kg). The degree of lung injury after monocrotaline was assessed by bronchoalveolar lavage, by histological and ultrastructural examination, and by measurement of right ventricular hypertrophy. To assess the effects of monocrotaline on metastasis, animals were injected iv with 2 X 10(7) [125I]iododeoxyuridine-labeled or unlabeled Walker 256 carcinosarcoma cells at various periods of time (1 day to 20 days) after monocrotaline. The retention of labeled cells was determined by gamma counts of lungs 24 hr after injection. There was a direct correlation between the severity of lung injury and the number of cancer cells retained in the lung 24 hr after injection. Metastasis was quantified by morphometric analysis of histologic sections prepared from lungs 1 week after an injection of unlabeled cells. The median area of lung involved by tumor after iv injection was 39% for rats injected with cancer cells 10 days after monocrotaline vs 3% for controls. In studies on spontaneous metastasis, rats were given an intramuscular injection of Walker 256 cells 5 days after monocrotaline and metastasis was quantified by morphometry 7 days after tumor transplantation. The median tumor burden of animals pretreated with monocrotaline was 37% vs 8% for controls. We conclude that lung injury initiated by monocrotaline can facilitate the spread of the rat Walker 256 carcinosarcoma.

Effects of neutrophil-mediated pulmonary endothelial injury on the localization and metastasis of circulating Walker carcinosarcoma cells.

The lung, a frequent site of cancer metastases, is also a susceptible target in several models of endothelial injury. In previous studies we have demonstrated that such injury, induced by bleomycin or by exposure to high concentrations of atmospheric oxygen, can facilitate the localization and metastasis of circulating tumor cells. Here we have tested the hypothesis that neutrophil-mediated injury to pulmonary endothelium has a similar effect. In Sprague-Dawley rats, intravenous injection of cobra venom factor resulted in complement activation, rapid sequestration of neutrophils in the lung, and endothelial damage, demonstrated by morphology, and by increased protein content and leakage of intravenous 125I-albumin into bronchoalveolar lavage fluids. When 125I-iododeoxyuridine-labeled Walker carcinosarcoma cells were injected intravenously during the period of endothelial injury, the pulmonary capillaries contained aggregates of neutrophils and tumor cells 2 h later, and there was a 3-fold increase in pulmonary tumor cell localization after 24 h in treated animals, compared to controls. Enhancement of tumor cell localization was prevented by pretreatment of the rats with catalase or by antineutrophil antisera. When animals were examined 2 weeks after cell injection, treatment groups had significantly more metastatic tumor nodules and a greater area of lung tissue involved by metastatic tumors. We conclude that neutrophil-mediated damage to the pulmonary endothelium can significantly increase the trapping of circulating tumor cells, and is likely to be clinically important since the large vascular bed of the lung is susceptible to host-mediated injury.