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We evaluated the electrophoretic deposition of nanohydroxyapatite/superhydrop hilic multiwalled carbon nanotube composites (nHAp/MWCNT) onto stainless steel biomedical alloys for applications in bone tissue engineering. First, nHAp/MWCNT composites were dispersed into 0.042 mol·L-1 of Ca(NO3)2·4H2O + 0.025 mol·L-1 NH4H2PO4 electrolytes (pH = 4.8) at two different concentrations. Next, a voltage of -2 V was applied using 316L stainless steel as a working electrode (0.27 cm²), a high-purity platinum coil wire was used as the auxiliary electrode, and an Ag/AgCl (3 M) electrode was used as the reference electrode. The nHAp/MWCNT composites were characterized by transmission electron microscopy. The deposited nHAp and nHAp/MWCNT films were characterized by profilometry, scanning electron microscopy, X-ray diffractometry and Raman spectroscopy. Human osteoblast cells were cultivated with the different materials and in vitro cytotoxicity was evaluated using lactate dehydrogenase (LDH) assay. The osteogenesis process was evaluated by mRNA levels of the three genes that are directly related to bone repair: Alkaline Phosphatase, Osteopontin and Osteocalcin. We showed that rough, crystalline apatite thin films containing phases of nHAp were successfully deposited onto 316L stainless steel alloys. Also, we noticed that nHAp/MWCNT thin films deposited onto 316L stainless steel alloys upregulated the expression of important genes related to bone mineralization and maturation. Our results strongly support the possibility of this new alternative to modify the surface of metallic biomedical alloys to promote bone tissue regeneration.
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RESUMEN Objetivos Analizar: 1) el perfil lipídico en personas con glucemia de ayunas alterada (GAA) y 2) su posible asociación con parámetros clínico-metabólicos. Material y métodos Se reclutaron 101 personas de ambos sexos asistentes a consultorios de la Carrera Universitaria de Medicina Interna UNLP, incluyéndose personas >15 años que firmaron consentimiento informado para participar en el estudio; se excluyeron aquellos tratados con fármacos que afectaran el metabolismo lipídico y con diabetes tipo 2. En ellos se registraron antecedentes personales, heredofamiliares, hábitos de vida y ocurrencia de eventos cardiovasculares previos, índice de masa corporal (IMC), circunferencia de cintura (CC) y tensión arterial. En muestras de sangre se determinó glucemia, HbA1c y perfil lipídico; en la mayoría se agregó insulinemia e índice HOMA-IR. La evaluación estadística incluyó ANOVA y test de Tukey, considerándose significativas diferencias con valor de p ≤0,05. Resultados: 67,32% de los participantes presentaron glucemias ≤100 mg/dl (grupo control) y el 32,67% disglucemias compatibles con el estado de GAA. La edad promedio, el IMC y la CC, los valores de HbA1c, insulina y HOMA-IR al igual que el porcentaje de personas con hipertensión arterial fueron significativamente mayores en este último grupo. Los valores del perfil lipídico registrados fueron mayores en el grupo de GAA excepto el c-HDL en el que fueron menores. Conclusión La dislipemia presente en personas con GAA sería simultáneamente un marcador de ateroesclerosis obliterante y un promotor de la transición a DT2, por lo que requiere su diagnóstico y tratamiento precoz.
ABSTRACT Aims To analyze: 1) the lipid profile in people with impaired fasting glucose (IFG) and 2) its potential association with clinical and metabolic parameters. Materials and methods: 101 people were recruited from those attending the University of Internal Medicine UNLP clinic, including people of both sexes, >15 years who sign informed consent to participate in the study; those treated with drugs that affect lipid metabolism and with type 2 diabetes were excluded. In all of them had we recoded body mass index (BMI), abdominal circumference (AC) and blood pressure. Their personal history, inherited relatives, life habits and occurrence of cardiovascular events were also recorded. In their blood samples, blood glucose, HbA1c and lipid profile were measured as well as insulin and HOMA-IR index in most of them. Statistical evaluation included ANOVA and Tukey's test; significant differences were considered when their p value was ≤0.05. Results 67.32% of the participants presented glycemias ≤100 mg/dl (control group) and 32.67% values compatible with IFG status. Mean age, BMI and WC, HbA1c, insulin and HOMA-IR values, as well as the percentage of people with hypertension, were significantly higher in the latter group. The values of the lipid profile recorded were higher in the GAA group except the HDL-c in which they were lower. Conclusion Since the dyslipidemia present in people with IFG would simultaneously be a marker of atherosclerosis obliterans and a promoter of the transition to DT2, it requires its early diagnosis and treatment.
