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1 ete prevention of infection occurring in one foal.
2 etween SCID foals and the reconstituted SCID foal.
3 m an immune-reconstituted EIAV-infected SCID foal.
4 rhodococcal pneumonia, CTL were evaluated in foals.
5 ntly killed infected targets from 3-week-old foals.
6 ined from four EIAV-infected immunocompetent foals.
7 iate between that seen in SCID mice and SCID foals.
8  causes severe pyogranulomatous pneumonia in foals.
9 rology for diagnosis of R. equi pneumonia in foals.
10 bronchopneumonia when inhaled by susceptible foals.
11 were affected as severely as immunocompetent foals.
12 her SCID or immunocompetent thrombocytopenic foals.
13 onary lesions when compared to non-nebulized foals.
14 T helper type 1 response compared to control foals.
15 als worldwide, most commonly affecting horse foals.
16 death in immunocompromised hosts, especially foals.
17  (1 Arabian and 1 Arabian-pony cross), and 2 foals (1 Arabian and 1 Arabian-pony cross) with severe c
18  young adult Arabian horses, two 1-month-old foals (1 Arabian and 1 Arabian-pony cross), and 2 foals
19 g infection in both SCID and immunocompetent foals: 51 and 68%, respectively, relative to the preinfe
20   In severe combined immunodeficiency (SCID) foals, a 5 bp deletion at codon 9480 results in a frames
21                                In three SCID foals, a novel neutralization-resistant variant arose th
22  and the treatment of subclinically affected foals, a significant increase in the incidence of macrol
23        Plasma was infused into young horses (foals) affected with severe combined immunodeficiency (S
24  of pneumonia were examined in 22 additional foals after intrabronchial challenge with R. equi.
25 ell-mediated immune responses and protecting foals against experimental pneumonia challenge.
26           Our goal was to passively immunize foals against R. equi by nebulizing mRNA encoding an equ
27     These antibodies cross-reacted with both foal and adult PBAC.
28 virus was isolated from feces of a diarrheic foal and serially propagated in human rectal adenocarcin
29         All strains of R. equi isolated from foals and approximately a third isolated from humans con
30                      Immunocompetent Arabian foals and Arabian foals with severe combined immunodefic
31 differences between SCID and immunocompetent foals and between SCID foals and the reconstituted SCID
32 ere recognized by sera from R. equi-infected foals and immune adult horses.
33  severe, life-threatening pneumonia in young foals and in people with underlying immune deficiencies.
34 ival within macrophages and for virulence in foals and mice.
35  growth of the organism and for virulence in foals and murine in vivo model systems.
36 D and immunocompetent foals and between SCID foals and the reconstituted SCID foal.
37 pneumonia with abscessation in young horses (foals) and in immunocompromised people, such as persons
38 rd of care for treating R. equi pneumonia in foals, and adjunctive therapies are needed.
39  genetic immunodeficiencies in mice, Arabian foals, and recently in Jack Russell terriers have been a
40 ere than its murine counterpart in that SCID foals are incapable of forming either coding or signal j
41 nt CTL activity was present in three of five foals at 6 weeks of age, and significant specific lysis
42  specific lysis was induced by PBMC from all foals at 8 weeks of age.
43 threatening pyogranulomatous pneumonia, most foals develop a protective immune response that lasts th
44 mained healthy, whereas 67% (4/6) of control foals developed clinical pneumonia.
45 the most common viral agents associated with foal diarrhea.
46 data on the impact of antibiotic exposure of foals during the first month of life.
47 f abortion in pregnant mares, death in young foals, establishment of the carrier state in stallions,
48 to 89% in three SCID and two immunocompetent foals examined.
49                                    Immunized foals exhibit changes in the epigenetic profile of blood
50 ce in DNA-PK(CS) expression in SCID mice and foals explains the more severe phenotype of equine SCID,
51 d effectively produced intrapulmonary mAb in foals for at least 5 days following nebulization.
52 h node tissues of two horses (a mare and its foal) from Italy that succumbed to an acute respiratory
53 tion of all available information about each foal, including clinical presentation, diagnostic test r
54                                              Foals infected and nebulized with PUL-042 or vehicle alo
55  five severe combined immunodeficient (SCID) foals infected with EIAV.
56                                              Foals infected with equine infectious anemia virus becom
57                            In contrast, SCID foals infused with nonimmune plasma developed acute dise
58 s is that the mutant DNA-PKCS allele in SCID foals inhibits signal end resolution.
