The Concept of the Human in the Works of Carl Schmitt

Diese Arbeit befasst sich mit der politischen Anthropologie Carl Schmitts. Sie zeigt mit Blick auf sein ganzes Werk, dass seine Anthropologie keineswegs rein negativ zu verstehen ist. Vielmehr liegt der Gehalt und das Potenzial seiner Anthropologie in einem umfassenden Begriff des Menschlichen (the human), der weniger damit zu tun hat, ob der Mensch guter oder böser Natur ist, und vielmehr den Gegenstand seines politischen und philosophischen Denkens überhaupt bildet. Dieses Argument wird auf drei Hauptfeldern entfaltet: Schmitts Rationalitätstheorie, seinem Begriff des Politischen und seiner Geschichtsphilosophie, die dem dreiteiligen Aufbau der Arbeit zugrunde liegen. Durch eine Analyse seiner Rationalitätstheorie wird der Begriff des Menschlichen überhaupt erst sichtbar. Schmitts Begriff des Menschlichen hängt eng mit seiner Auffassung einer besonders menschlichen, römisch-katholischen Rationalität zusammen. Diese besonders menschliche Rationalität zeichnet sich durch ihren stetigen Bezug zum Sozialen sowie ihren vermittelnden Charakter aus. Zwei Eigenschaften, die sie ebenfalls von der herrschenden, ökonomisch-technischen Rationalität unterscheidet. Anhand dieses Rationalitätsbegriffs wird im zweiten Kapitel Schmitts Werk Der Begriff des Politischen untersucht. Dabei wird deutlich, dass sein "anthropologisches Bekenntnis" im 7. Kapitel vom Begriff des Politischen weniger die Funktion einer Aussage über den Menschen als solchen hat, sondern vielmehr dazu dient, das Politische als einen Bereich der menschlichen Freiheit zu etablieren. Die Erkenntnis dieser Freiheit sowie das Phänomen des Politischen sind der menschlichen Rationalität zugänglich, weil nur diese die politische (Selbst-)Behauptung des Menschen zulässt, ohne sie auf ein tieferliegendes Phänomen hinter der Sphäre der menschlichen Prätentionen zurückführen zu wollen. Das dritte Kapitel widmet sich Schmitts Geschichtsphilosophie und zeigt, dass diese auf zweierlei Art und Weise vom Begriff des Menschlichen strukturiert wird. Zuerst handelt es sich bei Schmitts Interpretation der neueren europäischen Geschichte (ab dem 16. Jh.) stets um ein (tragisches) Narrativ der menschlichen Rationalität. In einem zweiten Schritt wird Schmitts Begriff des Katechons untersucht. Indem seine vereinzelten Aussagen zu dieser Figur, die die Aufgabe hat, das jüngste Gericht fernzuhalten, in Zusammenhang mit seinen Überlegungen zum Begriff der Kreatur gesetzt werden, zeigt sich, dass seine Geschichtsphilosophie stets die Intention hat, dem freien und menschlichen Handeln einen Platz zwischen Determinismus und Sinnlosigkeit einzuräumen. Die Arbeit schließt mit einer Zusammenfassung des Begriffs des Menschlichen sowie Überlegungen zum kulturellen Kontext des Begriffs ab.This study is devoted to the political anthropology of Carl Schmitt (1888-1985). It argues with regard to his entire oeuvre, that his anthropology can in no way be understood in a purely negative manner. Rather, the meaning and potential of his anthropology lies in a far broader concept of the human as such. This concept of the human, not the human being, exceeds the question of whether the human being is by nature good or bad. It constitutes the central object of Schmitt's political and philosophical thought and is the attempt to identify and describe a particularly human sphere of existence. This argument is unfolded across three main fields of his thought: his theory of rationality, his concept of the political and his philosophy of history, from which follows the three-part structure of this study. The first part of this study makes visible the concept of the human by examining Schmitt's theory of rationality. By looking more closely at his work Roman Catholicism and Political Form, it becomes clear that Schmitt sees in the Roman Catholic Church a particularly human form of rationality. By using the term of the human to describe a form of rationality, Schmitt makes clear that the human as such is, for him, not merely a question of the individual human being. This particularly human, Roman-Catholic rationality distinguishes itself through its constant social orientation and its mediating character from the dominant economic-technical rationality. Having worked out a relationship between Schmitt's concept of rationality and his concept of the human, the second part of this study revisits the "anthropological confession" in chapter seven of The Concept of the Political in order to show that Schmitt's insistence upon the human being's evil or problematic nature is less a statement about the individual human being and much more what Schmitt sees as the necessary presupposition for the theoretical establishment of a sphere of free human action. Both the recognition of this freedom as well as the phenomenon of the political are only accessible for the particularly human rationality because it is the only form of rationality that can accept the idea of political activity in the name of freedom, justice and the good without reducing them to some non-political phenomenon that supposedly lies behind the political. The third chapter focuses on Schmitt's philosophy of history and the two central roles played in it by the concept of the human. The first of these is the fact that Schmitt's interpretation of modern European history is always actually the tragic narrative of human rationality. In order to preserve something of this human rationality, Schmitt formulated an eschatological philosophy of history based on the biblical figure of the katechon (2 Thess.), a numinous force charged with holding back the Last Judgment. By examining his theory of the katechon in its relationship to the 'creature' as well as Schmitts ever-recurrent Roman fixation and christology, Schmitt's philosophy of history reveals itself as the attempt to create a place for free human action, between determinism and meaninglessness. The study closes with considerations concerning the cultural context of the concept of the human in the early 20th century

