Komentarze do artykułu Antoniego Kuklińskiego

Krzysztof Porwit’s article polemicizes with the thinking expressed in Antoni Kukliński’s article, saying that the new paradigm of associations between a KBE and a KBS is meant to apply to all aspects of the economy and society. The obstacles and conflicts in these associations are pointed out, and doubts are expressed about the rate of progress along the road to a KBE and KBS described in the article, creating a circle of progress and success. The article relates to Antoni Kukliński’s thesis about the reasons behind the stoppage of the development of a KBE in countries that are poorer than the countries of the European Union. In his article, Kukliński presents the chances of a remedy; but Porwit claims that first it is necessary to remove the causes of the malady by means of work from the very bottom - by means of an improvement to the institutional order and moral renewal. Only on such foundations is it possible to attain a high quality of formal-legal characteristics and institutional order.Roman Galar’s paper relates to the basic thesis of Antoni Kukliński’s article, i.e. the trap of low-level efficiency equilibrium. While underlining the appropriateness of this diagnosis, he nevertheless undermines it by noting that cause-effect mechanisms operate on a different level. He offers his own interpretation for the causes of this “ low level” trap, pointing out, among other things, the dangers of copying institutional standards from “high level” countries, and suggests a solution to the problem by creating a network of social enclaves which the processes of creating a KBE may function safely. He supports the idea of forming a Society of Friends of a Knowledge-Based Economy, providing exhaustive arguments in its favour, and indicates the need for such a Society to explain what a KBE really means, because misunderstandings of the purpose of a KBE may discredit the entire idea of such an economy. Krzysztof PORWIT:Autor polemizuje z tezą artykułu Antoniego Kuklińskiego, iż nowy paradygmat sprzężeń między gospodarką opartą na wiedzy a społeczeństwem opartym na wiedzy ma dotyczyć zarówno gospodarki, jak i społeczeństwa. Zwraca uwagę na przeszkody i konflikty w tym współdziałaniu, a także podaje w wątpliwość stan zaawansowania na drodze do gospodarki i społeczeństwa opartych na wiedzy nakreślony w komentowanym artykule, stwarzający magiczny krąg postępu i sukcesu. Autor ustosunkowuje się do tezy Antoniego Kuklińskiego na temat przyczyn blokady rozwoju gospodarki opartej na wiedzy krajach biedniejszych niż państwa Unii Europejskiej. Kukliński w swym artykule zarysował szanse terapii; według Porwita konieczne jest najpierw usunięcie przyczyn schorzeń poprzez pracę od podstaw, ulepszanie ładu instytucjonalnego, moralną odnowę i dopiero na takich fundamentach możliwe będzie osiąganie wysokiej jakości cech formalnoprawnych i ładu instytucjonalnego.Roman GALAR:Autor ustosunkowuje się do podstawowej tezy artykułu Antoniego Kuklińskiego, tzn. pułapki równowagi niskiego poziomu efektywności. Podkreśla trafność diagnozy, ale jednocześnie podważa ją, zauważając, iż mechanizmy przyczynowo-skutkowe funkcjonują na innym poziomie. Podaje własną interpretację przyczyn pułapki „niskiego poziomu” , zwracając uwagę m.in. na niebezpieczeństwa związane z kopiowaniem standardów instytucjonalnych z krajów „wysokiego poziomu” i proponuje jako rozwiązanie problemu tworzenie sieci społecznych enklaw, w ramach których procesy kreowania gospodarki opartej na wiedzy będą mogły bezpiecznie funkcjonować. Wspiera pomysł powołania Towarzystwa Przyjaciół Gospodarki Opartej na Wiedzy, podając rozwiniętą argumentację, zwraca także uwagę na znaczenie wyjaśnienia przez to Towarzystwo, o co naprawdę chodzi w idei tworzenia tego rodzaju gospodarki, gdyż nieporozumienia wokół kwestii związanych z gospodarką opartą na wiedzy grożą dyskredytacją całej idei

The Regulation of Commodity Options

To outline further genetic mechanisms of transformation from follicular lymphoma (FL) to diffuse large B-cell lymphoma (DLBCL), we have performed whole genome array-CGH in 81 tumors from 60 patients [29 de novo DLBCL (dnDLBCL), 31 transformed DLBCL (tDLBCL), and 21 antecedent FL]. In 15 patients, paired tumor samples (primary FL and a subsequent tDLBCL) were available, among which three possessed more than two subsequent tumors, allowing us to follow specific genetic alterations acquired before, during, and after the transformation. Gain of 2p15-16.1 encompassing, among others, the REL, BCL11A, USP34, COMMD1, and OTX1 genes was found to be more common in the tDLBCL compared with dnDLBCL (P < 0.001). Furthermore, a high-level amplification of 2p15-16.1 was also detected in the FL stage prior to transformation, indicating its importance during the transformation event. Quantitative real-time PCR showed a higher level of amplification of REL, USP34, and COMMD1 (all involved in the NF kappa B-pathway) compared with BCL11A, which indicates that the altered genes disrupting the NF kappa B pathway may be the driver genes of transformation rather than the previously suggested BCL11A. Moreover, a 17q21.33 amplification was exclusively found in tDLBCL, never in FL (P < 0.04) or dnDLBCL, indicating an upregulation of genes of importance during the later phase of transformation. Taken together, our study demonstrates potential genomic markers for disease progression to clinically more aggressive forms. We also confirm the importance of the TP53-, CDKN2A-, and NF kappa B-pathways for the transformation from FL to DLBCL

