Performance Differences Between the Sexes in the Boston Marathon From 1972 to 2017

Knechtle, B, Di Gangi, S, Rüst, CA, and Nikolaidis, PT. Performance differences between the sexes in the Boston Marathon from 1972 to 2017. J Strength Cond Res XX(X): 000-000, 2018-The differences between the sexes in marathon running have been investigated for athletes competing in world class-level races. However, no information exists about changes in these differences since the first women officially began participating in marathons. We examined trends in participation and performance in the Boston Marathon from 1972 to 2017. A total of 371,250 different finishers (64% men) and 553,890 observations-with 187,998 (34%) being of women and 365,892 (66%) of men-were analyzed using Generalized Additive Mixed Models. The number of finishers increased over the years. Female participation started at 2.81% in 1972 and reached 45.68% in 2016. Considering all finishers, men (03:38:42 ± 00:41:43 h:min:s) were overall faster than women (04:03:28 ± 00:38:32 h:min:s) by 10.7%. Average performance worsened over the years, but the differences between the sexes decreased. For the annual 10 fastest runners, performance improved with a decrease in speed difference (18.3% overall, men: 02:13:30 ± 00:04:08 h:min:s vs. women: 02:37:42 ± 00:17:58 h:min:s). For the annual winners, performance improved with a decrease in speed difference (15.5% overall, men: 02:10:24 ± 00:03:05 h:min:s vs. women: 02:30:43 ± 00:11:05 h:min:s). For the near-elite finishers from the 21st to the 100th place and from the 101st to the 200th place, women's performance improved with a decrease in the difference to men. In summary, the trend in performance over the years depended on the methodological approach (i.e., all vs. annual 10 fastest finishers vs. annual winners), but the difference between the sexes decreased in all instances. Although men were 10.7% faster than women, the fastest men (i.e., top 10 and winners) increased the gap between men and women by an average of 18.3% for the annual 10 fastest and 15.5% for the annual winners

World Records in Half-Marathon Running by Sex and Age

The relationship between age and elite marathon race times is well investigated, but little is known for half-marathon running. This study investigated the relationship between half-marathon race times and age in 1-year intervals by using the world singe age records in half-marathon running and the sex difference in performance from 5-91 years in men and 5-93 years in women. We found a 4 order-polynomial relationship between age and race time for both women and men. Women achieve their best half-marathon race time earlier in life than men, 23.89 years compared with 28.13, but when using a non-linear regression analysis, the age of the fastest race time does not differ between men and women with 26.62 years in women and 26.80 years in men. Moreover, women increase the sex difference in half-marathon running performance to men with advancing age

Midline brain structures in adult niemann-pick type c disease: A cross-sectional study

Objective: A range of neuropathological changes occur in the brains of individuals with adult Niemann-Pick type C disease (NPC), a recessive disorder of cholesterol trafficking that results in accumulation of cholesterol and gangliosides in lysosomes, particularly in neurons. One of the most significant regions of grey matter loss occurs in the thalami, which abut the midline. What is not known is whether these are neurodevelopmental in origin well prior to symptomatic onset. We aimed to examine other markers of midline developmental anomalies in adults with NPC. Method: We examined the size of adhesio interthalamica (AI) and cavum septum pellucidum (CSP) (if present) in nine individuals diagnosed with NPC and nine healthy comparison subjects, matched for age and gender, using a 3T magnetic resonance volumetric sequence and measured the length of the AI and CSP in mm. Results: We found that 5/9 NPC patients and 0/9 controls had a missing AI. AI length was significantly shorter in the patient group. No subject in other group had a large CSP, and CSP length did not differ. Duration of illness showed a trend to a negative correlation with AI length in patients. Conclusions: Our findings suggest that adult NPC patients show some markers of early neurodevelopmental disturbance, matching findings seen in psychotic disorders. The differences in AI, but not CSP, suggest neurodevelopmental change may occur early in gestation rather than post-partum. The relationship with duration of illness suggests that there may be atrophy over time in these structures, consistent with prior analyses of grey matter regions in NPC

