Reflexões sobre o projeto ético-político profissional do serviço social e a democratização

O presente artigo apresenta reflexões sobre o projeto ético-político profissional e a defesa das conquistas democráticas brasileiras, tendo como fio condutor a análise sobre democracia e democratização, e o desafio de reafirmar a democracia como princípio do Código de Ética Profissional na defesa de um projeto profissional vinculado à construção de uma nova ordem societária

On the Relationships between Minor Tremor and Ballistocardiogram in Man

The minor tremor (MT), or microvibration, of the thenar muscles was recorded over in normal adults under various physiological conditions. In addition to MT, the ballistocardiogram (BCG), electrocardiogram (EKG) and respiratory movements were also traced simultaneously to determine the correspondence between MT and the pulsation of the heart. In. the relaxed awake state, the dominant vibrations of MT were found out to appear in corresponding very well to I, J and K and L, M and N waves of BCG as well as R and T waves of EKG. These changes corresponding to BCG or EKG were, on the other hand, demonstrated to be potentiated and weakened by deepening and stopping breathing, respectively. In addition, both MT and BCG were shown to cause a marked increase in amplitude and frequency in cases of Master two step test as the load of EKG, in which facilitatory changes of circulatory and respiratory systems can be provoked. From the above-mentioned results, it seems likely that the facilitatory and inhibitory changes in the pulsation of the heart besides those in muscle tonus play an important role in the augmentation and inhibition in MT under various physiological conditions, and furthermore the respiratory changes in MT might be caused by respiratory changes of cardiac output in inspiratory and expiratory phases of respiration as well

MicroRNA Deregulation in Anaplastic Thyroid Cancer Biology

Anaplastic thyroid cancer (ATC) is among the most lethal types of cancers, characterized as a fast-growing and highly invasive thyroid tumor that is unresponsive to surgery and radioiodine, blunting therapeutic efficacy. Classically, genetic alterations in tumor suppressor TP53 are frequent, and cumulative alterations in different signaling pathways, such as MAPK and PI3K, are detected in ATC. Recently, deregulation in microRNAs (miRNAs), a class of small endogenous RNAs that regulate protein expression, has been implicated in tumorigenesis and cancer progression. Deregulation of miRNA expression is detected in thyroid cancer. Upregulation of miRNAs, such as miR-146b, miR-221, and miR-222, is observed in ATC and also in differentiated thyroid cancer (papillary and follicular), indicating that these miRNAs’ overexpression is essential in maintaining tumorigenesis. However, specific miRNAs are downregulated in ATC, such as those of the miR-200 and miR-30 families, which are important negative regulators of cell migration, invasion, and epithelial-to-mesenchymal transition (EMT), processes that are overactivated in ATC. Therefore, molecular interference to restore the expression of tumor suppressor miRNAs, or to blunt overexpressed oncogenic miRNAs, is a promising therapeutic approach to ameliorate the treatment of ATC. In this review, we will explore the importance of miRNA deregulation for ATC cell biology

MiRNA-146b-5p upregulates migration and invasion of different Papillary Thyroid Carcinoma cells

Abstract\ud \ud Background\ud Tumor invasiveness is directly related to the ability of tumor cells to migrate and invade surrounding tissues, usually degrading extracellular matrix. Despite significant progress in the knowledge about migration and invasion, there is much more to elucidate about their regulatory mechanisms, especially in cancer cells. MicroRNAs (miRs) were recently described as important regulators of migration. Differential expression of miRs in cancer is frequently associated with progression, invasion and metastasis. In papillary thyroid carcinoma (PTC), miR-146b-5p is highly expressed and positively correlated to the degree of malignancy.\ud \ud \ud Methods\ud This study aimed to investigate the role of miR-146b-5p on the migratory and invasive behaviors of thyroid cells, using a non tumor rat thyroid follicular cell line (PCCl3) transfected with the miR-146b-5p genomic region, and two PTC cell lines (TPC-1 and BCPAP, bearing distinct oncogenic backgrounds), which express high levels of miR-146b-5p, after miR-146b inhibition by antagomiR and miR-146b overexpression by mimics-miR. Migration and invasion were studied by time-lapse and transwell assays (with and without Matrigel®). Gelatin degradation assays were also employed, as well as F-actin staining.\ud \ud \ud Results\ud Migration and invasion of PCCl3 were increased 2-3x after miR-146b-5p overexpression (10X) and large lamellipodia were evident in those cells. After miR-146b-5p inhibition, TPC-1 and BCPAP migration and invasion were significantly reduced, with cells showing several simultaneous processes and low polarity. Gelatin degradation was inhibited in TPC-1 cells after inhibition of miR-146b-5p, but was unaffected in BCPAP cells, which did not degrade gelatin. The inhibition of miR-146b-5p in PCCl3 also inhibited migration and invasion, and additional (exogenous) overexpression of this miR in TPC-1 and BCPAP cells increased migration and invasion, without effects on cell morphology or gelatin degradation. The overexpression of SMAD4 in BCPAP cells, a validated target of miR-146b-5p and key protein in the TGF-β signaling pathway, inhibited migration similarly to the effects observed with the antagomiR 146b-5p.\ud \ud \ud Conclusions\ud miR-146b-5p positively regulates migration and invasion of thyroid normal and tumor follicular cells (independently from their original mutation, either BRAF or RET/PTC), through a mechanism that involves the actin cytoskeleton but not an increased capacity of matrix degradation.This research was supported by Fundação de Amparo à Pesquisa do Estado\ud de São Paulo (FAPESP, Grants # 2011/18936-7 and #2012/03990-9),\ud Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES,\ud PNPD), Conselho Nacional de Desenvolvimento Científico e Tecnológico\ud (CNPq grants #307452/2012-3 and #448052/2014-8) and Pró-Reitoria de\ud Pesquisa da Universidade de São Paulo (NAPMiR)

