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Biomedical subjects

F Bureau

Publications and source records attributed to F Bureau.

At least 19 recordsLinked to original sources

Prolactin-induced activation of nuclear factor kappaB in bovine mammary epithelial cells: role in chronic mastitis.

We sought to determine whether prolactin (PRL) could influence the neutrophilic inflammation that characterizes chronic mastitis. Most of the genes encoding inflammatory proteins depend on the nuclear factor kappaB (NF-kappaB) for their expression. We addressed the hypothesis that immunomodulatory activities of PRL might arise from an increase in NF-kappaB activity. MAC-T cells, a bovine mammary epithelial cell line, were stimulated with increasing concentrations of bovine PRL (1, 5, 25, 125, and 1,000 ng/mL). Level of NF-kappaB binding activity was measured and mRNA was evaluated for IL-1beta, IL-6, IL-8, granulocyte-macrophage colony-stimulating factor (GMCSF), IFN-gamma, and tumor necrosis factor (TNF)-alpha, cytokines known to require NF-kappaB for their maximal transcription. Prolactin activated NF-kappaB; maximal NF-kappaB activation was weaker with PRL than with TNF-alpha at 30 or 180 min poststimulation. In addition, PRL significantly amplified, in a dose-dependent manner, mRNA expression of IL-1beta, IL-6, IL-8, GMCSF, and TNF-alpha. We measured PRL concentrations in blood and milk from healthy and chronic mastitis-infected cows, and studied the relationship between the PRL concentration and the degree of inflammation in the mammary gland as indirectly assessed by somatic cell counts (SCC). Plasma PRL did not differ significantly between healthy and chronic mastitis-affected cows (63.7 and 67.5 ng/mL, respectively). Milk PRL concentration was significantly increased in chronic mastitis-affected quarters with the highest SCC, and had a positive significant correlation between SCC, as well as between the number of neutrophils present in milk samples. The present findings show that PRL promotes an inflammatory response in bovine mammary epithelial cells via NF-kappaB activation, and suggest a role for PRL in the pathogenesis of chronic mastitis.

Animals↗

Helenalin reduces Staphylococcus aureus infection in vitro and in vivo.

Staphylococcus (S.) aureus is a major udder pathogen causing bovine mastitis. Some pro-inflammatory cytokines, including tumor necrosis factor-alpha (TNF-alpha), enhance extracellular and intracellular growth of S. aureus, indicating that the inflammatory process favors S. aureus infection. Helenalin is a sesquiterpene lactone with potent anti-inflammatory properties. This study was designed to evaluate the effects of helenalin on S. aureus infection. First, in vitro experiments were conducted. These studies revealed that proliferation of S. aureus in bovine mammary epithelial MAC-T cells treated in the presence or absence of TNF-alpha was markedly reduced in the presence of helenalin. Secondly, in vivo effects of helenalin were investigated. Lactating mice treated in the presence or absence of helenalin were challenged by the intramammary route with S. aureus and the bacteria in the mammary glands were counted 12 h after infection. Significantly less numbers of bacteria were recovered from the infected glands of helenalin-treated mice compared with untreated mice. Moreover, histological examination of mammary tissue from helenalin-treated mice that were challenged with S. aureus indicated that helenalin is able to significantly reduce leukocyte infiltration in the mammary gland following S. aureus inoculation. Our results show that helenalin reduces S. aureus intracellular growth and experimental S. aureus infection. We conclude that helenalin may be of potential interest in the treatment of S. aureus-induced mastitis in the bovine species.

Animals↗

Iron availability and consumption of tea, vervain and mint during weaning in Morocco.

BACKGROUND/AIMS: Iron deficiency impairs growth and psychomotor development of infants. In Morocco, infusions are introduced very early in infant diet, and could contribute to iron deficiency, due to their high polyphenol content. METHODS: The availability of tea, mint and vervain infusions was assessed using an in vitro model of digestion and dialysis. Two gastric pHs were used: pH 4 as in the first week life, and pH 2.5 as in older infants. Six repetitions of each experiment were made. The total polyphenol content of infusions was measured. RESULTS: At pH 4 and at pH 2.5, iron availability was decreased by tea and vervain, and increased by mint and ascorbic acid. At both pHs it was increased by addition of ascorbic acid to tea and vervain. In addition, at pH 2.5 it was increased by addition of ascorbic acid to mint. The highest value was observed in the presence of both ascorbic acid and mint (33.1 +/- 4.1%). In any case, iron availability was higher at pH 2.5 than at pH 4 (with single compounds or combinations with ascorbic acid). The polyphenol contents (mg/l) of tea, vervain and mint infusions were 2,236.1, 771.1, and 16.5. CONCLUSIONS: Tea and vervain infusions inhibited iron availability. In contrast, mint improved it; vitamin C helped in preventing these inhibiting properties. It could be proposed to discourage tea and vervain drinking at early weaning and to replace them by mint infusion, or at least to promote the consumption of vitamin C-rich fruit juice to counteract these inhibiting effects.