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Humanos , Masculino , Feminino , Glicemia/metabolismo , Diabetes Mellitus Tipo 2/complicações , Dislipidemias/complicações , Glicemia/análise , Resistência à Insulina/fisiologia , Análise de Variância , Dislipidemias/diagnósticoRESUMO
BACKGROUND: Ozone exposure could increase lung damage induced by airborne particulate matter. Particulate matter lung toxicity has been attributed to its metallic content. AIM: To evaluate the acute effect of intratracheal administration of copper sulfate (CuSO4) on rat lungs previously damaged by a chronic intermittent ozone exposure. MATERIAL AND METHODS: Two-months-old male Sprague-Dawley rats were exposed to 0.5 ppm ozone four h per day, five days a week, during two months. CuSO4 was intratracheally instilled 20 h after ozone exposure. Controls breathed filtered air or were instilled with 0.9% NaCl or with CuSO4 or were only exposed to ozone. We evaluated lung histopathology. F2 isoprostanes were determined in plasma. Cell count, total proteins, γ glutamyl-transpeptidase (GGT) and alkaline phosphatases (AP) were determined in bronchoalveolar lavage fluid (BALF). RESULTS: Ozone increased total cell count, macrophages, proteins and AP in BALF (p < 0.05), and induced pulmonary neutrophil inflammation. CuSO4 plus air increased plasma F2 isoprostane levels and total cell count, neutrophils and proteins in BALF (p < 0.05). Histopathology showed foamy macrophages. Ozone plus CuSO4 exposed animals showed a neutrophil inflammatory lung response and an increase in total cell count, proteins, GGT and AP in BALF (p < 0.05). Foamy and pigmented alveolar macrophages were detected in all lungs of these animals (p < 0.001). CONCLUSIONS: Intratracheal instillation of a single dose of CuSO4 in rats previously subjected to a chronic and intermittent exposure to ozone induces a neutrophil pulmonary inflammatory response and cytoplasmic damage in macrophages.
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Sulfato de Cobre/administração & dosagem , Ozônio/toxicidade , Pneumonia/prevenção & controle , Animais , Modelos Animais de Doenças , Pulmão/patologia , Masculino , Modelos Animais , Material Particulado/toxicidade , Pneumonia/induzido quimicamente , Pneumonia/patologia , Ratos , Ratos Sprague-Dawley , Fatores de TempoRESUMO
Background: Ozone exposure could increase lung damage induced by airborne particulate matter. Particulate matter lung toxicity has been attributed to its metallic content. Aim: To evaluate the acute effect of intratracheal administration of copper sulfate (CuSO4) on rat lungs previously damaged by a chronic intermittent ozone exposure. Material and Methods: Two-months-old male Sprague-Dawley rats were exposed to 0.5 ppm ozone four h per day, five days a week, during two months. CuSO4 was intratracheally instilled 20 h after ozone exposure. Controls breathed filtered air or were instilled with 0.9% NaCl or with CuSO4 or were only exposed to ozone. We evaluated lung histopathology. F2 isoprostanes were determined in plasma. Cell count, total proteins, γ glutamyl-transpeptidase (GGT) and alkaline phosphatases (AP) were determined in bronchoalveolar lavage fluid (BALF). Results: Ozone increased total cell count, macrophages, proteins and AP in BALF (p < 0.05), and induced pulmonary neutrophil inflammation. CuSO4 plus air increased plasma F2 isoprostane levels and total cell count, neutrophils and proteins in BALF (p < 0.05). Histopathology showed foamy macrophages. Ozone plus CuSO4 exposed animals showed a neutrophil inflammatory lung response and an increase in total cell count, proteins, GGT and AP in BALF (p < 0.05). Foamy and pigmented alveolar macrophages were detected in all lungs of these animals (p < 0.001). Conclusions: Intratracheal instillation of a single dose of CuSO4 in rats previously subjected to a chronic and intermittent exposure to ozone induces a neutrophil pulmonary inflammatory response and cytoplasmic damage in macrophages.
