Search

IntroductionThe end of the coronavirus disease 2019 (COVID-19) pandemic has been declared by the World Health Organization on May 5, 2023. Several vaccines were developed, and new data is being published about their effectiveness. However, the clinical trials for the vaccines were performed before the Omicron variant appeared and there are population groups where vaccine effectiveness still needs to be tested. The overarching goal of the present study was to analyze the effects of COVID-19 vaccination before and after the Omicron variant in patients considering comorbidities in a population from Nuevo Leon, Mexico.MethodsEpidemiological COVID-19 data from the Mexican Social Security Institute were collected from 67 hospitals located in northeastern Mexico, from July 2020 to May 2023, and a total of 669,393 cases were compiled, 255,819 reported a SARS-CoV-2 positive reverse transcription quantitative polymerase chain reaction (RT-qPCR) test or a positive COVID-19 antigen rapid test.ResultsBefore Omicron (BO, 2020-2021), after 14 days of two doses of COVID-19 vaccine, BNT162b2 and ChAdOx1 vaccines were effective against infection in non-comorbid and all comorbid subgroups, whereas after Omicron (AO, 2022- 2023) there was no significant effectiveness against infection with none of the vaccines. Regarding hospitalization BO, BNT162b2, ChAdOx1, CoronaVac and mRNA-1273 significantly protected non-comorbid patients whereas BNT162b2, ChAdOx1, and mRNA-1273, protected all comorbid subgroups against hospitalization. AO, BNT162b2, ChAdOx1, CoronaVac and mRNA-1273 were effective against hospitalization in non-comorbid patients whereas for most comorbid subgroups BNT162b2, ChAdOx1 and CoronaVac were effective against hospitalization. Non-comorbid patients were protected against death as an outcome of COVID-19 during the BO period with most vaccines whereas a reduction in effectiveness was observed AO with mRNA-1273 vaccines in patients with hypertension, and diabetes mellitus.DiscussionBO, COVID-19 vaccines were effective against infection, hospitalization, and death whereas AO, COVID-19 vaccines failed to protect the population from COVID-19 infection. A varying effectiveness against hospitalization and death is observed AO.

Summary: Background: Neuroimaging-based brain-age delta has been shown to be a mediator linking cardiovascular risk factors to cognitive function. We aimed to assess the mediating role of brain-age delta in the association between modifiable risk factors of dementia and longitudinal cognitive decline in middle-aged and older individuals who are asymptomatic, stratified by Alzheimer's disease pathology. We also explored whether the mediation effect is specific to cognitive domain. Methods: In this cohort study, we included participants from the ALFA+ cohort aged between 45 years and 65 years who were cognitively unimpaired and who had available structural MRI, cerebrospinal fluid β-amyloid (Aβ)42 and Aβ40 measurements obtained within 1 year of each other, modifiable risk factors assessment, and cognitive evaluation over 3 years. Participants were recruited from the Barcelonaβeta Brain Research Center (Barcelona, Spain). Included individuals underwent a first assessment between Oct 25, 2016, and Jan 28, 2020, and a follow-up cognitive assessment 3·28 (SD 0·27) years later. We computed brain-age delta and composites of different cognitive function domains (preclinical Alzheimer's cognitive composite [PACC], attention, executive function, episodic memory, visual processing, and language). We used partial least squares path modelling to explore mediation effects in the associations between modifiable risk factors (including cardiovascular, mental health, mood, metabolic or endocrine history, and alcohol use) and changes in cognitive composites. To assess the role of Alzheimer's disease pathology, we computed separate models for Aβ-negative and Aβ-positive individuals. Findings: Of the 419 participants enrolled in ALFA+, 302 met our inclusion criteria, of which 108 participants were classified as Aβ-positive and 194 as Aβ-negative. In Aβ-positive individuals, brain-age delta partially mediated (percent mediation proportion 15·73% [95% CI 14·22–16·66]) the association between modifiable risk factors and decline in overall cognition (across cognitive domains). Brain-age delta fully mediated (mediation proportion 28·03% [26·25–29·21]) the effect of modifiable risk factors on the PACC, wherein increased values for risk factors correlated with an older brain-age delta, and, consequently, an older brain-age delta was linked to greater PACC decline. This effect appears to be primarily driven by memory decline. Mediation was not significant in Aβ-negative individuals (3·52% [0·072–4·17]) on PACC, although path coefficients were not significantly different from those in the Aβ-positive group. Interpretation: Our findings suggest that brain-age delta captures the association between modifiable risk factors and longitudinal cognitive decline in middle-aged and older people. In asymptomatic middle-aged and older individuals who are Aβ-positive, the pathology might be the strongest driver of cognitive decline, whereas the effect of risk factors is smaller. Our results highlight the potential of brain-age delta as an objective outcome measure for preventive lifestyle interventions targeting cognitive decline. Funding: La Caixa Foundation, the TriBEKa Imaging Platform, and the Universities and Research Secretariat of the Catalan Government. Translation: For the Spanish translation of the abstract see Supplementary Materials section.

