Evaluating our progress with trauma transfer imaging: repeat CT scans, incomplete imaging, and delayed definitive care.

PURPOSE: Many trauma patients present at non-trauma centers and require transfer. CT imaging obtained at the initial hospital (IH) may lead to delays in definitive trauma care, and previous studies have shown imaging is often repeated at the trauma center (TC). METHODS: A retrospective review was performed of all tier 1 trauma patients transferred to our TC between May 2018 and April 2019. Patients that did and did not undergo CT imaging at the IH were compared (n = 147). Of those with IH CT imaging (n = 68), we identified 4 imaging "inadequacies": (1) repeat CT scans: CT scan of the same body region performed at IH and at TC; (2) C-spine inadequacies: severely injured patients who underwent head CT without a C-spine CT; (3) incomplete chest-abdomen-pelvis (CAP): patients with partial CAP CT imaging at IH that underwent an additional portion of CAP imaging at TC; (4) CAP CT without IV contrast. RESULTS: IH time was significantly prolonged when CT imaging was obtained. Of those that had IH imaging, 13 patients (19%) required repeat CT, ten (15%) had a C-spine inadequacy, 11 (16%) had incomplete CAP, and 28 (41%) had one or more inadequacy. Patients with any inadequacy underwent more CT imaging. Most patients (76%) with imaging at the IH returned to the CT scan at the TC. CONCLUSION: In severely injured trauma patients transferred to our TC, we identified many continuing issues with IH CT imaging. The imaging inadequacies detailed above lead to delays in definitive care and subject patients to increased radiation.

Contributing factors of teenage pregnancy among African-American females living in economically disadvantaged communities.

AIM: To identify contributing factors that increased the risk of pregnancy among African-American adolescent females living in economically disadvantaged communities and to evaluate the current pregnancy prevention programs addressing these factors in order to provide suggestions for the development of tailored pregnancy prevention programs for this target population. BACKGROUND: Pregnancy rates among adolescents in the United States have declined over the past several years. Despite this trend, the pregnancy rate for African-American adolescent females is disproportionately higher than the adolescent pregnancy rates for other ethnicities. Limited attempts have been made to compile and synthesize the factors that increase risk of pregnancy in this population or to evaluate the effectiveness of intervention programs for African-American females that incorporate these risk factors. METHOD: An integrative literature review was conducted to identify the major contributing factors of pregnancy among African American adolescents living in economically disadvantaged areas. RESULTS: Of the identified contributing risk factors for early pregnancy among African-American adolescent females, the five most supported risk factors were: parental influence, peer influence, social messages, substance use including alcohol, and pregnancy desire. Twelve pregnancy prevention programs were identified that addressed one or more of the five contributing factors to pregnancy. Parental influence and social messages were the most addressed factors among these programs. CONCLUSIONS: This review found five contributing factors related to teenage pregnancy; however, current intervention programs are not well addressed substance use as a component of alcohol use. Thus, development of a tailored pregnancy prevention program incorporating those factors will help decrease the high pregnancy rate among this target population.

Activation of brain endothelial cells by interleukin-1 is regulated by the extracellular matrix after acute brain injury.

The extracellular matrix (ECM) of the central nervous system (CNS) is essential for normal brain function, whilst ECM remodelling is associated with cerebrovascular inflammation driven by the cytokine interleukin-1 (IL-1) after acute brain injury. The effect of ECM remodelling on endothelial activation during neuroinflammation remains unknown. Here we report that ECM remodelling in the cerebrovasculature critically regulates IL-1-induced endothelial cell activation after cerebral ischaemia; Expression levels of ECM molecules associated with the cerebrovasculature, namely fibronectin (FN) and collagen IV (Col IV), strongly increased in brain blood vessels after middle cerebral artery occlusion (MCAo) in a time-dependent manner, reaching a peak of vascular expression 48 h after MCAo. In cultures, FN and Col IV (but also laminin-1 and fibrillin-1) promoted strong attachment of the GPNT endothelial cell line and primary rat brain endothelial cells, which was markedly inhibited by RGD (Arg-Gly-Asp) peptide, or specific integrin ß1, α4, α5 and αv blockade. IL-1ß-induced activation of extracellular-regulated kinase 1/2 (ERK1/2) and nuclear factor κB (NFκB), and synthesis of cytokine-induced neutrophil chemoattractant (CINC-1) were enhanced in cells plated onto ECM molecules, and these responses were inhibited by selective integrin blockade. Finally, increased ECM expression in vessels after MCAo was found associated with vinculin clustering, increased integrin ß1 expression, and increased IL-1 receptor associated kinase-1 (IRAK-1) activity in endothelial cells and perivascular astrocytes. Therefore, our data indicate a novel function for the ECM in the regulation of cerebrovascular inflammation triggered by IL-1 during acute brain injury.

Adhesion to the extracellular matrix is required for interleukin-1 beta actions leading to reactive phenotype in rat astrocytes.

