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Ninth-century Alī Abū Nāfi, famously known as Ziryāb, fled Baghdad and established himself as the most celebrated musician and arbiter of high style and sophisticated dining in the Cordovan courts of Muslim Spain. While this should not be surprising as he left when Abbasid gastronomy had already reached a high level of sophistication, the modern narratives of him extolling the role he played in revolutionising the dining experiences he had on al-Andalus and the rest of Europe ever after are exaggeratedly portrayed and even fallacious at times. The aim of the article, therefore, is to sift through some of the representative modern accounts of him - they are largely based on early modern translations of Arabic sources - and try to figure out how inaccuracies and misinformation could have crept in. A primary source is used in straightening the record. It is the account of Ibn Ḥayyān al-Qurṭubī, the most detailed and the closest to Ziryāb's time but the latest to have been discovered. It is edited in Arabic only and has not been made use of regarding the role he played in shaping the Andalusi cuisine. That is in addition to what we know of it today through the two medieval Andalusi cookbooks that survived from the region. [ABSTRACT FROM AUTHOR]

INTRODUCTION: Anti‐amyloid antibody therapies such as lecanemab are increasingly being used to treat Alzheimer's disease (AD). These therapies are associated with a high rate of amyloid‐related imaging abnormalities (ARIA). METHODS: We review the case history of a patient who developed ARIA associated with lecanemab treatment. RESULTS: In addition to microhemorrhages and cerebral edema that are recognized features of ARIA, the patient developed several ischemic strokes. The patient also experienced frequent electrographic seizures without overt clinical seizures. The patient demonstrated clinical and radiographic improvement after steroid treatment. DISCUSSION: Our case suggests that ischemic strokes may be a feature of ARIA and highlights the importance of having a high clinical suspicion for seizures in ARIA. As anti‐amyloid therapies are likely going to be increasingly used to treat AD, it is important to appreciate the spectrum of clinical and radiographic findings that can result as side effects from this class of therapies. Highlights: We report a patient who developed severe amyloid‐related imaging abnormalities (ARIA) after treatment with lecanemab.Our report suggests that ischemic strokes may be a novel imaging feature of ARIA.Our report highlights the need for high clinical suspicion for seizures in ARIA. [ABSTRACT FROM AUTHOR]

INTRODUCTION: Typical MRI measures of neurodegeneration have limited sensitivity in early disease stages. Diffusion MRI (dMRI) microstructural measures may allow for detection in preclinical stages. METHODS: Participants had dMRI and either beta‐amyloid PET or plasma biomarkers of Alzheimer's pathology within 18 months of MRI. Microstructure was measured in portions of the medial temporal lobe (MTL) with high neurofibrillary tangle (NFT) burden based on a previously developed post mortem 3D‐map. Regressions examined relationships between microstructure and markers of Alzheimer's pathology in preclinical disease and then across disease stages. RESULTS: There was higher isometric volume fraction in amyloid‐positive compared to amyloid‐negative cognitively unimpaired individuals in high tangle MTL regions. Similarly, plasma biomarkers and 18F‐flortaucipir were associated with microstructural changes in preclinical disease. Additional microstructural effects were seen across disease stages. DISCUSSION: Combining a post mortem atlas of NFT pathology with microstructural measures allows for detection of neurodegeneration in preclinical Alzheimer's disease. Highlights: Typical markers of neurodegeneration are not sensitive in preclinical Alzheimer's.dMRI measured microstructure in regions with high NFT.Microstructural changes occur in medial temporal regions in preclinical disease.Microstructural changes occur in other typical Alzheimer's regions in later stages.Combining post mortem pathology atlases with in vivo MRI is a powerful framework. [ABSTRACT FROM AUTHOR]

