Perceptions of the effect of parental deportation on adult intimate relationships.

Research has shown that children of undocumented Latinx parents in the United States are at greater risk for negative long-term effects on their mental health and overall well-being. Chief among these concerns are the negative effects of disrupted attachment processes, as deported parents are often taken from their families by force and required to parent from afar, if they can continue parenting at all. Despite the ubiquity of deported families, little is known about the effects of deportation on the attachment of left-behind children and the subsequent potential disruptive effect of deportation on their adult relationships. This phenomenological study aims to understand how adults who have experienced parental deportation in their childhood describe the effects of that event on their adult intimate relationships. Themes of (1) ambiguous loss; (2) inability to trust others; (3) fear of separation from loved ones; and (4) shame emerged and are discussed considering existing literature on attachment theory, immigration, and the Latinx population. Treatment implications are also discussed.

The autophagy protein Def8 is altered in Alzheimer's disease and Aß42-expressing Drosophila brains.

Alzheimer's disease (AD) is the most common neurodegenerative disorder, characterized by protein accumulation in the brain as a main neuropathological hallmark. Among them, Aß42 peptides tend to aggregate and create oligomers and plaques. Macroautophagy, a form of autophagy characterized by a double-membrane vesicle, plays a crucial role in maintaining neuronal homeostasis by degrading protein aggregates and dysfunctional organelles as a quality control process. Recently, DEF8, a relatively uncharacterized protein, has been proposed as a participant in vesicular traffic and autophagy pathways. We have reported increased DEF8 levels in lymphocytes from mild cognitive impairment (MCI) and early-stage AD patients and a neuronal profile in a murine transgenic AD model. Here, we analyzed DEF8 localization and levels in the postmortem frontal cortex of AD patients, finding increased levels compared to healthy controls. To evaluate the potential function of DEF8 in the nervous system, we performed an in silico assessment of its expression and network profiles, followed by an in vivo evaluation of a neuronal Def8 deficient model using a Drosophila melanogaster model of AD based on Aß42 expression. Our findings show that DEF8 is an essential protein for maintaining cellular homeostasis in the nervous system, and it is upregulated under stress conditions generated by Aß42 aggregation. This study suggests DEF8 as a novel actor in the physiopathology of AD, and its exploration may lead to new treatment avenues.

Evaluation of Three Vaccination Schemes Against Clostridium perfringens Alpha Toxin and Their Effects on the Performance, Level of Intestinal Lesions, and Serum Antibody Titers in Broilers.

The objective of the trial was to evaluate three vaccination schemes against Clostridium perfringens (CP) alpha-toxoid through drinking water to determine if they can protect against clinical signs of necrotic enteritis and coccidiosis in broiler chickens. Three hundred 1-day-old Cobb 500 male chicks were used in 4 treatments with 10 repetitions. Each group received 1 of the following treatments over the course of 29 days: T1, no vaccination; T2, vaccination on Day 1; T3, vaccination on Day 7; and T4, vaccination on Days 7 and 17. The birds were vaccinated with inactivated CP toxoid type A, administered via drinking water. During the first 14 days, a high-protein diet (27%) consisting of corn, soy, and fish meal was fed. On Day 14 Eimeria acervulina (EA), Eimeria maxima (EMx), Eimeria tenella (ET), Eimeria necatrix, and Eimeria brunetti were used in a coccidial challenge. The field isolate CP type A was then inoculated on Days 18, 19, and 20. Ten birds were slaughtered by treatment to obtain serology samples for antibody titers and intestine samples for CP and Eimeria lesion score and gut integrity indicators. Productive performance was assessed using complete randomized design and compared statistically using the Tukey test, whereas intestinal integrity variables and antibodies against CP alpha toxin were assessed using a Kruskal-Wallis nonparametric method. The results revealed that the treatments had an effect on productive performance (P < 0.05); T3 had better body weight and weight gain than T1. In terms of lesion score at Day 21, T4 had a lower lesion score by EA, EMx, and ET than T1. Cell desquamation in T2 was lower than in T4, and excess mucus (EM) in T1 was the worst in gut integrity indicators at Day 21. On the other hand, T2 had more EM than T3 and T4 at Day 25. In the measurement of antibodies, no statistical differences (P > 0.05) were found. These findings indicate that vaccination on Day 7 (T3) outperformed double vaccination on Days 7 and 17 (T4) and single on Day 1 (T2), in terms of productive performance, gut integrity, and lesion scores; and on the last day of the experiment T3 had the best performance in immunology response.