World Single Age Records in Running From 5 km to Marathon

This study investigated the relationship between race times and age, in 1-year intervals, by using the world single age records, from 5 km to marathon running (i. e., 5 km, 4 miles, 8, 10, 12, 15 km, 10 miles, 20 km, half-marathon, 25 km, 30 km, and marathon). For each race, a regression model was fitted. Effects of sex, alone and in interaction with age, and the effect of country of origin on performance were examined in a multi-variable model. The relationship between age and race time was modeled through a 4th order-polynomial function. Women achieved their best half-marathon and marathon race time, respectively, 1 year and 3 years earlier in life than men. On the contrary, in the other races, the best women performances were achieved later in life than men (i.e., 4 miles and 30 km: 2 years later, 8 km: 3 years later, 15–20–25 km: 1 year later, 10 miles: 4 years) or at the same age (i.e., 5, 10, 12 km). Moreover, age of peak performance did not change monotonically with the distance of race. For all races, except 12 km, sex differences had an absolute maximum at old ages and a relative maximum near the age of peak performance. From 8 km onward, estimated sex differences were increasing with increasing race distance. Regarding country, runners from Canada were slower than runners from the United States of America in 5 km by 00:10:05 h:min:s (p < 0.001) and in half-marathon by 00:18:43 h:min:s (p < 0.01). On the contrary, in marathon, they were 00:18:43 h:min faster (p < 0.05). Moreover, in 10 miles, runners from Great Britain were 00:02:53 h:min:s faster (p < 0.05) than runners from the United States of America. In summary, differences seem to exist in the age of peak performance between women and men and for nearly all distances sex differences showed an absolute maximum at old ages and relative maximum near the age of peak performance. Thus, these findings highlight the need for sex-specific training programs, especially near the age of peak performance and for elder runners

PET imaging of putative microglial activation in individuals at ultra-high risk for psychosis, recently diagnosed and chronically ill with schizophrenia

We examined putative microglial activation as a function of illness course in schizophrenia. Microglial activity was quantified using [11C](R)-(1-[2-chrorophynyl]-N-methyl-N-[1-methylpropyl]-3 isoquinoline carboxamide (11C-(R)-PK11195) positron emission tomography (PET) in: (i) 10 individuals at ultra-high risk (UHR) of psychosis; (ii) 18 patients recently diagnosed with schizophrenia; (iii) 15 patients chronically ill with schizophrenia; and, (iv) 27 age-matched healthy controls. Regional-binding potential (BPND) was calculated using the simplified reference-tissue model with four alternative reference inputs. The UHR, recent-onset and chronic patient groups were compared to age-matched healthy control groups to examine between-group BPND differences in 6 regions: dorsal frontal, orbital frontal, anterior cingulate, medial temporal, thalamus and insula. Correlation analysis tested for BPND associations with gray matter volume, peripheral cytokines and clinical variables. The null hypothesis of equality in BPND between patients (UHR, recent-onset and chronic) and respective healthy control groups (younger and older) was not rejected for any group comparison or region. Across all subjects, BPND was positively correlated to age in the thalamus (r=0.43, P=0.008, false discovery rate). No correlations with regional gray matter, peripheral cytokine levels or clinical symptoms were detected. We therefore found no evidence of microglial activation in groups of individuals at high risk, recently diagnosed or chronically ill with schizophrenia. While the possibility of 11C-(R)-PK11195-binding differences in certain patient subgroups remains, the patient cohorts in our study, who also displayed normal peripheral cytokine profiles, do not substantiate the assumption of microglial activation in schizophrenia as a regular and defining feature, as measured by 11C-(R)-PK11195 BPND.M A Di Biase, A Zalesky, G O'keefe, L Laskaris, B T Baune, C S Weickert, J Olver, P D McGorry, G P Amminger, B Nelson, A M Scott, I Hickie, R Banati, F Turkheimer, M Yaqub, I P Everall, C Pantelis and V Crople