INTRODUCTION: We investigate pathological correlates of plasma phosphorylated tau 181 (p‐tau181), glial fibrillary acidic protein (GFAP), and neurofilament light chain (NfL) across a clinically diverse spectrum of neurodegenerative disease, including normal cognition (NormCog) and impaired cognition (ImpCog). METHODS: Participants were NormCog (n = 132) and ImpCog (n = 461), with confirmed β‐amyloid (Aβ+/‐) status (cerebrospinal fluid, positron emission tomography, autopsy) and single molecule array plasma measurements. Logistic regression and receiver operating characteristic (ROC) area under the curve (AUC) tested how combining plasma analytes discriminated Aβ+ from Aβ‐. Survival analyses tested time to clinical dementia rating (global CDR) progression. RESULTS: Multivariable models (p‐tau+GFAP+NfL) had the best performance to detect Aβ+ in NormCog (ROCAUC = 0.87) and ImpCog (ROCAUC = 0.87). Survival analyses demonstrated that higher NfL best predicted faster CDR progression for both Aβ+ (hazard ratio [HR] = 2.94; p = 8.1e‐06) and Aβ‐ individuals (HR = 3.11; p = 2.6e‐09). DISCUSSION: Combining plasma biomarkers can optimize detection of Alzheimer's disease (AD) pathology across cognitively normal and clinically diverse neurodegenerative disease. Highlights: Participants were clinically heterogeneous, with autopsy‐ or biomarker‐confirmed Aβ.Combining plasma p‐tau181, GFAP, and NfL improved diagnostic accuracy for Aβ status.Diagnosis by plasma biomarkers is more accurate in amnestic AD than nonamnestic AD.Plasma analytes show independent associations with tau PET and post mortem Aβ/tau.Plasma NfL predicted longitudinal cognitive decline in both Aβ+ and Aβ‐ individuals. [ABSTRACT FROM AUTHOR]

This cohort study investigates the patterns of morphological brain changes that are reproducibly detectable with artificial intelligence (AI) in cognitively unimpaired populations and their genetic, clinical, lifestyle, and cognitive features. Key Points: Question: What patterns of morphological brain changes are reproducibly detectable in cognitively unimpaired populations, and what are their genetic, clinical, lifestyle, and cognitive features? Findings: In this multistudy harmonized cohort of 27 402 individuals aged 45 to 85 years without diagnosed cognitive impairment, 3 subgroups of structural brain measures in decade-spanning groups in a data-driven manner were found: 1 typical and 2 accelerated aging subgroups, displaying distinct associations with genetics, cognitive decline, cardiovascular risk factors, and amyloid pathology. Meaning: Three genetically distinct and longitudinally stable subgroups display brain changes reflecting differential susceptibility to Alzheimer disease and other neurodegenerative diseases, cognitive decline, and clinical progression. Importance: Brain aging elicits complex neuroanatomical changes influenced by multiple age-related pathologies. Understanding the heterogeneity of structural brain changes in aging may provide insights into preclinical stages of neurodegenerative diseases. Objective: To derive subgroups with common patterns of variation in participants without diagnosed cognitive impairment (WODCI) in a data-driven manner and relate them to genetics, biomedical measures, and cognitive decline trajectories. Design, Setting, and Participants: Data acquisition for this cohort study was performed from 1999 to 2020. Data consolidation and harmonization were conducted from July 2017 to July 2021. Age-specific subgroups of structural brain measures were modeled in 4 decade-long intervals spanning ages 45 to 85 years using a deep learning, semisupervised clustering method leveraging generative adversarial networks. Data were analyzed from July 2021 to February 2023 and were drawn from the Imaging-Based Coordinate System for Aging and Neurodegenerative Diseases (iSTAGING) international consortium. Individuals WODCI at baseline spanning ages 45 to 85 years were included, with greater than 50 000 data time points. Exposures: Individuals WODCI at baseline scan. Main Outcomes and Measures: Three subgroups, consistent across decades, were identified within the WODCI population. Associations with genetics, cardiovascular risk factors (CVRFs), amyloid β (Aβ), and future cognitive decline were assessed. Results: In a sample of 27 402 individuals (mean [SD] age, 63.0 [8.3] years; 15 146 female [55%]) WODCI, 3 subgroups were identified in contrast with the reference group: a typical aging subgroup, A1, with a specific pattern of modest atrophy and white matter hyperintensity (WMH) load, and 2 accelerated aging subgroups, A2 and A3, with characteristics that were more distinct at age 65 years and older. A2 was associated with hypertension, WMH, and vascular disease–related genetic variants and was enriched for Aβ positivity (ages ≥65 years) and apolipoprotein E (APOE) ε4 carriers. A3 showed severe, widespread atrophy, moderate presence of CVRFs, and greater cognitive decline. Genetic variants associated with A1 were protective for WMH (rs7209235: mean [SD] B = −0.07 [0.01]; P value = 2.31 × 10−9) and Alzheimer disease (rs72932727: mean [SD] B = 0.1 [0.02]; P value = 6.49 × 10−9), whereas the converse was observed for A2 (rs7209235: mean [SD] B = 0.1 [0.01]; P value = 1.73 × 10−15 and rs72932727: mean [SD] B = −0.09 [0.02]; P value = 4.05 × 10−7, respectively); variants in A3 were associated with regional atrophy (rs167684: mean [SD] B = 0.08 [0.01]; P value = 7.22 × 10−12) and white matter integrity measures (rs1636250: mean [SD] B = 0.06 [0.01]; P value = 4.90 × 10−7). Conclusions and Relevance: The 3 subgroups showed distinct associations with CVRFs, genetics, and subsequent cognitive decline. These subgroups likely reflect multiple underlying neuropathologic processes and affect susceptibility to Alzheimer disease, paving pathways toward patient stratification at early asymptomatic stages and promoting precision medicine in clinical trials and health care. [ABSTRACT FROM AUTHOR]