Evaluación de tres esquemas de vacunación contra la toxina alfa de Clostridium perfringens y sus efectos sobre el rendimiento, el nivel de lesiones intestinales y los títulos de anticuerpos séricos en pollos de engorde. El objetivo del ensayo fue evaluar tres programas de vacunación contra Clostridium perfringens (CP) con un alfa-toxoide a través del agua de bebida para determinar si protegían contra signos clínicos de enteritis necrótica y coccidiosis en pollos de engorde. Para ello se emplearon 300 pollitos machos Cobb 500 de un día de edad, distribuidos en 4 tratamientos con 10 repeticiones. Cada grupo recibió, durante 29 días, uno de los siguientes tratamientos: T1: sin vacunación; T2: vacunación en el día uno; T3: vacunación en el día siete y T4, vacunación en los días siete y 17. Las aves fueron vacunadas con toxoide inactivado de C. perfringens tipo A, que se administró en el agua de bebida. Durante los primeros 14 días se alimentó con una dieta alta en proteína (27%) que consistía en maíz, soya y harina de pescado. El desafío coccidial se realizó en el día 14 con Eimeria acervulina (EA), Eimeria maxima (EMx), Eimeria tenella (ET), Eimeria necatrix and Eimeria brunetti. Posteriormente, en los días 18, 19 y 20 se inoculó una cepa aislada de campo de C. perfringens tipo A. Se sacrificaron diez aves por tratamiento para obtener muestras de sueros para determinar los títulos de anticuerpos y muestras de intestino para determinar la puntuación de lesiones por C. perfringens, por Eimeria y los indicadores de integridad intestinal. El comportamiento productivo se analizó bajo un diseño completamente al azar (DCA) y la comparación estadística se realizó mediante la prueba de Tukey, mientras que para las variables de integridad intestinal y los títulos de anticuerpos contra alfa toxina de C. perfringens se utilizó el método no paramétrico Kruskal-Wallis. Los resultados mostraron que el comportamiento productivo fue influenciado por los tratamientos (P < 0.05); el tratamiento T3 mostró el mejor peso corporal y ganancia de peso en comparación con el tratamiento T1. Con relación al puntaje de lesiones en el día 21, el tratamiento T4 tuvo el menor puntaje de lesiones por E. acervulina, E. maxima y E. tenella en comparación con el tratamiento T1. La descamación celular en el tratamiento T2 fue menor que en el T4 y el exceso de moco en el tratamiento T1 fue peor entre los indicadores de integridad intestinal en el día 21. Por otro lado, el tratamiento T2 tenía más exceso de moco en comparación con los tratamientos T3 y T4 en el día 25. No se encontraron diferencias estadísticas (P > 0.05) en la medición de títulos de anticuerpos. Estos hallazgos indican que la vacunación en el día siete (T3) superó a la vacunación doble en los días 7 y 17 (T4) y única en el día uno (T2), en términos de rendimiento productivo, integridad intestinal y puntajes de lesiones, además en el último día del experimento, el tratamiento T3 tuvo el mejor desempeño en la respuesta inmunológica.

The unfolded protein response transcription factor XBP1s ameliorates Alzheimer's disease by improving synaptic function and proteostasis.

