Care management improves total cost of care for patients with dementia.

OBJECTIVES: To examine a 12-month dementia care management program's effect on health care cost, utilization, and overall return on investment in a Medicare managed care population. STUDY DESIGN: Pre-post analysis of participants (n = 121) enrolled in Ochsner's Care Ecosystem program from 2019 through 2021 compared with propensity-matched controls (n = 121). The primary outcome comparison was total cost of care. Secondary outcomes included components of total cost of care (eg, inpatient, outpatient, emergency department [ED] costs), health care utilization (eg, number of ED visits), and differences in Hierarchical Condition Category (HCC) risk scores. METHODS: Difference-in-differences analyses were conducted from baseline through 12 months comparing various financial metrics and utilization between groups. RESULTS: Care Ecosystem participants had significantly lower total cost of care at 12 months, mean savings of $475.80 per member per month compared with controls. Care Ecosystem participants had fewer ED, outpatient, and professional visits. HCC risk scores were also better relative to matched controls. CONCLUSIONS: A collaborative dementia care program demonstrated significant financial benefit in a managed Medicare population.

Performance of the Modified Caregiver Strain Index in a Sample of Black and White Persons Living With Dementia and Their Caregivers.

BACKGROUND AND OBJECTIVES: This study examined the performance of the Modified Caregiver Strain Index (MCSI) in a sample of Black and White caregivers of persons living with dementia. RESEARCH DESIGN AND METHODS: Data on 153 dyads enrolled in the Care Ecosystem dementia care management program were analyzed, including sociodemographic variables, dementia severity, and caregiver burden and wellbeing. Factor structure, item-response patterns, and concurrent validity were assessed across racial groups. RESULTS: Differences between Black and White caregivers included gender, dyad relation, and socioeconomic disadvantage. Factor structure and item loadings varied by racial cohort, with parameters supporting a 3-factor model. For Black caregivers, finances and work, emotional and physical strain, and family and personal adjustment items loaded together on individual factors. For White caregivers physical and emotional strain items loaded on separate factors, although personal and family adjustment items loaded with work and financial strain items. Item-level analysis revealed differences between groups, with Black caregivers endorsing physical strain to a greater degree (p = .003). Total MCSI scores were positively correlated with concurrent measures like the PHQ-9 (White: r = 0.67, Black: r = 0.54) and the GAD-2 (White: r = 0.47, Black: r = 0.4), and negatively correlated with self-efficacy ratings (White: r = -0.54, Black: r = -0.55), with a p < .001 for all validity analysis. DISCUSSION AND IMPLICATIONS: The MCSI displayed acceptable statistical performance for Black and White caregivers of persons living with dementia and displayed a factor structure sensitive to cultural variations of the construct. Researchers results highlight the inherent complexity and the relevance of selecting inclusive measures to appropriately serve diverse populations.

Immediate effects and duration of a short and single application of transcutaneous auricular vagus nerve stimulation on P300 event related potential.

Introduction: Transcutaneous auricular vagus nerve stimulation (taVNS) is a neuromodulatory technique that stimulates the auricular branch of the vagus nerve. The modulation of the locus coeruleus-norepinephrine (LC-NE) network is one of the potential working mechanisms of this method. Our aims were 1-to investigate if short and single applications of taVNS can modulate the P300 cognitive event-related potential (ERP) as an indirect marker that reflects NE brain activation under control of the LC, and 2-to evaluate the duration of these changes. Methods: 20 healthy volunteers executed an auditory oddball paradigm to obtain P300 and reaction time (RT) values. Then a 7 min active or sham taVNS period was initiated and simultaneously a new P300 paradigm was performed. We successively repeated the paradigm on 4 occasions with different time intervals up to 56 min after the stimulation onset. Results: During active taVNS an immediate and significant effect of increasing the amplitude and reducing the latency of P300, as well as a shortening in the RT was observed. This effect was prolonged in time up to 28 min. The values then returned to pre-stimulation levels. Sham stimulation did not generate changes. Discussion: Our results, demonstrate differential facilitating effects in a concrete time window after taVNS. Literature about the modulatory effect of taVNS over P300 ERP shows a wide spread of results. There is not a standardized system for taVNS and currently the great heterogeneity of stimulation approaches concerning targets and parameters, make it difficult to obtain conclusions about this relationship. Our study was designed optimizing several stimulation settings, such as a customized earbud stimulator, enlarged stimulating surface, simultaneous stimulation over the cymba and cavum conchae, a Delayed Biphasic Pulse Burst and current controlled stimulation that adjusted the output voltage and guaranteed the administration of a preset electrical dose. Under our stimulation conditions, targeting vagal nerve fibers via taVNS modulates the P300 in healthy participants. The optimal settings of modulatory function of taVNS on P300, and their interdependency is insufficiently studied in the literature, but our data provides several easily optimizable parameters, that will produce more robust results in future.

