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PubMed2003

Source motion mitigation for adaptive matched field processing.

Application of adaptive matched field processing to the problem of detecting quiet targets in shallow water is complicated by source motion, both the motion of the target and the motion of discrete interferers. Target motion causes spreading of the target peak, thereby reducing output signal power. Interferer motion increases the dimensionality of the interference subspace, reducing adaptive interference suppression. This paper presents three techniques that mitigate source motion problems in adaptive matched field processing. The first involves rank reduction, which enables adaptive weight computation over short observation intervals where motion effects are less pronounced. The other two techniques specifically compensate for source motion. Explicit target motion compensation reduces target motion mismatch by focusing snapshots according to a target velocity hypothesis. And time-varying interference filtering places time-varying nulls on moving interferers not otherwise suppressed by adaptive weights. The three techniques are applied to volumetric array data from the Santa Barbara Channel Experiment and are shown to improve output signal-to-background-plus-noise ratio by more than 3 dB over the standard minimum-variance, distortionless response adaptive beam-former. Application of the techniques in some cases proves to be the difference between detecting and not detecting the target.

Acoustics↗
PubMed1958

Ultraviolet mitigation of x-ray lethality in dividing yeast cells.

The lethal effect of x-rays on dividing yeast cells can be decreased by small ultraviolet exposures delivered before or after x-ray exposure. This mitigating action can be decreased by exposure to visible light concomitant with photoreactivation of ultraviolet lethality. The results suggest considerable overlap between x-ray and ultraviolet lethality sites in dividing cells.

Light↗
PubMed2006

Intestinal Shiga toxin-producing Escherichia coli bacteria mitigate bovine leukemia virus infection in experimentally infected sheep.

Ruminants often carry gastrointestinal Shiga toxin (Stx)-producing Escherichia coli (STEC). Stxs belong to a large family of ribosome-inactivating proteins (RIPs), found in many plants and some bacteria. Plant RIPs, secreted into extracellular spaces, limit the spread of viruses through plant tissues by penetrating and killing virally infected cells. Previously, we showed Stx activity against bovine leukemia virus (BLV)-infected cells in vitro and hypothesized that STEC bacteria have antiviral activity in ruminant hosts. Here, we investigated the impact of STEC on the initial phases of BLV infection in sheep. Sheep were treated with biweekly oral doses of E. coli O157:H7 (an STEC) or an isogenic stx mutant strain. A different group of sheep were similarly treated with five naturally occurring ovine STEC isolates or stx-negative E. coli. Intestinal STEC bacteria were enumerated and identified by standard fecal culture and DNA hybridization. Oral STEC treatment did not always result in carriage of STEC, although many animals consistently presented with >10(4) CFU/g feces. BLV viremia was assessed by spontaneous lymphocyte proliferation (SLP) in cultures of blood mononuclear cells and by syncytium formation in cocultures of the same with F-81 indicator cells. SLP was lower (P < 0.05) and syncytia were fewer (P < 0.05) in STEC-treated sheep than in untreated sheep. Both lower SLP and fewer syncytia positively correlated with fecal STEC numbers. Average weight gain post-BLV challenge was higher in STEC-treated sheep than in untreated sheep (P < 0.05). These results support the hypothesis that in ruminants, intestinal STEC bacteria have antiviral activity and mitigate BLV-induced disease.

Animals↗
PubMed2025

Strategies for mitigating emerging artemisinin-based antimalarial drug resistance in Rwanda: a promising approach for managing therapies in malaria-endemic countries.

Malaria treatment failures associated with reduced efficacy of chloroquine (CQ) and amodiaquine (AQ) antimalarial drugs emerged in Rwanda during the 1980s, prompting the policy shift towards adopting artemisinin-based combination therapies in 2006 as an alternative. However, recent findings from malaria surveillance and therapeutic efficacy studies have revealed a countrywide increase in antimalarial drug resistance. Particularly, artemether-lumefantrine (AL) efficacy has significantly decreased, probably due to the emergence of Plasmodium falciparum (Pf) genomic mutations. To mitigate the current drug resistance, Rwanda has adopted targeted multiple first-line therapies. Through the national malaria control program, antimalarial drugs were deployed in accordance with the reported resistance profile. A significant rise in Pfkelch13 mutations, particularly A675V associated with AL resistance, was mainly reported in the western region; therefore, artesunate-pyronaridine was recommended. Dihydroartemisinin-piperaquine was considered in eastern and central regions, where R561H mutations were predominant. On the contrary, AL was maintained in the southern region, where the prevalence of the R561H mutation was low. Insights from this data-driven model will inform its extension to other malaria-endemic countries facing emerging Pf genetic diversity.