Nestin expression in the kidney with an obstructed ureter

Nestin is an intermediate filament protein originally identified in neuroepithelial stem cells. This cytoskeletal-associated protein is also expressed in some non-neuronal organs including renal tubular cells and glomerular endothelial cells during kidney development. Little is known, however, about nestin expression in the kidney during injury. In this study, we find nestin expression induced in renal tubular and interstitial myofibroblasts in the adult rat kidney following unilateral ureteral obstruction. The degree of nestin expression was well correlated with the degree of tubulointerstitial fibrosis. Immunohistochemical identification of specific nephron segments showed that nestin was primarily expressed by proximal tubules, partially by distal tubules and thick ascending limbs of Henle but not by collecting ducts. The nestin-positive tubular cells also expressed vimentin and heat-shock protein 47 (HSP47) suggesting these cells reverted to a mesenchymal phenotype. Not all vimentin- or HSP-expressing cells expressed nestin; however, suggesting that nestin is distinct from these conventional mesenchymal markers. Nestin expression was also found associated with phenotypical changes in cultured renal cells induced by hypoxia or transforming growth factor-β. Nestin expression was located in hypoxic regions of the kidney with an obstructed ureter. Our results indicate that nestin could be a novel marker for tubulointerstitial injury

Mitotic cell cycle proteins increase in podocytes despite lack of proliferation

Mitotic cell cycle proteins increase in podocytes despite lack of proliferation.BackgroundPodocyte proliferation is an uncommon response to glomerular injury and its lack may underlie the development of glomerulosclerosis. However, whether podocytes have the capacity to enter and finish mitosis and cytokinesis is not known.MethodsThe expression of mitotic cell cycle proteins (phosphorylated Histone 3, Cdc2, cyclin B1 and B2) was examined by immunohistochemistry in kidneys of embryonal mice, transgenic HIV-mice, and rats with experimental membranous nephropathy (passive Heymann nephritis, PHN). Mitotic proteins also were measured by Western blot in glomerular protein from PHN-rats and the activity of mitotic cyclins was quantified by histone kinase assay.ResultsMitotic proteins were increased in embryonal mouse glomeruli during the S- and comma-shaped stages and were absent at the capillary loop stage and in mature rodent glomeruli. There was an increase in podocyte expression of Cdc2, cyclin B1 and B2 and phosphorylated histone 3 in PHN rats, and in HIV transgenic mice.ConclusionsPodocytes have the ability to increase cell cycle proteins required for mitosis. Without obvious differences in the expression of the major mitotic proteins in PHN- and HIV-nephropathy, a regulatory disturbance in cytokinesis might be responsible for the development of polynucleated cells and a lack of podocyte proliferation in experimental glomerular disease

