Measuring fiscal sustainability on the municipal level: A German case study

The consequences of ageing populations for federal and state fiscal policies are, due to the research efforts of the last two decades, well known. However, it is rather less well known how the municipal level is affected. Therefore, by using a modification of the sustainability definition formulated by Blanchard, Chouraqui, Hagemann, and Sartor (1990) and the concepts of Auerbachs, Kotlikoffs and Gokhales Generational Accounting (1991) we define a new framework focusing on capital stock, financial management and depreciation of municipal assets. This papers purpose is to deliver a concept which is able to provide sound indicators for long-term budgeting by local authorities. We apply this framework to three German cities with different typologies, Munich, Freiburg and Schwäbisch Hall. --Fiscal sustainability,demographic transition,municipalities

Well-Being in Germany: GDP and Unemployment Still Matter

"This paper examines regional differences in subjective well-being (SWB) in Germany. Inferential statistics indicate a diminishing but still significant gap between East and West Germany, but also differing levels of SWB within both parts. The observed regional pattern of life satisfaction reflects macroeconomic fundamentals, where labor market conditions play a dominant role. Differing levels of GDP and economic growth have contributed rather indirectly to regional well-being such that the years since the German reunification can be considered as a period of joyless growth. Approximately half of the "satisfaction gap" between East and West Germany can be attributed to differing macroeconomic conditions. Moreover, we argue that it is advisable for governments to collect more data on aspects that presumably influence the well-being of society. For example, it is highly probable that reliable data on regional income inequality would lead to several important and influential studies. This, in turn, can help to design indicators for those characteristics which are known for affecting SWB. In total, we do not perceive any fundamental caveat for using data on SWB in order to measure welfare directly, at least within culturally and linguistically homogenous regions. To reduce statistical uncertainty, however, it would be helpful to include subjective information of this kind into larger cross-sectional surveys such as common census data." [author's abstract

Zum Kostenanstieg im Gesundheitswesen 2009: Wie teuer waren die Reformen?

Das faktisch umlagefinanzierte Gesundheitswesen der Gesetzlichen Krankenversicherung steht in Anbetracht der demografischen Entwicklung nach wie vor massiven Finanzierungsproblemen gegenüber. Das Wettbewerbsstärkungsgesetz sollte daher ursprünglich nicht nur Ausgangspunkt für weitere Reformen etwa in Richtung eines Prämiensystems sein, sondern sich vor allem effizienzsteigernd und kostendämpfend auswirken. Tatsächlich jedoch sind die öffentlichen Ausgaben im Gesundheitswesen im Krisenjahr 2009 um mehr als sechs Prozent angestiegen. Dieser Beitrag wirft einen detaillierten Blick auf die zurückliegende Kostensteigerung und misst den ursächlichen Einflussfaktoren ihre jeweilige Bedeutung zu. Die Analyse konzentriert sich dabei insbesondere auf demografische, technologische und politische Faktoren. --

Ehrbare Staaten? Die Ergebnisse der Generationenbilanzierung im internationalen Vergleich

Ein fiskalischer Vergleich entwickelter Staaten geschieht häufig über jährliche Indikatoren wie etwa den Maastricht-Kriterien Defizit-und Schuldenquote. Um jedoch die Tragfähigkeit einer jeweiligen Fiskalpolitik einschätzen zu können, bedarf es der Erweiterung der Perspektive um langfristige implizite Verpflichtungen, welche hauptsächlich in Sozialversicherungssystemen begründet sind. Die vorliegende Arbeit untersucht mit Hilfe von Generationenbilanzen die fiskalische Nachhaltigkeit von acht Staaten (Deutschland, Frankreich, Großbritannien, Norwegen, Österreich, Schweiz, Spanien und die Vereinigten Staaten). Dabei ergibt sich ein relativ komplexes Bild. Während die anglosächsischen Staaten zwar die absolut gesehen höchsten impliziten Lasten aufweisen, sähen sich bei einer nachhaltigen Steuerpolitik Österreich, Frankreich und Deutschland Abgabenquotienten von fast bzw. über 50 Prozent gegenübergestellt. --

Unsecured Intracranial Aneurysms and Induced Hypertension in Cerebral Vasospasm: Is Induced Hypertension Safe?

