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Nonadditive genetic effects are currently ignored in national genetic evaluations of farm animals because of ignorance of thelevel of dominance variance for traits of interest and the difficult computational problems involved. Potential gains fromincluding the effects of dominance in genetic evaluations include “purification” of additive values and availability ofpredictions of specific combining abilities for each pair of prospective parents. This study focused on making evaluation withdominance effects feasible computationally and on ascertaining benefits of such an evaluation for dairy cattle, beef cattle,and swine. Using iteration on data, computing costs for evaluation with dominance effects included costs could be less thantwice expensive as with only an additive model. With Method Â, variance components could be estimated for problemsinvolving up to 10 millions equations. Dominance effects accounted for up to 10% of phenotypic variance; estimates werelarger for growth traits. As a percentage of additive variance, the estimate of dominance variance reached 78% for 21-d litterweight of swine and 47% for post weaning weight of beef cattle. When dominance effects are ignored, additive evaluationsare “contaminated”; effects are greatest for evaluations of dams in a single large family. These changes in ranking wereimportant for dairy cattle, especially for dams of full-sibs, but were less important for swine. Specific combining abilitiescannot be included in sire evaluations and need to be computed separately for each set of parents. The predictions of specificcombining abilities could be used in computerized mating programs via the Internet. Gains from including the dominanceeffect in genetic evaluations would be moderate but would outweigh expenditures to produce those evaluations.

Estimates of genetic parameters for number of stillborns (NSB) in relation to litter size (LS) were obtained with random regression models (RRM). Data were collected from 4 purebred Duroc nucleus farms between 2004 and 2008. Two data sets with 6,575 litters for the first parity (P1) and 6,259 litters for the second to fifth parity (P2-5) with a total of 8,217 and 5,066 animals in the pedigree were analyzed separately. Number of stillborns was studied as a trait on sow level. Fixed effects were contemporary groups (farm-year-season) and fixed cubic regression coefficients on LS with Legendre polynomials. Models for P2-5 included the fixed effect of parity, Random effects were additive genetic effects for both data sets with permanent environmental effects included for P2-5. Random effects modeled with Legendre polynomials (RRM-L), linear splines (RRM-S), and degree 0 B-splines (RRM-BS) with regressions on LS were used. For P1, the order of polynomial, the number of knots, and the number of intervals used for respective models were quadratic, 3, and 3, respectively. For P2-5, the same parameters were linear, 2, and 2, respectively. Heterogeneous residual variances were considered in the models. For P1, estimates of heritability were 12 to 15%, 5 to 6%, and 6 to 7% in LS 5, 9, and 13, respectively. For P2-5, estimates were 15 to 17%, 4 to 5%, and 4 to 6% in LS 6, 9, and 12, respectively. For P1, average estimates of genetic correlations between LS 5 to 9, 5 to 13, and 9 to 13 were 0.53, -0.29, and 0.65, respectively. For P2-5, same estimates averaged for RRM-L and RRM-S were 0.75, -0.21, and 0.50, respectively. For RRM-BS with 2 intervals, the correlation was 0.66 between LS 5 to 7 and 8 to 13. Parameters obtained by 3 RRM revealed the nonlinear relationship between additive genetic effect of NSB and the environmental deviation of LS. The negative correlations between the 2 extreme LS might possibly indicate different genetic bases on incidence of stillbirth. Key words: litter size, pig, random regression, stillbirth doi: 10.2527/jas.2009-2413

The objective of this study was to quantify the effect of heat stress during the life of a pig on its final weight, as a first step toward a genetic evaluation for heat tolerance. Data included carcass weights of 23,556 crossbred pigs [Duroc x (Landrace x Large White)] raised on 2 farms in North Carolina and slaughtered from May 2005 through December 2006. Weather data were available from a nearby weather station. Lifetime of a pig was assumed to be partitioned into 2 periods. During an initial period, the effect of heat stress was assumed to be negligible or compensated for later. During the second period ending in slaughtering, the ADG was assumed to be affected linearly by heat load. Weekly heat load was calculated as degrees of average temperature-humidity index in excess of a threshold (18[degrees]C). The total heat load (H) was the sum of weekly heat loads during the second period. During the months of January to May H was 0; H reached a peak in September. The final BW during the peak of heat stress decreased about 6 kg compared with BW during months of non-heat stress. Weekly and monthly averages of carcass weight generally moved similarly to H. However, there were large fluctuations unrelated to H; the fluctuations were different on the 2 farms. The model included the effects of farm-year of slaughter, sex, age at slaughter, and H, where age at slaughter and H were linear regressions. In analyses, the threshold was varied from 16 to 20[degrees]C, and the second period was varied from 8 to 16 wk. The greatest [R.sup.2] (10.4%) was at the threshold of temperature-humidity index = 18[degrees]C for a period of 10 wk. Varying the threshold and the length of time reduced [R.sup.2] less than 1%. Least squares means of year-month and year-week of carcass weight were calculated using a model with the fixed effects farm-year-month or farm-year-week of slaughter, sex, and age at slaughter (linear covariate), and the random effect of birth litter. Changes in BW of finisher pigs due to heat stress can be quantified by H during the last 10 wk of the life of the pig. Key words: carcass weight, heat stress, pig

The objective of this study was to describe genetic variability of pig carcass weight as a function of heat stress. Data included carcass weights of 23,556 crossbred pigs [Duroc x (Landrace x Large White)] raised on 2 farms in North Carolina and harvested from May 2005 through December 2006. Weather data were obtained from a weather station located about 20 km from the furthest farm. Weekly heat load was calculated as degrees of average temperature-humidity index (THI) in excess of 18[degrees]C. The total heat load (H) was the sum of heat loads for 10 wk before harvest. Variance components were estimated with 3 models: univariate (UNI)--not accounting for heat stress, 2-trait (MT2), and random regression (RR). In all of the models, effects included contemporary group, sex, age at harvest, sire, and litter. In MT2, observations in months in which heat stress was observed ('hot') and not observed ('cold') were treated as separate traits. Heat stress was observed in the months of August to November 2005, as well as July to October 2006. No heat stress was observed in the months of May to July 2005, January to June 2006, and November to December 2006. The RR model added a random regression on heat load for the sire effect. Heat load was adjusted to a scale ranging from 0 (no heat stress) to 5 (greatest heat stress). The heritability estimate [+ or -] SE of carcass weight in UNI was 0.17 [+ or -] 0.01. In MT2, the estimates were 0.14 [+ or -] 0.01 for 'cold' and 0.28 [+ or -] 0.01 for 'hot'; the genetic correlation between carcass weight in 'hot' and 'cold' months was 0.42 [+ or -] 0.13. The heritability estimates obtained with RR were 0.20 [+ or -] 0.11, 0.19 [+ or -] 0.15, and 0.51 [+ or -] 0.17 for H = 0, 2.5, and 5, respectively. The genetic correlation between the performance in 'cold' months (H = 0), and performance under maximum heat load (H = 5) was 0.02, between H = 0 and intermediate heat load (H = 2.5) was 0.52, and between H = 2.5 and H = 5 was 0.86. Rank correlations between EPD derived from the different models ranged from 0.82 to 0.94 between carcass weights under similar H, 0.18 to 0.54 between carcass weights under high and low H, and 0.66 to 0.91 between carcass weights of intermediate and high/low H. Heritability for growth was greater under heat stress. Selection for crossbred performance would be optimal when data for periods both in the absence and presence of heat stress were considered. Key words: carcass weight, genetic parameter, heat stress, pig, random regression

