Four common diagnostic problems that inhibit radon mitigation.
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Air Pollutants↗
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Field validation of sound mitigation models and air pollutant emission testing in support of missile motor disposal activities.
The U.S. Department of Defense approved activities conducted at the Utah Test and Training Range (UTTR) include both operational readiness test firing of intercontinental ballistic missile motors as well as the destruction of obsolete or otherwise unusable intercontinental ballistic missile motors through open burn/open detonation (OB/ OD). Within the Utah Division of Air Quality, these activities have been identified as having the potential to generate unacceptable noise levels, as well as significant amounts of hazardous air pollutants. Hill Air Force Base, UT, has completed a series of field tests at the UTTR in which sound-monitoring surveillance of OB/OD activities was conducted to validate the Sound Intensity Prediction System (SIPS) model. Using results generated by the SIPS model to support the decision to detonate, the UTTR successfully disposed of missile motors having an aggregate net explosive weight (NEW) of 56,500 lbs without generating adverse noise levels within populated areas. These results suggest that, under appropriate conditions, missile motors of even larger NEW may be detonated without exceeding regulatory noise limits. In conjunction with collecting noise monitoring data, air quality data was collected to support the development of air emission factors for both static missile motor firings and OB/OD activities. Through the installation of 15 ground-based air samplers, the generation of combustion fixed gases, hazardous air pollutants, and chlorides were monitored during the 56,500-lb NEW detonation event. Comparison of field measurements to predictions generated from the U.S. Navy's energetic combustion pollutant formation model, POLU4WN, indicated that, as the detonation fireball expanded from ground zero, organic compounds as well as carbon monoxide continued to oxidize as the hot gases reacted with ambient air. Hazardous air pollutant analysis of air samplers confirmed the presence of chloromethane, benzene, toluene, 1,2-propadiene, and 2-methyl-l-propene, whereas the absence of hydrogen chloride gas suggested that free chlorine is not generated during the combustion process.
Air Pollutants↗
Electromagnetic fields: principles of exposure mitigation.
Basic principles of reducing exposure to electromagnetic fields are reviewed in this article. Measures to reduce exposure can be divided into organisational/administrative and technical/engineering actions. Both strategies are briefly analysed and the basic principles of the theory of shielding are presented. A definition of shielding effectiveness (SE) is given, and the results from the general Transmission Lines Theory are presented. Practical situations of shielding static and time-varying electric and magnetic fields are discussed on the basis of the physical properties of the fields and of the shield.
Electric Conductivity↗
Valproate and HDAC inhibition: a new epigenetic strategy to mitigate phenotypic severity in ALS?
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Amyotrophic Lateral Sclerosis↗
Mitigating Charge Transfer Inefficiency in the Chandra X-Ray Observatory Advanced CCD Imaging Spectrometer.
The ACIS front-illuminated CCDs on board the Chandra X-Ray Observatory were damaged in the extreme environment of the Earth's radiation belts, resulting in enhanced charge transfer inefficiency (CTI). This produces a row dependence in gain, event grade, and energy resolution. We model the CTI as a function of input photon energy, including the effects of detrapping (charge trailing), shielding within an event (charge in the leading pixels of the 3x3 event island protects the rest of the island by filling traps), and nonuniform spatial distribution of traps. This technique cannot fully recover the degraded energy resolution, but it reduces the position dependence of gain and grade distributions. By correcting the grade distributions as well as the event amplitudes, we can improve the instrument's quantum efficiency. We outline our model for CTI correction and discuss how the corrector can improve astrophysical results derived from ACIS data.
Journal Article↗
Mitigation of hookworm disease by immunization with soluble extracts of Ancylostoma ceylanicum.
