Myśl liberalna a dylematy rozwoju w dobie kryzysu gospodarczego

The idea of liberalism in economics has generated an enormous range of scientific discussions and sparked explosive disputes as to its economic effectiveness. Doubts centre around three questions. The first addresses the dilemma whether economic resources are universal, i.e. independent from stages of development of the particular economies, institutional and social conditions. The second concerns the role of the state in an economy. The third expresses doubts as to distribution, thus, equality of opportunities and social justice. The most recent financial crisis has led to a widespread acceptance of profound state intervention in the economy. Many financial authorities, central banks and international financial institutions have undertaken monetary and fiscal interventions on an unprecedented scale. Establishment of a tight system of banking regulation and supervision (sequencing) has cast doubts on value of liberalism as one of the best ways to achieving economic success

Spór o drogi wyjścia z pułapki płynności i deflacji

This paper addresses the issue of liquidity trap. The term is adopted from J. Keynes to define an economy in the state of zero bound interest rate and imminent deflation. The discussion is based on findings from  P. Krugman’s theoretical model of an endowment economy (1998). Critical analysis is applied to recommendations for escaping from the liquidity trap which involves introduction of negative real interest rate by appropriate decisions of financial authorities aiming at structural reforms, fiscal and monetary expansion. This analysis, outlined in general terms by P. Krugman and his critics, focuses on critical assessment of theoretical consequences of discussed proposals, particularly those formulated as calls for “credible promises to be irresponsible”, and practical effects of escaping from the liquidity trap which has been undertaken by Japan, so far largely to no avail. Also, this paper presents the author’s evaluation of ways out of the liquidity trap attempted over the years and related to the current financial crisis, highlighting  the issues of inflation targeting, exchanges rates, and debt.Artykuł podejmuje kwestię pułapki płynności. Termin ten został zastosowany przez J. Keynesa na oznaczenie gospodarki w stanie charakteryzującym się stopami procentowymi bliskimi zeru i zagrożonej deflacją. Podstawą dyskusji są tezy wynikające z teoretycznego modelu tzw. endowmenteconomy  P. Krugmana (1998). Analiza krytyczna zaleca wyjście z pułapki płynności  poprzez doprowadzenie przez władze finansowe do negatywnej realnej stopy procentowej w wyniku reform strukturalnych oraz ekspansji fiskalnej i monetarnej. Analiza ta, zarysowana ogólnie przez P. Krugmana i jego krytyków, koncentruje się na krytycznej ocenie teoretycznych skutków dyskutowanych propozycji, zwłaszcza tych sformułowanych jako „wiarygodne postanowienie bycia nieodpowiedzialnym”  i praktycznych skutków prób wyjścia z pułapki płynności, podjętych przez Japonię, dotąd wszakże bez większego sukcesu. Artykuł zawiera także ocenę odautorską dotycząca dróg wyjścia z pułapki płynności podejmowanych na przestrzeni  ubiegłych lat i nawiązuje do bieżącego kryzysu finansowego w odniesieniu do celu inflacyjnego, kursu wymiennego i zadłużenia

Kreatywność kapitału intelektualnego - kooperacja czy konkurencja w B+R

The paper is devoted to the choice between cooperative and competitive R&D models. It consists of 3 sections. The discussion is based on two models of the intellectual capital, advanced by T. Steward and P. Sullivan. This capital consists of human capital (knowledge, skills, capabilities, motivations) and infrastructural capital (software, data bases, and telecommunication solutions) (section 1). The intellectual capital, which often constitutes the most valuable asset of a company, is created as part of a complicated, costly, and long-lasting process of accumulation and transfer of knowledge and technology via free and commercial channels, and as a result of R&D activity as well. It activates a secondary and multi-directional process of diffusion of knowledge (spillovers) (section 2). R+D activities are realized in cooperative or competitive (independent) ways. S. A. Hörte (2004) discusses applicability of both the models in relation to results of the Prisoner’s Dilemma (Axelrod 1984) simulation by analyzing a three-dimensional matrix of variables (a firm’s strategy, phase of R&D, and its knowledge level). The conclusions, although not unequivocal, are, for some matches of variables, useful in practical decision-making. (section 3)