To study the genetic relationship between three grouped reasons for sow removal (SR) in consecutive parities, accounting for censoring, 13,838 records from Large White sows were analyzed. Data were from seven pure-line farms having, on average, 5.9% unknown SR. Three traits were subjectively defined, each corresponding to a classification of SR (reproductive [RR], nonreproductive [RN], and others [RO]). Records for each trait could take one of five categories, according to parity at removal (0 to 4 or later). A multivariate linear censored model was implemented. The model to estimate (co)variance components and parameters included the effects of year-season, region, contemporary group, and additive genetic effects. The most common SR was related to reproduction (48.5%). Diseases of different origin and cause, old age/parity, and sow death or loss accounted for about 18, 7, and 4% of total culls, respectively. Estimates of variance components showed heterogeneity of additive genetic and residual variances for the three traits. Estimates of heritability were 0.18, 0.13, and 0.15 for RR, RN, and RO, respectively. Genetic correlations between removal codes were high ([greater than or equal to] 0.90). Results suggest sizeable additive genetic variances exist for parity at removal and different codes of removal. Different SR reasons seem to operate similarly or as a closely related genetic trait associated with fitness. In particular, RN and RO seem to be genetically indistinguishable. Data structure, definition, and volume are major limitations in studies of sow survival. A multiple-trait censored model is preferred to evaluate reasons of sow disposal. Grouped removal causes seem to be strongly genetically correlated but with heterogeneous variances, suggesting that combining all removal causes and treating the trait as parity at disposal is an alternative approach. Key Words: Sow Culling, Sow Disposal, Sow Removal, Survival, Swine

Records of on-test ADG of Large White gilts were analyzed to estimate variance components of direct and associative genetic effects. Models included the effects of contemporary group (farm-barn-batch), birth litter, pen group, and direct and associative additive genetic effects. The area of each pen was 14 [m.sup.2]. The additive genetic variance was a function of the number of competitors in a group, the additive relationships between the animal performing the record and its pen mates, and the additive relationships between pen mates. To partially account for differences in the number of pen mates, a covariable ([q.sub.i] = 1, 1/n, or [1/n.sup.1/2]) was added to the associative genetic effect. There were 4,946 records from 2,409 litters and 362 pen groups. Pen group size ranged from 12 to 16 gilts. Analyses by REML converged very slowly. A grid search showed that the likelihood function was almost flat when the additive genetic associative effect was fitted. Estimates of direct and associative heritability were 0.15 and 0.03, respectively. Within the BLUPF90 family of programs, the mixed-model equations can be set up directly. For variance component estimation, simple programs (REMLF90 and GIBBSF90) worked without modifications, but more optimized programs did not. Estimates obtained using the three values of [q.sub.i] were similar. With the data structure available for this study and under an environment with relative low competition among animals, accurate estimation of associative genetic effects was not possible. Estimation of competitive effects with large pen size is difficult. The magnitude of competition effects may be larger in commercial populations, where housing is denser and food is limited. Key Words: Competition, Genetic Effects, Growth, Swine

Up to 109,447 records of 49,656 Large White sows were used to evaluate the genetic relationship between number of pigs born dead (BD) and number born alive (BA) in first and later parities. Performance data (n = 30,832) for ultrasound backfat (BF) at the end of the test and days to reach 113.5 kg (AD) were used to estimate their relationships with BD and BA at first parity in a four-trait threshold-linear analysis (TL). Effects were year-farm, contemporary group (CG: farm-farrowing year-farrowing month) and animal additive genetic. At first parity, estimates of heritability were 0.09, 0.09, 0.37, and 0.31 for BA, BD, AD, and BF, respectively. The estimate of genetic correlation between BD and litter size was -0.04 (BD-BA). Corresponding values with test traits were both -0.14 (BD-AD, BD-BF). Estimates of genetic correlation between BA and performance traits were 0.08 (BA-AD) and 0.05 (BA-BF). The two test traits were moderately negatively correlated (-0.22). For later parities, a six-trait (BD, BA in three parities) TL model was implemented. The estimates of additive genetic variances and heritability increased with parity for BD and BA. Estimates of heritabilities were: 0.09, 0.10, and 0.11 for BD, and 0.09, 0.12, and 0.12 for BA in parities one to three, respectively. Estimates of genetic correlations between different parities were high (0.91 to 0.96) for BD, and slightly lower (0.74 to 0.95) for BA. Genetic correlations between BD and BA were low and positive (0.02 to 0.17) for BA in Parities 1 and 2, but negative (-0.04 to -0.10) for BA in Parity 3. Selection for increased litter size should have little effect on farrowing piglet mortality. Intense selection for faster growth and increased leanness should increase farrowing piglet mortality of first-parity sows. A repeatability model with a simple correction for the heterogeneity of variances over parities could be implemented to select against farrowing mortality. The genetic components of perinatal piglet mortality are independent of the ones for litter size in the first parity, and they show an undesirable, but not strong, genetic association in second parity. Key Words: Backfat, Farrowing Mortality, Genetic Correlations, Growth, Litter Size

