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La deficiencia de vitamina D representa una de las condiciones carenciales más comunes a nivel mundial, afectando a millones de personas en todos los grupos etarios y en múltiples contextos clínicos. A pesar de su alta prevalencia, continúa siendo subdiagnosticada y subtratada, en parte debido a su curso silencioso, a la escasa incorporación de su tamizaje en la práctica médica rutinaria y a la persistente percepción de que sus consecuencias clínicas se limitan al metabolismo óseo. Esta mirada reduccionista ha contribuido a que se desaproveche una herramienta terapéutica segura, accesible y con amplio potencial preventivo y pronóstico en distintas enfermedades crónicas.Durante décadas, el déficit de vitamina D estuvo principalmente vinculado al raquitismo infantil y a la osteomalacia en adultos, sin embargo, avances en la investigación han demostrado que la vitamina D posee receptores en múltiples tejidos, ejerciendo funciones endocrinas, paracrinas e inmunomoduladoras que trascienden su rol en la homeostasis del calcio y el fósforo. Actualmente, se reconoce que niveles bajos de 25-hidroxivitamina D están asociados no solo a fragilidad ósea, caídas y fracturas, sino también a sarcopenia, debilidad muscular, alteraciones inmunológicas, disfunción metabólica, neurocognitiva y emocional, entre otros desenlaces adversos.

One of the significant obstacles to the growth of sugarcane production is the infection by phytopathogens, mainly by the bacterium Leifsonia xyli subsp. xyli (Lxx) causal agent of Ratoon stunting disease. Thus, this research aimed to evaluate the effects of kasugamycin on the in vitro growth of sugarcane, as well as its effect on the bacterium Lxx. Explants of strain SP791011 from sugarcane were inoculated in MS culture medium supplemented with the antimicrobial kasugamycin at concentrations of 0.00; 0.87; 1.08; 1.74 and 3.48 mL.L-1, where they remained for 30 days. After this period, the survival rate, shoot number per explant, height of the explants, phytomass, dry phytomass and phytosanitary were evaluated based on the presence of genomic DNA of Lxx. It was verified that the culture in kasugamycin influenced the morphological variables negatively; nevertheless, the antimicrobial did not demonstrate phytotoxicity to the plants. All treatments tested in this experiment were diagnosed as positive, with DNA amplification for Lxx, despite it was observed a reduction in bacterial load, suggesting that kasugamycin at higher doses can be evaluated as an attempt to eliminate the bacterium in the in vitro cultivation of sugarcane. RESUMO: Um dos maiores entraves para o crescimento da produção de cana-de-açúcar é a infecção por fitopatógenos, principalmente pela bactéria Leifsonia xyli subsp. xyli (Lxx), agente causal do raquitismo-da-soqueira, doença que mais causa perdas a cultura. Assim, este trabalho teve como objetivo, avaliar os efeitos do antimicrobiano casugamicina sobre o crescimento in vitro, bem como seu efeito sobre a infecção endógena por Lxx em cana-de-açúcar. Explantes da variedade SP791011 de cana-de-açúcar foram inoculados em meio de cultura MS suplementados com o antimicrobiano nas concentrações de 0,00; 0,87; 1,08; 1,74 e 3,48 mL.L-1, em que permaneceram por 30 dias. Após este período, foi avaliada a taxa de sobrevivência, número de brotações por explante, altura dos explantes, fitomassa, fitomassa seca e fitossanidade em relação à presença de DNA genômico de Lxx. Foi verificado que o cultivo em casugamicina influenciou de forma negativa nas variáveis morfológicas, apesar disso, o antimicrobiano não mostrou fitotoxidade às plantas. Todos os tratamentos testados neste experimento foram diagnosticados como positivos, com amplificação de DNA para Lxx, apesar de ter sido observada uma redução na carga bacteriana, sugerindo que a casugamicina em doses superiores pode ser avaliada como alternativa na tentativa de eliminar completamente a bactéria no cultivo in vitro de cana-de-açúcar.