Reformy strukturalne jako antidotum na nierówności społeczne

Poland, like other countries worldwide, experiences substantial income inequalities and constantly expanding gaps in wealth. This causes adverse macroeconomic consequences by restricting dynamics of domestic demand. Levels of the inequalities are decided by tax, welfare and educational systems and, above all, by nature of a labour market. A desirable fiscal consensus becomes an urgent necessity. Although a degree of inequality is an immanent characteristic of capitalism, the question is, what levels of inequalities are acceptable and when do such inequalities become harmful rather than useful?W Polsce, podobnie jak w innych krajach świata, występują duże nierówności dochodowe i stale rosnące nierówności majątkowe. Wywołuje to negatywne konsekwencje makroekonomiczne, ograniczając dynamikę krajowego popytu. O poziomie nierówności decyduje system podatkowy, zabezpieczeń socjalnych, edukacyjny oraz przede wszystkim charakter rynku pracy. Poszukiwanie pożądanego konsensusu podatkowego staje się pilną koniecznością. I chociaż pewien sto-pień nierówności jest immanentną cechą kapitalizmu, powstaje pytanie, jaki poziom nierówności jest do zaakceptowania oraz kiedy nierówności czynią więcej szkody niż pożytku? &nbsp

Periostin regulates collagen fibrillogenesis and the biomechanical properties of connective tissues

Periostin is predominantly expressed in collagen-rich fibrous connective tissues that are subjected to constant mechanical stresses including: heart valves, tendons, perichondrium, cornea, and the periodontal ligament (PDL). Based on these data we hypothesize that periostin can regulate collagen I fibrillogenesis and thereby affect the biomechanical properties of connective tissues. Immunoprecipitation and immunogold transmission electron microscopy experiments demonstrate that periostin is capable of directly interacting with collagen I. To analyze the potential role of periostin in collagen I fibrillogenesis, gene targeted mice were generated. Transmission electron microscopy and morphometric analyses demonstrated reduced collagen fibril diameters in skin dermis of periostin knockout mice, an indication of aberrant collagen I fibrillogenesis. In addition, differential scanning calorimetry (DSC) demonstrated a lower collagen denaturing temperature in periostin knockout mice, reflecting a reduced level of collagen cross-linking. Functional biomechanical properties of periostin null skin specimens and atrioventricular (AV) valve explant experiments provided direct evidence of the role that periostin plays in regulating the viscoelastic properties of connective tissues. Collectively, these data demonstrate for the first time that periostin can regulate collagen I fibrillogenesis and thereby serves as an important mediator of the biomechanical properties of fibrous connective tissues.Peer reviewe

Periostin is up-regulated in high grade and high stage prostate cancer

BACKGROUND: Expression of periostin is an indicator of epithelial-mesenchymal transition in cancer but a detailed analysis of periostin expression in prostate cancer has not been conducted so far. METHODS: Here, we evaluated periostin expression in prostate cancer cells and peritumoural stroma immunohistochemically in two independent prostate cancer cohorts, including a training cohort (n = 93) and a test cohort (n = 325). Metastatic prostate cancers (n = 20), hormone refractory prostate cancers (n = 19) and benign prostatic tissues (n = 38) were also analyzed. RESULTS: In total, strong epithelial periostin expression was detectable in 142 of 418 (34.0%) of prostate carcinomas and in 11 of 38 benign prostate glands (28.9%). Increased periostin expression in carcinoma cells was significantly associated with high Gleason score (p < 0.01) and advanced tumour stage (p < 0.05) in the test cohort. Whereas periostin expression was weak or absent in the stroma around normal prostate glands, strong periostin expression in tumour stroma was found in most primary and metastatic prostate cancers. High stromal periostin expression was associated with higher Gleason scores (p < 0.001). There was a relationship between stromal periostin expression and shortened PSA relapse free survival times in the training cohort (p < 0.05). CONCLUSIONS: Our data indicate that periostin up-regulation is related to increased tumour aggressiveness in prostate cancer and might be a promising target for therapeutical interventions in primary and metastatic prostate cancer

A novel HSF4 gene mutation (p.R405X) causing autosomal recessive congenital cataracts in a large consanguineous family from Pakistan

