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The goal of this study was to evaluate survival of important viral pathogens of livestock in animal feed ingredients imported daily into the United States under simulated transboundary conditions. Eleven viruses were selected based on global significance and impact to the livestock industry, including Foot and Mouth Disease Virus (FMDV), Classical Swine Fever Virus (CSFV), African Swine Fever Virus (ASFV), Influenza A Virus of Swine (IAV-S), Pseudorabies virus (PRV), Nipah Virus (NiV), Porcine Reproductive and Respiratory Syndrome Virus (PRRSV), Swine Vesicular Disease Virus (SVDV), Vesicular Stomatitis Virus (VSV), Porcine Circovirus Type 2 (PCV2) and Vesicular Exanthema of Swine Virus (VESV). Surrogate viruses with similar genetic and physical properties were used for 6 viruses. Surrogates belonged to the same virus families as target pathogens, and included Senecavirus A (SVA) for FMDV, Bovine Viral Diarrhea Virus (BVDV) for CSFV, Bovine Herpesvirus Type 1 (BHV1) for PRV, Canine Distemper Virus (CDV) for NiV, Porcine Sapelovirus (PSV) for SVDV and Feline Calicivirus (FCV) for VESV. For the remaining target viruses, actual pathogens were used. Virus survival was evaluated using Trans-Pacific or Trans-Atlantic transboundary models involving representative feed ingredients, transport times and environmental conditions, with samples tested by PCR, VI and/or swine bioassay. SVA (representing FMDV), FCV (representing VESV), BHV-1 (representing PRV), PRRSV, PSV (representing SVDV), ASFV and PCV2 maintained infectivity during transport, while BVDV (representing CSFV), VSV, CDV (representing NiV) and IAV-S did not. Notably, more viruses survived in conventional soybean meal, lysine hydrochloride, choline chloride, vitamin D and pork sausage casings. These results support published data on transboundary risk of PEDV in feed, demonstrate survival of certain viruses in specific feed ingredients (“high-risk combinations”) under conditions simulating transport between continents and provide further evidence that contaminated feed ingredients may represent a risk for transport of pathogens at domestic and global levels.

BackgroundIdiopathic inflammatory myopathies (IIM) are a group of rare, heterogeneous diseases in which the hallmark feature is chronic inflammation of skeletal muscle leading to muscle weakness. Initial conventional therapy is based on expert opinion and includes glucocorticoids in combination with methotrexate, azathioprine, or mycophenolate. If this therapy is not sufficiently effective, second line therapy (calcineurin inhibitors or IVIG) may be considered. If still insufficient, escalation to rituximab or cyclophosphamide is considered. Agents not included in conventional recommended therapies have also been used and are being studied in the management of IIM.ObjectivesTo characterize real-world treatment trajectories among individuals with IIM.MethodsData were provided by adults with IIM enrolled in FORWARD, The National Databank for Rheumatic Diseases. Participants with a co-occurring RA, SLE, or SSc diagnosis were excluded. Participant characteristics were assessed at baseline (study entry) by treatment category and significance was assessed by one way ANOVA and Fisher’s exact tests, as appropriate (p<0.05). Treatment category (none, steroid alone, first line without steroid, first line, second line, third line, and other DMARD) was assessed at baseline and for ultimate line of treatment reported during observation. First, second, and third line treatments were considered “conventional” and others were considered “nonconventional.”ResultsA total of 126 participants met inclusion criteria. At baseline, 43% of participants were on first line therapy. Most of the remaining participants were either on a corticosteroid alone (23%) or were on first line therapy but without a corticosteroid (17%). A relatively small number of participants (2%) were on second line therapy, and none were on third line therapy at baseline. About 9% reported use of a nonconventional DMARD, and the remaining 6% reported no treatment. Those who reported no therapy were more likely to be male and had higher global severity scores. Across 504 person-years