Purpose – The purpose of this paper s to study the financing behavior of family firms (FF), as these differ from their small- and medium-sized enterprise (SME) counterparts in their capital structure decision, mainly due to an increased risk aversion and the desire to maintain control over the firm. Design/methodology/approach – A sample of 470 SMEs from a bank-based environment is examined for the period of 2005-2010. A dynamic panel data model is utilized to assess both the role of several capital structure determinants and the target-adjusting behavior for different subsamples of firms. Findings – The results show that FF, whether controlled by founders or not, are relatively more leveraged. The aim to maintain long-term control and limited financing options and other factors seem crucial to the observed differences in leverage and dominate risk considerations associated with higher debt. Presumed differences in agency costs across generations do not drive capital structure decisions, as overall leverage does not differ between founder- and descendant-controlled family firms (FCFF and DCFF, respectively). Firms with a founder-chief executive officer (CEO), however, adjust faster to deviations from a target debt ratio. The effects of many proposed capital structure determinants differ across firm types, but are highly consistent with predictions from the pecking order theory. Practical implications – Based on the results of this study, we suggest policy-makers in bank-based economies like Austria to strongly focus on mechanisms that facilitate the access to bank debt to ensure adequate allocation of finances to SMEs. This is especially important to stimulate growth and further innovation for the dominant group of FF, as they rely on debt the most to maintain family control. Originality/value – This paper makes a novel contribution to the literature, as it combines an analysis of the capital structure of non-listed family firms (NFF) in a bank-based economy, the respective role of founder management, the dynamic adjustment to a presumed debt target and joint tests of capital structure theories.

BackgroundCattle breeding populations are susceptible to the propagation of recessive diseases. Individual sires generate tens of thousands of progeny via artificial insemination. The frequency of deleterious alleles carried by such sires may increase considerably within few generations. Deleterious alleles manifest themselves often by missing homozygosity resulting from embryonic/fetal, perinatal or juvenile lethality of homozygotes.ResultsA scan for homozygous haplotype deficiency in 25,544 Fleckvieh cattle uncovered four haplotypes affecting reproductive and rearing success. Exploiting whole-genome resequencing data from 263 animals facilitated to pinpoint putatively causal mutations in two of these haplotypes. A mutation causing an evolutionarily unlikely substitution in SUGT1 was perfectly associated with a haplotype compromising insemination success. The mutation was not found in homozygous state in 10,363 animals (P = 1.79 × 10−5) and is thus likely to cause lethality of homozygous embryos. A frameshift mutation in SLC2A2 encoding glucose transporter 2 (GLUT2) compromises calf survival. The mutation leads to premature termination of translation and activates cryptic splice sites resulting in multiple exon variants also with premature translation termination. The affected calves exhibit stunted growth, resembling the phenotypic appearance of Fanconi-Bickel syndrome in humans (OMIM 227810), which is also caused by mutations in SLC2A2.ConclusionsExploiting comprehensive genotype and sequence data enabled us to reveal two deleterious alleles in SLC2A2 and SUGT1 that compromise pre- and postnatal survival in homozygous state. Our results provide the basis for genome-assisted approaches to avoiding inadvertent carrier matings and to improving reproductive and rearing success in Fleckvieh cattle.Electronic supplementary materialThe online version of this article (doi:10.1186/s12864-015-1483-7) contains supplementary material, which is available to authorized users.

Infection with bovine viral diarrhea virus (BVDV) results in major economic losses either directly through decreased productive performance in cattle herds or indirectly, such as through expenses for control programs. The aim of this systematic review was to review financial and/or economic assessment studies of prevention and/or mitigation activities of BVDV at national, regional and farm level worldwide. Once all predefined criteria had been met, 35 articles were included for this systematic review. Studies were analyzed with particular focus on the type of financially and/or economically-assessed prevention and/or mitigation activities. Due to the wide range of possible prevention and/or mitigation activities, these activities were grouped into five categories: i) control and/or eradication programs, ii) monitoring or surveillance, iii) prevention, iv) vaccination and v) individual culling, control and testing strategies. Additionally, the studies were analyzed according to economically-related variables such as efficiency, costs or benefits of prevention and/or mitigation activities, the applied financial and/or economic and statistical methods, the payers of prevention and/or mitigation activities, the assessed production systems, and the countries for which such evaluations are available. Financial and/or economic assessments performed in Europe were dominated by those from the United Kingdom, which assessed mostly vaccination strategies, and Norway which primarily carried out assessments in the area of control and eradication programs; whereas among non-European countries the United States carried out the majority of financial and/or economic assessments in the area of individual culling, control and testing. More than half of all studies provided an efficiency calculation of prevention and/or mitigation activities and demonstrated whether the inherent costs of implemented activities were or were not justified. The dairy sector was three times more likely to be assessed by the countries than beef production systems. In addition, the dairy sector was approximately eight times more likely to be assessed economically with respect to prevention and/or mitigation activities than calf and youngstock production systems. Furthermore, the private sector was identified as the primary payer of prevention and/or mitigation activities. This systematic review demonstrated a lack of studies relating to efficiency calculations, in particular at national and regional level, and the specific production systems. Thus, we confirmed the need for more well-designed studies in animal health economics in order to demonstrate that the implementation and inherent costs of BVDV prevention and/or mitigation activities are justified.

