The Rationale of Crisis Management – On the Handling of Coincidence in Economic Situation

The subject of this essay is too complex a problem as to cover all details in depth and, thus, draws its attention only to core aspects of the handling of coincidence leaving out sophisticated studies and analytic findings as well as detailed reference to economic literature though there is not very much. On the other hand, for a lot of actual as well as general reasons, the subject is too important a matter as to ignore the serious methodological problems of crisis management, which are rooted in some politically still active bias hidden in orthodox neo-classical economics (Stiglitz 2010). If crisis management continues to follow traditional rationales, it will fail realizing the increasing dynamic of crises within the globalising economies of the world. No existing economy can be considered as an isolated system of its own embedded in a stable composition of societal surroundings. Obviously, many a critical situation has its origin in the sphere of civilization, of political discrepancies, and of administrative inflexibilities. On the other hand, any grave amplitude of markets would touch the entire social surrounding. The belief in the markets’ strength of self-regulation is a dangerous construction of orthodox economics (Bendixen 2009b, 2010). The view on crises suggested here is that of a holistic approach to understand a critical situation. Any interpretation of a situation includes empirical dates and figures based on analytic research, but solving a problem is not an act of logical derivation from findings, as if a solution can be excavated in the mud of reality by empirical studies only. Empirical figures report events of the past; the future does not reveal any empiricism. This would be a contradiction in itself. The end of a crisis as well as the search for solutions to fight the problems revealed is unavoidably a view into the future. Therefore, the rationale of crisis management cannot be made of pure empiricism but should include a far reaching vision of the future emerging from holistic understanding of the situation as a whole

Molecular characterisation of the early response in pigs to experimental infection with Actinobacillus pleuropneumoniae using cDNA microarrays

<p>Abstract</p> <p>Background</p> <p>The bacterium <it>Actinobacillus pleuropneumoniae </it>is responsible for porcine pleuropneumonia, a widespread, highly contagious and often fatal respiratory disease of pigs. The general porcine innate immune response after <it>A. pleuropneumoniae </it>infection is still not clarified. The objective of this study was hence to characterise the transcriptional response, measured by using cDNA microarrays, in pigs 24 hours after experimental inoculation with <it>A. pleuropneumoniae</it>.</p> <p>Methods</p> <p>Microarray analyses were conducted to reveal genes being differentially expressed in inflamed versus non-inflamed lung tissue sampled from inoculated animals as well as in liver and tracheobronchial lymph node tissue sampled from three inoculated animals versus two non-inoculated animals. The lung samples were studied using a porcine cDNA microarray with 5375 unique PCR products while liver tissue and tracheobronchial lymph node tissue were hybridised to an expanded version of the porcine microarray with 26879 unique PCR products.</p> <p>Results</p> <p>A total of 357 genes differed significantly in expression between infected and non-infected lung tissue, 713 genes differed in expression in liver tissue from infected versus non-infected animals and 130 genes differed in expression in tracheobronchial lymph node tissue from infected versus non-infected animals. Among these genes, several have previously been described to be part of a general host response to infections encoding immune response related proteins. In inflamed lung tissue, genes encoding immune activating proteins and other pro-inflammatory mediators of the innate immune response were found to be up-regulated. Genes encoding different acute phase reactants were found to be differentially expressed in the liver.</p> <p>Conclusion</p> <p>The obtained results are largely in accordance with previous studies of the mammalian immune response. Furthermore, a number of differentially expressed genes have not previously been associated with infection or are presently unidentified. Determination of their specific roles during infection may lead to a better understanding of innate immunity in pigs. Although additional work including more animals is clearly needed to elucidate host response to porcine pleuropneumonia, the results presented in this study demonstrate three subsets of genes consistently expressed at different levels depending upon infection status.</p

Microarray Expression Profiles of 20.000 Genes across 23 Healthy Porcine Tissues

BACKGROUND: Gene expression microarrays have been intensively applied to screen for genes involved in specific biological processes of interest such as diseases or responses to environmental stimuli. For mammalian species, cataloging of the global gene expression profiles in large tissue collections under normal conditions have been focusing on human and mouse genomes but is lacking for the pig genome. METHODOLOGY/PRINCIPAL FINDINGS: Here we present the results from a large-scale porcine study establishing microarray cDNA expression profiles of approximately 20.000 genes across 23 healthy tissues. As expected, a large portion of the genes show tissue specific expression in agreement with mappings to gene descriptions, Gene Ontology terms and KEGG pathways. Two-way hierarchical clustering identified expected tissue clusters in accordance with tissue type and a number of cDNA clusters having similar gene expression patterns across tissues. For one of these cDNA clusters, we demonstrate that possible tissue associated gene function can be inferred for previously uncharacterized genes based on their shared expression patterns with functionally annotated genes. We show that gene expression in common porcine tissues is similar to the expression in homologous tissues of human. CONCLUSIONS/SIGNIFICANCE: The results from this study constitute a valuable and publicly available resource of basic gene expression profiles in normal porcine tissues and will contribute to the identification and functional annotation of porcine genes

