13 research outputs found

    ICAM-1 expression on immune cells in chronic villitis

    Get PDF
    AbstractIntroductionICAM-1 expression on the villous syncytiotrophoblast (ST) is believed to participate in migration of maternal cells into the inflamed villi regardless of villitis etiology. However, its expression on immune cells in chronic villitis (CV) has yet to be analyzed. ICAM-1 induces cell–cell adhesion allowing intercellular communication, T cell-mediated defense mechanism, and inflammatory response.Material and methods21 cases of CV (all without an identifiable etiologic agent) and 3 control placentas were analyzed using ICAM-1, and for immune cells CD45, CD3 and CD68. These cells were subdivided according to their location in inflamed villi: a) within the inflamed villi and b) outside forming perivillous aggregates.ResultsLarge amounts of CD45, CD3 and CD68 were found within the inflamed villi and forming perivillous aggregates attached to areas of trophoblastic loss. Inflamed villi usually showed ICAM-1+ ST. The majority of immune cells surrounding areas of trophoblastic rupture presented marked expression of ICAM-1. In contrast, a small number of immune cells within the inflamed villi exhibited ICAM-1 expression. Only some (<5%) inflamed villi without trophoblastic rupture and with ICAM-1+ ST presented adherence of immune cells.DiscussionIn inflamed villi of chronic villitis, the level of ICAM-1 expression on immune cells depends on their location: high in number of cells in the perivillous region and low within the villi. The strongest expression of ICAM-1 on immune cells attached to areas of trophoblastic rupture suggests that the loss of trophoblast can lead to an amplification of the inflammatory response

    Genomic profile of a squamous cell carcinoma Ex pleomorphic adenoma compared to a head and neck squamous cell carcinoma

    Get PDF
    [No abstract available]sem informação843393397FAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULO2011/23204-5; 2011/23366-

    Pervasive gaps in Amazonian ecological research

    Get PDF
    Biodiversity loss is one of the main challenges of our time, and attempts to address it require a clear understanding of how ecological communities respond to environmental change across time and space. While the increasing availability of global databases on ecological communities has advanced our knowledge of biodiversity sensitivity to environmental changes, vast areas of the tropics remain understudied. In the American tropics, Amazonia stands out as the world's most diverse rainforest and the primary source of Neotropical biodiversity, but it remains among the least known forests in America and is often underrepresented in biodiversity databases. To worsen this situation, human-induced modifications may eliminate pieces of the Amazon's biodiversity puzzle before we can use them to understand how ecological communities are responding. To increase generalization and applicability of biodiversity knowledge, it is thus crucial to reduce biases in ecological research, particularly in regions projected to face the most pronounced environmental changes. We integrate ecological community metadata of 7,694 sampling sites for multiple organism groups in a machine learning model framework to map the research probability across the Brazilian Amazonia, while identifying the region's vulnerability to environmental change. 15%–18% of the most neglected areas in ecological research are expected to experience severe climate or land use changes by 2050. This means that unless we take immediate action, we will not be able to establish their current status, much less monitor how it is changing and what is being lost

    Sclerotherapy Followed By Surgery For The Treatment Of Oral Hemangioma: A Report Of Two Cases

