Viscoelastic surfactants (VES) have been widely used in acidizing and acid fracturing. They are used as diversion agents during matrix acid treatments and leakoff control agents during acid fracturing. At high temperatures, viscoelastic surfactants hydrolyze, resulting in phase separation after a certain time. Their viscosities significantly decrease and it is much easier for them to flow back causing much less damage to the formation. In this study, 4 to 8 wt% of a new VES-acid system was tested at temperatures of up to 250°F over hydrolysis times of 0 to 6 hours. Then, the solutions were neutralized by calcium carbonate until the pH reached 4.5. An HP/HT rheometer was used to measure the viscosity of the spent acids. Mass spectrometry (MS) was conducted to analyze the hydrolysis products of the VES. Coreflood tests were also conducted on Indiana limestone to determine the effects of the hydrolysis products on the permeability of these cores. The temperature was set at 250°F and the flow rate at 2.5 cm^(3)/s. The viscosities of all VES-acid systems remained high at the beginning of hydrolysis, which was good for acid diversion. After that, the VES acid systems experienced a significant viscosity reduction due to phase separation; it became much easier for the spent acid to flow back. Coreflood experiments caused little damage to the Indiana limestone. MS results indicated hydrolysis of peptide bonds. Fatty acids formed the top oil layer, and amine-based molecules formed the aqueous phase. This study will summarize and discuss the details of viscosity changes of the acid systems of this kind of viscoelastic surfactant, the damage caused by hydrolysis products, and how this kind of viscoelastic surfactant can be used to improve treatments.

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A major challenge for the pig industry is to formulate starter diets that primarily fit the digestive capacity, maintain GIT health and promote growth without recourse to in-feed antimicrobials. Experiments were conducted to evaluate the efficacy of carbohydrase enzymes (CE) targeting non-starch polysaccharides (NSP) in enhancing gut health and function in piglets. First, an experiment was conducted to evaluate the effects of adding CE in piglet diets on growth performance, GIT bacterial activity and nutrient digestibility. Pigs fed diets containing CE had a higher ileal lactobacilli count, total organic acids concentrations, NSP digestibility and low ammonia compared with control. The effectiveness of CE targeting NSP was further evaluated using enterotoxigenic E. coli (ETEC) in a challenge model to evaluate the impact on gut health and function. Two approaches for the ETEC challenge were adopted; an in situ small intestine segments perfusion model and an in vivo model. Initially, a pilot study was conducted to establish and validate the in situ model. In the pilot study, conventional anti-diarrhea agents; fumaric acid, ZnO, egg yolk antibodies against ETEC K88 fimbriae and carbadox, attenuated fluid losses in ETEC-infected jejunal segments. Following the establishment of the in situ model, four experiments were conducted to study the effects NSP hydrolysis products (HP) from various feedstuffs (i.e. wheat, soybean meal, canola meal and flaxseed) on ETEC-induced secretory diarrhea. The results demonstrated that HP protected against ETEC-induced fluid and electrolyte losses. A further study was conducted to investigate the response of piglets fed diets containing HP and EYA singly or in combination upon oral challenge with ETEC. Feeding HP and EYA alone or in combination attenuated ETEC-enteritis symptoms such that piglets fed additives showed less pronounced acute phase responses and superior performance. Piglets fed diets containing additives had lower gastric pH, fewer ETEC adhered to ileal mucosa and lower incidence of diarrhea. Overall, reduction of intestinal pathogens or toxic bacterial metabolites contributes to enhanced GIT health and function. These novel results expand the scope of enzyme technology in animal nutrition within the new paradigm of dietary approaches to gut health and function.

A major challenge for the pig industry is to formulate starter diets that primarily fit the digestive capacity, maintain GIT health and promote growth without recourse to in-feed antimicrobials. Experiments were conducted to evaluate the efficacy of carbohydrase enzymes (CE) targeting non-starch polysaccharides (NSP) in enhancing gut health and function in piglets. First, an experiment was conducted to evaluate the effects of adding CE in piglet diets on growth performance, GIT bacterial activity and nutrient digestibility. Pigs fed diets containing CE had a higher ileal lactobacilli count, total organic acids concentrations, NSP digestibility and low ammonia compared with control. The effectiveness of CE targeting NSP was further evaluated using enterotoxigenic E. coli (ETEC) in a challenge model to evaluate the impact on gut health and function. Two approaches for the ETEC challenge were adopted; an in situ small intestine segments perfusion model and an in vivo model. Initially, a pilot study was conducted to establish and validate the in situ model. In the pilot study, conventional anti-diarrhea agents; fumaric acid, ZnO, egg yolk antibodies against ETEC K88 fimbriae and carbadox, attenuated fluid losses in ETEC-infected jejunal segments. Following the establishment of the in situ model, four experiments were conducted to study the effects NSP hydrolysis products (HP) from various feedstuffs (i.e. wheat, soybean meal, canola meal and flaxseed) on ETEC-induced secretory diarrhea. The results demonstrated that HP protected against ETEC-induced fluid and electrolyte losses. A further study was conducted to investigate the response of piglets fed diets containing HP and EYA singly or in combination upon oral challenge with ETEC. Feeding HP and EYA alone or in combination attenuated ETEC-enteritis symptoms such that piglets fed additives showed less pronounced acute phase responses and superior performance. Piglets fed diets containing additives had lower gastric pH, fewer ETEC adhered to ileal mucosa and lower incidence of diarrhea. Overall, reduction of intestinal pathogens or toxic bacterial metabolites contributes to enhanced GIT health and function. These novel results expand the scope of enzyme technology in animal nutrition within the new paradigm of dietary approaches to gut health and function.

