Effect of trauma quality improvement initiatives on outcomes and costs at community hospitals: A scoping review.

BACKGROUND: Due to complex geography and resource constraints, trauma patients are often initially transported to community or rural facilities rather than a larger Level I or II trauma center. The objective of this scoping review was to synthesize evidence on interventions that improved the quality of trauma care and/or reduced healthcare costs at non-Level I or II facilities. METHODS: A scoping review was performed to identify studies implementing a Quality Improvement (QI) initiative at a non-major trauma center (i.e., non-Level I or II trauma center [or equivalent]). We searched 3 electronic databases (MEDLINE, Embase, CINAHL) and the grey literature (relevant networks, organizations/associations). Methodological quality was evaluated using NIH and JBI study quality assessment tools. Studies were included if they evaluated the effect of implementing a trauma care QI initiative on one or more of the following: 1) trauma outcomes (mortality, morbidity); 2) system outcomes (e.g., length of stay [LOS], transfer times, provider factors); 3) provider knowledge or perception; or 4) healthcare costs. Pediatric trauma, pre-hospital and tele-trauma specific studies were excluded. RESULTS: Of 1046 data sources screened, 36 were included for full review (29 journal articles, 7 abstracts/posters without full text). Educational initiatives including the Rural Trauma Team Development Course and the Advanced Trauma Life Support course were the most common QI interventions investigated. Study outcomes included process metrics such as transfer time to tertiary care and hospital LOS, along with measures of provider perception and knowledge. Improvement in mortality was reported in a single study evaluating the impact of establishing a dedicated trauma service at a community hospital. CONCLUSIONS: Our review captured a broad spectrum of trauma QI projects implemented at non-major trauma centers. Educational interventions did result in process outcome improvements and high rates of self-reported improvements in trauma care. Given the heterogeneous capabilities of community and rural hospitals, there is no panacea for trauma QI at these facilities. Future research should focus on patient outcomes like mortality and morbidity, and locally relevant initiatives.

Deploy the proboscis!: Functional morphology and kinematics of a novel form of extreme jaw protrusion in the hingemouth, Phractolaemus ansorgii (Gonorynchiformes).

Premaxillary protrusion and the performance advantages it confers are implicated in the success of diverse lineages of teleost fishes, such as Cypriniformes and Acanthomorpha. Although premaxillary protrusion has evolved independently at least five times within bony fishes, much of the functional work investigating this kinesis relates to mechanisms found only in these two clades. Few studies have characterized feeding mechanisms in less-diverse premaxilla-protruding lineages and fewer yet have investigated the distinctive anatomy underlying jaw kinesis in these lineages. Here, we integrated dissection, clearing and staining, histology, micro-CT, and high-speed videography to investigate an isolated and independent origin of jaw protrusion in the hingemouth, Phractolaemus ansorgii, which employs a complex arrangement of bones, musculature, and connective tissues to feed on benthic detritus via a deployable proboscis. Our goals were to provide an integrative account of the underlying architecture of P. ansorgii's feeding apparatus and to assess the functional consequences of this drastic deviation from the more typical teleost condition. Phractolaemus ansorgii's cranial anatomy is distinct from all other fishes in that its adducted lower jaw is caudally oriented, and it possesses a mouth at the terminal end of an elongated, tube-like proboscis that is unique in its lack of skeletal support from the oral jaws. Instead, its mouth is supported primarily by hyaline-cell cartilage and other rigid connective tissues, and features highly flexible lips that are covered in rows of keratinous unculi. Concomitant changes to the adductor musculature likely allow for the flexibility to protrude the mouth dorsally and ventrally as observed during different feeding behaviors, while the intrinsic compliance of the lips allows for more effective scraping of irregular surfaces. From our feeding videos, we find that P. ansorgii is capable of modulating the distance of protrusion, with maximum anterior protrusion exceeding 30% of head length. This represents a previously undescribed example of extreme jaw protrusion on par with many acanthomorph species. Protrusion is much slower in P. ansorgii-reaching an average speed of 2.74 cm/s-compared to acanthomorphs feeding on elusive prey or even benthivorous cypriniforms. However, this reorganization of cranial anatomy may reflect a greater need for dexterity to forage more precisely in multiple directions and on a wide variety of surface textures. Although this highly modified mechanism may have limited versatility over evolutionary timescales, it has persisted in solitude within Gonorynchiformes, representing a novel functional solution for benthic feeding in tropical West African rivers.