    No full text
    Hemangiomas, vascular malformations, and varices are common benign vascular lesions in the head and neck region. They can occur in the mouth and primarily affect the lips, tongue, buccal mucosa, and palate. The main types of treatments are surgery and intralesional injection of sclerosant agents. However, other therapies have been considered, such as systemic corticosteroids, laser therapy, interferon a, and cryotherapy. Currently, sclerotherapy is employed largely because of its efficiency and ability to conserve the surrounded tissues. Surgery can be used exclusively or associated with sclerotherapy in lesions that do not show complete resolution. This article describes the cases of two patients with oral hemangiomas that were submitted to sclerotherapy with ethanol-amine oleate. Although an important decrease was detected after seven applications in both cases, surgical resection of the residual lesion was performed to achieve optimal results.593e121e125Moukaddam, H., Pollak, J., Haims, A.H., MRI characteristics and classification of peripheral vascular malformations and tumors (2009) Skeletal Radiol, 38 (6), pp. 535-547Finn, M.C., Glowacki, J., Mulliken, J.B., Congenital vascular lesions: Clinical application of a new classification (1983) Journal of Pediatric Surgery, 18 (6), pp. 894-900Takahashi, K., Mulliken, J.B., Kozakewich, H.P.W., Rogers, R.A., Folkman, J., Ezekowitz, R.A.B., Cellular markers that distinguish the phases of hemangioma during infancy and childhood (1994) Journal of Clinical Investigation, 93 (6), pp. 2357-2364Al Buainian, H., Verhaeghe, E., Dierckxsens, L., Naeyaert, J.M., Early treatment of hemangiomas with lasers (2003) A review, Dermatology, 206 (4), pp. 370-373Liu, Y., Liu, D., Wang, Y., Zhang, W., Zhao, F., Clinical study of sclerotherapy of maxillofacial venous malformations using absolute ethanol and pingyangmycin (2009) J Oral Maxillofac Surg, 67 (1), pp. 98-104Mulliken, J.B., Glowacki, J., Thomson, H.G., Hemangiomas and vascular malformations in infants and children: A classification based on endothelial characteristics (1982) Plastic and Reconstructive Surgery, 69 (3), pp. 412-422Brunelle, F.O., Chaumont, P., Jeillac, D., Manach, Y., Lallemand, D., Facial vascular malformations in children. Conventional and digital, diagnostic and therapeutic angiography (1988) Pediatr Radiol, 18 (5), pp. 377-382Selim, H., Selim, A., Khachemoune, A., Metwally, S.A.F.A., Use of sclerosing agent in the management of oral and perioral hemangiomas: Review and case reports (2007) Medical Science Monitor, 13 (9), pp. CS114-CS119. , http://www.medscimonit.com/pub/vol_13/no_9/10040.pdfCorrea, P.H., Nunes, L.C., Johann, A.C., Aguiar, M.C., Gomez, R.S., Mesquita, R.A., Prevalence of oral hemangioma, vascular malformation and varix in a Brazilian population (2007) Braz Oral Res, 21 (1), pp. 40-45Corbet, E.F., Holmgren, C.J., Phillipsen, H.P., Oral mucosal lesions in 65-74-year-old Hong Kong Chinese (1994) Community Dent Oral Epidemiol, 22 (5 PART 2), pp. 392-395Espinoza, I., Rojas, R., Aranda, W., Gamonal, J., Prevalence of oral mucosal lesions in elderly people in Santiago, Chile (2003) Journal of Oral Pathology and Medicine, 32 (10), pp. 571-575. , DOI 10.1034/j.1600-0714.2003.00031.xAl-Khateeb, T., Hamasha, A.A.-H., Almasri, N.M., Oral and maxillofacial tumours in North Jordanian children and adolescents: A retrospective analysis over 10 years (2003) International Journal of Oral and Maxillofacial Surgery, 32 (1), pp. 78-83. , DOI 10.1054/ijom.2002.0309Barrett, A.W., Speight, P.M., Superficial arteriovenous hemangioma of the oral cavity (2000) Oral Surg Oral Med Oral Pathol Oral Radiol Endod, 90 (6), pp. 731-738Legiehn, G.M., Heran, M.K., Venous malformations: Classification, development, diagnosis, and interventional radiologic management (2008) Radiol Clin North Am, 46 (3), pp. 545-597Van Doorne, L., De Maeseneer, M., Stricker, C., Vanrensbergen, R., Stricker, M., Diagnosis and treatment of vascular lesion of the lip (2002) British Journal of Oral and Maxillofacial Surgery, 40 (6), pp. 497-503. , DOI 10.1016/S0266-4356(02)00153-5Rodrigues Johann, A.C.B., Ferreira Aguiar, M.C., Vieira Do Carmo, M.A., Gomez, R.S., Castro, W.H., Mesquita, R.A., Sclerotherapy of benign oral vascular lesion with ethanolamine oleate: An open clinical trial with 30 lesions (2005) Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology and Endodontology, 100 (5), pp. 579-584. , DOI 10.1016/j.tripleo.2004.12.021, PII S1079210405000338Deveikis, J.R., Percutaneous ethanol sclerotherapy for vascular malformations in the head and neck (2005) Arch Facial Plast Surg, 7 (5), pp. 322-325Berenguer, B., Burrows, P.E., Zurakowski, D., Mulliken, J.B., Sclerotherapy of craniofacial venous malformations: Complications and results (1999) Plast Reconstr Surg, 104 (1), pp. 1-11Jin, Y., Lin, X., Li, W., Hu, X., Ma, G., Wang, W., Sclerotherapy after embolization of draining vein: A safe treatment method for venous malformations (2008) J Vase Surg, 47 (6), pp. 1292-1299Boye, E., Jinnin, M., Olsen, B.R., Infantile hemangioma: Challenges, new insights, and therapeutic promise (2009) J Craniofac Surg, 20 (SUPPL. 1), pp. 678-684Zhao, J.H., Zhang, W.F., Zhao, Y.F., Sclerotherapy of oral and facial venous malformations with use of pingyangmycin and/or sodium morrhate (2004) Int J Oral Maxillofac Surg, 33 (5), pp. 463-466Kaplan, I., Gassner, S., Shindel, Y., Carbon dioxide laser in head and neck surgery (1974) Am J Surg, 128 (4), pp. 543-544Andrews, G.C., Kelly, R.J., Treatment of vascular nevi by injection of sclerosing solutions (1932) Arch Dermatol, 26, pp. 92-94O'Donovan, J.C., Donaldson, J.S., Morello, F.P., Pensler, J.M., Vogelzang, R.L., Bauer, B., Symptomatic hemangiomas and venous malformations in infants, children, and young adults: Treatment with percutaneous injection of sodium tetradecil sulfate (1997) AJR Am J Roentgenol, 169 (3), pp. 723-729Winter, H., Drager, E., Sterry, W., Sclerotherapy for treatment of hemangiomas (2000) Dermatologic Surgery, 26 (2), pp. 105-108. , DOI 10.1046/j.1524-4725.2000.98012.xMatsumoto, K., Nakanishi, H., Koizumi, Y., Seike, T., Kanda, I., Kubo, Y., Sclerotherapy of hemangiomas with late involution (2003) Dermatol Surg, 29 (6), pp. 668-671Kaessler, H.W., Vascular birth marks (1934) J Am Med Assoc, 110, pp. 1644-1647Choi, Y.H., Han, M.H., O-Ki, K., Cha, S.H., Chang, K.-H., Craniofacial cavernous venous malformations: Percutaneous sclerotherapy with use of ethanolamine oleate (2002) Journal of Vascular and Interventional Radiology, 13 (5), pp. 475-482Bordas, J.M., Feu, F., Vilella, A., Rodes, J., Anaphylactic reaction to ethanolamine oleate injection in sclerotherapy of esophageal varices (1989) Endoscopy, 21 (1), p. 5

