Factors that Affect Patient Wait Times at a Free Clinic.

Free clinics may present long wait times. A retrospective chart review was conducted at a free clinic to understand contributing factors. Three wait times (total visit time, lobby wait time, and triage time) were analyzed across 349 patients. Variables included in the models were the total number of patients, providers, and volunteers; interpreter services; social work involvement; medical complexity; new vs. returning patient; scheduled vs. walk-in appointment; transportation provision; medical volunteer training level; and on-site medications and labs. Data analysis with multiple regressions was conducted. Factors that significantly affected wait times included the level of medical complexity (p<.001), medical volunteer training levels (p<.001), in-house labs (p<.001), in-house medications (p=.04), and new patients (p=.01). An intervention involving time benchmarks at the beginning of clinics reduced first-wave lobby wait times (p<.001). Future interventions addressing these factors may reduce wait times at other clinics.

The Costs of Operating a Student-run Free Clinic.

INTRODUCTION: Free clinics provide care for those who may otherwise not have access. While this care is often free for patients, it is not free to operate such clinics. This review will provide a budget and breakdown of all expenditures at a student-run free clinic along with average costs of services provided to patients. METHODS: Accounting data was used to categorize all expenses and generate an annual budget. An inventory tracking system was developed to measure the costs of all medical supplies and services accurately, providing information on costs per clinic and costs per patient for each provided service. RESULTS: The average cost per clinic was $53.55 (per patient: $2.14) for general clinic supplies, $43.74 (per patient: $7.29) for telehealth, $278.47 (per patient: $12.66) for laboratory services, $247.25 (per patient: $10.75) for pharmacy services, and $8.30 (per patient: $1.19) for social work. These costs contributed to a relative minority (< 33%) of the total costs to run a free clinic, where the highest costs were for volunteer appreciation and administrative overhead. Twelve categories of expenditures (administrative overhead, volunteer appreciation, medical and lab supplies, conferences and special projects, advertising and marketing, telehealth, pharmacy, specialty clinics, chronic care, patient transportation, social work, and accounting services) were ranked in order of necessity, and methods for cost reduction were discussed for each category. CONCLUSIONS: Categorizing costs can show where cost savings and cost-effective additions may be implemented. This study may serve as a financial and budgeting reference for other clinics.

Peptidomimetic-Based Vesicles Inhibit Amyloid-ß Fibrillation and Attenuate Cytotoxicity.

An interruption in Aß homeostasis leads to the deposit of neurotoxic amyloid plaques and is associated with Alzheimer's disease. A supramolecular strategy based on the assembly of peptidomimetic agents into functional vesicles has been conceived for the simultaneous inhibition of Aß42 fibrillation and expedited clearance of Aß42 aggregates. Tris-pyrrolamide peptidomimetic, ADH-353, contains one hydrophobic N-butyl and two hydrophilic N-propylamine side chains and readily forms vesicles under physiological conditions. These vesicles completely rescue both mouse neuroblastoma N2a and human neuroblastoma SH-SY5Y cells from the cytotoxicity that follows from Aß42 misfolding likely in mitochondria. Biophysical studies, including confocal imaging, demonstrate the biocompatibility and selectivity of the approach toward this aberrant protein assembly in cellular milieu.

Sub-stoichiometric inhibition of IAPP aggregation: a peptidomimetic approach to anti-amyloid agents.

Membrane-catalysed misfolding of islet amyloid polypeptide is associated with the death of ß-cells in type II diabetes (T2D). Most active compounds so far reported require high doses for inhibition of membrane bound IAPP fibrillation. Here, we describe a naphthalimide-appended oligopyridylamide-based α-helical mimetic, DM 1, for targeting membrane bound IAPP. DM 1 completely inhibits the aggregation of IAPP at doses of 0.2 equivalents. DM 1 is also effective at similarly low doses for inhibition of seed-catalyzed secondary nucleation. An NMR based study demonstrates that DM 1 modulates IAPP self-assembly by stabilizing and/or perturbing the N-terminus helix conformation. DM 1 at substoichiometric doses rescues rat insulinoma cells from IAPP-mediated cytotoxicity. Most importantly, 0.2 equivalents of DM 1 disaggregate preformed oligomers and fibrils and can reverse cytotoxicity by modulating toxic preformed oligomers and fibrils of IAPP into non-toxic conformations.