Vitamin D, the major steroid hormone that controls mineral ion homeostasis, exerts its actions through the vitamin D receptor (VDR). The VDR is expressed in many tissues, including several tissues not thought to play a role in mineral metabolism. Studies in kindreds with VDR mutations (vitamin D-dependent rickets type II, VDDR II) have demonstrated hypocalcemia, hyperparathyroidism, rickets, and osteomalacia. Alopecia, which is not a feature of vitamin D deficiency, is seen in some kindreds. We have generated a mouse model of VDDR II by targeted ablation of the second zinc finger of the VDR DNA-binding domain. Despite known expression of the VDR in fetal life, homozygous mice are phenotypically normal at birth and demonstrate normal survival at least until 6 months. They become hypocalcemic at 21 days of age, at which time their parathyroid hormone (PTH) levels begin to rise. Hyperparathyroidism is accompanied by an increase in the size of the parathyroid gland as well as an increase in PTH mRNA levels. Rickets and osteomalacia are seen by day 35; however, as early as day 15, there is an expansion in the zone of hypertrophic chondrocytes in the growth plate. In contrast to animals made vitamin D deficient by dietary means, and like some patients with VDDR II, these mice develop progressive alopecia from the age of 4 weeks.

Five- and six-day-old broilers from two flocks experiencing excessive mortality were submitted for necropsy. Rickets was diagnosed based on clinical signs of lameness and on gross and histopathologic lesions. Because of a confirmed feed mill error, these flocks had been fed a starter ration with a high calcium/phosphorus ratio (either 7.7:1 or 3.5:1). After debate concerning the profitability of salvaging the remaining birds in the affected flocks, the starter feed was replaced at 7 days of age. At processing, the affected flocks had weighted averages of body weight and feed conversion of 1.71 kg and 1.88, respectively; these averages compared favorably with the company averages of 1.72 kg and 1.87. The majority of the mortality in the affected flocks occurred during the first week. This case report demonstrates that it may be advantageous for a producer to salvage chicks that have been affected severely with rickets at less than 1 week of age

Young female broiler chickens fed diets amended with 0, 35, 75, and 150 mg fusaric acid (FA)/kg diet for 3 weeks showed no aberrations in behavior, feed intake, weight gain, or appearance of the visceral organs. Furthermore, there was no correlation between the dietary concentration of FA and incidence of tibial dyschondroplasia and leg-shape deformities. Ash content of dry fat-free tibiae was not influenced by FA; thus, no rickets was present in these chickens. FA enhanced the humoral response to sheep erythrocytes but significantly reduced cell-mediated cutaneous response to phytohemagglutinin-P

Phosphorus-deficient diets fed to broiler chicks from day 1 to day 21 induced rickets. Some chicks were stunted, but most grew well, though they had increased respiratory rates, high arterial carbon dioxide partial pressure, and low oxygen partial pressure and were polycythemic. Most of the broilers that died showed signs of pulmocardiovascular abnormalities, some died from hypoxia, and some died from right ventricular failure with or without ascites. Many broilers had mild to marked right ventricular hypertrophy and dilation with or without ascites when examined at 21 days. It is suggested that right ventricular hypertrophy and dilation was a response to pulmonary arterial hypertension caused by chronic hypoxia, which resulted from inability to breathe normally because of poor rib strength and infolding. When right ventricular failure occurred, it was secondary to right ventricular hypertrophy and dilation. /// Dietas deficientes en fósforo administradas a pollitos de engorde del día 1 al 21 causaron raquitismo. Aunque la mayoría de los pollitos creció bien, algunos presentaron enanismo. Todos mostraron un aumento en la frecuencia respiratoria, niveles arteriales altos de bióxido de carbono y bajos de oxígeno, además de policitemia. La mayoría de los pollos que murieron mostraron signos de alteraciones pulmocardiovasculares, algunos murieron por hipoxia y otros por falla ventricular derecha con o sin ascitis. El exámen al dia 21 de edad reveló que muchos pollos tenían una ligera a marcada hipertrofia ventricular derecha y dilatación con o sin ascitis. Se sugiere que la hipertrofia y dilatación ventricular derecha fué en respuesta a la hipertensión arterial pulmonar causada por la hipoxia crónica resultante de la incapacidad para respirar normalmente debido a la baja resistencia y deformación de las costillas. La falla ventricular derecha fué secundaria a la hipertrofia y dilatación ventricular derecha.

Reported rates of maternal mortality and childhood rickets in Mongolia are comparatively high and are a major health problem. This paper reviews recent literature on the causes of high maternal mortality and childhood rickets, and suggests that seasonally variable nutrition underlies risk factors for these conditions. These factors are likely to operate over an inter-generational time-scale.