Alteration in the buffering capacity of the proteostasis network is an emerging feature of Alzheimer's disease (AD), highlighting the occurrence of endoplasmic reticulum (ER) stress. The unfolded protein response (UPR) is the main adaptive pathway to cope with protein folding stress at the ER. Inositol-requiring enzyme-1 (IRE1) operates as a central ER stress sensor, enabling the establishment of adaptive and repair programs through the control of the expression of the transcription factor X-box binding protein 1 (XBP1). To artificially enforce the adaptive capacity of the UPR in the AD brain, we developed strategies to express the active form of XBP1 in the brain. Overexpression of XBP1 in the nervous system using transgenic mice reduced the load of amyloid deposits and preserved synaptic and cognitive function. Moreover, local delivery of XBP1 into the hippocampus of an 5xFAD mice using adeno-associated vectors improved different AD features. XBP1 expression corrected a large proportion of the proteomic alterations observed in the AD model, restoring the levels of several synaptic proteins and factors involved in actin cytoskeleton regulation and axonal growth. Our results illustrate the therapeutic potential of targeting UPR-dependent gene expression programs as a strategy to ameliorate AD features and sustain synaptic function.

Neuronal Rubicon Represses Extracellular APP/Amyloid ß Deposition in Alzheimer's Disease.

Alzheimer's disease (AD) is the most prevalent age-associated neurodegenerative disease. A decrease in autophagy during aging contributes to brain disorders by accumulating potentially toxic substrates in neurons. Rubicon is a well-established inhibitor of autophagy in all cells. However, Rubicon participates in different pathways depending on cell type, and little information is currently available on neuronal Rubicon's role in the AD context. Here, we investigated the cell-specific expression of Rubicon in postmortem brain samples from AD patients and 5xFAD mice and its impact on amyloid ß burden in vivo and neuroblastoma cells. Further, we assessed Rubicon levels in human-induced pluripotent stem cells (hiPSCs), derived from early-to-moderate AD and in postmortem samples from severe AD patients. We found increased Rubicon levels in AD-hiPSCs and postmortem samples and a notable Rubicon localization in neurons. In AD transgenic mice lacking Rubicon, we observed intensified amyloid ß burden in the hippocampus and decreased Pacer and p62 levels. In APP-expressing neuroblastoma cells, increased APP/amyloid ß secretion in the medium was found when Rubicon was absent, which was not observed in cells depleted of Atg5, essential for autophagy, or Rab27a, required for exosome secretion. Our results propose an uncharacterized role of Rubicon on APP/amyloid ß homeostasis, in which neuronal Rubicon is a repressor of APP/amyloid ß secretion, defining a new way to target AD and other similar diseases therapeutically.

Thematic analysis of therapists' experiences integrating EMDR and EFT in couple therapy: Theoretical and clinical complementarity, and benefits to client couples.

In this article, we present partial findings from a thematic analysis study that examined integrating emotionally focused therapy (EFT) and eye-movement desensitization and reprocessing (EMDR) as clinical frameworks in couple therapy. The purpose of the study is to better understand how therapists integrate EFT and EMDR therapy in their clinical work. Thirteen licensed therapists (n = 13) trained in EFT and EMDR were interviewed about their experiences integrating these two models in their couple therapy practice. The findings included in this article are related to how these models complement each other as well as the clinical benefits associated with their integration. Findings provide preliminary evidence that there are benefits and challenges when integrating both models, although we emphasize complementarity in this article. Limitations and implications for future research on the integration and efficacy of these two models are also discussed.

DEF8 and Autophagy-Associated Genes Are Altered in Mild Cognitive Impairment, Probable Alzheimer's Disease Patients, and a Transgenic Model of the Disease.

BACKGROUND: Disturbances in the autophagy/endolysosomal systems are proposed as early signatures of Alzheimer's disease (AD). However, few studies are available concerning autophagy gene expression in AD patients. OBJECTIVE: To explore the differential expression of classical genes involved in the autophagy pathway, among them a less characterized one, DEF8 (Differentially expressed in FDCP 8), initially considered a Rubicon family member, in peripheralblood mononuclear cells (PBMCs) from individuals with mild cognitive impairment (MCI) and probable AD (pAD) and correlate the results with the expression of DEF8 in the brain of 5xFAD mice. METHOD: By real-time PCR and flow cytometry, we evaluated autophagy genes levels in PBMCs from MCI and pAD patients. We evaluated DEF8 levels and its localization in brain samples of the 5xFAD mice by real-time PCR, western blot, and immunofluorescence. RESULTS: Transcriptional levels of DEF8 were significantly reduced in PBMCs of MCI and pAD patients compared with healthy donors, correlating with the MoCA and MoCA-MIS cognitive tests scores. DEF8 protein levels were increased in lymphocytes from MCI but not pAD, compared to controls. In the case of brain samples from 5xFAD mice, we observed a reduced mRNA expression and augmented protein levels in 5xFAD compared to age-matched wild-type mice. DEF8 presented a neuronal localization. CONCLUSION: DEF8, a protein proposed to act at the final step of the autophagy/endolysosomal pathway, is differentially expressed in PBMCs of MCI and pAD and neurons of 5xFAD mice. These results suggest a potential role for DEF8 in the pathophysiology of AD.

