Evolución histórica del Sistema Nacional de Salud venezolano(1909-2023) / Historical evolution of the Venezuelan National Health System (1909-2023)

Se hace un análisis de la Evolución Histórica del Sistema Nacional de Salud en Venezuela desde 1909 hasta el año 2023. Se realizó un desglose de seis etapas: etapa "A" o Gomecista (1905 ­ 1935), etapa "B" o de la Segunda Guerra Mundial (1936- 1945), etapa "C" o de la División de Hospitales(1946-1949), etapa "D" o Perezjimenista (1950 ­ 1958), etapa "E" o de inicio de la Democracia (1959 ­ 1963), etapa "F" de Modelo Curativo y de Expansión Hospitalaria (1963 ­ 1998),etapa "G" de la Revolución Bolivariana (1999 ­ 2023). Se analizó también el Plan Nacional de Salud 2019 ­ 2025(AU)

An analysis of the Historical Evolution of the National Health System in Venezuela is made from 1909 to the year 2023. A breakdown of six stages is made: stage "A" or Gomez (1905 - 1935), stage "B" or Second World War (1936-1945),stage "C" or the Hospital Division (1946-1949), stage "D" or Perezjimenista (1950-1958), stage "E" or the beginning of Democracy (1959-1963), stage "F" of the Curative Model and Hospital Expansion (1963-1998), stage "G" of the Bolivarian Revolution (1999 - 2023). The National Health Plan 2019 -2025 is also analyzed(AU)

Microbiota gastrointestinal aeróbica en niños con trastorno del espectro autista. Estudio preliminar / GASTROINTESTINAL MICROBIOTA AEROBIC IN CHILDREN WITH AUTISM SPECTRUM DISORDERS. PRELIMINARY STUDY

Introducción: la alteración de la microbiota intestinal o Dis- biosis ha sido implicada en los cambios de comportamiento del neurodesarrollo y problemas gastrointestinales en pacientes con trastorno del espectro autista (TEA). Objetivo: evaluar la micro- biota intestinal aeróbica (MGIA) y clasificarla en beneficiosa, transitoria y enteropatógena en niños con TEA en la Unidad de Autismo-Maternidad Concepción Palacios. Pacientes y métodos: desde el 26/02/2015 al 12/05/2015 se estudiaron de forma experimental y prospectiva 39 niños diagnosticados con TEA; en el estudio de la MGIA se utilizaron muestras de heces. Se aplicó una encuesta para recopilar datos epidemiológicos, clínicos y comportamientos del neurodesarrollo. Se propone la clasificación de severidad de la disbiosis en grado I,II,III o ausente para la evaluación de la MGIA. Resultados: Fueron 27 niños (69,23%) y 12 niñas (30,77%), con una edad media de 6,3. Disbiosis 31 (79,5%), Disbiosis ausente 8 (20,5%). Según el grado de disbiosis, 5 (16,13%) Grado I, 7 (22,58%) Grado II, 19 (61,29%) Grado III. Los principales agentes causales de disbiosis fueron Klebsiella spp. 16, Proteus mirabilis 8, Streptococcus sp, 6, Serratia marcensces 5, Candida spp. 4. Dos niños presentaron Campylobacter coli como MGIA patógena. Manifestaciones gastrointestinales: 25,80% dolor abdominal, 16,13% diarrea y 38.7% estreñimiento. Trastornos del neurodesarrollo: 50% aleteos, 34% autoagresión, 61% berrinches, insomnio un 34.3%. Conclusiones: Se hace necesario comparar esta investigación con un grupo de niños sin TEA para confirmar que la presencia de disbiosis como causante de alteración de la MGIA se presenta con más frecuencia en niños con TEA.

Background: altering the intestinal microbiota or Dysbiosis has been implicated in the changes the behavior of neurodevelopmen- tal and gastrointestinal problems in patients with autism spectrum disorder (ASD). Objective: To evaluate aerobic intestinal micro- biota (AMGI) and rank it beneficial, transitory and enteropathogenic in children with ASD, the Autism Unit-Maternidad Concepcion Palacios. Patients and Methods: From 26/02/2015 to 05/12/2015 were studied experimentally and prospectively 39 children diagnosed with ASD; in this study the AMGI stool samples were used. A survey to collect epidemiological, clinical and neurodevelopmental behavior was applied. Severity classification dysbiosis proposed in grade I, II, III or absent for evaluating the AMGI. Results: There were 27 kids (69.23%) and 12 girls (30.77%) with a mean age of 6.3. Dysbiosis 31 (79.5%), Dysbiosis absent eight (20.5%). Depending on the degree of dysbiosis, 5 (16.13%) Grade I, 7 (22.58%) Grade II, 19 (61.29%) Grade III. The main causative agents of dysbiosis were Klebsiella spp. 16, Proteus mirabilis 8, Streptococcus sp. 6, Serratia marcensces 5, Candida spp. 4. Two children presented MGIA pathogenic Campylobacter coli. Gastrointestinal symptoms: 25,80% abdominal pain, 16.13% diarrhea and 38.7% constipation. Neurodevelopmental disorders: 50% flapping, 34% self-harm, 61% tantrums and 34.3% insomnia. Conclusion: It is necessary to compare this research with a group of children without ASD to confirm the presence of dysbiosis to cau- se impaired MGIA occurs most often in children with ASD.

High plasma phospholipase A2 activity, inflammation markers, and LDL alterations in obesity with or without type 2 diabetes.

Plasma phospholipases A(2) (PLA(2)) hydrolyze phospholipids of circulating lipoproteins or deposited in arteries producing bioactive lipids believed to contribute to the atherosclerotic inflammatory response. PLA(2)(s) are elevated in obesity and type 2 diabetes (T2D) but it is not clear which of these conditions is the cause since they frequently coexist. This study attempts to evaluate if high plasma PLA(2)(s) activities and markers of their effects in lipoproteins are associated with obesity or T2D diabetes, or with both. Total PLA(2) and Ca(2+)-dependent and -independent activities, lipids, lipoproteins, apoAI, and apoB apolipoproteins and affinity of apoB-lipoproteins for arterial proteoglycans were measured, as well as Inflammation markers. These parameters were evaluated in plasma samples of four groups: (i) apparently healthy controls with normal BMI (nBMI), (ii) obese subjects with no T2D, (iii) patients with T2D but with nBMI, and (iv) obese patients with T2D. PLA(2) activities were measured in the presence and absence of Ca(2+) and in the presence of specific inhibitors. Obese subjects, with or without T2D, had high activities of total PLA(2) and of Ca(2+)-dependent and Ca(2+)-independent enzymes. The activities were correlated with inflammation markers in obese subjects with and without diabetes and with alterations of low-density lipoproteins (LDLs) that increased their affinity for arterial proteoglycans. Ca(2+)-dependent secretory (sPLA(2)) enzymes were the main responsible of the obesity-associated high activity. We speculate that augmented PLA(2)(s) activity that increases affinity of circulating LDL for arterial intima proteoglycans could be another atherogenic component of obesity.