Neurocitoma central: relato de dois casos

Neurocitoma central é um tumor neuroectodérmico raro, geralmente localizado nos ventrículos laterais. Uma mulher de 26 anos e um homem de 33 anos apresentaram-se com hipertensão intracraniana. Exames de imagem revelaram tumor intraventricular heterogêneo, que impregnava por contraste, ocupando os ventrículos laterais e causando hidrocefalia. A mulher faleceu no pós-operatório e o homem está livre de recidiva após três anos. Ambos os tumores eram sólidos, com células arredondadas, lembrando oligodendroglia, positivas para sinaptofisina, cromogranina e NSE e algumas para GFAP, vimentina e proteína S-100. Microscopia eletrônica mostrou neurópilo entre os corpos celulares, mas sinapses eram raras63410841089Central neurocytomas are rare neuroectodermal tumors believed to arise from the subependymal matrix of the lateral ventricles. Case reports: A 26-year-old woman and a 33-year-old man each had a large, heterogeneous, contrast enhancing mass in the lateral ventricles at the foramen of Monro causing bilateral hydrocephalus. The woman died after surgery, but the man is asymptomatic after three years. Histopathology: Both tumors were composed of isomorphic rounded cells positive for synaptophysin, chromogranin and NSE, while some reacted for GFAP, vimentin and S-100 protein. Electron microscopy revealed neuropil-like tissue between cells, but synapses were rar

Mri Shows Dorsal Lesions And Spinal Cord Atrophy In Chronic Sensory Neuronopathies

