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Background: Mental disorders in university students are a growing attention problem in the international community due to their high prevalence and serious consequences. One possible reason is university students' difficulties in coping with stress. Repetitive negative thinking (RNT) is a transdiagnostic process that, when combined with stress, can lead to the development of various disorders. We aim to determine the effect of stress and RNT on predicting various mental health syndromes in university students across 7 days. Method: Prospective observational study using Momentary Ecological Assessment (EMA) with the OURMIND Mobile App. On day one, 238 university students responded to the SCL-90R questionnaire for symptoms of depression, anxiety, hostility, obsession, psychoticism, paranoia, somatization, and interpersonal sensitivity; RNT styles questionnaires, RRS for rumination and negative reflection, PSWQ for worry; SISCO-II for term academic stress, and sociodemographic. EMA consisted of five assessments a day for 6 days; each time, the students answered items about academic and non-academic stress (EMA-stress), reactive RNT duration and intrusiveness (EMA-RNT process), and reactive RNT rumination, reflection, and worry (EMA-RNT content). On day eight, symptoms were re-assessed. Seven hierarchical stepwise linear regression models were used to test the predictive power of the study variables in the development of SCL-90R symptoms. Results: When comparing models, adding baseline symptoms increased the models' predictive power in all symptom groups. In most cases, including EMA-stress generated greater predictive power, except for paranoia and interpersonal sensitivity. Adding the EMA-RNT process increased the prediction of paranoia and obsessive symptoms; for hostility symptoms, RNT styles increased predictive power. For the final regression models, considering the initial symptoms, the EMA-RNT process predicted the progression of symptoms in six out of eight groups, while EMA-non-academic stress predicted the remaining two. Additionally, living with other relatives or friends was a predictor of depressive symptoms. Discussion: The stress of university life impacts the development of psychiatric symptoms in university students. These results provide evidence of RNT as a transdiagnostic process in several syndromic groups. Universal preventive programs should consider the impact of academic and non-academic stress on university students' mental health. Targeting RNT would also benefit selective preventive interventions.

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Core-shell micro/nanomotors have garnered significant interest in biomedicine owing to their versatile task-performing capabilities. However, their effectiveness for photothermal therapy (PTT) still faces challenges because of their poor tumor accumulation, lower light-to-heat conversion, and due to the limited penetration of near-infrared (NIR) light. In this study, we present a novel core-shell micromotor that combines magnetic and photothermal properties. It is synthesized via the template-assisted electrodeposition of iron (Fe) and reduced graphene oxide (rGO) on a microtubular pore-shaped membrane. The resulting Fe-rGO micromotor consists of a core of oval-shaped zero-valent iron nanoparticles with large magnetization. At the same time, the outer layer has a uniform reduced graphene oxide (rGO) topography. Combined, these Fe-rGO core-shell micromotors respond to magnetic forces and near-infrared (NIR) light (1064 nm), achieving a remarkable photothermal conversion efficiency of 78% at a concentration of 434 µg mL-1. They can also carry doxorubicin (DOX) and rapidly release it upon NIR irradiation. Additionally, preliminary results regarding the biocompatibility of these micromotors through in vitro tests on a 3D breast cancer model demonstrate low cytotoxicity and strong accumulation. These promising results suggest that such Fe-rGO core-shell micromotors could hold great potential for combined photothermal therapy.

