Senior Mentorship and Scholarly Success: Assessing Influences on Successful Neurosurgery Residency Applicant's H-index.

BACKGROUND: Research productivity is on the rise as neurosurgical residency positions become increasingly competitive. OBJECTIVE: We explored the relationship between neurosurgical residency applicant's senior author's research productivity and matching into a neurosurgery residency program. METHODS: A retrospective analysis of bibliometric data for applicants who matched into neurosurgery in 2022-2023 and their senior authors was conducted using Scopus. RESULTS: Logistic regression revealed a significant association between h-index values and top 40 match outcomes (p=0.038). The maximum h-index of senior authors significantly predicted matches at top 40 programs (p=0.003). Affiliation with a top 40 medical school increased both applicant and senior author h-indices (p=0.05, p<0.001 respectively). Linear regression of the maximum h-index of senior authors in pre-residency publications explained 42% of this variability (p<0.001). A multiple linear regression model incorporating this with publication number elucidated 69% of the variance in interns' h-index. Authorship data categorized as first, second, and third author positions showed 1847 first author, 1417 second author, and 118 third author publications over two-years. Applicants at top 40 residency programs had more first and second author publications compared to those from non-top 40 programs (p=0.0158, p=0.0275). CONCLUSION: There is a strong correlation between a neurosurgical applicant's academic output and that of their senior authors. The number of publications and the maximum h-index of senior authors significantly predict applicant h-indices. We also demonstrated that there is a significant difference in the academic productivity of applicants and senior authors of applicants who successfully match into a top 40 i(h)5 rated neurosurgical residency.

Real-World Outcomes of Canaloplasty and Trabeculotomy Combined with Cataract Surgery in Eyes with All Stages of Open-Angle Glaucoma.

Purpose: To evaluate the long-term safety and efficacy of sequential canaloplasty and trabeculotomy combined with cataract surgery in patients with mild, moderate, and advanced open-angle glaucoma. Patients and Methods: Case records of 171 consecutive patients (171 eyes) who had undergone cataract surgery followed by canaloplasty (≥180°) and trabeculotomy (≥90°) for mild, moderate, or advanced open-angle glaucoma (Shaffer grade ≥3) using the OMNI Surgical System (Sight Sciences, Inc., Menlo Park, CA) were analyzed retrospectively. Efficacy endpoints included change in mean IOP and number of medications from baseline to postoperative 12- and 24-months for the overall dataset and stratified by each stage of glaucoma. Kaplan-Meier survival analysis of success (eyes that did not require secondary surgical interventions (SSI)) by postoperative 24 months was also performed. Results: Postoperatively, there was a statistically significant reduction in IOP (baseline of 17.2 mmHg on 1.3 medicines reduced to 14.3 on 0.8 medicines (12 months) and 14.0 on 0.9 medicines (24 months), p<0.001 for both time points). Eyes with advanced glaucoma (N=63) maintained significant IOP reduction (17.8 mmHg on 1.6 medicines at baseline reduced to 13.6 mmHg on 1.3 medicines (12 months) and 13.0 on 1.5 medicines (24 months), p<0.001). Kaplan-Meier analysis showed a 93.0% survival probability for the avoidance of SSI at 2 years after surgery. Conclusion: Canaloplasty and trabeculotomy combined with cataract surgery provided effective IOP reduction for eyes with all stages of glaucoma at postoperative 12 and 24 months, and the procedure yielded a 93% survival rate for SSI avoidance at 2 years.

Delivering progranulin to neuronal lysosomes protects against excitotoxicity.

Loss-of-function mutations in progranulin (GRN) are a major genetic cause of frontotemporal dementia (FTD), possibly due to loss of progranulin's neurotrophic and anti-inflammatory effects. Progranulin promotes neuronal growth and protects against excitotoxicity and other forms of injury. It is unclear if these neurotrophic effects are mediated through cellular signaling or through promotion of lysosomal function. Progranulin is a secreted proprotein that may activate neurotrophic signaling through cell-surface receptors. However, progranulin is efficiently trafficked to lysosomes and is necessary for maintaining lysosomal function. To determine which of these mechanisms mediates progranulin's protection against excitotoxicity, we generated lentiviral vectors expressing progranulin (PGRN) or lysosome-targeted progranulin (L-PGRN). L-PGRN was generated by fusing the LAMP-1 transmembrane and cytosolic domains to the C-terminus of progranulin. L-PGRN exhibited no detectable secretion, but was delivered to lysosomes and processed into granulins. PGRN and L-PGRN protected against NMDA excitotoxicity in rat primary cortical neurons, but L-PGRN had more consistent protective effects than PGRN. L-PGRN's protective effects were likely mediated through the autophagy-lysosomal pathway. In control neurons, an excitotoxic dose of NMDA stimulated autophagy, and inhibiting autophagy with 3-methyladenine reduced excitotoxic cell death. L-PGRN blunted the autophagic response to NMDA and occluded the protective effect of 3-methyladenine. This was not due to a general impairment of autophagy, as L-PGRN increased basal autophagy and did not alter autophagy after nutrient starvation. These data show that progranulin's protection against excitotoxicity does not require extracellular progranulin, but is mediated through lysosomes, providing a mechanistic link between progranulin's lysosomal and neurotrophic effects.