El posgrado constituye uno de los procesos universitarios de mayor importancia para la formación de profesionales competentes en función de lograr una sociedad más próspera y sostenible, por su incidencia en la actualización de conocimientos y en el desarrollo de habilidades en temas priorizados del desarrollo local, en aras de ganar en productividad y calidad de forma sistemática y oportuna. El presente artículo tiene como objetivo: diseñar un procedimiento para evaluar la calidad del posgrado en el Centro Universitario Municipal Jobabo (CUM Jobabo) de la Provincia de Las Tunas. Como resultado de la aplicación de métodos y técnicas científicas, se sistematizaron referentes teóricos y herramientas metodológicas valiosas para el diseño del procedimiento, el cual constituye un aporte metodológico para la evaluación de la calidad del posgrado y favorece la gestión de la calidad de este proceso en la referida institución. Como resultado de la valoración de la pertinencia del procedimiento, se obtuvo una opinión muy favorable de los especialistas en el tema, y se propone su generalización total en el CUM Jobabo. La herramienta diseñada constituye un referente importante de las investigaciones en el objeto y el campo investigado.

Abstract Background Mortality due to tuberculosis (TB) has increased due to the development of drug resistance, the mechanisms of which have not been fully elucidated. Our research group identified a low expression of lipF gene in Mycobacterium tuberculosis clinical isolates with drug resistance. The aim of this work was to evaluate the effect of lipase F (LipF) expression on mycobacterial drug resistance. Results The effects of expressing lipF from Mycobacterium tuberculosis in Mycobacterium smegmatis on resistance to antituberculosis drugs were determined with resazurin microtiter assay plate and growth kinetics. Functionality of ectopic LipF was confirmed. LipF expression reduced the rifampicin (RIF) and streptomycin (STR) minimum inhibitory concentration (MIC) from 3.12 μg/mL to 1.6 μg/mL and 0.25 μg/mL to 0.06 μg/mL respectively, moreover a reduced M. smegmatis growth in presence of RIF and STR compared with that of a control strain without LipF expression (p

The emergence of multidrug-resistant (MDR) Mycobacterium tuberculosis strains threaten the control of tuberculosis. New antitubercular dihydrosphingosine analogs, named UCIs, have been evaluated in preclinical studies but their cellular and molecular mechanisms of action against M. tuberculosis are still unknown. The aim of this study was to evaluate the effect of UCI exposure on gene expression of drug-sensitive H37Rv and MDR CIBIN:UMF:15:99 clones of M. tuberculosis which were isolated, phenotypically, and genetically characterized, cultured to log phase and treated with UCI compounds; followed by total RNA isolation, reverse transcription and hybridization assays on Affymetrix genomic microarrays. Data were validated with RT-qPCR assays. As results, UCI-05 and UCI-14 exposure increased gltA1 expression in drug-sensitive H37Rv clones. Furthermore, UCI-05 increased lprQ expression in MDR CIBIN:UMF:15:99 M. tuberculosis clones while UCI-14 reduced the expression of this gene in drug-sensitive H37Rv clones. In addition, UCI-05 reduced rpsO expression in drug-sensitive H37Rv clones. We found gene expression alterations that suggest these molecules may alter carbon and lipid metabolism as well as interfere in the protein-producing machinery in M. tuberculosis.