Contributions of Adaptive Laboratory Evolution towards the Enhancement of the Biotechnological Potential of Non-Conventional Yeast Species.

Changes in biological properties over several generations, induced by controlling short-term evolutionary processes in the laboratory through selective pressure, and whole-genome re-sequencing, help determine the genetic basis of microorganism's adaptive laboratory evolution (ALE). Due to the versatility of this technique and the imminent urgency for alternatives to petroleum-based strategies, ALE has been actively conducted for several yeasts, primarily using the conventional species Saccharomyces cerevisiae, but also non-conventional yeasts. As a hot topic at the moment since genetically modified organisms are a debatable subject and a global consensus on their employment has not yet been attained, a panoply of new studies employing ALE approaches have emerged and many different applications have been exploited in this context. In the present review, we gathered, for the first time, relevant studies showing the ALE of non-conventional yeast species towards their biotechnological improvement, cataloging them according to the aim of the study, and comparing them considering the species used, the outcome of the experiment, and the employed methodology. This review sheds light on the applicability of ALE as a powerful tool to enhance species features and improve their performance in biotechnology, with emphasis on the non-conventional yeast species, as an alternative or in combination with genome editing approaches.

Virus-Induced Membrane Fusion in Neurodegenerative Disorders.

A growing body of epidemiological and research data has associated neurotropic viruses with accelerated brain aging and increased risk of neurodegenerative disorders. Many viruses replicate optimally in senescent cells, as they offer a hospitable microenvironment with persistently elevated cytosolic calcium, abundant intracellular iron, and low interferon type I. As cell-cell fusion is a major driver of cellular senescence, many viruses have developed the ability to promote this phenotype by forming syncytia. Cell-cell fusion is associated with immunosuppression mediated by phosphatidylserine externalization that enable viruses to evade host defenses. In hosts, virus-induced immune dysfunction and premature cellular senescence may predispose to neurodegenerative disorders. This concept is supported by novel studies that found postinfectious cognitive dysfunction in several viral illnesses, including human immunodeficiency virus-1, herpes simplex virus-1, and SARS-CoV-2. Virus-induced pathological syncytia may provide a unified framework for conceptualizing neuronal cell cycle reentry, aneuploidy, somatic mosaicism, viral spreading of pathological Tau and elimination of viable synapses and neurons by neurotoxic astrocytes and microglia. In this narrative review, we take a closer look at cell-cell fusion and vesicular merger in the pathogenesis of neurodegenerative disorders. We present a "decentralized" information processing model that conceptualizes neurodegeneration as a systemic illness, triggered by cytoskeletal pathology. We also discuss strategies for reversing cell-cell fusion, including, TMEM16F inhibitors, calcium channel blockers, senolytics, and tubulin stabilizing agents. Finally, going beyond neurodegeneration, we examine the potential benefit of harnessing fusion as a therapeutic strategy in regenerative medicine.

Manejo anestésico y perioperatorio en paciente pediátrico con hiperglicinemia no cetósica / Anesthetic and perioperative management in children with non-ketotic hyperglycinemiawith non-ketotic hyperglycinemia

Presentación del caso: se reporta un paciente pediátrico con diagnóstico de hiperglicinemia no cetósica (HNC), enfermedad neurometabólica poco frecuente ocasionada por una deficiencia en el sistema de segmentación de la glicina, codificada por los genes GLDC, GCSH, AMT y GCSL que conduce a niveles elevados de glicina en la sinapsis generando un efecto agonista prolongado en los receptores N-metil-D-aspartato (NMDA). Discusión y conclusiones: se asocia con hipotonía, convulsiones y trastornos de la deglución, los cuales dependerán de la edad de presentación. Se revisa la literatura actual para el abordaje perioperatorio.

