Modernisierung contra Demokratisierung : Putins russischer Weg

Die Jukos-Affäre, die Abschaffung der Direktwahl der Gouverneure, die jüngste Reform zur Wahl der Staatsduma, die neuen Verfahren zur Bestellung von Richtern und einiges mehr haben die Zweifel am politischen Kurs Wladimir Putins und an der demokratischen Entwicklung in Russland erheblich verstärkt. Schon in seiner ersten Amtszeit hatte sich Putin bevorzugt autoritärer Machtmittel bedient. Doch konnte dies damit gerechtfertigt werden, den unter Boris Jelzin massiv geschwächten russischen Staat zu seinem Recht verhelfen und die Wirtschaft aus ihrer schweren Krise führen zu müssen. Beides gilt heute so nicht mehr, gleichwohl schreitet der autoritäre Kurs weiter voran. Der Report diskutiert die möglichen Gründe und die westlichen Reaktionen. Erklärungen reichen vom historisch-kulturellen Erbe, das Russland immer wieder auf autoritäre Sonderwege führt, über die Normalität autoritärer Modernisierung bis hin zu falschen politischen und wirtschaftlichen Weichenstellungen am Beginn des Übergangs zu einer demokratischen und marktwirtschaftlichen Ordnung in den frühen 1990er Jahren. Aus den unterschiedlichen Erklärungen folgen unterschiedliche Empfehlungen für die westliche Politik. Sie reichen von einem kooperativen business as usual bis hin zu verstärkter Abgrenzung. Dabei stehen im ersten Fall die eigenen sicherheitspolitischen und wirtschaftlichen Interessen im Mittelpunkt, während im zweiten eine erfolgreiche Demokratisierung zum Schlüssel stabiler Beziehungen erhoben wird

Paradoxe Kontinuitäten : die deutsche Russlandpolitik und die koalitionären Farbenlehren

Die deutsch-russischen Beziehungen sind über die letzten beiden Jahrzehnte einem kontinuierlichen Muster gefolgt, ungeachtet aller Regierungswechsel. Während die Oppositionsparteien der jeweiligen Regierung „Saunafreundschaften“ oder einen „Schmusekurs“ vorwarfen und im Fall der Regierungsübernahme grundlegende Änderungen ankündigten, stellte sich zwischen den Regierungsspitzen immer wieder innerhalb kurzer Zeit Harmonie und Freundschaft ein. Dies galt für das Duo Kohl/Jelzin ebenso wie für Schröder und Putin. Und auch Angela Merkel betonte nun bei ihrem Antrittsbesuch in Moskau, sie wolle außenpolitische Kontinuität. Hans-Joachim Spanger untersucht im vorliegenden HSFK-Report die Gründe für diese nachhaltige Annäherung nach dem Kalten Krieg. Nach seinem Befund erlauben die deutschen Interessen kaum eine Alternative zur Pflege der guten Beziehungen, auch wenn diese vordergründig mit dem deutschen Selbstverständnis als „Zivilmacht“ kontrastieren. Dabei stehen wirtschaftliche Interessen im Mittelpunkt, doch legt auch das sicherheitspolitische Interesse an Stabilität in Russland und Europa eine Kooperation nahe. Differenzen in Bezug auf die demokratischen Werte, wie sie etwa im Tschetschenien-Konflikt deutlich werden oder bei der zunehmenden Beschränkung der Pressefreiheit in Russland, stören zwar dessen Bild in der deutschen Öffentlichkeit, hatten bislang aber keinen nennenswerten Einfluss auf die „strategische Partnerschaft“ beider Länder. Es bleibt jedoch eine Dissonanz, da in der öffentlichen Meinung bei nahezu jeder Gelegenheit antirussische Reflexe aufleben, die durchaus Störfeuer in den deutsch-russischen Beziehungen darstellen. Hier ruht das absehbar größte Risiko für die Kontinuität der Beziehungen

Die Wiederkehr des Staates : Staatszerfall als wissenschaftliches und entwicklungspolitisches Problem