Aging is commonly accompanied by increased cardiovascular risk and diet plays a crucial role in health condition. The aim of this study was to determine cardiovascular risk factors as predictors of nutritional risk in Mexican older adults. A cross-sectional study on Mexican patients aged ≥60 years with cardiovascular risk factors affiliated with a medical unit in Northeast Mexico was performed from July to December 2021. The nutritional risk evaluations were performed using the Mini Nutritional Assessment (MNA) questionnaire. After a multivariate analysis, the cardiovascular risk factors identified as independent predictors of risk of malnutrition were hypertriglyceridemia (adjusted OR (AOR): 1.8; 95% CI: 1.03–3.14; p = 0.04) and systolic hypertension I (AOR: 2.28; 95% CI: 1.04–5.02; p = 0.041); age over 80 years (AOR: 5.17; 95% CI: 1.83–14.65, p = 0.002) and elementary school education (AOR: 2.34; 95% CI: 1.20–4.55; p = 0.013) were also related. The cross-sectional design and single-center approach of this study limits the generalizability of the results; however, conducting timely evaluations of blood pressure, triglyceride levels, and risk of malnutrition using the MNA tool for patients aged ≥60 years could prevent illness and reduce mortality within this population group. [ABSTRACT FROM AUTHOR]

INTRODUCTION: In 2013, the ALzheimer's and FAmilies (ALFA) project was established to investigate pathophysiological changes in preclinical Alzheimer's disease (AD), and to foster research on early detection and preventive interventions. METHODS: We conducted a comprehensive genetic characterization of ALFA participants with respect to neurodegenerative/cerebrovascular diseases, AD biomarkers, brain endophenotypes, risk factors and aging biomarkers. We placed particular emphasis on amyloid/tau status and assessed gender differences. Multiple polygenic risk scores were computed to capture different aspects of genetic predisposition. We additionally compared AD risk in ALFA to that across the full disease spectrum from the Alzheimer's Disease Neuroimaging Initiative (ADNI). RESULTS: Results show that the ALFA project has been successful at establishing a cohort of cognitively unimpaired individuals at high genetic predisposition of AD. DISCUSSION: It is, therefore, well‐suited to study early pathophysiological changes in the preclinical AD continuum. Highlights: Prevalence of ε4 carriers in ALzheimer and FAmilies (ALFA) is higher than in the general European populationThe ALFA study is highly enriched in Alzheimer's disease (AD) genetic risk factors beyond APOEAD genetic profiles in ALFA are similar to clinical groups along the continuumALFA has succeeded in establishing a cohort of cognitively unimpaired individuals at high genetic AD riskALFA is well suited to study pathogenic events/early pathophysiological changes in AD [ABSTRACT FROM AUTHOR]

INTRODUCTION: Detection of Alzheimer's disease (AD) pathophysiology among individuals with mild cognitive changes and those experiencing subjective cognitive decline (SCD) remains challenging. Plasma phosphorylated tau 217 (p‐tau217) is one of the most promising of the emerging biomarkers for AD. However, accessible methods are limited. METHODS: We employed a novel p‐tau217 immunoassay (University of Gothenburg [UGOT] p‐tau217) in four independent cohorts (n = 308) including a cerebrospinal fluid (CSF) biomarker‐classified cohort (Discovery), two cohorts consisting mostly of cognitively unimpaired (CU) and mild cognitively impaired (MCI) participants (MYHAT and Pittsburgh), and a population‐based cohort of individuals with SCD (Barcelonaβeta Brain Research Center's Alzheimer's At‐Risk Cohort [β‐AARC]). RESULTS: UGOT p‐tau217 showed high accuracy (area under the curve [AUC] = 0.80–0.91) identifying amyloid beta (Aβ) pathology, determined either by Aβ positron emission tomography or CSF Aβ42/40 ratio. In individuals experiencing SCD, UGOT p‐tau217 showed high accuracy identifying those with a positive CSF Aβ42/40 ratio (AUC = 0.91). DISCUSSION: UGOT p‐tau217 can be an easily accessible and efficient way to screen and monitor patients with suspected AD pathophysiology, even in the early stages of the continuum. [ABSTRACT FROM AUTHOR]