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BACKGROUND: Tumor-derived small extracellular vesicles (sEVs) can promote tumorigenic and metastatic capacities in less aggressive recipient cells mainly through the biomolecules in their cargo. However, despite recent advances, the specific molecules orchestrating these changes are not completely defined. Lactadherin is a secreted glycoprotein typically found in the milk fat globule membrane. Its overexpression has been associated with increased tumorigenesis and metastasis in breast cancer (BC) and other tumors. However, neither its presence in sEVs secreted by BC cells, nor its role in sEV-mediated intercellular communication have been described. The present study focused on the role of lactadherin-containing sEVs from metastatic MDA-MB-231 triple-negative BC (TNBC) cells (sEV-MDA231) in the promotion of pro-metastatic capacities in non-tumorigenic and non-metastatic recipient cells in vitro, as well as their pro-metastatic role in a murine model of peritoneal carcinomatosis. RESULTS: We show that lactadherin is present in sEVs secreted by BC cells and it is higher in sEV-MDA231 compared with the other BC cell-secreted sEVs measured through ELISA. Incubation of non-metastatic recipient cells with sEV-MDA231 increases their migration and, to some extent, their tumoroid formation capacity but not their anchorage-independent growth. Remarkably, lactadherin blockade in sEV-MDA231 results in a significant decrease of those sEV-mediated changes in vitro. Similarly, intraperitoneally treatment of mice with MDA-MB-231 BC cells and sEV-MDA231 greatly increase the formation of malignant ascites and tumor micronodules, effects that were significantly inhibited when lactadherin was previously blocked in those sEV-MDA231. CONCLUSIONS: As to our knowledge, our study provides the first evidence on the role of lactadherin in metastatic BC cell-secreted sEVs as promoter of: (i) metastatic capacities in less aggressive recipient cells, and ii) the formation of malignant ascites and metastatic tumor nodules. These results increase our understanding on the role of lactadherin in sEVs as promoter of metastatic capacities which can be used as a therapeutic option for BC and other malignancies.

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PURPOSE: Oral squamous cell carcinoma (OSCC) is commonly preceded by potentially malignant lesions, referred to as oral dysplasia. We recently reported that oral dysplasia is associated with aberrant activation of the Wnt/ß-catenin pathway, due to overexpression of Wnt ligands in a Porcupine (PORCN)-dependent manner. Pharmacologic inhibition of PORCN precludes Wnt secretion and has been proposed as a potential therapeutic approach to treat established cancers. Nevertheless, there are no studies that explore the effects of PORCN inhibition at the different stages of oral carcinogenesis. EXPERIMENTAL DESIGN: We performed a model of tobacco-induced oral cancer in vitro, where dysplastic oral keratinocytes (DOK) were transformed into oral carcinoma cells (DOK-TC), and assessed the effects of inhibiting PORCN with the C59 inhibitor. Similarly, an in vivo model of oral carcinogenesis and ex vivo samples derived from patients diagnosed with oral dysplasia and OSCC were treated with C59. RESULTS: Both in vitro and ex vivo oral carcinogenesis approaches revealed decreased levels of nuclear ß-catenin and Wnt3a, as observed by immunofluorescence and IHC analyses. Consistently, reduced protein and mRNA levels of survivin were observed after treatment with C59. Functionally, treatment with C59 in vitro resulted in diminished cell migration, viability, and invasion. Finally, by using an in vivo model of oral carcinogenesis, we found that treatment with C59 prevented the development of OSCC by reducing the size and number of oral tumor lesions. CONCLUSIONS: The inhibition of Wnt ligand secretion with C59 represents a feasible treatment to prevent the progression of early oral lesions toward OSCC.

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BACKGROUND: Tumor-derived small extracellular vesicles (sEVs) can promote tumorigenic and metastatic capacities in less aggressive recipient cells mainly through the biomolecules in their cargo. However, despite recent advances, the specific molecules orchestrating these changes are not completely defined. Lactadherin is a secreted 0protein typically found in the milk fat globule membrane. Its overexpression has been associated with increased tumorigenesis and metastasis in breast cancer (BC) and other tumors. However, neither its presence in sEVs secreted by BC cells, nor its role in sEV-mediated intercellular communication have been described. The present study focused on the role of lactadherin-containing sEVs from metastatic MDA-MB-231 triple-negative BC (TNBC) cells (sEV-MDA231) in the promotion of pro-metastatic capacities in non-tumorigenic and non-metastatic recipient cells in vitro, as well as their pro-metastatic role in a murine model of peritoneal carcinomatosis. RESULTS: We show that lactadherin is present in sEVs secreted by BC cells and it is higher in sEV-MDA231 compared with the other BC cell-secreted sEVs measured through ELISA. Incubation of non-metastatic recipient cells with sEV- MDA231 increases their migration and, to some extent, their tumoroid formation capacity but not their anchorage-independent growth. Remarkably, lactadherin blockade in sEV-MDA231 results in a significant decrease of those sEV-mediated changes in vitro. Similarly, intraperitoneally treatment of mice with MDA-MB-231 BC cells and sEV-MDA231 greatly increase the formation of malignant ascites and tumor micronodules, effects that were significantly inhibited when lactadherin was previously blocked in those sEV-MDA231. CONCLUSIONS: As to our knowledge, our study provides the first evidence on the role of lactadherin in metastatic BC cell-secreted sEVs as promoter of: (i) metastatic capacities in less aggressive recipient cells, and ii) the formation of malignant ascites and metastatic tumor nodules. These results increase our understanding on the role of lactadherin in sEVs as promoter of metastatic capacities which can be used as a therapeutic option for BC and other malignancies.