Background: Induced hypertension is an established therapy to treat cerebral vasospasm (CVS) following subarachnoid hemorrhage (SAH) to prevent delayed ischemic deficits. Currently, there is minimal evidence available assessing the risk of induced hypertension in the presence of unsecured aneurysms. The aim of this study was to investigate the impact of induced hypertension on the rupturing of unsecured aneurysms in treating CVS. Methods: We conducted a retrospective analysis between 1999 and 2009. Patients with unsecured aneurysms treated with induced hypertension were identified and stratified as having (1) additional unruptured unsecured aneurysms or (2) ruptured unsecured aneurysms. Hemodynamic parameters were analyzed and any bleeding recorded. Results: Forty-five patients were included. Of those, 41 had 71 additional unruptured unsecured aneurysms and four patients had four ruptured unsecured aneurysms. The mean size of unsecured aneurysms was: 4.0±1.9mm (additional unruptured) and 5.3±2.2mm (ruptured), respectively. No aneurysm ruptured during therapy. Combining our data with previously published studies, there appears to be no increase of risk for aneurysm rupture by induced hypertension when compared to the natural history (0.5% for group 1, 2.9% for group 2). Conclusion: These data corroborate that induced hypertension may be a safe treatment option to prevent cerebral infarction in CVS, even in the presence of unsecured aneurysms. Our findings suggest that induced hypertension does not increase rupture of unsecured aneurysms. Given the high risk for cerebral infarction in severe CVS, we conclude that induced hypertension should not be omitted due to the presence of unsecured aneurysm

Levosimendan, a new therapeutic approach to prevent delayed cerebral vasospasm after subarachnoid hemorrhage?

BACKGROUND Under physiological cerebral conditions, levosimendan, a calcium-channel sensitizer, has a dose-dependent antagonistic effect on prostaglandin F2alpha (PGF)-induced vasoconstriction. This circumstance could be used in antagonizing delayed cerebral vasospasm (dCVS), one of the main complications after subarachnoid hemorrhage (SAH), leading to delayed cerebral ischemia and ischemic neurological deficits. Data already exist that identified neuroprotective effects of levosimendan in a traumatic brain injury model and additionally, it has been proven that this compound prevents narrowing of the basilar artery (BA) luminal area after SAH in an in vitro rabbit model. Takotsubo cardiomyopathy, a severe ventricular dysfunction, is also a well-known complication after SAH, associated with pulmonary edema and prolonged intubation. METHODS The polypeptide endothelin-1 (ET-1) plays a key role in the development of dCVS after SAH. Therefore, the aim of the present investigation was to detect functional interactions between the calcium-sensitizing and the ET-1-dependent vasoconstriction after experimental-induced SAH; interactions between levosimendan and a substrate-specific vasorelaxation in the BA were also examined. It was reviewed whether levosimendan has a beneficial influence on endothelin(A) and/or endothelin(B1) receptors (ET-(A) and ET-(B1) receptors) in cerebral vessels after SAH. We also examined whether this drug could have antagonistic effects on a PGF-induced vasoconstriction. RESULTS Under treatment with levosimendan after SAH, the endothelin system seems to be affected. The ET-1-induced contraction is decreased, not significantly. In addition, we detected changes in the nitric oxide-cyclic guanosine monophosphate (NO-cGMP) pathway. Preincubation with levosimendan causes a modulatory effect on the ET-(B1) receptor-dependent vasorelaxation. It induces an upregulation of the NO-cGMP pathway with a significantly increased relaxation. Even after PGF-induced precontraction a dose-dependent relaxation was registered, which was significantly higher (Emax) and earlier (pD2) compared to the concentration-effect curve without levosimendan. CONCLUSIONS After experimental-induced dCVS, levosimendan seems to restore the well-known impaired function of the vasorelaxant ET-(B1) receptor. Levosimendan also reversed the PGF-induced contraction dose-dependently. Both of these mechanisms could be used for antagonizing dCVS in patients suffering SAH. Levosimendan could even be used additionally in treating patients developing takotsubo cardiomyopathy

Mean Platelet Volume/Platelet Count Ratio and Risk of Progression in Glioblastoma