The extracellular matrix (ECM) of the brain is essential for homeostasis and normal functions, but is rapidly remodelled during acute brain injury alongside the development of an inflammatory response driven by the cytokine interleukin (IL)-1. Whether the ECM regulates IL-1 actions in astrocytes is completely unknown. The aim of this study was to test the hypothesis that cellular attachment to the ECM is a critical mediator of IL-1beta-induced signalling pathways and development of reactive phenotype in astrocytes. Primary rat astrocytes adhered to fibronectin, laminin and fibrillin-1 in an integrin-dependent manner. Attachment to these ECM molecules significantly increased IL-1beta-induced activation of extracellular signal-regulated kinase 1/2 (ERK1/2) and inhibition of RhoA and Rho kinase (ROCK), coincident with loss of focal adhesions and cellular morphological changes. Our data demonstrate that the ECM regulates IL-1 actions in astrocytes via cross-talk mechanisms between ERK1/2 and RhoA/ROCK, which could have important implications in brain inflammatory disorders.

Development of metabolic inflammation during pre-hibernation fattening in 13-lined ground squirrels (Ictidomys tridecemlineatus).

Obesity is a worldwide pandemic with significant comorbidities. It is often accompanied by mild inflammation of the intestine followed by inflammation of metabolic tissues such as liver, adipose tissue, and skeletal muscle. Several laboratory models of obesity exist, but seasonal models like hibernators may be valuable for understanding the pathogenesis of obesity independent of genetic or high-fat diet-induced changes. As part of their annual cycle, obligate hibernators, like the 13-lined ground squirrel (Ictidomys tridecemlineatus), undergo a rapid shift from a lean to an obese state to store energy in the form of fat for their prolonged winter fast. Here, we show that ground squirrels gained mass steadily throughout the active season despite a drop in energy intake starting around 9 weeks post-hibernation. Glucose tolerance tests revealed a significant decrease in tolerance late in the active season. In visceral adipose, we found increases in adipocyte size, tumor necrosis factor (TNF)-α and interleukin (IL)-6 levels. IL-6 levels also increased in liver and muscle and TNF-α increased in the ileum late in the active season. Levels of the anti-inflammatory cytokine, IL-10, decreased in visceral adipose and colon tissues around the same time. These data suggest metabolic inflammation develops along with adiposity late in the squirrels' active season.

Adhesion to fibronectin regulates interleukin-1 beta expression in microglial cells.

The extracellular matrix (ECM) of the central nervous system (CNS) is rapidly degraded following acute brain injury, leading to inflammation and neuronal death. Under these conditions, the pro-inflammatory cytokine interleukin-1beta (IL-1beta) is primarily produced by microglial cells and is a key mediator of neuroinflammation, but whether the ECM regulates microglial IL-1 synthesis after CNS injury remains unknown. This study aimed to investigate whether cell attachment to ECM molecules modulated IL-1beta production in activated microglia in vitro. We found adhesion to fibronectin, fibrillin-1 and laminin promoted microglial cell adhesion and spreading, potentiated by bacterial lipopolysaccharide (LPS) treatment. Adhesion to fibronectin (but not fibrillin-1 or laminin) regulated IL-1beta expression via a cell density-dependent mechanism, whereby fibronectin-induced cell proliferation resulted in less IL-1beta being produced. These data suggest an important regulatory mechanism of IL-1 production, associated with microglial migration and proliferation, driven by ECM degradation and/or synthesis in an injured brain.

Colloids engineering and filtration to enhance the sensitivity of paper-based biosensors.

Paper-based biosensors represent a disruptive technology by providing instantaneous and low-cost diagnostics for health and environmental applications. The lack of sensitivity can be an obstacle for this technology to compete with traditional analytical instrumentations. Aiming to improve the sensitivity of a paper-based colorimetric biosensor, we have applied colloids engineering in combination with filtration to lower the paper substrate backgrounds and optimize the immobilization of bio-molecules on paper. A model system consisting of an enzyme, alkaline phosphatase (ALP), and an inorganic colloid, calcium carbonate (CC), flocculated by a cationic dimethylamino-ethyl-methacrylate polyacrylamide (CPAM), demonstrated that the optimized CC flocs are best for enhancing the detecting sensitivity of ALP. The CC floc structure on paper was optimized by modulating its structure in suspension. Subsequently, the filtration process and the wicking ability of paper enabled to freeze the deposited CC structure inherited from the suspension. The incorporation of biomolecules into the CC before immobilizing on paper through filtration provided not only a better microenvironment, but also a higher surface density of immobilized biomolecules. The ALP detection limit of 117 fmol per zone (5mm circle) in the current study was fifty times lower than that of the common soaking method for biomolecule immobilization. The minimum amount of biomolecules per unit substrate area required for detection was lowered by over an order of magnitude, compared with spotting methods (i.e. inkjet printing). The improvement was also demonstrated by the steepest slope of standard curve, the lowest background, and the highest activity of the bioactive paper probed with the diluted BCIP/NBT liquid substrates.