The effects of vetrabutin chlorhydrate and oxytocin on stillbirth rate and asphyxia in swine

Oxytocin and vetrabutin chlorhydrate (VC) are used to reduce the duration of farrowing in swine. The objective of the present study was to evaluate the use of these products on intra-partum stillbirth (IPS) rate and asphyxia. At the onset of parturition, sows (n=180) were allocated to receive 2 mL of saline (control group), oxytocin (40 IU i.m.) or 100mg of VC per 60 kg of body weight, with all treatments given i.m. Oytocin-treated sows had a higher number of IPS than the VC and Control groups (means, 1.2, 0.8 and 0.6, respectively; P<0.001), and the highest percentage of ruptured umbilical cords (76.0, 9.4 and 37.5%; P<0.003). There were differences among groups for duration of farrowing (means, 163.0, 211.2 and 306.9 min in the oxytocin, VC and control groups; P<0.001), interval between piglets (13.9, 19.2 and 28.1 min; P<0.001), and in IPS, the incidence of ruptured umbilical cords was 76.0, 9.4 and 37.5% (P<0.003) and absence of a fetal heartbeat was 53.3, 16.9 and 12.5% (P<0.05). Although oxytocin decreased both duration of farrowing and interval between piglets by approximately 50% relative to control sows, it resulted in a significantly higher rate of IPS, in association with a much higher incidence of ruptured umbilical cord and absence of a fetal heartbeat. Treatment with VC reduced farrowing duration by approximately 1.5h, with an IPS rate that was not significantly different from controls but significantly lower than that of oxytocin-treated sows.     

Rapid warming is associated with population decline among terrestrial birds and mammals globally

Animal populations have undergone substantial declines in recent decades. These declines have occurred alongside rapid, human‐driven environmental change, including climate warming. An association between population declines and environmental change is well established, yet there has been relatively little analysis of the importance of the rates of climate warming and its interaction with conversion to anthropogenic land use in causing population declines. Here we present a global assessment of the impact of rapid climate warming and anthropogenic land use conversion on 987 populations of 481 species of terrestrial birds and mammals since 1950. We collated spatially referenced population trends of at least 5 years’ duration from the Living Planet database and used mixed effects models to assess the association of these trends with observed rates of climate warming, rates of conversion to anthropogenic land use, body mass, and protected area coverage. We found that declines in population abundance for both birds and mammals are greater in areas where mean temperature has increased more rapidly, and that this effect is more pronounced for birds. However, we do not find a strong effect of conversion to anthropogenic land use, body mass, or protected area coverage. Our results identify a link between rapid warming and population declines, thus supporting the notion that rapid climate warming is a global threat to biodiversity.     

Alterations of plasma lipids in mice via adenoviral-mediated hepatic overexpression of human ABCA1

ATP binding cassette transporter A1 (ABCA1) is a widely expressed lipid transporter essential for the generation of HDL. ABCA1 is particularly abundant in the liver, suggesting that the liver may play a major role in HDL homeostasis. To determine how hepatic ABCA1 affects plasma HDL cholesterol levels, we treated mice with an adenovirus (Ad)-expressing human ABCA1 under the control of the cytomegalovirus promoter. Treated mice showed a dose-dependent increase in hepatic ABCA1 protein, ranging from 1.2-fold to 8.3-fold using doses from 5 x 108 to 1.5 x 109 pfu, with maximal expression observed on Day 3 posttreatment. A selective increase in HDL cholesterol occurred at Day 3 in mice treated with 5 x 108 pfu Ad-ABCA1, but higher doses did not further elevate HDL cholesterol levels. In contrast, total cholesterol, triglycerides, phospholipids, non-HDL cholesterol, and apolipoprotein B levels all increased in a dose-dependent manner, suggesting that excessive overexpression of hepatic ABCA1 in the absence of its normal regulatory sequences altered total lipid homeostasis. At comparable expression levels, bacterial artificial chromosome transgenic mice, which express ABCA1 under the control of its endogenous regulatory sequences, showed a greater and more specific increase in HDL cholesterol than Ad-ABCA1-treated mice. Our results suggest that appropriate regulation of ABCA1 is critical for a selective increase in HDL cholesterol levels.     

Control of the bifunctional O2-sensor kinase NreB of Staphylococcus carnosus by the nitrate sensor NreA: Switching from kinase to phosphatase state

The NreB–NreC two-component system of Staphylococcus carnosus for O₂ sensing cooperates with the accessory nitrate sensor NreA in the NreA–NreB–NreC system for coordinated sensing and regulation of nitrate respiration by O₂ and nitrate. ApoNreA (NreA in the absence of nitrate) interacts with NreB and inhibits NreB autophosphorylation (and activation). NreB contains the phosphatase motif DxxxQ. The present study shows that NreB on its own was inactive for the dephosphorylation of the phosphorylated response regulator NreC (NreC-P), but co-incubation with NreB and NreA stimulated NreC-P dephosphorylation. Either the presence of instead of apoNreA or mutation of the phosphatase motif (D160 or Q164) of NreB abrogated phosphatase activity of NreB. Phosphatase activity was observed for anoxic (active) NreB as well as oxic NreB, therefore the functional state of NreB is not relevant for phosphatase activity. Thus, NreB is a bifunctional sensor kinase with an integral cryptic phosphatase activity. Activation of phosphatase activity and dephosphorylation of NreC-P requires NreA as a cofactor. Accordingly, NreA and nitrate have major and dual roles in NreA–NreB–NreC regulation by (i) inhibiting NreB phosphorylation and (ii) triggering a kinase/phosphatase switch of NreB when present as apoNreA.