Ascorbic Acid↗

Cysteinyl-leukotrienes contribute to sputum eosinophil chemotactic activity in asthmatics.

BACKGROUND: Cysteinyl-leukotrienes are lipid derived mediators involved in asthma. They are able to stimulate eosinophil chemotaxis in vitro. Induced sputum from asthmatics has been shown to contain eosinophil chemotactic activity. The purpose of our study was to evaluate the contribution of cysteinyl-leukotrienes to sputum eosinophil chemotactic activity in asthmatics and to seek whether there might be differences between asthmatics free of inhaled corticosteroids vs those regularly receiving this treatment. METHODS: Twenty-two patients (11 corticosteroid free, mean FEV1 99% predicted, 11 corticosteroid-treated, mean FEV1 77% predicted) recruited from our asthma clinic underwent a sputum induction. Sputum was processed according to standard procedure. Eosinophil chemotactic activity contained in the fluid phase was assessed using Boyden microchamber model and expressed as chemotaxis index (CI). Cysteinyl-leukotrienes were measured in sputum supernatant by ELISA and their role in sputum eosionophil chemotactic activity was evaluated by using montelukast, a selective antagonist of a cys-LT1 receptor. RESULTS: Cysteinyl-leukotrienes were well detectable in sputum supernatants from both steroid-naive (247 +/- 42 pg/ml) and steroid-treated (228 +/- 26 pg/ml) asthmatics. Sputum eosinophil chemotactic activity was indiscriminately present in both corticosteroid-naive (CI: 2.61 +/- 0.22) and corticosteroid-treated (2.98 +/- 0.35) asthmatics. Montelukast (100 microM) significantly inhibited the eosinophil chemotactic activity in both groups achieving a mean inhibition of 54.2 +/- 9.2% (P < 0.001) and 64.7 +/- 7.8% (P < 0.001) in steroid-naive and steroid-treated asthmatics respectively. CONCLUSION: Cysteinyl-leukotrienes actively participate in sputum eosinophil chemotactic activity found in asthmatics irrespective of whether they are or not under treatment with inhaled corticoids.

Adult↗

[Control of gene transcription as a new therapeutic target in asthma].

The recent advances in the knowledge of the molecular mechanisms underlying asthma have lead to a significant improvement of the current treatments of the disease and opened new perspectives for the development of therapeutic alternatives to inhaled corticosteroids. The selective targeting of transcription factors controlling the expression of the genes implicated in the pathogenesis of asthma is one of these privileged strategies. This review aims at describing the most promising new therapeutic targets in the control of asthmatic inflammation at the gene transcription level.

Asthma↗

Delayed neutrophil apoptosis in bovine subclinical mastitis.

Bovine subclinical mastitis can be defined as a moderated inflammatory disease characterized by a persistent accumulation of neutrophils in milk. As GMCSF-mediated delay of neutrophil apoptosis contributes to the accumulation of inflammatory cells at the site of inflammation in many human diseases, we sought to determine whether subclinical mastitis in cows is also associated with a GMCSF-dependent increase in milk-neutrophil survival. We first addressed the hypothesis that GMCSF delays bovine neutrophil apoptosis by activation of the signal transducer and activator of transcription (STAT) family members STAT3 and STAT5, which are critical regulators of the expression of various Bcl-2 family proteins. Granulocyte-macrophage colony-stimulating factor significantly delayed apoptosis of blood neutrophils obtained from healthy cows. In these cells, GMCSF activated STAT5, but not STAT3, and induced an increase in the mRNA of the antiapoptotic Bcl-2 member, Bcl-xL. Granulocyte-macrophage colony-stimulating factor-dependent STAT5 activation and up-regulation of Bcl-xL mRNA were blocked by the Jak inhibitor, AG-490. This inhibition was associated with abrogation of the prosurvival effect of GMCSF, demonstrating a key role for STAT5 in delayed neutrophil apoptosis. We further found that GMCSF expression was increased in milk cells from cows affected with subclinical mastitis. Neutrophils from these cows demonstrated a significant delay of apoptosis as compared with neutrophils obtained from healthy cows and were unresponsive to GMCSF. Active STAT5 complexes were detected in these neutrophils. Finally, in the presence of AG-490, apoptosis was induced and a time-dependent down-regulation of Bcl-xL mRNA was observed in milk neutrophils from mastitis-affected cows. These results indicate that neutrophil survival is enhanced in milk of subclinical mastitis-affected cows and suggest a role for a GMCSF-activated STAT5 signaling pathway in this phenomenon. This pathway could thus represent a target for the control of persistent accumulation of neutrophils in the bovine mammary gland.