BACKGROUND AND PURPOSE: Sensory neuronopathies (SN) represent a specific subgroup of peripheral nervous system diseases, characterized by degeneration of dorsal root ganglia (DRG) and its projections. We tried to estimate the frequency and extent of spinal cord MRI abnormalities in a group of patients with SN and correlate these with clinical and neurophysiological features. METHODS: We performed spinal cord MRI scans in 16 chronic SN patients. Images were analyzed for the presence of posterior hyperintense lesions on T2WI and cord areas at C3 level were obtained using a previously validated method. A group of 14 healthy controls with similar age and gender distribution was used for comparison. ANOVA was employed for statistical analysis. RESULTS: Posterior T2WI lesions were found in 13 out of 16 patients. Cord areas were significantly smaller in SN patients than controls (84.3 × 97.2 mm2, P <.05). Atrophy correlated with severity of sensory ataxia and neurophysiologic abnormalities but not with duration of disease. CONCLUSIONS: These findings support volumetric spinal cord MRI as a useful tool in the assessment of chronic SN. © 2008 by the American Society of Neuroimaging.182168172Sghirlanzoni, A., Pareyson, D., Lauria, G., Sensory neuron diseases (2005) Lancet Neurol, 4, pp. 349-361Lauria, G., Pareyson, D., Sghirlanzoni, A., Neurophysiological diagnosis of acquired sensory ganglionopathies (2003) Eur Neurol, 50, pp. 146-152Mori, K., Koike, H., Misu, K., Hattori, N., Ichimura, M., Sobue, G., Spinal cord magnetic resonance imaging demonstrates sensory neuronal involvement and clinical severity in neuronopathy associated with Sjogren's syndrome (2001) J Neurol Neurosurg Psychiatry, 71, pp. 488-492Lauria, G., Pareyson, D., Grisoli, M., Sghirlanzoni, A., Clinical and magnetic resonance imaging findings in chronic sensory ganglionopathies (2000) Ann Neurol, 47, pp. 104-109Carnevalle, A.D., Rondina, J.M., Kobayashi, E., Cendes, F., Validation of a semiautomated system for MRI-based hippocampal volumetry in patients with temporal lobe epilepsy (2003) J Epilepsy Clin Neurophysiol, 9, pp. 97-104Franca Jr., M.C., D'Abreu, A., Maurer-Morelli, C.V., Seccolin, R., Appenzeller, S., Alessio, A., Damasceno, B.P., Lopes-Cendes, I., Prospective neuroimaging study in hereditary spastic paraplegia with thin corpus callosum (2007) Mov Disord, 22, pp. 1556-1562Beucher, S., Meyer, F., The morphological approach to segmentation: The watershed transform (1993) Mathematical Morphology in Image Processing., pp. 433-481. , In: Dougherty, E.R., ed, New York: Marcel Dekker, chapter 12, pLin, C., Dyck, P., Spinner, R., Krauss, W., Dyck, P.J.B., Diagnostic yield of nerve rootlet biopsy [abstract] (2006) Neurology, 66 (5), pp. A44-A45Lauria, G., Sghirlanzoni, A., Lombardi, R., Pareyson, D., Epidermal nerve fiber density in sensory ganglionopathies: Clinical and neurophysiologic correlations (2001) Muscle Nerve, 24, pp. 1034-1039Bang, M.S., Han, T.R., Lim, J.Y., Acute sensory neuronopathy: Identified with electrodiagnosis and magnetic resonance imaging (1998) Am J Phys Med Rehabil, 77, pp. 494-497Takahashi, Y., Takata, T., Hoshino, M., Sakurai, M., Kanazawa, I., Benefit of IVIG for long-standing ataxic sensory neuronopathy with Sjogren's syndrome (2003) Neurology, 60, pp. 503-505Hemmer, B., Glocker, F.X., Schumacher, M., Deuschl, G., Lucking, C.H., Subacute combined degeneration: Clinical, electrophysiological, and magnetic resonance imaging findings (1998) J Neurol Neurosurg Psychiatry, 65, pp. 822-827Kumar, N., Crum, B., Petersen, R.C., Vernino, S.A., Ahlskog, J.E., Copper deficiency myelopathy (2004) Arch Neurol, 61, pp. 762-766Mascalchi, M., Salvi, F., Piacentini, S., Bartolozzi, C., Friedreich's ataxia: MR findings involving the cervical portion of the spinal cord (1994) AJR Am J Roentgenol, 163, pp. 187-191Gilmore, C.P., Deluca, G.C., Bo, L., Owens, T., Lowe, J., Esiri, M.M., Evangelou, N., Spinal cord atrophy in multiple sclerosis caused by white matter volume loss (2005) Arch Neurol, 62, pp. 1859-1862Bieniek, M., Altmann, D.R., Davies, G.R., Ingle, G.T., Rashid, W., Sastre-Garriga, J., Thompson, A.J., Miller, D.H., Cord atrophy separates early primary progressive and relapsing remitting multiple sclerosis (2006) J Neurol Neurosurg Psychiatry, 77, pp. 1036-1039Laura, M., Leong, W., Murray, N.M., Ingle, G., Miszkiel, K.A., Altmann, D.R., Miller, D.H., Reilly, M.M., Chronic inflammatory demyelinating polyradiculoneuropathy: MRI study of brain and spinal cord (2005) Neurology, 64, pp. 914-916Hedera, P., Eldevik, O.P., Maly, P., Rainier, S., Fink, J.K., Spinal cord magnetic resonance imaging in autosomal dominant hereditary spastic paraplegia (2005) Neuroradiology, 47, pp. 730-734Bakshi, R., Dandamudi, V.S., Neema, M., De, C., Bermel, R.A., Measurement of brain and spinal cord atrophy by magnetic resonance imaging as a tool to monitor multiple sclerosis (2005) J Neuroimaging, 15, pp. 30S-45SBarkhof, F., McKinstry, R.C., Quantifying spinal cord demyelination with magnetic transfer imaging (2005) Neurology, 64, pp. 1677-167

