[Kouri: bovine race from Chad lake. I. General introduction to its zootechnical and biochemical study: origins and ecology of the race].
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OBJECTIVE: To identify race-start characteristics associated with catastrophic musculoskeletal (MS) injury in Thoroughbred racehorses at 2 racetracks in Florida during 1995 through 1998. DESIGN: Matched case-control study. ANIMALS: 97 Thoroughbreds (case horses) that incurred a catastrophic MS injury during racing and 388 Thoroughbreds (control horses) randomly selected from noninjured participants and matched on the basis of racetrack and year. PROCEDURE: Incidence of MS injury was calculated for all race meets at 2 racetracks in Florida from 1995 through 1998. Race-start characteristics were compared among case and control horses, using conditional logistic regression. RESULTS: Overall incidence of MS injury was 1.2/1,000 race starts (97/79,416 starts). Incidence of injury was significantly higher for turf races (2.3/1,000 starts) than for dirt races (0.9/1,000 starts). Sex, number of days since last race, and racing surface were associated with risk of injury; geldings, > or = 33 days since the last race, and turf racing surface were associated with a higher risk of injury. CONCLUSIONS AND CLINICAL RELEVANCE: Incidence of injury among Thoroughbreds in Florida was associated with sex, number of days since last race, and racing surface. Days since last race may have been an indicator of previous health and lameness problems. Racing surface may have been a risk factor for MS injury because turf races tended to be more competitive than dirt races. Horses running in turf races were more likely to participate in races with a large field, handicap races, long races, and races with high purses.
OBJECTIVE: To determine whether sex or foaling period were associated with time to first race start and whether sex, age at time of first race start, or inter-race period were associated with career duration for Thoroughbred racehorses in Australia. ANIMALS: 553 Thoroughbred racehorses. PROCEDURE: Race records through to the end of the 6-year-old racing season were obtained for each horse. Product-limit survival analysis was used to determine whether sex or foaling period was associated with time to first race start and whether sex or age at first race was associated with career duration. A Cox proportional hazards model was used to determine whether sex, age at first possible race, age at first race, or inter-race period was associated with time to first race start or career duration. RESULTS: 472 horses (85.4%) raced. Time to first race start was not associated with sex or foaling period. However, males, who had their first race at a younger age and a greater mean number of rest days between races, had longer careers. The hazard ratio for career duration of males versus females, controlling for age at time of first race and inter-race period (0.27), confirmed that males had a higher probability of a long racing career. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that for Thoroughbred racehorses, sex and time of birth during the foaling season were not associated with time to first race. Male Thoroughbred racehorses that were raced less intensively or raced at a younger age were more likely to have long racing careers.
OBJECTIVE: To characterize and contrast data from Thoroughbreds that incurred a fatal musculoskeletal injury (FMI; injury resulting in death or euthanasia) during racing or training and data from all California race entrants during a 9-month period in 1991. DESIGN: Case-control study. ANIMALS: Thoroughbreds that incurred a FMI during racing or training at a California race-meet and all California race entrants from January through June and October through December 1991. PROCEDURE: Age and sex were compared with chi 2 and Fisher's exact tests among horses fatally injured while racing and training. A log-linear model was fit to assess the relationship between race-meet and age and sex of California race entrants. Incidence risk of racing FMI was estimated per 1,000 race entrants, and the relationship between the occurrence of FMI during racing with race-meet, age, and sex was evaluated by logistic regression. RESULTS: Injury type and sex-specific age distributions differed among the horses fatally injured during racing and training. Age and sex distributions of the race entrants were not independent and varied among race-meets. Overall incidence risk of racing FMI was estimated at 1.7/1,000 race entrants. Risk of racing FMI in male horses was about twofold that in female horses, and in 4-year-olds was twofold that in 3-year-olds. CLINICAL IMPLICATIONS: Age and sex-related differences in risk of incurring a FMI during racing should be considered when comparing fatal injury rates among race-meets.