INTRODUCTION: We studied how biomarkers of reactive astrogliosis mediate the pathogenic cascade in the earliest Alzheimer's disease (AD) stages. METHODS: We performed path analysis on data from 384 cognitively unimpaired individuals from the ALzheimer and FAmilies (ALFA)+ study using structural equation modeling to quantify the relationships between biomarkers of reactive astrogliosis and the AD pathological cascade. RESULTS: Cerebrospinal fluid (CSF) amyloid beta (Aβ)42/40 was associated with Aβ aggregation on positron emission tomography (PET) and with CSF p‐tau181, which was in turn directly associated with CSF neurofilament light (NfL). Plasma glial fibrillary acidic protein (GFAP) mediated the relationship between CSF Aβ42/40 and Aβ‐PET, and CSF YKL‐40 partly explained the association between Aβ‐PET, p‐tau181, and NfL. DISCUSSION: Our results suggest that reactive astrogliosis, as indicated by different fluid biomarkers, influences the pathogenic cascade during the preclinical stage of AD. While plasma GFAP mediates the early association between soluble and insoluble Aβ, CSF YKL‐40 mediates the latter association between Aβ and downstream Aβ‐induced tau pathology and tau‐induced neuronal injury. Highlights: Lower CSF Aβ42/40 was directly linked to higher plasma GFAP concentrations.Plasma GFAP partially explained the relationship between soluble Aβ and insoluble Aβ.CSF YKL‐40 mediated Aβ‐induced tau phosphorylation and tau‐induced neuronal injury. [ABSTRACT FROM AUTHOR]

Background: In this study, we evaluated the association between tau PET and fluid biomarkers and explored biological mechanisms associated with elevated tau in cognitively unimpaired(CU) individuals. Method: Seventy‐nine CU individuals from the ALFA+ cohort had [18F]RO‐948 and [18F]flutemetamol PET, T1‐weighted MRI, CSF and plasma biomarkers. Longitudinal changes in cognition were measured using cognition composites(Table1). Participants were categorized into AT stages using CSF biomarkers and pre‐established cut‐offs(Table 1). [18F]RO‐948 SUVR was measured in entorhinal(BraakI/II), limbic(BraakIII/IV), and neocortical(BraakV/VI) regions using the inferior cerebellum as reference. Regional positivity thresholds per Braak region were calculated as mean+2SD of the A‐T‐ group. [18F]flutemetamol PET scans were quantified in Centiloids(CL). Associations between [18F]RO‐948 SUVRs and AD biomarkers (Figure1) were assessed using Pearson correlations. Receiver Operating Curve(ROC) analyses were conducted to determine the capacity of biomarkers to predict BraakI/II positivity. In those with CL>cut‐off for tau‐PET positivity, differences in non‐core AD fluid biomarkers(Figure2) and longitudinal cognition were sought between tau BraakI/II positive and negative individuals. The mediating effect of non‐core AD biomarkers on the AD pathophysiological cascade were sought. FDR‐corrected p‐values<0.05 were considered significant. Result: Nine cases(11.4%) were positive in BraakI/II. Following a hierarchical pattern, four of them were also positive for BraakIII/IV and one for BraakV/VI. Fluid biomarkers presented correlations with tau PET SUVR in all Braak stages (Figure1) and predictive capacity for tau‐PET positivity in BraakI/II(Table2). In individuals with CL>32.53, BraakI/II positives had higher levels of CSF‐GFAP(p<0.01) and CSF‐NFL(p = 0.03), and presented declines in PACC and in visual, attention, and memory composites (Figure1). CSF‐GFAP partially mediated the association between CL and tau‐PET (16%) and between tau‐PET and CSF‐NfL (30%). Conclusion: Early in the AD continuum, [18F]RO‐948 PET conformed to the Braak hierarchical model. CSF and plasma biomarkers showed moderate associations with tau PET SUVR but good capacity to predict tau PET positivity in BraakI/II. Tau‐PET positivity in this region was associated with higher astrogliosis, neurodegeneration and cognitive decline as compared to tau‐PET negatives with similar levels of amyloid deposition. Astrogliosis partially explained the observed associations between amyloid deposition and the presence of tau tangles in medial temporal regions and, even strongly, between the latter and neurodegeneration. [ABSTRACT FROM AUTHOR]