of observation, 47% reported first line treatment, 10% reported second line, and 3% reported third line as the most advanced conventional therapy received. The remaining 40% reported either nonconventional or no treatment.ConclusionDespite published recommendations to combine glucocorticoids with another immunosuppressive drug as part of first line therapy for IIM, many individuals with IIM are not prescribed concomitant DMARDs. In this cohort, there were no significant differences in IIM subtype, disease duration, or calendar year by conventional vs nonconventional therapy at study entry. A relatively small number of individuals with IIM reported receiving no treatment during observation, which may be due to significantly shorter follow up time in that subgroup. Future work should examine treatment response and changes in disease activity with changing lines of treatment.Table 1.Characteristics of included participants at study entry by baseline treatment category.Conventional TherapyNonconventional TherapyNo Therapyn=57n=61n=8pAge, years54.6 (14.3)57.2 (14.2)57.0 (8.3)0.61Female sex, %77.882.837.50.02White race, %90.688.575.00.62IIM subtypeDM41.144.137.5PM42.932.212.50.19Unspecified16.123.750.0Time since symptom onset, years6.5 (6.0)8.3 (6.3)4.1 (5.2)0.20Study entry prior to 2010, %55.466.137.50.50Observation time, years3.6 (3.4)4.4 (4.8)2.0 (2.4)0.01Rural residence, %30.421.137.50.41Hx smoking, %42.940.775.00.18Pain VAS, 0-103.1 (2.8)3.2 (2.9)5.1 (3.5)0.71Global severity, 0-103.6 (2.8)3.4 (2.7)6.3 (2.8)0.03HAQ-II, 0-31.0 (0.7)0.9 (0.6)1.2 (0.7)0.48PAS-II, 0-33.5 (2.3)3.3 (2.3)5.1 (2.6)0.86Figure 1.Treatment progression among individuals in FORWARD with IIM. Baseline (at study entry) treatment category is shown on the left, and ultimate treatment category (during observation) is shown on the right. First line = glucocorticoid + methotrexate, azathioprine, or mycophenolate. Second line = calcineurin inhibitors or IVIG. Third line = rituximab or cyclophosphamide.REFERENCES:NIL.Acknowledgements:NIL.Disclosure of InterestsKristin Wipfler: None declared, Urbano Sbarigia Shareholder of: Johnson & Johnson, Employee of: Janssen, Federico Zazzetti Shareholder of: Johnson & Johnson, Employee of: Janssen, Anna Sheahan Employee of: Janssen, Iris Lin Shareholder of: Johnson & Johnson, Employee of: Janssen, Evo Alemao Shareholder of: Johnson & Johnson, Employee of: Janssen, Kaleb Michaud: None declared.

BackgroundDespite major advances in rheumatoid arthritis (RA) treatment and the improved outcomes that have been associated with the expanding number of advanced therapies available, a substantial number of patients are refractory to multiple biologics. To understand the mechanisms behind refractory RA (reRA) and ultimately improve therapies tailored to individuals, a better understanding of associated factors is necessary. The shared epitope (SE) is an amino acid sequence motif coded by several HLA-DRB1 alleles that are overrepresented among people with RA and is associated with the production of anti-citrullinated protein antibodies.ObjectivesTo characterize the relationship between SE status and risk of developing refractory RA.MethodsParticipants in FORWARD, The National Databank for Rheumatic Diseases, with RA, high-resolution HLA-DRB1 typing, no history of biologic use at study entry, and subsequent exposure to one or more biologics were included. The reRA group included participants with exposure to at least three biologics while under observation. Those who used a single biologic with continued use for at least two years during observation comprised the comparison non-refractory group. Descriptive statistics for each group were calculated at initiation of first biologic. Significance was assessed with Fisher’s exact tests and Mann-Whitney U tests (p<0.05), as appropriate. Logistic regression was used to determine the relationship between shared epitope status and baseline odds of becoming refractory.ResultsCharacteristics of the 70 participants that met inclusion criteria are presented in Table 1. Several covariates varied significantly by refractory group, but these differences were attenuated in adjusted models. SE positive individuals had significantly lower odds of becoming refractory, a