Animals↗

Increased nuclear factor kappaB activity in milk cells of mastitis-affected cows.

Bacterial mastitis is accompanied by a drastic increase in milk somatic cell count (SCC), with neutrophils being the predominant cell type found in the infected quarters. Accumulation and activation of neutrophils at the site of infection require local expression of many inflammatory genes encoding adhesion molecules, chemokines and cytokines. Most of the inflammatory genes contain binding sites for the nuclear factor kappaB (NF-kappaB) within their promoter and therefore partly depend on NF-kappaB for their expression. We thus hypothesized that an increase in NF-kappaB activity in the mammary gland could contribute to development of the neutrophilic inflammation that characterizes mastitis. In an attempt to verify this hypothesis, we first assessed milk cells from healthy and acute and chronic mastitis-affected cows for NF-kappaB activity using electrophoretic mobility shift assays. We next studied the relationships between the intensity of NF-kappaB activity in these cells and the degree of udder inflammation. Active NF-kappaB complexes were undetectable in milk cells from healthy cows, whereas high levels of NF-kappaB activity were always found in cells from cows with acute mastitis. In milk cells obtained from chronic mastitis-affected cows, NF-kappaB activity varied from low to high. Finally, the level of NF-kappaB activity measured in milk cells from chronic mastitis-affected cows was not correlated to SCC or to the proportion of neutrophils present in milk samples, but was highly correlated with the expression level of interleukin-8 and granulocyte/macrophage colony-stimulating factor, two NF-kappaB-dependent cytokines crucially involved in initiation and perpetuation of neutrophilic inflammation. These results suggest that NF-kappaB might play a role in mastitis pathogenesis.

Animals↗

Imbalance between lipoxin A4 and leukotriene B4 in chronic mastitis-affected cows.

Persistent accumulation of inflammatory cells in the udder, with neutrophils being the predominant cell type, is a characteristic feature of chronic mastitis in dairy cows. Leukotriene (LT) B4 is a potent chemotactic agent, known to induce recruitment and accumulation of neutrophils in the bovine mammary gland. The LTB4-stimulated neutrophil functional responses are closely opposed by lipoxin (LX) A4, which promotes the resolution of inflammation. We thus hypothesized that the chronic inflammation of the udder could be associated with an unfavorable ratio between these two eicosanoids and that the persistence of neutrophil accumulation could be due to an increase in LTB4 synthesis and/or an impaired LXA4 production. In an attempt to verify this hypothesis, we first measured LXA4, LTB4, and their ratio in the milk of healthy and acute and chronic mastitis-affected quarters. Next, we studied the relationships between these variables and the degree of udder inflammation as assessed by somatic cell count measurement. The LTB4 concentration was low in healthy quarters, drastically increased in acute mastitis, and reached intermediate levels in chronic mastitis-affected quarters. However, whereas LXA4 concentration was highly increased in acute mastitis, healthy and chronic quarters had similarly low values. The LXA4:LTB4 ratio was thus significantly lower in chronic mastitis-affected cows. The LTB4 concentrations measured in chronic quarters were highly correlated to somatic cell count and to milk neutrophil and macrophage numbers. A weaker correlation was observed between LXA4 and these variables. For both eicosanoids, the highest correlation was observed with the number of neutrophils. These results show the existence of an LXA4:LTB4 imbalance in chronic mastitis-affected cows because of low LXA4 concentrations. Further studies are needed to determine whether administration of LX or stable analogs could have therapeutic potential in the control of chronic bovine mastitis.

