A Concussion-U educational program led to an immediate improvement in concussion knowledge and attitudes among elite male Bantam and Midget AAA hockey players. Increased knowledge was maintained at long-term follow-up, but improved attitude was not. Future studies should investigate whether similar educational programs influence symptom reporting and concussion incidence. In addition, they should focus on how to maintain improved concussion attitudes.

Here we examine the role of the exchange protein directly activated by cAMP (Epac) in b-adrenergic-dependent associative odor preference learning in rat pups. Bulbar Epac agonist (8-pCPT-2-O-Me-cAMP, or 8-pCPT) infusions, paired with odor, initiated preference learning, which was selective for the paired odor. Interestingly, pairing odor with Epac activation produced both short-term (STM) and long-term (LTM) odor preference memories. Training using b-adrenergic-activation paired with odor recruited rapid and transient ERK phosphorylation consistent with a role for Epac activation in normal learning. An ERK antagonist prevented intermediate-term memory (ITM) and LTM, but not STM. Epac agonist infusions induced ERK phosphorylation in the mitral cell layer, in the inner half of the dendritic external plexiform layer, in the glomeruli and, patchily, among granule cells. Increased CREB phosphorylation in the mitral and granule cell layers was also seen. Simultaneous blockade of both ERK and CREB pathways prevented any long-term b-adrenergic activated odor preference memory, while LTM deficits associated with blocking only one pathway were prevented by stronger b-adrenergic activation. These results suggest that Epac and PKA play parallel and independent, as well as likely synergistic, roles in creating cAMP-dependent associative memory in rat pups. They further implicate a novel ERK-independent pathway in the mediation of STM by Epac.

OBJECTIVEAcute kidney injury (AKI) is associated with death in critically ill patients, but this complication has not been well characterized after aneurysmal subarachnoid hemorrhage (aSAH). The purpose of this study was to determine the incidence of AKI after aSAH and to identify risk factors for renal dysfunction. Secondary objectives were to examine what effect AKI has on patient mortality and functional outcome at 12 weeks post-aSAH.METHODSThe authors performed a post hoc analysis of the Clazosentan to Overcome Neurological Ischemia and Infarction Occurring After Subarachnoid Hemorrhage (CONSCIOUS-1) trial data set (clinical trial registration no.: NCT00111085, https://clinicaltrials.gov). The primary outcome of interest was the development of AKI, which was defined according to the Kidney Disease: Improving Global Outcomes (KDIGO) guidelines. Secondary outcomes of interest were death and a modified Rankin Scale score greater than 2 at 12 weeks post-aSAH. Propensity score matching was used to assess for a significant treatment effect related to clazosentan administration and AKI. Univariate analysis, locally weighted scatterplot smoothing (LOWESS) curves, and stepwise logistic regression models were used to evaluate for associations between baseline or disease-related characteristics and study outcomes.RESULTSOne hundred fifty-six (38%) of the 413 patients enrolled in the CONSCIOUS-1 trial developed AKI during their ICU stay. A history of hypertension (p < 0.001) and the number of nephrotoxic medications administered (p = 0.029) were independent predictors of AKI on multivariate analysis. AKI was an independent predictor of death (p = 0.028) but not a poor functional outcome (p = 0.21) on multivariate testing. Unresolved renal dysfunction was the strongest independent predictor of death in this cohort (p < 0.001).CONCLUSIONSAKI is a common complication following aSAH. Patients with premorbid hypertension and those treated with nephrotoxic medications may be at greater risk for renal dysfunction. AKI appears to confer an increased probability of death after aSAH.

