The impact of within-litter weight variation on the productivity of pig enterprises is poorly understood. The objective of the study was to determine the effect of within-litter birth weight variation on litter performance at three weeks of age and at weaning. The study was conducted using records from 1 788 litters, collected between January 1998 and September 2010, from a pig herd at the Agricultural Research Council (ARC), Irene. The records consisted of piglet identity, breed of sow, breed of boar, parity number, date of farrowing, number of piglets born alive (NBA), individual piglet weight at birth, three weeks and at weaning. From these records, mean birth weight (MBWT), litter weight at birth (TBWT), within-litter birth weight coefficient of variation (CVB), minimum birth weight (MinB) and maximum birth weight (MaxB) were calculated. Mean weight at three weeks (MWTT), litter weight at three weeks (LWTT), within-litter weight coefficient of variation at three weeks (CVT), percent survival to three weeks (SURVT), mean litter weaning weight (MWWT), litter weight at weaning (LWWT), within-litter weaning weight coefficient of variation (CVW) and percent survival at weaning (SURVW) were computed as derivatives. The factors affecting CVB were analysed using the General Linear Model procedures (SAS, 2008). For the relationships between CVB and litter performance at three weeks and weaning, PROC STEPWISE was used. The PROC REG (SAS, 2008) was then used to test whether the relationships between CVB and CVT, SURVT, MWTT, LWTT, CVW, SURVW, MWWT, LWWT and LWWT. Multiparous sows farrowed litters with higher (P<0.05) CVB than gilts. The litter weight (TBWT) and NBA, fitted as covariates, also affected (P<0.05) CVB. The correlation between CVB and NBA was 0.30. The CVB had a linear relationship (P<0.05) with SURVT (SURVT = 83.21 - 0.20 CVB), CVT (CVT = 16.71 + 0.50 CVB), SURV (SURW = 87.9 – 0.04CVB) and CVW (CVW= 15.8 + 0.5CVB). An increase of CVT with CVB depended on parity (P<0.05). The rate of increase of CVT with CVB was highest in Parity 1 (b=0.41) followed by Parity 2 (b=0.36) then middle aged (Parity 3-5) sows (b=0.32). The CVB had no effect on MWTT, LWTT, MWWT and LWWT (P>0.05). The CVB was shown to be an important determinant of SURVT and SURVW. A uniform litter at birth is likely to lead to a homogenous litter at three weeks and weaning, thereby reducing costs of production. Pig producers should, therefore aim at producing homogenous litters at birth. / Thesis (M.Sc.Agric.)-University of KwaZulu-Natal, Pietermaritzburg, 2011.

This thesis tests the hypothesis that increased neuronal cell death in SIDS infants is related to the ability of risk factors, such as prone sleeping, to expose infants to intermittent hypercapnic hypoxia (IHH). Based on the hypothesis that the NMDA system is linked to neuronal death, by way of excitotoxicity, correlations were also sought between cell death and changes in NMDA receptor (NR1) expression in brainstem nuclei controlling cardiorespiratory function. The first aim of this study was to verify that increased neuronal cell death occurs in SIDS infants. To verify a piglet model of SIDS risk factors, brainstem changes were examined in piglets exposed to IHH, and comparisons were made to changes seen in SIDS infants. The NMDA receptor was characterised in controls for both the human infant and the piglet groups. Comparisons of neuronal changes were made with SIDS infants, and piglets exposed to IHH. Non-radioactive in-situ hybridisation and immunohistochemistry were performed on formalin fixed and paraffin embedded brainstem tissue to identify markers of cell death (caspase-3, active caspase-3, and TUNEL), and to examine NR1 mRNA and protein expressions. Staining was quantified using computerised image analysis software. Eight nuclei from the brainstem medulla (caudal in piglets, and mid in infants), and two nuclei from the rostral pons (infants) were studied. The first dataset included human infants aged 1-6 months with a diagnosis of SIDS (n=15) or non-SIDS (n=10). The second dataset comprised developing piglets aged 13-14 days, with controls (n=6), against those exposed to IHH for 2 (n=6) or 4 (n=5) days. Increased neuronal cell death was not verified in the SIDS infants, but abnormalities in NR1 expression were present in selected nuclei of the medulla. Piglets exposed to IHH had increased neuronal cell death and changes in NR1 in selected nuclei of the medulla. There was also a positive correlation between increased cell death and high NR1 levels. Preliminary data showed that SIDS infants who usually slept prone had some differences in NR1 compared to those who did not usually sleep prone. From these findings, it was concluded that IHH may underlie the abnormalities in NMDA receptor expression that are present in the brainstem of SIDS infants. Although IHH can induce an increase in neuronal cell death, its significance in the aetiology of SIDS is not known. In piglets, IHH induced cell death correlated with high NMDA expression in some brainstem nuclei, supporting the hypothesis that excitotoxicity may be involved in the mechanism for cell death. Moreover, this thesis presents for the first time, �preliminary pathological proof� of an association between prone sleeping and abnormal NMDA receptor expression in SIDS infants.

Diss. (sammanfattning). Uppsala : Sveriges lantbruksuniv., 2003. / Härtill 4 uppsatser.

Diss. (sammanfattning) Uppsala : Sveriges lantbruksuniv. / Härtill 5 uppsatser.

Diss. (sammanfattning) Uppsala : Sveriges lantbruksuniv. / Härtill 4 uppsatser.

Diss. (sammanfattning) Alnarp : Sveriges lantbruksuniv. / Härtill 6 uppsatser.

Diss. (sammanfattning) Uppsala : Sveriges lantbruksuniversitet, 2004. / Härtill 5 uppsatser.

Diss. (sammanfattning) Uppsala : Sveriges lantbruksuniv., 2008. / Härtill 4 uppsatser.

Thesis (M.S.)--Ohio State University, 2009. / Title from first page of PDF file. Includes bibliographical references (p. 85-94).

Thesis (M.Sc.)--University of Alberta, 2009. / A thesis submitted to the Faculty of Graduate Studies and Research in partial fulfillment of the requirements for the degree of Master of Science in Experimental Surgery, Department of Surgery, University of Alberta. Title from pdf file main screen (viewed on July 28, 2009). Includes bibliographical references.