Acute Disease↗

[Value of induced sputum in the investigation of asthma].

INTRODUCTION: The technique of induced expectoration generates sputum by the inhalation of hypertonic saline. On account of its non-invasive character, its simplicity, its relative harmlessness, its cost effectiveness and its reproducibility this technique, that appeared in the early 1990's, has rapidly established itself as the technique of choice in the investigation of bronchial inflammation in asthma. STATE OF THE ART: We present the results of our studies that have contributed to the validation of the technique at the methodological level and to the exploitation of the cellular contents as much as the fluid phase of the expectorations in characterising bronchial inflammation in asthmatics. Our results confirm an infiltration of the airways of asthmatics with eosinophils that appears to be proportional to the severity of the illness. We evaluate the effect of inhaled steroids and of theophylline on sputum eosinophilia and bronchial reactivity and discuss the role of eosinophils on bronchial hyperreactivity. Finally we discuss the use of induced expectoration in clinical practice in asthma. PERSPECTIVES: The analysis of induced sputum could well become a valuable tool in the clinical evaluation and monitoring of asthma in the same way as symptoms and abnormalities of lung function. CONCLUSIONS: Induced expectoration has certainly contributed to the understanding of the cellular and molecular mechanisms of asthma as well as the role of bronchial inflammation in the clinical manifestations of the disease.

Asthma↗

Influence of short-chain fatty acids on iron absorption by proximal colon.

BACKGROUND: Short-chain fatty acids produced by bacterial fermentation in the colon enhance the local absorption of cations, such as calcium, that could be used to improve the bioavailability of iron if a significant colonic absorption of iron were to occur. METHODS: Iron (iron gluconate, 100 microM) absorption by the caecum of the rat was compared with that in proximal sites of the small bowel using the Ussing chamber model; the influence of probiotic bacteria (Propionibacterium freudenreichii) on iron absorption was assessed and compared with that of two of their fermentation products (acetic and propionic acids) using the Ussing chamber and the ligated colon with gamma emitting iron as experimental models. RESULTS: The caecum absorbed less iron than the duodenum, but significantly more than the jejunum and ileum. This occurred mainly through an enhanced mucosal transfer of iron uptake. Propionibacteria enhanced iron absorption from the proximal colon; the same effect was observed in the presence of viable bacteria, or the culture medium free of viable bacteria, or acetate and propionate or propionate alone. CONCLUSIONS: The proximal colon could be a significant site available for iron absorption; this absorption can be enhanced by local production of short-chain fatty acids such as propionate.

Animals↗

Impaired accumulation of granulocytes in the lung during ozone adaptation.

Respiratory alterations induced by an acute exposure to ozone (O(3)) paradoxically resolve during multiday exposure. This adaptation is characteristically accompanied by a gradual attenuation of lung neutrophilia. As maintenance of neutrophilia at the site of inflammation is due to cytokine-mediated delayed neutrophil apoptosis, which is associated with reduced levels of Bax, a proapoptotic protein, we sought to determine whether defects in these mechanisms could account for O(3) adaptation. Lung granulocytes obtained at different time points from calves exposed to 0.75 ppm O(3) for 12 h/d for 7 consecutive days neither showed enhancement of survival nor Bax deficiency, when compared to blood granulocytes. To further investigate the effects of an exogenous oxidative stress on neutrophil survival, human granulocytes were treated with hydrogen peroxide alone, or in combination with granulocyte/macrophage colony-stimulating factor, an antiapoptotic cytokine. Both treatments led to rapid apoptosis associated with downregulation of Bcl-x(L) and Bcl-2, two antiapoptotic proteins. This study shows that O(3) adaptation is associated with a failure in the mechanisms leading to accumulation of neutrophils at the site of inflammation, and suggests that this defect is due to direct proapoptotic effects of exogenous oxidative stress on granulocytes.

Adaptation, Physiological↗

p65 Homodimer activity in distal airway cells determines lung dysfunction in equine heaves.

