Circulating growth hormone (GH) concentrations increase in pregnancy and administration of GH during early-mid pregnancy increases fetal growth in well-fed pigs. To determine whether increased maternal GH could promote fetal growth when feed availability is restricted, fifteen cross-bred primiparous sows (gilts) were fed at approximately 30% of ad libitum intake, from mating onwards and were injected daily i.m. with recombinant porcine GH (pGH) at doses of 0, 13·4 0·3 and 25·6 0·5 µg/kg live weight from day 25 to day 51 of pregnancy (term 115 days). Treatment with pGH increased maternal backfat loss between day 25 and day 51 of pregnancy, and increased maternal plasma IGF-I concentrations measured at day 51 of pregnancy. Fetal body weight, length and skull width at day 51 of pregnancy were increased by maternal treatment with pGH. Fetal plasma glucose concentrations were increased and maternal/fetal plasma glucose concentration gradients were decreased by maternal pGH treatment at 13·4, but not 25·6 µg/kg.day. Fetal plasma concentrations of urea were decreased by both levels of pGH treatment. Overall, fetal weight was negatively correlated with fetal plasma concentrations of urea, positively correlated with maternal plasma -amino nitrogen concentrations and unrelated to glucose concentrations in either maternal or fetal plasma. This suggests that the availability of amino acids, not glucose, limits fetal growth in the first half of pregnancy in underfed gilts, and that maternal GH treatment may improve amino acid delivery to the fetus.
Treatment of pigs with porcine ST (pST) in early to mid-pregnancy increases body weight and length of their fetuses by mid-pregnancy, but this increased weight may not persist to birth. We investigated the effects of short- (25 d) and long-term (75 d) treatment with pST, and interactions between long-term pST treatment and crude protein content of diet, in restricted-fed gilts. In both experiments, Large White x Landrace gilts were bred at first estrus to Large White x Duroc boars and allowed to farrow naturally. In the first experiment, gilts were fed 1.8 kg/d of a diet containing 13.5 MJ DE/kg of DM and 15.05% CP (as-fed basis) throughout pregnancy, and were injected daily with 0, 2, or 4 mg pST from d 25 to 50 of pregnancy. Maternal treatment with pST from d 25 to 50 of pregnancy did not affect the number of piglets born per litter or progeny size at birth. In the second experiment, gilts were injected daily with 0 or 2 mg of pST and fed 2.2 kg/d of a diet containing 14.5 MJ DE/kg and either (as-fed basis) 16.6% (0.81% lysine) or 22.2% CP (1.16% lysine) from d 25 to 100 of pregnancy. All gilts were then fed 3.0 kg/d of the lower protein diet from d 100 of pregnancy to farrowing. Treatment with 2 mg pST/d from d 25 to 100 of pregnancy increased live weight of all gilts during the treatment period (P = 0.016), but the change in maternal live weight from d 25 to 100 of pregnancy was only increased (P = 0.001) by pST in gilts fed the higher protein diet. Live weight of gilts 1 d after farrowing was increased by pST treatment (P = 0.007), but was not altered by protein content of diet during pregnancy. In gilts fed the lower protein diet, but not in those fed the higher protein diet, pST treatment decreased maternal backfat depth during treatment (P < 0.020) and 1 d after farrowing (P = 0.002). Treatment with pST during pregnancy did not affect the number of piglets born per litter but independently increased body weight by 11.6% (P < 0.001) and length by 3.4% (P = 0.005) of progeny at birth and decreased (P < 0.01) the negative effect of litter size on body weight at birth. We conclude that in feed-restricted gilts, fetal weight gains in response to 25 d of pST treatment before mid-pregnancy are not maintained to term but that treatment with pST during most of pregnancy increases progeny size at birth and reduces maternal constraint of fetal growth.
Twenty-seven sows were allocated at their first farrowing to 3 experimental treatments in which their sucking pigs had access to no supplemental milk, liquid cow milk (CM), or a synthetic milk supplement (SM). Liquid cow milk contained 128 g total solids/kg, 24·2 g CP/kg, 30·4 g fat/kg, and 1·8 g lysine/kg, whereas the supplemental synthetic milk contained 200 g total solids/kg, 102·6 g CP/kg, 36·0 g fat/kg, and 9·0 g lysine/kg. All litters contained 12 pigs and the supplemental milk products were offered ad libitum from Day 4 of lactation until weaning at 28 days of age. Between Days 0 and 14 of lactation, there was no effect of treatment on supplemental milk intake or average piglet growth rate but between Days 14 and 28 of lactation, litters given milk supplements grew faster than litters receiving no supplemental milk. Overall, piglet growth rates between Days 0 and 28 of lactation were greater for litters receiving supplemental milk (297 and 277 g/day for CM and SM litters, respectively) than for litters receiving no supplemental milk (239 g/day). Piglets offered cow milk drank more milk between Days 4 and 28 of lactation than piglets offered the synthetic milk (5·48 v. 2·38 kg/day). Piglets in litters which had access to cow milk visited the supplemental feeder more often (5·5 v. 2·7 visits per suckling interval) and spent longer at the feeder (45·4 v. 14·5 s) than pigs in litters which had access to the synthetic milk supplement. Average sow milk production was 15·4 and 15·3 kg/day between Days 11 and 14 and between Days 25 and 28 of lactation, respectively, and was unaffected by treatment. Treatment also had no significant effect on average suckling interval on Day 21 of lactation (51·7 min) or carcass composition of representative pigs from each litter killed at 28 days of age. Between Days 14 and 28, female pigs grew faster than male pigs (304·3±9·3 v. 292·0±9· 2 g/day). These results demonstrate that provision of supplemental milk to sucking pigs can improve preweaning growth rate and the response increased as lactation proceeded.
Hospital, by the senior author were included. Data was collected from statistics department, theatre database, discharge registry, ICU and HDU register and patient clinical notes. Study end-points included operative time, shunt use, perioperative stroke, 30 day mortality, restenosis and re intervention. Results: 114 cCEA procedures were undertaken from July 2008 to December 2011, while 63 eCEA performed during Jan 2012 to July 2014. Results are shown in Table 1. Intraarterial shunts were used in 19 % of cCEA and 1.6% of eCEA cases. Patients were followed postoperatively by Duplex imaging. Death and stroke rate in both groups was 0 %. Operative time for eCEA was significantly less that the cCEA. There were 5 restenosis in cCEA and only one in eCEA (range 20 to 70%). Conclusion: eCEA is safe and effective technique for carotid endarterectomy. It significantly reduces the operative time with low re-stenosis rate.
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