A Multidisciplinary Model for Reviewing Severe Maternal Morbidity Cases and Teaching Residents Patient Safety Principles.

The Joint Commission recommends that severe maternal morbidity (SMM) cases involving peripartum ICU admissions and blood transfusion > 4 units undergo systematic reviews to determine opportunities for improvement in care. This article describes a retrospective study of an SMM multidisciplinary committee review using a published template. METHODS: Residents attend a patient safety and quality improvement (PSQI) course at orientation, learn in serial PSQI educational sessions, and receive individual training on the SMM review. The multidisciplinary SMM review process determines contributory factors, identifies best practices, recognizes care improvement opportunities, and facilitates adoption of appropriate interventions. How the process educated residents on the Clinical Learning Environment Review (CLER) focus areas was explored. RESULTS: From January 2015 to June 2017, 45 SMM cases were reviewed. Reviewers were primarily residents/fellows (64.4% of cases), nurses (11.1%), and maternal-fetal medicine faculty (24.4%). Transfusion > 4 units occurred in 44.4% of cases, and ICU admission in 68.9%. Causes of SMM included obstetric bleeding (57.8%), hypertensive crisis (42.2%), and cardiac disease (24.4%). Preterm delivery occurred in 60.0% of cases; 71.1% were postpartum, and 80.0% had cesarean deliveries. Contributory provider factors included diagnostic delays (55.6%) and treatment delays or errors (44.4%). Contributory patient factors included psychiatric/behavioral health (20.0%) and health care barriers (22.2%). Morbidity could have been prevented by provider factors in 53.3% of cases and by patient factors in 37.8%. Interventions initiated included recruiting a safety nurse, TeamSTEPPS® training, and adoption of hypertension and postpartum hemorrhage safety bundles. CONCLUSION: SMM reviews can be successfully implemented and provide training on safety and quality.

First Biochemical Characterization of a Methylcitric Acid Cycle from Bacillus subtilis Strain 168.

The genome of Bacillus subtilis strain 168 contains the mother cell metabolic gene (mmg) operon that encodes homologues from the methylcitric acid cycle. We showed that the three genes, mmgDE and yqiQ(mmgF), provide three of the five steps of the methylcitric acid cycle. We also showed that the fourth step can be supplied by citB (aconitase), and we suggest that the fifth missing step, the propionyl-CoA synthetase, is probably skipped because the ß-oxidation of methyl-branched fatty acids by the enzymes encoded by mmgABC should produce propionyl-CoA. We also noted interesting enzymology for MmgD and MmgE. First, MmgD is a bifunctional citrate synthase/2-methylcitrate synthase with 2.3-fold higher activity as a 2-methylcitrate synthase. This enzyme catalyzes the formation of either (2S,3R)- or (2R,3S)-2-methylcitrate, but reports of 2-methylcitrate synthases from other species indicated that they produced the (2S,3S) isomer. However, we showed that MmgD and PrpC (from Escherichia coli) in fact produce the same stereoisomer. Second, the MmgE enzyme is not a stereospecific 2-methylcitrate dehydratase because it can dehydrate at least two of the four diastereomers of 2-methylcitrate to yield either (E)-2-methylaconitate or (Z)-2-methylaconitate. We also showed for the first time that the E. coli homologue PrpD exhibited the same lack of stereospecificity. However, the physiological pathways proceed via (Z)-2-methylaconitate, which served as the substrate for the citB enzyme in the synthesis of 2-methylisocitrate. We completed our characterization of this pathway by showing that the 2-methylisocitrate produced by CitB is converted to pyruvate and succinate by the enzyme YqiQ(MmgF).

Location and functional analysis of the Aspergillus nidulans Aurora kinase confirm mitotic functions and suggest non-mitotic roles.

Filamentous fungi have devastating negative impacts as pathogens and agents of food spoilage but also have critical ecological importance and are utilized for industrial applications. The characteristic multinucleate nature of filamentous fungi is facilitated by limiting if, when and where septation, the fungal equivalent of cytokinesis, occurs. In the model filamentous fungus Aspergillus nidulans septation does not occur immediately after mitosis and is an incomplete process resulting in the formation of a septal pore whose permeability is cell cycle regulated. How mitotic regulators, such as the Aurora kinase, contribute to the often unique biology of filamentous fungi is not well understood. The Aurora B kinase has not previously been investigated in any detail during hyphal growth. Here we demonstrate for the first time that Aurora displays cell cycle dependent locations to the region of forming septa, the septal pore and mature septa as well as the mitotic apparatus. To functionally analyze Aurora, we generated a temperature sensitive allele revealing essential mitotic and spindle assembly checkpoint functions consistent with its location to the kinetochore region and spindle midzone. Our analysis also reveals that cellular and kinetochore Aurora levels increase during a mitotic spindle assembly checkpoint arrest and we propose that this could be important for checkpoint inactivation when spindle formation is prevented. We demonstrate that Aurora accumulation at mature septa following mitotic entry does not require mitotic progression but is dependent upon a timing mechanism. Surprisingly we also find that Aurora inactivation leads to cellular swelling and lysis indicating an unexpected function for Aurora in fungal cell growth. Thus in addition to its conserved mitotic functions our data suggest that Aurora has the capacity to be an important regulator of septal biology and cell growth in filamentous fungi.