Commercial swine production has become an increasingly globalised industry, with global meat trade demanding that all regions compete on cost and differentiation of pork products. The utilisation of continually improving genetic populations can be one input that helps maintain, or increases, the competitiveness of an individual producer or regional industry. So as to deliver these improving genetic populations, genetic providers of today must focus on developing and implementing best science that delivers improvement on traits affecting commercial profitability. Providers must also efficiently multiply and disseminate the improved merit to the commercial hog production level. The swine-genetics industry has made considerable progress in driving a faster genetic gain over the past 30 years by systematically combining ever-changing computing power, accurate data capture and emerging genomics information. The combination of these technologies today has resulted in hundreds of thousands of animals being genotyped for tens of thousands of markers, and this information is being combined with extensive phenotypic data to deliver rates of genetic gain nearly double what we were able to achieve 20 years ago. As importantly, this scientific advancement can then be combined with the ability to continue to understand and evaluate emerging traits related to animal robustness, well-being and consumer demand, resulting in the most comprehensive definition of selection targets in the history of modern animal improvement. Finally, managing the dissemination of these genes through boar stud and multiplication systems helps ensure that the commercial level minimises lag and utilises the highest-merit genetics available. [ABSTRACT FROM AUTHOR]

The Beef Improvement Federation recommends residual feed intake (RFI) be calculated from 70-d tests preceded by a 21-d adjustment period. Individual animal feed intake and gain measurements are expensive and time consuming, which limits the number of animals available for national genetic evaluation of feed intake. If a shorter test period of comparable accuracy could be used, the cost would decrease and more animals could be tested annually. The objective of this study was to determine if data from shortened tests is equally as predictive of average daily DMI (ADMI) and RFI values from 70-d tests. Feed intake and weight measures were collected after weaning from Bos taurus bulls, steers, and heifers (n = 612) during four 70-d performance tests. For each individual, ADMI and RFI were calculated. Residual feed intake was calculated by regressing ADMI on metabolic midweight (MMWT) and ADG with the effect of breed included where appropriate. Based on four 70-d intake tests, ADMI, RFI, ADG, and MMWT were evaluated using shortened test lengths in a post hoc analysis where shortened test lengths were imposed on the full-period tests. The ADMI, RFI, ADG, and MMWT values from the full 70-d test were regressed on ADMI, RFI, ADG, and MMWT values resulting from the constructed shorter data subsets. The 8 subsets ranged from 14 to 56 d in length. The fixed effects of test, breed, animal's origin, and sex were included in each comparison for ADMI, ADG, and MMWT. Estimates for regression coefficients of ADMI values from a full test on various subsets ranged from 0.63 to 1.02. Likewise, estimated coefficients obtained from the regression of full test RFI, ADG, and MMWT values on subsets ranged from 0.50 to 1.00, 0.09 to 0.85, and 0.48 to 1.02, respectively. We conclude that ADMI values from a 42-d test (P < 0.0001) and RFI values from a 56-d test (P < 0.0001) adequately predict ADMI and RFI when compared to a 70-d test. These results suggest that testing periods of 42 d for determining ADMI and 56 d for RFI could ultimately reduce testing costs and result in collection of data on a larger number of animals per year, in turn resulting in more data for genetic evaluation. [ABSTRACT FROM AUTHOR]

Genetic parameters for daily feed intake (DFI, g/day) and daily gain (DG, g/day) were estimated using records of 1916 Duroc boars from electronic feeder stations. Management was limited and resulted in varied ranges of age and weight on test. Boars were housed in 102 pens, each equipped with one feeder, and allowed ad libitum feeding. Weekly averages of DFI and DG were used due to large variation in daily records. Six traits were defined as DFI and DG during 85–106 (period 1), 107–128 (period 2) and 129–150 days of age (period 3). A six-trait model included age as a linear and a quadratic covariate for DFI and a linear covariate for DG with a fixed effect of year–week–pen and random effects of litter, additive genetic animal and permanent environmental animal. Variance components were estimated by a Bayesian approach using Gibbs sampling algorithm. Estimates of heritability for respective periods were 18%, 12% and 10% for DFI and 21%, 11% and 10% for DG. Genetic correlations between DFI and DG in the same period were 0.70, 0.73 and 0.32 for the respective periods. DFI and DG obtained from automatic feeders can be analysed to reveal variation across testing periods by using weekly averages when many monthly averages are incomplete. [ABSTRACT FROM AUTHOR]

This study examined the utility of serial weights from FIRE (Feed Intake Recording Equipment, Osborne Industries, Inc., Osborne, KS, USA) stations for an analysis of daily gain. Data included 884 132 body weight records from 3888 purebred Duroc pigs. Pigs entered the feeder station at age 77–149 days and left at age 95–184 days. A substantial number of records were abnormal, showing body weight close to 0 or up to twice the average weight. Plots of body weights for some animals indicated two parallel growth curves. Initial editing used a robust regression, which was a two-step procedure. In the first step, a quadratic growth curve was estimated assuming small or 0 weights for points far away from the curve; the process is iterative. In the second step, weights more than 1.5 SD from the estimated growth curve were treated as outliers. The retained body weight records (607 597) were averaged to create average daily weight (170 443) and then used to calculate daily gains (152 636). Additional editing steps included retaining only animals with ≥50 body weight records and SD of the daily gain ≤2 kg, followed by removing records outside 3 SD from the mean for given age, across all the animals – the resulting data set included 69 068 records of daily gain from 1921 animals. Daily gain based on daily, weekly and bi-weekly intervals was analysed using repeatability models. Heritability estimates were 0.04, 6 and 9%, respectively. The last two estimates correspond to heritability of 28% for a 12 week interval. For daily gain averaged weekly, the estimate of heritability obtained with a random regression model varied from 0.07 to 0.10. After extensive editing, body weight records from automatic feeding stations are useful for genetic analyses of daily gain from weekly or bi-weekly but not daily intervals. [ABSTRACT FROM AUTHOR]

Social genetic relationships among average daily gain (ADG, g) and feeding pattern as daily feed intake (DFI, g), daily feeder occupation time (DOT, min), and daily feeding rate (DFR, g/min) were examined using records of 547 Duroc boars. Single-trait animal models were fitted differently for traits, including or excluding social genetic effects, random or fixed pen effects, with covariates of pen sizes and initial age or weight. Genetic parameters for feeding pattern were estimated by restricted maximum likelihood. Six sets of parameters for ADG based on literature estimates were used due to difficulty in untangling confounded effects. Positive and negative signs of direct-social genetic covariances were interpreted as heritable cooperation and competition, respectively. Dominant and subordinate pigs were classified as pigs with higher direct and social genetic values, respectively. Correlations of estimated breeding values between ADG and DFI, DOT, and DFR were 0.46, 0.04 and 0.29 for dominant pigs. Given heritable cooperation, subordinate pigs tended to increase feed intake ( r = 0.36) and eating rate ( r = 0.25). Given heritable competition, subordinate pigs fail to compensate for the competition with decreased feed intake ( r = −0.53). The slow eating rate ( r = −0.31) was considered as a consequence of eating during less busy hour of feeding. [ABSTRACT FROM AUTHOR]