Antimalarials↗
PubMed1997

Surfactant improves lung function and mitigates bacterial growth in immature ventilated rabbits with experimentally induced neonatal group B streptococcal pneumonia.

AIMS: To study the influence of surfactant on lung function and bacterial proliferation in immature newborn rabbits with experimental group B streptococcal (GBS) pneumonia. METHODS: Preterm rabbit fetuses (gestational age 28 days) underwent tracheotomy and were mechanically ventilated in a warmed body plethysmograph that permitted measurement of lung-thorax compliance. Fifteen minutes after the onset of ventilation the animals received either GBS or saline intratracheally; at 30 minutes, a bolus of saline or 200 mg/kg of a porcine surfactant (Curosurf) was administered via the airway. Bacterial proliferation was evaluated in lung homogenate at the end of the experiments and the results expressed as mean log10 cfu/g lung (SD). Animals receiving only saline (n = 20) or saline and surfactant (n = 20) served as controls. RESULTS: The average survival time was about three hours in all groups. Infected animals receiving surfactant (n = 22) had significantly less bacterial growth (9.09 (0.45) vs 9.76 (0.91)) and improved lung function (compliance: 0.61 (0.14) vs 0.34 (0.19) ml/kg. cm H2O) than infected rabbits receiving saline at 30 minutes (n = 22). CONCLUSION: Surfactant improves lung function and mitigates bacterial growth in preterm rabbits infected with group B streptococci.

Animals↗
PubMed1985

Mitigation of the response of Friesian calves to live Babesia bovis vaccine by treatment with long acting oxytetracycline.

Forty 11- to 13-month-old Friesian calves were inoculated with live Babesia bovis vaccine. Twenty of the calves were treated with long acting oxytetracycline seven and 15 days after receiving the vaccine. Parasites were detected in nine of the treated calves compared with all 20 of the untreated control group. Treated calves were less febrile and had higher packed cell volumes than control animals. All calves from both groups developed a considerable antibody titre to B bovis. It appears that long acting oxytetracycline can mitigate the response of sensitive cattle breeds to live antibabesial vaccine and prevent damage caused by excessive multiplication of B bovis parasites.

Animals↗
PubMed2007

Cockroach allergen biology and mitigation in the indoor environment.

For nearly a half century, cockroaches have been recognized as a major cause of asthma morbidity in the urban, inner-city environment. Several cockroach-produced allergens have been identified and characterized, and a few have been produced as recombinant proteins. Recent research has moved beyond clinical, patient-based investigations to a more entomological perspective that addresses the production, physiological regulation, and developmental expression of cockroach allergens, thus providing insight into their functional biology and their relationship to current cockroach control strategies. Although successful removal of cockroach allergens from the infested environment has been difficult to accomplish with remedial sanitation, large-scale reductions in cockroach allergens below clinically relevant thresholds have recently been realized through suppression of cockroach populations. Here we review the current understanding of cockroach allergen biology and the demographics associated with human exposure and sensitization. We also critically evaluate allergen mitigation studies from an entomological perspective, highlighting disparities between successful and failed attempts to lessen the cockroach allergen burden in homes.

Air Pollution, Indoor↗
PubMed1997

The pinewood nematode: regulation and mitigation.

In North America, the native pinewood nematode (PWN), Bursaphelenchus xylophilus, kills exotic pines. When inadvertently introduced to Japan and other Asian countries, PWN became a destructive pest of pines. The PWN has been intercepted in pine shipments from North America to Europe, where there is concern that it may also kill pines and other conifers. To protect their forests from the PWN and other pests, the European Union and other countries now regulate the import of all coniferous chips, sawn wood, and logs. Several species of Bursaphelenchus have a phoretic relationship with Monochamus spp., which carry them to recently felled logs and dead or dying conifers, particularly pines. As a result, species of Monochamus, Bursaphelenchus, or both may be found in chips, unseasoned lumber, and logs. During the past decade, procedures to disinfest transported unprocessed wood have been investigated. These mitigation measures include prevention, host selection, and treatment by fumigation, irradiation, chemical dips, and elevated temperatures.