Objective The aim of this work was to evaluate the hypothesis that the distribution of circulating immune cell subsets, or their activation state, is significantly different between peripartum cardiomyopathy (PPCM) and healthy postpartum (HP) women. Background PPCM is a major cause of maternal morbidity and mortality, and an immune-mediated etiology has been hypothesized. Cellular immunity, altered in pregnancy and the peripartum period, has been proposed to play a role in PPCM pathogenesis. Methods The Investigation of Pregnancy-Associated Cardiomyopathy (IPAC) study enrolled 100 women presenting with a left ventricular ejection fraction of <0.45 within 2 months of delivery. Peripheral T-cell subsets, natural killer (NK) cells, and cellular activation markers were assessed by flow cytometry in PPCM women early (<6 wk), 2 months, and 6 months postpartum and compared with those of HP women and women with non–pregnancy-associated recent-onset cardiomyopathy (ROCM). Results Entry NK cell levels (CD3−CD56+CD16+; reported as % of CD3− cells) were significantly (P < .0003) reduced in PPCM (6.6 ± 4.9% of CD3− cells) compared to HP (11.9 ± 5%). Of T-cell subtypes, CD3+CD4−CD8−CD38+ cells differed significantly (P < .004) between PPCM (24.5 ± 12.5% of CD3+CD4−CD8− cells) and HP (12.5 ± 6.4%). PPCM patients demonstrated a rapid recovery of NK and CD3+CD4−CD8−CD38+ cell levels. However, black women had a delayed recovery of NK cells. A similar reduction of NK cells was observed in women with ROCM. Conclusions Compared with HP control women, early postpartum PPCM women show significantly reduced NK cells, and higher CD3+CD4−CD8−CD38+ cells, which both normalize over time postpartum. The mechanistic role of NK cells and “double negative” (CD4−CD8−) T regulatory cells in PPCM requires further investigation.

Despite guidelines, many individuals are not routinely tested for HIV within healthcare settings. Our objective was to quantify and characterize preceding clinical encounters by newly-diagnosed persons living with HIV in southern Alberta, Canada. We discuss the clinical impact of missed HIV testing, and options for remediation. Clinical encounters prior to HIV diagnosis including the discharge diagnosis were collected between 1 April 2011 and 1 April 2016. We followed the HIV Indicator Diseases across Europe Study criteria to identify HIV Clinical Indicator Conditions (HCICs) present at clinical encounters. Patients accessing prior care were compared to those who had not previously accessed care. Of 393 individuals, 231 (58.7%) had ≥1 encounter prior to diagnosis; 224 (57%) of encounters occurred in outpatient clinics, 130 (33.1%) in emergency departments, and 39 (9.9%) in urgent care clinics. Approximately 25% (n = 57) of patients who engaged healthcare had ≥ 1 recognized HCIC but did not receive HIV testing. The most frequent HCICs were infection (n = 34; 60%) and hematological disorders (n = 12; 21%). The median CD4 cell count at HIV diagnosis for patients with an HCIC was 127 cells/mm3. In this population, three of five patients had accessed healthcare prior to diagnosis with one of four presenting with HCICs but were not offered HIV testing. Protocols beyond the current recommendations are urgently required to address missed HIV diagnostic opportunities who engaged healthcare.

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Background The economic consequences of a missed opportunity for HIV testing at an earlier stage of infection within a healthcare setting are poorly described. Methods For all newly diagnosed HIV patients followed at the Southern Alberta HIV/AIDS Clinic (SAC), Calgary, Canada, between 1 April 2011 and 1 April 2016, all clinical encounters occurring < 3 years prior to diagnosis within the region were obtained. The direct costs of HIV care after diagnosis to 31 March 2019 were determined from a payers’ perspective and reported as mean cost per patient per month (PPPM) in 2019 Canadian dollars (CDN$). Patients with no encounters for 3 years prior to diagnosis were compared with patients with encounters, with special attention to patients with HIV clinical indicator conditions (HCICs). Results Of 388 patients, 60% had one or more prior encounter without HIV testing; 14% had been treated for an HCIC. Females, older patients and heterosexuals were more likely to have prior encounters. At diagnosis, patients with previous encounters presented with lower CD4 counts and higher rates of AIDS. The mean PPPM costs for patients with any prior encounter or for an HCIC‐based encounter were 16% and 33% higher, respectively, than for patients with no prior encounters. While mean PPPM costs for antiretroviral drugs and outpatient visits were slightly higher, in‐patient costs were 10 times higher for people with HIV who had a previous HCIC encounter vs. those with no encounters (CDN$316 vs. $31, respectively). Conclusions Any healthcare visit, especially for an HCIC, represents relatively easy opportunities for HIV testing. Not testing can result in poorer health and higher costs. Targeted clinical testing and novel interventions to correct overlooked testing opportunities within healthcare settings may be an easy way to implement cost savings.

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