A hereditary disposition for bovine peripheral nerve sheath tumors in Danish Holstein cattle

BACKGROUND: Peripheral nerve sheath tumors (PNSTs) are frequently found in Danish cattle at slaughter. Bovine PNSTs share several gross and histopathological characteristics with the PNSTs in humans with heritable neurofibromatosis syndromes. The aim of the present study was to investigate a possible hereditary disposition to PNSTs in dairy cattle by statistical analysis performed on data from 567 cattle with PNSTs. Furthermore, a preliminary genome-wide association study (GWAS) was performed on DNA isolated from 28 affected and 28 non-affected Holstein cows to identify loci in the bovine genome involved in the development of PNSTs. RESULTS: PNSTs were significantly more common in the Danish Holstein breed than in other breeds with 0.49% of Danish Holsteins slaughtered during an eight-year-period having PNSTs. PNSTs also occurred significantly more frequently in the offspring of some specific Holstein sires. Examination of three generation pedigrees showed that these sires were genetically related through a widely used US Holstein sire. The PNSTs included in GWAS were histologically classified as neurofibroma-schwannoma (43%), schwannoma (36%) and neurofibroma (21%) and derived from Holstein cows with multiple PNSTs. A single SNP on chromosome 27 reached genome-wide significance. CONCLUSIONS: Gross and histological characteristics of bovine PNSTs are comparable to PNSTs in humans (schwannomatosis). Danish Holsteins are genetically disposed to develop PNSTs but the examined materials are insufficient to allow determination of the mode of inheritance

Characterisation of five candidate genes within the ETEC F4ab/ac candidate region in pigs

BACKGROUND: Enterotoxigenic Escherichia coli (ETEC) that express the F4ab and F4ac fimbriae is a major contributor to diarrhoea outbreaks in the pig breeding industry, infecting both newborn and weaned piglets. Some pigs are resistant to this infection, and susceptibility is inherited as a simple dominant Mendelian trait. Indentifying the genetics behind this trait will greatly benefit pig welfare as well as the pig breeding industry by providing an opportunity to select against genetically susceptible animals, thereby reducing the number of diarrhoea outbreaks. The trait has recently been mapped by haplotype sharing to a 2.5 Mb region on pig chromosome 13, a region containing 18 annotated genes. FINDINGS: The coding regions of five candidate genes for susceptibility to ETEC F4ab/ac infection (TFRC, ACK1, MUC20, MUC4 and KIAA0226), all located in the 2.5 Mb region, were investigated for the presence of possible causative mutations. A total of 34 polymorphisms were identified in either coding regions or their flanking introns. The genotyping data for two of those were found to perfectly match the genotypes at the ETEC F4ab/ac locus, a G to C polymorphism in intron 11 of TFRC and a C to T silent polymorphism in exon 22 of KIAA0226. Transcriptional profiles of the five genes were investigated in a porcine tissue panel including various intestinal tissues. All five genes were expressed in intestinal tissues at different levels but none of the genes were found differentially expressed between ETEC F4ab/ac resistant and ETEC F4ab/ac susceptible animals in any of the tested tissues. CONCLUSIONS: None of the identified polymorphisms are obvious causative mutations for ETEC F4ab/ac susceptibility, as they have no impact on the level of the overall mRNA expression nor predicted to influence the composition of the amino acids composition. However, we cannot exclude that the five tested genes are bona fide candidate genes for susceptibility to ETEC F4ab/ac infection since the identified polymorphism might affect the translational apparatus, alternative splice forms may exist and post translational mechanisms might contribute to disease susceptibility

Congenital bovine spinal dysmyelination is caused by a missense mutation in the SPAST gene