Journal Article↗
PubMed2006

Preemptive, but not reactive, spinal cord stimulation mitigates transient ischemia-induced myocardial infarction via cardiac adrenergic neurons.

Our objective was to determine whether electrical neuromodulation using spinal cord stimulation (SCS) mitigates transient ischemia-induced ventricular infarction and, if so, whether adrenergic neurons are involved in such cardioprotection. The hearts of anesthetized rabbits, subjected to 30 min of left anterior descending coronary arterial occlusion (CAO) followed by 3 h of reperfusion (control), were compared with those with preemptive SCS (starting 15 min before and continuing throughout the 30-min CAO) or reactive SCS (started at 1 or 28 min of CAO). For SCS, the dorsal C8-T2 segments of the spinal cord were stimulated electrically (50 Hz, 0.2 ms, 90% of motor threshold). For preemptive SCS, separate groups of animals were pretreated 15 min before SCS onset with 1) vehicle, 2) prazosin (alpha(1)-adrenoceptor blockade), or 3) timolol (beta-adrenoceptor blockade). Infarct size (IS), measured with tetrazolium, was expressed as a percentage of risk zone. In controls exposed to 30 min of CAO, IS was 36.4 +/- 9.5% (SD). Preemptive SCS reduced IS to 21.8 +/- 6.8% (P < 0.001). Preemptive SCS-mediated infarct reduction was eliminated by prazosin (36.6 +/- 8.8%) and blunted by timolol (29.4 +/- 7.5%). Reactive SCS did not reduce IS. SCS increased phosphorylation of cardiac PKC. SCS did not alter blood pressure or heart rate. We conclude that preemptive SCS reduces the size of infarcts induced by transient CAO; such cardioprotection involves cardiac adrenergic neurons.

Animals↗
PubMed2006

Beta1-adrenoceptor blockade mitigates excessive norepinephrine release into cardiac interstitium in mitral regurgitation in dog.

Mitral regurgitation (MR) is associated with increased neuronal release of norepinephrine (NE) and epinephrine (EP) into myocardial interstitial fluid (ISF) that may be necessary in sustaining left ventricular (LV) function via activation of cardiomyocyte beta-adrenergic receptors (ARs). However, activation of neuronal beta-ARs on cardiac neurons may lead to further catecholamine release, with an attendant risk of functional deterioration. We hypothesize that a beneficial effect of beta-AR blockade may therefore mitigate excessive catecholamine release from cardiac adrenergic neurons in dogs with MR. We measured the effects of chronic beta-receptor blockade (beta-RB) on ISF NE and EP release using in vivo microdialysis in open-chest anesthetized dogs after 4 wk of MR with or without extended release of metoprolol succinate (100 mg/day) as well as in control dogs. Fractional shortening increased by 30% in both MR and MR + beta-RB dogs after 4 wk of MR. In MR + beta-RB dogs, stellate-stimulated heart rate change was attenuated compared with control and MR dogs, whereas peak change of LV pressure over time (+dP/dt) increased equally in all groups. Stellate-stimulated ISF NE increased fivefold over baseline in MR versus twofold in control dogs (< 0.05), but the NE release was significantly attenuated in MR + beta-RB dogs. In contrast, stellate-stimulated increases in ISF EP did not differ in control, MR, and MR + beta-RB dogs. This study demonstrates that beta-RB attenuates ISF NE release from cardiac neurons and that the LV functional response to MR is not dependent on an excess increase in ISF NE. Thus beta1-RB may exert a beneficial effect by attenuating untoward effects of excessive sympathetic efferent neural NE release while sustaining early LV functional adaptation to MR.

Adrenergic beta-1 Receptor Antagonists↗
PubMed1987

Mitigation of pulmonary hyperoxic injury by administration of exogenous surfactant.

