Some approaches to the analysis of market structure's impact in milk commodity chain

The nowadays development in agribusiness can be characterised as shifting of power to the finalising levels and distribution in food commodity chains, which influence as well as form competitive environment of farm and also food-processing companies. The dependence of producers (farmers) on finalising stage is increasing, as well as the risk is transferred and the marked power is enforced in food commodity chains. Those factors are changing proportions, conditions of approach and share of individual stages of commodity chain on value added launched in final product. Possible approach to the identification of market power within food commodity chains is the approach based on price transmission analysis; inelastic price transmission (especially in case of price growth) can imply the existence of market power at certain market level of the commodity chain. This approach - with the distinction of dairy products with low or high value added - is applied on dairy commodity chain in conditions of the Czech Republic.commodity chain, market structure, milk and milk products, price transmission, value added, Agribusiness, Livestock Production/Industries,

Empirical Risk Factors in Realized Stock Returns

Measuring risk in the stock market context is one of the key challenges of modern finance. Despite of the substantial significance of the topic to investors and market regulators, there is a controversy over what risk factors should be used to price the assets or to determine the cost of capital. We empirically investigate the ability of several commonly proposed risk factors to predict Swedish stock returns. We consider the sensitivity of an asset returns to the variation in market returns, the market value of equity, the ratio of market value of equity to book value of equity and the short-term historical stock returns. We conclude that none of these factors is clearly significant for explaining stock returns at the Stockholm Stock Exchange, which casts doubt on their use as universal risk factors in various corporate governance contexts. It seems that the previously documented relationship is contingent on the data sample used and on the time period.stock returns, asset pricing, risk, multifactor models, CAPM, size, book-to-market, momentum, Sweden

CAPM Beta, Size, Book-to-Market, and Momentum in Realized Stock Returns

Measuring risk in the stock market context is one of the key challenges of modern finance. Despite the substantial significance of the topic to investors and market regulators, there is a controversy over what risk factors should be used to price assets or to determine the cost of capital. We empirically investigate the ability of several commonly proposed risk factors to predict Swedish stock returns. We consider the sensitivity of asset returns to the variation in market returns (beta), the market value of equity (size), the ratio of the market value of equity to the book value of equity, and short-term historical stock returns (momentum). We conclude that none of these factors is clearly significant for explaining stock returns on the Stockholm Stock Exchange, which casts doubt on their use as universal risk factors in various corporate governance contexts. It seems that the previously documented relationship is contingent on the data sample used and on the time period.stock returns, asset pricing, risk, multifactor models, CAPM, size, book-to-market, momentum, Sweden

European Citizens Initiative - EU Fact Sheets

The European Citizens' Initiative (ECI) is an important instrument of participatory democracy in the European Union, allowing one million EU citizens residing in at least one quarter of the Member States to invite the Commission to submit a proposal for a legal act to implement the EU Treaties. Since the application of Regulation (EU) No 211/2011 establishing detailed procedures and conditions for the ECI, four initiatives have been successfully submitted to the Commission

Genetic background modifies neurodegeneration and neuroinflammation driven by misfolded human tau protein in rat model of tauopathy: implication for immunomodulatory approach to Alzheimer's disease

<p>Abstract</p> <p>Background</p> <p>Numerous epidemiological studies demonstrate that genetic background modifies the onset and the progression of Alzheimer's disease and related neurodegenerative disorders. The efficacious influence of genetic background on the disease pathway of amyloid beta has been meticulously described in rodent models. Since the impact of genetic modifiers on the neurodegenerative and neuroinflammatory cascade induced by misfolded tau protein is yet to be elucidated, we have addressed the issue by using transgenic lines expressing the same human truncated tau protein in either spontaneously hypertensive rat (SHR) or Wistar-Kyoto (WKY) genetic background.</p> <p>Methods</p> <p>Brains of WKY and SHR transgenic rats in the terminal stage of phenotype and their age-matched non-transgenic littermates were examined by means of immunohistochemistry and unbiased stereology. Basic measures of tau-induced neurodegeneration (load of neurofibrillary tangles) and neuroinflammation (number of Iba1-positive microglia, their activated morphology, and numbers of microglia immunoreactive for MHCII and astrocytes immunoreactive for GFAP) were quantified with an optical fractionator in brain areas affected by neurofibrillary pathology (pons, medulla oblongata). The stereological data were evaluated using two-way ANOVA and Student's t-test.</p> <p>Results</p> <p>Tau neurodegeneration (neurofibrillary tangles (NFTs), axonopathy) and neuroinflammation (microgliosis, astrocytosis) appeared in both WKY and SHR transgenic rats. Although identical levels of transgene expression in both lines were present, terminally-staged WKY transgenic rats displayed significantly lower final NFT loads than their SHR transgenic counterparts. Interestingly, microglial responses showed a striking difference between transgenic lines. Only 1.6% of microglia in SHR transgenic rats expressed MHCII in spite of having a robust phagocytic phenotype, whereas in WKY transgenic rats, 23.2% of microglia expressed MHCII despite displaying a considerably lower extent of transformation into phagocytic phenotype.</p> <p>Conclusions</p> <p>These results show that the immune response represents a pivotal and genetically variable modifying factor that is able to influence vulnerability to neurodegeneration. Therefore, targeted immunomodulation could represent a prospective therapeutic approach to Alzheimer's disease.</p