Day-old broiler chicks were fed a calcium-deficient diet for 30 days. Gross, microscopic, and radiographic examinations of the proximal tibiotarsus were done at 2, 3, and 4 weeks of age. In 2-week-old chicks, the growth-plate proliferating-prehypertrophied zone (P-PHZ) was variably lengthened and disorganized, cartilage columns of the degenerating hypertrophied zone and metaphyseal primary spongiosa were shortened, and bone spicules of the secondary spongiosa were bordered by increased osteoid. In 3-week-old chicks, lesions were either similar or more pronounced, with the additional finding of metaphyseal peritrabecular fibrosis. In 4-week-old chicks, the P-PHZ decreased in relative length, osteoid seams and fibrous connective tissue were less prominent, and tibial dyschondroplasia-like lesions were present. Results demonstrated that dietary calcium deficiency produced rachitic lesions, that the lesions were very different from those of phosphorus deficiency or calcium excess, and that the lesions were variable over time. /// Pollos de engorde de un día de edad fueron alimentados con una dieta deficiente en calcio durante 30 días. A las 2, 3 o 4 semanas de edad se realizaron examenes macroscópicos, microscópicos y radiográficos de la parte proximal de la articulación tibiotarsiana. En los pollos de 2 semanas de edad la zona del cartílago hipertrófico de la línea epifisiaria se encontraba alargada y desorganizada, las columnas cartilaginosas de la zona hipertrófica y la metáfisis de la zona primaria espongiosa estaban acortadas y las espículas óseas de la espongiosa secundaria se encontraban rodeadas por un aumento del tejido osteoide. En pollos de 3 semanas de edad las lesiones fueron similares o más pronunciadas, presentándose además fibrosis peritrabecular. En pollos de 4 semanas la línea epifisiaria del cartílago hipertrófico disminuyó en su longitud relativa, las uniones osteoideas y el tejido conectivo fibroso eran menos prominentes. Se encontraron lesiones similares a las observadas en la discondroplasia de la tibia. Los resultados demostraron que una dieta deficiente en calcio produce lesiones de raquitismo y que estas lesiones son muy diferentes a aquellas inducidas por deficiencias de fósforo o por excesos de calcio. Así mismo, estas lesiones varían dependiendo del período de desarrollo de la enfermedad.

Day-old broiler chicks were fed a vitamin D-deficient diet for 30 days. Gross, microscopic, and radiographic examinations of the proximal tibiotarsus were done at 2, 3, and 4 weeks of age. In 2-week-old chicks, there was variable lengthening and disorganization of the proliferating-prehypertrophied zone (P-PHZ), resorption of cartilage spicules in the degenerating hypertrophied zone and primary spongiosa, and lengthening of bone spicules in the secondary spongiosa; many bone surfaces were lined with increased osteoid. In 3-week-old chicks, there was a tendency for the P-PHZ to decrease in relative length and for cartilage spicules to increase in length. In 4-week-old chicks, however, there was marked lengthening of the P-PHZ, resorption of cartilage spicules, and replacement of the metaphysis with irregularly oriented islands of woven bone, osteoid, and loose fibrous connective tissue. /// Pollos de engorde de un día de edad fueron alimentados con una dieta deficiente en vitamina D durante 30 días. A las 2, 3 o 4 semanas de edad se realizaron examenes macroscópicos, microscópicos y radiográficos de la parte proximal de la articulación tibiotarsiana. En pollos de 2 semanas se observó que la zona del cartílago hipertrófico de la línea epifisiaria se encontraba alargada y desorganizada; la espongiosa primaria y la zona hipertrófica presentaban reabsorción de las espículas cartilaginosas; la espongiosa secundaria presentaba alargamiento de las espículas óseas y muchas superficies óseas estaban rodeadas de tejido osteoide. En pollos de 3 semanas se observó una tendencia a disminuír en longitud de la zona del cartílago hipertrófico de la línea epifisiaria mientras que las espículas cartilaginosas aumentaban en longitud. Sin embargo, en los pollos de 4 semanas se observó un marcado alargamiento de la zona del cartílago hipértrofico de la línea epifisiaria, hubo reabsorción de las espículas cartilaginosas y reemplazo de la metáfisis con islotes trabeculares orientados irregularmente, tejidos osteoide y conectivo fibroso.