We studied the effects of surfactant supplementation on the progression of lung injury in rabbits exposed to 100% O2 for 64 h and returned to room air for 24 h. At this time, rabbits not treated with surfactant exhibit a severe lung injury with hypoxemia, increased alveolar premeability to solute, decreased total lung capacity (TLC) and lung edema. For surfactant treatment, 125 mg of calf lung surfactant extract (CLSE), suspended in 6-8 ml of normal saline, were instilled intratracheally at 0 and 12 h posthyperoxic exposure. At 24 h postexposure, these CLSE-treated rabbits compared with saline controls had significantly higher amounts of lung phospolipids (34 +/- 4 vs. 4.5 +/- 0.6 mumol/kg body wt) and increased TLC (42 +/- 2 vs. 27 +/- 1 ml/kg), with significantly lower amounts of alveolar protein (36 +/- 3 vs. 56 +/- 3 mg/kg) and decreased lung wet weight-to-dry weight ratios (5.6 +/- 0.1 vs. 6.3 +/- 0.3). Surfactant supplementation also decreased the degree of lung atelectasis as reflected by the increase in arterial O2 partial pressure (PaO2) after breathing 100% O2 for 20 min (PaO2 = 460 +/- 31 vs. 197 +/- 52 Torr). These findings indicate that instillation of exogenous surfactant mitigates the progression of hyperoxic lung injury in rabbits.

Animals↗
PubMed2001

Efficacy of nasal strip and furosemide in mitigating EIPH in Thoroughbred horses.

The purpose of this investigation was to study the effects of an equine nasal strip (NS), furosemide (Fur), and a combination of both (NS + Fur) on exercise-induced pulmonary hemorrhage (EIPH) at speeds corresponding to near-maximal effort. Five Thoroughbreds (526 +/- 25 kg) were run on a flat treadmill from 7 to 14 m/s in 1 m x s(-1) x min(-)1 increments every 2 wk (treatment order randomized) under control (Con), Fur (1 mg/kg iv 4 h prior), NS, or NS + Fur conditions. During each run, pulmonary arterial (Ppa) and esophageal (Pes) pressures were measured. Severity of EIPH was quantified via bronchoalveolar lavage (BAL) 30 min postrun. Furosemide (Fur and NS + Fur trials) reduced peak Ppa approximately 7 mmHg compared with Con (P < 0.05) whereas NS had no effect (P > 0.05). Maximal Pes swings were not different among groups (P > 0.05). NS significantly diminished EIPH compared with the Con trial [Con, 55.0 +/- 36.2; NS, 30.8 +/- 21.8 x 10(6) red blood cells (RBC)/ml BAL fluid; P < 0.05]. Fur reduced EIPH to a greater extent than NS (5.2 +/- 3.0 x 10(6) RBC/ml BAL; P < 0.05 vs. Con and NS) with no additional benefit from NS + Fur (8.5 +/- 4.2 x 10(6) RBC/ml BAL; P > 0.05 vs. Fur, P < 0.05 vs. Con and NS). In conclusion, although both modalities (NS and Fur) were successful in mitigating EIPH, neither abolished EIPH fully as evaluated via BAL. Fur was more effective than NS in constraining the severity of EIPH. The simultaneous use of both interventions appears to offer no further gain with respect to reducing EIPH.

Animals↗
PubMed2006

Oxidative stress in renal anemia of hemodialysis patients is mitigated by epoetin treatment.

BACKGROUND/AIMS: Oxidative stress often occurs in chronic hemodialysis (HD) patients. The objective of our study was to investigate the interrelationship between oxidative stress and the degree of renal anemia. METHODS: In 107 consecutive HD patients, serum concentrations of two major aldehydic lipid peroxidation (LPO) products, 4-hydroxynonenal (HNE) and malondialdehyde (MDA), and of protein carbonyls were analyzed as parameters of oxidative stress and related to the degree of renal anemia. Additionally, in 76 patients treated with epoetin long-term changes in the serum levels of aldehydic LPO products were observed. RESULTS: In HD patients, serum levels of HNE, MDA, and protein carbonyls are increased in comparison to controls. The lower the hemoglobin, i.e. the stronger the degree of renal anemia, the higher the serum concentrations of HNE, MDA, and protein carbonyls. The HNE and MDA levels decreased during HD. Long-term studies on the correction of renal anemia by epoetin demonstrated a mitigation of oxidative stress during this therapy. During periods of 1 and 2 years, it was observed that the serum levels of HNE and MDA could be reduced. CONCLUSION: Chronic renal failure is connected with oxidative stress which correlates with the degree of renal anemia, and the serum levels of aldehydic LPO products could be reduced during correction of renal anemia by epoetin.