ObjectiveThe mean platelet volume/platelet count (MPV/PC) ratio is an emerging biomarker in selected types of cancer. The objective of this study is to analyze the association of MPV/PC ratio with progression and survival in glioblastoma (GB) patients, with consideration of patient demographics, tumor morphology, extent of resection, molecular pathology, and oncological therapy.MethodsOne hundred ninety-one patients with newly diagnosed GB were analyzed retrospectively. MPV/PC ratio groups (≤ or >0.0575) were dichotomized into low-MPV/PC ratio (≤0.0575) and high-MPV/PC ratio (>0.0575) groups according to the most significant split in the log-rank test.ResultsA two-sided Fisher’s exact test showed no significant differences in the confounders between the low- and high-MPV/PC ratio groups. The median progression-free survival (PFS) was 9.0 months (95% CI=8.0–10.0) in the low-MPV/PC ratio group (n=164) and 6.0 months (95% CI=3.0–8.9) in the high-MPV/PC group (n=28) (p=0.013). Multivariate Cox regression analysis including the O-6-methylguanine-DNA methyltransferase (MGMT) status, age (≤/>65 years), baseline Karnofsky Performance Status (KPS), and MPV/PC ratio showed high-MPV/PC ratio as a predictor of progression (p =0.04, HR=1.61, 95% CI=1.01–2.57). In the subgroup of IDH1 wild-type GBs, high MPV/PC ratio was still a significant predictor for shortened PFS (p=0.042, HR=1.60, 95% CI=1.02–2.52). MPV/PC ratio showed no significant effect in the overall survival (OS) analysis. Median OS was 15.0 months in the high-MPV/PC ratio group and 21.0 months in the low-MPV/PC ratio group (p=0.22).ConclusionMPV/PC ratio may independently predict the progression-free survival rates of patients with glioblastoma multiforme

Spreading depolarization and angiographic spasm are separate mediators of delayed infarcts

In DISCHARGE-1, a recent Phase III diagnostic trial in aneurysmal subarachnoid haemorrhage patients, spreading depolarization variables were found to be an independent real-time biomarker of delayed cerebral ischaemia. We here investigated based on prospectively collected data from DISCHARGE-1 whether delayed infarcts in the anterior, middle, or posterior cerebral artery territories correlate with (i) extravascular blood volumes; (ii) predefined spreading depolarization variables, or proximal vasospasm assessed by either (iii) digital subtraction angiography or (iv) transcranial Doppler-sonography; and whether spreading depolarizations and/or vasospasm are mediators between extravascular blood and delayed infarcts. Relationships between variable groups were analysed using Spearman correlations in 136 patients. Thereafter, principal component analyses were performed for each variable group. Obtained components were included in path models with a priori defined structure. In the first path model, we only included spreading depolarization variables, as our primary interest was to investigate spreading depolarizations. Standardised path coefficients were 0.22 for the path from extravascular bloodcomponent to depolarizationcomponent (P = 0.010); and 0.44 for the path from depolarizationcomponent to the first principal component of delayed infarct volume (P < 0.001); but only 0.07 for the direct path from bloodcomponent to delayed infarctcomponent (P = 0.36). Thus, the role of spreading depolarizations as a mediator between blood and delayed infarcts was confirmed. In the principal component analysis of extravascular blood volume, intraventricular haemorrhage was not represented in the first component. Therefore, based on the correlation analyses, we also constructed another path model with bloodcomponent without intraventricular haemorrhage as first and intraventricular haemorrhage as second extrinsic variable. We found two paths, one from (subarachnoid) bloodcomponent to delayed infarctcomponent with depolarizationcomponent as mediator (path coefficients from bloodcomponent to depolarizationcomponent = 0.23, P = 0.03; path coefficients from depolarizationcomponent to delayed infarctcomponent = 0.29, P = 0.002), and one from intraventricular haemorrhage to delayed infarctcomponent with angiographic vasospasmcomponent as mediator variable (path coefficients from intraventricular haemorrhage to vasospasmcomponent = 0.24, P = 0.03; path coefficients from vasospasmcomponent to delayed infarctcomponent = 0.35, P < 0.001). Human autopsy studies shaped the hypothesis that blood clots on the cortex surface suffice to cause delayed infarcts beneath the clots. Experimentally, clot-released factors induce cortical spreading depolarizations that trigger (i) neuronal cytotoxic oedema and (ii) spreading ischaemia. The statistical mediator role of spreading depolarization variables between subarachnoid blood volume and delayed infarct volume supports this pathogenetic concept. We did not find that angiographic vasospasm triggers spreading depolarizations, but angiographic vasospasm contributed to delayed infarct volume. This could possibly result from enhancement of spreading depolarization-induced spreading ischaemia by reduced upstream blood supply.Peer Reviewe