Case presentation: we report a child with a diagnosis of non-ketotic hyperglycinemia (NKGH), a rare neurometabolic disease caused by a defect in the glycine cleavage system, encoded by the GLDC, GCSH, AMT and GCSL genes resulting in elevated synaptic glycine levels generating a prolonged agonist effect on N-methyl-D-aspartate (NMDA) receptors. Discussion and conclusions: it is associated with hypotonia, seizures and swallowing disorders, which will depend on the age at presentation. A literature review was conducted to tailor perioperative approach.

Social determinants of health and community assets: Their importance for context analysis / Determinantes sociales de la salud y activos comunitarios: importancia para el análisis de contexto

ABSTRACT Public health, from alternative perspectives on the approach to positive health, seeks to overcome the deficit in recognizing the resources possessed by people and their communities as proposed in the Salutogenesis assets model. Therefore, this paper aims to establish the relationship between the Social Determinants of Health (SDH) and community assets. A two-stage sequential transformative mixed methods design, quantitative and qualitative, was used. Family files, mapping techniques, interviews, and participant observation were used as instruments. Older adults, women, and leaders have a history that creates opportunities based on education, work, and potential, developed individually or by coexistence between the same families and in the neighborhood. The SDH and community assets converge in the understanding of the territory as a social, historical, and eco-environmental space. There, the macro-policies are reflected, sometimes isolated from people's perceived, conceived, and lived spaces. In the construction of a healthy life, the main elements are people and their relationships. It is in this context that their talents, skills, and abilities are discovered. The results show a bilateral relationship between community assets and the SDH to understand the health-disease process. While the determinants focus on external conditions, risk, and vulnerability, depending on the disease, the assets do so in a positive health perspective that strengthens the resources of people and their communities. In this sense, they complement each other.

RESUMEN La salud pública, desde miradas alternativas con acercamiento a la salud positiva, busca superar el déficit para reconocer los recursos que tienen las personas y sus comunidades, a partir de la Salutogénesis - Modelo de activos. Así, pues, el escrito establece la relación de los determinantes sociales de la salud (DSS) y los activos comunitarios. Se utilizó un diseño mixto transformativo recurrente con dos fases: cuantitativa y cualitativa. Como instrumentos, las fichas familiares, técnicas cartográficas, la entrevista y la observación participante. Los adultos mayores, mujeres y líderes poseen una historia que crea oportunidades basadas en la educación, el trabajo y sus potencialidades, desarrolladas individualmente o por la convivencia entre las mismas familias y el barrio. Los DSS y los activos comunitarios convergen en la comprensión del territorio, como un espacio social, histórico y ecoambiental. Allí, se reflejan las macro políticas, en ocasiones aisladas de los espacios percibidos, concebidos y vividos de las personas. En la construcción de una vida sana, los principales elementos son las personas y sus relaciones; en ese contexto, se descubren sus talentos, las habilidades y las capacidades. Los resultados evidenciaron relación bilateral entre los activos comunitarios y los DSS, para comprender el proceso salud-enfermedad; mientras los determinantes se centran en condiciones externas, de riesgo y de vulnerabilidad en función de la enfermedad, los activos lo hacen en una mirada de salud positiva, que fortalece los recursos de las personas y sus comunidades. En este sentido, se complementan de manera recíproca.

PTSD as an Endothelial Disease: Insights From COVID-19.

SARS-CoV-2 virus, the etiologic agent of COVID-19, has affected almost every aspect of human life, precipitating stress-related pathology in vulnerable individuals. As the prevalence rate of posttraumatic stress disorder in pandemic survivors exceeds that of the general and special populations, the virus may predispose to this disorder by directly interfering with the stress-processing pathways. The SARS-CoV-2 interactome has identified several antigens that may disrupt the blood-brain-barrier by inducing premature senescence in many cell types, including the cerebral endothelial cells. This enables the stress molecules, including angiotensin II, endothelin-1 and plasminogen activator inhibitor 1, to aberrantly activate the amygdala, hippocampus, and medial prefrontal cortex, increasing the vulnerability to stress related disorders. This is supported by observing the beneficial effects of angiotensin receptor blockers and angiotensin converting enzyme inhibitors in both posttraumatic stress disorder and SARS-CoV-2 critical illness. In this narrative review, we take a closer look at the virus-host dialog and its impact on the renin-angiotensin system, mitochondrial fitness, and brain-derived neurotrophic factor. We discuss the role of furin cleaving site, the fibrinolytic system, and Sigma-1 receptor in the pathogenesis of psychological trauma. In other words, learning from the virus, clarify the molecular underpinnings of stress related disorders, and design better therapies for these conditions. In this context, we emphasize new potential treatments, including furin and bromodomains inhibitors.