Aged↗
PubMed2003

Mitigation of neutrophil infiltration in a rat model of early Staphylococcus aureus endophthalmitis.

PURPOSE: Infectious endophthalmitis is characterized by neutrophil migration into the eye. The purpose of this study was to determine whether systemic neutrophil depletion mitigates the ocular influx of neutrophils during the early phases of experimental endophthalmitis. METHODS: Endophthalmitis was induced in rats by intravitreal injection of Staphylococcus aureus. Animals received a single systemic dose of an anti-neutrophil-depleting antibody (dAb) or normal rabbit serum (NRS) 6 or 12 hours after intravitreal injection. Inflammation was graded both in vivo and by histopathology. Myeloperoxidase (MPO) was used as a biomarker of neutrophil infiltration. Bacterial clearance was evaluated by determining the amount of viable bacteria recovered from ocular specimens. RESULTS: Rats that received dAb 6 hours after bacterial injection exhibited significantly lower clinical scores, MPO activity, fewer vitreous exudates, and higher vitreous bacterial counts at 24 hours (P < 0.05). As the neutrophil population returned in this group, measured by the number in the peripheral blood, increasing intraocular inflammation was observed. Rats receiving dAb 12 hours after vitreous injection also demonstrated significantly lower clinical scores, MPO activity and less vitreous exudates at the 24-hour time point (P < 0.05). No significant differences from the control were detected at any of the subsequent time points, except in bacterial counts and MPO activity. CONCLUSIONS: Depletion of neutrophils early in the inflammatory response delayed the onset of severe ocular inflammation but also prevented adequate bacterial clearance. These results confirm the important role of neutrophils in ocular host defense during the early stages of experimental endophthalmitis.

Animals↗
PubMed1996

Mitigation of nitrofurantoin-induced toxicity in the perfused rat liver.

1. Nitrofurantoin is an antimicrobial agent which produces hepatotoxicity caused by the redox cycling of the nitro group and its radical anion. This futile cycling triggers a complex series of events known collectively as oxidative stress. 2. Our goal was to determine treatment strategies which could mitigate nitrofurantoin-induced toxicity in the isolated perfused rat liver. We co-infused various agents which blocked early or late events in the progression to toxicity. Tissue levels of glutathione and protein thiols were measured as indicators of the progression to toxicity and lactate dehydrogenase leakage into the perfusate was used as a marker of irreversible cell death. 3. Five treatments significantly (P < 0.05) decreased LDH leakage (reported as thousands of units accumulated in perfusate at 300 min, mean+/-standard error, n = 3-4) when compared to nitrofurantoin alone (274 +/- 37). These treatments were adenosine-2'-monophosphate (120 +/- 53), penicillamine (90 +/- 29), N-(2-mercaptopropionyl)-glycine (120 +/- 49) and bromosulfophthalein with (80 +/- 29) or without 5,5'-difluro-1,2-bis(O-aminophenoxy)ethane-N,N,N'N'-tetraace tic acid (101 +/- 46). Two other treatments, N-acetylcysteine (183 +/- 7) and dithiothreitol (166 +/- 59) delayed the onset of toxicity. Finally, calpeptin (319 +/- 34) which blocks activation of nonlysosomal proteases was ineffective. 4. We concluded that early intervention on the pathway to toxicity was most effective. The strategies detailed here may prove beneficial in treating hepatotoxicity seen following nitrofurantoin therapy.

Acetylcysteine↗
PubMed1997

Mitigation of nitrofurantoin-induced toxicity in the perfused rat lung.