    Carcinoma Ex-adenoma Pleomórfico Derivado De Adenoma Pleomórfico Recorrente Mostra Diferença Importante Por Array Cgh Em Comparação Com Adenoma Pleomórfico Recorrente Sem Transformação Maligna

    No full text
    A key step of cancer development is the progressive accumulation of genomic changes resulting in disruption of several biological mechanisms. Carcinoma ex-pleomorphic adenoma (CXPA) is an aggressive neoplasm that arises from a pleomorphic adenoma. CXPA derived from a recurrent PA (RPA) has been rarely reported, and the genomic changes associated with these tumors have not yet been studied. Objective We analyzed CXPA from RPAs and RPAs without malignant transformation using array-comparative genomic hybridization (array-CGH) to identify somatic copy number alterations and affected genes. Methods DNA samples extracted from FFPE tumors were submitted to array-CGH investigation, and data was analyzed by Nexus Copy Number Discovery Edition v.7. Results No somatic copy number alterations were found in RPAs without malignant transformation. As for CXPA from RPA, although genomic profiles were unique for each case, we detected some chromosomal regions that appear to be preferentially affected by copy number alterations. The first case of CXPA-RPA (frankly invasive myoepithelial carcinoma) showed copy number alterations affecting 1p36.33p13, 5p and chromosomes 3 and 8. The second case of CXPA-RPA (frankly invasive epithelial-myoepithelial carcinoma) showed several alterations at chromosomes 3, 8, and 16, with two amplifications at 8p12p11.21 and 12q14.3q21.2. The third case of CXPA-RPA (minimally invasive epithelial-myoepithelial carcinoma) exhibited amplifications at 12q13.3q14.1, 12q14.3, and 12q15. Conclusion The occurrence of gains at chromosomes 3 and 8 and genomic amplifications at 8p and 12q, mainly those encompassing the HMGA2, MDM2, WIF1, WHSC1L1, LIRG3, CDK4 in CXAP from RPA can be a significant promotional factor in malignant transformation. © 2016 Associação Brasileira de Otorrinolaringologia e Cirurgia Cérvico-Facial82668769

