Effect of temperature on raw whole milk density and its potential impact on milk payment in the dairy industry

The objective of this study was to determine the effect of temperature on whole milk density measured at four different temperatures: 5, 10, 15, and 20 °C. A total of ninety-three individual milk samples were collected from morning milking of thirty-two Holstein Friesian dairy cows, of national average genetic merit, once every two weeks over a period of 4 weeks and were assessed by Fourier transform infrared spectroscopy for milk composition analysis. Density of the milk was evaluated using two different analytical methods: a portable density meter DMA35 and a standard desktop model DMA4500M (Anton Paar GmbH, UK). Milk density was analysed with a linear mixed model with the fixed effects of sampling period, temperature and analysis method; triple interaction of sampling period x analysis method x temperature; and the random effect of cow to account for repeated measures. The effect of temperature on milk density (ρ) was also evaluated including temperature (t) as covariate with linear and quadratic effects within each analytic method. The regression equation describing the curvature and density–temperature relationship for the DMA35 instrument was ρ = 1.0338−0.00017T−0.0000122T² (R² = 0.64), while it was ρ = 1.0334 + 0.000057T−0.00001T² (R² = 0.61) for DMA4500 instrument. The mean density determined with DMA4500 at 5 °C was 1.0334 g cm⁻³, with corresponding figures of 1.0330, 1.0320 and 1.0305 g cm⁻³ at 10, 15 and 20 °C, respectively. The milk density values obtained in this study at specific temperatures will help to address any bias in weight–volume calculations and thus may also improve the financial and operational control for the dairy processors in Ireland and internationally.     

The impacts of cattle access points on deposited sediment levels in headwater streams in Ireland

Cattle access to streams has been linked globally with degradation of stream water quality, driven largely by bank erosion and resultant instream, fine sediment deposition. The majority of evidence on such effects is however based in arid and semiarid regions of the United States and Australia, with few studies relating to cool temperate climates such as Northwest Europe. In this study, “Quorer” resuspendable sediment samples were taken from riffle geomorphic units upstream (control) and at two points downstream (pressure and recovery) of cattle access points in headwater streams in agricultural catchments in Ireland to assess levels of deposited stream sediment. Samples were taken in April/May (2016) prior to the grazing season and in October (2016) at the end of the grazing season. Sites in good‐high ecological status catchments and less than good ecological status catchments were included in the study. Higher levels of sediment were found downstream of cattle access points in both good‐high status and less than good status catchments; however, the impacts of access points were spatially confined to, in most cases, the area immediately downstream of the point of access. There was a strong correlation between deposited sediment mass and organic matter (OM) mass, with levels of OM increasing linearly with deposited sediment mass. Levels of measured sediment were negatively correlated with riparian habitat health (measured using a qualitative habitat assessment). The results of this study highlight the need for measures to prevent cattle access to headwater streams where access points can be many in order to manage local habitat quality and downstream water quality issues.     

A noncompetitive peptide inhibitor of the nicotinic acetylcholine receptor from Conus purpurascens venom

A paralytic peptide, psi-conotoxin Piiie has been purified and characterized from Conus purpurascens venom. Electrophysiological studies indicate that the peptide inhibits the nicotinic acetylcholine receptor (nAChR). However, the peptide does not block the binding of alpha-bungarotoxin, a competitive nAChR antagonist. Thus, psi-conotoxin Piiie appears to inhibit the receptor at a site other than the acetylcholine-binding site. As ascertained by sequence analysis, mass spectrometry, and chemical synthesis, the peptide has the following covalent structure: HOOCCLYGKCRRYOGCSSASCCQR* (O = 4-trans hydroxyproline; * indicates an amidated C-terminus). The disulfide connectivity of the toxin is unrelated to the alpha- or the alphaA-conotoxins, the Conus peptide families that are competitive inhibitors of the nAChR, but shows homology to the mu-conotoxins (which are Na+ channel blockers).     