Timeline: Mitochondria.

Mitochondria perform diverse yet interconnected cellular functions and are dynamically regulated by complex signaling pathways. Interest in this fascinating organelle has recently undergone a renaissance due to a series of discoveries revealing that mitochondrial function goes beyond the generation of molecular fuel. This Timeline highlights some of the groundbreaking events over the last 30 years in our understanding of how mitochondria are made and turned over, and how they integrate and signal within the cell and organism. To view this Timeline, open or download the PDF.

Greetings from the planet croton.

In this issue of Molecular Cell, Sabari et al. (2015) discover that levels of intracellular crotonyl-CoA impact the histone acylation landscape, providing deeper insight into the exotic histone modification, crotonylation, and exploring new avenues by which cellular metabolism can influence gene expression.

The E3 ligase PARC mediates the degradation of cytosolic cytochrome c to promote survival in neurons and cancer cells.

The ability to withstand mitochondrial damage is especially critical for the survival of postmitotic cells, such as neurons. Likewise, cancer cells can also survive mitochondrial stress. We found that cytochrome c (Cyt c), which induces apoptosis upon its release from damaged mitochondria, is targeted for proteasome-mediated degradation in mouse neurons, cardiomyocytes, and myotubes and in human glioma and neuroblastoma cells, but not in proliferating human fibroblasts. In mouse neurons, apoptotic protease-activating factor 1 (Apaf-1) prevented the proteasome-dependent degradation of Cyt c in response to induced mitochondrial stress. An RNA interference screen in U-87 MG glioma cells identified p53-associated Parkin-like cytoplasmic protein (PARC, also known as CUL9) as an E3 ligase that targets Cyt c for degradation. The abundance of PARC positively correlated with differentiation in mouse neurons, and overexpression of PARC reduced the abundance of mitochondrially-released cytosolic Cyt c in various cancer cell lines and in mouse embryonic fibroblasts. Conversely, neurons from Parc-deficient mice had increased sensitivity to mitochondrial damage, and neuroblastoma or glioma cells in which PARC or ubiquitin was knocked down had increased abundance of mitochondrially-released cytosolic Cyt c and decreased viability in response to stress. These findings suggest that PARC-mediated ubiquitination and degradation of Cyt c is a strategy engaged by both neurons and cancer cells to prevent apoptosis during conditions of mitochondrial stress.

Role of Rap1 in promoting sickle red blood cell adhesion to laminin via BCAM/LU.

Vaso-occlusion is a hallmark of sickle cell disease. Agonist-induced activation of sickle red blood cells (SS RBCs) promotes their adhesion to vascular proteins, potentially contributing to vasoocclusion. Previously, we described a cyclic adenosine monophosphate (cAMP)-dependent increase in SS RBC adhesion to laminin. Here, we investigated whether Rap1, a small guanosine triphosphatase (GTPase) known to promote integrin-mediated adhesion in other cells, was involved in this signaling pathway. We found that agonists known to induce cAMP signaling promoted the GTP-bound, active state of Rap1 in SS RBCs. The cAMP-dependent exchange factor Epac (exchange protein directly activated by cAMP) is a likely upstream activator of Rap1, since Epac is present in these cells and the Epac-specific cAMP analog 8CPT-2-Me (8-(4-cholorophenylthio)-2'-O-methyl-cAMP) activated Rap1 and promoted SS RBC adhesion to laminin. This 8CPT-2-Me-stimulated adhesion was integrin independent, since it was insensitive to RGD peptide or antibodies against the only known integrin on SS RBCs, alpha4beta1. However, this adhesion was completely inhibited by either a soluble version of basal cell adhesion molecule/Lutheran (BCAM/LU) or a BCAM/LU adhesion-blocking anti-body. Surprisingly, 8CPT-2-Me-activated Rap1 did not promote SS RBC adhesion to a known alpha4beta1 ligand, vascular cell adhesion molecule 1 (VCAM-1). These results demonstrate that Epac-induced Rap1 activation in SS RBCs promotes BCAM/LU-mediated adhesion to laminin. Thus, Epac-mediated Rap1 activation may represent an important signaling pathway for promoting SS RBC adhesion.