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Animais , Masculino , Ratos , Ozônio/toxicidade , Pneumonia/prevenção & controle , Sulfato de Cobre/administração & dosagem , Pneumonia/induzido quimicamente , Pneumonia/patologia , Fatores de Tempo , Ratos Sprague-Dawley , Modelos Animais , Modelos Animais de Doenças , Material Particulado/toxicidade , Pulmão/patologiaRESUMO
Measures to control maize white spot (MWS) caused by Pantoea ananatis are preferentially based on resistant cultivars. A lack of knowledge on the genetic variability of pathogens could interfere with the development and utilization of controlling strategies in this pathosystem. The main goals of this study were to investigate the genetic variability of 90 P. ananatis isolates from three different eco-geographical regions of Brazil by amplified fragment length polymorphism (AFLP), and to determine the presence of a universal P. ananatis plasmid in isolates from tropical Brazil. Analysis of genetic similarity by AFLP allowed us to categorize the 90 isolates into two groups. However, no correlation between the collecting sites and genetic groupings was observed. The polymorphism percentage found in P. ananatis ranged between 24.64 and 92.46%, and genetic diversity was calculated to be 0.07-0.09. The analysis of molecular variance showed that 99.18% of genetic variability was within the populations, providing evidence that evolutionary forces were acting on these populations. All P. ananatis isolates showed the P. ananatis universal plasmid (280 or 352 kb). This is the first report on the presence of a universal P. ananatis plasmid from MWS lesions in the tropical area.
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Pantoea/classificação , Doenças das Plantas/microbiologia , Zea mays/microbiologia , Análise do Polimorfismo de Comprimento de Fragmentos Amplificados , Brasil , DNA Bacteriano/genética , DNA Ribossômico/genética , Evolução Molecular , Variação Genética , Pantoea/genética , Pantoea/isolamento & purificação , Doenças das Plantas/genética , Plasmídeos/genéticaRESUMO
Maize White Spot (MWS), a foliar disease caused by Pantoea ananatis, could cause up to 60% yield loss. Some strains of P. ananatis harboring the ice nucleation gene inaA catalyze the formation of ice nuclei, causing tissue damage at temperatures slightly below freezing. Little is known about the relationship between the presence of the ina gene in this maize pathogen and its expression during the phenomenon of ice nucleus formation. Here, we attempted to verify the presence of the inaA gene and the expression of phenotype in vitro. The identity of the isolates and the presence of the inaA gene were determined by P. ananatis species-specific primers. The expression of the inaA gene was assessed in vitro by the visualization of ice-crystal formation in water at subzero temperatures. A total of ninety P. ananatis isolates from MWS lesions were characterized. The presence of the inaA gene was confirmed by gel electrophoresis of the 350-400-bp PCR products. The inaA primers did not lead to DNA fragment amplification in three isolates. The ice nucleation phenotype was expressed in 83.34% of the isolates carrying the inaA gene. Our study showed that the ice nucleation in P. ananatis isolated from MWS lesions was dependent on the presence of a functional ina gene in the genome. We also found evidence indicating that some P. ananatis strains have a mutated form of the inaA gene, producing a non-functional ice nucleation protein. This is the first report on inaA gene characterization in P. ananatis isolates from Maize White Spot.
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Proteínas de Bactérias/genética , Proteínas de Membrana/genética , Pantoea/metabolismo , Doenças das Plantas/microbiologia , Zea mays/microbiologia , Proteínas de Bactérias/metabolismo , Temperatura Baixa , Expressão Gênica , Proteínas de Membrana/metabolismo , Mutação , Pantoea/genéticaRESUMO
El ozono (O3) troposférico es el principal oxidante del esmog fotoquímico. Como es un contaminante aéreo, sus efectos están relacionados con la dosis efectiva = [Concentración] x [tiempo de exposición] x [ventilación minuto]. Objetivo: Determinar si el ejercicio físico -que aumenta la ventilación minuto- puede aumentar el daño pulmonar inducido por la exposición a O3 en ratas en reposo. Material y Métodos: Se usó 4 series de ratas Sprague-Dawley juveniles. Dos series fueron expuestas a 0,5 ppm de O3 (4 h diarias por 2 días) en reposo (n = 13) o durante ejercicio (n = 12). Dos series control respiraron aire filtrado (AF) en reposo (n = 13) o durante sesiones de ejercicio (n = 13), en una rueda vertical giratoria (15 min de ejercicio alternados con 15 min de descanso hasta completar 4 h diarias durante 2 días). Las ratas fueron eutanasiadas y se determinó la razón peso húmedo/peso seco (PH/PS) en el pulmón izquierdo. En el lavado broncoalveolar (LBA) del pulmón derecho, se determinó recuento total de células, proteínas totales y actividad de gamma-glutamiltraspeptidasa (GGT). Resultados: la razón PH/PS y el recuento de células y las proteínas del LBA aumentaron en las ratas en reposo expuestas a O3 comparadas con las ratas en reposo que respiraron AF (p < 0,05 ANOVA & Newman-Keuls). La actividad de GGT en el LBA fue mayor en las ratas que en ejercicio respiraron AF en comparación con las ratas que respiraron AF en reposo (p < 0,05). Hubo aumento de GGT, proteínas y recuento de células en el LBA de la serie [ejercicio + O3] comparada con la serie [reposo + O3] (p < 0,05). Conclusión: El ejercicio físico aumenta el daño pulmonar inducido por la exposición aguda e intermitente a 0,5 ppm de O3 en ratas juveniles.