Nuclear factor-kappaB (NF-kappaB) activity, which is a key regulator of inflammatory gene expression, is increased in bronchial epithelial cells from horses suffering from heaves (a hypersensitivity-associated inflammatory condition of the lung). To determine whether this increased activity extends to distal airways and to other pulmonary cells, cells recovered by broncho-alveolar lavage (BAL) in healthy and heaves-affected horses were assessed for NF-kappaB activity. NF-kappaB activity was much higher in BAL cells from heaves-affected horses, especially during crisis (disease exacerbation), than in cells from healthy horses. Moreover, the level of NF-kappaB activity found in BAL cells was positively correlated to total lung resistance and to the proportion of neutrophils present in BAL fluid. Finally, prototypical p65-p50 NF-kappaB heterodimers were absent from BAL cells, which mostly contained p65 homodimers. These results (1) show that increased NF-kappaB activity is a general feature of heaves lung; (2) demonstrate the importance of p65 homodimers in neutrophilic inflammation; and (3) suggest that the use of specific NF-kappaB inhibitors could improve lung function in heaves-affected horses.

Animals↗

Inhibition of zinc absorption by iron depends on their ratio.

Previous studies upon zinc-iron interactions gave conflicting results that could come from differences in protocol design or in trace element status of subjects. The present work assessed the influence of zinc : iron ratio and iron deficiency upon zinc absorption. The digestive absorption of zinc sulphate (100 micromol Zn/l) in presence of iron gluconate was studied in perfused jejunal loops (n = 6/group) of normal rats (range 0-1000 micromol Fe/l) and iron deficient rats (200-750 micromol Fe/l). In normal rats no significant iron inhibition on zinc absorption occurred at Fe:Zn ratio below 2:1. At higher ratios zinc uptake and net absorption decreased significantly (p<0.05). Between 2:1 and 5:1 a dose dependent inhibition of zinc absorption occurred and reached a plateau beyond this ratio. In iron deficient animals no changes in zinc uptake, mucosal retention and absorption compared to normal animals occurred at ratio 2:1. At higher ratios differences were observed at every zinc absorption step except for mucosal retention at 7.5:1 ratio. Iron-zinc interactions depend on their ratio and on previous trace elements status of subjects. Due to the wide and unknown variations that were likely to occur between the subjects of previous human and experimental studies, these results could explain some of the discrepancies between their results.

Animals↗

Aluminium increases xanthine oxidase activity and disturbs antioxidant status in the rat.

The mechanisms responsible for the neurotoxic effects of Al remain poorly understood. In order to determine whether Al promotes oxidative stress in vivo, we measured the enzymatic activity of xanthine oxidase (XO), superoxide dismutase (SOD), glutathione peroxidase (GPX), glutathione-S-transferase (GST) and glutathione reductase (GR) in four groups of rats after eight days of intraperitoneal administration of variable concentrations of Al (0, 5, 10, and 15 mg/kg body weight, respectively). XO activity was measured in both plasma and liver samples, and the activities of the remaining enzymes were further determined in the brain and red blood cells (RBC). The most significant changes were observed in XO and GPX activities, that were enhanced and depressed, respectively. In both instances, the enzyme activities were correlated with Al concentrations, either positively (XO) or negatively (GPX). Enhancement of XO and inhibition of GPX activity may lead to the accumulation of intermediate toxic compounds such as hydrogen peroxide and hydroxyl radicals, since SOD activity is increased as well. The latter finding must be taken with some caution because previous studies have shown contradictory results in this field. Our data suggest that Al toxicity could be mediated by its action on both pro- and anti-oxidant enzymes. The biological significance of these findings remains to be established.

Aluminum↗

Agreement between patients' and proxies' reports of quality of life in Alzheimer's disease.

Agreement between self reports and proxy reports of health-related quality of life (H RQoL) was examined in a sample of 76 patients with mild to moderate Alzheimer's disease and their proxies. Patients and proxies completed an '17-item Duke health profile'. The items were rephrased for the proxy. The proportion of exact agreement between patients and proxies on the 17 items ranged from 26.3 to 52.6%. Results reveal poor to moderate agreement (intraclass correlation coefficients (ICCs) from 0.00 to 0.61 for 10 subscales) between patients' and proxies' reports. Agreement was higher for measures of function that are directly observable (physical health, disability) and relatively poor for more subjective measures. Proxy reliability varied according to the relationship of the proxy to the index subject. Spouses and nurses agreed more closely with index subjects than did children or nurses' aides. Agreement decreased with increasing severity of dementia. Statistically significant differences in mean scores were noted for several dimensions, with proxies tending to rate the patients as having a lower quality of life than the patients themselves. This study indicates the importance of considering the information source of a patient's HRQoL. However, assessments by proxies should be used with caution.