Hookworms are a leading cause of anemia in developing countries, and a strategy aimed at reducing pathology caused by blood-feeding adult parasites would be a valuable addition to global control efforts. This article describes experiments designed to induce resistance to the major clinical sequelae (weight loss and anemia) of Ancylostoma ceylanicum hookworm infection in Syrian golden hamsters of the outbred LVG strain. Previously infected animals acquired long-lived resistance to weight loss and anemia caused by a secondary hookworm infection. Furthermore, transfer of pooled serum from twice-infected hamsters to animals undergoing a primary infection was associated with partial resistance to growth delay and anemia. Active vaccination of hamsters with soluble adult hookworm antigens emulsified in alum led to partial protection from hookworm-associated pathology in the absence of reductions in adult worm burden. This intriguing result may have important implications for human vaccine development.
Ancylostoma↗
A review of the cost effectiveness of radon mitigation in domestic properties in Northamptonshire.
The costs of remedial work, and the radon level reduction achieved, have been studied in a series of domestic properties in Northamptonshire, which is a radon affected area. The cost-effectiveness of the series is similar to published theoretical estimates for proposed national remediation programmes, and five times more effective than our similar analysis for the National Health Service workplace, if it is assumed that 100% of householders discovering levels above 300 Bq m-3 implement remediation. In practice, in the UK, far fewer of those who arrange an initial radon test proceed to remediation, but this domestic programme could be cost effective if more than 5% carry out remediation. Our series confirms that a considerable number of householders with radon levels in the 200 to 300 Bq m-3 range do not seek or implement remediation work.
Air Pollution, Indoor↗
Adenovirus-mediated utrophin gene transfer mitigates the dystrophic phenotype of mdx mouse muscles.
Utrophin is a close homolog of dystrophin, the protein whose mutations cause Duchenne muscular dystrophy (DMD). Utrophin is present at low levels in normal and dystrophic muscle, whereas dystrophin is largely absent in DMD. In such cases, the replacement of dystrophin using a utrophin gene transfer strategy could be more advantageous because utrophin would not be a neoantigen. To establish if adenovirus (AV)-mediated utrophin gene transfer is a possible option for the treatment of DMD, an AV vector expressing a shortened version of utrophin (AdCMV-Utr) was constructed. The effect of utrophin overexpression was investigated following intramuscular injection of this AV into mdx mice, the mouse model of DMD. When the tibialis anterior (TA) muscles of 3- to 5-day-old animals were injected with 5 microl of AdCMV-Utr (7.0 x 10(11) virus/ml), an average of 32% of fibers were transduced and the transduction level remained stable for at least 60 days. The presence of utrophin restored the normal histochemical pattern of the dystrophin-associated protein complex at the cell surface and resulted in a reduction in the number of centrally nucleated fibers. The transduced fibers were largely impermeable to the tracer dye Evans blue, suggesting that utrophin protects the surface membrane from breakage. In vitro measurements of the force decline in response to high-stress eccentric contractions demonstrated that the muscles overexpressing utrophin were more resistant to mechanical stress-induced injury. Taken together, these data indicate that AV-mediated utrophin gene transfer can correct various aspects of the dystrophic phenotype. However, a progressive reduction in the number of transduced fibers was observed when the TA muscles of 30- to 45-day-old mice were injected with 25 microl of AdCMV-Utr. This reduction coincides with a humoral response to the AV and transgene, which consists of a hybrid mouse-human cDNA.
Adenoviridae↗
Beer mitigates some effects of copper deficiency in rats.
Because of an epidemiologic association of decreased risk of death from ischemic heart disease with moderate use of alcoholic beverages, and because numerous abnormalities found in people with ischemic heart disease are also found in animals deficient in copper, rats were fed a diet deficient in copper and were given either beer or water to drink. Rats drinking beer lived nearly six times as long and had lower plasma cholesterol, less cardiac enlargement, and higher liver copper. Apparent absorption and biological half-life of oral radiocopper were increased by beer. The effects were not attributable to alcohol, chromium, or copper in beer. Beer intakes were similar to those of some people in the United States. Results may explain seasonal cycles in plasma cholesterol and may be germane to the epidemiology of ischemic heart disease because diets in the United States seem to be low in copper.
Animals↗
Selenium deficiency mitigates hypothyroxinemia in iodine-deficient subjects.