Cytokine profiles of stimulated blood lymphocytes in asthmatic and healthy adolescents across the school year

T cell cytokines play an important role in mediating airway inflammation in asthma. The predominance of a Th2 cytokine profile, particularly interleukin (IL)-4 and IL-5, is associated with the pathogenesis and course of asthma. The aim of this study was to test the hypothesis that a stressful life event alters the pattern of cytokine release in asthmatic individuals. Thirteen healthy controls and 21 asthmatic adolescents gave blood samples three times over a semester: midsemester, during the week of final examinations, and 2-3 weeks after examinations. Interferon-gamma (IFN-gamma), IL-2, IL-4, and IL-5 were measured from supernatants of cells stimulated with PHA/PMA for 24 h. Cells from asthmatic subjects released significantly more IL-5 during the examination and postexamination periods, whereas cells from healthy controls released significantly more IL-2 during the midsemester and examination periods, thereby indicating a bias for a Th2-like pattern in asthmatics and a Th1-like pattern in healthy controls. IL-4 and IL-5 production showed a marked decrease during and after examinations in healthy controls, whereas this decline was absent in asthmatics. The ratios of IFN-gamma:IL-4 and IFN-gamma:IL-5 also revealed significant changes in the profile of cytokine release across the semester. These results indicate differential cytokine responses in asthmatics that may become pronounced during periods of cellular activation.     

Effects of the glucocorticoid agonist, RU28362, and the antagonist RU486 on lung phosphatidylcholine and antioxidant enzyme development in the genetically obese Zucker rat

The biochemical maturation of the lung in late gestation and in the young animal is regulated by glucocorticoids. The present study was aimed at dissociating the different glucocorticoid receptor sites involved in these regulatory functions. The obese Zucker rat was selected as a model for this study as it exhibits hypersensitivity to glucocorticoid hormone action by virtue of its elevated receptor numbers and activity. Two synthetic steroid analogues were administered to obese animals; RU28362, a specific type II receptor agonist, and the type II antagonist RU486. RU28362 promoted a strong catabolic effect, which was associated with reduced food intake and the abolition of growth in the rats. The agonist, RU28362, attenuated developmental increases in antioxidant enzyme activities, and altered the growth of the tissue. At the age studied, development of the lung phosphatidylcholine (PC) system was almost complete, but RU28362 increased disaturated PC 16:0/16:0 concentrations by almost 2-fold, and altered the molecular composition of total pulmonary PC. RU486 attenuated the growth of the rats and reduced their food intake. Treatment with the type II antagonist attenuated lung growth and increased the activities of pulmonary copper zinc (Cu/Zn) and manganese (Mn) superoxide dismutases. RU486 had no effect on lung PC concentrations and molecular composition. The data suggest a role for type I glucocorticoid receptors in the regulation of the antioxidant enzyme system in the lung, as type II antagonism will channel endogenous glucocorticoid binding to the type I site. Type II receptor binding would appear to play a role in regulating the lung PC content.     

Long-term follow-up of a randomized post-induction therapy trial in acute myelogenous leukemia (a Southeastern Cancer Study Group trial)

A phase III clinical trial was designed to determine if more intensive induction and consolidation therapy for acute myeloblastic leukemia increases the remission rate and prolongs survival. A minor objective was to determine if the use of non-cross resistant drugs was more effective than the same drugs used for induction. Patients with untreated leukemia between the ages of 15 and 50 were given daunorubicin 45 mg/m2 for the first 3 days of a 10-day continuous infusion of cytosine arabinoside, initially at a dose of 2000 mg/m2 but reduced to 100 mg/m2 because of toxicity. Those under 36 achieving a complete remission and with an histocompatible donor were assigned to a transplant arm. The rest were randomized to receive one of three consolidation arms: A, cytosine arabinoside, 200 mg/m2 daily for 7 days and daunorubicin 45 mg/m2 daily for 3 days for three courses; B, one course as in Arm A followed by amsacrine, 120 mg/m2 daily for 5 days followed by a 5-day continuous infusion of azacytidine, 150 mg/m2/day; C, thioguanine and cytosine arabinoside, 100 mg/m2 every 12 h and daunorubicin 10 mg/m2 daily for 5 days for three courses followed by four maintenance courses of cytosine arabinoside, 100 mg/m2 daily for 5 days and daunorubicin, 45 mg/m2 for 2 days every 13 weeks. From 1981 to 1986, 398 eligible patients were enrolled and 219 achieved a complete remission. The initial induction dose of cytosine arabinoside was reduced after five of 29 patients exhibited fatal gastrointestinal toxicity. Only 11 patients were assigned to the transplant arm. There were no significant differences in the consolidation arms. The 5 year disease-free survivals were 38, 31 and 27% in arms A, B, and C respectively. Intensive consolidation therapy with the same or different drugs used in induction was as effective as lower dose consolidation followed by maintenance therapy.