Nereis garwoodi n. sp. is described on the basis of eight syntype specimens (six atokous and two heteronereis) collected in Bahía Chetumal, Mexican Caribbean coast, and the variability in the paragnath numbers in the pharynx is established using 180 specimens; paragnath numbers are I:10(SD=1.9); II:30 (SD=2.6); III:41 (SD=5.2); IV:29 (SD=3.5), V:1, VI:4, VII-VIII: >30. Its eyes are big and its longest tentacular cirri reaches setiger 11. A revised key to species of Nereis recorded from the Grand Caribbean Sea is included.Se describe N. garwoodi n. sp. con base en ocho ejemplares sintipos (seis atokos y dos heteronereis) recolectados en el sublitoral (1 m) en la bahía de Chetumal y se define la variación en los paragnatos de las áreas diag-nósticas de la faringe usando 180 ejemplares, las cuáles son I:10(SD=1.9); II:30 (SD=2.6); III:41 (SD=5.2); IV:29 (SD=3.5), V:1, VI:4, VII-VIII:>30. Se caracteriza por tener un cirro tentacular que alcanza el setígero 11. Se incluye una clave revisada para las especies de Nereis registradas en el Gran Caribe.

Background: Glial fibrillary acidic protein (GFAP) and chitinase‐3‐like protein 1 (YKL‐40) are biomarkers of different astrocyte phenotypes, both of which are elevated in the dementia phase of Alzheimer's disease (AD). However, the specific contribution of these astrocyte phenotypes early in the AD continuum is not fully understood. Here, we studied how these two astrocyte phenotypes mediate the early pathogenic cascade in the preclinical stage of AD. Method: We assessed 384 cognitively unimpaired individuals from the ALFA+ study with amyloid‐β (Aβ)42/40, phosphorylated tau (p‐tau181), neurofilament light (NfL) and YKL‐40 measured in cerebrospinal fluid (CSF) and GFAP measured in plasma, as well as [18F]flutemetamol positron emission tomography (PET) and neuropsychological testing (Annual change in the Preclinical Alzheimer's Cognitive Composite [PACC]). Path analysis using structural equation modelling was used to quantify the relationships between biomarkers of reactive astrogliosis and Amyloid‐Tau‐Neurodegeneration biomarkers, while incorporating age, sex, and apolipoprotein E (APOE) ε4 effects. Direct effects with FDR‐corrected p‐values below.05 were considered significant. Result: CSF Aβ42/40 was associated with Aβ aggregation as measured by PET and with CSF p‐tau181, respectively. The latter was associated with CSF NfL, but no associations were found between any biomarkers and PACC changes in this early sample (Figure 1; Table 1). Plasma GFAP mediated the association between CSF Aβ42/40 and Aβ‐PET. Additionally, CSF YKL‐40 mediated the association between Aβ‐PET and p‐tau181 and between p‐tau181 and NfL. APOE ε4 had a direct association with CSF Aβ42/40 only, whereas age had independent associations with CSF Aβ42/40, NfL, GFAP and YKL‐40. Male sex was associated with higher CSF NfL levels, independently of other variables tested. Conclusion: Our results suggest that astrocyte phenotypes that release GFAP into the blood influence the aggregation of soluble Aβ into fibrillary plaques. On the other hand, those releasing YKL‐40 into the CSF appear to play a role later in the pathological cascade, mediating downstream tau pathology and neuronal damage. These results indicate that different astrocyte phenotypes are specifically involved in distinct stages of the early pathological cascade in preclinical AD. Interventions targeting astrocyte dysfunction in preclinical stages may prevent or delay the onset of AD dementia. [ABSTRACT FROM AUTHOR]

Copyright of Opuntia Brava is the property of Universidad de Ciencias Pedagogicas de Las Tunas, Centro de Documentacion e Informacion Pedagogica and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)