Reproduction performances and conditions of group-housed non ...

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- Appendix 1 - Figure 2. A pig embryo approximately 30 days old (Maddox-Hyttel, 2003) The major part of prenatal mortality occurs in the first 35 days of pregnancy and perhaps especially before day 18 of pregnancy (Pope & First, 1985; van der Lende et al., 1994). The average embryo mortality is in the range of 20-30 % but with large variation between and within populations (van der Lende et al., 1994). The last mentioned is illustrated in a study by van der Lende (1989) where the embryo mortality varied from 0 to 67 % in 71 gilts. Hormonal control of reproduction The above-mentioned physiological events are under sharp endocrine control of the hypothalamo-piturity-ovarian axis (Turner et al., 2002). Gonadotrophin-releasing hormone (GnRH) is released from the hypothalamus and transported to the anterior pituitary gland where it stimulates the release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH). Luteinizing hormone and FSH act on the ovaries to stimulate the development of the pre-ovulatory follicle (Foxcroft & Hunter, 1985). FSH is necessary to support follicular growth up to 5-6mm whereas LH is necessary for the final stages of follicle maturation (Britt et al., 1985). These developing follicles produce oestrogen, which is the primary trigger of oestrus behaviour (Hughes et al., 1996). The increased level of oestrogen influences the hypothalamus to increase the secretion of LH. The LH peak introduces changes in the follicle wall eventually leading to ovulation (Hughes et al., 1996). The ratio of oestrogen and progesterone and the level of prostaglandin influence the transport of the released ova to the site of fertilisation by causing contractions of the oviduct (Frandson & Spurgeon, 1992). Oestrogen and prostaglandin increase uterine activity and progesterone decreases uterine activity (Langendijk, 2001). Prostaglandin is also involved in the transport of semen from the uterus to the site of fertilisation (Soede, 1993). This transport is furthermore depending on small amounts of oxytocin, released from the posterior gland at the onset of oestrus, causing strong contractions of the uterus (Hughes & Varley, 1980). The oxytocin release is augmented by both external (the presence of a boar) and internal stimulation (from seminal oestrogens) (Soede, 1993). 114
- Appendix 1 - Soon after ovulation the granulosa cells lining the follicle wall begins to multiply to form a corpus luteum (CL) (Anderson, 2000). If fertilisation does not occur, prostaglandin produced by the uterus is transferred to the ovary were it induces regression of CL. Corpus Luteum is essential for maintenance of pregnancy because CL is the only source of progesterone in the sow and progesterone is essential during the whole period of pregnancy (van der Lende, 1989). The main function of CL is the secretion of progesterone. Progesterone stimulates uterine secretions (among other things IGF-1) and progesterone is the primary director of uterine development and secretion (Geisert & Yelich, 1997). Furthermore progesterone is necessary to prevent contractions of the uterus, which would be caused by ele- vated levels of oestrogen (Hughes et al., 1996). Both oestrogen (Stroband & Lende, 1990) and progesterone are involved in preparing the uterine wall for the attachment of the em- bryos (Hughes & Varley, 1980). There are indications that LH is essential for maintenance of the CL beyond the first 12 days of pregnancy but that this requirement for LH decreases after day 29 of pregnancy (Peltoniemi et al., 1995; Hughes et al., 1996). To avoid regression of CL at day 16 in oestrus cycle the embryo around day 11-12 secretes oestrogen (Bazer et al., 1982; Geisert & Yelich, 1997). This is also called ‘the embryonic signal’ (Peltoniemi et al., 2000) or ‘the maternal recognition signal’ (Geisert et al., 1987). Accord- ing to Bazer et al. (1982;1984) oestrogen produced by the embryo directs the prostaglandin synthesised in the uterus into the uterine lumen which prevent their release to the uterine vascular bed and therefore prevents the regression of CL. Oxytocin (Geisert & Yelich, 1997), which secretion from the endometrium is stimulated by oestrogen, and prolactin (Gross et al., 1990 cf Geisert et al., 1994) may also play a role in this redirection of prostaglandin. Bazer et al. (1984) suggested that prostaglandin is only luteolytic on day 12 or later after onset of oestrus. However, Estill et