Studies were performed to assess the role of combined selenium and iodine deficiency in the etiology of endemic myxedematous cretinism in a population in Zaire. One effect of selenium deficiency may be to lower glutathione peroxidase activity in the thyroid gland, thus allowing hydrogen peroxide produced during thyroid hormone synthesis to be cytotoxic. In selenium-and-iodine-deficient humans, selenium supplementation may aggravate hypothyroidism by stimulating thyroxin metabolism by the selenoenzyme type I iodothyronine 5'-deiodinase. Selenium supplementation is thus not indicated without iodine or thyroid hormone supplementation in cases of combined selenium and iodine deficiencies.
Adolescent↗
Immunization of Dahl SS/jr rats with an ouabain conjugate mitigates hypertension.
Inhibition of the Na+/K(+)-ATPase by a circulating endogenous digitalis- or ouabain-like substance has been associated with the pathogenesis of several forms of clinical and experimental hypertension. Inbred salt-sensitive Dahl SS/jr rats were immunized with either urease or a ouabain-urease conjugate, then challenged with a high salt diet. The salt-induced increase in blood pressure in the ouabain-urease-immunized animals was significantly less than that of the urease-inoculated rats. Sera of the ouabain-urease immunized animals cross-reacted with ouabagenin, digoxigenin, digoxin, and digitoxin, but not with aldosterone, corticosterone, deoxycorticosterone (DOC), 18-hydroxy DOC, or 19-nor DOC. The fact that hypertension was not completely blocked by immunization supports ample evidence that the disease in these animals is multifactorial with several genes involved.
Animals↗
Inhaled vitamin A mitigates hyperoxia-induced acute and chronic lung damage in a neonatal rat model of bronchopulmonary dysplasia.
RATIONALE: Prevention of bronchopulmonary dysplasia (BPD) remains a critical unmet need. OBJECTIVES: We continued evaluating aerosolized vitamin A in a neonatal rat hyperoxia-injury model of BPD, testing whether lung-targeted inhalation yields superior outcomes compared to enteral or intramuscular (IM) delivery. METHODS: Rat pups were exposed to continuous 95% hyperoxia for seven days to induce lung damage. Vitamin A was administered from post-natal day (PD) 1-7 by inhalation, enteral or IM dosing. Persisting effectiveness of inhaled vitamin A was examined at PD 21, dwelling in normoxia after all interventions were discontinued at PD 7. MEASUREMENTS AND MAIN RESULTS: Comprehensive analyses include alveolar morphometrics, in vivo pulmonary function testing, assessment of hepatic vitamin A level, and quantitating gene and protein expression of relevant biomarkers of lung maturation, inflammation and damage/repair, employing singlex and multiplexed assays and whole-genome gene expression. CONCLUSIONS: Inhaled vitamin A suppressed hyperoxia-induced lung damage, with key hallmarks of BPD, including lung morphometrics and biomarkers associated with lung damage and inflammation, being effectively indistinguishable from healthy controls at both PD 7 and 21, Natural reparative processes were enhanced, with normal alveolarization and pulmonary function at PD 21. Despite raising hepatic vitamin A levels, enteral dosing was ineffective in restoring alveolar morphology at PD 7. Consistent with previous reporting, IM dosing yielded modest effect at PD 7 but with little evidence of benefit to pulmonary function at PD 21. Observation of dose-dependent effects with aerosolized vitamin A strengthens the evidence of the benefits of lung-targeted delivery, supporting further development of inhaled vitamin A as a BPD preventive strategy.
Journal Article↗
Environmental antibiotic contamination and AMR: Integrating pathways, impacts, and artificial intelligence-driven mitigation.
