Increasing Your Calf Crop by Management, Pregnancy Testing, and Breeding Soundness Examination of Bulls

Percent calf crop weaned is influenced more by man¬agement decisions than by any other single factor in a cow herd, and therefore can be a very important factor in annual returns for a cow-calf operation. Percent calf crop weaned is calculated by dividing the number of calves weaned by the total number of females exposed during the breeding season. As shown in Table 1, as percent calf crop weaned increases, pounds of calf weaned per cow exposed increas¬es and production cost per hundred pounds of calf produced decreases. Increasing weaning weights approximately 50 pounds is equal to an increase of 10% in calf crop weaned

Feeding Natural Cattle

Some consumers are willing to pay a premium for “natural” beef products from production systems not utilizing implants, ionophores, or antibiotics. Producers marketing to these systems can attain substantial premiums. The term “natural” as defined by the USDA, is extremely loose, and all fresh beef qualifies as a natural product. However, “natural” is more strictly defined by the marketplace. Claims, which vary from company to company, are regulated by the Food and Drug Administration and must be verifiable. It is generally accepted that cattle qualifying for natural programs have never received antibiotics or hormones at any time from birth to harvest

Definitions and Descriptions: Conventional, Natural, and Organic Beef Production and Consumption

Natural and organic beef production was only 1.1% of total beef production and 1.6% of total U.S. beef sales in 2006 but is the fastest growing sector in the beef industry. With demand continuing to surge in these markets, you will find that terminology used in these marketing strategies is confusing. Beef that is produced following “natural” or “organic” protocols is assumed to have been raised without hormones or antibiotics. But “natural” and “organic” are not the same, and “natural” also is variable

Effect of Supplementing Distillers Grain or Corn on Performance of Cows Grazing Spring Pasture during the Breeding Season

In a 2 yr study 180 lactating cows (2 to 10 yr old) grazing pastures dominated by smooth bromegrass and Kentucky bluegrass near Brookings, SD received 3 supplemental treatments for 48 d beginning in mid May. Cows received 4.6 lb DM of dried distillers grains with solubles (DDGS), 4.3 lb corn DM, or no supplement daily, starting approximately 14 d prior to the start of the breeding season. Cows were bled weekly for 5 wk beginning 1 wk prior to the beginning of the treatment period. Serum was analyzed for progesterone concentration to determine the onset of cyclicity. While supplemented cows did tend to have higher ADG than cows that received no supplement, supplementation did not improve any measure of reproduction. Calf growth rate was not affected by supplementation. The results were similar when only 2 and 3 yr olds were included in the analysis. Under the conditions of this study, it is not beneficial to supplement cows with DDGS or corn to improve cow reproductive performance or calf performance

The Varicella-Zoster Virus ORF47 Kinase Interferes with Host Innate Immune Response by Inhibiting the Activation of IRF3

The innate immune response constitutes the first line of host defence that limits viral spread and plays an important role in the activation of adaptive immune response. Viral components are recognized by specific host pathogen recognition receptors triggering the activation of IRF3. IRF3, along with NF-κB, is a key regulator of IFN-β expression. Until now, the role of IRF3 in the activation of the innate immune response during Varicella-Zoster Virus (VZV) infection has been poorly studied. In this work, we demonstrated for the first time that VZV rapidly induces an atypical phosphorylation of IRF3 that is inhibitory since it prevents subsequent IRF3 homodimerization and induction of target genes. Using a mutant virus unable to express the viral kinase ORF47p, we demonstrated that (i) IRF3 slower-migrating form disappears; (ii) IRF3 is phosphorylated on serine 396 again and recovers the ability to form homodimers; (iii) amounts of IRF3 target genes such as IFN-β and ISG15 mRNA are greater than in cells infected with the wild-type virus; and (iv) IRF3 physically interacts with ORF47p. These data led us to hypothesize that the viral kinase ORF47p is involved in the atypical phosphorylation of IRF3 during VZV infection, which prevents its homodimerization and subsequent induction of target genes such as IFN-β and ISG15

The Nitric Oxide Pathway Provides Innate Antiviral Protection in Conjunction with the Type I Interferon Pathway in Fibroblasts