The Highly Expressed FAM83F Protein in Papillary Thyroid Cancer Exerts a Pro-Oncogenic Role in Thyroid Follicular Cells

Thyroid cancer is the most common endocrine cancer with predominant prevalence of papillary thyroid cancer (PTC) histotype. MAPK signaling genetic alterations are frequent in PTC, affecting more than 80% of cases. These alterations constitutively activate MAPK signaling cross-regulating different pro-oncogenic pathways. However, additional molecular alterations associated with thyroid cancer are not completely understood. In this extent, the new family of proteins named FAM83 (FAMily with sequence similarity 83) was recently identified as mediator of oncogenic signaling in different types of cancer. Here we report FAM83F as a novel highly expressed protein in PTC. We evaluated FAM83F levels in 106 PTC specimens, 34 goiter, and 41 adjacent non-tumoral human thyroid, and observed FAM83F cytoplasmic overexpression in 71% of PTC (76 of 106) while goiter tissues showed nuclear positivity and normal thyroid showed no staining by immunohistochemistry. Moreover, TSH-induced goiter and BRAFT1799A-induced PTC animal models also showed FAM83F activation. In vitro, we generated a stable thyroid cell line PCCL3 with FAM83F overexpression and observed that FAM83F deregulates thyroid follicular cell biology leading to loss of thyroid differentiation genes such as Sodium-Iodide Symporter (NIS), reactivation of stem cell markers such as LIN28B and SOX2, induction of cell migration and resistance to doxorubicin-induced apoptosis. Moreover, FAM83F activates MAPK signaling through interaction with BRAF and RAF while impairs TGFβ antiproliferative signaling transduction. In this study, we showed FAM83F as a new pro-oncogenic protein overexpressed in thyroid cancer that modulates thyroid follicular cell biology and differentiation through cross-regulation of MAPK and TGFβ signaling

国民栄養調査に基づくビタミンK, B_6, B_<12>の摂取状況に関する研究

In this study, vitamin (K, B_6, B_) intakes per capita per day were calculated on the basis of the results of the National Nutrition Survey, using the Weighted Average Tables of vitamins in foods. The daily intake of vitamin K was 376μg. The major sources of vitamin K from foods were green, yellow vegetables, other vegetables, and pulses. The daily intake of vitamin B_6 was 1.62mg. It\u27s major sources were fishes and shellfishes, meats, and cereals. The daily intake of vitamin B_ was 10.9μg. The major sources of vitamin B_ were fishes and shellfishes, meats, and seaweeds. Therefore, these vitamin (K, B_6, B_) intakes were seemed to be sufficient for their adequate dietary intakes

Functional toll-like receptor 4 overexpression in papillary thyroid cancer by MAPK/ERK-induced ETS1 transcriptional activity