59 the genetic SCID disease observed in Arabian foals is explained by a defect in V(D)J recombination th
60 B-17 SCID mice, the molecular defect in SCID foals is in the catalytic subunit of the DNA-dependent p
61 on for the differences between SCID mice and foals is that the mutant DNA-PKCS allele in SCID foals i
62 standard for preventing R. equi pneumonia in foals is transfusion of hyperimmune plasma, which is exp
63 trasonography (i.e., subclinically pneumonic foals) is common in the United States.
64  pathogen that primarily causes pneumonia in foals less than six months in age and immunocompromised
65  protein carbonyls, during chill storage, of foal liver pate reflects the intense oxidative degradati
66 nd protein changes, during chill storage, of foal liver pate was studied.
67 on) increased during refrigerated storage of foal liver pate, with the contents in the HF group being
68                                              Foal meat is considered a healthy alternative to other m
69 sed several candidate protein biomarkers for foal meat quality that are worthy to evaluate in the fut
70                                Using a horse foal model, we show that enteral immunization of newborn
71 olic rates of chronically catheterized fetal foals (n = 24) were measured at different gestational ag
72                                     Neonatal foals (n = 48) were nebulized with either PUL-042 or veh
73 ess effects of plasma or serum from infected foals on megakaryocyte (MK) growth and maturation in vit
74 matode species including a major pathogen of foals, Parascaris univalens.
75 ficant differences in lipid oxidation, since foal pates with higher fat content (HF) showed significa
76 arrheal pathogens in young animals including foals, piglets, calves, goats, sheep, cats, and dogs alo
77  annual prevalence of rotavirus in diarrheic foals ranged between 18 and 28% in Haryana (India).
78 ies resulted in larger placentae and heavier foals relative to PinP (P < 0.05).
79       TinP had smaller placentae and lighter foals relative to TinT (P < 0.05).
80              Post-challenge, all 5 immunized foals remained healthy, whereas 67% (4/6) of control foa
81                       Growth-enhanced (PinT) foals showed elevated basal arterial blood pressure and
82         Conversely, growth-restricted (TinP) foals showed no change in basal arterial blood pressure,
83 s the likely cause of ectopia lentis in this foal, the first genetic explanation for this condition i
84 case in C.B-17 SCID mice and in Arabian SCID foals, the defective factor in these SCID puppies is DNA
85 n and deletion of 83 amino acids; as in SCID foals, the mutant protein is unstable.
86  and resistome of 38 subclinically pneumonic foals treated with either MaR (n = 19) or gallium maltol
87 rect evidence of multi-drug resistance among foals treated with MaR.
88 tively transfect the bronchial epithelium of foals using naked mRNA (i.e., mRNA formulated in a sodiu
89      Whole genome sequencing of the affected foal was conducted, and forty-six candidate genes were e
90                                 The affected foal was confirmed by Sanger sequencing to be heterozygo
91  between immunocompetent and immunodeficient foals was not statistically significant.
92 ophages and in the lungs of R. equi-infected foals, we hypothesized that vapG could be an important v
93                      Values for maternal and foal weights and placental area at birth were larger in
94                                 Maternal and foal weights and placental microscopic area were measure
95  young adult Arabian-pony crosses and 1 SCID foal were then inoculated with plasma containing only EH
96 s not dependent on the immune response: SCID foals were affected as severely as immunocompetent foals
97                          At age 28 days, all foals were challenged intrabronchially with R. equi.
98                            Four of five SCID foals were completely protected against homologous chall
99                                              Foals were immunized twice via gavage of R. equi (immuni
100                                 Treated SCID foals were protected against clinical disease, with comp
101 ood mononuclear cells (PBMC) from 3-week-old foals were unable to lyse either autologous perinatal or
102                                              Foals with lower faecal bacterial diversity at one month
103 ole blood samples, and serum samples from 56 foals with pneumonia were analyzed.
104 al with rifampin (MaR) to apparently healthy foals with pulmonary lesions identified by thoracic ultr
105 we show that enteral immunization of newborn foals with Rhodococcus equi overcomes neonatal vaccinati
106    Immunocompetent Arabian foals and Arabian foals with severe combined immunodeficiency (SCID), whic
107 Rhodococcus equi isolated from young horses (foals) with R. equi pneumonia, carry an 80-90 kb virulen
108  neutralizing immune plasma in young horses (foals) with severe combined immunodeficiency (SCID).
109  nebulization with TLR agonists (PUL-042) in foals would improve innate immunity and reduce the sever

 
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