The innate host response to virus infection is largely dominated by the production of type I interferon and interferon stimulated genes. In particular, fibroblasts respond robustly to viral infection and to recognition of viral signatures such as dsRNA with the rapid production of type I interferon; subsequently, fibroblasts are a key cell type in antiviral protection. We recently found, however, that primary fibroblasts deficient for the production of interferon, interferon stimulated genes, and other cytokines and chemokines mount a robust antiviral response against both DNA and RNA viruses following stimulation with dsRNA. Nitric oxide is a chemical compound with pleiotropic functions; its production by phagocytes in response to interferon-γ is associated with antimicrobial activity. Here we show that in response to dsRNA, nitric oxide is rapidly produced in primary fibroblasts. In the presence of an intact interferon system, nitric oxide plays a minor but significant role in antiviral protection. However, in the absence of an interferon system, nitric oxide is critical for the protection against DNA viruses. In primary fibroblasts, NF-κB and interferon regulatory factor 1 participate in the induction of inducible nitric oxide synthase expression, which subsequently produces nitric oxide. As large DNA viruses encode multiple and diverse immune modulators to disable the interferon system, it appears that the nitric oxide pathway serves as a secondary strategy to protect the host against viral infection in key cell types, such as fibroblasts, that largely rely on the type I interferon system for antiviral protection

Self Protection from Anti-Viral Responses – Ro52 Promotes Degradation of the Transcription Factor IRF7 Downstream of the Viral Toll-Like Receptors

Ro52 is a member of the TRIM family of single-protein E3 ligases and is also a target for autoantibody production in systemic lupus erythematosus and Sjögren's syndrome. We previously demonstrated a novel function of Ro52 in the ubiquitination and proteasomal degradation of IRF3 following TLR3/4 stimulation. We now present evidence that Ro52 has a similar role in regulating the stability and activity of IRF7. Endogenous immunoprecipitation of Ro52-bound proteins revealed that IRF7 associates with Ro52, an effect which increases following TLR7 and TLR9 stimulation, suggesting that Ro52 interacts with IRF7 post-pathogen recognition. Furthermore, we show that Ro52 ubiquitinates IRF7 in a dose-dependent manner, resulting in a decrease in total IRF7 expression and a subsequent decrease in IFN-α production. IRF7 stability was increased in bone marrow-derived macrophages from Ro52-deficient mice stimulated with imiquimod or CpG-B, consistent with a role for Ro52 in the negative regulation of IRF7 signalling. Taken together, these results suggest that Ro52-mediated ubiquitination promotes the degradation of IRF7 following TLR7 and TLR9 stimulation. As Ro52 is known to be IFN-inducible, this system constitutes a negative-feedback loop that acts to protect the host from the prolonged activation of the immune response

Herpes Simplex Virus 1 Has Multiple Mechanisms for Blocking Virus-Induced Interferon Production

In response to viral infection, host cells elicit a number of responses, including the expression of alpha/beta interferon (IFN-α/β). In these cells, IFN regulatory factor-3 (IRF-3) undergoes a sequence of posttranslational modifications that allow it to act as a potent transcriptional coactivator of specific IFN genes, including IFN-β. We investigated the mechanisms by which herpes simplex virus 1 (HSV-1) inhibits the production of IFN-β mediated by the IRF-3 signaling pathway. Here, we show that HSV-1 infection can block the accumulation of IFN-β triggered by Sendai virus (SeV) infection. Our results indicate that HSV-1 infection blocks the nuclear accumulation of activated IRF-3 but does not block the initial virus-induced phosphorylation of IRF-3. The former effect was at least partly mediated by increased turnover of IRF-3 in HSV-1-infected cells. Using mutant viruses, we determined that the immediate-early protein ICP0 was necessary for the inhibition of IRF-3 nuclear accumulation. Expression of ICP0 also had the ability to reduce IFN-β production induced by SeV infection. ICP0 has been shown previously to play a role in HSV-1 sensitivity to IFN and in the inhibition of antiviral gene production. However, we observed that an ICP0 mutant virus still retained the ability to inhibit the production of IFN-β. These results argue that HSV-1 has multiple mechanisms to inhibit the production of IFN-β, providing additional ways in which HSV-1 can block the IFN-mediated host response