Emerging evidence suggests that unregulated Toll-like receptors (TLRs) signaling promotes tumor survival signals, thus favoring tumor progression. Here, the mechanism underlying TLR4 overexpression in papillary thyroid carcinomas (PTCs) mainly harboring the BRAFV600E mutation was studied. TLR4 was over expressed in PTCs compared to non-neoplastic thyroid tissue. Moreover, paired clinical specimens of primary PTC and its lymph node metastasis showed a significant up regulation of TLR4 levels in the metastatic tissues. In agreement, conditional BRAFV600E expression in normal rat thyroid cells and mouse thyroid tissue up regulated TLR4 expression levels. Furthermore, functional TLR4 expression was demonstrated in PTC cells by increased NF-κB transcriptional activity in response to the exogenous TLR4-agonist lipopolysaccharide (LPS). Of note, The Cancer Genome Atlas (TCGA) data analysis revealed that BRAFV600E-positive tumors with high TLR4 expression were associated with shorter disease-free survival. Transcriptomic data analysis indicated a positive correlation between TLR4 expression levels and MAPK/ERK signaling activation. Consistently, chemical blockade of MAPK/ERK signaling abrogated BRAFV600E-induced TLR4 expression. A detailed study of the TLR4 promoter revealed a critical MAPK/ERK-sensitive Ets binding-site involved in BRAFV600E responsiveness. Subsequent investigation revealed that the Ets-binding factor ETS1 is critical for BRAFV600E-induced MAPK/ERK signaling-dependent TLR4 gene expression. Together, these data indicate that functional TLR4 over expression in PTCs is a consequence of thyroid tumor-oncogenic driver dysregulation of MAPK/ERK/ETS1 signaling.Fil: Peyret, Victoria. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Departamento de Bioquímica Clínica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba; ArgentinaFil: Nazar, Magalí. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; ArgentinaFil: Martín, Mariano. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba; ArgentinaFil: Quintar, Amado Alfredo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; ArgentinaFil: Fernandez, Elmer Andres. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba; Argentina. Area de Ciencias Agrarias, Ingeniería, Ciencias Biológicas y de la Salud de la Universidad Católica de Córdoba; ArgentinaFil: Geysels, Romina Celeste. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; ArgentinaFil: Fuziwara, Cesar. Universidade de Sao Paulo; BrasilFil: Montesinos, Maria del Mar. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; ArgentinaFil: Maldonado, Cristina Alicia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; ArgentinaFil: Santisteban, Pilar. Consejo Superior de Investigaciones Científicas. Universidad Autónoma de Madrid. Centro de Investigación Biomédica en Red Cáncer; EspañaFil: Kimura, Edna T.. Universidade de Sao Paulo; BrasilFil: Pellizas, Claudia Gabriela. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; ArgentinaFil: Nicola, Juan Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; ArgentinaFil: Masini, Ana María. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentin

MicroRNAs miR-146-5p e let-7f como ferramenta de prognóstico para o carcinoma papilífero de tiroide: relato de caso

Papillary thyroid cancer (PTC) is the most incident histotype of thyroid cancer. A certain fraction of PTC cases (5%) are irresponsive to conventional treatment, and refractory to radioiodine therapy. The current prognostic factors for aggressiveness are mainly based on tumor size, the presence of lymph node metastasis, extrathyroidal invasion and, more recently, the presence of the BRAFT(1799A) mutation. MicroRNAs (miRNAs) have been described as promising molecular markers for cancer as their deregulation is observed in a wide range of tumors. Recent studies indicate that the over-expression of miR-146b-5p is associated with aggressiveness and BRAFT(1799A) mutation. Furthermore, down-regulation of let-7f is observed in several types of tumors, including PTC. In this study, we evaluated the miR146b-5p and let-7f status in a young male patient with aggressive, BRAFT(1799A)-positive papillary thyroid carcinoma, with extensive lymph node metastases and short-time recurrence. The analysis of miR-146b-5p and let-7f expression revealed a distinct pattern from a cohort of PTC patients, suggesting caution in evaluating miRNA expression data as molecular markers of PTC diagnosis and prognosis. Arq Bras Endocrinol Metab. 2012;56(8):552-7O carcinoma papilífero (PTC) é o histotipo mais prevalente de câncer de tiroide. Cerca de 5% dos casos são refratários ao tratamento convencional e à radioiodoterapia. Os fatores prognósticos para agressividade mais utilizados atualmente são o tamanho do tumor, a presença de metástases linfonodais ao diagnóstico, a presença de invasão extratiroideana e, mais recentemente, a presença da mutação BRAFT1799A. A análise de perfil de expressão de microRNAs (miRNA) mostra que esses pequenos RNAs são marcadores moleculares promissores para o câncer, por apresentarem desregulação de sua expressão em uma ampla gama de tumores, includindo o PTC. Estudos recentes revelam a associação entre o aumento da expressão do miRNA e miR-146b-5p e a presença da mutação BRAFT1799A como um fator de pior prognóstico no PTC. Além disso, observa-se a diminuição da expressão de let-7f em diversos tipos de tumores, incluindo tumores tiroideanos. Neste relato de caso, realizamos a quantificação da expressão de miR-146b-5p e let-7f em um paciente jovem, de sexo masculino, apresentando PTC positivo para a mutação BRAFT1799A com extensas metástases linfonodais ao diagnóstico e recidiva precoce. A análise da expressão de miR-146b-5p e let-7f mostrou um padrão diferente do observado em um grupo de pacientes PTC, sugerindo a necessidade de cautela na interpretação da expressão de miRNAs como marcador molecular no diagnóstico e prognóstico de PTC. Arq Bras Endocrinol Metab. 2012;56(8):552-7Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (Fapesp)Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP)Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq)Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq)Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES)Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (Capes