Afghanistan ist das aktuelle Beispiel für ein Phänomen, das Außenminister Joschka Fischer als "schwarze Löcher der Ordnungslosigkeit, der Unterentwicklung und der Verzweiflung" beschrieb. Seit dem 11. September stehen der Zerfall von Staaten und die damit verbundenen Gefahren transnationaler Gewalt ganz oben auf der weltpolitischen Agenda. Nicht nur militärisch, sondern vor allem entwicklungspolitisch stellt dieses Problem eine zentrale globale Herausforderung dar. Ist der Staat für die staatlichen Gebilde der Dritten Welt, die zunehmend Zerfallserscheinungen aufweisen, überhaupt noch die adäquate Organisationsform? Hat das internationale Staatensystem nicht bereits seinen historischen Zenith überschritten? Ist es zudem sinnvoll, zerfallene Staaten wieder zusammenzufügen, und damit einen erneuten Zerfallsprozess einzuleiten? Der Autor skizziert in seiner Untersuchung die Traditionen von Modellen der Staatenbildung und diskutiert die Konsequenzen der etatistisch-universalistischen Position auf der einen und des partikularistischen Ansatzes auf der anderen Seite. Die Praxis fortschreitenden Staatszerfalls zeigt, dass eine externe Intervention zumeist unumgänglich ist, um u. a. Gewaltexzesse zu stoppen; doch dürfen solche Kriseneinsätze keine dauerhaften Protektorate oder gar neuen Kolonialismus zur Folge haben. Vielmehr gilt es, Strukturen für nachhaltige Lösungen zu schaffen, die an die funktionierenden Selbstverwaltungsprozesse auf lokaler und regionaler Ebene anknüpfen. Diese national zu vernetzen, wäre die wichtige Aufgabe einer langfristig engagierten Entwicklungskooperation

Poverty reduction through democratisation? : PRSP: challenges of a new development assistance strategy

The unpretentious acronym, “PRSP”, embodies a concept of thorough reform in the policies of international development. With the adoption of the Poverty Reduction Strategy Paper Initiative in September 1999, the World Bank and the IMF declared the notions of national ownership and social participation to be the fundamental principles for both their loan policies and the extension of debt relief to highly indebted poor countries (HIPC II). Since then, the recipient countries have to set up their own development plans, i.e. PRSPs. And “civil society” and in particular “the poor” themselves have to assist in the setting up, operation and control of such programmes. In principle, with the PRSP approach democratisation has finally been integrated in IMF and World Bank strategy. The following report considers the extent of this conceptual change. As a concept, PRSP embraces far-reaching changes and opens up far-reaching chances. However, in the reality of PRSP processes ownership collides with the still dominant role of IMF and World Bank, participation appears as mere consultation steered by respective governments, while the macro-economic framework largely remains excluded from public debate . A review of the debate on experiences with PRSP as well as two case studies on Bolivia and Tanzania demonstrate that these inconsistencies, contradictions and limitations are as far reaching as to query the concept itself

Clinical outcome of a patient with lysosomal acid lipase deficiency and first results after initiation of treatment with Sebelipase alfa: A case report

We report on a case of very rare autosomal recessive cholesteryl ester storage disease due to lysosomal acid lipase deficiency (LALD). LALD is caused by mutations in the lysosomal acid lipase A (LIPA) gene resulting in cholesteryl ester accumulation in liver, spleen, and macrophages. It can lead to liver failure, accelerated atherosclerosis and premature death. Until recently, treatment options were limited to lipid-lowering medications to control dyslipidemia. Presently, a long-term enzyme replacement therapy with Sebelipase alfa, a recombinant human lysosomal acid lipase, is available for patients with LALD. Our patient's condition became conspicuous at the age of two due to a xanthogranuloma of the chin together with increased lipid levels, elevated liver enzymes and hepatomegaly. It took another five years until our patient was diagnosed with LALD after genetic testing. A bi-weekly therapy with intravenous Sebelipase alfa was started at the age of 26 years. It led to normalization of lipid levels, reduction of liver enzymes and beginning regression of hepatomegaly in the absence of adverse drug reactions after 46 infusions. Since LALD can take a fatal course even in patients with a long-term stable condition, it is essential to identify affected patients early and to treat them appropriately by enzyme replacement therapy. LALD should be suspected in patients with low high-density lipoprotein cholesterol (HDL-C) and high low-density lipoprotein cholesterol (LDL-C) in conjunction with elevated liver enzymes or hepatomegaly. A registry for LALD patients shall help to advance our understanding of the disease as well as improve patient care (NCT01633489)