Aged↗

Enhanced survival of lung granulocytes in an animal model of asthma: evidence for a role of GM-CSF activated STAT5 signalling pathway.

BACKGROUND: As granulocyte/macrophage colony stimulating factor (GM-CSF) mediated delay of granulocyte apoptosis contributes to the accumulation of inflammatory cells at the site of inflammation in many diseases, we sought to determine whether asthma is also associated with a GM-CSF dependent increase in lung granulocyte survival. Moreover, because GM-CSF mediates its effects through activation of signal transducer and activator of transcription 5 (STAT5), we also investigated the potential role of STAT5 in allergic inflammation. METHODS: Blood granulocytes were recovered from six healthy and six heaves affected horses, a model of asthma. Lung granulocytes were obtained by bronchoalveolar lavage (BAL) from the same horses. Granulocytes were cultured in the presence or absence of anti-GM-CSF receptor antibodies for different times and apoptosis was determined using the Annexin-V/propidium iodide detection method. Nuclear protein extracts from cultured granulocytes were analysed for STAT5 binding activity by electrophoretic mobility shift assay. RESULTS: BAL fluid granulocytes from heaves affected horses demonstrated a significant delay in apoptosis compared with blood granulocytes from the same horses and blood and BAL fluid granulocytes from healthy horses. Conversely, the rate of apoptosis in blood granulocytes from healthy and heaves affected horses was comparable. The enhanced survival of BAL fluid granulocytes from affected horses was suppressed in the presence of antibodies directed against GM-CSF receptors. Increased levels of active STAT5 were found in BAL fluid granulocytes from heaves affected horses and were markedly reduced after treatment with anti-GM-CSF receptor antibodies. CONCLUSIONS: These data indicate that granulocyte survival is enhanced in the lung of heaves affected horses and suggest a role for a GM-CSF activated STAT5 pathway in delaying apoptosis of lung granulocytes in this model of asthma.

Animals↗

Spirometric performance in Belgian Blue calves: II. Analysis of environmental factors and estimation of genetic parameters.

Genetic parameters and environmental effects for spirometric variables (SV) in calves were estimated using 734 Belgian Blue calves (15 to 297 d of age), sired by 20 AI bulls. For each calf, the following SV were measured: 1) the average ventilation (l/min) recorded during the 15 s of maximal ventilatory changes induced by lobeline administration (0.25 mg/kg, i.v.) (15-s MV(L)); 2) the vital capacity, and the maximal peak expiratory and inspiratory flows recorded after lobeline administration; and 3) the ventilatory reserve (15-s MV(L) - ventilation at rest). Analysis of environmental factors showed age of calf, herd, sex, and vaccination status had significant effects on SV. A sire model and a multiple-trait derivative-free REML procedure were used to estimate genetic parameters for SV, body weight, and muscling score. Heritabilities for SV ranged from 0.28 +/- 0.11 to 0.44 +/- 0.16. Genetic correlations among SV varied from 0.76 to 0.98 and environmental correlations from 0.69 to 0.80. Genetic correlations of SV with body weight (0.25 to 0.56) and with muscling score (0.21 to 0.76) were positive, as were environmental correlations of SV with body weight (0.44 to 0.70) and muscling score (0.09 to 0.25). These results suggest that selection may improve SV without impairing other traits of economic importance.

Animals↗

Spirometric performance in Belgian Blue calves: I. Effects on economic losses due to the bovine respiratory disease complex.

The aim of this study was to determine whether high spirometric performances in calves are associated with low economic losses due to the bovine respiratory disease complex (BRDC). Five spirometric variables (SV) were measured in 909 double-muscled Belgian Blue calves from 15 to 60 d of age. Afterward, calves were monitored for 6 mo to determine whether they developed BRDC and to determine the costs due to BRDC (i.e., medicine costs and veterinarians' fees, plus estimated financial losses due to mortality in case of death). To analyze the effects of spirometric performances on BRDC cost, a fixed linear model was used for each SV. In addition to SV, each model included the effects of sex, dam's parity, vaccination status, muscular development score, herd-period, and BW. Only herd-period and the maximal ventilation and the vital capacity had significant effects on costs due to BRDC, indicating that these two SV are major physiological determinants of economic losses associated with BRDC. Accordingly, it is assumed that an amelioration of maximal ventilation and vital capacity could result in increased resistance to BRDC in calves.

Airway Resistance↗