Tropospheric ozone (O3) is the major oxidant of photochemical smog. Being an air pollutant, its effects are related to effective dose = [Concentration] x [exposure time] x [pulmonary ventilation]. Objective: Determine whether physical exercise -that increases pulmonary ventilation- is able to augment the pulmonary damage induced by O3 exposure in resting rats. Material and Methods: Four series of juvenile Sprague-Dawley rats were used. Two series were exposed to 0.5 ppm O3 (4 hours a day for 2 days) at rest (n=13) or during exercise (n=12). Two control series breathed filtered air (FA) at rest (n=13) or during exercise sessions (n=13), in a vertical rotary wheel (15 min exercise alternated with 15 min resting until to completing 4 hours a day for 2 days). Rats were euthanized and wet weight / dry weight ratio (W/D ratio) was determined in left lung. Total cell counting, total protein content and γ-glutamyltraspeptidase (GGT) activity were determined in the right lung bronchoalveolar lavage fluid (BALF). Results: W/D weight ratio as well as total cell counting and protein content increased in BALF from resting rats exposed to O3 as compared with resting rats breathing FA (p < 0.05 ANOVA & Newman-Keuls test). GGT activity in BALF increased in rats under exercise breathing FA as compared with resting rats breathing FA (p<0.05). GGT, proteins and cells counting increased in BALFfrom series [exercise + O3] as compared to series [resting + O3] (p< 0.05). Conclusion: Physical exercise increases lung damage induced by intermittent and acute 0.5 ppm O3 exposure in juvenile rats.
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Animais , Ratos , Exercício Físico , Pneumopatias/induzido quimicamente , Oxidantes Fotoquímicos/efeitos adversos , Ozônio/efeitos adversos , Análise de Variância , Pneumopatias/fisiopatologia , Fatores de Tempo , Lavagem Broncoalveolar , Ratos Sprague-Dawley , gama-GlutamiltransferaseRESUMO
A new species belonging to the Dothideomycete genus Acanthostigma is described from bark of two Nothofagus species from Argentina. Its identity as a new species is based on both morphology and molecular sequence data. Acanthostigma patagonica differs from other species in the genus by having larger ascomata and setae and wider, asymmetrical ascospores. An amended key to Acanthostigma species is provided along with a discussion of other species previously described from South America.
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Ascomicetos/classificação , Fagaceae/microbiologia , Ascomicetos/genética , Ascomicetos/ultraestrutura , DNA Fúngico/análise , DNA Fúngico/genética , DNA Ribossômico/análise , DNA Ribossômico/genética , Geografia , Dados de Sequência Molecular , Filogenia , Análise de Sequência de DNA , América do Sul , Esporos Fúngicos/ultraestruturaRESUMO
Intermittent exposure of rats to Santiago's traffic pollution is associated to a decrease in growth after more than 100 days (range: 101-111) and to histological lung damage after 90 and particularly after 180 days. Our aim was to assess whether a 90 days exposure of rats to air from a Santiago's heavy traffic avenue, is able to induce a systemic proinflammatory reaction. Thirty-days-old Sprague-Dawley rats (n = 7) were directly exposed to air from a heavy traffic avenue (8 h, 5 days a week, from April 27 to July 29, 2009). Controls (n = 7) breathed animal room air. Rats were weighed twice a week and after completing 90 days of observation, lungs were subjected to histopathology and C reactive protein, viscosity and F2-isoprostane in plasma and microhematocrit were determined in blood samples. Exposure to PM10, PM2.5, ozone, NO2 and CO were estimated from registrations of 4 Santiago's monitoring stations. Plasmatic C reactive protein and viscosity and microhematocrit were significantly increased after 90 days of exposure as compared to controls (p < 0.05). No significant changes were observed in F2-isoprostane, nor in lung histopathology, nor in body weight curve versus time in exposed as compared to control series. Hourly mean value of PM25 in the 8 h of exposure was high: 38.9 ug/m³. It is concluded that 90 days of intermittent exposure of rats to Santiago's air pollution would promote a systemic inflammatory reaction. This response to air pollution might precede the decrease in body growth and the histological lung damage reported previously by our laboratory in the same species after intermittent Santiago's urban air pollution exposure.