INTRODUCTION: Vascular risk factors contribute to cognitive decline suggesting that maintaining cerebrovascular health could reduce dementia risk. The objective of this study is to evaluate the association of cerebrovascular reactivity (CVR), a measure of brain blood vessel elasticity, with mild cognitive impairment (MCI) and dementia. METHODS: Participants were enrolled in the Systolic Blood Pressure Intervention Trial Memory and Cognition in Decreased Hypertension (SPRINT‐MIND) magnetic resonance imaging substudy. Baseline CVR in Alzheimer's disease (AD) signature regions were primary variables of interest. The occipital pole and postcentral gyrus were included as control regions. RESULTS: Higher AD composite CVR was associated with lower MCI risk. No significant associations between inferior temporal gyrus, occipital pole, or postcentral gyrus CVR and MCI risk, or any regional CVR–combined risk associations were observed. DISCUSSION: CVR in AD signature regions is negatively associated with occurrence of MCI, implicating CVR in AD signature regions as a potential mechanism leading to cognitive impairment. [ABSTRACT FROM AUTHOR]

INTRODUCTION: Variability in relationship of tau‐based neurofibrillary tangles (T) and neurodegeneration (N) in Alzheimer's disease (AD) arises from non‐specific nature of N, modulated by non‐AD co‐pathologies, age‐related changes, and resilience factors. METHODS: We used regional T‐N residual patterns to partition 184 patients within the Alzheimer's continuum into data‐driven groups. These were compared with groups from 159 non‐AD (amyloid "negative") patients partitioned using cortical thickness, and groups in 98 patients with ante mortem MRI and post mortem tissue for measuring N and T, respectively. We applied the initial T‐N residual model to classify 71 patients in an independent cohort into predefined groups. RESULTS: AD groups displayed spatial T‐N mismatch patterns resembling neurodegeneration patterns in non‐AD groups, similarly associated with non‐AD factors and diverging cognitive outcomes. In the autopsy cohort, limbic T‐N mismatch correlated with TDP‐43 co‐pathology. DISCUSSION: T‐N mismatch may provide a personalized approach for determining non‐AD factors associated with resilience/vulnerability in AD. [ABSTRACT FROM AUTHOR]

INTRODUCTION: Heart rate (HR) fragmentation indices quantify breakdown of HR regulation and are associated with atrial fibrillation and cognitive impairment. Their association with brain magnetic resonance imaging (MRI) markers of small vessel disease is unexplored. METHODS: In 606 stroke‐free participants of the Multi‐Ethnic Study of Atherosclerosis (mean age 67), HR fragmentation indices including percentage of inflection points (PIP) were derived from sleep study recordings. We examined PIP in relation to white matter hyperintensity (WMH) volume, total white matter fractional anisotropy (FA), and microbleeds from 3‐Tesla brain MRI completed 7 years later. RESULTS: In adjusted analyses, higher PIP was associated with greater WMH volume (14% per standard deviation [SD], 95% confidence interval [CI]: 2, 27%, P = 0.02) and lower WM FA (–0.09 SD per SD, 95% CI: –0.16, –0.01, P = 0.03). DISCUSSION: HR fragmentation was associated with small vessel disease. HR fragmentation can be measured automatically from ambulatory electrocardiogram devices and may be useful as a biomarker of vascular brain injury. [ABSTRACT FROM AUTHOR]