Long-term impact of the metabolic status on weight loss-induced health benefits

Background: While short-term effects of weight loss on quality of life and metabolic aspects appear to be different in metabolically healthy (MHO) and metabolically unhealthy obese (MUO), respective long-term data is still missing. Given the high relevance of long-term changes, we aimed to address these in this post-hoc analysis of the MAINTAIN trial. Methods: We analyzed 143 overweight/obese subjects (BMI >= 27 kg/m(2), age >= 18 years) before and after a 3-month weight loss program (>= 8% weight loss), after a 12-month period of a randomized weight maintenance intervention (n =121), and after another 6 months without intervention (n=112). Subjects were retrospectively grouped into MHO and MUO by the presence of metabolic syndrome and secondarily by estimates of insulin sensitivity (HOMA-IR and ISIclamp). Quality of life (QoL), blood pressure, lipids, HOMA-IR, and ISIclamp were assessed and evaluated using mixed model analyses. Results: Despite similar short- and long-term weight loss, weight loss-induced improvement of HOMA-IR was more pronounced in MUO than MHO after 3 months (MHO: 2.4[95%-CI: 1.9-2.9] vs. 1.6[1.1-2.1], p= 0.004; MUO: 3.6[3.2-4.0] vs. 2.0[1.6-2.4], p < 0.001; p= 0.03 for inter-group comparison). After 21 months, the beneficial effect was no longer seen in MHO (2.0[1.5-2.6], p= 1.0), while it remained partially preserved in MUO (2.9[2.4-3.3], p= 0.002). QueryShort-term improvements of lipid parameters were similar in both groups. However, long-term improvements of HDL-cholesterol and triglycerides were only seen in MUO (44.4[41.5-47.4] vs. 49.3[46.2, 52.3] mg/dl, p < 0.001; 176.8[158.9-194.8] vs. 138.8[119.4-158.3] mg/dl, p < 0.001, respectively) but not in MHO. Weight loss-induced improvements in the QoL and particularly the physical health status were maintained in MUO until the end of the trial, while benefits disappeared over time in MHO. Group allocation by HOMA-IR and ISIclamp revealed higher benefits for MUO mainly in parameters of the glucose metabolism and QoL. Conclusions: Our data demonstrates stronger and longer-lasting improvements of metabolism and QoL in MUO after weight loss

Fetuin-B, a potential link of liver-adipose tissue cross talk during diet-induced weight loss–weight maintenance

BACKGROUND/OBJECTIVES: Numerous hepatokines are involved in inter-organ cross talk regulating tissue-specific insulin sensitivity. Adipose tissue lipolysis represents a crucial element of adipose insulin sensitivity and is substantially involved in long-term body weight regulation after dietary weight loss. Thus, we aimed to analyze the impact of the hepatokine Fetuin-B in the context of weight loss induced short- and long-term modulation of adipose insulin sensitivity. SUBJECTS/METHODS: 143 subjects (age > 18; BMI >= 27 kg/m(2)) were analyzed before (T-3) and after (T0) a standardized 12-week dietary weight reduction program. Afterward, subjects were randomized to a 12-month lifestyle intervention or a control group. After 12 months (T12) no further intervention was performed until 6 months later (T18) (Maintain-Adults trial). Tissue-specific insulin sensitivity was estimated by HOMA-IR (predominantly liver), ISIClamp (predominantly skeletal muscle), and free fatty acid suppression during hyperinsulinemic-euglycemic clamp (FFA(Supp)) (predominantly adipose tissue). Fetuin-B was measured at all concomitant time points. RESULTS: Circulating Fetuin-B levels correlated significantly with estimates of obesity, hepatic steatosis as well as HOMA-IR, ISIClamp, FFA(Supp) at baseline. Fetuin-B decreased during dietary weight loss (4.2 (3.5-4.9) vs. 3.8 (3.2-4.6) mu g/ml; p = 2.1 x 10(-5)). This change was associated with concomitant improvement of HOMA-IR (r = 0.222; p = 0.008) and FFA(Supp) (r = -0.210; p = 0.013), suggesting a particular relationship to hepatic and adipose tissue insulin sensitivity. Weight loss induced improvements of insulin resistance were almost completely preserved until months 12 and 18 and most interestingly, the short and long-term improvement of FFA(Supp) was partially predicted by baseline level of Fetuin-B. CONCLUSIONS: Our data suggest that Fetuin-B might be a potential mediator of liver-adipose cross talk involved in short- and long-term regulation of adipose insulin sensitivity, especially in the context of diet-induced weight changes

