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Though they have comparable prevalence of mental illness, American racial and ethnic minorities are less likely to receive mental health services than white Americans. Minorities are often part of racial and ethnic social networks, which may affect mental health service utilization in two ways. While these networks can encourage service utilization by working as a channel of knowledge spillover and social support, they can also discourage utilization by stigmatizing mental illness. This study examined the association of racial and ethnic social networks with mental health service utilization and depression diagnosis in the USA. Using the 2012 Behavioral Risk Factor Surveillance System (BRFSS) data, a multilevel mixed-effect generalized linear model was adopted, controlling for predisposing, need, and enabling factors of mental health service utilization. The association of racial and ethnic social networks with mental health service utilization and depression diagnosis was significant and negative among African Americans. Despite having a comparable number of bad mental health days, the association was insignificant among Hispanic, Asian, and non-Hispanic white respondents. An African American living in a county where all residents were African American was less likely to utilize mental health services by 84.3-86.8% and less likely to be diagnosed with depression by 76.0-84.8% than an African American living in a county where no residents were African American. These results suggest racial and ethnic social networks can discourage mental health service utilization and should be engaged in efforts to improve mental health, particularly among African American communities in the USA.

ObjectiveTo provide recommendations on how to most effectively implement advanced features of acute care patient portals, including: (1) patient-provider communication, (2) care plan information, (3) clinical data viewing, (4) patient education, (5) patient safety, (6) caregiver access, and (7) hospital amenities.RecommendationsWe summarize the experiences of 6 organizations that have implemented acute care portals, representing a variety of settings and technologies. We discuss the considerations for and challenges of incorporating various features into an acute care patient portal, and extract the lessons learned from each institution’s experience. We recommend that stakeholders in acute care patient portals should: (1) consider the benefits and challenges of generic and structured electronic care team messaging; (2) examine strategies to provide rich care plan information, such as daily schedule, problem list, care goals, discharge criteria, and post-hospitalization care plan; (3) offer increasingly comprehensive access to clinical data and medical record information; (4) develop alternative strategies for patient education that go beyond infobuttons; (5) focus on improving patient safety through explicit safety-oriented features; (6) consider strategies to engage patient caregivers through portals while remaining cognizant of potential Health Insurance Portability and Accountability Act (HIPAA) violations; (7) consider offering amenities to patients through acute care portals, such as information about navigating the hospital or electronic food ordering.

Parkinson's disease (PD) involves both motor and non-motor disturbances. Non-motor features include alterations in sensory olfactory function which may constitute a viable biomarker for the disorder. It is not clear what causes olfactory dysfunction but it appears to coincide with the development of synucleopathy within the olfactory bulb (OB). Elevation in alpha-synuclein (a-syn) is indeed a risk factor for development of the sporadic disorder. The multifactorial nature of the idiopathic disease combined with variability in its presentation suggests that it is likely to be influenced by several factors and that in vivo models that explore the synergistic effect of alpha-synuclein elevation with other potential contributing factors are likely to be of importance in understanding the disease etiology. Using a dual transgenic (DTg) mouse model of dopaminergic alpha-synuclein overexpression coupled with doxycycline (Dox)-inducible glutathione (GSH) depletion in these same cells, we demonstrate an age-related loss in behavioral olfactory function coupled with a significant neurodegeneration of glomerular dopaminergic neurons. This is accompanied by increase in alpha-synuclein levels in non-dopaminergic cells in the granule cell layer (GCL). In addition, isolated olfactory bulb synaptosomes from dual transgenic lines with Dox consistently showed a slight but significant reduction in maximum mitochondrial respiration compared to controls. These results suggest that in the presence of increased oxidative stress, increased alpha-synuclein expression within dopaminergic OB neurons results in neurodegeneration in the glomerular layer (GL) and increased alpha-synuclein levels in the granular cell layer which coincide with olfactory dysfunction.

