Characteristics of biter and victim piglets apparent before a tail biting outbreak

Little is known about the characteristics of biters and victims before the appearance of a tail-biting outbreak in groups of pigs. This study aimed to characterise biters and victims (according to gender and performance) and to quantify their behavioural development during the 6 days preceding the tail-biting outbreak. The hypotheses tested were: (a) biters are more often female, are the lighter pigs in the group, are more restless and perform more aggressive behaviour; and (b) victims are more often male, heavier and less active. Using video recordings we carried out a detailed study of 14 pens with a tail-biting outbreak among the weaned piglets. All piglets were individually marked and we observed the behaviour of biters, victims and control piglets (piglet types). In every pen, each piglet type was observed every other day from 6 days before (D-6) to the day of the first visible tail damage (i.e. day of tail biting outbreak; D0). While the number of male biters (6 of the 14 biters) and male victims (11 of the 14 victims) was not significantly different (P = 0.13), this numerical contrast was considerable. The start weight of victims was significantly (P = 0.03) higher (8.6 kg) than those of biters (7.5 kg) and control piglets (8.0 kg). Biters tended (P = 0.08) to spend longer sitting/kneeling (3.1 min/h) than controls (1.7 min/h), but no differences were seen in the time spent lying or standing. Victims tended (P = 0.07) to change posture more often (restlessness) than controls and chased penmates more (P = 0.04) than biters. Victims also performed more (P = 0.04) aggressive behaviour than biters and controls. In contrast, biters tended (P = 0.08) to be chased by penmates more often and tended (P = 0.06) to receive more aggressive behaviour than controls. Furthermore, biters spent longer manipulating the enrichment device (P = 0.01) and the posterior/tail (P = 0.02) of their penmates than controls and tended (P = 0.06) to perform more tail bites than victims. Victims received more posterior/tail manipulation (P = 0.02) and tail bites (P = 0.04) than controls. It was also noticed that, independent of piglet type, restlessness (P = 0.03) increased and the frequency of performed tail bites tended (P = 0.08) to increase in the 6 days preceding a tail-biting outbreak. These findings may contribute to the early identification of biters or victims and support the development of strategies to minimise the occurrence of tail bitin

French responses to the Prague Spring: connections, (mis)perception and appropriation

Looking at the vast literature on the events of 1968 in various European countries, it is striking that the histories of '1968' of the Western and Eastern halves of the continent are largely still written separately.1 Nevertheless, despite the very different political and socio-economic contexts, the protest movements on both sides of the Iron Curtain shared a number of characteristics. The 1968 events in Czechoslovakia and Western Europe were, reduced to the basics, investigations into the possibility of marrying social justice with liberty, and thus reflected a tension within European Marxism. This essay provides an analysis specifically of the responses by the French left—the Communist Party, the student movements and the gauchistes—to the Prague Spring, characterised by misunderstandings and strategic appropriation. The Prague Spring was seen by both the reformist and the radical left in France as a moderate movement. This limited interpretation of the Prague Spring as a liberal democratic project continues to inform our memory of it

Activation of the E-cadherin/catenin complex in human MCF-7 breast cancer cells by all-trans-retinoic acid.

All-trans-retinoic acid (RA), like insulin-like growth factor I (IGF-I) and tamoxifen, inhibit invasion of human MCF-7/6 mammary cancer cells in vitro. For tamoxifen and for IGF-I, activation of the invasion-suppressor function of the E-cadherin/catenin complex was shown to be the most probable mechanism of the anti-invasive action. We did a series of experiments to determine whether the anti-invasive effect of RA also implicated the invasion-suppressor E-cadherin/catenin complex. Human MCF-7/6 mammary and HCT-8/R1 colon cancer cells, both with a dysfunctional E-cadherin/catenin complex, were treated with RA and the function of the complex was evaluated through Ca(2+)-dependent fast aggregation. Fast aggregation of both MCF-7/6 and HCT-8/R1 cells was induced by 1 microM RA. This effect was abolished by antibodies against E-cadherin. RA-induced fast aggregation was not sensitive to cycloheximide, tyrosine kinase inhibitors or antibodies against IGF-I or against the IGF-I receptor. RA did not stimulate IGF-I receptor phosphorylation or alter the E-cadherin/catenin complex, as evidenced by immunoprecipitation. RA up-regulates the function of the invasion-suppressor complex E-cadherin/catenin. Its action mechanism is different from that of IGF-I. RA may act as an anti-invasive agent with unique mechanisms of action

The New RF Control System for the CERN SPS Accelerator

The old SPS RF control system designed in 1972 has been replaced completely, i.e. both hardware and software. The new system has to control both RF equipment conceived during the last 23 years and future (modern) equipment. Using information analysis methods, we derived a model of an RF command and designed a data base accordingly (ORACLE®). Information from this data base is used for command generation and processing and also for archiving settings. The advantage is purely generic software, i.e. the same computer code is used for switching on an RF amplifier, as for setting a frequency synthesizer. New equipment is added very simply by entering new records in the data base. Additional features include a reservation scheme whereby a user can take private control of any piece of equipment, a reporting facility notifying the user of the simultaneous control activity by other users on RF equipment, and a capability scheme assigning a level of expertise to each user restricting action on the equipment

Cowel-model geeft bedrijven een welzijnsscore

ASG ontwerpt baanbrekende houderijsystemen voor de melkveehouderij – het betreft stallen inclusief de belangrijke schakels in de keten, zoals de aanvoer van krachtvoer en kunstmest. Dit in opdracht van LNV. Het project kreeg de naam Kracht van Koeien. De onderzoekers bouwden onlangs een rekenmodel (Cowel) om de risico- of welzijnsscore van stalsystemen te bepale

Altered Cigarette Smoke-Induced Lung Inflammation Due to Ablation of Grx1

Glutaredoxins (Grx) are redox enzymes that remove glutathione bound to protein thiols, know as S-glutathionylation (PSSG). PSSG is a reservoir of GSH and can affect the function of proteins. It inhibits the NF-κB pathway and LPS aspiration in Grx1 KO mice with decreased inflammatory cytokine levels. In this study we investigated whether absence of Grx1 similarly repressed cigarette smoke-induced inflammation in an exposure model in mice. Cigarette smoke exposure for four weeks decreased lung PSSG levels, but increased PSSG in lavaged cells and lavage fluid (BALF). Grx1 KO mice had increased levels of PSSG in lung tissue, BALF and BAL cells in response to smoke compared to wt mice. Importantly, levels of multiple inflammatory mediators in the BALF were decreased in Grx1 KO animals following cigarette smoke exposure compared to wt mice, as were levels of neutrophils, dendritic cells and lymphocytes. On the other hand, macrophage numbers were higher in Grx1 KO mice in response to smoke. Although cigarette smoke in vivo caused inverse effects in inflammatory and resident cells with respect to PSSG, primary macrophages and epithelial cells cultured from Grx1 KO mice both produced less KC compared to cells isolated from WT mice after smoke extract exposure. In this manuscript, we provide evidence that Grx1 has an important role in regulating cigarette smoke-induced lung inflammation which seems to diverge from its effects on total PSSG. Secondly, these data expose the differential effect of cigarette smoke on PSSG in inflammatory versus resident lung cells