Endothelial Senescence and Chronic Fatigue Syndrome, a COVID-19 Based Hypothesis.

Myalgic encephalomyelitis/chronic fatigue syndrome is a serious illness of unknown etiology, characterized by debilitating exhaustion, memory impairment, pain and sleep abnormalities. Viral infections are believed to initiate the pathogenesis of this syndrome although the definite proof remains elusive. With the unfolding of COVID-19 pandemic, the interest in this condition has resurfaced as excessive tiredness, a major complaint of patients infected with the SARS-CoV-2 virus, often lingers for a long time, resulting in disability, and poor life quality. In a previous article, we hypothesized that COVID-19-upregulated angiotensin II triggered premature endothelial cell senescence, disrupting the intestinal and blood brain barriers. Here, we hypothesize further that post-viral sequelae, including myalgic encephalomyelitis/chronic fatigue syndrome, are promoted by the gut microbes or toxin translocation from the gastrointestinal tract into other tissues, including the brain. This model is supported by the SARS-CoV-2 interaction with host proteins and bacterial lipopolysaccharide. Conversely, targeting microbial translocation and cellular senescence may ameliorate the symptoms of this disabling illness.

Impact on Antibiotic Resistance, Therapeutic Success, and Control of Side Effects in Therapeutic Drug Monitoring (TDM) of Daptomycin: A Scoping Review.

Antimicrobial resistance (AR) is a problem that threatens the search for adequate safe and effective antibiotic therapy against multi-resistant bacteria like methicillin-resistant Staphylococcus aureus (MRSA), and vancomycin-resistant Enterococci (VRE) and Clostridium difficile, among others. Daptomycin is the treatment of choice for some infections caused by Gram-positive bacteria, indicated most of the time in patients with special clinical conditions where its high pharmacokinetic variability (PK) does not allow adequate plasma concentrations to be reached. The objective of this review is to describe the data available about the type of therapeutic drug monitoring (TDM) method used and described so far in hospitalized patients with daptomycin and to describe its impact on therapeutic success, suppression of bacterial resistance, and control of side effects. The need to create worldwide strategies for the appropriate use of antibiotics is clear, and one of these is the performance of therapeutic drug monitoring (TDM). TDM helps to achieve a dose adjustment and obtain a favorable clinical outcome for patients by measuring plasma concentrations of an administered drug, making a rational interpretation guided by a predefined concentration range, and, thus, adjusting dosages individually.

COVID-19, ferrosenescence and neurodegeneration, a mini-review.

Exacerbation of cognitive, motor and nonmotor symptoms have been described in critically ill COVID-19 patients, indicating that, like prior pandemics, neurodegenerative sequelae may mark the aftermath of this viral infection. Moreover, SARS-CoV-2, the causative agent of COVID-19 disease, was associated with hyperferritinemia and unfavorable prognosis in older individuals, suggesting virus-induced ferrosenescence. We have previously defined ferrosenescence as an iron-associated disruption of both the human genome and its repair mechanisms, leading to premature cellular senescence and neurodegeneration. As viruses replicate more efficiently in iron-rich senescent cells, they may have developed the ability to induce this phenotype in host tissues, predisposing to both immune dysfunction and neurodegenerative disorders. In this mini-review, we summarize what is known about the SARS-CoV-2-induced cellular senescence and iron dysmetabolism. We also take a closer look at immunotherapy with natural killer cells, angiotensin II receptor blockers ("sartans"), iron chelators and dipeptidyl peptidase 4 inhibitors ("gliptins") as adjunct treatments for both COVID-19 and its neurodegenerative complications.

The Other Obesity Epidemic-Of Drugs and Bugs.