The objective of this study was to determine the Standardized Ileal Digestible (SID) threonine:lysine ratio on nursery pigs performance under commercial conditions. A total of 2,262 pigs (PIC 359×Camborough®, 5.7 ± 0.1 kg) were used in a 39-d trial. Pens were assigned to dietary treatments in a randomized complete block based on initial BW and room (13 pens/treatment). Lysine was kept below the requirement to ensure that the Thr:Lys ratio was not underestimated (1.30, 1.30, 1.25, and 1.15% SID Lys for 5.7 to 6.4, 6.4 to 9.1, 9.1 to 12.2, and 12.2 to 18.8 kg, respectively). Dietary treatments were 53, 56, 59, 62, 65, and 68% SID Thr:Lys and were fed throughout the entire study. The levels of zinc oxide in the first and second diet were 1600 and 800 mg/kg, respectively. Diet analysis matched formulated values. Data was analyzed using the MIXED procedure of SAS. Linear and quadratic polynomial contrasts were used to evaluate the dose response effect. BW and room were considered random effects in the models. The NLMIXED procedure was used to evaluate competing models: linear (LN), quadratic polynomial (QP), broken-line linear (BLL), and broken-line quadratic (BLQ). From 0 to 21 d, ADG and G:F increased (linear, P = 0.016) with the increase in SID Thr:Lys, whereas ADFI and BW were not statistically affected (P = 0.236). From d 21 to 39, G:F increased (quadratic, P = 0.006) with the increase in SID Thr:Lys. However, ADG, ADFI, and BW were not statistically different (P = 0.179) between treatments. Overall, G:F increased significantly (quadratic, P = 0.001) and ADG was not statistically different (P = 0.103) as SID Thr:Lys increased, whereas ADFI was not statistically different (P = 0.236). Based on the dose-response estimation models with the best fit, the levels that maximized performance were >68% for ADG [LN; (ADG=0.64686 + 0.0014932×SID Thr:Lys)/2.2046] and 65% for G:F [QP; G:F=1/(3.56512–0.0661676×SID Thr:Lys+0.0005089×(SID Thr:Lys)2)]. In conclusion, formulating diets to 65% SID Thr:Lys should maximize G:F while capturing 99.4% of ADG. SID Threonine:Lysine SEM 53 56 59 62 65 68 d 0 to 39 ADGa, g 327 336 331 340 331 345 10.4 ADFI, g 490 481 476 481 472 485 16.8 G:Fb 0.667 0.685 0.694 0.699 0.699 0.699 0.008 BW, kg d 0 5.6 5.7 5.6 5.7 5.7 5.6 0.13 d 39 18.5 18.7 18.7 19 18.6 19.1 0.45 aLinear,P=0.103. bQuadratic, P=0.001. [ABSTRACT FROM AUTHOR]

A method was developed to assess the functional significance of a sequence motif in yeast Upf3p, a protein required for nonsense-mediated mRNA decay (NMD). The motif lies at the edge of the Upf3p-Upf2p interaction domain, but at the same time resembles the canonical leucine-rich nuclear export sequence (NES) found in proteins that bind Crm1p exportin. To test the function of the putative NES, site-directed mutations that cause substitutions of conserved NES-A residues were first selected to identify hypermorphic alleles. Next, a portable Crm1p-binding NES from HIV-1 Rev protein that functions in yeast was fused en masse to the C-terminus of variant Upf3 proteins using loxP sites recognized by bacterial cre-recombinase. Finally, variant Upf3-Rev proteins that were functional in NMD were selected and examined for the types of amino acid substitutions present in NES-A. The mutational analysis revealed that amino acid substitutions in the Upf3 NES impair both nuclear export and the Upf2p-Upf3p interaction, both of which are required for Upf3p to function in NMD. The method described in this report could be modified for the genetic analysis of a variety of portable protein domains.

Cattle living at altitudes greater than 1,500 m are susceptible to the development of high altitude disease (HAD) and a higher risk of death. Pulmonary arterial pressure (PAP) is used as an indicator of an animal's susceptibility to HAD. Measurements of PAP on cattle at lower elevations are generally considered less reliable indicators of HAD when compared to measurements taken at higher elevations, yet little evidence has been published evaluating this relationship. Therefore, the objective of this study was to evaluate PAP measurements from high and low elevations using a multivariate approach. We hypothesized that PAP measurements from lower elevations have a less than perfect relationship to PAP measurements from high elevations. Data collected from 2009 to 2017 was obtained from a multi-breed seedstock database that included PAP measurements and associated information (i.e., PAP testing date and elevation). The average PAP measurement was 44.08 ± 10.75 mmHg, with minimum and maximum observations of 32 and 149 mmHg, respectively. The age when PAP measurements were taken ranged from 9 to 21 months with an average age of 15.9 ± 2.8 months. Elevation ranged from 1,555 m to 2,407 m with a bimodal distribution. Therefore, animals with PAP measurements from elevations above 2,000 m were classified as high elevation (HPAP; n = 1,369) and animals with PAP measurements below 2,000 m were considered low elevation (LPAP; n = 1,243). A two-trait animal model was used to estimate genetic parameters and EBV for both LPAP and HPAP traits. The model contained the fixed effects of degree of outcross, breed percent, and PAP age as covariates, and sex and contemporary group (PAP date and yearling management combined) categories. Breed effects were included as covariates of breed percentages for Angus, Charolais, South Devon, Gelbvieh, Simmental, and "Other" breeds. Animal was included as a random effect and a 3-generation pedigree consisting of 11,573 animals was used. Heritability for LPAP and HPAP were 0.26 ± 0.08 and 0.37 ± 0.10, respectively, with a genetic correlation of 0.79 ± 0.23. Sire EBV for HPAP were regressed on corresponding sire EBV for LPAP, resulting in a regression coefficient of 0.705 ± 0.002 (P < 0.0001). These results suggest that a strong relationship exists between LPAP and HPAP, but the relationship is not perfect. The high genetic correlation between the traits suggest that measurements taken at lower elevations can still serve as an indicator of PAP measurements collected at higher elevations. [ABSTRACT FROM AUTHOR]