IRE1 signaling exacerbates Alzheimer's disease pathogenesis.

Altered proteostasis is a salient feature of Alzheimer's disease (AD), highlighting the occurrence of endoplasmic reticulum (ER) stress and abnormal protein aggregation. ER stress triggers the activation of the unfolded protein response (UPR), a signaling pathway that enforces adaptive programs to sustain proteostasis or eliminate terminally damaged cells. IRE1 is an ER-located kinase and endoribonuclease that operates as a major stress transducer, mediating both adaptive and proapoptotic programs under ER stress. IRE1 signaling controls the expression of the transcription factor XBP1, in addition to degrade several RNAs. Importantly, a polymorphism in the XBP1 promoter was suggested as a risk factor to develop AD. Here, we demonstrate a positive correlation between the progression of AD histopathology and the activation of IRE1 in human brain tissue. To define the significance of the UPR to AD, we targeted IRE1 expression in a transgenic mouse model of AD. Despite initial expectations that IRE1 signaling may protect against AD, genetic ablation of the RNase domain of IRE1 in the nervous system significantly reduced amyloid deposition, the content of amyloid ß oligomers, and astrocyte activation. IRE1 deficiency fully restored the learning and memory capacity of AD mice, associated with improved synaptic function and improved long-term potentiation (LTP). At the molecular level, IRE1 deletion reduced the expression of amyloid precursor protein (APP) in cortical and hippocampal areas of AD mice. In vitro experiments demonstrated that inhibition of IRE1 downstream signaling reduces APP steady-state levels, associated with its retention at the ER followed by proteasome-mediated degradation. Our findings uncovered an unanticipated role of IRE1 in the pathogenesis of AD, offering a novel target for disease intervention.

[Estimation of costs caused by cystic echinococcosis]. / Estimación del impacto económico de la equinococosis quística en Chile y análisis de las posibles causas que han dificultado su erradicación.

BACKGROUND: Hydatid disease or cystic echinococcosis, caused by the parasite Echinococcus granulosus, has a worldwide distribution, affecting people of working age and can cause high levels of morbidity and even death. AIM: To estimate the economic impact at the human and animal level caused by the disease in Chile. MATERIAL AND METHODS: We analyzed information about the disease obtained from reports and publications emanated from the Chilean Ministry of Health, United Nations Food and Agriculture Organization, the U.S. National Institute of Statistics and the National Agricultural Service. Animal derived costs were estimated evaluating the expenses for pharmacological treatment of infected dogs and animal production losses derived from confiscations and reductions in meat production. RESULTS: The total number of patients who underwent surgery to remove a hydatid cyst in Chile during 2012, was estimated as 767 individuals. The annual costs derived only from surgical treatment, were estimated in USD 2.46 million. Summing the costs of sick leaves and loss of productivity, the costs at the human level ascended to USD 3.13 million. Considering human and animal costs, the annual economic burden of the disease was estimated in USD 14.35 million. CONCLUSIONS: The Analysis of the regional distribution of human and animal hydatidosis, suggests a significant environmental contamination with parasite eggs in high incidence regions such as Aysén, Araucanía, BioBío and Coquimbo. The efficiency of control programs for the disease would be greatly improved if the causes for these regional contaminations are elucidated.