In humans, the clinical and molecular characterization of sporadic syndromes is often hindered by the small number of patients and the difficulty in developing animal models for severe dominant conditions. Here we show that the availability of large data sets of whole-genome sequences, high-density SNP chip genotypes and extensive recording of phenotype offers an unprecedented opportunity to quickly dissect the genetic architecture of severe dominant conditions in livestock. We report on the identification of seven dominant de novo mutations in CHD7, COL1A1, COL2A1, COPA, and MITF and exploit the structure of cattle populations to describe their clinical consequences and map modifier loci. Moreover, we demonstrate that the emergence of recessive genetic defects can be monitored by detecting de novo deleterious mutations in the genome of bulls used for artificial insemination. These results demonstrate the attractiveness of cattle as a model species in the post genomic era, particularly to confirm the genetic aetiology of isolated clinical case reports in humans.

BackgroundHaplotypes with reduced or missing homozygosity may harbor deleterious alleles that compromise juvenile survival. A scan for homozygous haplotype deficiency revealed a short segment on bovine chromosome 19 (Braunvieh haplotype 2, BH2) that was associated with high juvenile mortality in Braunvieh cattle. However, the molecular genetic underpinnings and the pathophysiology of BH2 remain to be elucidated.ResultsThe frequency of BH2 was 6.5 % in 8,446 Braunvieh animals from the national bovine genome databases. Both perinatal and juvenile mortality of BH2 homozygous calves were higher than the average in Braunvieh cattle resulting in a depletion of BH2 homozygous adult animals (P = 9.3x10−12). The analysis of whole-genome sequence data from 54 Braunvieh animals uncovered a missense mutation in TUBD1 (rs383232842, p.H210R) that was compatible with recessive inheritance of BH2. The availability of sequence data of 236 animals from diverse bovine populations revealed that the missense mutation also segregated at a low frequency (1.7 %) in the Fleckvieh breed. A validation study in 37,314 Fleckvieh animals confirmed high juvenile mortality of homozygous calves (P = 2.2x10−15). Our findings show that the putative disease allele is located on an ancestral haplotype that segregates in Braunvieh and Fleckvieh cattle. To unravel the pathophysiology of BH2, six homozygous animals were examined at the animal clinic. Clinical and pathological findings revealed that homozygous calves suffered from chronic airway disease possibly resulting from defective cilia in the respiratory tract.ConclusionsA missense mutation in TUBD1 is associated with high perinatal and juvenile mortality in Braunvieh and Fleckvieh cattle. The mutation is located on a common haplotype likely originating from an ancient ancestor of Braunvieh and Fleckvieh cattle. Our findings demonstrate for the first time that deleterious alleles may segregate across closed cattle breeds without recent admixture. Homozygous calves suffer from chronic airway disease resulting in poor growth performance and high juvenile mortality. The respiratory manifestations resemble key features of diseases resulting from impaired function of airway cilia.Electronic supplementary materialThe online version of this article (doi:10.1186/s12864-016-2742-y) contains supplementary material, which is available to authorized users.

Creating the ideal nutrition program for calves is a demanding task that has undergone tremendous change in recent years. Products and technologies including novel milk replacers and automated calf feeding systems have been developed to facilitate the ability of dairy producers to feed for higher growth rates before weaning. The creation of new feeding programs and milk replacers has to be looked at carefully, not only from a nutrition point of view but also from the perspective of a potential effect on physiologic digestion and calf health. Abomasal emptying is a critical factor that may link nutrition and disease. The purpose of this article is to review both intrinsic and extrinsic factors that are responsible for abomasal emptying. Predominant extrinsic factors controlling abomasal emptying include meal volume, energy density, and osmolality along with the content and source of protein. This article also reviews experimental methods used to measure abomasal emptying in the calf including those that would be appropriate for use under field conditions. Among these methods, the use of ultrasonography and different absorption tests (d-xylose, acetaminophen) as tools to measure abomasal emptying are discussed. The relationship between abomasal emptying and disease is explored, particularly as it relates to abomasal bloat. Abomasal bloat is a complex syndrome that seems to be increasing in frequency and whose etiology likely at least partially involves slowing of abomasal emptying. Suggestions for minimizing the effect of feeding programs on abomasal emptying are explored as well as needs for future research.

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