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1.
Rev. neuro-psiquiatr. (Impr.) ; 84(1): 11-18, ene-mar 2021. tab
Article in Spanish | LILACS-Express | LILACS | ID: biblio-1251972

ABSTRACT

RESUMEN Objetivo: Sistematizar el proceso de formulación de diagnósticos y planes de tratamiento en grupos participativos de profesionales y usuarios, denominados Grupos de Acogimiento, como alternativa al modelo convencional de consultas psiquiátricas individuales y secuenciales, en el ámbito de la salud mental comunitaria. Material Métodos : El estudio se realizó en un centro de salud mental comunitaria (CSMC) de Lima durante el periodo enero-diciembre de 2018. Se siguió una metodología de investigación-acción en la que propuestas surgidas de la experiencia se implementaban para, luego, analizar críticamente sus resultados y ajustarlos sucesivamente hasta lograr un punto de estandarización o de consenso entre los participantes. Resultados: El modelo participativo se aplicó en 97% de los usuarios durante el periodo de observación y se llegó a la formulación de diagnósticos y planes de tratamiento durante la sesión del Grupo de Acogimiento, en el 85% de los pacientes. Las sesiones se estandarizaron en cuatro momentos concatenados y semi-estructurados: Presentación horizontal de participantes, comprensión empática mutua, exploración colectiva de causas, y decisiones terapéuticas compartidas. Conclusiones: El modelo participativo de Grupos de Acogimiento fue una alternativa viable y eficaz para la formulación inicial de diagnósticos y planes terapéuticos en el CSMC, con fases semiestructuradas convenientemente estandarizadas y replicables.


SUMMARY Objective: To systematize the process of diagnosis and treatment plan formulations in participatory groups of users and professionals, called Fostering Groups, as an alternative to the conventional model of individual and sequential psychiatric consults, in the field of community mental health. Material and Methods : The study was carried out in a community mental health center (CMHC) in Lima throughout the period January-December 2018. An action-research methodology was followed, in which proposals arising from the experiences were put into action to, then, critically analyze the and adjust them successively until reaching a point of standardization or consensus among the participants. Results : The participatory model was applied in 97% of the users during the observation period and the formulation of diagnoses and treatment plans during the Foster Group session was successfully reached in 85% of the patients. The sessions were standardized in four concatenated and semi-structured moments: Horizontal presentation of participants, mutual empathetic understanding, collective exploration of causes, and shared therapeutic decisions. Conclusions : The Fostering group model was a viable and effective alternative for the initial formulation of diagnoses and therapeutic plans in the CMHC, with semi-structured phases conveniently standardized and replicable.

2.
Rev Fac Cien Med Univ Nac Cordoba ; 76(4): 233-237, 2019 12 03.
Article in Spanish | MEDLINE | ID: mdl-31833747

ABSTRACT

Background: Malnutrition at admission of paediatric hospitalization is a risk factor for negative evolution and is associated with increased morbidity and mortality. The main objective was to learn about the frequency of malnutrition and undernourishment as well as the nutritional risk at hospital admission, through a sample of paediatric patients. Material and Methods: A descriptive cross-sectional was taken, chosen from long term patients in Hospital Dr. Humberto Notti. A nutritional screening (Strong Kids) was applied, assessing nutritional risk within 48 hours. of hospital admission and nutritional diagnosis was obtained with the corresponding anthropometric data. For the statistical analysis, Fisher Test and Student test were used. Results: 134 patients were admitted (59% women), 4 years of age, (1 to 9 years) (medium sized and IQR), and hospitalization lasted 4 days (3 to 7 days). At the ingress, 17% presented acute malnutrition, and 60% presented moderate nutritional risk. Those who suffered from high nutritional risk, went through more frequent pain, change of weight, less eating, diarrhea, and signs of undernourishment, than those who suffered from moderated nutritional risk. (Fisher < 0, 0001). Conclusion: Malnutrition or undernourishment at hospital admission affects about the 20% of patients and more than half presents moderated nutritional risk. These two observations justify the systematic carrying out of an evaluation of the nutritional status