Meat quality traits and palatability characteristics were evaluated on 240 barrows and gilts subjected to one of eight dietary regimens: (1) control (no supplement), (2) vitamin D3(D3), (3) vitamin E (E), (4) magnesium (Mg), (5) vitamins D3 and E (D3/E), (6) vitamin D3 and magnesium (D3/Mg), (7) vitamin E and magnesium (E/Mg), and (8) vitamins D3 and E, and magnesium (D3/E/Mg). Barrows supplemented with D3/E/Mg had the highest (P>0.05) ultimate pH. Those supplemented with E had a higher ultimate pH than those supplemented with D3/Mg or the control. Gilts supplemented with Mg had the highest ultimate pH of all of the gilts while those supplemented with D3 had the lowest. Barrows supplemented with Mg or E had more marbling than those supplemented with D3 or D/E. Gilts supplemented with Mg had the most marbling when compared to other gilts. At 48 h postmortem, no differences due to dietary treatment were observed in L&ast;, a&ast; or b&ast; value, drip loss or purge loss. At 14 days postmortem, no differences due to diet existed in sensory characteristics. Results suggest that supplementation of swine diets with some dietary supplement combinations of containing Mg may have some potential benefit for increasing ultimate pH. [Copyright &y& Elsevier]

Porcine reproductive and respiratory syndrome (PRRS) is one of the world's most persistent viral pig diseases, with a significant economic impact on the pig industry. PRRS affects pigs of all ages, causing late-term abortions and stillbirths in sows, respiratory disease in piglets, and increased susceptibility to secondary bacterial infection with a high mortality rate. PRRS disease is caused by a positive single-stranded RNA PRRS virus (PRRSV), which has a narrow host-cell tropism limited to monocyte-macrophage lineage cells. Several studies demonstrated that the removal of CD163 protein or, as a minimum, its scavenger receptor cysteine-rich domain 5 (SRCR5) precludes the viral genome release, conferring resistance to PRRSV in live animals. Today, very limited information exists about the impact of such edits on animal performance from birth to maturity in pigs. Using CRISPR-Cas9 with dual-guide RNAs and non-homologous end joining (NHEJ), first-generation (E0) pigs were produced with a deletion of exon 7 in the CD163 gene. The selected pigs were bred to produce the next three generations of pigs to establish multiple lines of pigs homozygous for the edited allele, thereby confirming that the CD163 gene with removed exon 7 was stable during multiple breeding cycles. The pigs were evaluated relative to non-edited pigs from birth to maturity, including any potential changes in meat composition and resistance to PRRSV. This study demonstrates that removing the SRCR5 domain from the CD163 protein confers resistance to PRRSV and, relative to unedited pigs, resulted in no detected differences in meat composition and no changes in the growth rate, health, and ability to farrow. Together, these results support the targeted use of gene editing in livestock animals to address significant diseases without adversely impacting the health and well-being of the animals or the food products derived from them., Competing Interests: Authors CN, BB, SR, and ER were employed by Genus plc Research and Development. Authors LGP, C-YC, MC, PH, JH, AS, and MR were employed by Genus plc PIC., (Copyright © 2024 Nesbitt, Galina Pantoja, Beaton, Chen, Culbertson, Harms, Holl, Sosnicki, Reddy, Rotolo and Rice.)

Disease resistance genes in livestock provide health benefits to animals and opportunities for farmers to meet the growing demand for affordable, high-quality protein. Previously, researchers used gene editing to modify the porcine CD163 gene and demonstrated resistance to a harmful virus that causes porcine reproductive and respiratory syndrome (PRRS). To maximize potential benefits, this disease resistance trait needs to be present in commercially relevant breeding populations for multiplication and distribution of pigs. Toward this goal, a first-of-its-kind, scaled gene editing program was established to introduce a single modified CD163 allele into four genetically diverse, elite porcine lines. This effort produced healthy pigs that resisted PRRS virus infection as determined by macrophage and animal challenges. This founder population will be used for additional disease and trait testing, multiplication, and commercial distribution upon regulatory approval. Applying CRISPR-Cas to eliminate a viral disease represents a major step toward improving animal health.

Several bat species act as asymptomatic reservoirs for many viruses that are highly pathogenic in other mammals. Here, we have characterized the functional diversification of the protein kinase R (PKR), a major antiviral innate defense system. Our data indicate that PKR has evolved under positive selection and has undergone repeated genomic duplications in bats in contrast to all studied mammals that have a single copy of the gene. Functional testing of the relationship between PKR and poxvirus antagonists revealed how an evolutionary conflict with ancient pathogenic poxviruses has shaped a specific bat host-virus interface. We determined that duplicated PKRs of the Myotis species have undergone genetic diversification, allowing them to collectively escape from and enhance the control of DNA and RNA viruses. These findings suggest that viral-driven adaptations in PKR contribute to modern virus-bat interactions and may account for bat-specific immunity.

Background: There has been a renewed interest in the pathomechanics of elbow dislocation, with recent literature having suggested that the medial ulnar collateral ligament is more often disrupted in dislocations than the lateral ligamentous complex. The purpose of this serial sectioning study was to determine the influence of the posterior bundle of the medial ulnar collateral ligament (pMUCL) as a stabilizer against elbow dislocation., Methods: An elbow dislocation was simulated in 5 cadaveric elbows by mechanically applying an external rotation moment and valgus force. Medial ulnohumeral joint gapping was measured at 30°, 60°, and 90° of flexion in an intact elbow after sectioning of the medial collateral ligament's anterior bundle (aMUCL) and then after sectioning of the pMUCL as well., Results: After sectioning of the aMUCL, the pMUCL was able to stabilize the joint against dislocation. After aMUCL sectioning, the proximal joint space significantly increased by 4.2 ± 0.6 mm at 30° of flexion and 2.6 ± 0.3 mm at 60° of flexion, although it did not dislocate. The gapping increase of 0.9 ± 0.6 at 90° of flexion did not reach significance. After sectioning of the pMUCL (after having already sectioned the aMUCL), all of the specimens frankly dislocated at all flexion angles., Conclusions: An intact pMUCL can prevent elbow dislocation and limited joint subluxation to within 6.6 mm. Our findings indicate that repair or reconstruction may be warranted in certain circumstances (ie, residual instability after operative management of a terrible triad injury or after aMUCL reconstruction)., (Copyright © 2016 Journal of Shoulder and Elbow Surgery Board of Trustees. Published by Elsevier Inc. All rights reserved.)