TP53 mutations in myelodysplastic syndromes with deletion of 5q

The myelodysplastic syndromes (MDS) constitute a heterogeneous group of malignant bone marrow disorders characterized by peripheral cytopenia(s) and increased risk of progression to acute myeloid leukemia (AML). International Prognostic Scoring system (IPSS) Low- or Intermediate (INT)-1 risk MDS with a deletion of 5q (del5q) were considered to have an indolent course and a low risk for progression to AML as compared to other MDS subtypes. However, more recent studies have shown that overall survival (OS) and risk for AML progression vary greatly in del(5q) MDS patients indicating that factors beyond established risk scoring systems impact patient outcome. Molecular abnormalities have emerged as putative prognostic markers. We performed molecular studies in a patient with classical 5q-syndrome who unexpectedly evolved to high-risk MDS with complex karyotype (Paper I). Immunohistochemistry (IHC) of pre-treatment marrow biopsies revealed a small fraction of progenitors with strong p53 expression and sequencing confirmed a TP53 mutation. TP53 mutated subclones had not been described in MDS with isolated del(5q) and indicated a previously unknown heterogeneity. In a subsequent study of 55 patients with lower-risk del(5q) MDS, 18% of the patients were found to have TP53 mutated subclones at diagnosis which rendered them at higher risk for progression (Paper II). Interestingly, the association with outcome was even stronger for p53 IHC indicating a high sensitivity of this method for early identification of patients with adverse outcome. As a next step, we assessed p53 protein expression in a cohort of 85 lower-risk del(5q) MDS patients treated with lenalidomide within a clinical trial (Paper IV). P53 IHC positive patients showed significantly shorter overall survival, higher risk for leukemic transformation, and lower cytogenetic response rate to lenalidomide, hence validating the results from Paper II. Importantly, pyrosequencing analysis of microdissected IHC stained cells confirmed that cells with strong staining carried TP53 mutations, while moderate staining reflected wild-type TP53. Due to the apparently exquisite sensitivity of the del(5q) clone to len, we hypothesized that higher doses of lenalidomide may induce cytogenetic and clinical responses also in patients with high-risk MDS/AML with chromosome 5 abnormalities who were refractory or ineligible for standard treatment (Paper III). In this study, we demonstrated that treatment was able to inhibit the del(5q)tumor clone in a cohort of patients with extremely advanced disease, which suggests that the selective inhibitory effect of len in vitro may be translated into a therapeutic response in vivo. Importantly, TP53 mutations were common (62%) in this cohort, and uniformly associated with treatment failure. Altogether, our findings suggest an important role of the p53 pathway in both low- and high-risk del(5q) MDS, and in relation to treatment with lenalidomide. These findings will have major implications for risk stratification and the choice of therapy

The Desire to wipe the slate green, or why the world is in need of a hard reset

Esej jest próbą analizy niektórych popularniejszych trendów ideologicznych „zielonego” dyskursu, ze szczególnym uwzględnieniem zagadnień czystości oraz powrotu świata do wyidealizowanego stanu z czasów przedindustrialnych, niedotkniętego problemami współczesnej egzystencji. Omawia on dążenie do czystości pod kątem ekopolityki oraz ekopoetyki, jednocześnie sprzeciwiając się stanowi czystości, samemu noszącemu znamiona kulturowej manipulacji, jako pożądanemu. Po krytycznym odczytaniu fragmentów Oryksa i Derkacza Margaret Atwood, wysunięta zostaje teza, że uporczywe faworyzowanie wyższości Natury nie różni się w skutkach od innych apokaliptycznych scenariuszy, w których ludzkość przymusowo powraca do czasów przedtechnologicznych, tym samym podkreślając wagę kontekstu ludzkiej kondycji, która czerpie garściami ze swojego podwójnego, kulturowo-naturalnego rodowodu

T2K experiment neutrino cross sections results

The understanding of neutrino–nucleus interactions is crucial for the precise measurement of neutrino oscillations phenomenon. Moreover, it is important for Monte Carlo modeling of neutrinos interactions, which at this moment is simplified. For this reason, a variety of cross-section measurements on different target materials and at different neutrino beam energies are performed worldwide. The goal of this paper is to review the recent results from neutrino cross-section measurements from the T2K experiment