Ehlers-danlos Syndrome Type Iv And Multiple Aortic Aneurysms. A Case Report

Beside atherosclerosis, aortic aneurysms can be part of the clinical spectrum of many systemic diseases, including infectious, inflammatory, genetic and, less often, congenital disorders. A 48-year-old white man presented with multiple large aneurysms of the aorta and its main branches. Medical history was unremarkable except for the presence of a softened abdominal mass since he was 28 years old. On the physical examination, an arterial murmur was heard over the left carotid artery and a palpable mass was noted in the whole right side of the abdomen. No skin or joint abnormalities were noted. Aortography, computed tomography, and magnetic resonance angiography showed multiple large aneurysms of the descending thoracic and abdominal aorta. Aneurysms of the innominate, left subclavian, and carotid arteries were also seen. This case resembles those previously reported, in which multiple aortic aneurysms were associated with abnormalities of the type III procollagen gene (COL3A1). Although the classic stigmas of the Ehlers-Danlos syndrome type IV were lacking, this genetic disease may be the cause of the multiple aneurysms in this patient.523223228Desforges, J., Abdominal aortic aneurysm (1993) N Engl J Med, 328, pp. 1167-1172Reed, D., Reed, C., Stemmermann, G., Are aortic aneurysms caused by atherosclerosis? (1992) Circulation, 85, pp. 205-211Allins, A.D., Wagner, W.H., Cossman, L.V., Tuberculous infection of the descending thoracic and abdominal aorta: Case report and literature review (1999) Ann Vasc Surg, 13, pp. 439-444Jackman J.D., Jr., Radolf, J.D., Cardiovascular syphilis (1989) Am J Med, 87, pp. 425-433Kerr, G.S., Hallahan, C.W., Giordano, J., Takayasu arteritis (1994) Ann Intern Med, 120, pp. 919-929Kuivaniemi, H., Tromp, G., Prockop, D.J., Genetic causes of aortic aneurysms (1991) J Clin Invest, 88, pp. 1441-1444Santos-Ocampo, A., Hoffman, G.S., Aneurysms and hypermobility in a 45-year-old woman (1999) Cleve Clin J Med, 66, pp. 426-433Narcisi, P., Wu, Y., Tromp, G., Single base mutation that substitutes glutamic acid for glycine 1021 in the COL3A1 gene and causes Ehlers-Danlos syndrome type IV (1993) Am J Med Genet, 46, pp. 278-283Byers, P.H., Holbrook, K.A., Barsh, G.S., Altered secretion of type III procollagen in a form of type IV Ehlers-Danlos syndrome (1981) Lab Invest, 44, pp. 336-341Tromp, G., Kuivaniemi, H., Shikata, H., A single base mutation that substitutes serine for glycine 790 of the alpha 1 (III) chain of the type III procollagen exposes an arginine and causes Ehlers-Danlos syndrome IV (1989) J Biol Chem, 264, pp. 1349-1352Superti-Furga, A., Gugler, E., Gitzelmann, R., Ehlers-Danlos syndrome type IV: A multi-exon deletion in one of the two COL3A1 alleles affecting structure, stability, and processing of type III procollagen (1988) J Biol Chem, 263, pp. 6226-6232Pope, F.M., Martin, G.R., McKusick, V.A., Inheritance of Ehlers-Danlos type IV syndrome (1977) J Med Genet, 14, pp. 200-204Pope, F.M., Martin, G.R., Lichetenstein, J.R., Patients with Ehlers-Danlos syndrome type IV lack type III collagen (1975) Proc Natl Acad Sci USA, 72, pp. 1314-1316Tsipouras, P., Silverman, D.I., The genetic basis of aortic disease. Marfan syndrome and beyond (1999) Cardiol Clin, 17, pp. 683-696Francke, U., Berg, M., Tynan, K., A Gly 1127 Ser mutation in an EGF-like domain of the fibrillin-1 gene is a risk factor for ascending aortic aneurysm and dissection (1995) Am J Hum Genet, 56, pp. 1287-1296Engle, J., Safi, H.J., Abbassi, O., Mucopolysaccharidosis presenting as a pediatric multiple aortic