al. (1993) found that repeated treatment with prostaglandin from day five to day ten also resulted in luteolysis. Geisert et al. (1994) hy- pothesise that, before the first embryonic signal, progesterone controls the release of prostaglandin. It seems that a second prolonged embryonic oestrogen signal is required after day 14 to maintain pregnancy beyond day 30 (Geisert et al., 1987). At the time of parturition foetal cortisol stimulate the prostaglandin production in the uterus, which causes regression of the CL followed by a drop in progesterone level (Hughes et al., 1996; Anderson, 2000). Discussion The above-mentioned emphasize that a successful reproduction depends upon a series of precisely timed physiological and endocrine events. These events may be disturbed by various factors. There are thus indications that the endocrine regulation may be disturbed by e.g. stress, as indicated by increased cortisol. In several studies, administration of corti- 115
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Reproduction performances and condi
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Contents Summary………………
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Paper II - Summary - A review of 15
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- Sammendrag - SAMMENDRAG Antallet
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- Sammendrag - søgt. Positive korr
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- Background and aim - systems and
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- Outline of this thesis - OUTLINE
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- How does group housing vary in pr
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- How does group housing vary in pr
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- Paper I - Effect of energy intake
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- Paper I - 1. Introduction The num
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- Paper I - Therefore, the aim of t
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Refer ence Table 1. Effect of energ
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- Paper I - Therefore, low energy s
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Table 2. Effect of energy intake in
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- Paper I - However, this does not
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Table 3. Effect of energy intake in
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- Paper I - Feeding sows 16, 27 or
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- Paper I - gonadotrophins (LH, FSH
Page 46 and 47:
- Paper I - the first four weeks af
Page 48 and 49:
- Paper I - Cosgrove, J.R., Foxcrof
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- Paper I - Matschke, G.H., 1964. T
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- Paper I - Tribble, L.F., Orr, D.E
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- Paper III - Indicators of feed in
Page 57 and 58:
- Paper III - 1. Introduction The n
Page 59 and 60: Table 1. Applied feeding and housin
Page 61 and 62: - Paper III - performed. The sow ha
Page 63 and 64: - Paper III - proximately three wee
Page 65 and 66: - Paper III - Table 3. Overall mean
Page 67 and 68: Table 5. Correlations between all c
Page 69 and 70: Back fat W, mm Back fat gain, AM-F,
Page 71 and 72: - Paper III - from three weeks afte
Page 73 and 74: - Paper III - Number of skin lesion
Page 75 and 76: - Paper III - In herds practising g
Page 77 and 78: - Paper III - Previous work have fo
Page 79 and 80: References - Paper III - Andersen,
Page 81 and 82: - Paper III - Kongsted, A.G. 2004a.
Page 83 and 84: - Paper IV - Relation between repro
Page 85 and 86: - Paper IV - 1. Introduction Group
Page 87 and 88: - Paper IV - ing compared to number
Page 89 and 90: - Paper IV - mixed model using the
Page 91 and 92: Table 2. Estimates and standard err
Page 93 and 94: - Paper IV - cial effect on high ra
Page 95 and 96: References - Paper IV - Aherne, F.X
Page 97 and 98: - Paper IV - Olsson, A.-C., Svendse
Page 99 and 100: - General discussion - GENERAL DISC
Page 101 and 102: - General discussion - However, an
Page 103 and 104: References - General discussion - A
Page 105 and 106: - Conclusions - 6. CONCLUSIONS Two
Page 107 and 108: - Appendix 1 - APPENDIX 1 LITTER SI
Page 109: - Appendix 1 - they are mature i.e.
Page 113 and 114: - Appendix 1 - Crombie, P.L., 1970.
Page 115: - Appendix 1 - Scott, M.A., 2000. A
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