Estimación del impacto económico de la equinococosis quística en Chile y análisis de las posibles causas que han dificultado su erradicación / Estimation of costs caused by cystic echinococcosis

Background: Hydatid disease or cystic echinococcosis, caused by the parasite Echinococcus granulosus, has a worldwide distribution, affecting people of working age and can cause high levels of morbidity and even death. Aim: To estimate the economic impact at the human and animal level caused by the disease in Chile. Material and Methods: We analyzed information about the disease obtained from reports and publications emanated from the Chilean Ministry of Health, United Nations Food and Agriculture Organization, the U.S. National Institute of Statistics and the National Agricultural Service. Animal derived costs were estimated evaluating the expenses for pharmacological treatment of infected dogs and animal production losses derived from confiscations and reductions in meat production. Results: The total number of patients who underwent surgery to remove a hydatid cyst in Chile during 2012, was estimated as 767 individuals. The annual costs derived only from surgical treatment, were estimated in USD 2.46 million. Summing the costs of sick leaves and loss of productivity, the costs at the human level ascended to USD 3.13 million. Considering human and animal costs, the annual economic burden of the disease was estimated in USD 14.35 million. Conclusions: The Analysis of the regional distribution of human and animal hydatidosis, suggests a significant environmental contamination with parasite eggs in high incidence regions such as Aysén, Araucanía, BioBío and Coquimbo. The efficiency of control programs for the disease would be greatly improved if the causes for these regional contaminations are elucidated.

Detection of the G3 genotype of Echinococcus granulosus from hydatid cysts of Chilean cattle using COX1 and ND1 mitochondrial markers.

For a deeper understanding of the phylogenetic relationships of Echinococcus genotypes and species in different intermediate hosts, we analyzed samples from human and bovine hydatid cysts. For this, segments of the cytochrome oxidase (COX1) and NADH dehydrogenase (ND1) mitochondrial genes were used. To obtain sufficient amounts of the ND1 marker to be sequenced properly, a new variant of the PCR assay was implemented. Phylogenetic analysis with both markers showed that most of the analyzed samples correspond to genotype G1. However, a sample from cysts of a bovine lung (Q21), with the COX1 marker, was grouped in a node together with a sample belonging to genotype G3. In the phylogenetic tree obtained with the ND1 marker, this sample was grouped with sequences of genotypes G3, G2, and G4. Analyzing the single nucleotide polymorphic (SNP) sites of both markers, it was observed that the Q21 sequence is almost identical to the G3 sequence and differ in only one SNP from the G2 sequence, and is completely different from G4. These results are noteworthy, since neither G2 nor G3 genotypes have been described previously in Chile, raising the possibility that the G3 genotype is present in these latitudes. This information is highly relevant; it can be employed to uncover additional unknown details of transmission cycles of this important parasite.

Regulation of cardiac autophagy by insulin-like growth factor 1.

Insulin-like growth factor-1 (IGF-1) signaling is a key pathway in the control of cell growth and survival. Three critical nodes in the IGF-1 signaling pathway have been described in cardiomyocytes: protein kinase Akt/mammalian target of rapamycin (mTOR), Ras/Raf/extracellular signal-regulated kinase (ERK), and phospholipase C (PLC)/inositol 1,4,5-triphosphate (InsP3 )/Ca(2+) . The Akt/mTOR and Ras/Raf/ERK signaling arms govern survival in the settings of cardiac stress and hypertrophic growth. By contrast, PLC/InsP3 /Ca(2+) functions to regulate metabolic adaptability and gene transcription. Autophagy is a catabolic process involved in protein degradation, organelle turnover, and nonselective breakdown of cytoplasmic components during nutrient starvation or stress. In the heart, autophagy is observed in a variety of human pathologies, where it can be either adaptive or maladaptive, depending on the context. We proposed the hypothesis that IGF-1 protects the heart by rescuing the mitochondrial metabolism and the energetics state, reducing cell death and controls the potentially exacerbate autophagic response to nutritional stress. In light of the importance of IGF-1 and autophagy in the heart, we review here IGF-1 signaling and autophagy regulation in the context of cardiomyocyte nutritional stress.

