Background: Non-invasive micro-ultrasound was evaluated as a method to quantify intrauterine growth phenotypes in mice. Improved methods are required to accelerate research using genetically-altered mice to investigate the interactive roles of genes and environments on embryonic and placental growth. We determined (1) feasible age ranges for measuring specific variables, (2) normative growth curves, (3) accuracy of ultrasound measurements in comparison with light microscopy, and (4) weight prediction equations using regression analysis for CD-1 mice and evaluated their accuracy when applied to other mouse strains.
The present study examined the effects of feeding gilts a high fibre diet from the third post-pubertal oestrus until either day 19 of the same cycle or insemination at the following oestrus on oocyte maturity, embryo survival and associated changes in reproductive hormone concentrations. Gilts fed with the high fibre diet had lower circulating oestradiol concentrations on days 17, 18 and 19 of the cycle and increased LH pulse frequency on day 18. More oocytes recovered on day 19 from gilts receiving the high fibre diet were at metaphase II after 46-h culture in medium containing 10% of their own follicular fluid, despite fewer large (O7 mm) follicles in these gilts when compared with control animals. There was no effect of diet on ovulation rate, corpora lutea size or progesterone concentrations on days 10-12 after insemination, but embryo survival on days 27-29 after insemination was higher in gilts that received the high fibre diet. This study demonstrates that a high fibre diet that increases embryo survival also improves oocyte maturity and provides information on endocrine correlates that may shed light on underlying mechanisms.
A retrospective cohort study of 116 British pig farms was undertaken to investigate the epidemiological risk factors associated with herd breakdowns with postweaning multisystemic wasting syndrome (PMWS). Farmers reported the PMWS status of their herd (case definition 1) and, where applicable, when the disease was first suspected and what they observed; they described a prolonged increase in mortality in six to 16-week-old pigs that was not attributable to any disease known to be on their farm. There was over 90 per cent agreement on the farmers' PMWS status between the farmers and their veterinarians. Approximately 70 per cent of the breakdowns were confirmed at the laboratory (case definition 2) except during the outbreak of foot-and-mouth disease (FMD) in 2001 when it was reduced to 30 per cent. Porcine circovirus type 2 antigen was detected in pigs examined postmortem (case definition 3) in approximately 90 per cent of the farms with increased mortality. The breakdowns occurred initially in the south of England and spread west and north, as well as locally in a radial pattern from the affected farms, and there was strong statistical evidence that there was non-random space-time clustering. The risk of herd breakdowns with PMWS was not constant; therefore, for each case definition, three survival models were developed with outcome variable time to breakdown of between January 2000 and January 2001, February 2001 to September 2001 (during FMD) or October 2001 to December 2003. Exposures with a bivariable significance of P<0.20 were tested in three multivariable Cox proportional hazard models. From January 2000 to January 2001 the risk of a herd breakdown with PMWS for definitions 1, 2 and 3 was greater for farms with 600 or more breeding sows, and for definitions 1 and 3 there was an increased risk associated with the purchase of replacement gilts rather than using homebred replacements. For definitions 1 and 3 the farms where the nearest pig farm had no breeding pigs were at greater risk of a breakdown than those where the nearest farm had breeding stock, as were the farms where visitors were not requested to avoid pigs for more than three days before visiting the farm during the FMD outbreak. From October 2001, the associated risks were identical for all three case definitions; farms were at greater risk when they had 600 or more breeding sows, if visitors had not avoided contact with pigs for more than three days before visiting the farm, and when there was a farm with PMWS less than five miles away. The affected farms were more likely to have disease associated with porcine parvovirus, porcine reproduction and respiratory syndrome virus, erysipelas, Escherichia coli and salmonella. These exposures were positively associated with large herds and the farm being close to other pig farms, but did not remain in the final models for breakdown with PMWS, indicating that such farms may be at greater risk of many infectious diseases.
Background: In utero microinjection has proven valuable for exploring the developmental consequences of altering gene expression, and for studying cell lineage or migration during the latter half of embryonic mouse development (from embryonic day 9.5 of gestation (E9.5)). In the current study, we use ultrasound guidance to accurately target microinjections in the conceptus at E6.5-E7.5, which is prior to cardiovascular or placental dependence. This method may be useful for determining the developmental effects of targeted genetic or cellular interventions at critical stages of placentation, gastrulation, axis formation, and neural tube closure.
Data from a cross-sectional study of 113 British pig herds carried out in 2004 were used to investigate the associations between postweaning multisystemic wasting (PMWS) in pigs and herds and porcine circovirus 2 (PCV2) antigen score and antibody titre, and associated histological signs in lymph nodes. The sensitivity and specificity of published herd definitions for PMWS were tested on the study farms to consider the role of PCV2 in PMWS. Herds were defined as PMWS-affected, -unaffected or -recovered based on current and past postweaning mortality (PWM), grower pigs with clinical signs of rapid wasting, hairiness and pallor and no other known cause of death on the farm. PCV2 antigen and antibody were not used in the definition of PMWS. In each PMWS-affected herd, up to three sick pigs with the clinical signs above and one healthy pig of a similar age were taken for postmortem examination (PME). In all other herds at least one healthy pig was taken for PME. Lymph nodes were analysed for PCV2 antigen and histological changes, and serum samples were analysed for PCV2 antibody. PCV2 antibody was present in all the herds sampled. There was a non-linear association between PCV2 antigen and antibody. There was no association between the presence of high scores of PCV2 antigen in pigs and the presence of high PWM in herds. PCV2 antigen score was significantly higher in sick than healthy pigs within farms, and high PCV2 score was associated with giant cells, coalescence and absence of germinal centres in lymph nodes. These results did not vary by PMWS-affected, -unaffected or -recovered farms. PCV2 antigen was present at high scores in approximately 10% of healthy pigs on all farms. All three herd definitions of PMWS were highly sensitive, defining PMWS-affected herds as affected, but had a specificity ranging from 23% to 43%. We conclude that the current diagnostic tests for PCV2 indicated higher scores of virus in sick pigs but were not useful to define pigs or herds with PMWS. The ubiquity of PCV2 and the lack of specificity of the PCV2 tests indicate that PCV2 may be a necessary but not sufficient cause of PMWS disease. Linking this with the knowledge that the herd breakdowns occurred in a space time epidemic indicates that another infectious co-factor may be necessary for disease to occur.
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