Evaluation of a Hybrid Medication Synchronization Training Module for Pharmacy Technicians.

BACKGROUND: Medication synchronization involves coordinating a patient's medications to a single date each month. Medication synchronization programs close gaps in care and improve adherence compared to automatic refill-processing programs. Patients are two to six times more adherent to medications when enrolled in a medication synchronization program. Medication synchronization has historically been driven by pharmacists; however, pharmacy technicians are in a unique position to logistically run this service. OBJECTIVE: To develop a training program for pharmacy technicians regarding medication synchronization and assess changes in knowledge and confidence before and after implementing a training program. PRACTICE DESCRIPTION: An independent community pharmacy in North Carolina. Pharmacists provide medication therapy management, reimbursed clinical services, medication synchronization, and immunizations. PRACTICE INNOVATION: The training program included medication synchronization basics, patient enrollment process, processing a synced patient, and a hands-on practice session. EVALUATION METHODS: Technicians took a pre-training questionnaire assessing knowledge and confidence before immediately completing a one-on-one pharmacist-led training session with a hands-on component on medication synchronization. Technicians took the same post-training questionnaire 2 weeks after completing the training session and utilizing medication synchronization in daily workflow. Pre- and post-training scores were assessed using a paired samples t-test. RESULTS: 10 technicians completed the training program; 40% of the technicians were certified and 30% were enrolled in a PharmD program. The mean pre-training knowledge score was 78% (7.1/9 points), the mean post-training knowledge score was 92% (8.3/9 points), the mean difference between the pre- and post- training knowledge scores was 13.4% (1.2 points), a statistically significant difference (p=0.0026). Confidence with conducting a medication synchronization call increased from 7.2 to 9.6 on a 10-point Likert scale and confidence scores increased regarding incorporating medication synchronization into workflow from 6.9 to 8.7. CONCLUSION: The standardized technician training program increased knowledge and confidence in technicians regarding managing a medication synchronization program.

Early surgery improves survival after femoral fractures in the elderly: A retrospective review of 502 fragility fractures.

AIMS: Fragility fractures are a growing global healthcare burden; fragility fractures of the femur have been shown to occur in a highly comorbid patient group, with parallels to hip fracture patients. This study aimed to investigate if early surgery for femoral fractures, distal to the hip, resulted in a reduction in mortality in patients over 65 years of age. METHODS: A retrospective review of prospectively collected data for all consecutive femoral fractures in patients aged over 65 years who underwent surgical management between January 2000 and December 2018. Data was extracted from the Fracture Outcomes Research Database (FORD) and analysed to assess if early surgery, defined as occurring within 48 h of hospital admission with a fragility femur fracture, had an effect on 30 day and 1 year mortality. RESULTS: 502 eligible patients were included; median follow up time was 57 months. 24 patients (4.7%) died within 30 days of surgery and 105 patients (20.9%) had died within 1 year of surgery. Patients who underwent surgery within 48 h of admission had a significantly reduced chance of mortality within 1 year of surgery compared to patients who had surgery more than 48 h after admission (OR = 0.401, 95% CI 0.25-0.65, p<0.001). Following Multivariate Cox Regression analysis the hazard ratio of 1 year mortality following early surgery remained significantly reduced (HR = 0.57, 95% CI 0.36-0.92, p = 0.020). CONCLUSIONS: This study demonstrates that fragility femoral fracture patients represent a similar cohort to hip fracture patients, with high mortality rates. We recommend that hip fracture management principles are also employed for fragility femoral fractures in patients over 65 years, with rapid pre-operative optimisation to ensure these patients undergo early surgical intervention.

In vitro placenta barrier model using primary human trophoblasts, underlying connective tissue and vascular endothelium.

Fetal development may be compromised by adverse events at the placental interface between mother and fetus. However, it is still unclear how the communication between mother and fetus occurs through the placenta. In vitro - models of the human placental barrier, which could help our understanding and which recreate three-dimensional (3D) structures with biological functionalities and vasculatures, have not been reported yet. Here we present a 3D-vascularized human primary placental barrier model which can be constructed in 1 day. We illustrate the similarity of our model to first trimester human placenta, both in its structure and in its ability to respond to altered oxygen and to secrete factors that cause damage cells across the barrier including embryonic cortical neurons. We use this model to highlight the possibility that both the trophoblast and the endothelium within the placenta might play a role in the fetomaternal dialogue.

Nanoparticle-induced neuronal toxicity across placental barriers is mediated by autophagy and dependent on astrocytes.

The potential for maternal nanoparticle (NP) exposures to cause developmental toxicity in the fetus without the direct passage of NPs has previously been shown, but the mechanism remained elusive. We now demonstrate that exposure of cobalt and chromium NPs to BeWo cell barriers, an in vitro model of the human placenta, triggers impairment of the autophagic flux and release of interleukin-6. This contributes to the altered differentiation of human neural progenitor cells and DNA damage in the derived neurons and astrocytes. Crucially, neuronal DNA damage is mediated by astrocytes. Inhibiting the autophagic degradation in the BeWo barrier by overexpression of the dominant-negative human ATG4BC74A significantly reduces the levels of DNA damage in astrocytes. In vivo, indirect NP toxicity in mice results in neurodevelopmental abnormalities with reactive astrogliosis and increased DNA damage in the fetal hippocampus. Our results demonstrate the potential importance of autophagy to elicit NP toxicity and the risk of indirect developmental neurotoxicity after maternal NP exposure.

Treating the placenta to prevent adverse effects of gestational hypoxia on fetal brain development.

Some neuropsychiatric disease, including schizophrenia, may originate during prenatal development, following periods of gestational hypoxia and placental oxidative stress. Here we investigated if gestational hypoxia promotes damaging secretions from the placenta that affect fetal development and whether a mitochondria-targeted antioxidant MitoQ might prevent this. Gestational hypoxia caused low birth-weight and changes in young adult offspring brain, mimicking those in human neuropsychiatric disease. Exposure of cultured neurons to fetal plasma or to secretions from the placenta or from model trophoblast barriers that had been exposed to altered oxygenation caused similar morphological changes. The secretions and plasma contained altered microRNAs whose targets were linked with changes in gene expression in the fetal brain and with human schizophrenia loci. Molecular and morphological changes in vivo and in vitro were prevented by a single dose of MitoQ bound to nanoparticles, which were shown to localise and prevent oxidative stress in the placenta but not in the fetus. We suggest the possibility of developing preventative treatments that target the placenta and not the fetus to reduce risk of psychiatric disease in later life.