Psammocarcinoma of ovary with serous cystadenofibroma of contralateral ovary: a case report

<p>Abstract</p> <p>Introduction</p> <p>Psammocarcinoma of ovary is a rare serous neoplasm characterized by extensive formation of psammoma bodies, invasion of ovarian stroma, peritoneum or intraperitoneal viscera, and moderate cytological atypia. Extensive medlar search showed presence of only 28 cases of psammocarcinoma of ovary reported till date.</p> <p>Case presentation</p> <p>We herein report a case of psammocarcinoma of ovary with serous cystadenofibroma of contralateral ovary in a 55 year old Asian Indian female.</p> <p>Conclusion</p> <p>To the best of author's knowledge, ours is the rare case describing coexistence of this very rare malignant serous epithelial tumor with a benign serous cystadenofibroma of contralateral ovary.</p

A human glomerular SAGE transcriptome database

Background: To facilitate in the identification of gene products important in regulating renal glomerular structure and function, we have produced an annotated transcriptome database for normal human glomeruli using the SAGE approach. Description: The database contains 22,907 unique SAGE tag sequences, with a total tag count of 48,905. For each SAGE tag, the ratio of its frequency in glomeruli relative to that in 115 non-glomerular tissues or cells, a measure of transcript enrichment in glomeruli, was calculated. A total of 133 SAGE tags representing well-characterized transcripts were enriched 10-fold or more in glomeruli compared to other tissues. Comparison of data from this study with a previous human glomerular Sau3A-anchored SAGE library reveals that 47 of the highly enriched transcripts are common to both libraries. Among these are the SAGE tags representing many podocyte-predominant transcripts like WT-1, podocin and synaptopodin. Enrichment of podocyte transcript tags SAGE library indicates that other SAGE tags observed at much higher frequencies in this glomerular compared to non-glomerular SAGE libraries are likely to be glomerulus-predominant. A higher level of mRNA expression for 19 transcripts represented by glomerulus-enriched SAGE tags was verified by RT-PCR comparing glomeruli to lung, liver and spleen. Conclusions: The database can be retrieved from, or interrogated online at http://cgap.nci.nih.gov/SAGE. The annotated database is also provided as an additional file with gene identification for 9,022, and matches to the human genome or transcript homologs in other species for 1,433 tags. It should be a useful tool for in silico mining of glomerular gene expression

Genetic and Pharmacological Inhibition of MicroRNA-92a Maintains Podocyte Cell Cycle Quiescence and Limits Crescentic Glomerulonephritis

Crescentic rapidly progressive glomerulonephritis (RPGN) represents the most aggressive form of acquired glomerular disease. While most therapeutic approaches involve potentially toxic immunosuppressive strategies, the pathophysiology remains incompletely understood. Podocytes are glomerular epithelial cells that are normally growth-arrested because of the expression of cyclin-dependent kinase (CDK) inhibitors. An exception is in RPGN where podocytes undergo a deregulation of their differentiated phenotype and proliferate. Here we demonstrate that microRNA-92a (miR-92a) is enriched in podocytes of patients and mice with RPGN. The CDK inhibitor p57Kip2 is a major target of miR-92a that constitutively safeguards podocyte cell cycle quiescence. Podocyte-specific deletion of miR-92a in mice de-repressed the expression of p57Kip2 and prevented glomerular injury in RPGN. Administration of an anti-miR-92a after disease initiation prevented albuminuria and kidney failure, indicating miR-92a inhibition as a potential therapeutic strategy for RPGN. We demonstrate that miRNA induction in epithelial cells can break glomerular tolerance to immune injury