The expanding therapeutic use of thalidomide (TD) remains limited by its species-specific teratogenicity in humans and rabbits, but not rodents. The R and S isomers of TD may be selectively responsible for its respective therapeutic and teratogenic effects, but rapid in vivo racemization makes this impossible to confirm. Fluorothalidomide (FTD), a fluorinated TD analogue with stable, non-racemizing isomers, may serve as a model compound for determining stereoselective effects. In vivo, FTD was undetectable in plasma, suggesting rapid breakdown, as confirmed in vitro, where FTD hydrolyzed up to 22-fold faster than TD. Unlike TD, FTD in pregnant rabbits and mice was highly toxic and lethal to both dams and fetuses. In rabbit embryo culture, FTD initiated optic (eye) vesicle and hindbrain but not classic limb bud embryopathies. Chemical instability, potent general toxicity and absence of limb bud embryopathies make FTD an unsuitable stereoselective model for TD teratogenesis. TD teratogenesis may involve its bioactivation by embryonic prostaglandin H synthases (PHSs) to a free radical intermediate that increases embryopathic reactive oxygen species (ROS) formation. However, the teratogenic potential of rapidly formed TD hydrolysis products and the determinants of species-specific teratogenesis are unclear. For some teratogens, mouse strains that are resistant in vivo are susceptible in embryo culture, suggesting maternal and/or placental determinants of risk. However, TD and two hydrolysis products, 2-phthalimidoglutaramic acid (PGMA) and 2-phthalimidoglutaraic acid (PGA), were non-embryopathic in CD-1 mouse embryo culture. Also, mice deficient in oxoguanine glycosylase 1 (OGG1), which repairs oxidatively damaged DNA, were resistant to TD embryopathies in culture and in vivo. Therefore, murine resistance to TD teratogenesis is dependent on embryonic factors, rather than maternal/placental determinants or increased DNA repair. In contrast, rabbit embryos exposed in culture to TD, PGMA and PGA exhibited head/brain, otic (ear) vesicle and classic limb bud embryopathies, validating the first mammalian embryo culture model for TD teratogenesis and providing the first evidence of a teratogenic role for TD hydrolysis products. Pretreatment with eicosatetraynoic acid (ETYA), a dual PHS/lipoxygenase inhibitor, or phenylbutylnitrone (PBN), a free radical spin trapping agent, completely blocked TD, PGMA and PGA-initiated embryopathies, implicating a PHS-dependent, ROS-mediated embryopathic mechanism.

The expanding therapeutic use of thalidomide (TD) remains limited by its species-specific teratogenicity in humans and rabbits, but not rodents. The R and S isomers of TD may be selectively responsible for its respective therapeutic and teratogenic effects, but rapid in vivo racemization makes this impossible to confirm. Fluorothalidomide (FTD), a fluorinated TD analogue with stable, non-racemizing isomers, may serve as a model compound for determining stereoselective effects. In vivo, FTD was undetectable in plasma, suggesting rapid breakdown, as confirmed in vitro, where FTD hydrolyzed up to 22-fold faster than TD. Unlike TD, FTD in pregnant rabbits and mice was highly toxic and lethal to both dams and fetuses. In rabbit embryo culture, FTD initiated optic (eye) vesicle and hindbrain but not classic limb bud embryopathies. Chemical instability, potent general toxicity and absence of limb bud embryopathies make FTD an unsuitable stereoselective model for TD teratogenesis. TD teratogenesis may involve its bioactivation by embryonic prostaglandin H synthases (PHSs) to a free radical intermediate that increases embryopathic reactive oxygen species (ROS) formation. However, the teratogenic potential of rapidly formed TD hydrolysis products and the determinants of species-specific teratogenesis are unclear. For some teratogens, mouse strains that are resistant in vivo are susceptible in embryo culture, suggesting maternal and/or placental determinants of risk. However, TD and two hydrolysis products, 2-phthalimidoglutaramic acid (PGMA) and 2-phthalimidoglutaraic acid (PGA), were non-embryopathic in CD-1 mouse embryo culture. Also, mice deficient in oxoguanine glycosylase 1 (OGG1), which repairs oxidatively damaged DNA, were resistant to TD embryopathies in culture and in vivo. Therefore, murine resistance to TD teratogenesis is dependent on embryonic factors, rather than maternal/placental determinants or increased DNA repair. In contrast, rabbit embryos exposed in culture to TD, PGMA and PGA exhibited head/brain, otic (ear) vesicle and classic limb bud embryopathies, validating the first mammalian embryo culture model for TD teratogenesis and providing the first evidence of a teratogenic role for TD hydrolysis products. Pretreatment with eicosatetraynoic acid (ETYA), a dual PHS/lipoxygenase inhibitor, or phenylbutylnitrone (PBN), a free radical spin trapping agent, completely blocked TD, PGMA and PGA-initiated embryopathies, implicating a PHS-dependent, ROS-mediated embryopathic mechanism.