Dictatorial Institutions and their Impact on Economic Growth

Non-democratic regimes vary in the degree to which domestic groups threaten their rule and the extent to which they, need the cooperation of these groups. To both neutralize threats to their rule and solicit cooperation, some dictators coopt potential domestic opposition by providing rents and policy concessions within nominally-democratic institutions, such as legislatures and political parties. These institutions, designed as instruments of cooptation, facilitate cooperation between the regime and outside groups which promotes economic growth

Dictatorial Institutions and their Impact on Policies

Abstract Dictators use legislatures and parties to coopt groups within society. In exchange for their support for the regime and their participation within these institutions, dictators must make some policy concessions and offer spoils to these groups. In this paper, I test whether institutions affect government expenditures in 138 countries that experienced dictatorship during the 1946-1996 period. The results show that when dictators are constrained by institutions, they are forced to allocate more resources to public goods, such as education, and less to the armed forces. In addition, institutions facilitate the distribution of rents in the form of government employment

Platelet Inhibitors in Non-ST-Segment Elevation Acute Coronary Syndromes and Percutaneous Coronary Intervention: Glycoprotein IIb/IIIa Inhibitors, Clopidogrel, or Both?

The role of glycoprotein (Gp) IIb/IIIa receptor antagonists remains controversial and these agents are infrequently utilized during non-ST-segment elevation acute coronary syndromes (NSTE-ACS) despite American Heart Association/American College of Cardiology guidelines. Despite recommendations, the NRMI-4 (National Registry of Myocardial Infarction 4) and CRUSADE (Can rapid risk stratification of unstable angina patients suppress adverse outcomes with early implementation of the ACC/AHA guidelines?) registries observed that only 25%–32% of eligible patients received early Gp IIb/IIIa therapy, despite a 6.3% absolute mortality reduction in NRMI-4 and a 2% absolute mortality reduction in CRUSADE. A pooled analysis of Gp IIb/IIIa data from these registries suggest a major reduction in mortality (Odds Ratio = 0.43, 95% Confidence Index 0.25–0.74, p = 0.002) with early Gp IIb/IIIa therapy, yet clinicians fail to utilize this option in NSTE-ACS. The evidence-based approach to NSTE-ACS involves aspirin, clopidogrel, low-molecular weight heparins, or unfractionated heparin in concert with Gp IIb/IIIa receptor antagonists, however, newer percutaneous coronary intervention (PCI)-based trials challenge current recommendations. Novel strategies emerging in NSTE-ACS include omitting Gp IIb/IIIa inhibitors altogether or using Gp IIb/IIIa inhibitors with higher doses of clopidogrel in selected patients. The ISAR-REACT (Intracoronary stenting and antithrombotic regimen–Rapid early action for coronary treatment) and ISAR-SWEET (ISAR–Is abciximab a superior way to eliminate elevated thrombotic risk in diabetics) trials question the value of abciximab when 600 mg of clopidogrel concurrently administered during PCI. The CLEAR-PLATELETS (Clopidogrel loading with eptifibatide to arrest the reactivity of platelets) and PEACE (Platelet activity extinction in non-Q-wave MI with ASA, clopidogrel, and eptifibatide) trials suggest more durable platelet inhibition when Gp IIb/IIIa inhibitors are used with higher doses clopidogrel. The ISAR-COOL (ISAR: Cooling off strategy) trial found no difference in ischemic outcomes when Gp IIb/IIIa inhibitors were excluded and ARMYDA-2 (Antiplatelet therapy for reduction of myocardial damage during angioplasty) suggested higher doses of clopidogrel are more appropriate during PCI when Gp IIb/IIIa inhibitors are not utilized. This constellation of new trials forces reconsideration of current recommendations in regards to patient risk stratification, choice of antithrombotic therapy, doses, and timing. These new data will impact emerging guidelines and updates are currently in progress

Suppression of ion-implantation induced porosity in germanium by a silicon dioxide capping layer

Ion implantation with high ion fluences is indispensable for successful use of germanium (Ge) in the next generation of electronic and photonic devices. However, Ge readily becomes porous after a moderate fluence implant (∼1×1015 ion cm−2) at room temperature, and for heavy ion species such as tin (Sn), holding the target at liquid nitrogen (LN2) temperature suppresses porosity formation only up to a fluence of 2×1016 ion cm−2. We show, using stylus profilometry and electron microscopy, that a nanometer scale capping layer of silicon dioxide significantly suppresses the development of the porous structure in Ge during a Sn − implant at a fluence of 4.5×1016 ion cm−2 at LN2 temperature. The significant loss of the implanted species through sputtering is also suppressed. The effectiveness of the capping layer in preventing porosity, as well as suppressing sputter removal of Ge, permits the attainment of an implanted Sn concentration in Ge of ∼15 at.%, which is about 2.5 times the maximum value previously attained. The crystallinity of the Ge-Sn layer following pulsed-laser-melting induced solidification is also greatly improved compared with that of uncapped material, thus opening up potential applications of the Ge-Sn alloy as a direct bandgap material fabricated by an ion beam synthesis technique

Molecular Sequence of Events and Signaling Pathways in Cerebral Metastases

Brain metastases are the leading cause of morbidity and mortality among cancer patients, and are reported to occur in about 40% of cancer patients with metastatic disease in the United States of America. Primary tumor cells appear to detach from the parent tumor site, migrate, survive and pass through the blood brain barrier in order to establish cerebral metastases. This complex process involves distinct molecular and genetic mechanisms that mediate metastasis from these primary organs to the brain. Furthermore, an interaction between the invading cells and cerebral milieu is shown to promote this process as well. Here, we review the mechanisms by which primary cancer cells metastasize to the brain via a mechanism called epithelial-to-mesenchymal transition, as well as the involvement of certain microRNA and genetic aberrations implicated in cerebral metastases from the lung, breast, skin, kidney and colon. While the mechanisms governing the development of brain metastases remain a major hindrance in treatment, understanding and identification of the aforementioned molecular pathways may allow for improved management and discovery of novel therapeutic targets