Background: We sought to validate two structural MRI‐based brain health models: Spatial Pattern of Atrophy for REcognition of Alzheimer's disease (SPARE‐AD) and SPARE‐Brain Age Gap (SPARE‐BAG), which estimates the discrepancy between biological brain age and chronological age. These models' generalization to non‐amnestic AD (naAD) syndromes and associations with positron emission tomography (PET) and plasma biomarkers remain underinvestigated. We hypothesized that SPARE‐AD scores in naAD would be lower (less abnormal) than in amnestic AD (aAD) but elevated (more abnormal) relative to controls; and that SPARE‐AD but not SPARE‐BAG scores would be associated with PET and plasma biomarkers of AD. Method: SPARE‐AD and SPARE‐BAG scores were estimated for each of 1607 MRI scans from 277 cognitively normal adults (62.8% female; mean age = 69.5 years) and 902 clinical participants (54.2% female; mean age = 73.1 years), including 585 with amnestic mild cognitive impairment (aMCI) or aAD; 56 with naAD syndromes; 28 with vascular disease; 28 with Lewy body disorders (LBD); 18 with suspected frontotemporal lobar degeneration (FTLD); 56 with non‐amnestic MCI of uncertain etiology; and 131 with other clinical diagnoses. We used mixed effects models adjusting for age, sex, and global cognition to test group differences in SPARE‐AD and SPARE‐BAG. Additionally, we assessed associations with tau (n = 122) and amyloid‐beta (n = 199) PET imaging and plasma‐based phosphorylated tau‐181 (p‐tau181) and glial fibrillary acidic protein (GFAP) (n = 358). Result: SPARE‐AD scores were elevated vs. controls in aMCI/aAD, naAD, vascular disease, FTLD, and naMCI (all p<0.003) but not in LBD or other diagnoses (p>0.1). NaAD patients had lower SPARE‐AD (p<0.02) but higher SPARE‐BAG scores (p<0.02) than aMCI/aAD patients. SPARE‐AD scores were positively associated with mean cortical tau PET uptake, amyloid PET positivity, and plasma p‐tau181 and GFAP (all p<0.001). In contrast, SPARE‐BAG scores were not associated with PET or plasma biomarkers (all p>0.05). Conclusion: SPARE‐AD values for naAD syndromes were intermediate between those of controls and aMCI/AD patients, likely reflecting divergent, partially overlapping cortical atrophy relative to aAD. PET and plasma biomarkers of AD neuropathologic change were associated with SPARE‐AD but not with SPARE‐BAG scores, suggesting SPARE‐BAG reflects age‐related atrophy that is largely independent of AD. [ABSTRACT FROM AUTHOR]

Background: Brain functional connectivity (FC) measures derived from resting‐state fMRI (rsfMRI) data have advanced our understanding of the brain organization. However, most existing studies investigate the brain functional networks (FNs) at a specific scale, ignoring potentially complementary FC information at different levels of spatial granularity as well as the cross‐scale information. Given that the brain is a multi‐scale, hierarchical system, FCs between FNs at different spatial scales may provide complementary information to those measured within‐scales for characterizing the aging brain. Method: We computed multiscale FNs to capture their FC measures across multiple scales and investigated the associations between cross‐scale FCs and the brain aging based on rsfMRI data of a diverse cohort (n = 4186, aged 22 to 97 years) from seven sites of the iSTAGING study [1]. For each subject, we computed the FNs at seven scales, yielding seven sets of k (k = 17, 25, 50, 75, 100, 125 and 150) FNs, same as our previous study [2‐3]. We estimated FC measures between the 542 FNs using Pearson's correlation, yielding the cross‐scale FC matrices that were harmonized across sites in the tangent space using ComBat‐GAM [4] with sex and age as covariates. The harmonized FC measures were used as features to build an age prediction model using Ridge regression as illustrated in Figure 1. The brain age prediction model was compared with that built on harmonized FC measures between FNs of the same scales, with the performance estimated with a nested five‐fold cross‐validation. Result: The cross‐scale FC measures performed significantly better than the within‐scale FC measures for the brain age prediction, as summarized in Table 1. Figure 2 shows the most informative FC measures for the brain age prediction. Specifically, FC measures computed both cross‐ and within‐scales between the visual, somatomotor, and frontoparietal networks provided relatively more useful information for the brain age prediction than FC measures between other FNs. Conclusion: Our study demonstrated that the cross‐scale FC measures provided complementary information to the within‐scale FC measures for predicting the brain age, facilitating enhanced understanding of aging related changes of the brain functional organization. [ABSTRACT FROM AUTHOR]