    Genomic Copy Number Alterations Of Primary And Secondary Metastasizing Pleomorphic Adenomas

    No full text
    Aims: Metastasizing pleomorphic adenoma (MPA) is a rare tumour, and its mechanism of metastasis still is unknown. To date, there has been no study on MPA genomics. We analysed primary and secondary MPAs with array comparative genomic hybridization to identify somatic copy number alterations and affected genes. Methods and results: Tumour DNA samples from primary (parotid salivary gland) and secondary (scalp skin) MPAs were subjected to array comparative genomic hybridization investigation, and the data were analysed with NEXUS COPY NUMBER DISCOVERY. The primary MPA showed copy number losses affecting 3p22.2p14.3 and 19p13.3p123, and a complex pattern of four different deletions at chromosome 6. The 3p deletion encompassed several genes: CTNNB1, SETD2, BAP1, and PBRM1, among others. The secondary MPA showed a genomic profile similar to that of the primary MPA, with acquisition of additional copy number changes affecting 9p24.3p13.1 (loss), 19q11q13.43 (gain), and 22q11.1q13.33 (gain). Conclusion: Our findings indicated a clonal origin of the secondary MPA, as both tumours shared a common profile of genomic copy number alterations. Furthermore, we were able to detect in the primary tumour a specific pattern of copy number alterations that could explain the metastasizing characteristic, whereas the secondary MPA showed a more unbalanced genome

    Levels And Patterns Of Expression Of Hypoxia-inducible Factor-1α, Vascular Endothelial Growth Factor, Glucose Transporter-1 And Cd105 In Adenoid Cystic Carcinomas With High-grade Transformation

