The Effect of Mandated Planning on Plan Quality

Problem: What is a “good plan”? Among their key goals, plans aim to communicate, influence and engage. Persuasiveness (the ability to engage and motivate) is, therefore, an essential plan quality. Unfortunately, all too many comprehensive plans lack this important quality. In addition, state planning mandates intended to strengthen planning can instead worsen this shortcoming.

Purpose: To develop a methodology to measure and compare the communicative and persuasive qualities of plans in states with and without planning mandates.

Methods: A specially designed protocol was developed to measure the communicative and persuasive qualities of comprehensive plans. Plans of 20 municipalities in states with planning mandates were compared with those of 20 municipalities in states without planning mandates. Statistical analyses of the results were conducted using the Wilcoxon–Mann–Whitney (U) test and simple t tests.

Results and conclusions: Requiring local governments to prepare plans did not result in better plans—at least as measured by a protocol tailored specifically to assess the persuasiveness and communicative quality of plans. Plans prepared in mandate states were much more rigid and standardized than those prepared in nonmandate states. Nonmandated plans also scored much higher in terms of their narrative and storytelling qualities than mandated plans. Private consultant involvement in plan making significantly increased the communicative and persuasive qualities of plans.

Takeaway for practice: Plans in all 40 municipalities fell far short of the ideal communicative and persuasive qualities set forth in the protocol. The deficiency was greatest in states with planning mandates. The involvement of private consultants had a positive impact on plan quality, while the provision of state funding for planning did not.

Research support: None.     

Diskitis caused by Actinobacillus actinomycetemcomitans

A 32-year-old man with acquired immunodeficiency syndrome (AIDS) admitted to the hospital for treatment of visceral leishmaniasis was inadvertently given 10 times the prescribed first dose of sodium stibogluconate ([Sb] 6.5 g instead of 0.65 g). He experienced no immediate major toxicity during the first 48 hours, but a significant rise of pancreatic enzyme activities was observed (amylase at 10 times the upper limit of normal, lipase at 50 times the upper limit of normal) without clinical signs or indications on computed tomography (CT) of pancreatitis. The third day after the overdose, he developed appendicitis, which appeared coincidental; he recovered uneventfully from surgery. Most of the overdose of Sb was eliminated within the first few hours. Pharmacokinetics remained linear; the rapid, long elimination half-lives (2.7 hours and 54 hours, respectively) were similar to those in previously published results. The administration of a chelating agent, dimercaptosuccinic acid (DMSA), 72 hours after the Sb overdose did not modify the pharmacokinetics of the medication.     

Factor XI activation by meizothrombin: stimulation by phospholipid vesicles containing both phosphatidylserine and phosphatidylethanolamine

The activation of factor XI by meizothrombin was investigated using recombinant meizothrombin (R155A meizothrombin) that is resistant to autocatalytic removal of fragment 1. Meizothrombin was capable of activating factor XI at an activation rate similar to that of thrombin. Dextran sulphate and heparin, known cofactors of thrombin-mediated factor XI activation, did not stimulate the activation of factor XI by meizothrombin. However, the activation of factor XI by meizothrombin was markedly enhanced by vesicles containing phosphatidylcholine (PC), phosphatidylserine (PS) and phosphatidylethanolamine (PE), whereas PC/PS or PC/PE vesicles only had a minor effect on the activation. Thrombin-mediated factor XI activation was not influenced by phospholipids. The effect of PC/PS/PE and PC/PS vesicles was studied in a factor XI dependent clot lysis assay. In this assay, factor XI inhibits clot lysis by a feedback loop in the intrinsic pathway via thrombin-mediated factor XI activation. Removal of endogenous phospholipids in plasma by centrifugation resulted in an increased clot lysis, which could be restored to the pre-centrifugation level by the addition of PC/PS/PE vesicles, but not by PC/PS vesicles. When clot lysis was initiated by factor IXa in the presence of a factor XIa blocking antibody, there was no difference in inhibitory effect of PC/PS/PE or PC/PS vesicles. These data suggested that the differences in clot lysis inhibition observed between PC/PS/PE and PC/PS vesicles were caused by factor XI activation by meizothrombin. Meizothrombin-mediated factor XI activation may therefore play an important role in the antifibrinolytic feedback loop in the intrinsic pathway.