OBJECTIVE: To investigate relationships of several racehorse characteristics and race conditions with risk of a catastrophic musculoskeletal injury (CMI) resulting in euthanasia in Thoroughbreds during racing in California in 1992. DESIGN: Retrospective longitudinal study. ANIMALS: Thoroughbreds that incurred CMI during racing and all California race entrants in 1992. PROCEDURE: Necropsy records were reviewed, and race start information was obtained. Incidence risk of CMI/1,000 race entrants was estimated. Relationships between CMI during racing and race-meet, entrant age and sex, race type and length, and racing surface type and condition were evaluated by use of logistic regression. RESULTS: Incidence risk of CMI was 1.7/1,000 entrants. A higher risk of CMI was found at 2 fair race-meets, with incidence risks of 4.9 and 5.5/1,000 entrants. Risk of injury in male horses was 1.7 times greater than that in female horses, and influence of age on risk depended on race type. Risk of injury for horses 2 to 5 years old was two times greater for claiming horses than for maiden horses. Race length or racing surface type (dirt vs turf) or condition (fast, muddy, yielding) were not significantly associated with risk of CMI. CLINICAL IMPLICATIONS: Incidence of CMI was similar among 12 of 14 major and fair race-meets and among various race lengths and racing surface types and conditions, whereas incidence of CMI was influenced by entrant age and sex as well as race type. Investigators should consider controlling for age and sex, race-meet, and race type whenever possible in studies of risk of CMI.
Geneticists in England and the United States clearly reversed their published remarks on the effects of race crossing between 1930 and 1950. The reversal occurred in two steps. First came the change in the 1930's from a condemnation of wide race crosses to an agnostic view. The second change, from the agnostic view to the belief that wide race crosses were at worst biologically harmless, took place during and shortly after World War II. The entire reversal occurred in the light of little new compelling data from studies of actual human race crosses. The lack of new data is unsurprising. Few geneticists wished to initiate experiments that took three human generations to complete. And controlled race crosses are hard to arrange, even with government grants. What might be more surprising was the willingness of geneticists to make such positive statements about race crossing when they had so little reliable genetic evidence. I interviewed or wrote to ten prominent geneticists who worked on human genetics between 1930 and 1950. Not one believed that new evidence on race crossing was the primary reason why geneticists changed their minds about the effects of race crossing. One plausible explanation, that the rise of "population thinking" (44) caused geneticists to change their minds, does not fit the evidence. Castle was no more of a "population" thinker than East, yet they differed radically in their conclusions about race crossing. What, then, did cause geneticists to change their minds? Most important was the revulsion of educated people in the United States and England to Nazi race doctrines and their use in justifying extermination of Jews. Few geneticists wanted to argue, as had the Nazis, that biology showed race crossing was harmful. Instead, having witnessed the horrible toll, geneticists naturally wanted to argue that biology showed race crossing was at worst harmless. No racist nation could misuse that conclusion. And geneticists did revise their biology to fit their feelings of revulsion. Geneticists' ideas about the related question of hereditary mental differences between races is perhaps undergoing a similar development to that seen earlier in their ideas about race crossing. In 1951, judging from the response to the Unesco second statement on race and comments in genetics literature, most geneticists agreed with Muller that races probably differed in significant average mental traits. By 1969, when Arthur Jensen advocated this view in his controversial article (45), most geneticists who spoke publicly on the issue had adopted an agnostic position. Knowledge of hereditary racial differences in IQ had scarcely changed since 1951, but society had changed considerably in racial attitudes. It will be interesting to see if during the next several decades geneticists will argue, on the basis of little additional evidence, that hereditary mental differences between races do not exist. I am not condemning geneticists because social and political factors have influenced their scientific conclusions about race crossing and race differences. It is necessary and natural that changing social attitudes will influence areas of biology where little is known and the conclusions are possibly socially explosive. The real danger is not that biology changes with society, but that the public expects biology to provide the objective truth apart from social influences. Geneticists and the public should realize that the science of genetics is often closely intertwined with social attitudes and political considerations.