    No full text
    Aims: To compare the expression of proteins regulated by hypoxia between adenoid cystic carcinoma (ACC) with and without high-grade transformation (HGT). Methods and results: In eight ACC-HGT and 18 ACC without HGT, expression of hypoxia-inducible factor-1 (HIF-1α), vascular endothelial growth factor (VEGF), glucose transporter-1 (GLUT-1) and microvascular density (MVD) by CD105 (a hypoxia-inducible protein expressed in angiogenic endothelial cells) was determined. Expression levels of HIF-1α and VEGF as well as CD105-MVD did not differ significantly between: (i) transformed and conventional areas (TA and CA, respectively) of ACC-HGT, (ii) CA and ordinary ACC. HIF-1α was detected in 100% of cases and presented a diffuse expression pattern. No significant association was found between levels of HIF-1α expression and tumour size, metastasis and recurrence. GLUT-1 showed a prostromal expression pattern and was observed exclusively in TA (three of six cases) and in only three of 14 ACC. Conclusions: Both the absence of significant alterations in levels of expression of HIF-1α, VEGF and CD105 and the patterns of expression of HIF-1α and GLUT-1 suggest that hypoxia may not play a key role in the process of high-grade transformation of ACC. Although HIF-1α expression is a common finding in ACC, it cannot be used as a marker of tumour aggressiveness. © 2012 Blackwell Publishing Limited.605816825El-Naggar, A.K., Huvos, A.G., Adenoid cystic carcinoma (2005) World Health Organization classification of tumour. Pathology and genetics. Head and neck tumours, pp. 223-224. , Barnes L, Eveson JW, Reichart P, Sidransky D eds. Lyon: IARC PressSimpson, R.H., Pereira, E.M., Ribeiro, A.C., Abdulkadir, A., Reis-Filho, J.S., Polymorphous low-grade adenocarcinoma of the salivary glands with transformation to high-grade carcinoma (2002) Histopathology, 41, pp. 250-259Nagao, T., Gaffey, T.A., Serizawa, H., Dedifferentiated adenoid cystic carcinoma: a clinicopathologic study of 6 cases (2003) Mod. Pathol., 16, pp. 1265-1272Seethala, R.R., Hunt, J.L., Baloch, Z.W., Livolsi, V.A., Leon Barnes, E., Adenoid cystic carcinoma with high-grade transformation: a report of 11 cases and a review of the literature (2007) Am. J. Surg. Pathol., 31, pp. 1683-1694Skalová, A., Sima, R., Vanecek, T., Acinic cell carcinoma with high-grade transformation: a report of 9 cases with immunohistochemical study and analysis of TP53 and HER-2/neu genes (2009) Am. J. Surg. Pathol., 33, pp. 1137-1145Roy, P., Bullock, M.J., Perez-Ordoñez, B., Dardick, I., Weinreb, I., Epithelial-myoepithelial carcinoma with high-grade transformation (2010) Am. J. Surg. Pathol., 34, pp. 1258-1265Costa, A.F., Altemani, A., Vékony, H., Genetic profile of adenoid cystic carcinomas (ACC) with high-grade transformation versus solid type (2011) Cell. Oncol., 34, pp. 369-379Costa, A.F., Altemani, A., Hermsen, M., Current concepts on dedifferentiation/high-grade transformation in salivary gland tumors (2011) Patholog. Res. Int., 2011, p. 325965Cheuk, W., Chan, J.K., Ngan, R.K., Dedifferentiation in adenoid cystic carcinoma of salivary gland. An uncommon complication associated with an accelerated clinical course (1999) Am. J. Surg. Pathol., 23, pp. 465-472Harris, A.L., Hypoxia - a key regulatory factor in tumour growth (2002) Nat. Rev. Cancer, 2, pp. 38-47Jögi, A., Øra, I., Nilsson, H., Poellinger, L., Axelson, H., Pahlman, S., Hypoxia-induced dedifferentiation in neuroblastoma cells (2003) Cancer Lett., 197, pp. 145-150Axelson, H., Fredlund, E., Ovenberger, M., Landberg, G., Pahlman, S., Hypoxia-induced dedifferentiation of tumor cells: a mechanism behind heterogeneity and aggressiveness of solid tumors (2005) Semin. Cell Dev. Biol., 16, pp. 554-563Semenza, G.L., HIF-1: mediator of physiological and pathophysiological responses to hypoxia (2000) J. Appl. Physiol., 88, pp. 1474-1480Gatenby, R.A., Gillies, R.J., Why do cancers have high aerobic glycolysis? (2004) Nat. Rev. Cancer, 4, pp. 891-899Behrooz, A., Ismail-Beigi, F., Stimulation of glucose transport by hypoxia: signals and mechanisms (1999) News Physiol. Sci., 14, pp. 105-110Chen, C., Pore, N., Behrooz, A., Ismail-Beigi, F., Maity, A., Regulation of glut1 mRNA by hypoxia-inducible factor-1. Interaction between H-ras and hypoxia (2001) J. Biol. Chem., 276, pp. 9519-9525Gillies, R.J., Gatenby, R.A., Adaptive landscapes and emergent phenotypes: why do cancers have high glycolysis? (2007) J. Bioenerg. Biomembr., 39, pp. 251-257Haber, R.S., Rathan, A., Weiser, K.R., GLUT1 glucose transporter expression in colorectal carcinoma: a marker for poor prognosis (1998) Cancer, 83, pp. 34-40Kalir, T., Wang, B.Y., Goldfischer, M., Immunohistochemical staining of GLUT1 in benign, borderline, and malignant ovarian epithelia (2002) Cancer, 94, pp. 1078-1082Burstein, D.E., Nagi, C., Kohtz, D.S., Lee, L., Wang, B., Immunodetection