aneurysm: First reported case (1997) J Vasc Surg, 26, pp. 704-710Fikar, C.R., Amrhein, J.A., Harris, J.P., Dissecting aortic aneurysm in childhood and adolescence. Case report and literature review (1981) Clin Pediatr (Phila), 20, pp. 578-583Wahl, W.L., Michaels, A.J., Wang, S.C., Blunt thoracic aortic injury: Delayed or early repair? (1999) J Trauma, 47, pp. 254-259Roth, S.M., Wheeler, J.R., Gregory, R.T., Blunt injury of the abdominal aorta: A review (1997) J Trauma, 42, pp. 748-755Tromp, G., Wu, Y., Prockop, D.J., Sequencing of cDNA from 50 unrelated patients reveals that mutations in the triple-helical domain of type III procollagen are an infrequent cause of aortic aneurysms (1993) J Clin Invest, 91, pp. 2539-2545Wilmink, A.B., Quick, C.R., Epidemiology and potential for prevention of abdominal aortic aneurysm (1998) Br J Surg, 85, pp. 155-162Curci, J.A., Liao, S., Huffman, M.D., Expression and localization of macrophage elastase (matrix matalloproteinase-12) in abdominal aortic aneurysms (1998) J Clin Invest, 102, pp. 1900-1910Sternbergh III, W.C., Gonze, M.D., Garrard, C.L., Abdominal and thoracoabdominal aortic aneurysm (1998) Surg Clin North Am, 78, pp. 827-843St Jean, P., Hart, B., Webster, M., Alpha-1-antitrypsin deficiency in aneurysmal disease (1996) Hum Heredity, 46, pp. 92-97Kita, Y., Shimizu, M., Sugihara, N., Abdominal aortic aneurysms in familial hypercholesterolemia - Case reports (1993) Angiology, 44, pp. 491-499Kontusaari, S., Tromp, G., Kuivaniemi, H., Inheritance of an RNA splicing mutation (G+ 1IVS20) in the type III procollagen gene (COL3A1) in a family having aortic aneurysms and easy bruisability: Phenotypic overlap between familial arterial aneurysms and Ehlers-Danlos syndrome type IV (1990) Am J Hum Genet, 47, pp. 112-120Khan, A.S., Spiera, H., Association of aortic aneurysm in patients with systemic lupus erythematosus: A series of case reports and a review of the literature (1998) J Rheumatol, 25, pp. 2019-2021Gedalia, A., Shetty, A.K., Ward, K., Abdominal aortic aneurysm associated with childhood sarcoidosis (1996) J Rheumatol, 23, pp. 757-759Tuzuner, A., Uncu, H., A case of Behçet's disease with an abdominal aortic aneurysm and two aneurysms in the common carotid artery (1996) Angiology, 47, pp. 1173-1180Gravallese, E.M., Corson, J.M., Coblyn, J.S., Rheumatoid aortitis: A rarely recognized but clinically significant entity (1989) Medicine, 68, pp. 95-106Cipriano, P.R., Alonso, D.R., Baltaxe, H.A., Multiple aortic aneurysms in relapsing polychondritis (1976) Am J Cardiol, 37, pp. 1097-1102Evans, J.M., O'Fallon, W.M., Hunder, G.G., Increased incidence of aortic aneurysm and dissection in giant cell (temporal) arteritis. A population-based study (1995) Ann Intern Med, 122, pp. 502-507Tseng, J.F., Cambria, R.P., Aretz, H.T., Thoracoabdominal aortic aneurysm in Cogan's syndrome (1999) J Vasc Surg, 30, pp. 565-568Baron, J.H., Aortitis and ankylosing spondilitis (1969) Lancet, 1 (7585), p. 106Kontusaari, S., Tromp, G., Kuivaniemi, H., A mutation in the gene for type III procollagen (COL3A1) in a family with aortic aneurysms (1990) J Clin Invest, 86, pp. 1465-1473Hamano, K., Minami, Y., Fujimura, Y., Emergency operation for thoracic aortic aneurysm caused by Ehlers-Danlos syndrome (1994) Ann Thorac Surg, 58, pp. 1180-1182Hamano, K., Kuga, T., Takahashi, M., The lack of type III collagen in a patient with aneurysms and an aortic dissection (1998) J Vasc Surg, 28, pp. 1104-1106Gatalica, Z., Gibas, Z., Martinez-Hernandes, A., Dissecting aortic aneurysm as a complication of generalized fibromuscular dysplasia (1992) Hum Pathol, 23, pp. 586-58