The widespread contamination of the environment with antibiotic residues is a significant factor contributing to the global crisis of antimicrobial resistance (AMR). Antibiotics from various sources, such as effluents from municipal and hospital wastewater treatment plants, agricultural runoffs, discharges from pharmaceutical manufacturing and improper disposal of expired or unused medicines, create selective pressures in the spread of antibiotic resistance genes. These environmental reservoirs act as hotspots for horizontal gene transfer, facilitating the emergence of multidrug-resistant pathogens. Conventional detection methods including culture-based assays, chromatographic quantification, and molecular diagnostics, provide essential insights but are limited by low throughput, reduced sensitivity to new Antibiotic Resistance Genes, and challenges in real-time monitoring across complex environments. Recent advances, such as whole-genome sequencing, metagenomics, and biosensor-based detection, help to address these gaps by enabling more comprehensive surveillance of the resistome. Artificial intelligence further enhances these approaches by improving data interpretation and pattern recognition, thus complementing traditional and molecular methods rather than replacing them. This review examines the pathways of environmental antibiotic contamination, ecological and health impacts of AMR, and limitations of conventional detection methods. It aims to clarify how these pathways contribute to the AMR crisis, assess the effectiveness of existing surveillance techniques, and identify gaps in current research.
Anti-Bacterial Agents↗
Evidence that inactivated oral cholera vaccines both prevent and mitigate Vibrio cholerae O1 infections in a cholera-endemic area.
In a randomized, placebo-controlled field trial of B subunit-killed whole cell (BS-WC) and killed whole cell only (WC) inactivated oral cholera vaccines in rural Bangladesh, active surveillance of selected neighborhoods during the first year after vaccination identified 127 Vibrio cholerae O1 infections among 3285 three-dose recipients. For each vaccine, protective efficacy was greater against symptomatic (57%, P < .05 for BS-WC; 58%, P < .05 for WC) than against asymptomatic infections (46%, P < .05 for BS-WC; 32%, P = .09 for WC), and protection against each grade of infection was demonstrable for both the classical and El Tor biotypes. Although vaccine protection against symptomatic infections was evident in both young children and older persons, only persons vaccinated at age > 5 years were protected against asymptomatic infections. These results suggest that the inactivated oral vaccines acted both to protect against intestinal colonization by V. cholerae O1 and to interrupt the pathogenic sequence of established infections.
Adolescent↗
Meropenem-Colistin Combination Mitigates Porin-Associated Carbapenem Resistance Development in Ertapenem-Mono-Resistant Enterobacterales.
BACKGROUND: Non-carbapenemase-producing Enterobacterales with isolated ertapenem resistance (ETP-mono-R) may represent an early stage in the evolution toward broader carbapenem resistance, but whether further resistance induction occurs and its underlying mechanisms remain poorly understood. METHODS: Resistance induction was assessed in three Escherichia coli, four Klebsiella pneumoniae, and two Enterobacter cloacae isolates through serial exposure to subinhibitory concentrations of meropenem (MEM), imipenem, ceftazidime-avibactam, or colistin (COL), with antibiotic-free passaging for reversion. Resistance induction under MEM+COL was evaluated separately. Whole-genome sequencing (WGS), targeted porin-gene Sanger sequencing, and transcriptional analysis were used to characterize resistance mechanisms across induction stages. RESULTS: Subinhibitory MEM exposure rapidly selected for carbapenem resistance through porin-associated alterations in a species-specific manner. E. coli accumulated loop-region mutations in ompC, while K. pneumoniae predominantly developed disruptive mutations in ompK36, both accompanied by marked transcriptional downregulation. In contrast, E. cloacae retained wild-type porins but showed increased MEM MICs, suggesting a non-porin-mediated mechanism. Subinhibitory exposure to COL alone rapidly induced colistin resistance but was associated with decreased carbapenem MICs. Co-exposure to MEM and COL significantly delayed resistance development and reduced MIC increases (all P < 0.05). Targeted sequencing of 26 non-carbapenemase-producing K. pneumoniae isolates resistant to all carbapenems revealed widespread disruptive ompK36 alterations, including the S337P substitution identified experimentally, consistent with a shared permeability-loss pathway. CONCLUSIONS: In ETP-mono-R Enterobacterales, subinhibitory carbapenem exposure promotes carbapenem resistance, with porin-associated mechanisms predominating in E. coli and K. pneumoniae. Co-exposure to COL attenuates this process, suggesting a potential strategy to delay the emergence of carbapenem resistance.