OBJECTIVE: To determine the frequency of epistaxis during or after racing among racehorses and identify factors associated with development of epistaxis. DESIGN: Retrospective study. SAMPLE POPULATION: 247,564 Thoroughbred and 4,045 Anglo-Arab race starts. PROCEDURE: Race start information (breed, age, sex, racing distance, and race type) was obtained for Thoroughbred and Anglo-Arab horses racing in Japan Racing Association-sanctioned races between 1992 and 1997. All horses that raced were examined by a veterinarian within 30 minutes of the conclusion of the race; any horse that had blood at the nostrils was examined with an endoscope. If blood was observed in the trachea, epistaxis related to exercise-induced pulmonary hemorrhage (EIPH) was diagnosed. RESULTS: Epistaxis related to EIPH was identified following 369 race starts (0.15%). Frequency of EIPH-related epistaxis was significantly associated with race type, age, distance, and sex. Epistaxis was more common following steeplechase races than following flat races, in older horses than in horses that were 2 years old, following races < or =1,600 m long than following races between 1,601 and 2,000 m long, and in females than in sexually intact males. For horses that had an episode of epistaxis, the recurrence rate was 4.64%. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggested that frequency of EIPH-related epistaxis in racehorses is associated with the horse's age and sex, the type of race, and the distance raced. The higher frequency in shorter races suggests that higher intensity exercise of shorter duration may increase the probability of EIPH.
The small GTPase racE is essential for cytokinesis in Dictyostelium but its precise role in cell division is not known. To determine the molecular mechanism of racE function, we undertook a mutational analysis of racE. The exogenous expression of either wild-type racE or a constitutively active V20racE mutant effectively rescues the cytokinesis deficiency of racE null cells. In contrast, a constitutively inactive N25racE mutant fails to rescue the cytokinesis deficiency. Thus, cytokinesis requires only the activation of racE by GTP and not the inactivation of racE by hydrolysis of GTP. To determine the spatial distribution of racE, we created a fusion protein with GFP at the amino terminus of racE. Remarkably, GFP-racE fusion protein was fully competent to rescue the phenotype of racE null cells and, therefore, must reside in the same location as native racE. We found that GFP-racE localized to the plasma membrane of the cell throughout the entire cell cycle. Furthermore, constitutively active and inactive GFP-racE fusion proteins also localized to the plasma membrane. We mapped the domain required for plasma membrane localization to the carboxyl-terminal 40 amino acids of racE. This domain, however, is not sufficient to confer racE function onto a closely related GTPase. Taken together, these results suggest that racE functions at the cell cortex but it is not involved in determining the timing or placement of the contractile ring.
The effects of furosemide on the racing times of 79 horses without exercise-induced pulmonary hemorrhage (EIPH) and 52 horses with EIPH were investigated. Racing times were adjusted to 1-mile equivalent racing times by 2 speed handicapping methods, and analysis of covariance was used to adjust actual racing times by winning time and distance for each race. All 3 methods of determining racing time indicated that geldings without EIPH had significantly faster racing times (P less than 0.05) when given furosemide before racing than when furosemide was not given before racing. Females and colts without EIPH were determined to have faster racing times when furosemide was given before racing, but the difference was not significant. Geldings with EIPH had significantly faster racing times (P = 0.0231) when given furosemide before racing, as determined by one of the speed handicapping methods. There was a strong correlation (range 0.9314 to 0.9751) between the 1-mile equivalent racing times, as determined by the 2 speed handicapping methods for horses with and without EIPH. Furosemide failed to prevent the development of EIPH in many horses that were previously considered to be EIPH-negative. When given furosemide, 62 (25.3%) of 235 EIPH-negative horses were EIPH-positive after racing. Furosemide had questionable efficacy for prevention of EIPH in known EIPH-positive horses. Thirty-two (61.5%) of 52 EIPH-positive horses given furosemide before a race remained EIPH-positive after that race.
