Assessment of clinical continuity strategies offered by dual-degree training programs in the USA.

Background: Integration of clinical skills during graduate training in dual-degree programs remains a challenge. The present study investigated the availability and self-perceived efficacy of clinical continuity strategies for dual-degree trainees preparing for clinical training. Methods: Survey participants were MD/DO-PhD students enrolled in dual-degree-granting institutions in the USA. The response rate was 95% of 73 unique institutions surveyed, representing 56% of the 124 MD-PhD and 7 DO-PhD recognized training programs. Respondents were asked to indicate the availability and self-perceived efficacy of each strategy. Results: Reported available clinical continuity strategies included clinical volunteering (95.6%), medical grand rounds (86.9%), mentored clinical experiences (84.2%), standardized patients/ practice Objective Structured Clinical Examinations (OSCEs) (70.3%), clinical case reviews (45.9%), clinical journal clubs (38.3%), and preclinical courses/review sessions (37.2%). Trainees rated standardized patients (µ = 6.98 ± 0.356), mentored clinical experiences (µ = 6.94 ± 0.301), clinical skills review sessions (µ = 6.89 ± 0.384), preclinical courses/review sessions (µ = 6.74 ± 0.482), and clinical volunteering (µ = 6.60 ± 0.369), significantly (p < 0.050) higher than clinical case review (µ = 5.34 ± 0.412), clinical journal club (µ = 4.75 ± 0.498), and medicine grand rounds (µ = 4.45 ± 0.377). Further, 84.4% of respondents stated they would be willing to devote at least 0.5-1 hour per week to clinical continuity opportunities during graduate training. Conclusion: Less than half of the institutions surveyed offered strategies perceived as the most efficacious in preparing trainees for clinical reentry, such as clinical skills review sessions. Broader implementation of these strategies could help better prepare dual-degree students for their return to clinical training.

Leadless Pacemaker Implantation in a Patient With Diminutive Subclavian Veins.

BACKGROUND: Conventional pacemakers have a longstanding history of preventing morbidity and mortality in patients with bradyarrhythmia and conduction disorders. While decades of advancements have improved pacemaker technology and implantation technique, insertion of transvenous leads and formation of a pectoral pocket can lead to complications, including pocket hematoma, pneumothorax, or infection. Leadless pacemakers were introduced in 2012 to address these complications; however, early leadless systems only provided single-chamber ventricular pacing. In 2020, an accelerometer-based atrial sensing feature was developed to allow for atrioventricular (AV) synchrony with these devices. Early evidence suggests that patients with sinus rhythm and AV block can benefit from single-chamber leadless pacing systems with an AV synchrony algorithm. As availability of these devices continues to broaden, identification of appropriate recipients has become increasingly relevant.

Computational Analysis of Therapeutic Neuroadaptation to Chronic Antidepressant in a Model of the Monoaminergic Neurotransmitter and Stress Hormone Systems.

The clinical practice of selective serotonin reuptake inhibitor (SSRI) augmentation relies heavily on trial-and-error. Unfortunately, the drug combinations prescribed today fail to provide relief for many depressed patients. In order to identify potentially more effective treatments, we developed a computational model of the monoaminergic neurotransmitter and stress-steroid systems that neuroadapts to chronic administration of combinations of antidepressant drugs and hormones by adjusting the strengths of its transmitter-system components (TSCs). We used the model to screen 60 chronically administered drug/hormone pairs and triples, and identified as potentially therapeutic those combinations that raised the monoamines (serotonin, norepinephrine, and dopamine) but lowered cortisol following neuroadaptation in the model. We also evaluated the contributions of individual and pairs of TSCs to therapeutic neuroadaptation with chronic SSRI using sensitivity, correlation, and linear temporal-logic analyses. All three approaches revealed that therapeutic neuroadaptation to chronic SSRI is an overdetermined process that depends on multiple TSCs, providing a potential explanation for the clinical finding that no single antidepressant regimen alleviates depressive symptoms in all patients.

Computational Model of Antidepressant Response Heterogeneity as Multi-pathway Neuroadaptation.

Current hypotheses cannot fully explain the clinically observed heterogeneity in antidepressant response. The therapeutic latency of antidepressants suggests that therapeutic outcomes are achieved not by the acute effects of the drugs, but rather by the homeostatic changes that occur as the brain adapts to their chronic administration. We present a computational model that represents the known interactions between the monoaminergic neurotransmitter-producing brain regions and associated non-monoaminergic neurotransmitter systems, and use the model to explore the possible ways in which the brain can homeostatically adjust to chronic antidepressant administration. The model also represents the neuron-specific neurotransmitter receptors that are known to adjust their strengths (expressions or sensitivities) in response to chronic antidepressant administration, and neuroadaptation in the model occurs through sequential adjustments in these receptor strengths. The main result is that the model can reach similar levels of adaptation to chronic administration of the same antidepressant drug or combination along many different pathways, arriving correspondingly at many different receptor strength configurations, but not all of those adapted configurations are also associated with therapeutic elevations in monoamine levels. When expressed as the percentage of adapted configurations that are also associated with elevations in one or more of the monoamines, our modeling results largely agree with the percentage efficacy rates of antidepressants and antidepressant combinations observed in clinical trials. Our neuroadaptation model provides an explanation for the clinical reports of heterogeneous outcomes among patients chronically administered the same antidepressant drug regimen.