Alternating Hemisphere Tumefactive Demyelinating Disorder [2]

[No abstract available]129737738Dagher, A.P., Smirniotopoulus, J., Tumef-active demyelinating lesion (1996) Neuroradiology, 38, pp. 560-565Dale, R.C., De Sousa, C., Chong, W.K., Cox, T.C.S., Harding, B., Neville, B.G.R., Acute disseminated encephalomyelitis, multiphasic disseminated encephalomyelitis and multiple sclerosis in children (2000) Brain, 123, pp. 2407-2422Ernst, T., Chang, L., Walot, I., Huff, K., Physiologic MRI of a tumefactive multiple sclerosis lesion (1998) Neurology, 51, pp. 1486-1488Hynson, J.L., Kornberg, A.J., Coleman, L.T., Shield, L., Harvey, A.S., Kean, M.J., Clinical and neuroradiological features of acute disseminated encephalomyelitis in children (2001) Neurology, 56, pp. 1308-1312Kepes, J.J., Large focal tumor-like demyelinating lesions of the brain: Intermediate entity between multiple sclerosis and acute disseminated encephalomyelitis? A study of 31 patients (1993) Ann Neurol, 33, pp. 18-27Khan, S., Yaqub, B.A., Poser, C.M., Al Deeb, S.M., Bholega, S., Multiphasic disseminated encephalomyelitis presenting as alternating hemiplegia (1995) J Neurol Neurosurg Psychiatry, 58, pp. 467-470Law, M., Meltzer, D.E., Cha, S., Spectroscopic magnetic resonance imaging of a tumefactive demyelinating lesion (2002) Neuroradiology, 44, pp. 986-989Metafratzi, Z., Argyropoulou, M.I., Tzoufi, M., Papadopoulou, Z., Efremidis, S.C., Conventional MRI and magnetization transfer imaging of tumor like multiple sclerosis in a child (2002) Neuroradiology, 44, pp. 97-99Reis, F., Kobayashi, E., Maciel, E.P., Magnetic resonance imaging and clinical features in adults with monophasic demyelinating disease. Acute disseminated encephalomyelitis or a variant of multiple sclerosis? (1999) Arq Neuropsiquiatr, 57, pp. 853-859Schwartz, S., Mohr, A., Knauth, M., Wildemann, B., Storch-Hagenlocher, B., Acute disseminated encephalomyelitis. A follow-up of 40 adult patients (2001) Neurology, 56, pp. 1313-1318Scolding, N., The differential diagnosis of multiple sclerosis (2001) J Neurol Neurosurg Psychiatry, 71 (SUPPL. 2), pp. 9-15Simone, I.L., Federico, F., Trojano, M., High resolution proton spectroscopy of cerebrospinal fluid in MS patients - Comparison with biochemical changes in demyelinating plaques (1996) J Neurol Sci, 144, pp. 182-19

Central Neurocytoma: Report Of Two Cases

Introduction: Central neurocytomas are rare neuroectodermal tumors believed to arise from the subependymal matrix of the lateral ventricles. Case reports: A 26-year-old woman and a 33-year-old man each had a large, heterogeneous, contrast enhancing mass in the lateral ventricles at the foramen of Monro causing bilateral hydrocephalus. The woman died after surgery, but the man is asymptomatic after three years. Histopathology: Both tumors were composed of isomorphic rounded cells positive for synaptophysin, chromogranin and NSE, while some reacted for GFAP, vimentin and S-100 protein. Electron microscopy revealed neuropil-like tissue between cells, but synapses were rare.63410841089Hassoun, J., Gambarelli, D., Grisoli, F., Central neurocytoma: An electron-microscopic study of two cases (1982) Acta Neuropathol, 56, pp. 151-156. , BerlVon Deimling, A., Janzer, R., Kleihues, P., Wiestler, O.D., Patterns of differentiation in central neurocytoma: An immunohistochemical study of eleven biopsies (1990) Acta Neuropathol, 79, pp. 473-479. , BerlTsuchida, T., Matsumoto, M., Shirayama, Y., Imahori, T., Kasai, H., Kawamoto, K., Neuronal and glial characteristics of central neurocytoma: Electron microscopical analysis of two cases (1996) Acta Neuropathol, 91, pp. 573-577. , BerlIshiuchi, S., Tamura, M., Central neurocytoma: An immunohistochemical, ultrastructural and cell culture study (1997) Acta Neuropathol, 94, pp. 425-435. , BerlRobbins, P., Segal, A., Narula, S., Central neurocytoma: A clinicopathological, immunohistochemical and ultrastructural study of 7 cases (1995) Pathol Res Pract, 191, pp. 100-111Schmidt, M.H., Gottfried, O.N., Von Koch, C.S., Chang, S.M., McDermott, M.W., Central neurocytoma: A review (2004) J Neurooncol, 66, pp. 377-384Zhang, B., Luo, B., Zhang, Z., Sun, G., Wen, J., Central neurocytoma: A clinicopathological and neuroradiological study (2004) Neuroradiology, 46, pp. 888-895Nishio, S., Morioka, T., Suzuki, S., Fukui, M., Tumours around the foramen of Monro: Clinical and neuroimaging features and their differential diagnosis (2002) J Clin Neurosci, 9, pp. 137-141Shin, J.H., Lee, H.K., Khang, S.K., Neuronal tumors of the central nervous system: Radiologic findings and pathologic correlation (2002) Radiographics, 22, pp. 1177-1189Soylemezoglu, F., Onder, S., Tezel, G.G., Berker, M., Neuronal nuclear antigen (NeuN): A new tool in the diagnosis of central neurocytoma (2003) Pathol Res Pract, 199, pp. 463-468Figarella-Branger, D., Pellissier, J.F., Daumas-Duport, C., Central neurocytomas: Critical evaluation of a small-cell neuronal tumor (1992) Am J Surg Pathol, 16, pp. 97-109Kubota, T., Hayashi, M., Kawano, H., Central neurocytoma: Immunohistochemical and ultrastructural study (1991) Acta Neuropathol, 81, pp. 418-427. , BerlRades, D., Fehlauer, F., Treatment options for central neurocytoma (2002) Neurology, 59, pp. 1268-1270Kulkarni, V., Rajshekhar, V., Haran, R.P., Chandi, S.M., Long-term outcome in patients with central neurocytoma following stereotactic biopsy and radiation therapy (2002) Br J Neurosurg, 16, pp. 126-132Ashkan, K., Casey, A.T., D'Arrigo, C., Harkness, W.F., Thomas, D.G., Benign central neurocytoma (2000) Cancer, 89, pp. 1111-1120Christov, C., Adle-Biassette, H., Le Guerinel, C., Recurrent central neurocytoma with marked increase in MIB-1 labelling index (1999) Br J Neurosurg, 13, pp. 496-499Soylemezoglu, F., Scheithauer, B.W., Esteve, J., Kleihues, P., Atypical central neurocytoma (1997) J Neuropathol Exp Neurol, 56, pp. 551-556Kuchiki, H., Kayama, T., Sakurada, K., Saino, M., Kawakami, K., Sato, S., Two cases of atypical central neurocytomas (2002) Brain Tumor Pathol, 19, pp. 105-110Coelho, M.N., Ramina, R., Meneses, M.S., Arruda, W.O., Milano, J.B., Peritoneal dissemination from central neurocytoma: Case report (2003) Arq Neuropsiquiatr, 61, pp. 1030-1034Hanel, R.A., Montano, J.C., Gasparetto, E., Ditzel, L.F., Torres, L.F., Araujo, J.C., Neurocitoma central com apresentação incomum por hemorragia intraventricular: Relato de caso (2001) Arq Neuropsiquiatr, 59, pp. 628-63

