Symposium review: Omics in dairy and animal science-Promise, potential, and pitfalls.

Sequencing the first genome took 15 yr and $3 billion to complete. Currently, a genome can be sequenced in a day for a few thousand dollars. Comparing the relative abundance of nearly every mRNA transcript and small RNAs from cells and tissues from different experimental conditions has become so easy that it can take longer to transfer the data between computers than to perform the experiment. Nucleotide sequencing techniques have become so sensitive that the greatest concern is not detecting a gene or transcript but rather, falsely identifying one. Better genome sequencing has led to more complete transcriptomic and proteomic databases and, combined with more sensitive instrumentation and separation techniques, is bringing us closer to detecting complete transcriptomes and proteomes. The promise of these powerful omics techniques is to lead us to new and unexpected connections between molecular processes in the context of animal health. This promise cannot be achieved without hypothesis-driven research that connects omics data with animal health experiments. Any researcher who wishes to invest the time and resources in omics experiments should be aware of the common pitfalls and limitations of these techniques so they can avoid these issues and maximize the use of these research tools. Several important questions must be asked: What is the quality of the databases and how they are annotated? Are the annotations based on experimental results or computational predictions? What assumptions are made by the analysis algorithms, and how will this affect the result? Finally, how can the research community use the vast amount of data being generated by omics experiments in ways to achieve the goals of better animal health and production (which is the promise of omics technologies)? Until the observations shown in omics data sets are used to achieve the goals of better animal health and production, the potential of omics technology will not be fully realized.

The effect of pegylated granulocyte colony-stimulating factor treatment prior to experimental mastitis in lactating Holsteins.

Neutrophils are the first-acting and most prominent cellular defense against mastitis-causing pathogens. This makes neutrophil activation and expansion obvious candidates for targeted therapeutics. The granulocyte colony-stimulating factor (G-CSF) cytokine stimulates the bone marrow to produce granulocytes and stem cells and release them into the bloodstream, which results in neutrophilia as well as increasing the presence of other progenitor cells in the bloodstream. A pegylated form of G-CSF (PEG-gCSF) has been shown to significantly decrease naturally occurring mastitis rates in cows postpartum. The use of PEG-gCSF had not been evaluated in response to an experimental mastitis challenge. In an effort to examine the effect and mechanism of PEG-gCSF treatment, we challenged 11 mid-lactation Holsteins with ∼400 cfu Escherichia coli P4 by intramammary infusion. Five cows received 2 PEG-gCSF injections, one at 14 d and the other at 7 d before disease challenge, and 6 cows remained untreated. To evaluate the response of cows to the PEG-gCSF treatment, we measured complete blood counts, somatic cell counts, bacterial counts, milk yield, and feed intake data. The PEG-gCSF-treated cows had significantly increased circulating levels of neutrophils and lymphocytes after each PEG-gCSF injection, as well as following mastitis challenge. The PEG-gCSF-treated cows had significantly lower bacterial counts and lower milk BSA levels at the peak of infection. In addition, control cows had significant decreases in milk yield postinfection and significantly reduced feed intake postinfection compared with PEG-gCSF-treated cows. Collectively, PEG-gCSF treatment resulted in reduced disease severity when administered before a bacterial challenge. Mechanistically, we show that G-CSF treatment increases cell surface expression of an E-selectin ligand before infection on neutrophils and monocytes found in the blood. These cells quickly disappear from the blood shortly after infection, suggesting a mechanism for the reduced mastitis severity by priming immune cells for quick targeting to the site of infection.

Racial variation in spontaneous fetal deaths at 20 weeks or older in upstate New York, 1980-86.

The distribution of spontaneous fetal deaths (at age 20 weeks or more) by maternal race has received considerably less study than other adverse pregnancy outcomes. The purpose of this study was twofold--(a) to describe spontaneous fetal deaths among white, black, and American Indian women and (b) to determine if there was any variation by International Classification of Diseases, Ninth Revision (ICD-9) cause of death, gestational age at death, or maternal age at loss among these groups of mothers. Using the fetal death certificate registry maintained by the New York State Department of Health, 8,592 spontaneous fetal deaths at age 20 weeks or more were identified among upstate (exclusive of New York City) mothers between 1980 and 1986. By race it was 7,300 for white women, 1,257 for black women, and 27 for American Indian women. Spontaneous fetal death rates varied by maternal race as listed on vital records--black, 13.5 per 1,000 total births, white, 8.3, and American Indian, 8.1. The three leading causes of death (ICD-9,779, 762, and 761) did not vary by maternal race. Gestational age at death, imputed from last menstrual period, did vary by maternal race. Fetal deaths to white and black mothers were observed to occur most often between 24 weeks of pregnancy (39 percent) and 32 weeks (43 percent), while American Indian fetal deaths generally occurred later (more than 33 weeks) in pregnancy (41 percent). Most spontaneous fetal deaths occurred to mothers ages 20-29 regardless of race. Black teenage mothers, however, experienced the largest proportion of losses(23 percent) compared with white (10 percent) and American Indian (I I percent) teenage mothers.

Comparison of Native American births in upstate New York with other race births, 1980-86.

The purpose of this study was to describe the neonatal characteristics of Native American (Indian) infants and the antenatal characteristics of their mothers as compared with white, black, and other race infants. The study population comprised 979,444 live births to upstate New York (exclusive of New York City) resident mothers between 1980 and 1986. Data were abstracted from vital records (birth certificates) and analyzed using a variety of descriptive statistics. Mothers of Native American and black infants had similar antenatal profiles (that is, younger, higher parity, lower educational attainment, and delayed initiation of prenatal care), which differed from mothers of white or other race infants. Despite having at-risk mothers, Native American infants were similar to white and other race infants with respect to the percentage of births that were considered low birth weight or premature. Black infants were twice as likely as the other three groups of infants to be low birth weight or premature. These findings suggest that other factors appear to be important in determining neonatal outcome and that typical at-risk antenatal profile of mothers may not be consistent across all racial groups.