Scaffolds are devices with interconnected pores that favor cell interaction and proliferation. They play a significant role in tissue engineering, as they mimic the conditions of tissue production in vivo. The aim of this study was to synthesize scaffolds of chitosan, collagen, and Jatropha mollissima by lyophilization and characterize their chemical/biodegradability and morphological properties. For that, techniques of optical microscopy, infrared spectrometry, biodegradation test, and degree of swelling were performed. A 2% (m/v) chitosan/collagen (1:9) in lactic acid solution was produced. Then, Jatropha mollissima crude extract was added to this solution in different proportions of mass (5, 10, and 15%). Optical microscope images indicated the three-dimensional network formation with interconnected pores and predominantly lamellar shape. Through infrared spectrometry, characteristic bands indicated a physical mixture. Also, the swelling degree of all samples was proportional to the amount of Jatropha mollissima extract with the highest percentage of 1852%. Biodegradation test also revealed a proportional ratio between the amount of sap used and the degraded percentage with the lowest value of around 35% in 28 days. In conclusion, it can be inferred that the scaffolds produced show potential to be used in tissue engineering as dressings. proliferation vivo chitosan collagen chemicalbiodegradability chemical biodegradability properties microscopy spectrometry performed 2 m/v mv m v (m/v chitosancollagen 19 1 9 (1:9 Then 5, 5 (5 10 15%. 15 15% . 15%) threedimensional three dimensional shape mixture Also 1852 1852% 35 days conclusion dressings (1: ( 185 3 (1 18

Ipomoea sericophylla e Ipomoea riedelii causam uma doença de armazenamento de glicoproteínas em caprinos. Este trabalho relata a intoxicação experimental em caprinos por I. sericophylla e I. riedelii contendo 0,05% e 0,01% de swainsonina, respectivamente. Foram utilizados três grupos de quatro animais. O Grupo 1 recebeu doses diárias de 2g/kg peso vivo (pv) de I. sericophylla dessecada (150mg de swainsonina/kg). Os caprinos deste grupo apresentaram sinais clínicos 36-38 dias após o início da ingestão. O Grupo 2 ingeriu diariamente 2g/kg de I. riedelii dessecada (30mg de swainsonina/kg) por 70 dias. Como não foram observados sinais clínicos a dose de suainsonina foi aumentada para 60mg/kg por outros 70 dias. Os caprinos do Grupo 2 apresentaram sinais clínicos 26-65 dias após o aumento da dose de swainsonina para 60mg/kg. O Grupo 3 foi utilizado como controle. Neste experimento, a menor dose tóxica de swainsonina foi de 60mg/kg, que representa 0,0004% da matéria seca, em caprinos ingerindo 1,5% pv de matéria seca. Para caprinos ingerindo 2%-2,5% pv de matéria seca essa dose corresponderia a 0,00024%-0,0003 % da matéria seca. Após o final do experimento dois caprinos foram eutanasiados e outros seis foram observados para conferir a recuperação dos sinais clínicos. Quatro caprinos que continuaram ingerindo as plantas contendo suainsonina por 39-89 dias após os primeiros sinais clínicos permaneceram com sinais clínicos irreversíveis, enquanto que dois caprinos que ingeriram as plantas por 15 e 20 dias após os primeiros sinais clínicos se recuperaram totalmente. Estes resultados e os de trabalhos anteriores sugerem que as lesões irreversíveis, devidas à perda neuronal, ocorrem quando os caprinos continuam ingerindo a planta por aproximadamente 30 dias após o início dos sinais clínicos. Os sinais clínicos e as lesões histológicas foram similares às descritas anteriormente em animais intoxicados por plantas contendo swainsonina. Não foram observadas alterações significantes no hematócrito, número de eritrócitos e leucócitos, hemoglobina, volume corpuscular médio, concentrações séricas de glicose, proteínas totais e albumina e nas atividades séricas de gama glutamiltransferase e aspartato aminotransferase. As concentrações de swainsonina de 0,05% em I. sericophylla e 0,01% em I. riedelii são diferentes de amostras de essas plantas utilizadas em experimentos prévios, que continham 0.14% e 0,5% de swainsonina, respectivamente, demonstrando uma marcada variação entre amostras.