Chronic psychiatric patients with schizophrenia and related disorders are frequently treatment-resistant and may require higher doses of psychotropic drugs to remain stable. Prolonged exposure to these agents increases the risk of weight gain and cardiometabolic disorders, leading to poorer outcomes and higher medical cost. It is well-established that obesity has reached epidemic proportions throughout the world, however it is less known that its rates are two to three times higher in mentally ill patients compared to the general population. Psychotropic drugs have emerged as a major cause of weight gain, pointing to an urgent need for novel interventions to attenuate this unintended consequence. Recently, the gut microbial community has been linked to psychotropic drugs-induced obesity as these agents were found to possess antimicrobial properties and trigger intestinal dysbiosis, depleting Bacteroidetes phylum. Since germ-free animals exposed to psychotropics have not demonstrated weight gain, altered commensal flora composition is believed to be necessary and sufficient to induce dysmetabolism. Conversely, not only do psychotropics disrupt the composition of gut microbiota but the later alter the metabolism of the former. Here we review the role of gut bacterial community in psychotropic drugs metabolism and dysbiosis. We discuss potential biomarkers reflecting the status of Bacteroidetes phylum and take a closer look at nutritional interventions, fecal microbiota transplantation, and transcranial magnetic stimulation, strategies that may lower obesity rates in chronic psychiatric patients.

Intoxication With Endogenous Angiotensin II: A COVID-19 Hypothesis.

Severe acute respiratory syndrome coronavirus 2 has spread rapidly around the globe. However, despite its high pathogenicity and transmissibility, the severity of the associated disease, COVID-19, varies widely. While the prognosis is favorable in most patients, critical illness, manifested by respiratory distress, thromboembolism, shock, and multi-organ failure, has been reported in about 5% of cases. Several studies have associated poor COVID-19 outcomes with the exhaustion of natural killer cells and cytotoxic T cells, lymphopenia, and elevated serum levels of D-dimer. In this article, we propose a common pathophysiological denominator for these negative prognostic markers, endogenous, angiotensin II toxicity. We hypothesize that, like in avian influenza, the outlook of COVID-19 is negatively correlated with the intracellular accumulation of angiotensin II promoted by the viral blockade of its degrading enzyme receptors. In this model, upregulated angiotensin II causes premature vascular senescence, leading to dysfunctional coagulation, and immunity. We further hypothesize that angiotensin II blockers and immune checkpoint inhibitors may be salutary for COVID-19 patients with critical illness by reversing both the clotting and immune defects (Graphical Abstract).

Determinantes sociales de la salud y riesgo familiar en población de dos municipios de caldas, colombia

Introducción: Los determinantes sociales de la salud son condiciones en las que las personas se desarrollan y tienen impacto sobre las familias. Objetivo: Determinar la relación de los determinantes sociales de la salud y el riesgo familiar en los municipios de Neira y Villamaría del departamento de Caldas. Métodos: Estudio descriptivo y correlacionai La población fue 314 fichas familiares. Resultados: El estado de la vivienda fue buena, estrato socioeconómico 2, casa o apartamento en arriendo; en mayor porcentaje, eran hombres entre 29 y 59 años, afiliados al régimen contributivo, no trabajaban y de bajo nivel educativo secundaria incompleta y completa. Los determinantes sociales de la salud que se asociaron p<0,05 con el riesgo familiar fueron: barrio, escolaridad, trabajo, tipo, condición de la vivienda y el hacinamiento. Conclusiones: Existe relación entre los determinantes sociales de la salud y el riesgo familiar. Se sugiere priorizar determinantes de acuerdo con situaciones concretas de los sujetos.

Introduction: Social determinants of health are the conditions in which people grow, and they impact families. Objective: To determine the relationship between social determinants of health and familiar risk in Neira and Villamaría municipalities in the Caldas department. Method: A descriptive and correlational study with 314 familiar records. Results: Housing condition was good, level 2 in socioeconomic strata, rented house or apartment, mostly men between 29 and 59 years old, affiliated to contributive social regime, unemployed, and low education level. The associated social determinants (p < 0,05) were: neighborhood, education level, work, type, and housing condition, and overcrowding. Conclusions: There is a relationship between social determinants of health and familiar risk. So, it is suggested to prioritize determinants according to the situations of the subjects.