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Caveolin-1 (CAV1) is a membrane-bound protein that suppresses tumor development yet also promotes metastasis. E-cadherin is important in CAV1-dependent tumor suppression and prevents CAV1-enhanced lung metastasis. Here, we used murine B16F10 and human A375 melanoma cells with low levels of endogenous CAV1 and E-cadherin to unravel how co-expression of E-cadherin modulates CAV1 function in vitro and in vivo in WT C57BL/6 or Rag-/- immunodeficient mice and how a pro-inflammatory environment generated by treating cells with prostaglandin E2 (PGE2) alters CAV1 function in the presence of E-cadherin. CAV1 expression augmented migration, invasion, and metastasis of melanoma cells, and these effects were abolished via transient co-expression of E-cadherin. Importantly, exposure of cells to PGE2 reverted the effects of E-cadherin expression and increased CAV1 phosphorylation on tyrosine-14 and metastasis. Moreover, PGE2 administration blocked the ability of the CAV1/E-cadherin complex to prevent tumor formation. Therefore, our results support the notion that PGE2 can override the tumor suppressor potential of the E-cadherin/CAV1 complex and that CAV1 released from the complex is phosphorylated on tyrosine-14 and promotes migration/invasion/metastasis. These observations provide direct evidence showing how a pro-inflammatory environment caused here via PGE2 administration can convert a potent tumor suppressor complex into a promoter of malignant cell behavior.

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The aim of this study was to evaluate, for the first time, the antiproliferative, apoptotic and diminishing effects of the anchored growth-independent capacity of an ethanol macerate extract from the Annona cherimola seed (EMCHS) in the human gastric cancer cell line SNU-1. The cells treated with EMCHS (20 µg/mL) significantly reduced the capacity to form clones of the tumor cell. Moreover, 50 µg/mL of EMCHS extract induced apoptosis, as was shown by the Annexin-V assay. UHPLC-MS/MS analysis detected two acetogenins (Annonacinone and Annonacin) in the EMCHS, which could be largely responsible for its selective antiproliferative effect. The identification of fatty acids by GC-FID showed the presence of eight fatty acids, among which was, oleic acid, which has recognized activity as an adjuvant in antitumor treatments. Taken together, our results indicate that the EMCHS seems promising for use as a natural therapy against gastric cancer disease.

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This study protocol aims to analyze and compare the effects of combined movement and storytelling intervention (CMSI) on fundamental motor skills (locomotor skills and object control), language development (language comprehension, language expression, vocabulary and language description), and physical activity levels (light intensity, moderate-to-vigorous intensity and sedentary time) in children aged 3 to 6 years. The sample will consist of 144 children from 12 class groups, randomly assigned to 3 experimental groups (n = 72 children) and 3 control groups (n = 72 children), belonging to 4 class groups of upper-middle-level classes (2 experimental and 2 control; 3 to 4 years), 4 transition level 1 classes (2 experimental and 2 control; 4 to 5 years) and 4 transition level 2 classes (2 experimental and 2 control; 5 to 6 years). The experimental groups will perform CMSI for 3 sessions per week (40 min per session) over 12 weeks (using one motor story per week), while the control groups will not receive any treatment. The main outcome will provide information about fundamental motor skills, language development, and physical activity levels. Our hypothesis indicates that CMSI has the potential to generate significant increases in selected assessments. If this intervention proves to be beneficial, it could contribute to preschool and school curricula.