Background: Understanding heterogeneity of structural brain changes in aging may provide insights into susceptibility to neurodegenerative diseases. We characterize the genetics underlying brain structural heterogeneity within cognitively unimpaired (CU) individuals using data‐driven machine learning applied to a diverse dataset of 27,402 individuals from 11 neuroimaging studies from the iSTAGING consortium. Method: Structural brain morphologic patterns of CU individuals were independently examined in four decade‐long intervals spanning ages 45 to 85. Within each interval, Smile‐GAN (Yang et al., 2021) was trained on baseline anatomic and white matter hyperintensity (WMH) volumes. Smile‐GAN probability scores were used as phenotypes in genome‐wide association studies (GWAS). Specifically, we performed multiple linear regressions controlling for confounders (e.g., age) via Plink (Purcell et al., 2007). We observed longitudinal clustering stability across decades, so individuals from adjacent age groups were combined into broader age groups ([45,65), [65,85)) due to the large sample requirement of GWAS. Genomic loci, represented by the top leading single nucleotide polymorphisms (SNPs), were defined considering linkage disequilibrium. We investigated associations of SNPs with clinical traits and mapped them to genes using the GWAS Catalog (Buniello et al., 2019). Result: Three structural brain aging patterns, relative to resilient agers (A0), consistent across decades, emerged: A1, or 'typical' aging with low atrophy and WMHs, and two 'advanced' aging patterns, one showing elevated WMHs and modest atrophy (A2) and the other displaying severe, widespread atrophy and moderate WMH load (A3) (Figure 1). GWAS discovered eight and six genomic loci in [45,65) and [65,85) age groups, respectively (Table 1, Figure 2). The lead SNPs for A1 and A2 were previously associated with several cardiometabolic risk factors, WMHs, and regional brain volumes. Interestingly, rs4843552, previously associated with white matter microstructure and regional brain volumes, showed opposite effects for A1 (protection) and A2 (risk), consistent with the neuroimaging patterns. WDR41 in A3 group was previously associated with the age of Alzheimer's disease onset (Herold et al., 2016). Conclusion: Reproducible neuroimaging patterns defined by regional atrophy and WMH burden were identified across CU individuals and demonstrated unique genetics. Further research is needed to elucidate the neuropathological pathways that mediate these relationships. [ABSTRACT FROM AUTHOR]

Background: We sought to validate two structural MRI‐based brain health models: Spatial Pattern of Atrophy for REcognition of Alzheimer's disease (SPARE‐AD) and SPARE‐Brain Age Gap (SPARE‐BAG), which estimates the discrepancy between biological brain age and chronological age. These models' generalization to non‐amnestic AD (naAD) syndromes and associations with positron emission tomography (PET) and plasma biomarkers remain underinvestigated. We hypothesized that SPARE‐AD scores in naAD would be lower (less abnormal) than in amnestic AD (aAD) but elevated (more abnormal) relative to controls; and that SPARE‐AD but not SPARE‐BAG scores would be associated with PET and plasma biomarkers of AD. Method: SPARE‐AD and SPARE‐BAG scores were estimated for each of 1607 MRI scans from 277 cognitively normal adults (62.8% female; mean age = 69.5 years) and 902 clinical participants (54.2% female; mean age = 73.1 years), including 585 with amnestic mild cognitive impairment (aMCI) or aAD; 56 with naAD syndromes; 28 with vascular disease; 28 with Lewy body disorders (LBD); 18 with suspected frontotemporal lobar degeneration (FTLD); 56 with non‐amnestic MCI of uncertain etiology; and 131 with other clinical diagnoses. We used mixed effects models adjusting for age, sex, and global cognition to test group differences in SPARE‐AD and SPARE‐BAG. Additionally, we assessed associations with tau (n = 122) and amyloid‐beta (n = 199) PET imaging and plasma‐based phosphorylated tau‐181 (p‐tau181) and glial fibrillary acidic protein (GFAP) (n = 358). Result: SPARE‐AD scores were elevated vs. controls in aMCI/aAD, naAD, vascular disease, FTLD, and naMCI (all p<0.003) but not in LBD or other diagnoses (p>0.1). NaAD patients had lower SPARE‐AD (p<0.02) but higher SPARE‐BAG scores (p<0.02) than aMCI/aAD patients. SPARE‐AD scores were positively associated with mean cortical tau PET uptake, amyloid PET positivity, and plasma p‐tau181 and GFAP (all p<0.001). In contrast, SPARE‐BAG scores were not associated with PET or plasma biomarkers (all p>0.05). Conclusion: SPARE‐AD values for naAD syndromes were intermediate between those of controls and aMCI/AD patients, likely reflecting divergent, partially overlapping cortical atrophy relative to aAD. PET and plasma biomarkers of AD neuropathologic change were associated with SPARE‐AD but not with SPARE‐BAG scores, suggesting SPARE‐BAG reflects age‐related atrophy that is largely independent of AD. [ABSTRACT FROM AUTHOR]