La exposición intermitente de ratas centinela a la contaminación del tráfico vehicular de Santiago se ha asociado a disminución del crecimiento corporal después de cien días de exposición (rango: 101-111) y a daño histopatológico del pulmón a los 90 días y más, especialmente a los 180 días de exposición. Nuestro objetivo fue evaluar si la exposición al aire de una avenida con elevado tráfico vehicular durante 90 días era capaz de inducir en la rata una respuesta inflamatoria sistémica. Ratas Sprague-Dawley de 30 días de edad (n = 7) fueron directamente expuestas a respirar el aire de una avenida con elevado flujo vehicular (8 h, 5 días por semana, desde el 27 de abril hasta el 29 de julio de 2009). Las ratas control (n = 7) respiraron aire del bioterio. Las ratas se pesaron dos veces por semana y después de completar 90 días de observación, los pulmones se destinaron a estudio histopatológico. Se realizó microhematocrito y se determinó proteína C reactiva, viscosidad y F2-isoprostano plasmáticos en muestras de sangre. La exposición a PM10, PM2,5, ozono, NO2 y CO se calculó de los registros de cuatro estaciones de monitoreo de Santiago. Después de 90 días de exposición se observó un aumento significativo (p < 0,05) de la proteína C reactiva y de la viscosidad plasmática y también del microhematocrito, en relación a la serie control. No se observaron cambios significativos en F2-isoprostano plasmático, ni en la histopatología pulmonar, ni en la curva de peso corporal versus tiempo al comparar la serie expuesta con la serie control. El promedio horario de PM2,5 en las 8 horas de exposición fue alto: 38,9 ug/m³. Concluimos que 90 días de exposición intermitente a la contaminación aérea de Santiago en el modelo experimental promueve una reacción inflamatoria sistémica. Esta respuesta a la contaminación aérea podría preceder a la disminución del crecimiento corporal y al daño histológico pulmonar encontrado en otro de nuestros estudios en esta misma especie después...
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Animais , Ratos , Poluição do Ar/efeitos adversos , Dióxido de Nitrogênio/efeitos adversos , Inflamação , Material Particulado/efeitos adversos , Monóxido de Carbono/efeitos adversos , Viscosidade Sanguínea , Poluentes Ambientais/análise , Exposição Ambiental , Pneumopatias/induzido quimicamente , /análise , Proteína C-Reativa/análise , Ratos Sprague-Dawley , Fatores de TempoRESUMO
This work reports the experimental volumetric properties and also the saturated solubility of indomethacin and ethylhexyl triazine in ethyl acetate + ethanol mixtures at 293.15 to 313.15 K and evaluates the validity of the Jouyban-Acree (J & A) model to correlate the solubility of these compounds in ethyl acetate + ethanol solvent mixtures. The solubility correlation is studied as a function of temperature and cosolvent composition. The J & A model requires only the experimental solubility values in the pure solvents at all the temperatures under study. The calculated values by using both compounds deviate as mean in 30% from experimental solubility values.
En este trabajo se evalúa la validez del modelo de Jouyban-Acree (J A) para la correlación de la solubilidad de estos dos agentes de uso farmacéutico en mezclas acetato de etilo + etanol, en función de la composición solvente y de la temperatura, en el intervalo entre 293,15 y 313,15 K. El modelo J A requiere únicamente de los valores experimentales de solubilidad de los fármacos en los solventes puros en función de la temperatura. Se encuentra que los valores obtenidos con los dos compuestos presentan desviaciones cercanas al 30% respecto a los valores experimentales de solubilidad.