1. Nitrofurantoin is an antimicrobial agent which produces pulmonary toxicity via the redox cycling of the nitro group and its radical anion. This futile cycling triggers a complex series of events known collectively as oxidative stress. 2. In the isolated perfused rat lung, nitrofurantoin induced a decrease in tissue levels of glutathione but not protein thiols by the end of the 180 min experiment. There was no decline in tissue levels of angiotensin converting enzyme (a marker of cell disruption). However, edema was extensive as monitored in real time by weight gain (2.71 +/- 0.56 g vs 0.63 +/- 0.53 g in control, P < 0.05, n = 4) and lung mechanical functioning. The edema was matched by an increase in lavage proteins (85 +/- 15 mg vs 16 +/- 9 mg in controls, P < 0.05, n = 4). Electron microscopic examination of tissue indicated that the endothelial cells were detached from the basement membrane which would account for the edema. 3. Co-infusion of penicillamine, N-acetylcysteine or N-(2-mercaptopropionyl)-glycine which can protect tissue from oxidative stress failed to mitigate NFT-induced edema. Allopurinol, an inhibitor of xanthine oxidase and a metal chelator, significantly decreased weight gain but did not prevent the loss of glutathione. These results suggested that allopurinol was not blocking metabolic activation of NFT by xanthine oxidase but scavenging metal cations which can initiate and/or propagate the oxidative stress cascade. 4. We concluded that, in the isolated perfused rat lung, the classic pathway of oxidative stress induced by NFT is interrupted at the stage of GSH loss. These experiments demonstrated that organ function was compromised more than the individual cells. They also suggested that allopurinol may prove beneficial in modulating NFT pulmonary toxicity.

Animals↗
PubMed2006

CD40 deficiency mitigates Alzheimer's disease pathology in transgenic mouse models.

We have previously shown that transgenic mice carrying a mutant human APP but deficient in CD40L, display a decrease in astrocytosis and microgliosis associated with a lower amount of deposited Abeta. Furthermore, an anti-CD40L treatment causes a diminution of Abeta pathology in the brain and an improved performance in several cognitive tasks in the double transgenic PSAPP mouse model. Although these data suggest a potential role for CD40L in Alzheimer's disease pathology in transgenic mice they do not cast light on whether this effect is due to inhibition of signaling via CD40 or whether it is due to the mitigation of some other unknown role of CD40L. In the present report we have generated APP and PSAPP mouse models with a disrupted CD40 gene and compared the pathological features (such as amyloid burden, astrocytosis and microgliosis that are typical of Alzheimer's disease-like pathology in these transgenic mouse strains) with appropriate controls. We find that all these features are reduced in mouse models deficient for CD40 compared with their littermates where CD40 is present. These data suggest that CD40 signaling is required to allow the full repertoire of AD-like pathology in these mice and that inhibition of the CD40 signaling pathway is a potential therapeutic strategy in Alzheimer's disease.

Journal Article↗
PubMed2002

Relationship of perception of radon as a health risk and willingness to engage in radon testing and mitigation.

PURPOSE/OBJECTIVES: To gather data on radon levels and determine correlations among subjects' characteristics, willingness to test for radon, and perceptions of radon as a health risk. DESIGN: Descriptive correlational. SETTING: Rural DeKalb County in northern Illinois. SAMPLE: 473 respondents from a group of 1,620 randomly selected county residences. METHODS: Participants were surveyed via telephone using the Community Radon Program questionnaire. Radon measurements were taken with home radon test kits. MAIN RESEARCH VARIABLES: Gender, income, age, educational level, smoking status, race, home ownership, willingness to test for radon, and radon risk perception. FINDINGS: Most participants were familiar with radon but did not view it as an immediate health hazard and would not have screened for radon on their own. 88% of the radon measurements exceeded the U.S. Environmental Protection Agency's moderate risk potential level, and 53% exceeded the action level (i.e., 4 pCi/L). CONCLUSIONS: Perception of radon as a health risk was correlated positively with planning to conduct further radon testing and to employ radon mitigation methods. More research is needed on people's willingness to obtain radon emission levels and the cancer rates in areas that have high potential for radon. IMPLICATIONS FOR NURSING: According to the environmental literature, the effect of household radon emissions on the development of lung cancer is as great a health risk as secondhand smoke. Virtually no nursing literature on the subject has been published. As the primary source of health information in many rural counties, nurses, especially public health nurses, are at the forefront in public health educational efforts. Nurses are the most likely healthcare professionals to enter patients' homes and can play a significant role in disseminating information about radon as a potential carcinogen.

Adult↗