<p>Abstract</p> <p>Background</p> <p>Hereditary cataracts are most frequently inherited as autosomal dominant traits, but can also be inherited in an autosomal recessive or X-linked fashion. To date, 12 loci for autosomal recessive cataracts have been mapped including a locus on chromosome 16q22 containing the disease-causing gene <it>HSF4 </it>(Genbank accession number <ext-link ext-link-id="NM_001040667" ext-link-type="gen">NM_001040667</ext-link>). Here, we describe a family from Pakistan with the first nonsense mutation in <it>HSF4 </it>thus expanding the mutational spectrum of this heat shock transcription factor gene.</p> <p>Methods</p> <p>A large consanguineous Pakistani family with autosomal recessive cataracts was collected from Quetta. Genetic linkage analysis was performed for the common known autosomal recessive cataracts loci and linkage to a locus containing <it>HSF4 </it>(OMIM 602438) was found. All exons and adjacent splice sites of the heat shock transcription factor 4 gene (<it>HSF4</it>) were sequenced. A mutation-specific restriction enzyme digest (H<it>ph</it>I) was performed for all family members and unrelated controls.</p> <p>Results</p> <p>The disease phenotype perfectly co-segregated with markers flanking the known cataract gene HSF4, whereas other autosomal recessive loci were excluded. A maximum two-point LOD score with a Zmax = 5.6 at θ = 0 was obtained for D16S421. Direct sequencing of HSF4 revealed the nucleotide exchange c.1213C > T in this family predicting an arginine to stop codon exchange (p.R405X).</p> <p>Conclusion</p> <p>We identified the first nonsense mutation (p.R405X) in exon 11 of <it>HSF4 </it>in a large consanguineous Pakistani family with autosomal recessive cataract.</p

Association of CDX1 binding site of periostin gene with bone mineral density and vertebral fracture risk

Summary Periostin (POSTN) as a regulator of osteoblast differentiation and bone formation may affect susceptibility to osteoporosis. This study suggests POSTN as a candidate gene for bone mineral density (BMD) variation and vertebral fracture risk, which could better our understanding about the genetic pathogenesis of osteoporosis and will be useful in clinic in the future. Introduction The genetic determination of osteoporosis is complex and ill-defined. Periostin (POSTN), an extracellular matrix secreted by osteoblasts and a regulator of osteoblast differentiation and bone formation, may affect susceptibility to osteoporosis. Methods We adopted a tag-single nucleotide polymorphism (SNP) based association method followed by imputationbased verification and identification of a causal variant. The association was investigated in 1,572 subjects with extremeBMD and replicated in an independent population of 2,509 subjects. BMD was measured by dual X-ray absorptiometry. Vertebral fractures were identified by assessing vertebral height from X-rays of the thoracolumbar spine. Association analyses were performed with PLINK toolset and imputation analyses with MACH software. The top imputation finding was subsequently validated by genotyping. Interactions between POSTN and another BMD-related candidate gene sclerostin (SOST) were analyzed using MDR program and validated by logistical regression analyses. The putative transcription factor binding with target sequence was confirmed by electrophoretic mobility shift assay (EMSA). Results Several SNPs of POSTN were associated with BMD or vertebral fractures. The most significant polymorphism was rs9547970, located at the -2,327bpupstream(P06.8×10-4)of POSTN. Carriers of the minor allele G per copy of rs9547970 had1.33higherriskofvertebralfracture(P00. 007). An interactive effect between POSTN and SOST upon BMD variation was suggested (P<0.01). A specific binding of CDX1 to the sequence of POSTN with the major allele A of rs9547970 but not the variant G allele was confirmed by EMSA. Conclusions Our results suggest POSTN as a candidate gene for BMD variation and vertebral fracture risk. © 2012 International Osteoporosis Foundation and National Osteoporosis Foundation.published_or_final_versionSpringer Open Choice, 28 May 201

Midkine expression correlating with growth activity and tooth morphogenesis in odontogenic tumors

Midkine (MK; a low molecular weight heparin-binding growth factor) is a multifunctional cytokine. MK plays a role in morphogenesis of many organs including teeth through epithelial-mesenchymal interactions. We immunohistochemically examined MK expression in various human odontogenic tumors. There was no difference in positive rate and intensity of MK between benign odontogenic tumors and their malignant counterparts. Ameloblastoma showed MK localization in the peripheral columnar cells in budding processes from the parenchyma, which frequently expressed proliferating cell nuclear antigen. MK was also preferentially expressed in keratinized cells in acanthomatous ameloblastoma and keratocystic odontogenic tumor. In odontogenic mixed tumors except for odontoma, intense immunoreactivity to MK was found in epithelial follicles, the surrounding odontogenic ectomesenchymal tissue, and the basement membrane between them. Intensity in the odontogenic ectomesenchyme decreased in relation to distance from the epithelial follicles. No expression was found in tumor cells associated with production of dental hard tissues in odontogenic mixed tumors including odontoma. These findings suggested that MK is involved in the reciprocal interaction between odontogenic epithelium and odontogenic ectomesenchymal tissue in areas without dental hard tissue formation in odontogenic mixed tumors. Coexpression of MK and proliferating cell nuclear antigen was also observed in epithelial follicles and highly cellular nodules in the ectomesenchyme of odontogenic mixed tumors. MK is considered to mediate growth activity of odontogenic tumors and cell differentiation of odontogenic mixed tumors through molecular mechanisms similar to those involved in morphogenesis of the tooth