The impact of prior malignancies on second malignancies and survival in MM patients: a population-based study

To access publisher's full text version of this article, please click on the hyperlink in Additional Links field or click on the hyperlink at the top of the page marked FilesIn the present study, we aimed to evaluate 2 hypotheses. First, we hypothesize that prior malignancy is a proxy for genetic susceptibility that could be a risk factor for subsequent malignancy development in multiple myeloma (MM) patients. Second, we hypothesize that survival after MM is influenced by a prior malignancy. All patients diagnosed with MM from 1 January 1973 to 31 December 2010 were identified from the Swedish Cancer Register. Cox regression model was used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) where prior malignancy was compared in MM patients who developed a subsequent malignancy and MM patients who did not. In another Cox regression model, survival was compared in MM patients with and without a prior malignancy diagnosis. A total of 19 791 patients were diagnosed with MM. Patients with a prior malignancy diagnosis had a significantly increased risk of developing a subsequent malignancy compared with MM patients without (HR 1.42, 95% CI 1.23-1.65, P 1 prior malignancy reduces survival even further.Asrun Einarsdottir Foundation in Iceland Blodcancerfonden Swedish Cancer Society Stockholm County Council Karolinska Institutet Foundation University of Iceland Research Fund Icelandic Centre for Research Landspitali University Hospital Research Fund Marie Curie Career Integration Grant Memorial Sloan Kettering Cancer Center Core Grant by the National Cancer Institute, National Institutes of Healt

A Minimal Model of Signaling Network Elucidates Cell-to-Cell Stochastic Variability in Apoptosis

Signaling networks are designed to sense an environmental stimulus and adapt to it. We propose and study a minimal model of signaling network that can sense and respond to external stimuli of varying strength in an adaptive manner. The structure of this minimal network is derived based on some simple assumptions on its differential response to external stimuli. We employ stochastic differential equations and probability distributions obtained from stochastic simulations to characterize differential signaling response in our minimal network model. We show that the proposed minimal signaling network displays two distinct types of response as the strength of the stimulus is decreased. The signaling network has a deterministic part that undergoes rapid activation by a strong stimulus in which case cell-to-cell fluctuations can be ignored. As the strength of the stimulus decreases, the stochastic part of the network begins dominating the signaling response where slow activation is observed with characteristic large cell-to-cell stochastic variability. Interestingly, this proposed stochastic signaling network can capture some of the essential signaling behaviors of a complex apoptotic cell death signaling network that has been studied through experiments and large-scale computer simulations. Thus we claim that the proposed signaling network is an appropriate minimal model of apoptosis signaling. Elucidating the fundamental design principles of complex cellular signaling pathways such as apoptosis signaling remains a challenging task. We demonstrate how our proposed minimal model can help elucidate the effect of a specific apoptotic inhibitor Bcl-2 on apoptotic signaling in a cell-type independent manner. We also discuss the implications of our study in elucidating the adaptive strategy of cell death signaling pathways.Comment: 9 pages, 6 figure

New limits on neutrino non-unitary mixings based on prescribed singular values

Singular values are used to construct physically admissible 3-dimensional mix- ing matrices characterized as contractions. Depending on the number of singular values strictly less than one, the space of the 3-dimensional mixing matrices can be split into four disjoint subsets, which accordingly corresponds to the minimal number of additional, non-standard neutrinos. We show in numerical analysis that taking into account present experimental precision and fits to different neutrino mass splitting schemes, it is not pos- sible to distinguish, on the level of 3-dimensional mixing matrices, between two and three extra neutrino states. It means that in 3+2 and 3+3 neutrino mixing scenarios, using the so-called α parametrization, ranges of non-unitary mixings are the same. However, on the level of a complete unitary 3+1 neutrino mixing matrix, using the dilation procedure and the Cosine-Sine decomposition, we were able to shrink bounds for the \light-heavy" mixing matrix elements. For instance, in the so-called seesaw mass scheme, a new upper limit on jUe4j is about two times stringent than before and equals 0.021. For all considered mass schemes the lowest bounds are also obtained for all mixings, i.e. |Ue4|, |Uμ4|, |Uτ4|. New results obtained in this work are based on analysis of neutrino mixing matrices obtained from the global fits at the 95% CL

Studies of Non-standard Particle Mixings Through Singular Values

Singular values provide a method to study mixing matrices in particle physics. The methods of unitary dilations and the cosine–sine matrix decomposition are discussed in the framework of the Standard Model neutrinos mixing with one non-standard neutrino. We show that the mixings are continuous functions of singular values. It implies that the magnitude of non-standard mixing can be estimated from below and above unambiguously from the experimentally determined interval PMNS mixing matrix