Negotiations to restructure sovereign debts are protracted, taking on average almost 8 years to complete. In this paper we construct a new database (the most extensive of its kind covering ninety recent sovereign defaults) and use it to document that these negotiations are also ineffective in both repaying creditors and reducing the debt burden countries face. Specifically, we find that creditor losses average roughly 40 per-cent, and that the average debtor exits default more highly indebted than when they entered default. To explain this apparent large inefficiency in negotiations, we present a theory of sovereign debt renegotiation in which delay arises from the same commitment problems that lead to default in the first place. A debt restructuring generates surplus for the parties at both the time of settlement and in the future. However, a creditor's ability to share in the future surplus is limited by the risk that the debtor will default on the settlement agreement. Hence, the debtor and creditor find it privately optimal to delay restructuring until future default risk is low, even though delay means some gains from trade remain unexploited. We show that a quantitative version of our theory can account for a number of stylized facts about sovereign default, as well as the new facts about debt restructurings that we document in this paper. Finally, we argue that our findings shed light on the existence of delays in bargaining in a wider range of contexts.

Today, reducing medication errors and improving patient safety have become common topics of discussion for the president of the United States, federal and state legislators, the insurance industry, pharmaceutical companies, health care professionals, and patients. But this is not news to clinical pharmacologists. Improving the judicious use of medications and minimizing adverse drug reactions have always been key areas of research and study for those working in clinical pharmacology. However, added to the older terms of adverse drug reactions and rational therapeutics, the now politically correct expression of medication error has emerged. Focusing on the word error has drawn attention to "prevention" and what can be done to minimize mistakes and improve patient safety. Webster's New Collegiate Dictionary has several definitions of error, but the one that seems to be most appropriate in the context of medication errors is "an act that through ingnorance, deficiency, or accident departs from or fails to achieve what should be done." What should be done is generally known as "the five rights": the right drug, right dose, right route, right time, and right patient. One can make an error of omission (failure to act correctly) or an error of commission (acted incorrectly). This article now summarizes what is currently known about medication errors and translates the information into case studies illustrating common scenarios leading to medication errors. Each case is analyzed to provide insight into how the medication error could have been prevented. "System errors" are described, and the application of failure mode effect analysis (FMEA) is presented to determine the part of the "safety net" that failed. Examples of reengineering the system to make it more "error proof" are presented. An error can be prevented. However, the practice of medicine, pharmacy, and nursing in the hospital setting is very complicated, and so many steps occur from "pen to patient" that there is a lot to analyze. Implementing safer practices requires developing safer systems. Many errors occur as a result of poor oral or written communications. Enhanced communication skills and better interactions among members of the health care team and the patient are essential. The informed consent process should be used as a patient safety tool, and the patient should be warned about material and foreseeable serious side effects and be told what signs and symptoms should be immediately reported to the physician before the patient is forced to go to the emergency department for urgent or emergency care. Last, reducing medication errors is an ongoing process of quality improvement. Faculty systems must be redesigned, and seamless, computerized integrated medication delivery must be instituted by health care professionals adequately trained to use such technological advances. Sloppy handwritten prescriptions should be replaced by computerized physician order entry, a very effective technique for reducing prescribing/ordering errors, but another far less exp...

The 5-year EFS rate of patients with AML is 31% and has improved. The five-drug induction regimen is no better than standard induction, BMT appears superior to chemotherapy, and maintenance therapy was not beneficial.

Results suggest that aggressively timed induction therapy followed by marrow ablation and BMT rescue with either autologous or allogeneic grafts for children with newly diagnosed AML or MDS is both feasible and effective.