of GLUT1, p63 and phospho-histone H1 in invasive head and neck squamous carcinoma: correlation of immunohistochemical staining patterns with keratinization (2006) Histopathology, 48, pp. 717-722Ferrara, N., Gerber, H.P., LeCouter, J., The biology of VEGF and its receptors (2003) Nat. Med., 9, pp. 669-676Adams, R.H., Alitalo, K., Molecular regulation of angiogenesis and lymphangiogenesis (2007) Nat. Rev. Mol. Cell Biol., 8, pp. 464-478Li, C., Issa, R., Kumar, P., CD105 prevents apoptosis in hypoxic endothelial cells (2003) J. Cell Sci., 116, pp. 2677-2685Duff, S.E., Li, C., Garland, J.M., Kumar, S., CD105 is important for angiogenesis: evidence and potential applications (2003) FASEB J., 17, pp. 984-992Li, C., Guo, B., Bernabeu, C., Kumar, S., Angiogenesis in breast cancer: the role of transforming growth factor beta and CD105 (2001) Microsc. Res. Tech., 52, pp. 437-449Seeber, L.M., Horrée, N., van der Groep, P., van der Wall, E., Verheijen, R.H., van Diest, P.J., Necrosis related HIF-1alpha expression predicts prognosis in patients with endometrioid endometrial carcinoma (2010) BMC Cancer, 10, pp. 307-317Bonfitto, V.L., Demasi, A.P., Costa, A.F., Bonfitto, J.F., Araujo, V.C., Altemani, A., High-grade transformation of adenoid cystic carcinomas: a study of the expression of GLUT1 glucose transporter and of mitochondrial antigen (2010) J. Clin. Pathol., 63, pp. 615-619Iyer, N.V., Kotch, L.E., Agani, F., Cellular and developmental control of O 2 homeostasis by hypoxia-inducible factor 1 alpha (1998) Genes Dev., 12, pp. 149-162Zhong, H., De Marzo, A.M., Laughner, E., Overexpression of hypoxia-inducible factor 1alpha in common human cancers and their metastases (1999) Cancer Res., 59, pp. 5830-5835Bos, R., Zhong, H., Hanrahan, C.F., Levels of hypoxia-inducible factor-1alpha during breast carcinogenesis (2001) J. Natl. Cancer Inst., 93, pp. 309-314Mabjeesh, N.J., Amir, S., Hypoxia-inducible factor (HIF) in human tumorigenesis (2007) Histol. Histopathol., 22, pp. 559-572Sivridis, E., Giatromanolaki, A., Gatter, K.C., Harris, A.L., Koukourakis, M.I., Association of hypoxia-inducible factors 1alpha and 2alpha with activated angiogenic pathways and prognosis in patients with endometrial carcinoma (2002) Cancer, 95, pp. 1055-1063Vleugel, M.M., Greijer, A.E., Shvarts, A., Differential prognostic impact of hypoxia induced and diffuse HIF-1alpha expression in invasive breast cancer (2005) J. Clin. Pathol., 58, pp. 172-177Tomes, L., Emberley, E., Niu, Y., Necrosis and hypoxia in invasive breast carcinoma (2003) Breast Cancer Res. Treat., 81, pp. 61-69Moreno-Sánchez, R., Rodríguez-Enríquez, A., Marín-Hernández, A., Saavedra, E., Energy metabolism in tumour cells (2007) FEBS J., 274, pp. 1393-1418Mazurek, S., Boschek, C.B., Eigenbrodt, E., The role of phosphometabolites in cell proliferation, energy metabolism, and tumor therapy (1997) J. Bioenerg. Biomembr., 29, pp. 315-330Li, C., Hampson, I.N., Hampson, L., Kumar, P., Bernabeu, C., Kumar, S., CD105 antagonizes the inhibitory signaling of transforming growth factor beta1 on human vascular endothelial cells (2000) FASEB J., 14, pp. 55-64Neufeld, G., Cohen, T., Gengrinovitch, S., Poltorak, Z., Vascular endothelial growth factor (VEGF) and its receptors (1999) FASEB J., 13, pp. 9-22Kimura, H., Weisz, A., Ogura, T., Identification of hypoxia-inducible factor 1 ancillary sequence and its function in vascular endothelial growth factor gene induction by hypoxia and nitric oxide (2001) J. Biol. Chem., 276, pp. 2292-2298Sánchez-Elsner, T., Botella, L.M., Velasco, B., Langa, C., Bernabéu, C., Endoglin expression is regulated by transcriptional cooperation between the hypoxia and transforming growth factor-beta pathways (2002) J. Biol. Chem., 277, pp. 43799-4380

    Silver nanoparticles coated with dodecanethiol used as fillers in noncytotoxic and antifungal PBAT surface based on nanocomposites

    No full text
    In the present study, we report the preparation of antifungal and non-cytotoxic polymer nanocomposites with potential application in biomedical materials. Dodecanethiol-protected silver nanoparticles (AgNPs-DDT) were synthesized by a reduction/precipitation method and dispersed in chloroform to obtain stable colloidal dispersions. PBAT-based nanocomposites containing 0.25, 0.5 and 2 wt% AgNPs-DDT were prepared by casting method. The incorporation of AgNPs-DDT in PBAT matrix resulted in nanocomposites which combine improved mechanical performance and antifungal properties with a non-cytotoxic characteristic988008072016/09588-9; 2016/08595-1NÃO TEMNÃO TEMFAPESP – Fundação de Amparo à Pesquisa Do Estado De São PauloFAPESP – Fundação de Amparo à Pesquisa Do Estado De São PauloCAPES - Coordenação de Aperfeiçoamento de Pessoal e Nível SuperiorCNPQ - Conselho Nacional de Desenvolvimento Científico e Tecnológic
    corecore