Introducción: La desnutrición al ingreso de la internación pediátrica es un factor de riesgo de mala evolución y está asociado a mayor morbimortalidad. El principal objetivo fue conocer la frecuencia de desnutrición y riesgo nutricional al inicio de la hospitalización en una muestra de pacientes pediátricos. Población y métodos: Diseño descriptivo, transversal. Se incluyeron pacientes de 1 mes a 14 años internados entre marzo y julio de 2016, en el Hospital Dr. Humberto Notti. Se aplicó un tamizaje nutricional (Strong Kids) valorando riesgo nutricional dentro de las 48hs. de ingreso hospitalario y se obtuvo diagnóstico nutricional con los datos antropométricos correspondientes. Para el análisis estadístico se utilizó Test de Fisher y t de Student. Resultados: Ingresaron 134 pacientes, edad 4 (1 a 9) años (mediana e IQR) y la duración de la internación fue de 4 (3 a 7) días. Al momento del ingreso el 17% presentaba desnutrición aguda y el 60% un riesgo nutricional moderado. Los pacientes con alto riesgo nutricional al ingreso tuvieron más frecuentemente dolor, cambio de peso, menor ingesta, diarrea y signos de desnutrición que los que tuvieron un riesgo nutricional moderado (Fisher < 0,0001). Conclusión: La desnutrición al ingreso de la hospitalización afecta a casi la quinta parte de los pacientes y más de la mitad presenta riesgo nutricional moderado lo que justifica la realización sistemática de la evaluación del riesgo nutricional. Conclusión: La desnutrición al ingreso de la hospitalización afecta a casi la quinta parte de los pacientes y más de la mitad presenta riesgo nutricional moderado lo que justifica la realización sistemática de la evaluación del riesgo nutricional.


Subject(s)
Hospitalization/statistics & numerical data , Malnutrition/diagnosis , Child , Child, Preschool , Cross-Sectional Studies , Female , Humans , Infant , Length of Stay , Male , Malnutrition/epidemiology , Nutrition Assessment , Pilot Projects , Risk Factors
3.
Kidney Int ; 80(4): 358-68, 2011 Aug.
Article in English | MEDLINE | ID: mdl-21389977

ABSTRACT

Enhanced transforming growth factor-ß1 (TGF-ß1) expression in renal cells promotes fibrosis and hypertrophy during the progression of diabetic nephropathy. The TGF-ß1 promoter is positively controlled by the E-box regulators, upstream stimulatory factors (USFs), in response to diabetic (high glucose) conditions; however, it is not clear whether TGF-ß1 is autoregulated by itself. As changes in microRNAs (miRNAs) have been implicated in kidney disease, we tested their involvement in this process. TGF-ß1 levels were found to be upregulated by microRNA-192 (miR-192) or miR-200b/c in mouse mesangial cells. Amounts of miR-200b/c were increased in glomeruli from type 1 (streptozotocin) and type 2 (db/db) diabetic mice, and in mouse mesangial cells treated with TGF-ß1 in vitro. Levels of miR-200b/c were also upregulated by miR-192 in the mesangial cells, suggesting that miR-200b/c are downstream of miR-192. Activity of the TGF-ß1 promoter was upregulated by TGF-ß1 or miR-192, demonstrating that the miR-192-miR-200 cascade induces TGF-ß1 expression. TGF-ß1 increased the occupancy of activators USF1 and Tfe3, and decreased that of the repressor Zeb1 on the TGF-ß1 promoter E-box binding sites. Inhibitors of miR-192 decreased the expression of miR-200b/c, Col1a2, Col4a1, and TGF-ß1 in mouse mesangial cells, and in mouse kidney cortex. Thus, miRNA-regulated circuits may amplify TGF-ß1 signaling, accelerating chronic fibrotic diseases such as diabetic nephropathy.


Subject(s)
Diabetes Mellitus, Experimental/metabolism , Diabetes Mellitus, Type 1/metabolism , Diabetes Mellitus, Type 2/metabolism , Diabetic Nephropathies/metabolism , Mesangial Cells/metabolism , MicroRNAs/metabolism , Transforming Growth Factor beta1/metabolism , 3' Untranslated Regions , Animals , Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/metabolism , Binding Sites , Cells, Cultured , Collagen Type I/metabolism , Collagen Type IV/metabolism , Diabetes Mellitus, Experimental/chemically induced , Diabetes Mellitus, Experimental/genetics , Diabetes Mellitus, Experimental/pathology , Diabetes Mellitus, Type 1/chemically induced , Diabetes Mellitus, Type 1/genetics , Diabetes Mellitus, Type 1/pathology , Diabetes Mellitus, Type 2/genetics , Diabetes Mellitus, Type 2/pathology , Diabetic Nephropathies/genetics , Diabetic Nephropathies/pathology , Fibrosis , Homeodomain Proteins/metabolism , Homeostasis , Kruppel-Like Transcription Factors/metabolism , Mice , Mutation , Oligonucleotides/metabolism , Promoter Regions, Genetic , Time Factors , Transfection , Transforming Growth Factor beta1/genetics , Up-Regulation , Upstream Stimulatory Factors/metabolism , Zinc Finger E-box-Binding Homeobox 1
4.
Clin J Am Soc Nephrol ; 4(7): 1255-66, 2009 Jul.
Article in English | MEDLINE | ID: mdl-19581401

