Search

Abstract Background Isg15 covalently modifies murine endometrial proteins in response to early pregnancy. Isg15 can also be severed from targeted proteins by a specific protease called Ubp43 (Usp18). Mice lacking Ubp43 (null) form increased conjugated Isg15 in response to interferon. The Isg15 system has not been examined in chorioallantoic placenta (CP) or mesometrial (MM) components of implantation sites beyond 9.5 days post coitum (dpc). It was hypothesized that deletion of Ubp43 would cause disregulation of Isg15 in implantation sites, and that this would affect pregnancy rates. Methods Heterozygous (het) Ubp43 mice were mated and MM and CP implantation sites were collected on 12.5 and 17.5 days post-coitum (dpc). Results Free and conjugated Isg15 were greater on 12.5 versus 17.5 dpc in MM. Free and conjugated Isg15 were also present in CP, but did not differ due to genotype on 12.5 dpc. However, null CP had greater free and conjugated Isg15 when compared to het/wt on 17.5 dpc. Null progeny died in utero with fetal genotype ratios (wt:het:null) of 2:5:1 on 12.5 and 2:2:1 on 17.5 dpc. Implantation sites were disrupted within the junctional zone and spongiotrophoblast, contained less vasculature based on lectin B4 staining and contained greater Isg15 mRNA and VEGF protein in Ubp43 null when compared to wt placenta. Conclusion It is concluded that Isg15 and its conjugates are present in implantation sites during mid to late gestation and that deletion of Ubp43 causes an increase in free and conjugated Isg15 at the feto-maternal interface. Also, under mixed genetic background, deletion of Ubp43 results in fetal death.

The article focuses on study of materno-placental microbiome of gravid beef cows under feed intake restriction. Topics discussed include existence of reproductive microbiome as evidence in cattle, matured bovine rumen influenced by feed intake restriction, and counts of phyla presented in abundance in mature rumen being impacted.

Background: Human milk contains appetite-regulating hormones that may influence infant growth and obesity risk. Research aims: We evaluated whether leptin, peptide tyrosine-tyrosine (PYY), glucagon-like peptide-1 (GLP-1), and ghrelin concentrations in human milk (1) changed during feeding (from foremilk to hindmilk) and during the first 6 months of infancy; (2) were explained by maternal factors; and (3) were associated with infant anthropometrics and growth. Methods: Mother–infant dyads (N = 22) participated. Samples of foremilk and hindmilk at 1 month postpartum were collected and analyzed for leptin, PYY, GLP-1, and ghrelin via radioimmunoassay and milkfat percentage estimated via creamatocrit. Samples were also collected in mothers (n = 15) who breastfed through 6 months. Anthropometrics were obtained on all mother–infant dyads at 1 month and all infants at 6 months and 12 months. Results: At 1 month, milk GLP-1 and milkfat concentration increased from foremilk to hindmilk (p ≤.05) while leptin and PYY concentrations remained stable during feeding. Milk hormone concentrations and milkfat tended to decline overtime, with lower leptin, PYY, and ghrelin at 6 months versus 1 month (p <.05). At 1 month, milk leptin and milkfat content were associated with maternal markers of adiposity (r = 0.49–0.78, p <.001); whereas, milk PYY was correlated with maternal serum PYY concentration (r = 0.672, p =.001). Average 1-month milk concentrations of GLP-1 and leptin were negatively associated with weight-for-age z -scores at 6 months (r = −0.46, p <.05) and 12 months (r = −0.49, p <.05), respectively. Conclusion: The content of certain appetite-regulating hormones in human milk may be influenced by maternal factors and play a role in infant growth; much needs to be learned about their role in the obesity protection of breastfed infants. [ABSTRACT FROM AUTHOR]

The article presents a study examine the effect of aflatoxin B1 treatment on expression of transient receptor potential melastatin 8 in mouse ovary and testes. Topics discussed include use of Aa oats, barley, wheat, and other livestock feeds; and aflatoxin B1 (AFB1), that can lead to reproductive deficiencies in a variety of species, including humans, livestock, and mice.

In endurance-trained men, an acute bout of exercise is shown to suppress post-exercise appetite, yet limited research has examined this response in women. The purpose of this study was to investigate the effect of exercise intensity on appetite and gut hormone responses in endurance-trained women. Highly-trained women (n = 15, 18-40 years, 58.4 ± 6.4 kg, VO2MAX = 55.2 ± 4.3 mL/kg/min) completed isocaloric bouts (500 kcals or 2093 kJ) of moderate-intensity (MIE, 60% VO2MAX) and high-intensity (HIE, 85% VO2MAX) treadmill running at the same time of day, following a similar 48-h diet/exercise period, and at least 1-week apart. Blood was drawn pre-exercise (baseline), immediately post-exercise and every 20-min for the next 60-min. Plasma concentrations of acylated ghrelin, PYY3-36, GLP-1 and subjective appetite ratings via visual analog scale (VAS) were assessed at each time point. Acylated ghrelin decreased (p = 0.014) and PYY3-36 and GLP-1 increased (p = 0.036, p < 0.0001) immediately post-exercise, indicating appetite suppression. VAS ratings of hunger and desire to eat decreased immediately post-exercise (p = 0.0012, p = 0.0031, respectively), also indicating appetite suppression. There were no differences between exercise intensities for appetite hormones or VAS. Similar to males, post-exercise appetite regulatory hormones were altered toward suppression in highly-trained women and independent of energy cost of exercise. Results are important for female athletes striving to optimize nutrition for endurance performance. [ABSTRACT FROM AUTHOR]