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Cancer research has prioritized the study of the tumor microenvironment (TME) as a crucial area of investigation. Understanding the communication between tumor cells and the various cell types within the TME has become a focal point. Bidirectional communication processes between these cells support cellular transformation, as well as the survival, invasion, and metastatic dissemination of tumor cells. Extracellular vesicles are lipid bilayer structures secreted by cells that emerge as important mediators of this cell-to-cell communication. EVs transfer their molecular cargo, including proteins and nucleic acids, and particularly microRNAs, which play critical roles in intercellular communication. Tumor-derived EVs, for example, can promote angiogenesis and enhance endothelial permeability by delivering specific miRNAs. Moreover, adipocytes, a significant component of the breast stroma, exhibit high EV secretory activity, which can then modulate metabolic processes, promoting the growth, proliferation, and migration of tumor cells. Comprehensive studies investigating the involvement of EVs and their miRNA cargo in the TME, as well as their underlying mechanisms driving tumoral capacities, are necessary for a deeper understanding of these complex interactions. Such knowledge holds promise for the development of novel diagnostic and therapeutic strategies in cancer treatment.

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Identifying risk factors associated with COVID-19 lethality is crucial in combating the ongoing pandemic. In this study, we developed lethality predictive models for each epidemiological wave and for the overall dataset using the Extreme Gradient Boosting technique and analyzed them using Shapley values to determine the contribution levels of various features, including demographics, comorbidities, medical units, and recent medical information from confirmed COVID-19 cases in Mexico between February 23, 2020, and April 15, 2022. The results showed that pneumonia and advanced age were the most important factors predicting patient death in all cohorts. Additionally, the medical unit where the patient received care acted as a risk or protective factor. IMSS medical units were identified as high-risk factors in all cohorts, except in wave four, while SSA medical units generally were moderate protective factors. We also found that intubation was a high-risk factor in the first epidemiological wave and a moderate-risk factor in the following waves. Female gender was a protective factor of moderate-high importance in all cohorts, while being between 18 and 29 years old was a moderate protective factor and being between 50 and 59 years old was a moderate risk factor. Additionally, diabetes (all cohorts), obesity (third wave), and hypertension (fourth wave) were identified as moderate risk factors. Finally, residing in municipalities with the lowest Human Development Index level represented a moderate risk factor. In conclusion, this study identified several significant risk factors associated with COVID-19 lethality in Mexico, which could aid policymakers in developing targeted interventions to reduce mortality rates.

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Using a novel mathematical tool called the Te-gram, researchers analyzed the energy distribution of frequency components in the scale-frequency plane. Through this analysis, a frequency band of approximately 12 Hz is identified, which can be isolated without distorting its constituent frequencies. This band, along with others, remained inseparable through conventional time-frequency analysis methods. The Te-gram successfully addresses this knowledge gap, providing multi-sensitivity in the frequency domain and effectively attenuating cross-term energy. The Daubechies 45 wavelet function was employed due to its exceptional 150 dB attenuation in the rejection band. The validation process encompassed three stages: pre-, during-, and post-seismic activity. The utilized signal corresponds to the 19 September 2017 earthquake, occurring between the states of Morelos and Puebla, Mexico. The results showcased the impressive ability of the Te-gram to surpass expectations in terms of sensitivity and energy distribution within the frequency domain. The Te-gram outperformed the procedures documented in the existing literature. On the other hand, the results show a frequency band between 0.7 Hz and 1.75 Hz, which is named the planet Earth noise.