Oxidative stress is frequently implicated in the pathology of neurodegenerative disease. The chief source of this stress is from mitochondrial respiration, via the passage of reducing equivalents through the respiratory chain resulting in a small but potentially pathological production of superoxide. The superoxide that is produced during normal respiration is primarily detoxified within the mitochondria by superoxide dismutase 2 (Sod2), a key protein for maintaining mitochondrial function. Mitochondria are distributed throughout the soma of neurons, as well as along neuronal processes and at the synaptic terminus. This distribution of potentially independent mitochondria throughout the neuron, at distinct subcellular locations, allows for the possibility of regional subcellular deficits in mitochondrial function. There has been increasing interest in the quantification and characterization of messages and proteins at the synapse, due to its importance in neurodegenerative disease, most notably Alzheimer’s disease. Here, we report the transcriptomic and proteomic changes that occur in synaptosomes from frontal cortices of Sod2 null mice. Constitutively null Sod2 mice were differentially dosed with the synthetic catalytic antioxidant EUK-189, which can extend the lifespan of these mice, as well as uncover or prevent neurodegeneration due to endogenous oxidative stress. This approach facilitated insight into quantification of trafficked messages and proteins to the synaptosome. We used two complementary methods to investigate the nature of the synaptosome under oxidative stress; either whole genome gene expression microarrays or mass spectrometry-based proteomics using isobaric tagging for relative and absolute quantitation (iTRAQ) of proteins. We have characterized the relative enrichments of gene ontologies at both gene and protein expression that occur due to mitochondrial oxidative stress in the synaptosome, which may lead to new avenues of investigation in understanding the regulation of the synaptic function in normal and diseased states. As a result of using these approaches, we report for the first time an activation of the mTOR pathway in synaptosomes isolated from Sod2 null mice, confirmed by an upregulation of the phosphorylation of 4E-BP1.

Objective Our objective was to determine whether autologous endothelial progenitor cells (EPCs) delivered into the pericardial space will migrate to and incorporate into ischemic myocardium in a porcine model. Background Use of EPCs to enhance neovascularization and preserve myocardial function in ischemic tissue is undergoing intense scrutiny as a potential therapy. Delivery into the pericardial sac may overcome some of the limitations of currently employed cell delivery techniques. Methods EPCs were immunopurified from peripheral blood of Yorkshire pigs by selecting for the CD31 surface antigen, and adherent cells were cultured for 3–5 days. After myocardial ischemia was induced in the left anterior descending (LAD) artery, either autologous DiI (1,1′-dioctadecyl-1-3,3,3′,3′-tetramethylindocarbocyanine perchlorate)-labeled EPCs ( n =10) or serum-free medium (SFM; n =8) was delivered into the pericardial space using a percutaneous transatrial approach. Animals were sacrificed on Day 7 or 21. Echocardiography was performed at baseline, during ischemia, and on Day 7 in six SFM group animals and six EPC group animals. Results On Day 7, EPCs were identified in the left ventricular (LV) anterior wall or anterior septum in all six EPC-treated animals (cell density of 626±122/mm 2 ). On Day 21, EPCs were identified in the LV anterior wall or anterior septum in three of four EPC-treated animals (cell density of 267±167/mm 2 ). These cells showed dual staining for DiI and Bandeiraea simplicifolia lectin I (a marker of both native and exogenous endothelial cells). At the Day 7 follow-up, echocardiography demonstrated that fractional shortening in the EPC-treated group was 30.6±3.4, compared with 22.6±2.8 in SFM controls ( P =.05). Conclusions EPCs can migrate from the pericardial space to incorporate exclusively into areas of ischemic myocardium and may have favorable effects on LV function.

Successful treatment of infants with gastrointestinal involvement in Langerhans cell histiocytosis (LCH) has been poor, with no specific chemotherapeutic regimen of clear benefit. An 8-month-old male, diagnosed with LCH by skin and gastrointestinal biopsies, was treated with several cycles of 2-chlorodeoxyadenosine, vinblastine and prednisone with only partial response. Ultimately, two cycles of 2-chlorodeoxyadenosine concomitant with high-dose cytarabine led to a durable complete response. Twenty-seven months since the last course of chemotherapy, the patient continues to thrive free of disease. Treatment with 2-chlorodeoxyadenosine and cytarabine should be considered for further study in patients with poor-prognosis LCH.