Gender Distribution Associated With the Journal Wilderness & Environmental Medicine.

INTRODUCTION: Publication and peer review are fundamental to career advancement in science and academic medicine. Studies demonstrate that women are underrepresented in science publishing. We evaluated the gender distribution of contributors to Wilderness & Environmental Medicine (WEM) from 2010 through 2019. METHODS: We extracted author data from ScienceDirect, reviewer data from the WEM Editorial Manager database, and editorial board data from journal records. Gender (female and male) was classified using automated probability-based assessment with Genderize.io software. RESULTS: A total of 2297 unique authors were published over the 10-y span, generating 3613 authorships, of which gender was classified for 96% (n=3480). Women represented 26% (n=572) of all authors, which breaks down to 22% of all, 19% of first, 28% of second, and 18% of last authorships. Women represented 20% of peer reviewers (508/2517), 20% of reviewers-in-training (19/72), and 16% of editorial board members (7/45). The proportion of female authors, first authors, and reviewers increased over time. Women received fewer invitations per reviewer than men (mean 2.1 [95% CI 2.0-2.3] vs 2.4 [95% CI 2.3-2.5]; P=0.004), accepted reviews at similar rates (mean 73 vs 71%; P=0.214), and returned reviews 1.4 d later (mean 10.4 [CI 9.5-11.3] vs 9.0 d [95% CI 8.5-9.6]; P=0.005). CONCLUSIONS: While female representation increased over the study period, women comprise a minority of WEM authors, peer reviewers, and editorial board members. Gender equity could be improved by identifying and eliminating barriers to participation, addressing any potential bias in review processes, implementing strategies to increase female-authored submissions, and increasing mentorship and training.

Gender Equity in Membership, Leadership, and Award Recognition in the Wilderness Medical Society.

INTRODUCTION: Despite near gender parity for women entering medical careers, women remain underrepresented in medical societies. This study evaluated the gender distribution associated with Wilderness Medical Society (WMS) activities. METHODS: A retrospective review was performed on the gender breakdown of the following WMS members: a single-day 2020 snapshot, conference attendees 2012 through 2020, conference presenters from winter 2017 through winter 2021, and leadership and awards data from 1984 through 2021. Genderize.io was used to generate probability-based gender categorizations (male/female) based on first names or pronoun associations. RESULTS: Gender was assigned in 91% (4043/4461) of 2020 WMS members, 92% (6179/6720) of 2012-2020 conference attendees, and 100% of remaining categories. Women represented 28% (1143/4043) of members, 27% (1679/6179) of conference attendees, 31% (143/465) of all conference presenters, 20% (62/303) of mainstage presenters, 23% (17/75) of all board members, 38% (14/37) of committee chairs, and 10% (2/20) of board presidents. Women received 18% (42/228) of recognition awards and 31% (15/48) of research grants issued. CONCLUSIONS: Although women comprise a minority of WMS participants, gender distribution was similar across categories for membership, conference presenters, total board positions, and research grant awards. Relative underrepresentation was seen in the highest leadership levels, in recognition awards, and in mainstage presenters. Ongoing auditing may help to identify and address sources of bias and/or barriers to participation. Although it is only one of many components of equity, identifying successes and future opportunities for gender balance can strengthen the base of the WMS, promote growth, and ensure a strong leadership pipeline.

Spontaneous Variation in Electrocorticographic Resting-State Connectivity.

Prior studies using functional magnetic resonance imaging, electroencephalography, and magnetoencephalography have observed both structured patterns in resting-state functional connectivity and spontaneous longitudinal variation in connectivity patterns independent of a task. In this first study using electrocorticography (ECoG), we characterized spontaneous, intersession variation in resting-state functional connectivity not linked to a task. We evaluated pairwise connectivity between electrodes using three measures (phase locking value [PLV], amplitude correlation, and coherence) for six canonical frequency bands, capturing different characteristics of time-evolving signals. We grouped electrodes into 10 functional regions and used intraclass correlation (ICC) to estimate pairwise longitudinal stability. We found that stronger PLV (PLV ≥0.4) in theta through gamma bands and strong correlation in all bands (R2's ≥0.6) are linked to substantial stability (ICC ≥0.6), but that stability does not imply strong phase locking or amplitude correlation. There was no notable link between strong coherence and high ICC. All within-region PLVs are markedly stable across frequencies. In addition, we highlight interaction patterns across several regions: parahippocampal/entorhinal cortex is characterized by stable, weak functional connectivity except self-connections. Dorsolateral prefrontal cortex connectivity is weak and unstable, except self-connections. Inferior parietal lobule has little stability despite narrow connectivity bounds. We confirm prior studies linking functional connectivity strength and intersession variability, extending into higher frequencies than other modalities, with greater spatial specificity than scalp electrophysiology. We suggest further studies quantitatively compare ECoG to other modalities and/or use these findings as a baseline to capture functional connectivity and dynamics linked to perturbations with a task or disease state.

