The Morbidity and Mortality Assessment Tool (MMAT): Design and Proof of Concept.

BACKGROUND: Morbidity and Mortality Conference (MMC) is a traditional quality assessment tool among surgical residencies to evaluate complications within their care and to integrate and educate best practices. Unfortunately, it is difficult to validate and measure loop closure as a result of MMC. This may result in repeating past mistakes or worse, becoming a meeting of anecdotal experiences. The goal of this study is to present results from a morbidity and mortality assessment tool (MMAT) which provides a means of measuring and tracking factors related to those surgical complications discussed within the MMC. MATERIALS AND METHODS: Three years of MMC presentations were organized into a database and further divided and organized into variables which included case by the class year of the presenting resident, service line, month the case was presented, and potential contributing factors. Contributing factors considered for each case were categorized as: Systems-Based, Direct Patient Care, and Interpersonal Communication. Contributing factors were assigned to cases by a review committee consisting of residents and faculty members. RESULTS: The lack of knowledge, technical error, lack of experience, lack of supervision, failure to communicate with team members were present in greater than 10% of the presented cases. There was a "July Effect" in the Trauma service, where there was a statistically significant difference between the percentage of cases presented that involved Failure to Communicate errors when compared with the remainder of the year. CONCLUSIONS: MMAT allows longitudinal collection of data from each MMC to recognize patterns that facilitate improvements in systems of care and institutional memory.

Energetic response of Atlantic surfclam Spisula solidissima to ocean acidification.

In this study, we assessed the Atlantic surfclam (Spisula solidissima) energy budget under different ocean acidification conditions (OA). During 12 weeks, 126 individuals were maintained at three different ρCO2 concentrations. Every two weeks, individuals were sampled for physiological measurements and scope for growth (SFG). In the high ρCO2 treatment, clearance rate decreased and excretion rate increased relative to the low ρCO2 treatment, resulting in reduced SFG. Moreover, oxygen:nitrogen (O:N) excretion ratio dropped, suggesting that a switch in metabolic strategy occurred. The medium ρCO2 treatment had no significant effects upon SFG; however, metabolic loss increased, suggesting a rise in energy expenditure. In addition, a significant increase in food selection efficiency was observed in the medium treatment, which could be a compensatory reaction to the metabolic over-costs. Results showed that surfclams are particularly sensitive to OA; however, the different compensatory mechanisms observed indicate that they are capable of some temporary resilience.

Overexpression of NGF or GDNF alters transcriptional plasticity evoked by inflammation.

Transcriptional changes evoked in nociceptive sensory neurons by inflammatory injury play a substantial role in the generation of and recovery from painful hypersensitivity. Transgenic mice overexpressing nerve growth factor (NGF) or glial cell line-derived neurotrophic factor (GDNF) in the skin possess a greatly increased number of nociceptors. Surprisingly, NGF-overexpressers display reduced hypersensitivity and recovered more rapidly in response to inflammation, suggesting a compensatory suppression of nociceptive transmission in these mice. To determine whether these transgenic mice show changes in inflammation-evoked transcriptional plasticity, we examined the expression of a panel of genes implicated in nociceptive signaling in response to injection of complete Freund's adjuvant into the hindpaw. Relative mRNA levels were quantified 1, 4 and 15 days after injection using real-time PCR. In wild type mice CFA injection elicited a reproducible pattern of altered gene expression that returned to baseline over a 2-week period. In mice overexpressing NGF or GDNF the expression patterns for several genes were substantially altered; these changes in injury-evoked patterns of gene expression suggest the existence of endogenous regulatory mechanisms that can compensate for increased nociceptive input by modulating the expression of a limited subset of genes.

Transgenic mice possessing increased numbers of nociceptors do not exhibit increased behavioral sensitivity in models of inflammatory and neuropathic pain.

At least two classes of neciceptors can be distinguished based on their growth factor requirements: glial cell-line derived neurotrophic factor (GDNF)- and nerve growth factor (NGF)-dependent primary afferent neurons. Based on numerous anatomical and biochemical differences, GDNF- and NGF-dependent neurons have been proposed to be involved in the development of different types of persistent pain. To examine this hypothesis we used two lines of transgenic mice that contained a supernormal number of either NGF- or GDNF-dependent neurons (referred to as NGF-OE and GDNF-OE mice, respectively). These mice were tested in a model of inflammatory pain (induced by injection of complete Freund's adjuvant) and neuropathic pain (using a spinal nerve ligation protocol). Contrary to expectations, neither line of transgenic mice became more hyperalgesic following induction of persistent pain. In fact, NGF-OE mice recovered more rapidly and became hypoalgesic despite extensive paw swelling in the inflammatory pain model. In the neuropathic pain model, only wildtype mice became hyperalgesic. Real-time PCR analysis showed that the NGF-OE and GDNF-OE mice exhibited changes in neuronal-specific mRNAs in the dorsal root ganglia but not the spinal cord dorsal horn. These results indicate that increasing the number of nociceptors results in potent compensatory mechanisms that may begin with changes in the sensory neurons themselves.