Cell type-specific manifestations of cortical thickness heterogeneity in schizophrenia

Brain morphology differs markedly between individuals with schizophrenia, but the cellular and genetic basis of this heterogeneity is poorly understood. Here, we sought to determine whether cortical thickness (CTh) heterogeneity in schizophrenia relates to interregional variation in distinct neural cell types, as inferred from established gene expression data and person-specific genomic variation. This study comprised 1849 participants in total, including a discovery (140 cases and 1267 controls) and a validation cohort (335 cases and 185 controls). To characterize CTh heterogeneity, normative ranges were established for 34 cortical regions and the extent of deviation from these ranges was measured for each individual with schizophrenia. CTh deviations were explained by interregional gene expression levels of five out of seven neural cell types examined: (1) astrocytes; (2) endothelial cells; (3) oligodendrocyte progenitor cells (OPCs); (4) excitatory neurons; and (5) inhibitory neurons. Regional alignment between CTh alterations with cell type transcriptional maps distinguished broad patient subtypes, which were validated against genomic data drawn from the same individuals. In a predominantly neuronal/endothelial subtype (22% of patients), CTh deviations covaried with polygenic risk for schizophrenia (sczPRS) calculated specifically from genes marking neuronal and endothelial cells (r = −0.40, p = 0.010). Whereas, in a predominantly glia/OPC subtype (43% of patients), CTh deviations covaried with sczPRS calculated from glia and OPC-linked genes (r = −0.30, p = 0.028). This multi-scale analysis of genomic, transcriptomic, and brain phenotypic data may indicate that CTh heterogeneity in schizophrenia relates to inter-individual variation in cell-type specific functions. Decomposing heterogeneity in relation to cortical cell types enables prioritization of schizophrenia subsets for future disease modeling efforts

Reply to: New Meta- and Mega-analyses of Magnetic Resonance Imaging Findings in Schizophrenia: Do They Really Increase Our Knowledge About the Nature of the Disease Process?

This work was supported by National Institute of Biomedical Imaging and Bioengineering Grant No. U54EB020403 (to the ENIGMA consortium)

Psychosis brain subtypes validated in first-episode cohorts and related to illness remission:results from the PHENOM consortium

© The Author(s) 2023. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.Using machine learning, we recently decomposed the neuroanatomical heterogeneity of established schizophrenia to discover two volumetric subgroups—a ‘lower brain volume’ subgroup (SG1) and an ‘higher striatal volume’ subgroup (SG2) with otherwise normal brain structure. In this study, we investigated whether the MRI signatures of these subgroups were also already present at the time of the first-episode of psychosis (FEP) and whether they were related to clinical presentation and clinical remission over 1-, 3-, and 5-years. We included 572 FEP and 424 healthy controls (HC) from 4 sites (Sao Paulo, Santander, London, Melbourne) of the PHENOM consortium. Our prior MRI subgrouping models (671 participants; USA, Germany, and China) were applied to both FEP and HC. Participants were assigned into 1 of 4 categories: subgroup 1 (SG1), subgroup 2 (SG2), no subgroup membership (‘None’), and mixed SG1 + SG2 subgroups (‘Mixed’). Voxel-wise analyses characterized SG1 and SG2 subgroups. Supervised machine learning analyses characterized baseline and remission signatures related to SG1 and SG2 membership. The two dominant patterns of ‘lower brain volume’ in SG1 and ‘higher striatal volume’ (with otherwise normal neuromorphology) in SG2 were identified already at the first episode of psychosis. SG1 had a significantly higher proportion of FEP (32%) vs. HC (19%) than SG2 (FEP, 21%; HC, 23%). Clinical multivariate signatures separated the SG1 and SG2 subgroups (balanced accuracy = 64%; p < 0.0001), with SG2 showing higher education but also greater positive psychosis symptoms at first presentation, and an association with symptom remission at 1-year, 5-year, and when timepoints were combined. Neuromorphological subtypes of schizophrenia are already evident at illness onset, separated by distinct clinical presentations, and differentially associated with subsequent remission. These results suggest that the subgroups may be underlying risk phenotypes that could be targeted in future treatment trials and are critical to consider when interpreting neuroimaging literature.Supported by NIH grant R01MH112070 and the National Health and Medical Research Council (NHMRC) grant GA126980. Russel Shinohara was supported by the NIH grant R01M123550. RCG was supported by the NIH grant R01MH119219.Open Access funding enabled and organized by CAUL and its Member Institutions.Peer reviewe