This study performs a comprehensive bibliometric analysis of biomedical (i.e., non-brain) technology such as eye-tracking (ET), electromyography (EMG), galvanic skin response (GSR), implicit association test (IAT), and electrocardiogram (ECG) tools in studying consumer' behavior. To achieve this aim, we adopted the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) protocol and bibliometric analysis (VOSviewer software) for extracting the relevant documents from the Web of Science (WOS) database between 2013 and June 2023. A total of 58 documents (fifty-one articles and seven review articles) were included in the analysis. The results showed an increasing trend in publications over the years--the top countries in terms of publication outcome were Spain (13 papers) and the USA (10 papers). The analysis also identified the most influential authors, such as Babiloni, F. and Cherubino, P. It was further analyzed for the most cited article, which is titled "Neurophysiological Tools to Investigate Consumer's Gender Differences during the Observation of TV Commercials", and keywords related to neuromarketing and non-brain tools. Additionally, Frontiers in Psychology was determined as the most-productive journal. This bibliometric analysis reveals insights into the current state of non-brain tools research. It also provides insights into future research directions in the consumer neuroscience field. This study will provide general insights and details about current trends in consumer neuroscience research using biomedical technology. [ABSTRACT FROM AUTHOR]

Evidence on the effectiveness of vaccination-induced immunity compared to SARS-CoV-2 natural immunity is warranted to inform vaccination recommendations. In this study, we aimed to conduct a comparative assessment of antibody responses between vaccinated naïve (VN) and unvaccinated naturally infected individuals (NI) over 10 Months. The study comprised fully-vaccinated naïve individuals (VN; n = 596) who had no history of SARS-CoV-2 infection, and received two doses of either BNT162b2 or mRNA-1273, and naturally infected individuals who had a documented history of SARS-CoV-2 infection and no vaccination record (NI cohort; n = 218). We measured the levels of neutralizing total antibodies (NtAbs), anti-S-RBD IgG, and anti-S1 IgA titers among VN and NI up to ∼10 months from administration of the first dose, and up to ∼7 months from SARS-CoV-2 infection, respectively. To explore the relationship between the antibody responses and time, Spearman's correlation coefficient was computed. Furthermore, correlations between the levels of NtAbs/anti-S-RBD IgG and NtAbs/anti-S1 IgA were examined through pairwise correlation analysis. Up to six months, VN individuals had a significantly higher NtAb and anti-S-RBD IgG antibody responses compared to NI individuals. At the 7th month, there was a significant decline in antibody responses among VN individuals, but not NI individuals, with a minimum decrease of 3.7-fold (p < 0.001). Among VN individuals, anti-S1 IgA levels began to decrease significantly (1.4-fold; p = 0.007) after two months, and both NtAb and S-RBD IgG levels began to decline significantly (NtAb: 2.0-fold; p = 0.042, S-RBD IgG: 2.4-fold; p = 0.035) after three months. After 10 months, the most significant decline among VN individuals was observed for S-RBD-IgG (30.0-fold; P < 0.001), followed by NtAb (15.7-fold; P < 0.001) and S-IgA (3.7-fold; P < 0.001) (most stable). Moreover, after 5 months, there was no significant difference in the IgA response between the two groups. These findings have important implications for policymakers in the development of vaccination strategies, particularly in the consideration of booster doses to sustain long-lasting protection against COVID-19. [ABSTRACT FROM AUTHOR]

