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Eighty pigs (average weight of 60 kg) were allotted by weight and sex to pens and treatments. There were four dietary treatments, five pens per treatment, and four pigs per pen. Diets consisted of a typical corn-soybean mix containing 9% total fat, 3% from the corn-soybean mix and 6% added. The four dietary treatments included 1) 6% safflower oil, 2) 4% safflower oil and 2% tallow, 3) 2% safflower oil and 4% tallow, and 4) 6% tallow, resulting in 6.1, 4.6, 3.2, and 1.76% linoleic acid, respectively, in the diet. Pigs were slaughtered at an average weight of 100 kg. Proximate composition, tristimulus color coordinates (L, a, and b values), pH, and flavor difference of the longissimus muscle (LM) were evaluated. Fatty acid content (milligrams per 100 grams of tissue) of the subcutaneous fat and LM and headspace volatile content of the LM were determined by capillary gas liquid chromatography. Proximate composition, color, pH, and flavor of the LM were not influenced by diet. Fatty acid content of the subcutaneous fat and LM and volatile content of the LM were influenced by diet. Increased levels of safflower oil in the diet resulted in less C16:0 and C18:1 and more C18:2, C20:2, and C20:3 in the subcutaneous fat. The LM contained more C18:2 and less C18:3 and C24:0 due to increased levels of safflower oil in the diet. Compared with the 6% tallow diet, LM from pigs fed the 4 or 6% safflower diets contained more pentanal, hexanal, 2-heptanone, trans-2-heptenal, 2-pentyl furan, 2-ethyl-1-hexanol, decanal, and undecanal.(ABSTRACT TRUNCATED AT 250 WORDS)

Two experiments were conducted at separate commercial farms. In Exp. 1, all primiparous sows and an equal number of multiparous sows weaned each week were randomly assigned to one of four treatment groups. Treatments consisted of one i.m. injection on the day of weaning of 0, 50, 100, or 200 mg of beta-carotene. Sows were checked for estrus with boars once daily and mated at first estrus after weaning. A sample of sows (n = 100) was selected for determination of plasma beta-carotene and vitamin A. Blood samples were obtained from another group (n = 120) 14 d after injection to determine plasma progesterone. In Exp. 2, treatments consisted of i.m. injection of 200 mg of beta-carotene, 50,000 IU of vitamin A, or vehicle on the day of weaning, on the day of mating, and on d 7 after mating. In both experiments, the sow diet was supplemented with 11,000 IU/kg of vitamin A. In Exp. 1, there was no effect of dose of beta-carotene on the interval from weaning to estrus or on the repeat service rate. There was a dose x parity interaction on the number of pigs born dead (P < .01) and born alive (P < .10), because treatment with beta-carotene did not affect reproduction in primiparous sows, but litters subsequently farrowed by multiparous sows had more pigs born alive and fewer pigs born dead. There was a dose x day interaction (P < .05) on plasma beta-carotene; beta-carotene was elevated on d 6 and 13 after injection.(ABSTRACT TRUNCATED AT 250 WORDS)