Ipomoea sericophylla and Ipomoea riedelii cause a glycoprotein storage disease in goats. This paper reports the experimental poisoning in goats by dried I. sericophylla and I. riedelii containing 0.05% and 0.01% swainsonine, respectively. Three groups with four animals each were used. Group 1 received daily doses of 2g/kg body weight (bw) of dried I. sericophylla (150mg of swainsonine/kg). Goats from this group had clinical signs 36-38 days after the start of ingestion. Group 2 received dried I. riedelii daily doses of 2g/kg of I. riedelii (30mg of swainsonine/kg) for 70 days. No clinical signs were observed, therefore the swainsonine dose was increased to 60mg/kg for another 70 days. Goats from Group 2 had clinical signs 26-65 days after increase in swainsonine dose to 60mg/kg. Group 3 was used as control. In these experiments the minimum toxic dose was 60mg/kg which represents 0.0004% of the dry matter in goats ingesting 1.5% bw of the dry matter. For goats ingesting 2%-2.5% bw of dry matter this dose would be 0.00024%-0.0003% of the dry matter. After the end of the experiment two goats were euthanized and another six were observed for recovery of clinical signs. Four goats that continued to consume swainsonine containing plant for 39-89 days after the first clinical signs had non reversible signs, while two goats that ingested the plant for only 15 and 20 days after the first clinical signs recovered completely. These and previous results indicate that irreversible lesions due to neuronal loss occur in goats that continue to ingest the plants for about 30 days after the first clinical signs. Clinical signs and histological lesions were similar to those reported previously for goats poisoned by swainsonine containing plants. No significant alterations were found in packed cell volume, red and white blood cell counts, hemoglobin and mean corpuscular hemoglobin concentrations, mean corpuscular volume, and serum levels of glucose, total protein, and albumin, and the serum activities of gamma glutamyl transferase and aspartate aminotransferase. Swainsonine concentration of 0.05% in I. sericophylla and 0.01% in I. riedelii are different from samples of these plants used in previous experiments, which contained 0.14% and 0.5% swainsonine, respectively, demonstrating a wide variation in the toxicity of different samples.

Descrevem-se três surtos de intoxicação por nitratos e nitritos em bovinos na região semi-árida do estado da Paraíba, nordeste do Brasil. O primeiro surto foi causado por Echinochloa polystachya (capim-mandante) e os demais por Pennisetum purpureum (capim-elefante) e ocorreram após um período prolongado de seca, após o início das primeiras chuvas. Em um dos surtos causado por Pennisetum purpureum, uma parte da área onde estava o pasto que continha níveis altos de nitratos havia sido fertilizada com esterco de bovino. No primeiro surto morreram 5 bovinos de um total de 11, no segundo morreram 21 de um total de 81 e no terceiro morreram 3 de um total de 19 bovinos. Os sinais clínicos se caracterizaram por anorexia, dispnéia, ranger de dentes, depressão ou hiperexitabilidade, tremores, contrações abdominais, salivação, corrimento nasal, andar cambaleante, mucosas cianóticas e, finalmente, decúbito. A presença de nitratos e nitritos foi detectada no sangue dos animais e nos pastos por meio da prova de difenilamina. Parece que o principal fator que determinou a concentração de altos níveis de nitratos nas plantas foi a ocorrência de chuvas depois de um longo período de seca. Outro fator importante no surto causado por Pennisetum purpureum foi a fertilização do solo com esterco.

Three outbreaks of nitrate poisoning are reported from the semiarid region of the state of Paraíba, northeastern Brazil. One outbreak caused by Echinochloa polystachya (capim-mandante) and two others caused by Pennisetum purpureum (capim-elefante) occurred at the end of the dry season, after the first rains. In one of the outbreaks caused by Pennisetum purpureum part of the pasture had been fertilized with cattle manure. Five out of 11 cattle died on one farm, 27 out of 81 on another, and 3 out of 9 on a third one. Clinical signs were anorexia, respiratory distress, teeth grinding, depression or hyperexitability, tremors, abdominal contractions, salivation, nasal discharge, uncoordinated gait, cyanosis, and finally recumbency. Nitrates and nitrites in the blood of affected cattle and pastures were determined by the diphenylamine test. It is suggested that the main reason for nitrate accumulation in the grasses was the prolonged draught followed by rain. In one of the outbreaks caused by Pennisetum purpureum, another reason was probably the fertilization of the soil with cattle manure.