Introduction: Iron plays a significant role in energy production. However, it is not uncommon for athletes to be diagnosed with iron deficiency (ID), suggesting a correlation between performance and iron regulation. As a result, the International Olympic Committee has recommended iron screenings during health evaluations for elite athletes. Furthermore, athletes participating in esthetic sports are at increased risk for suboptimal iron intake due to disordered eating. Therefore, the purpose of this study was to investigate the distribution of serum ferritin (SF) in a cohort of elite ballet dancers and determine associations between vitamin D, anthropometric measures, stress injury, and dietary preferences. Methods: Electronic health records of 40 elite ballet dancers (22 female, 18 male), age 19 to 38 years old, from the 2020 to 2021 pre-participation physical screening were examined. Chi squared comparisons were calculated to evaluate the association between SF and additional variables (ie, gender, age, height, weight, body mass index, vitamin D, stress injury history, and dietary preferences). SF values were compared to published normal and athletic population data. Results: 58.97% of participants displayed normal or above SF values (>50 ng/ml), while 41.02% displayed minimal (<50 ng/ml) to depleted (<0.12/ng/ml) SF values. Approximately, 68% of the female dancers were ID and did not meet the minimal value needed for athletes. Females were more likely to have lower SF distributions (x² [4] = 15.6377, P = .004) compared to male dancers. Additionally, dancers who reported dietary preferences (ie, vegetarian) were more likely to display lower SF distributions (x² [4] = 13.3366, P = .010). Conclusion: Over half of the female elite ballet dancers were ID which is consistent with current research. Females were at a significant higher risk compared to male dancers who reported dietary preferences. These findings suggest iron screenings should be considered in elite dancer populations. [ABSTRACT FROM AUTHOR]

INTRODUCTION: Little is known about the epidemiology of brain microbleeds in racially/ethnically diverse populations. METHODS: In the Multi‐Ethnic Study of Atherosclerosis, brain microbleeds were identified from 3T magnetic resonance imaging susceptibility‐weighted imaging sequences using deep learning models followed by radiologist review. RESULTS: Among 1016 participants without prior stroke (25% Black, 15% Chinese, 19% Hispanic, 41% White, mean age 72), microbleed prevalence was 20% at age 60 to 64.9 and 45% at ≥85 years. Deep microbleeds were associated with older age, hypertension, higher body mass index, and atrial fibrillation, and lobar microbleeds with male sex and atrial fibrillation. Overall, microbleeds were associated with greater white matter hyperintensity volume and lower total white matter fractional anisotropy. DISCUSSION: Results suggest differing associations for lobar versus deep locations. Sensitive microbleed quantification will facilitate future longitudinal studies of their potential role as an early indicator of vascular pathology. [ABSTRACT FROM AUTHOR]

Glycine assisted self-combustion method resulted in fabrication of cobalt-manganese ferrite substituted by zinc (Zn) element. The as- synthesized Zn substituted Co- Mn ferrite was subjected to heat treatment at 600 oC and 800 oC for 2h. Effects of heat treatment on the structural, morphological, surface and magnetic properties of ZnCoMn ferrite were studied. These properties were characterized by using various techniques including TGA-DTGA, FTIR, XRD, SEM, EDX, TEM and VSM. The results showed that the used preparation route led to the formation of nano crystalline Zn0.2Co0.4Mn0.4Fe2O4 particle with cubic spinel type structure. The crystallinity of this ferrite increases as the heat treatment increases. However, the preparation method resulted to the creation of spongy, fluffy, foamy and fragile material with cubic type structure with some agglomerations. Increasing the calcination temperature from 600 oC to 800 oC, led to a decrease in the surface area (39.4 %) of the as- synthesized ferrite. This treatment causes an increase in the magnetization(40.3 %) of this ferrite. The heat treatment that led to various changes in the different properties of the manufactured ferrite was discussed. [ABSTRACT FROM AUTHOR]