Molecular and cellular identification of the immune response in peripheral ganglia following nerve injury.

BACKGROUND: Neuroinflammation accompanies neural trauma and most neurological diseases. Axotomy in the peripheral nervous system (PNS) leads to dramatic changes in the injured neuron: the cell body expresses a distinct set of genes known as regeneration-associated genes, the distal axonal segment degenerates and its debris is cleared, and the axons in the proximal segment form growth cones and extend neurites. These processes are orchestrated in part by immune and other non-neuronal cells. Macrophages in ganglia play an integral role in supporting regeneration. Here, we explore further the molecular and cellular components of the injury-induced immune response within peripheral ganglia. METHODS: Adult male wild-type (WT) and Ccr2 -/- mice were subjected to a unilateral transection of the sciatic nerve and axotomy of the superior cervical ganglion (SCG). Antibody arrays were used to determine the expression of chemokines and cytokines in the dorsal root ganglion (DRG) and SCG. Flow cytometry and immunohistochemistry were utilized to identify the cellular composition of the injury-induced immune response within ganglia. RESULTS: Chemokine expression in the ganglia differed 48 h after nerve injury with a large increase in macrophage inflammatory protein-1γ in the SCG but not in the DRG, while C-C class chemokine ligand 2 was highly expressed in both ganglia. Differences between WT and Ccr2 -/- mice were also observed with increased C-C class chemokine ligand 6/C10 expression in the WT DRG compared to C-C class chemokine receptor 2 (CCR2)-/- DRG and increased CXCL5 expression in CCR2-/- SCG compared to WT. Diminished macrophage accumulation in the DRG and SCG of Ccr2 -/- mice was found compared to WT ganglia 7 days after nerve injury. Interestingly, neutrophils were found in the SCG but not in the DRG. Cytokine expression, measured 7 days after injury, differed between ganglion type and genotype. Macrophage activation was assayed by colabeling ganglia with the anti-inflammatory marker CD206 and the macrophage marker CD68, and an almost complete colocalization of the two markers was found in both ganglia. CONCLUSIONS: This study demonstrates both molecular and cellular differences in the nerve injury-induced immune response between DRG and SCG and between WT and Ccr2 -/- mice.

Overexpression of the monocyte chemokine CCL2 in dorsal root ganglion neurons causes a conditioning-like increase in neurite outgrowth and does so via a STAT3 dependent mechanism.

Neuroinflammation plays a critical role in the regeneration of peripheral nerves following axotomy. An injury to the sciatic nerve leads to significant macrophage accumulation in the L5 DRG, an effect not seen when the dorsal root is injured. We recently demonstrated that this accumulation around axotomized cell bodies is necessary for a peripheral conditioning lesion response to occur. Here we asked whether overexpression of the monocyte chemokine CCL2 specifically in DRG neurons of uninjured mice is sufficient to cause macrophage accumulation and to enhance regeneration or whether other injury-derived signals are required. AAV5-EF1α-CCL2 was injected intrathecally, and this injection led to a time-dependent increase in CCL2 mRNA expression and macrophage accumulation in L5 DRG, with a maximal response at 3 weeks post-injection. These changes led to a conditioning-like increase in neurite outgrowth in DRG explant and dissociated cell cultures. This increase in regeneration was dependent upon CCL2 acting through its primary receptor CCR2. When CCL2 was overexpressed in CCR2-/- mice, macrophage accumulation and enhanced regeneration were not observed. To address the mechanism by which CCL2 overexpression enhances regeneration, we tested for elevated expression of regeneration-associated genes in these animals. Surprisingly, we found that CCL2 overexpression led to a selective increase in LIF mRNA and neuronal phosphorylated STAT3 (pSTAT3) in L5 DRGs, with no change in expression seen in other RAGs such as GAP-43. Blockade of STAT3 phosphorylation by each of two different inhibitors prevented the increase in neurite outgrowth. Thus, CCL2 overexpression is sufficient to induce macrophage accumulation in uninjured L5 DRGs and increase the regenerative capacity of DRG neurons via a STAT3-dependent mechanism.