Factor XI mutation in normally fertile and repeat breeding Holstein cows in the Middle Anatolian region of Turkey: a financial approach

2012 ◽  
Vol 52 (11) ◽  
pp. 1042 ◽  
Author(s):  
B. Akyuz ◽  
S. Sariozkan ◽  
D. Bayram

The aim of this study was to compare the prevalence of factor XI deficiency (FXID) carriers and potential financial losses depending on ‘extended calving interval’ and ‘extra service’ in normally fertile and repeat breeder cows in Turkey. For this purpose, a total of 161 Holstein cows were genotyped for the FXI gene mutation originating from various herds located in the Middle Anatolian region of Turkey. In the study, animals were divided into two groups – normally fertile (n = 118) and repeat breeding (n = 43) cows. In each group, one FXID carrier animal was identified and the prevalence of the FXID carrier was found to be 0.85 and 2.33% in normally fertile and repeat breeder cows, respectively. In a financial analysis, it was determined that extended calving interval in a normally fertile cow caused $246 losses and $546 losses in a repeat breeder cow. Additionally, financial losses due to extra service per conception were calculated as $12 and $36 per cow in normally fertile and repeat breeder cows, respectively. In normally fertile and repeat breeder cows, the sum of losses due to extended calving interval and extra service was calculated as $258 (246 + 12) and $582 (546 + 36). This study found that a repeat breeder cow causes an extra $324 ($582 – $258) financial loss compared with a normally fertile cow. Consequently, unlike other genetic disorders like BLAD and DUMPS, which do not decrease the performance of carrier animals, the mutant FXI allele could lead to repeat breeder syndrome in FXID carrier cows and cause important financial losses in dairy farms.

1984 ◽  
Vol 51 (03) ◽  
pp. 371-375 ◽  
Author(s):  
Kangathevy Morgan ◽  
Sandra Schiffman ◽  
Donald Feinstein

SummaryTwo patients with hereditary factor XI deficiency developed inhibitors following plasma transfusions. Neither had severe spontaneous bleeding. The patients’ plasmas neutralized both factor XI in plasma, purified factor XI, and purified factor XIa. The inhibitor in both patients’ plasmas adsorbed to Protein A- Sepharose. The inhibitors eluted from Protein A-Sepharose were partially neutralized by kappa and lambda light chain antisera indicating that they were polyclonal IgG antibodies. Both inhibitors markedly decreased adsorption of factor XI to glass surfaces. The cleavage of factor XI by trypsin was unaffected by the inhibitors. The lack of severe spontaneous bleeding in both of these patients strongly suggests that an alternate coagulation mechanism bypassing factor XI must compensate for this severe defect.


2020 ◽  
Vol 192 ◽  
pp. 100-102
Author(s):  
Donglei Zhang ◽  
Xian Zhang ◽  
Boyang Sun ◽  
Huiyuan Li ◽  
Feng Xue ◽  
...  

2007 ◽  
pp. 321-327 ◽  
Author(s):  
Uri Seligsohn

2019 ◽  
Vol 153 (10) ◽  
pp. 373-379
Author(s):  
Carlos Bravo-Perez ◽  
Teresa Ródenas ◽  
Julio Esteban ◽  
Maria Eugenia de la Morena-Barrio ◽  
Salam Salloum-Asfar ◽  
...  

2013 ◽  
Vol 28 (4) ◽  
pp. 618-620 ◽  
Author(s):  
Yohei Yamada ◽  
Kayoko Fujimoto-Ibusuki ◽  
Keiko Morikawa-Kubota

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