relationship that remained consistent with varying model complexity (Figure 1; OR [95% CI] 0.16 [0.05, 0.49] in univariate model; p=0.001). HLA-DRB1*04:01 was the only SE positive allele independently associated with nonrefractory status (p=0.036; data for other alleles not shown).ConclusionIn this cohort, individuals with RA who are SE positive were less likely to be refractory to multiple biologics. This relationship appears to be primarily the result of the HLA-DRB1*04:01 allele rather than any other alleles associated with SE positivity. These findings suggest that SE positive individuals with RA are more likely to find success with their first biologic, while SE negative individuals may be more likely to cycle through multiple biologics. Ongoing and future work will investigate this relationship further and assess whether these results remain consistent when using varying definitions of reRA.Table 1.Baseline (initiation of first biologic) characteristics of study participants. Values are mean (SD) unless otherwise noted.Non-RefractoryRefractoryn=48n=22pSE positive, %81.340.90.002≥1 copy of HLA-DRB1*04:01, %52.122.70.036Age, years57.2 (12.6)55.0 (9.7)0.266Female sex, %93.886.40.370White race, %95.785.70.167Time since symptom onset, years11.3 (11.3)7.3 (7.1)0.132Observation time, years6.9 (4.4)11.6 (5.5)<0.001Hx smoking, %27.136.40.575BMI, kg/m227.0 (5.5)32.4 (7.8)0.011Hx cancer, %14.69.10.709Hx pulmonary disorder, %18.827.30.532Hx GI disorder, %35.459.10.074Concomitant steroid use, %25.050.00.055Concomitant csDMARD use, %89.681.80.448Pain VAS, 0-102.5 (2.3)4.1 (2.8)0.011Global severity VAS, 0-102.7 (2.4)4.4 (2.5)0.013HAQ-II, 0-30.69 (0.56)1.01 (0.52)0.023Figure 1.Odds of becoming refractory by SE status. Odds ratios for becoming refractory when SE positive are shown for 9 unique models of increasing complexity. Each model includes a new covariate and all previously listed covariates. P-values for the SE positive covariate are displayed to the right of each associated OR and 95% CI.REFERENCES:NIL.Acknowledgements:NIL.Disclosure of InterestsKristin Wipfler: None declared, Sofia Pedro: None declared, Urbano Sbarigia Shareholder of: Johnson & Johnson, Employee of: Janssen, Federico Zazzetti Shareholder of: Johnson & Johnson, Employee of: Janssen, Anna Sheahan Employee of: Janssen, Iris Lin Shareholder of: Johnson & Johnson, Employee of: Janssen, Evo Alemao Shareholder of: Johnson & Johnson, Employee of: Janssen, Kaleb Michaud: None declared.

Background:Sjögren’s disease (SjD) is a chronic autoimmune condition that can affect the musculoskeletal system, nervous system, and/or vascular system. Autoantibodies anti–Sjögren’s-syndrome-related antigen A (anti-SSA/Ro) and B (anti-SSB/La) are hallmark autoantibodies in SjD [1], associated with earlier disease onset, extra-glandular manifestations, and more significant glandular dysfunction. Anti-SSA/Ro antibodies are associated with hematologic abnormalities, and extra-glandular disease such as lymphadenopathy [2].Objectives:The aim of this study is to describe the systemic disease activity of SjD patients with and without the presence of these autoantibodies.Methods:Data were drawn from the Adelphi Real World SjD Disease Specific Programme™, a cross-sectional survey of rheumatologists and their next six consecutively consulting patients with SjD conducted in France, Germany, Italy, Spain, and the United States in June – October 2018.Rheumatologists provided retrospective information regarding patient testing at diagnosis, including the serum anti-SSA/Ro and serum anti-SSB/La antibody tests, as well as patients’ current clinical characteristics and systemic involvement. These data were used for the calculation of a proxy clinical EULAR Sjögren’s syndrome disease activity index (clinESSDAI) score, calculated using physician-perceived severity scores of the individual organ domains.These same patients were asked to complete patient self-completion questionnaires which included the EQ-5D-3L, EuroQoL Visual Analogue Scale (EQ-VAS), Functional Assessment of Chronic Illness Therapy – Fatigue Scale (FACIT-Fatigue), and work productivity and activity impairment questionnaire (WPAI). All data are reported descriptively.Results:Rheumatologists (n=319) reported data on 1,879 patients; mean (SD) patient age was 53.2 (12.2) years, 89% of patients were female and 89% were white. Table 1 shows the clinical and patient-reported outcomes for both seropositive and seronegative anti-SSA/Ro and anti-SSB/La SjD patients, with a combined group of patients seropositive (49%) or seronegative (4%) for both antibody tests. Of patients with reported antibody test results for anti-SSA/Ro (n=1404), 92% were seropositive. For anti-SSB/La (n=1341) 73% were seropositive.Haematological involvement was reported for 22% of double seropositive patients but only 9% of double seronegative patients. Mean clinESSDAI scores for seropositive patients were 3.1 (anti-SSA/Ro) and 1.8 (anti-SSB/La) points higher than in seronegative patients (Table 1).Patient-reported EQ-5D-3L and WPAI scores are reported in Table 1. Mean (SD) EQ-VAS score for double seropositive patients was 61.5 (18.6), on a scale 0-100 where 100 is equal to the best imaginable health state. Mean (SD) EQ-VAS score for double seronegative patients was 73.4 (26.2). Mean (SD) FACIT-Fatigue scores for double seropositive and seronegative patients were 30.6 (10.46) and 36.3 (13.3) respectively, on a scale of 0-52 with higher scores indicating less fatigue.Conclusion:Patients who were seronegative had a similar level of organ involvement as seropositive patients, but seropositive patients had directionally higher clinESSDAI scores. Therefore, patients who had serum anti-SSA/Ro and/or serum anti-SSB/LA autoantibodies at diagnosis could represent a group of SjD patients likely to experience more clinical activity. Patient-reported outcome measures also suggest seropositive SjD patients may experience a lower health state and greater fatigue than in seronegative SjD patients. Further research is needed to better explore this potential indicator of clinical activity among SjD patients.REFERENCES:[1] Hernández-Molina G, et al. Autoimmun Rev. 2011;10(3):123-125.[2] Alexander EL, et al. Ann Int Med. 1983;98(2):155–159.Acknowledgements:Medical writing support was provided by Panita Maturavongsadit, PhD, of Lumanity Communications Inc., and was funded by Janssen Global Services, LLC.Disclosure of Interests:Jacques-Eric Gottenberg AbbVie, Janssen, BMS, UCB, MSD, Novartis, Pfizer, Gilead, Galapagos, Lilly, Sanofi, Nicola Massey Adelphi Real World, Megan Hughes Adelphi Real World, Victoria Barton Adelphi Real World, Sarah Weatherby Adelphi Real World, Federico Zazzetti May own shares/stock options of Johnson & Johnson, Johson & Johnson Innovative Medicine, Andras Borsi May own shares/stock options of Johnson & Johnson, Johson & Johnson Innovative Medicine, Wim Noel May own shares/stock options of Johnson & Johnson, Johson & Johnson Innovative Medicine, Evo Alemao May own shares/stock options of Johnson & Johnson, Johson & Johnson Innovative Medicine, Harman Dhatt May own shares/stock options of Johnson & Johnson, Johson & Johnson Innovative Medicine, Angelina Villasis-Keever May own shares/stock options of Johnson & Johnson, Johson & Johnson Innovative Medicine, Anna Sheahan May own shares/stock options of Johnson & Johnson, Johson & Johnson Innovative Medicine, Urbano Sbarigia May own shares/stock options of Johnson & Johnson, Johson & Johnson Innovative Medicine.

Background:Clinical EULAR Sjögren’s syndrome disease activity index (clinESSDAI) and EULAR Sjögren’s syndrome patient-reported index (ESSPRI) are commonly utilized clinical trial endpoints, reflecting disease activity and patient-reported symptomatology, respectively. The relationship between the thresholds for disease activity as measured by these clinical outcome assessments (COAs) reflecting physician and patient perspectives respectively, and their correlation with other patient-reported outcome measures (PROMs) remains to be elucidated.Objectives:This study aimed to evaluate the relationship between COAs and PROMs in Sjögren’s disease.Methods:Data were drawn from the Adelphi Real World Sjögren’s (SjD) Disease Specific Programme™, a cross-sectional survey, with retrospective data collection, of rheumatologists and their next six consecutively consulting patients with SjD in France, Germany, Italy, Spain, and the United States in June – October 