Today, reducing medication errors and improving patient safety have become common topics of discussion for the president of the United States, federal and state legislators, the insurance industry, pharmaceutical companies, health care professionals, and patients. But this is not news to clinical pharmacologists. Improving the judicious use of medications and minimizing adverse drug reactions have always been key areas of research and study for those working in clinical pharmacology. However, added to the older terms of adverse drug reactions and rational therapeutics, the now politically correct expression of medication error has emerged. Focusing on the word error has drawn attention to "prevention" and what can be done to minimize mistakes and improve patient safety. Webster's New Collegiate Dictionary has several definitions of error, but the one that seems to be most appropriate in the context of medication errors is "an act that through ingnorance, deficiency, or accident departs from or fails to achieve what should be done." What should be done is generally known as "the five rights": the right drug, right dose, right route, right time, and right patient. One can make an error of omission (failure to act correctly) or an error of commission (acted incorrectly). This article now summarizes what is currently known about medication errors and translates the information into case studies illustrating common scenarios leading to medication errors. Each case is analyzed to provide insight into how the medication error could have been prevented. "System errors" are described, and the application of failure mode effect analysis (FMEA) is presented to determine the part of the "safety net" that failed. Examples of reengineering the system to make it more "error proof" are presented. An error can be prevented. However, the practice of medicine, pharmacy, and nursing in the hospital setting is very complicated, and so many steps occur from "pen to patient" that there is a lot to analyze. Implementing safer practices requires developing safer systems. Many errors occur as a result of poor oral or written communications. Enhanced communication skills and better interactions among members of the health care team and the patient are essential. The informed consent process should be used as a patient safety tool, and the patient should be warned about material and foreseeable serious side effects and be told what signs and symptoms should be immediately reported to the physician before the patient is forced to go to the emergency department for urgent or emergency care. Last, reducing medication errors is an ongoing process of quality improvement. Faculty systems must be redesigned, and seamless, computerized integrated medication delivery must be instituted by health care professionals adequately trained to use such technological advances. Sloppy handwritten prescriptions should be replaced by computerized physician order entry, a very effective technique for reducing prescribing/ordering errors, but another far less exp...

A case of bronchioloalveolar carcinoma of the lung is described in a 19-year-old man who had had a lobectomy in infancy, for removal of a congenital cystic adenomatoid malformation. It is suggested that congenital cystic adenomatoid malformation may predispose a patient to development of epithelial malignancies of the lung, whereas mesenchymal hamartomas usually are associated with nonepithelial neoplasms.

Hepatobiliary dysfunction is a well recognized complication in infants and children on long-term total parenteral nutrition. This clinical-pathological study of fifteen patients with this syndrome suggests that cholestasis is the primary pathogenetic mechanism. The cause of the cholestasis is not well understood, but does not appear to be primarily related to the type of intravenous fluids or the occurrence of sepsis. It is suggested that the prolonged fasting results in disruption of the normal gastro-intestinal mechanisms responsible for bile production and flow. This is supported by the pathological findings, the fact that hepatobiliary dysfunction develops late (usually around 2-3 months), the observation that elevated bile acids and direct hyperbilirubinemia occurs prior to any evidence of hepatocellular necrosis and the occurrence of cholelithiasis in some patients.

Congenital absence of the midbrain and upper pons is a rare human malformation. We describe two unrelated infants with this anomaly and cerebellar hypoplasia who were born at term but died in early infancy from lack of central respiratory drive. MRI in both cases disclosed the lesions during life. Neuropathological examination, performed in one, included immunocytochemical studies of NeuN, synaptophysin, vimentin, and glial fibrillary acidic protein (GFAP). Autopsy revealed a thin midline cord passing through the clivus, in place of the midbrain; it corresponded to hypoplastic and fused corticospinal tracts with ectopic neural tissue in the surrounding leptomeninges. Some ectopia were immunoreactive for synaptophysin and NeuN and others were nonreactive. The neural surfaces facing the subarachnoid fluid-filled space left by the absent midbrain and upper pons were lined by an abnormal villous ependyma. The architecture of the cerebellar cortex was imperfect but generally normal, and Bergmann glial cells had normal radial processes shown by vimentin and GFAP. Structures of the telencephalon, diencephalon, lower brainstem, and spinal cord were generally well formed, but inferior olivary and dentate nuclei were rudimentary and the spinal central canal was dilated at lumbar levels. The cerebral cortex was normally laminated, but pyramidal neurons of layer 5 were sparse in the frontal lobes. The hippocampus, olfactory system, and corpus callosum were formed. An ectopic lingual thyroid was found and had been associated with hypothyroidism during life. A murine model resembling this dysgenesis is demonstrated by homozygous mutations of the organizer genes Wnt1 or En1, also resulting in cerebellar aplasia, and En2, associated with cerebellar hypoplasia. These genes are essential to the formation of the mesencephalic neuromere and rhombomere 1 (metencephalon or upper pons and cerebellum). Pax8 has binding sites in the promoter for En2 and is essential for thyroid development. We speculate that in the human, the failure to form a mesencephalon and metencephalon, with cerebellar hypoplasia, results from a mutation or deletion in the EN2 (Engrailed-2) gene.