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Objective: Describe a model for incorporating campus-based Sexual Assault Nurse Examiner (SANE) services. Describe differences in patient satisfaction and utilization of follow-up resources between patients seeking SANE services at a university health center (UHC) compared to an emergency department (ED). Participants: Patients seeking SANE services at the UHC or ED of a large Midwestern university from January 2016-April 2018. Fifty-eight participants completed a satisfaction survey, including 28 students. Twenty-eight participants completed a follow-up survey, including 15 students. Methods: A Qualtrics survey assessed--(1) satisfaction following the SANE exam and (2) use of follow-up services 4-6 weeks later. Descriptive analyses, exact logistic regressions, and OLS regressions were calculated. Results: There were no differences in satisfaction, services received, or follow-up services accessed between patients at the UHC and ED, including between students. Conclusions: Campus-based SANE services meet the expectations of survivors and do not differ significantly from services at the ED.

Dendritic morphology is a critical determinant of neuronal connectivity, and in postganglionic sympathetic neurons, tonic activity correlates directly with the size of the dendritic arbor. Thus, identifying signaling mechanisms that regulate dendritic arborization of sympathetic neurons is important to understanding how functional neural circuitry is established and maintained in the sympathetic nervous system. Bone morphogenetic proteins (BMPs) promote dendritic growth in sympathetic neurons; however, downstream signaling events that link BMP receptor activation to dendritic growth are poorly characterized. We previously reported that BMP7 upregulates p75(NTR) mRNA in cultured sympathetic neurons. This receptor is implicated in controlling dendritic growth in central neurons but whether p75(NTR) regulates dendritic growth in peripheral neurons is not known. Here, we demonstrate that BMP7 increases p75(NTR) protein in cultured sympathetic neurons, and this effect is blocked by pharmacologic inhibition of signaling via BMP type I receptor. BMP7 does not trigger dendritic growth in sympathetic neurons dissociated from superior cervical ganglia (SCG) of p75(NTR) nullizygous mice, and overexpression of p75(NTR) in p75(NTR) -/- neurons is sufficient to cause dendritic growth even in the absence of BMP7. Morphometric analyses of SCG from wild-type versus p75(NTR) nullizygous mice at 3, 6, and 12 to 16 weeks of age indicated that genetic deletion of p75(NTR) does not prevent dendritic growth but does stunt dendritic maturation in sympathetic neurons. These data support the hypotheses that p75(NTR) is involved in downstream signaling events that mediate BMP7-induced dendritic growth in sympathetic neurons, and suggest that p75(NTR) signaling positively modulates dendritic complexity in sympathetic neurons in vivo. © 2016 Wiley Periodicals, Inc. Develop Neurobiol 76: 1003-1013, 2016.

Inflammatory cytokines that act through glycoprotein (gp)130 are elevated in the heart after myocardial infarction and in heart failure. These cytokines are potent regulators of neurotransmitter and neuropeptide production in sympathetic neurons but are also important for the survival of cardiac myocytes after damage to the heart. To examine the effect of gp130 cytokines on cardiac nerves, we used [gp130.sup.DBH-Cre/lox] mice, which have a selective deletion of the gp130 cytokine receptor in neurons expressing dopamine [beta]-hydroxylase (DBH). Basal sympathetic parameters, including norepinephrine (NE) content, tyrosine hydroxylase expression, NE transporter expression, and sympathetic innervation density, appeared normal in [gp130.sup.DBH-Cre/lox] compared with wild-type mice. Likewise, basal cardiovascular parameters measured under isoflurane anesthesia were similar in both genotypes, including mean arterial pressure, left ventricular peak systolic pressure, dP/[dt.sub.max], and dP/[dt.sub.min]. However, pharmacological interventions revealed an autonomic imbalance in [gp130.sup.DBH-Cre/lox] mice that was correlated with an increased incidence of premature ventricular complexes after reperfusion. Stimulation of NE release with tyramine and infusion of the [beta]-agonist dobutamine revealed blunted adrenergic transmission that correlated with decreased [beta]-receptor expression in [gp130.sup.DBH-Cre/lox] hearts. Due to the developmental expression of the DBH-Cre transgene in parasympathetic ganglia, gp130 was eliminated. Cholinergic transmission was impaired in [gp130.sup.DBH-Cre/lox] hearts due to decreased parasympathetic drive, but tyrosine hydroxylase immunohistochemistry in the brain stem revealed that catecholaminergic nuclei appeared grossly normal. Thus, the apparently normal basal parameters in [gp130.sup.DBH-Cre/lox] mice mask an autonomic imbalance that includes alterations in sympathetic and parasympathetic transmission. cardiac; sympathetic; parasympathetic; ischemia-reperfusion