Background: There are little demographic data on finger dislocation injuries. This study examines the epidemiological characteristics of patients presenting for emergency care of finger dislocations within the United States., Methods: The National Electronic Injury Surveillance System was queried for finger dislocation injuries treated in US emergency departments between 2004 and 2008. Weighted estimates, in conjunction with Census data, were used to analyze patient demographics, injury locales, and incidence rates within and between, demographic groups., Results: During the 5-year study period, an estimated 166 561 finger dislocations were treated in 1 499 222 917 person-years: an incidence rate of 11.11 per 100 000 person-years. Males were predominantly affected (78.7%) at an incidence rate of 17.8 per 100 000. The rate in females was 4.65 per 100 000 person-years. Most dislocations occurred in the 15- to 19-year age group (38.6 dislocations per 100 000 person-years). Among racial groups, blacks (16.8) were affected more than whites (7.72) or patients characterized as "other" (4.90). In terms of injury venue, 35.9% of cases took place at a sporting or recreational facility. In addition, 44.7% of sports-related dislocations occurred while playing either basketball or football., Conclusions: In the United States, finger dislocations appear to occur most often in black males 15 to 19 years of age and among sports participants, particularly basketball and football players.

We investigated the influence of the bifunctional guidance molecule netrin-1 on axonal growth in the injured adult spinal cord. In the adult, netrin-1 is expressed on mature oligodendrocytes, cells of the central canal, and the meninges. Netrin-1 protein in white matter is selectively enriched adjacent to paranodal loops of myelin in nodes of Ranvier. The repulsion-mediating netrin-1 uncoordinated-5 (UNC5) receptors are expressed by neurons of the corticospinal and rubrospinal projections, and by intrinsic neurons of the spinal cord, both before and after spinal cord injury. Neutralization of netrin-1 in myelin prepared from adult rat spinal cord using UNC5 receptor bodies increases neurite outgrowth from UNC5-expressing spinal motor neurons in vitro. Furthermore, axon regeneration is inhibited in a netrin-1-enriched zone, devoid of other myelin-associated inhibitors, within spinal cord lesion sites in vivo. We conclude that netrin-1 is a novel oligodendrocyte-associated inhibitor that can contribute to axonal growth failure after adult spinal cord injury.

Olfactory ensheathing cells (OECs) have been reported to migrate long distances and to bridge lesion sites, guiding axonal regeneration after spinal cord injury (SCI). To understand mechanisms of OEC migration and axonal guidance, we injected lamina propria OECs 1 mm rostral and caudal to C4 SCI sites. One month later, OECs formed an apparent migrating cell tract continuously extending from the injection site through the lesion, physically bridging the lesion. Confocal immunolabeling demonstrated that, whereas this cell tract displaced host astrocytes, descending or ascending long tract axons did not preferentially extend into the cell tract and OECs failed to support bridging of corticospinal axons. Notably, the "bridging" tract of OECs formed within 1 h of cell injection, raising the possibility that cells passively spread from the pressure injection site rather than actively migrating. Control injections of bone marrow stromal cells (MSCs) or fibroblasts 1 mm from the lesion site also rapidly dispersed into the lesion cavity. Cell tracts extending into the lesion site were not seen when cells were injected either at low volumes, into spinal cord gray matter, or 3 d before or 9 d after SCI. OECs proliferated in injection sites, cell tracts, and lesion sites, indicating that OECs can also accumulate through cell proliferation. Thus, OECs do not appear to exhibit significant migratory properties when grafted to the spinal cord, exhibit no detectable difference in promoting axon growth into a SCI site compared with MSCs or fibroblasts, and do not support bridging of corticospinal axons beyond a dorsal column lesion.

Meat quality traits and palatability characteristics were evaluated on 240 barrows and gilts subjected to one of eight dietary regimens: (1) control (no supplement), (2) vitamin D(3)(D(3)), (3) vitamin E (E), (4) magnesium (Mg), (5) vitamins D(3) and E (D(3)/E), (6) vitamin D(3) and magnesium (D(3)/Mg), (7) vitamin E and magnesium (E/Mg), and (8) vitamins D(3) and E, and magnesium (D(3)/E/Mg). Barrows supplemented with D(3)/E/Mg had the highest (P>0.05) ultimate pH. Those supplemented with E had a higher ultimate pH than those supplemented with D(3)/Mg or the control. Gilts supplemented with Mg had the highest ultimate pH of all of the gilts while those supplemented with D(3) had the lowest. Barrows supplemented with Mg or E had more marbling than those supplemented with D(3) or D/E. Gilts supplemented with Mg had the most marbling when compared to other gilts. At 48 h postmortem, no differences due to dietary treatment were observed in L (∗), a (∗) or b (∗) value, drip loss or purge loss. At 14 days postmortem, no differences due to diet existed in sensory characteristics. Results suggest that supplementation of swine diets with some dietary supplement combinations of containing Mg may have some potential benefit for increasing ultimate pH.

The SUF13 and SUF14 genes were identified among extragenic suppressors of +1 frameshift mutations. SUF13 is synonymous with MBF1, a single-copy nonessential gene coding for a POLII transcription factor. The suf13-1 mutation is a two-nucleotide deletion in the SUF13/MBF1 coding region. A suf13::TRP1 null mutant suppresses +1 frameshift mutations, indicating that suppression is caused by loss of SUF13 function. The suf13-1 suppressor alters sensitivity to aminoglycoside antibiotics and reduces the accumulation of his4-713 mRNA, suggesting that suppression is mediated at the translational level. The SUF14 gene is synonymous with RPS3, a single-copy essential gene that codes for the ribosomal protein S3. The suf14-1 mutation is a missense substitution in the coding region. Increased expression of S3 limits the accumulation of SUF14 mRNA, suggesting that expression is autoregulated. A frameshift mutation in SUF14 that prevents full-length translation eliminated regulation, indicating that S3 is required for regulation. Using CUP1-SUF14 and SUF14-lacZ fusions, run-on transcription assays, and estimates of mRNA half-life, our results show that transcription plays a minor role if any in regulation and that the 5'-UTR is necessary but not sufficient for regulation. A change in mRNA decay rate may be the primary mechanism for regulation.

mRNAs are monitored for errors in gene expression by RNA surveillance, in which mRNAs that cannot be fully translated are degraded by the nonsense-mediated mRNA decay pathway (NMD). RNA surveillance ensures that potentially deleterious truncated proteins are seldom made. NMD pathways that promote surveillance have been found in a wide range of eukaryotes. In Saccharomyces cerevisiae, the proteins encoded by the UPF1, UPF2, and UPF3 genes catalyze steps in NMD and are required for RNA surveillance. In this report, we show that the Upf proteins are also required to control the total accumulation of a large number of mRNAs in addition to their role in RNA surveillance. High-density oligonucleotide arrays were used to monitor global changes in the yeast transcriptome caused by loss of UPF gene function. Null mutations in the UPF genes caused altered accumulation of hundreds of mRNAs. The majority were increased in abundance, but some were decreased. The same mRNAs were affected regardless of which of the three UPF gene was inactivated. The proteins encoded by UPF-dependent mRNAs were broadly distributed by function but were underrepresented in two MIPS (Munich Information Center for Protein Sequences) categories: protein synthesis and protein destination. In a UPF(+) strain, the average level of expression of UPF-dependent mRNAs was threefold lower than the average level of expression of all mRNAs in the transcriptome, suggesting that highly abundant mRNAs were underrepresented. We suggest a model for how the abundance of hundreds of mRNAs might be controlled by the Upf proteins.