Enterobacterales↗
Flavones mitigate tumor necrosis factor-alpha-induced adhesion molecule upregulation in cultured human endothelial cells: role of nuclear factor-kappa B.
Flavones have been classified as anti-atherogenic agents that inhibit monocyte adhesion to stimulated endothelium, possibly by blocking induction of cell adhesion molecules (CAM). This anti-atherogenic feature of these flavonoids appears to be related to their chemical structures. Flavones may interfere with key signaling events involved in endothelial cell activation by inflammatory mediators. This study examined the effects of flavones on the induction of CAM and the translocation and DNA binding of nuclear factor-kappa B (NF-kappa B) in TNF-alpha-activated human umbilical vein endothelial cells (HUVEC). The effects of flavones, luteolin and apigenin, on adhesion of THP-1 monocytes to the TNF-alpha-activated HUVEC, protein expression and mRNA levels of vascular cell adhesion molecule-1 (VCAM-1), intracellular cell adhesion molecule-1 (ICAM-1) and E-selectin, and nuclear appearance and DNA binding activity of NF-kappa B were determined. Flavanols, flavonols, and flavanones were used for comparison. TNF-alpha significantly induced HUVEC protein expression of VCAM-1, ICAM-1, and E-selectin with increasing mRNA levels. Luteolin and apigenin inhibited the TNF-alpha-induced upregulation of THP-1 adhesion and VCAM-1 expression; these inhibitory effects were dose-dependent. The flavones at doses of > or =25 micromol/L almost completely abolished the increased CAM protein and mRNA regardless of their anti-oxidative activity. With the exception of the flavonol quercetin, flavonoids had no such effect; quercetin substantially attenuated the CAM induction. The flavones inhibited nuclear translocation and DNA binding activity of the NF-kappa B-containing binding site in the promoter region of the CAM genes in TNF-alpha-activated HUVEC. The inhibition of endothelial CAM induction by flavones is mediated by their interference with the NF-kappa B-dependent transcription pathway. Thus, the flavones may hamper initial atherosclerotic events involving endothelial CAM induction.
Apigenin↗
Antimicrobial peptides in mucosal secretions: the importance of local secretions in mitigating infection.
The antimicrobial activity of the collective molecules comprising human milk reflects an evolutionarily successful paradigm for preventing and limiting microbial infection. Understanding the molecules that participate in this process and how they work can yield insight into potentially new antimicrobial therapies. Upon proteolytic processing, antimicrobial peptides can be derived from milk proteins, such as lactoferrin, casein, and lysozyme. Similarly, using the HIV-1 gp41 protein template, we have demonstrated that the 28-residue C-terminus, when produced as an independent peptide, exhibits selective toxicity for bacteria over eukaryotic cells. Upon optimizing this sequence for cationic charge and hydrophobic character presented as a alpha-helical structure, we show improved capability of the parent LLP1 sequence to selectively kill bacteria in the host environment and that this activity is increased by the inclusion of Trp residues on the hydrophobic face. We report that it is possible to (i) design de novo antimicrobial peptides that demonstrate optimal antimicrobial activity with minimal inflammatory activity and (ii) design antimicrobial peptides to function in a defined environment. In the end, we describe a de novo designed antimicrobial peptide, WLBU2, which is selectively toxic to microbial pathogens in complex environments and does not stimulate a significant immunomodulatory response. In spite of these properties, WLBU2 activity against Pseudomonas aeruginosa in human milk is inferior to the host peptide LL37 with regard to antimicrobial potency. These studies demonstrate that antimicrobial peptides can be engineered for greater potency in one medium but may not be optimal for working in a different medium such as human milk.
Amino Acid Sequence↗
Mitigation of secondary disease of allogeneic mouse radiation chimeras by modification of the intestinal microflora.
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Animals↗