2018. Rheumatologists reported on patients’ clinical characteristics, including subjective disease severity, and systemic involvement for the calculation of a clinESSDAI proxy score. Patients voluntarily completed questionnaires including components for ESSPRI proxy score calculations and other PROMs including EQ-5D-3L (US tariff) (0-1; MCID = 0.04) [1], EuroQoL Visual Analogue Scale (EQ-VAS), Functional Assessment of Chronic Illness Therapy – Fatigue Scale (FACIT-F) (0-52; MCID = 3-6 points) [2], and work productivity and activity impairment questionnaire (WPAI). Associations between clinESSDAI and ESSPRI, and PROM scores and subjective disease severity were examined through univariate linear and logistic regression modelling. Mean differences in PROM scores were determined by two-sample t-tests and compared with published values for minimal clinically important differences (MCID) [1,2]. Statistical significance was p<0.05 for all tests, and the published thresholds utilized for the purposes of this study were as follows: clinESSDAI (low <5, moderate 5-13, high >13); ESSPRI (<5, ≥5).Results:Rheumatologists (n=319) reported data on 1,879 SjD patients. All PROMs were significantly associated with both clinESSDAI and ESSPRI (Table 1). Mean EQ-5D-3L utility scores were 0.79, 0.74, and 0.66 for low, moderate, and high clinESSDAI respectively; and 0.82 and 0.64 for ESSPRI <5 and ≥5, respectively. Mean FACIT-F scores were 33.96, 30.76, and 29.10 for low, moderate, and high clinESSDAI respectively; and 36.19 and 24.62 for ESSPRI <5 and ≥5, respectively. All mean differences within clinESSDAI and ESSPRI groups were statistically significant.Conclusion:ClinESSDAI and ESSPRI are significantly associated with PROMs, suggesting a relationship with systemic disease activity and patient-reported symptomatology. ESSPRI’s greater incremental association with other PROMs suggests that patient experience focuses more on non-systemic aspects of disease, implying ESSPRI may be more closely associated with other PROMs. However, difference in COAs and their scales (clinESSDAI: 0-123; ESSPRI: 0-10) may impact the magnitude of the observed association. Existing clinESSDAI disease activity thresholds are generally consistent with MCIDs in low-moderate disease activity; however, mean differences beyond MCIDs at the moderate-high threshold suggest a broad range in outcome scores. Similarly, difference in PROM means beyond the MCID suggests that ESSPRI scores <5 and ≥5 may be too broadly grouped to comprehensively reflect differences in patient outcomes. These findings suggest that both clinESSDAI and ESSPRI require contextualised interpretation in clinical trial results and indicate that current published thresholds understate the difference in EQ-5D-3L and FACIT-F experienced by patients.REFERENCES:[1] Luo N, et al. Medical Care. 2010; 48(4):365-371.[2] Nordin Å, et al. BMC Med Res Methodol. 2016;16:62.Acknowledgements:Medical writing support was provided by Panita Maturavongsadit, PhD, of Lumanity Communications Inc., and was funded by Janssen Global Services, LLC.Disclosure of Interests:Jacques-Eric Gottenberg AbbVie, Janssen, BMS, UCB, MSD, Novartis, Pfizer, Gilead, Galapagos, Lilly, Sanofi, Nicola Massey Adelphi Real World, Megan Hughes Adelphi Real World, Victoria Barton Adelphi Real World, Sarah Weatherby Adelphi Real World, Federico Zazzetti May own shares/stock options of Johnson & Johnson, Johson & Johnson Innovative Medicine, Andras Borsi May own shares/stock options of Johnson & Johnson, Johnson & Johnson Innovative Medicine, Wim Noel May own shares/stock options of Johnson & Johnson, Johson & Johnson Innovative Medicine, Evo Alemao May own shares/stock options of Johnson & Johnson, Johson & Johnson Innovative Medicine, Harman Dhatt May own shares/stock options of Johnson & Johnson, Johnson & Johnson Innovative Medicine, Angelina Villasis-Keever May own shares/stock options of Johnson & Johnson, Johnson & Johnson Innovative Medicine, Anna Sheahan May own shares/stock options of Johnson & Johnson, Johnson & Johnson Innovative Medicine, Urbano Sbarigia May own shares/stock options of Johnson & Johnson, Johnson & Johnson Innovative Medicine.

[This corrects the article DOI: 10.1371/journal.pone.0194509.].