Messenger RNAs are monitored for errors that arise during gene expression by a mechanism called RNA surveillance, with the result that most mRNAs that cannot be translated along their full length are rapidly degraded. This ensures that truncated proteins are seldom made, reducing the accumulation of rogue proteins that might be deleterious. The pathway leading to accelerated mRNA decay is referred to as nonsense-mediated mRNA decay (NMD). The proteins that catalyze steps in NMD in yeast serve two roles, one to monitor errors in gene expression and the other to control the abundance of endogenous wild-type mRNAs as part of the normal repertoire of gene expression. The NMD pathway has a direct impact on hundreds of genetic disorders in the human population, where about a quarter of all known mutations are predicted to trigger NMD.

Sen1p from Saccharomyces cerevisiae is a nucleic acid helicase related to DEAD box RNA helicases and type I DNA helicases. The temperature-sensitive sen1-1 mutation located in the helicase motif alters the accumulation of pre-tRNAs, pre-rRNAs, and some small nuclear RNAs. In this report, we show that cells carrying sen1-1 exhibit altered accumulation of several small nucleolar RNAs (snoRNAs) immediately upon temperature shift. Using Northern blotting, RNase H cleavage, primer extension, and base compositional analysis, we detected three forms of the snoRNA snR13 in wild-type cells: an abundant TMG-capped 124-nucleotide (nt) mature form (snR13F) and two less abundant RNAs, including a heterogeneous population of approximately 1,400-nt 3'-extended forms (snR13R) and a 108-nt 5'-truncated form (snR13T) that is missing 16 nt at the 5' end. A subpopulation of snR13R contains the same 5' truncation. Newly synthesized snR13R RNA accumulates with time at the expense of snR13F following temperature shift of sen1-1 cells, suggesting a possible precursor-product relationship. snR13R and snR13T both increase in abundance at the restrictive temperature, indicating that Sen1p stabilizes the 5' end and promotes maturation of the 3' end. snR13F contains canonical C and D boxes common to many snoRNAs. The 5' end of snR13T and the 3' end of snR13F reside within C2U4 sequences that immediately flank the C and D boxes. A mutation in the 5' C2U4 repeat causes underaccumulation of snR13F, whereas mutations in the 3' C2U4 repeat cause the accumulation of two novel RNAs that migrate in the 500-nt range. At the restrictive temperature, double mutants carrying sen1-1 and mutations in the 3' C2U4 repeat show reduced accumulation of the novel RNAs and increased accumulation of snR13R RNA, indicating that Sen1p and the 3' C2U4 sequence act in a common pathway to facilitate 3' end formation. Based on these findings, we propose that Sen1p and the C2U4 repeats that flank the C and D boxes promote maturation of the 3' terminus and stability of the 5' terminus and are required for maximal rates of synthesis and levels of accumulation of mature snR13F.

In Saccharomyces cerevisiae, Upf3p is required for nonsense-mediated mRNA decay (NMD). Although localized primarily in the cytoplasm, Upf3p contains three sequence elements that resemble nuclear localization signals (NLSs) and two sequence elements that resemble nuclear export signals (NESs). We found that a cytoplasmic reporter protein localized to the nucleus when fused to any one of the three NLS-like sequences of Upf3p. A nuclear reporter protein localized to the cytoplasm when fused to one of the NES-like sequences (NES-A). We present evidence that NES-A functions to signal the export of Upf3p from the nucleus. Combined alanine substitutions in the NES-A element caused a re-distribution of Upf3p to a subnuclear location identified as the nucleolus and conferred an Nmd- phenotype. Single mutations in NES-A failed to affect the distribution of Upf3p and were Nmd+. When an NES element from HIV-1 Rev was inserted near the C terminus of a mutant Upf3p containing multiple mutations in NES-A, the cytoplasmic distribution typical of wild-type Upf3p was restored but the cells remained phenotypically Nmd-. These results suggest that NES-A is a functional nuclear export signal. Combined mutations in NES-A may cause multiple defects in protein function leading to an Nmd- phenotype even when export is restored.

The CTF13 gene codes for a subunit of the kinetochore in Saccharomyces cerevisiae. The temperature-sensitive mutation ctf13-30, which confers reduced fidelity of chromosome transmission, is a G --> A transition causing an amino acid substitution of Lys for Glu146. Strains carrying one chromosomal copy of ctf13-30 fail to grow at the restrictive temperature, whereas a haploid strain carrying two copies of ctf13-30 can grow. Four genes, UPF1, UPF2, UPF3, and ICK1, were represented among extragenic suppressors of ctf13-30. The UPF genes encode proteins that promote rapid decay of pre-mRNAs and mRNAs containing a premature stop codon. Suppressor mutations in these genes restore kinetochore function by causing increased accumulation of ctf13-30 mRNA. They also cause increased accumulation of CYH2 pre-mRNA, which is a natural target of UPF-mediated decay. Mutations in ICK1 restore kinetochore function but have no effect on ctf13-30 mRNA or CYH2 pre-mRNA accumulation. Most importantly, loss of UPF1 function causes increased accumulation of wild-type CTF13 mRNA but has no effect on the mRNA half-life. We propose that UPF-mediated decay modulates the mRNA level of one or more factors involved in CTF13 mRNA expression.