ABSTRACT

MicroRNAs (miRs) are a family of short non-coding RNAs. These endogenously produced factors have been shown to play important roles in gene regulation. The discovery of miRs has greatly expanded our knowledge of gene regulation at the posttranscriptional level. miRs inhibit target gene expression by blocking protein translation or by inducing mRNA degradation and therefore have the potential to modulate physiologic and pathologic processes. The imperative need to determine their cellular targets and disease relevance has sparked an unprecedented explosion of research in the miR field. Recent findings have revealed critical functions for specific miRs in cellular events such as proliferation, differentiation, development, and immune responses and in the regulation of genes relevant to human diseases. Of particular interest to renal researchers are recent reports that key miRs are highly expressed in the kidney and can act as effectors of TGF-beta actions and high glucose in diabetic kidney disease. Moreover, podocyte-specific deletion of Dicer, a key enzyme involved in miR biogenesis, led to proteinuria and severe renal dysfunction in mice. Hence, studies aimed at determining the in vitro and in vivo functions of miRs in the kidney could determine their value as therapeutic targets for progressive renal glomerular and tubular diseases. Translational approaches could be facilitated by the development of effective inhibitors of specific miRs and methods for optimal delivery of anti-miRs to the kidney. The major goal of this review is to highlight key functions of these miRs and their relationships to human diseases, with special emphasis on diabetic kidney disease.


Subject(s)
Kidney/physiology , MicroRNAs/physiology , Renal Insufficiency, Chronic/genetics , Renal Insufficiency, Chronic/physiopathology , Animals , Disease Progression , Humans
5.
BMC Cancer ; 9: 159, 2009 May 21.
Article in English | MEDLINE | ID: mdl-19460168

ABSTRACT

BACKGROUND: Drosophila Groucho and its human Transducin-like-Enhancer of Split orthologs (TLEs) function as transcription co-repressors within the context of Wnt signaling, a pathway with strong links to cancer. The current model for how Groucho/TLE's modify Wnt signaling is by direct competition with beta-catenin for LEF/TCF binding. The molecular events involved in this competitive interaction are not defined and the actions of Groucho/TLEs within the context of Wnt-linked cancer are unknown. METHODS: We used in vitro protein interaction assays with the LEF/TCF family member LEF-1, and in vivo assays with Wnt reporter plasmids to define Groucho/TLE interaction and repressor function. RESULTS: Mapping studies reveal that Groucho/TLE binds two regions in LEF-1. The primary site of recognition is a 20 amino acid region in the Context Dependent Regulatory domain. An auxiliary site is in the High Mobility Group DNA binding domain. Mutation of an eight amino acid sequence within the primary region (RFSHHMIP) results in a loss of Groucho action in a transient reporter assay. Drosophila Groucho, human TLE-1, and a truncated human TLE isoform Amino-enhancer-of-split (AES), work equivalently to repress LEF-1*beta-catenin transcription in transient reporter assays, and these actions are sensitive to the HDAC inhibitor Trichostatin A. A survey of Groucho/TLE action in a panel of six colon cancer cell lines with elevated beta-catenin shows that Groucho is not able to repress transcription in a subset of these cell lines. CONCLUSION: Our data shows that Groucho/TLE repression requires two sites of interaction in LEF-1 and that a central, conserved amino acid sequence within the primary region (F S/T/P/xx y I/L/V) is critical. Our data also reveals that AES opposes LEF-1 transcription activation and that both Groucho and AES repression require histone deacetylase activity suggesting multiple steps in Groucho competition with beta-catenin. The variable ability of Groucho/TLE to oppose Wnt signaling in colon cancer cells suggests there may be defects in one or more of these steps.


Subject(s)
Basic Helix-Loop-Helix Transcription Factors/metabolism , Histone Deacetylase Inhibitors , Histone Deacetylases/metabolism , Lymphoid Enhancer-Binding Factor 1/metabolism , Repressor Proteins/metabolism , Animals , Basic Helix-Loop-Helix Transcription Factors/genetics , COS Cells , Cell Line, Tumor , Chlorocebus aethiops , Colonic Neoplasms/genetics , Colonic Neoplasms/metabolism , Humans , Hydroxamic Acids/pharmacology , Mutation , Protein Binding , Protein Structure, Tertiary , Repressor Proteins/genetics , Transfection , beta Catenin/metabolism
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