The objective of this study was to determine whether the physiological response to an intravenous glucose challenge would be affected by genetic strain or concentrate supplementation in grazing Holstein-Friesian cows in early lactation. North American (NA; n=30) or New Zealand (NZ; n=30) cows were randomly allocated to 1 of 3 feeding treatments. All cows were offered a generous pasture allowance, and 4 of the 6 groups received either 3 or 6kg of dry matter (DM)/cow per day of concentrates. During wk 5 of lactation, all cows underwent an intravenous glucose challenge. Cows of NA origin produced more milk than NZ cows, but there was no significant strain effect on milk fat or protein yield. Milk yield and the yield of individual components increased with increasing level of concentrate eaten, but there were no significant strain×diet interactions. During wk 1 to 6, mean body weight and body condition score decreased in all treatments. Average body weight was greater in NA cows, but body condition score was greater for NZ cows. There was no strain or diet effect on the length of the postpartum anovulatory interval, with cows ovulating before 40 d postpartum on average. Glucose fractional turnover rate was greater in NZ cows compared with those of NA origin and in all cows receiving 6kg of DM concentrates, indicating a less severe insulin resistance in those treatments. Consistent with this, the time taken to dispose of half the peak glucose concentration was less when 6kg of DM concentrate was fed, and tended to be less in NZ than in NA cows. There was no effect of genetic strain on glucose area under the curve (AUC) at 60 or 120min, but AUC at both time points was less in cows receiving 6kg of DM concentrates per day. Neither genetic strain nor nutrition affected basal or peak insulin concentrations, insulin increment, or insulin AUC, and there were no strain×diet interactions for any of the glucose challenge response variables measured. In conclusion, differences in milk production between NA and NZ cows in early lactation can, at least in part, be explained by the greater degree of insulin resistance in the NA cows, and this insulin resistance can be overcome by supplementing grazing cows with 6kg of DM concentrates.

[This corrects the article DOI: 10.1371/journal.pone.0194509.].

Background In May 2021, the B.1.617 variant of SARS-CoV-2 emerged in Ireland, and both Delta and Kappa sub-lineages were initially deemed variants of concern (VOCs) on a precautionary basis. We describe a large outbreak of SARS-CoV-2 B.1.617.1 (Kappa mutation) linked to a private gathering among third level students in Cork, Ireland. Methods Surveillance data were available from the Health Service Executive COVID Care Tracker. The epidemiological sequence of infection for each new case in this outbreak was tracked and whole genome sequencing was requested on all linked cases. Enhanced public health control measures were implemented by the Department of Public Health HSE-South to contain onward spread of VOCs, including retrospective contact tracing, lengthy isolation and quarantine periods for cases and close contacts. Extensive surveillance efforts were used to describe and control onward transmission. Results There were 146 confirmed SARS-CoV-2 cases linked to the outbreak. All sequenced cases (53/146; 36%) confirmed Kappa mutation. The median age was 21 years (range 17–65). The majority (88%) had symptoms of SARS-CoV-2 infection. There were 407 close contacts; the median was 3 per case (range 0–14). There were no known hospitalisations, ICU admissions or deaths. Vaccination data was unavailable, but the outbreak pre-dated routine availability of COVID-19 vaccines among younger adults in Ireland. Conclusion Enhanced public health control measures for new and emerging variants of SARS-CoV-2 may be burdensome for cases and close contacts. The overall public health benefit of enhanced controls may only become apparent when evidence on disease transmissibility and severity becomes more complete.

The objective of this study was to investigate the relationship between nitrogen isotopic fractionation (δ(15)N) and nitrogen-use efficiency (milk nitrogen/nitrogen intake; NUE) in pasture-fed dairy cows supplemented with increasing levels of urea to mimic high rumen degradable protein pastures in spring. Fifteen cows were randomly assigned to freshly cut pasture and either supplemented with 0, 250, or 336 g urea/d. Feed, milk, and plasma were analyzed for δ(15)N, milk and plasma for urea nitrogen concentration, and plasma for ammonia concentration. Treatment effects were tested using ANOVA and relationships between variables were established by linear regression. Lower dry matter intake (P = 0.002) and milk yield (P = 0.002) occurred with the highest urea supplementation (336 g urea/d) compared with the other two treatments. There was a strong linear relationship between milk δ(15)N - feed δ(15)N and NUE: [NUE (%) = 58.9 - 10.17 × milk δ(15)N - feed δ(15)N (‰) (r(2) = 0.83, P < 0.001, SE = 1.67)] and between plasma δ(15)N - feed δ(15)N and NUE: [NUE (%) = 52.4 - 8.61 × plasma δ(15)N - feed δ(15)N (‰) (r(2) = 0.85, P < 0.001, SE = 1.56)] . This study confirmed the potential use of δ(15)N to predict NUE in cows consuming different levels of rumen degradable protein.