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Antecedentes: Se ha demostrado que la coinfección tu-berculosis y COVID-19 presenta peor evolución clínica. La inmunidad protectora se debilita frente a esta situación, generando fallo en el control de ambas infecciones, reac-tivación de formas latentes de tuberculosis y progresión exacerbada de los casos activos. Asimismo, la terapia con corticoides utilizada dentro del tratamiento de infecciones graves por COVID-19 puede generar inmunosupresión y precipitar la progresión de la tuberculosis.Objetivos: Describir las características clínicas, presenta-ción y evolución de los pacientes críticos con coinfección COVID-19 y tuberculosis. Evaluar la incidencia y letalidad de la asociación COVID-19 y tuberculosis en cuidados in-tensivos. Materiales y métodos: Se realizó un estudio retrospectivo, descriptivo. Se revisaron 12 historias clínicas de pacientes con coinfección COVID-19-tuberculosis sobre 1014 histo-rias clínicas de pacientes ingresados con diagnóstico de COVID-19, durante el periodo comprendido enero 2020 y junio 2022. Se utilizó estadística descriptiva. Resultados y discusión: Sobre un total de 1014 historias clínicas, se encontraron 12 pacientes con coinfección (in-cidencia de 0,011). La letalidad global en cuidados inten-sivos fue del 75%, a los 45 días fue del 83,3%, duplicando la letalidad general de los pacientes COVID-19 no coinfec-tados ingresados durante el mismo periodo (75% versus 37%). Los pacientes que requirieron ingreso a ventilación RESUMENARTÍCULO ORIGINALmecánica tuvieron una letalidad del 100% y aquellos que tenían infección por virus de inmunodeficiencia adquirida presentaron una letalidad de 100%. Resulta importante describir los hallazgos y alertar sobre la evolución desfavorable de aquellos pacientes que pre-sentan esta asociación a fin de optimizar el manejo y espe-cialmente recomendar la búsqueda de coinfección cuando el criterio clínico lo requiera

Background: Coinfection with tuberculosis and COVID-19 has been shown to have a worse clinical course. Protective immunity is weakened in this situation, leading to failure to control both infections, reactivation of latent forms of TB and exacerbated progression of active cases. Furthermore, corticosteroid therapy used in the treatment of severe COVID-19 infections can lead to immunosuppression and precipitate TB progression.Objectives: To describe the clinical characteristics, presentation and evolution of critically ill patients with COVID-19 and tuberculosis co-infection.To evaluate the incidence and lethality of COVID-19 and tuberculosis association in intensive care.Materials and methods: A retrospective, descriptive study was conducted. Twelve medical records of patients aged 18 years or older admitted to intensive care with a diagnosis of COVID-19 during the period January 2020 to July 2022 were reviewed. Descriptive statistics were used.Results and discussion: Out of a total of 1014 medical records, 12 patients were found with co-infection (incidence 0.011). The global intensive care case fatality was 75%, at 45 days it was 83.3%. This was twice the overall case fatality of non-co-infected COVID-19 patients admitted during the same period (75% versus 37%). Patients requiring admission to mechanical ventilation had a 100% case fatality and those with acquired immunodeficiency virus infection had a 100% case fatality.It is important to describe the findings and to alert to the worse evolution of those patients presenting with this association, in order to improve management and recommend searching for co-infection when clinical criteria require it

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BACKGROUND: Helicobacter pylori (Hp) infects the stomach of 50% of the world's population. Importantly, chronic infection by this bacterium correlates with the appearance of several extra-gastric pathologies, including neurodegenerative diseases. In such conditions, brain astrocytes become reactive and neurotoxic. However, it is still unclear whether this highly prevalent bacterium or the nanosized outer membrane vesicles (OMVs) they produce, can reach the brain, thus affecting neurons/astrocytes. Here, we evaluated the effects of Hp OMVs on astrocytes and neurons in vivo and in vitro. METHODS: Purified OMVs were characterized by mass spectrometry (MS/MS). Labeled OMVs were administered orally or injected into the mouse tail vein to study OMV-brain distribution. By immunofluorescence of tissue samples, we evaluated: GFAP (astrocytes), ßIII tubulin (neurons), and urease (OMVs). The in vitro effect of OMVs in astrocytes was assessed by monitoring NF-κB activation, expression of reactivity markers, cytokines in astrocyte-conditioned medium (ACM), and neuronal cell viability. RESULTS: Urease and GroEL were prominent proteins in OMVs. Urease (OMVs) was present in the mouse brain and its detection coincided with astrocyte reactivity and neuronal damage. In vitro, OMVs induced astrocyte reactivity by increasing the intermediate filament proteins GFAP and vimentin, the plasma membrane αVß3 integrin, and the hemichannel connexin 43. OMVs also produced neurotoxic factors and promoted the release of IFNγ in a manner dependent on the activation of the transcription factor NF-κB. Surface antigens on reactive astrocytes, as well as secreted factors in response to OMVs, were shown to inhibit neurite outgrowth and damage neurons. CONCLUSIONS: OMVs administered orally or injected into the mouse bloodstream reach the brain, altering astrocyte function and promoting neuronal damage in vivo. The effects of OMVs on astrocytes were confirmed in vitro and shown to be NF-κB-dependent. These findings suggest that Hp could trigger systemic effects by releasing nanosized vesicles that cross epithelial barriers and access the CNS, thus altering brain cells.