Activation of Cell Cycle Arrest and Apoptosis by the Proto-Oncogene Pim-2

Potent survival effects have been ascribed to the serine/threonine kinase proto-oncogene PIM-2. Elevated levels of PIM-2 are associated with various malignancies. In human cells, a single Pim-2 transcript gives rise mainly to two protein isoforms (34, 41 kDa) that share an identical catalytic site but differ at their N-terminus, due to in-frame alternative translation initiation sites. In this study we observed that the 34 kDa PIM-2 isoform has differential nuclear and cytoplasmic forms in all tested cell lines, suggesting a possible role for the balance between these forms for PIM-2's function. To further study the cellular role of the 34 kDa isoform of PIM-2, an N-terminally HA-tagged form of this isoform was transiently expressed in HeLa cells. Surprisingly, this resulted in increased level of G1 arrested cells, as well as of apoptotic cells. These effects could not be obtained by a Flag-tagged form of the 41 kDa isoform. The G1 arrest and apoptotic effects were associated with an increase in T14/Y15 phosphorylation of CDK2 and proteasom-dependent down-regulation of CDC25A, as well as with up-regulation of p57, E2F-1, and p73. No such effects were obtained upon over-expression of a kinase-dead form of the HA-tagged 34 kDa PIM-2. By either using a dominant negative form of p73, or by over-expressing the 34 kDa PIM-2 in p73-silenced cells, we demonstrated that these effects were p73-dependent. These results demonstrate that while PIM-2 can function as a potent survival factor, it can, under certain circumstances, exhibit pro-apoptotic effects as well

Characterization of Cyclin E Expression in Multiple Myeloma and Its Functional Role in Seliciclib-Induced Apoptotic Cell Death

Multiple Myeloma (MM) is a lymphatic neoplasm characterized by clonal proliferation of malignant plasma cell that eventually develops resistance to chemotherapy. Drug resistance, differentiation block and increased survival of the MM tumor cells result from high genomic instability. Chromosomal translocations, the most common genomic alterations in MM, lead to dysregulation of cyclin D, a regulatory protein that governs the activation of key cell cycle regulator – cyclin dependent kinase (CDK). Genomic instability was reported to be affected by over expression of another CDK regulator - cyclin E (CCNE). This occurs early in tumorigenesis in various lymphatic malignancies including CLL, NHL and HL. We therefore sought to investigate the role of cyclin E in MM. CCNE1 expression was found to be heterogeneous in various MM cell lines (hMMCLs). Incubation of hMMCLs with seliciclib, a selective CDK-inhibitor, results in apoptosis which is accompanied by down regulation of MCL1 and p27. Ectopic over expression of CCNE1 resulted in reduced sensitivity of the MM tumor cells in comparison to the paternal cell line, whereas CCNE1 silencing with siRNA increased the cell sensitivity to seliciclib. Adhesion to FN of hMMCLs was prevented by seliciclib, eliminating adhesion–mediated drug resistance of MM cells. Combination of seliciclib with flavopiridol effectively reduced CCNE1 and CCND1 protein levels, increased subG1 apoptotic fraction and promoted MM cell death in BMSCs co-culture conditions, therefore over-coming stroma-mediated protection. We suggest that seliciclib may be considered as essential component of modern anti MM drug combination therapy

CDK2 and PKA Mediated-Sequential Phosphorylation Is Critical for p19INK4d Function in the DNA Damage Response

DNA damage triggers a phosphorylation-based signaling cascade known as the DNA damage response. p19INK4d, a member of the INK4 family of CDK4/6 inhibitors, has been reported to participate in the DNA damage response promoting DNA repair and cell survival. Here, we provide mechanistic insight into the activation mechanism of p19INK4d linked to the response to DNA damage. Results showed that p19INK4d becomes phosphorylated following UV radiation, β-amyloid peptide and cisplatin treatments. ATM-Chk2/ATR-Chk1 signaling pathways were found to be differentially involved in p19INK4d phosphorylation depending on the type of DNA damage. Two sequential phosphorylation events at serine 76 and threonine 141 were identified using p19INK4d single-point mutants in metabolic labeling assays with 32P-orthophosphate. CDK2 and PKA were found to participate in p19INK4d phosphorylation process and that they would mediate serine 76 and threonine 141 modifications respectively. Nuclear translocation of p19INK4d induced by DNA damage was shown to be dependent on serine 76 phosphorylation. Most importantly, both phosphorylation sites were found to be crucial for p19INK4d function in DNA repair and cell survival. In contrast, serine 76 and threonine 141 were dispensable for CDK4/6 inhibition highlighting the independence of p19INK4d functions, in agreement with our previous findings. These results constitute the first description of the activation mechanism of p19INK4d in response to genotoxic stress and demonstrate the functional relevance of this activation following DNA damage