Determinantes sociales de la salud y riesgo familiar en población de dos municipios de Caldas / Social determinants of health and family risk in the population of two municipalities of Caldas / Determinantes sociais da saúde e risco familiar na população de dois concelhos das Caldas

Introducción: los determinantes sociales de la salud son condiciones en las que las personas se desarrollan y tienen impacto sobre las familias. Objetivo: determinar la relación de los determinantes sociales de la salud y el riesgo familiar en los municipios de Neira y Villamaría del Departamento de Caldas. Métodos: estudio descriptivo y correlacional. La población fue 314 fichas familiares. Resultados: el estado de la vivienda fue buena, estrato socioeconómico 2, casa o apartamento en arriendo; en mayor porcentaje eran hombres entre 29 y 59 años, afiliados al régimen contributivo, no trabajaban y de bajo nivel educativo secundaria incompleta y completa. Los determinantes sociales de la salud que se asociaron p<0,05 con el riesgo familiar fueron: barrio, escolaridad, trabajo, tipo, condición de la vivienda y el hacinamiento. Conclusiones: Existe relación entre los determinantes sociales de la salud y el riesgo familiar. Se sugiere priorizar determinantes de acuerdo con situaciones concretas de los sujetos.

Introduction: the social determinants of health are conditions in which people develop and have an impact on families. Objective: to determine the relationship between the social determinants of health and family risk in the municipalities of Neira and Villamaría in the Department of Caldas. Methods: descriptive and correlational study. The population was 314 family records. Results: the state of the housing was good, socioeconomic stratum 2, house or apartment for rent; the highest percentage were men between 29 and 59 years old, affiliated to the contributory regime, not working and with a low level of education, incomplete and complete secondary school. The social determinants of health that were associated p<0.05 with family risk were: neighborhood, schooling, work, type, condition of housing and overcrowding. Conclusions: There is a relationship between social determinants of health and family risk. It is suggested to prioritize determinants according to the specific situations of the subjects.

Introdução: os determinantes sociais da saúde são as condições em que as pessoas se desenvolvem e têm um impacto nas famílias. Objetivo: determinar a relação entre os determinantes sociais da saúde e o risco familiar nos municípios de Neira e Villamaría, no Departamento de Caldas. Métodos: estudo descritivo e correlacional. A população foi constituída por 314 registos familiares. Resultados: o estado da habitação era bom, estrato socioeconómico 2, casa ou apartamento alugado; a maior percentagem era de homens entre os 29 e os 59 anos, filiados no regime contributivo, não trabalhando e com baixo nível de escolaridade, ensino secundário incompleto e completo. Os determinantes sociais de saúde que se associaram p<0,05 com o risco familiar foram: vizinhança, escolaridade, trabalho, tipo, condição da moradia e superlotação. Conclusões: Existe uma relação entre os determinantes sociais da saúde e o risco familiar. Sugere-se a priorização dos determinantes de acordo com as situações específicas dos sujeitos.

The Post-amyloid Era in Alzheimer's Disease: Trust Your Gut Feeling.

The amyloid hypothesis, the assumption that beta-amyloid toxicity is the primary cause of neuronal and synaptic loss, has been the mainstream research concept in Alzheimer's disease for the past two decades. Currently, this model is quietly being replaced by a more holistic, "systemic disease" paradigm which, like the aging process, affects multiple body tissues and organs, including the gut microbiota. It is well-established that inflammation is a hallmark of cellular senescence; however, the infection-senescence link has been less explored. Microbiota-induced senescence is a gradually emerging concept promoted by the discovery of pathogens and their products in Alzheimer's disease brains associated with senescent neurons, glia, and endothelial cells. Infectious agents have previously been associated with Alzheimer's disease, but the cause vs. effect issue could not be resolved. A recent study may have settled this debate as it shows that gingipain, a Porphyromonas gingivalis toxin, can be detected not only in Alzheimer's disease but also in the brains of older individuals deceased prior to developing the illness. In this review, we take the position that gut and other microbes from the body periphery reach the brain by triggering intestinal and blood-brain barrier senescence and disruption. We also surmise that novel Alzheimer's disease findings, including neuronal somatic mosaicism, iron dyshomeostasis, aggressive glial phenotypes, and loss of aerobic glycolysis, can be explained by the infection-senescence model. In addition, we discuss potential cellular senescence targets and therapeutic strategies, including iron chelators, inflammasome inhibitors, senolytic antibiotics, mitophagy inducers, and epigenetic metabolic reprograming.