Higher levels of glutamate in the associative-striatum of subjects with prodromal symptoms of schizophrenia and patients with first-episode psychosis

The glutamatergic and dopaminergic systems are thought to be involved in the pathophysiology of schizophrenia. Their interaction has been widely documented and may have a role in the neurobiological basis of the disease. The aim of this study was to compare, using proton magnetic resonance spectroscopy (1H-MRS), glutamate levels in the precommissural dorsal-caudate (a dopamine-rich region) and the cerebellar cortex (negligible for dopamine) in the following: (1) 18 antipsychotic-naïve subjects with prodromal symptoms and considered to be at ultra high-risk for schizophrenia (UHR), (2) 18 antipsychotic-naïve first- episode psychosis patients (FEP), and (3) 40 age- and sex- matched healthy controls. All subjects underwent a 1H-MRS study using a 3Tesla scanner. Glutamate levels were quantified and corrected for the proportion of cerebrospinal fluid and percentage of gray matter in the voxel. The UHR and FEP groups showed higher levels of glutamate than controls, without differences between UHR and FEP. In the cerebellum, no differences were seen between the three groups. The higher glutamate level in the precommissural dorsal-caudate and not in the cerebellum of UHR and FEP suggests that a high glutamate level (a) precedes the onset of schizophrenia, and (b) is present in a dopamine-rich region previously implicated in the pathophysiology of schizophrenia.peer-reviewe

Cognitive functioning throughout adulthood and illness stages in individuals with psychotic disorders and their unaffected siblings

Important questions remain about the profile of cognitive impairment in psychotic disorders across adulthood and illness stages. The age-associated profile of familial impairments also remains unclear, as well as the effect of factors, such as symptoms, functioning, and medication. Using cross-sectional data from the EU-GEI and GROUP studies, comprising 8455 participants aged 18 to 65, we examined cognitive functioning across adulthood in patients with psychotic disorders (n = 2883), and their unaffected siblings (n = 2271), compared to controls (n = 3301). An abbreviated WAIS-III measured verbal knowledge, working memory, visuospatial processing, processing speed, and IQ. Patients showed medium to large deficits across all functions (ES range = –0.45 to –0.73, p < 0.001), while siblings showed small deficits on IQ, verbal knowledge, and working memory (ES = –0.14 to –0.33, p < 0.001). Magnitude of impairment was not associated with participant age, such that the size of impairment in older and younger patients did not significantly differ. However, first-episode patients performed worse than prodromal patients (ES range = –0.88 to –0.60, p < 0.001). Adjusting for cannabis use, symptom severity, and global functioning attenuated impairments in siblings, while deficits in patients remained statistically significant, albeit reduced by half (ES range = –0.13 to –0.38, p < 0.01). Antipsychotic medication also accounted for around half of the impairment in patients (ES range = –0.21 to –0.43, p < 0.01). Deficits in verbal knowledge, and working memory may specifically index familial, i.e., shared genetic and/or shared environmental, liability for psychotic disorders. Nevertheless, potentially modifiable illness-related factors account for a significant portion of the cognitive impairment in psychotic disorders