A longitudinal study of naloxone opioid overdose awareness and reversal training for first-year medical students: specific elements require reinforcement.

BACKGROUND: The opioid epidemic is a progressively worsening public health crisis that continues to impact healthcare system strategies such as overdose reversal and destigmatization. Even among healthcare professionals, there remains a lack of confidence in naloxone administration and a prevalence of stigma. While training can play a major impact in reducing these shortcomings, the long-term effectiveness has yet to be characterized in training healthcare professionals. This study examined the long-term retention of opioid overdose awareness and reversal training (OOART) by evaluating performance at two-time intervals, immediately post-training and at a 3-month follow-up. METHODS: Voluntary training was offered to first-year (M1) medical students at the Drexel University College of Medicine in 2021. At this training, 118 students completed training, 95 completed the post-training survey, and 42 completed the 3-month follow-up. RESULTS: Opioid reversal knowledge questions assessed significantly increased scores post-training and at the 3-month follow-up. In three of the attitude questions, scores were improved at both follow-up timepoints. In addition, three attitude questions indicating a participant's confidence to respond to an opioid overdose situation increased directly after the training, but regressed at the 3-month follow-up. The remaining questions did not show any statistical difference across the survey intervals. CONCLUSIONS: This study establishes that while OOART provides participants with the knowledge of how to respond to an opioid overdose, the retention of this knowledge at a 3-month interval is reduced. The results were mixed for longitudinal assessment of participant's attitudes toward people with opioid use disorder. Some positive increases in attitudes were retained at the 3-month interval, while others trended back toward pre-training levels. These results support the effectiveness of the training but also provide evidence that OOART must be reinforced often

Ophthalmology in North America: Early Stories (1491-1801)

New World plants, such as tobacco, tomato, and chili, were held to have beneficial effects on the eyes. Indigenous healers rubbed or scraped the eyes or eyelids to treat inflammation, corneal opacities, and even eye irritation from smoke. European settlers used harsh treatments, such as bleeding and blistering, when the eyes were inflamed or had loss of vision with a normal appearance (gutta serena). In New Spain, surgery for corneal opacity was performed in 1601 and cataract couching in 1611. North American physicians knew of contralateral loss of vision after trauma or surgery (sympathetic ophthalmia), which they called “sympathy.” To date, the earliest identified cataract couching by a surgeon trained in the New World was performed in 1769 by John Bartlett of Rhode Island. The American Revolution negatively affected ophthalmology, as loyalist surgeons were expelled and others were consumed with wartime activities. After the war, cataract extraction was imported to America in earnest and academic development resumed. Charles F Bartlett, the son of John, performed cataract extraction but was also a “rapacious privateer.” In 1801, a doctor in the frontier territory of Kentucky observed anticholinergic poisoning by Datura stramonium (Jimsonweed) and suggested that this agent be applied topically to dilate the pupil before cataract extraction. John Warren at Harvard preferred couching in the 1790s, but, after his son returned from European training, recommended treating angle closure glaucoma by lens extraction. Other eye procedures described or advertised in America before the 19th century included enucleation, resection of conjunctival lesions or periocular tumors, treatment of lacrimal fistula, and fitting of prosthetic eyes

New insights into the genetic etiology of Alzheimer’s disease and related dementias

Characterization of the genetic landscape of Alzheimer’s disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/‘proxy’ AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE ε4 allele

New insights into the genetic etiology of Alzheimer’s disease and related dementias

Characterization of the genetic landscape of Alzheimer’s disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/‘proxy’ AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE ε4 allele