Circulating vaspin is unrelated to insulin sensitivity in a cohort of nondiabetic humans

Objective: To study the association of vaspin with glucose metabolism. Design: Cross-sectional and intervention study. Subjects and methods: The association of serum vaspin with metabolic and anthropometric characteristics was investigated in 108 volunteers. Euglycemic–hyperinsulinemic clamps (EHC) were performed in 83 of the participants. Changes of circulating vaspin levels were additionally studied in a crossover study using 300 min EHC with lipid versus saline infusion (n=10). Results: Neither glucose tolerance status nor insulin sensitivity, both as measured using EHCs and using homeostasis model assessment for insulin resistance (HOMA-IR), was significantly associated with serum vaspin in the cross-sectional study. Furthermore, there was no effect of short-term lipid-induced insulin resistance due to a 300 min intravenous lipid challenge on circulating vaspin. However, circulating vaspin levels were significantly elevated in women using oral contraceptives (OC), both compared to women without OC intake (1.17±0.26 vs 0.52±0.09 ng/ml, P=0.02) and males (1.17±0.26 vs 0.29±0.04 ng/ml, P=0.01). After exclusion of OC using females and stratification according to body mass index (BMI), a significant sexual dimorphism in subjects with a BMI <25 kg/m2 was observed (males 0.21±0.04 ng/ml versus females 0.70±0.16 ng/ml, P=0.009). Conclusion: Our results support the existence of a sexual dimorphism regarding circulating vaspin. The lack of an association of serum vaspin with HOMA-IR and M value indicates, however, no major role for vaspin concerning insulin sensitivity in nondiabetic humans

Skeletal Muscle 11beta-HSD1 Controls Glucocorticoid-Induced Proteolysis and Expression of E3 Ubiquitin Ligases Atrogin-1 and MuRF-1

Recent studies demonstrated expression and activity of the intracellular cortisone-cortisol shuttle 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) in skeletal muscle and inhibition of 11beta-HSD1 in muscle cells improved insulin sensitivity. Glucocorticoids induce muscle atrophy via increased expression of the E3 ubiquitin ligases Atrogin-1 (Muscle Atrophy F-box (MAFbx)) and MuRF-1 (Muscle RING-Finger-1). We hypothesized that 11beta-HSD1 controls glucocorticoid-induced expression of atrophy E3 ubiquitin ligases in skeletal muscle. Primary human myoblasts were generated from healthy volunteers. 11beta-HSD1-dependent protein degradation was analyzed by [3H]-tyrosine release assay. RT-PCR was used to determine mRNA expression of E3 ubiquitin ligases and 11beta-HSD1 activity was measured by conversion of radioactively labeled [3H]-cortisone to [3H]-cortisol separated by thin-layer chromatography. We here demonstrate that 11beta-HSD1 is expressed and biologically active in interconverting cortisone to active cortisol in murine skeletal muscle cells (C2C12) as well as in primary human myotubes. 11beta-HSD1 expression increased during differentiation from myoblasts to mature myotubes (p<0.01), suggesting a role of 11beta-HSD1 in skeletal muscle growth and differentiation. Treatment with cortisone increased protein degradation by about 20% (p<0.001), which was paralleled by an elevation of Atrogin-1 and MuRF-1 mRNA expression (p<0.01, respectively). Notably, pre-treatment with the 11beta-HSD1 inhibitor carbenoxolone (Cbx) completely abolished the effect of cortisone on protein degradation as well as on Atrogin-1 and MuRF-1 expression. In summary, our data suggest that 11beta-HSD1 controls glucocorticoid-induced protein degradation in human and murine skeletal muscle via regulation of the E3 ubiquitin ligases Atrogin-1 and MuRF-1