Evaluating academic productivity and match outcomes in neurosurgery residents from medical schools without a neurosurgery residency program: a 2016-2022 bibliometric analysis.

OBJECTIVE: Transition of the United States Medical Licensing Examination Step 1 to a pass/fail structure has focused attention on medical student research in residency application. Previous studies have explored how various factors affect the neurosurgery match success, but none have focused on applicants from schools without a neurosurgery residency program. METHODS: The authors compiled a list of neurosurgery residents matched from 2016 to 2022 from schools lacking a neurosurgery program. They gathered demographic and bibliometric data, focusing on academic productivity before residency. The distinction between the top 40 and non-top 40 programs used the 5-year institutional h-index (ih[5]-index) of departments. RESULTS: Between 2016 and 2022, the gross number of students entering neurosurgery from schools without a home program rose from 15 to 26 in 2021, declining to 23 in 2022. The range of matched applicants per school was 0 to 10. The median number of publications per resident increased from 2 in 2016 to 5 in 2022 (p < 0.001). The lowest and highest numbers of publications by applicants were 0 and 40, respectively, with 22.5% reporting no publications. The lowest and highest h-indices by applicants were 0 and 11, respectively, with nearly one-third (31.2%) possessing an h-index of 0. Applicants from schools lacking a neurosurgery residency program who matched into top 40 programs had a publication range of 0-11, with a higher median of 3 compared with those who did not (median 2, range 0-8). While no significant differences were found in publication numbers (p = 0.084), a difference in h-index was observed (p = 0.024) between the two groups. Publications significantly correlated with the h-index, with each additional publication increasing the h-index by 0.19 (p < 0.001, adjusted R2 = 0.3348). CONCLUSIONS: Median publication counts have increased in this cohort, but they do not distinguish top 40 program matches. Conversely, the h-index, correlating with publication quantity and journal impact factor, does.

Evaluating Patient-reported Outcomes after Bilateral Reduction Mammoplasty: A Comparison of Reduction Techniques at a University Hospital.

Background: Macromastia, defined as the abnormal enlargement of breasts, burdens individuals physically and psychologically, impacting their daily lives beyond aesthetics. Reduction mammoplasty offers relief by restoring proportional breast volume and appropriate contour. Surgical success relies on choosing a suitable individualized operative technique tailored to the patient's presentation and postoperative goals. This study examines postoperative, patient-reported outcomes across different reduction techniques to gauge the impact of reduction technique on overall patient perspective of aesthetic and functional satisfaction. Methods: A retrospective review identified reduction mammoplasty patients by a single surgeon between 2018 and 2022. Exclusion criteria included augmentation-related or cancer reconstructive procedures. Phone interviews were conducted using a survey adapted from BREAST-Q to assess postoperative outcomes in patients. Data analysis included Pearson chi-square test in STATA 16.1. Results: Among 155 patients identified, 64 completed the survey. Average postsurgical interval was 24 months postoperative. After stratifying patients by operative technique, there was no significant difference in postoperative satisfaction among the cohorts with regard to nipple and breast appearance, sensation, symmetry, or shape. Conclusions: This study highlights no significant disparity in perceived aesthetic or functional outcomes among different reduction mammoplasty techniques. Personalized considerations, such as patient factors, surgical expertise, and anatomical specifics, should guide technique selection, emphasizing individualized approaches over presumed superior methods for optimal results.

Cross-species analysis identifies mitochondrial dysregulation as a functional consequence of the schizophrenia-associated 3q29 deletion.

The 1.6-megabase deletion at chromosome 3q29 (3q29Del) is the strongest identified genetic risk factor for schizophrenia, but the effects of this variant on neurodevelopment are not well understood. We interrogated the developing neural transcriptome in two experimental model systems with complementary advantages: isogenic human cortical organoids and isocortex from the 3q29Del mouse model. We profiled transcriptomes from isogenic cortical organoids that were aged for 2 and 12 months, as well as perinatal mouse isocortex, all at single-cell resolution. Systematic pathway analysis implicated dysregulation of mitochondrial function and energy metabolism. These molecular signatures were supported by analysis of oxidative phosphorylation protein complex expression in mouse brain and assays of mitochondrial function in engineered cell lines, which revealed a lack of metabolic flexibility and a contribution of the 3q29 gene PAK2. Together, these data indicate that metabolic disruption is associated with 3q29Del and is conserved across species.

Cross-species transcriptomic analysis identifies mitochondrial dysregulation as a functional consequence of the schizophrenia-associated 3q29 deletion.

Recent advances in the genetics of schizophrenia (SCZ) have identified rare variants that confer high disease risk, including a 1.6 Mb deletion at chromosome 3q29 with a staggeringly large effect size (O.R. > 40). Understanding the impact of the 3q29 deletion (3q29Del) on the developing CNS may therefore lead to insights about the pathobiology of schizophrenia. To gain clues about the molecular and cellular perturbations caused by the 3q29 deletion, we interrogated transcriptomic effects in two experimental model systems with complementary advantages: isogenic human forebrain cortical organoids and isocortex from the 3q29Del mouse model. We first created isogenic lines by engineering the full 3q29Del into an induced pluripotent stem cell line from a neurotypical individual. We profiled transcriptomes from isogenic cortical organoids that were aged for 2 months and 12 months, as well as day p7 perinatal mouse isocortex, all at single cell resolution. Differential expression analysis by genotype in each cell-type cluster revealed that more than half of the differentially expressed genes identified in mouse cortex were also differentially expressed in human cortical organoids, and strong correlations were observed in mouse-human differential gene expression across most major cell-types. We systematically filtered differentially expressed genes to identify changes occurring in both model systems. Pathway analysis on this filtered gene set implicated dysregulation of mitochondrial function and energy metabolism, although the direction of the effect was dependent on developmental timepoint. Transcriptomic changes were validated at the protein level by analysis of oxidative phosphorylation protein complexes in mouse brain tissue. Assays of mitochondrial function in human heterologous cells further confirmed robust mitochondrial dysregulation in 3q29Del cells, and these effects are partially recapitulated by ablation of the 3q29Del gene PAK2 . Taken together these data indicate that metabolic disruption is associated with 3q29Del and is conserved across species. These results converge with data from other rare SCZ-associated variants as well as idiopathic schizophrenia, suggesting that mitochondrial dysfunction may be a significant but overlooked contributing factor to the development of psychotic disorders. This cross-species scRNA-seq analysis of the SCZ-associated 3q29 deletion reveals that this copy number variant may produce early and persistent changes in cellular metabolism that are relevant to human neurodevelopment.