The objective of this study was to estimate the dominance variance for postweaning gain in Limousin cattle. Data included 215,326 records of postweaning gain from 205 to 365 d, provided by the North American Limousin Foundation. Parental dominance subclasses were formed and related using the method of Hoeschele and VanRaden. Variance components were estimated using Method R based on six samples of 50%. Fixed effects in the model included contemporary group and covariates for inbreeding and breed composition (percentage Limousin). Heterozygosity was negatively correlated with breed composition (< -.99) and was therefore not included in the model. Two types of contemporary groups used as original groups from the National Cattle Evaluation were partially based on breed composition. Original contemporary groups that were too homogeneous for breed composition were replaced by herd-year-sex classes. Two models were used with the two data sets. Model 1 contained the fixed effects described above and an additive genetic effect. Model 2 included a dominance effect in addition to the effects contained in Model 1. In total, four combinations of contemporary group x model were used. Dominance variance was computed as being four times the estimated parental subclass variance. Estimates for inbreeding depression and breed composition (percentage Limousin) were all small and not greatly affected by inclusion of dominance effects or changes in contemporary groups. Estimates of the additive variance (expressed as percentage of the phenotypic variance) were only slightly affected, with values between 20 and 21%. Dominance estimates were highly affected when passing from original (10%) and to alternative contemporary groups (18%). Such large values may indicate that dominance is important for postweaning gain. Results showed the advantage of an individual dominance approach based on sire-dam combinations; therefore, expected gains through the use of specific combination ability as a part of the mating selection criteria for growth might be high.

We used 179,485 Yorkshire reproductive and 239,354 Yorkshire growth records to estimate additive and dominance variances by Method Fraktur R. Estimates were obtained for number born alive (NBA), 21-d litter weight (LWT), days to 104.5 kg (DAYS), and backfat at 104.5 kg (BF). The single-trait models for NBA and LWT included the fixed effects of contemporary group and regression on inbreeding percentage and the random effects mate within contemporary group, animal permanent environment, animal additive, and parental dominance. The single-trait models for DAYS and BF included the fixed effects of contemporary group, sex, and regression on inbreeding percentage and the random effects litter of birth, dam permanent environment, animal additive, and parental dominance. Final estimates were obtained from six samples for each trait. Regression coefficients for 10% inbreeding were found to be -.23 for NBA, -.52 kg for LWT, 2.1 d for DAYS, and 0 mm for BF. Estimates of additive and dominance variances expressed as a percentage of phenotypic variances were, respectively, 8.8 +/- .5 and 2.2 +/- .7 for NBA, 8.1 +/- 1.1 and 6.3 +/- .9 for LWT, 33.2 +/- .4 and 10.3 +/- 1.5 for DAYS, and 43.6 +/- .9 and 4.8 +/- .7 for BF. The ratio of dominance to additive variances ranged from .78 to .11.

A single base change in the helicase superfamily 1 domain of the yeast Saccharomyces cerevisiae SEN1 gene results in a heat-sensitive mutation that alters the cellular abundance of many RNA species. We compared the relative amounts of RNAs between cells that are wild-type and mutant after temperature-shift. In the mutant several RNAs were found to either decrease or increase in abundance. The affected RNAs include tRNAs, rRNAs and small nuclear and nucleolar RNAs. Many of the affected RNAs have been positively identified and include end-matured precursor tRNAs and the small nuclear and nucleolar RNAs U5 and snR40 and snR45. Several small nucleolar RNAs co-immunoprecipitate with Sen1 but differentially associate with the wild-type and mutant protein. Its inactivation also impairs precursor rRNA maturation, resulting in increased accumulation of 35S and 6S precursor rRNAs and reduced levels of 20S, 23S and 27S rRNA processing intermediates. Thus, Sen1 is required for the biosynthesis of various functionally distinct classes of nuclear RNAs. We propose that Sen1 is an RNA helicase acting on a wide range of RNA classes. Its effects on the targeted RNAs in turn enable ribonuclease activity.

Number born alive (NBA) and litter weaning weight (LWT) can be influenced by many factors, including environment, parity, age at farrowing, lactation length, and genetic merit as well as number of pigs after transfer (NAT) and weaning age (WNAGE) for LWT. The objectives of this study were to estimate adjustment factors for NBA and LWT using all effects in the model and to refine parity effects by including age of the sow in parity 1 (P1) and parity 2 (P2). The models used included fixed effects of contemporary groups and parity/age class, random direct genetic and permanent environment effects, as well as the fixed effects of NAT and WNAGE for LWT. A large effect due to age of the sow at breeding within P1 and P2 was found and new adjustments were found to differ from previous studies. In the Yorkshire population, for example, the average P1 adjustment was 1.0 pig in this study, compared to the current .69; however, this ranges from 1.46 for the youngest P1 females to .57 for the oldest. Similarly, in P2 the average adjustment was found to be .50, with an adjustment of .99 for the youngest P2 and 0 for the oldest. Also, age of dam was found to contribute variation to P1 litter records for LWT. A residual analysis showed nonsignificant differences (P > .60) across the age classes after using the new adjustments; however, significant differences (P < .01) remained after using the current adjustments.

In yeast, the accelerated rate of decay of nonsense mutant mRNAs, called nonsense-mediated mRNA decay, requires three proteins, Upf1p, Upf2p, and Upf3p. Single, double, and triple disruptions of the UPF genes had nearly identical effects on nonsense mRNA accumulation, suggesting that the encoded proteins function in a common pathway. We examined the distribution of epitope-tagged versions of Upf proteins by sucrose density gradient fractionation of soluble lysates and found that all three proteins co-distributed with 80 S ribosomal particles and polyribosomes. Treatment of lysates with RNase A caused a coincident collapse of polyribosomes and each Upf protein into fractions containing 80 S ribosomal particles, as expected for proteins that are associated with polyribosomes. Mutations in the cysteine-rich (zinc finger) and RNA helicase domains of Upf1p caused loss of function, but the mutant proteins remained polyribosome-associated. Density gradient profiles for Upf1p were unchanged in the absence of Upf3p, and although similar, were modestly shifted to fractions lighter than those containing polyribosomes in the absence of Upf2p. Upf2p shifted toward heavier polyribosome fractions in the absence of Upf1p and into fractions containing 80 S particles and lighter fractions in the absence of Upf3p. Our results suggest that the association of Upf2p with polyribosomes typically found in a wild-type strain depends on the presence and opposing effects of Upf1p and Upf3p.

Purpose: The purpose of this paper was to discuss our experiences with an implantable bone conduction hearing prosthesis, the XOMED Audiant Bone Conductor (Jacksonville, FL)., Patients and Methods: Twenty-four patients who had been implanted with the Audiant Bone Conductor were interviewed by telephone following implantation. Questions were asked regarding use of the device and subjective benefit., Results: Eleven patients are using their devices, 12 patients are not using their devices, and one patient has been lost to follow-up. Patients using the device report satisfaction and prefer the Audiant to other amplification systems, whereas those not using the device indicate that insufficient amplification or weak magnetic attraction prevent its use., Conclusions: Analysis of failures has altered our criteria for implantation. With improvements that have been made by XOMED and stricter patient criteria, the Audiant should be considered a viable amplification alternative for certain hearing-impaired patients.