To produce a prolonged decrease m blood pressure, we have developed a nonpathogenic adeno-associated viral vector (AAV) with the antIsense DNA for AT1-R AAV has many advantages over other viral vectors AAV does not stimulate mflammallon or immune reaction AAV enters nondtvlchng cells and does not replicate Therefore, it IS an appropriate choice for gene therapy Recombinant AAV was prepared with a cassette contaumg a cytomegalovtrus promoter and the cDNA for the AT, receptor inserted m the annsense dire&on The cassette was packaged ohgonucleotides, directed to either AT,-R mRNA or to anglotensmogen mRNA, slgmfscantly reduce blood pressure m hypertensive animals with a single mJection mto the bram I-3 Although the adn-nmstration of antisense m the brain proved that antlsense can reduce high blood pressure of neurogemc orlgm, it obviously 1s not an acceptable route for treatment of human hypertension To demonstrate that antisense acts via a systemic route of delivery, we have shown that antisense delivered mtravenously4 or mtra-arterially5 can also reduce blood pressure m hypertensive rats. Antisense AT1 mRNA significantly decreased the blood pressure m 2&idney, 1 clip rats, m which circulating remn-Ang levels are high 4 Anglotensmogen mRNA-directed antIsense ohgonucleotide, in a hposome carrier inJected mtravenously m SHR, also decreased hypertension 5 The uptake of antisense was predommantly m the hver, as shown by fluorescent-tagged antisense. A sm-nlar approach was taken by Tomlta et al," who prepared three angiotensmogen mRNA-directed antisense ohgonucleotides and delivered them m hposomes and Sendal virus by direct mJectlon mto the hepatlc portal vem They also noted a decrease m blood pressure m SHR While these results have been encouraging for the use of antisense as a poFrom the Department of Physiology, College of Medicine, Unlversity of Florlda, Gamesvllle, Fla, and Harvard Medical School (P W ), Boston, MassCorrespondence to Dr M I Pixlhps, Department of Physiology, College of Medicine, Utuverslty of Flonda, Gamesvllle, FL 32610 E-mad MIP@phys med ufl edu 0 1997 American Heart Assoclatron, Inc tential treatment of hypertension, the maximum effectlveness of a single injection lasts for 7 days. Although this 1s Impressively longer than the response to a single dose of any antlhypertenslve drug currently available, it 1s our hope that we can extend the effectiveness of the antisense approach by delivering antisense m a viral vector that will produce a prolonged reduction m blood pressure for weeks or months There are several vu-al vectors to choose from, mcludmg retrovlruses, adenovlrus, herpes virus, polo virus, and AAV All have disadvantages and some advantages, but the AAV offers the most attractive advantages and the fewest disadvantages AAV 1s safe to use It does not induce any pathogenic response and does not replicate mslde cells The AAV 1s a defective parvovlrus and cannot replicate m cells without the presence of wild-type adenovlrus 73 The AAV IS effective as a vector because it either mt...

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The experiment investigated the effects of a supplemental candy coproduct (Chocolate Candy Feed [CCF]; International Ingredient Corp., St. Louis, MO), an alternative carbohydrate source to dietary lactose, on growth performance and on health status of nursery pigs. Crossbred pigs ( = 1,408; 21 d of age and 7.1 ± 0.3 kg BW; Smithfield Premium Genetics, Rose Hill, NC) were randomly assigned to 4 treatments (16 pens/treatment and 22 pigs/pen) in a randomized complete block design: 0, 15, 30, and 45% of lactose replaced by CCF based on equal amounts of total sugars. The experimental period was divided into 3 phases: phase I (1.8 kg diet/pig for 11 ± 1 d), phase II (6.8 kg diet/pig for 17 ± 2 d), and phase III (until 49 d after weaning). Pigs received a common phase III diet. The levels of lactose, supplied by whey permeate (79.3 ± 0.8% lactose), were 20, 8, and 0% in phase I, II, and III, respectively. All experimental diets contained the same levels of essential AA and energy (ME) for each phase. Fecal scores were observed on d 5, 7, and 9 after weaning. Blood samples were taken at the end of phase I and II to measure blood urea N. The duration of phase I tended to linearly decrease ( = 0.063) with increasing CCF. In phase I, the ADFI increased ( < 0.05) with increasing CCF whereas ADG and G:F did not change. In phase II, the duration and ADFI did not change whereas ADG linearly decreased ( < 0.05) with increasing CCF. However, the G:F was not changed as CCF increased. During phase I and II together, the duration was linearly decreased ( < 0.05) as CCF increased, whereas no difference in growth performance was observed. Overall, ADFI, ADG, and G:F were not affected by replacing whey permeate with CCF in diets, indicating no adverse effects of a candy coproduct as a carbohydrate substitute to lactose on growth performance of nursery pigs. Blood urea N did not change in phase I but tended to linearly increase ( = 0.088) in phase II as CCF increased. There were no differences in fecal scores and mortality as CCF increased. However, increasing CCF tended to linearly decrease ( = 0.083) morbidity, which implies no adverse effects of a candy coproduct replacement on health status of nursery pigs. In conclusion, a candy coproduct can be used to replace up to 45% of dietary lactose for nursery pigs without negative effects on growth performance or health status. A candy coproduct could be an economical alternative to partly replace the use of lactose in swine production.