Bovine spinal dysmyelination (BSD) is a recessive congenital neurodegenerative disease in cattle (Bos taurus) characterized by pathological changes of the myelin sheaths in the spinal cord. The occurrence of BSD is a longstanding problem in the American Brown Swiss (ABS) breed and in several European cattle breeds upgraded with ABS. Here, we show that the disease locus on bovine chromosome 11 harbors the SPAST gene that, when mutated, is responsible for the human disorder hereditary spastic paraplegia (HSP). Initially, SPAST encoding Spastin was considered a less likely candidate gene for BSD since the modes of inheritance as well as the time of onset and severity of symptoms differ widely between HSP and BSD. However, sequence analysis of the bovine SPAST gene in affected animals identified a R560Q substitution at a position in the ATPase domain of the Spastin protein that is invariant from insects to mammals. Interestingly, three different mutations in human SPAST gene at the equivalent position are known to cause HSP. To explore this observation further, we genotyped more than 3,100 animals of various cattle breeds and found that the glutamine allele exclusively occurred in breeds upgraded with ABS. Furthermore, all confirmed BSD carriers were heterozygous, while all affected calves were homozygous for the glutamine allele consistent with recessive transmission of the underlying mutation and complete penetrance in the homozygous state. Subsequent analysis of recombinant Spastin in vitro showed that the R560Q substitution severely impaired the ATPase activity, demonstrating a causal relationship between the SPAST mutation and BSD

Reduced prediction error responses in high-as compared to low-uncertainty musical contexts

Abstract Theories of predictive processing propose that prediction error responses are modulated by the certainty of the predictive model or precision . While there is some evidence for this phenomenon in the visual and, to a lesser extent, the auditory modality, little is known about whether it operates in the complex auditory contexts of daily life. Here, we examined how prediction error responses behave in a more complex and ecologically valid auditory context than those typically studied. We created musical tone sequences with different degrees of pitch uncertainty to manipulate the precision of participants’ auditory expectations. Magnetoencephalography was used to measure the magnetic counterpart of the mismatch negativity (MMNm) as a neural marker of prediction error in a multi-feature paradigm. Pitch, slide, intensity and timbre deviants were included. We compared high-entropy stimuli, consisting of a set of non-repetitive melodies, with low-entropy stimuli consisting of a simple, repetitive pitch pattern. Pitch entropy was quantitatively assessed with an information-theoretic model of auditory expectation. We found a reduction in pitch and slide MMNm amplitudes in the high-entropy as compared to the low-entropy context. No significant differences were found for intensity and timbre MMNm amplitudes. Furthermore, in a separate behavioral experiment investigating the detection of pitch deviants, similar decreases were found for accuracy measures in response to more fine-grained increases in pitch entropy. Our results are consistent with a precision modulation of auditory prediction error in a musical context, and suggest that this effect is specific to features that depend on the manipulated dimension—pitch information, in this case. Highlights The mismatch negativity (MMNm) is reduced in musical contexts with high pitch uncertainty The MMNm reduction is restricted to pitch-related features Accuracy during deviance detection is reduced in contexts with higher uncertainty The results suggest a feature-selective precision modulation of prediction error Materials, data and scripts can be found in the Open Science Framework repository: http://bit.ly/music_entropy_MMN DOI: 10.17605/OSF.IO/MY6T

Increased sinusoidal flow is not the primary stimulus to liver regeneration

Background: Hemodynamic changes in the liver remnant following partial hepatectomy (PHx) have been suggested to be a primary stimulus in triggering liver regeneration. We hypothesized that it is the increased sinusoidal flow per se and hence the shear-stress stimulus on the endothelial surface within the liver remnant which is the main stimulus to regeneration. In order to test this hypothesis we wanted to increase the sinusoidal flow without performing a concomitant liver resection. Accordingly, we constructed an aorto-portal shunt to the left portal vein branch creating a standardized four-fold increase in flow to segments II, III and IV. The impact of this manipulation was studied in both an acute model (6 animals, 9 hours) using a global porcine cDNA microarray chip and in a chronic model observing weight and histological changes (7 animals, 3 weeks). Results: Gene expression profiling from the shunted segments does not suggest that increased sinusoidal flow per se results in activation of genes promoting mitosis. Hyperperfusion over three weeks results in the whole liver gaining a supranormal weight of 3.9% of the total body weight (versus the normal 2.5%). Contrary to our hypothesis, the weight gain was observed on the non-shunted side without an increase in sinusoidal flow. Conclusions: An isolated increase in sinusoidal flow does not have the same genetic, microscopic or macroscopic impact on the liver as that seen in the liver remnant after partial hepatectomy, indicating that increased sinusoidal flow may not be a sufficient stimulus in itself for the initiation of liver regeneration