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La fibrosis quística (FQ) es un trastorno hereditario, de las glándulas de secreción exocrina, considerada la causa más frecuente de insuficiencia pancreática exocrina (IPE) en la infancia. Esta revisión resume el panorama del tratamiento de reposición enzimática en la IPE asociada a la FQ, las formulaciones disponibles, su dosificación y modo de administración, así como las limitaciones y desafíos actuales y las posibles áreas del desarrollo futuro

Cystic fibrosis (CF) is an inherited disorder of the exocrine secretion glands, considered the most frequent cause of exocrine pancreatic insufficiency (EPI) in childhood. This review summarizes the landscape of enzyme replacement therapy in PEI associated with CF, the available formulations, their dosage and mode of administration, as well as the current limitations and challenges and potential areas for future development.

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Potential drug-eluting scaffolds of electrospun poly(acrylic acid-co-styrene sulfonate) P(AA-co-SS) in clonogenic assays using tumorigenic gastric and ovarian cancer cells were tested in vitro. Electrospun polymer nanofiber (EPnF) meshes of PAA and PSSNa homo- and P(AA-co-SS) copolymer composed of 30:70, 50:50, 70:30 acrylic acid (AA) and sodium 4-styrene sulfonate (SSNa) units were performed by electrospinning (ES). The synthesis, structural and morphological characterization of all EPnF meshes were analyzed by optical and electron microscopy (SEM-EDS), infrared spectroscopy (FTIR), contact angle, and X-ray diffraction (XRD) measurements. This study shows that different ratio of AA and SSNa of monomers in P(AA-co-SS) EPnF play a crucial role in clonogenic in vitro assays. We found that 50:50 P(AA-co-SS) EPnF mesh loaded with antineoplastic drugs can be an excellent suppressor of growth-independent anchored capacities in vitro assays and a good subcutaneous drug delivery system for chemotherapeutic medication in vivo model for surgical resection procedures in cancer research.

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One of the recent attractive therapeutic approaches for cancer treatment is restoring downregulated microRNAs. They play an essential muti-regulatory role in cellular processes such as proliferation, differentiation, survival, apoptosis, cell cycle, angiogenesis, and metastasis, among others. In this study, a gold nanoplatform (GNPF) carrying miR-145, a downregulated microRNA in many cancer types, including epithelial ovarian cancer, was designed and synthesized. For targeting purposes, the GNPF was functionalized with the FSH33 peptide, which provided selectivity for ovarian cancer, and loaded with the miR-145 to obtain the nanosystem GNPF-miR-145. The GNPF-mir-145 was selectively incorporated in A2780 and SKOV3 cells and significantly inhibited cell viability and migration and exhibited proliferative and anchor-independent growth capacities. Moreover, it diminished VEGF release and reduced the spheroid size of ovarian cancer through the damage of cell membranes, thus decreasing cell viability and possibly activating apoptosis. These results provide important advances in developing miR-based therapies using nanoparticles as selective vectors and provide approaches for in vivo evaluation.

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INTRODUCTION: The population living in conditions of poorness has a heavier pathological burden than social strata with better economic possibilities. OBJECTIVE: To determine the influence of socioeconomic and demographic factors on COVID-19 morbidity, mortality and lethality in municipalities and states of Mexico. METHODS: Morbidity, mortality and lethality associated with COVID-19 were analyzed according to the human development index and its indicators, and type of population. Descriptive statistical analyses, correlations between developmental variables and morbidity, mortality and lethality, association tests and hierarchical groupings were carried out. RESULTS: Positive correlations were observed between morbidity and mortality and the human development index; COVID-19 fatality increased as the values of said index decreased. There was a significantly higher risk of elevated mortality in localities with moderate and low development, and in those with less than 49,999 inhabitants. The main factors associated with fatality were lack of access to health services, income vulnerability and social deprivation. CONCLUSIONS: The evidence generated should lead to decisions aimed at improving the quality of life of the population with social deprivations and vulnerabilities, which needs to be protected against the consequences of current COVID-19 pandemic.