El cuidado de sí, conocimiento actitudes y prácticas preventivas del cáncer cervicouterino, en enfermeras en formación / The care of it's, knowledge attitudes and preventive practices of the cervicouterine cancer in nurses in training

Aplicación de una encuesta con tres cuestionarios sobre lo que conocen creen e implementan como práctica cotidiana y de prevención del cáncer de cuello uterino, 158 enfermeras en formación de una universidad privada y 186 de una universidad pública, de Manizales, Colombia entre octubre de 2016 y octubre de 2017. METODOLOGÍA: descriptiva correlacional. OBJETIVOS: Describir y analizar los principales cuidados de sí, conocimientos actitudes y prácticas de las enfermeras en formación, sobre el autocuidado frente al cáncer cervicouterino. El análisis de datos se realizó con Correlación de Pearson, coeficientes de determinación y razón de momios. RESULTADOS Y CONCLUSIONES: Determinación de comportamientos deficitarios, de creencias y prácticas de prevención, necesidad de modificar los marcos cognitivos para la comprensión de la neoplasia, factores de riesgo e implicaciones en el estado de salud. El cuidado de si es un concepto fundamental para modificar modelos de representación, fortalecer actitudes y aptitudes que mejoren las capacidades de autorreflexión sobre la enfermedad.

Application of a survey with three questionnaires about what they know and implement as daily practice and prevention of cervical cancer, 158 nurses in training from a private university and 186 from a public university, from Manizales, Colombia between October 2016 and October 2017. METHODOLOGY: descriptive correlational. OBJECTIVES: Describe and analyze the main care of themselves, knowledge attitudes and practices of nurses in training, on self-care against cervical cancer. The data analysis was performed with Pearson correlation, coefficients of determination and odds ratio. RESULTS AND CONCLUSIONS: Determination of deficient behaviors, of beliefs and practices of prevention, need to modify the cognitive frameworks for the understanding of the neoplasm, risk factors and implications in the state of health. Caring for yourself is a fundamental concept for modifying models of representation, strengthening attitudes and skills that improve self-reflection abilities about the disease.

Rusty Microglia: Trainers of Innate Immunity in Alzheimer's Disease.

Alzheimer's disease, the most common form of dementia, is marked by progressive cognitive and functional impairment believed to reflect synaptic and neuronal loss. Recent preclinical data suggests that lipopolysaccharide (LPS)-activated microglia may contribute to the elimination of viable neurons and synapses by promoting a neurotoxic astrocytic phenotype, defined as A1. The innate immune cells, including microglia and astrocytes, can either facilitate or inhibit neuroinflammation in response to peripherally applied inflammatory stimuli, such as LPS. Depending on previous antigen encounters, these cells can assume activated (trained) or silenced (tolerized) phenotypes, augmenting or lowering inflammation. Iron, reactive oxygen species (ROS), and LPS, the cell wall component of gram-negative bacteria, are microglial activators, but only the latter can trigger immune tolerization. In Alzheimer's disease, tolerization may be impaired as elevated LPS levels, reported in this condition, fail to lower neuroinflammation. Iron is closely linked to immunity as it plays a key role in immune cells proliferation and maturation, but it is also indispensable to pathogens and malignancies which compete for its capture. Danger signals, including LPS, induce intracellular iron sequestration in innate immune cells to withhold it from pathogens. However, excess cytosolic iron increases the risk of inflammasomes' activation, microglial training and neuroinflammation. Moreover, it was suggested that free iron can awaken the dormant central nervous system (CNS) LPS-shedding microbes, engendering prolonged neuroinflammation that may override immune tolerization, triggering autoimmunity. In this review, we focus on iron-related innate immune pathology in Alzheimer's disease and discuss potential immunotherapeutic agents for microglial de-escalation along with possible delivery vehicles for these compounds.

Ferrosenescence: The iron age of neurodegeneration?

Aging has been associated with iron retention in many cell types, including the neurons, promoting neurodegeneration by ferroptosis. Excess intracellular iron accelerates aging by damaging the DNA and blocking genomic repair systems, a process we define as ferrosenescence. Novel neuroimaging and proteomic techniques have pinpointed indicators of both iron retention and ferrosenescence, allowing for their early correction, potentially bringing prevention of neurodegenerative disorders within reach. In this review, we take a closer look at the early markers of iron dyshomeostasis in neurodegenerative disorders, focusing on preventive strategies based on nutritional and microbiome manipulations.