The balance between norepinephrine (NE) synthesis, release, and reuptake is disrupted after acute myocardial infarction, resulting in elevated extracellular NE. Stimulation of sympathetic neurons in vitro increases NE synthesis and the synthetic enzyme tyrosine hydroxylase (TH) to a greater extent than it increases NE reuptake and the NE transporter (NET), which removes NE from the extracellular space. We used TGR(ASrAOGEN) transgenie rats, which lack postinfarct sympathetic hyperactivity, to test the hypothesis that increased cardiac sympathetic nerve activity accounts for the imbalance in TH and NET expression in these neurons after myocardial infarction. TH and NET mRNA levels were identical in the stellate ganglia of unoperated TGR(ASrAOGEN) rats compared with Sprague Dawley (SD) controls, but the threefold increase in TH and twofold increase in NET mRNA seen in the stellate ganglia of SD rats 1 wk after ischemia-reperfusion was absent in TGR(ASrAOGEN) rats. Similarly, the increase in TH and NET protein observed in the base of the SD ventricle was absent in the base of the TGR (ASrAOGEN) ventricle. Neuronal TH content was depleted in the left ventricle of both genotypes, whereas NET was unchanged. Basal heart rate and cardiac function were similar in both genotypes, but TGR(ASrAOGEN) hearts were more sensitive to the 13-agonist dobutamine. Tyramine-induced release of endogenous NE generated similar changes in ventricular pressure and contractility in both genotypes, but postinfarct relaxation was enhanced in TGR(ASrAOGEN) hearts. These data support the hypothesis that postinfarct sympathetic hyperactivity is the major stimulus increasing TH and NET expression in cardiac neurons. ischemia-reperfusion; sympathetic hyperactivity; autonomic

Cardiac sympathetic nerves stimulate heart rate and force of contraction. Myocardial infarction (MI) leads to the loss of sympathetic nerves within the heart, and clinical studies have indicated that sympathetic denervation is a risk factor for arrhythmias and cardiac arrest. Two distinct types of denervation have been identified in the mouse heart after MI caused by ischemia-reperfusion: transient denervation of peri-infarct myocardium and sustained denervation of the infarct. Sustained denervation is linked to increased arrhythmia risk, but it is not known whether acute nerve loss in peri-infarct myocardium also contributes to arrhythmia risk. Peri-infarct sympathetic denervation requires the p75 neurotrophin receptor (p75NTR), but removal of p75NTR alters the pattern of sympathetic innervation in the heart and increases spontaneous arrhythmias. Therefore, we targeted the p75NTR coreceptor sortilin and the p75NTR-induced protease tumor necrosis factor-α-converting enzyme/A disintegrin and metalloproteinase domain 17 (TACE/ADAM17) to selectively block peri-infarct denervation. Sympathetic nerve density was quantified using immunohistochemistry for tyrosine hydroxylase. Genetic deletion of sortilin had no effect on the timing or extent of axon degeneration, but inhibition of TACE/ADAM17 with the protease inhibitor marimastat prevented the loss of axons from viable myocardium. We then asked whether retention of nerves in peri-infarct myocardium had an impact on cardiac electrophysiology 3 days after MI using ex vivo optical mapping of transmembrane potential and intracellular Ca 2+ . Preventing acute denervation of viable myocardium after MI did not significantly alter cardiac electrophysiology or Ca 2+ handling, suggesting that transient denervation at this early time point has minimal impact on arrhythmia risk. NEW & NOTEWORTHY Sympathetic denervation after myocardial infarction is a risk factor for arrhythmias. We asked whether transient loss of nerves in viable myocardium contributed to arrhythmia risk. We found that targeting protease activity could prevent acute peri-infarct denervation but that it did not significantly alter cardiac electrophysiology or Ca 2+ handling 3 days after myocardial infarction.

Objective: To understand patient participation in interactive voice response (IVR) depression monitoring and self-management support calls and estimate the workload from clinical alerts based on patients' IVR reports., Study Design: Observational study from program implementation in 13 community- and university-based primary care practices., Methods: Patients with depression were identified using electronic records and enrolled by telephone. Patients were asked to complete IVR assessments weekly; those with significantly improved symptoms had the option of completing assessments monthly. Patients could enroll with an informal caregiver who received automated feedback based on patients' IVR reports. Clinicians received alerts regarding significant changes in the scores on the Patient Health Questionnaire 9-item depression measure, antidepressant adherence problems, or suicidal ideation., Results: A total of 387 patients were followed for 12,042 weeks. More than half (59%) opted to participate with a caregiver. Patients completed 68% of 7912 attempted IVR assessments. Assessment completion was unrelated to patients' depressive symptoms and was higher among those who participated with a caregiver, were married, had more comorbidities, or reported missing a prior appointment. Assessment completion was lower when patients received monthly versus weekly assessment attempts. Clinical alerts were generated during 4.9% of follow-up weeks; most represented medication adherence problems (2.8%). Alerts indicating suicidal ideation were rare (0.2% of patient-weeks)., Conclusions: IVR support calls represent a viable strategy for increasing access to depression monitoring and self-management assistance in primary care. These programs generate a manageable number of alerts, most of which can be triaged with limited physician involvement.