Common bean (Phaseolus vulgaris L.) cultivars are distinguished morphologically, agronomically and ecologically into specific races within each of the two gene pools found for the species (Andean and Mesoamerican). The objective of this study was to describe the race structure of the Mesoamerican gene pool using microsatellite markers. A total of 60 genotypes previously described as pertaining to specific Mesoamerican races as well as two Andean control genotypes were analyzed with 52 markers. A total of 267 bands were generated with an average of 5.1 alleles per marker and 0.297 heterozygosity across all microsatellites. Correspondence analysis identified two major groups equivalent to the Mesoamerica race and a group containing both Durango and Jalisco race genotypes. Two outlying individuals were classified as potentially of the Guatemala race although this race does not have a defined structure and previously classified members of this race were classified with other races. Population structure analysis with K = 1-4 agreed with this classification. The genetic diversity based on Nei's index for the entire set of genotypes was 0.468 while this was highest for the Durango-Jalisco group (0.414), intermediate for race Mesoamerica (0.340) and low for race Guatemala (0.262). Genetic differentiation (G (ST)) between the Mesoamerican races was 0.27 while genetic distance and identity showed race Durango and Jalisco individuals to be closely related with high gene flow (N (m)) both between these two races (1.67) and between races Durango and Mesoamerica (1.58). Observed heterozygosity was low in all the races as would be expected for an inbreeding species. The analysis with microsatellite markers identified subgroups, which agreed well with commercial class divisions, and seed size was the main distinguishing factor between the two major groups identified.
OBJECTIVES: The 2000 Census, which provides denominators used in calculating vital statistics and other rates, allowed multiple-race responses. Many other data systems that provide numerators used in calculating rates collect only single-race data. Bridging is needed to make the numerators and denominators comparable. This report describes and evaluates the method used by the National Center for Health Statistics to bridge multiple-race responses obtained from Census 2000 to single-race categories, creating single-race population estimates that are available to the public. METHODS: The authors fitted logistic regression models to multiple-race data from the National Health Interview Survey (NHIS) for 1997-2000. These fitted models, and two bridging methods previously suggested by the Office of Management and Budget, were applied to the public-use Census Modified Race Data Summary file to create single-race population estimates for the U.S. The authors also compared death rates for single-race groups calculated using these three approaches. RESULTS: Parameter estimates differed between the NHIS models for the multiple-race groups. For example, as the percentage of multiple-race respondents in a county increased, the likelihood of stating black as a primary race increased among black/white respondents but decreased among American Indian or Alaska Native/black respondents. The inclusion of county-level contextual variables in the regression models as well as the underlying demographic differences across states led to variation in allocation percentages; for example, the allocation of black/white respondents to single-race white ranged from nearly zero to more than 50% across states. Death rates calculated using bridging via the NHIS models were similar to those calculated using other methods, except for the American Indian/Alaska Native group, which included a large proportion of multiple-race reporters. CONCLUSION: Many data systems do not currently allow multiple-race reporting. When such data systems are used with Census counts to produce race-specific rates, bridging methods that incorporate geographic and demographic factors may lead to better rates than methods that do not consider such factors.
The 1997 standard for race and ethnicity data from the Office of Management and Budget requires the collection of data for multiple race groups. The aims of this study were to compare characteristics of multiple race children and describe race reporting for children within interracial and multiple race families. Descriptive statistics were estimated using the 1993-1995 National Health Interview Surveys. In this time period, 2.6% of children had more than one race reported. Multiple race children were a diverse group who differed from each other and their single race counterparts. For example, the percent of children reported as both Black and White who lived in a two-parent household (58.9%), was significantly less than the corresponding percents for other multiple race children (65.8%-79.6%), and between the corresponding percents for single race Black (42.7%) and single race White children (83.2%). The relationships between parental race and child's race varied. Although 3.1% of children in two-parent households lived with interracial parents, fewer than half of these children had more than one race reported. Sociodemographic variables were not associated with child's reported race among interracial families. These findings indicate that generalizations about multiple race children for research or policy purposes will be problematic.