Clinicopathological correlations in behavioural variant frontotemporal dementia.

Accurately predicting the underlying neuropathological diagnosis in patients with behavioural variant frontotemporal dementia (bvFTD) poses a daunting challenge for clinicians but will be critical for the success of disease-modifying therapies. We sought to improve pathological prediction by exploring clinicopathological correlations in a large bvFTD cohort. Among 438 patients in whom bvFTD was either the top or an alternative possible clinical diagnosis, 117 had available autopsy data, including 98 with a primary pathological diagnosis of frontotemporal lobar degeneration (FTLD), 15 with Alzheimer's disease, and four with amyotrophic lateral sclerosis who lacked neurodegenerative disease-related pathology outside of the motor system. Patients with FTLD were distributed between FTLD-tau (34 patients: 10 corticobasal degeneration, nine progressive supranuclear palsy, eight Pick's disease, three frontotemporal dementia with parkinsonism associated with chromosome 17, three unclassifiable tauopathy, and one argyrophilic grain disease); FTLD-TDP (55 patients: nine type A including one with motor neuron disease, 27 type B including 21 with motor neuron disease, eight type C with right temporal lobe presentations, and 11 unclassifiable including eight with motor neuron disease), FTLD-FUS (eight patients), and one patient with FTLD-ubiquitin proteasome system positive inclusions (FTLD-UPS) that stained negatively for tau, TDP-43, and FUS. Alzheimer's disease was uncommon (6%) among patients whose only top diagnosis during follow-up was bvFTD. Seventy-nine per cent of FTLD-tau, 86% of FTLD-TDP, and 88% of FTLD-FUS met at least 'possible' bvFTD diagnostic criteria at first presentation. The frequency of the six core bvFTD diagnostic features was similar in FTLD-tau and FTLD-TDP, suggesting that these features alone cannot be used to separate patients by major molecular class. Voxel-based morphometry revealed that nearly all pathological subgroups and even individual patients share atrophy in anterior cingulate, frontoinsula, striatum, and amygdala, indicating that degeneration of these regions is intimately linked to the behavioural syndrome produced by these diverse aetiologies. In addition to these unifying features, symptom profiles also differed among pathological subtypes, suggesting distinct anatomical vulnerabilities and informing a clinician's prediction of pathological diagnosis. Data-driven classification into one of the 10 most common pathological diagnoses was most accurate (up to 60.2%) when using a combination of known predictive factors (genetic mutations, motor features, or striking atrophy patterns) and the results of a discriminant function analysis that incorporated clinical, neuroimaging, and neuropsychological data.

Network degeneration and dysfunction in presymptomatic C9ORF72 expansion carriers.

Hexanucleotide repeat expansions in C9ORF72 are the most common known genetic cause of familial and sporadic frontotemporal dementia and amyotrophic lateral sclerosis. Previous work has shown that patients with behavioral variant frontotemporal dementia due to C9ORF72 show salience and sensorimotor network disruptions comparable to those seen in sporadic behavioral variant frontotemporal dementia, but it remains unknown how early in the lifespan these and other changes in brain structure and function arise. To gain insights into this question, we compared 15 presymptomatic carriers (age 43.7 ± 10.2 years, nine females) to matched healthy controls. We used voxel-based morphometry to assess gray matter, diffusion tensor imaging to interrogate white matter tracts, and task-free functional MRI to probe the salience, sensorimotor, default mode, and medial pulvinar thalamus-seeded networks. We further used a retrospective chart review to ascertain psychiatric histories in carriers and their non-carrier family members. Carriers showed normal cognition and behavior despite gray matter volume and brain connectivity deficits that were apparent as early as the fourth decade of life. Gray matter volume deficits were topographically similar though less severe than those in patients with behavioral variant frontotemporal dementia due to C9ORF72, with major foci in cingulate, insula, thalamus, and striatum. Reduced white matter integrity was found in the corpus callosum, cingulum bundles, corticospinal tracts, uncinate fasciculi and inferior longitudinal fasciculi. Intrinsic connectivity deficits were detected in all four networks but most prominent in salience and medial pulvinar thalamus-seeded networks. Carrier and control groups showed comparable relationships between imaging metrics and age, suggesting that deficits emerge during early adulthood. Carriers and non-carrier family members had comparable lifetime histories of psychiatric symptoms. Taken together, the findings suggest that presymptomatic C9ORF72 expansion carriers exhibit functionally compensated brain volume and connectivity deficits that are similar, though less severe, to those reported during the symptomatic phase. The early adulthood emergence of these deficits suggests that they represent aberrant network patterning during development, an early neurodegeneration prodrome, or both.