Subclinical mastitis, a common intramammary disease in sheep production, can be costly to producers due to compromised performance and decreased longevity. Our research focused on preventative and therapeutic measures on mammary health where the objectives were to identify (1) the impact of Zn supplementation on the milk microbiome and (2) the impact of management practices at lambing and weaning on prevalence and cure rate of subclinical mastitis, the milk microbiome, and levels of antimicrobial resistance in milk bacteria. In study 1, the milk microbiome was characterized during the first 3 wk of lactation and at weaning in ewes divergent in dietary Zn supplementation (1× = CON or 3× recommendations = ZnTRT). Mammary health was assessed using somatic cell count (SCC) class. Amplicon sequencing revealed the presence of Staphylococcus, Mannheimia, Corynebacterium, and Pseudomonas, all major mastitis pathogens. Effects of breed, dietary Zn concentration, and SCC class on diversity were limited to early lactation, where CON milk had greater composition stability than ZnTRT milk (P = 0.02). In study 2, milk bacteria were characterized by culture; Staphylococcus spp. and Streptococcus spp. were tested for antimicrobial susceptibility. Subclinical mastitis prevalence ranged from 22–66% where coagulase-negative staphylococci (CoNS; 59%), bacilli (35%), Mannheimia haemolytica (10%), S. aureus (8%), streptococci (5%), and Corynebacterium spp. (5%) were common. Milk samples were compared by jug bedding treatment: jugs were cleaned and dried with barn lime before adding fresh straw (CLEAN) or fresh straw was added atop soiled bedding (SOILED). Bedding had no effect on subclinical mastitis (P = 0.57), but CoNS had greater sulfadimethoxine resistance in SOILED isolates (P = 0.03). Additional mastitis control methods at weaning were evaluated: penicillin injection (PENN), restricted feed access (FAST), or their combination (COMBO). Weaning treatment did not affect cure rate from weaning to 3-d post- weaning (P = 0.21). Further characterization of these samples via microbial sequencing are underway with source tracking analyses to investigate an exogenous route via retrograde transfer and environmental bacteria or endogenous route via an entero-mammary pathway. Results support that breed, animal husbandry, and mammary health variably affect the milk microbiome and provide novel insight to the impact of management practices in a milk microbiome longitudinal study. [ABSTRACT FROM AUTHOR]

Adequate maternal nutrient supply is critical for normal fetal organogenesis. We previously demonstrated that a global 50% nutrient restriction during the first half of gestation causes compensatory growth of both the left and right ventricles of the fetal heart by day 78 of gestation. Thus, it was hypothesized that maternal nutrient restriction significantly altered gene expression in the fetal cardiac left ventricle (LV). Pregnant ewes were randomly grouped into control (100% national research council (NRC) requirements) or nutrient-restricted groups (50% NRC requirements) from day 28 to day 78 of gestation, at which time fetal LV were collected. Fetal LV mRNA was used to construct a suppression subtraction cDNA library from which 11 cDNA clones were found by differential dot blot hybridization and virtual Northern analysis to be up-regulated by maternal nutrient restriction: caveolin, stathmin, G-1 cyclin, α-actin, titin, cardiac ankyrin repeat protein (CARP), cardiac-specific RNA-helicase activated by MEF2C (CHAMP), endothelial and smooth muscle derived neuropilin (ESDN), prostatic binding protein, NADH dehydrogenase subunit 2, and an unknown protein. Six of these clones (cardiac α-actin, cyclin G1, stathmin, NADH dehydrogenase subunit 2, titin and prostatic binding protein) have been linked to cardiac hypertrophy in other species including humans. Of the remaining clones, caveolin, CARP and CHAMP have been shown to inhibit remodelling of hypertrophic tissue. Compensatory growth of fetal LV in response to maternal undernutrition is concluded to be associated with increased transcription of genes related to cardiac hypertrophy, compensatory growth or remodelling. Counter-regulatory gene transcription may be increased, in part, as a response to moderating the degree of cardiac remodelling. The short- and long-term consequences of these changes in fetal heart gene expression and induction of specific homeostatic mechanisms in response to maternal ... [ABSTRACT FROM AUTHOR]

A correction is presented to the article "Ruminant Nutrition Symposium: Tiny but mighty: the role of the rumen microbes in livestock production" which appeared in the 2018 issue.