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http://dx.doi.org/10.1097/AOG.0b013e3181fa4596 | DOI Listing |
J Am Assoc Nurse Pract
January 2025
Division of Cardiology, Department of Medicine, Duke Health Integrated Practice, Duke University Health System, Durham, North Carolina.
Background: Increasing patient demand and clinician burnout in rheumatology practices have highlighted the need for more efficient models of care (MOC). Interprofessional collaboration is essential for improving patient outcomes and clinician satisfaction.
Local Problem: Our current MOC lacks standardization and formal integration of Nurse Practitioners (NPs) and Physician Assistants (PAs), resulting in reduced clinician satisfaction and limited patient access.
Elife
January 2025
Department of Neurosciences, Case Western Reserve University School of Medicine, Cleveland, United States.
Sensory experience during developmental critical periods has lifelong consequences for circuit function and behavior, but the molecular and cellular mechanisms through which experience causes these changes are not well understood. The antennal lobe houses synapses between olfactory sensory neurons (OSNs) and downstream projection neurons (PNs) in stereotyped glomeruli. Many glomeruli exhibit structural plasticity in response to early-life odor exposure, indicating a general sensitivity of the fly olfactory circuitry to early sensory experience.
View Article and Find Full Text PDFJ Psychosoc Oncol
January 2025
University of Minnesota Medical School, Minneapolis, MN, USA.
Background/purpose: Immunotherapies, such as CAR-T, have revolutionized cancer treatment for some cancers. However, these treatments often require active participation of a family member or friend to act as a caregiver at home for several weeks after infusion. Given the novelty of CAR-T, there is a need to better understand the experience of patients receiving these treatments and their caregivers.
View Article and Find Full Text PDFEndocrine
January 2025
Pediatric Unit, IRCCS AOU of Bologna, Bologna, Italy.
J Nephrol
January 2025
Department of Nephrology, Beaumont Hospital, Dublin, Ireland.
Background: Autosomal dominant polycystic kidney disease (ADPKD) is caused primarily by pathogenic variants in the PKD1 and PKD2 genes. Although the type of ADPKD variant can influence disease severity, rare, hypomorphic PKD1 variants have also been reported to modify disease severity or cause biallelic ADPKD. This study examines whether rare, additional, potentially protein-altering, non-pathogenic PKD1 variants contribute to ADPKD phenotypic outcomes.
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