INTRODUCCIÓN: La población en situación de pobreza presenta una carga patológica mayor que los estratos sociales con mejores posibilidades económicas. OBJETIVO: Determinar la influencia de los factores socioeconómicos y demográficos en la morbilidad, mortalidad y letalidad de COVID-19 en municipios y estados de México. MÉTODOS: Se analizó la morbilidad, mortalidad y letalidad asociadas a COVID-19 conforme el índice de desarrollo humano y sus indicadores, así como el tipo de población. Se realizaron análisis estadísticos descriptivos, de correlación entre variables de desarrollo versus morbilidad, mortalidad y letalidad, pruebas de asociación y agrupaciones jerárquicas. RESULTADOS: Se observaron correlaciones positivas entre la morbilidad y mortalidad y el índice de desarrollo humano; la letalidad por COVID-19 aumentó conforme disminuyó dicho índice. Existió riesgo significativamente superior de alta letalidad en las localidades con moderado y bajo desarrollo, así como en aquellas con menos de 49 999 habitantes. Los principales factores asociados a la letalidad fueron la falta de acceso a los servicios de salud, la vulnerabilidad por ingreso y la carencia social. CONCLUSIONES: La evidencia generada debe llevar a decisiones tendentes al mejoramiento de la calidad de vida de la población con carencias y vulnerabilidades sociales, que necesita ser protegida contra las consecuencias de la actual pandemia de COVID-19.

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La creciente epidemia de obesidad ha sido uno de los retos más importantes de salud pública en México durante los últimos años. Con apoyo de la Federación Mundial de Obesidad, en 2021 formamos un grupo de profesionales para identificar y resumir las acciones prioritarias en las que puede enfocarse nuestro país para hacer frente a esta epidemia. Al proceso de desarrollo y discusión de este grupo se sumaron más de 1 000 profesionales de la salud para retomar recomendaciones de documentos y guías de alto nivel previamente publicados. En conmemoración del Día Mundial de la Obesidad, en este 2022 se presenta esta postura como insumo para el desarrollo de acciones en el ámbito profesional y de los diferentes sectores, en la que se incluyen 10 recomendaciones de acción, desde la perspectiva poblacional hasta la atención individualizada, y se enfatiza en la importancia de la participación social, de las intervenciones integrales con visión centrada en la persona y de la sostenibilidad planetaria, además de mejorar la educación y las campañas de difusión, propiciar un ambiente promotor de entornos activos y blindar de conflictos de interés los esfuerzos de prevención y control. La postura hace un llamado para abordar la obesidad de manera seria, con base en la evidencia científica, oportuna e integral, con enfoque de curso de vida, de forma ética y sensible, y sin perpetuar las barreras del estigma de peso en la sociedad.

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Lactadherin is a secreted glycoprotein associated with the milk fat globule membrane, which is highly present in the blood and in the mammary tissue of lactating women. Several biological functions have been associated with this protein, mainly attributable to its immunomodulatory role promoting phagocyte-mediated clearance of apoptotic cells. It has been shown that lactadherin also plays important roles in cell adhesion, the promotion of angiogenesis, and tissue regeneration. On the other hand, this protein has been used as a marker of breast cancer and tumor progression. Recently, high levels of lactadherin has been associated with poor prognosis and decreased survival, not only in breast cancer, but also in melanoma, ovarian, colorectal, and other types of cancer. Although the mechanisms responsible for the tumor-promoting effects attributed to lactadherin have not been fully elucidated, a growing body of literature indicates that lactadherin could be a promising therapeutic target and/or biomarker for breast and other tumors. Moreover, recent studies have shown its presence in extracellular vesicles derived from cancer cell lines and cancer patients, which was associated with cancer aggressiveness and worse prognosis. Thus, this review will focus on the link between lactadherin and cancer development and progression, its possible use as a cancer biomarker and/or therapeutic target, concluding with a possible role of this protein in cellular communication mediated by extracellular vesicles.

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