Una aproximación a la relación familia, envejecimiento y política social en México / An approach to the relationship family, aging and social policy in Mexico

En México, como en otros países, el envejecimiento demográfico ha sido un tema abordado en diversas investigaciones y con distintos énfasis disciplinares. Las implicaciones que traerá consigo contar con un gran número de personas con 65 años o más es un tema que ha adquirido gran relevancia en la actualidad. No obstante, hay que indicar que el envejecimiento no se vive igual en todas las latitudes, mientras que en muchos países europeos se cuentan con sistemas de salud y seguridad social para la población envejecida, en algunos países latinoamericanos el derecho a servicios de salud y la obtención deingresos una vez que se ha concluido la vida laboral siguen siendo temas de preocupación para los gobiernos. México forma parte de los países que enfrentan dificultades para atender a la población envejecida actual y la futura. Frente a este panorama las redes informales de apoyo, como la familia, son de gran importancia para aliviar las dificultades económicas y de salud a las que se enfrenta la población envejecida. Es en este contexto que el arreglo familiar en el que se encuentran las personas con 65 años o más podría responder a una “estrategia” para aliviar situaciones socioeconómicas precarias. En particular en este trabajo se tiene por objetivo ofrecer un panorama de la cobertura social de la población adulta mayor en México y su vinculación con el tipo de arreglo familiar en el que residen.

In Mexico, as in other countries, demographic ageing has been an issue studied from diverse areas and with different disciplinary emphasis. Implications which will bring with it having a large number of people 65 years or older is a matter which has gained great relevance nowadays. However, it is important to indicate that aging is not living equal in all latitudes, while many European countries have strong health systems and social security for older persons, in some Latin American countries the right to health care and income once work has been completed remain matters of concern to Governments. Mexico is part of the countries that face difficulties addressing the present and the future ageing population. Faced with this panorama, informal networks of support, such as the family, are important to relieve economic hardship and health facing the older people. It isin this context that family arrangement in which are persons age 65 or older could respond to a "strategy" relieving precarious socio-economic situations. In particular the aim of this work is to provide an overview of the social coverage of the adult population in Mexico and linking it to the type of family arrangement in which they reside.

Sindrome neurotóxico secundario a mordedura de araña: a propósito de un caso / Nerve syndrome secondary to spider bites: a case

Se presenta el caso de una mujer de 19 años de edad, víctima de mordedura de araña 72 horas previas a su ingreso hospitalario, cuando se encontraba en una excursión en la selva ecuatoriana. Horas más tarde presentó parestesias de miembros inferiores, vesículas y fiebre. A las 24 horas de la mordedura acudió a una cUnica particular en la ciudad de Quito, donde presentó cuatro convulsiones tónico-c1ónicas generalizadas. Recibió corticoide IV, analgesia, vitamina K. Posteriormente transferida al Hospital Vozandes Quito, donde se evidencia episodio de contractura muscular de dorso y región cervical posterior, sin pérdida de la conciencia, pero con dolor importante. Evolución hospitalaria satisfactoria.

Loss of escape-related giant neurons in a spiny lobster, Panulirus argus.

When attacked, many decapod crustaceans perform tailflips, which are triggered by a neural circuit that includes lateral giant interneurons, medial giant interneurons, and fast flexor motor giant neurons (MoGs). Slipper lobsters (Scyllaridae) lack these giant neurons, and it has been hypothesized that behavioral (e.g., digging) and morphological (e.g., flattening and armor) specializations in this group caused the loss of escape-related giant neurons. To test this hypothesis, we examined a species of spiny lobster, Panulirus argus. Spiny lobsters belong to the sister taxon of the scyllarids, but they have a more crayfish-like morphology than scyllarids and were predicted to have escape-related giant neurons. Ventral nerve cords of P. argus were examined using paraffin-embedded sections and cobalt backfills. We found no escape-related giant neurons and no large axon profiles in the dorsal region of the nerve cord of P. argus. Cobalt backfills showed one fewer fast flexor motor neuron than in species with MoGs and none of the fast flexor motor neurons show any of the anatomical specializations of MoGs. This suggests that all palinuran species lack this giant escape circuit, and that the loss of rapid escape behavior preceded, and may have driven, alternative predator avoidance and anti-predator strategies in palinurans.