Ten Years of Tau-Targeted Immunotherapy: The Path Walked and the Roads Ahead

Neurofibrillary pathology comprised of pathological tau protein is closely tied to a range of neurodegenerative disorders, the most common of which is Alzheimer’s disease. While they are individually rarer, a range of other disorders, the tauopathies (including Pick’s disease, progressive supranuclear palsy, corticobasal degeneration, primary progressive aphasia, and ∼50% of behavioral variant frontotemporal dementia cases) display pronounced underlying tau pathology. In all cases, the distribution and amount of tau pathology closely correlates with the severity and phenotype of cognitive impairment, and with the pattern and degree of brain atrophy. Successfully counteracting tau pathology is likely to halt or slow the progression of these debilitating disorders. This makes tau a target of prime importance, yet an elusive one. The diversity of the tau proteome and post-translational modifications, as well as pathophysiology of tau are reviewed. Beginning 2013, a range of tau-targeted immunotherapies have entered clinical development; these therapies, and their common themes and differences are reviewed. The manuscript provides an extensive discussion on epitope selection for immunotherapies against tau pathology, on immunological mechanisms involved in their action, and challenges such as immune senescence, vaccine design, or evolution of epitopes. Furthermore, we provide methodological recommendations for the characterization of active vaccines and antibodies, animal models, and the target itself – the diseased tau proteome

p53 induces distinct epigenetic states at its direct target promoters

<p>Abstract</p> <p>Background</p> <p>The tumor suppressor protein p53 is a transcription factor that is mutated in many cancers. Regulation of gene expression by binding of wild-type p53 to its target sites is accompanied by changes in epigenetic marks like histone acetylation. We studied DNA binding and epigenetic changes induced by wild-type and mutant p53 in non-malignant hTERT-immortalized human mammary epithelial cells overexpressing either wild-type p53 or one of four p53 mutants (R175H, R249S, R273H and R280K) on a wild-type p53 background.</p> <p>Results</p> <p>Using chromatin immunoprecipitation coupled to a 13,000 human promoter microarray, we found that wild-type p53 bound 197 promoters on the microarray including known and novel p53 targets. Of these p53 targets only 20% showed a concomitant increase in histone acetylation, which was linked to increased gene expression, while 80% of targets showed no changes in histone acetylation. We did not observe any decreases in histone acetylation in genes directly bound by wild-type p53. DNA binding in samples expressing mutant p53 was reduced over 95% relative to wild-type p53 and very few changes in histone acetylation and no changes in DNA methylation were observed in mutant p53 expressing samples.</p> <p>Conclusion</p> <p>We conclude that wild-type p53 induces transcription of target genes by binding to DNA and differential induction of histone acetylation at target promoters. Several new wild-type p53 target genes, including <it>DGKZ</it>, <it>FBXO22 </it>and <it>GDF9</it>, were found. DNA binding of wild-type p53 is highly compromised if mutant p53 is present due to interaction of both p53 forms resulting in no direct effect on epigenetic marks.</p

Expression of selected pathway-marker genes in human urothelial cells exposed chronically to a non-cytotoxic concentration of monomethylarsonous acid

AbstractBladder cancer has been associated with chronic arsenic exposure. Monomethylarsonous acid [MMA(III)] is a metabolite of inorganic arsenic and has been shown to transform an immortalized urothelial cell line (UROtsa) at concentrations 20-fold less than arsenite. MMA(III) was used as a model arsenical to examine the mechanisms of arsenical-induced transformation of urothelium. A previous microarray analysis revealed only minor changes in gene expression at 1 and 2 months of chronic exposure to MMA(III), contrasting with substantial changes observed at 3 months of exposure. To address the lack of information between 2 and 3 months of exposure (the critical period of transformation), the expression of select pathway marker genes was measured by PCR array analysis on a weekly basis. Cell proliferation rate, anchorage-independent growth, and tumorigenicity in SCID mice were also assessed to determine the early, persistent phenotypic changes and their association with the changes in expression of these selected marker genes. A very similar pattern of alterations in these genes was observed when compared to the microarray results, and suggested that early perturbations in cell signaling cascades, immunological pathways, cytokine expression, and MAPK pathway are particularly important in driving malignant transformation. These results showed a strong association between the acquired phenotypic changes that occurred as early as 1–2 months of chronic MMA(III) exposure, and the observed gene expression pattern that is indicative of the earliest stages in carcinogenesis

Neural correlates of compassion - An integrative systematic review

Compassion is a psychological construct that has received increasing attention in recent years. Even though a lot of work has been done to identify neural correlates of empathy across studies, such work has not been properly done on neural correlates of compassion. Therefore, the aim was to systematically review the literature on neural correlates of compassion.We have searched through PsycINFO, PubMed and Web of Science for relevant articles published between 1985 and 2020. We included the studies (n = 35) examining the relationship between brain structure or function and compassion. Screening was performed by two authors, between whom a level of agreement was calculated. The quality of the studies was assessed by measures used in other studies as well by measures specific for our study aims. This study was conducted under PRISMA guidelines.Our analysis revealed that the most frequent neural associations with compassion across all analysed studies can be found in the orbital part of the left inferior frontal gyrus, in the right cerebellum, the bilateral middle temporal gyrus, in the bilateral insula and the right caudate nucleus.Our findings suggest that people displaying a lower compassion tend to have either lower neural activity or a grey matter volume in neural areas associated with reward