Influence of a native strain of Staphylococcus xylosus on the microbiological, physicochemical and sensorial characteristics on milano salami type

In this work, the influence of native starter cultures on the microbiological, physicochemical and sensorial characteristics of Milano salami type was studied. Two batches of Milano salami type were produced: Batch A, with the addition of Staphylococcus xylosus U5 and Batch B (control) without the starter culture. The Milano salami type was characterized by an important microbial activity of coagulase-negative staphylococci (CNS) that resulted in substantial growth in Batch A during the ripening with an initial count of 7.60 log cfu.g-1 and reached 9.84 log CFU.g-1 after 14 days. Bacterial enzymes that showed efficient activity under the conditions found in Milano salami type were catalase, nitrite and nitrate reductase, contributing for sensory and physicochemical properties of the product. There were no significant differences in general free fatty acids composition among the batches, while the color parameters (L *, a * and b *) in the Batch A presented significantly higher values in relation to Batch B. Moreover, batch A had the higher preference in sensorial analysis.<br>A análise da influência de culturas iniciadoras nativas nas características microbiológicas, físicoquímicas e sensoriais de salame tipo Milano foi o objeto deste estudo. Foram produzidos dois grupos de salame tipo Milano: Grupo A - com aplicação de linhagem Staphylococcus xylosus U5 enquanto o controle, Grupo B, foi produzido sem culturas iniciadoras. O salame tipo Milano foi caracterizado pela importante atividade microbiana de estafilococos coagulase negativo (SCN), que resultou significativo crescimento no Grupo A durante a maturação, com contagem inicial de 7,60 ufc.g-1 e alcançando um crescimento de 9,84 cfu.g-1 depois de 14 dias. As enzimas bacterianas que mostraram eficiente atividade sob as condições encontradas no salame tipo Milano foram catalase, nitrito e nitrato redutase, contribuindo para as propriedades físicoquímicas e sensoriais do produto. Não houve diferenças significativas na composição geral dos ácidos graxos livres entre as amostras, enquanto os parâmetros de cor (L*, a* e b*) obtidos no salame inoculado (Grupo A) diferiram significativamente em relação ao controle (Grupo B) e foi o grupo preferido pelos degustadores